MODULE-1: INTRODUCTION TO PRODUCTION / METABOLIC

DISEASES

Learning objectives

 To understand the metabolic/ production disorders and nutritional deficiency

diseases
 To know the significance of metabolic profile test in the diagnosis of metabolic
disorders
 To know about the clinical significance, diagnosis and prevention of metabolic
and nutritional deficiency disorders.
 To know the inter relationship of metabolic disorders/ production disorders
with health , production and reproduction in animals.
 To have a better knowledge about the agroclimatic conditions associated with
metabolic/ nutritional deficiency disorders.
 To enable to understand the treatment, managemental and control measures
to prevent the metabolic/ nutritional deficiency disorders

 BASIC CONCEPTS OF PRODUCTION DISEASES

BASIC CONCEPTS OF METABOLIC PROFILE TEST

 It is a laboratory aid to preventive medicine

 Veterinary diagnostic aid in the investigation of production disease /
nutritional deficiency diseases

1|Page
  It is an aid in
selection of superior individual
 Detect qualitative and quantitative adequacy of the diet
 Recognize limiting factors for growth in young animals
 Assessment of tolerance to exercise and training in horse
 To monitor fertility and health (in domestic and wild ruminants) in relation to
metabolic status
 To monitor ill effects of stress and welfare
 For early detection of problems associated with seasonal changes and
agricultural system adopted
 To detect and control inherited congenital defects associated with micro-
nutrients

WHEN METABOLIC PROFILE TEST IS NEEDED?

 When the animal is high producing

 When there is need to change diet
 At the end of winter
 At the end of summer
 Preferably every month in problematic herds

HOW TO CHOOSE THE METABOLITE?

 A reliable automated analytical method for metabolite under test is preferred

 The concentration of metabolite in blood must be sufficiently stable.
 A valid statistical model should be available for assessment
 Sufficient breed and location specific database should be made available for
interpretation of the result

 BLOOD COMPONENTS

Chosen to assess major metabolic pathways in production

Blood glucose Energy metabolism

Urea, Albumin, Hb Protein metabolism
Ca, P, Mg Major mineral metabolism
Na, K Electrolyte metabolism
Cu, Co, Iodine Trace elements
TYPES OF METABOLIC PROFILE TESTS
Compton Mini metabolic Individual preventive
examination
Hb Only to assess energy and protein Blood glucose

2|Page
PCV intake Cholesterol
BUN SGOT
Glucose Blood glucose

Serum Inorganic Serum urea Nitrogen

Ca, P, Mg

K & Na Albumin
Total serum protein  Between 4-10 weeks after
calving
A:G  Done at the interval of 4-
6 weeks.

SUPPLEMENTARY INFORMATION FOR MPT

 Individual
o Age
o Date of calving
o Milk yield and mastitis status
o Amount and type of concentrate and fodder fed/day
o Body condition
o Consistency of feces

 Whole herd
o Average daily forage intake.
o Analysis of forage and grains
o Total herd production & number of cows in milk & milk quality data.
o Individual daily yield of 6 cows during 3 consecutive peaks.
o Presence of clinical signs if any

 INTERPRETATION OF METABOLIC PROFILE TEST

The nutritional status of the animal in terms of energy , protein and mineral status is
being interpreted based on the data available on various blood components

ENERGY STATUS - GLUCOSE

 Indicator of energy sufficiency in lactating and late pregnant animals

 Glucose has a fairly a precise homeostatic control and marginally low values
are unreliable
 Lower in early lactation and winter months
 An index of adequacy of energy intake

3|Page
  Decrease at the time of milk secretion
 Influenced by chemical nature of carbohydrate, physical form of feed &
roughage content of ration.
 Stress, excitement, low environment temperature and corticosteroids increase
the glucose level
 Low blood glucose produces ketosis and is responsible for poor conception
rate

PROTEIN STATUS

 Urea, albumin, total protein, PCV & Hb reflect the protein status
 Globulin and total protein increase with age.
 Albumin, urea decrease with increasing age.
 Urea and Hb with PCV: Increase during summer.
 Hb and PCV inversely related to current milk yield.
 Low urea reflects low protein status
 Albumin and Hb decrease reflects long standing low protein status
 Albumin concentration related to conception rate.

MINERAL STATUS

 P: Tend to fall following long term insufficient dietary intake,

hyperphosphatemia occur while grazing on higher fertilized pasture.
 Ca: Vary within narrow limits. Abnormally low levels in late pregnancy
indicate a dangerous situation.
 Mg: Deprivation of feed and fall in environmental temperature produces
clinical hypomagnesaemia. Supplementation of Mg salt is protective.
 Na, K, Cu & selenium: Assessed by sampling pregnant animals receiving no
supplemental concentrates

Physiological

 Season, milk yield & stage of lactation produce significant fluctuations.

CONCLUSION

Conclusion

 M.P.T establishes whether or not the blood composition of a dairy herd or an

individual cow is normal
 Blood composition becomes abnormal only when homeostasis is apparently
upset.

4|Page
  A satisfactory way to monitor blood composition routinely will be to use mini
profile or individual preventive examination at regular interval, between
full Compton metabolic profile tests performed say bi-annually.

Limitations

 Must be carefully planned

 Expensive
 Regional laboratory with automated analytical equipment and trained staff is
needed
 Local population data base (means) for each parameter should be available

MODULE-2: MILK FEVER

Learning objectives

 To understand about the calcium homeostasis in periparturient animals

 To know about the etio-pathogenesis of milk fever in production animals
 To get knowledge about the diagnosis, treatment, control and prevention of
milk fever

DEFINITION FOR MILK FEVER

 A disease of adult female bovine occurring

around the parturition and caused
by hypocalcemia , characterised by weakness, recumbency, paresis, shock
and death.

 BODY CALCIUM AND THEIR TYPES

5|Page
 CALCIUM HOMEOSTASIS

INCIDENCE OF MILK FEVER

 5-10 yrs age group most commonly affected

6|Page
  High prevalence during 3 rd – 7th calving
 Jerseys breed is the most susceptible than other breeds.
 High susceptibility when animals are fed with high protein diet before and
after calving.
 No specific seasonal occurrence
 Complete milking in first 48 hrs- precipitating factor
 Certain families with in the breed – more susceptible
 Cases may occur during the last few days of pregnancy and immediately after
parturition.
 Majority cases occur within 72 hours postpartum
 Acid - diet decreases the incidences
 Alkaline diet increases the incidence

FACTORS PRECIPITATING OCCURRENCE OF MILK FEVER

 Failure of mobilizationof Ca to circulation from body reserves

 Depletion of reserves by development of negative Ca balance in late pregnancy
 Increased estrogen levels – interfere with Ca mobilization from bone
 Hypomagnesaemia – decrease Ca mobilization from bone
 Coliform mastitis – toxin decreases serum Ca and P levels

PATHOGENESIS OF MILK FEVER

 Hyperaesthesia instead of hypersensitivity, tetany of head and limbs instead

of convulsions
 Decrease of muscle tone – vulnerability increases for prolapse of uterus or
vagina
 Hypothermia , depression of consciousness
 Ca:Mg is 6:1 - If serum Mg decreases these sign continues during second stage
of milk fever
 Phosphorus decrease, prolong the duration of recumbency

SIGNS OF MILK FEVER

Clinical signs of milk fever varies with the stage of the disease

 I Stage - prodromal stage

 II Stage - Sternal recumbency
 III Stage - Lateral recumbency

STAGE I OF MILK FEVER

 Excitement and tetany

 Hypersensitiveness

7|Page
  Muscular tremor of head and limbs
 Disinclined to eat and move
 Grinding of teeth
 Protruding tongue
 Stiff hind limb
 Animals ataxic and falls easily

STAGE II OF MILK FEVER

 Sternal recumbency with lateral kink

 No tetany but unable to get up
 Muzzle – dry
 Skin and extremities – cold
 Temperature – Subnormal (97-101ºF)
 Pupil – dilated – no reflex
 Eyes – disparity in the size of pupils staring and dry – pupillary light reflex
decrease or absent
 Relaxation of anus and loss of anal reflex-dung in rectum
 Circulatory system - decrease heart sound – veins cannot be raised
 Weak pulse, ruminal stasis, forced expiratory grunt

STAGE III OF MILK FEVER

 Lateral recumbency
 Coma
 Limbs – flaccid, unable to get up
 Pulse – impalpable
 Heart sounds – inaudible 120/min
 Unable to raise the vein
 Bloat if without treatment – animal dies within a period of 12 – 24 hrs
 Milk fever with hypomagnesaemia and hyperphosphatemia
 Tetany and hypersensitiveness beyond 1st stage
 Excitement and fibrillary and twitching of the eyelids
 Tetanic convulsion by touch or sound
 Trismus
 Heat and respiratory rate-accelerated
 Heart sound – increased
 Death occurs due to respiratory failure

Reproductive tract

 Dilated cervix, normal presentation of fetus, uterine prolapse, dystocia,

retained placenta

8|Page
 DIAGNOSIS OF MILK FEVER

 Characteristic clinical signs

 Sign related with serum levels of Ca, Mg, P
 Estimation of serum levels of Ca, Mg, P
 Ketosis (concurrent) – animal rise after Ca therapy but continue to
have signs of ketosis
 Ischemic muscle necrosis (Degenerative myopathy)
o Post mortem – pale muscle surrounded by normal color
o SGOT increase
 History of access to plant rich in oxalates

TREATMENT AND CONTROL MEASURES FOR

HYPOCALCAEMIC ANIMALS

Treatment

 Treatment during I stage – ideal

 Longer the interval between recumbency and treatment, greater the incidence
of downer cow due to ischemic muscle necrosis
 Temperature > 39ºC – indication of existing complication – higher mortality
rate
 To be placed in sternal recumbency until the treatment ends to avoid
aspiration pneumonia.
 Calborogluconate 500 ml to 1 liter – 3 g/10 lb, 50% i/v, 50% s/c
 Shifting to non slippery ground or pure rubber mat
 Do not milk for 6 hours.
 Do not urge the cow to stand too soon

Dose of Calcium

 1 gm Ca / 45kg (100 lb)

 25 % calcium borogluconate = 10.4 gm /500ml
 Cattle – 400-500ml i/v , 100-200 gm s/c
 Goat- 15-20 gm i/v, 5-10 g s/c

Response to Calcium therapy

 Belching
 Muscle tremor – flanks→ whole body
 Pulse rate decreases and amplitude improves
 Heart sound intensity is increased
 Sweating of muzzle
 Defecation – firm stool with mucous

9|Page
  Urination does not follow until cow rises
 Wait for 5-8 hrs until it stands. If not repeat the dose
 If it doesn’t stand after 24 hrs – use hip lifters.

Unfavourable Response to Calcium therapy

 Cardiac irregularities
 Heart rate increased
 Shallow respiration.

Prevention

Dietary management during the transition period

 Feed low Ca (<20 g Ca /day) and normal level of P for 2 weeks prior to
parturition
 Avoid drastic change in the diet (3 or 4 days time for change)
 Dietary cation- anion difference programme

Parentral vitamin D and analogs

 Vitamin D2 20-30 million units / day for 3-7 days antepartum (predicting the
date of parturition is a problem)
 1,25 (OH2)D3 – 10,000 IU i/m / 24 hrs prior to parturition. If no delivery
repeat at 24 hrs interval 270 mg until delivery

Calcium gel oral dosing before calving, at calving and 12 and 24 h after
calving

 CaCl2 40-50 g

MODULE-3: ACUTE PARTURIENT HYPOCALCAEMIA

Learning objectives

 To study the etio-pathogenesis of hypocalcemia in goat, sows, dogs and mares.

 To get a knowledge about the diagnosis, treatment, control and prevention of
acute parturient hypocalcemia in goats, sows, mares.

ACUTE PARTURIENT HYPOCALCEMIA IN GOATS

Etiology

 A depression of ionised calcium in tissue fluid is the basic biochemical defect

in acute parturient hypocalcaemia.

10 | P a g e
Epidemiology

 Occurrence of acute parturient hypocalcaemia in goats is apparently rare.

 There is fall in serum calcium and phosphorus levels in all goats at kidding
due to onset of lactation
 In heavy milking goats, an absolute deficiency of calcium at any stage of
lactation will precipitate the disease.
 Milking goats get affected mostly during 4-6 years of age
 Cases occur before and after kidding, some even 3 weeks after parturition.

Pathogenesis: Similar to dairy cows

Clinical signs

 Slight tremors
 Twitching
 Hyper excitability
 Slight ataxia
 Lethargy
 Incordination of limbs
 Paresis
 Recumbency
 Bloat
 Coma and death

Dignosis

 Based on clinical signs

 Rapid response to calcium therapy
 Serum calcium 2 to 6 mg/dl

Treatment: 25% Calcium Borogluconate 80-100ml slow I/V

Control: Similar to dairy cows

ACUTE PARTURIENT HYPOCALCEMIA IN BITCHES

Synonym: Eclampsia, Peurperal tetany

Definition

 It is a metabolic disease occurring

commonly in young bitches within 2-10
days of whelping and clinically characterized by restlessness, excitement,
panting and tonic-clonic convulsions.

11 | P a g e
Etiology: Hypocalcaemia

Predisposing factors

 Atony of smooth muscle and skeletal muscle

 Improper prenatal nutrition
 In appropriate calcium supplementation
 Improper prenatal nutrition
 Heavy litter size
 Lactation in young bitches
 Toy breeds
 Neuromuscular tetany
 Concurrent hypoglycemia is the cause of signs of tonoclonic convulsions.

Clinical signs

 Restlessness
 Excitement
 Poor maternal care
 Salivation
 Dyspepsia
 Increased respiratory rate
 Panting
 Stiffness of joints
 Ataxia and staggering gait
 Tonoclonic convulsions
 Opisthotonus
 Hyperthemia
 Stiff tilted gait due to muscular tetany

Dignosis

 History of late pregnancy and early lactation

 Clinical signs are always observed in nourshing bitches
 Characterstic symptoms
 Low serum calcium level - less than 7 mg/dl
 Low blood glucose - less than 80 mg/dl

Treatment

 Remove the sucking puppies

 25% calcium borogluconate 1ml/kg b.wt slow I/V
 20% dextrose 30-50ml slow I/V
 To control Fits - Diazepam 0.5 mg /kg b.wt slow I/V

12 | P a g e
 LACTATION TETANY IN MARES

Synonyms: Eclampsia, Transit tetany.

 Common occurrence in draft horses breeding, mortality rate is high i.e.> 60%
 Occurs in lactating mares- at about 10th day of foaling or 1-2 days after
weaning
 Mares grazing on lush pasture - heavy flow of milk - more susceptible
 Hard physical work , housing wild ponies and prolonged transport are
precipitating factors
 Sometimes- no apparent cause

CLINICAL SIGNS OBSERVED IN LACTATION TETANY

 Severe cases -sweat profusely, difficulty in moving because of tetany and in-
coordination, stiff gait, tail is slightly raised, rapid violent respiration, wide
dilatation of nostrils, distinct thumping sound from chest(due to spasm of
diaphragm), muscular fibrillation-massseter trismus, no prolapse of
membrane nictitans.
 Hyper sensitive to sound.
 Handling precipitates tetany.
 Temperature normal or increased slightly.
 Pulse rate-normal early, later elevated and irregular.
 Attempts to eat and drink, but unable to swallow.
 Urination and defecation kept in abeyance.
 Peristalsis is reduced.
 Recumbency with in 24 hrs-convulsions- die after 48 hrs of illness.
 Serum Ca: > 8mg% - excitability ; 5-8 mg% -spasm ; <5 mg % -
recumbency and stupor

DIFFERENTIAL DIAGNOSIS AND TREATMENT OF

LACTATION TETANY

Differential diagnosis

 Tetanus -prolapse of membrane nictitans, no relationship to recent foaling or

weaning or physical exertion.
 Laminitis - anxiety, muscle tremor, pain in the foot.

Treatment

 Inj. Calcium solutions- complete recovery.

 Main sign of recovery-voiding large volumes of urine.

13 | P a g e
 MODULE-4: OSTEODYSTROPHIA FIBROSA

Learning objectives

 To study the diagnosis and treatment of osteodystrophia fibrosa in animals

 To understand the etiology of osteodystrophia fibrosa in animals

INTRODUCTION

 This is a general term for the diseases of bone which may be due to failure of
normal development or abnormal metabolism of mature bone.

Characteristic clinical signs

 Distortion and enlargement of bone

 Susceptibility to fracture
 Interference with gait & posture.

ETIOLOGY

 Ca, P & vit D deficiency

o Absolute deficiency
o Imbalance of Ca : P in diet
 Deficiency of Ca/ P leads to
o Hypoplasia which causes rickets in young animal
o Atropy resulting in Osteomalacia in adult ruminants
o Osteodystrophia fibrosa in adult pig & horses
o Perosis is a condition in chicks, due to Osteodystrophy
 Inadequate nutrition
 Hypo & Hyper vitaminosis A results in Osteodystrophic changes in cattle &
swine
 Prolonged feeding of High Ca diet in Bulls leads to Hypercalcitonism.
 Multiple vitamin & mineral deficiency results in Osteodystrophy in cattle
 Chemical agents eg. chronic lead poisoning, fluorine poisoning
 Inherited & congenital cause eg. Achondroplasia, chondrodystrophy &
osteogenesis imperfecti.
 In Chronic interstitial Nephritis there is High P, So4.
 'Rubber Bone' in dogs is a condition which is due to hyper activity of
parathyroid, resulting in demineralization (Fibrous Osteodystrophy).
 Deficiency of P in Horse → Big head or mandible disease

DIAGNOSIS AND TREATMENT

Diagnosis

14 | P a g e
  Detailed history
 Clinical signs
 Radiographic examination

Treatment

 Supplementation of Ca, P & vitamin D

 Vitamin D 10,000 I.U. /kg
 Di calcium Po4
 Adequate bedding

MODULE-5: DOWNER COW SYNDROME

Learning objectives

 To study the etiology, pathogenesis and diagnosis of downer cow syndrome

 To get knowledge about the treatment, control and prevention of downer cow
syndrome

DEFINITION OF DOWNER COW SYNDROME

 Downer - unable to rise after 24 hrs and after 2 Calcium treatments.

 Usually occurs as a complication following hypocalcaemic parturient paresis.
 Characterised clinically by,
o Prolonged recumbency even after 2 successive Ca therapy
o Down at least for 24 hrs without any apparent reason
o Traumatic injury to limb muscles and nerves
o Ischemic necrosis of limb muscles
o Myocarditis
o Fatty infiltration and degeneration of liver

CREEPER COW

15 | P a g e
  Alert & can support on fore quarters but unable to use hind quarters after
therapy for Milk fever.
 May occur due to hypokalemia.

ETIOLOGY OF DOWNER COW SYNDROME

 As a complication of hypocalcemic parturient paresis

 Traumatic injuries of muscles especially
medial thigh muscle. Rupture of
gastrocnemius tissues around hip joint muscle, Obturator muscles & tendon
spread eagling of hind legs, dystocia.
 Traumatic injuries to nerves of the limbs viz., sciatic, obturator, radial
and peroneus.
 Prolonged recumbency after an over long delay (> 4 hrs) in the treatment of
milk fever may result in ischemic necrosis.
 Serum electrolyte imbalance or deficit
 Persistent hypophosphatemia.
 Insufficient amount of Ca (ischemic necrosis) as treatment for milk fever
 Hypokalemia with hypophosphatemia is a typical manifestation in creeper
cow (alert, bright, crawl about but couldn’t raise).
 Toxemia in per acute or acute mastitis, acute diffuse peritonitis, uterine
rupture, aspiration pneumonia, traumatic reticulitis / pericarditis.
 Managemental causes: malnutrition, over fat, slippery floors, epidural
anaesthesia.

EPIDEMIOLOGY OF DOWNER COW SYNDROME

16 | P a g e
  Occurs as a sequele of milk fever 2 or 3 days after calving in heavy milk
producers
 Concurrently with milk fever in many cases
 Common during peak lactation years of high producers
 It is a complication arising due to delayed or incomplete treatment of various
diseases after parturition
 Poor housing conditions , excess body fat, septic conditions and malnutrition
may act as predisposing factors.

CLINICAL SIGNS OF DOWNER COW SYNDROME

 Bright and alert

 Eats and drinks moderately well
 Normal temperature
 Heart rate is usually normal or elevated to 80-100/minute, tachycardia and
arrhythmia immediately following i/v Calcium administration.
 Respiration not affected
 Normal defecation and urination
 Preoteinuria indicate extensive muscle damage
 Some animals make no effort to rise
 Many make frequent effort to rise but unable to get up ( creeper) - frog like
attitude on non slippery surface (bare ground or damp bedding)
 Some cases are able to stand with assistance (lifting on tail head or hip slings)
 In some cases, hind legs are extended on each side and reach up to elbow joint
(due to dislocation of hip joint or traumatic injuries surrounding hip with or
without rupture of ligaments)

17 | P a g e
 CLINICO-PATHOLOGICAL CHANGES IN DOWNER COW
SYNDROME

 Serum Ca, P, Mg, Glucose - normal

 Hematological examination - normal as in recently calved. Neutropenia with
left shift
 Serum CPK increased
 SGOT increased
 Moderate ketonuria
 Proteinuria and brown colour turbid urine in severe cases due to
myoglobinuria
 Low arterial B.P.
 Abnormal E.C.G.

NECROPSY FINDINGS IN DOWNER COW SYNDROME

 Haemorrhage and edema of skin and damage to nerves of limbs

 Haemorrhage and degeneration of thigh muscles, haemorrhage around hip
joint, ischemic necrosis of musculature
 Eosinophilic infiltration of ruptured necrotic muscles
 Heart dilated and flabby. Histopathology shows focal myocarditis
 Fatty degeneration of liver
 Adrenal glands enlarged
 Histopathology of kidney reveals degenerative changes of glomerular and
tubular epithelium

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS OF DOWNER

COW SYNDROME

Diagnosis

 A thorough clinical and laboratory examination is required

 Arrived at after eliminating all known causes of recumbency in a cow which
had milk fever and failed to rise with in 24 hrs following 2 successive course
of treatment

Differential diagnosis

Medical cases

 Diseases of bones – osteoporosis, Osteomalacia

 Carpal extensor myositis - fore limb stretched internally
 Diseases of joints - acute arthritis especially hip joint
 Foot diseases – laminitis, fissured feet

18 | P a g e
  Diseases of brain and CNS - sporadic bovine encephalitis.
 Peripheral nerve paralysis - Obturator, femoral
 Metabolic - milk fever, hypomagnesaemia, transit fever, ketosis, fatty liver, P
deficiency and paralytic myoglobinuria.
 Nutritional –rickets, mineral deficiency & vitamin A deficiency
 Poisonings – ergot poisoning
 Toxemic conditions
 Infectious diseases - black quarter, tetanus, botulism, rabies
 Parasitic diseases - tick paralysis, babesiosis
 Others- weakness, ephemeral fever, acidosis, foreign body, pneumonia,
Pyelonephritis and heat stroke

Surgical cases

 Trauma, dislocation, ruptures of ligaments and muscles

O & G cases

 Calving injury, metritis, damage to spinal cord, rupture of uterus

TREATMENT FOR DOWNER COW SYNDROME

 Treatment is not specific but symptomatic

 Inj. Magnesium salts, Po4, corticosteroids.
 Stimulant tonics - tripelenamine Hcl
 Vitamin E and Se - vetienzyme 0.5 mg/ kg slow i/v
 Solutions containing K, P, Ca, Mg
 Fluid therapy- oral and parental
 Comfortable bedding
 Turn the cow from side to side
 Physiotherapy to avoid muscle damage
 Non slippery ground surface
 Antibiotic for septic conditions
 Anti inflammatory
 Lifting devices- Danish aqua lift and power cow cradle

19 | P a g e
 CONTROL MEASURES FOR DOWNER COW SYNDROME

 Measures to prevent milk fever

 Early detection and treatment of milk fever
 Good bedding like straw bedding and soft ground surface
 Well bedded box stall for calving and then upto 48 hrs
 Rolled from one side to other on hourly basis if possible
 Avoid lateral recumbency by placing bales of straw, to prevent hydro static
congestion and Ruminal tympany
 Avoid exposure to hot sun to prevent heat stroke
 Be sympathetic to the animal; provide non - slippery surface, keep out door
and tie a rope between 2 pasterns to avoid the hind feet slipping apart

MODULE-6: KETOSIS

Learning objectives

 To study the etio-pathogenesis and clinical signs in ketosis of cattle

 To get a knowledge about the diagnosis, treatment , control and prevention of
ketosis in cattle.

ETIOLOGY OF BOVINE KETOSIS

 Nutritional or metabolic insult in high yielding cows in early lactation results

in negative energy balance.

20 | P a g e
  Failure to provide sufficient glucose when the animals are subjected to heavier
demands on their resource of glucose and glycogen, than can be met by
their digestive and metabolic activity.
 Dysfunction of adrenal gland. Stress of parturition, lactation (cattle) and
stress of late pregnancy (in ewes) and stress of malnutrition leads to
decreased ACTH activity.
 Relative hypothyroidism.
 Composition of ration - ensilage (high in butyric acid) are more ketogenic than
hay.
 Composition of ruminal flora influences digestive process and thus changes in
end products of digestion and their relative concentrations. Hence, there is
difference in ketogenicity between feeds. Eg. High protein diets produces
more butyric acid.
 Factors those decrease energy supply, increase demand for glucose and
increase utilization of body fat will lead to ketosis.
 Animals in 4 -10 weeks post-partum, peak milk yield and decreased dry mater
intake are prone for ketosis.
 Starvation decrease propionic acid (relative) resulting in excessive utilization
of fat.
 From quantitative and qualitative estimations of ketone bodies in rumen
liquor and body fluids, it appears that abnormal ruminal conditions may
play an important part in the production of clinical ketosis.
 Hepatic insufficiency - primary or secondary . Hypoglycemia results in
mobilization of fat & its deposition in liver - perpetuation of hepatic
insufficiency.

OVINE KETOSIS

 A disease of intensive farming system and relatively rare in grazing units.

 Ketosis in goats - identical with ovine ketosis

Etiology

 Increased plasma cortisol due to environmental and nutritional stress, failure

by liver to metabolize the cortisol.
 Decline in plane of nutrition during last 2 months of pregnancy.
 Exposure to inclement weather
 Worm load Eg. Haemonchus contortus.

Epidemiology

 Highly fatal, may occur as out break, mostly during last month of pregnancy
 Ewes carrying more than 1 lamb are more susceptible

21 | P a g e
  Precipitating factor - fall in plane of nutrition precipitated by sudden short
periods of starvation up to 48 hours (by management), cold inclement
weather.

EPIDEMIOLOGY OF KETOSIS

 Ketosis is of two types - Primary (Estate acetonemia) and secondary

 Primary (estate acetonemia)
o Ketosis of heavily fed high producing cows
o Inheritance may be there
o Tendency to reoccur in individual animals is probably due to variation
in digestive capacity or metabolic efficiency
o Excessive feeding of ensilage
o Inadequate exercise
o Over fatness at calving time
o Inadequate energy intake during early lactation
o Specific dietary deficiency of cobalt (essential for metabolising
propionic acid), phosphorous and vitamin B12
 Secondary ketosis is caused by
o Reduction in appetite
o Abomasal displacement
o Traumatic reticulitis
o Metritis
o Mastitis
o Fluorosis
 Occur in animals mainly housed during winter and occasionally in animals at
pasture
 Death of animal is rare
 Morbidity variable and difficult to measure
 Economic losses due to individual ketosis
 Prevalence of sub clinical ketosis - 10 % in under nourished cows
 Ketosis of pregnant ewes is highly fatal and may occur as outbreak
 Ketosis in cows is mostly sporadic
 Regardless of specific etiology bovine ketosis is
o Most common during 1st month of lactation
o Less common during 2nd month of lactation
o Occasionally during late pregnancy
o Higher frequency in 20 - 30 days of calving
o Low prevalence at 1st calving
o Peak prevalence at 4th calving

CLINICAL FINDINGS IN KETOSIS

Bovine ketosis

22 | P a g e
Wasting form

 Gradual but moderate decrease in appetite and decreased milk yield over 2-4
days
 First refuse grains, ensilage but continue to eat hay.
 Loss of body weight is rapid due to off-feed
 Woody appearance (due to loss of cutaneous elasticity and s/c fat)
 Feces firm and dry
 Cow moderately depressed
 Disinclined to move
 Normal temperature, pulse and respiratory rates.
 Rate and amplitude of ruminal movements normal and may be decreased in
prolonged cases
 Ketone odour from mouth and milk
 Staggering and partial blindness may occur transiently.
 Severely affected animal die.
 Spontaneous recovery in about a month, but milk yield never return to normal
level; sharp drop in SNF content of milk in wasting form.

Nervous form

 Suddenly appear Bizarre, delirium, walking in circles, straddling or crossing of

legs, head pushing or leaning onto stanchion, apparent blindness, aimless
movements, wandering, vigorous licking of the skin and inanimate objects
 Depraved appetite
 Chewing movements with salivation
 Hyperaesthetic- bellowing on pinching or stroking
 Moderate tremor and tetany
 Gait is usually staggering.
 Nervous sign usually occur in short episodes which last for 1 or 2 hrs and may
recur at intervals of about 8 to 12 hrs
 Affected cows may injure themselves during the nervous episodes

Ovine and Caprine ketosis

 Similar to nervous form of ketosis in cows

 Separate from flock and apparent blindness (alert but disinclined to move).
 Stand still when approached by man or dog and no attempt to escape, head
pressed against obstacle, stand in water trough all day and lap the water.
 Feces - constipation, dry and scanty
 Grinding of teeth
 Later stages - more severe nervous signs, tremors of muscles of head,
twitching of lips, champing of jaws and salivation

23 | P a g e
  Clonic contraction of cervical muscles,dorsal flexion or lateral deviation of
head, circling, convulsions spread to the whole body.

 Recurrent attack and drowsiness between convulsions

 Star gazing,incordination, falling when attempting to walk
 Smell of ketone in breath.

 Course: become recumbent in 3-4 days and then coma for 3-4 days

CLINICAL PATHOLOGY OF KETOSIS

Metabolite Level when Normal
diseased
Primary hypoglycemia 20-40mg/dl 50mg/dl

24 | P a g e
Secondary hypoglycemia
>40 mg or above
normal

Ketones - Primary 10-100mg/dl Up to 10 mg / dl

Ketones - Secondary < 50 mg /dl

Urinary ketones 80-130 mg/dl 10-70 mg/dl

(primary/secondary)

Milk ketones Average 40mg/dl 3 mg/dl

Liver glycogen Low

Glucose curve Normal

VFA in blood and rumen Increased

 Field test (Rothera’s reaction) : Milk and urine can be tested. It measures only
Aceto acetic acid.
o ß hydroxybutyric acid – no reaction
o Acetone - very little reaction
o Primary ketosis - strong colour
o Secondary ketosis - moderate reaction

DIAGNOSIS OF KETOSIS

 History with reference to time of calving, duration of pregnancy in ewes,

feeding program
 Biochemical examination reveals hypoglycemia, ketonemia and ketonuria
 In cases of sub clinical ketosis: Ketonemia with absence of clinical signs
 Differentiate secondary ketonuria due to
o TRP,
o Bovine pyelonephritis,
o Indigestion,
o Abomasal displacement,
o Metritis and
o Mastitis.
 Nervous form of ketosis should be differentiated from Listeriosis and Rabies.
 Ovine ketosis: die within 6-7 days

TREATMENT OF OVINE KETOSIS

25 | P a g e
  Response is less satisfactory. It depends on severity of cases and duration of
the disease. Neither replacement therapy nor hormonal therapy have any
effect.
o Oral- glucose 45 g, NaCl 8.5 g , glycine 6.17 g, and electrolytes in 160
ml every 4-8 hrs.
 The flock should be examined for any evidence of ketosis and to be treated
with propylene glycol or glycerol.
 Increased carbohydrate intake in flock.
 In clinical cases - caesarian section, glucocorticoids parentally, glucose or
glycerol.

REPLACEMENT THERAPY

 50 % glucose 500ml I/V, 20 % glucose I/P,

 Propylene glycol or glycerine @ 225 mg / day for 2 days then 110 mg / day for
2 days.
 In sheep, common complication is acidosis. So sodium bicarbonate is to be
given along with replacement therapy.
 Sodium propionate 110 -225 mg/ day, but shows very slow response.
 Lactates: Ca or sodium lactate 1 kg initially, later ½ kg / day for 7 days or
 Sodium acetate 110-500 g/day.
 Ammonium lactate 200g/day for 5 days.
 Ewes: Sodium ethyl oxaloacetae I/V (costly).
 Anabolic steroids: Effective treatment for pregnancy toxemia of cows.
Trenbolone acetate @ 60mg to 100 mg as single injection.
 Insulin with glucose or glucocorticoids 200 – 300 I.U. Repeat every 24 – 48
hrs. There is no marked therapeutic advantage.

MISCELLANEOUS TREATMENTS

 Chloral hydrate- Initially, 30 g orally as capsule, later 7 g bid for several days
as drench in molasses or water. It breaks the starch in the rumen and
stimulates production and absorption of glucose. Also, selectively influence
rumen fermentation to produce more of sodium propionate.
 Potassium chlorate can also be given but in some cases it causes severe
diarrhea.
 Vitamin B12 and cobalt - for the activation of coenzyme A.
 Cysteamine (precursor of co-enzyme A)- 750 mg i/v
 Sodium fumerate (precursor of co-enzyme A) 3 doses at 1-3 days interval.
 Provide adequate food and water.
 Sheep at pasture are to be driven to shade to avoid heat stroke.
 Caesarian or corticosteroid to induce parturition.
 Monensin sodium enhances the propionate production in the rumen. Dose
25mg/day in grain feed mix.

26 | P a g e
 CONTROL MEASURES FOR KETOSIS

Cattle

 Should not be starved or over fat at calving.

 Adequate calorie intake at early lactation.
 Feeding in preparation for the next lactation should not begin until about 4
weeks to calving.
 4 weeks prior to calving: silage or hay or pasture maintenance + 1 Kg
concentrate/ day; gradually increase to 5 kg concentrate/day at calving.
 After calving, increase concentrate as production increases i.e. 3 kg hay/ 100
kg b.wt. or 9 kg ensilage/ 100kg b.wt. as maintenance + 1 kg concentrate /3
kg milk produced.
 Protein should not exceed 16-18 %.
 Exercise is must in intensive rearing.
 Ration should contain Co, P and I2.
 Avoid wet ensilage or mouldy hay or dusty hay ( as they have increased levels
of butyrate).
 Prophylactic feeding of sodium propionate @ 110g daily for 6 weeks.
 Sodium propionate 110 g/ day for 6 weeks
 Propylene glycol @ 350 ml / day for 10 days after serving or 6% of concentrate
ration for 2 months.
 Blood glucose and milk ketone estimation during 6th week of lactation.

Sheep

 Same as in cows. Monensin sodium @ 25 mg/day as feed mix.

 Ensure that the plane of nutrition is raising in 2nd half of pregnancy.
 During last 2 months: concentrates containing 10% protein @ 0.25 kg/ day,
increasing to 1 kg/ day during last 2 weeks.
 Avoid sudden change in feed.
 Ensure extra food during bad weather.
 Shelter should be available in pasture.
 Ewes should be driven out for ½ hr twice daily in well fed flocks.
 If pasture is available, only concentrate should be fed.

General

 Manipulation of ration to produce more of propionate in the rumen (ration of

finely ground roughage, cooked grain, cod liver oil with certain unsaturated
fatty acid are anti ketogenic and produces less of milk fat thereby reducing
energy loss).
 Blood glucose estimation at 2-6 weeks of lactation( < 35 mg % needs
attention). Regular tests for ketone in urine are to be done from 2nd week.

27 | P a g e
  Estimation of β hydroxy-butyrate levels in early lactation.
 Palatable feeds and frequent feeding.
 1/3rd of total D.M consumption through good quality roughage helps to
maintain appetite.

MODULE-7: HYPOMAGNESAEMIA

Learning objectives

 To understand the magnesium homeostasis in periparturient animal.

 To study the etio-pathogenesis, clinical signs , diagnosis, treatment and
control of hypomagnesaemia in cattle.

CHARACTERISTICS OF HYPOMAGNESEMIC TETANY

Characterised by

 Hypomagnesaemia.
 Hypocalcaemia.
 Clinically clonic-tonic muscular spasms and convulsions, death due to
respiratory failure.
 Tetany associated with depression of Mg.

Two types

 Whole milk tetany -due to specific deficiency of Mg in diet.

 Lactation tetany- due to partial dietary deficiency i.e. nutritional / metabolic
factors that decrease availability or increase body loss.

ETIOLOGY AND EPIDEMIOLOGY OF HYPOMAGNESEMIC

TETANY

Etiology of hypomagnesemic tetany

 Short period of starvation (24-48 hrs) which may occur in association with
transport also.
 High Po4 intake competes with Mg absorption (cereals rich in K, lush green).
 No readily mobilizable large storage of Mg in the body.
 No efficient homeostatic mechanism.
 Loss of Mg in milk, urine & digestive secretions.
 Reasonably low level along with starvation may precipitate the disease.
 During inclement weather (cold, wet, windy weather), hyper activity of thyroid
leads to inadequate calorie intake.
 Variation in susceptibility between individual animals .

28 | P a g e
  Cows turned out to lush pasture during spring after closed housing in winter.
 Grazing on young green cereal crops may cause wheat pasture poisoning.
 Dry cattle or beef cattle running at pasture in winter time, when nutrition is
usually inadequate.

Epidemiology hypomagnesemic tetany

 Occur throughout the world. Commonly occurs in winter and in conditions

where there is no proper shelter.
 Morbidity 2-12%.
 Case fatality is high (about 30%) – difficult to determine the cause as the
affected animals are found dead.
 Can also occur in sheep, but less common.

CLINICAL SIGNS OF HYPOMAGNESEMIC TETANY

Acute

 Cease to graze, posture of unusual alertness, twitching of muscles and ears.

 Severe hyperesthesia - even a slight disturbance can precipitate attack,
continuous bellowing, frenzied galloping.
 Staggering gait
 Falls with tetany of limbs, clonic convulsions, nystagmus, champing of jaws,
frothing at the mouth, pricking of ears, retraction of eyelids
 The animal lies calm between episodes frequently, but sudden noise or touch
precipitates another attack.
 Temperature - 40 to 40.5ºC.
 Pulse and respiratory rates increased.
 Intensity of heart sounds audible at some distance from cow.
 Death in ½ - 1 hr.
 Mortality is high.

Sub acute

 Gradual onset - 3 to 4 days.

 Inappetence.
 Wildness of facialexpression.
 Exaggerated limb movements.
 Resist being driven.
 Spasmodic urination and defecation.
 Decreased milk yield .
 Ruminal movements decreased.
 Wild tetany of hind legs and tail showing unsteady, straddling gait, retraction
of head and trismus.

29 | P a g e
  Sudden movement, noise, restraint and injections can precipitate violent
convulsions.
 May recover spontaneously within days or the disease progress to a stage of
recumbency.
 Treatment is usually effective with marked tendency to relapse.

Chronic

 Serum Mg decreased
 No clinical signs, but sudden death.
 Few animals show vague syndrome - dullness, unthriftiness (more obvious
syndrome), indifferent appetite and reduced milk yield.
 Paresis / milk fever like syndrome (in lactating cattle) but not responding to
Calcium treatment.
 May also occur from the sub-acute form.

CLINICO-PATHOLOGICAL CHANGES IN HYPOMAGNESEMIC

TETANY

Clinical pathology

 In clinical cases- serum Mg level will be from 0.3 to 0.7 mg%. (Normal: 1.7 to
3 mg.)
 Estimation of Ca:Mg ratio in bone. Normal is 70:1, If Ca <70 – safe , >70 –
problem Eg. 90:1 could be taken as a severe case.
 Serum creatinine phosphokinase increased.
 SGOT increased (marginally).
 Decreased levels of CSF Mg (sample can be collected upto 12 hrs after death).
Normal being 2 mg%. i.e similar to plasma level. In clinical cases: 1.25
mg%
 There may be clinically normal cows with hypomagnesaemia (0.4 mg% - 1.84
mg%)
 Low Urine Mg is a good presumptive evidence.

Postmortem examination

 Extravasation of blood
in subcutaneous area, endocardium, pleura,
peritoneum and intestinal mucosa.

DIAGNOSIS OF HYPOMAGNESEMIC TETANY

Diagnosis

 Clinical signs - incoordination, hyperaesthesia and tetany

30 | P a g e
  Laboratory measurement of blood magnesium levels
 CSF magnesium concentration
 Herd diagnosis done by assessing urine magnesium concentration

Differential diagnosis

 Acute lead poisoning - blindness, mania. History will reveal possibility of

access to lead.
 Bovine spongiform encephalopathy - longer clinical course.
 Rabies - straining, ascending paralysis, no tetany.
 Nervous form of ketosis - marked ketonuria.
 Poisoning by claviceps purpurea - cerebellar ataxia.
 Tetanus - prolonged duration, bloat, prolapse of 3rd eyelid.
 Strychnine poisoning- no protrusion but retraction of eye ball.
 Polio encephalomalacia - history and clinical signs
 Enterotoxaemia - history of endemicity with clinico-pathological findings.
 Avitaminosis -A - Analysing composition of ration
 Poisoning by organic mercurials and arsenics - history of access to poison

TREATMENT OF HYPOMAGNESEMIC TETANY

 10% MgSo4 - 100 ml s/c gives only a transient effect and should be followed
with feed supplement
 Narcosis with chloral hydrate
 Tranquilizers
 Morphine to avoid respiratory paralysis
 50% MgSo4 50-100 ml s/c on one side and Ca borogluconate -150 ml on other
side
 Calcium magnesium preparation - 25%: 500 ml i/v followed by concentrated
solution of 50 % MgSo4 200 ml s/c (or) 20 % Mg So4: 200-300 ml i/v

MODULE-8: POSTPARTURIENT HAEMOGLOBINURIA IN

CATTLE AND BUFFALO

Learning objectives

 To understand the etio-pathogeneis and clinical signs of nutritional

haemoglobinuria in postparturient dairy animals.
 To study the diagnosis, treatment, control and prevention of nutritional
haemoglobinuria in postparturient cows.

DEFINITION OF NUTRITIONAL HAEMOGLOBINURIA

31 | P a g e
  A disease of high producing dairy cows occurring soon after calving.
It is also
called postparturient haemoglobinuria and is characterised by intravascular
hemolysis, haemoglobinuria and anemia.

ETIOLOGY AND EPIDEMIOLOGY NUTRITIONAL

HAEMOGLOBINURIA

Etiology

 Ration low in P, hay and grass from low P area, draught

 Cu deficiency (incidence reduced when supplemented)

Precipitating factor

 Grazing Brassica sp. plants, rape and turnip and other cruciferous plants,
large quantity of beet pulp, sugar cane top (low in p).
 Exposure to cold weather, cold water - erythrocytes becomes more sensitive to
hemolysis when there is hypophosphatemia & hypocupremia

Epidemiology

 Prolonged hypophosphatemia is an important predisposing factor

 'P' deficient soil and drought condition act as precipitating factors
 50% mortality and 40% morbidity
 Adult cow & she buffalo 3-6 weeks after delivery are more prone.
 Animals in 3-6th Lactation are more prone
 Geographical distribution: Throughout the world including India
 In India: It is very common in North India – Punjab, Haryana, M.P,
Rajasthan, Western part of Maharashtra.
 In Europe & North America the diseases is more common during prolonged
period of housing.

PATHOGENESIS OF NUTRITIONAL HAEMOGLOBINURIA

32 | P a g e
  Haemoglobinuria and hemolysis does not occur always. Death is mainly due
to anemic anoxia.
 The possible role of Cu and Se deficiency in hypophosphatemia is unclear. In
cases of Cu deficiency, there will be microcytic hypochromic anemia.
 Cu and Se provide protection against effects of orally acquired hemolytic
agents of cruciferous plants.

CLINICAL SIGNS IN NUTRITIONAL HAEMOGLOBINURIA

Acute cases

 Rapid onset after 2-4 weeks of calving, course is 3-5 days, red coloured urine,
anorexia, weakness, severe depression of milk yield.

Less acute cases

 Eats and gives milk for 24 hours after red coloured urine.
 Dehydration occurs quickly.
 Haemoglobinuria, inappetence, severe depression of milk yield.
 Heart rate is increased and bounding.
 Augmented irregular pulse.
 Temperature – Normal or raised (40ºC).
 Mucous membrane – pallor, later yellow.
 Dyspnoea is obvious.
 Diarrhoea; sometimes constipation.
 Mastitis.
 Gangrenous necrosis of tail, feet, pastern, ear and teeth (occasionally).
 Milk yield reduced.

33 | P a g e
  Suffer for 2-3 days and then recumbent followed by death in few hours /days.

If survive

 Weakness and Pica only during convalescence.

 There may be additional sign of 'P' deficiency is recumbency.
 Affects ruminal digestion.
 Lame and bone disease
 Infertility.
 Pica.
 Fall of milk yield.
 Retarded growth and unthriftiness.
 Weakness and convalescence

In marginal deficiency- general condition of the herd is normal

CLINICO PATHOLOGICAL CHANGES IN NUTRITIONAL

HAEMOGLOBINURIA

 Non-lactating animals of the affected herd in marginal 'P' deficiency

area may
have normal range of inorganic P (4-7 mg %).But, lactating animal my have
moderately low levels of 2-3 mg. Affected animal may also have extremely
low levels of 0.4 to 1.5mg.
 R.B.C decreased – Heinz body seen.
 Urine: Dark red brown to black, moderately turbid, No R.B.C.
 Low Cu in blood & liver.

PM changes

 Jaundiced carcass
 Blood: Dark and thin
 Swelling of spleen
 Liver: Fatty infiltration, swollen
 Dropsy in lower part of the body
 Discolored urine in bladder

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS OF

NUTRITIONAL HEMOGLOBINURIA IN ANIMALS

 Characteristic clinical signs like hemolytic anemia, haemoglobinuria within 4

weeks of parturition.
 Deficiency of P

Differential diagnosis

34 | P a g e
  Parasite – Babesia, Theileria
 High altitudes
 Copper Poisoning
 Plant – Rape
 Bacteria: Anthrax, Leptospira, Bacillary Haemoglobinuria
 Virus – Rinderpest
 Cold water
 Enzootic nutritional muscular dystrophy
 Drug induced Eg. Phenothiazine
 Enzootic haematuria
 Myoglobinuria
 Chronic hill haematuria
 Blood transfusion
 Metabolic ketosis
 Pyelonephritis

TREATMENT FOR NUTRITIONAL HAEMOGLOBINURIA

Treatment

 Keep in quiet and warm place.

 Avoid laxatives and purgatives.
 Blood Transfusion (5 to 10 liters) → followed by fluid therapy to prevent
haemoglobinuric nephrosis.
 Acid sodium phosphate 60 gm in 300 ml i/v very slow+ same dose s/c .
Further s/c inj at 12 hours interval for 3 times.
 Orally drench 30 gm Sodium acid Po4 BID.
 Copper glycinate 500mg i/v in copper deficiency cases
 Haematinics during convalescence.
 Bone meal 120 g BID / Dicalcium Po4.– orally for 5 days

Prevention

 Copper gluconate 120 mg s/c.

 Remove the cruciferous plants.
 Adequate intake of 'P' during early lactation.

MODULE-9: AZOTURIA IN EQUINES

Learning objectives

 To study the etio-pathogenesis and clinical signs of azoturia in horses

 To get knowledge about the diagnosis, treatment, control and prevention of
azoturia in horses

35 | P a g e
 DEFINITION OF AZOTURIA

 Synonyms: Paralytic myoglobinuria.

 It is a disease of horses occurring during exercise after a period of inactivity on
full ration. It is characterized by myoglobinuria and muscular degeneration.

ETIOLOGY OF AZOTURIA

 Large stores of glycogen are laid down in muscles during a period of idleness
and when exercise is taken the glycogen is rapidly metabolized into lactic acid.

 Nutritional deficiency of vitamin E and Selenium have also been suggested as

a cause.
 Occurrence of enzymatic defects in individual horses.

EPIDEMIOLOGY OF AZOTURIA

 Sporadic cases occur particularly in race horses fed heavily on grains.

 In most instances, history of complete inactivity for 2 or more days
immediately preceding the onset of disease.
 Draft horses on rest because of minor injuries are often maintained on full
work ration and become affected when taken back to work.

