CHAPTER-1: GENERAL INTRODUCTION ON POULTRY DISEASES; VIRAL

DISEASES

 1) Ranikhet disease
HISTORY

 The first outbreak of the disease was recorded in 1926, in Java, Indonesia and in
1927 by Doyle in Newcastle -upon- Tyne , England .
 In India , the disease was first recorded at Ranikhet (U.P.) in Kumoan hills (Nainital
District, Uttaranchal) by Edward in 1927. Hence the name Ranikhet disease.
 The name, Newcastle disease was coined by Doyle as a temporary measure to avoid
a descriptive name that might be confused with other diseases. Later, it became clear
that other less severe diseases were caused by viruses indistinguishable from NDV.
 In the United States , a relatively mild respiratory disease, often with nervous signs,
was first described in the 1930 and subsequently termed pneumoencephalitis.
 It was caused by a virus indistinguishable from NDV in serological tests.
Subsequently, numerous NDV isolations that produced extremely mild or no disease
in chickens was made around the world. In India , it is the most important disease of
poultry.

ETIOLOGY

 Causative agent: Paramyxovirus type1 (PMV-1 belongs to the genus Avulavirus,

family Paramyxoviridae).
 Based on the disease produced in chickens, NDVs have been classified into five
pathotypes
o Viscerotropic velogenic: The NDVs cause a highly virulent form of the disease.
Haemorrhagic lesions are characteristically present in the intestinal tract.
o Neurotropic velogenic: These NDVs cause high mortality following respioratory
and nervous signs.
o Mesogenic: These NDVs cause low mortality following respiratory and some
times nervous signs.
o Lentogenic: These respiratory NDVs cause mild or inapparent respiratory
infection.
o Asymptamatic: The enteric NDVs cause inapparent enteric infection.

SUSCEPTIBLE SPECIES

 ND occurs in domestic fowl, turkeys, pheasants, pigeons, quail and guinea fowl.
 Ducks and geese are susceptible but severe disease is rare.
 Many species of wild birds are also susceptible.
 Chickens are the most and waterfowl the least susceptible of domestic poultry.
 Psittacines (parrots) are highly susceptible and can excrete virus for long periods.
 Human infections, with flu-like symptoms and conjunctivitis, have been reported.
 EPIDEMIOLOGY AND TRANSMISSION

Epidemiology

 Virulent NDV strains are endemic in poultry in most of Asia , Africa , and some
countries of North, Central, and South America.
 Other countries, including the USA and Canada , are free of those strains and
maintain that status with import restrictions and eradication by destroying diseased
poultry.
 Cormorants, pigeons, and imported psittacine species have also been sources of
virulent NDV infections of poultry.
 Low virulence NDV is prevalent in poultry and wild birds, especially waterfowl.
 Infection of domestic poultry with low virulence NDV contributes to lower
productivity.

Transmission

 Infected birds shed virus in exhaled air, respiratory discharges, and feces.
 Virus is shed during incubation, during the clinical stage, and for a varying but
limited period during convalescence.
 Virus may also be present in eggs laid during clinical disease and in all parts of the
carcass during acute virulent infections.
 Chickens are readily infected by aerosols and by ingesting contaminated water or
food.
 Infected chickens are the primary source of virus, but other domestic and wild birds
may be sources of NDV.

 The virus has been found to survive for several days on the mucous membrane of the
human respiratory tract and has been isolated from sputum.

P PATHOGENESIS
 CLINICAL FINDINGS

 Clinical manifestations vary from high morbidity and mortality to asymptomatic

infections.
 The severity of an infection is dependent on the nature of the infecting virus, its
virulence and the age, immune status, and susceptibility of the host species.
 Onset is rapid, and signs appear throughout the flock within 2-12 days (average 5)
after aerosol exposure.
 Spread is slower if the fecal-oral route is the primary means of transmission,
particularly for caged birds.
 Young birds are the most susceptible.
 Observed signs depend on whether the infecting virus has a predilection for
respiratory, digestive, or nervous systems. They are

Velogenic (high virulent) viruses

 Sudden death
 Depression
 Prostration
 Diarrhoea
 Facial edema
 Cyanosis of comb (See the picture)
 Mortality - 100%

Mesogenic viruses (Moderately virulent) viruses

 Severe respiratory signs

 Decreased nervous signs

 Increased drop in egg production
 Mortality - 50%

Lentogenic or low virulent viruses.Mild respiratory sigbe for short period

LESIONS

Macroscopic lesions (Velogenic form)

 Young chickens and those dying peracutely may have no lesions especially in birds
that only show nervous signs.
 Remarkable lesions are usually observed only with VVND and they include
 Haemorrhage in intestine
 Petechial haemorrhage in proventiculus
 Enlarged and necrotic caecal tonsils
 Necrosis and haemorrhage in lymphoid aggregates in intestine
 Splenic necrosis on capsular surface
 Nervous system lesions are not seen regardless of pathotypes
 In contrast, the lesions in birds infected with lower virulence NDV strains may be
limited to respiratory tract
 Congestion and mucoid exudates seen in the respiratory tract, especially in trachea
(see the picture below) with opacity and thickening of the air sacs (airsacculitis).
 Secondary bacterial infections will increase the severity of the respiratory lesions.
 Ovarian follicle - Flaccid, haemorrhagic stigmata
 Oviduct - haemorrhage and discolouration.

MICROSCOPIC LESIONS

 Microscopic lesions are as variable

 They are, therefore, of no value in the diagnosis
 Lesions in the central nervous system are those of non-purulent encephalomyelitis
with neural degeneration, foci of glial cells, perivascular infiltration of lymphocytes,
and proliferation of endothelial cells.
 Lesions usually occur in the cerebellum, medulla, mid brain, brain stem and spinal
cord, but rarely in cerebrum.
 Lesions in the vascular system include hyperaemia, oedema, and haemorrhage in
many organs.
 Regressive changes in the lymphopoietic system consist of disappearance of
lymphoid tissue.
 Necrotic lesions are found through out the spleen.
 Marked degeneration of the medullary region of bursa.
 The haemorrhagic necrotic lesions in the intestinal tract develop in lymphoid
aggregates.
 Lesions in the upper respiratory tract may be severe and related to the degree of
respiratory distress.
 Lesions may extend through out the length of the trachea. Cilia may be lost within 2
days of infection.
 In the mucosa, congestion, edema, and dense cellular infiltration of lymphocytes
and macrophages may be seen.
 Edema, cell infiltration, and increased thickness and density of the air sacs may
occur.

DIAGNOSIS

 None of the clinical signs or lesions can be regarded as specific or pathognomonic.

 Confirmation test - Haemagglutination-inhibition test. A rise in haemagglutination-
inhibition antibodies in paired serum samples also confirms the disease.
 Other serological test - Single radial immunodiffusion, Agar gel precipitin, Virus
neutralization (VN) in chick embryos, and plaque neutralization.
 ELISA has become popular, especially as part of flock screening procedure.
 At present the only definite method of diagnosis is isolation of virus using suitable
samples and its characterization using a group of monoclonal antibodies.
 Samples
o Live birds - Both cloacal/ faeces or tracheal swabs, regardless of clinical signs.
o Dead birds - Intestines, intestinal contents and trachea should be collected
together with affected organs and tissues.
 While examining the carcasses of ND affected chicken the other diseases like a vian
influenza, Infectious laryngotracheitis, infectious bronchitis, EDS-76,
encephalomyelitis, pneumovirus infection, infectious coryza, fowl cholera,
encephalomalacia, intoxications, middle ear infection/skull osteitis, and
salmonellosis should be considered as some lesions of these diseases may mimic
those of ND.

PREVENTION

 Live lentogenic vaccines, chiefly B1 and LaSota strains, are widely used and typically
administered to poultry by mass application in drinking water or by spray.
 Alternatively, individual administration is via the nares or conjunctival sac.
 Healthy chicks are vaccinated as early as day 1-4 of life. However, delaying
vaccination until the second or third week avoids maternal antibody interference
with an active immune response.
 Mycoplasma, some other bacteria, and other viruses affecting the respiratory tract, if
present, may act synergistically with some vaccines to aggravate the vaccine reaction
after spray administration.
 Oil-adjuvanted inactivated vaccines are also used following live vaccine in breeders
and layers and may be used alone in situations where use of live virus may be
contraindicated.
 In countries where virulent NDV is endemic, a combination of live virus and
inactivated vaccine can be used; or alternatively, if permitted by law, a live
mesogenic strain vaccine may be used in older birds.
 The frequency of revaccination to protect chickens throughout life largely depends
on the risk of exposure and virulence of the field virus challenge.

ZOONOTIC RISK

 Newcastle disease viruses, whether virulent field viruses or live vaccine, can produce
a transitory conjunctivitis in humans, but the condition has been limited primarily
to laboratory workers and vaccination teams exposed to large quantities of virus.
 Before poultry vaccination was widely practiced, conjunctivitis from NDV infection
occurred in crews eviscerating poultry in processing plants.
 The disease has not been reported in people who rear poultry or consume poultry
products.
 2) Infectious bursal disease (Gumboro disease)
INTRODUCTION

 Other names
o Gumboro disease
o Infectious Bursal Disease (1972)
o Infectious bursitis
o Avian nephrosis (1962)
 Acute highly contagious infection of chickens
 Birna virus ( ds RNA) - Birna = two
 B- Lymphocytes are the primary target cells
 Bursa, lymphoid organ, is severely affected
 First report in Gumboro (Delware District of USA)
 Economically significant, because
o Heavy mortality in 3 – 6 wks old chickens and older
o Severe prolonged immunosuppression of chickens infected at an early age
 Immunosuppression leads to
o Vaccination failures
o Escherichia coli infection
o Gangrenous dermatitis
o Inclusion Body hepatitis – anaemia syndrome

ETIOLOGY AND TRANSMISSION

Etiology

Serotype 1 IBDV

 World wide distribution

 Antigenic variation
 Variation in virulence - from apathogenic to highly virulent strains
 50 % mortality
 Tropism for B-Lymphocytes of the bursa and their depletion

Serotype 2 IBDV

 Wide spread
 No pathogenic/ Immunosuppressive
 Affects chickens, turkeys, ducks
 Serotype 1 and 2 IBDV infects turkeys and ducks but no disease

Transmission

 IBD is highly contagious

  Affected birds excrete the virus in faeces for 10-14 days
 Virus is very stable
o Remains highly infectious for many months (up to 122 days) in the poultry
environment
o Remains infectious even after 52 days in water, feed and droppings.
o Hardy nature of this virus survives heat, cleaning and disinfectant procedures
o Survival in the environment between outbreaks
 Role of mechanical vectors (Human, wild birds, insects)
 Meal worms and litter mites remains infective for up to 8 weeks
 No vertical transmission and carriers
 Young chicks with MDA are immune to infection (but not to virulent strain)
 Older birds (due to bursal regression) are more resistant to infection

IBD: PATHOGENESIS

B - cells and their precursors are the main target cells

 T- Lymphocytes are relatively unaffected

 Renal pathology (swollen with urate deposits and cell debris) are due to severely
swollen bursa
 Mechanism for muscular haemorrhage is not known (may be due to interference of
virus with the normal blood clotting mechanism)
 Bursal infection in early life can result in impaired immune responses
 Consequences
o Lowered resistance to diseases
o Suboptimal ( inadequate) responses to vaccination
 Susceptible age - 3 -6 wks of age
 Subclinical infection in younger than 3 wks —> immunosuppression
o Chemical bursectomy (using cyclophosphamide) in 3 day old chicks and
subsequent challenge at 4 wks —> Resistant to disease
o Similar results in surgically bursectamised 4 wks old chickens ( with mild
necrosis of lymphatic tissue and 1000 times less viral production) but 100%
mortality in control non-bursectamised birds

CLINICAL SIGNS

 Severity depends upon age, breed, and MDA level of the chick as well as the
virulence of virus
 Acute form
o Incubation period: 2- 3 days
o 3 -6 wks old chicks are affected
 Signs
o Depression
o White watery diarrhoea
o Soiled vent
o Anorexia
o Ruffled feathers
 o Reluctance to move
o Closed eyes and death
 Morbidity - 10 – 100%
 Mortality
o 0 - 20% (Normally)
o 90 – 100% (VVIBDV)
 Milder form - Little or No signs Suboptimal (growth) / response to vaccination
 Course of the disease
o Short, leading to death or recovery (in individual bird)
o Mortality reaches a peak 3-5 days after infection

GROSS PATHOLOGY

 Dehydration of carcass
 Muscular haemorrhage (thigh and pectoral) (see the picture - below), some times at
the junction of proventriculus and gizzard (see the picture - below).
 Haemorrhages of pectoral leg muscles are typical of IBD
 Intestine with excess mucus

Bursa

 Enlarged, inflamed, edematous and cream coloured (early)

 Atrophy (after 3 – 8 days)
 Haemorrhage on the internal and serosal surfaces (see the picture below)
 Caseous core within the lumen from sloughed epithelium

Other organs

 Liver- Hepatomegaly and peripheral infarcts

 Spleen- Splenomegaly
 Kidneys- Swelling and white appearance, dilatation of tubules with urates ( cell
debris, occasionally).
MICROSCOPICAL LESIONS

 Spleen - Moderate lymphoid cell necrosis

 Thymus and caecal tonsil - Lymphoid cellular reaction (early stage), but less
extensive damage
 Harderian gland - Depletion of plasma cells
 Kidneys - Non - specific
 Liver - Mild perivascular infiltration of monocytes.

DIAGNOSIS

 Based on history, clinical signs and gross lesions ( for acute disease)
 Differential diagnosis is required (for subclinical IBD)

Serological test

 AGPT (using macerated bursa)

 ELISA (against a known positive antiserum)

To identify the presence of antigen

 Immunoperoxidase staining
 Immunofluorescence (in frozen bursal sections or smears)
 Virus isolation (rarely) - Time consuming process
 Inoculation of suspected bursa into 10 – 11 days old embryonated eggs
 Some strains grow on Chick embryo fibroblast, vero cells or certain lymphoblastoid
cell cultures
 Abs may develop after infection (detected by NT,ELISA, Precipitation test). It is
useful when MDA declines below detectable levels)
 Nucleic acid probe, Ag-capture ELISA (using MCAbs.,), RT-PCR

DIFFERENTIAL DIAGNOSIS

 Coccidiosis
 Ranikhet disease
 Haemorrhagic syndrome of muscles and other haemorrhages
 Avitaminosis A
 FLKS
 Water deprivation with swollen kidneys
 Excess renal urates.
 CHAPTER-2: INFECTIOUS BRONCHITIS AND INFECTIOUS
LARYNGEOTRACHEITIS

 3) Infectious bronchitis

INTRODUCTION

 Highly infectious and contagious respiratory disease of chicks

 Also affect the oviduct, and some strains have a tendency for the kidneys
 Great economic importance due to its adverse effect on egg production and egg
quality in layers, and on production in broilers
 Other pathogens such as mycoplasma or E.coli increases the severity and duration of
the disease

ETIOLOGY

 Different serotypes (Respiratory, Nephrotoxic)

o Respiratory tract - massachusetts and connecticut
o Nephrotoxic - T, Gray and Holte serotype
 Concurrent infection with more than one serotype occurs

HOST

 Virus affects respiratory , renal and reproductive system 3Rs = ( R+R+R)

 Adverse effects on egg production/ quality in layers on weight gain in broilers
 Complications due to secondary bacterial infections (Mycoplasma / E.coli)
 Host : Young chicks – Respiratory form. Under 10 weeks - Nephritic form
 Intercurrent infections (RD, ILT, Coryza, CRD, E.coli, IBD ) aggravate respiratory
form

SPREAD

 Direct
 Airborne transmission (common)
 Faeces
 Fomites
 Eggs
 IB - PATHOGENECITY


 New virus appear 3-4 hours after infection
 Maximum out put per cell within 12 hours
 Recovery occurs ( if no secondary complications)
 Virulence (of IBV strains of respiratory tract) towards reproductive tract varies

CLINICAL SIGNS

 Signs may be asymptamatic/ signs of respiratory/ reproductive tract

Respiratory form

 Rales, gasping, sneezing, watery nasal discharge, facial edema, lachrymation

 Early appearance due to rapid spread (incubation period: 1-3 days)
No mortality (if no secondary infection)

Reproductive form

 Damage to functional oviduct in adults(most common)

o Egg production quality ( more than 50 %) watery albumin
o Egg abnormalities (smaller, misshapen, corrugations and leathery)
 Abnormal development of oviduct in young chicks (after infection)
o Partial / complete failure - Blind layer

Renal (Nephritic) form

 Young growing birds

 Respiratory signs seen
 Mortality – 30 % ( in severe form)
 Little / No mortality ( in mild form)
 MACRO AND MICROSCOPIC LESIONS

Macroscopical lesions

Respiratory tract

 Serous, catarrhal, or Caseous exudates in the trachea and bronchi, generally without
haemorrhage

 Caseous plugs may be found in the lower trachea and bronchi of chicks that die
 Air sacs are thickened and opaque
 Secondary bacterial infections in meat-type birds, especially with coli form bacteria,
produce caseous airsacculitis, perihepatitis, and pericarditis. Small areas of
pneumonia may be observed around the large bronchi.

Reproductive tract

 Fluid yolk material may be found in the abdominal

 Abnormal ovary having the misshapen follicles

 Egg
o Outer surface - Ridges or concretions
o Watery albumin

Kidney

 Swollen, pale kidneys, with tubules and ureters distended with urates

 In layers, urolithiasis is associated with virus infection and certain dietary factors

Microscopical lesions

 Trachea & Bronchi: Inflammatory and degenerative changes

 Air sac: Edema, epithelial desquamation, fibrinous exudate
 Kidney: Interstitial nephritis, Degenerative changes, Urolithiasis , urates in ureter
 Oviduct: Epithelial damage, dilatation of tubular glands, infiltration of onuclear
cells, proliferation of lymphoid follicles

DIAGNOSIS

 Based on clinical signs

 Gross and microscopic lesions
 Serological test includes
o Virus neutralisaton (VN)
o Immunodiffusion (ID)
 o Haemagglutination inhibition (HI)
o Immunofluorescence (IF) and ELISA
o ELISA - more sensitive

 4) Infectious laryngeotracheitis

ETIOLOGY

 Acute viral disease of chickens and pheasants

 Dyspnoea, coughing, gasping and expectoration of bloody exudate
 All age groups are susceptible (very young chicks)
 Concurrent infections (RD,IB,FP,IC,CRD) complicates the disease
 Predisposition by Vit.A and ammonia
 Spread by aerosol, ingestion, mechanical (carriers) and fomites

ILT - PATHOGENECITY

CLINICAL SIGNS
  Peracute form : Death without any signs/Dyspnoea/ Severe coughing/Expectoration
of bloody exudate
 Acute form
o Nasal discharge/Ocular/Conjunctivitis
o Obstruction of trachea with bloody exudate —> Drawn out gasps (stretching of
neck) —> Wide open beak (Oral breathing)
o Death in 3-4 days / Recovery in 2-3 wks (in some cases)
 Mild form : Moist rales, head shaking, mild coughing/ conjunctivitis
 Asymptomatic form : Unnoticed in a flock

MACROSCPICAL LESIONS

Peracute form

 Haemorrhagic tracheitis —> obstruction

Acute form

 Caseous/Diphtheritic exudate —> obstruction

 Tracheal congestion

Mild form

 Caseous exudate
 Excess mucous
 Conjunctivitis

MICROSCOPICAL LESIONS

Degenerative changes

 Swollen cells
 Loss of cilia
 Desquamation

Inflammatory changes

 Infiltration of Lymphocytes, Macrophages in sub (mucosa)

 Desquamation ( Lack of epithelium + Rupture of capillaries) —> Haemorrhage
 Intranuclear inclusions in tracheal epithelium
 Seen in early stage of infection (1-5 days)
 Disappear as they desquamate
 DIAGNOSIS

 Clinical signs
 Demonstration of inclusion bodies
 Serological tests includes FAT,IP,ELISA,PCR,AGID,VN,IFA
 Virus on CAM

CHAPTER-3: FOWL POX AND AVIAN INFLUENZA

 5) Fowl pox
INTRODUCTION

 Largest virus known in birds

 Genome is double stranded DNA
 It is, unusually, capable of replication in the cell cytoplasm
 Complete virions (Borrel granules) accumulate within the inclusion bodies- i.e.
Bollinger bodies (inside the cytoplasm of the cells)
 When the infected cells sloughed off into the environment in the scab, the virus
remains in the inclusion and is resistant to desiccation

ETIOLOGY AND EPIDEMIOLOGY

 Virus does not penetrate intact skin

 Some break in the skin is required for the virus to enter the epithelial cells, replicate
and cause disease
 Direct contact
o It is the major factor
o During vaccination, the individuals may transfer the virus from affected to
healthy birds
o Deposition of virus in eyes —> Through lachrymal duct it goes to larynx —>
Upper respiratory tract infection
 In a contaminated environment, aerosols (droplets) generated from feather follicles
and dried scabs carry the virus and spread the disease
 Biting insects, like mosquitoes spread the disease
 Can be transmitted by the respiratory tract
 PATHOGENESIS

 Complete virions (Borrel granules) accumulate within

the inclusion bodies (Bollinger bodies)
 Virus —> Epithelial cells —> Proliferation ( Cell to
cell)
 Entry of virus into blood —> Viraemia
 No gross pathology of organs, but viral multiplication
in liver, spleen —> Secondary viraemia

CLINICAL SIGNS

Cutaneous form ( Dry pox)

 Nodular proliferative skin lesions in non feathered parts – Head, Neck, Legs, Feet
 Spread is gradual
 Poor weight gain , poor egg production
 Papule —> vesicles —> pustules —> crust/scab —> scar
 Less mortality (may be high due to complications)

Diphtheretic form (Wet pox)

 Fibrino-necrotic and proliferative lesion in the mucous membrane of URT/ mouth/

esophagus
 Small white nodules in upper respiratory /digestive tract —> Raised yellow plaques
on the mucous membranes
 Lesions are present in
o Mouth- Inappetance (lack of desire for food)
o Larynx/ trachea- Difficulty in breathing (Dyspnoea)
o Esophagus- Difficulty in swallowing
o Nares- Nasal discharge
o Conjunctiva- Discharge/ Blindness
 Mortality as high as 50% . But usually low.

 Gross lesions
 Cutaneous form- Nodules (due to hyperplasia involving epidermis and underlying
hair follicles) and other features as in signs.
 Diphtheretic form- Slightly elevated white opaque nodules develop on mucous
membranes —> Yellow, cheesy, necrotic pseudo-diphtheretic or diphtheretic
membrane —> on removal bleeding ulcers.
Microscopical lesions

 Most important lesion is hyperplasia of epithelium ( irrespective of the form ) and

enlargement of the cells, with associated inflammatory changes
 Characteristic eosinophilic cytoplasmic inclusion bodies ( Bollinger bodies ) are seen
under light microscopy
 Tracheal mucosa
o Initial, hyperplasia and hypertrophy with subsequent enlargement of epithelial
cells which contain eosinophilic cytoplasmic inclusion bodies
o The inclusion bodies may occupy the entire cytoplasm, with resulting cell
necrosis
 Immunity
o Actively acquired immunity against fowl pox occurs after recovery from naturally
occurring infection or vaccination
o Both cell mediated and humoral immunity provide protection
o CMI develops earlier than the HI

DIAGNOSIS

 Cutaneous form
o Based on clinical signs (Easy)
o Demonstration of intracytoplasmic eosinophilic inclusions - Borrel bodies
(virions) - By scrapping from the lesions and smears made on glass slides with
suitable stain
 Diphtheretic form
o Based on clinical signs (Difficulty)
o Formation of ulcer, on removal of lesions, helps to differentiate it from ILT and
Hypovitaminosis - A
 Inoculation test

o Identification of inclusion bodies under light microscope

 Serological tests - To detect antibodies
o Agar gel precipitation test ( AGPT )
o Passive haemagglutination
o Serum neutralisation( SA )
 o Indirect fluorescent antibody
o Immunoperoxidase ( IP )
o ELISA
 Titre
o Transitory {AGPT)
o Low (SN)
o ELISA (Most sensitive)

DIFFERENTIAL DIAGNOSIS

 Pantothenic acid
 Biotin deficiency
 Vitamin A deficiency
 Infectious Laryngotracheitis
 Other respiratory diseases in poultry
 Injuries caused by external parasites and cannibalism.

 6) Avian influenza
INTRODUCTION

 Avian influenza (AI) viruses infect domestic poultry and wild birds.
 In domestic poultry, AI viruses are typically of low pathogenicity (LP), causing
subclinical infections, respiratory disease, or drops in egg production.
 However, a few AI viruses cause severe systemic infections with high mortality.
 This highly pathogenic (HP) form of the disease has historically been called fowl
plague.
 In most wild birds, AI viral infections are subclinical.

ETIOLOGY

 Avian influenza viruses are type A orthomyxoviruses characterized by antigenically

homologous nucleoprotein and matrix internal proteins, which are identified by
serology in agar gel immunodiffusion (AGID) tests.
 AI viruses are further divided into 15 haemagglutinin (H1-15) and 9 neuraminidase
(N1-9) subtypes based on haemagglutinin inhibition and neuraminidase inhibition
tests, respectively.
 Most AI viruses (H1-15 subtypes) are of LP, but some of the H5 and H7 AI viruses
are HP for chickens, turkeys, and related gallinaceous domestic poultry.

EPIDEMIOLOGY AND TRANSMISSION

 LP viruses are distributed worldwide and are recovered frequently from clinically
normal shorebirds and migrating waterfowl. Occasionally, LP viruses are recovered
from imported pet birds and ratites.
 The viruses may be present in backyard flocks and other birds sold through live-
poultry markets, but most commercially raised poultry in developed countries are
free of AI viruses.
 The HP viruses arise from mutation of some H5 and H7 LP viruses and cause
devastating epizootics.
 Depopulation and quarantine programs are used to quickly eliminate the HP
viruses.
 The incubation period is highly variable and ranges from a few days to 1 wk.
 Transmission between individual birds is by ingestion or inhalation. Experimentally,
cats have been infected with 1 strain of H5N1 Asian HP AI following respiratory
exposure, ingestion of infected chickens, or contact with infected cats.
 Potentially, domestic house cats could serve as a transmission vector between farms,
but the ability of other AI viruses, including other H5N1 strains, to infect cats is
unknown.
 Transmission between farms is the result of breaches in biosecurity practices,
principally by movement of infected birds or contaminated feces and respiratory
secretions on fomites such as equipment or clothing.
 Airborne dissemination may be important over limited distances.

LOW PATHOGENIC AVIAN INFLUENZA (LPAI)

 These AI viruses typically produce respiratory signs such as ocular and nasal
discharge and swollen infraorbital sinuses.
 Sinusitis is common in domestic ducks, quail, and turkeys.
 Lesions in the respiratory tract typically include congestion and inflammation of the
trachea and lungs.
 In layers and breeders, there may be decreased egg production or fertility, ova
rupture (evident as yolk in the abdominal cavity) or involution, or mucosal edema
and inflammatory exudates in the lumen of the oviduct.
 Some layer and breeder chickens may have acute renal failure and visceral urate
deposition (visceral gout).
 The morbidity and mortality is usually low unless accompanied by secondary
bacterial or viral infections or aggravated by environmental stress factors.

HIGH PATHOGENIC AVIAN INFLUENZA(HPAI) VIRUS

 Even in the absence of secondary pathogens, HP viruses cause severe, systemic

disease with high mortality in chickens, turkeys, and other gallinaceous birds.
 In peracute cases, clinical signs or gross lesions may be lacking before death.
 However, in acute cases, lesions may include:
 Cyanosis and edema of the head, comb, and wattle;
 Edema and discoloration of the shanks and feet due to subcutaneous ecchymotic
hemorrhages;
 Petechial haemorrhages on visceral organs and in muscles; and
 Blood-tinged oral and nasal discharges.
 In severely affected birds, greenish diarrhoea is common.
  Birds that survive the fulminating infection may develop CNS involvement evident
as torticollis, Opisthotonus, or incoordination.
 The location and severity of microscopic lesions are highly variable and may consist
of edema, hemorrhage, and necrosis in parenchymal cells of multiple visceral
organs, skin, and CNS.

CLINICAL FINDINGS AND LESIONS

 Clinical signs, severity of disease, and mortality rates vary depending on AI virus
strain and host species.

