ANIMAL POISONS

SCORPIONS
Scorpions have a crab-like appearance comprises of
various segmented with venom secreting glands.
The venom contains toxalbumin having neurotoxic and hemotoxic [that destroy
red blood cells (that is, cause hemolysis)] actions.
Red scorpion(Mesobuthus tamulus) venom contains a potent cardiotoxin.
Action: The venom is a potent autonomic stimulator, resulting in the release of
massive amounts of catecholamines from the adrenals. It has also some direct effect
on the myocardium.

Symptoms and signs:

The local irritation is characterized by redness and burning pain radiating from the
site.
There may be headache, giddiness, nausea, profuse perspiration and muscular
cramps followed in some cases by coma.
Although the duration of symptoms is ordinarily 24-48 hrs, neurologic
manifestations may persist for upto 1 week.
 Findings in case of death are widespread hemorrhage.
 Myocardial damage is found in deaths from red scorpion.
 Complications- Tacchycardia, hypertension, arrhythmias,
hyperthermia, rhabdomyolysis(rapid disintegration of striated
muscle tissue accompanied by the excretion of myoglobin in the
urine) and acidosis.
PM findings
Affected site is swollen. Sting may be found at the site. The area may
show eccymosis(skin discoloration due to bleeding underneath the
skin). Pulmonary edema and myocardial infraction may be seen.

Medicolegal aspects:
 Scorpion poisoning is accidental.
 SNAKES
Phylum : Chordata
Class : Reptilia
Order : Squamota
Suborder : Serpentes
 Snakes are classified into 2 groups,
poisonous and non-poisonous
 Poisonous snakes are further divided
3 types on the basis of poison secreted by them:
 Elapids (secreting neurotoxic venom)
 Vipers (vasculotoxic venom)
 Sea snakes (myotoxic venom)
 Neurotoxic venom causes muscular weakness of legs and
paralysis of muscles of face, throat and respiration. Neurotoxins of
cobra venom produce both convulsions and paralysis, whereas
krait venom causes only muscular paralysis.
 Vasculartoxic venom :
 It causes coagulation disorders.
As a result, endothelium of blood vessels is destroyed,
red cells are lysed and other tissue cells are destroyed.

 Myotoxic venom produces muscular pain, followed by

myoglobinuria (presence of myoglobin in the urine), 3-5
hrs later, ending in respiratory failure in fatal cases.
 The hallmark of attack of a venomous snake is presence
of fang marks.

 In contrast bites by non-venomous snake produce a

characteristic U-shaped set of teeth marks.
Snake Venom
Snake venom is highly concentrated, clear amber coloured digestive juice of the
snake. When it is dried, it becomes like fine needles which are soluble in water.

• It has got proteolytic enzymes, phosphatidases, and neurotoxins.

• Proteolytic enzymes cause tissue destruction by liberating histamines by
damaging muscular epithelium of blood vessels leading to release of RBCs and
serum in tissues.
• Phosphatidases cause haemolysis and toxic effects on heart and circulation.
• Neurotoxins produce curare-like effect on CNS leading to paralysis. The snake
venom also contains other enzymes like proteases, erepsin, choline esterases,
hyaluronidase, ribonucleases and ophio oxidases.

Poison apparatus: It is a modified salivary gland consisting of:

• Gland : lies just below or behind the eyes, one on each side, above the upper jaw.
• Duct: Arises from the gland to carry the poisonous venom from gland to the fangs.
• Fangs: Two in number. These are curved teeth situated on the maxillary bones and
lies along the jaws. They are like hollow hypodermic needles (solid in non-
poisonous snakes).
Symptoms and signs:
 Poisoning may occur from bite (injection) or absorption of venom
through cuts or scratches.
 In some cases, instantaneous death occurs from shock due to fright,
even before any symptoms commence.
 The degree of toxicity depends upon:
Potency of venom
Main toxic principles it contains.
Amount injected (depends upon age, size, sex and species of
snake)
Whether the bite is on bare skin or through clothing
Local Reaction

• They are present more in viper snake bite. There is local swelling due to
leakage of fluid as a result of damage of capillary endothelium. Pain and
discolouration develop at the site of the bite. Within fifteen minutes
nausea, vomiting and signs of collapse supervene. There is a cold
clammy skin, hypersalivation, weak feeble, rapid pulse with low blood
pressure is seen. The necrosis develops at the site.

• In cases of bite from snake such as cobra or krait, the immediate local
actions are burning or tingling pain, irritation, swelling and
inflammation. But the local reaction is very less as compared to viper
snake bite. Within 15 minutes, constitutional symptoms develop in the
form of giddiness, lethargy, muscular weakness, drowsiness and a feeling
of intoxication. Nausea and vomiting may also be there. Weakness of
muscles increases and paralysis of limbs develop. It spreads on to
involve trunk and rest of the body. Breathing becomes slow and
laboured. The death occurs due to coma.
• Snake venom whether it is from cobra or viper group of snakes, it has
haemolytic action on blood. It reduces coagulability of blood leading
to oozing of blood from the site of the bite. Spontaneous oozing of
blood into vital organs such as brain can occur up to several days after
the bite. It is due to direct endothelial damage caused by venom
component. Acute renal failure may follow within one week.