36 | P a g e
  Outbreaks have also been recorded in horses grazing on pasture but taking no
exercise.
 Mycotoxins were also suggested as a predisposing factor, but supporting
evidence was not available.

PATHOGENESIS OF AZOTURIA

 Gluteal muscles are commonly involved due to their high content of glycogen.
 Myopathic lesion cause pressure on the sciatic nerve and other crural nerve.
 Necrotic muscle fibers, hard, painful swelling of the large muscle masses
result in secondary neuropathic degeneration of rectus femoris and vastus
muscles leading to myoglobin liberated from the necrotic muscle fibers
followed by dark red brown urine.
 Death due to decubital septicemia or myohemoglobinuric nephrosis and
uremia and degeneration of myocardium.

CLINICAL SIGNS OF AZOTURIA

 Signs develop within 15 minutes to 1 hour on work. Signs may disappear in

few hours if the horse is given complete rest immediately, but the condition
usually progress to recumbency.
 First assume a dog sitting posture followed by lateral recumbency.
 Severe pain, restlessness, struggling and repeated attempt to rise.
 Respiration rapid.
 Small pulse.
 Temperature increased in severe cases.
 One or all four limbs may be affected; commonly both hind limbs are
involved.
 Quadriceps femoris and gluteal muscles are hard and board like.
 Urine-dark brown colour.
 Lameness-restriction of hind limbs movement. If exercise is stopped as soon
as lameness occurs the horse may recover in 2-4 days.
 Prognosis is good if the animal remains standing.

TREATMENT FOR AZOTURIA

 Further exercise should be avoided.

 Keep the horse in a loose box or box stall.
 Effort should be made to keep the horse standing.
 Slinging may be advisable.
 Narcosis or chloral hydrate (if pain).
 Corticosteroids I/V.
 Thiamine Hcl 0.5 gm I/M- gives favorable results.
 Antihistamines, vitamin E injection.

37 | P a g e
  Sodium bicarbonate orally or I/V- to keep the urine alkaline to avoid
putrificaton of myoglobin in renal tubules.
 Hot fomentation to affected part.

MODULE-10: HYPOTHYROIDISM AND DIABETES IN DOGS

Learning objectives

 To study the etiology, pathogenesis, clinical signs, diagnosis, treatment and

control of hypothyroidism in dogs
 To know about the etio-pathogenesis, clinical signs, diagnosis, treatment and
control of Diabetes mellitus and Diabetes insipidus.

DEFINITION ETIO-PATHOGENESIS AND EPIDEMIOLOGY OF

HYPOTHYROIDISM

Definition

 Hypothyroidism is the result of decreased production of thyroxine (T4) and

Triiodothyronine (T3) by the thyroid gland.

Etio-pathogenesis

 Hypothyroidism may result from dysfunction of any part of the hypothalamic

– pituitary – thyroid axis.
 Primary acquired canine hypothyroidism is due to lymphocytic thyroiditis.
 In idiopathic follicular atropy, there is loss of thyroid parenchyma and
replacement by adipose connective tissue.
 Less commonly, hypothyroidism is caused by bilateral thyroid neoplasia.
 Secondary hypothyroidism (deficiency of TSH) is rarely described in dogs.
Causes of acquired secondary hypothyroidism include pituitary
malformations and pituitary neoplasia.
 Tertiary Hypothyroidism (deficiency of TRH) is yet to be documented in the
dog.
 Congenital hypothyroidism (cretinism) is rarely diagnosed in dogs.
 Congenital primary hypothyroidism includes iodine deficiency, thyroid
dysgenesis and dyshormonogenesis.
 Secondary congenital hypothyroidism due to apparent isolated TSH or TRH
deficiency was reported in a family of young giant schnangers and in a
young boxer.
 Iatrogenic causes of hypothyroidism include iodine treatment, administration
of anti-thyroid drugs and surgical thyroidectomy.

Epidemiology

38 | P a g e
  The reported prevalence of canine hypothyroidism is from 0.2% to 0.8%.
Mean age at diagnosis is 7 years, with range of 0.5 to 15 years. Golden
retrievers and Doberman pinschers are among the breeds reported to be at
higher risk for hypothyroidism.
 In one study, Neutered males and females were reported to be at increased
risk for developing hypothyroidism compared with sexually intact animals.

CLINICAL SIGNS AND CLINICO-PATHOLOGICAL CHANGES

OF HYPOTHYROIDISM

Clinical signs

 Clinical signs of hypothyroidism may be non-specific and insidious in onset.

Common clinical signs attributable to decreased metabolic rate include
lethargy, mental dullness, weight gain, unwillingness to exercise and cold
intolerance. Obesity occurs in approximately 40% of hypothyroid dogs.

Dermatological changes

 Dermatologic changes occur in 60% to 80% of hypothyroid dogs. Common

findings include dry scaly skin, changes in hair coat quality or color,
alopecia, seborrhea and superficial pyoderma. Hyperkeratosis,
hyperpigmentation, comedone formation, hypertrichosis, ceruminous
otitis, poor wound healing, increased bruising and myxedema may also
occur.
 Alopecia is usually bilaterally symmetric and is first evident in areas of
wear and tear such as the lateral trunk, ventral thorax and tail. The hair is
often brittle, easily epilated and loss of under-coat may result in a coarse
appearance or puppy – like hair coat.
 Signs of decreased metabolic rate in conjunction with dermatologic
abnormalities should increase suspicion of hypothyroidism.
 Hypothyroid dogs are predisposed to recurrent bacterial infections of the skin
such as folliculitis, pyoderma and furunculosis.
 Malassezia spp infections and demodicosis are associated with
hypothyroidism. Pruritus may occur with concurrent infection.

Reproductive abnormalities

 Female reproductive abnormalities attributed to hypothyroidism include

prolonged interestrous interval, silent estrus, failure to cycle, spontaneous
abortion, low-birth weight litters, uterine inertia and stillborn puppies.
 Inappropriate galactorrhea apparently due to hyperprolactinemia has been
reported in sexually intact hypothyroid bitches.

39 | P a g e
  Male reproductive problems attributed to hypothyroidism include low libido,
testicular atrophy, hypospermia and azoospermia.

Nervous system abnormalities

 Both the peripheral and central nervous systems may be affected by

hypothyroidism. Peripheral neuropathy is the best documented neurologic
manifestation. Affected dogs have exercise intolerance, weakness, ataxia,
paralysis, deficits of conscious proprioception and decreased spinal
reflexes.
 Unilateral lameness reported in hypothyroid dogs may be a manifestation of
generalized neuromyopathy.
 Dysfunction of multiple cranial nerves and abnormal gait and postural
reactions.
 In myxedema, coma, profound mental dullness or stupor is accompanied by
non pitting edema, hypothermia with a lack of shivering, bradycardia,
weakness and inappetence.
 Abnormalities of the cardiovascular system such as sinus bradycardia, weak
apex beat, low QRS voltages and inverted T waves occur in hypothyroid
dogs. Reduced left ventricular pump function has also been documented.
 Ocular abnormalities reported in canine hypothyroidism include corneal
lipidosis, corneal ulceration, uveitis, lipid effusion into the aqueous humor,
secondary glaucoma, lipemia, retinitis, retinal detachment and
keratoconjunctivitis sicca.
 Congenital hypothyroidism results in mental retardation and stunted
disproportionate growth due to epiphyseal dysgenesis and delayed skeletal
maturation. Affected dogs are mentally dull and have large broad heads,
short thick necks, short limbs, macroglossia, hypothermia, delayed dental
eruption, ataxia and abdominal distention. Dermatologic findings are
similar to those seen in the adult hypothyroid dog. Other clinical signs may
include gait abnormalities, stenotic ear canals, sealed eyelids and
constipation.

Clinicopathologic changes

 Results of hemogram, biochemical panel and urinalysis often support a

diagnosis of hypothyroidism.
 A mild non regenerative anemia occurs in 30% of hypothyroid dogs
 Fasting hypercholesterolemia occurs in 75% of hypothyroid dogs where as
hypertriglyceridemia occurs in up to 88% cases
 In rare cases hyperlipidemia may lead to atherosclerosis.

40 | P a g e
 

DIAGNOSIS AND TREATMENT OF HYPOTHYROIDISM

Diagnosis

 A complete history
 Physical examination
 Minimum data base: T4 concentration - 1.5 – 3.5 µg/dL; TSH response test
; TRH response test

41 | P a g e
  Antithyroglobulin antibody is found in 36% to 50% of hypothyroid dogs.
 Thyroid biopsy

Treatment

 The initial treatment of choice regardless of the underlying

cause of the
disease is synthetic sodium L-thyroxine (T4) 0.02 mg/kg P.O, every 12 hr
 In myxedema coma, T4 should be administered initially intravenously
(5mg/kg) because of poor gastrointestinal absorption due to hypo motility.
Other supportive therapy including appropriate fluid therapy, passive
rewarming and ventilatory support may also be necessary.

DIABETES INSIPIDUS

 A functional disturbance of the kidney (decreased tubular reabsorption) due

to pituitary dysfunction so that ADH is not secreted in adequate amount to
control water excretion, leading to watery urine, free from albumin and
sugar.

Etiology

 More in horse especially stallion (Bed wetting).

 More in summer than in winter.
 Cats: Cancerous growth of pituitary and injuries to skull.
 Rare in farm animals.

Symptoms

 Polyuria: Horse 40 to 60 liters. Dog 3 to 4 liters.

o Urine: Watery with odour: Low sp. Gr. 1.001 to 1.002.
o In early: Easy voiding.
o In Late: Some what painful.
 Polydipsia: Horse 100 Liters; Dog 10-15 lit/day. When sufficient water not
available – Drink urine.
 Appetite – slowly decrease.
 Mucous membrane and skin – dry.
 Hair: dull and coarse.
 In Dogs: cataract, abscess in the perenial glands and prostate.
 Sooner or later emaciation.
 Neglected cases: Absolute cachexia.

Differential diagnosis

 Diabetes mellitus.

42 | P a g e
Treatment

 Horse: Best food free from albumin and salt.

 Reduce water to 20-24 liter / day.
 Pitressin tannate in oil.

DIABETES MELLITUS

 Diabetes mellitus is a complex metabolic disorder as result of insufficient

insulin secretion or excessive insulin antagonism leading to wide
aberrations in carbohydrate, fat and protein metabolism with secondary
disturbances in water and electrolytes.

Insulin non-availability

 Degenerative changes in β cells in pancreatic islets.

 Reduced effectiveness of hormone due to anti-insulin antibodies or inactive
complex.
 Autoimmune mediated islets cytotoxicity.
 Inappropriate secretion of hormones by neoplasms in other organs.

Incidence

 1:200 total canine patients

 Spontaneous in mature dogs (8-9 yrs female more affected than male)
 Susceptibility: miniature Poodle, Dacshunds and Terriers.

Pathogenic mechanism

 Destruction of islet cells due to severe pancreatitisand subsequent

replacement by fibrous tissues. So, the gland becomes firm, multinodular
and often has scattered areas of haemorrhage and necrosis.
 Selective degeneration of Islet cells (more in cats): Stress, obesity,
administration of cortisol.

Causes

 Idiopathic atrophy
 Virus

Clinical signs

 Onset is insidious – chronic.

 Polydipsia, polyuria, increased food consumption but loss of body weight.
 Bilateral cataract.

43 | P a g e
  In diabetes increased concentration of glucose in aqueous and vitreous
humour. So glucose penetrates into lens. There, it is metabolized into
sorbitol and further into fructose. The increased concentration in lens leads
to entry of water into lens fiber and causing swelling.
 Weakness.
 Diminished resistance to bacteria and fungal infection. So, recurrent or
chronic infection such as suppurative cystitis, prostatitis,
Bronchopneumonia and dermatitis.
 Hepatomegaly due to cirrhosis or accumulation of fat. Rough palpation leads
to intra abdominal haemorrhage.
 Chronic renal disease.
 Blindness due to microangiopathy.
 Gangrene.
 Ketone bodies accumulate in blood. Loss of sodium through urine – H+
conserved – so, acidosis leading to coma.

Laboratory diagnosis

 Glycosuria (urine more viscid, sweety odour & specific gravity increase.
 Fasting hyperglycemia - increases to 140 mg/ 100ml.
 Glucose tolerance test (GTT) (i/v or oral).
 Ketone in blood and urine and smell in respiratory tract.
 Elevated serum cholesterol and triglycerides.

Differential diagnosis

 Chronic nephritis: urine - Low specific gravity, increased protein, no sugar.

 Diabetes insipidus: Urine - low specific gravity which increase after the
administration of antidiuretic hormone.
 Pyometra: Polyuria, No glucose. Abdominal distension.
 Acute nephritis: Increased temperature, vomition, occasionally urine contains
sugar.
 Adreno cortical hyper function: Alopecia, hyperkeratosis.
 Prolonged steroid therapy.

Treatment

 Uncomplicated - Control hyperglycemia by insulin.

 Complicated - Correction of dehydration with plasma expanders, electrolyte
replacement.
 Infusion of bicarbonate to control acidosis.
 If hypokalemia , 'K' to be given.
 For obese animal - no insulin.

44 | P a g e
  In milder cases - Soluble insulin- absorbed quickly, act within 20-30 minutes;
reach peak levels within 4 hrs and maintained at these levels for maximum
of 8 hrs
 Protamine Zn insulin s/c : reach peak in 8-12 hrs and this level is maintained
for nearly 24-36 hrs
 Intermediate action: - Lente insulin, Globulin insulin and Isophan insulin.
They start acting in 4 hrs, reach peak in 8hrs and maintained for 18-26 hrs.
 NPH (Neutral Protamine Hagedorn) : 1 unit /kg in morning along with food.
 Stabilize the patient: To start with 2 units of soluble insulin + 2 units of other
types; then 4 + 4; then 6+6 units
 Check the urine daily.
 In advanced case – several hundred units i/v.
 Good grade of canned food and green vegetables + pancreatin – 2 tablet.
 Oral therapy – unsuccessful.

MODULE-11: DISEASES CAUSED DUE TO DEFICIENCY OF

IRON

Learning objectives

 To study the etiology, pathogenesis and clinical signs in iron deficiency in

animals
 To get knowledge about the diagnosis, treatment and control of iron
deficiency in animals

DEFICIENCIES OF MINERAL NUTRIENTS

Macro minerals

Calcium, phosphorus, potassium, sodium, magnesium, chlorine, sulfur.

Micro minerals or trace elements

 Copper, selenium, zinc, cobalt, iron, iodine, manganese and molybdenum

 At least 15 mineral nutrients are nutritionally essential for ruminants.
 Trace elements involved as component of many tissues and enzyme activities.

Evidence of existence of deficiency

 Diet prior to the occurrence of the disease must be considered.

 Specific deficiencies are associated with particular soil type and geological
maps may predict the probable occurrence for nutritional deficiencies.
 Diseases of plants may also indicate specific soil deficiencies. Eg. Reclamation
disease of oats indicate copper deficiency

45 | P a g e
  Heavy application of nitrogen fertilizer can reduce the Cu, Co, Mo and Mn
content of the plants.
 Heavy application of lime reduces the plant Cu, Co and Mn level but increase
in Mo level.

Abnormal absorption

 Excess phosphate reduces calcium absorption.

 Excess Ca reduces absorption of iodine.
 Chronic enteritis reduces the absorption of most dietary essentials.
 Abnormal utilization of ingested nutrients:
o Mo and sulfate reduces Cu storage.
o Thiamine reduces the dietary requirement of essential fatty acids.

ETIOLOGY AND EPIDEMIOLOGY OF IRON DEFICIENCY

Etiology

 Mostly newborn is affected due to lack of iron in milk.

 Deposition in liver is low to maintain normal haemopoiesis for more than 2-3
weeks.
 In piglets, iron deficiency is dietetic leading to anemia and failure to thrive.

Epidemiology

 Not common in farm animals.

 Mostly piglets are affected.
 Continued blood loss may lead to sub clinical anemia with iron deficiency.
 Cattle with chronic tick infestation - Non-regenerative anemia with subnormal
serum iron.
 Horse with strongyloides (suck blood) – subnormal Hb level.
 Calves only on Milk- develop Fe deficiency ; when start eating roughage it is
rectified.

In piglets

 When they grow in indoors, they develop iron deficiency.

 Black is affected more than white.

PATHOGENESIS OF IRON DEFICIENCY

46 | P a g e
  Piglets at birth have 9-11 gm/dl of Hb.
 Physiological fall at 8-10th day to 4-5 g/dl.
 If iron is sufficiently given the Hb returns to normal starting from 10th day;
otherwise, develop anaemia due to fast growth.

CLINICAL SIGNS IN IRON DEFICIENCY

 Decreased food intake.

 Diarrhea with normal colour.
 Servere dyspnoea, lethargy and increase in amplitude of apex beat with
exercise.
 Skin and mucous membrane become pale and often quite yellow in white pigs.
 Edema of head and fore quarters → fat puffed up appearance and they die
quickly.
 A lean, white hairy look , thin and unthrifty condition → sudden death or
recovery.
 High incidence of infectious disease ( esp. E coli, Streptococcus) associated
with iron deficiency.

PATHOLOGICAL CHANGES IN IRON DEFICIENCY

 Normal pig and cats: Post-natal fall of 8 gm/dl Hb- (Physiological fall) some
times as low as 4-5 gm/dl in first 10 days.
 In deficient animals 2-4 gm / dl during 3rd week.
 When 4 gm /dl Hb – clinical sign appears.

47 | P a g e
  Blood picture – RBC decreased to 3-4 million/µl with microcytic hypochromic
anemia.
 Postmortem examination
o Pallor and thin watery blood, moderate anasarca, dilated heart.
o Liver – Enlarged, Mottled appearance and fatty infiltration.

DIFFERENTIAL DIAGNOSIS OF IRON DEFICIENCY

 Diagnosis :It is very easy. Clinical examination and haematological

examination are very helpful in determining the anaemia and its severity.

Differential diagnosis

 Copper deficiency – also cause anaemia.

 Isoimmunization hemolytic anaemia – Haemoglobinuria and jaundice in
young pigs.
 Protozoan parasites.
 Eperythrozoonosis – all ages.

TREATMENT AND CONTROL OF IRON DEFICIENCY

Treatment

 Cattle: Oral Iron sulphate / gluconate 2-4 gm daily for 2 weeks. As iron is
unpalatable, mix with feed or molasses as liquid.
 Horse: Individual Idiosyncratic reactions are common.
o Dose: 0.5-1 gm elemental iron in one injection /week.
o Organic iron preparation – Iron dextran.
o Iron – sorbital acid complex: Iron saccharase /gluconate.
o Inj. vit B12 5000 µg /week as single dose.

Prevention

 Only to baby piglets not to sows.

 Piglets: Allow suckers access to pasture or dirt yard.
 Oral dosing: Daily 4 ml of 1.8% solution of ferrous sulphate, iron
pyrophosphate 300 mg /day for 7 days. Oral therapy essential within 12hrs of
birth.
 Reduced Iron 0.5 – 1 gm once weekly.

Prepare the following iron Paint and apply on the mammary gland for the baby
piglets to suckle
Ferrous 450G -

48 | P a g e
sulphate
CuSo4 75oG -
Sugar 450G -

Water 2 lit -
Excess oral iron cause diarrhea

Spray
Iron 9G For every 50 lb of soil and throw it in the pen
CuSo4 1.5 G -
Injections

Iron dextran 3rd and 7th day i/m

Iron fumarate / -
glutamate
MODULE-12: DISEASES CAUSED DUE TO DEFICIENCY OF
COPPER

Learning objectives

 To study the etio-pathogenesis of copper deficiency syndrome in animals

 To get
knowledge about the clinical signs, diagnosis, differential
diagnosis,treatment and control of copper deficiency syndrome.

CHARACTERISTICS OF COPPER DEFICIENCY

 Occurs primarily in young ruminants.

 Characterized by
o Retarded growth rate
o Unthriftiness
o Diarrhea
o lameness
o Change in the hair colour
o Demyelination of the CNS in neonates
o Anemia in the later stages
o Falling disease
o Osteoporosis
o changes in the coat (achromotrichia)
o Rough and depigmented hair

49 | P a g e
 ETIOLOGY AND EPIDEMIOLOGY OF COPPER DEFICIENCY

 Cu deficiency may be primary, when the intake in the diet is inadequate or

secondary, when the dietary intake is sufficient but the utilization of the Cu
by tissues is impeded.
 In ruminants, Cu deficiency causes interference with tissue oxidation resulting
in various clinical manifestations including those associated with anemia
and demyelination in the central nervous system.
 Cu deficiency causes diseases of economic importance in many parts of the
world. Although heavy mortalities occur in affected areas the major loss is
due to failure of animals to thrive.
 Enzootic ataxia may affect up to 90% of a lamb flock in badly affected areas
and most of these lambs die of inanition.
 In falling disease up to 45% of cattle in affected herds may die.
 Young animals are much more susceptible to primary Cu deficiency than
adults. The signs are severe in calves and yearlings, less severe in 2 year
olds and of minor degree in adults.
 Enzootic ataxia is primarily a disease of suckling lambs whose dams receive
insufficient dietary Cu.
 Milk is always a poor source of Cu and when it is the solo source of
nourishment, the intake of Cu will be low. Milk from normal ewes contains
0.2-0.6 mg of Cu/ liter, but under conditions of severe Cu deficiency this
may be reduced to 0.01-0.02 mg/liter.
 Both primary and secondary Cu deficiency occur most commonly in spring
and summer coinciding with the time at which the Cu content of the pasture
is the lowest

PRIMARY COPPER DEFICIENCY

 The amount of Cu in the diet may be inadequate when the forage is grown on
deficient soils or on soils in which the Cu is unavailable. In general there are
2 types of soil on which Cu deficient plants are produced.
o Sandy soils –poor in organic matter.
o Peat or muck soils –reclaimed from swamps.
 Pasture containing less than 3 ppm DM of Cu will produce signs of deficiency
in grazing ruminants.
 Levels of 3 -5 ppm DM can be considered as dangerous and levels greater than
5 ppm DM ( preferably 7-12) can be considered as safe unless complicating
factors cause secondary Cu deficiency.
 The diseases caused by a primary deficiency of Cu in ruminants are enzootic
ataxia of sheep in Australia, New Zealand and USA; Licking sickness of
cattle in Holland and falling disease of cattle in Australia.
 In pigs Cu deficiency may cause anaemia in sucking pigs.

50 | P a g e
  Adult horses are unaffected but there have been reports of abnormalities of
limbs and joints of foals reared in Cu deficient area.
 A concurrent deficiency of both Cu and Co occurs in Australia (coast disease),
Florida and USA (salt sickness) and is characterized by the appearance of
clinical signs of both deficiencies. The disease is controlled by
supplementation of the diet with Cu and Co.
 Cu deficiency of ruminants in India usually results in infertility and low
production.

SECONDARY COPPER DEFICIENCY

Disease Country Species Cu level Probable
affected in liver conditioning
factor
Sway back Britain, Sheep Low Unknown
USA
Renguerra Peru Sheep Low Unknown
Teart Britain Sheep & Unknown Mo
cattle

Scouring Holland Cattle Unknown Unknown

disease

Peat scours New cattle Low Mo

Zealand

Peat scours Britain Cattle Low Unknown

Peat scours Canada Cattle Unknown Mo

Salt Florida, Cattle Unknown Unknown

sickness USA

Pine Scotland Calves Low Unknown

 The conditioning factor is known only in some instances. A dietary excess of

Mo being most frequently incriminated. Zinc, iron, lead and calcium
carbonate are also considered to be conditioning agents.
 A high Mo intake can induce Cu deficiency even when the Cu content of the
pasture is high and a higher Cu intake can overcome the effect of the Mo.
 The disease caused by the secondary Cu deficiency is mostly due to high
dietary intakes of Mo and sulfate. They include syndromes characterized by
diarrhea or by unthriftiness.
 Another syndrome is yellow calf- a disease of nursing calves where Cu content
of forages ranges from 2.6 to 11.8 ppm and the Mo from 1 to 39 ppm.

51 | P a g e
  Sway back of lambs in UK has been classified as a secondary Cu deficiency but
no conditioning factor has been determined.
 Mo appears to be the conditioning agents in enzootic ataxia in the United
States.
 A dietary excess of Mo is known to be the conditioning factor in the diarrheic
diseases. Peat scours in New Zealand, California and Canada and teart in
Britain.

COPPER METABOLISM

Cu-Mo-sulfate relationship

 Secondary Cu deficiency occurs when the dietary intake of Cu is considered to

be adequate, but absorption and utilization of Cu are inadequate because of
the presence of interfering substances in the diet. Mo and sulfate alone or in
combination can affect Cu metabolism. This also affects the foetus and
interferes with the Cu storage in the foetal liver.
 Selenium administration to sheep on Cu deficient pastures causes
improvement in Cu absorption.
 Molybdate reacts with sulfides to produce thiomolybdates ( copper tetra
thiomolybdate) in rumen.

Cu absorption

 Absorption of Cu is interfered in a sheep on high Mo intake.

 Molybdate may affect the pool of sulfide in the rumen by two routes.
o If the diet contains sulfides, the Molybedate decreases the
concentration of sulfides. Cu can become unavailable to the animal
in the rumen by formation of cupric Molybedate or formation of
cupric sulfide.
o If the diet contain sulfate as a major sulphur source, Molybedate
alleviate clinical Cu deficiency.
o If the diet contain sulphur amino acids as the major source of
sulphur, Molybedate aggravate clinical Cu deficiency.

Cu utilization

 It can be affected by sulfate and Molybedate by interference with mobilization

of Cu from the liver, inhibition of Cu intake by the tissues and inhibition of Cu
transport both into and out of the liver and inhibition of the synthesis of Cu
storage complexes and ceruloplasmin.

Hepatic storage

52 | P a g e
  When sheep are fed a Cu deficient diet both molybdate alone or sulfate alone
will decrease the levels of Cu in plasma, liver and kidney as well as
decreasing ceruloplasmin activity.
 With adequate dietary levels, the liver Cu level are less in the presence of
molybdate and sulfate.
 Molybdate and sulfate together impair the movement of Cu into or out of the
liver, possibly by affecting Cu transport. Sulfate alone exerts an effect. An
increase in intake reduces hepatic storage of both Cu and Mo.

Tissue utilization

 Clinical sign of hypocuprosis (such as steely wool) can occur in sheep where
blood Cu levels are high. Under these circumstances Cu is not utilizable in
tissues and the blood Cu raises in response to the physiological needs of the
tissues.

PATHOGENESIS OF COPPER DEFICIENCY

Bone

 The osteoporosis which occurs in natural cases of Cu deficiency is caused by

the depression of osteoblastic activity.
 There is marked overgrowth of epiphyseal cartilage especially at
costochondral junction and in metatarsal bones. There is also an
impairment of collagen formation.

Heart

 The myocardial degeneration of falling disease may be terminal manifestation

of anemic anoxia or due to interference with tissue oxidation.
 In this disease, it is thought that the stress of calving and lactation contribute
to the development of heart block and ventricular fibrillation, when there
has already been considerable decrease in cardiac reserve.

Blood vessels

 Experimentally produced Cu deficiency has also caused a sudden death due to

rupture of heart and great vessels in a high proportion of pigs fed a Cu
deficient diet. The basic defect is degeneration of the internal elastic
laminae.

Nervous tissue

 The mechanism by which Cu deficiency halts the formation of myelin and

causes demyelination has not been established. In experimental animals it

53 | P a g e
 has been shown that Cu deficiency does interfere with the synthesis of
phospholipids.
 Anoxia is cause of demyelination. Anemic anoxia is likely to occur in highly
deficient ewes, and anemic ewes do produce a higher proportion of lambs
with enzootic ataxia. However, there is often no anemia in ewes which
produce lambs with the more common sub acute form of the disease.
 Severely deficient ewes have lambs which are affected at birth and in which
myelin formation is likely to have been prevented. The lambs of ewes less
severely deficient have normal myelination at birth and develop
demyelination in postnatal life.

Effects on tissues

 Cu plays an important role in tissue oxidation by either supplementing

cytochrome oxidase system or entering into their formation.
 Ceruloplasmin is the Cu containing enzyme through which Cu exerts its
physiological functions.

Wool

 The straightness and stringiness of the wool is due to inadequate

keratinization due to imperfect oxidation of free thiol groups.
 Provision of Cu to such sheep is followed by oxidation of these free thiol
groups and a return to normal keratinization within a few hours.

GENERAL SYNDROME - PRIMARY Cu DEFICIENCY - CATTLE

 Primary Cu deficiency causes unthriftiness, loss of milk production and

anemia in adult cattle. An increased occurrence of post parturient
haemoglobinuria is also recorded. The coat colour is affected, red and black
cattle changing to bleached, rusty red and becomes rough and staring.
 Calves grow poorly, sometimes have chronic diarrhea and there is an
increased tendency for bone to fracture, particularly the limb bones
including the scapula. In some cases ataxia develops after exercise, there
being loss of control limbs with the animal falling or subsiding into a sitting
posture. Itching and hair licking is also recorded as a manifestation of Cu
deficiency in cattle.
 Although diarrhea occurs, persistent scouring is not characteristic of primary
Cu deficiency.
 Calves may develop stiffness and enlargement of the joints and contraction of
the flexor tendons causing the affected animals to stand on their toes.
 These signs may be present at birth or occur before weaning.

SECONDARY Cu DEFICIENCY - CATTLE

54 | P a g e
  The syndrome caused by secondary Cu deficiency includes the signs of
primary Cu deficiency except that anemia occurs less commonly.
 In addition to the other signs, there is a general tendency for scouring to
occur, particularly in cattle. Diarrhea is a prominent sign in experimental
Cu deficiency.

Falling disease of cattle

 The characteristic behavior in falling disease is that the cows are apparently
healthy, but throw up their heads below and fall.
 Death is instantaneous in most of the cases, but some fall and struggle feebly
on their sides for minutes with intermittent bellowing and running
movements and attempt to rise. Rare cases show signs for up to 24 hours or
more.

Peat scours (teart) of cattle and sheep

 Persistent diarrhea with the passage of watery, yellow, green to black feaces
with an offensiveness odour occurs soon after the cattle go on to affected
pasture, in some cases with in 8-10 days.
 Debility, rough hair coat and depigmentation manifested by reddening or grey
flecking especially around the eyes in black cattle.
 Affected animal usually recover in a few days following treatment with Cu.

Unthriftiness (pine) of calves

 The earliest sign are stiffness of gait and unthriftiness.

 The epiphyses of the distal ends of the metacarpus and metatarsus may be
enlarged and resemble the epiphysitis of calves deficient in calcium and
phosphorous or vitamin D.
 The epiphyses are painful on palpation and some calves are severely lame.

Anemia

 Cu is essential for formation of hemoglobin, but it is not marked in the

secondary form.
 In view of the heavy hemosiderin deposits in tissues of copper deficient
animals, Cu is necessary for the reutilization of iron liberated from the
normal breakdown of hemoglobin.

ENZOOTIC ATAXIA AND SWAY BACK IN LAMBS

Enzootic ataxia

55 | P a g e
  Affect only unweaned lambs. Lamb may be affected at birth. Most cases occur
in the 1-2 month age group. Severity of the paresis decreases with
increasing age at onset.
 Lambs affected at birth or within the first month usually die within 3-4 days.
The diseases in older lambs may lost for 3-4 weeks. Inco-ordination of the
hind limbs occur.
 Respiratory rate and heart rate greatly accelerated by exertion. As the disease
progresses, the incoordination become more severe and may be apparent
after walking only a few yards.
 Excessive flexion of joints, wobbling of the hind quarters and finally falling.
Hind legs are affected first and the lambs may be able to drag itself about in
a sitting position. Then once forelimbs are involved, recumbency persists
and lamb die of inanition. There is no true paralysis; the lambs able to kick
vigorously even in the recumbent stage. Appetite remains unaffected.

Sway back

Congenital form

 Cerebrospinal swayback occurs only when the Cu deficiency is extreme.

Affected lamb is born dead or weak and unable to stand and suck.
Incoordination and erratic movements are evident than in enzootic ataxia.
 Spastic paralysis and occasionally blindness. Softening and cavitation of the
cerebral white matter commences by 120th day of gestation.

Progressive (delayed) spinal sway back

 Begins to develop some weeks after birth with lesions and clinical signs
appearing at 3-6 weeks of age.

Postnatal acute fatal sway back

 It is a 3 rd form of the disease that appears to occurs only in wales. This

develops suddenly.
 Sudden onset of recumbency with death occurring 1-2 days later due to
swelling of the cerebrum.

CLINICAL SIGNS OF COPPER DEFICIENCY

 Profuse watery diarrhea and weight loss.

 Epiphyseal enlargement, stiffness and unthriftiness seen in young ruminants
are the result of Cu deficiency.
 Spontaneous fractures in ruminants

56 | P a g e
  Enzootic ataxia - characterized by (lambs, deers and pigs)inco-ordination,
recumbency begins with hindlegs progress to the fore limbs.
 Inadequate keratinization of wool due to imperfect oxidation of free thiol
group during hair growth and keratinization.
 Copper containing enzyme, tyrosinase is needed to convert L- tyrosine to
melanin. With Cu deficiency this conversion is slow and hair is lighter in
colour than normal
 Cu deficiency leads to decreased immune function in ruminants. Also
associated with anaemia (altered iron metabolism), decreased weight gain
or weight loss.
 Clinical signs of Cu deficiency are more prominent in young animals and may
include retarded growth rate, rough depigmented hair, diarrhea,
osteoporosis with spontaneous fractures, anaemia and changes in the coat
colour.
 In lambs- sway back or enzootic ataxia, demyelination syndrome.
 Cu deficiency has also been associated with hemolytic anaemia in post
parturient dairy cattle.
 Cu plays an important role in the transport of iron from the gut to the marrow
and in the incorporation of iron into the heme moiety.
 Anemia - moderate, slowly progressive and closely resembles iron deficiency.
 Cu deficiency can be documented by measuring serum Cu as ceruloplasmin,
erythrocyte-superoxide-dismutase or the Cu content of hair, liver and
kidney.
 Serum iron is low in ruminants with Cu deficiency. Cu can be supplied as a
dietary supplement or as injectable Cu glycinate preparations.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS OF COPPER

DEFICIENCY

Diagnosis

 By symptoms and response to treatment with Cu.

 Estimation of Cu content of tissues and body fluids.
 Estimation of ceruloplasmin in the serum

Differential diagnosis

 Unthriftiness due to internal parasites.

 Peat scours and Johne’s disease.
 Malnutrition due to energy and protein deficiency.
 Lameness caused by osteodystrophy due to Ca, P and vitamin D imbalance.
 Anemia due to pediculosus.
 Sudden death due to other causes.

57 | P a g e
 TREATMENT AND CONTROL MEASURES IN COPPER
DEFICIENCY

 Oral dosingwith 4 gm of CuSo4 for calves from 2-6 months of age and 8-10 gm
for adult cattle given weekly for 3-5 weeks is recommended for primary or
secondary Cu deficiency.
 The diet of the affected animals should also be supplemented with Cu. Cu
sulfate may be added to the mineral salt mixture at a level of 3-5 % of the
total mixture.
 A commonly recommended mixture for cattle is 50 % Ca- P mineral
supplement, 45% of cobalt iodized salt and 3-5 % Cu sulfate. This mixture is
offered free of choice or can be added to a complete diet at the rate of 1 % of
the total diet.
 Prognosis is guarded to good.
 Excess Mo and sulfate can be over come by increasing the dietary Cu or by
injecting Cu.
 Parentral injection of Cu glycinate may also be used. Brisket region is suitable
for injection site.
 Cu So4 can be added to molasses at 0.363 g / head / day for mature cattle.
 In some countries, EDTA (Cu disodium edeate) solution is used as injectable
Cu supplements. Dose: Adult- 400 mg (120 mg Cu) S/C ; Calves: 100-200
mg .One injection is effective as a treatment for 4-6 months in primary Cu
deficiency.
 Oral administration of Cu oxide needle (fine rods of 1-10 mm long) placed in
gelatin capsules that dissolve in the reticulorumen and liberate the CuO
wires. These wires reside in the reticulum and abomasum and slowly
release Cu for absorption.
 In case of excess Mo / sulfates repeat the injection for 4-6 weeks

MODULE-13: DISEASES CAUSED DUE TO DEFICIENCY OF

COBALT

Learning objectives

 To study the etiopathogenesis, clinical signs and diagnosis of cobalt deficiency

in cattle
 To get a knowledge about the differential diagnosis, treatment and control of
cobalt deficiency in cattle.

CHARACTERISTICS OF COBALT DEFICIENCY

 Anorexia and wasting

 Reduced milk yield

58 | P a g e
  Sheep: Pine in Britain
 Bush sickness in Newzealand
 Grand Traverse Disease – USA

EPIDEMIOLOGICAL FACTORS IN COBALT DEFICIENCY

 Cattle are less susceptible than sheep

 Young ones are more susceptible than adult
 Frank deficiency
is rare in carnivores and omnivores
 Horses are not susceptible (vit B12 present in meat)
 Soil: Less than 0.25 ppm in soil lead to less pasture content
 Grazing cattle show secondary ketosis in areas of Co deficiency.

PATHOGENESIS OF COBALT DEFICIENCY

 Cobalt stored only in limited amount.

 Its action is only in rumen. So, it is required continuously in feed.
 Co is required in rumen to produce B12 (cyanocobalamin)which is required
for conversion of methylmalonyl coenzyme A to succinyl coenzyme A.
 Both enzymes intermediates the utilization pathway of propionate
 In cobalt deficiency there is inability to metabolize propionic acid leading to
failure of appetite which results in inanition and death.

In sheep

 Hepatic dysfunction causes “white Liver disease”.

 Clinically “ Photosensitization”, become greyish color and show anemia.

CLINICAL SIGNS OBSERVED IN COBALT DEFICIENCY

 Less severe in cattle than in sheep.

 Gradual decrease in appetite leads to loss of body weight, emaciation
and
weakness inspite of availability of abundant green fodders.
 Pica in cattle
 Mucous membrane pallor
 Easily fatigued.
 Reduction of growth and milk yield.
 Decreased wool production which become tender and broken.
 Infertility and diarrhea and lacrimation in later stage.
 Clinical signs appear in 6 months of age. Death occurs 3-12 months after the
appearance of first symptoms.

CLINICO PATHOLOGICAL CHANGES IN COBALT DEFICIENCY

59 | P a g e
  Estimation of Co or vit B12 content of liver (0.3 ppm).
 Hematology: Animal anemic, but Hb and RBC are normal due to hemo
concentration. Normocytic normochromic anemia.
 Methylmalonic acid (MMA) in plasma and urine, Forminoglutamic acid
(FIGLU) in urine are diagnostic and prognostic indicators of cobalt
deficiency
 Hypoglycemia, usually <60mg / gm/dl plasma.
 Low serum alkaline phosphatase (<20 I.U / liter).

DIFFERENTIAL DIAGNOSIS

 Nutritional deficiency of Cu, selenium and vitamin D.

 Internal parasites – Co deficiency predispose to heavy infestation.
 Johne’s disease in sheep.
 Rule out other causes of anemia

TREATMENT AND CONTROL MEASURES IN COBALT

DEFICIENCY

Treatment

 Sheep: Cobalt sulphate 1mg/day/sheep,orally or can be given in accumulated

dose / week.
 Cattle: 0.5 gm orally / daily or 10 times of Prophylactic dose orally.
 To give 1 mg of Co , it is necessary to give 5mg of cobalt chloride or cobalt
sulphate in water. Parental injection has no use.
 Vitamin B12 (costly). Vitamin B12( hydroxy cobalamine) @ 1 mg i/m for 14
weeks to lambs.

Control

 Safe level: Sheep 0.06mg/kg/DM or 5 mg/day.

 Cattle 0.07 mg/kg/DM or 25 mg/day.
 Top dressing of cobalt sulphate 400-600 g / ha / annually as pellets.

MODULE-14: DISEASES CAUSED DUE TO DEFICIENCY OF

ZINC AND MANGANESE

Learning objectives

 To study the etiopathogenesis and clinical signs of zinc deficiency in animals

 To have knowledge on manganese deficiency in animals.
 To study the diagnosis, differential diagnosis, treatment and control of zinc
deficiency in animals.

60 | P a g e
 CHARACTERISTICS OF ZINC DEFICIENCY

 Parakeratosis in swine.
 Depression of productivity and parakeratosis in pig, less in other ruminants.
 Characteristics: Parakeratosis, alopecia, wool eating, abnormal hoof growth,
lameness and unthriftiness.

ETIOLOGY OF ZINC DEFICIENCY

Swine

Primary

 When ration contain less than 40mg Zn/kg DM

Secondary (Conditioned)

 Excess Ca i.e. more than 7gm of Ca /kg D.M for growers.

 Protein of vegetable origin eg. Soybean meal- unavailable because of its
presence in bound form.
 Deficiency of unsaturated fatty acids (EFA) (High Ca decrease the digestibility
of fat).
 High levels of copper will decrease the zinc requirement.
 Enteric infection (diarrhea) exacerbates the disease.
 Increased requirement in pregnancy and lactation, especially in gilts.
 Occur during period of rapid growth, after weaning, 7-10 weeks of age.

Ruminants

Primary

 Degree of compaction of soil.

 Increase in N2 and P concentration in soil increase the incidence of disease.
 Soil PH of more than 6.5 precipitates Zn deficiency. Because, Zn solubility
decreases as the pH increases.
 Legumes contain less amount of zinc.
 Zn concentration decreased with aging of plant.

Secondary

 Immature grass → affects digestibility.

 Late cut hay – poor digestibility.
 Excess dietary sulphur.

61 | P a g e
 PATHOGENESIS OF ZINC DEFICIENCY

 Not well understood. Zn is a component of carbonic anhydrase. It

is associated with RNA function, insulin, glucagons and other hormones.
 Young ones are affected more than the adults.

Mildly affected

 Reduced appetite.
 Sub optimal weight gains.
 Poor feed utilization.

Severely affected

 Thrive badly.
 Parakeratosis of lower
parts of legs, within the thighs or scrotum and face.
 Decreased cell mediated immune function.

CLINICAL SIGNS IN ZINC DEFICIENCY

Ruminants

 Parakeratosis involving more than 40% of skin area.

 Alopecia.
 Stunted growth.
 Stiff gait in experimental cases.

Cattle

 Rough coated. The affected skin is thick, wrinkled and partially fissured.
 Leg joints may swell and excess salivation may occur because of hemorrhage
in teeth and ulcers on dental pad.
 Lesions usually involves udder, muzzle, vulva, scrotum, anus and tail head
 Milk yield decreased.
 Low zinc may cause infectious pododermatitis.
 In sub clinical cases there is ‘depression of reproductivity'.

Sheep

 Loss of wool/ Fleece , crimp thin, stained, and easily shed.

 Hooves softens & distorted
 Leg joints may swell.
 Skin lesions around eyes, hoof and nose.
 Wool eating may occur.
 Testicular size and spermatogenesis affected

62 | P a g e
  Infertility in ewes.

Pigs

 Rate and efficiency of body weight gain decreased.

 Lesions on the lower part of extremities, limbs, joints, ear, face, tail, abdomen,
inside of thigh and side of the body. Belly, Hams & Back are also affected.
 The lesion progress in 2 to 3 weeks from small red spots through papules to
dry patches with fissured crusts of several millimeters deep.
 Mild diarrhea often occurs.
 Sub clinical deficiency occurs in sows with small litters, little scratching and
rubbing, secondary S/C abscess. They recover spontaneously if deficiency is
corrected.

DIFFERENTIAL DIAGNOSIS FOR ZINC DEFICIENCY

Pigs

 Exudative epididymitis – caused by Staphylococcus hyos or Staphhylococcus

hycus – occur in unweaned pigs.
 Dry crumbly lesions or greasy lesions - more mortality.
 Pityriasis rosea (erythematous skin covered by scale).

Sheep

 Contagious pustular dermatitis (viral disease).

Cattle

 Scrapie, mange – itching and rubbing.

 Ringworm and mycosis.
 Vitamin- A deficiency.
 Chronic selenosis – emaciation, lameness and loss of hair.
 Photosensitization.

TREATMENT AND CONTROL MEASURES OF ZINC

DEFICIENCY

Treatment

Pig

 200 gm ZnSo4 or carbonate/ tonne of feed.

 Inj zinc 2-4 mg /kg daily for 10 days or inj ZnO in olive oil @ 200 mg for adult
sheep or 50 mg/lambs, IM.

63 | P a g e
  0.5 g ZnS04 in water once in a week for 3 months.
 In calves, 2-4 gm Zn So4 once in a week.
 Ca content of feed must be corrected (restricted to 0.65 to 0.75% in diet) to 50
mg /kg of diet for pigs.

Sheep

 Oral Zinc 200 mg daily for 4 weeks.

Prevention

 Give salt lick to calves (2.5 to 5 g Zn/kg).

 Oils containing unsaturated fatty acids
 Zn containing fertilizers to pasture.
 Intra ruminal pellets.
 S/c depots of ZnO/Zn metal dust.

ETIOLOGY AND PATHOGENESIS OF MANGANESE

DEFICIENCY

A dietary deficiency of manganese (Mn) may cause infertility and skeletal deformities
both congenitally and after birth.

Etiology

 A primary deficiency occurs endemically in some areas because of a geological

deficiency in the local rock formations.
 Apart from primary dietary deficiency of manganese
 Poorly absorbed from intestine
 An excess calcium and/or phosphorus in the diet is known to increase the
requirements of manganese in the diet of calves and is considered to reduce
the availability of dietary manganese to cattle.
 Congenital chondrodystrophy in calves has been associated with manganese
deficiency.
 An outbreak of congenital skeletal defects in Holstein calves due to manganese
deficiency has been reported.

Pathogenesis

 Manganese plays an active role in bone matrix formation, and in the synthesis
of chondroitin sulfate which is responsible for maintaining the rigidity of
connective tissues.
 In manganese deficiency, these are affected deleteriously and result in skeletal
abnormalities.

64 | P a g e
  Only 1 % of manganese is absorbed from the diet and the liver removes most
of it, leaving very low blood levels of the element.

EPIDEMIOLOGY OF MANGANESE DEFICIENCY

 Manganese-responsive infertility occurs in areas where soils on farms have

contained less than 3 mg/kg of manganese.
 A secondary soil deficiency is thought to occur and one of the factors
suspected is high alkalinity, which reduces the availability of manganese in
the soil to plants.
 There are three main soil types on which the disease occurs:
o Soils low in manganese have low output even when pH is less than
5.5
o Sandy soils where availability starts to fall
o Heavy soils where availability starts to fall at pH of 7.0.
 Heavy liming of soils reduce the manganese intake of grazing animals.
 Pasture containing less than 80 mg/kg of manganese is incapable of
supporting normal bovine fertility, and herbage containing less than 50
mg/kg is often associated with infertility and anestrus.
 According to Agricultural Research Council, levels of 40 mg/kg dry matter
(DM) in the diet should be adequate.
 There are important variations in the manganese content of seeds, an
important matter in poultry nutrition.
o Maize and barley have the lowest content.
o Wheat or oats have three to five times as much, and
o Bran and pollard are the richest natural sources with 10-20 times the
content of maize or wheat.
 Cows' milk is exceptionally low in manganese.

CLINICAL FINDINGS AND CLINICAL PATHOLOGY OF

MANGANESE DEFICIENCY

Clinical findings

In cattle

 The common syndromes are

o Infertility, which is manifested by slowness to exhibit estrus, and
failure to conceive, often accompanied by subnormal size of one or
both ovaries. Subestrus and weak estrus have also been observed.
o Calves with congenital limb deformities
o The deformities include knuckling at the fetlocks, enlarged joints
and, possibly, twisting of the legs.

65 | P a g e
 o The bones of affected lambs are shorter and weaker than normal and
there are signs of joint pain, hopping gait, and reluctance to move.
o Affected calves manifest poor growth, dry coat, and loss of coat color.
o An outbreak of congenital skeletal malformations in Holstein calves
was characterized clinically by small birth weights (average 15 kg).
Abnormalities included joint laxity, doming of the foreheads,
superior brachygnathia, and a dwarf like appearance due to the short
long-bones. The features of the head were similar to those of the wild
beast. The majority of affected calves were dyspneic at birth, and
snorting and grunting respiratory sounds were common. Affected
calves failed to thrive and most were culled due to poor performance.