DIAGNOSIS

 AI viruses can be readily isolated from tracheal and cloacal swabs.

 They grow well in the allantoic sac of embryonating chicken eggs and agglutinate
RBC.
 The haemagglutination is not inhibited by Newcastle disease or other paramyxoviral
antiserum.
 AI viruses are identified by demonstrating the presence of,
o influenza A matrix or nucleoprotein antigens using AGID or other suitable
immunoassays, or
o viral RNA using an influenza A specific RT-PCR tests.

Differential diagnosis
ETIOLOGY

 LP AI must be differentiated from other respiratory diseases or causes of decreased

egg production including,
o acute to sub acute viral diseases such as infectious bronchitis, infectious
laryngotracheitis, lentogenic Newcastle disease, and infections by other
paramyxoviruses
o bacterial diseases such as mycoplasmosis, infectious coryza, ornithobacteriosis,
turkey coryza, and the respiratory form of fowl cholera, and
o fungal diseases such as aspergillosis.
 HP AI must be differentiated from other causes of high mortality such as
velogenic Newcastle disease, peracute septicaemic fowl cholera, heat exhaustion,
and severe water deprivation.

PREVENTION AND CONTROL

 Vaccines can prevent clinical signs and death. Furthermore, viral replication and
shedding from the respiratory and GI tracts may be reduced in vaccinated birds.
 Specific protection is achieved through autogenous virus vaccines or from vaccines
prepared from AI virus of the same haemagglutinin subtype.
  Antibodies to the viral neuraminidase antigens may provide some protection.
Currently, only inactivated whole AI virus and recombinant fowlpox - AI-H5
vaccines are licensed in the USA .
 The use of AI vaccine requires approval of the state veterinarian.
 In addition, use of H5 and H7 AI vaccines in the USA requires USDA approval.
 Treating LP-affected flocks with broad-spectrum antibiotics to control secondary
pathogens and increasing house temperatures may reduce morbidity and mortality.
 Treatment with antiviral compounds is not approved or recommended. Suspected
outbreaks should be reported to appropriate regulatory authorities.

ZOONATIC RISK

 Avian influenza viruses exhibit host adaptation and rarely infect humans, usually as
isolated individual cases without human-to-human transmission.
 In the 1997 Hong Kong outbreak, the risk factor for human infection was direct
contact with infected poultry, but not the handling, cooking, or consumption of
poultry meat.
 In 2004, HP AI of strain H5N1 infected poultry and wild birds in 9 Asian countries.
 In Thailand and Vietnam , 37 human cases were confirmed, with a case fatality rate
of 68%.
 CHAPTER-4: MAREK'S DISEASE AND AVIAN LEUCOSIS COMPLEX

7) MAREK'S DISEASE

INTRODUCTION

 Chickens are the most important natural host for Marek’s disease virus, a highly
cell-associated but readily transmitted alpha herpes virus with lymphotropic
properties of gamma herpes viruses.
 Quail can be naturally infected and turkeys can be infected experimentally.
However, severe clinical outbreaks of Marek’s disease in commercial turkey flocks,
with mortality from tumors reaching 40-80% between 8-17 wk of age, were reported
recently in France, Israel, and Germany.
 In some of these cases, the affected turkey flocks were raised in proximity to
broilers.
 Turkeys are also commonly infected with turkey herpes virus, an avirulent strain
related to Marek’s disease virus. Other birds and mammals appear to be refractory
to the disease or infection.
 Marek’s disease is one of the most ubiquitous avian infections; it is identified in
chicken flocks worldwide.
 Every flock, except for those maintained under strict pathogen-free conditions, may
be presumed to be infected.
 Although clinical disease is not always apparent in infected flocks, a subclinical
decrease in growth rate and egg production may be economically important.

 ETIOLOGY

 Three serotypes of the cell-associated herpes virus are recognized. Serotypes 1 and 2
designate virulent and avirulent chicken isolates, respectively; serotype 3 designates
the related avirulent turkey herpes virus. Serotypes 2 and 3, as well as attenuated
serotype 1 viruses, have been used as vaccines.
 Serotypes are identified by reaction with type-specific monoclonal antibodies or by
biological characteristics such as host range, pathogenicity, growth rate, and plaque
morphology.
 Currently, virulent serotype 1 strains are further divided into pathotypes, which are
often referred to as mild (m), virulent (v), very virulent (vv), and very virulent plus
(vv+) Marek’s disease virus strains.

TRANSMISSION AND EPIDEMIOLOGY

 The disease is highly contagious and readily transmitted among chickens.

 The virus matures into a fully infective, enveloped form in the epithelium of the
feather follicle, from which it is released into the environment.
 It may survive for months in poultry house litter or dust. Dust or dander from
infected chickens is particularly effective in transmission.
 Once the virus is introduced into a chicken flock, regardless of vaccination status,
infection spreads quickly from bird to bird.
 Infected chickens continue to be carriers for long periods and act as sources of
infectious virus. Shedding of infectious virus can be reduced, but not prevented, by
prior vaccination.
 Unlike serotypes 1 and 2, which are highly contagious, turkey herpes virus is not
readily transmissible among chickens (although it is easily transmitted among
turkeys, its natural host).
 Attenuated serotype 1 strains vary greatly in their transmissibility among chickens;
the most highly attenuated are not transmitted. Marek’s disease virus is not
vertically transmitted.
 The incidence of Marek’s disease is quite variable in commercial flocks and depends
on strain and dose of virus, age at exposure, maternal antibody, host gender and
genetics, other concurrent diseases, and several environmental factors including
stress.

PATHOGENESIS

 Currently, 4 arbitrary phases of infection in vivo are recognized,

o early productive-restrictive virus infection causing primarily degenerative
changes
o latent infection
o a second phase of cytolytic, productive-restrictive infection coincident with
permanent immunosuppression and
o a proliferative phase involving nonproductively infected lymphoid cells that may
or may not progress to the point of lymphoma formation
  Productive infection may occur transiently in B lymphocytes within a few days after
infection with virulent serotype 1 strains and is characterized by antigen production,
which leads to cell death.
 Productive infection also occurs in the feather follicle epithelium, in which
enveloped virions are produced.
 Latent infection of activated T cells is responsible for the long term carrier state.
 No antigens are expressed, but virus can be recovered from lymphocytes by co-
cultivation with susceptible cells in tissue cultures.
 Some T cells, latently infected with oncogenic serotype 1 strains, undergo neoplastic
transformation.
 These transformed cells, provided they escape the immune system of the host, may
multiply to form characteristic lymphoid neoplasms.
 Cell-mediated and humoral immune responses are both directed against viral
antigens, with cell-mediated immunity probably being the most important

CLINICAL SIGNS AND LESIONS

 Typically, affected birds show only depression before death, although emaciation
may be noted.
 A transient paralysis syndrome (unilateral leg paresis) has been associated with
Marek’s disease, causing a characteristic posture of one leg held forward and the
other held backward as lesions progress.
 Chickens become ataxic for periods of several days and then recover. This syndrome
is rare in immunized birds.
 Enlarged nerves are one of the most consistent gross lesions in affected birds
 Various peripheral nerves, but particularly the vagus, brachial, and sciatic, become
enlarged and lose their striations.
 Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the
liver , spleen, gonads, heart, lung, kidney, muscle, and proventriculus.

Lymphoid infiltrates may expand the iris muscle and distort the shape of the
pupil (Enlarged feather follicles (commonly termed skin leukosis) may be noted in broilers
after defeathering during processing and are a cause for condemnation

 The bursa is only rarely tumorous and more frequently is atrophic. Histologically,
the lesions consist of a mixed population of small, medium, and large lymphoid cells
plus plasma cells and large anaplastic lymphoblasts.
 These cell populations undoubtedly include both tumor cells and reactive
inflammatory cells. When the bursa is involved, the tumor cells typically appear in
interfollicular areas.

DIAGNOSIS

 Usually, diagnosis is based on enlarged nerves and lymphoid tumors in various

viscera.
  The rareness of bursal tumors helps distinguish this disease from lymphoid leukosis
also, Marek’s disease can develop in chickens as young as 3 wk of age, whereas
lymphoid leukosis typically is seen in chickens >14 wk of age. Reticuloendotheliosis,
although rare, can easily be confused with Marek’s disease because both diseases
feature enlarged nerves and T-cell lymphomas in visceral organs.
 A diagnosis based on typical gross lesions may be confirmed histologically, or better,
by demonstration of predominant T-cell populations and Marek’s viral DNA in
lymphomas by histochemistry and PCR, respectively.
 Furthermore, Marek’s disease lymphomas will usually lack evidence of clonally
integrated avian retroviruses or alteration of the cellular oncogene c-myc.

CONTROL

 Vaccination is the central strategy for the prevention and control of Marek’s disease.
 The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay
exposure and by breeding for genetic resistance.
 Probably the most widely used vaccine consists of turkey herpes virus.
 Bivalent vaccines consisting of turkey herpes virus and either the SB-1 or 301B/1 strains of
serotype 2 Marek’s disease virus has been used to provide additional protection against
challenge with virulent serotype 1 isolates.
 Several attenuated serotype 1 Marek’s disease vaccines are also available; of these, the
CV1988/Rispens strains appears particularly effective.
 A synergistic effect on protection, noted mainly between serotype 2 and 3 strains, has
prompted the empirical use of other virus mixtures.
 Because vaccines are administered at hatching and require 1-2 wk to produce an effective
immunity, exposure of chickens to virus should be minimized during the first few days after
hatching.
 Vaccines are also effective when administered to embryos at the 18th day of incubation.
 In ovo vaccination is now performed by automated technology and is widely used for
vaccination of commercial broiler chickens, mainly because of reduced labor costs and greater
precision of vaccine administration.
 Proper handling of vaccine during thawing and reconstitution is crucial to ensure that
adequate doses are administered.
 Cell-associated vaccines are generally more effective than cell-free vaccines because they are
neutralized less by maternal antibodies.
 Under typical conditions, vaccine efficacy is usually >90%. Since the advent of vaccination,
losses from Marek’s disease have been reduced dramatically in broiler and layer flocks.
 However, disease may become a serious problem in individual flocks or in selected geographic
areas (eg, the Delmarva broiler industry).
 Of the many causes proposed for these excessive losses, early exposure to very virulent virus
strains appears to be among the most important.
 Using fowl pox virus and herpes virus of turkeys as vectors, experimental recombinant vaccines
have been shown to be effective against challenge with virulent Marek’s disease virus.



 8) Avian leucosis complex
INTRODUCTION

 Under natural conditions, lymphoid leukosis has been the most common form of the
leukosis / sarcoma group of diseases seen in chicken flocks, although recently
myeloid leukosis has become prevalent.
 Members of the leukosis / sarcoma group of avian retroviruses, including avian
leukosis viruses that were formerly placed in a subgenus termed avian type C
oncorna viruses have recently been termed alpha retroviruses.
 Members of this group of viruses have similar physical and molecular characteristics
and share a common group-specific antigen.
 Avian leukosis occurs naturally only in chickens. Experimentally, some of the viruses
of the leukosis/sarcoma group can infect and produce tumors in other species of
birds or even mammals.
 The infection is known to exist in virtually all chicken flocks except for some SPF
flocks from which it has been eradicated.
 The frequency of infection has been reduced substantially in the primary breeding
stocks of several commercial poultry breeding companies.
 In recent years this control program has expanded, and infection has become
infrequent or absent in certain commercial flocks.
 The frequency of avian leukosis tumors even in heavily infected flocks is typically
low (<4%), and disease is often inapparent.
 Up to 1.5% excess mortality per wk has been reported in commercial broiler- breeder
flocks naturally infected with subgroup J avian leukosis virus.

ETIOLOGY

 Avian leukosis is caused by certain members of the leukosis/sarcoma group of avian

retroviruses.
 These viruses are commonly called avian leukosis viruses and belong to subgroups
A, B, C, D, E, and J.
 Subgroups A and B have been most prevalent in western countries, until the
emergence of subgroup J.
 Since the initial isolation of subgroup J virus in England, the virus has been isolated
from broiler-breeder stocks experiencing myeloid neoplasms (myelocytoma) in
many other countries.
 Subgroup E avian leukosis viruses are endogenous viruses produced by viral genes
integrated into the host cell DNA and are only rarely oncogenic.
 The subgroups have distinct antigenicities and cellular host ranges that are
determined by viral envelope glycoproteins.
 Some antigenic variation, demonstrated by cross-neutralization, also occurs within
subgroups.
 All field strains of avian leukosis virus are oncogenic, although some differences in
oncogenicity and replicative ability have been recognized.
 TRANSMISSION AND EPIDEMIOLOGY

 Chickens are the natural hosts for all viruses of the leukosis/sarcoma group; these
viruses have not been isolated from other avian species except pheasants, partridges,
and quail.
 Avian leukosis virus is shed by the hen into the albumen or yolk, or both; infection
probably occurs after the onset of incubation.
 Congenitally infected chickens fail to produce neutralizing antibodies and usually
remain viraemic for life.
 Horizontal infection after hatching is also important, especially when chicks are
exposed immediately after hatching to high doses of virus, eg, in feces of
congenitally infected chicks or in contaminated vaccines.
 Horizontally infected chickens have a transient viraemia followed by antibody
production.
 The earlier the infection, the more likely it is to lead to tolerance, persistent
viraemia, and tumors.
 Other factors known to increase the susceptibility of chickens to horizontal infection
include the absence of maternal antibodies and the presence of endogenous
retroviruses, especially those associated with the late feathering (K) gene.
 Tumors are more frequent in congenital than in horizontal infections, but many
more chickens are exposed horizontally than congenitally.
 Rates of embryo transmission typically are 1-10%; virtually all chicks in an infected
flock are exposed by contact.
 Congenital and, in some cases, early horizontal infection can induce permanent
carrier states characterized by shedding of virus or antigen into the environment and
into eggs.
 Late infection (ie, inoculation at 12-20 wk of age) is unlikely to lead to virus
shedding.
 The virus is not highly contagious compared with other viral agents and is readily
inactivated by disinfectants.
 Transmission can be reduced or eliminated by strict sanitation.
 After the infection is eradicated, standard disease control and sanitation practices
can keep chicken flocks free of the disease.
 The role of males in transmission of avian leukosis virus is uncertain.
 Infected cocks apparently do not influence the rate of congenital infection of
progeny.
 Cocks may act only as virus carriers and sources of contact or venereal infection to
other birds.

PATHOGENESIS

 Lymphoid leukosis is a clonal malignancy of the bursal-dependent lymphoid system.

 Transformation invariably occurs in the intact bursa, often as early as 4-8 wk after
infection.
 These tumors require 14-16 wk to develop. Death rarely occurs before 14 wk of age
and is more frequent around the time of sexual maturity.
 The disease can be prevented, even up to 5 mo of age, by treatments that destroy the
bursa.
 The tumors are composed almost entirely of B lymphocytes that, in many instances,
have IgM on their surfaces.
 No antitumor immune response has been recognized. Antibodies are readily induced
after infection, except when tolerance occurs.
 The induction of lymphoid leukosis tumors can be enhanced in chickens co infected
with serotype 2 Marek’s disease virus, a common vaccine virus.
 This enhancement requires a genetically susceptible chicken and early infection with
lymphoid leukosis virus in addition to serotype 2 Marek’s disease vaccination.
 Because most commercial chicken strains are resistant and lymphoid leukosis virus
infection has been largely eradicated from susceptible stocks, enhancement is not
currently recognized as a field problem.
 A subclinical disease syndrome characterized by depressed egg production in the
absence of tumor formation is more important economically than mortality from
lymphoid leukosis.
 Chickens with subclinical disease usually shed virus or viral antigen into the
albumen of eggs. The pathogenic mechanisms are poorly understood.
 Myeloid leukosis is a malignancy of myeloid precursors arising from the bone
marrow. Its pathogenesis is not well understood.

CLINICAL FINDINGS AND LESIONS

 Chickens with lymphoid leukosis show nonspecific clinical signs including

inappetence, weakness, diarrhea, dehydration, and emaciation.
 Infected chickens become depressed before death. Palpation often reveals an
enlarged bursa and sometimes an enlarged liver.
 Infected birds may not necessarily develop tumors, but they may lay fewer eggs.
 Diffuse or nodular lymphoid tumors are common in the liver (see the picture
below) spleen, and bursa, and are found occasionally in the kidneys, gonads, and
mesentery.
 Involvement of the bursa has been considered virtually pathognomonic, although
bursal lymphomas are now known to also be induced by reticuloendotheliosis virus.
 Sometimes the bursal tumors are small and observed only after careful examination
of the mucosal surface of the organ.
 Usually, no enlargement of peripheral nerves is apparent, although such lesions
have been noted after experimental inoculation of subgroup J virus.
 Microscopically, the tumor cells are uniform, large lymphocytes. Mitotic figures are
frequent.
 Outbreaks of neoplasms other than lymphoid leukosis such as myelocytomas,
haemangiomas, and renal tumors have also been noted in meat-type chickens
infected with subgroup J avian leukosis virus.
 Myelocytomatosis and skeletal myelocytomas may cause protuberances on the head,
thorax, and shanks.
 Myelocytomas may develop in the orbit of the eye, causing hemorrhage and
blindness.
 Haemangiomas may be seen in the skin, appearing as “blood blisters,” which may
rupture causing hemorrhage.
 Renal tumors may cause paralysis due to pressure on the sciatic nerve.
Microscopically, especially in cases of myelocytomas induced by subgroup J avian
leukosis virus, the liver shows a massive intravascular and extravascular
accumulation of myelocytes characterized by the presence of cytoplasmic
eosinophilic granules.
 Most strains of leukosis/sarcoma viruses also induce non lymphoid tumors
(including sarcomas), erythroblastosis, myeloblastosis, myelocytomas,
haemangiomas, nephroblastomas, osteopetrosis, and related neoplasms.
 The nature of the tumors and their frequency depend on virus and chicken strain,
age, dose, and route of infection.
 Occasional outbreaks of predominantly one type of tumor are seen in the field. The
Rous sarcoma virus, a member of this group, has been widely studied in the
laboratory.
 Each strain usually causes a predominantly neoplastic disease and can be
distinguished on the basis of pathogenicity.
 Some viruses (eg, Rous sarcoma and erythroblastosis viruses) contain a viral
oncogene that leads to neoplasm induction within a short incubation period, but
such viruses are rare in the field.
 Viruses with a viral oncogene are often defective for replication and require the
presence of a non defective helper virus to replicate.

DIAGNOSIS

 Because avian leukosis virus is widespread among chickens, virus isolation and the
demonstration of antigen or antibody have limited or no value in diagnosing field
cases of lymphomas.
 Gross characteristics of diagnostic significance include the tumorous involvement of
the liver, spleen, or bursa in the absence of peripheral nerve lesions. Tumors occur
in birds >14 wk old.
 In lymphoid leukosis, the lymphoid cells are histologically uniform in character,
large, and contain IgM and B-cell markers on their surface.
 Tumors can be differentiated from those of Marek’s disease by gross and
microscopic pathology (although this can be difficult in practice) and by molecular
techniques that demonstrate the characteristic clonal integration of proviral DNA
into the tumor cell genome with the associated disruption of the c-myc oncogene.
 Lymphoid leukosis cannot easily be differentiated from B-cell lymphomas caused by
reticuloendotheliosis virus except by virologic assays; however, such tumors
probably are extremely rare.
 ELISA kits for detection of antibodies to avian leukosis virus subgroups A, B, and J
are available commercially.
 CONTROL

 Lymphoid leukosis appears to be controlled best by reduction and eventual

eradication of the causative virus.
 Breeder flocks are evaluated for viral shedding by testing for viral antigens in the
albumen of eggs with enzyme immunoassays or by biologic assays for infectious
virus.
 Eggs from shedder hens are discarded, so that progeny flocks typically have reduced
levels of infection. If raised in small groups, infection-free flocks can be derived with
relative ease.
 These control measures are applied only to primary breeder flocks.
 Voluntary programs to reduce viral infection have already reduced mortality from
lymphoid leukosis and improved egg production in most layer strains; similar
programs are underway in certain meat strains.
 Some breeders favor, and have virtually achieved, total eradication, while others
favor a reduced level of viral infection.
 Some chickens have specific genetic resistance to infection with certain subgroups of
virus.
 Although genetic cellular resistance will unlikely replace the need for reduction or
eradication of the virus, the cellular receptor gene has been cloned, and quick
molecular assays for viral susceptibility could be developed.
 Thus far, vaccination for tumor prevention has not been promising.
 However, recombinant vaccines lacking infectious avian leukosis virus can induce
antibodies in breeders to ensure protective maternal antibodies in progeny chicks
and may be an attractive adjunct to eradication programs.

CHAPTER-5: AVIAN ENCEPHALOMYELITIS, INCLUSION BODY AND

HYDROPERICARDIUM SYNDROME

9) AVIAN ENCEPHALOMYELITIS

INTRODUCTION

 Avian encephalomyelitis (AE) is an infectious viral disease of young chickens,

turkeys, pheasants, and quail.
 It is characterised by ataxia and rapid tremors, especially of the head and neck. AE
occurs worldwide.
 The causative picornavirus is a single-stranded RNA (ss RNA). All strains appear to
be antigenically uniform, but there are variations in neurotropism and virulence.
 Field strains are mainly enterotropic, whereas egg-adated strains are mainly
neurotropic.
 The immune status of the affected bird appears to be the main factor influencing the
outcome of infection.
 Antobodies are transferred to progeny from the dam through the egg, and can be
demonstrated in egg yolk.
 Maternal antibodies can protect young birds against systemic infection.
 SPREAD

 Ingestion is the usual route of entry. Virus is shed in the faeces for a period of
several days and it is quite resistant to environmental conditions.
 It appears that some birds are enteric carriers and excrete virus in their droppings.
Infected litter is a source of the virus which is easily transmitted horizontally by
fomites and mechanical carriers. Vertical transmission is a very important means of
virus dissemination.
 Transmission of the virus occurs through the egg, from infected to susceptible stock.
 Egg transmission occurs during the period from the infection of susceptible laying
hens to the development of immunity, a period of 3-4 weeks.

PATHOGENESIS

 In young chicks exposed to field strains, primary infection of the alimentary tract,
especially duodenum, is rapidly followed by a viraemia, and subsequent infection of
the pancreas and other visceral organs (liver, heart, kidney, spleen) and skeletal
muscle, and finally central nervous system.
 Viral antigen is abundant in the CNS, where Purkinje cells and molecular layer of the
cerebellum are the favoured sites of virus replication.
 Persistence of the viral infection is common in the CNS, alimentary tract and
pancreas. CNS and the pancreas are the only sites uniformly infected by egg-adapted
strains.
 Age at exposure is especially important in the pathogenesis. Birds infected at one
day of age generally die, where as those infected at 8 days develop paresis (partial
paralysis) but usually recover.
 Infection at 28 days causes no clinical signs. Bursectomy but not thymectomy
abolished the age resistance. This indicated that humoral immunity was the basis of
age resistance.
 It is found that young age correlates with prolonged viraemia, persistence of virus in
the brain, and development of clinical disease

AVIAN ENCEPHALMYELITIS: CLINICAL SIGNS

 AE usually makes it appearance when chicks are 1-2 week of age. Affected chicks
first show a slightly dull expression of the eyes.
 This is followed by a progressive ataxia from incoordination of the muscles, which
may be detected readily by exercising the chicks.
 As the ataxia becomes more pronounced, chicks show an inclination to sit on their
hocks and finally, they come to rest, or fall on their sides
 Fine tremors of the head and neck may become noticeable.
 Ataxia usually progresses until the chick is incapable of moving about, and this stage
is followed by inanition (loss of vitality from lack of food and water), prostration,
and finally death.
 Some chicks may survive and grow to maturity. Survivors may later develop
blindness from an opacity giving a bluish discolouration to the lens
 LESIONS

 The only gross lesions in chicks are whitish areas in the muscles of ventriculus,
which are due to masses of infiltrating lymphocytes.
 In adult birds, no changes have been described except the lens opacities.
 Microscopically, the main changes are in the CNS and some viscera. The peripheral
nervous system is not involved.
 In the CNS, the lesions are those of a disseminated non-purulent encephalomyelitis,
and a ganglionitis of the dorsal root ganglia.
 The most finding is a striking perivascular infiltration in all portions of the brain and
spinal cord, except cerebellum. Microgliosis occurs as diffuse and nodular
aggregates. The glial lesion is seen chiefly in the cerebellar molecular layer.
 In the mid-brain, two nuclei- nucleus rotundus and nucleus ovoidalis – are always
affected with a loose microgliosis which is considered Pathognomonic. Another
lesion of Pathognomonic importance is central chromatolysis (axonal reaction) of
the neurons in the nuclei of thebrain stem, particularly those of the medulla
oblongata.
 The dying neuron is surrounded by satellite oligodendroglia.Later, microglia
phagocytize the remains. The central chromatolysis is never seen without an
accompanying cellular reaction.
 Visceral lesions appear to be hyperplasia of thelymphocytic aggregates. In the
proventriculus, there only a few small lymphocytes in the muscular wall.
 In AE, theses become dense lymphocytic foci (aggregates). This lesion is
Pathognomonic. Similar lesions occur in the ventriculus muscle, but unfortunately
they also occur in mArek’s disease.
 In the pancreas, circumscribed lymphocytic follicles are normal, but in AE
thenumber increases several times.
 In the myocardium, particularly in the atrium, there are aggregates of lymphocytes.
These are considered to be the result of AE.

DIAGNOSIS

 The clinical signs, absence of gross lesions, and microscopic findings in the brain,
spinal cord and visceral organs together with the absence of other virus infections
and nutritional deficiencies affecting the nervous system, are strongly suggestive of
avian encephalomyelitis and are frequently used for presumptive diagnosis.
 A definitive diagnosis requires demonstration of the virus by isolation and
identification or by other means.
 Examination of smears from the brain, or cryostat sections stained by direct
immunofluorescence may also be used to demonstrate virus; positive results are
confirmatory and often unreliable.
 A number of serological tests are available for determining the infection. These
include virus neutralization (VN) test, an indirect immunofluorescence test,
immunodiffusion and an ELISA test. Because of its specificity and sensitivity,
rapidity of performance and amenability to large-scale screening, the ELISA has
replaced other tests for antibody, including the assessment of efficacy of vaccination.
 DIFFERENTIAL DIAGNOSIS

 It is necessary to consider other causes of neurological disorders such as nutritional

encephalmalacia and virus infections Ranikhet disease, and Marek’s disease.

 10) Inclusion body hepatitis

INTRODUCTION

 This disease is usually seen in meat-producing chickens aged 3-7 weeks. However it
has also been recorded in birds as young as 7 days old, and as old as 20 weeks.
 It is a rare disease in turkeys. It is characterised by a sudden increase in mortality.
This is normally between 2 and 10% of the flock but upto 30% has been described.
 Significant mortality persists for only a few days.

ETIOLOGY

 The etiology of the disease has not been properly established. There is no separate
inclusion body hepatitis virus.
 Virtually every serotype of fowl Aviadenovirus group I have been isolated from the
naturally occurring cases of IBH.
 Furthermore, all the adenovirus serotypes produce hepatitis when young SPF chicks
are inoculated parenterally.
 Most experimental adenovirus infections produce basophilic inclusion bodies in the
hepatocytes whereas most natural cases produce eosinophilic intranuclear inclusion
bodies. If adenoviruses are involved in producing IBH, they appear to acta with
some other factor.
 It has been suggested that immunosuppression produced by infectious bursal
disease (IBD) helps adenovirus to produce IBH. However many flocks undergoing
combined infections with these viruses remain healthy. Furthermore, outbreaks of
IBH occurred in both Northern Ireland and Newzealand before IBD virus was into
those countries. Some outbreaks of disease described as IBH closely resemble
haemorrhagic syndrome/ infectious anaemia caused by Chicken anaemia virus.
 Outbreaks of IBH which occurred in Australia in the early 1990s differ significantly
from the above. They occurred in much younger chicks (i.e. under 3 weeks of the
age), have caused higher mortality and predominantly basophilic inclusion bodies
were present in hepatocytes.
 Adenoviruses have been isolated from field cases and have reproduced the disease
experimentally in chickens. In India, the disease has appeared as seasonal,
especially after monsoon, in the cold season. The mycotoxin stress seems to be
another predisposing factor besides IBD.

