In this article we will discuss about Poisonous Snakes:- 1. Biting Mechanism of Poisonous Snakes 2. Indian Poisonous Snakes and Venom 3. Effects 4. Treatment.
Biting Mechanism of Poisonous Snakes:
Boltt and Ewer (1964) studied the biting mechanism on Puff adder (Bitis arietans). Recently Bellairs (1969), Bellairs and Attridge (1975) concluded that the biting mechanism of puff odder is applicable in all poisonous snakes.
The mechanism also entails the same story in case of Indian poisonous snakes, specially the cobra and viper groups. The mechanism of biting is a complicated process and the sequences of biting may be discussed in three observable steps.
These are:
(a) Opening of the mouth:
Just before striking the digastric muscle contracts, as a result the mouth opens (Fig. 8.32B).
(b) Rotation of maxilla:
As the mouth opens, the lower jaw moves forward and a rotation of the squamosal, quadrate and mandible in relation to each other occurs. Now the sphenopterygoid muscles contract. This contraction results in the forward movement of pterygoid and up-pushing of the ectopterygoid.
The upward movement of the ectopterygoid brings about a rotation of the maxilla on its own axis round the lacrimal and as the end result the fang is raised and comes to its striking position (Fig. 8.32C, D). The fang is nearly horizontal in position when the mouth remains closed. But during opening of the mouth to bite, the fang assumes almost vertical position.
Boltt and Ewer (1964) have suggested that the quadrate is loosely attached to the posterior part of the pterygoid and the weak force which is generated by the rotation of the lower end of quadrate, could not help in the forward movement of pterygoid and ectopterygoid.
They suggest that the movement of the pterygoid and ectopterygoid is effected by the contraction of their own muscles the protractor and levator pterygoidei (Fig. 8.33) which jointly act to push the pterygoid and ectopterygoid directly forward.
As a result the maxilla rotates in its own axes. Boltt and Ewer also believe that the erection of fangs is not related to the opening and closing of the mouth. The fangs can be erected independently.
(c) Closing of mouth:
This is brought about by the contraction of the temporalis muscles and sphenopterygoid muscles. The point of the fang is directed backward while the mouth is closed. It takes a longer time to open the mouth than to close it.
Indian Poisonous Snakes and Venom:
(i) Common Krait (Bungarus caeruleus):
The bite of common krait is fatal to man. The snake is considered to be the second most poisonous in the world and first in Asia. The secretion per strike varies from 8 to 2 mg of dried venom.
The venom is more toxic than that of cobra and is considered to be 15 times more virulent than the Cobra’s. 1 mg dried poison becomes the lethal dose for man. Death may result in 5 to 12 hours after the bite.
(ii) Banded Krait (Bungarus fasciatus):
The bite of banded krait is also lethal as other kraits. The venom is less toxic than cobra poison. Rarely there is any record of the bite by this species but a bullock died in about 20 minutes after the bite of this species.
(iii) Indian Cobra (Naja naja):
The amount of venom secreted per strike is about 211 mg. 12 mg dose of venom becomes lethal for a man. The poison glands contain about 317 mg venom. The cobra venom is 5 times more virulent than viper.
(iv) King Cobra (Ophiophagus hannah):
The poison is less virulent than that of cobra. The amount of venom that is discharged at a bite, equivalent to ten lethal doses to man. Death has been recorded in 15 to 20 minutes. The glands yield about 650 mg venom. An adult elephant dies dead at a single bite.
(v) Russell’s Viper (Vipera russelli):
72 mg may be injected at per strike. 15 mg dose of venom thought to be the fatal dose for man. The fangs are largest in length among Indian poisonous snakes and are about 16 mm. The gland contains about 108 mg venom.
(vi) Saw Scaled Viper (Echis carinatus):
The average yield of dry venom by weight is about 18 mg with a recorded maximum yield of about 72 mg. About 12 mg can be injected per strike. 8 mg is believed to be fatal dose for a man. The venom is 5 times more virulent than that of cobra and 16 times as toxic as Russell’s Viper venom. The length of the fang is 5 mm as compared with the length of the body of 380 mm.
Table 30 shows the venom yield in different poisonous snakes of the world and lethal dose for human beings.
Effects of Snake’s Poison:
The venom is generally introduced into the subcutaneous tissue and then it reaches the general circulation. When introduced directly into the vein the effect is instantaneous. Table 29 shows the components of venoms and their effects on human beings. The venom of different snakes acts differently.
(i) Cobra poison:
The effects are observed within half an hour. Symptoms are giddiness, high pulse rate, extreme salivation, partial paralysis of tongue and larynx, vomiting and contraction of pupil. The eyes remains sensitive to light and consciousness remains undisturbed. Respiration is shallow, ultimately ceases and death follows. It is a neurotoxin.
(ii) Viper poison:
The effects are observed within quarter of an hour. Symptoms are swelling of the wounded region, discolouration due to extravasation, acute burning pain, pupil dilatation, high pulse rate, profuse vomiting and watery discharge from rectum.
Eyes lose sensitivity to light and consciousness is affected. Extravasation becomes extensive, swelling spreads and death comes. The poison of the two groups differs in properties though a viperine can poison a colubrine and vice versa. The poison is effect less on members of same family. It is haemo-toxic.
(iii) Krait poison:
The kraits are highly poisonous but the absence of local pain, swelling, oozing or bleeding raise doubt of bite in first hours. Even fangs mark do not reveal any visible spot. Symptoms are very similar with the signs of neurotoxicity of cobras.
The first sign of neurotoxicity is ptosis. The other signs are severe abdominal pain, drooping, dribbling of saliva, cyanosis and respiratory failure. The krait venom acts both as a neurotoxin and haemo-toxin. The cause of death is asphyxia through paralysis of the respiratory centre.
(iv) Sea snake’s poison:
The sea snake is highly venomous. The poison acts as myotoxic which effects on muscles, causing release of myoglobin that is excreted through the kidneys. The first symptoms are weakness and soreness in the muscles.
The eyelids droop and jaws become stiff. Weakness gradually increases in such condition that the patient is unable to lift a finger. The muscles are damaged, release myoglobin which stains urine red. Heart beat shows irregularity and death may happen within 12 hours after the bite. Sometimes death is delayed by several days.
Treatment of a Poisonous Snake Bite:
After snake bite, the first aid treatment and medical or surgical care are necessary as far as possible.
The following methods are recommended for the victims:
(i) Stop the spread of venom in the body by applying a tourniquet or ligature 5 to 10 cm above the wound in the direction of the heart.
(ii) Wash the spot with clean water.
(iii) An incision about 1 cm deep should be done near about the wound with the help of a sterilized knife or blade.
(iv) First let out some blood by pressure and suck out some blood with a suction cup but never by mouth.
(v) Always help the victims to keep in relaxed mood.
(vi) Seek a physician and neutralize the venom by injecting antivenin (the exact dosage can be from 10-100 ml).
(vii) Control the complications caused by the antivenin, such as the fever “serum disease”, an allergic reaction to the foreign proteins of the serum, severe shock conditions such as anaphylactic shock (caused by release of histamines) and others.
(viii) Handle the victim cautiously, because the general handling may speed up the circulation of blood,
(ix) In case of cobras, kraits, viper’s bite the polyvalent serum should be injected preferably intravenously as soon as possible after the bite. If necessary, a placebo injection may be recommended to reassure the patient.