In pigs

 reduction in skeletal growth

 muscle weakness
 obesity
 irregular, diminished or absent estrus,
 agalactia
 resorption of fetuses or the birth of stillborn pigs.
 Leg weakness, bowing of the front legs and shortening of bones also occur.

Clinical pathology

Cattle: Normal values

 In blood - 18-19 flg/dL (3.3-3.5 flmol/L), although considerably lower levels

are sometimes quoted.
 Liver - 12 mg/kg (0.21 mmol/kg) and down to 8 mg/kg (0.15 mmol/kg) in
newborn calves, which also have a lower content in hair.
 Hair - about 12 mg/kg (0.21 mmol/kg) and infertility is observed in
association with levels of less than 8 mg/kg (0.15 mmol/kg). In normal
cows, the manganese content of hair falls to 4.5 mg/kg (0.08 mmol/kg) at
calving.
 Tissue - between 2 and 4 mg/kg (0.04 and 0 . 0 7 mmol/kg) in most tissue

DIAGNOSIS, TREATMENT AND CONTROL OF MANGANESE

DEFICIENCY

Diagnosis

 There is no simple, single diagnostic test permitting detection of manganese

deficiency in animals.

66 | P a g e
  Reproductive functions in male and female, are most sensitive to manganese
deficiency and are affected before possible biochemical criteria, e.g. blood
and bone alkaline phosphatase, and liver arginase levels are significantly
changed.
 The only certain way of detecting moderate deficiency status is by measuring
response to supplementation.

Necropsy findings

 In congenital chondrodystrophy in calves, the limbs are shortened and all the
joints are enlarged.
 Histologically, there is poor cartilage maturation with excessive amounts of
rarefied cartilage matrix.
 There are degenerative changes in the chondrocytes and severe reduction in
the mucopolysaccharide content of all body hyaline cartilage.

Treatment and control

 Assuming typical DMI, a diet with approximately 14 mg Mn/kg DM will meet

the requirement for a 700 kg non -lactating cow during the last month of
lactation.
 For pigs, the recommended dietary intakes are 24-57 mg manganese per 45 kg
BW. Expressed as a proportion of food intake, the recommended dietary
level is 40 mg/kg DM in feed. The manganese requirements for gestation
and lactation are 20 ppm of the diet.

MODULE-15: DISEASES CAUSED DUE TO DEFICIENCY OF

CALCIUM, PHOSPHORUS AND MAGNESIUM

Learning objective

 To study the etiopathogenesis, clinical findings, treatment and control of Ca, P

& Mg deficiencies in animals.

CALCIUM DEFINICIENCY

Calcium

 About 99% of total body Calcium and 75% of body Phosphorus are found in
skeleton
 Teeth contains 80-85% of total P.
 70% Ash of the body contains Ca & p.
 Most of the calcium is present in extracellular fluid. Only minor portions are
in the body fluids.

67 | P a g e
Normal calcium metabolism

Functions in the Body

 Normal neuromuscular excitation.

 Capillary & cell membrane permeability
 Normal transmission of nerve impulse
 Normal blood coagulation
 Maintaining total body health
 Normal growth and development
 Keeping the heart beating
 Regulating blood pressure
 Metabolising iron
 In the physiological actions of a number of hormones (particularly those
associated with the thyroid and parathyroid glands)
 Cell structure and
 Absorbtion of vitamin B12.

Factors affecting calcium absorption

 As calcium level in the diet increases, serum calcium level increases.

 During pregnancy & Lactation, calcium absorption increases.
 As Age increases, absorption decreases
 Oxalate forms insoluble salt. So absorption is reduced
 Increased acidity increases absorption
 Ca : P ratio (in diet) also influences absorption

Factors affecting serum calcium levels

 Higher Estrogen levels interfere with Ca metabolism in bone.

 Hypomagnesaemia decrease Ca mobilization from bone
 Coliform mastitis – toxin decrease serum Ca & P levels.
 Parathyroid deficiency (fever, foot and mouth disease, trauma, aging, excess
Ca for prolonged period)
 Deficiency of vit D
 Unfavoured Ca/P ratio due to soil conditions
 Interference of acid pH

Disease conditions

 Rickets & Osteomalacia - Discussed under Vit D deficiency

 Osteoporosis: Osteoporosis occurs when the composition of the bone is
normal, but the mass is so reduced that the skeleton looses its strength and
becomes unable to perform its supporting role in the body. In this case,

68 | P a g e
 fractures may occur due to minor falls and bumps, or bones may even break
under their own weight.

PHOSPHORUS DEFICIENCY

 It is present in 4 forms in blood (Total phosphorus 14-15 mg.)

1. Ester phosphorous: ATP, Hexophosphate, Glycerophosphate
(in.R.B.C) and Diphosphoglycerate
2. Lipid phosphorous (5-8mg): Phosphatides, lecithin, cephalin,
sphingomyelin
3. Nucleic acid phosphorous : DNA & R.N.A
4. Inorganic phosphorous: Distributed in cell & plasma

Functions of phosphorous

 It is present 15-20% outside skeleton in soft tissue as organic ester

1. It is involved in vital cellular structure
2. Serves in degradation and synthesis of carbon compounds
3. High energy PO4 bonds play role in storage, liberation & transfer of
energy
4. Maintain acid – base balance by excreting as H2 PO4 or HPO4.
5. Bone formation

Epidemiology

 Widespread under natural conditions.

 Milking cows are more commonly affected.
 Heavy leaching by rain and constant removal by cropping may reduce P in soil
 Presence of phytic acids in plant tissues render phosphate unavailable.
 It is significant in carnivores and pig but not in herbivores.
 Deficiency is less in sheep than in cattle
 Excess Ca++ interfere as insoluble Ca2 (Po4)2
 Excess Mg++ also interferes
 Excreted in dung of cattle and in urine of Dog

Deficiency signs

 Common in cattle.
 Young animals grow slowly and develop rickets.
 Retarded growth, low milk yield and reduced fertility
 Cows in late pregnancy often become recumbent. Although, they continue to
eat but are unable to rise.
 Characteristic conformation – leggy appearance, narrow & slab sided chest,
small girth, small pelvis, fragile bones and rough & stairy coat

69 | P a g e
Control

 Daily requirements
o Cattle: 3-20 G/day
o Sheep: 2.5 – 3.5 G/day
o Ewes in lactation: 5G/150 lb
o Swine: 5-10 G / day twice daily during pregnancy.
 Provision of P supplements. (Bone meal, Dicalcium phosphate, Disodium
phosphate, Sodium pyrophosphate with feed or salt mixure).
 Monosodium dihydrogen phosphate (Monosodium orthophosphate): 10-20 g
/ 20 lit. water to drink
 Super juice: Plain Super phosphate @ 2.5 Kg / 40 lit water is mixed and
stirred vigorously and allowed to settle. 100-200 ml supernatant is
sprinkled on the feed of each cow.
o High phosphate containing sources: Bran, cottonseed, Linseed
meal, milk, gluten, Soya bean.

MAGNESIUM DEFICIENCY

 Common diseases due to hypomagnesemia in cattle are:

 Lactation tetany in cattle (please ref. chaper 6)
 Hypomagnesemic tetany ( please refe. chapter 7)

MODULE-16: DISEASES CAUSED DUE TO DEFICIENCY OF

SELENIUM AND VITAMIN E

Learning objectives

 To learn the diseases caused by Selenium and vitamin deficiency in domestic

animal species.
 To study the details about etiopathogenesis, clinical findings, diagnosis,
differential diagnosis, treatment, prevention and control of vit E and
selenium deficiency diseases.

SELENIUM DEFICIENCY

 Selenium is essential nutrient for animals. Diseases due to selenium

inadequacy are of world wide distribution and of economic importance.
 The biochemical role of selenium is as a component of the enzyme glutathione
peroxidase.
 The enzyme from the erythrocytes of both cattle and sheep contain 4 gm
atoms of selenium per mole of enzyme

70 | P a g e
 ETIOLOGY OF SELENIUM DEFICIENCY

 Selenium and vitamin E deficiency diseases of farm animals are caused by

diets which are deficient in selenium.
 Excessive poly unsaturated fatty acids in the diet is a conditioning factor
 Interaction between selenium and trace minerals may occur. Selenium and
vitamin E supplementation can provide protection against cobalt induced
cardiomyopathy. These diseases are associated with diets which are low in
selenium because of the selenium deficiency of soil on which they were
grown.
 Heavy neonatal mortality, unthriftiness in weaner calves, goat and lambs,
chronic diarrhea in calves, infertility due to foetal resorption in ewes,
dietetic hepatosis in swine are the important non specific diseases which
often responds to dietary supplementation with selenium and vitamin E.
 The pH of the soil: Alkalinity encourages selenium absorption by plants.
 Legumes take up less selenium than grasses.
 Seasonal conditions also influence the selenium content of the pasture.

PATHOGENESIS OF SELENIUM DEFICIENCY

 Dietary selenium, sulphur containing amino acids and vitamin E act

synergistically to protect losses from oxidative damage. Both vitamin E and
selenium deficiency in diet causes hyaline degeneration and calcification of
muscle fibers. Regeneration of skeletal muscle is rapidly followed by
invasion phagocytes and regeneration.
 Vitamin E (α tocopherol) serves as a biological anti-oxidant.
 During normal cellular metabolism-highly reactive forms of O2 (free radicals)
are produced. These include H2O2, hydro peroxides, lipoperoxides,
superperoxide, various hydroxyl radicals and single oxygen.
 Selenium is essential component of 5 selenoproteins. Glutathione peroxidase
enzyme, a deiodinase in liver and kidney converts T4 to T3 and
selenoprotein P.
 Anaemia is also caused by this deficiency in swine and affects the bone
marrow.
 Nutritional muscular dystrophy occurs commonly in young calves, lambs and
foals.
 Vitamin E is active within the cell membranes as a lipid soluble anti oxidant
scavenging free radicals that otherwise might react with unsaturated fatty
acids to form lipid hydro peroxidases.
 PUFA s contain high concentration of linolenic acid.
 Increased concentration of PUFAs in the plasma enhance the chance of free
radical formation and tissue damage.
 Vitamin E or selenium deficient animals may be at a greatly increased risk of
tissue oxidative damage when exposed to such diets.

71 | P a g e
  The myocardial and diaphragmatic form of the disease results in acute heart
failure, respiratory distress and rapid death inspite of treatment. Acute
muscular dystrophy results in liberation of myoglobin into the blood
resulting in myoglobinuria.
 Selenium and vitamin E deficiency in swine results in hepatic necrosis,
degenerative myopathy of cardiac and skeletal muscles, edema,
microangiopathy and yellowish discolouration of adipose tissue.

CLINICAL SIGNS AND PATHOLOGICAL CHANGES IN

SELENIUM DEFICIENCY

Clinical signs

 Acute muscular enzootic dystrophy affected animals die without premonitory

signs especially after exercise.
 Nutritional muscular dystrophy

Cardiac form

 Sudden onset, present with lesion in the heart, diaphragm and intercostal
muscles.
 Depression, respiratory distress-Dyspnoea, nasal discharge,blood stained-
pulmonary edema, profound weakness, recumbency, rapid often irregular
heart beat.
 Cardiac murmurs-occasionally on auscultation.
 Rectal temperature normal, but may be elevated because of increased
muscular work associated with respiratory efforts.
 Calves are depressed with dyspnoea, tachycardia and increased rectal
temperature.
 Differential diagnosis: pneumonia
 Death with in 24 hours despite medical therapy

Skeletal form

 Slower onset. Characterized by muscular weakness or stiffness, may be

recumbent, unable to stand. Those that are able to rise on their own or with
assistance show muscle weakness. Trembling of limb muscles or stiffness.
Supporting muscles of fore and hind limbs swollen, hard and painful on
palpation.
 Commonly affected muscles: Gastronemius, semitendinosus,
semimembranosus, biceps femoris and muscles of the lumbar, gluteal and
neck region.
 If diaphragm and intercostal muscles are affected- respiratory distress.
 Dysphagia-due to the involvement of tongue muscles, cardiomyopathy occurs

72 | P a g e
 often.
 Heart rate may be increased, but heart sounds are normal.
 Animals with skeletal NMD often responded to rest and treatment within 3-5
days; animals can often stand and walk.
 Differential diagnosis: Pneumonia, septicemia and toxemia may have similar
presenting signs.
 In calves: dullness and severe respiratory distress accompanied by frothy or
blood stained nasal discharge. Affected calves and foals are in lateral
recumbency and unable to sit in sternal recumbency even when assisted.
Heart rate increased to 150-200/minute. Affected calves are thirsty and die
within 6-12 hours after onset of signs. Temperature is normal.
 Sub acute enzootic muscular dystrophy in calves - 'white muscle disease' and
in young lambs- 'stiff lamb disease'. Affected animals will be in sternal
recumbency. Unable to stand, trembling of limbs, weakness, shoulder muscle
and gluteal muscles are swollen bilaterally, major involvement of diaphragm
and inter costal muscles occur in many cases and causes Dyspnoea and
abdominal type of respiration. Heart rate increased. In severe cases upper
border of the scapula protrude above the vertebral column and widely
separated from chest the toes are spread.
 In foals - edema of the head and neck are common. The horses may be
presented initially with clinical signs of colic.

Clinical pathology

 Plasma creatinine phosphokinase in muscular dystrophy of calves, lambs and

foals is of diagnostic value. The SGOT activity is also an indication of muscle
damage but not as reliable as CPK.

VITAMIN E AND SELENIUM DEFICIENCY IN SWINES

Mulberry heart disease

 Deficiency of selenium and vitamin E occur in rapidly growing feeder

pigs also recorded in piglets and sows.
 Affected animals are commonly found dead without premonitory signs.
 The stress of movement, inclement weather or transportation will precipitate
further acute deaths.

Hepatosis dietetica, exudative diathesis

 Most pigs found dead.Before death- Dyspnoea, depression, vomiting,

staggering, diarrhea, collapse.

73 | P a g e
  Muscular dystrophy
 Oesophago gastric ulcers cause ulcerations
 Exudative diathesis.

VITAMIN E AND SELENIUM DEFICIENCIES IN OTHER

ANIMALS

 Retained foetal membranes may be due to deficiency of selenium and / or

vitamin E deficiency
 Blood abnormalities - anaemia, decreased PCV and Hb.
 Myeloencephalopathy: associated with vitamin E deficiency.
 Neurological defects and degenerative myeloencephalopathy.
 Generalized steatitis associated with vitamin E and selenium- horses and
recently weaned foals.
 Fat necrosis, yellow fat disease, poly myositis and muscular dystrophy.

NECROPSY FINDINGS IN SELENIUM AND VITAMIN E

DEFICIENT ANIMALS

 Bilaterally symmetric myodegeneration is a consistent finding inNMD.

 Skeletal muscle degeneration is characterized by pale discoloration and a dry
appearance of affected muscles.
 White streaks in muscle bundles- represent bands of coagulation necrosis,
fibrosis and calcification.
 Cardiac muscles undergo changes similar to those of skeletal muscle.
 In calves, the left ventricle and septum are more frequently involved.
 Myocardial degeneration extends through full thickness of the ventricular
wall.

DIAGNOSIS OF SELENIUM DEFICIENCY

 By characteristic symptoms.
 By laboratory findings of CPK and SGOT.
 Confirmed by analysis of glutathione peroxidase.
 Estimation of selenium content in soil, feed samples and animal lesions.
 Enzootic muscular dystrophy may be easily confused with other diseases when
the myocardial or diaphragmatic involvement is severe. Dyspnoea and with
fever is difficult to distinguish from pneumonia.
 Differentiation from infectious diseases which cause septicemia, pneumonia
and toxemia is necessary.
 In acute muscular dystrophy, the serum CPK and SGOT levels are moderately
elevated.

74 | P a g e
  In lambs, differentiation from enzootic ataxia and sway back is necessary.

TREATMENT FOR SELENIUM AND VITAMIN E DEFICIENCY

 Combined mixture of selenium and α tocopherol is used in treatment.

 For muscular dystrophy in calves, lambs and foals - mixture of 3 mg selenium
(sodium selenite) and 150 I.U / ml of DL- α tocopherol acetate @2 ml / 45
kg body weight i/m
 Depending on the species and type of production, supplementation may be
accompanied in several ways.
o Selenium fertilization of soil
o Selenium top dressing of plants
o Addition of Selenium in feeds
o Oral drenching
o Selenium pellets
o Intramuscular injection
 Cardiac form: myocardial damage is extensive and incompatible with life.
 Skeletal form: amenable to treatment, but secondary complication due to
respiratory diseases develope.
 Supplementation with selenium and vitamin E. Injectable selenium products
is available with variable concentration.
o 1 mg to 5 mg /ml with 50 mg (68 I.U) of vitamin E.
o 0.055 to 0.067 mg / kg (2.50 to 3 mg / 45 kg body weight-
intramuscularly or S/C injection.
 Oral α tocopherol is now available for all species and contains 500 I.U vitamin
E / ml. The recommended dosage of this product is 1 to 3 I.U / lb body
weight (1 to 3 I.U / lb).
 Supportive therapy-antibiotics for secondary pneumonia and decubital
lesions. Fluids and electrolytes
 Properly prepared and stored hay grain (high quality green forage) should
ensure adequate vitamin E intake.

MODULE-17: VITAMIN B COMPLEX AND VITAMIN C

DEFICIENCY

Learning objectives

 To study the etiopathogenesis, clinical findings and diagnosis of vitamin B

complex and Vit C deficiency in animals
 To learn the differential diagnosis, treatment, prevention and control of
vitamin B complex and C deficiency in animals

THIAMIN DEFICIENCY

75 | P a g e
Etiology

 Thiamin deficiency may be primary, due to deficiency of the vitamin in the

diet, or secondary, because of destruction of the vitamin in the diet by
thiaminase.
 A primary deficiency is unlikely under natural conditions because most plants,
especially seeds, yeast, and milk contain adequate amounts.
 Thiamin is normally synthesized in adequate quantities in the rumen of cattle
and sheep on a well-balanced roughage diet. The degree of synthesis is
governed to some extent by the composition of the ration; a sufficiency of
readily fermentable carbohydrate causing an increase of synthesis of most
vitamins of the B complex and a high intake in the diet reducing synthesis.
 Microbial synthesis of thiamin also occurs in the alimentary tract of
monogastric animals and in young calves and lambs, but not in sufficient
quantities to avoid the necessity for a dietary supply, so that deficiency
states can be readily induced in these animals with experimental diets.

Pathogenesis

The only known function of thiamin is its activity as a co-carboxylase in the

metabolism of fats, carbohydrates and proteins and a deficiency of the vitamin leads
to the accumulation of endogenous pyruvates. Polio encephalomalacia has been
produced experimentally in preruminant lambs on a thiamin -free diet. There are
other prodromal indications of deficiency disease. For example, there is a decrease in
erthrocyte precursors and in erythrocyte transketolase. Additional clinical signs also
in the circulatory and alimentary systems, but their pathogenesis cannot be clearly
related to the known functions of thiamin. Subclinical thiamin deficiency due to
thiaminases in the alimentary tract is associated with low erythrocyte transketolase
activities and elevated thiamin pyrophosphate effects, which may explain the poor
growth rate.

Clinical findings

 Bracken fern (Pteridium aquilinum) and horsetail (Equisetum arvense)

poisoning in the horse - Incoordination and falling and bradycardia due to
cardiac irregularity, are the cardinal clinical signs of bracken fern poisoning
in the horse. These signs disappear after the parenteral administration of
thiamin.
 Swaying from side to side occurs first, followed by pronounced
incoordination, including crossing of the forelegs and wide action in the
hindlegs. When standing, the legs are placed well apart and crouching and
arching of the back are evident. Muscle tremor develops.
 Clonic convulsions and opisthotonos are the terminal stage.
 Appetite is good until late in the disease when somnolence prevents eating.

76 | P a g e
  Temperature is normal and the heart rate is slow until the terminal period
when both rise to above normal levels.

Clinical pathology

 Blood pyruvic acid levels in horses are raised from normal levels of 2-3
microg/dL to 6-8 microg/dL.
 Blood thiamin levels are reduced from normal levels of 8-10 microg/dL to 2.5-
3.0 microg/dL.
 Electrocardiograms show evidence of myocardial insufficiency.
 In pigs, blood pyruvate levels are elevated and there is a fall in blood
transketolase activity. These changes occur very early in the disease.

Differential diagnosis

 Diagnosis of secondary thiamin deficiency in horses must be based on the

signs of paralysis and known access to bracken fern or horsetail. A similar
syndrome may occur with poisoning by
o Crotalaria spp.
o Perennial ryegrass
o Indigofera enneaphylla
o Ragwort (Senecio jacobaea).
 It is accompanied by hepatic necrosis and fibrosis. The encephalomyelitides
are usually accompanied by signs of cerebral involvement, by fever and
failure to respond to thiamin therapy.

NICOTINIC ACID DEFICIENCY

 Nicotinic acid or niacin is essential for normal carbohydrate metabolism.

Because of the high content in most natural animal feeds, deficiency states
are rare in ordinary circumstances, except in pigs fed rations high in corn..
 A low protein intake exacerbates the effects of the deficiency, but a high
protein intake is not fully protective. In ruminants, synthesis within the
animal provides an adequate source.
 The daily requirements of niacin for mature pigs are 0.1-0.4 mg/kg BW, but
growing pigs appear to require rather more (0.6-1 mg/kg BW) for optimum
growth.
 At necropsy, hemorrhages in the gastric and duodenal walls, congestion and
swelling of the small intestinal mucosa, and ulcers in the large intestine are
characteristic and closely resemble those of necrotic enteritis caused by
infection with Salmonella spp.
 Experimental production of the disease in pigs by the administration of an
antimetabolite to nicotinamide causes ataxia or quadriplegia, accompanied
by distinctive lesions in the gray matter of the cervical and lumbar

77 | P a g e
 enlargements of the ventral horn of the spinal cord. The identical lesions
and clinical picture have been observed in naturally occurring disease.
 The oral therapeutic dose rate of nicotinic acid in pigs is 100-200 mg; 10-20
g/tonne of feed supplies sufficient nicotinic acid for pigs of all ages. Niacin
is low in price and should always be added to pig rations based on corn.

PYRIDOXINE (VITAMIN B6) DEFICIENCY

 A deficiency of pyridoxine in the diet is not known to occur under natural

conditions.
 Experimental deficiency in pigs is characterized by periodic epileptiform
convulsions and at necropsy by generalized hemosiderosis with a microcytic
anemia, hyperplasia of the bone marrow, and fatty infiltration of the liver.
 The daily requirement of pyridoxine in the pig is of the order of 100 microg/kg
BW or 1 mg/kg of solid food, although higher levels have been
recommended on occasions.
 Certain strains of chickens have a high requirement for pyridoxine and the
same may be true of pigs.

PANTOTHENIC ACID DEFICIENCY (HYPOPANTOTHENOSIS)

 Pantothenic acid is a dietary essential in all species other than ruminants,

which synthesize it in the rumen.
 Deficiency under natural conditions has been recorded mainly in pigs on
rations based on corn. Decrease in weight gain due to anorexia and
inefficient food utilization occurs first.
 Dermatitis develops with a dark brown exudate collecting around the eyes and
there is a patchy alopecia.
 Diarrhea and incoordination with a spastic, goose-stepping gait are
characteristic.
 Calcium pantothenate (500 microg/kg BW/d) is effective in treatment and
prevention. As a feed additive, 10-12 g/tonne is adequate.

BIOTIN (VITAMIN H) DEFICIENCY (HYPOBIOTINOSIS)

 Biotin or vitamin H has several important biochemical functions. It is a

cofactor in several enzyme systems involved in carboxylation and
transcarboxylation reactions and consequently has a significant effect on
carbohydrate metabolism, fatty acid synthesis, amino acid deamination,
purine synthesis, and nucleic acid metabolism.
 Biotin is found in almost all plant and animal materials and, being required in
very small quantities, is unlikely to be deficient in diets under natural
conditions, especially as microbial synthesis occurs in the alimentary tract.

78 | P a g e
 CATTLE BIOTIN

 Cattle Biotin is now considered a significant factor in lameness of cattle. Biotin

is important for the differentiation of epidermal cells which are required for
normal production of keratin and hoof horn tissue. Biotin also acts as a co-
factor in carboxylase enzymes and is an important factor in both
gluconeogenesis and fatty acid synthesis.
 Significant differences in the fatty acid profile of horn tissue of cattle with claw
lesions have been observed. Biotin supplementation reduces clinical white
line disease, reduces horn lesions, and improves horn quality by
strengthening the intercellular cementing material between keratinocytes.
 Improved hoof integrity in intensively managed dairy cows has occurred
following biotin supplementation. However, a long period of
supplementation is required before the effect of the vitamin on hoof health
care is expressed. In addition, there may be improved milk production, milk
composition, and cow fertility with biotin supplementation.
 Biotin is synthesized in the rumen and absolute biotin deficiency has not been
recognized. However, ruminal synthesis of biotin may be compromised by
acidic conditions in the rumen, which may increase the need for
supplementation of biotin in the diet of high-producing dairy cows.

DIARY COW BIOTIN

 In the dairy cow in the periparturient period and early lactation, the levels
of biotin may decrease. A decrease in plasma biotin levels of dairy cows at
25 days in milk (DIM), returning to constant levels from 100 DIM until the
end of lactation.
 Feeding supplemental biotin at 20 g/d during the last 16 days postpar tum
and at 30 g/d from calving through to 70 days postpartum elevated
concentrations of plasma and milk compared with cows unsupplemented
with biotin.
 Supplemental biotin also elevated plasma glucose and lowered nonesterified
fatty acids, which indicates that supplemental biotin is involved in hepatic
gluconeogenesis. The triacylglycerol concentration in liver tended to
decrease at a faster rate within 2 days after parturition.
 The supplementation of Holstein cows in the Atherton Tablelands in
Australia, with biotin at 20 mg/head per day resulted in improved
locomotion scores compared to unsupplemented cows in the wet summer
period. The number of lame cows observed by the farmer were significantly
fewer during the rainy period for the biotin-supplemented herds and
required fewer antibiotic treatments than unsupplemented herds.
 Supplementation with biotin reduced white line disease lameness by 45% in
multiparous cows down to 8.5 cases per 100 cow years, whereas the effect of
biotin supplementation in primiparous cows was not significant. A

79 | P a g e
 supplementation length of at least 6 months was required to reduce the risk
of white line lameness in multiparous cows. The overall incidence rate of
lameness (per 100 cows per year) was 68.9 with a range of 31.6 to 111.5 per
farm.
 Approximately 130 days of biotin supplementation is required before a
significant difference in white line lesion lameness occurs.
 A controlled 14- month field trial evaluated the effect of biotin
supplementation on hoof lesions, milk production and reproductive
performance of dairy cows housed in the same free-stall facility With the
same environment, base diet, and management.
 It is possible that biotin improves the quality of claw horn, which encourages
the replacement of defective horn, improves healing and makes it less likely
for sole lesions to develop from laminitis in its early stages.
 The administration of biotin at 40 mg per day for 50 days to dairy cows with
uncomplicated sole ulcers, resulted in significant improvement in
histological horn quality of the newly formed epidermis covering the sole
ulcer. Biotin supplementation at 20 mg/d did not affect the tensile strength
of the white line.
 Supplementary dietary biotin at 10 mg/head per day significantly increased
serum levels of biotin and increased claw hardness compared with
unsupplemented cows. After 18 months, only 15% of the biotin
supplemented cows had vertical fissures compared with 35 % in the
unsupplemented cows.

BIOTIN FOR PIG

 The principal source of biotin for the pig is the feed. Diets based on cereals
with a low available biotin content may provide insufficient dietary biotin
for the maintenance of hoof horn integrity in pigs.
 Continuous feeding of sulfonamides or antibiotics may induce a deficiency.
 An antivitamin to biotin (avidin) occurs in egg white and biotin deficiency can
be produced experimentally by feeding large quantities of uncooked egg
white.
 In pigs, experimental biotin deficiency is manifested by alopecia, dermatitis,
and painful cracking of the soles and the walls of the hooves.
 Supplementation of the diet of breeding sows with biotin at an early stage of
development makes a significant contribution to the maintenance of horn
integrity.
 Affected animals become progressively lame after being on a biotin-deficient
ration for several months. Arching of the back and a haunched stance with
the hindlegs positioned forward occurs initially. This posture has been
described as a 'kangaroo-sitting posture'. The foot pads become softer and
the hoof horn less resilient. The feet are painful and some sows will not
stand for breeding.

80 | P a g e
  The dewclaws also are affected by cracks and the accumulation of necrotic
tissue.
 Skin lesions also develop in affected gilts and sows. There is gradual alopecia,
particularly over the back, the base of the tail, and the hindquarters. The
hairs are more bristly than normal and break easily.
 As the lesions of the feet and skin develop there is a marked drop in the serum
biotin concentrations, which is considered as a sensitive index of biotin
deficiency. Adequate biotin status may be indicated by serum biotin levels
(ng/L) >700; marginal, 600-700; inadequate, 400-600; and deficient
below 400.
 Compression and hardness tests made on external hoof have also been used as
an indirect measure of biotin adequacy in pigs. The tests indicate that
significant improvements in the strength and hardness of pig hoof horn are
produced by biotin.
 Reproductive performance of sows is also influenced by their biotin status.
Supplementation of the diet with biotin may increase litter size, increase the
number of pigs weaned, decrease the mean interval in days from weaning to
service and improve conception rate. Over a period of four parities, piglet
production increased by 1.42 pigs/sow year.

BIOTIN FOR HORSE

 The dietary supplementation of horses with 10-30 mg biotin /day for 6-9
months is considered to be effective as an aid in the treatment of weak horn
hoof in horses.
 The hoof horn quality of more than two-thirds of the Lippizaner horses had
moderate to severe changes: microcracks visible in the transition from the
middle to the inner zone of the coronary horn; separation of the sole from
the coronary horn in the region within the white zone.
 Biotin supplementation for 19 months improved horn quality. Continuous
dietary supplementation with biotin at a daily dose of 20 mg is necessary to
improve and maintain hoof horn quality in horses

FOLIC ACID DEFICIENCY (HYPOFOLICOSIS)

 Folic acid (pteroylglutamic acid) is necessary for nucleic acid metabolism and
its deficiency in humans leads to the development of pernicious anemia. A
dietary source is necessary to all species and an adequate intake is provided
by pasture.
 The vitamin has a particular interest for equine nutritionists. Permanently
stabled horses and some horses in training may require additional folic
acid, preferably on a daily basis by the oral route.

81 | P a g e
  Folic acid deficiency can be induced in fetal foals and adult horses by
administration of folate orally coincident with administration of inhibitors
of folate metabolism (pyrimethamine trimethoprim, sulfonamides).

CHOLINE DEFICIENCY (HYPOCHOLINOSIS)

 Choline is a dietary essential for pigs and young calves. Calves fed on a
synthetic choline-deficient diet from the second day of life develop an acute
syndrome in about 7 days. There is marked weakness and inability to get
up, labored or rapid breathing, and anorexia. Recovery follows treatment
with choline.
 Older calves are not affected.
 On some rations, the addition of choline increases daily gain in feedlot steers,
particularly during the early part of the feeding period. Supplementation of
20 g/day of rumen protected choline to dairy cows 14 days before
parturition increased milk production during the first month of lactation
and the concentration of choline in milk.
 Choline increased tocopherol plasma concentrations. The NEFA
concentrations at the time of parturition were lower in treated animals than
in controls, indicating improved lipid metabolism.
 In choline deficient pigs, ataxia, fatty degeneration of the liver and a high
mortality rate occur. Enlarged and tender hocks have been observed in
feeder pigs.
 For pigs, 1 kg/tonne of food is considered to supply sufficient choline.
 Congenital splayleg of piglets has been attributed to choline deficiency but
adding choline to the ration of the sows does not always prevent the
condition.

VITAMIN B12 DEFICIENCY (HYPOCYANOCOBALAMINOSIS)

 Vitamin B12 deficiency is unlikely to occur under natural conditions other

than because of a primary dietary deficiency of cobalt, which is an
important disease in many countries of the world. Although microbial
synthesis of the vitamin occurs in the rumen in the presence of adequate
cobalt and in the intestines of other herbivores such as the horse, it is
probably a dietary essential in the pig and young calf. Animal protein is a
good source.
 A deficiency syndrome has been produced in young calves on a synthetic
ration. Signs include anorexia, cessation of growth, loss of condition, and
muscular weakness. The daily requirement under these conditions is 20-40
microg of vitamin B12.
 Sows vary in their ability to absorb the vitamin and those with poor
absorption ability, or on deficient diets, show poor reproductive

82 | P a g e
 performance. For pigs, 10-50 mg/tonne of feed is considered to be
adequate.
 The vitamin is used empirically in racing dogs and horses to alleviate parasitic
and dietetic anemias at a dose rate of 2 microg/kg BW.
 Cyanocobalamin zinc tannate provides effective tissue levels of vitamin B12
for 2-4 weeks after one injection.
 It is also used as a feed additive for fattening pigs, usually in the form of fish
or meat meal or as ' animal protein factor'.
 It is essential as a supplement if the diet contains no animal protein and
maximum results from the feeding of antibiotics to pigs are obtained only if
the intake of vitamin B12 is adequate.

VITAMIN C

 Vitamin C is synthesized by all species. Not an important dietary essential in

any of the domestic animals. Synthesis occurs in tissues and, although
blood levels fall after birth, in the newborn calf they begin to rise again at
about 3 weeks of age. Dermatosis of young calves has been associated with
low levels of ascorbic acid in their plasma and responds to a single injection
of 3 g of ascorbic acid.
 A heavy dandruff, followed by a waxy crust, alopecia and dermatitis
commences on the ears and spreads over the cheeks, down the crest of the
neck and over the shoulders.
 A single oral dose of 20 g of ascorbic acid does not result in any increase in
plasma concentrations. However, daily administration of either 4.5 g or 20
g results in significant increases in plasma concentrations.

MODULE-18: VITAMIN A, D AND K DEFICIENCY

Learning objectives

 To learn the diseases caused by vit A,D & K deficiencies in animals

 To study in detail about the etiology, epidemiology, pathogenesis, clinical
findings, diagnosis , differential diagnosis, treatment, prevention and
control of vit A,D & K deficiencies in animals

VITAMIN A DEFICIENCY

 Vitamin A and its metabolites play diverse roles in physiology, ranging from
incorporation into vision pigments to controlling transcription of a host of
important genes.
 Health depends on maintaining vitamin A levels within a normal range, as
either too little or too much of this vitamin lead to serious disease.

83 | P a g e
 AETIOLOGY AND PATHOGENESIS OF VITAMIN A
DEFICIENCY

Hypovitaminosis - A

 Insufficient supply of the vitamin A in the ration (or) defective absorption

from the alimentary canal.

Etiology

 Primary Vitamin A deficiency

o Major economic importance in groups of animals on pasture or fed
diets deficient in the Vitamin A or its precursors.
o Ruminants on pasture or dry range pasture during periods of
drought.
o Maternal deficiency of Vitamin A can result in herd outbreak of
congenital hypovitaminosis A in calves.
o Adequacy of supplements to diets not always be sufficient to prevent
deficiency.
 Secondary Vitamin A deficiency
o Occur in cases of chronic disease of the liver or intestines because of
lack of conversion of carotene to Vitamin A occur in the intestinal
epithelium and the liver is the main site of storage of the vitamin.
o Intake of inorganic P also affects Vitamin A storage.
o Vitamin E and C help to prevent loss of Vitamin A in feed stuffs.

Pathogenesis

 Night vision
o Ability to see in dim light is reduced because of interference with
regeneration of visual purple.
 CSF fluid pressure
o Increase in CSF pressure is due to impaired absorption of the CSF
due to reduced tissue permeability of the arachnoid villi and
thickening of the connective tissue matrix of cerebral duramater.
 Bone growth
o Vitamin A is necessary to maintain normal position and activity of
osteoblasts and osteoclasts.
o If deficiency occurs there is no retardation of endochondral bone
growth in that shaping, especially the finer molding of bones, does
not proceed normally.
o Overcrowding of the cranial activity occur with resulting distortion
and herniation of the brain and an increase in CSF pressure upto 4-6
times normal.

84 | P a g e
  Epithelial tissues
o Vitamin A deficiency leads to atrophy of all epithelial cells.
o The secretory cells are gradually replaced by the stratified,
keratinizing epithelial cells common to non-secretary epithelial
tissues.
o This replacement of secretory epithelium by keratinized epithelium
occurs chiefly in the salivary glands, the urogenital tract the para-
ocular gland and teeth.
 Embryological development
o Vitamin A essential for organ formation during growth of the fetus.
o Constriction of the optic canal with thickening of the duramater
results in ischemic necrosis of the optic nerve and optic disc edema
resulting in blindness.
 Immune mechanisms
o Vitamin A and β carotene afford protection against infection by
influencing both specific and non specific host defense mechanisms.

CLINICO-PATHOLOGICAL FINDINGS IN VITAMIN A

DEFICIENCY

Clinical findings

 Night blindness
 Xerophthalmia -- thickening and clouding of the cornea in calf
 Thin, serous mucoid discharge, corneal keratinization, clouding, ulceration
and photophobia in other animals.
 Changes in the skin
o A rough, dry coat with a shaggy appearance and splitting of the bristle
tips in pigs.
o Heavy deposits of bran like scales on the skin-cattle
o Dry, scaly hooves – horse.
 Body weight
o Inappetance, weakness, stunted growth and emaciation.
 Reproductive efficiency
o In male – libido is retained but degeneration of the germinative
epithelium of the seminiferous tubules cause reduction in the number
of motile, normal spermatozoa produced.
o In female – placental degeneration leads to abortion the birth of dead
or weak young one.

Nervous system

 Paralysis of skeletal muscle due to damage of peripheral nerve roots.

 Encephalopathy

85 | P a g e
  Blindness.
 Convulsion -Common in beef calves at 6-8 months
 Affected calves are usually not blind and the menace reflex may be slightly
impaired.
 Some calves are hyper-aesthetic to touch or sound.
 Blindness -- Usually occur up to 2-3 years of age. Both pupils are widely
dilated and fixed and will not respond to light.
 Varying degrees of peripapillary retinal detachment, papillary and
peripapillary retinal hemorrhage and disruption of the retinal pigment
epithelium.
 Menace reflex totally absent.
 Palpebral and corneal reflex present.

Congenital defects

 In pigs

Clinical pathology

 Plasma Vitamin A
o Cattle - 25-60 mg / dl
o pigs - 23-29 mg/dl
o Lambs - 45.1 mg/dl
 Plasma retinol
o Useful for horses - normal 16.5 mg/dl
 Plasme carotene
o Useful for cattle – normal 150 mg/dl
 CSF
o Vitamin A deficiency increases CSF pressure . In cattle :-Normal < 100
; in deficiency, it will rise to 200 mm
o Pig -normal 80-145 mm it will rise above 200 mm
o Sheep - normal 55-65 mm; it will rise to 70-150 mm.

Necropsy

o Squamous metaplasia of interlobular ducts of parotid gland

o Compression of optic nerve tracts and spinal nerve root
o Degeneration of testes

DIAGNOSIS, TREATMENT AND CONTROL IN VITAMIN A

DEFICIENCY

Diagnosis

86 | P a g e
The condidtions to be included in differential diagnosis are:

 Cattle
o Polioencephalomalacia
o Hypo-magnesemic tetany
o Lead poisoning
o Rabies
o Meningo-encephalitis.
o Peripheral blindness due to bilateral opthalmitis.
 Swine
o Salt poisoning
o Pseudo rabies
o Viral encephalomyelitis
o Spinal cord compression.

Treatment

 Vitamin A deficiency is treated immediately at a dose rate equivalent to 10-20

times the daily maintenance
 440 IU/kg b.wt.

Control

 Daily requirement – 40 IU/kg b.wt.

 During pregnancy & Lactation by 50-75% of the requirements.
 Supplementation method.
 By parentral inj- I/m injection of Vitamin A at an interval of 50-60 days at the
rate of 3000-6000 IU/kg b.wt.
 Oral vitamin A- Single bolus of Vitamin A at a dose of 2.8 mg /Kg B.wt. in dry
season.
 To raise milk levels – adding 10g of powder to the drinking water.

VITAMIN D DEFICIENCY

Diseases due to Vit. D deficiency

 Rickets in calves.
 Osteomalacia in adults.

Vitamin D or its precursors enter the body by 3 routes

 By solar radiation.
 Vitamin D can be added to the milk or in milk replacers fed to calves and in
concentrates for adult cattle.
 Ultra violet irradiation .

87 | P a g e
Signs

 Clinically the important effect of vitamin D deficiency is defective growth and

mineralization of bones.
 Non specific signs include poor productivity, stunted growth and lameness.
 The joints enlarged and the growth plate thickens with uncalcified cartilage.

RICKETS

 A disease of growing animals.

 Man, apes, birds and rats but not in swine .
 It is due to failure of calcium salts to be deposited promptly in the newly
formed bone matrix.
 Defective encdochondral mineralization of the zone of provisional calcification
of the long bones.
 Miscellaneous group of Ca and P deficiency

Causes

 In adequate supply of Ca and/or P and / or vit D. For proper mineralization of

bones, osteoid requires ions of Ca & ionised P as HPO4 in blood.
 Low calcium absorption due to Gastroenteritis, lack of Vit.D and formation of
insoluble calcium salts.
 Absorption of Ca is influenced by dietary Ca:P ratio.
 Skeletal deformities due to other diseases eg. Canine distemper

Clinical signs

 G.I disorders.
 Bronchitis.
 Generalised tenderness.
 Restlessness.
 Emaciation.
 Tiredness in puppies.
 Occasional convulsion or tetany.
 Walking in wrist than toes due to weakness of flexor tendons.
 Recumbency.
 Failure to grow.
 Bone: Bowing of legs outward, , knobs on ribs (racketty rosary)
 Body is too heavy to legs.
 Epiphyses of long bones are swollen.
 Long bones bend; Metacarpus – thin and crouching in goat.
 Ribs – bend inwards – so on both the side of thorax, there is longitudinal
shallow groove.

88 | P a g e
  Pelvis – Acetabulum is pressed upwards & inwards by head of femur so,
constriction of pelvis.
 Vertebrae- various deformities. Hence, it is called Rachitis.
 Scoliosis, kyphosis, lordosis or 2 or 3 antagonistic curves.
 Skull: Thickening and deformity of Ramii of inferior maxillary region,
difficulty in respiration, Asphyxia as facial bone bulges.

Differential diagnosis

 Distemper: Nasal or ocular discharge if there is involvement of G.I. tract

 Muscular Rhematism: No enlargement in bones
 Tumour: Individual bone only involved.

Treatment

 Ration containing Calcium 1.2% and Phosphorus 0.8%. (Ratio 1.5:1) with
vitamin D supplement.
 Add 0.5 gm Calcium carbonate for every 100 gm of meal fed.
 Feed with organic meats like liver, kidney & heart
 Give cod liver oil
 Cortisone and Calcium supplements.
 Avoid Continuous yeast or Liquid paraffin.

RICKETS

 A disease of growing animals.

 Man, apes, birds and rats but not in swine .
 It is due to failure of calcium salts to be deposited promptly in the newly
formed bone matrix.
 Defective encdochondral mineralization of the zone of provisional calcification
of the long bones.
 Miscellaneous group of Ca and P deficiency

Causes

 In adequate supply of Ca and/or P and / or vit D. For proper mineralization of

bones, osteoid requires ions of Ca & ionised P as HPO4 in blood.
 Low calcium absorption due to Gastroenteritis, lack of Vit.D and formation of
insoluble calcium salts.
 Absorption of Ca is influenced by dietary Ca:P ratio.
 Skeletal deformities due to other diseases eg. Canine distemper

Clinical signs

 G.I disorders.

89 | P a g e
  Bronchitis.
 Generalised tenderness.
 Restlessness.
 Emaciation.
 Tiredness in puppies.
 Occasional convulsion or tetany.
 Walking in wrist than toes due to weakness of flexor tendons.
 Recumbency.
 Failure to grow.
 Bone: Bowing of legs outward, , knobs on ribs (racketty rosary)
 Body is too heavy to legs.
 Epiphyses of long bones are swollen.
 Long bones bend; Metacarpus – thin and crouching in goat.
 Ribs – bend inwards – so on both the side of thorax, there is longitudinal
shallow groove.
 Pelvis – Acetabulum is pressed upwards & inwards by head of femur so,
constriction of pelvis.
 Vertebrae- various deformities. Hence, it is called Rachitis.
 Scoliosis, kyphosis, lordosis or 2 or 3 antagonistic curves.
 Skull: Thickening and deformity of Ramii of inferior maxillary region,
difficulty in respiration, Asphyxia as facial bone bulges.

Differential diagnosis

 Distemper: Nasal or ocular discharge if there is involvement of G.I. tract

 Muscular Rhematism: No enlargement in bones
 Tumour: Individual bone only involved.

Treatment

 Ration containing Calcium 1.2% and Phosphorus 0.8%. (Ratio 1.5:1) with
vitamin D supplement.
 Add 0.5 gm Calcium carbonate for every 100 gm of meal fed.
 Feed with organic meats like liver, kidney & heart
 Give cod liver oil
 Cortisone and Calcium supplements.
 Avoid Continuous yeast or Liquid paraffin.

OSTEOMALACIA

 Horses, cattle and pigs

are affected.
 Pregnant and lactating
animals are more prone.
 Lameness and pathological fracture are common clinical findings.

90 | P a g e
Etiology

 Horse - dietetic: wide Ca:P ratio 1

:2.
 Cattle: It is primary not secondary; Vit D is not having much role.;Mostly
animals kept in stall.

Pathogenesis

 Softening of mature bone due to extensive resorption and failure of

mineralization of newly formed matrix.
 There are no enlargement at the ends of long bones but spontaneous fracture.
 Osteodystrophia fibrosa: - excessive resorption of bones and replacement by
connective tissue.
 Secondary hyperthyroidism resulting in swelling of mandible, maxilla &
frontal bone (Big Head) and spontaneous fracture of long bones & ribs.

Physical changes

 Cattle: Epiphysitis, vertebral exostosis usually T2 and T12 ,

L2 – L3.
 Old bulls which will have more pressure during breeding – Fusing of vertebrae
(spondylitis) occurs.
 Horse also fusing of vertebrae degeneration of intra vertebral disc.

Symptoms

Cattle

 First licking the soil , faeces and urine then formation of body deformities.
 Stunted, head is bigger, perverted appetite, crooked legs, cracking sound in
points.
 Lack of growth and production, stiff Limb and swollen joints and easy fracture
in hip and ribs.
 Tail will become soft and it can be coiled like rope, sterility, peculiar gait,
arched back in lumbar vertebrae, recumbent due to pain or due to fracture
of pelvic bones.

Horse

 Head larger.
 Roof of the mouth bulging in oral cavity not able to
close, look like maxillary
paralysis difficult mastication, some time Blood stain in the tongue.
Narrowing of Nasal passage – snoring asphyxia.

Diagnosis

91 | P a g e
  X-ray – Horse Extreme porosity of entire skeleton.
 Blood chemistry: Ca:P normal for long time in severe cases alkaline
phosphatase increased. serum inorganic P 1.3 to 1.6 mmol/L to 0.48 to 1.13
mmol/L.
 Histopathology of bone biopsy.

Treatment

 Dicalcium Po4 @ 3-4 times the daily requirement for 6 days, orally. The slow
reduction until 10th day with vit D @ 10,000 I.U / kg b.wt.

VITAMIN K DEFICIENCY

 A primary deficiency of vitamin K is unlikely under natural conditions in

domestic animals because of the high content of substances with vitamin K
activity in most plants and the substantial synthesis of these substances by
microbial activity in the alimentary canal.
 Sporadic cases may occur when impairment of the flow of bile reduces the
digestion and absorption of this fat-soluble vitamin.
 Experimental vitamin K deficiency in piglets is manifested by hypersensitivity,
anemia, anorexia, weakness, and a marked increase in prothrombin time.
The minimum daily requirement for newborn pigs is 5 micro g/kg BW and
the minimum curative injection dose is four times larger.
 A hemorrhagic disease of recently weaned pigs from 6 to 15 weeks of age is
considered to be associated with vitamin K deficiency. Affected pigs fail to
grow, pale, develop large subcutaneous hematomas, lameness and epistaxis.
Excessive and fatal hemorrhage following routine castration may occur in
pigs from 30 to 40 days of age, but not at 15-20 days of age. Subcutaneous
massive hemorrhage is more common in pigs at 40-70 days of age.
 Prothrombin time and activated partial thromboplastin time are prolonged
along with decreased levels of vitamin K-dependent factors II, VII, IX, and
X.
 At necropsy, hemorrhages are extensive in the muscles of the hindlimbs,
forelimbs, and axillary and mandibular region.
 Vitamin K, or vitamin K2, given at a dose of 3 mg/kg BW IM as a single dose
will restore the blood coagulation defects to normal. Vitamin K3 added to
the feed at a rate of 25 mg/kg for 4 days was also effective.
 The most important therapeutic use of vitamin K in domestic animals is in
sweet clover poisoning where toxic quantities of coumarin severely depress
the prothrombin levels of the blood and interfere with its clotting
mechanism.
 Industrial poisons used in rodent control which contain anticoagulants of the
coumarin type, e.g. warfarin, cause fatal hypothrombinemia; vitamin K is
an effective antidote.

