Karnataka Veterinary, Animal and Fisheries Sciences

University, Bidar

Identification of poisonous and non

poisonous snakes

Dr. Prashantkumar Waghe

M.V.Sc., Ph.D
Assistant Professor
Veterinary College, Bidar

Department of Veterinary Pharmacology & Toxicology

 Classification of snakes

Poisonous snakes belong to three Families on the basis of

poison secreted :
1. Elapidae: Neurotoxic
2. Viperidae: Vasculotoxic / haemotoxic
3. Hydrophidae : Myotoxic
4. Colubridae
5. Crotalidae
 ELAPINES
Examples:
A. Common Cobra / Nag or Kalsap or Naja naja
B. King Cobra – Raj Nag or Naja hanna or Naja bangarus
C. Krait : Subgrouped into :
a) Common krait or Bangarus caeruleus
b) Banded krait or Bangarus fasciatus
c) Coral snake
d) Tiger snake
e) Mambas
f) Death adder
 Common Cobra / Nag or Kalsap or Naja naja
• Seen through out India,
Burma, Srilanka
• Well marked hood
• Single (monocellate) or
double spectacle mark
Monocellate Cobra
Naja Naja Kaouthia
 COBRA KING COBRA
Very common Very rare
Found in cervices, dark and open places Found in dense forest

Length up to 1.8 m 5.4 m

Hood is large Hood is small

Caudal scales are in pairs
Food - frogs, lizards, birds, snakes and
small mammals – rats and hare
Sometime – their own kid
Caudal scale near the vent are single
Eat only other snakes: Rat snake
Cobras
Malabar pit vipers
Occasionally feeds on monitor lizards
Common krait

Bungarus
Caeruleus
Neurotoxic
Banded krait or Bangarus fasciatus
Coral snake

Tiger snake
Mambas

Death adder
 VIPERINES
They are grouped into:
A) Pitless Vipers/True Viper: They are
a) Russel ‘s Viper
b) Puff Adder

B) Pit Vipers : They are [Crotalidae]

a) Rattle snakes
b) Copper head
Russell’s viper Puff Adder

Haemotoxic
Rattle snakes Copper head
 HYDROPHIDAE

• 20 types of sea snakes found in India.

• All are poisonous.

• They are myotoxic

DIFFERENCES BETWEEN COBRA AND VIPER
TRAITS COBRA VIPER
1. Body Usually long and cylindrical Usually short and stout with narrow neck
2. Head Small, rarely broader than body, Larger and broader than body, usually
usually of same width as that of wider than the neck, covered with small
neck, covered with large scales scales
3.Maxillary Carry other teeth beside the Carry only the poison fangs
bones poison fangs
4. Eye Round pupil Vertical pupil
5. Fangs. Grooved short, fine and fixed Long, movable and strong
6. Eggs Oviparous Viviparous
7. Tail Round Tapering
8.Venom Neurotoxic mainly Haemotoxic usually
 Snake Bite and Snake Venom

 When a snake bites, it may excrete venom but this is

dependent on the type of snake - venomous or non
venomous.

 Snake Venom is a Toxin (Haematotoxin, Neurotoxin, or

Cytotoxin)

 It is a varied form of saliva and excreted through a modified

parotid salivary gland
– Located on each side of the skull, behind the eye
– Produced through a pumping mechanism from a
sac that stores the venom, proceeds through a
channel, down a tubular fang, hollow in the center
to project the venom
Proteins
Composition of snake venom
- Enzymes:
1. Proteolytic enzymes /proteases : digest protein, anticoagulant
2. Hyaluronidases: facilitates venom spread through out the body
3. Phospholipases A, B, C: degrade lipids, Strong haemolytic and mycotoxic agents – cardiotoxicty
4. Phosphodiesterases: lowering the BP
5. ATPases: metabolise the ATP
6. AchE : Hydrolyse the Ach
7. Lipases: Hydrolysis of Lipid
8. Collagenase: digest collagen
9. Ribonuclease: against RNA
10. Deoxyribonuclase : against DNA
11. Ophio-oxidase: helps in autolysis and putrefatcion
12. Thrombin like enzyme: fibrinogen clot formation
13. L -Aminoacid oxidase: it give yellow colour to venom, tiggers some other enzymes
Non Enzymatic Proteins:
 Neurotoxins
 Haemorrhagins - vasculotoxic
 Cardiotoxins
 Myotoxins – muscle necrosis
 Cytolisins – tissue necrosis
 Toxalbumins

