ZOOTOXINS

Zootoxins
The toxins produced by animals e.g. snakes,
fish, toads, scorpions, bees, wasps, spider,
ticks etc.
Venom : It is the poison or toxin secreted by
specialized glands of an animal.

Venomous animals : Animals or creatures that
are capable of producing a poison in a highly
developed secretory gland or group of cells
and deliver the toxin during a stinging or
biting act.


VENOMOUS ANIMALS

Venomous animals are found in most groups or classes of the Animal
Kingdom and in most habitats, both terrestrial and marine.
Overview of venomous animals
Of the approximately 26 Phyla of animals, at least 6 contain species
that use venom or internal poison, as either pure defense, or both for
offence and defense
A few groups, however, account for the vast majority of cases of
human envenoming or poisoning by animals:
Venomous snakes >125,000 deaths/year.
Scorpions approximately 5,000 deaths/year.
Stinging insects hundreds of deaths/year due to anaphylactic
reactions to venom.
Puffer fish several hundred deaths/year.
Jellyfish possibly scores of deaths/year.
Spiders perhaps 10-50 deaths/year.
Stinging fish perhaps 1-10 deaths/year.
Venomous molluscs perhaps 1-10 deaths/year.
VENOMS
Venoms are nearly always complex mixtures of varied
biologically active substances (toxins) which may work
independently or synergystically and each of which may have
one or more quite distinct target sites and actions.
In many venoms a single component or group of closely
related components may be responsible for most or all major
effects in envenomed humans, but in other venoms,
particularly snake venoms, a multitude of diverse components
may each cause distinct major effects, resulting in a complex,
multisystem disease process.
TOXIN/VENOM COMPOSITION

PROTEIN CONTAINING COMPONENT - polypeptides
Enzyme - phospholipase, hyaluronidase, Ach-
esterase (ants, bees, lizards, snakes)
- histamine, serotonin, acetylcholine, norepinephrin
- dopamine( ants, snakes)
Saponins
Alkaloids(ants)
Volatile oils(bees)
OTHER formic acid (Ant), phenol, hydrogen cyanide


SPECIFIC TOXINS

Saxitoxin, gonyautoxin, brevetoxin(shellfish)
Mellitin , apomin (bees)
Ciguatoxin, maitotoxin(fish)
Tetrodotoxin(fish, newts)
Bufagin, bufotoxin, bufotenine (frogs, toads)
Gilatoxin (lizard)
AmmodytoxinA, caudoxin, taipoxin(snakes)

PHARMACODYNAMICS OF ENVENOMING
Factors affecting Rate Of Absorption, Clinical Effectiveness And
Elimination Of Venom :
The way venoms are introduced by a bite or sting
Depth of injection
Quantity involved
The size and action of venom components
Size, age, pre-existing disease
Post envenoming activity of the victim will all influence the
rate of absorption
In general terms, however, the speed of onset of action of a
particular component will be determined by its size and target
tissue location.
Thus necrotoxins and other locally active toxins may commence
clinical effects almost immediately after the bite or sting, as they
are already at their target site, while systemically active toxins
must first reach the bloodstream

ANTIVENOMS
are specific antidotes to venoms.
Virtually all are whole or fractionated animal IgG raised against a
target whole venom, not specific venom components.
Antivenoms are polyclonal and may contain far more
neutralising activity against some venom components than
others.
The choice of venoms may strongly influence the clinical efficacy
of an antivenom; if only a narrow range of species or species
from a small part of a geographic range is used, then the
antivenom may lack efficacy against bites from a wider range of
species or against bites from the target species from other parts
of its geographic range.
ANTIVENOMS
Antivenoms may be
Truly monovalent (raised against the venom of a single
species of animal), monovalent to genus level (cover all or
several species within a genus, or ocasionally closely related
genera)
Polyvalent (raised against a venoms from a variety of species,
usually unrelated apart from a common geographic
range).
Most commonly, the animal used for immunising is the horse,
but sheep, goats, rabbits and even chicken egg yolk have
been used.
Horse based antivenoms, in particular, have a generally high
incidence of adverse reactions, but the rate of reactions will
also be determined by the degree and quality of refining,
particularly removal of non-IgG components such as albumin
and where IgG has been fractionated
Three Principles of antivenom therapy
To tailor the dose to the individual situation.
To give as soon as possible, once it is indicated. (most situations
of acute envenoming, the IV route is preferred, but there are
exceptions, which will be noted for particular animals as they
apply)
To monitor carefully for the effect of antivenom therapy.
(monitoring both effectiveness in counteracting envenoming
and observing for adverse effects of therapy)
SNAKES

Snake bite in animals generally occurs
while grazing or hunting.
In India 2,00,000 bites and 15-20,000
snake bite deaths per every
year{humans}
There are more than 3500 different
species of snakes out which more than
400 have been found to be poisonous and
dangerous.