92 | P a g e
  For warfarin - inducedanticoagulation in the horse, the administration of
300-500 mg of vitamin K S/C every 4-6 h until the prothrombin time
retums to baseline values is recommended.

MODULE-19: DISEASES OF NEONATES

Learning objectives

 To learn the etio-pathogenesis and clinical findings of neonatal diseases

 To study various neonatal diseases in calves, lambs and dogs
 To understand the diagnosis, treatment , prevention and control of neonatal
diseases

NEONATAL DISEASES

 This chapter considers the principle of the diseases which occur during the
first month of life in animals born alive at term.
 The need for the chapter arises out of the special sensitivities which the
newborns have
o Their immunological incompetence.
o Their dependence on adequate colostrum containing adequate
antibodies at the right time.
o Their dependence on frequent intake of readily available
carbohydrate to maintain energy.
o Their relative inefficiency in maintaining normal body temperature,
upwards or downwards.

Diseases

o Calf hood diseases

o Diseases of neonatal lambs and kids
o Neonatal diseases of foals
o Diseases of neonatal pups
o Neonatal diseases of piglets

CALF HOOD DISEASES

 These are divided into

o Early postnatal diseases (within 48 hours of birth)
o Delayed postnatal diseases (2-7 days of age)
o Late postnatal diseases (1-4 weeks of age)

Early postnatal diseases

93 | P a g e
  Most diseases occurring in this period are non-infectious and metabolic. Eg.
Hypoglycemia and hypothermia due to poor mothering.
 Hypothermia due to exposure to cold and low vigor in neonates due to
malnutrition
 Congenital diseases
o Neonatal rickets
o Goiter
o Croocked calf disease

Delayed postnatal disease

 It is due to failure of passive transfer of colostral immunoglobins.

o Colibacillosis
o Joint ill
o Salmonellosis
o Viral enteric Infections
 Rota virus
 Corona virus

Late postnatal diseases

 Septicemic disease
 Enteric disease
 Respiratory disease
 Cryptosporidiosis
 White muscle disease
 Ascariasis

GENERAL EPIDEMIOLOGY

 Determine the duration of pregnancy to ensure that the animals were born at
term
 Collect the epidemiological information on the problem
o What is the abnormality?
o What is the apparent age at onset? And the age at death.
o What clinical signs are consistently associated with the problem?
o What is the prevalence in particular group?
o What is the birth history of affected animals? Has there been any
difference in management of the dams of the affected animals?
o What is the farm policy for feeding of colostrum?
o What have been the environmental conditions during the past 48
hours; conduct a post mortem examination of all available dead
neonates.

94 | P a g e
 DIAGNOSIS

 Anamnesis
 Clinical signs
 Hematology
 Serum biochemical profile
 Urinalysis
 Imaging techniques
 Serology
 Blood culture

CRITICAL CARE OF THE NEWBORN CALF

Critical care of the newborn calf

General principles are:

 Initial assessment and monitoring

 Nursing care
 Nutritional support
 Antimicrobial treatment (aminopenicillins and cephalosporin)
 Fluid therapy
 Respiratory support
 Intestinal protectant

Principles of control and prevention of infectious diseases of neonatal calves

 Removal of the cause of the disease from the environment of the new born.
 Removal of the newborn calf from the infectious environment if necessary.
 Increasing and maintaining the non specific resistance of the newborn
through colostrum as soon as possible.
 Increasing the specific resistance of the newborn through the use of vaccines.

DISEASES OF NEONATAL LAMBS

 Hypothermia / hypoglycemia / starvation complex

 Lamb dysentery
 Enteric disease
 Septicemic disease
 Respiratory disease

NEONATAL DISEASES OF FOALS

 Neonatal isoerythrolysis

95 | P a g e
  Neonatal mal adjustment syndrome

NEONATAL ISOERYTHROLYSIS

 Definition
o Hemolytic anemia of newborn foals occurs because of immune –
mediated destruction of the neonate’s red blood cells by antibodies
acquired from the dam.
 Etiology
o Maternal alloantibodies to neonate's blood group antigens are
transferred to the neonate in colostrum and cause lysis of the
neonate’s red blood cells.
 Epidemiology
o Disease in progeny of multiparous mares. The dam lacks blood group
antigens possessed by the sire and inherited by the foal.
o The majority of cases in foals are due to the presence of Aa or Qa
antigens
 Pathogenesis
o The interaction between the antibody and the red cells of the
newborn is followed by hemolysis with resultant anemia,
hemoglobinuria and jaundice.
 Clinical signs
o Peracute cases develop within 8-36 hours of birth and the first
indication of the disease may be collapse. Severe hemoglobinuria and
pallor are evident but icterus is not apparent initially. The mortality
rate is high.
o In acute cases, signs do not develop until 2-4 days after birth and
jaundice is marked, with only moderate pallor and hemoglobinuria.
o Subacute cases may not show signs until 4-5 days after birth.
Jaundice is marked but there is no hemoglobinuria and only mild
pallor of mucosae.
o General signs include lassitude, weakness and disinclination to suck.
The foal lies down in sternal recumbency for long periods. There is
no febrile reaction but tachycardia and tachypnea. Terminally
dyspnea and convulsions may develop.
 Clinical pathology
o Hematological examination reveals acute anemia ( decreased Hb,
PCV and TEC).
o Depending on the severity of the disease and its duration, there may
be leukocytosis, neutrophilia, monocytosis and the presence of
nucleated red blood cells
o Serum biochemical analysis reveals an increased serum
concentration of unconjugated bilirubin.
 Diagnosis

96 | P a g e
 Anamnesis
o
o Clinical signs
o Clinico- pathological findings
o Direct Coomb’s test:
 A positive direct antiglobulin test, confirming the presence of
antibodies on the surface of red blood cells in foals with
anemia.
 Treatment
o The aim of treatment is to
 Prevent the deleterious effects of anemia
 Prevent or treat hemoglobinuric nephrosis
 Prevent secondary infection in severely ill animals
 Restore normal fluid, electrolyte and acid – base status
 Provide adequate nutrition
 Minimize stress
 Control
o The principles of control are
 Identification of incompatible matings by blood group typing
 Identification of risk foals by testing of mare serum or colostrum
for the presence of alloantibodies directed against blood
factors possessed by the foal

NEONATAL MAL ADJUSTMENT SYNDROME OF FOALS

 Synonyms – dummy foal, barkers and wanderers

 Definition
o This is a disease of foals less than 36 hours of age characterized by
changes in mentation, failure to suckle and abnormal behavior
occurring as a result of peri-partum hypoxia or cerebrovascular
accidents.
 Etiology
o The etiology is unknown, but is believed to involve antenatal, natal or
postnatal hypoxia due to placental abnormalities, intracranial
hemorrhages or thoracic trauma during birth
 Epidemiology
o The disease is sporadic and occur world wide with annual incidence
of approximately 1%. The case fatality rate for foals affected at birth
is as high as 80% while for those with delayed onset of signs it is
approximately 50%.
 Pathogenesis
o It is speculated that hypoxia resulting from intracranial vascular
accidents, asphyxia at birth or placental insufficiency before birth
damages the central nervous system. Neurological abnormalities and
failure to nurse causes failure of transfer of maternal

97 | P a g e
 immunoglobulin, predisposing the foal to septicemia and
hypoglycemia.
 Clinical signs
o Foals that are abnormal at birth can display a range of behavioral
abnormalities from lack of suckle reflex to convulsions with extensor
rigidity.
o Aimless wandering and a characteristic barking vocalization is
sometimes present.
o Recumbent foals may struggle wildly and in an uncoordinated
fashion to stand.
o Convulsive foals usually display opisthotonos with extensor rigidity.
Other signs of convulsive activity include facial twitching,
nystagmus, rapid blinking, chewing and drooling.
o Convulsive foals are tachypnic, tachycardic and hyperthermic during
and immediately after convulsions.
o Foals that are normal at birth may develop signs by 24 hours of age.
The signs are similar to those described above.
 Clinical pathology
o There are no hematological or serum biochemical abnormalities
characteristic of the disease
 Diagnosis
o Definitive diagnosis of the disease is difficult and is based on
exclusion of other diseases that can cause similar signs and at
necropsy demonstration of intracranial lesions consistent with the
disease.
 Treatment
 The principles of treatment are
o Control of convulsion
o Treatment of cerebral edema and hemorrhage
o Correction of failure of transfer of passive immunity
o Nutritional support and general nursing care
 Control
o Prevention of hypoxia in neonates by close monitoring of the health of
the mare and of parturition may reduce the incidence of the disease.

FADING PUPPY SYNDROME / FADING PUPPY COMPLEX

 Definition
o Fading puppy syndrome is a term used to describe the failure of
young puppies to survive in the first 2-3 weeks of life and their
ensuring death without any obvious cause.
 Etiology
o Known causes – 45%
o Unknown causes – 55%

98 | P a g e
  Known causes
o Nutritional – maternal / management linked causes leadind to
starvation
o Infection – (Bacterial, viral and parasitic)
o Very low birth weight
o Hypothermia
o Prematurity
o Congenital abnormality
o Low lung surfactant (phosphatidylcholine)
 Pathogenesis: Not known
 Clinical signs
o Lassitude
o Absence of sucking reflex
o Restlessness
o Crying
o Lateral recumbency with limb peddling
o General weakness
o Death
 Diagnosis
o History
o Physical examination
o Hematology
o Serum bio-chemical profile
o Pm findings
o Urinalysis
o Urine and blood culture
o Estimation of lung surfactant in dead puppies
 Treatment
o Specific treatment for infection
 Amoxicillin clavulanate 12.5 – 25 mg / kg- orally BID
o Proper management practice
o Supportive therapy

NEONATAL DISEASES OF PIGLETS

 Baby pig disease / neonatal hypoglycemia

 Piglet anemia

BABY PIG DISEASE/NEONATAL HYPOGLYCEMIA

Etiology

 An inadequate intake of milk is the primary cause of hypoglycemia in piglets.

This may be due to failure of the piglets to suck. Failure to suck may be due

99 | P a g e
 to such disease as coliform septicemia, transmissible gastroenteritis (TGE),
streptococcal infections, myoclonia, congenital and hemolytic disease of the
newborn.
 Piglets under 4 days of age rapidly develop hypoglycemia under fasting
conditions

Pathogenesis

 The piglet is born with

o Liver glycogen level 20mg / gww
o Muscle glycogen level 120mg/ gww
o Blood glucose at a low level of 30-60 mg/dL.

Clinical findings

 The disease is most characteristic in piglets under a few days of age.

o Incoordination
o Shivering
o Dullness
o Anorexia
o Subnormal temperature
o Cold, clammy skin
o Marked pallor and ruffling of the hair
o The heart beat may fall as low as 80/min
o Tetanic convulsion
o Aimless movements
o Opisthotonos

100 | P a g e
 o Champing of the jaws
o Tortuous movements
o Rigidity of the neck and trunk
o Terminally coma and death

Diagnosis

 Anamnesis : below 4 days piglet

 Clinical signs
 Clinical pathology
o Blood glucose < 40 mg/dl
o Significant rises in blood urea nitrogen

Treatment

 20% dextrose 15ml I.P.

 protection from cold is important and environmental temperature of 27-32oC
will improve the survival rate of piglets.

Control

 Avoidance of the causative factors described earlier constitutes prevention.

PIGLET ANEMIA

Definition

 Iron deficiency causes anemia and failure to thrive occurs commonly in young
sucking piglets maintained indoor with no access to iron/ supplementation
in diet.

Etiology

 Dietary deficiency of Iron

 Iron deficiency anemia occurs in nursing piglets for three reasons
o They do not have access to soil, which is a main source of iron for
young farm animals
o They grow rapidly and their absolute requirements for iron are high
o Milk is a poor source of iron

Pathogenesis

101 | P a g e
  Iron deficient piglets appear to be more susceptible to diarrhea at about 2
weeks
 A marked impairment of gastric acid secretion leading to atrophic gastritis
occurs in iron deficient piglets
 Villous atrophy of small intestine and changes in gastro intestinal flora also
occur in iron deficient piglets

Clinical signs

 Growth rate is reduced

 Feed intake is reduced
 A mild diarrhea may occur
 Dyspnea, lethargy and marked increase in amplitude of the apex beat of the
heart can be felt after exercise
 The skin and mucosa are pale
 Edema of the head and fore quarters, giving the animal a fat, puffed – up
appearance may be present
 Sudden death

Diagnosis

 Nutritional history
 Clinical signs
 Clinico-pathological findings
o Decreased Hb 8g / dl
o TEC 3-4 x 1012/L

102 | P a g e
Treatment

 Inj. Imferon 15mg / piglet/day (For 3-7 days of age).

Control

 Allow the piglets on pasture

 Feeding of sow with feeds containing 20 g iron/day
 Painting of the sow udder
o FeSO4 - 450 gr
o CuSO4 - 75 gr
o Sugar - 450 gr
o Water - 2 liters
 The administration of iron dextron to the piglets at a few days of age is
preventive and is a routine health management strategy in modern swine
production
 Feeding sows a diet supplemented with 200 mg iron/kg DM of diet will
satisfactorily prevent iron deficiency anemia in the piglets.

MODULE-20: DISEASES OF MUSCLES

Learning objectives

 To learn the etiopathogenesis of the muscle diseases

 To study the clinical findings, diagnosis and treatment of muscle diseases in
animals

MYASTHENIA (SKELETAL MUSCLE ASTHENIA)

 The common causes of myasthenia in farm animals are

o Ischemia in iliac thrombosis in the horse and after recumbency in
cows with parturient paresis. The end stage of myonecrosis and not
reversible.
o Toxins: general toxemia is a cause
 Metabolic effect on muscle fibers include hypokalemia, hypocalcemia and
possibly hypophosphatemia, hypoglycemia in new born pigs and lactic
acidemia after engorgement of grains.

ETIOLOGY AND PATHOGENESIS OF MYOPATHY

Myopathy

103 | P a g e
  The term myopathy describes the non inflammatory degeneration of skeletal
muscles which is characterized clinically by muscle weakness and
pathologically by hyaline degeneration of the muscle fibers.

Etiology

 A nutritional deficiency of vitamin E and selenium ( enzootic nutritional

muscular dystrophy) is a common cause in calves, lambs, foals and piglets.
 Exertional or post exercise rhabdomyolysis in horses after unaccustomed
exercises or insufficient training.
 Degenerative myopathy – in new born calves, sheep and goats.
 Toxic agents
 Ischemia
 Neurogenic
 Neoplasms

Pathogenesis

 The characteristic change in most cases of primary myopathy varies from

hyaline degeneration to coagulative necrosis, affecting particularly the heavy
thigh muscles and the muscles of the diaphragm.
 Myocardial lesions are also commonly associated with the degeneration of
skeletal muscles and when severe will cause rapid death within a few hours
or days.
 The visible effects of the lesions are varying degree of muscle weakness,
muscle pain, recumbency, stiff gait, inability to move the limbs and
development of respiratory and circulatory insufficiency.
 Because of the necrosis of the muscle, myoglobin is excreted in the urine and
myoglobinuric necrosis is an important complication, particularly of acute
primary myopathy.
 In Exertional rhabdomyolysis in horses there is enhanced glycolysis with
depletion of muscle glycogen, the accumulation of large amount of lactate in
muscle and in blood and development of hyaline degeneration of myofibers.
 In Secondary myopathy due to ischemia, there may be multiple focal areas
of necrosis which cause muscle weakness and results in an increase of
muscle enzymes in the serum.
 In neurogenic atrophy of muscle, there is flaccid paralysis, a marked
decrease in total muscle mass and degeneration of myofibers with failure to
regenerate unless the nerve supply is atleast partially restored.

CLINICAL FINDINGS OF MYOPATHY

Primary myopathy

104 | P a g e
  Sudden onset of weakness and pseudoparalysis of the affected muscles,
causing paresis and recumbency and in many cases accompanying
respiratory and circulatory insufficiencies.
 Cardiac irregularity and tachycardia may be evident, and myoglobinuria
occurs in horse and yearling cattle.
 The affected skeletal muscles in acute cases may feel swollen, hard and
rubbery but in most cases it is difficult to detect significant abnormality by
palpation.
 Acute cases of primary myopathy may die within 24 hours after the onset of
signs.

Acute nutritional myopathy

 Muscle stiffness and pain, myoglobinuria, edema of the head and neck,
recumbency and death in a few days.
 Lethargy and stiffness of gait are characteristic of less acute cases.

Tying-up

 In Tying – up in horses there is a very sudden onset of muscle soreness 10 -20

minutes following the exercise. There is profuse sweating and the degree of
soreness varies from mild, in which the horse moves with a short, shuffling
gait, to acute, in which there is a great disinclination to move at all. In
severe cases horses are unable to move their hind legs and swelling and
rigidity of the croup muscles develops. Myoglobinuria is common.

Post anaesthetic myositis

 Recovery is prolonged and when initial attempts are made to stand there is
lumbar rigidity, pain and reluctance to bear weight. The limbs may be rigid
and the muscle firm on palpation.

Hyperkalemic periodic paralysis

 Initially there is brief period myotonia with prolapse of the third eyelid. In
severe cases the horse becomes recumbent and myotonia is replaced by
flaccidity. Sweating occurs, and generalized muscle fasciculations are
apparent, with large groups of muscle fibers contracting simultaneously at
random.
 The animal remains bright and alert and responds to noise and painful
stimuli. In milder cases, affected horse remain standing and generalized
muscle fasciculations are prominent over the neck, shoulder and flank.
When the horse is asked to move, the limb may buckle and the animal
appears weak. The horse is unable to lift its head, usually will not eat and
may yawn repeatedly early in the course of an episode.

105 | P a g e
  In secondary myopathy due to ischemia – the affected animal is unable to
raise and the affected hind limbs are commonly directed behind the cow in
the foreleg attitude.
 In neurogenic atrophy there is marked loss of function in the total mass of
muscle - flaccid paralysis, loss of tendon reflexes and failure of
regeneration.

CLINICAL PATHOLOGY OF MYOPATHY

 Creatinine kinase is a highly specific indication of both myocardial and

skeletal muscle degeneration. CK has a half-life of about 4-6 hours.
 The level of AST is also increased following myopathy but because the enzyme
is present in other tissues such as liver, it is not a reliable indicator of
primary muscle tissue degeneration. Because AST has longer half-life than
CK, the level of AST may remain elevated for several days following acute
myopathy.

TREATMENT FOR MYOPATHY

 Vitamin E and selenium are indicated for the treatment of nutritional

muscular dystrophy.
 Supportive therapy for any case of myopathy, particularly severe cases in
which there is persistent recumbency, consists of:
o Liberal quantities of thick bedding
o Removal from solid floors to softer ground.
o Frequent turning from side to side to minimize secondary myopathy.
o Provision of fluid therapy to prevent myoglobinuric necrosis.
o Palatable nutritious diet.

MODULE-21: DISEASES OF BONES

Learning objectives

 To learn the etiopathogenesis of diseases of bones

 To study the clinical findings, diagnosis, differential diagnosis and treatment
of diseases of bones.

AETIOLOGY AND PATHOGENESIS OF OSTEOMYELITIS

 Inflammation of bone is uncommon in farm animals except when infection is

introduced by traumatic or by the haematogenous route. Bacteria can reach
bone by any of the three routes.

106 | P a g e
 o Haematogenously
o By extension from an adjacent focus of infection
o By direct inoculation through trauma or surgery.
 The infection occur commonly in the metaphysis, physis and epiphysis which
are sites of bony growth and thus susceptible to blood borne infections. The
metaphyseal blood vessels loop towards the physis and ramify into
sinusoids which spread throughout the metaphyseal region.
 Haematogenous osteomyelitis in cattle can be of
o Physeal type in which an infection generally of metaphyseal bone
orginates at or near the growth plate usually affecting the distal
metacarpus, metatarsus, radius or tibia.
o Epiphyseal type in which an infection originates near the junction of
the subchondral bone and the immature epiphyseal joint cartilage
most often affecting the distal femoral condyle epiphysis, the patellar
and the distal radius.
 The epiphyseal osteomyelitides are usually due to infection with Salmonella
spp and are most common in calves under 12 weeks of age. The physeal
infection are usually due to Actinomyces pyogenes and occur most
commonly in cattle over 6 months of age.

CLINICAL FINDINGS OF OSTEOMYELITIS

 In general, the signs are:

o Lameness
o Generalized soft tissue swelling and inflammation
o Pain on palpation of the affected area
o Chronic persistent drainage
o Secondary muscle atrophy of the affected limb
 Erosion of bone occurs and pus discharges into surrounding tissues, causing a
cellulitis or phlegmon and to the exterior through the sinuses which persist
for long periods.The affected bone is often swollen and may fracture easily
because of weakening of its structure.
 When the bones of the jaw are involved, the teeth are often shed and this,
together with pain and the distortion of the jaw, interferes with prehension
and mastigation.
 Involvement of vertebral bodies may lead to the secondary involvement of the
meninges and the development of paralysis.
 Lameness and local swelling are the major manifestations of involvement of
the limb bones.
 Cervico-thoracic vertebral osteomyelitis in calves between 2-9 weeks of age is
characterized by difficulty in raising with a tendency to knuckle or kneel on
forelimbs which are hypotonic and hyporeflexic. Pain can be elicited on
manipulation of the neck. The lesion usually involve one or more of the

107 | P a g e
 vertebrae from C6 – T1. Salmonella dublin is commonly isolated from the
vertebral lesion.

CLINICAL PATHOLOGY AND DIAGNOSIS OF OSTEOMYELITIS

Clinical pathology

 Radiographic changes include:

o Necrotic sequestrum initially
o New bone formation
o Loss of bone density

Differential diagnosis

 Healing fracture
 Traumatic periosteitis or osteitis
 Bone tumor
 Nutritional osteodystrophy
 Infection of the bone due to external trauma and fracture.

TREATMENT FOR OSTEOMYELITIS

 In case of long term infection or those with extensive bone necrosis, surgery is
generally recommended to remove sequestra, devitalized tissue and sinus
tracts which are harboring large numbers of bacteria.
 In septic physitis, the implantation of homologous cancellous bone grafts
following debridement of necrotic bone, and the application of a walking
cast for 4 -5 weeks and antimicrobial therapy for 2 weeks are highly
successful.

ETIOLOGY OF OSTEODYSTROPHY

Nutritional causes

 Calcium, phosphorous and Vitamin D – absolute deficiencies or imbalances in

calcium and phosphorous ratio in diets cause:
o Rickets in young animals –e.g. growing lambs fed a diet rich in wheat
bran.
o Absolute deficiencies of calcium
o Osteomalacia in adult ruminants, osteodystrophia fibrosa in the
horse occur most commonly in animals receiving a diet low in
calcium and high in phosphorous.
 Copper deficiency : Osteoporosis in lambs ; Epiphysitis in young cattle

108 | P a g e
  Inadequate dietary nutrition and general under-nutrition of cattle and sheep
can result in
o Severe osteoporosis and a great increase in case of fracture
o Chronic parasitism can lead to osteodystrophy in young growing
ruminants
o Hypovitaminosis A and hypervitaminosis can cause osteodystrophic
changes in cattle and swine.
o Prolonged feeding of a diet high in calcium to bulls can cause
nutritional hypercalcitoninism.
o Multiple vitamin and mineral deficiencies and be a cause of
osteodystrophy in cattle.

Inherited and congenital causes

 Achondroplasia and chondrodystrophy in dwarf calves and some cases of

prolonged gestation.
 Angular deformities of joints of long bones due to asymmetric growth plate
activity are common in foals.
 Physitis is dysplasia of growth plate, characterized by an irregular border
between the cartilage and the metaphysical zone of ossification, an increase
in the latero medial diameter of the physis, and disto proximally oriented
fissures at the medial aspect of the metaphysis, which originate at the
physis.
 Abnormal modeling of trabecular bone has been recognized in prenatal and
neonatal calves.

PATHOGENESIS OF OSTEODYSTROPHY

 Osteodystrophy is a general term used to describe those diseases of bones in

which there is a failure of normal bone development or abnormal
metabolism of bone which is already mature.
 Rickets is a disease of young growing animals, in which there is a failure of
provisional calcification of the osteoid plus a failure of mineralization of the
cartilaginous matrix of the developing bone.
 Failure of provisional calcification of cartilage results in an increased depth
and width of the epiphyseal plates particularly of the long bones and costal
cartilages of the ribs.
 There is a decreased rate of longitudinal growth of long bones and
enlargement of the ends of long bones due to the effects of weight causing
flaring of the diaphysis adjacent to the epiphyseal plate. Within the
thickened and widened epiphyseal plate there may be hemorrhages, minute
fracture of adjacent trabecular bone of the metaphysis and in chronic cases
the hemorrhagic zone may be largely replaced by fibrous tissues. These
changes can be seen radiographically as epiphyseitis and clinically as a

109 | P a g e
 enlargements of the ends of long bones and costochondral junction of the
ribs. These changes at the epiphyses may result in separation of the
epiphysis which commonly affects the femoral head.
 The articular cartilage may remain normal or there may be sub-articular
collapse resulting in grooving and folding of the articular cartilage and
ultimately degenerative arthropathy and osteochondrosis.
 Eruption of the teeth in rickets is irregular and dental attrition is rapid.
 Osteomalacia is a softening of mature bone due to excessive resorption of
mineral deposits in bone and failure of mineralization of newly formed
matrix.
 Osteodystrophiafibrosa may be super imposed on rickets or osteomalacia
and occurs in secondary hyperparathyroidism. Diets low in calcium or
which contain a relative excess of phosphorus cause secondary
hyperparathyroidism.
 Osteoporosis is due to failure or inadequacy of the formation of the organic
matrix of the bone. The bone becomes porous, light, fragile and fracture
easily.
 Congenital defects of bone include complete (achondroplasia) and partial
(chondrodystrophy) failure of normal development of cartilage.

CLINICAL FINDINGS OF OSTEODYSTROPHY

 In general terms there is weakening of the bones due to defective

mineralization and osteoporosis, which results in the bending of bones
which probably causes pain and shifting lameness.
 The normal weight and tension stresses cause distortion of the normal axial
relationships of the bones which results in the bowing of long bones.
 The distal ends of the long bones are commonly enlarged at the level of the
epiphyseal plates and circumscribed swelling of the soft tissue around the
epiphysis may be prominent and painful on palpation.
 Spontaneous fractures occur commonly and usually in mature animals.
Common sites for fractures include the long bones of the limb, pelvic girdle,
femoral head, vertebra, ribs and transverse process of the vertebrae.
 Ordinary hand pressure or moderate restraint of animals with osteomalacia
and osteodystrophiafibrosa is often sufficient to cause a fracture.
 Calcinosis of cattle is characterized clinically by chronic wasting, lameness,
ectopic calcification of cardiovascular system, lungs and kidneys, ulceration
of joint cartilage and extensive calcification of bones.

CLINICAL PATHOLOGY OF OSTEODYSTROPHY

 The laboratory analyses which are indicated include the following:

o Serum calcium and phosphorus
o Serum alkaline phosphatase

110 | P a g e
 o Feed analysis for calcium, phosphorus, vitamin D and other
minerals.
o Bone ash chemical analysis
o Histopathology of bone biopsy
o Radiographic examination of the skeleton.

 TREATMENT FOR OSTEODYSTROPHY

The oral administration of dicalcium phosphate @ 3-4 times the daily requirement,
daily for 6 days followed by a reduction to the daily requirement by the 10th day,
combined with one injection of vitamin D @ 10,000 IU/kg body weight is
recommended.

MODULE-22: DISEASES OF JOINTS

Learning objectives

 To learn the etiopathogenesis of diseases of joints in animals

 To study the clinical findings, diagnosis and treatment of diseases of joints

ARTHROPATHY (OSTEOARTHROPATHY, DEGENERATIVE

JOINT DISEASE

 The term osteoarthropathy and degenerative joint disease are used here to
describe non inflammatory lesions of the articular surfaces of the joints
characterized by:
o Degeneration and erosion of the articular joints
o Eburnation of subchondral bones
o Hypertrophy of bone surrounding the articular cartilage resulting in
lipping and spur formation at the joint margins.

Aetiology

Nutritional causes

 Secondary to or associated with rickets, osteomalacia, bowie and

osteodystrophiafibrosa.
 Coxo-femoral arthropathy in dairy cattle associated with aphosphorosis
 Copper, manganese and magnesium deficiency.

Steroid induced

111 | P a g e
  The intra-articular injection or prolonged parenteral administration of
corticosteroid in horse may lead to degenerative joint disease.

Biochemical trauma

Acute traumatic injury

 Repeated sub-acute trauma to joint surface can lead to degenerative

arthropathy.
 Growth rate, body size and genetic predisposition.
 Degenerative coxo-femoral arthropathy occurs in young beef bulls as early as
9 months of age. A congenital shallow acetabulam may predispose.
 Osteochondrosis is an important cause of lameness in horses. The stifle, hock
and shoulder joints are more commonly affected.

PATHOGENESIS OF ARTHROPATHY

 Articular cartilage is a tissue consisting of chondrocytes scattered in a matrix

of collagen fibres and an amorphous intercellular substance containing
proteoglycans. Articular cartilage contains no nerves, is avascular and has a
high matrix – to – cell ratio.
 The chondrocytes are the only living mater in the cartilage and produce the
fine strands of collagen and are engaged in protein and proteoglycan
synthesis.
 The matrix of the cartilage consists of water soluble proteoglycans
interspersed with collagen fibers which are arranged in parallel rows
superficially and crisscross rows closer to the calcified layer. This enables
the cartilage to withstand the shearing stresses superficially and
compression more deeply.
 The proteoglycans are glycosamino-glycan-protein complexes, bound by link
glucoprotein to a linear hyaluronic acid molecule. The glycosaminoglycan in
articular cartilages are chondroitin 4- sulfate and chondroitin-6-sulfate and
keratin sulfate.
 About 75% of the proteoglycans exist on aggregates which protect from
degradation and because of their high content of water, form large poly
anionic complexes which have considerable elastic resistant to
compression.
 Nutrition of the articular cartilage is provided via the synovial fluid and is
dependent on the capillary flow to synovial membrane.

PRIMARY AND SECONDARY OSTEO-ARTHROPATHY

Primary osteo-arthropathy

112 | P a g e
  This is due to normal aging processes and ordinary joint usage. The initial
lesions occur in the superficial layer of the articular cartilages where, with
increasing age, there is loss of normal resilience of the cartilage, a lowering
of the content of chondrointin sulfate and reduction in the permeability of
the cartilaginous matrix which results in progressive degeneration of the
articular cartilage.

Secondary osteoarthropathy

 This appears to be initiated by injuries or congenital conformational defects.

 Following acute trauma, the initial changes are often characterized by acute
synovitis and capsulitis. As a result of the inflammatory response,
leukocyte, prostaglandins, lysosomal enzymes and hyaluronidase enter the
synovial fluid which becomes less viscous and affects the nutrition of the
cartilage.

CLINICAL FINDINGS OF ARTHROPATHY

 Chronic lameness which becomes progressively worse over a long period of

time and usually does not repond to the treatment. The disease is insidious
and generally not clinically apparent in the early stages.
 A common clinical history is that the affected animal becomes progressively
more lame over a period of weeks and months and prefers long periods of
recumbency. There is usually a difficulty in flexing affected joints, normally
which results in a stiff or stilted gait.
 The bony prominences of the joint eventually appear more prominent than
normal which is due to the disuse muscle atrophy of the affected limbs.
 Pigs: The common clinical findings are hyper-flexion of the carpus, limb
bowing and adduction of both forelegs at the level of carpus,
hyperextension of the fore and hind phalanges and anterior curvature of the
tarsus.
 Osteochondrosis in cattle is characterized by chronic long standing lameness
either with or without joint effusions. The stifle joint is most commonly
affected followed by the hock joint. In young growing bulls there is
reluctance to move, stiffness, enlargement of the ends of long bones and
straightened joints.
 Osteochondrosis in horse is characterized by non-painful distension of an
affected joint. This is accompanied by joint swelling and stiffness

 CLINICAL PATHOLOGY OF ARTHROPATHY

Synovial fluid Normal Degenerative Infectious arthritis

analysis joint arthropathy

113 | P a g e
Gross Colourless, Pale yellow, may contain Turbid, yellow
appearence clear flocculent debris

Total volume - Normal or slight increase Usually marked

increase

Clot formation No clot May clot within

No clot minutes after
collection
Erythrocytes < 4000 6000-12000 4000-8000

leukocytes < 250 250-1000 50000-1.5lakhs

Neutrophils 7 10-15 80-90

lymhocytes 35-40 45-50 4-8

Monocytes 45-50 35-40 1-3
Total protein 1.2 – 1.8 1.6-1.8 3.2-4.5

Relative - Slightly reduced Decreased

viscosity
pH - - Decreased
TREATMENT OF ARTHROPATHY

 The treatment of active disease particularly in soft tissues which is

contributing to articular degeneration includes rest, immobilization,
physical therapy, intra-articular injections of corticosteroids, non- steroidal
anti-inflammatory agents, joint lavage, and intra articular injection of
sodium hyaluronate.
 Polysulfated glycosaminoglycans have been reported to induce articular
cartilage matrix synthesis and to decrease matrix degradation.

ARTHRITIS AND SYNOVITIS

 Inflammation of the synovial membrane and articular surfaces as result of

infection. Occurs commonly in farm animals.
 It is characterized by varying degrees of lameness and a warm and swollen
painful joint.
 The synovial fluid is usually abnormal, containing an increased leukocyte
count and the pathogens causing the arthritis.

 AETIOLOGY OF ARTHRITIS AND SYNOVITIS

114 | P a g e
Calves Caused by Actinomyces pyogenes, Fusobacterium necroforum,
Staphylococcus spp

Lambs Caused by Erysipelothrix insidiosa,Fusobacterium necroforum,

Staphylococcus spp, Haemophilus agni and Pasteurella haemolytica

Foals Actinobacillus equii, Salmonella abortivoequina

Piglets Streptococci lancefields groups – C,E and L.
Cattle Haemophilus somnus, Mycoplasma agalactiavarbovis, M. mycoides,
Brucella abortus.

Sheep and Mycoplasma spp, Streptococcus dysgalactiae

goats

Pigs Glasser’s disease, Mycoplasma and Brucella suis

PATHOGENESIS OF ARTHRITIS AND SYNOVITIS

 In infectious arthritis which is haematogenous in orgin, there is usually a

sinovitis initially, followed by changes in the articular cartilages and
sometimes in the bone. With almost any systemic infection there may be
localization of infectious agent in the synovial membrane and joint cavity.
The synovial membrane is inflamed, edematous and there are varying
degrees of villus hypertrophy and deposition of fibrin.
 The synovitis causes distension of the joint capsule with fluid and joint is
painful and warm.
 A progressive infectious synovitis commonly results in pannus formation
between the articular surfaces with erosion of articular cartilages, infection
of subchondral bone and osteomyelitis. In the chronic stages, there is
extensive granulation tissue formation, chronic synovitis and degenerative
joint disease with osteophyte formation and ankylosis is possible.
Depending on the organism the arthritis may be suppurative or
serofibrinous.
 Suppurative arthritis is particularly destructive of cartilage and bone and
commonly there is rupture of the joint capsule.
 Septicaemic foals may develop infectious arthritis and concurrent poly
osteomyelitis, because of the patency of transphyseal vessels in the newborn
foals, which allows spread of infection across the physes with the
development of lesions in the metaphysis, epiphysis and adjacent to the
articular cartilage.

CLINICAL FINDINGS OF ARTHRITIS AND SYNOVITIS

115 | P a g e
  Inflammation of the synovial membrane causes pain and lameness in the
affected limb, sometimes to the point that the animal will not put it to the
ground.
 Pain and heat are usually detectable on palpation.
 Pyogenic bacteria cause the greatest degree of swelling and may result in the
rupture of joint capsule.
 Some enlargement of the epiphysis is usual and this may be the only
enlargement in non-pyogenic infections, particularly that caused by
Erysipelothrix insidiosa.
 Fever, inappetence to anorexia, endotoxemia, loss of body weight and
discomfort may occur in animals with only one severely affected joint. In
many of the neonatal infection there will also be an accompanied
omphalophlebitis.
 Arthritis in older animals may also be accompanied by signs of inflammation
of the serous membrane and endocardium when the infection is result of
haematogenous localization.
 The joint most commonly involved are the hock, stifle and knee but infection
of the fetlock, interphalangeal and intervertebral joints is not uncommon.
In chronic cases, there may be physical impairment of joint movement
because of fibrous thickening of the joint capsule, periarticular ossification
and rarely ankylosis of the joint.

CLINICAL PATHOLOGY AND DIFFERENTIAL DIAGNOSIS OF

ARTHRITIS AND SYNOVITIS

Clinical pathology

 Arthrocentesis
 Analysis of joint fluid
 Culture of joint fluid
 Serology of joint fluid
 Radiography
 Ultrasonography

Differential diagnosis

 Degenerative joint disease

 Osteo dystrophy and epiphysitis
 Osteomyelitis
 Degenerative myopathy
 Myositis
 Traumatic injuries of tendons and ligaments
 Disease of the nervous system, especially the peripheral nerve and spinal cord.

116 | P a g e
 TREATMENT FOR ARTHRITIS AND SYNOVITIS

 The antimicrobials which perfuse into the joint in therapeutic concentrations

include the natural and synthetic penicillins, tetracyclins, trimethoprim –
potentiated suphonamides, neomycin, gentamicin and kanamycin.
 Intra-articular antimicrobials: the combined intra articular and i.v.
administration of gentamicin to normal horse can result in concentration 10
– 100 times greater than after i.v. administration alone.
 Antimicrobial impregnated polymethylmethacrylate beads have been used for
the treatment of chronic arthritis.
 Lavage of joint – aspiration and distention – irrigation of the joint cavity using
poly-ionic electrolyte solutions buffered to 7.4 is recommended. The
irrigation removes exudates and lysozymes which destroy articular
cartilage.
 Surgical drainage and arthrotomy – failure to respond to parenteral and intra
articular medication may require surgery of the joint capsule.
 Open drainage and intra articular and parenteral antimicrobial has been used
to treat persistent or severe septic arthritis or tenosynovitis.

MODULE-23: DERMATOLOGY

Learning objectives

 To learn the etiopathogenesis of dermatological disorders

 To study the clinical signs, diagnosis, differential diagnosis and treatment of
skin disorders

SARCOPTIC MANGE

117 | P a g e
Aetiology

 Sarcoptes scabiei var. canis.

Clinical signs

 The clinical signs may appear within one week after infection. They result
from mechanical irritation and hypersensitivity.
 Severe and constant pruritus often leading to a rapid appearance of extensive
excoriations

Primary lesions

 Erythematous and crusted papules.

Secondary lesions

 Crusts, excoriation, hyperpigmentation and lichenification.

Associated dermatological findings

 Scaling and seborrhoea, alopecia, pyotraumatic dermatitis, otitis externa

affecting the margin of the ear flaps.

Lesion distributions

118 | P a g e
  Margins of the ear pinnae and the bony prominence, especially elbows and
hocks, and the ventral portion of the chest and abdomen.

Diagnosis

 Pinna pedal reflex is highly suggestive and positive in more than 80% of the
cases and rare in other pruritic dermatosis.
 Examination of scrapings from crusted papule (elbow and hocks) and ear
margins. This is the only way to obtain absolute confirmation of the
diagnosis.
 Procedure
o Put a drop of liquid paraffin or mineral oil on a microscopic slide,
lubricate the scalpel blade and soften the skin. Then scrape until
capillary bleeding results and examine the entire sample present
under the cover slip under 10X objective. Every field must be
examined carefully.
o Skin biopsies: At best these are only suggestive, with parasites only
rarely observed.

Differential diagnosis

 Atopic dermatitis, food allergy, folliculitis and Malassezia dermatitis.

Treatment

 Topical: Acaricidal dips twice a week for a minimum of 6 applications.

oLime sulphur 2-3%,
o Amitraz 0.05 % three times at 15 days interval.
 Systemic treatment: Ivermectin 250 to 400 mcg /kg, 2 or3 times at 10 or 15
days interval by subcutaneous injection.
 Milbemycin oxime – 2mg/kg three times at one week interval orally.
 Additional therapy: keratolytic, anti seborrhoeic, antipruritic and emollient
topical shampoos and lotions.
 Systemic corticosteroid treatment for the first week in cases with very intense
pruritis (prednisolone 0.5 to 1mg/kg/day) orally 2 or 3 days.

DEMODECOSIS AND PYODEMODICOSIS

 It is associated with proliferation of the mite, Demodex canis, which are

normal inhabitants of the hair follicle and sebaceous glands.
 Classically, two forms of demodicosis are described - localised and
generalized.

119 | P a g e
  Their habitat is restricted to skin, but in severe demodicosis all stages may be
found in the lymphoid tissues and in many other internal organs. It is
assumed that they reach these sites by simple drainage via the lymphatics.
 High incidence of demodicosis in malnourished puppies and also in
association with severe internal parasitism.
 Adult onset of generalized demodicosis is usually associated with a serious
internal disease and is not infrequently seen with multicentric lymphoma,
hyperadrenocorticism and hypothyroidism. It may also develop secondarily
to chronic corticosteroid or immunotherapy.
 Proliferation of mites within the hair follicle interferes with the normal
clearing mechanism of the follicle and predisposes to infection with
staphylococcus intermedius. Subsequent rupture of the hair follicle leads to
a bacterial furunculosis and free mites in the dermis initiate a foreign body
reaction.
 In long standing cases the infection can go deeper and cellulitis develops. This
is particularly serious when it involves the interdigital area, leading to
severe pododermatitis.

Epidemiology

 Three different types

 Juvenile onset of localized demodicosis
o Peak age of onset is 3 -6 months; generally thought of as being a
relatively common disease, but without any inherited predisposition.
 Juvenile onset of generalised demodicosis
o Onset is usually from 3-6 months and it is rare for this to commence
after puberty and the disease is less common. It usually commences
as localized demodicosis of which some 10% of cases may progress to
the generalized form.
o Breeds commonly quoted as being predisposed include German
Shepherd, great Dane, collie, Doberman, English Bulldog, Boxer,
Afghan Hound, Dalmatian, Daschund and Beagle.
 Adult onset of generalised demodicosis
o This is far less common and is usually associated with a severe
internal disease (eg., endocrine disorder or the use corticosteroids or
immunosuppressive drugs).

CLINICAL SIGNS OF DEMODECOSIS AND PYODEMODICOSIS

 Areas of predilection are the face particularly the periocular area and
commissures of the lips, and the forelegs. Focal, demarcated areas of
alopecia accompanied by a fine scale. Such areas may be erythematous.
 Focal or generalized areas of seborrhoeas manifested by excessive scales and a
waxy surface lipid film.

120 | P a g e
  Most cases of demodicosis are non pruritic unless there is a secondary
pyoderma. Some cases, usually those with marked follicular plugging,
develop a bacterial folliculitis and show pustule which tend not to progress
to the development of marked epidermal collarettes.
 Deep pyoderma, either furunculosis or cellulitis is often a sequel and indeed
this may be the only presenting signs.

DIAGNOSIS OF DEMODECOSIS AND PYODEMODICOSIS

Diagnosis

Examination of scrapings

TREATMENT FOR DEMODECOSIS AND PYODEMODICOSIS

 Localised demodicosis is usually a self-limiting that cure spontaneously.

Generalised demodicosis

 Aggressive acaricidal therapy is necessary.

 Amitraz is used at 250ppm applied every two weeks.
 Antibiotic therapy: concomitant antibiotic should be used in case of pustular
demodicosis. Generally an antibiotic that is appropriate for staphylococcus
intermedius is used, irrespective of whether gram negative organisms are
also isolated.

Resistant cases

 Oral ivermectin at 400 -600 mcg/kg daily for upto 8 months as required.

121 | P a g e
  Milbimycin – orally at the dose of 0.5 – 2 mg/kg
 Moxidectin has also been used orally at 200 -400 mcg/kg daily for upto 6
months.

 Some three to five sites selected for skin scraping. The hair, if present, is
clipped. The skin is gently squeezed between thumb and forefinger to force
the mites more superficially in the hair follicle.
 Put a drop of liquid paraffin or mineral oil on a microscopic slide, lubricate the
scalpel blade and use it to soften the skin. Then scrape until capillary
bleeding results and examine the entire sample present under the cover slip
under the 10X objective. Every field must be examined carefully.

Other diagnostic aids

 Examination of hair pluckings as the mites are deep in the hair follicles. They
are often readily observed around the hair bulb of hairs plucked from the
periphery of the lesions.
 Skin biopsies of affected skin are an effective method of diagnosis, but are
unnecessary for routine cases.

Differential diagnosis

 The localised form is readily confused clinically with dermatophytosis.

 The pustular form resembles any other form of deep pyoderma.

MALASSEZIA DERMATITIS

122 | P a g e
Aetiology

 Malassezia dermatitis is a fungal skin infection. The pathogenic agent,

Malassezia pachydermatis is lipophilic yeast belonging to the cutaneous
microflora of the normal dog, along with Staphylococcus intermedius.
 Malassezia dermatitis is frequent in dogs, and is usually very pruritic.
 Malassezia pachydermatis – The malassezia genus includes unicellular
lipophilic yeast. Their growth is favoured by the presence of the lipids.
 Malasseziapachydermatis is characterized by a monopolar budding from a
broad base. This type of reproduction leads to its characteristic peanut
shaped appearance under microscope.

Pathogenesis

 Normal canine respond to yeast present on the skin surface.

o Non specific response mechanism (neutrophil phagocytosis)
o Specific cell mediated response mechanism
 Some pathogenic alteration favours the development of the normal
saprophytic Malassezia pachydermatis into a pathogenic status.
 Disruption of the cutaneous ecological equilibrium, modify the capacity and
the mechanism of host defence.
 Skin factors enhancing the multiplication of Malasseziapachydermatis:
excessive production or modification of the nature of sebum or cerumen,
excessive humidity, disruption of the epidermal barrier and presence of skin
folds.

CLINICAL SIGNS OF MALASSEZIA DERMATITIS

 Pruritis is always present and is usually intense.

 Primary lesions - generalized or localized erythema, papules and
erythematous maculae.
 Secondary lesions – greasy seborrhea, crust, diffuse alopecia,
hyperpigmentation and lichenification when chronic.
 Lesions are preferentially localized on the ventral aspect of the body (neck,
axilla, abdomen and inguinal area) and the perianal region. Other areas also
frequently affected are the face and the limbs (medial thighs and the
extremities)
 An offensive odour of rancid grease is also frequently present.
 Erythemato - ceruminous otitis externa is frequently associated.

DIGNOSIS OF MALASSEZIA DERMATITIS

Cytology

123 | P a g e
  Cytology is reliable, allows the rapid performance and interpretation and
inexpensive.
 Various sampling techniques exist:
o Direct impression smear, cellophane tape test, smear from a skin
scraping and swab smear.

Direct impression smear

 A slide is placed and rubbed against the lesional areas. The edge of the slide
may be sufficient if the area to sample is small.
 Perform several smears in different lesional areas.
 Let the samples dry for 1 – 2 minutes in open air.
 Immerse the slides in the three different dyes used for classic hematological
fast acting dye (generally 30 seconds each).
 Rinse the slides thoroughly with clear water and blot them carefully with an
absorbent paper, examination side upwards, until the water is completely
absorbed.
 A hair dryer may be used for final drying.