CLINICAL SIGNS

 The disease is characterised by sudden onset of mortality, reaching highest after 3-4
days, and dropping on the 5th day, but some times continuing for 2-3 weeks.
  Morbidity is low. Sick birds adopt a crouching position with ruffled feathers and die
within 48 hours, or recover.
 Mortality may reach 10%, and sometimes as high as 30%. Overall feed conversion
and weight gain are usually decreased.
 Anaemia, jaundice of the skin and subcutaneous fat, haemorrhages in various
organs, especially the muscles, and bone marrow degeneration are usually present,
but vary in severity.
 In some outbreaks the bone marrow lesions are most prominent, and it has been
suggested that the disease should be called, “Hepato-myeloporetic disease”.

LESIONS

 The liver in diseased birds is pale, friable and swollen, and frequently has
haemorrhages. Petechial or ecchymotic haemorrhagesmay be present in the liver
and skeletal muscles.
 Microscopically, there is a diffuse and generalized hepatitis, with intranuclear
inclusion bodies in the hepatocytes, which are often eosinophilic.
 In the Australian outbreaks, basophilic inclusions predominated. Virus particles
were detected only in cells with basophilic inclusions.
 Eosinophilic inclusions were composed of fibrillar granular material. IN the New
zealand outbreaks, inclusions were eosinophilic.

DIAGNOSIS

 This depends on isolation and identification of the virus, and on serological tests.
Specimens of choice are faeces, pharynx, kidney, and affected organs, e.g. livers.
 Virus isolation is best achieved by inoculating both a 10% suspension of the affected
organ and a a faeces suspension into cell cultures. Chicken embryo liver or lung
cells, or chick kidney cells, are all sensitive but chick embryo fibroblatss are
relatively insensitive.
 Antibody to the conventional adenovirus group antigen can be detected using the
double immunodiffusion (DID) test. The indirect immunofluorescent test is much
more sensitive and rapid, and is inexpensive. ELISA has been used to detect group
antibodies, and it is expensive and sensitive.
 Demonstration of eosinophilic intranuclear inclusion body in Haematoxylin and
eosin staining in the hepatocytes of chickens in naturally occurring inclusion body
hepatitis is diagnostic.

 11) Hydropericardium syndrome

INTRODUCTION

 A viral disease, which was reported from Pakistan, affecting particularly broilers and
the losses varies from 10-20%.

 CAUSE AND TRANSMISSION

 An incomplete virus which requires another adenovirus for its multiplication and
growth is the cause of this disease and certain viral diseases such as adenovirus,
IBH, aflatoxicosis are said to be responsible for the outbreak of this disease.

CLINICAL SIGNS AND POSTMORTEM LESIONS

 The affected chicks died suddenly.

On postmortem examination

 The pericardial sac is filled with straw color fluid,

 Swollen and discolored liver,

 Swollen kidneys with distended ureters
 Due to malfunctioning of liver and kidneys, there is reduction in osmotic pressure
resulting in seepage of fluid in pericardial sac.
 The pericardial sac becomes distended due to excessive accumulation of fluid giving
rise the appearance of LICHI.

TREATMENT AND CONTROL

 No specific treatment of the disease.

 An auto vaccine, prepared form the liver of affected broiler chicks given at 2 or 3
week of age, is found to be satisfactory in immunizing the chicks against this disease.
 Proper care should be taken for the control of contributing factors.
 CHAPTER-6: CHICKEN INFECTIOUS AGENT, EGG DROP SYNDROME AND
AVIAN NEPHRITIS

 12) Chicken infectious agent

INTRODUCTION

 Chicken infectious anaemia (CIA) is a disease of young chickens caused by a unique

small virus.
 The disease is characterised by aplastic anaemia and generalized lymphoid atrophy,
with an accompanying immunosuppression. As a result, CIA is usually complicated
by secondary viral, bacterial, or fungal infections.
 The agent was first described in Japan in 1979 and was designated chicken anaemia
agent (CAA).Following its characterization as a non-enveloped virus containing a
single stranded circular DNA, it was renamed as “Chicken anaemia virus (CAV)” and
classified under Circaviridae. Because the disease caused by it is commonly called
chicken infectious anaemia, the virus is now called "Chicken infectious anaemia
virus(CIAV)”.
 CAV is a remarkably resistant virus; its infectivity resists heating at 80®c for 15
minutes and exposure to pH3.
 CAV has been isolated from chickens in an increasing number of countries
worldwide and serological surveys indicate that CAV infection is common in
chickens through out the world.
 It is not known if avian species other than domestic fowl are infected. All isolates of
CIAV isolated to date belong to a single.

SPREAD

 The virus spreads both horizontally and vertically.

 Vertical transmission through the hatching egg is considered to be most important
means of dissemination.
 Embryo infection can also be caused by semen of infected cocks.
 The virus is present in high concentrations in the faeces of chickens 5-7 weeks after
infection.
 Horizontal infection by direct or indirect contact usually occurs through the oral
route by ingesting infected material, but infection through respiratory route may
also be possible.

PATHOGENESIS

 Experimental studies have shown that anaemia and pathological changes associated
with CAV are produced only following parentral inoculation of high doses of CAV
into neonatal , fully susceptible (i.e. having no maternal antibody) chicks.
 Chicks infected by contact with parenterally inoculated chicks are also resistant to
experimental disease but become infected and shed the virus.
 Maternal antibody is protective. Chicks with maternal antibody usually show no
disease or anaemia following parentral inoculation, but may become infected and
shed the virus.
 Experimental dual infection of CIAV and immunosuppressive viruses such as
reticuloendotheliosis virus, virulent Marek’s disease virus and infectious bursal
disease(IBD) virus enhances the apparent pathogenicity of CAV, resulting in greater
mortality and more persistent anaemia and histological lesions.
 In such dual infections the protective effect of maternal antibody to CAV may be
overcome.
 In chicks dually infected with CAV and IBD virus, the age résistance was overcome
and contact-infected chicks also developed anaemia. CIAV has been shown to be
immunosuppressive.
 Functional changes were detected in splenic lymphocytes and splenic and bone
marrow macrophages from both clinically affected and sub clinically infected chicks.
 Following intramuscular inoculation of susceptible day- old chicks, CAV was
consistently recovered from all organs for upto 21 days after inoculation.
 The principal sites of CAV replication are precursor T cells in the thymic cortex and
in haemocytoblasts in the bone marrow.
 Destruction of these cells accounts for the immunosuppression and anaemia.
However, the virus also replicates in all lymphoid aggregates through out the body.

SIGNS

 Disease occurs in theprogeny of breeder flocks which are infected for the first time
with the the virus fater they come into lay.
 CIAV is vertically transmitted to the progeny. No clinical signs are seen in the
parents. However, around two weeks of age, the young chicks show variable
mortality. This can be as great as 60% but usually averages around 10%. The most
characteristic changes in infected are anaemia, aplasia of the bone marrow and
atrophy of thymus, spleen and bursa of Fabricius.
 Anaemia is characterised by watery blood, increased clotting time and paler plasma.
 Low haematocrit values ranging from 6-27% is due to pancytopaenia with markedly
decreased numbers of erythrocytes, white blood cells, and thrombocytes.
 Affected birds are depressed and more or less pale. Haemorrhages may occur under
the skin and through out the skeletal muscles.
 Enlarged livers and gangrenous dermatitis may also be present. Other names for this
condition are anaemia dermatitis syndrome, infectious anaemia syndrome,
haemorrhagic syndrome, and blue-wing disease.
 Surviving chicks completely recover from anaemia by 20-28 days after infection.
However, retarded recovery and increased mortality may be associated with
secondary bacterial and viral infections. Secondary infections cause more severe
clinical signs.
 Subclinical infection of the progeny of immune breeder flocks is common. This
occurs soon after maternally acquired antibodies have disappeared at about 3 weeks
of age.
 MACROSCOPIC LESIONS

 Though thymic atrophy is the most consistent lesion, bone marrow atrophy is the
most characteristic lesion. Femoral bone marrow is fatty, and yellowish and pink.
 Thymic atrophy may result in a complete regression of the organ.
 As infected chicks develop age resistance, thymic atrophy is a much more consistent
lesion than grossly visible bone marrow lesions. Bursal atrophy is less noticeable.
 Haemorrhages in the proventricular mucosa, and subcutaneous and muscular
haemorrhages are some times associated with severe anaemia.

MICROSCOPIC LESIONS

 In the anaemic chicks, microscopicchanges have been characterised as

panmyelophthisis (wasting away of the the bone marrow), and generalized lymphoid
atrophy.
 In the bone marrow, atrophy and aplasia involve all compartments and all
haematopoietic cells.
 Haematopoietic cells are replaced by adipose tissue proliferating stroma cells.
Severe lymphoid depletion is seen in thymus, bursa of Fabricius, spleen and caecal
tonsils, as well as in a wide range of other tissues.
 The thymus cortex and medulla become equally atrophic. Lesions in the bursa of
Fabricius consist of atrophy of the lymphoid follicles.
 In the spleen also, there is atrophy of lymphoid tissue.
 In the liver, kidneys, lungs, proventriculus, duodenum, and caecal tonsils, lymphoid
foci are depleted of cells.

DIAGNOSIS

 Outbreaks of clinical disease are normally diagnosed on the basis of the

characteristic signs and pathology. There is also usually a history of a common
breeder flock, which is often close to peak egg production.
 Laboratory diagnosis is base on immunofluorescent or immunocyto
chemicaldetection of CIAV antigens in thymus or bone marrow. Viral DNA can also
be detected in thymus or bone marrow by insitu hybridization, dot blot
hybridization or polymerase chain reaction (PCR).
 Virus isolation is not recommended because it is slow and expensive. Serum
antibody to CIAV can be detected by a variety of serological tests including serum
neutrolisation, indirect immunofluorescence and enzyme-linked immunosorbent
assay (ELISA).

DIFFERENTIAL DIAGNOSIS

 Runting and Stunting Syndrome, field rickets and Salmonella enteritidis

septicaemia were the conditions most likely to produce low weights and mortality in
this age group.
 All of these were excluded on the absence of typical pathology.
  Sulphonamide toxicity and severe aflatoxicosis can induce haemorrhagic lesions and
aplastic anaemia, though these would not be expected to occur in the progeny of
only 1 parent flock.

 13) Egg drop syndrome

ETIOLOGY

 The cause of EDS is an adenovirus that differs from aviadenoviruses and

siadenoviruses in that it agglutinates avian but not mammalian red blood cells to
high titres.
 Although EDS virus apparently shares the Aviadenovirus group antigen, this can be
detected only by indirect means. It is now classified as a species, duck adenovirus A,
in the genus Atadenovirus.
 In fact, EDS virus is a naturally occurring adenovirus of ducks, geese and other
water fowl that has infected domestic fowl.
 It grows best in duck and geese cell cultures but also grows well in chick embryo
liver and chick kidney cells. All virus isolates belong to one serotype (DAdV-1).

SPREAD

 EDS outbreaks are divided into three patterns.

o In the classical form, Primary breeders are infected and the main method of
spread is vertical through embryonated egg.Although the number of infected
embryos is low, spread is very efficient.
o The second pattern is the endemic form. It has resulted from lateral spread
between flocks. Spread is primarily associated with contaminated eggs or egg
trays and is sually seen in commercial egg layers. Any age of laying flock may be
affected and there is often an association between affected flocks and an egg
packing station.
o The third pattern is sporadic form. It is also seen in any age or breed of chicken.
It results from introduction of infection from ducks, geese or any infected wild
bird, either through direct or indirectly through drinking water contaminated
with droppings.
 The main source of virus in the droppings is secretion from the oviduct. Lateral
spread between flocks via contaminated personnel or fomites, other than egg trays
can occur, but does not appear to be a major hazard. Other methods of spread could
be via contaminated needles and possibly, by biting insects.

PATHOGENESIS

 Following experimental infection of laying infection, the virus grows to a limited

extent in the nasal mucosa. This is followed by a transient viraemia, with virus
growth in lymphoid tissue through out the body, especially spleen and thymus.
 The infundibulum of the oviduct is consistently affected. At 8 days after infection
there is massive viral replication in the pouch shell gland region of the oviduct, and
 to a much lesser extent , in other parts of the oviduct. This coincides with the
occurrence of egg shell changes. Both the eggs with normal and affected shells
contain virus, both externally and internally, for the next 2 -3 weeks.
 Chicks hatched from these infected eggs often do not develop antibody but they may
be latently infected. At around peak egg production, the virus is reactivated and
horizontal spread occurs.
 In a minority of cases there is horizontal spread of the virus between birds during
the growing period, but, as the amount of virus excreted is small, this spread is
limited.

LINICAL SIGNS

 The first sign is usually loss of shell pigmentation. This is quickly followed by
production of thin-shelled, soft-shelled and shell-less eggs.
 Egg shells may have focal thickening due to mineral deposits. However, ridging and
misshapen eggs are not a feature. There is a drop in egg production.
 The birds are normally healthy but some times appear slightly depressed. Diarrhoea
may be noticed due to an excess of oviduct secretion in droppings.
 Classical EDS is manifested by a sudden apparent fall in egg production around peak
production or by a failure to achieve or hold expected production.

MACROSCOPIC PATHOLOGY

 Inactive ovaries and atrophied oviducts are often the only recognized lesons, and
these are not consistently present.

MICROSCOPIC PATHOLOGY

 The main pathological changes occur in the pouch shell gland of oviduct. Virus
replicates in epithelial cell nuclei, and produces intranuclear inclusion bodies.
 Many affected cells are sloughed into the lumen. There is a severe inflammatory
response involving macrophages, plasma cells and lymphocytes, together with
variable numbers of heterophils in the lamina propria and epithelium.

DIAGNOSIS

 The combination of a sudden fall in egg production, associated with thin-shelled and
shell-less eggs in a apparently healthy birds, is almost diagnostic.
 Virus isolation can be difficult because it is very difficult to identify the correct bird
to sample. The easiest method is to feed the affected eggs to susceptible hens.
 Once they produce abnormal eggs, the pouch shell gland is harvested, and samples
inoculated into either duck kidney, or fibroblast cell cultures, or embryonated eggs.
Virus growth is detected by testing for haemagglutinins.
 Detection of antibodies to EDS virus by the haemagglutination inhibition (HI) test
using fowl erythrocytes is sensitive and easy and is the diagnostic method of choice
in unvaccinated flocks.. ELISA is now also used
 DIFFERENTIAL DIAGNOSIS

 EDS can be distinguished from Newcastle disease and influenza virus infections by
the absence of illness, and from infectious bronchitis by the eggshell changes that
occur at or just before the drop in egg production and by the absence of ridges and
malformed eggs sometimes seen in infectious bronchitis.

 15) Avian nephritis

INTRODUCTION

 Avian nephritis, caused by enterovirus, is an acute, highly contagious, typically

subclinical disease of young chickens that produces lesions in the kidneys.
 The virus called, Avian nephritis virus (ANV), was firstdescribed in Japan in 1979. It
is a single stranded RNA (ss RNA) virus.
 ANV is distinct from avian encephalomyelitis virus and duck hepatitis viruses.

SPREAD

 ANV is distributed worldwide in the domestic fowl. Transmission readily occurs by

direct or indirect contact.
 The most common method is probably through ingestion of faecally contaminated
material.
 Egg transmission (vertical transmission) has been suggested on the basis of field
observations.

PATHOGENESIS

 Only young chickens are known to develop clinical disease and distinct kidney
lesions when exposed to ANV. Following infection, the virus is first detected in
faeces within 2 days, with maximum virus shedding at 4-5 days.
 The virus is widely distributed, with maximum titres in the kidney and jejunum and
low titres in the bursa of Fabricius, spleen and liver.
 The virus is consistently isolated from kidney, jejunum, and rectum, but not from
brain and trachea.

CLINICAL SIGNS

 The clinical sign in one-day old chicks is only transient diarrhoea, but not all chicks
show the signs. Weight gain is depressed.
 In the broiler chickens, symptoms vary from none ( subclinical) to outbreaks of the
so-called “runting syndrome” and baby chick nephropathy”.
 LESIONS

 Gross lesions in dead chicks are mild to severe discolouration and swelling in the
kidneys, and visceral urate deposits.
 Chalk- like urate crystals are seen on the surface of the peritoneum and liver. The
heart is white due to heavy urate deposits on the surface of epicardium.
 Microscopically, the primary changes consist of necrosis and degeneration of
epithelial cells of the proximal convoluted tubules with infiltration of granulocytosis
and interstitial nephritis of varying severity.
 The degenerating epithelial cells show acidiphilic granules of various sizes in the
cytoplasm. Also, there is interstitial lymphocytic infiltration and moderate fibrosis.
 In the later stages, lymphoid follicles develop. Virus particles and viral antigens can
be demonstrated in the degenerating epithelium by electron microscopy, and also by
immunofluorescence.

DIAGNOSIS

 Antibodies against the virus can be detected by indirect immunofluorescence, serum

neutralization tests, and ELISA. Of these serum neutralization is the most sensitive,
but is costly and laborious.
 For isolation and identification of the virus, samples of faeces and/or kidney should
be inoculated into cultures of chick kidney cells or into chick embryos.

DIFFERENTIAL DIAGNOSIS

 Certain nephrotoxic strains of infectious bronchitis virus cause interstitial nephritis.

 It is difficult to separate the two conditions on the basis of the microscopic lesions.
However, with infectious bronchitis there are some changes in the trachea, and
infections in kidneys are usually preceded by respiratory signs.

CHAPTER-7: INFECTIOUS STUNTING SYNDROME AND REO VIRUS

INFECTIONS

 15) Viral arthritis (Teno synovitis)

INTRODUCTION

 Reoviruses are ubiquitous in chickens and turkeys; some strains become viraemic
and localize in the large joints, resulting in arthritis, tendinitis, and synovitis.
 Most birds are thought to be susceptible to respiratory-intestinal strains of reo
viruses.
 Chickens and, to a lesser degree, turkeys are susceptible to viral arthritis, which is
seen worldwide.
 Reoviruses also have been associated with pericarditis and myocarditis,
hydropericardium, pasting, malabsorption, and femoral head necrosis, although
further study is needed to define their role.
 TRANSMISSION AND PATHOGENESIS

 The disease is egg-transmitted and is of short duration except when lateral

transmission in a flock is prolonged.
 Respiratory and digestive infections may occur but are of short duration; however,
the virus survives in tendon sheaths for extended periods.
 The virus is spread via aerosols, fomites, and mechanical means, and is resistant to
heat and chemical inactivation.
 Several antigenic subtypes of avian reoviruses have been identified; however, there
appears to be significant cross-protection among most of the isolates or subtypes.
 Pathogenicity of the isolates varies widely. Serious outbreaks of viral arthritis are
followed by a decreased incidence in later hatch groups of birds from the same
parent flock.
 This may be related to decreased egg transmission and development of parental
immunity.
 Day-old chicks are more susceptible than older birds when exposed by natural
means.
 The earlier in life the chick is infected, the longer the virus persists in the tissues.

CLINICAL FINDINGS

 The arthritic form (tenosynovitis) usually is seen in broilers 4-8 wk old as unilateral
or bilateral swellings of the tendons of the shank and above the hock; it can also be
found in much older chickens.
 The birds walk with a stilted gait. In severely affected flocks, rupture of the
gastrocnemius tendon is frequent, and many cull birds are seen around the feeders
and waterers.
 Mortality is 2-10% and morbidity 5-50%. Severely affected birds rarely recover; less
severely affected birds recover in 4-6 wk.
 The infection is inapparent in many birds. Feed efficiency and rate of gain are
decreased.

LESIONS

 An acute, fulminating infection is occasionally seen in young chicks and embryos

with cardiomegaly, hepatomegaly, and splenomegaly with necrotic foci.
 Edema of the tendons of the leg is marked, petechial hemorrhages develop in the
synovial membranes above the hock, and fusion and calcification of the tendon
bundles are common.
 Blood clots and hemorrhages are seen with rupture of the gastrocnemius tendon.
 Pitted erosions of the cartilage of the distal tibiotarsus are seen with flattening of the
condyles.
 Histologically, the synovial cells are hypertrophied, hyperplastic, and infiltrated by
lymphocytes and macrophages.
 The synovia contain heterophils and macrophages. Infiltration of heterophils or
lymphocytes, or both, between myocardial fibers is a constant finding.
  However, the infiltrating heterophils are difficult to distinguish from the clusters of
young, proliferating heterophils (ectopic myelopoiesis) that are present in the heart
muscle of all young, rapidly growing broiler chickens.

DIAGNOSIS

 A presumptive diagnosis can be based on unilateral or bilateral swelling of the tendons of the
shank and tendon bundle above the hock and on the inflammatory changes in the tendons and
synovia described above.
 Virus from affected tissues can be isolated in primary kidney, liver, or lung cells, or in the yolk
sac or chorioallantoic membrane of embryonating chicken eggs.
 The agar-gel-precipitin test is usually positive, and most birds are positive early in the
infection.
 Virus neutralization tests and challenge of immunized chickens are used to detect the specific
serotype.
 Culture procedures should be used to differentiate mycoplasmal and other bacterial infections.
Other causes of lameness should be considered.

TREATMENT AND CONTROL

 There is no treatment. Maternal antibody prevents early infection in chicks and

should reduce or prevent egg transmission.
 Because egg transmission is the principal means of spread, it is desirable to have the
breeder flock immune.
 Such a program should be directed to the serotypes present in the flock.
 Adult birds are less susceptible to clinical disease if exposed by natural routes

 16) Infectious stunting syndrome

INTRODUCTION

 Infectious stunting Syndrome (ISS) is a transmissible disease that is seen worldwide

and results in a variable percentage of runted and stunted birds.
 It is also sometimes known as, ‘pale bird syndrome’, malabsorption syndrome’, ‘
infectious runting’ and ‘runting and stunting syndrome’.
 The financial losses are caused by an increased number of culled birds, poor feed
conversion, reduced weight for age, and greater than expected variations in weight
at slaughter.
 The disease has now been reported from most broiler growing countries of the
world, including India.

CAUSE

 ISS is probably caused by a number of viruses, which include calciviruses,

enteroviruses,parvovirus, coronavirus, FEW virus, reovirus, or toga-like particles,
reo- viruses, and Rotavirus have been detected in affected flocks, but none of them
 has been shown to be capable of causing the disease on its own. This strongly
suggests that ISS has a multifactorial cause.
 ISS occurs at least three different forms( main problem in small intestines, pancreas
or proventriculus). Recent studies have revelaed picornavirus-like particles in the
cytoplasm of degenerating enterocytes and associated macrophages in acute
intestinal lesions.
 All breeds and strains of chickens are susceptible, but suppression of growth is most
noticeable in broilers because of their rapid growth rates.

PATHOGENESIS

 Following infection, the lesions are most pronounced in the mid-jejunum.

o Piconavirus –like particles are detected in the cytoplasm of enterocytes on the
villi. These viruses are associated with necrosis of enterocytes, and there is
marked infiltration of macrophages and lymphocytes into the vilus.
o The viruses are then spread through macrophages to the lamina propria
surrounding the crypts, and multiplication of the virus in crypt enterocytes lead
to necrosis and loss of crypts. At this stage there is significant villus atrophy. By
second week, the lost enterocytes are replaced through crypt cell proliferation,
but the villi are populated by biochemically immature enterocytes. This results in
impaired digestive capability, and leads to poor growth, the characteristic feature
of the disease.
o Retarded feathering is probably the result of reduced digestion and absorption of
sulphur-containing amino acids.

CLINICAL SIGNS

 The percentage of affected chickens in a flock with ISS can vary from a few percent
to more than 90%. At 4-8 days, the stunted chickens are characterised by the
retarded feathering on their heads and necks, and pendulous abdomens. At about
two weeks, affected chickens are often called as, “yellow heads” because of the
prominence of the retained down feathers on the head and neck.
 Broken and displaced primary wing feathers have given the disease names like”
helicopter feathering” or “ helicopter disease”. AT 2-4 weeks clinical signs include
lameness due to secondary osteodystrophy, poor weight gain, opisthotonous due to
secondary encephalomalacia and pale shanks.
 One of the important features if the disease is the presence of severely stunted
(runted) chickens, which remain small despite their huge appetites.

MACROSCOPIC LESSIONS

 Affected birds can be relatively small for their age and pale. The subcutaneous fat is
pale compared to normal, hence the name” pale bird syndrome”. They are not
anaemic. Intestines are distended and pale with poorly digested contents. This
phenomenon has been referred to as “malabsorption syndrome”. In chickens that
have not recently eaten,the intestine s contain clear watery or mucoid fluid and
hence it is described as”mucoid” or catarrhal enteritis. The thymus is reduced to a
 chain of small dark lobes, and the bursa of Fabricius is usually swollen. Depending
on the form of ISS, the pancreas can be hard, atrophic and very pale.
 In all forms of ISS, osteodystrophy is commonly seen in the affected birds of a few
weeks of age. Because of the osteodystrophy, the disarticulation of the hips during
the necropsy can easily result in a separation of femur head from the femur. This can
also happen during catching, transport and handling of the birds for slaughter.

MICROSCOPIC LESIONS

 Intestinal lesions include villus atrophy, and necrosis and degeneration of

enterocytes on the sides of villi and crypts, associated with significant infiltration of
lymphocytes and macrophages into the villus and lamina propria.
 Lesions are most pronounced in the mid-jejunum. Enterocytes and degenerate
macrophages reveal small cytoplasmic inclusions.

DIAGNOSIS

 The etiological agent has not been characterised, and serological tests are not
available. Therefore, diagnosis depends upon characteristic features of the disease,
namely severely stunted ( runted) but active chickens with retained down feathers
on the head and neck at 2-3 weeks of age; and poor growth in a variable percentage
of the remaining flock at 2-4 weeks.

CHAPTER-8: BACTERIAL DISEASES

 1) Colibacillosis
INTRODUCTION

 Escherichia coli is a normal inhabitant of the digestive tract of mammals and birds,
and most strains are non-pathogenic. Certain serotypes can cause disease in poultry.
 Colisepticaemia, egg peritonitis, yolk sac infection, and coligranuloma ( Hjarre’s
disease) are the well recgnised results of E.coli infection infection. These conditions
are collectively grouped under the heading “ Colibacillosis”.

a) Colisepticaemia
INTRODUCTION

Colibacillosis occurs as an acute fatal septicemia or subacute pericarditis and

airsacculitis.It is a common systemic disease of economic importance in poultry and
is seen worldwide.
 ETIOLOGY AND PATHOGENESIS

 Escherichia coli is a gram-negative, rod-shaped bacterium normally found in the

intestines of poultry and most other animals; although most are nonpathogenic, a
limited number produce extraintestinal infections.
 Pathogenic strains are commonly of the O1, O2, and O78 serotypes, but serotypes
O11, O15, O18, O51, O115, and O132 have also been reported for E coli isolates
associated with cellulitis and colibacillosis.
 There is considerable diversity of serogroups among clinical isolates, and only a
small percentage of these isolates belong to serotypes O1, O2, or O78.
 In fact, 18-29% of avian E coli isolates cannot be typed.
 Therefore, no single E coli serotype used as a bacterin can provide full protection
against all of the serotypes that cause E coli infections.
 Virulence factors include the ability to resist phagocytosis, utilization of highly
efficient iron acquisition systems, resistance to killing by serum, production of
colicins, and adherence to respiratory epithelium. Virulent E. coli are generally
nontoxigenic, poorly invasive, and do not possess common adhesins.
 Large numbers of E coli are maintained in the poultry house environment through
fecal contamination.
 Initial exposure to pathogenic E coli may occur in the hatchery from infected or
contaminated eggs, but systemic infection usually requires predisposing
environmental factors or infectious causes.
 Mycoplasmosis, infectious bronchitis, Newcastle disease, hemorrhagic enteritis, and
turkey bordetellosis precede colibacillosis.
 Poor air quality and other environmental stresses may also predispose to E coli
infections.
 Systemic infection occurs when large numbers of pathogenic E coli gain access to the
bloodstream from the respiratory tract or intestine.
 Bacteremia progresses to septicemia and death, or the infection extends to serosal
surfaces, pericardium, joints, and other organs.

CLINICAL FINDINGS AND LESIONS

Colisepticaemia

 Signs are nonspecific and vary with age, organs involved, and concurrent disease.
 Young birds dying of acute septicemia have few lesions except for enlarged,
hyperemic liver and spleen with increased fluid in body cavities.
 Birds that survive septicemia develop subacute fibrinopurulent airsacculitis,
pericarditis, perihepatitis, and lymphocytic depletion of the bursa and thymus.