• Myotoxic effects - main features in sea snake bite. Generalised muscle

pain is seen in all skeletal muscles of the body. Pituitary failure in the
form of pituitary haemorrhage may be seen in Russell’s viper bites.
Sweating, cold extremities, tachycardia, hypotension and ECG changes
(S-T changes) are the features of cardiovascular depression seen in
cobra and viper bites. Hyperkalaemia (higher than normal levels of
potassium in the circulating blood; associated with kidney failure)
leading to cardiac arrest is seen in sea snake poisoning. Hyperkalaemia
occurs as a result of muscle damage.

• As snake venom can cross placenta, when pregnant women is bitten by

snake, her foetus can die too due to venom effect.
Specific symptoms in various Snake bites
1. Common Krait: Venom is neurotoxic. Not much pain or swelling at local site but
within 1 hour the victim feels sleepy and neurotoxicity develops.

2. Cobra: Swelling at local site develops not before 2–3 hours. Necrosis develops more
rapidly and may be seen as wet gangrene in 2–3 days. Local symptoms include reddish
tender spot with burning pain. The neurotoxic effects start within 30–60 minutes.

3. Sea Snakes: Venom is most toxic as compared to cobra and vipers. Snake bite is
small pin-head puncture usually 1–8 in number, without much local pain. Paralysis and
rhabdomyolysis are seen. Painful muscular movement, ascending paralysis, slurred
speech, dysphagia, ptosis (drooping of the upper eyelid due to paralysis) and
myoglobulinuria are seen.
4. Russell’s Viper:
Severe local reaction is followed by swelling in 15–20 minutes. Local necrosis appears
slowly over weeks and present as dry gangrene. The death is caused due to shock
developing within one week.
Fatal dose: 15 mg – dried cobra venom
20 mg – viper venom
6 mg – krait venom
8 mg – saw-scaled viper venom
Fatal period:
Death may occur instantaneously from shock due to fright.
Death from
 Cobra venom- within a few min to few hours
 Viper venom- in a few days
 Sea snake bite is mostly not fatal

Postmortem appearances:
1 or 2 bite marks about 1 cm deep in case of elapid and 2.5 cm deep in case
of viper may be found.
There is some swelling about the bitten part.
There is no definite appearances indicating cause of death except the signs
of asphyxia.
In case of viper bite, the local appearances are more striking due to severe
oozing of blood from puncture site.
The blood is fluid and hemolyzed causing early staining of blood vessels.
There are hemorrhages in lungs membranes.
Endocardial hemorrhage are seen especially in left ventricle.
Petechiae are also found within kidney and mucosa of urinary
bladder, stomach and intestines.
Blood fails to clot normally even after addition of thrombin
because of extremely low levels of fibrinogen.
Arterioles and capillaries are characterized by blurred walls
and swollen endothelial cells.
Other findings include necrosis of renal tubules and cloudy
swelling of other organs.

Medicolegal aspects:
Generally accidental
Rarely homicidal and still rarely suicidal.
Sometimes used to kill cattles.
Difference between Poisonous Snake and Non-Poisonous Snake

Belly Scales
 Head Scales

A. Poisonous Snake B. Non-Poisonous Snake

(a) Side view of Poisonous snake, (b) Fangs Points to be noted in
Features of common Poisonous Snakes
Common Krait Banded Krait

Russel Viper Sea Snakes

Differentiate : Cobra and Viper
Differentiate : Sign &Symptoms Elapinae and Viperine bite
CANTHARIDES
The Spanish fly(Cantharis vesicatoria) or blister
beetle is a green coloured insect which is widely
present. When the insect is dried up and turned into
a powder, a brown coloured powder with green
particles is obtained.
Active principle is cantharidin. This principle is
freely soluble in alcohol but not in water. It is a
very strong vesicant(causing blistering to the skin).
The Spanish fly is known as cantharis vesicatoria.
In India, teleni makhi (Mylabriscichorii) is widely
prevalent in north India and Kashmir. It also contains
cantharidin. Other species of teleni makhi are also
present throughout India.
Action – It is locally irritant and nephrotoxic agent.
Absorption – Canthridin is readily absorbed from all the surfaces,
including the skin.
Sign & Symptoms –
 On local application - cantharidin initially does not cause any side
effects but after 2–3 hours, local redness and inflammation is seen
which is followed by multiple blisters formation. Later, all blisters
may combine and form a large area of necrosis.
 On ingestion, within 2 hours it produces severe burning in mouth,
throat and stomach. It causes blistering of tongue, swollen tongue,
intense thirst, increased salivation due to inflammation of salivary
glands, nausea, vomiting and diarrhoea. There is a pain in loins,
increased frequency of urine, painful priapism with swelling and
inflammation of genital organs. The patient becomes very restless.
 The person may die of peripheral shock with slow, feeble pulse along
with low blood pressure. The voice of the person may become hoarse
due to the vocal cord spasm.
• Fatal Dose - About 1–2 gm.
• Fatal period- 24–36 hours.
Treatment
Gastric lavage should be done immediately. Fluids should be started
intravenously to avoid dehydration. The patient should be managed by
supportive treatment.
Postmortem Findings
External: Inflammation and vesicles are seen in mouth.
Internal:
i. GIT: The mucous membrane of the oesophagus and stomach is often
swollen and engorged, and may show patches of ulceration and
haemorrhages. Stomach may contain shiny greenish particles of insect.
ii. Kidneys: Kidneys are congested. Acute tubular necrosis may be seen.
iii. Lungs: congested and oedematous.

Medico-legal Significance
The cantharides are used as aphrodisiac due to their tendency to cause
priapism. They can also be used to produce criminal abortion. It is rarely
used for suicidal and homicidal purposes. Accidental poisoning can occur
due to application of blistering paper (Charta epispastica).