Cellophane tape test

 A clear cellophane tape is pressed firmly on the lesions. Sample several times
in different lesional areas. Make a loop with the piece of cellophane tape by
fixing it at the end of a slide, the adhesive side carrying the material
sampled outwards.
 Immerse the slides in the three different dyes used for classic hematological
fast acting dye (generally 30 seconds each).
 Rinse the slides thoroughly with clear water and blot them carefully with an
absorbent paper, examination side upwards, until the water is completely
absorbed.
 A hair dryer may be used for final drying.
 Unroll the adhesive tape and stick it on the slide.

Microscopic observations

 Locate microscopically well stained areas and centre them under the
microscope lens. Take care to position the slide on the right side with
materials sampled or cellophane upward.
 Look for the areas with most cells under low magnification, particularly
epidermal cell debris malassezia tend to cluster.
 Semi quantitatively scale (from 0 - +++) the number of the malassezia
present.

Differential diagnosis

124 | P a g e
  Hypersensitivity skin conditions (atopy, FAD,food allergy or even contact
dermatitis) which are also the most frequent primary causes.
 Parasitic dermatosis
 Any other cause of kerato-seborrhoeic disorders combined with a dermatitis.

TREATMENT FOR MALASSEZIA DERMATITIS

 In general the therapy of malassezia dermatitis is based on the sole use of

topical therapy or combined with a systemic anti-fungal treatment.

Sytemic therapy

 Ketoconazole – 5mg/kg SID or BID or 10 mg/kg SID.

 Itrakonazole may be used at 5 -20mg/kg every 24 to 48 hours. The initial
prescription must lost a minimum of 2 weeks. A treatment of 1 or 2 months
is generally necessary and must be continued after clinical recovery (7-10
days)
 Corticosteroids are contraindicated in Malassezia dermatitis, even in the
presence of pruritis, for there is a risk of rebound effects i.e. severe relapse.

Topical therapy

 The topical agents include antiseptic or antifugal agents (chlorhexidine,

miconazole, econazole, enilconazole and ketaconazole)
 The use of antiseptic or antifungal shampoos, 2 or 3 times a week for 2 weeks
and then every week until healing. First enables the mechanical removal of
a large quantities of debris and yeast and then directly counteracts the
microbial proliferation.

FLEA ALLERGIC DERMATITIS (FAD)

 Flea allergic dermatitis is a pruritic dermatitis arising from a hypersensitivity

to the bites of fleas (essentially Ctenocephalides felis). Very frequently, it is
one of the commonest cause of pruritus in dogs.

Aetiology

 Fleas are extremely common in temperate and warmer climates, with varying
levels of infestation of pets and their environment closely linked to ambient
temperature and humidity.
 Dogs that are atopic and suffer from atopic dermatitis are predisposed to the
development of flea allergy.

The pathogenesis in a hypersensitive dog

125 | P a g e
  Hypersensitive dogs can develop their disease via number of
immunopathogenic pathways, which are :
 The majority of sensitive dogs develop IgE antibodies (type I hypersensitivity),
and thus mast cell- derived mediators are involved.
 In additions, some dogs manifest cutaneous basophil hypersensitivity with an
influx of basophils armed with IgE antibody in to the site of application of
allergens.
 Most dogs also have cell mediated, delayed or type IV hypersensitivity.
Injection of the allergen causes an influx of lymphocytes and macrophages
and a variety of interleukins are involved. In a certain number of
cases(probably 15-30%), delayed hypersensitivity alone exists.

CLINICAL SIGNS OF FLEA ALLERGIC DERMATITIS

 FAD is still sometimes called summer eczema.

 The primary eruption is an erythematous papule, which may develop a crust
before disappearing in 2-4 days.
 The distribution involves mainly the lower back and posterior and inner
thighs. These are also the sites most favored by the fleas.
 Secondary lesions resulting from self trauma due to the intense pruritus.
 Changes seen in chronic cases include seborrhea, crusting, alopecia and
eventually lichenification.

DIAGNOSIS OF FLEA ALLERGIC DERMATITIS

 Age of onset: young adult dogs(1-6 year in 75% of cases)

 Demonstration of fleas or flea excreta supports the diagnosis but absence of
those elements don’t exclude it.
 The area of pruritus is also an impacting consideration.
 More likely appear in favorableseason (e.g. late spring, summer and early
autumn in temperate climate).
 May however be present during the whole year in favorable climate, with the
constituent part of the life cycle surviving indoors in the winter.
 Clinical signs may also persist year –round, even in the absence of fleas, if the
FAD is associated with a concomitant diseases (e.g. atopic dermatitis due to
house mites).

HYPOTHYROIDISM

 Hypothyroidism, a condition in which there are low levels of thyroid

hormones in the blood, is the most commonly diagnosed endocrine
disorder in dogs but rare in cats.
 Hypothyroidism is the result of decreased production of thyroxine (T4) and
triiodothyronine (T3) by the thyroid gland.

126 | P a g e
  Common causes of Hypothyroidism in dogs include
oLymphocytic thyroditis
o Idiopathic follicular atrophy
 Many cases of hypothyroidism have a genetic basis and many breeds are
prone to developing hypothyroidism.
 Hypothyroidism may result from dysfunction of any part of the hypothalamic-
pituitary - thyroid axis.
 Canine thyroiditis is believed to be immune mediated, but the immunologic
and molecular pathogenesis has not been well characterized.
 Because thyroid hormone influence the functions of many organs,
hypothyroidisim is considered in the differential diagnosis of a wide range
of problems.

Clinical signs

 Clinical signs attributable to decreased metabolic rate include lethargy, mental

dullness, weight gain, unwilling to exercise and cold intolerance.
 Obesity occurs in approximately 40% of hypothyroid dogs.
 Common dermatological findings include bilateral alopecia, spares the
extremities, hairs easily epilates, alopecia on the bridge of the nose and tail
(rat tail), dry dull brittle hair coat,dry scaly skin, changes in hair coat
quality or color, alopecia, seborrhea and superficial pyoderma,
hyperkeratosis, hyperpigmentation, cereminous otisis, poor wound healing
and Myxedema.
 Hypothyroid dogs are predisposed to recurrent bacterial infections such as
folliculitis, pyoderma and furunculosis.
 Variable pigmentation to the skin and coat.
 Seborrhoea, poor hair growth after clipping and hypertrichosis- a rare finding
especially in Boxer and Irish Setter.

Diagnosis

 Over 50% of hypothyroid dogs have high blood cholesterol and often
increased triglycerides and lipoproteins. Thyroid hormones commonly
measured include total T4, total T3 and free T4.
 Skin Biopsy reveals non-specific endocrine changes- follicular keratitis,
follicular dilatation, telogenisation of hair follicles, evidence of pyoderma ,
malazessia and demodicosis.
 TSH response test is a test of thyroid gland reserve and is the criterian
standard for diagnosis of canine hypothyroidism. TRH response test is
sometimes used to evaluate thyroid function in dogs.
 Scintigraphy and thyroid ultrasonography may also be useful in evaluation of
dogs with suspected hypothyroidism.

127 | P a g e
Treatment

 The initial treatment of choice, regardless of the underlying causes of

hypothyroidism, is synthetic sodium l-thyroxine (T4).
 A dose of 0.02mg/ kg every 24 hrs. normalizes TSH concentration in most
dogs; higher doses (0.04m/kg q 12 hr) are required to consistently
normalize T3 concentration.
 Adequacy of therapy should be confirmed by therapeutic monitoring 4 to 8
weeks after beginning l-thyroxine supplementation.
 An incorrect diagnosis of hypothyroidism is the most common reason for
treatment failure.
 Diseases such as hyperadrenocorticism, atopy and flea hyper sensitivity may
have clinical signs similar to those of hypothyroidism and may be
associated with decreased thyroid hormone concentrations.
 Prognosis for return to normal function following treatment is excellent in
most adult hypothyroid dogs. Prognosis in myxedema coma is dependent
on early recoginition.

128 | P a g e
 MODULE-24: DISEASES OF THE EPIDERMIS AND DERMIS

Learning objectives

 To study the etiopathogenesis of diseases of epidermis and dermis

 To get a knowledge about the clinical sings, diagnosis, differential diagnosis
and treatment of diseases of epidermis and dermis

PITYRIASIS

 Primary pityriasis: Excessive bran-like scales on the skin, characterized by

overproduction of keratinized epithelial cells and can be caused by:
o Hypovitaminosis A

129 | P a g e
 o Nutritional deficiency of B vitamins, especially of riboflavin and
nicotinic acid in pigs, or linolenic acid, and probably other essential
unsaturated fatty acids
o Poisoning by iodine
 Secondary pityriasis: characterized by excessive desquamation of epithelial
cells and usually associated with:
o Scratching in flea, louse and mange infestations
o Keratolytic infection, e.g. with ringworm fungus.
 Pityriasis scales are accumulations of keratinized epithelial cells, sometimes
softened and made greasy by the exudation of serum or sebum.
Overproduction, when it occurs, begins around the orifices of the hair
follicles and spreads to the surrounding stratum corneum.
 Primary pityriasis scales are superficial, accumulate where the coat is long,
and are usually associated with a dry, lusterless coat. Itching or other skin
lesions are not the features. Secondary pityriasis is usually accompanied by
the lesions of the primary disease.
 Pityriasis is identified by the absence of parasites and fungi from skin
scrapings.

Treatment

 Primary treatment requires correction of the primary cause.

 Supportive treatment commences with a thorough washing, followed by
alternating applications of a bland, emollient ointment and an alcoholic
lotion.
 Salicylic acid is frequently incorporated into a lotion or ointment with a
lanolin base.

HYPERKERATOSIS

 Epithelial cells accumulate on the skin as a result of excessive keratinization of

epithelial cells and intercellular bridges, interference with normal cell
division in the granular layer of the epidermis and hypertrophy of the
stratum corneum.
 Lesions may be local at pressure points, e.g. elbows, when animals lie
habitually on hard surfaces.
 Generalized hyperkeratosis may be caused by:
o Poisoning with highly chlorinated naphthalene compounds
o Chronic arsenic poisoning
o Inherited congenital ichthyosis
o Inherited dyserythropoiesis dyskeratosis
 The skin is dry, scaly, thicker than normal, usually corrugated, hairless and
fissured in a gridlike pattern.

130 | P a g e
  Secondary infection of deep fissures may occur if the area is continually wet.
However, the lesion is usually dry and the plugs of hyperkeratotic material
can be removed, leaving the underlying skin intact.
 Confirmation of the diagnosis is by the demonstration of the characteristically
thickened stratum corneum in a biopsy section, which also serves to
differentiate the condition from parakeratosis and inherited ichthyosis.
 Primary treatment depends on correction of the cause. Supportive treatment
is by the application of a keratolytic agent (e.g. salicylic acid ointment).

PARAKERATOSIS

 Parakeratosis, a skin condition characterized by incomplete keratinization of

epithelial cells, can be caused by nonspecific chronic inflammation of
cellular epidermis associated with dietary deficiency of zinc
 The initial lesion comprises , edema of the prickle cell layer, dilatation of the
intercellular lymphatics and leukocyte infiltration.
 The lesions may be extensive and diffuse but are often confined to the flexor
aspects of joints (referred to historically in horses as mallenders and
sallenders).
 Initially the skin is reddened, followed by thickening and gray discoloration.
Large, soft scales accumulate, are often held in place by hairs and usually
crack and fissure, and their removal leaves a raw, red surface.
 Hyperkeratosis scales are thin, dry and accompany an intact, normal skin.

Treatment

 Primary treatment requires correction of any nutritional deficiency.

 Supportive treatment includes removal of the crusts by the use of keratolytic
agent (e.g. salicylic acid ointment) or by vigorous scrubbing with soapy
water, followed by application of an astringent (e.g. white lotion paste),
which must be applied frequently and for some time after the lesions have
disappeared.

PACHYDERMA

 Pachyderma, including scleroderma, is thickening of the skin affecting all

layers, often including subcutaneous tissue, and usually localized but often
extensive as in lymphangitis and greasy heel in horses.There are no specific
causes, most cases being due to nonspecific chronic or recurrent
inflammation.
 In affected areas the hair coat is thin or absent and the skin is thicker and
tougher than usual. It appears tight and, because of its thickness and
reduced volume of subcutaneous tissue, cannot be picked into folds or

131 | P a g e
 moved easily over underlying tissue. The skin surface is unbroken and there
are no lesions and no crusts or scabs as in parakeratosis and hyperkeratosis.
 Confirmation of the diagnosis depends on histopathological examination of a
biopsy. The cells in all layers are usually normal but the individual layers
are increased in thickness. There is hypertrophy of the prickle cell layer of
the epidermis and enlargement of the interpapillary processes.

Differential dianosis

 Parakeratosis
 Cutaneous neoplasia
 Papillomatosis

Treatment

 Primary treatment requires removal of the causal irritation but in well-

established cases little improvement can be anticipated, and surgical
removal may be a practical solution when the area is small. In early cases
local or systemic corticosteroids may effect a recovery.

IMPETIGO

A superficial eruption of thin-walled, small vesicles, surrounded by a zone of

erythema, that develop into pustules, then rupture to form scabs.

 In animals the main organism found is usually a staphylococcus. The

causative organism appears to gain entry through minor abrasions, with
spread resulting from rupture of lesions causing contamination of
surrounding skin and the development of secondary lesions. Spread from
animal to animal occurs readily.

132 | P a g e
  The only specific examples of impetigo in large animals are
o Udder impetigo of cows
o Q Infectious dermatitis or 'contagious pyoderma' of baby pigs
associated with unspecified streptococci and staphylococci
 Small (3-6 mm) vesicles appear chiefly on the relatively hairless parts of the
body and do not become confluent. No irritation is evident. Vesicle rupture
occurs readily but some persist as yellow scabs. Involvement of hair follicles
is common and leads to the development of acne and deeper, more
extensive lesions. Individual lesions heal rapidly in about a week but
successive crops of vesicles may prolong the duration of the disease.
 Confirmation of the diagnosis is by culture of vesicular fluid and identification
of the causative bacterium and its sensitivity.

Differential dianosis

 Cowpox, in which the lesions occur almost exclusively on the teats and pass
through the characteristic stages of pox.
 Pseudocowpox, in which lesions are characteristic and also restricted in
occurrence to the teats.

Treatment

 Primary treatment with antibiotic topically is usually all that is required

because individual lesions heal so rapidly.
 Supportive treatment is aimed at preventing the occurrence of secondary
lesions and spread of the disease to other animals. Twice daily bathing with
efficient germicidal skin wash is usually adequate.

URTICARIA

 An allergic condition characterized by cutaneous wheals. It is most common in

horses.

Etiology

 Primary urticaria results directly from the effect of the pathogen, examples
are:
o Insect stings
o Contact with stinging plants
o Ingestion of unusual food with the allergen, usually a protein
o Occasionally an unusual feed item, e.g. garlic to a horse
o After a recent change of diet
o Administration of a particular drug, e.g. penicillin; possibly
guaifenesin or other anesthetic agent

133 | P a g e
 Allergic reaction in cattle following vaccination for foot-and mouth
o
disease
o Death of warble fly larvae in tissue
o Milk allergy when Jersey cows are dried off
o Transfusion reaction
 Secondary urticaria occurs as part of a syndrome
o Respiratory tract infections in horses, including strangles and the
upper respiratory tract viral infections
o Erysipelas in pigs .

Pathogenesis

 The lesions are characteristic of an allergic reaction. There is degranulation of

mast cells followed by liberation of chemical mediators, inflammation,
resulting in the subsequent development of dermal edema. A primary
dilatation of capillaries causes cutaneous erythema. Exudation from the
damaged capillary walls causes local edema in the dermis and a wheal
develops.
 Only the dermis, and sometimes the epidermis, is involved. In extreme cases
the wheals may expand to become seromas, when they may ulcerate and
discharge. The lesions of urticaria usually resolve in 12-24 hours but in
recurrent urticaria an affected horse may have persistent and chronic
eruption of lesions over a period of days or months

CLINICAL FINDINGS OF URTICARIA

 Wheals, mostly circular, well delineated, steep-sided, easily visible elevations

in the skin, appear very rapidly and often in large numbers, commencing
usually on the neck but being most numerous on the body. They vary from
0.5-5 cm in diameter, with a flat top and are tense to the touch.
 There is often no itching, except with plant or insect stings, nor discontinuity
of the epithelial surface, exudation or weeping. Pallor of the skin in wheals
can be observed only in unpigmented skin.
 Other allergic phenomena, including diarrhea and slight fever, may
accompany the eruption. The onset of the lesions is acute to peracute with
the wheals developing within minutes to hours after exposure to the
triggering agent. When associated with severe adverse systemic responses,
including apnea, respiratory arrest, atrial fibrillation, cardiac arrest or
sudden death, the case qualifies as one of anaphylaxis. Subsidence of the
wheals within 24-48 hours is usual but they may persist for 3-4 days
because of the appearance of fresh lesions.
 Urticaria lasting 8 weeks or longer is classified as chronic or recurrent
urticaria, which may require testing for atopic disease using intradermal
skin testing and serum testing for antigen-specific IgE.

134 | P a g e
  Adverse reactions in dairy cattle following annual vaccination for foot-and-
mouth disease are characterized by wheals (3-20 mm in diameter) covering
most of the body, followed by exudative and necrotic dermatitis. The
affected areas become hairless and the wheals exude serum and become
scabbed over. Edema of the legs is common and vesicles occur on the teats.
The lesions appear 8-12 weeks postvaccination and may persist for 3-5
weeks. Loss of body weight and lymphadenopathy also occur. Pruritus,
depression and a drop in milk yield are common.

TREATMENT FOR URTICARIA

Primary treatment

 A change of diet and environment, especially exposure to the causal insects or

plants, is standard practice. Spontaneous recovery is common.

Supportive treatment

 Corticosteroids, antihistamines, or epinephrine by parenteral injection

provide the best and most rational treatment, especially in the relief of the
pruritus, which can be anonying in some cases. One treatment is usually
sufficient but lesions may recur. The local application of cooling astringent
lotions such as calamine or white lotion or a dilute solution of sodium
bicarbonate is favored. In large animal practice parenteral injections of
calcium salts are used with apparently good results.
 Long-term medical management of persistent urticaria involves the
administration of corticosteroids and or antihistamines.
 Oral administration of prednisone or prednisolone at the lowest possible dose
on alternate days is the method of choice. The antihistamine of choice is
oral hydroxyzine hydrochloride initially at 600 mg three times daily,
followed by gradual reduction to a minimum maintenance dose required to
keep the horse free of lesions.

DERMATITIS

Etiology

Cattle

 Udder impetigo - S. aureus

 Cutaneous botryomycosis of the udder caused by a combination of trauma and
infection by Pseudomonas aeruginosa
 Cowpox
 Ulcerative mammillitis - udder and teats only

135 | P a g e
  Foot-and-mouth disease – vesicles around natural orifices.
 vesicular stomatitis with lesions on teats and coronet
 Rinderpest, bovine virus diarrhea, bovine malignant catarrh, bluetongue -
erosive lesions around natural orifices, eyes, coronets.
 Dermatitis on legs - potato poisoning, topical application of irritants
 Plaque-like and cracked skin lesions on the udder, hindquarters, lips and
muzzle of cattle bedded on straw heavily contaminated with Fusarium
sporotrichioides
 Slurry

Sheep and goats

 Strawberry footrot – Dermatophilus pedis

 Sheep pox - Contagious ecthyma, Ulcerative dermatosis
 Rinderpest. peste de petits mminants, bluetongue - as for cattle
 Foot-and-mouth disease and vesicular stomatitis
 Fleece rot - constant wetting and associated with P aeruginosa
 Blowfly infestation (cutaneous myiasis)
 Ovine atopic dermatitis
 Caprine idiopathic dermatitis a Post dipping necrotic dermatitis

Pigs

 Ulcerative granuloma - Borrelia suilla a Exudative epidennitis –

Staphylococcus hyicus (greasy pig disease) a Pig pox
 Swine vesicular disease, vesicular exanthema of swine, foot-and-mouth
disease - vesicles around natural orifices
 Sunburn
 Porcine necrotic ear syndrome
 Nonspecific nutritional dermatitis - experimental nutritional deficiency of
nicotinic acid, riboflavin, pantothenic acid, biotin
 Pityriasis rosea - cause unknown
 Idiopathic chronic recurrent dermatoses.

Horses

 Viral papular dermatitis

 Vesicular stomatitis - vesicles around natural orifices
 Sporotrichosis
 Dermatophytes, including ringworm, follicular dermatitis, hyphomycosis
(pythiosis), tinea versicolor dermatitis
 Scald - constant wetting
 Atopic dermatitis (IgE-mediated hypersensitivity)
 Chronic eosinophilic dermatitis

136 | P a g e
  Pemphigus, lupus erythematosus, erythema multiforme, eosinophilic
dermatitis and stomatitis
 Molluscum contagiosum
 Linear hyperkeratosis
 Nodular necrobiosis
 Ear plaque
 Cutaneous habronemiasis
 Tropical lichen

Pathogenesis

 Dermatitis is basically an inflammation of the deeper layers

of the skin
involving the blood vessels and lymphatics. It may be acute or chronic,
suppurative, weeping, seborrheic, ulcerative or gangrenous. In all cases,
there is increased thickness and increased temperature of the part. Pain or
itching is present and erythema is evident in unpigmented skin.

CLINICAL FINDINGS AND DIFFERENTIAL DIAGNOSIS OF

DERMATITIS

Clinical findings

 Initially erythema and increased warmth; later, may vary from discrete
vesicular lesion to diffuse weeping lesion depending on the severity of the
causative agent.
 Edema of the skin and soft tissue in severe cases.
 Necrosis and gangrene of the affected skin in much more severe cases.
 Diffuse cellulitis and phlegmonous lesion if infection involves s/c tissues
 Pyoderma
 Systemic reaction when affected skin area is extensive
o shock with peripheral circulatory failure
o Toxemia / septicemia

Differential diagnosis

 Hyperhidrosis and anhidrosis are dysfunctions of sweating and have no

cutaneous lesion
 Cutaneous neoplasm is differentiable on histopathological examination
 Epitheliogenesis imperfecta is a congenital absence of all layers of skin
 Vascular nevus is a congenital lesion commonly referred to as 'birth mark'

TREATMENT FOR DERMATITIS

137 | P a g e
  Primary treatment must be to remove the noxious physical or chemical
agent from the environment or to supplement the diet to repair a
nutritional deficiency. The choice of a suitable treatment for infectious skin
disease will depend upon the accurate identification of the etiological agent.
 Supportive treatment includes both local and systemic therapy. Local
applications may need to be astringent either as powders or lotions in the
weeping stage or as greasy salves in the scabby stage. The inclusion of
corticosteroids or antihistamine preparation is recommended in allergic
states and it is desirable to prescribe sedative or anesthetic agents when
pain or itching is severe.
 If shock is present, parenteral fluids should be administered. If the lesions are
extensive or secondary bacterial invasion is likely to occur, parenterally
administered antibiotics or antifungal agents may be preferred to topical
applications. A high protein diet or the administration of protein
hydrolysates or amino acid combinations may find a place in the treatment
of valuable animals. Nonspecific remedies such as gold-containing remedies
(e.g. aurothioglucose) are commonly used in autoimmune diseases such as
pemphigus.
 The use of vaccines as prophylaxis in viral and bacterial dermatitides must
not be neglected. Autogenous vaccines may be most satisfactory in bacterial
infections. An autogenous vaccine is particularly recommended in the
treatment of staphylococcal dermatitis in horses and bovine udder impetigo
in which long and repeated courses of treatment with penicillin produce
only temporary remission. An autogenous vaccine produces a cure in many
cases.

ALOPECIA AND HYPOTRICHOSIS

Etiology

 Alopecia is complete absence of the hair or wool coat; hypotrichosis is less

than the normal amount of hair or wool. Both may be caused by the
following conditions.
o Failure of follicles to develop
o Congenital hypotrichosis
o Loss of follicles
 Cicatricial alopecia due to scarring after deep skin wounds that destroy
follicles. Cicatricial alopecia occurs following permanent destruction of the
hair follicles, and regrowth of hair will not occur. Examples include
physical, chemical or thermal injury, severe furunculosis, neoplasia and
certain infections such as cutaneous onchocerciasis.
 Failure of the follicle to produce a fiber:
o Inherited symmetrical alopecia,
o Congenital hypotrichosis.

138 | P a g e
 o Congenital hypothyroidism (goiter) due to iodine deficiency in the
dam.
o After viral infection of the dam, alopecia congenitally in the
newborn, e.g. after bovine virus diarrhea in cattle
 Metabolic alopecia: subsequent to a period of malnutrition or severe illness -'a
break in the wool', e.g. excessive whale, palm or soya oil in milk replacers to
calves; the fibers grown during the period of nutritional or metabolic stress
have a zone of weakness and are easily broken.
 Traumatic alopecia: due to excessive scratching or rubbing associated with
louse, tick or itch-mite infestations; rubbing against narrow doors, feed
troughs or tethers in confined housing, against harness in working animals.
 Poisoning by thallium, selenium, arsenic, mercury or the tree Leucaena
leucocephala
 Idiopathic hair loss from the tail switch of well- fed beef bulls. In sterile
eosinophilic folliculitis of cattle.
 Wool slip: In many primary skin diseases, e.g. parakeratosis, hyperkeratosis,
dermatitis, cutaneous neoplasia, sarcoid; pythiosis. Hair is lost at the site of
local lesions.

Pathogenesis

 Normal shedding of hair fibers is a constant but largely unexplained process,

especially during significant changes in environmental temperature. The
long winter coat is shed in response to warmer spring temperatures and
increased hours of sunlight, and rapidly regrows as environmental
temperatures fall in the autumn.
 In inherited hair defects there may be a reduction in follicle numbers or a
reduced capacity of each follicle to produce fibers.
 Chemical depilation produced by cytotoxic agents, such as cyclophosphamide,
occurs as a result of induced cytoplasmic degeneration in some of the
germinative cells of the bulb of the wool follicle.

Clinical findings

 When alopecia is due to breakage of the fiber, the stumps of old fibers or
developing new ones may be seen.
 When fibers fail to grow the skin is shiny and in most cases is thinner than
normal.
 In cases of congenital follicular aplasia, the ordinary covering hairs are absent
but the coarser tactile hairs about the eyes, lips and extremities are often
present.
 Absence of the hair coat makes the animal more susceptible to sudden
changes of environmental temperature. There may be manifestations of a
primary disease and evidence of scratching or rubbing.

139 | P a g e
Treatment

 Primary treatment consists of removing the causes of trauma or other damage

to fibers.
 In cases of faulty follicle or fiber development treatment is not usually
attempted.

ACHROMOTRICHIA

 It is a deficient pigmentation in hair or wool fiber and may result

as follows
o Bands of depigmentation in an otherwise black wool fleece are the
result of a transitory deficiency of copper in the diet
o Cattle on diets containing excess molybdenum and deficient copper
show a peculiar speckling of the coat caused by an absence of
pigment in a proportion of hair fibers. The speckling is often most
marked around the eyes, giving the animal the appearance of
wearing spectacles.
o General loss of density of pigmentation in all coat colors, e.g.
Hereford cattle shade off from their normal deep red to a washed-out
orange.

VITILIGO

 Patchy depigmentation of the skin with premature graying of the local hair is
not uncommon in cattle and horses. The usual manifestation is the
appearance of patches of gray or white hair -'snowflakes' in an otherwise
pigmented coat. The defect is esthetic only.
 Histopathological examination reveals a complete absence of melanocytes
from affected areas but the cause is unknown in most cases. A genetic
etiology is suspected in Arabian horses and Holstein-Friesian cattle.
 It can also be caused by
o Application of'supercooled' instruments that selectively destroy
melanocytes, the basis for freeze branding.
o Prolonged pressure, e.g. by poorly fitting harness
o An idiopathic state in horses, usually during a debilitating disease,
with patchy depigmentation of skin appearing on the prepuce,
perineum, underneath the tail, and on the face.There is no
discontinuity of the skin.

SEBORRHEA

Etiology

140 | P a g e
  Seborrhea is an excessive secretion of sebum on to the skin surface. In large
animals it is always secondary to dermatitis or other skin irritation, e.g.:
Exudative epidermitis of pigs associated with S. hyicus, Greasy heel of
horses including infection with S. hyicus.

Pathogenesis

 Increased blood supply to the skin and increased hair growth appear to
stimulate the production of sebum, but why seborrhea is provoked in some
individuals and not in others is unknown.

Clinical findings

 In primary seborrhea there are no lesions, only excessive greasiness of the

skin. The sebum may be spread over the body surface like a film of oil or be
dried into crusts, which can be removed easily. Sebaceous glands may be
hypertrophied.
 Flexural seborrhea: Flexural seborrhea is most common in young,
periparturient dairy cows. Severe inflammation and a profuse outpouring of
sebum appear in the groin between the udder and the medial surface of the
thigh, or in the median fissure between the two halves of the udder.
Extensive skin necrosis follows, causing a pronounced odor of decay, which
may be the first sign observed by the owner. Irritation may cause lameness
and the cow may attempt to lick the part. Shedding of the Oily, malodorous
skin leaves a raw surface beneath; healingfollows in 3-4 weeks.
 Greasy heel of cows: Cows grazing constantly irrigated, wet pastures, or in
very muddy conditions in tropical areas may develop local swelling, with
deep fissuring of the skin and an outpouring of evil-smelling exudate, on
the back of the pastern of all four feet but most severely in the hind limbs.
Affected animals are badly lame and their milk yield declines sharply.
Removing the cows to dryland and treating systemically with a
broadspectrum antibiotic effects a rapid recovery.
 Greasy heel of horses (scratches): Creasy heel occurs mostly on the hind
pasterns of horses that stand conlinuously in wet, insanitary stables. Some
cases do occur in well managed stables. It has been suggested that
secondary infections associated with either S. aureus and D. congolensis
may be causative factors. Dermatophytosis, chorioptic mange and
photosensitization arc also possible causative factors.

Treatment

 The skin must be kept clean and dry. Affected areas should be defatted with
hot soap and water washes, then properly dried, and an astringent lotion,
e.g. white lotion, should be applied daily. In acute cases of greasy heel, the

141 | P a g e
 application at 5-day intervals of an ointment made up of five parts salicylic
acid, three parts boric acid, two parts phenol, two parts mineral oil and two
parts petroleum jelly is recommended.
 Long-standing cases profit from the twice-daily washing of the part and
covering with an ointment containing an antibiotic, a fungistat and a
corticosteroid, e.g. gentamicin, clotrimazole, betametasone.

FOLLICULITIS

Etiology

 Infection and inflammation of hair follicles associated with suppurative

organisms, including staphylococci. Identifiable forms of folliculitis as
individual diseases include:
o Staphylococcal dermatitis of horses
o Contagious acne of horses
o Benign facial folliculitis of sucking lambs
o Demodectic mange
o Bovine sterile eosinophilic folliculitis.

Pathogenesis

 Sebaceous gland ducts blocked by inspissated secretion and epithelial debris

or by pressure become infected. Folliculitis is also a sequel to seborrhea,
with hypertrophy of sebaceous glands and dilatation of their ducts.

Clinical findings

 The sequence of lesion development is: nodules around the base of the hair,
then pustules, then crusts, finally hair fiber loss. Itching may occur, but
pain and rupture of pustules under pressure are more common.
 Pustule rupture leads to contamination of the surrounding skin and
development of further lesions. In bovine sterile eosinophilic folliculitis, the
multiple lesions are crusted, alopecic, 3-5 cm diameter nodules on all parts
of the body except the limbs. They are composed largely of eosinophils and
are negative on culture.

Treatment

 Primary treatment commences with cleaning the skin by washing followed

by a disinfectant rinse. Affected areas should be treated with antibacterial
ointments or lotions. If the lesions are extensive the parenteral
administration of antibiotics is recommended. The course of treatment
should last 1 week; in chronic cases this may need to be at least 1 month; a

142 | P a g e
 broad-spectrum preparation such as trimethoprim-sulfadiazine is
recommended.
 Supportive treatment – infected animals should be isolated and grooming
tools and blankets disinfected.

MODULE-25: MANAGEMENT OF COMMON CLINICAL

POISONINGS

Learning objectives

 To study the common poisonings in animals

 To learn the clinical findings, diagnosis and treatment of common posoning
in animals.

PRINCIPLES OF TREATMENT IN CASES OF POISONING

 There are certain principles which apply to all cases of poisoning and they are
listed briefly below. The three main principles are,
o Removal of the residual poison from the alimentary tract or skin
o Provision of chemical and physiological antidotes to the poison that
has been absorbed. Effective supportive care, nursing, and
convalescent care.
o In farm animals, gastric lavage and emetics are of little or no
practical value and the removal of residual poison from the
alimentary tract depends largely upon the use of adsorbents and
purgatives. The only effective adsorbent is activated charcoal. The
dose rate is 1-3 g/kg BW repeated as necessary. It adsorbs
chlorinated hydrocarbons, organophosphorus compounds,
mycotoxins and plant alkaloids, the common feed additives,
antibacterial agents and bacterial toxins. It does not adsorb cyanide,
heavy metals, halogens, nitrite, alcohols, caustics, sodium chloride or
chlorate.
 A purgative is necessary to remove the combined adsorbent and poison; it can
be administered simultaneously with the adsorbent. The use of irritant
purgatives is not advisable when the poison is an irritant and has already
been associated with gastroenteritis, and non-absorbable oily purgatives
(e.g.mineral oil) are preferable in these cases.Saline purgatives (sodium
sulfate) are of value in the treatment of non-irritant poisons such as
cyanogenetic glucosides.
 Neutralization of residual poison in the alimentary tract includes use of
Oxidizing agents or tannic acid preparations for precipitating alkaloids.
Proteins, including milk and eggs, are effective chemical antidotes for
poisons that coagulate proteins. Lead is precipitated by the addition of
sulfates to the alimentary tract contents.

143 | P a g e
  Poison that has already been absorbed can in some instances be inactivated or
its excretion facilitated by the provision of chemical antidotes. For instance,
sodium nitrite and sodium thiosulfate are effective systemic antidotes to
hydrocyanic acid, and calcium versenate is an effective antidote against
lead.
 Treatment of the effects of a poison includes provision of physiological
antidotes, e.g. the injection of a calcium salt in cases of overdosing with
magnesium salts.
 Ancillary or supportive treatment, include the provision of fluids in
dehydration due to diarrhea, demulcents in gastroenteritis, sedatives in
excitement, stimulants in cases of central nervous system depression.
 It is essential when undertaking the treatment of animals for poisoning;
especially those which are producing milk or which are destined to become
meat in a short time, to take into account the possible unsuitability of the
product for human consumption because of the presence of the poison or
the antidote.

LEAD POISONING (PLUMBISM)

Treatment

 The case fatality rate of acute lead poisoning of cattle is high because of their
high susceptibility and the nature of the material ingested. Sedation by i.v
injection of anesthetic doses of pentobarbital sodium in calves and chloral
hydrate in adults temporarily relieves the convulsions.
 Calcium versenate (calcium dis odium ethylenediamine tetra-acetate,
CaEDTA) at a dose of 110-220 mg/kg BW i/v over 12 hours, which is
approached by rapid i.v. injections of two doses of 110 mglkg BW weight, 6
hours apart. This can be done daily for 3-5 days. CaEDTA is available as a
6.6% solution for i.v. administration.
 CaEDTA removes lead directly from bone-sensitive sites and not from
parenchymatous organs because cell membranes form a barrier to the
therapeutic removal of intracellular lead. The lead is removed from soft
tissues by equilibration with bone. The process takes time and thus
necessitates multiple treatment.
 An increase in the heart and respiratory rates and the development of muscle
tremors during injection indicates a toxic reaction but can be avoided by
slow administration. Recovery may take 5-15 days and parenteral or
stomach tube alimentation may be required. Blindness may persist for
several days after general recovery and may continue indefinitely.
 Oral dosing with small amounts of magnesium sulfate has been used on the
basis that soluble lead salts will be precipitated as the insoluble sulfate and
excreted in the feces.

144 | P a g e
Control

 Adequate nutrition and consistent feeding practices will minimize pica or

abnormal feeding behavior in livestock.
 Only lead-free paints should be used on surfaces and fixtures to which
livestock have access.
 All pastures should be inspected before cattle are introduced to them.

ARSENIC POISONING

Treatment

 In acute cases treatment is of little value because of the large amounts

ingested and the delay between ingestion and the appearance of illness, but
affected animals are unsuitable for human consumption so that treatment is
not usually undertaken.

Primary treatment

 BAL (2,3-dimercaptopropranol) is an efficient antidote for poisoning by

organic arsenicals, but is often disappointing in cases of poisoning by
inorganic salts, unless therapy is begun before clinical signs appear. Dosing
at 4- hourly intervals is necessary and the oily injection is associated with
some local pain.
 Sodium thiosulfate is a practicable and frequently used treatment. The
compound is almost completely non-toxic and can be given in large
amounts and without accurate measurement. Intravenous injection is
desirable as an initial treatment using 15-30 g of the salt in 100-200 mL of
water and this should be followed by oral dosing of 30-60 g at 6-hour
intervals. Treatment should be continued until recovery occurs which may
require 3-4 days.

Supportive treatment

 Attempts should be made to adsorb the residual arsenic in the gut by

administering charcoal (1-4 g/kg BW) and then removed by the
administration of an oil demulcent, or osmotic purgative like magnesium
sulfate.
 Severe dehydration occurs and supportive treatment must include the
provision of ample fluids preferably by parenteral injection.
 An adequate supply of drinking water containing electrolytes should be
provided and the animals should be disturbed as little as possible and
provided with shelter from the sun.

145 | P a g e
  Astringent preparations given by mouth may help to reduce the loss of body
fluids.
 At least 10 days should be permitted between ceasing to feed the arsanilate
and slaughter to avoid poisoning of humans.
 Therapeutic preparations containing arsenic should be labelled 'Poison' and
strict instructions given on dosage, particularly the length of time for which
administration should continue.
 Animals to be dipped in arsenical solutions should be watered before dipping
to prevent them drinking the dip.

MERCURY POISONING

Treatment

 In acute cases large amounts of coagulable protein such as eggs should be

given by mouth immediately, followed by mild purgatives to facilitate
removal from the gut before digestion and absorption occur. In acute and
chronic cases treatment with sodium thiosulfate as described in arsenic
poisoning is recommended.
 BAL can be used but has the same limitations here as in arsenic poisoning,
and delay in treatment of any sort is likely to be fatal. An injection of BAL
(6.5 mg/kg BW) should be given every 4 hours.
 Dimercapto succinic acid (DMSA) at 10 mg/kg BW. t.i.d. is reported effective
in hastening the elimination of mercury in urine. Suppportive treatment
includes astringents given orally to control the gastroenteritis and fluids
given parenterally to correct the dehydration.

Control

 Seed grains dusted with mercury compounds should not be fed to animals.

FLUORINE POISONING

Treatment

 Primary treatment, apart from removing the animals from the source of
fluorine, is largely impractical. Acute cases require gastrointestinal
sedatives. Supportive treatment to neutralize residual fluorine in the
alimentary tract and calcium salts intravenously is recommended.
 Aluminum salts act as neutralizers of the hydrofluoric acid produced in the
stomach and because of their insolubility they are safe even in large
quantities (30 g of aluminum sulfate daily for prevention, more for
treatment).

146 | P a g e
  The calcium salts given intravenously should be given to effect, using the
disappearance of tetany and hyperesthesia as a guide. These treatments will
probably have to be repeated.
 The parenteral administration of glucose solutions is recommended because
of the interference by fluorine with glucose metabolism. Irrespective of
treatment used, no improvement in dental or osseous lesions can be
anticipated but there may be amelioration of the other clinical signs.

Control

 Fluorine content of feed: Phosphatic feed supplements should contain not

more than 0.2% fluorine for milking or breeding cattle or 0.3% for slaughter
cattle, and should not comprise more than 2 % of the grain ration if the
fluorine content is of this order.
 Inspite of this recommendation the feeding of rock phosphate containing 1-
1.5% fluorine to cattle for long periods is maintained in some areas without
major deleterious effects on health. Some deposits of rock phosphate have
much higher contents of fluorine than others and commercial
defluorination makes these toxic deposits safe for animal feeding.
 Bone meal in some areas may contain excessive quantities of fluorine and
should be checked for its fluorine content. Access to super phosphate made
from rock phosphate with high fluorine content should be avoided. Water
from deep wells and artesian bores should be assayed for fluorine content
before use.

MOLYBDENUM POISONING

Primary treatment

 Molybdenum toxicity can be treated by the administration of copper, and

controlled by increasing the copper content of the diet by 5 mg/kg. But the
administration of copper to large numbers of animals presents a number of
problems.
 For longterm control, the recommended ratio of Cu:Mo is 4:1 to 10:1, and a
Sulfur:Mo ratio of <100:1 is considered safe vs.copper accumulation.

COPPER POISONING

Treatment

 Diagnostic confirmation is by demonstration of high blood and liver levels of

copper plus histological evidence of liver damage. The history and the
examination of feedstuffs and pastures are valuable aids in determining the
cause.

147 | P a g e
  1g anhydrous sodium sulfate significantly reduces the copper content of
tissues and appears to prevent deaths in lambs known to have toxic
amounts of copper. The mode of action is by increasing the fecal excretion
of copper. Under experimental conditions injection intravenously or
subcutaneously has an ameliorating effect on copper poisoning by reducing
the capacity of circulating copper to enter erythrocytes and cause their lysis.
 Injection of ammonium tetrathiomolybdate (three to six times) intravenously
at 2-3-day intervals at a dose rate of 2.7 mg/kg BW is also effective. So too is
the daily intravenous injections of sodium calcium edetate (70 mg/kg BW)
for 2 days to calves.
 Supportive treatment should include blood transfusion. In acute cases
gastrointestinal sedatives and symptomatic treatment for shock are
recommended.

SODIUM CHLORIDE POISONING

Treatment

 Primary treatment of both acute and chronic salt poisoning is the immediate
removal of the toxic feed or water. Serum sodium levels should not be
reduced by more than 0.5 mEq/hour. If possible, serum sodium should be
measured and a formula used to calculate the free water deficit is as follows:

Free water deficit (L) = 0.6 x body weight (kg) x ([current serum sodium
concentrationl reference range serum sodium concentration] - 1)

 Initially access to fresh water should be restricted to small amounts at

frequent intervals; unlimited access may be associated with a sudden
increase in the number of animals affected.
 In advanced cases, animals may be unable to drink and water may have to be
administered by stomach tube.
 Supportive treatment includes alimentary tract sedatives when gastroenteritis
is present and administration of isotonic fluids when dehydration has
occurred.
 When there is evidence of cerebral edema it may be necessary to administer a
sedative, and cerebral decompression may be attempted by the use of
diuretics or hypertonic solutions injected parenterally.

Control

 Drinking water for all classes of livestock should not contain more than 0.5%
sodium chloride or total salts, although sheep and beef cattle can survive on
water containing as much as 1.7 % sodium chloride or total salts.

148 | P a g e
  Both salt and water should be freely available at all times. Diets fed to pigs
should not contain more than 1 % salt. The way in which whey is fed to pigs
- with minimum water intake – makes prevention difficult unless the whey
can be kept free of salt at the cheese factory.

ZINC POISONING

Treatment

 Primary: Other than removal of the source of the zinc, none are
recommended.
 Supportive treatment is limited to symptomatic treatment.

Control

 Galvanized utensils and piping should be rinsed after each use in carrying
milk.

CHLORINATED HYDROCARBONS (ORGANOCHLORIDES)

Treatment

 There is no specific primary treatment.

 Supportive treatment includes sedation with pentobarbital sodium; repeated
until signs disappear.
 Intravenous injections of glucose and calcium and the administration of a
non-oily purgative.
 Activated charcoal (2 g/kg) given early by stomach tube will bind pesticide in
rumen and reduce further absorption.
 Residual chemical should be removed from the coat, and this may be
facilitated by judicious washing with soap and copious water rinse.
 After the source of contamination is removed, drenching of cows with up to 2
kg of activated charcoal followed by daily incorporation in their feed for 2
weeks, or small amounts of mineral oil by mouth at short intervals, have
been recommended for this purpose.

Control

 Mixed enterprise farms, especially vegetablecropping and cattle farming, are

the main sources for contamination incidents. Avoidance of the use of the
compounds is recommended.

ORGANOPHOSPHORUS COMPOUNDS AND CARBAMATES

(ORGANOPHOSPHATES)

149 | P a g e
Treatment

 Primary treatment is urgent and critical, especially in cattle because of the

usually high case fatality rate. Atropine in large (about double the normal)
doses is the rational and approved treatment.
 Recommended doses are 0.25 mg/kg BW in cattle and 1 mg/kg BW in sheep.
In very sick animals about one-third of this dose should be given very slowly
intravenously in a dilute (2%) solution and the remainder by intramuscular
injection. Injections may have to be repeated at 4-5-hourly intervals as
signs return, and continued over a period of 24--48 hours.
 Atropine appears to have low efficacy in sheep. This is not a serious drawback
as sheep are much less susceptible than cattle to larger doses of atropine.
 Oximes have some efficiency in the treatment of OP compounds, but not all
carbamates some of which may have their toxicity enhanced. Oxime
trimedoxime bromide is superior to 2-pyridine aldoxime methiodide (2-
PAM) and diacetylmonoxime (DAM). Recommended dose rates for 2-
pyridine aldoxime methiodide are 5O-100 mg/kg BW given intravenously
and for trimedoxime bromide 10-20 mg/kg BW. These dose rates can also
be used for subcutaneous and intraperitoneal injection.
 Administration by any route is as a 10% solution in normal saline. In horses 2-
pyridine aldoxime methiodide at doses of 20 mg/kg BW has given good
results.
 Combined oxime and atropine, e.g. 2,3- butanedione monoxime and atropine,
is recommended as superior to either drug alone. The value of the
treatment is greatest if it is carried out early, before 24 hours after
poisoning.
 Removal of residual toxin: Animals that have been dipped or sprayed should
be washed with water to which soap, soda or a detergent is added to remove
residual organophosphorus material. When oral intake has occurred
activated charcoal will adsorb residual toxin in the gut.

Control

 Most outbreaks occur after accidental access to compounds and this cannot
always be avoided. Animals to be treated orally with organophosphorous
insecticides should be permitted ample fresh drinking water beforehand.
 Chlorpyrifos is restricted to use in beef cattle and then not in calves less than
12 weeks old nor in bulls over 8 months of age.

RODENTICIDES

 The commonly used rodenticides in some countries are sodium fluoroacetate

and alphanaphthylthiourea (ANTU), but their use is banned in other
countries. Anticoagulants, include warfarin ((3-acetonylbenzyl -4-

150 | P a g e
 hydroxycoumarin) and its analogs, as well as newer 'second generation'
anticoagulants (brodificoum, bromodiolone, chlorphacinone).
 Zinc phosphide is often used as an alternative to anticoagulant rodenticides.
They are all toxic to domestic animals and may cause death when ingested
accidentally. 'Quintox', a rodenticide containing cholecalciferol (0.75 g/kg),
has been associated with hypercalcemia, hyperphosphatemia, and death in
dogs, and could cause death in farm animals .

UREA

Treatment

 No primary treatment is likely to be effective but the oral administration of a

weak acid such as vinegar (0.5-1 L to a sheep, 4 L to a cow), or 5% acetic
acid is recommended.
 Cold water (10-30 L for adult cattle) will dilute excess urea and temporarily
lower rumen pH. This may reduce the amount of ammonia absorbed but it
must be administered as soon as the first clinical signs appear and repeated
asmay be necessary as clinical signs tend to recur about 30 minutes after
treatment.
 The only really effective treatment is prompt and efficient emptying of the
rumen, either via a large bore stomach tube or by rumenotomy, but the
results are indifferent because the damage has usually been done already.

COMMON POISONING IN DOGS AND CATS

 Common poisoning in dogs

 Common poisoning in cats

COMMON POISONING IN DOGS-I

Acetaminophen

1. How does the pet get them?

o Acetaminophen is presented as tablets/ capsules/ liquids either
single or combined
2. What happens if ingested?
o Hepatotoxicosis occurs with doses of 50 to 100 mg/kg
o Methemoglobinemia occurs with dose200 mg/kg.
o Facial and paw edema
o Transient keratoconjunctivitis sicca
3. How to treat?
1. Initiate gastric decontamination procedures followed with 5% N-
acetylcysteine (NAC) * solution administered 140 mg/kg NAC orally

151 | P a g e
 as a loading dose, followed by 70 mg/kg every six hours for at least
seven doses.
2. Fluids to maintain hydration
3. Adjunctive therapies
4. Ascorbic acid, which helps reduce methemoglobin to hemoglobin
5. Cimetidine, which inhibits cytochrome P-450 oxidation in the liver
and may help reduce acetaminophen metabolism;
S-adenosylmethionine (SAM-e) in patients in which long-term
treatment of hepatic injury is needed.
6. Monitor serum chemistry profile parameters
7. Monitor tear production - administer artificial tears and cyclosporine
if needed.
8. The facial and paw edema will resolve on its own
9. *NAC is not labeled for intravenous administration, it can be given
intravenously in life-threatening situations by using a bacteriostatic
filter (0.2 µm).