 (Unusually pathogenic salmonellae produce similar lesions in chicks.) Although

airsacculitis is a classic lesion of colibacillosis, whether it results from primary
respiratory exposure or from extension of serositis is unclear.
 Sporadic lesions include pneumonia, arthritis, osteomyelitis, and salpingitis
 DIAGNOSIS

 Unlike pathogenic E coli associated with illnesses in other animal species, avian
isolates are generally nonhemolytic on sheep (5%) blood agar.
 Isolation of a pure culture of E coli from heart blood, liver, or typical visceral lesions
in a fresh carcass indicates primary or secondary colibacillosis.
 Consideration should be given to predisposing infections and environmental factors.
 Pathogenicity of isolates is established when parenteral inoculation of young chicks
or poults results in fatal septicemia or typical lesions within 3 days.
 Pathogenicity can also be detected by inoculation of the allantoic sac of 12-day-old
chick embryos.
 Resulting gross lesions include cranial and skin hemorrhages in addition to
encephalomalacia in embryos inoculated with virulent isolates.

TREATMENT AND CONTROL

 Treatment strategies include attempts to control predisposing infections or

environmental factors and early use of antibacterials indicated by susceptibility
tests.
 Most isolates are resistant to tetracyclines, streptomycin, and sulfa drugs, although
therapeutic success can sometimes be achieved with tetracycline.
 In fact, 90% of clinical isolates are resistant to tetracycline, with 60% of isolates
resistant to 5 or more antibiotics.
 Fluoroquinolone use is controversial because the use of these drugs in commercial
broilers is believed to select for resistant Campylobacter spp associated with human
foodborne infections.
 Commercial bacterins, administered to breeder hens or chicks, have provided some
protection against homologous E coli serotypes.

B) Yolk sac infection

INTRODUCTION

 Also known as “mushy chick disease” and “omphalitis’. This condition is one of the
common causes of mortality in chicks during the first week after hatching.E.coli can
be involved either as the primary and sole causative agent or as a secondary
opportunist.
 Yolk sac infection can be associated with a thickened navel , where the route of
infection is via the unhealed navel, orbacteria can multiply in the hatching egg
following faecal contamination of the shell.
 Yolk sac infection can cause 100% mortality in a batch of chicks in the first week of
life, but deaths are usually between 5% and 10%. Other bacteria, such as Bacillus
cereus, staphylococci, Pseudomonas aeruginosa,Proteus Spp. And clostridia, can
also cause yolk sac infection, either on their own, or, more commonly together with
E.coli.
  E.coli multiplies rapidly in the intestines of newly hatched chicks and infection
spreads rapidly from chick to chick in the hatchery and brooders.
 A hatching environment that is not sufficiently humid is often associated with a high
incidence of yolk sac infection.

CLINICAL SIGNS AND LESIONS

Yolk sac infection (Omphalitis, Mushy chick disease)

 Affected chicks appear depressed and have distended abdomen and a tendancy to
huddle.
 Sometimes the navel is visibly thickened, prominent and necrotic. Affected carcasses
may show a distinctive, purifying smell.
 Post-mortem examination reveals a septicaemic carcass with the subcutaneous and
yolk sac blood vessels engorged and dilated.
 The lungs are usually congested and the liver and kidneys dark and swollen.
 The striking finding is an inflamed unabsorbed yolk sac with the yolk abnormal in
colour and consistency.

Yolk sac infection (Mushy chick disease,

Omphalitis) Abdominal cavity revealing the inflammed
"unabsorbed" yolk sac with abnormal colour and consistency of
its content (arrows)
The striking finding is an inflamed unabsorbed yolk sac with the yolk abnormal in colour and consistency.

 The yolk may be yellow and insipissated or brownish green and watery, and is often
fetid.
 Peritonitis with haemorrhages in the serosal surfaces of the intestines is a regular
feature.
 A profuse pure growth of nonhaemolytic E.coli may be recovered from the
abdominal viscera and particularly the yolk sac on direct culture.
 EGG PERITONITIS

 The term, "egg peritonitis" covers a number of reproductive disorders of poultry.

These include peritonitis, salpingitis and impaction of the oviduct.
 Postmortem examination reveals egg debris, inspissated yolk. caseous material or
milky fliuid in the abdominal cavity (see the pictures below), along with
inflammation and distortion of the ovaries, and salpingitis.
Alternatively, the oviduct may be obstructed by a core of inspissated inflammatory
debris, which may sometimes result in rupture of oviduct wall.

 At times, rupture of the ovarina follicless are visible (see the pictures below).
 A whole or partly formed egg may be impacted in the oviduct (see the pictures
below).

Impaction of oviduct: Oviduct showing Impaction of oviduct: Incised oviduct

varying distension at different segments due (red arrow) showing varying amount of
to accumulation of yolk materials in a solid whitish yolk materials at different
natural case. segments in a natural case.

Egg bound: Oviduct showing retention of Egg bound: Oviduct showing a "leathery
fully formed egg inside. egg" retained in the lumen.
  A profuse pure growth of E.coli can be isolated from the oviduct and caseous
inspissated material.

Impaction of oviduct

 A large oval mass may be seen in the abdominal cavity.

 The mass, probably an impacted oviduct, was firm and adhered to peritoneum and
visceral organs.
 The abdominal mass contains several masses of yolk, each surrounded with
concentric rings (see the pictures below-A).
 Cut surfaces of the mass were laminated, and loosely attached to one another(see
the pictures below-B).
 Each layer was composed of fibrous connective tissue, heterophils, macrophages,
cellular debris, and fibrin clots.

A) Impaction of oviduct: On incision, B) Impaction of oviduct: Cut surface of the

distended oviduct (red arrow) revealing the mass revealing concentric appearance (arrows)
solid yolk mass (blue arrow) in the lumen. of the impacted yolk material.
COLIGRANULOMA

Coligranuloma (Hjarre’s Disease):

 The condition usually occurs as the cause of sporadic death in adult hens.
 The clinical signs are non-specific and affected birds are usually found dead or die
after depression and loss of condition.
 Post-mortem examination typically shows hard, yellow, nodular granulomas in the
mesentery and wall of the intestine ( see the picture), and particularly the caecum.
 o Some times the liver is similarly affected and is hard, blotchy, discoloured and
swollen.

 2) Infectious coryza
INTRODUCTION

 Infectious coryza is an acute, highly contagious disease of the upper respiratory tract
of chickens.
 A chronic respiratory disease can develop when complicated by other pathogens.
 The disease occurs worldwide and causes economic losses due to an increased
culling rate in meat chickens and significant reduction of egg production in laying
and breeding fowl.

CAUSE

 The disease is caused by Haemophilus paragallinarum.

 The disease is limited to chickens. Chickens of all ages are susceptible but older
birds tend to react more severely.

SPREAD

 The main source of infection is clinically affected and carrier birds. As only a few
viable organisms are necessary for the infection, it can be transmitted by drinking
water contaminated by nasal discharge as well as by airborne means over a short
distance.
 Lateral transmission occurs readily by direct contact.

PATHOGENESIS

 Adherence of the organism to the ciliated mucosa of the upper respiratory tract
seems to be the first step of the infection.
 The capsule and the haemagglutination antigen play an important role in the
colonization.
 Toxic substances released from the organism during the proliferation are associated
with production of lesions in the mucosa and appearance of the clinical signs.
 The capsule may act as a natural defence substance against the bactericidal power of
complement through the alternate pathway.
 As paragallinarum is a noninvasive bacterial agent with a strong tropism for ciliated
cells and migrates into the lower respiratory tract ( lungs, air sac) only after
synergistic interaction with other infectious agents and/or if encouraged by
immunosuppression.
 Factors that predispose to more severe and prolonged disease ( chronic respiratory
disease) include intercurrent infections with microorganisms such as infectious
bronchitis virus, laryngotracheitis virus, Mycoplasma gallisepticum, Escherichia
coli orPasteurella spp. and unfavourable environmental conditions.
 CLINICAL SIGNS

 The disease in flocks on floor management is characterised byrapid spread, high

morbidity and low mortality.
 The period of incubation is 1-3 days after contact infection and all susceptible birds
in the flock show signs within 7 – 10 days. If not complicated by other infections, the
course of the disease is not more than 10 days in the mild form and approximately
about 3 weeks in the more severe form.
 The first typical signs include sero-mucoid nasal and ocular discharge and facial
edema

Infectious coryza: Chicken showing watery discharge

from the eye and swollen sinuses(blue arrow)
resulting the closure of eyes and adhesion of dust
particles on the nasal discharge (green arrow).

 In severe cases, marked conjunctivitis with closed eyes, swollen wattles (wattle
disease) and difficulty in breathing can be seen.

 Feed and water consumption is usually decreased resulting in a drop in egg

production or an increase in the rate of culls.
 A reduction of egg production of more than 20% indicates multifactorial disease.
 If complicated with other infectious agents a more severe and prolonged disease
may develop with the clinical picture of a chronic respiratory disease.
 LESIONS

 In acute cases, lesions may be limited to the infraorbital sinuses.

 Affected chickens have catarrhal to fibrinopurulent inflammation of the nasal
passage and infraorbital sinus and conjunctivae.
 As the disease becomes chronic or other pathogens become involved, the sinus
exudate may become consolidated and turn yellowish

 The upper trachea may be involved but the lungs and airs sacs are only affected in
chronic complicated cases.
 Subcutaneous edema of the face and wattles is prominent.
 Microscopically, marked loss of cilia and microvilli, cell edema, degeneration and
desquamation of mucosal and glandular epithelium, infiltration of leukocytes and
deposition of mucopurulent substances can be seen and followed by infiltration of
mast cells into the lamina propria of the mucous membrane.

DIAGNOSIS

 The history of a rapidly spreading disease, its clinical signs and lesions may allow a
tentative diagnosis.
 The diagnosis has to be confirmed by cultural identification of the causal agent.
Swabs from an infraorbital sinus ( the nasal exudates is usually contaminated) of 2
or 3 diseased chickens should be cultured on blood agar plates cross-streaked with a
feeder organism such as Staphylococcus epidermidis.Swabs form the trachea and
airsacs may be taken, althoughH.paragallinarum is less frequently isolated from
thes areas.
 The organism should be identified by morphology, biochemistry and
immunofluorescence.
 A number of serological tests are used for the examination of sera for specific
antibodies against H.paragallinarum. These include agglutination,
haemagglutination inhibition, and fluorescent antibody test.

CHAPTER-9: CLOSTRIDIAL DISEASES AND SALMONELLOSIS

BOTULISM (LIMBERNECK)

 Botulism is caused by exotoxin of rapidly proliferating C lostridium botulinum.

 The disease affects poultry worldwide. There are 8 antigenically different toxigenic
groupin gs (A, B, C-alpha, C-beta, D, E, F and G).
 Almost all outbreaks in poultry are caused by type C-alpha. Occasionally,
however, types A, B, and E are involved. Botulism toxins are among the most potent
toxins known.
 Type C toxin is produced under anaerobic conditions. Type C-alpha cultures produce
three toxins: CI, C2, and small amounts of type D toxin.

 SPREAD

 C. botulinum type C is distributed worldwide. Type C organisms grow in the

gastrointestinal tract of normal birds. Type C spores are
 commonly found in and around poultry farms. Presence of organisms in the
gastrointestinal tract, and resistance of spores to inactivation, favour spread of this
organism. Outbreaks occur in chickens when the toxin is consumed, usually in
decaying poultry carcasses, or toxin-containing maggots or beetles.
 Maggots are eaten up greedily by chickens, which can lead to outbreaks.
 Toxin is produced by bacterial growth in rotting vegetation exposed during dry
summers.
 The toxin may sometimes be both produced in, and absorbed from, the caeca of
chickens, without any external source of toxin being available.
 Botulism is fairly rare in domestic poultry kept under good standards of
management and hygiene in which carcasses are regularly and frequently removed.

PATHOGENESIS

 Type C botulism can be caused by ingestion of preformed toxin. Because, the

organism is widely distributed in the gut, as indicated, dead birds provide conditions
for C . botulinum growth and toxin production.
 Birds scavanging (i.e., searching for decaying flesh as food) such carcasses can
readily obtain enough toxin to become affected.
 Botulism caused by A, B, and E rarely, and generally has been associated with
consumption of spoiled human food products fed to backyard chicken flocks.
 The pathogenesis of botulism was once thought exclusively to be ingestion of
preformed toxin. There is growing evidence that C. botulinum type C produces toxin
in the gut to cause disease.
 The term “toxico-infection” has been used to describe this form of the disease in
broiler chickens. Experimental evidence suggests caecum as the site of toxin
production.

SIGNS

 Clinical signs appear within a few hours of ingestion of the toxin. In chickens,
flaccid paralysis (i.e., lacking firmness of muscles) of legs, wings, neck and eyelids
are main features of the disease.
 Initially, affected birds are found sitting and reluctant to move. If forced to walk,
they appear lame. Wings droop when paralysed.
 Affected birds have ruffled feathers. Limberneck, the original and common name for
botulism, precisely describes paralysis of the neck. Because of eyelid paralysis, birds
appear comatose (in coma, unconscious), and may look dead.
 Death results from cardiac and respiratory failure.
 LESIONS

 There are no gross or microscopic lesions. Sometimes, maggots or feathers may be

found in the crop.

DIAGNOSIS

 The presumptive diagnosis of botulism is based on clinical signs and lack of gross or
microscopic lesions.
 Definitive diagnosis requires detection of in serum, crop, or gastrointestinal
washings from sick birds.
 The presence of toxin is confirmed by the injection of serum, or extracts of crop, or
intestinal contents, into mice.
 Since toxin can be produced in decaying body tissues, material for examination
should be from living birds, or fresh Carcasses.

Necrotic enteritis
INTRODUCTION

 Necrotic enteritis (NE) is found worldwide, and is a disease of increasing importance

owing to ever increasing restrictions on the preventive use of in-feed antimicrobials.
 Clinical disease may have devastating effects on production. Milder forms, including
subclinical disease, are most common, and may exert a significantly negative impact
on production.
 The most common form of C.perfringens –associated liver disease is
cholangiohepatitis. C.perfringens has also been implicated in wet litter problems
and impaired production performance but without the detection of specific lesions.
 The disease is most common in broiler chickens and meat turkeys. Broilers aged 2-5
weeks are most frequently affected. It is also fund regularly found in layers, mostly
in pullets and young birds kept on litter.

CAUSE

 The disease is caused by Clostridium perfringens type A or C in the large intestine

and caeca, and subsequent migration to small intestine where it produces toxins.
 Alpha toxin produced by C.perfringens types A and C, and beta toxin produced by
type C, are believed responsible for intestinal and mucosal necrosis, the
characteristic lesion of the disease.
 Both have been detected in faeces of chickens with NE. Predisposing factors include
outbreaks of coccidiosis, especially mild or subclinical, changes in diet, and
inadequate cleaning of houses, utensils and equipment.
 SPREAD

 Clostridium perfringens can be found i n faeces, soil, dust, contaminated feed and
litter, or intestinal contents.
 Contaminated feed or litter are the main source of infection.
 Fish meal is considered a particularly likely source of Clostridium
perfringens contamination.

CLINICAL SIGNS

 Clinical signs are variable and non-specific. Acute NE is characterised by increased

mortality but few visibly sick birds, indicating that affected birds die rapidly.
 The signs include depression, decreased feed intake, and reluctance to move, ruffled
feathers and diarrhoea.
 The mildest form of NE induces no visible illness of the birds but is associated with
temporarily reduced weight gain, impaired feed conversion ratio and increased
condemnation rates at slaughter due to liver lesions.

NECROTIC ENTERITIS: LESIONS

 The characteristic gross lesion of necrotic enteritis is a pseudo membrane attached

to the intestinal mucosa, primarily the small intestine.
 The mucosa of the caecal pouches are not changed but the caecal tonsils and
adjoining narrow segments of the caeca may occasionally be affected.
 The pseudo membrane which varies in entent, may be partly or entirely detached
from the viable mucosa, leaving behind a depression or a more extended smooth
surface.
 The membrane may be white, yellow, green, brown or red. A yellow or green
discolourations is the most commonly found.
 The affected gut segment may be dilated and soft with fluid contents, or the wall
appear turgid and rigid with dry and sparse luminal contents.
 A detached pseudo membrane is occasionally found in the gut lumen. The contents
of the caecal pouches are often dark and dry.
 Birds dying with NE often show a dark liver with dilated gall bladder, pale kidneys
with prominent lobular outlines, and dark and dry pectoral musculature indicating
dehydration.
 The body condition depends on the course of disease. Birds dying with acute NE are
in good bodily condition.
 Three main types of liver lesion may be found. The most common and most
characteristic is cholangiohepatitis.
 Livers with the second type of lesion show light, randomly localized nodules ( focal
necroses and granulomas) of the liver parenchyma, and the third and most rare
type is massive liver necrosis causing a smaller or larger part of a liver lobe to be
homogenously discoloured.
 PATHOGENESIS

 The pathogenesis of NE is incompletely understood. The presence of the organisms

in the intestine alone is not sufficient to induce necrotic enteritis.
 The following two requirements have been proposed for induction of necrotic
enteritis.
o The presence of some factor causing damage to the intestinal mucosa, and
o The presence of higher than normal numbers of intestinal C.
perfringens organisms.
 If these two requirements are fulfilled, lesions may develop, often starting at the tips
of the villi.
 Bacterial cells adhere to damaged epithelium and denuded lamina propria where
they prolifetae and induce coagulative necrosis.
 Attraction and lysis of heterophils granulocytes as well as further tissue necrosis and
bacterial proliferation proceed rapidly.
 The alpha-toxin, a necrotizing toxin produced by all the toxin types, has been
assumed to be an important virulence factor involved in the process. This toxin
destroys cell membranes by recognition and hydrolysis of membrane phospholipids.
Toxins may also enter the blood stream, causing systemic effects and death.

MICROSCOPIC LESIONS

 The characteristic feature is an aggregation of large, Gram-positive, rod-shaped

bacteria surrounded by necrotic tissue delineated from viable tissue by a zone of
granulocytic infiltration containing pyknotic cell nuclei.
 The lesions are usually located within the lamina propria of the gut mucosa.
 The least extensive lesions are limited to focal necroses comprising some epithelial
and stromal cells on the villus tips.
 The deepest lesions may even affect the muscular wall of the gut.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis

 The gross and microscopic lesions of the disease are adequate.

 In doubtful cases, bacteriology, histopathology and examination for coccidian will be
helpful.

Differential Diagnosis

 The similar lesions producing disease like coccidiosis and ulcerative enteritis should
be considered.

 GANGRENOUS DERMATITIS (MALIGNANT DEDEMA)

 Gangrenous dermatitis occurs worldwide in chickens and turkeys.

 The syndrome is precipitated by various detrimental microbial, nutritional and
environmental factors.
 The disease is characterized by a sudden onset, sharp increase in mortality, and
gangrenous necrosis of the skin over the wings, thighs, breast, and head.
 It occurs sporadically in chickens 4-16 wk old, affects broiler and layer replacement
stocks, and occasionally causes outbreaks in turkeys.

CAUSE

 Gangrenous skin necrosis may be associated with various aerobic and anaerobic
bacteria; however, Clostridium septicum ,Clostridium perfringens type A,
and Staphylococcus aureus , either singly or in combination are most often
involved. Combined infections are often more severe.
 Young chicks immunosuppressed by infectious bursal disease or chick anemia virus
are predisposed. The disease may occur secondary to avian adenovirus or
reticuloendothelial virus infections as well.
 Skin lesions due to trauma, wet litter, picking, or treading wounds may provide
entry sites for causative bacteria.
 Systemic effects arise from invading bacteria and their elaborated exotoxins.

CLINICAL SIGNS

 The first sign is usually a sudden dramatic increase in mortality in the affected flock.
 Overall mortality is 10-60%. Affected chickens are extremely depressed, lethargic,
and prostrate, and die within 8-24 hr.
 Red to black patches of moist, gangrenous skin are seen over the breast, abdomen,
wing tips, or thighs.
 Feather loss or sloughing of the epidermis is common. When clostridial infection
occurs, palpation of the affected areas often reveals crepitation due to gas bubbles in
the subcutis and musculature.

LESIONS

 At necropsy, there is an accumulation of gaseous, serosanguineous fluid in the

subcutis, and the musculature has a pale cooked appearance.
 The liver and spleen are enlarged and may contain infarcts or pale focal areas of
necrosis.
 The kidneys are usually swollen, and the lungs may be congested and edematous or
necrotic.
 Atrophy of the bursa of Fabricius may be found in birds that were exposed to
infectious bursal disease virus in the first few weeks after hatching.
  Histopathologic demonstration of gangrenous necrosis with numerous coccoid
bacteria or large, gram-positive rods with or without spores in affected tissues is
sufficient to confirm a clinical diagnosis.

DIAGNOSIS

 Isolation of the etiologic agent ( C. septicum , C. perfringens, or S aureus ), together

with the history and clinical findings.

DIFFERENTIAL DIAGNOSIS

 Differentiate gangrenous dermatitis from exudative diathesis and other diseases

involving the skin.
 Some times, squamous cell carcinoma of the skin of chickens may induce gross
lesions similar to those of gangrenous dermatitis and histopathology may be
necessary to differentiate.

 Ulcerative enteritis
INTRODUCTION

 Ulcerative enteritis (UE) is an bacterial infection of young chickens and turkeys

characterised by sudden onset and rapidly increasing mortality.
 The disease was first seen in enzootic proportions in quail, and was therefore
called”quail disease”.
 It has since been established that many avian species other than quail are
susceptible. Therefore, the earliest name has been replaced by ”ulcerative enteritis“.

CLINICAL SIGNS

 In acute disease there may be increased mortality without any obvious signs.
 In other case signs may include depression, huddling, with ruffled feathers, anorexia
and watery droppings. Mortality in chickens vary from 2% to as high as 12%.

LESIONS

Gross lesions

 Birds dying with acute disease show good condition and may have feed in the crop.
More protracted disease may lead to emaciation.
 The most important lesions are found in the intestine, liver and spleen.
 First, there are small, circular to lenticular mucosal ulcers affecting the small
intestine, caeca and upper large intestine.
  The ulcers may penetrate as deep as the serosa, which may become perforated and
result in peritonitis. The ulcers may coalesce to form large areas with a
pseudomembrane.
 Small ulcers have a haemorrhagic border, which may be seen on the serosal and
mucosal surfaces.
 A haemorrhagic border is less frequently found in larger lesions. Lesions with raised
edges may also be found.
 In the liver, usually there are yellowish to grey necrotic lesions of varying size. The
spleen is enlarged and haemorrhagic.
 Quail with acute disease may show haemorrhagic enteritis of the duodenum, with
small red spots visible on the serosal surface.

Microscopical lesions

 Intestinal ulcers consist of small haemorrhagic and necrotic areas, often with clumps
of Gram-positive bacteria.
 The ulcers involve villi and excreted into the the submucosa.
 The ulcers sometimes reach as deep as the muscular coat and serosa.
 Affected tissue is surrounded by granulocytes and mononuclear inflammatory cells.
 Liver lesions consist of multifocal foci of coagulative necrosis that are often poorly
demarcated and with minimal inflammatory reaction.
 Gram-positive bacteria are occasionally found within the necrotic foci.

DIAGNOSIS

 The gross lesions are often sufficient to make presumptive diagnosis.

 A definitive diagnosis requires detection of the bacterium in specimens from
affected birds. The liver is the most suitable organ for isolating C.colinum.
 Slide smears of liver and spleen tissues may be Gram-stained fo detection of Gram-
positive bacilli and subterminal and free spores.
 The organism can be demonstrated from a direct fluorescent antibody test in
cryostat sections of liver and intestine.

DIFFERENTIAL DIAGNOSIS

 Differential diagnosis should be made for necrotic enteritis, coccidiosis and

histomoniasis because of the similarity of the lesions in intestine.

 Salmonellosis

INTRODCUTION

Salmonella infection in poultry

 Salmonella pullorum - Pullorum disease

 Salmonella gallinarum - Fowl typhoid
  Salmonella typhimurium - Paratyphoid infections (Salmonellosis) - Relatively
common and public health significance because of the consumption of contaminated
poultry products.
 Salmonella arizonae - Arizonosis
 S.pullorum and S.gallinarum are highly host-adapted to chickens and turkeys.
 S.arizonae is most important in turkeys, with chickens occasionally affected.

PULLORUM
INTRODCUTION

Salmonella infection in poultry

 Salmonella pullorum - Pullorum disease

 Salmonella gallinarum - Fowl typhoid
 Salmonella typhimurium - Paratyphoid infections (Salmonellosis) - Relatively
common and public health significance because of the consumption of contaminated
poultry products.
 Salmonella arizonae - Arizonosis
 S.pullorum and S.gallinarum are highly host-adapted to chickens and turkeys.
 S.arizonae is most important in turkeys, with chickens occasionally affected.

CLINICAL SIGNS

 Disease occurs mainly in chicks under 3 weeks of age.

 First indication is excessive numbers of dead-in-shell chicks & death soon after
hatching
 Chicks - Depression with a tendency to huddle, respiratory distress, lack of appetite
and white viscous (thick and sticky) droppings - that adhere to the feathers around
the vent (pasty vent) Mortality varies considerably, and 100% in severe cases.
 Growers - Sub acute form: Lameness and swollen hock joint Poor growth rate.
 In older birds: pale & shrunken comb, Listless (depressed, dull).
 Layers - Reduced egg production ( the only sign).

PATHOLOGY

Chicks

 If death soon after hatching,

o Peritonitis with an inflamed, unabsorbed yolk sac
o Lungs: congested
o Liver: Dark, swollen, haemorrhages on the surfaces
 If die in the acute phase,
o No specific lesions, or those of septicaemia
 If death after showing signs for 1 or 2 days
o Typhilitis: enlarged and distended with casts of hard, dry necrotic material.
 o Discrete small, white, necrotic foci in the liver, lungs, myocardium, and
gizzard wall.
 In general, the lesions in chicks are neither characteristic nor consistent.

Growers

 Arthritis - Hock joint - Enlarged due to the presence of excess orange coloured
gelatinous material around the joints.

Adults

 Abnormal ovary: Irregular ova cystic misshapen discoloured pedunculated with

prominent thickened stalks.
 Inactive ovary with the small, pale, and undeveloped (in some cases)
 Peritonitis, arthritis and pericarditis.

DIAGNOSIS

 Tentative diagnosis - History, signs and lesions

 Clinical signs and lesions are not consistent. So, not dependable.
 Confirmatory diagnosis - Isolation of the causative agents by cultural examination.
 Detection of antibodies
o Rapid slide agglutination test on whole blood using stained antigen.
o Tube agglutination test on serum
 ELISA - Can be employed for screening large number of samples.

TREATMENT AND CONTROL

 Treatment of infected flocks to alleviate the perpetuation of the carrier state is

not recommended.
 Control is based on routine serologic testing of breeding stock to assure freedom
from infection.

Paratyphoid
ETIOLOGY

 Motile Salmonella serotypes, other than those in the S.arizonae sub genus are
often referred to as, “Paratyphoid (PT) salmonellae”.
 These organisms can infect a wide variety of hosts , including humans.
 In some cases they result in asymptomatic intestinal carriers and in some cases
they produce clinical diseases .
 The most commonly isolated serotypes from chickens (i.e. PT salmonellae)
are: S.typhimurium , S. entritidis, S. hadar, S. montevideo, S.kentucky
and , S. heidelberg.
 SPREAD

 Paratyphoid salmonellae can be introduced into poultry from the following

sources,
o Contaminated feed - Animal proteins containing feed : Fish meal, meat and
bone meal and poultry offal and feather meal.
o Vegetable proteins - They become contaminated with organisms either
before or after processing.
o Biological vectors - They can disseminate and amplify the organisms in
poultry flock.
o Insects - Cockroaches and meal worms (larvae of various beetles)
o Rats and mice - Important vectors of S.enteritidis in laying flocks.