Non Protein Toxins

 Peptide- Pyroglutamyl peptide
 Nucleoside-Adenine, Guanine, Inosine
 Lipid - Phospholipid,Cholestrol
 Amine-Histamine,Serotonin,Spermin
 Metal - Cu, Zn, Ni, Mg, Fe, Co
 Difference between poisonous and non-poisonous
snakes
Points Poisonous snakes Non Poisonous

Saliva Contains toxic peptides and enzymes Non-toxic

Ventral (belly) scales Broad and always extends across the entire width Small/ moderately large, never
of the belly extends across the belly
Head scales a) Usually small in vipers Are usually large with exceptions as
b) May be large in pit vipers (A pit between eye and nose) outlined under poisonous snakes
c) Cobras, King Kobras and Coral snakes where
third labial touches the eye and nasal shields
d) Kraits, where there is no pit and the third labial
does not touch the nose and eye

Teeth Two grooved or tubular fangs or poison teeth All teeth are uniform and small in
size and there are no fangs.
4 longitudinal rows of teeth in upper jaw
2 rows in lower jaw.

3. Fangs Hollow like hypodermic needle Short and solid

4. Tail Compressed Not markedly compressed

5. Habits Usually nocturnal Not so

6. Teeth bite marks Two fang marks with or without marks of other Two fang marks with number of
teeth small teeth marks
 Factor affecting snake bite toxicity
Factor Effect

Body weight Bigger the size lesser toxicity

Bite Not all bites by snake result in envenomation, so called dry bites 30-
70% of total bites depending upon the species and condition.
Horse ≥ Cattle ≥ Goats ≥ Dogs ≥ pig ≥ Cats
Part bitten Bite on face and trunk are most lethal

Site Injected directly in blood stream

Individual Sensitivity of individual to venom modified clinical outcome

sensitivity
Bite Type of bite (business or defence), Bite number , depth, duration of
characteristic when snake clinges to body, bite through clothes, amount of venom,
condition of fangs, different species & their lethal dose
 Mechanism of Toxicity of Venom

The most common types of enzymes are proteolytic, phospholipases and

hyaluronidases
– Proteolytic Enzymes: digestive properties

– Phospholipases: degrade lipids

– Hyaluronidases: facilitates venom spread through out the body

 Haemotoxicity:
 Attack circulatory system, muscle tissue causing coagulopathies,

cardiotoxicty and haemolysis

 Bleeding disorders: Venous constituent of snake venom interfere
with activation of clotting factors like fibrinolytic and
finrinogenolytic
 Directly /indirectly activate plasminogen
 Directly act on phospholipids
 Interfere with cascade to activate clotting factor or prothrombin
directly
Cardiotoxins:

Cardiotoxins are components that are specifically toxic

to the heart. They bind to particular sites on the surface
of muscle cells and cause depolarisation ==> the toxin
prevents muscle contraction.
These toxins may cause the heart to beat irregularly or
stop beating, causing death.
Viperines bite:
Local features :
 Rapid swelling and severe local tissue damage at bite site
 Pain – Spreads rapidly – restleness, anxiety, excitement, which is
followed by incardination of movement and lameness.
 Marked Discoloration of tissue – few min.
 Bloody fluid oozes from fang wounds
 Blister formation
 Bleeding from bite site
 Skin become cold, pupils are dilated – poorly respond to light
 Animals does not respond to the external stimuli – Pinching &
Pricking
 Followed by unconsciousness and collapse
 Systemic features:
 Generalized bleeding : Epistaxis, hemoptysis, hemetemesis,
bleeding gums, hematuria, malena, hemaorrhagic areas over
skin and mucosa
 Pulmonary edema, salivation, diarrhea
 Shock
 Renal failure
 Death – Resp. / Circu. failure
Clinical Signs
Elapines: Neurotoxic
Local Features :
 Fang marks
 Burning pain
 Swelling and discoloration
 Serosanguinous discharge
 Local symptoms are milder in comparison to that in Viperine bite.
Neurological Features :
 Muscular weakness – paralysis
 Difficulty in swallowing, viscid saliva and food collect in mouth
 Pharyngeal paralysis result in aspiration pneumonia
 Calves – marked pupillary dilation, excitement, incordination and later
paralysis
 Krait – Severe abdominal pain and convulsion - death
 Summary of Manifestations