RODENTICIDES

1. What are they?

o The three main types of rodenticides
1. Products containing anticoagulants (warfarin,brodifacoum,
diphacinone [also called diphenadione]),
2. Products containing bromethalin, and
3. Products containing cholecalciferol
2. What happens if ingested?
o Anticoagulant rodenticides
 Most common
 Ingestion can block vitamin K-dependent clotting factor
synthesis by inhibiting the 2,3-epoxide reductase enzyme,
which results in a coagulopathy three to five days after
ingestion (possibly sooner in immature animals).
o Bromethalin-containing rodenticide
 Signs ranges from tremors and seizures (convulsant syndrome)
to weakness and paralysis (paralytic syndrome) due to
vacuolization and severe spongiosis of the white matter within
the CNS and cerebral edema
 Convulsant syndrome usually occurs at doses of 2.3 mg/kg and
higher.
 Ingesting lower doses causes paralytic syndrome
o Cholecalciferol-containing rodenticides
 Can cause acute renal failure and tissue mineralization due to
increase in dogs' serum calcium and phosphorus
concentrations

152 | P a g e
 3. How to treat?
o Aticoagulant rodenticides
 Induce emesis and administer activated charcoal with a cathartic
as soon as possible. Do not induce emesis in symptomatic
animals (e.g. bleeding or seizing animals).
 Vitamin K1 orally for 14 to 30 days, depending on the specific
active ingredient.
 Evaluate the one-stage prothrombin time at 48 hours after the
last dose of vitamin K1. or alternatively monitor the
prothrombin time at 48 and 72 hours after ingestion, and if
elevated, initiate vitamin K1 therapy.
 If coagulopathy develops animals require whole blood or plasma
transfusion and oxygen and in these animals prognosis is
guarded and depends on the bleeding site.
o Bromethalin-containing rodenticide
 No specific treatment
 Aggressive decontamination is critical
 Prognosis is guarded when clinical signs are exhibited
 Resolve cerebral edema and seizures are treated by
administering corticosteroids, furosemide, mannitol, and
diazepam.
 The cerebral edema is intramyelinic, it does not respond well to
standard therapy.
 Mannitol, corticosteroids, and furosemide may temporarily
lower cerebrospinal fluid pressure
 If treatment are discontinued the clinical signs recurs
o Cholecalciferol-containing rodenticide
 Serum calcium and phosphorus concentrations and the renal
function parameters are to be monitored for 72 to 96 hours.
 Perform saline diuresis, and administer corticosteroids,
furosemide, or phosphate-binding agents.
 Salmon calcitonin or pamidronate may also be needed.
 Pamidronate, a bisphosphonate used in people to treat
hypercalcemia of malignancy, is a preferred agent in treating
cholecalciferol toxicosis. It is expensive, a single dose of
pamidronate is often sufficient to lower calcium
concentrations

CHOCOLATE

1. What is toxic?
o Chocolate contains two types of methylxanthine, theobromine and
caffeine, with their amounts varying depending on the type of
chocolate.

153 | P a g e
 Methylxanthine content in
o
 milk chocolate - 60 mg/oz
 dark chocolate - 150 mg/oz, and
 baking chocolate - 450 mg/oz
2. What happens?
o GI upset - vomiting and diarrhea can occur with any amount because
of chocolate's high fat and sugar content.
o cardiovascular effects (e.g. tachycardia, hypertension or hypotension,
arrhythmias)
o CNS signs (e.g. agitation, pacing, hyperactivity, tremors, seizures).
o How much is toxic and how?
 The toxicity depends on
 type of chocolate
 the amount ingested,
 the size of the animal, and
 the animal's sensitivity to methylxanthines.
o Ingestion of around 20 mg/kg methylxanthine causes mild
stimulation such as hyperactivity, agitation, and restlessness.
o Ingestion of around 40 mg/kg methylxanthine leads to
cardiotoxicosis and
o Ingesting more than 60 mg/kg causes severe CNS signs, such as
tremors and seizures.
3. How will you treat?
o Induce emesis or perform gastric lavage, use activated charcoal
o Monitor the patient's vital signs
o If cardiotoxicosis suspected - Continuous electrocardiogram (ECG)
o Perform baseline serum chemistry profiles
o Monitor electrolytes
o With intravenous fluids methylxanthine excretion is expected.
o If tachycardia-beta-blockers (e.g. propranolol, metoprolol)
o If nervous signs -diazepam
o To avoid reabsorption of methylxanthines from urinary bladder
avoid urine in bladder preferably catheterize and remove urine
catheter to keep the bladder empty.

IBUPROFEN

1. What is it and how does the dog get the access?

o Ibuprofen, a nonsteroidal anti-inflammatory drug with analgesic,
anti-inflammatory, and antipyretic effects
o It is available as 200 mg can contain up to 800 mg ibuprofen.
o It can be taken by dog either accidentally or when medicated by
owners for pain
2. What happens at various doses?

154 | P a g e
 GI, renal, and central nervous system (CNS) effects.
o
o 25 mg/kg or more often lead to gastrointestinal (GI) problems and
ulceration, manifested as vomiting, diarrhea, or abdominal pain.
o 175 mg/kg increase a dog's risk of developing acute renal failure
whereas aged dogs and dogs with history of renal failure may exhibit
renal failure at lower doses.
o More than 400 mg/kg, CNS effects such as depression, seizures, and
comas may occur.
3. How do you manage?
o Induce emesis, administering activated charcoal (multiple charcoal
doses are indicated to reduce enterohepatic recirculation in dogs that
have ingested high doses of ibuprofen)
o GI protectants (H2-blockers, sucralfate, misoprostol),
o Induce diuresis with intravenous fluids at twice the maintenance rate
o Monitor renal function

ANT AND ROACH BAITS

 What happens and how to manage?

o Common insecticides used in ant and roach baits today are boric
acid, avermectin, fipronil, hydramethylnon, propoxur, and
sulfluramid and have an attractant (often peanut butter), a
sweetening agent, and bread.
o Low concentration of the insecticide and the small size of the bait no
much serious toxicity is expected except for foreign body obstruction
from the parts of the container.
o Signs of ingestion are usually limited to mild GI upset and do not
require specific treatment.

COMMON POISONING IN DOGS-II

Pseudoephedrine

1. What is it? and What does it cause?

o Pseudoephedrine is a sympathomimetic drug structurally similar to
amphetamines and is present in most of the cold medications.
o Clinical signs
 Ingestion can lead to dose-dependent stimulation of the
cardiovascular system and the CNS.
o Signs include
 Agitation
 Hyperactivity
 Panting
 Hyperthermia

155 | P a g e
  Hypertension
 Tachycardia
 Head bobbing, or mydriasis.
 Ingesting as little as 10 to 12 mg/kg pseudoephedrine can cause
life-threatening signs.
2. How will you manage?
o gastric decontamination in asymptomatic animals
o patient monitoring, and symptomatic care.
o Acepromazine is used to control agitation and hyperactivity (Since
diazepam may aggravate the agitation avoid it)
o Phenobarbital to control severe tremors and seizures
o Fluid therapy enhances excretion of pseudoephedrine
o Hypertension is likely hence avoid exceed fluid rates of one and a
half to two times the maintenance rate unless the dog is in shock or
dehydrated.
o Tachycardia - use beta-blockers, such as propranolol

THYROID HORMONES

1. How is it toxic?
o Thyroid hormones are used to treat hypothyroidism in animals and
people, is avialable as desiccated thyroid (Natural) and levothyroxine
(synthetic) derivatives
o The liver and kidneys can act as buffers by releasing small or large
amounts of hormones, depending on what the body needs, back into
the plasma.
o In an overdose situation, these buffer organs can concentrate the
extra hormone and not release the already stored hormone.
2. What happens? and How will you mange?
o 0.2 mg/kg levothyroxine - mild signs
o 1 mg/kg or more - need treatment
o Hyperactivity and tachycardia are the most common signs
o Manage by the following steps:
 Initiate gastric decontamination
 Monitor the patients' ECGs, blood pressures, and serum T4
concentrations.
 Diazepam can be given to control hyperactivity
 Beta-blockers can be given to control tachycardia

BLEACH

1. What do they contain?

o Commercial bleaches are much more concentrated than regular
household bleaches (3% to 6% sodium hypochlorite);

156 | P a g e
 Fabtric bleaches contain sodium peroxide, sodium perborates, or
o
enzymatic detergents.
2. What happens when contacted/ingested/inhaled?
o Household bleaches can cause skin or eye irritation, mild oral or
esophageal burns, or GI irritation.
o Commercial bleaches can be corrosive and lead to severe stomatitis,
pharyngitis, esophagitis, or esophageal ulcerations.
o Inhalation exposure to bleach can cause respiratory irritation,
coughing, and bronchospasm.
o Damage can occur more seriuosly when bleach is mixed with
ammonia-containing agents, forming chloramine and chlorine gases
causing chemical pneumonitis.
3. How will you manage?
o To treat dermal exposure, bathe the dog with mild dishwashing
detergent.
o Bleach ingestion initial treatment includes oral dilution with milk or
water. Dilution is most effective if it is performed early.
o Emesis is contraindicated because of the irritating and potential
corrosive effects.
o GI protectants such as sucralfate or H2-blockers can also be used to
symptomatically treat bleach ingestion.
o Treating corrosive damage may also require pain medications,
antibiotics and nutritional support.
o Oxygen and bronchodilators may be needed to treat respiratory signs
in cases of inhalation exposure.

FERTILIZER

1. What do they contain?

o Fertilizer products generally contain varying amounts of nitrogen
(N), phosphorus (P), and potassium (K) compounds.
o Product ingredients are often listed as N-P-K 10-8-8, where each
number is the corresponding ingredient's concentration percentage.
o Presented as liquid, granular, and solid (e.g. stakes), and fertilizer
additives may include herbicides, insecticides, fungicides, iron,
copper, or zinc.
2. What happens? and How do you manage?
o Clinical signs
 Fertilizers have a wide margin of safety.
 GI signs such as vomiting, hypersalivation, diarrhea, or lethargy
 Signs are self-limiting and resolve within 12 to 24 hours in most
of the cases
o Management

157 | P a g e
  Treat animals with GI signs supportively with antiemetics,
fluids, and GI protectants.
 Heavy metals, such as iron, are generally not bioavailable but
can cause problem when large amounts are ingested.

HYDROCARBONS

1. Where are they present?

o Hydrocarbons are in numerous products, including paints,
varnishes, engine cleaners, furniture polish, lighter fluid, lamp oils,
paint removers, and fuel oil (e.g. acetone, xylene, kerosene, gasoline,
naphtha, mineral oil).
2. What are the signs?
o Vomiting and diarrhea
 Mild to moderate eye irritation and reversible ocular injury may
occur after contact with most hydrocarbons.
o Derrmal burns
 Highly volatile hydrocarbons (e.g. those found in kerosene,
gasoline, liquid furniture polish) are aspiration hazards
leading to pulmonary damage, transient CNS depression or
excitement, hypoxia, inflammation, and, potentially,
secondary infection (pneumonia) can occur.
 Hepatic, renal damage and even complete cardiovascular
complications occur.
3. How do you manage?
o Dilution is preferred than emesis because of complications of
aspiration
 Skin exposure - bathe the dog with a liquid dishwashing
detergent.
 Flush the eyes copiously with saline in cases of ocular exposure

4. COMMON POISONING IN CATS

Introduction

Cats are choosy and can reach places considered to be out of reach they are
characteristic nibblers and groomers hence likely to get access for poisonous agents
in and around and also those applied on skin.

RODENTICIDE

How do you approach?

158 | P a g e
  Various types have been dealt in our previous topic Common poisononing in
dogs.
 Clinical signs in cats generally occur three to seven days after exposure when
circulating clotting factors are depleted.
 Signs may be nonspecific like weakness, lethargy, and dyspnea due to bleeding
in any site.
 cough or respiratory difficulty as bleeding in lungs is common.
 Frank hemorrhage or ecchymoses may be seen.
 Lameness may occur if bleeding occurs in a joint
 Various neurologic signs may be noted if bleeding occurs in the brain or spinal
cord.
 Perform prothrombin time (PT) estimation
 Induce emesis and administering activated charcoal is effective at reducing
the amount absorbed systemically if presented immediately.
 If not Vitamin K1 (3 to 5 mg/kg orally divided twice daily) is antidotal.
 Vitamin K1 should be given for 14 days after warfarin exposure
 21 days after bromadiolone exposure
 30 days after brodifacoum and unknown anticoagulant exposure
 PT is done about 48 hours after vitamin K1 treatment to check the
effectiveness of treatment
 Whole blood or plasma transfusions are done bleeding and also administer
Vitamin K.
 If bleeding tendency occurs prognosis is poor.

ACETAMINOPHEN

What happens and How will you manage and How do they get access?

 Often administered to sick cats by their owners

 Acetaminophen has a narrow margin of safety in cats. One adult tablet (325 to
500 mg) could be lethal.
 Clinical signs such as
o Depression
o Vomiting
o Dyspnea
 Brown discoloration of the mucous membranes and blood due to
methemoglobinemia
 Respiratory distress
o Swelling of the face and paws
 Hepatic necrosis can develop at almost any level of exposure.
 Treatment
o Induce emesis and activated charcoal administered

159 | P a g e
 o Start oxygen therapy combined with a blood transfusion or
polymerized bovine hemoglobin solution administration for
methhaemoglobinemia
o Oral administration of N-acetylcysteine solution is diluted to a 5%
concentration with 5% dextrose or sterile water; this will yield a 50-
mg/ml solution.
o The loading dose is 140 mg/kg followed by 70 mg/kg every six hours
for seven additional doses.
o Intravenous fluids
o Cimetidine (to inhibit CP450 liver enzymes that activate
acetaminophen to the toxic metabolite), and ascorbic acid, which
may be used to help reduce methemoglobin to hemoglobin.
o The prognosis in these cases is fair to be guarded.

PERMETHRIN INSECTICIDES

What will they do and How to manage?

 These products used on dogs when applied on cats cause tremors and seizures
 Bathing the cat in a liquid hand dishwashing detergent as they remove the
agents from the sebum
 The tremors are best treated with slow intravenous boluses of methocarbamol
(total initial dose 55 to 220 mg/kg).
 Barbiturates, propofol, or both can be used if methocarbamol is ineffective.
 Diazepam is preferred if seizures are present.
 Body temperature is monitored.
 Administering intravenous fluids.
 No antidote.
 Prognosis is good if aggressive supportive care is done.

OTHER TOPICAL INSECTICIDES

 S-methoprene and pyriproxyfen insect growth regulators(used as topical flea

control)
 Organophosphates or carbamates, pyrethroids, imidacloprid, fipronil, and
selamectin - Insecticide ingredients
 If skin exposure occurs wash the product off with a mild detergent. Use
corticosteroid cream on local area of irritation. Use systemic corticosteroid
/ antihistamine if the irritation is more.
 Hypersalivation, agitation, and vomiting – if ingested occurs due to taste so
feed or simply remove clean the tongue.

GLITTER AND GLOW TOYS

160 | P a g e
How do you manage?

 Main ingredient dibutyl phthalate, an oily liquid that has a wide margin of
safety.
 Unpleasant taste shows hypersalivation, agitation, and, occasionally,
vomiting.
 Wipe the tongue and give some food for ingestion to remove taste.

ORNAMENTAL PLANTS AND FLOWERS

What to do?

 Ingesting any part of the plant may cause signs and should be aggressively
treated
 Ingestion causes vomiting and depression within two to four hours
 Polyuria, polydipsia, and more severe depression occurs after a day
 Renal blood profile like Creatinine, BUN and phosphorus are elevated
 Urinalysis may show cellular casts beginning about 18 hours after exposure.
 Induce emesis and activated charcoal.
 For 2 days put the cat on diuretics
 Immediate treatment gives good prognosis if oliguria or anuria sets then poor
prognosis is given.

NONSTEROIDAL ANTI-INFLAMMATORY DRUGS

How to act, when ingested?

 Ingested when owner administ or self-ingestion with canine formulations.

 Cats have a low tolerance for NSAIDs.
 Gastrointestinal - vomiting, diarrhea, ulceration, hemorrhage, and ulcer
perforation.
 Higher doses cause acute renal failure.
 CNS signs - seizures and comas at high doses.
 The more common drugs that can cause this syndrome include carprofen,
ibuprofen, deracoxib, naproxen, etodolac, meloxicam, and indomethacin.
 If ingsted 4 hours before nad there is vomiting signs induce vomiting and
activated charcoal.
 H2blocker (e.g. ranitidine or famotidine) or proton-pump inhibitor (e.g.
omeprazole), as well as sucralfate and misoprostol (1 to 3 µg/kg orally
b.i.d.) for seven to 10 days.
 Fluid therapy at twice the maintenance rate for at least 48 hours to prevent
renal damage.

CAT VACCINE PROTOCOL-I

161 | P a g e
American association of feline practitioners 2006 feline vaccination guidelines.
Summary: Vaccination ingeneral practice.

Vaccine Primary Primary series- Booster Comments

series- Adolescent/Ad
Kittens ult (>16 weeks)
(< 16
weeks)

Panleuk openia Begin as 2 doses, 3to4 A single Core

virus early as 6 weeks apart. dose is
(FPV)/Feline weeks of given 1  Killed vaccines
Herpesvirus-1 age , then year are preferred
and Feline every 3-4 followin for use in
Calcivirus(FHV- weeks g the last pregnant cats
1/ FCV) until 16 dose of (and only if
weeks of the absolutely
Injectable age. initial necessary)
series, and in FeLV
 MLV, non then no and/or FIV
adjuvan more infected cats
ted frequentl especially
 Killed y than those
adjuvan every 3 showing
ted years. evidence of
 Killed, immunosupr
non- ession.
adjuvan  Killed
ted panleukopeni
a vaccines
Intranasal should be
used in
 MLV non-
kittens less
adjuvan than 4 weeks
ted of age.
 All kittens and
cats should
atleast one
injectable
panleukopeni
a injection.

162 | P a g e
Rabies Administe Administer 2 Annual Core
r a single doses, 12 months booster
Injectable dose as apart. is  In states and
early as 8 required. municipalitie
 Canary or 12 s where feline
pox weeks of Vs. every rabies
virus- age 3 years vaccination is
vectored depending or as required
recombi on the required veterinarians
nant product by state must follow
(rabies), label. or local applicable
non- ordinanc statutes
adjuvan Revaccina e for 3  Booster
ted. te 1 year year. vaccination
 1-year later. with a 1 year
killed, rabies
adjuvan vaccine is
ted only
 3-year appropriate
killed, in states and
adjuvan municipalitie
ted s where
permitted by
law.
 Any rabies
vaccine can
be used for
revaccination
, even if the
product is not
the same
brand or type
of product
previouslt
administered.
 No laboratory
or
epidemiologi
c data exist to
support the
annual or
biennial
administratio

163 | P a g e
 n of 3 year
vaccines
following the
initial series

CAT VACCINE PROTOCOL-II

American association of feline practitioners 2006 feline vaccination guidelines.

Summary: Vaccination ingeneral practice.

Vaccine Primary Primary series- Booster Comments

series- Adolescent/Ad
Kittens (< ult (>16 weeks)
16 weeks)
Feline Leukemia Administer 2 doses, 3to4 When Non-core
Virus (FeLV) an initial weeks apart. indicated,
dose as a single FeLV vaccination is
Transdermal early as 8- dose is highly recommended
12 weeks of given 1 for all kittens
 Canary age, year
pox depending following  Booster
virus- on the last inoculation
vectore products; a dose of is
d second the initial recommend
recombi dose series, ed only in
nant should be then cats
(rFeLV) administer annually considered
, non- ed 3-4 in cats to be at risk
adjuvan weeks determine of exposure.
ted. later. d to have  In the United
sustained States, the
Injectable risk of 0.25 ml
exposure. rFeLV
 Or killed vaccine
adjuvan dose may
ted only be
administere
d via the
manufactur
er’s
transdermal
administrati

164 | P a g e
 on system.
 Only FeLV
negative
cats should
be
vaccinated;
FeLv testing
prior to
vaccine
administrati
on is
recommend
ed.
 Cats should be
tested for
FeLV
infection
before their
initial
vaccination
and where
there is a
possibility
that they
have been
exposed to
FeLV since
they were
last
vaccinated.

Feline immuno When When indicated, When Non-core

deficiency virus indicated, 3 3 doses are indicated,
(FIV) doses are required. a single  FIV vaccine
required. dose is should be
Injectable Each dose is given 1 restricted
administered, 2-3 year for cats at
 Killed, weeks apart following high risk of
adjuvan the last infection.
ted dose of  Vaccination
the initial induces
series, production
then of

165 | P a g e
 annually antibodies
in cats indistinguis
determine hable from
d to have those
sustained developed
risk of in response
exposure. to FIV
infection
and
interferes
with all
antibody
based FIV
diagnostic
tests for
atleast a
year
following
vaccination.
 Cats with
positive FIV
antibody
assay
results may
have
antibodies
as a result
of
vaccination,
infection or
both.
 FIV antibodies
are passed
from
vaccinated
queens to
their kittens
in
colostrums.
Colostrum
derived
antibodies
interfere

166 | P a g e
 with FIV
diagnosis
past the age
of weaning
in the
majority of
kittens, but
the
interference
appears to
wane by 12
weeks of
age.
 Cats should
test FIV
antibody
negative
immediately
prior to
vaccination
 Permanent
identificatio
n of
vaccinated
cats (e.g.,
using a
microchip)
will help
clarify
vaccination
status, but
will not
indicate
that such
cats are free
of infection.
 This vaccine
has been
shown to
provide
protection
from some,
but not all,

167 | P a g e
 strains of
FIV.

CAT VACCINE PROTOCOL-III

American association of feline practitioners 2006 feline vaccination guidelines.

Summary: Vaccination in general practice.

Vaccine Primary Primary Booster Comments

series- series-
Kittens (< Adolescent/Ad
16 weeks) ult (>16 weeks)
Feline infectious If If administered, Annual Not generally
peritonitis (FIP) administere give 2-3 doses, 3- booster is recommended
d, give a 4 weeks apart. recommend
 MLV, non- single dose ed by the  According
adjuvante as early as manufactur to the
d. early as 16 er. limited
 Intranasal weeks of studies
age, and a available,
second dose only cats
3-4 weeks known to be
later feline
coronavirus
antibody
negative at
the time of
vaccination
are likely to
develop
some level
of
protection.
 Vaccination
of cats
living
within
households
in which
FIP is
known to
exist or cats

168 | P a g e
 that are
known to be
feline
corona virus
antibody
positive is
not
recommend
ed.

Chlamydophila Administer Administer 2 Annual Non-core

felis the initial doses, 3-4 weeks booster is
dose as apart indicated  Vaccination
 Avirulent early as 9 for cats with reserved as
live, non weeks of sustained part of a
adjuvante age; a exposure control
d second dose risk. regime for
 Or killed, is cats in
adjuvante administere multiple-
d d 3-4 weeks cats
 Injectable later. environmen
ts where
infections
associated
with clinical
disease
have been
confirmed.
 Inadvertent
conjunctival
inoculation
of vaccine
has been
reported to
cause
clinical
signs of
infection.

Bordetella Administer Administer a Annual Non-core

bronchiseptica a single single dose booster is
dose intransally. indicated  Vaccination

169 | P a g e
  Avirulent intranasally for cats with may be
live, non as early as sustained considered
adjuvante 8 weeks of risk. in cases
d age where cats
 Intranasal are likely to
be at
specific risk
of infection.

Feline giardia Administer 2 doses 2-4 Annual Not generally

a single weeks apart. booster is recommended
 Killed dose at 8 recommend
adjuvante weeks of ed by the  There are
d age; a manufactur insufficient
 Injectable second dose er. studies
is available to
administere support the
d 2-4 weeks role of
later Giardia
vaccination
in
preventing
clinical
disease in
cats .
 Whether
the giardia
vaccine is
an effective
therapeutic
agent in
naturally
infected
cats is
currently
unknown.

 Injectable adjuvanted vaccine have been associated with local inflammatory

reactions at injection sites, with a degree of inflammation varying among
products. The potential role of local inflammatory reactions in the genesis
of vaccine-associated sarcomas remains controversial.

170 | P a g e
  Cats allowed outdoors, cats residing in open multiple-cat environments, cat
living with FeLV infected cats and cats residing in households with cats of
unknown FeLV infection status or where introduction of new cats is
common. Booster inoculation is not generally recommended for cats
housed strictly indoors.
 A recombinant FeLV vaccine available in Europe is designed to be
administered by subcutaneous injection; this product differs from the one
licensed in the United States.
 For example, outdoor fighting cats and FIV uninfected cats living with FIV
infected cats.
 For example, prior to confinement in multiple-cat environments such as
rescue shelters, boarding facilities orcatteries where bordetellosis has been
confirmed.

MODULE-26: DISEASES OF SENSE ORGANS

Learning objectives

 To study the common diseases of sense organs like ear and eyes , which are
affecting the domestic animal species.
 To learn the aetiology, pathogenesis, clinical findings, diagnosis and treatment
in diseases of sense organs.

EAR DISEASES

 Ear infections are one of the most commonly diagnosed problems in dogs and
are generally not difficult to detect. Around 10 - 20% of the dogs presented
to the pet clinic have ear disease. The ear disease may involve external ear,
middle ear or internal ear.
 There are many different causes and numerous treatment regimens to effect a
cure. Hygiene is of major importance both in curing the problem and
prevention of recurrence.
 Ear infections can easily become chronic in nature. So proper therapy early in
the course of the disease is important, along with long term commitment to
keep the ears clean.

Anatomy of the ear

 Ears of canines and felines differ from human significantly. The main
difference is the shape and length of the ear canal. It is longer in animals
and has a downward and then inward direction.
 Compared to human ear, cleaning the ear canal of a dog requires more efforts.
During the cleaning of dogs’ ears gently pull the external ear to straighten
the canal which will allow the deeper penetration of medication.

171 | P a g e
 CAUSES OF EAR DISEASES

It can be classified as follows

Primary causes

 A primary cause is an actual inciting agent that causes ear disease by itself
without predisposing or perpetuating causes.

 Parasites: Common parasites found in ears include:

Ticks
o
o Ear mites (Otodectes cynotis)
o Demodex mites (Demodex canis, Demodex cati)
o Sarcoptes mites (Sarcoptes scabiei)
o Notoedres mites (Notoedres cati)
 Ear mites are the most common cause of ear disease being
responsible for more than 50% of the cases in cats and 5-10%
of the cases in dogs.
 An allergic reaction to the mites is the primary reason for the
itching rather than few mites.
 Mite infections are highly contagious, and there is a possibility
that asymptomatic carrier dogs may be re-infecting the
patient with persistent ear disease.
 Cats with chronic, waxy ears have been found to have Demodex
cati infections.
 Micro-organisms
o In most cases, bacteria and yeast are perpetuating causes and not
primary causes of otitis externa. Bacteria will only become

172 | P a g e
 pathogenic when it reaches into the ear with liquid media eg.
Swimming in unclean water.
o Ringworm (dermatophyte) is a common cause of disease of the
earflap (pinna).
o Yeast infection, likewise, is pathogenic only when inoculated with a
broth type media. This can happen in a grooming saloon with poor
hygiene.
o The ears, which are warm, moist, and dark are a good place for
bacteria and yeast to grow. Therefore, changing the conditions of the
ear canal may be more important than killing the bacteria or yeast.
 Hypersensitivity (Allergies)
o Allergies to pollens in the air (atopy)
o Food allergy and contact-allergy Eg. Atopy
o Contact allergic dermatitis of the ear canal can occur from medications
used in the ear.
 Seborrhea
o Seborrheic disorders are common in dogs and denote a defect in the
normal maturation cycle of the skin as well as excessive oil
production.
o Breeds prone to seborrhea are: cocker spaniel, Irish setter, Beagle
and Basset hound.
 Other causes include hormonal disorders like
o Hypothyroidism - the most common cause of ear related hormonal
dysfunction.
o Male feminizing syndrome
o Sertoli cell tumors
o Some ovarian imbalances.
 Nasopharyngeal Polyp
o Nasopharyngeal polyps are fleshy benign masses of fibrous
connective tissue that arise from the respiratory epithelium of the
nasopharynx, eustachian tube, or tympanic cavity of cats.
o Young cats are more frequently affected than older cats.
 Auto immune diseases
o This is a group of rare diseases that are characterized by immune
dysfunction.
o The immune system attacks normal tissues causing inflammation
and ulceration.
o The ears may be involved in this type of reaction.
 Neoplasms: Ceruminous gland adenocarcinoma
 Uncommon causes
o Less common causes of otitis externa in dogs or cats include
immune-mediated dermatitis such as pemphigus, lupus or juvenile
cellulitis, adverse drug reactions, erythema multiforme, canine
distemper virus and traumatic injury to cartilage.

173 | P a g e
 PREDISPOSING AND PERPETUATING FACTORS OF EAR
DISEASES

Predisposing factors

 Hairin the ear canal eg. poodles, schnauzers.

 Pendulous ears eg. Basset hound
 Moisture in the ear eg. Labradors
 Inappropriate treatment

Perpetuating factors

 Perpetuating factors are those that prevent the resolution of the ear disease. In
all chronic cases, one or more of these factors will be present. Perpetuating
factors may be the reason for poor response to therapy, regardless of the
predisposing factors or primary cause.
 Once bacteria like Pseudomonas spp., Staphylococcus intermedius, Gram-
negative infections, Proteus spp, Escherichia coli, and Klebsiella spp.
establish infections, they cause a self-perpetuating course of inflammation
and damage.
 Malassezia pachydermatis is the most common perpetuating yeast infection. It
is a budding organism that is peanut, bottle-shaped or footprint-shaped. It
is found in one-third of the normal dogs' ears. It becomes pathogenic when
the ear micro environment is changed.
 Chronic inflammation stimulates the lining of the ear canal to undergo several
pathological changes resulting in a perpetuating disease process. These
changes include
o Increased production of ear secretions (oils, waxes, sebum)
o Excessive production of skin that becomes folded, thickened and
hyperplastic.
o Thickened skin leads to narrowing of the ear canal. The folds that the
skin forms prevent effective cleaning and medicating the ear canal
and also act as sites of perpetuating bacterial and yeast growth.
Inflammatory debris accumulates in the ear canal including dead,
exfoliated cells and the waxy secretions. This combination feeds
growing numbers of bacteria and yeast. These organisms produce
toxins as metabolic by-products that further initiate inflammatory
changes seen in chronic otitis.

OTITIS EXTERNA AND MEDIA

Otitis Externa

174 | P a g e
  Otitis Externa is classified as either Reactive or Infective in nature. Reactive is
characterized by acute erythematous reaction and also with chronic
proliferative and verrucous forms of the disease. In contrast, infective
includes acute and chronic inflammations, chronic ulcerative disease and
parasitic or fungal infections.
 Inflammation of the external ear canal, otitis externa, is a symptom of many
diseases and not a disease or diagnosis in itself.
 In cats, it is much less common and usually involves parasites (ear mites).
 In most of the chronic cases, the ear drum is ruptured and extension of the
infection into the middle ear is expected. This middle ear infection becomes
the source for otitis externa recurrence.
 Otitis media is also a common cause for failure of lateral ear re-section
surgery.

Otitis Media (Middle Ear Infection)

 Anything past the tympanic membrane (eardrum) is considered the middle

ear.
 Infection and pus within the tympanic cavity is difficult to treat with topical
therapy and often remains the source of infection and perpetuating
inflammation to the outer ear.
 Disease of the middle ear commonly results in calcification of the ear canal as
well as accumulations of plugs of debris in the middle ear and bulla. These
plugs must be removed by surgery. This inflammatory reaction may extend
to affect the temporo-mandibular joint (jaw joint) causing pain when
chewing or opening the mouth or palpating this area.

DIAGNOSIS OF EAR DISEASE

 By observation and physical examination. The clinical signs of ear infections

in dogs can range from mild to quite severe signs and includes
o shaking the head, scratching at the ears, pain, an odor from within
the ear canal, a discharge from the ear canal, redness, inflammatory
swelling inside the ear canal, scaling, crusting, hair loss (alopecia)
and broken hairs, aural hematoma and inflammation in the skin
surrounding the ear.
o Palpation may reveal a thickened, hard and calcified ear canal or a
soft ear canal that makes squishy sounds when squeezed.
o Presence of allergic disease on the rest of the body, feet, elbows, face
or rump may be noticed.
o Pruritus or pain associated with progressive inflammatory changes
may cause the animal to moan when ear is palpated.
 Otoscopic examination: The procedure is as follows:

175 | P a g e
 o The otoscope cones should be kept clean and soaked in disinfectant
between patients to prevent transmission of disease.
o The examination of the ear canal should be done on the good ear
first, then the bad ear.
o If the ear is very swollen and painful, anesthesia may be necessary.
o If the ear is so swollen, it is obvious that examination will be
impossible, even with anesthesia. Medications are used to reduce the
inflammation and then anesthesia is used to examine the ear.
 The type of discharge may help to indicate the type of disease
o Black, crumbly discharges - ear mites.
o Dark brown, creamy, sweet smelling discharge with itching - yeast
infection.
o Reddened earflap with scant discharge - allergies.
o Golden to brown, creamy discharge (ceruminous) - chronic, allergic
or seborrheic or hormonal problems.
o Yellow pus (purulent) discharge - bacterial infection.
o Red, painful, moist, ulcerated ear canals with a thin layer of whitish
ooze - acute moisture related bacterial infection secondary to bathing
or "swimmers ear".
 The interpretation of the normalcy of the eardrum (tympanic membrane) is
difficult to assess. The membrane becomes opaque, gray or brown due to
disease and thickens, losing its characteristic fish-scale appearance. The
presence of a tympanic membrane can be determined under anesthesia
with a soft, red, rubber feeding tube placed through the otoscope under
direct visualization. If the tip of the tube stops its progression down the ear
canal with the tip still visible, then the eardrum is still present. If the tip of
the tube disappears, then the eardrum is gone and the tube has passed into
the middle ear.
 Radiographs: Indicated if disease of the middle ear is suspected.
 Ear Swab Stain: This is a very important diagnostic step in all patients with
ear disease prior to medication. The sample should be taken with cotton-
tipped applicators.
 Performing a Roll Smear
o Cotton swabs and slides are needed to perform a roll smear.
o The cotton swab is gently placed in the ear canal to recover a sample
of the exudates. If otodectic mange is suspected, mineral oil should
be placed on the cotton swab. The cotton swab is then rolled on the
slide. A consistently thin smear should be made for bacteria and
yeast. A thick smear should be made for Otodectes. The slide is now
ready for examining mites. For microbiologic or cytologic evaluation,
the slide must be stained.
o The slide is labeled on the same side as the sample.
 Culture and Sensitivity: A culture of the discharge from the ear is sometimes
used as an aid to determine what bacteria or fungus is causing the problem.

176 | P a g e
 Since many organisims are usually grown in a culture, and some of them
are normal inhabitants, this test is not always advantageous.

THERAPY FOR EAR DISEASE

 Therapy for ear disease comprises of topical and systemic therapy.

 Topical medications may include,
o Cleansing and drying agents
o Topical acidifying agents
o Topical anti-inflammatory agents
o Topical antibacterial agents
o Topical antifungal agents
o Topical antiparasitical agents.
 Based on the diagnosis of the causative agent, the topical medication must be
chosen.
 Consideration of the vehicle or the carrier is very important in the treatment
of ear disease.
o Moist, exudative otitis externa should be treated with solutions or
lotions.
o In contrast dry, scaly or crusty ears should be treated with oil or
ointment based medication for best results.
 Systemic anti-inflammatory treatment is needed in many cases of systemic
disease that show manifestations in the ears.
 Corticosteroids: Powerful steroid action may be necessary for a short period in
allergic diseases. Systemic corticosteroids are also used in injectable form to
reduce inflammation initially so that the ear is easier to treat.The beneficial
effects of corticosteroids are:
o Potent anti-inflammatory effect reduce itching.
o Decrease exudation and swelling.
o Cause atrophy of wax producing glands.
o Reduce scar tissue formation and proliferative changes associated
with hyperplastic otitis externa.
 Antibacterials
o Systemic antibacterial therapy can be an invaluable aid in the
treatment of bacterial otitis externa. Patients with chronic recurrent
problems that have been properly treated at least twice with topical
medication are candidates for systemic therapy.
 Cefpodoxime – A new derivative of cephalosporin. It acts against
Pseudomonas and administered once a day.
 Fluroquinolone eg. Enrofloxacin
 Beta lactamases - penetrate Pseudomonas cell wall better than
other antibiotics -Increase gram negative activity but less
activity on gram positive and anaerobes compared to other
penicillins.

177 | P a g e
  Carboxypenicillin eg. Ticarcillin
 Ureidopenicillins eg. Piperacillin
 Silver sulfadiazine - inactivated by purulent debris; so they must
be applied in a clean ear. Spectrum also includes yeast.
 Tris-EDTA :EDTA is a binder of metals which are important to
the bacterial cell wall. Tris is used to buffer the EDTA to a pH
that is not irritating to the ear and to maximize the anti-
bacterial effect. Using Tris-EDTA gives extra power to the
topical antibiotics used concurrently.
 Anti-fungal
o In severe yeast infections, Chlorhexidine helps to kill both bacteria
and yeast and is commonly used.
o Ketoconazole is a systemic medication that may be used orally @ 5 -
10 mg /kg q 12-24 hr for yeast infections that are present in the
middle ear.
o Topically, Clotrimazole 1%, Miconazole 1 % and Ketoconazole 2% are
commonly used.
o If severe yeast infection is observed, medications such as
Ketoconazole, Itraconazole, and Fluconazole may be administered
for two to four weeks.
 Parasiticidal
o Ivermectin injection ( HITEK ) or ivermectin mixed with DMSO is
also used to kill ear mites in some exotic animals. Most Ivermectin
injectable protocols involve shots weekly or every two weeks.
o The treatment schedule for ear mites involves applying a product
that contains an antibiotic for any secondary bacterial infections, a
cortisone derivative for the inflammation, and thiabendazole to kill
yeasts and mites - 4 drops twice daily for 10 days; then, skip 10 days,
and then, repeat for 10 more days. At the beginning and end of each
treatment period, flea baths are given to kill mites that may be on the
external coat.
o There are currently several prescription products available that
reliably eradicate an ear mite infection with one single use, though a
thorough ear cleaning is still needed to remove the wax and debris
from the ear. These may be applied directly in the ear or to the pet's
skin behind the shoulders eg. topical version of ivermectin, and
topical version of milbemycin oxime, the same active ingredient as in
the heartworm preventive Interceptor.

TREATMENT OF OTITIS MEDIA

 The following steps may be adapted

o Access middle ear.
o Perform cytology and culture.

178 | P a g e
 o Flush bulla.
o Infuse topical medications into the bulla.
o Reduce inflammation with corticosteroids.
o Administer systemic and topical antimicrobials.
o Recheck weekly, and retreat 2 to 3 times.
o Consider surgery if necessary.
 Surgical
o Lateral ear canal resection
o Lateral Ear Removal
o Total ablation - Bulla Osteotomy 2 types
o Modified ablation technique

Medical management

 The earcanal can never be cleaned with cotton tip applicator. Two major
problems occur when these are used for cleaning.
o The applicator irritates the delicate otic epithelium allowing
colonization of damaged tissues by bacteria and yeasts.
o Secondly, material in the vertical canal is usually pushed into
horizontal canal where it lodges against tympanic membrane.
 The material acts as a nidus for infection or may cause pressure damage to the
tympanic membrane with the potential for development of middle ear
disease .

Irrigating /Flushing procedure

 A rubber-bulb syringe is used to flush the ear canal.

 The ear is then aspirated free of water for examination. The eardrum is tested
for patency (to detect a hole) as described earlier. If needed additional
application of the ceruminolytic solution may be necessary if there is still
wax or debris blocking the eardrum.
 A soft, red, rubber feeding tube and syringe is used to flush the debris from
the middle ear. Flushing the solution in, and aspirating it out, is very
effective
 For large chunks that cannot be flushed out or to scrape the middle ear free of
lodged debris, ear curettes or cerumin loops are used. Alligator forceps can
also be used to remove hair, foreign objects and plugs of debris if necessary
 The ear canal is suctioned and flushed with water as a final rinse, then
suctioned and dried gently with cotton swabs
 Medicaments that can be used during irrigation / flushing and cleaning
o Ethylene diamine tetra acetic acid-tris (EDTA-tris) can be used at
concentrations between 1.0 - 5.0% as a flush and is available as a
proprietary veterinary ear wash. A concentration of 2.5% acetic acid

179 | P a g e
 is effective at killing Pseudomonas spp. Acetic-acid-based products
should be used with care in ulcerated ear canals.
o Chlorohexidine is recommended by some authors as a flush solution
but must be used at low concentration (0.05%) to avoid ototoxicity.
(Harvey et al, 2001). . If the eardrum is suspected to be ruptured
chlorhexidine should not be used as it is toxic to the auditory nerve.
o A warm solution of Povidone iodine diluted 10:1 with tap water
(resulting in a tea-colored solution) may be used. However, some
consider Povidone iodine as unsuitable as a flushing agent.
o Ears with waxy, thick debris are best cleaned by applying few drops
of any one of the following ceruminolytic agents which are available
in the market.Viz:- Docusate sodium solution, Triethanolamine
polypeptide oleate condensate, Dioctyl sodium sulfosuccinate,
combination of Dioctyl sulfosuccinate with urea peroxide and
lidocaine hydrochloride and hexamethyltetracosane in mineral oil.
Massage with ceruminolytic agent in the ear canal for five to fifteen
minutes. Allow15 minutes to 24 hours and then use an antibacterial.
o Though, many products with various combinations are available in
the market it is ideal to choose the combination of lactic acid and
salicylic acid ( EPIOTIC ), since they are keratolytic or keratoplasstic
agents. Isopropyl alcohol is the active agent used as the base for most
drying products. This is usually accompanied by weak, astringent
acids such as lactic acid, malic acid, benzoic acid, salicyclic acid and
boric acid, or salicylic acid and phenoxy ethanol (Epiotic).

Home care tips

 Many dogs having chronic skin disorders have chronic otitis externa as well.
These pets benefit from ear flushing as a part of their overall care.
 The ears might have been waxy or dirty on examination and a preventative
measure is indicated to reduce inflammation and wax production.
 The debris from the ears is rinsed away when the shampoo for the coat is
rinsed.
 At the end of the bath, the ears are given a final rinse and a drying solution is
applied.
 Ear Drying Solution is an astringent, antiprutic and anti-inflammatory.
Drying formulation which is placed in the ear while bathing is allowed to
soak. After the pet is lathered, the ears are flushed with a 50/50 mixture of
white vinegar and water. Detergents should not be used due to incomplete
rinsing as well as irritation
 EPIOTIC is an home care product to clean the ears of their pet, if they have
some knowledge on anatomy of the dogs’ ear. Clients often do not
understand the need for inserting the nozzle of the medication tube deep

180 | P a g e
 into the ear. They are often concerned about the pain or head shaking after
medication is applied

EXAMINATION OF EYE

 The ophthalmic examination, combined with history and signalment, provides

the foundation for obtaining an accurate diagnosis. Ophthalmic diagnosis is
achieved by a combination of basic knowledge, the mastering of simple
instrumentation and critical observation. Basic equipment and simple
technifques, including a magnifying loupe, bright focal illumination,
Schirmer tear test strips, diagnostic dyes, cytology, direct ophthalmoscopy,
and Schiotz tonometry should be readily available in any practice. More
expensive and sophisticated instrumentation and technologiesf, including
the slit-lamp biomicroscope, indirect ophthalmoscope, applanation
tenometry, electrophysiology, gonioscopy, ultrasonography, and other
imaging modalities, fluorescein angiography, keratoscopy, and retinoscopy
represent the next level of diagnostics and are available to specialists or to
those with a particular interest in the field. Click here to know more about
visual pathway
 A binocular magnifying loupe of x 2 to x 4 magnification and a focal length of
15-25 cm is useful not only for diagnostics but also for surgery; it allows
freedom of both hands for manipulation and a loupe-mounted diffuse
illuminator facilitates observation.
 The gross appearance of the eye and surrounding structures is observed to
determine the presence of periorbital swelling, lacrimation, abnormal
discharge, and the size and position of the eye. Both eyes must always be
considered, even if only one is obviously affected. In such instances it is
preferable to examine the normal (or less obviously affected ) eye first.
 A magnifying loupe and focal illumination are used to assess the adnexa and
anterior segment structures.
 Pupil light reflex (PLR), menace response, blinking, and ocular and periocular
sensation should then be evaluated. PLR can be tested in ambient light;
repeat the procedure in a darkened room prior to the instillation of dilating
agents if abnormalities are noted. First each eye is directly stimulated with a
bright focal light and the completeness and briskness of PLR is noted. This
is the direct reflex, while the pupil of the opposite eye constricts due to the
consensual reflex.
 The menace response should be tested next, paying attention not to cause air
movement toward the patient’s eye and a consequent blink (mediated by
the trigeminal nerve). Bear in mind that absence of the menace response is
normal in very young animals and problematic to interpret in cats.
 Manipulate the head and neck to evaluate ocular motility.
 Critically evaluate globe size and position, observe the symmetry of the globes
from above, palpate around the orbital rim and the orbital fossa, and

181 | P a g e
 retropulse both globes simultaneously. Distinction between exophthalmos
and globe enlargement is critical.
 Then consider the eyelids, third eyelid, conjunctiva, sclera, and cornea, and
anterior chamber, iris, lens and anterior vitreous, using the magnifying
loupe and the focal light.
 If the adnexa is inflamed and there is discharge, Schirmer Tear Test is
indicated, and cytology and culture should be considered.
 If a serous discharge is bilateral without evidence of inflammation, or the
discharge is concentrated on the medial aspect and the hyperemia is
particularly evident in the medial canthus, the lacrimal drainage system
should be investigated, with a suspicion of obstruction and/or
dacryocystitis. In these cases palpation over the lacrimal sac may be painful
and induce the expression of exudates through the punctuate.
 If the patient exhibits blepharospasm, look for corneal ulcers, a foreign body,
entropion, or ectopic cilia, and stain with fluorescein. Chronic disorders of
the cornea manifested by neovascularization and melanosis may be
associated with trichiasis, districhiasis, lagophthalmos, lacrimal secretory
disorders or immune-mediated disease.
 If intraocular disease is suspected, based on the presence of episcleral/ scleral
injection, corneal edema, aqueous cells or flare, or abnormal PLRs,
tonometry is a requisite.
 Congestion of episcleral vessels may be differentiated from conjunctival
injection by applying one drop of phenylephrine; in cases of conjunctivitis
the hyperemic pattern will almost completely disappear. Episcleral injection
is an indication of episcleritis, glaucoma, or uveitis.
 Because papillary dilatation is necessary for the remainder of the ophthalmic
exam, one drop of 1.0% tropicamide should be applied to each eye at this
point; perform the rest of the general physical examination in the interim.
Gonioscopy is optimally performed prior to mydriasis.
 When the pupils are completely dilated as an effect of the previously instilled
mydriatic, the lens, vitreous, and the ocular fundus may be carefully
examined. The lens can be examined by moving the transilluminator to the
right and to the left from the frontal position in such a way as to shift the
incident light and better visualize any opacity with the magnification loupe.
 Using the direct ophthalmoscope with a lens setting between 0 and +2 D and
the eye examined from arm’s length it is possible to evaluate the fundus
reflex as a relatively sensitive indicator of opacities within the media, which
appear as a dark shadow when using this technique of distant direct
ophthalmoscopy. The fundus should then be examined using the indirect or
direct ophthalmoscope.
 Schirmer tear test (STT): This test is used quantitatively to evaluate the
aqueous component of the tear film and thus aid in the diagnosis of
keratoconjunctivitis sicca (KCS).