CLINICAL SIGNS

 Disease is uncommon
 Young chicks, poults or ducklings are commonly affected
 Rarely in birds over 4 weeks of age
 Mortality is usually less than 20% but exceptional case it reaches 100%.
 Clinical signs are not specific, but similar irrespective of the serotypes
 Ruffled feathers and drooping wings , depression, closure of eyes and reluctance
to move
 Diarrhoea with pasting of feathers around the (pasty) vent is common
 Visual impairment due to corneal opacity or caseous plaques in the eye ball

MACROSCOPIC LESIONS

 Lesions vary from the complete absence to a septicaemic carcass- with the
congestion of lung, liver, spleen and swollen kidney
 Chicks - Unabsorbed yolk sac is a common feature.
 Birds survive the acute septicaemic phase.
o Discrete (separate) necrotic lesions in the lungs, liver and heart
o Peritonitis
o Haemorrhagic enteritis
 The most characteristic lesion is typhilitis (inflammation of caeca) with the caeca
distended by hard white necrotic cores.

DIAGNOSIS

 Isolation and identification for confirmation by of the causative agents.

 Chicks - Materials can be collected from liver, gall bladder, or yolk sac.
 Older birds - Often from the intestine; the caeca being the most likely site.
 Serological tests - Detection of antibodies,
o The value of serological tests depends on the salmonella serovar, to certain
extent.
  Whole blood test (WBT) using stained antigen
 Serum agglutination (SAT) tests.
 ELISA : can be done for screening large number of samples
 S.enteritidis possess the same group D somatic antigen as S.pullorum

PUBLIC HEALTH SIGNIFICANCE

 Salmonellae remain among the leading sources of food-borne illness throughout

much of the world
 The paratyphoid infection in birds (salmonellosis) acquire great importance
because of the human illness caused from the consumption of contaminated
poultry products.

TREATMENT AND CONTROL

Treatment

 Salmonella enteritidis (a paratyphoid Salmonella serotype) is a major food safety

concern, primarily for the egg-laying industry.
 Possible sources in commercial layers include transmission from breeders,
contaminated environments, infected rodents, and contaminated feed.
 Transmission to progeny from breeders is mainly through eggshell
contamination, although, unlike other paratyphoid Salmonella , transovarial
transmission may also occur.

Control

 Strict sanitation in the hatchery, fumigation of hatching eggs, pelleting of feed to

destroy salmonellae, cleaning and disinfection of poultry houses, rodent control,
and use of competitive exclusion products.
 Several antibacterial agents help prevent mortality but cannot eliminate flock
infection.
 Maintenance of poultry in confinement and exclusion of all pets, wild birds, and
rodents help prevent introduction of infection.

PATHOGENESIS

 Three categories of toxins play roles in pathogenicity

o Endotoxins
o Enterotoxins
o Cytotoxins
Endotoxins

 Associated with the lipid A portion of Salmonella cell wall lipopolysaccharide

(LPS)
 Endotoxin of S.enteritidis causes hepatic and splenic lesions
 LPS also contribute the resistance of cell wall to attack and digestion by host
phagocytes
 Hence, the loss of the ability to synthesize complete LPS is associated with
o a loss of virulence of S.enteritidis and
o an impaired ability of S.typhimurium to colonize the caeca and invade to
the spleen

Proteinaceous toxin

Paratyphoid general pathogenesis

 The overall virulence of salmonella depends mainly on the initial degree of

mucosal invasiveness

CHAPTER-10: FOWL CHOLERA, SPIROCHAETOSIS AND TUBERCULOSIS

1) FOWL CHOLERA

INTRODUCTION

 It is a contagious disease affecting domestic and wild birds.

 Causative agent - Pasteurella multocida.
 The disease is worldwide in distribution.
 All species of birds are susceptible, although turkeys are more so than fowl.
 Ducks and geese are also highly susceptible.
 Adult birds or those in growing stage are more frequently affected than younger
stock.
 Immune status of the bird may be associated with protection against the strain of
organisms to which the birds have previously been exposed.

SOURCE OF INFECTION

 Source of infections include,

o Carrier birds ( survivors of natural outbreak)
o ailing birds and their excretions
o carcasses of birds which have died of the infection
 Rats are reservoirs for Pasteurella multocida
 However, the organisms are not usually found in normal poultry or wild birds
 Airborne spread of infection does occur between pens, but spread through water
and feed troughs is more important
 No vertical transmission through eggs
 Route of entries - oral, nasal, and conjunctival routes, and through wounds.

PATHOGENESIS

 Virulence of the organisms in relation to fowl cholera is complex

 Virulence varies with the strain, host species, and variations within the species or
host and some chemical substance associated with the capsule, rather than with
its physical presence

CLINICAL SIGNS

 The disease occurs in several forms,

o peracute
o Acute
o Chronic and localized disease.
 Peracute: No warning signs but more mortality with good bodily condition.
 Acute: Marked depression, anorexia, mucous discharge from the orifices, foetid
(foul smelling) diarrhoea)
 Chronic
o Seen in the birds which survive the acute form. caused by the low virulent
organisms
o Depression, conjunctivitis, dyspnoea, and in few cases lameness, torticollis
and swelling of the wattle

PATHOLOGY

 Peracute
o Marked congestion of the carcass
 Acute disease
o Multiple petechiae through out the viscera
o Multiple pin-point necrotic foci in the liver
 Sub acute
o Edema of lungs (especially in turkeys)
o Pneumonia
o Perihepatitis
 Chronic
o Caseous arthritis of hock and foot joint swelling,
o Induration of one or both wattles (in chicken) Caseous exudate in the
middle ear ( torticollis)
 DIAGNOSIS

 Presumptive diagnosis can be made from clinical signs, lesions or isolation of the
organisms.
 Confirmative diagnosis can also be made on the above three.
 Demonstration of the organisms confirms the disease
o In peracute disease : Impression smears the liver or smears of heart will
reveal bipolar organisms in methylene blue stain.
o In pneumonic form : Smears from lungs will reveal the organisms.
 Isolation and identification of the organisms
o Depends on cultural and biochemical procedures
o Laboratory animal inoculation

TREATMENT

 Sulfonamides and antibiotics are commonly used; early treatment and adequate
dosages are important.
 Sulfaquinoxaline sodium in feed or water usually controls mortality, as do
sulfamethazine and sulfadimethoxine.
 Sulfas should be used with caution in breeders because of potential toxicity.
 High levels of tetracycline antibiotics in the feed (0.04%), drinking water, or
administered parenterally may be useful.
 Penicillin is often effective for sulfa-resistant infections.

PREVENTION

 Good management practices are essential to prevention

 Rodents, which are often carriers of P multocida, must be excluded from poultry
houses
 Adjuvant bacterins are widely used and generally effective; autogenous bacterins
are recommended when polyvalent bacterins are found to be ineffective.
 Attenuated vaccines are available for administration in drinking water to turkeys
and by wing-web inoculation to chickens.
 These live vaccines can effectively induce immunity against different serotypes of
P. multocida.
 They are recommended for use in healthy flocks only.

Spirochaetosis
INTRODUCTION

 It is acute, septicaemic disease characterized by marked illness, variable

morbidity, and high mortality
 It is caused by Borrelina anserina
 The disease is transmitted by the soft tick , Argus persicus . Hence its occurrence
is limited in its distribution to areas where the tick is common
 Spirochaetosis is endemic in certain parts of India and causes significant
economic losses
 The spirochaete can infect a wide variety of birds but the disease mainly occurs in
young fowl.

SPREAD OF INFECTION

 Soft ticks of the genus Argas are the main reservoirs of the organisms.
 The organisms must depend on the ticks for its continued existence.
 Not all the species of Argas act as biological vector of spirochaete.
 Argus persicus is the important vector.
 B.anserina is capable of surviving in either the bird or environment for long
periods.

PATHOGENESIS

 Ticks become infective 6-7 days after biting a host and remain infective up to 488
days. Birds gets organism from salivary gland through bite of the infected ticks
 Outbreaks are common during warm, humid seasons
 Recovered birds are not carriers
 CLINICAL SIGNS

 Birds are visibly sick with cyanosis or pallor, especially of comb and wattle
 Dullness, anorectic, ruffled feathers, huddled-up appear
 Greenish diarrhoea (containing excess bile and urates, probably resulting from
anorexia and increased water consumption)
 Characteristic feature: An abrupt elevation in body temperature due to the
presence of spirochaetes in the circulation
 Rapid loss of body weight
 Later, Paresis (partial paralysis) or paralysis, anaemia and coma
 Body temperature is subnormal just prior to death
 Recovered birds: Emaciated and may have paralysis of one orboth wings or legs

LESIONS

Macroscopic lesions

 Most characteristic: Marked enlargement and mottling of the spleen.

Splenomegaly may not be visible when the birds are infected with low virulent
strains or in early stage
 Liver: Enlargement with small haemorrhages and pale foci
 Kidney: Swollen and pale with urates visible in ureters
 Intestine: Contents are usually green and mucoid and there is variable degree of
haemorrhage, especially at the proventriculus and gizzard junction
 Pericardium: Mild pericarditis (some times) by sparing other serous memb.

Microscopic lesions

Spleen

 Inflammatory reaction is characterised by increased macrophage response ,

mono-nuclear- phagocyte system(MPS) hyperplasia , erythrophagocytosis, and
haemosiderin deposits
 Massive areas of haemorrhage (in some birds)

Liver

 Congestion, increased periportal infiltration of mixed lymphocytes ,

haemocytoblasts, and phagocytic cells with vacuolated cytoplasm
 Erythrophagocytosis and haemosiderin in Kupffer cells
 Extramedullary haemopoiesis may be present

Organisms in tissue

 Silver stains reveal spirochaetes in intercellular spaces and bile canaliculi

  Organisms within hepatocytes are usually fragmented or coiled, forming small
rings

Kidneys and intestine

 Lympho-plasmocytic infiltration (Infiltration of L & P)

Brain

 Mild to moderate meningo-encephalitis

DIAGNOSIS

 Presumptive diagnosis : Based on clinical signs and characteristic lesions

 Confirmative diagnosis
o Demonstration of the casual organisms : B. anserina
 Stained blood: Giemsa stain ( but Aniline and Romanowsky stain)
 Tissue sections: Silver impregnation technique
 Wet mounts: Dark-field microscopy is the diagnostic method
o Demonstration of antigen: In liver and spleen
 By serological tests and immunofluorescencea
o Demonstration of antibodies
 Serological examinations: Serum plate agglutination test
 Slide agglutination and immobilisation tests
 Agar gel precipitation test and IFT.

 Tuberculosis
INTRODUCTION

Mycobacterium avium - Avian tuberclosis

 Avian tuberculosis occurs throughout the world in many avian and some
mammalian species and in domestic poultry it is generally seen in mature stock
kept in conditions of poor management.
 It usually runs a protracted course, causing reduction in condition, reduced egg
production and eventually death.
 Although loss in a flock is intermittent it is invariably in adult fowls and this,
together with the culling of unthrifty birds and the depression in egg production,
can cause serious economic loss.
 The infection is of importance also because the disease occurs in wild birds, pigs,
rabbits and mink.
 EPIDEMIOLOGY

Cause

 Mycobacterium avium is the name given to a complex group of mycobacterial

organisms that, according to current taxonomy, consists of four subtypes,
o M. avium subsp. avium consists of three serotypes (1, 2 and 3) and several
genotypes: this subtype is fully virulent for birds and small terrestrial
mammals
o M avium subsp. hominissuis consists of serotypes 4-6, 8-fl and 21, and
several genotypes, and is found mainly in the external environment, dust,
water, soil and invertebrates but some are virulent for birds
o M avium subsp. paratuberculosis consists of a number of genotypes and
affects ruminants and other animals
o M. avium subsp. silvaticum is isolated rarely and can be virulent for birds.
 These mycobacteria are acid- and alcohol-fast whcn stained by the Ziehl -
Neelsen method and the organisms often appear beaded. Of this large number of
serotypes it is types I, 2 and 3 that are most virulent and are mainly responsible
for the disease in poultry. Even among these serotypes there is considerable
variation in virulence.
 M. avium, compared with other mycobacteria, is relatively resistant to
antimicrobials and relatively resistant to a number of disinfectants but is
sensitive to ionic detergents.
 Outside the body it can survive for many years but the unprotected organism is
killed by direct sunlight and within the carcass the organism survives for no more
than a few weeks.
 It does not show tropism for any particular tissue but gross lesions of the liver,
spleen, intestine and bone marrow are most commonly seen.

HOSTS

 It is probable that all species of bird can be infected but susceptibility among
domestic species seems to be in the following order: chickens, ducks, geese and,
least susceptible, turkeys, in which it is relatively uncommon.
 Ike disease is observed most commonly in older poultry because of the greater
opportunity for infection with age and the generally long incubation period.
However, occasionally, heavy losses may occur in pullets on multiage sites where
the infection is endemic and the standards of hygiene poor.
 Came birds, particularly pheasants, are also susceptible. Some birds kept in
zoological gardens seem to be prone to tuberculosis, perhaps because of the
difficulty in adequately cleaning and disinfecting pens.
 Cage birds may also succumb to avian tuberculosis but tuberculosis in parrots
and canaries may also be caused by M. bovis or M. tuberculosis.
 Surveys show that many species of wild bird become naturally infected and in
some instances a predisposing factor is their close association with infection in
domestic stock.
 Among mammals Al. avium can cause progressive disease in swine, rabbits and
mink and can cause sensitivity in cattle to the skin tuberculin rest.

SPREAD

 In the transmission of infection the most important source of the organism is the
infected host, including domestic poultry, game birds and per or wild birds. Next
in importance, because of the prolonged survival of Al avium outside the body of
the host, are items contaminated with the droppings and excrement of such
birds. These commonly include litter, contaminated pens and pasture, equipment
and implements that come into contact with infected hosts, and the hands, feet
and clothing of attendants.
 ‘Swill’ containing offal or trimmings from ruberculous fowl or pigs can also be a
source of infection.
 Eggs would seem to be only of minor importance in the spread of avian
tuberculosis.
 Tubercular lesions have occasionally been noted in the reproductive tract (ovary
and oviduct of the female and testes of the male) and tubercie bacilli have been
reported, rarely, in the eggs laid by tuberculous hens. However, there is no
evidence to suggest that chicks hatched from such eggs are likely to be infected or
that disease is likely to be introduced into a flock by this means.

INFUENCING FACTORS

 The infections are worldwide but disease varies between and within countries. In
domestic poultry lack of hygiene in management and the age of the birds
influence the appearance of the disease since the organism is highly resistant in
the environment and within the host is generally associated with a long
incubation period.

SIGNS

 Signs may be prolonged over a period of weeks or months before death. There is
generally progressive but slow loss of condition and accompanying loss of energy
and increasing lethargy.
 Although the appetite usually remains good, there is eventually gross emaciation
with marked atrophy of the sternal muscles, with the ‘keel’ becoming prominent
or even ‘knife-edged’.
 The face and comb become pale and sometimes jaundiced and the comb is
shrunken and often there is persistent diarrhoea with soiling of the tail feathers.
 Occasionally a bird will show a hopping, jerky type of locomotion, which is
usually unilateral and is thought to be associated with tubercular lesions of the
bone marrow of the leg bones or joints. Some may adopt a sitting position.
 Occasionally, birds may die suddenly in good bodily condition and yet show
advanced lesions of tuberculosis.
 In such eases rupture of the affected liver or spleen with consequent internal
haemorrhage is often the precipitating cause of death.

LESIONS

 Gross lesions, in the chicken, are most commonly seen in the intestines, liver,
spleen and bone marrow but may be found in any organ or tissue.
 Irrespective of the organ involved, the lesions are typical tubercular granulomata.
They are irregular, grey-white nodules, varying in size from pinpoint to large
masses of coalescing tubercular material.
 ‘When cut through, the nodules are firm and caseous and the centres may be a
pale yellow colour, particularly those from the bone marrow. Those in the liver
and intestine may show bile staining. llae liver and spleen are often grossly
enlarged and occasionally rupture, resulting in blood in the body cavity and
sudden death.
 The smaller tubercles in these organs can be readily enucleated from the
surrounding tissue, particularly when they protrude from the surface. Such
protrusion of tubercles from the surface of the spleen gives rhe organ an
irregular, ‘knobbly’ appearance.
 The wall of the intestine is invariably studded with similar lesions, varying in size
from a millimetre to several centimetres in diameter. They usually involve the
whole thickness of the intestinal wall and eventually ulcerate into the lumen of
the intestine, with consequent discharge of bacilli and probably constituting the
major source of infection within the droppings.
 The bone marrow of the long bones of the legs frequently contains tubercular
nodules, which can best be seen macroscopically if the bones are split
longitudinally, particularly in the region of the femoro-ribiotarsal and
tibiotarsal—tarsometatarsal joints. They are pale yellow in colour and vary in size
and number. This is one of the distinctive features of tuberculosis in the chicken.
 The lungs are less frequently affected in the domestic chicken but more
commonly in waterfowl. Tubercle bacilli have been isolated from some eases of
arthritis affecting the phalangeal joints (‘bumble foot’) in the fowl.

DIAGNOSIS

 The clinical signs and gross lesions are strongly indicative of avian tuberculosis
and the demonstration of acid/alcohol-fast tubercle bacilli in lesions or sections
is supportive of this. There is seldom any difficulty in demonstrating the
organisms, which are often present in very large numbers, particularly in young
lesions and those from the bone marrow.
 Cultural examination, or even chick inoculation of suspect material, may be
necessary when organisms are few or for isolation and identification of the causal
agent. The agent can also be identified by DNA techniques.
 Immunological tests are also of value in the recognition of infected birds during
life. They include the tuberculin test, an agglutination test and ELISA.
 The tuberculin test in the fowl consists of injection of 0.05-0.1 mL of avian
tuberculin into one wattle using a needle about 1 cm long and of 25 gauge.
 The other wattle remains uninjected as the control. When testing a flock it is
usual to inject the tuberculin into the wattle on the same side for each bird.
 The needle is introduced at the lower edge of the wattle and is directed upwards
into the centre.
 The test is read 48 h after the injection of tuberculin, although some positive
reactions may be observed sooner than this.
 The test is read by palpating the two wattles simultaneously between the first
finger and thumb of each hand.
 A positive reaction is recognized by a hot, soft, edematous swelling of the injected
wattle, which maybe twice the size of the uninjected one or even larger.
 Most uninfected birds will show no reaction in the injected wattle and occasional
small, firm, pea-like swellings can usually be ignored.
 The accuracy of the test, relative to gross lesions seen at necropsy, in detecting
infected birds is about 80%. However, birds in an advanced stage of infection
may give no reaction. It is possible, however, that such birds would be thin or
emaciated on handling during the testing of a flock and thus arouse suspicion of
tuberculosis.
 Various modifications of the site of inoculation of tuberculin have been suggested
for turkeys, ducks and other birds but this test has not yet proved to be reliable
for these species. For these the whole-blood, stained antigen agglutination rest
may be preferable.
 In this test a drop of antigen (a suspension of avian tubercle bacilli) is mixed with
a drop of blood from the bird under test. A positive reaction is indicated by
agglutination within 1 mm. The distinct advantage of this test is that birds have
only to be handled once; however, its lack of specificity must be considered.

DIFFERENTIAL DIAGNOSIS

 In differential diagnosis, at necropsy, most difficulty might be in differentiation

from neoplasia but the simple enucleation of tubercular lesions from the
surrounding tissues and the demonstration of typical acid fast organisms should
be adequate.
 CHAPTER-11: MYCOPLASMAL DISEASES AND AVIAN CHLAMYDIOSIS
(PSITTACOSIS)

 Mycoplasmal diseases
INTRODUCTION

 Several Mycoplasma spp have been isolated from avian hosts; M. gallisepticum ,
M. iowae , M. meleagridis , and M. synoviae are the most important.
 Mycoplasmas are fastidious bacteria, 0.3-0.8 µm in diameter; they lack a cell wall
and require a rich growth medium containing serum.
 They do not survive for more than a few days outside the host and are vulnerable
to common disinfectants. Each has distinctive epidemiologic and pathologic
characteristics.
 M. gallisepticum infection is commonly designated as chronic respiratory disease
in chickens and as infectious sinusitis in turkeys.
 Infection may also be seen in pheasants, chukar partridges, and peafowl.
Infection in pigeons, quail, ducks, geese, and psittacine birds should be
considered.
 Passerine-type birds are quite resistant, although M. gallisepticum is the major
cause of natural outbreaks of conjunctivitis in wild house finches (Carpodacus
mexicanus) in the eastern USA.
 The disease is worldwide. Its effects are most severe in large commercial
operations during winter.
 M. gallisepticum is the most pathogenic avian mycoplasma; however, strains may
differ markedly in virulence. Primary isolation is made in enriched broth medium
containing 10-15% serum, then plated on agar.
 Typical colonies are identified by immunofluorescence.

TRANSMISSION, EPIDEMIOLOGY AND PAHTOGENESIS

 In the USA, most breeder flocks are free of M. gallisepticum , and outbreaks are
due to lateral transmission from infected chickens; however, in some parts of the
world, egg transmission is a major source of infection.
 The incidence of egg transmission is highly variable, ranging up to 30-40%
during the first 2 mo after infection of susceptible birds in production.
 The transmission rate then lessens and is inconsistent (0-5%) until the end of
production.
 Birds infected before the onset of production transmit through the egg at a much
lower rate, if at all.
 The infection may be dormant in the infected chick for days to months, but when
the flock is stressed, aerosol transmission occurs rapidly and infection spreads
through the flock.
 Live virus vaccination, natural virus infection, cold weather, or crowding may
initiate the spread.
 In addition, the infection may be carried by personnel (especially from an
infected to a clean flock), fomites, or introduction of infected birds.
 In many flocks, the source of infection cannot be determined.
 The epithelium of the upper air passages is most susceptible to infection;
however, in severe, acute disease the infection is also found in the lower
respiratory tract.
 There is a marked interaction between respiratory viruses, Escherichia coli ,
and M. gallisepticum in the pathogenesis of chronic respiratory disease.
 Once infected, birds remain carriers for life.

CLINICAL FINDINGS

 In chickens, infection may be inapparent or result in varying degrees of respiratory distress,

with slight to marked rales, difficulty breathing, coughing, and/or sneezing.

 Morbidity is high and mortality low in uncomplicated cases.

 Nasal discharge and frothiness about the eyes may be present. In turkeys, the
disease is generally more severe than in chickens, and swelling of the paranasal
sinus is common.
 Feed efficiency and weight gains are reduced. Broilers and market turkeys may
suffer high condemnations at processing due to airsacculitis.
 In laying flocks, birds may fail to reach peak egg production, and the overall
production rate is lower than normal.

CHRONIC RESPIRATORY DISEASE (CRD):LESIONS

 Uncomplicated M. gallisepticum infections in chickens result in relatively mild

sinusitis, tracheitis, and airsacculitis.
 E coli infections are often concurrent and result in severe air sac thickening and
turbidity, with exudative accumulations, fibrinopurulent pericarditis, and
perihepatitis, particularly in broilers.
 Turkeys develop severe mucopurulent sinusitis and varying degrees of tracheitis
and airsacculitis.
 The mucous membranes are thickened, hyperplastic, necrotic, and infiltrated
with inflammatory cells. Lymphofollicular areas are found in the submucosa.

DIAGNOSIS

 Agglutination reactions and ELISA are commonly used for diagnosis.

 M gallisepticum should be confirmed by isolation and identification, PCR, or
haemagglutination-inhibition because nonspecific false agglutination reactions
 are common, especially after the inoculation of inactivated, oil-emulsion vaccines
or M synoviae infection.
 Isolates must be identified, because birds may also be infected with
nonpathogenic Mycoplasma spp .
 PCR is commonly used to rapidly detect the organism in upper respiratory
tissues.
 Newcastle disease, infectious bronchitis, influenza, and other respiratory
pathogens should be considered in the differential diagnosis.

TREATMENT AND CONTROL

 In the field, many cases of M. gallisepticum infection are complicated by other

pathogenic bacteria; thus, effective treatment must also attack the secondary
invader.
 Most strains of M. gallisepticum are sensitive to a number of antibiotics, such as
chlortetracycline, erythromycin, oxytetracycline, spectinomycin, tiamulin,
tylosin, or a fluoroquinolone such as enrofloxacin.
 Antibiotic is usually given in the feed or water for 5-7 days; however, in turkeys,
antibiotic may be given initially by injection, followed by feed or water
medication.
 Antibiotics may alleviate the clinical signs and lesions but do not eliminate
infection.
 Eradication of M. gallisepticum from chicken and turkey breeding stock is well
advanced in the USA and several other countries.
 The most effective control program is to identify breeders without serum
agglutination or ELISA titers and to maintain seronegative stock.
 In valuable breeding stock, treatment of eggs, usually with tylosin or heat, may be
used to eliminate egg transmission to progeny.
 Medication is not a good long- term control method but is of value in treating
individual infected flocks.
 The use of birds free of M. gallisepticum is desirable, but infection in multiple-
age commercial egg farms where depopulation is not feasible is a problem.
 An inactivated, oil-emulsion bacterin is available in most countries; it prevents
egg production losses but not infection.
 A live vaccine has been licensed in the USA for use in infected, multiple-age layer
flocks but may be used only with permission of the state veterinarian.
 The vaccine consists of a mild strain of M. gallisepticum (F-strain) and is usually
given at ~10-14 wk of age. F-strain is of low pathogenicity for chickens but is fully
virulent for turkeys.
 Vaccinated birds remain carriers, and immunity lasts through the laying season.
 Recently, 2 nonpathogenic live vaccine strains (6/85 and ts-11) have been
introduced; these strains offer the advantage of improved safety and are in
widespread use in commercial layers.

 Mycoplasma synoviae infection (Infectious synovitis)
INTRODUCTION

 M synoviae was first recognized as an acute to chronic infection of chickens and

turkeys that produced an exudative tendinitis and bursitis; it now occurs most
frequently as a subclinical infection of the upper respiratory tract.
 M synoviae infection is also a complication of airsacculitis in association with
Newcastle disease or infectious bronchitis.
 It is seen primarily in chickens and turkeys, but ducks, geese, guinea fowl,
parrots, pheasants, and quail may also be susceptible.
 Serum (preferably swine serum) and nicotinamide adenine dinucleotide are
required for growth on artificial media.

ETIOLOGY

 M. synoviae is egg-transmitted, but the rate is low (probably <5%), and some
hatches of progeny may be free of infection.
 Egg transmission is greatest during the first 1-2 mo after infection of susceptible
breeders.
 Lateral transmission is similar to that of M. gallisepticum , but the rate of spread
is generally more rapid.
 M. synoviae isolates vary widely in pathogenicity. Isolates from cases of
airsacculitis are more apt to produce air sac lesions than isolates from synovial
fluid or membranes.
 Some strains produce the typical clinical disease of synovitis.
 The paucity of natural outbreaks of clinical synovitis in chickens in recent years
may be related to the adaptation of M synoviae to the respiratory tract; however,
clinical synovitis in turkeys is relatively common.

CLINICAL FINDINGS

 Although slight rales may be present in birds with respiratory infection, usually
no signs are noticed.
 Younger birds, especially those under stress or suffering concurrent infections,
are more likely to be affected.
 Outbreaks of infectious synovitis occur most commonly in chickens at 4-6 wk and
in turkeys at 10-12 wk. Lame birds tend to sit.
 The more severely affected birds are depressed and are found around the feeders
and waterers. Swellings of the hocks and footpads are seen.
 Morbidity is 2-15%, and mortality 1-10%. The effect on egg production is
minimal, but instances of egg production losses have occurred.


LESIONS
  In the respiratory syndrome, airsacculitis occurs when the bird is stressed from
Newcastle disease, infectious bronchitis, or improper ventilation.
 In many cases, air sac lesions resolve after 1-2 wk. Early in synovitis, the liver is
enlarged and sometimes green.
 The spleen is enlarged, and the kidneys are enlarged and pale.
 A yellow to gray, viscid exudate is present in almost all synovial structures; it is
most commonly seen in the keel bursa, hock, and wing joints.
 In chronic cases, this exudate may become inspissated and orange.

DIAGNOSIS

 A presumptive diagnosis can be based on the lesions and clinical signs, but
laboratory confirmation is necessary.
 Skeletal abnormalities must be eliminated as the cause of lameness.
 The disease must be differentiated from viral tenosynovitis and from
staphylococcal and other bacterial infections.
 The serum plate agglutination or ELISA test is used to detect infected flocks, but
cross-reactions with M gallisepticum and other nonspecific reactions may occur.
 Reactors are confirmed as positive by haemagglutination-inhibition or by
isolation and identification of the organism.
 PCR may be used to rapidly detect the organism in infected tissues.
 In turkeys, the agglutination test for M synoviae may not be reliable.