Classification
(i) Elapidae: Coral snakes, COBRAS, KRAITS,
mombas.
(ii) Crotalidae: Rattle snakes, water moccasins,
copper heads, bush master, pitvipers.
(iii) Viperidae : The RUSSELS VIPERS, SAW
SCALED VIPER
(iv) Hydrophidae: The true sea snakes.
(v) Laticaudidae: Sea kraits.
(vi) Colubridae: Boomslang, bird snake,
rednecked, keel back
Toxicity due to snake bite generally
depends on

Toxicity of the venom and the quantity of venom
injected.
Ratio of animal i.e. size of the animal and venom
injected.
Species of snake.
Location of bite.
Sensitivity pattern:
Horse > Man > Sheep > Cattle > Goat > Dog > Pig > Cat.


Big Four Poisonous (Indian snakes)

Indian cobra, Naja naja, the most
famous of all Indian snakes.
Common krait, Bungarus
caeruleus
Russell's viper, Daboia russelii.
Saw-scaled viper, Echis carinatus.

Indian cobra, Naja naja
Common krait, Bungarus
caeruleus

Russell's viper, Daboia
russelii.

Saw-scaled viper, Echis
carinatus.

King Cobra
The king cobra
(Ophiophagus hannah) is
the worlds longest
venomous snake, growing
up to 5.5 m (18.5 ft).
The main constituent of
king cobra venom is a
postsynaptic neurotoxin,
and a single bite can
deliver up to 400500 mg
of venom
Fangs can grow to 20 mm
Venom discharge
Snake Discharge /bite LD
Cobra 200 mg 12-15 mg

Krait 20 mg 6 8 mg

Russell viper 150 mg 15 18 mg
King Cobra 500mg

Difference between venomous & non
venomous

Venom composition
Elapidae

Acetylcholinesterase(AChE)
Neurotoxin
(blocks nicotinic receptor)
Hyaluronidase
Phospholipase-A
2
Phosphodiesterse

NEUROTOXIC
FLACCID PARALYSIS


Viperidae

Thrombine like
enzymes
Proteolytic enzymes
5-Nucleotidase
Collagenase
Phospholipase-A
2
Phosphodiesterse

HAEMOTOXIC
C-V COLLAPSE
NEPHROTOXIC

Snake venom, the most complex of all poisons is a mixture of enzymatic
and non-enzymatic compounds as well as other non-toxic proteins
,carbohydrates and metals.
20 different enzymes- phospholipases A2, B, C, D , hydrolases,
phosphatases (acid as well as alkaline), proteases, esterases,
acetylcholinesterase, transaminase, hyaluronidase, phosphodiesterase,
nucleotidase and ATPase and nucleosidases (DNA & RNA) .
The non-enzymatic components are categorized as neurotoxins and
haemorrhagens .
Different species have differing proportions of most if not all of the above
mixtures- this is why poisonous species were formerly classified
exclusively as neurotoxic, haemotoxic or myotoxic.
The pathophysiologic basis for morbidity and mortality is the disruption of
normal cellular functions by these enzymes and toxins.
enzymes such as hyaluronidase disseminate venom by breaking down
tissue barriers leads to increase in the capillary permeability which may
cause loss of blood and plasma volume into the extravascular space.---
oedema.
Enzymes
Hyaluronidase splits acidic mucopolysaccharides and
promotes the distribution of venom in the extracellular
matrix of connective tissue.
phospholipases A
2
are esterolytic enzymes which break
down membrane phospholipids such as lecithin (=
phosphatidylcholine) into fatty acids and lysolecithin.
This causes cellular membrane damage leads to oedema,
blister formation and local tissue necrosis.
Proteases destroy endothelium of blood vessels.
Phosphatides cause haemolysis. Cholinesterases
neurotoxic.
Other peptides, polypeptides, glycoproteins etc


Paralysis

The neurotoxins block the stimulus transmission from nerve cell
to muscle and cause paralysis.
The venom does not penetrate the blood-brain barrier.
Some venom (cobra, mamba, krait alpha-bungarotoxin) works on
the nicotinic acetylcholine receptor present on muscle
(neuromuscular junction).
The postsynaptic effects are reversible with antivenom and
neostigmin.
Other types of venom work on the presynaptic nerve terminal,(
e.g. beta-bungarotoxin) and here neostigmin will not be effective.
Presynaptic neurotoxins inhibit the fusion of the vesicles
containing acetylcholine, with the nerves membrane of the
neuromuscular junction.

Mongoose

The acetylcholine receptor in the mongoose
has a slightly different protein sequence than
that of animals who are easily paralyzed by
(alpha)-bungarotoxin.
In laboratory experiments, the reconstituted
mongoose achr alpha-subunit of the
acetylcholine receptor did not bind (alpha)-
bungarotoxin

This is an example of natural resistance of the
mongoose to a component of cobra venom
Haemorrhages
Snake venom can interfere with blood coagulation{procoagulant &
anticoagulant}.
procoagulant--Venom can either activate prothrombin or have a
direct effect on fibrinogen and convert it into fibrin and thus itself
have a thrombin-like activity,
such as crotalase (rattlesnake venom), ancrod from Calloselamsa
rhodostoma batroxobin (reptilase) from Bothrops atrox moojeni.
Anticoagulant
Certain enzymes in venom activate factor V & X (e.g. Russells viper
and Vipera lebetina), or promote fibrinolysis (e.g. the enzyme
lebetase from V. lebetina).
Diluted venom of Russells viper contains a specific activator of
factor X which is used in some laboratory tests for lupus
anticoagulant.
Endothelial damage can be caused by venom containing so-called
"haemorrhagins


Types of snake venom toxins
1. Blood circulation toxin:-
HAEMOTOXIN
Eg: Vipers
The skin will become
purplish, black and necrotic.
After 6-8 hours, it could be
spread to the head, neck,
limbs and lower back.
If not treated, within 4
hours, death - due to heart
failure or shock.