182 | P a g e
 DISEASES OF EYE

 Diseases of the eye may be divided into three main categories

o Diseases that involve the accessory structures
 Conjunctivitis
 Epiphora
 Keratoconjunctivitis sicca (KCS)
 “Cherry eye”
o Diseases that involve the structures within the globe
 Corneal ulcers
 Cataracts
 Glaucoma
 Uveitis
 Trauma
o Diseases that involves the retina and the neural pathways
 Progressive retinal atrophy

COMMON EYE DISEASES

Conjunctivitis

 Trauma, allergic, mechanical irritants, parasites (Thalazia), orbital

inflammation, tear Deficienciesand other ocular and systemic infectious
agents (bacteria, virus, ehrlichia, Rickettsia rickettsii )can cause
conjunctivitis.
 Conjunctival ulceration, while uncommon in dogs, can occur secondary to
different kinds of trauma, including alkali burns.

Dermoids

 A dermoid is a choristoma, which are normal cells or tissues in an abnormal,

unnatural position.
 Dermoids most commonly occur at the temporal limbus and can involve the
eyelids, conjunctiva, cornea, or all the three.
 These lesions contain keratinized epithelium, hair, blood vessels, fibrous
tissue, fat, nerves, glands, smooth muscle and cartilage.
 Dermoids are present at birth, but they may not be recongnized clinically until
the animal are several weeks old.
 Dermoids are best treated by surgical removal, and if on the cornea, the
procedure of choice is most commonly a superficial keratectomy.

Inflammatory keratopathies

183 | P a g e
  Inflammatory corneal disorders can be further classified into ulcerative and
nonulcerative keratitis.
o Ulcerative Keratitis:- Corneal ulceration, or ulcerative keratitis, is
one of the most common ocular diseases in the dog. A corneal ulcer
is present when there is a break in the corneal epithelium that
exposes the underlying corneal stroma. Clinically, this results in
lacrimation, blepharospasm, photophobia, conjunctival hyperemia,
corneal edema, and possibly miosis and aqueous flare.
o The diagnosis of a corneal ulcer is made on the basis of these clinical
signs and the retention of topically applied fluorescein dye by the
corneal stroma.
o Uncomplicated superficial ulcers usually heal rapidly, with minimal
scar formation.

Uveal inflammation

 Uveitis occurs commonly in conjunction with many intraocular and systemic

diseases.
 Uveitis refers to inflammation of the uveal tissue, which is composed of the
iris, the ciliary body, and choroids.
 Anterior uveitis is inflammation of the iris and ciliary body; posterior uveitis is
inflammation of the choroids, and panuveitis is inflammation of all three
portions of the uvea.
 Anterior uveitis can manifest with many clinical signs. Some of these signs are
specific for uveitis, such as aqueous flare and hypopyon, while others are
general ocular responses, such as blepharospasm and ocular hyperemia.
 Anterior uveitis can also be a secondary component of other ocular diseases,
such as corneal ulceration and glaucoma.
 Treatment: Corticosteroids are the primary therapy for the treatment of
anterior uveitis. Prednisolone acetate- 1% suspension, is the most
commonly prescribed ophthalmic corticosteroid because of its potency and
availability.

Rickettsial diseases

 Ocular signs may occur in both the acute and chronic forms of the natural or
experimentally induced E. canis infections.
 Anterior uveitis is the most consistent ocular finding.
 Additional findings may include conjunctivitis, conjunctival or iridal
petechiations, corneal opacity, panuveitis often with hyphema, diffuse
retinitis or vasculitis, retinal detachment or hemorrhage papilledema, and
optic neuritis.

Hyphema

184 | P a g e
  Hyphema, or blood in the anterior chamber, occurs when uveal or retinal
vessels are damaged or abnormally formed. There are multiple causes of
hyphema in the dog, including trauma, neoplasia, retinal detachments,
blood dyscrasias, preiridal fibrovascular membranes, hypertension,
infectious disease, severe uveitis, and congenital anomalies.

Edema of the eyelids

 Edema of the eyelids is seen occasionally in the bovine, most frequently in

association with urticaria from an unknown cause.

Carcinoma

 Squamous cell carcinomas are the most common malignant neoplasms of the
bovine eyelids, but sarcomas sometimes are found.
 In the early stages new growths frequently have the pimple-like
granulomatous tissue, and often are attributed either to warts or to a
probable wound.
 The rapid extension may quickly hide the eyeball from view.
 The diagnosis may be substantiated by biopsy and sectioning whenever
feasible.

Glaucoma

 Normal canine and feline IOP ranges from 12 to 22 mm Hg.

 Values greater than 30 mm Hg are diagnostic for glaucoma. Most canine
glaucoma cases result from decreased outflow of aqueous fluid as opposed
to increased production.
 IOP may be measured by using a Schiotz tonometer or a Tono-Pen (Tono-Pen
Vet, Medtronic). Glaucoma may be primary or secondary.
 Glaucoma may also be acute or chronic.

MODULE-27: GENERAL PRINCIPLES IN THE DIAGNOSIS

AND TREATMENT OF NERVOUS DISEASES

Learning objectives

 To study the clinical neuro- anatomy and neuro- physiology of nervous system
 To learn about neurological examination in animals
 To study the CSF analysis, EEG and other diagnostic procedures in the
diagnosis of neurological disorders.

CLINICAL NEURO - ANATOMY AND NEURO - PHYSIOLOGY

185 | P a g e
  The function of nervous system is performed by three basic functional
divisions of nervous system viz., sensory system, integrative system and
motor system. The animal receives information (sensory), integrates it with
either stored information (memory) or presently coming information,
formulates a proper response (integration) and reacts (motor).
Anatomically this function is carried out by two major divisions, the central
nervous system (brain and spinal cord) and the peripheral nervous system
(cranial and spinal nerves, their ganglia, end organs and autonomic nervous
system).
 The brain and spinal cord are situated within the neural canal of the vertebral
column. It is covered by 3 layers of meninges viz., piamater, arachnoid
membrane and duramater from inside to outside. The subarachnoid space
contains cerebrospinal fluid. The central nervous system mainly comprised
of cerebrum, thalamus, hypothalamus, cerebellum, midbrain, pons,
medulla and reticular formation and spinal cord

Cerebrum

 It is composed of two cerebral hemispheres united by a mass of white matter

called corpus callosum. The various parts of cerebrum and their functions
are as follows.

Part Function

Frontal lobe Psychic activity, motor activity

Parietal lobe Sensory area for tactile cutaneous modalities
Temporal lobe Auditory sensation, psychomotor activity

Occipital lobe Visual activity

 In general, the cerebral cortex is responsible for consciousness, memory,

learning, voluntary action and reception and evaluation of sensory
information. The sub-cortical nuclei consist of basal nuclei and limbic
system. Basal nuclei are collection of nerve centers that exert a controlling
influence on the somatic motor activity of an animal. Limbic system
receives input form olfactory, optic, auditory, extraceptive and intraceptive
senses and from cerebral cortex. In fact, it receives and associates almost all
sensory modalities in some way and is also directly involved in emotion and
behaviour.
 Thalamus: It consists of two avid masses of grey matter connected at the mid
line and located in the central portion of diencephalons and acts as a relay
centre for all sensory inputs (thermal, tactile and pain) to the cerebral
cortex.

186 | P a g e
  Hypothalamus: It is the most ventral diencephalons and is a collection of
nuclei located ventral to thalamus. The afferent pathways are connected to
subcortical structures and efferent pathways are connected to pituitary,
thalamus, tegmentum, lower brain levels and limbic system.
 Cerebellum: It is the second largest part of brain and the projection tract
connect cerebellum with other parts of brain and spinal cord. It maintains
the control of skeletal muscle activity by co-ordinating movements of
groups of muscles, maintaining equilibrium and by control of posture. For
maintaining equilibrium, the cerebellum works very closely with the
vestibular apparatus. All activities of cerebellum are carried out below the
level of consciousness.
 Mid brain, pons, medulla and reticular formation: These structures connect
cerebrum, cerebellum and spinal cord. The cranial nerve nuclei are located
in these structures (3rd, 4th and 5th in mid brain, 5th, 6th, 7th and 8th in pons
and 8th, 9th, 10th, 11th and 12th in medulla.
 The nuclei for many vital centers like cardiac, vasomotor and respiratory
centre are located in medulla. Many reflexes such as swallowing, vomiting,
coughing, sneezing and hiccuping are regulated by medulla. All projection
tracts between spinal cord and brain pass through medulla.
 The reticular formation is a system of interlacing fibres and nerve cells that
form the central nerve core of brain stem. It is considered essential for
arousal from sleep, wakefulness, alertness, focusing attention and
perception.
 Spinal cord: It is a cylindric continuation of medulla and extends posteriorly
up to lumbo-sacral region. In general, the spinal cord tapers gradually in
caudal direction except at brachial and lumbo-sacral plexus, where it is
slightly enlarged. From these plexuses, the nerves of limbs originates. The
terminal end of spinal cord tapers to a point where it is surrounded by the
roots of sacral and coccygeal nerves which extends caudally in the neural
canal forming cauda equine. The cross section of spinal cord shows two
fissures one dorsally and the other ventrally; they are respectively called
dorsal and ventral fissures. The outer portions of spinal cord are composed
of white matter and contain the ascending and descending nerve tracts.
This portion may be divided into dorsal, lateral and ventral white columns.
The more centrally located grey matter is made up of nerve cell bodies and
their connective synaptic processes. This region in the form of letter H can
be subdivided into dorsal, lateral and ventral grey horns. Most of the cells in
ventral grey horns is motor in function whereas that of dorsal grey horn is
sensory. There is a narrow central canal running through the middle of grey
matter. It communicates with the fourth ventricle of the medulla oblongata.
 Peripheral nerves: They consist of 12 pairs of cranial nerves and 36 to 42 pairs
(according to species) of spinal nerves.

187 | P a g e
  The cranial nerves may be divided according to their function into three
groups.
o Afferent nerve: First (olfactory); Second (optic); Eighth (auditory)
o Efferent nerve: Seventh (facial); Eleventh (spinal accessory); Twelth
(hypoglossal)
o Mixed nerve: Third (oculomotor); Fourth (Trochlear); Fifth
(Trigeminal); Sixth (Abducent); Ninth (Glossopharyngeal); and
Tenth (Vagus). Third, fourth and sixth cranial nerves supply motor
and sensory fibres to muscles of eye.

188 | P a g e
  Autonomic nervous system: It consists of
o cranial and sacral divisions comprising the parasympathetic section
and
o thoracolumbar or sympathetic division. The fibres of autonomic
nervous system innervate the glands and visceral musculature of the
body. Many of the structures are supplied by both sympathetic and
parasympathetic components which are frequently mutually
anatagonistic. The overall function of autonomic nervous system is
to maintain internal homeokinesis.

NERVE CELL

 The basic units of nervous system are nerve cells viz., neurons and glial cells.
Neurons are the cells capable of transmitting an electrical impulse and are
responsible for the master control provided by the nervous system. Glial
cells are the supporting cells. Neurons may be unipolar, bipolar and
multipolar.
 Unipolar neurons have a common dendrite and axon stalk leading to and from
the cell body. The single dendrite is very long and is located in peripheral
cranial or spinal sensory nerve. Most of the cell bodies are located in the
ganglia exterior to spinal cord or brain stem. From the cell bodies in
peripheral nerve ganglia, the axons enter spinal cord or brain stem and
synapse on other neurons. The unipolar neurons carry sensory or afferent
information such as proprioception, touch and pain from the exterior body
into central nervous system. Bipolar neurons have one dendrite and one
axon from separate areas of the cell body and transmit sensory information
for olfaction, vision, audition and equilibrium.
 Most neurons are multipolar with multiple dendrites and one major axon.
They can be sensory or afferent neurons and transmit information from

189 | P a g e
 spinal cord and brain stem to the higher centres of cerebellum and
cerebrum. They can also be motor or efferent neurons and carry
information from higher brain centres to lower brain stem and spinal cord
centres and from the spinal cord through peripheral nerves to glands and
muscles. Multipolar neurons with short axons form internuncial neurons of
central nervous system which transmit information for short distances.
Multipolar neurons with long axons form the tracts of central nervous
system and peripheral nerves.
 A lower motor neuron (LMN) is a multipolar neuron with its dendrites and
cell body in brain stem nucleus or in the grey matter of spinal cord. The
axon of LMN travels out of the central nervous system (CNS) through
peripheral nerves to synapse on a gland or muscle. Spinal cord or brain
stem reflexes are composed of two or more neurons. A unipolar neuron
carries information from the body to a lower motor neuron directly or
indirectly through an internuncial neuron.
 The upper motor neurons (UMN) have their dendrites and cell bodies in
cerebral cortex grey matter or nuclei of brain stem. Their axons travel
through the brain stem and spinal cord in bundles of fibers called tracts,
which form part of the white matter of brain stem and spinal cord. UMN
has an overall inhibitory or calming effect on the LMN reflexes.

NEUROLOGICAL EXAMINATION

 Neurological examination is most rewarding in dog and cat since all the
techniques can be easily employed. However, in farm animals, many of the
techniques are not applicable because of their size and poor response to
many of the neurological tests. Young lambs and piglets are satisfactory in
this respect.
 Examination of nervous system includes history taking, preliminary general
clinical and detailed systematic examination of nervous system,
cerebrospinal fluid examination, radiographic examination, interpretation
of electroencephalogram and electromyogram and brain biopsy.

HISTORY

 The primary complaint and natural history of an illness provide the most
information about the cause and special attention should be given to record
the accurate history. Duration of signs, mode of onset (acute or chronic),
progression of disease and description of signs which occur only
intermittently should be ascertained. When the disease is a herd
problem,morbidity, mortality, case fatality rates and epidemiological
pattern should be known.
 Changes in behaviour and mental state can often be assessed only on history.
Access to some poison and traumatic injury are often causes of nervous

190 | P a g e
 disease and they can be known only from history. The details on
convulsions like its duration, frequency and pattern are important in the
diagnosis.
 Occurrence of pallor or cyanosis during convulsions is of particular
importance in differentiating cardiac syncope and a convulsion originating
in the nervous system.
 Abnormalities of gait or reluctance to walk detected soon after the puppy has
gained its feet may be ascribed to a congenital condition present at birth,
whereas if the signs are delayed until 3-6 months of age, the animal may be
suffering from hereditary lysosomal condition leading to progressive
deterioration.
 Documenting an animal’s description narrows down the differential diagnosis
eg.,
o idiopathic epilepsy commonly occurs before the age of 3 years;
o convulsions due to intracranial neoplasia and hypoglycaemic
episodes due to tumour of pancreatic islet cells are more common in
dogs over 3-5 years old;
o inherited epilepsy is common in miniature poodles, beagle, cocker
spaniel, dachshund and Alsatian.

GENERAL CLINICAL EXAMINATION

 General clinical examination consists largely of observations of clinical sings

manifested by the animal by inspection and other physical methods of
examination. It helps in initial location of the system involved so that
further detailed examination of the same can be undertaken.
 The clinical signs referable to diseases of nervous system include:
o manifestations of mental state (mania, frenzy, aggression, dullness
or depression, narcolepsy, coma, syncope, head pressing, aimless
wandering and various other psychological disturbances);
o abnormalities of posture and gait;
o disturbances in sensation (skin, smell, hearing and sight);
o nystagmus;
o balance;
o muscle tone; paralysis; neurogenic muscular atrophy;
o autonomic disturbances (e.g. colic, incontinence of faeces and urine
etc.,)
 The preliminary inspection of animal should be performed whenever possible
without the animal being aware of the clinician’s presence or at least in an
undisturbed state.

EXAMINATION OF CRANIAL NERVES (CN)

191 | P a g e
  Olfactory nerve (1st Cranial Nerve): Tests of senses of smell in animals usually
fail to give an unequivocal result because they are conditioned to sounds
and movements associated with feed preparation and presentation.
 Optic nerve: Particular side contain outer half fibres of same side optic nerve
and inner half fibres of opposite side optic nerve. The optic tracts terminate
in optic centres and from there, a system of nerve fibres known as optic
radiation originates and conducts impulses to the cortex. Field of vision
from an eye reaches the contralateral cortex. Lesions anterior to optic
chiasma result in loss of vision of the same side; whereas, lesions posterior
to optic chiasma cause loss of vision in both eyes. Visual activity can be
tested by observing
o the movement of eye while looking at the movement of an object or
person in front of the animal,
o menace response and
o ability to avoid objects in its path or ascend or descend an unfamiliar
staircase.
 Oculomotor, trochlear and abducent nerves (3rd, 4th and 6th CN): They control
the movements of eye ball as they supply fibres to the muscles of eye ball as
follows:

Nerves Muscles of eyeball Signs of dysfunction

Oculomotor Sphincter pupillae muscles and ciliary Power of accommodation
muscles affected.
Trochlear External rectus and Retractor oculi Inward movement of eye ball.

Abducent Superior oblique Inability to move eye ball

outward

 Trigeminal nerve (5th CN): It supplies

o sensory fibres to eye, both eyelids, lips, hard and soft palate, upper
and lower teeth, nasopharynx, larynegeal gland, tongue, forehead
and face and
o motor fibres to muscles of mastication.
o Sensory function can be tested by conjunctival and corneal reflexes,
wherein the conjunctiva and cornea respectively are to be touched
gently. In both cases the response is rapid and forceful closure of
eyelid occurs.
o Test for sense of taste is difficult to conduct in animals.
o Motor function to muscles of mastication can be evaluated by jaw
tone which can be assessed by resistance offered when attempting to
open the mouth. A dropped jaw that does stay closed implies
bilateral dysfunction of trigeminal nerve. In case of one side
paralysis, muscles of that side will not be prominent and while

192 | P a g e
 attempting to open mouth, lower jaw tends to deviate towards the
side on which nerve is paralysed.
 Facial nerve (7th CN) : It is otherwise called nerve of expression. It supplies
motor fibres to muscles of face, lips, cheeks, nostrils and external ears.
o Paralysis of one side results in dropping of ear with no response to
pinch, eye remaining open, menace response being weak or absent,
upper lip drawn towards healthy side, lower lip hangs down on the
affected side, saliva dribbles from mouth and face on the affected
side looking stupid with vacant look. In horse, in addition to above
signs, dilatation of nostrils can also be controlled by facial nerve.
o In bilateral paralysis, there is dyspnoea on strenuous exertion,
difficulty in prehension and dropping of food and saliva by chewing.
 Auditory nerve (8th CN): It consists of auditory and vestibular branches.
Auditory branch is concerned with the function of hearing while vestibular
branch is concerned with maintenance of equilibrium.
o Power of hearing can be tested by a fairly loud command. Animal
with normal hearing raises its head and turn towards the direction of
sound with movement of ear to catch the sound.
o Head tilt and nystagmus are indications of vestibular dysfunction.
Destruction of labyrinth or damage to vestibular nerve on one side
causes the animal to hold its head turned so that the affected side is
lower and animal tends to fall towards, the damaged side. Other
indications of vestibular dysfunction include ataxia, leaning or
circling to one side.
 Glossopharyngeal nerve (9th CN): It is mixed nerve consisting of sensory and
motor fibres. Sensory fibres supply to mucous membrane of tympanum,
Eustachian tube, pharynx, posterior 3rd of tongue, soft palate and tonsils
while, motor fibres supply to muscles of pharynx.
o Its function can be tested by swallow or gag reflex after opening
mouth and inserting a gloved finger at the back of throat or by
pinching throat or nose to elicit a swallow reflex. This procedure is
avoided in rabies suspected case. If the animal is aggressive, it
should be observed while swallowing water or food, instead. Cranial
nerves 9th and 10th contribute to this reflex.
 Vagus nerve (10th CN): The connections formed by vagus with neighbouring
nerves and with sympathetic are very extensive. Larynx, pharynx,
oesophagus and organs of thorax and abdomen are supplied by vagus.
Hence, the effects of dysfunction depend on the location of lesion. Some
significant effects are dysphagia, roaring in horse, tachycardia, digestive
dysfunction, etc.,
 Spinal accessory nerve (11th CN): It is a motor nerve and consists of two parts
viz., spinal and accessory. The spinal part arises from cervical part of spinal
cord and supply motor fibres to trapezius and sternocephalic muscles.
Dysfunction of this part of nerve results in dropping of scapula on affected

193 | P a g e
 side and head slightly turned to the affected side. The accessory part arises
from medulla and supplies motor fibres to vagus for pharynx and larynx.
 Hypoglossal nerve (12th CN): It is motor to the tongue. In unilateral paralysis,
tongue lies limply over the affected side while in bilateral paralysis, tongue
hangs limply from the mouth.

POSTURAL REACTIONS

 These reactions test the proprioceptive fibres of peripheral nerves, spinal cord,
brain stem, cerebrum, cerebellum and inner ear. They also test the long
motor pathways of UMN and their connections to LMN. The technique
involved is to either place the patient’s limb in an abnormal position to see
if the patient returns the limb to a normal position or to make the patient
carry more weight on a limb than normal and see if the limb can still be
used normally. The clinical deficit is contralateral in lesions of cerebrum
and ipsilateral in lesions of brain stem, spinal cord and peripheral spinal
nerves. Postural reactions are preserved in cerebellum and peripheral
vestibular injuries but ataxia is present. Co-ordination by vestibular nuclei -
Posture
 Proprioceptive positioning: It is performed by standing the limb knuckled
over at paw and observing ability of animal to correct this abnormal
position. The limb may also be abducted or adducted into abnormal
postures, which the animal with normal proprioceptive sense should
correct.
 Hemihopping / Hemistanding / Hemi walking: In this test, the patient’s limbs
on one side are held off the ground, while the patient is forced to walk
sideways on its remaining two limbs. This is an excellent test of strength as
a normal animal has no trouble in maintaining itself during the test. Weak
animals sag and / or collapse on the abnormal side. This test is also
excellent for detecting subtle asymmetries not detected on observation of
gait.

 Wheel barrowing: For it, initially patient’s thoracic and then pelvic limbs are
held off the ground while he is walked forward and backward on its two
weight bearing limbs. A normal animal usually supports itself during this
test and generally, the limbs move symmetrically.
 Hopping: Here, the clinician supports all limbs except one, making the patient
hop on one weight bearing limb. This test is excellent for detecting subtle
loss of strength, as well as for detecting the left to right asymmetry between
paired limbs.
 Tonic neck and eye reaction: They are tested when the animal is standing in
normal posture by flexing and extending the neck throughout its extreme
range. During flexion of neck, the animal’s eyes maintain their forward gaze

194 | P a g e
 but forelegs are extended and hind legs flexed. Function of these reflexes is
to maintain the direction of vision and position of head.
 Supporting or placing reaction: They are applicable either to forelimbs or hind
limbs and may be tested with or without a blind fold and accordingly called
tactile placing reaction or visual placing reaction. To test the reaction,
animal is held off the floor and slowly advanced until distal tibial or radial
region almost touches the edge of a table or chair. The normal dog or cat
immediately lifts the legs and place them on the table or chair before any
contact is made. Each leg can also be tested separately by grasping and
restraining one leg at a time. These reactions may aid in differentiating
between a lesion in anterior and posterior cortex; because visual placing
reaction necessitates an intact occipital cerebral lobe and the tactile
reaction does not so.
 Extensor postural thrust reaction: The test can be applied to both fore legs and
hind legs and performed by suspending and lowering the paws of animal
until they just touch the ground, upon which the animal shuffles its feet to
adjust its position. It may also be done by pressing down on the limbs and
noting the strength and symmetry of extension of limbs combating
downward pressure. Any loss of conscious proprioception seriously affects
this reaction which is used to determine the integrity of contralateral mid-
cerebral cortical function.
 Righting reaction: The dog or cat is blind folded and laid on its side and then
released in this test. The normal animal immediately assumes sternal
posture and gets up. It should be repeated with animal on its other side. A
weak or toxaemic animal may assume or remain in lateral recumbency and
then give the impression of loss of righting reaction. The reaction tests the
function of utricle, vestibular branch or auditory nerve, cerebellum and
portions of spinal cord.

SPINAL SEGMENTAL REFLEXES

 These reflexes directly test reflex arcs of spinal cord and injuries within a
reflex are cause dampening or total reflex loss. The reflex arc is also referred
to as a LMN and motor pathway connecting the brain centres to reflex arc is
called UMN.The signs or changes in the reflex is accordingly called UMN /
LMN sings or reflex change. Spinal reflexes may be divided into various
types based on the type of stimulation required to elicit them like
proprioceptive reflexes, nociceptive reflexes and special (released) reflexes.
Monosynaptic reflex arc and Polysynaptic reflex arc

195 | P a g e
  Proprioceptive reflexes: These reflexes are initiated by stretching of tendons
or muscle spindles and are strongly influenced by UMN. Hence, these
reflexes are diminished or absent in LMN lesion and exaggerated in UMN
lesion. As part of evaluation of proprioceptive reflexes, the muscle tone
should be evaluated.
 Triceps reflex: The reflex is elicited by striking the tendon of insertion of the
triceps muscle. A normal response is a slight extension of limb at the elbow.
This reflex is often difficult to obtain in normal animals and when present,
is hard to interpret. This reflex tests the radial nerve which arises from
spinal cord segmentsC1 – T1.
 Extensor caripi radialis reflex: This reflex is elicited by striking the muscle
belly of the extensor carpi radialis muscle, which results in extension of the
carpus. It is easier to elicit in many animals than the triceps reflex, but it is
also difficult to interpret. This reflex tests the radial nerve and spinal cord
segments C1 – T1.
 Biceps reflex: It is initiated by striking the tendon of insertion of biceps
muscle. A normal response is a slight flexion of the elbow. The reflex is
more difficult to obtain than triceps reflex and is also difficult to interpret.
It evaluates the musculocutaneous nerve which arises from spinal cord
segments C6-C8.
 Patellar reflex: It is the most important reflex in veterinary medicine and seen
only in recumbent animal. The reflex is elicited by striking straight patellar

196 | P a g e
 ligament with the handle of a percussion hammer or other suitable
instrument. When it is possible to apply the test in large animal, middle
patellar ligament is struck with the head of percussion hammer or back
edge of hand. Normal response is immediate contraction of quadriceps
femoris muscle with forward extension of the limb. The reflex is mediated
via femoral nerve in segments of the spinal cord L4-L6.
 Anterior tibialis reflex: It is initiated by striking belly of the cranial tibial
muscle. The normal response is flexion of tarsus but is not a reliable reflex.
This reflex tests the peroneal branch of sciatic nerve.
 Gastrocnemius reflex: It can be tested by striking tendon of gastrocnemius
muscle, with the limb partially flexed. The normal response is extension of
tarsus but it is also not a reliable reflex. It tests the tibial branch of sciatic
nerve, which originates from spinal cord segments L6 – S1.
 Nociceptive reflexes: They are initiated by nociceptive (painful) stimuli such
as pinching, compression of digits or pin pricks and do not have a large
UMN influence. Loss of nociceptive reflex indicates LMN lesion.
o Flexor reflexes; They are initiated by compressing a digit and normal
response is withdrawal of that limb. In fore limbs, this reflex tests
function of spinal cord segments C6-T2 and its peripheral nerves
while in pelvic limbs, it involves spinal cord segments L6-S and
sciatic nerve and its branches.
o Perineal reflex: It is tested by lightly pricking the perineal region and
the response is anal sphincter constriction and tail flexion. If a mild
weakness is suspected, the best way to test the reflex is doing a digital
rectal examination, so that the examiner can feel the sphincter’s
contracture strength. This reflex tests the peroneal and pudental
nerves, spinal cord segments S1-S3 and cauda equina.
 Panniculus reflex (Cutaneous trunci reflex ): It is initiated by stimulating
truncal skin with a pin or haemostat and normal response is contraction of
skin over entire thoracic trunk and cranial lumbar trunk. This reflex tests
the spinal cord segments C8-T1. It helps to distinguish between injuries to
the brachial plexus (reflex should be present) and thoracic limb nerve roots
(Reflex often absent). In some normal animals, this reflex may not be
present and so it must be interpreted cautiously.

View video

 Special (released) reflexes: If there is disconnection between reflex arc and

UMN, these reflexes become released. The ability to elicit these reflexes in
an adult animal indicates loss of UMN inhibition on the reflex arc and
presence of CNS lesion.
o Babinski reflex: It is elicited by lightly striking the plantar aspect of
metatarsus. In normal animal, the toes either do nothing or flex
slightly. In the presence of UMN lesion, toes spread apart and elevate

197 | P a g e
 (dorsi flex) which is known as positive babinski reflex and is
indicative of damage to UMN pathways to pelvic limb.
o Crossed extensor reflex: This can be seen in any limb and is
produced during the flexor reflex evaluation. In a normal animal, the
limb being stimulated flexes (a normal flexor reflex) and the
contralateral paired limb does nothing. In UMN disease, when there
is flexion of stimulated limb, the contralateral paired limb
involuntarily extends. This crossed extension is a consistent and
reliable sign that the limb that extends has lost some or all of its
UMN regulation.

SPINAL NERVES

 As lesions of spinal nerves affect function of LMN components, the resultant

paralysis is accompanied by muscle atrophy. Identification of the particular
nerve involved necessitates a sound knowledge of the anatomical
distribution and function of those spinal nerves likely to be affected. The
injury is usually unilateral except in cases of sacral or multiple pelvic
fracture.
 Location of lesion in central nervous system and the related clinical signs are
summarized in the following table.

Location Clinical signs

of lesion
Cerebrum Apathy/depression, disorientation, aggression, hyperexcitability, visual
impairment (contralateral), normal pupillary reflexes, compulsive
pacing, circling towards the lesion, view video contralateral hopping
and placing deficit, transient contralateral hemiparesis, little gait
deficit, seizures and papilloedema.
Midbrain Mental depression, coma, ventrolateral strabismus (ipsilateral),
mydriatic pupil, unresponsive to light with normal vision, ptosis,
spastic hemiparesis (contralateral)/rigid extension of all limbs
(opisthotonus), increased reflexes and muscle tone in contralateral/all
limbs and hyperventilation.
Vestibular Central Peripheral

Loss of balance Yes Yes

Head tilt Yes Yes

Falling / rolling Yes Yes

Nystagmus Horizontal, rotatory Yes Yes

198 | P a g e
 Vertifical, positional Yes No
Strabismus Yes Yes
Cranial nerve deficits Possible 5,6,7 Possible 7

Horner’s syndrome No Possible

Cerebellar signs Possible Not possible

Pons and Multiple cranial nerve deficits, hemiparesis (ipsilateral) to tetraplegia,

medulla increased reflexes and muscle tone in all limbs, irregular respiration,
mental depression may or may not be present.
Spinal cord Ataxia (Pelvic limbs often worse) reduced flexion / extension of head
C1 – C5 and neck, neck pain and rigidity, hyperactive spinal reflexes, postural
reactions depressed in all limbs, spastic hemiparesis to tetraplegia,
urinary incontinence (spastic) and respiratory difficulty may or may not
be present.
Spinal cord Monoparesis, hemiparesis or tetraplegia, depressed reflexes and
C6-T2 muscular atrophy in thoracic limbs, increased reflexes and muscle tone
without atrophy in pelvic limbs, depressed postural reactions in all four
limbs, urinary incontinence (spastic), increased sensitivity at the level
of lesion, reduced sensitivity behind the level of lesion, horner’s
syndrome (miosis, enopthalmos, ptosis and protrusion of 3rd eye lid),
depressed paniculus reflex (unilateral/ bilateral) and neck pain.

T3-L3 Spastic weakness / paralysis in pelvic limbs, normal thoracic limbs,

increased reflexes and muscle tone without atrophy in pelvic limbs,
urinary incontinence (spastic), increased sensitivity at the level of
lesion, reduced sensitivity caudal to the lesion, postural reaction
depressed in pelvic limbs, superficial sensory level, loss of panniculus
and deep pain alteration.

L4-Cd5 Flaccid weakness/paralysis of pelvic limbs, urinary incontinence (over

flow flaccid bladder), postural reaction depressed in pelvic limbs and
normal in thoracic limbs, reduced reflexes and muscle tone with
atrophy in pelvic limbs, dilated anus and faecal incontinence (S1 – S3),
atonic tail (Cd1-Cd5), superficial sensory level and deep pain alteration.
CEREBROSPINAL FLUID ANALYSIS

 Cerebrospinal fluid is collected from cisterna magna or sub-acrachnoid space

in the lumbar region using a suitable spinal needle (15 cm, 16 gauge for
horses and cattle; 7-9 cm, 22-20 gauge for cats and dogs).
 Cisterna magna site is preferred in dog and cat while lumbar site is selected in
horse and cattle.

199 | P a g e
  General anaesthesia is required for cisterna magna puncture but local
anaesthesia may be sufficient for lumbar puncture in cattle.
 For dog, a short acting barbiturate provides satisfactory anaesthesia.
 Procedure: The animal is placed in lateral recumbency and the site is prepared
as per surgical standard. The site of puncture is midline between occipital
crest and wings of atlas just cranial to dorsal spine of 2nd cervical vertebra.
Neck is fully flexed and nose held parallel to the table surface by an
assistant. The spinal needle is inserted through located site and tip is
directed towards the dog’s nose. As the needle penetration advances, a
sudden reduction in resistance indicates that sub-arachnoid space has been
reached. When stillet is withdrawn, fluid welling from the needle, confirms
that it is in the correct position and requisite sample can be collected by
attaching a sterile hypodermic syringe. To measure CSF pressure, a 3 way
tap and manometer are attached to the needle and reading is taken
immediately before collecting CSF.
 For cattle, site of lumbar puncture is located by determining point of
intersection of a line joining the cranial borders of tuber coxae with dorsal
sagittal line. Then, by palpation, the soft depression between dorsal process
of last lumbar vertebra and cranial end of median – sacral crest is located.
The puncture is made in standing position. Tranquilizer may be necessary
in horse but technique of collection is the same as described for cisternal
puncture. Lumbar puncture in sheep is more satisfactorily achieved with
the animal in sitting position. For pigs, lumbo – sacral puncture usually
gives more satisfactory results than cisternal puncture and it is done in
sitting position.
 Analysis of CSF: CSF is examined for various physical and chemical qualities
viz., colour, turbidity, coagulation, specific gravity, total and differential cell
counts, protein, chloride, glucose, blood urea nitrogen, etc. The normal
values for various species are given in table

Normal values of cerebrospinal fluid

Speci Pressu Physical Specif Cells Protei Gluco BUN Chlori

es re (mm appearanc ic / n se (mg% de
of e gravit cmm (mg% (mg%) ) (mg%)
H2O) y )
Cattle 88-330 Clear and 1.006 – 0-10 <40 35-70 11.0 620-760
watery 1.007
Horse 180-490 - 1.004 – 1-7 <70 40-78 2.3 – 388-792
1.008 3.2
Sheep 60-270 Clear and 1.004- 0-5 <40 39-109 5.62 750-868
colourless 1.008

200 | P a g e
Pig 80-145 Clear and - 0-7 <40 45-87 - -
colourless

Dog 24-172 Clear and 1.003- 1-8 <25 45-116 6-10 602-
colourless 1.0125 883

Cat 100 Clear and 1.005- 0-5 <20 53-67 2.3-3.2 670-723
colourless 1.007

 Normal CSF is clear, colourless, watery and does not coagulate. Bright red
colour indicates contamination with pure blood, which could have occurred
at the time of puncture. Yellow colouration is the result of haemorrhage
occurred sometime previously. In haemorrhage of inflammatory or
traumatic origin, CSF is dull red to brown in colour while in suppurative
conditions, it is greenish colour with more of neutrophils. Coagulation is a
feature in suppurative meningitis, internal haemorrhage and blood
contamination. Lymphocytes are increased in viral infections, chronic
infections, fungal infections and toxaemic states. Increased levels of protein
are observed in inflammatory and non-inflammatory diseases of CNS,
pneumonia, uraemia and convulsive states. Glucose concentration increases
in encephalities, spinal cord compression, brain neoplasm, brain abscess
and hyperglycaemia. In systemic hypoglycaemia and acute pyogenic
infections, glucose level is decreased while chloride is decreased in
meningitis.

ELECTROENCEPHALOGRAPHY (EEG)

 It may aid or confirm the localization of a lesion or provide support for a

diagnosis of hydrocephalus, encephalitis, asymmetrical lesions, acquired
epilepsy or brain death. EEG amplifies, filters and graphically records the
alterations over time of electrical potentials from cerebral cortex.
 Although there are seldom specific changes for a particular disease, an EEG is
indicated for many patients with signs of cerebral or head abnormalities.
Because of the high cost of the unit and a expertise necessary to interpret
the findings, availability is usually restricted to teaching hospitals.

OTHER DIAGNOSTIC PROCEDURES

 Radiography – myelography, cerebral arteriogrphy, cerebral venography and

ventriculography
 Computerised tomography
 Ultrasonography
 Magnatic resonance image
 Electromyography

201 | P a g e
  Spinal and brain evoked potentials
 Brain stem auditory evoked response
 Somato sensory evoked response
 Brain biopsy

GENERAL PRINCIPLES IN THE TREATMENT OF NERVOUS

DISEASES

 Blood-brain barrier is an important factor limiting elimination and control of

infection. It provides anatomic and physiological barrier to the movement
of materials into central nervous systems(CNS), thus limiting the entry of
therapeutic agents into CNS.
 Significant discrepancies exist between serum and cerebro-spinal fluid
concentration of drugs due to blood brain barrier. Macro molecules are
prevented from crossing this barrier. Hence, drugs with low albumin
binding should be selected for treatment.
 Drugs with low ionization and high lipid solubility more readily cross this
barrier eg., esterified ampicillin are more lipophilic and hence, cross the
blood-brain barrier (BBB) with ease.
 Inflammation of meninges increases the ability of anti-bacterial drugs to cross
BBB 5-10 folds. As inflammation subsides, the drug concentration drops.
 The ability of certain antibiotic / chemotherapeutic agents to cross the BBB is
given bellow:

Excellent with or without - Chloramphenicol, sulphonamide,

inflammation trimethoprim
Good only with inflammation - Ampicillin, Carbencillin, Cephalothin,
Cephaloridine
Minimal or not good with - Tetracycline, streptomycin, Kanamycin,
Inflammation Gentamycin
No passage with inflammation - Polymixin B, Colistin

 Failure to respond to antibiotic can be due to irreversibly advanced lesions

and in chronic suppurative process. The antibacterials can also be injected
directly into cisterna magna or lumbo-sacral space and should be given
daily for several days for cure. Preparations containing propylene glycol
should not be used for intrathecal administration, as it may cause rapid
death.
 Untreated brain oedema harms the brain by compression of axons and by
increasing intracranial pressure (ICP).

202 | P a g e
  Intracranial pressure elevation also compresses cerebral venous sinuses and
impairs cerebro – spinal fluid resorption and thus increase intracranial
pressure.

THERAPEUTIC APPROACH

 Several methods are used to alleviate brain oedema and / or lower ICP.
 Hyperventilation: There is a direct relationship between ICP and CO2 level as
its level reduces with low ICP. Hyperventilation is a simple and effective
means of lowering CO2 level.
 Mannitol: It is an osmotic diuretic commonly used to lower elevated ICP.
They are short – lived in their therapeutic effect and should never be
administered in hypovolaemia. The drug is used @ 0.5-2.0 gm/kg as 20%
solution IV over 30-60 minutes and repeated every 4-6 hr.
 Diuretic: It lowers ICP by both removing oedema and decreasing intracranial
volume. Furosemide is given @ 0.7 mg/kg IV and repeated every four
hours. If furosemide is administered in conjunction with mannitol, the
effect of both drugs are enhanced.
 Corticosteroids: These are used in high doses within 8 hr of trauma. It has
also been successfully used to treat oedema associated with brain tumours.
Prednisolone sodium succinate or phosphate @ 30 mg/kg is given initially
followed by repeated doses of 6-10 mg/kg once or twice daily. Alternatively
dexamethasone @ 0.5-2 mg/kg IV once daily or in two divided doses gives
very good results. In emergency, combination of mannitol with
corticosteroid is advisable.
 Hypertonic glucose solution: It also brings about decompression; but within
4-6 hr, there is again rise of cerebro-spinal fluid pressure. Hence, it is not
commonly used.
 Glycerol therapy: It is non-toxic and there is no rebound increase. It is used
@ 1.5 gm/kg every 24 hr in 3-4 divided doses orally (or) 500 ml of 10%
glycerol by slow IV in 3-4 hr time for 4-6 days.
 Dimethyl sulfoxide(DMSO): The drug is used @ 2 mg / kg as 40% solution
and response is seen in 6-8 hr.
 Anti-inflammatory therapy: Most effective therapy for inflammation is the
use of corticosteroids. It can be used even in infections since most of the
clinical signs are related to inflammation.
 CNS stimulants: They exert only transitory improvement and indicated
during nervous shock, anaesthetic accidents and short term reversible
anoxia. Eg., in anoxia due to cyanide or nitrite poisoning, CNS stimulants
are indicated.
o Doxapram HCI is given in dog @ 5.5-12 mg/kg IV every 15-20
minutes or in horse / cattle @0.2 mg/kg iv every 15-20 minutes.
o Bemegride @ 15 mg/kg iv or Coramine @ 22-44 mg/kg IV may also
be used

203 | P a g e
  CNS depressants: They are indicated in convulsions to avoid injuries.
Narcotics and genral anaesthetics are in common use to satisfactorily
control status epilepticus.
 Antineoplastic therapy: Treatment for tumour of nervous tissue consists of
surgical removal, radiation therapy, chemotherapy, or a combination of two
or more methods. Both radiation therapy and surgery have shown promise
in veterinary medicine. In general, they increase the length of life and
improve quality of life of animal.

MODULE-28: HYDROCEPHALUS, ENCEPHALITIS,

ENCEPHALOMALACIA AND MENINGITIS

Learning objectives

 To study the etiology and pathogenesis of hydrocephalus, encephalitis,

encephalomalacia and meningitis.
 To learn the clinical findings, diagnosis and treatment of hydrocephalus,
encephalitis, encephalomalacia and meningitis.

AETIOLOGY OF HYDROCEPHALUS

 In a broader sense, Hydrocephalus refers to as an increase in the volume of

cerebrospinal fluid and commonly seen in large ruminants and dogs. The
primary problem is often overlooked due to death of the animals by
complications.
 It can be classified into
o Normotensive hydrocephalus; and
o Hypertensive hydrocephalus.
 In Normotensive hydrocephalus, there is failure of cell growth or destruction
of tissue from degeneration associated with ischemia, inflammation or
injury. It is seen in bovine viral diarrhea, in vitro infection of foetus by blue
tongue virus, polioencephalomalacia, vitamin A deficiency in pregnant sow
and thrombosis of middle cerebral artery in calves..
 Hypertensive hydrocephalus occurs due to obstruction of CSF flow by
compression or lesions in the ventricular system or decreased cerebrospinal
fluid absorption.
o The obstructive pathology can be acquired or congenital. Acquired
lesions are seen in cerebral abscess, pachymeningitis, vitamin A
deficiency, coenurus cerebralis infestation, equine infectious
anaemia, etc.
o Congenital lesions occurs in malformation of skull bones resulting in
obstructive pathology and observed in certain breeds of cattle like
Ayrshire, Dexter, Jersey, Shothorn and Charolais.

204 | P a g e
 o Viral infections of foetus may also lead to congenital defects. It is also
common among small breeds of dogs with large skull (toy poodle,
Chihuahua, etc.) and among brachycephalic breeds (Boston terrier,
English bull dog, etc.)

PATHOGENESIS, CLINICAL AND NECROPSY FINDINGS OF

HYDROCEPHALUS

Pathogenesis of hydrocephalus

 The loss of neurons due to degeneration or necrosis of nervous tissue causes

arthrogryposis (flexural contraction of limbs).
 In obstructive type, there is embryological defects in drainage canals or in the
absorptive mechanism of arachnoid villi.
 Neoplasia may interfere indirectly with absorption through the arachnoid villi
because of its compressive effects on venous sinuses.

Clinical and necropsy findings in hydrocephalus

 Frequently young ones are born dead or born weak and die shortly after birth.
The clinical signs are referable to disturbance of cerebral hemispheres.
 There is disturbed consciousness varying from lethargy to severe depression,
tendency to sleep, hypoactivity, circling, head pressing, droopy head and
ears, head tremors, muscular fasciculation, spastic paresis, hypermetric
ataxia, blindness, ventrolateral strabismus, nystagmus, tongue flaccidity,
retention of food material in cheeks and lips, slow postural reaction, hyper
reflexia, psychomotor seizures, recumbency and coma.
 The clinical signs of hypertensive hydrocephalus may be unilateral or
bilateral. The unilateral sings include head tilt (towards lesion side),
ipsilateral mydriasis and contralateral menace deficit.
 Necropsy findings: Cholesterol clefts are interspersed with inflammatory cells
and blood vessels

DIAGNOSIS AND TREATMENT OF HYDROCEPHALUS

Diagnosis

 The history and clinical signs, radiography and electroencephalography (EEG)

are useful in the diagnosis of hydrocephalus. Plain radiograph reveals
‘ground glass’ opacity of cranial cavity due to fluid contents. Examination of
cerebrospinal fluid reveals normal findings. In EEG, there is diffuse slowing
of normal pattern with a remarkable increase in amplitude in all leads.
 Serum neutralization test is useful for diagnosis of blue tongue infection;
cerebrospinal fluid pressure is elevated in it.

205 | P a g e
  Congenital hydrochepalus may be mistaken for vitamin A deficiency in
newborn, if there is no distortion of cranium. Acquired hydrocephalus
needs to be differentiated from other diffuse diseases of brain including
encephalitis and encephalomalacia and from hepatic disease.
 The other clinical sings specific to the disease (fever in encephalitis and
jaundice in hepatic disease) will be of diagnostic value.

Treatment

 Direct lateral ventricular tap provides temporary relief.

 Inj. Dexamethasone 2.2-4.4 mg/kg initially followed by lower doses of 0.25 to
1 mg/day for several days or on alternate days may be given.

AETIOLOGY OF ENCEPHALITIS

Encephalitis

 Encephalitis is an inflammatory condition of brain caused from invasion by an

infectious agent and includes inflammation of nervous tissue or vessel wall.
It is characterized by irritational signs followed by sings of loss of nervous
function.

Aetiology

 Viruses like rabies, pseudorabies, Japanese B encephalitis, bovine malignant

catarrh, sporadic bovine encephalomyelitis, hog cholera, African swine
fever, Equine infectious encephalomyelitis, borna disease, scrapie, louping
ill, visna, viral caprine leucoencephalomyelitis, western encephalitis of dog,
infectious canine hepatitis, canine distemper, herpese canis encephalitis
and parvoviral encephalitis.
 Bacterial agents like listeria, necrobacillus, haemophilus, enterotoxaemia,
salmonella and erysipelas.
 Parasites like migratory larvae, multiceps multiceps and coccidiosis
 Fungal agents like cryptococcosis, coccidiomyces, histoplasma, blastomyces,
aspergillus and mucor sp.
 Ricketsial agent - toxoplasma
 Toxic agents like lead, arsenic, salt poisoning, ipomia plant, etc.
 Trauma, vaccinations, allergy, old dog encephalitis and infections spreading
from eyes, nasal sinus and external ears are also probable causes.

PATHOGENESIS, CLINICAL AND NECROPSY FINDINGS OF

ENCEPHALITIS

Pathogenesis

206 | P a g e
  Virus invasion causes death of neurons while bacteria and certain viruses (e.g
bovine malignant catarrh and sporadic bovine encephalomyelitis) affect
principally vasculature.
 Virus may enter the nervous tissue by progressive peripheral nerve trunk (e.g.
rabies, pseudo rabies and listeria monocytogenes).
 Entry of infectious agents can also occur via olfactory nerve.

Clinical findings

 Encephalitis is invariably associated with systemic sings like fever and its
attendant signs of anorexia and depression.
 Initially there is a period of excitement or mania which comprises viciousness
and uncontrolled activities like blind charging, bellowing and pawing. Later, it
is followed by mental depression including head pressing.
 The usual irritational sings include convulsions, nystagmus, photophobia,
champing of jaws, View video salivation and muscular tremors of face and
limbs.
 The signs of loss of nervous functions may vary from paresis with knuckling at
lower limb joints, spasticity of limbs with resultant ataxia to complete
paralysis.
 Deviation of head, circling, abnormalities of posture, ataxia and
incoordination occur more commonly as residual signs after recovery from
acute stage.
 In listeriosis, there is unilateral facial paralysis while in pseudorabies and
scrapie, paraesthesia and hyperaesthesia occur. Ataxia video

Necropsy findings

 There is no gross lesions of CNS but, lesions of other organs specific to the
disease can be seen. Histological lesions vary with the type and mode of
action of causative agent

DIAGNOSIS AND TREATMENT OF ENCEPHALITIS

Diagnosis

 Diagnosis depends to a great extent on the recognition of clinical signs of

specific encephalitides. History and clinical pathology are important in
poisoning cases.
 Encephalitis should be differentiated from acute cerebral oedema, focal space
occupying lesions, poisonings, hypovitaminosis A, hypoglycaemia,
encephalomalacia and meniningitis.