TREATMENT AND CONTROL

 Serologic testing and isolation similar to those for M gallisepticum have resulted
in eradication of the infection in most primary breeder flocks of chickens and
turkeys.
 Administration of a tetracycline antibiotic in the feed may be beneficial in
treatment or prevention of synovitis.
 When airsacculitis is a problem, preventive antibiotic therapy during the time of
respiratory reaction to Newcastle disease and infectious bronchitis vaccine may
be helpful.
 Medication of breeder flocks is of little value in preventing egg transmission.

Mycoplasma iowae infection

INTRODUCTION

 M. iowae was originally thought to be of low pathogenicity in producing air sac

lesions in chickens and turkeys, but it is a potentially important cause of reduced
hatchability in turkeys.
 Antigenicity and pathogenicity vary considerably among M iowae strains.
 M. iowae is resistant to 1% bile salts, and an enriched medium similar to those
used for other avian mycoplasmas is suitable.
 Infection was common in turkey flocks in Europe and North America, but the
infection rate has now been reduced by intensive eradication efforts in breeding
stocks.
 It is a relatively uncommon infection of chickens. M. iowae is egg transmitted,
but little is known of other aspects of its epidemiology.
 Many strains of M. iowae are lethal to turkey embryos.
 After experimental inoculation of young poults, stunting, poor feathering, and
various skeletal deformities such as tenosynovitis and chondrodystrophy develop,
but the mechanism is unknown.
 These effects have not been recognized in the field, probably because most
infected birds die before hatching. Older birds appear to be quite resistant.

CLINICAL FINIDINGS, LESIONS, AND DIAGNOSIS

 Affected turkey breeder flocks show no clinical signs other than reduced
hatchability (usually 2-5%).
 In many flocks, the hatchability returns to normal after 1-2 mo.
 Most embryos die during the mid to late stages of incubation.
 Dead turkey embryos are edematous, congested, and stunted; they may have
clubbed down.
 Poults challenged in ovo or at 1 day of age may develop various skeletal
deformities such as rotated tibia, deviated toes, chondrodystrophy, or erosion of
the articular cartilage of the hock joint.
 Feathers may also be poorly developed. Chicks challenged at 1 day of age may
develop tenosynovitis and ruptured tendons.
 Turkeys apparently have a poor antibody response, and no reliable serologic test
is available.
 Diagnosis relies on isolation and identification of the causative agent.

TREATMENT AND CONTROL

 The best method of control is to maintain flocks free of M. iowae ; however,

because serology is unreliable, this may be difficult.
 Dipping hatching eggs in solutions of enrofloxacin has significantly reduced
losses in hatchability.

 Avian chlamydiosis (Psittacosis, ornithosis and parrot fever)

INTRODUCTION

 Etiology: Chlamydia psittaci

 Gram negative coccoid organisms.
 Multiplies intracellularly within phagosomes.
 Multiplication is characterised by change from a small ring walled infectious form
(elementary form) to a larger flexible-walled non-infectious form (reticulate
body)
 The daughter reticulate bodies reorganise into elementary bodies. These are shed
extracellularly to infect new cell
 The organisms causes disease both in birds and humans
 Other names
o Parrot fever (in human): Febrile pulmonary disease (since it is from
parrot)
o Psittacosis: in humans, mammals, and psittacine birds (e.g.: Parrots,
parakeets etc.)
o Ornithosis: in birds other than psittacines.

PREVENTION AND TREATMENT

 Local governmental regulations should be followed wherever applicable. No

effective vaccine for use in birds is available.
 Treatment will prevent mortality and shedding but cannot be relied on to
eliminate latent infection; shedding may recur.
 Tetracyclines (chlortetracycline, oxytetracycline, and doxycycline) are the
antibiotics of choice.
 Drug resistance to tetracyclines is rare, but reduced sensitivity requiring higher
dosages is becoming more common.
 Tetracyclines are bacteriostatic and only effective against actively multiplying
organisms, making extended treatment times (from 2-6 wk, during which
minimum-inhibitory concentrations in blood are consistently maintained)
necessary.
 Outbreaks in poultry flocks are not common.
 Treating infected flocks with chlortetracycline at 400-750 g/ton for a minimum
of 2 wk before processing has effectively eliminated potential risk of infection for
plant employees.
 In companion birds, use of chlortetracycline-medicated feeds for 45 days is a
standard recommendation for imported birds.
 Difficulties in palatability of the feed itself or high level of antibiotic necessary for
adequate blood levels have limited its use.
 Long-acting oxytetracycline at 50-100 mg/kg, IM, every 2-3 days for 30 days,
provides adequate continuous blood levels and results in elimination of shedding
within 24 hr.
 However, muscle necrosis at injection sites may be extensive, which limits the
usefulness of this treatment.
 Doxycycline in a formulation for IM use has been given at 75-100 mg/kg as a
series of 7 injections over a 6-wk period.
 Supportive care for acutely affected birds also aids recovery.
 Appropriate biosecurity practices are necessary for controlling the introduction
and spread of chlamydiae in an avian population.
 Minimal standards include quarantine and examination of all new birds, traffic
control to minimize cross-contamination, isolation and treatment of affected and
contact birds, thorough cleaning and disinfection of premises and equipment
(preferably with small units managed on an all-in/all-out basis), provision of
uncontaminated feed, maintenance of records on all bird movements, and
continual monitoring for presence of chlamydial infection.
 The organism is susceptible to heat and most disinfectants (eg, 1:1,000
quaternary ammonium chloride, 1:100 bleach solution, 70% alcohol, etc), but is
resistant to acid and alkali.
 A voluntary cooperative improvement plan leading to certification of companion
birds derived from chlamydia-free breeders has been developed.

INCIDENCES

 Considerable variation in virulence among strains and also among species of host
 Turkeys are most susceptible and then ducks and pigeons
 Chickens are rarely affected
 The serotypes which infect birds are different from those of mammals. However,
avian strains of Chlamydia psittaci can infect humans
 Currently, six serotypes of Chlamydia psittaci are known to infect birds
 The disease in humans contracted from turkeys is usually more severe than that
from psittacine birds
 Avian chlamydiosis in birds is usually systemic and some times fatal.

INCIDENCES

 Considerable variation in virulence among strains and also among species of host
 Turkeys are most susceptible and then ducks and pigeons
 Chickens are rarely affected
 The serotypes which infect birds are different from those of mammals. However,
avian strains of Chlamydia psittaci can infect humans
 Currently, six serotypes of Chlamydia psittaci are known to infect birds
 The disease in humans contracted from turkeys is usually more severe than that
from psittacine birds
 Avian chlamydiosis in birds is usually systemic and some times fatal.
 PATHOGENESIS

CLINICAL SIGNS

 Human
o Sudden onset of febrile illness with upper respiratory involvement,
o Pneumonia and debility
o Although it is not usually fatal, significant death occurs
 Birds - Clinical signs vary with age, species of birds and strain of the organism
 Turkey, Duck, Pigeons
o Depression with ruffled feathers
o Anorexia, conjunctivitis, Purulent nasal discharge
o Tracheitis with rales (some times)
o Grey-green diarrhoea with blood
 Death may be sporadic or more in a flock.
 Mortality is likely to be higher in parrots than in parakeets.
 Recovered birds may excrete the organisms for longer period.
 Chickens are rarely affected (although susceptible).

PATHOLOGY

 Vary and are dependent on the severity and acute nature of the disease
 Mortality vary from 0 to 30%
 Gross lesions
o Serofibrinous exudate on serosal surfaces
o Pericardium - Inflammatory changes
o Lungs - Congestion
o Air sacs - Thickening due to clouding of walls
 o Liver and spleen- Enlargement & Softer and small necrotic foci and
petechiae

MICROSCOPIC LESIONS

 Organisms are present in various tissue cells in acute psittacosis.

Spleen

 Mononuclear cells containing organisms

 Hyperplasia of the reticulo-endothelial cells.

Liver

 Focal necrotic areas

 Infiltration of lymphocytes and plasma cells in portal areas

Kidneys

 Epithelium packed with large numbers of LCL bodies

Lungs

 Serous exudate in few alveoli

 No consolidation

Intestine

 Erosion of mucosa
 Infiltration of lamina propria and sub mucosa with lymphocytes an plasma cells

LCL (Levinthal, Coles, and Lillie) bodies

 Minute, spherical basophilic bodies.

 Frequently observed within the cytoplasms of macrophages and epithelial cells .

DIAGNOSIS

 Presumptive diagnosis: Based on clinical signs

 Confirmative diagnosis
o Demonstration of the casual organisms
o By fluorescent antibody or immunoperoxidase test
o Demonstration of chlamydial DNA using PCR
o Microscopical examination of smears, or sections of peritoneal, pericardial,
liver and spleen lesions for the presence of intracellular organisms in most
acute cases
 Isolation and identification of the organisms
o Reliable method
o Isolation of organisms in cell culture or embryonated hen eggs
o Mice inoculation with susceptible materials
 Serological examination: Demonstration of antibodies
o Complement fixation test (CFT): Modified or Indirect CF inhibitonT
o ELISA: More sensitive than CFT
o MAbs are used

ZOONOTIC IMPORTANCE

 The avian C.psittaci can infect humans

 Human infections are common after handling or processing of infected turkeys or
ducks
 The personnel employed in meat processing plant are at risk
 Hence precautions should be taken while handling them
 Most infections are through inhalation of infectious aerosols
 Pigeons may also may pose public health threats mainly to their producers
 Chickens are of lesser importance as potential health hazards

 CHAPTER-12: FUNGAL INFECTIONS AND MYCOTOXICOSIS –
INTRODUCTION
 Aspergillosis (Brooder pneumonia)
ETIOLOGY

 The two major species of fungus Aspergillus which cause aspergillosis in poultry
are,
o Aspergillus fumigatus
o Aspergillus flavus
 Other species include A.terreus, A.glaucus, A.niger, A.nidulans, A.amstelodami
and A.nigerscens
 These organisms are common soil saprophytes, occurring in decaying vegetative
matter and feed grains.
 They grow on organic matter in warm humid environments
 Fungal hyphae are 4 -12 m m in diameter and bear conidiopores producing
conidia (spores) 2 - 6 m m in diameter that are easily spread in air.

ASPERGILLOSIS: TRANSMISSION

 Aspergillosis is not a transmissible disease.

 Infections are acquired from environmental exposure.
 Infection is by inhalation of spores that usually originate from infected eggs.
 Contamination of the equipments may result in hatchery infection.
 ASPERGILLOSIS - TRANSMISSION

 Contaminated feed or poultry house litter also produce infection

 ASPERGILLOSIS - PATHOGENESIS

ASPERGILLOSIS - CLINICAL SIGNS IN CHICKS

 Signs are subtle even in cases in which severe airsacculitis is present

ASPERGILLOSIS: LESIONS
Macroscopical lesions

 Lungs and air sacs

o Granulomas appear as separate 1 -15 mm diameter white plaques or
caseous nodules.
o Composition: Necrotic centres containing branching, septate, 4-7 m m
diameter hyphae.
 Older lesions
o Contain pleomorphic hyphae up to 12 m m in dia.
o Air-filled cavities may appear green to black due to development of
pigmented conidiophores
o Fungi tend to proliferate within the granuloma and rarely invade adjacent
tissue in immunocompetent birds.
 Trachea: Yellow caseous plaques adherent to the mucosal surface that some
times occluding the lumina.
 Syrinx: Caseous, gelatinous, or less commonly mucopurulent exudate.
 Brain: white to yellow circumscribed areas either in cerebellum or cerebrum.
 Ocular form: Extensive keratoconjunctivitis

Microscopical lesions

Air sacs

 Thickening due to massive infiltration of heterophils, multinucleated giant cells

and other types of leukocytes
 Germinating conidia were seen in the membrane interstitium, and
lymphohistiocytic perivasculitisin less severely affected area
 Granulomas composing central necrotic cellular debris and heterophils with
peripheral palisade of epitheliod macrophages and aggregates of lymphocytes

DIAGNOSIS

 Aspergillosis can be made on PM lesions: Especially white caseous nodules in

lungs, or airsacs. Exudate plugs in tracheal and bronchial lumen
 Demonstration of branched, septate Aspergillus hyphae in the lesions
o Under microscopic, using impression smears of lesions
 o Using tissue sections
 Routine haematoxylin & eosin
 Periodic Acid-Schiff (PAS)
 Grocott’s Methenamine-Silver (GMS)
 Confirmation should also be made by cultural isolation and identification of the
causative fungus
 Although A.fumigatus is the most likely agent of avian aspergillosis, other species
of fungi can cause the disease. Therefore, isolates should be identified
 Granulomas or plaques may be cultured on Sabouraud dextrose agar with
antibiotics
 Serological tests are of limited value due to non-specific nature of the antigen.

DIFFERENTIAL DIAGNOSIS

 The clinical signs of avian aspergillosis are dependent upon the organ systems
involved
 Pulmonary aspergillosis is differentiated from other respiratory diseases by
granulamatous lesions at necropsy
o Exudative fibrinous or purulent air sacculitis and pneumonia are also
frequently seen in the following cases
 Mycoplasmosis
  Colibacillosis
 Fowl cholera
 Chlamydiosis
o If granulamatous lesions predominate , the following ones should also be
considered
 Mycobacteriosis
 Other mycoses

Favus infection
INTRODUCTION

 Dermatophytosis, dermatomycosis, ringworm, and favus are terms applied to the

condition of fungal infections of skin
 The term favus usually is used to denote the disease in poultry
 Favus has a world wide distribution but its occurrence is sporadic
 The disease is contagious and is transmissible in humans
 The primary etiologic agent of favus is Microsporum gallinae (previously,
Trichophyton gallinae)
 The incidence have been reported in the chicken, turkey, duck, quail, and canary
 M.gallinae favus may be more common in backyard, hobby, or game chicken
flocks.
 FAVUS - PATHOGENESIS

AFLATOXICOSIS

 Aflatoxin is the most prevalent and economically significant mycotoxin to be

consumed by poultry.

ETIOLOGY

 Aflatoxin is found in corn (maize), peanuts, cottonseed, millet, sorghum and

other feed grains. A. flavus produces the majority of the toxin and gives it its
name, but aflatoxin is also produced Aspergillus parasiticus.
 Both fungi are ubiquitous in the environment, contain toxigenic and nontoxigenic
strains, and produce aflatoxin in warm (30—35°C), high-humidity (0.90—0.99
activity) conditions.
 Handling or storage of grains in these conditions any where may also stimulate
production. Stressing host plants by insect damage, drought, poor nutrition or
delayed harvest increases afiatoxin production.
 Naturally occurring aflatoxin contains aflaroxins B1, B2, C1 and C2, but aflatoxin
B1 is usually in the highest concentration and is the most toxic.
 Aflatoxin is stable once formed in grain, and is not degraded during normal
milling and storage. Other toxins produced with aflatoxins under field conditions
may play a synergistic role in toxicity.

HOST
 Young poultry are most sensitive to afiatoxin than adults. There are also large
species differences, with ducks being 10 times more sensitive than chickens, and
turkeys intermediate between the two.

PATHOGENESIS

 After ingestion, aflatoxin B1 undergoes biotransformation to numerous highly

reactive metabolites with diverse adverse effects on metabolism.
 Metabolites bind to DNA and RNA, reduce protein synthesis and decrease cell-
mediated immunity and to a lesser extent humoral immunity. With continued
exposure intrahepatic biliary epithelial hyperplasia and extra medullary
haematopoiesis occur, the latter in response to a toxin-induced anaemia.
 Aflatoxin is rapidly excreted in the bile and urine and does not accumulate or
persist in body tissues. This perhaps explains the rapid recovery of egg
production and hatchability after cessation of to ingestion.

CLINICAL SIGNS

 Aflatoxicosis does not usually induce mortality directly, although high levels (>10
ppm) may be lethal.
 The most economically significant effects of aflatoxicosis on growing birds are
decreased growth and poor feed conversion (>1 ppm). There is also a marked
decrease in resistance to infections such as salmonellosis, coccidiosis, infectious
bursal disease and candidiasis, with resultant increased condemnations at
processing (>0.5 ppm). Poultry manifesting aflatoxicosis may also have failure of
normal pigmentation and increased bruising (>0.5 ppm).
 Intoxicated adult hens have decreased egg production and the hatchability of
those eggs that are produced is reduced (>2 ppm).
 In adult breeder males testicular weights and sperm counts are reduced.
 Insemination of hens with semen from affected males has shown decreased
fertility in some studies and no significant reduction in others.

LESIONS

 Lesions will depend on the age of the host and the dose of toxin and can include
enlarged Iivers which become friable and yellow with increasing dose, kidney and
spleen enlargement, diminution of the bursa of Fabricius, thymus and testes.
Petechial haemorrhages or bruises after trauma are also increased because of
decreased clotting factor synthesis and increased capillary fragility.
  Ochratoxicosis
ETIOLOGY

 Ochratoxicosis occurs less frequently in poultry than aflatoxicosis but is more

lethal because of its acute toxicity. Its name derives from Aspergillus
ochraceus, the first fungus shown to produce it.
 Most naturally occurring cases have been associated with ochratoxin produced
by P enicillium veridicatum but five other species of Aspergillus and six other
species of Penicilliumproduce it as well.
 Ochtatoxin is a dihydroisocoumarin derivative linked to L-3-phenylalanine.
 Ochratoxin A and the dechlorinated B form occur naturally but ochratoxin A is
the most toxic and is produced in greater quantities.

SPREAD

 Environmental conditions favouring ochratoxin production are similar to those

for aflatoxin, and simultaneous contamination with both is common.

HOST

 Young poultry are most sensitive to ochtatoxin ingestion and ducks are seven
times more sensitive to the acute effects than chickens.
 Quail and turkeys are also more sensitive to ochratoxicosis than chickens.

PATHOGENESIS

 Ochratoxin A inhibits protein synthesis, produces acute proximal tubular

epithelial necrosis in the kidneys and inhibits normal renal uric acid secretion.

SIGNS

 Acutely intoxicated birds are depressed, dehydrated and often polyuric (>4 ppm)
and die in acute renal failure.
 Survivors will be stunted, poorly feathered, and have increased clotting times,
anaemia and immunosuppression (>0.6 ppm). There may be loss of
pigmentation and reduced weight gain (>2 ppm).
 Laying hens may have delayed sexual maturity or develop wet droppings, causing
increased numbers of stained eggs. There is also a decrease in egg production and
hatchability (>2 ppm), and poor performance in progeny derived from
intoxicated hens.

LESIONS
 Affected kidneys are white to tan, swollen, hard and may have white pinpoint
urate crystals. If damage is extensive enough to cause renal failure there is
dehydration, hyperuricaemia and visceral urate deposition.
 Pasty white urates are deposited on pericardial, perihepatic, peritoneal and
articular surfaces. These deposits may be mistaken for inflammatory exudate but
their true nature can be determined by microscopic examination of impressions
or smears, or histological sections.
 More commonly, birds survive in compensated renal failure and kidneys appear
enlarged, fibrotic and pale.
 In addition to the renal lesions there is mild to moderate fatty change and
glycogen deposi tion in hepatocytes, resulting in yellow enlarged livers. There is
also some mild decrease in bursal and thymic size consistent with
immunosuppression.

 Trichothecene mycotoxicosis

INTRODUCTION

 Trichothecene mycotoxicosis occurs fairly frequently in commercial poultry but

at naturally occurring levels does not usually cause mortality.
 Losses result from reduced feed intake, decreased growth and
immunosuppression.

ETIOLOGY

 Trichothecene mycotoxins occur frequently in wheat, corn (maize) and other

grains used for poultry feed production and are produced by many species
of Fusarium, Stachybotrys and at least three other genera. They also produce
many nontrichothecene mycotoxins, some of which may exacerbate the clinical
effects of the trichothecenes present.
 Fusarium and Stachybotrys grow at many temperatures but toxin production is
highest in cold ( <20°C), moist conditions.
 Trichothecenes are therefore associated with cool climates, particularly when
grain harvests have been delayed into the winter months or infected grain has
been stored in cold conditions. This is distinct from aflatoxin or ochratoxin
production and thus simultaneous contamination with these toxins is rare. There
are approximately 80 chemically related sesquiterpinoid trichothecene
mycotoxins described, but most is known about the effects of the 1 2, 1 3-
epoxytrichothecenes T-2, hydroxy T-2 (HT-2), diacetoxyscirpenol (DAS,
anguidine) and deoxynivalenol (DON, vomitoxin). It is not known if these four
compounds cause most field cases of trichothecene mycotoxicosis. Zearalenone
(F2) also falls in this category but its effects in commercial poultry are minimal.
 HOST

 Young birds are more susceptible than older ones.

PATHOGENESIS

 Trichothecene mycotoxins of significance in poultry produce their pathogenic

effects by two mechanisms: direct epithelial necrosis and radiomimetic
effects that destroy rapidly dividing cells.
 T2 causes epithelial necrosis of mucous membranes on contact. Ulcers occur
where this contact is frequent or where contaminated feed becomes lodged. Thus
erosions and ulcers on the hard palate, tongue and rostral oropharynx, and
chemical burns of the rostral tip of the tongue are due to the direct caustic effects
of T-2.
 DAS is also epithelionecrotic but its effects are slightly less severe than those of T-
2.
 Depending on the dose, ulcers appear 3- 4 days after initial toxin intake and
continue to worsen as long as exposure persists.
 The radiomimetic effects result from trichothecenes severely inhibiting protein
synthesis and tissues with short cellular life spans and high turnover rates are
affected in trichothecenc mycotoxicosis. This accounts for the suppression by T-2
of haemaropoiesis, lymphopoiesis, normal immune responses and normal
replication of feather follicle epithelium and, in severe cases, replication of
enterocytes.
 Individual trichothecenes differ in their production of the above effects. 1-2 very
effectively produces oral ulcers at low doses and produces the radiomimetic
effects at slightly higher doses.
 DAS produces systemic radiomimetic effects at low doses but is an inefficient
producer of oral ulcers.
 In contrast, DON is relatively nontoxic in poultry and produces no oral ulcers, no
feed refusal and no radiomimetic effects at naturally occurring doses.

SIGNS

 There is reduced feed intake, weight gains and feed efficiency, also, anaemia and
poor feathering with broken feather shafts.
 Affected adult birds will develop oral ulcers, decreased egg production, decreased
shell quality and hatchability (>20 ppm 1-2).

LESIONS

 Ulcers are found at the commissures of the mouth, on the hard palate adjacent to
the beak and the palatine cleft, and on the dorsal surface of the tongue (>2ppmT-
2).
  Ulcers are not usually produced further down the oesophagus unless the birds eat
large amounts of feed rapidly. There may be reduction in size of the bursa of
Fabricius and thymus glands of young birds and birds may show anaemia and
pale bone marrow.
It should be noted that oral ulcers are not specific, since dietary copper sulphate
(>200 ppm) and other caustic or traumatic dietary ingredients induce identical
lesions.

Other mycotoxins
CITRININ

 Citrinin is a nephrotoxin produced in a variety of cereal grains by Penicillium

citrinum. During citrinin toxicosis, mortality is rare but water consumption is
increased and there is diffuse polyuria manifested as wet droppings (>300 ppm).
 Clinical signs begin within hours after initial exposure, persist as long as toxin-
containing feed is consumed and stop 8—10 h after cessation of exposure.
 Grossly, kidneys are slightly swollen but there are no microscopic lesions except
at very high dosages.

OOSPOREIN

 Oosporein is a nephrotoxic mycotoxin produced by Chaetomium

trilaterale. Ingestion by chicks (>300ppm) or turkeys (>500 ppm) produces
acute proximal tubular nephrosis and acute renal failure in severe cases.
 Effects are particularly severe in poultry less than 1 week old and lead to visceral
and articular urate deposits and mortality up to 20%.

FUSARIUM FUNGI

 Fusarium fungi produce a wide variety of other mycotoxins. Some strains

of Fusarium moniiforme produce fumonisins, a group of water-soluble
mycotoxins associated with equine encephalomalacia and swine pulmonary
edema. Poultry are apparently more resistant.
 Ingestion of 325 ppm by turkey poults and 250 ppm by broiler chicks is required
to decrease feed intake and bodyweights.

MONILIFORMIN

 Moniliformin is another mycotoxin produced by some F. moniliforme strains as

well as by Fusarium fujikuroi.
 It has been associated with acute myocardial necrosis and death in ducks,
chickens and turkey poults.
 Decreased feed intake and reduced body weights are seen in poults fed 50 ppm,
and in broiler chicks fed l00 ppm.
 FUSAROCHROMANONE (TDP-1)

 Fusarochromanone (TDP-1) is a rarely encountered mycotoxin produced by

multiple isolates of Fusarium.
 It produces leg deformities and tibial dyschondroplasia in chicks fed 20 ppm,
although the majority of naturally occurring tibial dyschondroplasia does not
appear to be due to this toxicosis.

ERGOTISM

 Ergotism is caused by the alkaloid toxins produced by Claviceps species,

particularly Clavicepa purpurea (‘ergot of rye’).
 The fungi grow on wild grasses and common cereal grains, including wheat,
barley and, more rarely, oats. Rye is most frequently affected.
 The acute disease takes the form of convulsions, ataxia and coma followed by
death.
 In the chronic form there is reduced growth or reduced egg production, poor
feathering, diarrhoea and gangrene affecting the comb- wattles, beak and feet
and sometimes vesicles and ulcers on the shanks and feet.

DIAGNOSIS OF MYCOTOXICOSES

 The clinical signs, gross and histopathological lesions may be helpful but not
specific.
 The results of feeding trials with the suspect feed to reproduce the field toxicosis
are also of value but it may be difficult to obtain replicate feed samples. Samples
of suspect feed and mouldy clumps for feeding trials and chemical analysis
should be collected directly from the trough in the poultry house.
 Samples can be rapidly screened for aflatoxin, ochraroxin, T-2, DON and
fumonisin with commercially available solid or liquid phase competitive enxyme-
linked immunosorbent assay (ELISA) tests.
 These inexpensive rapid tests can be done in minutes with material on the farm
or in the feed mill and yield generally excellent results. Positive tests should be
confirmed by most rigorous analytical chemical methods, including thin layer
chromatography, high-performance of liquid chromatography, grass
chromatography, mass spectrophotometry, or monoclonal antibody technology.
Such confirmation requires the capability of the diagnostic laboratory for both
analysis and interpretation.
CHAPTER-13: PARASITIC DISEASES

CLASSIFICATION OF PARASITES
INTRODUCTION

 Nematodes, cestodes, and trematodes are important parasites of poultry,

although modern rearing technology has dramatically changed the importance of
many species
 Parasites with complicated life cycles, involving intermediate hosts such as
insects or snails, were virtually eliminated when commercial poultry practices are
introduced
 Only a handful of these parasites are important in commercial poultry, although
many are found in small flocks reared in natural environments
 A few nematodes, such as the ascarids, caecal worms, and capillarids have direct
life cycles and are fecund enough to prosper in the poultry house environment,
particularly where management does not require frequent cleanouts
 Some cestodes are important, even though they use an intermediate host,
because the host also prospers in the poultry house environment

TREATODES

 Trematodes (flukes) are flat, leaflike, parasitic, organisms belonging to the

phylum Platyhelminthes, class Trematoda
 They differ from cestodes (class: Cestoda) in having a digestive system, and they
do not
form
proglott
ids
 T
he life
cycle of
all
tremato
des
parasiti
zing
birds
require
sa
mollusc
an as an
interme
diate
 host; some species also use a second intermediate host
 Since adult trematodes and larval metacercariae invade almost every cavity and
tissue of birds, they may show up unexpectedly at necropsy
 Flukes are less host-specific than tape worms. Therefore, wild birds often
introduce infection in areas where domestic poultry is reared
 Since many snails live in ponds and streams, ducks and geese are the most
frequently parasitized
 Out of all the trematodes, the oviduct fluke (Prosthogonimus sp.), which is a
frequent parasite of many species of wild birds, some times cause problems with
ducks and chickens.
 Prosthogonimus macrorchis , oviduct fluke has caused economic losses to poultry
producers by
o Drastically reducing egg production after a recent infection
o Occasionally being enveloped within a hen’s egg and later discovered by a
complaining customer
 Other organs invaded by the flukes include,
o Metacercarial cysts in the skin of chickens and turkeys ( Collyriclum faba )
o Small adult flukes in the conjunctival sac of the eye ( Philopthalmus gralli)
o Adults in the liver, pancreas, and bile duct of duct of ducks and turkeys (
Amphimerus elongatus )
o Adults in the collecting tubules of the excretory system of chickens, turkeys,
and pigeons ( Tanaisa bragai )
o Adults and eggs in the circulatory system of ducks by three species of blood
fluke; and
o Fourteen flukes that invade various areas of the digestive tract

IMPORTANT POULTRY TREMATODES

S.No Parasite Hosts Location
1 Echinostoma Ducks and geese Caeca and rectum
revolutum
2 Prosthogonimus sp. Fowl, duck and Bursa fabricius, oviduct, cloaca and
geese rectum

Cestodes
INTRODUCTION

 A high percentage of chickens and turkeys may be infected with tapeworms if

they are reared on range or in back yard flocks
 These parasites are found more frequently in warmer seasons., when
intermediate hosts are abundant
 Many species of tape worms are now considered rare in intensive poultry farming
because the birds do not come in contact with intermediate hosts
 Tape worms or cestodes are flattened, ribbon shaped, usually segmented worms.
 The term, proglottid is used to describe these individual segments
 Each proglottid contains one or more sets of reproductive organs, which may be
become overcrowded with eggs as the maturing proglottid becomes a gravid
proglottid
 Tape worms are characterised by complete absence of digestive tract and obtain
their nutritional nourishment by absorption from the intestinal contents of the
host
 Duodenum , jejunum or ileum are the usual site for attachment.But one
species, Hymenolepis megalops is found in the cloaca or bursa of Fabricius of
ducks

CESTODES - PATHOGENESIS

 Raillietina cesticillus and Choanotaenia infundibulum may block completely the

intestine of an infected bird
 Different species vary considerably in pathogenicity
 Some pathologically important species are,
o Davainea proglottina
 More harmful species in young birds
 Clinical signs : Emaciation, dull plumage, breathing difficulties, leg
weakness, paralysis, and death
o Raillietina tetragona - cause weight loss, and decreased egg production
o Raillietina echinobothrida
 One of the most pathogenic tapeworm
 Its presence has often associated with nodular disease of chickens
 It produces parasitic granuloma about 1-6 mm in diameter at the site
of attachment.
 The condition is associated with catarrhal hyperplastic enteritis as
well as lymphocytic, heterophilic and eosinophilic infiltration.