Feature Cobras Kraits Russells Saw Hump

Viper Scaled Nosed
Viper Viper
Local Pain/ Tissue Damage YES NO YES YES YES
Ptosis/ Neurological Signs YES YES YES! NO NO
Haemostatic abnormalities NO NO! YES YES YES
Renal Complications NO NO YES NO YES
Response to Neostigmine YES NO? NO? NO NO
Response to ASV YES YES YES YES NO
 PM findings
Two lacerated punctures :
 Fang marks about 1.25 cm deep in elapines
2.50 cm deep in Viperines
 Acute swelling , odema, hemorrhages and hematomas in the
affected area
Necropsy:
 Interstitial nephritis
 Toxic proliferative glomerulitis
 Intracerebral hemorrhages
 Necrosis of liver
 Diagnosis
Two lacerated punctures :
 Fang marks about 1.25 cm deep in elapines
2.50 cm deep in Viperines
 Very difficult long fur/wool
 Immunoassay – HB

Lab Findings:
 Creatine kinase released from degenerated muscle
 Extended clotting time
 Haemoglobinuria
 Myoglobinuria
 Whole Blood Clotting Test for viperine bite
 Urine Examination for Proteinuria, Myoglobinuria,
Haemoglobinuria
 First Aid
DOs-
 Assurance of patient
 Immobilisation
 Application of tourniquet????

DON’TS-
 Incision
 Suction
 Application of ice, massage or any chemical treatment
 General management of snake bite
1. Keep the animal undisturbed
2. To restrict the further absorption and distribution of venom,
apply a tight torniquet above the site of bite
3. Incise the local area of snake bite in the direction of blood
vessel and go for sucktion and infiltrate the area with 5% soap
solution.
4. Inject antivenin, antibiotics and antitoxins.
5. If snake has not been identified, give polyvalent antivenin
intravenously and also infiltrate the antivenin locally around
the site of bite.
6. Polyvalent antisnake venom should be administered
intravenously @ 10-20 ml per animal depending on the
weight of the animal.
7. Give supportive treatment for managing shock and cardio-
pulmonary disturbances by administering corticosteroids.
Precautions/contraindications:
(i) Do not use potassium permanganate.
(ii)Do not give extreme hot or cold treatment at
the site of bite or incision.
 TOADS
• Dog and cat may play with toads and get exposed
orally to the toxins of toad secreted by the glands
in their skin located above and posterior to the
eyes.
• Different toad toxins are bufogenins
(bufodienolides), bufotalin, bufotenidin,
bufotenin, bufoviridin, serotonin &
calecholamines
 Poisonous/toxic species of toads

• Bufo vulgaris (common toad)