207 | P a g e
  Encephalitis and meningitis are commonly associated with fever and
toxaemia, while it is not so with other conditions. CSF analysis will reveal
increased cell count in meningitis.

Treatment

 Treatment to the specific agent should be given.

 If there is fever, antipyrogens like analgin (cattle & horse 10-30 gm and dog &
cat 0.5 – 2.5 gm i/m or iv) or paracetamol (cattle & horse 1.5-3.0 gm i/m
and dog & cat 0.75 – 1.5 gm orally bid) are to be administered.
 Hyperthermia due to tremors or seizures can be controlled by cold water
application, ice packs or alcohol baths.
 In case of convulsions, anticonvulsants (Dog: phenobarbitone 1.5 – 5 mg/kg
i/v, 1-1.5 mg/kg i/m, 2.2 – 6.6 mg/kg orally; phenytoin 50 mg/kg/day in
two divided doses orally; sodium valproate 60 mg/kg orally tid) are
indicated while sedation (diazepam 2-5 mg tid) is done during excitement
stage.
 Corticosteroids (betamethasone or dexamethasone : cattle & horse 10-30 mg,
sheep & goat 2-5 mg, dogs & cats 0.25 – 0.5 mg i/m or i/v; prednisolone 1%
soln: cattle & horse 0.5 mg/kg or 10-20 ml i/m, dog& cats 1-3 ml i/m) help
in recovery of the case. The symptomatic treatments should be followed
until the disappearance of the clinical signs.
 Specific treatment to poisonings is necessary.
o In case of lead poisoning, calcium versenate (calcium di sodium
EDTA) as 6% solution @ 1 ml/kg/day in divided doses of two to three
times daily and thiamine hydrochloride @ 2mg/kg s/c may be given.
o In cases of arsenic poisoning, sodium thio sulfate 15-30 gm in 100-
200 ml of water i/v followed by oral dosing of 30-60 gm at 6th hourly
intervals is indicated. BAL (2,3, dimercapto propanol) is efficient
antidote for organic arsenical poisoning.
 Recumbent animals should be frequently turned to prevent decubital ulcers
and passive congestion of lungs. There may be need for expression of
bladder and use of suppositories to prevent constipation.

ETIOLOGY, EPIDEMIOLOGY AND PATHOGENESIS OF

ENCEPHALOMALACIA

 Encephalomalacia refers to softening and leucoencephalomalacia and

polioencephalamalacia refers to softening of white matter and grey matter,
respectively. Encephalomalacia includes the degenerative diseases of brain.

Aetiology

208 | P a g e
  Thiamine deficiency in simple stomach animal is often associated with the
disease.
 Nutritional deficiency of copper in lambs resulting in sway back and enzootic
ataxia,
 Grain overload,
 Clostridium perfringens type D toxin
 Hepatic encephalopathy
 Viral infection in-utero causing congenital defects like hypomyelinogenesis
and dysmyelinogenesis
 Feeding of mouldy corn infested with fusarium moniliformae causes
leukoencephalomalacia in horses.
 Organic mercurials, lead, selenium and organic arsenicals and mulberry heart
disease of pigs causes leukoencelphalomalcia.

Epidemiology

 Polioencephalomalacia is world wide in distribution and seen in individuals

and herd outbreaks. There is no sex or breed predilection and no seasonal
incidence.
 Animals above 18 months of age are commonly affected and predominantly
seen in high concentrate supplement. Mortality rate varies from 1-2 per
cent.

Pathogenesis

 Thiamine is involved in glucose metabolism and metabolism of the

neurotransmitters. There is reduction in the activity of ATP dependant
sodium and water transport mechanism in the neurons. Inward water
fluxes result in net neuronal swelling, which in turn results in increased
intracranial pressure and neuronal necrosis.
 In sway back, there is interference in phospholipids formation leading to
defective demyelination.
 In both leukoencephalomalacia and polioencephalomalacia, loss of nervous
function is noticed

CLINICAL AND NECROPSY FINDINGS OF

ENCEPHALOMALACIA

Clinical findings

 Polioencephalomalacia may be acute or develop slowly over several days.

 Dullness, detach from flock, somnolence, anorexia, walking with head held
erect or tilted, head pressing, circling, blindness, dorsomedial strabismus,
miosis, nystagmus, defective menace response, repetitive chewing,

209 | P a g e
 odontoprisis, hyperaesthesis, excitement, facial twitching, muscle tremors,
opisthotonus, convulsions and terminal coma are seen in most of the
animals.
 Untreated animals usually die after 3-4 days while survivors remain
irreversibly decorticated and are culled because of poor performance,
chronic anorexia, ataxia and blindness.
 If it is due to grain over load, fowl smelling watery stool, distended fluid filled
rumen, normal rectal temperature if no muscular fasciculation and
increased pulse and respiration may be seen. In case of excessive sulphur
diet, odour of hydrogen sulphide may be detected on the breath.

Necropsy findings

 Cortical swelling, softening, flattening and yellowish discolouration of grey

matter. Microscopically there is diffuse laminar necrosis

DIAGNOSIS AND TREATMENT OF ENCEPHALOMALACIA

Diagnosis

 History and clinical signs are important in detecting the disease.

 Cerebrospinal fluid reveals mild pleocytosis (5 to 50 wbc/dl) and increased
protein concentration (>50 mg/dl).
 Thiamine pyrophosphate (i.e. all phosphorylation forms of thiamine) can be
measured in erythrocytes and rumen.
 Blood levels of pyruvate and pyruvate kinase increase.
 If grain over load is the cause, gram positive organisms are drastically
increased in rumen fluid.
 Electroencephalography reveals constant high amplitude (50 to 60 V) and
slow activity (1 to 4Hz) while diffuse lowered activity is consistent with
diffuse necrosis.
 The syndrome should be differentiated from hydrocephalus, enterotoxaemia
type D, lead or other heavy metal poisoning, vitamin A deficienty, ethylene
glycol poisoning, rabies, infectious bovine rhinotrachetis, enecephalitis and
salt poisoning. Polioencephalomalacia due to high grain diet being a
common condition, it can be differentiated from the other conditions by
examination of rumen fluid.

Treatment

 Encephalomalacia is irreversible in later stages but if treated early, i.e. before

neuronal necrosis, response is good.
 Thiamine @ 10-20 mg/kg i/m or i/v may be infused along with 5% dextrose or
other isotonic fluids. Most patients show improvement by 24 hours of

210 | P a g e
 thiamine therapy. Inj. B complex containing equivalent dose of thiamine is
preferable. Thiamine propyl disulfide can be given orally – 1 gm in sheep
and 5 gm in cattle.It suppresses bacterial production of thaminase.
 Convulsion can be controlled by use of anticonvulsants as outlined under
encephalitis.
 Oedema and pressure related neuronal necrosis can be reduced by use of
corticosteroids as given under general principles of treatment.
 Dietary intake of carbohydrate and fibre should be examined and thiamine to
be supplemented for animals at risk.

Prevention and control

 Supplementation of thamine @ 3-10 mg/kg of feed if concentrate – fibre ratio

is high helps in its prevention.
 Addition of brewer’s yeast.
 Gradual adaptation to high concentrate ration ie. over 3 to 4 weeks.
 Supplementation of cobalt in trace mineral salt mixture.

AETIOLOGY AND PATHOGENESIS OF MENINGITIS

 Meningitis is inflammation of meninges and occurs due to bacterial or viral

invasion of central nervous system. It is seen most commonly as a
complication of a pre-existing disease and clinically manifested by fever,
cutaneous hyperaesthesisa and rigidity of muscles

Aetiology

 Septicaemia in young animals caused by streptococcus, coliform and

Salmonella infections, strangles in horses, listeriosis, haemophilus,
pasteurellosis, leptospirosis, tuberculosis, pseudomonas aeruginosa
mastitis of cattle and goats, Erysepelas.
 Cryptococcus and Actinomyces sp. in horses and Mycoplasma mycoides in
goats are the common bacterial agents associated with the disease.
Infections take place through haemotogenous route.
 Most cases of viral encephalitides also cause meningitis.
 Direct extension of infectious agents may occur from fracture of skull,
osteomyelitis, spinal cord disc protrusion, sinusitis, otitis, cauterization
during dehorning and haemorrhage into sub-arachnoid space.
 Metastasis or embolic showers to CNS in case of left sided endocarditis are
also probable causes of meningitis.

Pathogenesis

211 | P a g e
  The pyogenic bacteria cause inflammation around nerve trunk as they pass
across subarachnoid space.
 The inflammatory swelling interferes with blood supply to brain and spinal
cord.
 Inflammation of meninges also affects drainage of cerebrospinal fluid and
associated sings of increased cerebrospinal fluid pressure develop. Thus,
the clinical signs appear to be related to irritation of spinal nerve roots and
neurons of cerebral cortex and to hydrocephalus.

CLINICAL AND NECROPSY FINDINGS IN MENINGITIS

Clinical findings

 Acute meningitis develops suddenly and is accompanied by anorexia, fever

and toxaemia in addition to nervous signs.
 Vomiting is common in early stages in pigs.
 Nervous signs include generalized hyperaesthesisa, trismus, opisthotonus,
rigidity of neck and back leading to refusal to lower the head to eat and
disturbed consciousness varying from excitement or mania (in early stages)
to drowsiness and coma (in later stage). Blindness is common in cerebral
meningitis.
 Young animals suffer from ophthalmitis with hypopyon. Pupillary light reflex
is much slower than normal. Examination of fundus may reveal oedema of
optic disc, congestion of retinal vessels and exudation.
 Respiration is usually slow and deep. However, Cheyne-Stokes or Biot’s
respiration is often observed.
 Meningitis in farm animals is usually diffuse involving particularly brain stem
and upper cervical cord. However, it may also be localized involving one or
more cranial or spinal nerve. In such case, localized muscle tremor,
hyperaesthesia and rigidity are noticed. The affected muscles are board like
on palpation. Anaesthesia and paralysis may develop caudal to meningitis
area. Clinical signs of the specific aetiology are also seen.

Necropsy findings

 Macroscopically, meninges are thickened with hyperaemia and haemorrhages.

 On microscopic examination, infiltration of tissue by neutrophils and
lymphocytes is seen. Additional morbid changes specific to the cause may
also be seen.

DIAGNOSIS AND TREATMENT OF MENINGITIS

Diagnosis

212 | P a g e
  History and clinical signs are important in detecting the disease. There is
neutrophilic leukocytosis of peripheral blood.
 Cerebrospinal fluid is turbid, and has tendency to clot. It contains high protein
(20-270 mg/dl), increased cell count (>100 neutrophils/ m l) and normal
(80% of blood level) or decreased (less than 50% of blood level) glucose
levels. Bacteria may be seen on gram’s staining.
 Meningitis should be differentiated from encephalitis, acute cerebral oedema,
spinal cord compression, cervical inter vertebral disc protrusion,
hypoglycaemia and hypomagnesaemia.

Treatment

 Treatment of meningitis is difficult due to which high mortality rate is

observed.
 Antibiotics in large doses for several days intravenously or into cisterna
magna or lumbosacral space are given.
 Chloramphenicol :
o Cattle and Horse – 2-4 mg/kg iv bid, 20-40 mg/kg bid im;
o Sheep and Goat – 10 mg/kg iv bid, 30-40 mg/kg im bid;
o Dog - 25-50 mg/kg iv, im, oral, bid
 Tirimethoprim – Sulfa :
o Large Animals - 30 mg/kg iv, im, oral, bid
o Dog - 15 mg/kg iv, im, oral bid
 Ampicillin :
o Cattle, Horse - 5-10 mg/kg/iv, im, tid
o Sheep and Goat - 5-10 mg/kg iv, im, tid
o Dogs - 10 mg/kg iv, im, tid ; 20 mg/kg tid orally
 Cefotaxime : Dog - 25-50 mg/kg/day iv in divided doses
 Cephaloridine : Dog - 15-30 mg/kg/day/i/m or iv in divided doses

 Enrofloxacin : Dog - 5mg / kg once daily

 Corticosteroids are used to combat deleterious effect of inflammation as
outlined earlier.
 Muscle relaxants (glyceryl guaiacolate @ 90mg/kg as 10% solution in 5%
dextrose) and anaesthesia, anticonvulsants, supportive therapy with
intravenous fluids, antitoxin or toxin (immunization) and specific
monoclonal antibodies are also used to manage the affected cases.

MODULE-29: EPILEPSY

Learning objectives

 To study the etio-pathogenesis of epilepsy, coma, GID and ataxia

213 | P a g e
  To learn about the clinical findings, diagnosis and treatment of epilepsy,
ataxia, coma and GID

FORMS/TYPES OF EPILEPSY

 A seizure, ictus, fit or convulsion is a paroxysmal, uncontrolled transient

electrical discharge from the neurons of brain. The term epilepsy refers to a
condition of recurrent fits, which arise from non-progressive intracranial
disease and should not be reserved for idiopathic (true, primary or
inherited) epilepsy. Epilepsy is common in dogs and cats but rare in large
animals.

Forms / Types

 Two major forms of seizure are recognized on clinical, EEG and pathological
grounds.
o Generalized - Grandmal seizures, petitmal seizures
o Partial / Focal - Psychomotor seizure, Jacksonian seizure
 Generalized seizure
o Grandmal seizure: Grandmal seizure is the most common form of
convulsion in dogs and cats and it is characterized by behavioural
alteration followed by a combination of visceral and somatic motor
activity, as the dog loses contact with its environment and becomes
unconscious. Pupillary dilatation, excessive salivation and chewing
activity represent the visceral motor activity. The limbs become tonic
and are extended rigidly and animal falls on its side. A brief period of
opisthotonus, marked tonic limb extension and apnoea are followed
by or alternated with tonic limb activity and paddling or running
movements. This somatic motor activity is usually bilaterally
symmetric from the onset and throughout its course. Occasionally,
there are urinary and faecal excretions during or after convulsion.
The entire convulsion lasts 1-2 minutes but longer and severe
generalized seizures may be associated with toxicity and metabolic
disorders. The recovery period usually lasts a few minutes to an hour
but is variable.
o Petitmal seizure: It is much more common in man and occasionally
seen in dogs. It is characterized by a very brief loss of consciousness
and dog often does not collapse.
 Focal seizure or partial seizure: It may consist of tonic or clonic contractions
of isolated muscle groups without loss of consciousness. Focal lesions
within the crerbrum often result in episodic clinical signs that are related to
the specific region of the brain involved. It might be acquired due to trauma
at birth, neonatal hypoxia, postnatal intracranial trauma, encephalitis,

214 | P a g e
 neoplasia, etc. The seizure may not appear until months to years after
acquiring the epileptogenic foci.
o Psychomotor seizure: When the focus is in temporal lobe of cortex,
seizure consists of altered behaviour accompanied by complex motor
activity. This type of seizure activity is called as psychomotor seizure
and does not occur in animals.
o Jacksonian seizure: This type of epilepsy is very rare in animals and
is characterized by a spasm slowly spreading from one limb to
another.
 Extra cranial causes of seizure include hypoglycaemia, hypocalcaemia,
hyperlipoproteinaemia and gastro intestinal parasites while intracranial
causes include inflammation / degeneration, neoplasms, malformation and
trauma.

Phases

 There are four typical phases in epilepsy,

oProdromal phase: a period of mild behavioural change lasting for
hours or days just before a fits known as prodormal phase,
o Aura: it is very short usually lasting a few seconds and is
characterized by a more pronounced behavioural change
immediately preceding the onset of seizures.,
o Fit or ictus: the actual fit in most cases lasts only for 30 seconds to
two minutes and
o Postictal phase: a period lasting for hours in which animals seem
disoriented and may appear blind, hungry, thirsty, affectionate or
restless.
 Seizure activity results from the synchronization of large aggregates of
neurons that are driven, at least in the case of partial seizures, by abnormal
epileptic neurons in a seizure focus that recruit increasing numbers of
connected neurons. Generalized epileptic seizure activity may results from
subcortical pacing neurons acting through the excitatory amino acid
system. These neurons probably are heavily dependant on asparatate and
glutamate for facilitation. Microscopic abnormalities of brain may be
detectable in focal epilepsies but not usually in generalized epilepsies.

TREATMENT OF EPILEPSY

 Before therapy, every effort should be made to recognize the cause of epilepsy
by detailed history, physical examination including neurological
examination of the animal, laboratory examination, radiography, EEG,
scintigraphy and cerebral angiography. If no abnormality is detected in
these examinations, a diagnosis of idiopathic epilepsy can be arrived.

215 | P a g e
  Anticonvulsant therapy can be commenced when no extracranial causes for
seizure disorders are evident, seizure frequency greater than once in every
four to six weeks, cluster of seizures more than once during a period of eight
weeks, recurrent seizures accompanied by aggression and severe
generalized seizures concern the owner and he is willing to comply with
recommendation for treatment regimens and monitoring.
 Phenobarbitone Maximally suppresses spontaneous electrical discharge from
seizure foci at subhypnotic dosage and is most successful and inexpensive
anticonvulsant. Initial lower dosage of 3 to 5 mg/kg may give rise to
sedative side effects and slight ataxia during the first week, which
disappears in a short time on development of tolerance. The initial side
effects can be minimized by dividing the dose and later the drug can be
given as a single dosage in the evening on development of tolerance. Due to
long half-life of phenobarbitone, it takes about a fortnight to reach a steady
state of serum concentration and fits may occur during this period. Dosage
need to be raised up to 15 mg/kg in certain cases to control the seizures to
achieve the significant improvement. Increase in dose is finally limited by
sedative and hypnotic side effects to which tolerance no longer develops.
Polydipsia and polyphagia are common side effects. Clinical reports
indicate that 60 to 80% of epileptic dogs can be controlled effectively with
phenobarbitone as sole anticonvulsant agent.
 Primidone is a structural analogue of phenobarbitone that undergoes hepatic
oxidation to phenobarbitone and phenylethyl malanamide (PEMA). It is
estimated that phenobarbitone accounts for 80 to 85% of the
anticonvulsant activity of administered primidone and is effective in 52 to
87% of treated epileptic animals. The disadvantage with this drug is
frequent behavioural side effects and greater hepatotoxicity compared to
phenobarbitone. In most dogs, primidone dosage must be increased to 30
to 50 mg/kg daily for an acceptable improvement.
 The drung phenytoin is highly effective in the treatment of generalized motor
seizures in human beings. In the dog, however, it undergoes rapid
metahydroxylation, glycyronidation and renal excretion. It is a potent
microsomal enzyme inducer and stimulates its own degradation with
chronic administration. It leads to reduced half life on continued treatment.
On the basis of available clinical and pharmacokinetic data, it is not an
anticonvulsant of choice in dogs.
 Gastrointestinal absorption of valproic acid is rapid in dog, but the half – life
is only 1.2 to 3.7 hours.
 The use of diazepam as primary anticonvulsant in dog has been limited
because of significant fast hepatic clearance, rapid development of
functional tolerance to the anticonvulsant effects, short half life and high
cost. However, it has been very effective in control of feline seizure
disorders at a dose rate of 0.5 to 2.0 mg/kg orally and given every eight
hours.

216 | P a g e
Status Epilepticus

 It is a condition in which seizures are continual, one after the other,

with no
recovery between them. The condition can lead to irreversible coma or
death, and should be considered a medical emergency. Death in such cases
is caused by a combination of hyperthermia, circulatory collapse and
acidosis and hypoxia from muscle exertion and impaired respiration.
 Status epilepticus may resume from abrupt discontinuation of antiepileptic
medication.
 For the management of status epilepticus, the airway of the animal should be
established and oxygen be given, if necessary.
 If hypoglycaemia is suspected, after blood glucose estimation, 50% dextrose
should be administered.
 Anticonvulsive therapy consisting of Diazepam 2 mg for 5 kg dog /cat i/v, 5
mg for 10 kg dog i/v or 10 mg for 20 kg dog i/v be given.
 Local anaesthetic e.g. lignocaine 2 mg/kg slow intravenously can interrupt a
status epilepticus.
 Oral anticonvulsive therapy shall start as soon as the animal can swallow.
 If temperature remains elevated, ice water or alcohol bath may be given.
 If cerebral oedema is suspected, oxygen / mannitol /corticosteroids should be
used.

MODULE-30: ATAXIA, COMA AND GID (STURDY)

Ataxia

 Ataxia is synonymous with in co-ordination of muscular action or gait.

 If ataxia is due to lesions in geneal proprioceptive system, it is referred as
sensory ataxia as opposed to motor ataxia of cerebellar cortical disease.
 In animals, ataxia due to cerebellar dysfunction can be difficult to differentiate
from the proprioceptive defects (sensory ataxia) and partial motor paralysis
(weakness) which occurs with spinal cord lesions.

Aetiology

 In general, involvement of cerebellum and spinal cord causes ataxia. The

specific conditions include
o Inherited defects of cerebellar structure,
o congenital cerebellar defects (due to bovine viral diarrhea infection),
o injury due to parasitic larvae such as Hypoderma bovis,
o encephalomyelitis,
o encephalomalacia,
o compressing lesions in vertebral canal,
o trauma to spinal cord,

217 | P a g e
 o congenital defects of spinal cord,
o hydrocephalus,
o Infectious agents- blue tongue virus in calves and lambs,botulism,
enterotoxaemia, rabies, salmonellosis, tetanus, trypnasomiasis.
o deficiency of thiamine, nicotinic acid or vitaming A,
o certain fungal and plant toxins and
o poisoning of chlorinated hydrocarbon, crude oil, lead, metaldehyde
etc.,

CLINICAL FINDINGS IN ATAXIA

 During ataxia, there are defects in rate, range, force and direction of
movement. In true cerebellar ataxia, the abnormalities may include: base
wide stance (limb extremities placed more laterally), limbs swing to the side
and circumduct or abduct more than normal, delay in initiating protraction
of the limb on getting up, hind quarters appear slightly crouched (lower)
than usual, wobbly appearance, knuckling, hypermetria and hypometria
which may result in falling, unsuccessful attempts to reach food or drinking
bowl, head oscillates and cannot be maintained in normal spatial
relationship with rest of the body.
 Nystagmus, deficient menace response and blindness.
 Signs of weakness or ataxia or both may be elicited by gently pushing the hind
quarters or pulling the patient by tail to one side as it is standing and
walking.
 Weak animal can be pulled easily to weak side and may stumble or fall. In
companion animals, postural reactions such as placing, hopping,
proprioceptive positioning and tonic neck test may help to detect the signs
of ataxia.
 In-coordination of the hind legs is frequently a sign of a more generalized
ataxia in animal in which the lesions are located in cervical spinal cord.
Cerebellar ataxia should be differentiated from vestibular disease, which
produces varying degrees of loss of equilibrium causing imbalance and
ataxia. In vestibular disease, the strength is not interfered with and
therefore, no paresis is observed. As a rule, the disturbance is unilateral or
asymmetric and the sings are those of an asymmetric ataxia with
preservation of strength.

AETIOLOGY OF COMA

 A state of unconsciousness otherwise called coma, is a terminal point of

apathy or depression and even a painful stimulus is unable to elicit any
reaction.
 It is a pathologic abnormality caused by an interruption in the structural,
metabolic and / or physiologic integrity of the cerebrum or brain stem.

218 | P a g e
  It is considered as a neurological emergency and patients must be rapidly
assessed and possible causes be explored in order to begin the specific
treatment.
 Serial examinations are necessary to detect the changes in the condition of the
animal and to provide and accurate prognosis.

Aetiology

 Trauma including cerebral haemorrhage, cerebrovascular thrombosis and

sub-arachnoid haemorrhage, lesions of brain stem or cerebrum,
 viral, bacterial, fungal and protozoal infections. E.g. canine distemper, rabies,
ehrlichiosis, feline infectious peritonitis etc.,
 Inflammatory or degenerative lesions as observed in encephalitis,
encephalomyelitis, meniningoencephalitis, encephalomalacia,
 congenital defects like hydrocephalus, lysosomal storage disease and
lissencephaly, space occupying lesions,
 Metabolic diseases: hypoglycaemia and diabetes mellitus,
 Liver disease: hyperammonaemia and hypoglycaemia,
 Renal disease: uraemia, acidosis and hypocalcaemia,
 Myocardial disease: ischemic anoxia due to coronary thrombosis,
 Pulmonary disease: anoxic anoxia, acidosis, pulmonary infarction and
coenurosis,
 Adrenal disease: hypoadrenal cortical crisis and hyperkalaemia, haemorrhage,
heat stroke and nutritional deficiency diseases are usually associated with
coma.
 Poisonings: carbon monoxide, water intoxication, salt, lead , arsenic, zinc
phosphide, cannabinoids, mushroom poisoning, kikuyu grass, male fern,
hexachlorophene, cyanide, ethylene glycol, methyl alcohol, benzene
hexachloride, amphetamine sulphate, carbon tetrachloride, dinitrophennol,
kerosene, turpentine, barbiturates, bromides, amitraz in horses,
hallucinogeneic drugs that are available in patient’s environment and
accidental consumption of sedative drugs used by the owner are also the
probable cause of the disease.

PATHOGENESIS, CLINICAL SIGNS, DIAGNOSIS AND

TREATMENT IN COMA

Pathogenesis

 Pathophysiological aspects of coma include cerebral oedema, increased

intracranial pressure and herniation of brain tissue.
 Cerebral oedema is abnormal accumulation of fluid in brain parenchyma
which increases intracranial pressure and thus reduces cerebral perfusion.
Subsequently, cellular hypoxia is exacerbated causing more oedema and

219 | P a g e
 possible brain enlargement leading to herniation. Any increase in the
volume of neural tissue, spinal fluid or even blood can result in an increase
in intracranial pressure because, the brain is housed within a non-
distensible structure, the skull. Increased intracranial pressure can result in
herniation of a protion of the brain.

Diagnosis

 A thorough history and clinical examination of the patient coupled with a

minimum database on laboratory assessments covering the various
aetiologies are necessary for a precise diagnosis.

Prognosis

 It is generally guarded.If no improvement is noticed in 2 to 3 days despite

appropriate treatments, the prognosis is extremely poor.
 Signs of deterioration include development of arrhythmias, loss of the
oculocephalic response, and lack of pupil response to light.
 Should the animal’s condition improve, the owner should be informed of
possible sequelae such as permanent neurological deficits and epilepsy.

Treatment

 Before starting treatment, it is essential to establish patent airway. An

intravenous catheter is placed and blood samples are taken before giving
any treatment.
 Attempts are made to identify the specific aetiological agent and rational
treatment is given against it. Intragastric alimentation is usually provided.
 To correct the dehydration, parenteral fluids are given but care is taken not to
over-hydrate.
 Antibiotics are used to check the infections. Symptomatic treatemnt is
valuable in early response.
 Specific antidote is to be used for cases suspected to be due to poisoning.
 Cerebral oedema is treated.
 Good nursing to maintain fluid and electrolyte balance, proper nutrition and
prevention of hypostatic lung congestion and decubital ulcers are important
for managing the affected cases.

GID / STURDY

Aetiology

220 | P a g e
  It is caused by invasion of brain and spinal cord by intermediate stage of
Taenia parasite which inhabits the intestine of dog and wild canidae. The
syndrome is one of localized space occupying lesions of CNS.
 The disease is due to intermediate stage of Taenia multiceps. It is a disease
primarily of sheep and is occasionally recorded in cattle.

Pathogenesis

 The early stage of migration of larve through nervous tissue causes

encephalitis, especially in heavey infestation. Cyst like coenurus develops
gradullay and causes pressure on nervous tissue resulting in its irritation
and eventual destruction.

Clinical findings

 In acute outbreaks due to migration of larval stages, sheep show varying

degrees of blindness, ataxia, muscle tremors, nystagmus, excitability and
collapse.
 Sheep affected with mature coenurus show wild expression, salivation,
frenzied running, convulsions, circling and deviation of eyes and head.
Some animals may die in this stage.
 In those entering the second stage, slowly developing partial or complete
blindness is the most obvious sing.
 Dullness, clumsiness, head pressing, ataxia, incomplete mastication and
periodic epileptiform convulsions are other usual signs.
 Papilloedema, gradual development of paresis leading to paralysis and death
after a long course may also be recorded.

Necropsy

 Cysts are seen in brain or spinal cord. Local pressure atrophy of nervous tissue
and softening of overlying bone may occur.

Diagnosis

 Clinical signs and knowledge on local incidence of taeniasis may lead to

presumptive diagnosis.
 X-ray examination is useful to define the cyst.
 It should be differentiated from other space occupying lesions and
encephalitis.
 Demonstration of metacestode is essential for diagnosis.

Treatment and control

 Surgical drainage of cyst is necessary to reduce the cranial pressure.

221 | P a g e
  Mature tapeworm infestation in dogs within the farm should be controlled.
 Carcass of infested livestock should not be available to dogs.

MODULE-31: BRAIN ABSCESS AND BRAIN TUMOUR

Learning objectives

 To study etiopathogenesis of brain abscess and brain tumour

 To learn the clinical findings, diagnosis and treatment of brain abscess and
brain tumour

AETIOLOGY OF BRAIN ABSCESS

 Brain abscesses are focal accumulations of pus in central nervous system with
cortical signs of a steadily progressive mass lesion. They are relatively
uncommon in veterinary practices.
 Aetiology: Infections of Streptococcus equi, Actinobacillus mallei, actinomyces
pyogenes, Bacteroides sp. Pseudomonas peudomallei, Fusobacterium
necrophorum, Staphyloccus aureus or spread of infection from inner ear,
respiratory tract, oral cavity,dehorning site and nasal septal infection after
nose ringing may lead to development of brain abscess.

PATHOGENESIS OF BRAIN ABSCESS

 As the abscess grows in size, neurological dysfunction sets in slowly which is

asymmetric.
 Abscess also compress the cerebral cortex unilaterally leading to caudal
displacement of brain and functional loss of one occipital lobe which is
manifested in loss of vision in the contra lateral eye.
 CNS compression also causes ipsilateral mydriasis due to interference with
oculomotor nerve function.
 Abscess in the base of brain may damage the function of cranial nervs (III, V,
VII, and VIII).

CLINICAL FINDINGS OF BRAIN ABSCESS

 Slow onset of signs (asymmetric), vision loss in contralateral eye, blindness,

propulsive walking, circling, headtilt (towards the lesion side), depression,
coma, head pressing, sudden unexplained mania and papilloedema in the
ipsilateral eye are the common symptoms recorded.
 In later stages, animal goes to lateral recumbency and display a decerabrate
posture characterized by hypertonicity, hyper reflexia, opisthotonus, coma
and convulsions.

222 | P a g e
  The dogs suffering from brain abscess usually have a prior history of inner ear
and respiratory or oral infections.

DIAGNOSIS AND TREATMENT OF BRAIN ABSCESS

Diagnosis

 History and clinical signs are of some value for its detection.
 Cerebrospinal fluid examination reveals increased neutrophil counts and
protein content. Organisms are seen on gram’s staining and can also be
cultured.
 Computerised axial tomography (CAT) and magnetic resonance imaging
(MRI) are useful diagnostic procedures.
 Brain abscess should be differentiated from meningitis, encephalitis, tumour,
parasitic cysts, listeriosis, toxoplasmosis and otitis.
 Gram’s stained smear of CSF may be used for identifying the organisam.

Treatment

 Steroid or non-steroidal anti-inflammatory drugs along with antimicrobials,

preferably bactericidal are recommended.
 Fluid therapy and other supportive care helps in early response.
 Surgical drainage may also be tried to drain the pus.

AETIOLOGY OF BRAIN TUMOUR

 Primary neoplasia of brain in domestic species is most common in dogs,

usually over 3 years of age.
 Among the breeds, Boxer is particulary prone to tumours.

PATHOGENESIS OF BRAIN TUMOUR

 Growing lesions can result in destruction and loss of function of focal parts of
the brain.
 Pressure on the adjacent structures such as cranial nerves, pituitary and
cerebellum causes their dysfunction.
 Secondary hydrocephalus develops due to obstruction of flow of CSF. It may
also result from the expansion of lesion itself.
 Increased intracranial tension leads to papilloedema wherein the optic disc
becomes oedematous, raised, enlarged, and haemorrhagic. The presence of
papilloedema is a useful sign in detecting space occupying lesions.

CLINICAL FINDINGS OF BRAIN TUMOUR

223 | P a g e
  The affected dogs show signs of change of temperament and loss of acquired
habits and become lethargic, reluctant to react and soil indiscriminately.
 Blindness or hemianopia (righ or left visual field in both eyes are affected)
with papilloedema often follows.
 Other signs include epileptiform fits, circling with wide radius towards the
side of lesion, progress in the straight line if lesion is located in mid line,
tendency to fall on contralateral side and variable ataxia.
 Conscious reaction to pin prick is often depressed or absent on contralateral
side and hyperactive on ipsilateral side .
 The signs of impaired function of pituitary and hypothalamus and other signs
attributable to hydrocephalus and cranial nerve paralysis are also recorded.
 In case of mass at cerebro – pontine angle, there is a paradoxical vestibular
syndrome i.e head tilt/circling is away from lesion side.
 Farm animals reveal sings of hypermetric gait, ataxia, depression, facial
paresis or paralysis, facial anaesthesis or analgesia, head tilt, strabismus,
nystagmus, unilateral loss of menace response, exophthalmos, Horner’s
syndrome or asymmetiric air flow through nares.

DIAGNOSIS AND TREATMENT OF BRAIN TUMOUR

Diagnosis

 The diagnosis can be confirmed by air encephalography though there is no

pathagnomonic EEG pattern.
 Diagnostic imaging procedures are useful.

Treatment

 Palliative therapy includes use of glucocorticoids and anticonvulsants.

 Chemotherapy / radiation therapy or both are also valuable.
 In benign tumour, surgery is useful.

MODULE-32: POLYNEURITIS AND TRAUMATIC INJURY TO

SPINAL CORD

Equine polyneuritis

 Equine polyneuritis (Neuritis of cauda equina): The adult horses of either sex
and any breed are affected by this disease which may be acute or chronic.
There is profound loss of function of caudal nerves to tail and sacral nerves
to anus, perineum, rectum and bladder.
 Though the aetiology is unknown, the disease may follow outbreaks of
strangles.
 It is found to be related to equine herpes virus I or equine viral arteritis.

224 | P a g e
  Signs:
oThe affected horses reveal limp tail;
o rubbing the tail or buttocks on fixed objects;
o anus widely dialated and areflexic;
o rectum and bladder are full and require manual evacuation;
dribbling of urine;
o perianal desensitization surrounded by area of hyperaesthesis;
o normal sensation of external prepuce and sheath;
o mild paresis and ataxia of pelvic limbs;
o atrophy or increased sensitivity to palpation in gluteal muscles.
 The signs are symmetric.
 Thoracic limb deficits are rarely seen.
 There may be involvement of facial and trigeminal nerve dysfunction.

IDIOPATHIC POLYRADICULONEURITIS IN DOG

 It is an acute disease and involves inflammation of multiple portions of

peripheral nervous system.
 Raccoon bites are being incriminated as its cause.
 Clinical signs:Altered voice and symmetric flaccid tetraplegia with areflexia
and tetany.
 There is no specific therapy except persistent nursing care to prevent
infections of bladder and skin. Thick bedding of straw accompanied with
vigorous corticosteroid therapy at the onset enhance recovery rate.

CHRONIC CANINE POLYNEURITIS

 Slowly progressive weakness of one or more limbs and occasionally with facial
paresis and loss of voice volume.
 Asymmetry of signs is common but not constant.

Aetiology

 Polyneuritis may also be seen in other diseases like deficienty of vitamins B1,
B6 and B12,
 Diabetes mellitus
 Pyaemia, septicaemia, meningitis, myelitis, etc.,
 Rheumatoid disease e.g. rheumatic arthritis
 Polymyositis or
 Neurotoxin drugs like streptomycin, sulphur, nitrorurantoin, amprolsol,
antimony, arsenic etc., may induce polyneuritis if they are given in high
concentration for a long period of time.

AETIOLOGY AND PATHOGENESIS IN TRUMA TO SPINAL

225 | P a g e
 CORD

 A sudden severe trauma to spinal cord produces a syndrome of immediate

complete flaccid paralysis for a brief period caudal to injury because of
spinal shock. It is soon followed by flaccid paralysis in the area supplied by
injured segment and spastic paralysis develops caudal to it.
 The spinal cord injuries may vary greatly in the form of concussion, contusion,
laceration and compression.
o Concussion is a reversible physiological dysfunction without gross
pathology that follows mild injury.
o Contusion results from more severe trauma and is characterized by
neuronal degeneration, oedema and haemorrhage.
o Laceration denotes tearing of the spinal cord or meninges.
o In compression, spinal cord is under increased pressure from either
intramedullary or extramedullary force.

Aetiology

 Acute injury
ooccurs due to fracture or dislocation of vertebra,
ofracture of ligament,
o missile injury ,
o disc – protrusion in dogs,
o cerebrospinal nematodiasis,
o manual extraction of calf during dystocia,
o bite wounds,
o stretching due to hyperflexion or hyperextension,
o abnormal torsion and cord stretching over a bony ridge.
 Chronic injury is seen in spinal neoplasia and disck protrusion.

Pathogenesis

 The initial immediate effect of traumatic injury is a state of ‘spinal shock’,

where it is having complete paralysis. When the shock wears off, effect of
residual lesions remain.
 Slowly developing lesion results in chronic spinal cord compression.

CLINICAL FINDINGS

 During spinal shock, which develops immediately after severe injury, there is
flaccid paralysis of variable degree up and down the cord. Concurrently,
there is fall in local blood pressure due to vasodilatation, local sweating and
disappearance of stretch reflexes and cutaneous sensitivity.

226 | P a g e
  The reflexes and sensitivity may reappear after 30 minutes to several hours.
When shock passes off, the residual signs remain. They include:
o paralysis of varying degree,
o sternal or lateral recumbency,
o muscle wasting,
o anaesthesia at and caudal to the lesion,
o hyperaesthesia at anterior edge of the lesion (due to irritation of
sensory fibres by local inflammation and oedema) and
o paralysis of bladder and rectum.
 In case of fracture or dislocation of vertebra, other signs like mal-alignment of
spinous processes, pain on pressure and excessive mobility may be noticed.
 If nervous tissue is not destroyed, recovery takes place in 1 to 3 weeks. If a
large section of cord is damaged, there is no recovery.

DIAGNOSIS AND TREATMENT

Diagnosis

 History of trauma, speed of onset of clinical signs, a thorough neurological

examination, myelography and evoked spinal cord potential testing are
useful in arriving at the diagnosis.
 X-ray examination helps in locating the site and extent of injury.
 Cerebrospinal fluid analysis reveals normal to increased cell count and
increase in protein content.
 The condition should be differentiated from other causes of recumbency like
azoturia, acute rumen impaction and acute coliform mastitis. The existence
of signs specific to the disease helps in differentiation.

Treatment

 In spinal cord concussion, most recoveries are spontaneous.

 If no recovery is noticed in large animal, euthanasia is advised. Among
ruminants, goats are amenable to treatment.
 To relieve oedema, hyper osmolar solutions, oral glycerol and corticosteroids
are administered.
 Haemostasis is achieved by local hypothermia, anti-fibrinolytics
(aminocaproic acid), nor-epinephrine blockers,electrocautery and other
haemostatic agents such as gelfoam.
 Extramedullary compression should be removed by surgery.
 Foreign material, if any should be removed and bones and bone fragments be
stabilized.
 To overcome pain, analgesics, tranquilizers, narcotics and non – steroidal
anti-inflammatory drugs are recommended. Analgesics and tranquilizers
should be administered with care to ambulatory patients that have thoraco

227 | P a g e
 – lumbar spinal lesions, because the ataxic patient may slip and worsen the
contusion.
 Broad spectrum antibiotics to treat bladder infection in cases of retention of
bladder are recommended.
 Good nursing like deep bedding, turning at frequent intervals, massage of
bony prominence, periodical slinging, evacuation of bladder

MODULE-33: ETHNOVETERINARY MEDICINE

Learning objectives

 To study the ethnoveterinary practices concerned with animal health care

 To learn about the commonly used ethno plants in treating animal diseases by
animal owners.

ANIMAL KEEPING IN ANCIENT INDIA

 Before the advent of modern allopathic system of medicine, it seems possible

that the healing art was almost the same throughout the world including
India. This system of medicine has given the term ethno-medicine (when
implied to human treatment) and ethno-veterinary medicine (in the context
of animal treatment). In India, ethno-veterinary practices were in vogue
since time immemorial.
 In ancient India, the Vedic literature, particularly Atharvaveda is a repository
of traditional medicine including prescriptions for treatment of animal
diseases. Scriptures such as Skanda Purana, Devi Purana, Matsya Purana,
Agni Purana, Garuda Purana, Linga Purana, and books written by Charaka,
Susruta, Palakapya (1000 BC), and Shalihotra (2350 BC) documented
treatment of animal diseases using medicinal plants. Vedic texts also
describe divine healing powers.
 Yajurveda cites importance of growth and development of medicinal plants
and Atharvaveda mentions about the value of medicines in curing the
diseases. Shalihotra undoubtedly appears to be the first veterinarian of pre-
historic times. The ancient Indians were so apt with the knowledge of
herbals, even Alexander acquired some of the skills used by Indians,
particularly for treatment of snakebite.
 Ethno veterinary practices concern to animal healthcare is as old as the
domestication of various livestock species. They comprise belief,
knowledge, practices and skills pertaining to healthcare and management of
livestock. The Indian subcontinent has rich ethno veterinary health
traditions that are the products of decades of experiences. The traditional
medicines that are commonly used for animal healthcare can cut down
costs considerably. Moreover, they are readily available to the ordinary
farmer. The key challenges are to find out the effectiveness and

228 | P a g e
 contemporary relevance of these practices. Before the introduction of
western medicine, all livestock keepers relied on these traditional practices.
 Ethnoveterinary medicine deals with people’s knowledge, skills, methods,
practices and beliefs about the care of their animals. Ethnoveterinary
knowledge is acquired through practical experience and has traditionally
been passed down orally from generation to generation.
 Widespread interest in documenting and validating ethnoveterinary practices
arose in the early 1980s. Since then, several studies have been carried out,
many reports written and numerous conferences and workshops held.
These activities have saved ethnoveterinary knowledge from extinction.
 Most knowledge resided with elderly community members and disappeared as
they died. The introduction of modern practices also made it difficult for the
younger generations to appreciate and use the beliefs and practices of their
forefathers. Despite recent efforts to promote the use of ethnoveterinary
knowledge worldwide, much information is only documented in field
reports and scientific publications. Few practical manuals have been written
to help animal healthcare workers, farmer leaders and farmers to actively
train others in the use of effective and validated ethnoveterinary practices.
 According to the World Health Organization, at least 80% of people in
developing countries depend largely on indigenous practices for the control
and treatment of various diseases affecting both human beings and their
animals. Ethnoveterinary remedies are accessible, easy to prepare and
administer, at little or no cost at all to the farmer. These age-old practice
cover every area of veterinary specialization and all livestock species.
 The ethnoveterinary techniques include treatment and prevention of disease,
extensive materia-medica preparation, ecto- and endo-parasite control,
fertility enhancement, bone setting and poor mothering management.The
materia-medica consists mainly of plants in addition to other components
such as earth and minerals, and animal parts.
 Millions of people around the world have an intimate relationship with their
livestock. Many people depend on their livestock: animals provide them
with food, clothing, labour, fertilizers and cash, and act as a store of wealth
and a medium of exchange. Animals are a vital part of culture and in many
societies are regarded as equal to humans.
 To keep animals healthy, traditional healing practices have been applied for
centuries and have been passed down orally from generation to generation.
Before the introduction of western medicine, all livestock keepers relied on
these traditional practices. According to the World Health Organization, at
the moment, at least 80% of people in developing countries depend largely
on these practices for the control and treatment of various diseases that
affect both animals and humans. These traditional healing practices are
called ‘ethnoveterinary medicine’.

229 | P a g e
  Interest in ethnovet practices has grown recently because these practices are
much less prone to drug resistance and have fewer damaging side-effects on
the environment than conventional medicine.
 India has a rich heritage of ethno-veterinary medicinal practice but it has not
been utilized properly for the purpose of indigenous development i.e.
development from within, a case very much similar to Gaushala system in
the country.
 The potential of Gaushalas as breed improvement and conservation centers
and their role in rural development is yet to be exploited to the desired
extent. Existing infrastructure, committed private management and
leadership of devoted persons coupled with flow of resources in terms of
donations are some of the important factors which render Gaushalas as
ideal centers for their use in improving cattle productivity and conservation.
 Since there is huge gap between the demand and supply of veterinarians for
the adequate treatment of animals, the ethno-veterinary medicine sets this
imbalance right. It provides a sustainable, economically viable and eco-
friendly system of animal treatment and provides an opportunity to develop
a closer contact with Gaushalas and understand their problems.

ETHNO-VETERINARY MEDICINE IN RURAL INDIA

 Ethno-veterinary medicine is a systematic attempt to document the

indigenous traditional knowledge pertaining to animal health and
production. They are not new medicines. It could be argued that there is no
need for formal validation as users have already validated by using these
medicines. But it has to be integrated with modern Veterinary medicines.
Farmers are not ready to fully accept the advice of technocrats and continue
with their traditional practices. They have accepted only 30 percent of the
recommended practices in agriculture and animal husbandry sector since
independence. Many non-governmental organizations are involved in
systematic documentation and research on ethno-veterinary medicines.
Moreover it is sustainable due to low cost and its physical and cultural
compatibility. It is easy to administer, which is a major constraint in
majority of the recommended practices.
 State governments largely provide veterinary services in the country. It is
estimated that there is one veterinarian for every 7000 animals in the
country. The State controlled Animal husbandry departments provide
vaccination against major diseases such as foot and mouth disease,
rinderpest, haemorrhagic septicaemia and black quarter. Recent surveys
revealed that 75-85% of farmers use traditional or folk medicine for a
variety of conditions. But this system does not facilitate cure to all diseases.
More over the knowledge of a particular treatment is often restricted to a
community, or to some traditional healers. With the introduction of

230 | P a g e
 modern systems, many of these treatments are not validated "clinically" or
empirically and cannot be promoted on a large scale.
 Many of the medicinal plants are not available due to deforestation. Modern
medicine is technology dependent and needs skilled practitioners. Levels of
safety are low and care should be taken in dispensing antibiotics and
steroids. It can create health problems if improperly used. An integrated
livestock health care system that is economically viable and sustainable is
needed.

LIVESTOCK DISEASES AND ANIMAL HEALTH CARE

 Studies in six districts of Andhra Pradesh and Maharashtra revealed that

infectious diseases like FMD and black quarter are responsible for the
maximum losses. Other conditions like diarrhoea, tick infestation and
reproductive problems may not be fatal but lead to production losses. Even
though traditional medicine cannot eradicate infectious diseases it is useful
in many disease conditions.Some of the traditional medicines are more
useful against Anorexia. Digestive tonics, appetite stimulants and
stomachics are available in traditional medicine. These treatments do not
need further validation or recommendation and their use has been
empirically validated many times over generations of use. Improper feeding
and watering practices will result in bloat. Its incidence is more in monsoon
when animals are suddenly exposed to lot of fresh green fodder. Household
spices and herbs like ginger, asafoetida, etc, are very effective against
simple tympany and bloat.
 Many dermatological conditions are linked to ectoparasitsm, feeding
practices, hygienic standards and weather conditions. Combination of plant
oils like neem, coconut and debris along with sulphur powder can be used
for topical application.

WORM INFESTATIONS

 There are a number of plant and mineral derivatives, which are having
anthelmentic properties. If farmers could be taught to use these
preparations routinely it can considerably reduce the incidence of worm
infestation.
 Mixed farming, rotational grazing and quick composting of animal wastes will
reduce the incidence of anthelmintic resistance. Scientific feeding and water
management coupled with regular deworming will decrease the incidence of
diarrhoea.

231 | P a g e