DIAGNOSIS

 Demonstration of distinctive characteristic scolex , eggs, or individual proglottids

of different species of tapeworms
 Wet-mount preparations of the scolex may reveal enough characteristics to make
a species identification
 Distinctive egg characteristics can be demonstrated by teasing apart a gravid
proglottid under a cover slip
 Wet-preparations of mature or gravid proglottids ,under low magnification may
reveal diagnostic characteristics such as the
 If further details of the internal structures of the proglottid are required for
identification, it may be necessary to kill, fix, stain, destain, dehydrate, and
permanently mount the specimen
 IMPORTANT POULTRY CESTODES
Parasite Host Location
Raillietina sp. Chickens, turkeys, guinea fowls and pigeons Small intestine
Davainea proglottina Fowls and pigeons Small intestine
Choanotaenia infundibulum Fowls and turkeys Small intestine
Hymenolepis sp. Fowls, ducks and geese Small intestine
INTRODUCTION

 Nematodes constitute the most important group of helminthic parasites of

poultry
 In the number of species, the number of birds infected, and the amount of
damage done, they far exceed the trematodes and cestodes
 Avian nematodes usually have a broad host range. Therefore, nematodes found in
wild birds may constitute a hazard for commercially raised birds
 The nematodes are , with very few exceptions, sexually different
 The male can usually be differentiated from the female by the presence of two
(rarely one) chitinous (horny) structures known as spicules located in the
posterior end of the body
 The spicules are considered as intromittent (that which inserts) organs for use
during copulation. They keep the vulva and vagina open and guide the sperm into
the female
 Eggs or larvae are discharged through the vulva

DEVELOPMENT OF NEMATODES

 Eggs of some nematodes require only a few days to complete embryonation;

others require several weeks.
 In case of nematodes with direct life cycle, the final host becomes infected by
eating embryonated eggs containing second stage larvae or free larvae.
 In case of those with indirect life cycle, the intermediate host ingests the
embryonated eggs or free larvae, and retains the larvae within the body tissues.
 The final host becomes infected either by eating the infected intermediate hosts
or by injection of the larvae by a blood-feeding arthropod.
 Eggs of some nematodes require only a few days to complete embryonation ;
others require several weeks.
 In case of nematodes with direct life cycle, the final host becomes infected by
eating embryonated eggs containing second stage larvae., or free larvae.
 In case of those with indirect life cycle, the intermediate host ingests the
embryonated eggs or free larvae, and retains the larvae within the body tissues.
 The final host becomes infected either by eating the infected intermediate hosts
or by injection of the larvae by a blood-feeding arthropod.
 Nematodes
Ascaridia galli
INTRODUCTION

 Ascardia are the largest nematodes of poultry.

 The adults live in the lumen of the small intestine, but the larval stage invade the
mucosa.
 Ascardia galli occurs in chicken, turkey, duck and goose.
 It is usually found in the lumen of intestine, some times in the esophagus, crop,
gizzard, oviduct, and body cavity.
 Ascardia galli are large worms. The male is 50 -76 mm long, the female is 60-116
mm long.
 The eggs are oval-shaped, thick shelled, and not embryonated at the time of
deposition

ASCARIDIA GALLI - LIFE CYCLE

 A.galli eggs are ingested by grass hoppers or earth worms, hatch , and are infective
to chickens. However, no development of the larvae occurs.
 Under optimum conditions of temperature and moisture, eggs in the droppings
become infective in 10 – 12 days; under less favourable conditions, a long timer time
is necessary.
 Eggs are quite resistant to low (non-freezing) temperatures.
 ASCARIDIA GALLI - PATHOGENECITY

 Synergism with other diseases like coccidiosis, infectious bronchitis produce

harmful effects
 A.galli have also been shown to transmit avian reoviruses
 Some times, A.galli is found in the hen’s eggs as they migrate, from the cloaca, up
the oviduct with subsequent inclusion in the egg
 Infected eggs can be detected by candling

 Capillaria sp.
INTRODUCTION

 It infects chicken, turkey, duck, goose, guinea fowl, pigeon, and quail.
 They are seen in the small intestine and the caecum.
 They are the smallest of the nematodes.
 Highly pathogenic when they are present in large numbers.
 Different species parasitize different parts of the alimentary tract.
 Life cycle may be direct or indirect.
 The most common and pathogenic is Capillaria obsignata, a hair-like worm ,
which has a direct life cycle.
 CAPILLARIA INFECTION : PATHOGENECITY

 Gross lesions - In some cases, catarrhal exudate in the upper intestine and thickening of the wall

Heterakis gallinarum

INTRODUCTON

 Heterakis gallinarum (caecal worm) infects chicken, turkey, duck, goose pheasant
and quail
 The larval and adult H.gallinarum inhabit the caeca
 Adult worms are small and white
 The male is 7-13 mm long while the female is 10-15 mm long in length
 The eggs are thick-shelled, ellipsoidal, unsegmented when deposited, and
undistinguishable from those of A.galli.

HETERAKIS GALLINARUM - LIFE CYCLE

 The larvae are closely associated with and some times embedded in the caecal
tissue.
 At necropsy, most of the adult worms are found in the blind ends of caeca.
 Earth worms may also ingest the eggs of the caecal worms, and may be the means
of causing infection in poultry.

PATHOGENECITY

 Basically, H.gallinarum is not pathogenic

 The chief economic importance of the caecal worm lies in its role as a carrier of
the black head organism Histomonas meleagridis
 Histomoniasis may be produced in susceptible hosts by feeding embryonated
eggs of H. gallinarum taken from black head infected birds
 The protozoan parasites are found in the worm egg. Its presence has been
identified in the intestinal wall, in the reproductive systems of male and female,
and in the developing eggs of the caecal worms
 Gross lesions - The caeca show marked inflammation and thickening of walls
 In heavy infections, nodules form in the mucosa and sub mucosa, as the response
of already sensitized caeca to subsequent infection
 Hepatic granulomas containing the worms have also been reported in chicken
Respiratory tract nematodes-
 Syngamus trachea
INTRODUCTION

 Syngamus trachea is the only nematode of importance in the respiratory tract.

 It has been reported in chicken, turkey, goose, guinea fowl ,quail and other
species.
 It may be found in the trachea, bronchi, and bronchioles and causes the condition
of Gapes ( laboured breathing due to parasites).
 Therefore the worms are commonly known as gape worms.
 It is some times called as Red worm because if its colour , or forked worm
because the male and female are in permanent copulation so that they appear like
the letter ”Y”.
 The male is 2-6 mm long, and female 5-20 mm in length. The eggs are oval-
shaped and operculated.

SYNGAMUS TRACHEA - PATHOGENECITY

 Young birds are most seriously affected with gape worm.

 Turkey poults and baby chicks are most susceptible to infection.
 Turkey poults usually develop gapeworm signs earlier and begin to die sooner after
infection than young chickens.
  Protozoal diseases
Histomoniasis
INTRODUCTION

Other names: Black head and Infectious enterohepatitis

Etiology: Histomonas meleagridis - a protozoan parasite
Histomoniasis is a disease of caeca and liver
Although the disease is called as black head the signs are neither pathognomonic
nor characteristic of the disease, as many of the other diseases may produce a
similar appearance
Despite its occurrence in several species of birds, it is primarily a disease of
turkeys
The turkey is considered the most susceptible host because most affected turkeys
die
Sometimes, the disease also occurs in chickens but in a milder form
The disease is characterised by necrotic foci in the liver and ulceration of the
caeca.

LIFE CYCLE

 The existence of H.meleagridis is closely associated with caecal

nematode Heterakis gallinarum and several species of earthworms common in
the soil of poultry premises.
 Histomonads cannot survive outside the host for more than a few minutes unless
protected by heterakid egg or earthworm.
 Earthworm serve as transport hosts in which heterakid eggs hatch, and the young
worms survive in tissues in an infective stage.
 The parasite in th colony is flagellated and pleomorphic (in caecal lumen).
 It rounds up and loses its flagellum (in tissues).
 Histomonas do not form cysts, and there is no direct faeco-oral transmission.

TRANSMISSION

The most important natural route of transmission is within the egg of Heterakis
gallinarum.
Ingestion by caecal worms in the caecal lumen.
They enter into the nematode eggs which are ultimately shed in the host species
and are available to infect further hosts.
The role of heterakis as vectors is very important, because they are also parasites
of birds and protect the histomonads within their egg during transmission from
bird to bird.
The earthworm may also act as a transport host in which heterakis larvae may
hatch but remain viable and infected with histomonads in the earthworm tissues.
Besides the earthworms, insects such as flies, grass-hoppers, and crickets may
serve as mechanical vectors.

CLINICAL SIGNS

In turkeys
o Anorexia, drowsiness, dropping of the wings, closed eyes, and sulphur-
yellow droppings.
o Blackhead is an accurate term , since the head may or may not be cyanotic,
nor it is unique to histomoniasis.
o Mortality may be high, reaching a peak about a week after the onset of
signs.
In chicken
o Infection may be mild and go unnoticed or may be severe and cause high
mortality.
o Sulphur coloured droppings seen in turkeys are seldom found in chickens,
but blood caecal discharges have been observed.
o Sometimes, gross pathology in chickens may resemble caecal coccidiosis.

MACROSCOPIC LESION

 Lesions first occur in caeca and then in the liver

Liver

 Appear as circular depressed areas of necrosis up to 1 cm in diameter and are

surrounded by a raised ring - Pathognomonic lesion

MICROSCOPICAL LESION

Caecum

Earlier changes

 Hyperaemia and heterophilic infiltration in caecal wall

Later changes

 Infiltration with large numbers of lymphocytes and macrophages

 Caecal core consisting sloughed epithelium, fibrin, erythrocytes and
leukocytes along with trapped caecal ingesta
Liver

Earlier changes

 Small clusters of heterophils, lymphocytes, and monocytes near portal

vessels

Later changes

 Hepatocytes at the centre of lesions undergo necrosis and disintegration

 Necrosis becomes increasingly severe, resulting in large areas consisting of
only reticulum and cellular debris

DIAGNOSIS

Diagnosis can be made from the characteristic gross lesions which remain clearly
visible long after death.
If confirmation is required, stained sections from the periphery of liver lesions
will reveal rounded up organisms.
Identification of living organisms in the wet preparations from caecal lesions is a
little difficult. It requires fresh material and a heated microscope stage.

Cryptosporidiosis
INTRODUCTION

 Cryptosporidiosis is caused by protozoa of the phylum Apicomplexa, genus

Cryptosporidium.
 It have similarities with Eimeria, but also a number of important differences.
 In mammals, infections of intestine and diarrhoea are characteristic.
 But in birds the disease is usually associated with infection of the respiratory
tract.

ETIOLOGY

 Two species have been described in birds, Cryptosporidium baileyi and C.

meleagridis.
 Cryptosporidium baileyi causes both respiratory and intestinal disease, whereas
C. meleagridis is associated with enteric disease only.
 Cryptosporidia infect chickens, turkeys, ducks, geese, and several others.
 Isolates do not have rigid host specificity.

LIFE CYCLE

Excystation (Infective Sporozoite Release)

  Thick-walled oocysts are ingested by the host and reach the intestine where
sporozoites excyst and penetrate the microvillus borders of ileal enterocytes.
 This stage of development occurs in a parasitophorous vacuole, characterized as
an intracellular but extracytoplasmic space.
 Other Eimeriorina do not exhibit such behavior and confine themselves to
intracellular, intra-cytoplasmic domains

Merogeny (Asexual Multiplication)

 Once encysted within enterocytes, Cryptosporidium sp. sporozoites produce type

I meronts, each of which contains six to eight merozoites.
 This asexual development allows type I meronts to self replicate and help to
perpetuate the infection.
 Type I meronts may also continue development to type II meronts.
 Type II meronts contain only four merozoites.

Gametogeny (Gamete Formation)

 Microgametocytes (containing ~16 gametocytes), and the singular macrogametes

originate from the type II meronts. 2,12 These stages represent the sexual
reproduction ofCryptosporidium sp.

Fertilization

 A microgametocyte fertilizes the macrogamete to form a zygote.

 At this point in the life cycle, Cryptosporidium spp. also diverge from other
coccidia as
explained below

Oocyst Wall
Formation and
Sporogony
(Sporozoite
Formation)
  Approximately 80% of the zygotes formed during sexual reproduction continue
to develop as thick-walled oocysts.
 These oocysts sporulate within and are released from the host cell.
 Once free of the host cell, these oocysts pass from the body in the feces where
they are infective and can immediately transmit the infection to another host.
 The remaining ~20% of zygotes will form a unit membrane in place of an oocyst
wall that surrounds sporozoites.
 These zygotes will not be shed with the feces; they excyst within the intestinal
lumen releasing free sporozoites.
 These sporozoites continue the parasitic infection by penetrating another host
enterocyte (autoinfection).
 Cryptosporidiosis - Life cycle - Parasitic phas

CLINICAL SIGNS AND PATHOLOGY

 Infections can occur in very young chickens.

 Disease has been reported in chickens, turkeys, ducks, quails, pheasant and
others.

Intestinal infection

 Disease associated with enteric infection is rare.

 Even then, intestinal disease is usually mild.
 No clinical signs of gastrointestinal disease occur in chickens.

Respiratory infection

 It produces a variety of clinical signs depending on the particular site involved.

 There may be airsacculitis , pneumonia , sinusitis or conjunctivitis with coughing
, nasal discharges , and high morbidity and mortality.
 The affected birds show poor weight gain and higher feed/ gain ratios.

HISTOPATHOLOGY

Respiratory cryptosporidiosis

 A large number of parasites through out the epithelium lining the trachea and
bronchi.
 Epithelial hyperplasia.
 Thickening of the mucosa by mononuclear cell infiltrations with some
heterophils.
 Loss of cilia, and discharge of mucocellular exudate into the airways.

Intestinal cryptosporidiosis (i.e. of cloaca and bursa of Fabricius)

 It may produce microscopic lesions.

  But these do not result in gross lesions or in clinical signs of the disease.

DIAGNOSIS

 Both , respiratory and intestinal infections, can be diagnosed by,

o Identifying the oocysts from fluid obtained from the respiratory tract , or
from the faeces
 Diagnosis can also be made from demonstration of the,
o Organisms in sections of the affected mucosal epithelium
o Cysts in stained smears from the respiratory mucosa
o With a modified Ziehl-Neelsen stain , oocysts stain red and are 4-6 m m in
diameter, sub spherical.

TRANSMISSION

 Since C.baileyi can infect a variety of birds, it is possible that wild birds may serve
as carriers

CHAPTER-14: NUTRITIONAL AND METABOLIC DISEASES

INTRODUCTION

 There are a great variety of clinical conditions that are induced by nutritional
deficiencies and imbalances. These may arise from,
o Gross deficiency in the ration supplied to poultry
o Antagonism between nutrients
o Destruction or inactivation during feed manufacture
o Impaired absorption or metabolic disorder that renders supply inadequate
  A specific mineral or trace element deficiency generally produces characteristic
signs, reflecting specific metabolic functions; For eg,
o Fat soluble vitamins A and E are involved with membrane integrity
o Water soluble vitamins and trace elements with enzyme systems
o Very profound effects may be brought about by a deficiency of minute
amounts of these nutrients at the site required

VITAMIN- A

 The term vitamin A covers a number of physiological forms (retinol, retinoic acid,
retinaldehyde and retinyl ester)
 Retinol is the most common form in nature
 It is a fat-soluble vitamin found primarily in animal products such as liver and
fish oils
 Beta carotene is the precursor of vitamin A
 Maize containing more amount of beta carotene. Wheat based diets are assumed
to have no background vitamin A activity

KEY FUNCTION AND DEFICIENCY SYMPTOMS

VITAMIN- A

Key function

 Vitamin A is concerned with the maintenance of epithelial structure and function

Deficiency symptoms

 Epithelial/mucous membrane metaplasia, with secondary infection, particularly

of respiratory and intestinal tracts; the kidneys are affected, with impacted
ureters (nutritional nephropathy) and visceral urate deposition
 Reduce production and hatchability, production ceasing before hatchability is
severely affected
 Reduce appetite and growth, rough plumage
 Corneal hyperkeratosis, central and peripheral nerve lesions and hyperkeratosis
of mucous membranes of mouth and esophagus, which is the usual
pathognomonic sign

Hyperkeratosis of mucous membranes of mouth and esophagus is the

pathognomonic sign

VITAMIN- D

 The term vitamin D covers two main forms

o Ergocalciferol (Vitamin D2), which is poorly utilized by poultry
 o Cholecalciferol (Vitamin D3), Vitamin D3, is a fat-soluble vitamin and is
only found at any appreciable level in very specific tissues such as fish liver
oils
 Common feed ingredients contain little or no vitamin D and the required
supplement should be incorporated as cholecalciferol (Vitamin D3)

KEY FUNCTIONS

 Vitamin D, as the renal metabolite 1,25-dihydroxycholecalciferol (following initial

hydroxylation in the liver to the 25-hydroxy product), has the main function of
o Inducing the synthesis of calcium-binding proteins
o Controlling intestinal absorption
o Blood translation of calcium

DEFICIENCY SYMPTOMS

 Rachitic deformities in the legs - producing painful, hard joint swelling

 The bones, beak and claws become soft and pliable
 Growth is retarded and feather development is poor
 In the laying bird
o Moderate deficiency:
 causes osteomalacia, giving rise to brittle bones of reduced density
and cortical strength (osteoporosis) - such bones are light, porous and
fragile.
 As the deficiency progresses, eggshells become thinner, before soft
shells occur and then production falls.
 Hatchability also suffers and embryonic abnormalities are seen.
o Severe deficiency:
 Egg production stops rapidly, thereby sparing the hen from the effects
of calcium deficiency.
 Vitamin E
GENERAL INFORMATION

 The term vitamin E covers a range of tocopherols and tocotrienols that all have
vitamin E activity
o The key form for poultry is the a -tocopherol
o Sources: Cereal germs, most oilseeds and leafy plants
o Vitamin E may be described as a naturally occurring antioxidant

KEY FUNCTIONS

 Inter and intracellular antioxidant, preventing oxidation of unsaturated lipids

within cells; deficiency allows abnormal formation or accumulation of excessive
lipid hydroperoxides, with resulting cell tissue damage.
 There are a range of other functions
o Regulation of the pituitary-midbrain system (thus influencing thyroid and
adrenal hormone output)
o Nucleic acid metabolism
o Involvement in fertility
o Prevention of degenerative change in muscle and liver

DEFICIENCY SYMPTOMS

 As a fat-soluble intracellular antioxidant, a primary function of tocopherol is a

protective effect on cell membranes; hence, deficiency results in damage to blood
vessels and changes in capillary permeability
 Deficiency in breeders may give rise to early embryonic mortality associated with
vascular lesions( Usually around day 4 of incubation)
 In young growing birds deficiency conditions include
o Encephalomalacia
o Exudative diathesis
o Nutritional muscular dystrophy

ENCEPHLOMALACIA (CRAZY CHICK DISEASE)

 Encephalomalacia is seen in birds (Usually in good condition) up to the age of 5

weeks or so (Commonly weeks 2 and 3)
 Clinical signs - Muscular weakness, progressive ataxia with frequent falling,
spasmodic violent incoordination, head retraction and/or torticollis, paralysis
and death.
 Vascular lesions give rise to oedema and petechial haemorrhages in the
cerebellum, with ensuring neurone degeneration.
 Such gross lesions, seen in fresh brains in association with appropriate clinical
signs and history are virtually pathognomonic.
 On gross examination it may necessary to examine numerous birds for typical
‘diagnostic’ cerebellar lesions to be found.
 The condition is prevented by adequate vitamin E; selenium is said to have some
prophylactic effect. The usual treatment is vitamin E given via drinking water.

EXUDATIVE DIATHESIS

 Capillary wall lesions lead to increased vascular permeability, with resulting

blood and plasma leakage; this accumulates subcutaneously, particularly over the
breast and under the wings, also intramuscularly and in the pericardial sac.
 The condition is prevented by and responsive to vitamin E and selenium.
 The usual treatment is vitamin E via drinking water.

NUTRITIONAL MUSCULAR DYSTROPHY

 Nutritional muscular dystrophy frequently occurs with exudative diathesis and
tends to occur when vitamin E deficiency is accomplished by deficiency of
sulphur-containing amino acids (methionine and cysteine) in chicks, turkey
poults and duckling.
 Microthrombosis of arterioles and smaller capabilities cause occlusion, which
gives rise to degeneration and necrosis of muscle fibres, seen as pale streaks
mainly in breast and thigh muscles (hence the reference to white muscle
diseases).
 Prevention and treatment are by vitamin E supply, as previously described.

 Vitamin K

GENERAL INFORMATION

 The antihaemorrhagic vitamin K occurs in a number of forms as derivatives of

naphthoquinone.
 The most important, vitamin K1, is present in green plants, fruits and liver oils
 Vitamin K2 is present in animal and microbial materials
 The essential structure in all vitamin K analogues is menadione (known also as
vitamin K3), which has vitamin K activity
 Vitamin K3 is qualitatively different in that it is not an antagonist of the
anticoagulant drugs (e.g. dicoumarol, warfarin) and is water-soluble, whereas
vitamin K1 and K2 are fat-soluble

KEY FUNCTION

 Vitamin K is indispensable for blood coagulation, and participates in

prothrombin formation.
 It is also plays a role in calcium metabolism.
 Vitamin-K- dependent proteins are found in bones shell gland and eggshell.

DEFICIENCY SYMPTOMS

 Microbial synthesis occurs is the caecum and large intestine and as result
deficiency is very rare, especially in adult birds, although the supply of vitamin
derived from microbial synthesis is thought only to be of benefit if faeces are
consumed.
 Chicks can exhibit delayed blood clotting as a result of deficiency
 Oral administration of antibacterial drugs such as sulfaquinoxaline and some
other sulpha drugs are stated to be antagonistic to vitamin K activity
  Water soluble vitamins
 Vitamin B1

GENERAL INFORMATION

 The name is derived from the thiazole and pyrimidine rings in the structure.
 The synonym ‘aneurin’ relates to antineuritic properties, reflecting its important
function in carbohydrate metabolism (via several enzyme symtems).
 Vitamin B1is present in almost all living tissues, plant and animal. Brewer’s yeast
and cereal germs are good sources.
 Synthetically produced B1 is usually in the form of thiamine hydrochloride or
mononitrate.

DEFICIENCY SYMPTOMS

 Deficiency signs in poultry are not seen in the field, though theoretically it is
possible that the condition could occur in the presence of thiamine-splitting
enzymes (thiaminases) in feed ingredients such ad fishmeal.
 A deficiency will impair carbohydrate metabolism due to the role that thiamine
plays as a cofactor and therefore a reduction in energy availability will arise,
thereby affecting performance.
 A number of factors will influence the thiamine status of birds
o High temperatures increase requirement and it has been shown that the
level required to prevent polyneuritis is three times higher at 32 ˚ C than at
21˚ C
o The anticoccidial amprolium blocks thiamine while coccidia are
competitors for thiamine.
 In experimentally induced deficiency the signs are
o Deramatis
o Loss of appetite
o Growth weakness
o Polyneuritis
o Opisthotonus
o Paralysis
 Vitamin B2 (Riboflavin)

INTRODUCTION AND KEY FUNCTION

 Historically known by various names, such as lactoflavin and ovoflavin

 Milk and yeast products are good sources of vitamin B2

Key function

 Present in virtually all living cells, vitamin B2 derivatives function in several

enzyme systems as coenzymes that unite with specific protein elements to form
 flavoprotein enzymes, involved in
o Oxidation reduction
o Dehydrogenation
o Metabolism of carbohydrate, amino acid and fat and the regulation of
cellular metabolism. Hence, the vitamin is essential for growth and health.

DEFICIENCY SYMPTOMS

 In general terms, a lowered vitamin B2supply will lead to

o Reduced growth rate
o Non-specific conditions, such as
 Dermatitis
 Nervous disorders
 Reduced egg production occurs in severe deficiency but with marginally low
deficiency there is greatly reduced hatchability, with embtyonic death peaks in
mid and late incubation (dead-in-shell).
 Hatched chicks may be dwarfed and oedematous, show clubbed down, poor
feathering and leg paralysis and with similar degenerative changes in nerve
trunks to those found in older chicks with curled toe.

Curled toe paralysis

 Curled-toe paralysis may be seen in chicks around 10-14 days of age. Birds may
be unable to rise from their hocks, and the legs are outstretched with flaccid
paralysis and in-curling of the toes.
 The bird's head, wings and tail feathers droop, growth is retarded, birds are
recumbent, emaciated, and die.
 The sciatic and brachial nerves are swollen and discoloured, histologically
showing Schwann cell proliferation.
 They show degenerative changes in the myelin sheath and swelling and
fragmentation of the axis cylinder.
 Clubbed down in produced by a failure of the feathers to rupture their sheaths,
producing a club shape.

 Vitamin B6 (Pyridoxine)

GENERAL INFORMATION AND FUNCTION

 There are three compounds that have vitamin B6 activity

o Pyridoxine
o Pyridoxal
o Pyridoxamine
 Each of these has similar biological activity, although pyridoxine is the most
stable form.
 Sources: Red meat and tissue, egg yolk, yeast and cereals.
Key functions

 Vitamin B6 is involved in amino acid metabolism via numerous enzymes

DEFICIENCY SYMPTOMS

 Reduced appetite, growth and production

 Deficient skin and plumage
 Anaemia
 Demyelination
 Weakness
 Paresis
 Chondrodysrtophy

 Pantothenic acid
INTRODUCTION

 Pantothenic acid has been referred to as vitamin B5 (USA) and also as the chick
antidermatitis factor.
 Pantothenic acid is an unstable hygroscopic oil and is widely distributed in plant
and animal tissues.

KEY FUNCTIONS AND DEFICIENCY SYMPTOMS

Key functions

 Pantothenic acid is an essential part of coenzyme A(CoA), a vital element of

energy and fatty acid metabolism, the citric cycle, antibody formation and neural
function (via acetylcholine) and a precursor of cholesterol and thus of steroid
hormones.