• Bufo marinus (marine toad)
• Bufo regularis
• Bufo alvarius (river toad)
 Clinical signs
• Hyper salivation (some times foamy)
• Vomiting and pawing at the mouth
• Cardiac irregularities
• Pulmonary oedema
• Convulsions, prostration and collapse
• B. marinus - death occurs within 15 minutes
• B. regularis - paralysis as well and the
animals generally die within 2-6 days.
 Diagnosis
• History of pet playing with a toad.
• Clinical symptoms.
 Treatment
• No specific treatment
• Wash the mouth with plenty of water
• Give activated charcoal and osmotic purgatives
• Administer atropine sulfate intravenously to check
excessive salivation & bronchoconstriction
• Give antihistaminics, sedatives or tranquilizers
• Administer corticosteroids
• Administer cardioprotective agents
• Give large doses of propranolol (0.2 mg/kg) to control
cardiac arrythmias and myocardial fibrillation
 BEES, SCORPIONS AND WASPS
• Venom of bees, scorpion and wasps is a complex
mixture of peptides.
• Non-enzymatic proteins - apamin, melittin or kinins
• Enzymes such as phospholipase A and B.
hyaluronidase
• Formic acid and biologically active amines -histamine
and 5-HT etc.
• Melittin is protein mainly found in honey bees and is
antigenic in nature and produces allergic reactions
mainly in human beings and horses
• Anaphylaxis and death from a single sting occurs in
hypersensitive animals.
• Only mild to moderate inflammation and painful swelling is
observed.
• Following single insect bite, there is extreme serous exudation.
• Multiple bee or wasp stings - severe local inflammation and
oedema at the site of sting, intense pain and pronounced
excitement.
• In severe cases in horses - diarrhea, methaemoglobinemia,
bilirubinemia, jaundice, haemoglobinuria, tachycardia,
dyspnoea and followed by death, though in rare cases.
 Treatment
• No specific antidote is available.
• Only symptomatic treatment need to given
• Local application of weak solution of ammonia
and sodium bicarbonate
• Nervine tonics and stimulants, if there is
prostration.
• Tracheotomy, if asphyxia is severe.
• Emergency supportive therapy for restoration of
cardiopulmonary and management of anaphylaxis
 SPIDERS
• Black widow spider Desert violin spider
Arizona violin spider
• Brown widow spider Cobweb spiders
• Red legged spiders Jumping spiders,
• Brown recluse spider, Running spiders etc.
• In animals black widow spider (Latroductus mactalus)
has been mainly found to bite dogs and cats.
• Venom - alpha latrotoxin, is a potent and labile
neurotoxin which affects NMJ and also binds to calcium
channels and increases the membranes permeability to
calcium ions and enhances depolarization.
• High content of isoleucine and leucine and low of
tyrosine in addition to lipoproteins and hyaluronidase
• Spider venom is 10-15 times more potent than rattle
snakes.
 Clinical signs
• Intense pain at the sting site.
• Jelly like oedematous swelling around the bite
• Cramping spasms of abdominal muscles,
• CNS excitement due to reflex contraction of muscles,
rigidity of abdominal muscles
• Emesis, loss of appetite, weakness, dyspnoea and
hypertension.
• Paralysis occurs in acute cases and death in 4-6 hours
due to paralysis of respiratory muscles, but in mild
cases it may take days.
• Venom of brown recluse spider is rich in
hyaluronidase, proteases and other spreading
factors and haemolysins.
• Toxin probably damages endothelial cell
membranes.
• Toxin is known to cause local swelling, vascular
thrombosis and necrosis.
• Post mortem lesions : Post-mortem lesions are not
specific except for venous congestion.
• Treatment :
 No specific treatment is available
 Symptomatic treatment
 Give calcium gluconate, sodium pentobarbitone and
muscle relaxants
 Administer antihistaminic, intravenous fluids,
respiratory stimulants, corticosteroid, and atropine
sulphate.
 FISH (ICHTHYOTOXINS)

• All over world about 125 people are estimated to

die - puffer fish poisoning per annum
• Fish poisoning is not common in animals, though
dogs and certain animals and birds being fed fish
or fish meal in their feed
• About 700 different species of marine fishes are
known to be toxic. However, some are extremely
potent and highly toxic.
• Some of the poisonous fishes are
1. Shell fish – Saxitoxin – inhibits inward
movement of Na+ across the axonal membrane
2. Puffer fish - Tetrodotoxin - alters neuronal
membrane permeability to Na+ and K+
3. Moray eel - Ciguatoxin – increases membrane
permeability to Na+ and causing depolarization of
nerves. It has also anticholinesterase activity
4. Sting fish
5. Scombroid fish