Deficiency symptoms

 As with most B group vitamins, deficiency leads to loss of appetite and reduced
growth.
 Severe deficiency leads to dermatitis, with inflammatory changes in the corners
of the beak and the eyelids, vent and feet, depigmentation, and roughening and
loss of feathers.
 Deficiency in breeder feed leads to lowered egg production and impaired
hatchability, with embryo death peaks in early, mid or late incubation, depending
on the extent of deficiency.
 Embryos are oedematous and haemorrhagic, those which hatch being stunted
and weak. Poultry do not benefit from its bacterial synthesis in the intestine.
  Copper is the only common feed microingredient to antagonize pantothenic acid
activity, affecting the rate of production or function of CoA.

 Niacin
GENERAL INFORMATION AND KEY FUNCTION

General information

 Niacin (sometimes called vitamin B6) comprises nicotinic acid and nicotinamide,
both derived from pyridine
 Appreciable quantities of this vitamin occur in cereals but are in a bound form
and poor utilized
 Niacin can be synthesized by microbial action in the caecum and large intestines
but, as there is little absorption beyond this level, this is of limited value.
 In avian tissues a certain amount is synthesized from tryptophan
 Vitamins B1 and B2, pantothenic acid, folic acid and vitamin B12 have a sparing
and synergistic action on niacin.

Key function

 Niacin in its nicotinamide form is a critical part of the coenzymes involved n the
metabolism of proteins, fats and carbohydrates.

DEFICIENCY SYMPTOMS

 Loss of appetite
 Poor growth
 Skin and feather disorders
 Inflammation of mucous membranes of alimentary tract and nervous
degeneration (i.e a variety of non-specific abnormalities)
 In young growing birds, niacin is one of the primary nutritional deficiencies
(along with manganese, Zinc, choline, biotin, folic acid and pyridoxine) that can
cause chondrodystrophy.
 This is generalized disorder of the epiphyseal growth plates of long bones that
impairs linear growth but allows normal appositional growth and mineralization.
 This gives rise to bowing of the rapidly growing long bones with shortened
tibiotarsal bones, enlarged hocks,and slipped gastrocnemius tendon in severe
cases.
 There are characteristic changes in the growth plates.
 Biotin
INTRODUCTION

 Sometimes called vitamin H, biotin has a double ring structure with a number of
isomers.
 The D isomer is the biologically active form.
 Most feed components contain biotin but much is organically bound and
biologically unavailable. Such availability of biotin to poultry varies very widely
between raw material feed ingredients; for example, from maize it is 100%, from
wheat, 5%. The biotin molecule is sensitive to heat.

KEY FUNCTION

 In general, biotin is essential for growth, food utilization, epidermal tissue

maintenance, bone development and reproduction.
 It is a cofactor for various carboxylation enzymes, two of the most important
being pyruvate carboxylase (gluconeogenesis ) and acetyl CoA carboxylase
(lipogenesis), i.e. biotin is essential in carbohydrate and lipid metabolism, as well
as in protein synthesis, where, via effects on RNA formation, it is particularly
important in the control of scleroproteins ( hard proteins such as keratin).

DEFICIENCY SYMPTOMS

 In poultry, biotin deficiency leads clinically to reduced growth, epidermal and

sometimes bone lesions and, at the biochemical level, reduced biotin-dependent
enzyme activity.
 The complete biochemical role is not fully understood.
 In growing chickens and turkeys the first of biotin deficiency occur in epidermal
tissues.
 There is impaired feathering , periocular dermatitis, encrustations and fissures in
the angles of the beak and eyelids and on the foot pads and toes.
 Severe deficiency leads to growth depression, dry, sometimes villous, encrusted,
fissured, haemorrhagic skin on the feet, bone abnormality (chondrodystrophy),
leading to shortened, bowed legs with enlarged hocks.

BIOTIN BINDERS

 Antagonists or interfering substances (biotin binders), including avidin (from egg

albumen), streptavidin (from streptomycin moulds), peroxidizing fats and
mycotoxins (notably aflatoxin).
 The occurrence and age incidence of this condition in the young bird, due to
biotin deficiency, may be influenced by the biotin level in the egg (which in turn is
influenced by the dietary status of the hen), high levels having an ameliorating
effect.
 FATTY LIVER KIDNEY SYNDROME

 It is a metabolic disorder causing death of young broilers (and sometimes layer

pullets) commonly 10 -30 days of age.
 FLKS is a condition that is described as biotin responsive, rather than one of
uncomplicated biotin deficiency.
 It is usually associated with diets deficiency, as previously described.
 The syndrome is triggered by environmental factors rather than by nutrition.
 FLKS arises from a failures of hepatic gluconeogenesis (i.e. the metabolic
synthesis of glucose) and results in extensive fatty infiltration of body tissues,
with enlarged liver, kidneys and heart but with no inflammatory or degenerative
changes.
 Decreased hepatic gluconeogenesis caused by decreased pyruvate carboxylase
activity leads to severe hypoglycaemia.
 Biotin is a cofactor for both pyruvate carboxylase (gluconeogenesis) and acetyl
CoA carboxylase (lipogenesis).
 The amount of biotin required for prevention of FLKS may be greater than that
required for maximum growth rate.
 The condition can involve an interaction of nutritional, environmental, stress and
maternal factors, which may act in the following way:
o Biotin: the single most important nutritional factor
o Fat and protein: high levels offer protection by depressing the need for
lipogenesis (acetyl CoA carboxylase, which more readily sequesters biotin
than pyruvate carboxylase); decreased lipogenesis means more biotin
available for pyruvate carboxylase.
o Other vitamins: elevated levels increase the incidence of FLKS
o Pelleted feed: more rapid growth occurs than with mash feed
o Floor rearing: faecal biotin is available; not so on wire floors(e.g, in cages)
o Starvation and stress: deplete glycogen (glucose) reserve
o Age and biotin status of parent: eggs from older hens have more biotin
o Other diseases: cause stress and/or depress intestinal absorption.
 Clinical sings are of sudden onset, with well-grown birds becoming lethargic,
aphagic and recumbent. Mortality may range from below 5% up to 30%.
 Post-mortem findings are enlarged, pale, fat-infiltrated liver and kidneys, pink
adipose tissue (due to blood content) in the crop and intestinal tract.
 The pallor of the liver and kidneys results from the presence of excessive amounts
of fat (two or five times normal).

FOLIC ACID (FOLACIN)

 It is also a member of vitamin B group, and is particularly abundant in green

leaves, fresh vegetables, and fruits.
 Chemically, it is a complicated compound.
 Several related compounds with similar activity in amino acid metabolism are
grouped under this heading.
  Folic acid is necessary for growth, muscle formation, blood formation, and
feather growth. Diets are rarely low in this vitamin.

Functions

 Folic acid is a part of the enzyme system involved in single carbon metabolism.
 It is involved in the synthesis of methyl groups (CH3) of such important
metabolites as choline, methionine, and thymine.
 Folic acid is therefore required for cell mitosis.

CHOLINE

 Choline is sometimes referred to as vitamin B4 or B7, and is at times classed as a

necessary food substance rather than as a vitamin.
 It forms a part of the actual cell structure (in lecithin) and is therefore required in
considerably greater quantities than vitamins.
 The chick's requirement for choline is high.

Functions

 The primary role of choline is as a component of lecithin and other lipids.

Lecithin is a main component of cell structure.
 As such, choline is needed fot the structure of cell membranes.
 In tissues, choline forms the important neurotransmitter acetylcholine.
 Acetylcholine plays an important role in the transmission of nerve impulses in
the body. It also acts as a methyl donor.
 Choline has essential roles in fat metabolism. In liver, for transformation of
neutral fat to phospholipids, choline is needed.
 In choline deficiency, this transformation is interfered with and results in
accumulation of neutral fat in the hepatic cell (fatty change).
 Choline is therefore called a 'lipotropic factor' or 'lipotrope', because it promotes
mobilization of lipids out of the liver.
 Fatty livers in newborn pigs and calves that have been deprived of colostrum may
be due to choline deficiency.
 The choline requirements of these young animals are very high, and colostrum is
an excellent dietary source of choline.

DEFICIENT STATES

Poultry

 In chicks, apart from poor growth, the most important symptom of choline
deficiency is chondrodystrophy, a bone disorder, earlier known as 'perosis'.
 In egg-laying hens, choline deficiency causes fatty liver.
 In livers of chickens, fat content is higher in females than males.
 VITAMIN B12 (COBALAMIN)

 Vitamin B12 has the most complex structure of all the vitamins.
 It is abundant in all animal foods, including eggs, dairy products, but plants and
vegetables contain very little.
 Ruminants do not require dietary source because it is synthesized by bacteria
growing in the rumen.
 These bacteria require cobalt to produce vitamin B12.
 Lack of cobalt in the diet leads to vitamin B12 deficiency.
 However, the deficiency is important only in poultry.
 Functions: Vitamin B12 is involved in the metabolism of protein, carbohydrate,
and fat.
 In this action, it is closely associated with folic acid.
 Vitamin B12 is also involved in nucleic acid and methyl group synthesis, along
with folic acid.

DEFICIENCY STATES

 In poultry, the deficiency is associated with slow growth, decreased efficiency of

feed utilization, mortality, and reduced egg size and hatchability.
 Chondrodystrophy may occur in chicks when their diets lack choline and
methionine as source of methyl groups.
 In laying birds, hatchability may drop to zero in about 6 weeks.
 Vitamin B12-deficient embryos have maximum mortality on the 7th day of
incubation.

VITAMIN C

 Vitamin C is abundant in green leafy plants, green vegetables, and fresh fruits.
Citrus fruits contain the greatest amount of vitamin C.
 It is also present in milk and some animal products (liver, fish). Most animals
and buds synthesize sufficient amounts of vitamin C from glucose, because they
possess the required enzyme gluconolactone oxidase.
 Humans, monkeys, and guinea pigs lack this enzyme and therefore cannot
synthesize this vitamin.
 In mammals, ascorbic acid issynthesized in the liver, but in the chicken, it is
synthesized in the kidneys.
 Because domestic' animals consume an abundance of green feed, and since they
and poultry are capable of synthesizing vitamin C, a deficiency is seldom
observed.
Functions

 Ascorbic acid functions in a variety of biosynthetic pathways by accelerating

hydroxylation and amidation reactions.
 The most clearly established function of vitamin C is the activation of prolyland
Iysyl hydroxylases from inactive precursors, which in turn, bring
abouthydroxylation of the amino acids proline and lysine, respectively (see
tissuerepair (healing); Chapter 5). Collagen has the highest content
ofhydroxyproline in the body.
 Hydroxylation of proline and lysine impartsstructural stability and tensile
strength to collagen. Procollagen having unhydroxylated proline is unstable.
 Vitamin C also has antioxidant properties.Vitamin C can scavenge free radicals
directly in aqueous phases of the cell andcan act indirectly by regenerating the
antioxidant form of vitamin E. Thus,vitamin E and C act together.

DEFICIENCY STATES

 Deficiencies are important in humans, monkeys, and guinea pigs.

 In animals and birds, deficiency is seldom observed.
 However, even the high rate of synthesis of vitamin C in the chicken may be
inadequate during periods of severe stress of heat and physical trauma and in
infections.
 Also, there are no stores of vitamin C that are able toprotect chicken against
prolonged dietary deficiency.
 Moreover, in the chicken,vitamin C is not transported to the egg, but it is
synthesized by the young embryo.
 CHAPTER-15: MINERAL DEFICIENCES AND OTHER NUTRITIONAL
DISORDERS - INTRODUCTION

INTRODUCTION

 About 99% of body calcium and 80% of the phosphorus are present in the
skeleton, mainly as calcium hydroxyphosphate, which not only gives bones their
mechanical strength but also acts as a mineral reserve.
 Calcium carbonate is the major constituent of eggshells.
 Calcium and phosphate have important functions as electrolytes in body fluids,
calcium ions activating several hydrolytic enzymes and acting in nerve cell
excitation, neuromuscular transmission, muscular contraction and blood
clotting.
 Phosphate is a component of nucleic acids, phospholipids and certain protein and
coenzymes, as well as part of acids, phospholipids and certain and coenzymes, as
well as part of acids, phospholipids and certain proteins and coenzymes, as well
as part of acid-base balance and other biocgemical process, such as metabolic
energy transfer, protein synthesis and carbohydrate metabolism. Except for
animal products (e.g. meat and/or bonemeal and fishmeal), the raw material
 ingredients of poultry feeds are low in calcium; hence, supplementation (e.g. with
limestone) is included.
 Phosphate is mainly present in cereals and other plant products, largely as
phytate (i.e. Bound by phytic acid) and is poorly utilized. Phytate will also bind
other minerals strongly, making them unavailable.
 Phosphorus in animal byproducts is almost completely available but plant
phosphorus has a low biological availability for poultry, with only a minor part of
the total phosphorus present being inorganic and thus fully available to birds.
The majority, some 60-70%, is in the phytate form.
 There is a lack of phytase in the avian intestine, especially in young chicks, but
phytase is present in some grains. For these reasons, poultry feeds require
supplementation with phosphate, although the use of supplementary phytase
enzyme is becoming widespread in layer, broiler and turkey rations.
 The calcium and phosphorus should be in the ratio of 1.8 – 2.0: 1. A minimum 1%
calcium and 0.45% available phosphorus may now be expected for the starter
period.

 CALCIUM

DEFICIENCY SYMPTOMS

 Young growing birds suffer from rickets or osteomalacia leading to osteoporosis

in adult or laying birds
 Thin or soft-shelled eggs – Early sign of calcium deficiency in laying hens
 Cage layer fatigue is seen in caged hens that are producing well, in fair bodily
condition, and suddenly become recumbent (sometimes paralysed) with legs
extended.
 The bones are brittle, with thin cortices; ribs and sternum frequently deformed
and skeletal fractures are common. Spinal compression is the cause

 Sodium chloride
DEFICIENCY SYMPTOMS

 Deprivation of sodium in laying hens causes an,

o Abrupt fall in egg production
o Greatly increased bird activity with much increased pecking behavior and
cannibalism, especially at the everted cloaca of other birds ovipositing.
o In free-range and barn-laying flocks, where pecking can be more of a
problem, it is standard practice to use 0.18-0.20% sodium in the ration
while for caged birds 0.14% is adequate.

SALT POISONING

 Clinical signs of salt posoning include

 o Diarrhea
o Excessive thirst
o Loss of appetite
o Progressive muscular weakness
o Inability to stand
o Convulsions and death
o Ascites may be present
o Severe kidney damage occurs in young birds, with renal failure and death

 Manganese
DEFICIENCY SYPTOMS

 Young growing birds - growth is retarded and there is deformity of bone growth,
i.e. chondrodystrophy.
 Laying or breeding bird - deficiency causes a marked fall in egg production, with
greatly reduced hatchability (e.g. down 50%) in incubated eggs.
 Embryos frequently die in the last third of incubation, showing gross skeletal and
other defects including chondrodystrophy, micromelia, globular head, parrot
beak, odema of the cervicothoracic region and retarded down, feather and body
growth.
 Newly hatched chicks - Ataxia, titanic spasms and head retraction.

 Zinc
DEFICIENCY SYMPTOMS

 Poor growth and appetite

 Poor feathering and feather fraying,
 Scaly skin, especially on the legs and feet
 Young growing birds - the generalized growth plate disorder of chondrodystrophy
described earlier
 Reduced egg production occurs in deficiency and hatchability is impaired
 Embryonic mortality peaks around mid-incubation, with faulty trunk, spine and
limb formation and abnormal beak, head, brain and eye development,
presumably caused by zinc-dependant metabolic process involved in the
development of skeletal mesoderm.

 Selenium
DEFICIENCY SYMPTOMS

 Lack of dietary selenium limits production and function of GSH –Px, leading to
lipid hydroperoxide production in oxygen-laden cells with subsequent cell wall
 damage, the clinical effects including myopathy, microangiopathy and capillary
fragility
 In poultry, the well-recognized clinical conditions arising from these defects
include nutritional muscular dystrophy, exudative diathesis and
encephalomalacia.
 Exudative diathesis is known to respond clinically to selenium supplementation
in the presence of adequate vitamin E.

Fatty Liver - Haemorrhagic syndrome

 This is a metabolic disorder characterized by a very fatty liver, accompanied by
haemorrhages.
 The condition is sometimes seen in older laying hens kept in cages, particularly in
hot weather.
 There is usually a fall in egg production in the affected flock.
 Death occurs occasionally and is due to massive liver haemorrhages.

PATHOGENESIS

 There are important basic differences in carbohydrate and fat metabolism

between birds and mammals. Birds have several times (3-4 times) higher blood
glucose levels than mammals.
 Mammalian embryos obtain glucose through the placental circulation, whereas
the chicken embryo develops on yolk nutrients, the energy source being almost
all fat, not carbohydrate.
 The chicken embryo therefore has high levels of gluconeogenic enzymes, that is,
enzymes that form glucose from substances other than carbohydrates, such as
proteins and fats.
 These enzymes decrease after hatching as carbohydrate intake becomes available.
 Moreover, in contrast to mammals, where lipogenesis (fat formation) is mostly in
adipose tissue, in birds, it almost all occurs in the liver.
 Fat formation increases in the first week or two after hatching from almost zero
in the embryo (due to high yolk fat content) to much higher levels.
 As chickens reach sexual maturity and start laying, there is a further great
increase in liver lipogenesis.
 The laying hens then attain high blood lipid levels to supply the developing ova,
and the storage of fat in the liver enormously increases at this time.
 It is this lipogenic function of liver in the birds that forms basis for the occurrence
of conditions that involve excessive accumulation of fat in the liver, for example,
fatty liver and kidney syndrome (FLKS) in young broiler birds and fatty liver-
haemorrhagic syndrome (FLHS) in older laying hens.
 PATHOLOGY

 Macroscopically, FLHS is characterized by pronounced fatty liver accompanied

by haemorrhages.
 It occurs sporadically in older caged hens of heavier breeds in hot weather.
 There is usually a drop in egg production. The fat content of liver is usually
greater than 40% dry weight and may reach 70%.
 Death only occasionally occurs and is due to massive liver haemorrhage.
 The kidneys are pale and swollen, and the abdomen contains large accumulation
of fat.
 The exact cause of FLHS is not known, but contributory factors include high
carbohydrate and low-fat feed leading to fattiness; lack of exercise, for example,
in caged birds; stress, toxins, high egg production, high oestrogen, low thyroid
blood hormone levels; and strain of bird.
 Microscopically, hepatocytes are greatly distended with fat globules, which
eventually rupture cell membranes.
 There is also secondary inflammation, necrosis, and regenera tion.

FATTY LIVER AND KIDNEY SYNDROME

 Fatty liver and kidney syndrome (FLKS) is a metabolic disorder causing death of
young broilers, and sometimes growers (pullets) between 10-30 days of age.
 It is usually associated with diets that have marginal levels of biotin.

PATHOGENESIS

 FLKS arises from a failure of hepatic gluconeogenesis (metabolic synthesis of

glucose from fat) and results in extensive fatty infiltration of body tissues with
enlarged liver, kidneys, and heart, but not inflammatory or degenerative changes
 Decreased hepatic gluconeogenesis is caused by decreased pyruvate carboxylase
activity, and this leads to severe hypoglycaemia.
 Biotin is a cofactor for both pyruvate carboxylase (gluconeogenesis) and acetyl
CoA carboxylase (lipogenesis).
 High-fat feed decreases the need for lipogenesis (and, therefore, for biotin by
acetyl CoA carboxylase), so that biotin is available for pyruvate carboxylase and
gluconeogenesis.
 However, on low-fat feed, there is insufficient biotin for both the enzymes, but
acetyl CoA carboxylase has a greater access to biotin than pyruvate carboxylase.
 This means that fat formation (lipogenesis) will continue, but glucose formation
(gluconeogenesis) will suffer.
 Therefore, if normal fat intake is interrupted for even a short period of time,
hypoglycaemia develops, and may become serious due to low glycogen reserves of
the young chick.
 In response to the low blood glucose level, there is mobilization of free fatty acids
into the liver, from body tissues, for fat formation.
 The purpose being that fat so formed can be utilized to produce glucose to correct
the low blood level.
 However, as pyruvate carboxylase is a biotincontaining enzyme, its activity is
decreased in biotin deficiency.
 Biotin deficiency therefore prevents conversion of fat into glucose. This leads to
increased conversion of pyruvate to fatty acids.
 The net result is marked accumulation of fat in the liver.

CLINICAL SIGNS

 They are sudden in onset. Well-grown birds become dull and depressed, lose
appetite, lie down, and may die. Mortality may range between 5-30%.
 Postmortem findings include enlarged, pale, fat-rich liver and kidneys, and pink
adipose tissue due to congestion of blood vessels.
 Crop and intestine usually contain blackish fluid due to blood content.
 The paleness of the liver and kidneys is due to the presence of excessive amount
of fat (two to four times the normal). This is mostly triglycerides (neutral fat).

 CHAPTER-16: PATHOLOGY OF VICES AND MISCELLANEOUS

CONDITIONS

INTRODUCTION

 Cannibalism is a problem that is associated with large poultry flocks where the
birds kept in close confinement peck at associated birds.
 This can result in significant mortality within the flock when a wound is
generated and it will also cause a decrease in egg production as the hen pecked
birds become stressed.
 This is a vice which is usually precipitated by some aspect of management or
environment which the birds are subjected to
 Under the intensive management conditions , this condition can occur in all ages
of birds and in many species.
 It has been determined, however that the light breeds, such as the leghorns, are
more susceptible than the heavier breeds.
 These lighter breeds are characterized by their flighty nature and are
hypersensitive to environmental factors.

COMMON FORMS OF CANNIBOLISM

 The following are common forms of cannibalism seen in commercial poultry

operations.
Vent-picking

 Picking of the vent or region of the abdomen several inches below the vent is the
most severe form of cannibalism.
 This is generally more common in high-production or overweight pullet flocks.
 Predisposing factors are prolapse or tearing of the tissues by passage of an
abnormally large egg.
 Vent picking can result in anaemia.

Feather-pulling

 Frequently seen in flocks kept in close confinement resulting in lack of sufficient

exercise.
 Nutritional deficiencies may contribute to the problem.

Toe-picking
 Most commonly seen in young birds.
 Inadequate feeder space or inability of the chick to find the feed will lead to toe-
picking.

Head picking

 Follows injuries to the comb or wattles.

CAUSES OF CANNIBOLISM

 The problem may simply arise because of the normal pecking behavior of this
type of animal when searching for food or exploring an environment.
 The birds are kept in barren, crowded conditions and may have little else to peck
besides their pen mates.
 Once one hen has picked up this technique other hens, observing the behavior,
will learn from the initial pecker and a serious episode will develop.
 A lack or a deficiency of nutrients in a poultry ration may result in the birds
becoming irritated which can subsequently lead to cannibalism in the flock.
 Usually when diet formulation is involved in the outbreak the imbalance is in the
protein or the sodium level of the ration.
 Deficiencies can also be caused by insufficient feeding and water space.
 An abrupt change in the palatability or form of a flock's ration may also be a
contributing factor in the onset of cannibalism as the birds might impulsively
seek alternative sources of food.
  Poor ventilation, high temperature, low humidity , excessive population density,
and excess illumination are all factors in the flock's environment that may
precipitate an outbreak of this vice, especially with the lighter breeds.
 During egg laying the cloaca may become damaged and distended especially with
the passage of large eggs and this protrusion of the vent may be an attractant to
other birds due to its stark color difference against the white body.

PREVENTION OF CANNIBOLISM

 The onset of this vice can be prevented by paying particular attention to the
dietary factors (protein, sodium, and palatability), the environmental factors
(ventilation, temperature, humidity, population density, and lighting) and the
feeding and water space that is available for each bird.
 With highly intensive operations the light intensity should be reduced, perhaps
by changing to a light which is of a red hue.
 The most common and cost effective mode of prevention is the use of beak
trimming.
 Beak trimming is usually done at 4-6 weeks of age and the procedure requires
that two thirds of the upper mandible be removed.
 This procedure will not eliminate the abnormal behavior entirely but the birds
are less able to inflict damage.
 Other control methods include increasing feed availability, reducing group size,
adding litter, and providing distractants such as straw bales.
 Best method of control is to prevent it from starting at all, since once it has begun
it will be very difficult to stop.

 Feather picking

INTRODUCTION

 Feather picking is excessive self grooming, that includes picking at, plucking out,
or chewing on feathers.
 Preening is the behavior of birds in which they groom their feathers and skin free
from dirt or foreign particles and correct any feather distortions.
 In a severe case, the bird can be naked form the head down.
 Indicators of feather picking include feather loss, and / or mutilated feathers in
body areas accessible to a bird’s beak (including the wing skin fold, inner thighs,
and breast).
 Factors that can predispose a flock to feather pecking include.
o High levels of activity - these may be caused by environmental factors such
as high light levels or frequent disturbance and by genetic factors (eg. some
egg lines may be more active that some meat lines) among others.
o High stocking density - leads to frequent disturbance and bird to bird
interaction —> this in turn can lead to feather pecking.

 FEATHER PICKING - CAUSES

 The causes can be divided into strictly medical and non-medical in origin.
 It should be noted that medical causes for feather picking are rare in frequency
than non-medical, or psychological causes.

Medical origin

 Hypothyroidism
o This is a fairly rare occurrence, and signs include thickened dry skin and
excessive feather loss in combination with feather picking.
 Mineral deficiency or inadequate nutritional care
o Excessive feather pecking may be a consequence of a nutritional deficiency.

Non-medical origin

 Bird’s environment (Unsatisfactory housing)

o If the bird’s environmental needs are not met, boredom or stress can lead to
feather picking and mutilation.
o Also, if the cage size is inadequate (i.e. too small), feathers can be damaged
and this may result in forming a habit of feather picking
 Wing trimming
o Improper wing trimming can lead to damaged feather follicles, especially if
dull scissors are used and the ends of the feathers are left ragged or torn.
o When feathers are left like this, it can cause the bird discomfort and
aggravate feather picking.

SELF - MUTILATION

 Associated with feather picking

 Essentially, self-mutilation involves a bird chewing on its own flesh , often in the
breast area
 Unfortunately, as the area of mutilation becomes lacerated, nerve and tissue
damage can result, causing increased discomfort , and hence the bird chews on
itself even more
 Although the breast area is the most commonly seen area affected by self-
mutilation, some birds have been known to consume one or more of their own
toes
 Because self-mutilation leaves a chronically open wound on the bird, secondary
infections are also seen
 Self-mutilation can also be a formed habit when a bird has suffered some injury
to itself
 If for example, a severe wing clip causes a parrot to drop roughly to the floor,
wingtips or chests can be injured, and parrots especially seem naturally prone to
picking at the injury
 Aggression and biting are not uncommon and can often result in injuries leading
to self-mutilation as well

TREATMENT - FEATHER PICKING / SELF-MUTILATION

 There are four main methods by which feather picking and/or self-mutilation can
be treated
o Making changes to the bird’s environment by increasing cage size
o A physical barrier is required. i.e . Provision of Elizabethan collar while the
bird’s feathers grow out, or the wounds from mutilation heal
o Drug treatment
 Behavior modifying psychoactive drugs have been reported as an
effective treatment
 Clomipramine (an anti-depressant), Haloperidol (dopamine
antagonist) have been used with some degree of effectiveness in
reducing or curtailing feather picking and self-mutilation behavior
 The problem with using drugs to treat such behavior, is that the
underlying causes for the feather picking are never addressed , and
the birds are usually required to be on the drugs for the rest of their
lives.
 The proper dosage of the drugs can also be difficult to determine,
involving a trial and error approach.
o Behavioral modification techniques
 For example, feather picking in parrots can often be the result of
separation anxiety
 Keeping a favorite toy or food before the owner leaves
 Distractions such as leaving a radio or TV on for the bird may be
helpful. Birds often do respond to videotapes of their owners talking
to them in a normal, playful manner
 Feather picking can also be the result of some upheaval in the life of
either the owner or the bird.
 Companion birds, especially the psittacine species are highly attuned
to the attitudes and moods of their owners.
 Consequently, owners need to be aware of this, and in the event of
such upheavals, possible solutions should be discussed with the
owner.

CANNIBOLOSM - OTHER CONDITIONS

 Nose pecking
 Toe pecking
 Head pecking