2. nervetoxin: NEUROTOXIN
Eg: Krait
Local symptoms were not
obvious, less bleeding, swelling
and slight fever.
Within a few hours after injury,
the rapid systemic symptoms,
patients with anxiety
excitement, groaning with pain,
difficulty swallowing, difficulty
breathing, convulsions,
respiratory muscle paralysis and
the death will appear.


3. Mixed toxins: Both Eg: Cobra and King Cobra
General symptom -have the nerve symptom and harm
which were caused by blood circulation toxin.
CLINICAL SIGNS
The presence of a heavy hair coat and local
swelling obscures fang marks.
One or more fang puncture wounds may be
present on the animal.
The most common locations for fang marks
in small animals are the face and legs, head, neck.
Horses - nose, head, and neck.
Bites to the legs of horses are less common and
may present with minimal swelling
Cattle - Limbs and while grazing on the lip/jaw
Pre-paralytic signs:
Vomiting within 5 minutes and headache within two
minutes of bite, Syncope, decreased BP; abdominal colic.
Drowsiness is a cardinal sign. Bilateral ptosis (Paralysis of
eye muscles).
Disturbed vision.
Principally neurotoxic with muscles of eyes, tongue, throat
and chest paralyzed leading to respiratory failure and
death.
Calves:
Regurgitation of ruminal contents, paralysis of tongue,
pharynx and oesophagus are observed.
Edema and swelling are due to vasculotoxic action of
venom which has many proteolytic enzymes that affect
vasculature.


Generalised symptoms

General ---nausea, vomiting, malaise, weakness, dizziness
Cardiovascular --hypotension, shock, arrhythmia, pulmonary
oedema, heart failure
Haemostasis --haemorrhages from venipunctures, gums,
nose, vagina, subcutaneous haemorrhages, haematemesis
Neurological --paresthaesiae, ptosis, ophthalmoplegia,
dysphagia, aphonia, paralysis, respiratory arrest
Muscles --generalised myalgia, muscle stiffness, trismus,
myoglobinuria, hyperkalaemia
Kidneys --lumbar pain, haematuria, haemoglobinuria,
myoglobinuria, oliguria, uremia
Endocrine --shock and hypoglycaemia (early). Late weakness,
testes atrophy, amenorrhoea

Interval between snakebite and death

King Cobra -------- ()
Naja naja (cobra) -----8h (1/4-60h)

Crotalus species (rattlesnakes) ------16h (2h-26h)

Bungarus caerulus (Indian or common Krait) ----
18h (3h-63h)

Vipera (Daboia) russelli (Russells viper) ----
40h (1/4h-9 d)
Echis carinatus (saw-scaled viper) ------5 d (1-41d)


Diagnosis
History
Observing fang marks
Oozing of blood at the site of bite
Cyanosis
Identifying snake in the vicinity

Differential diagnosis.
Electrocution
Lightning shock
Anthrax

Rodenticides:
a. Warfarin group
b. Zinc phosphide

Strychnine/ Nux-vomica




PRECAUTIONS: TREATING SNAKEBITE
Do not excite and treat; Do not shift from herd
Apply a tourniquet (only for cobra/ krait bite) just above the site of bite. Release the
tourniquet periodically once in every 10-15 min to allow blood supplies.
In viper bite, application of tourniquet causes local necrosis
Mild soap water wash, Do not use antiseptics, KMNO
4
Sol.
The use of Alcohol to clean the wound is contraindicated because of its vasodilatory
effect, which would promote uptake and spread of venom
Excise inch area of bite, bleed with out excitement, after washing with soap.
No ice or any other type of cooling action on the bite.
No electric cable, string or rubber tourniquets to be used, this cuts off blood flow
completely and may result in amputation of the affected limb.
No electric shock, No incision in the bite site.
Do not burn the wound, as it would not have any effect on the venom, which has already
entered the bloodstream.
Do not suck the wound with mouth. A suction device may be applied over the bite to
help draw venom out of wound without making cuts.
Potassium permanganate should never be used.

GENERAL MANAGEMENT OF SNAKE BITE
Keep the animal undisturbed.
To restrict the further absorption and distribution of venom, apply
a tight torniquet above the site of bite,(NOT IN VIPERS)
Incise the local area of snake bite in the direction of blood vessel
and go for suction and infiltrate the area with 5% soap solution
Inject . A= Antivenom (Polyvalent) ; A= Antibiotic
(Broad spectrum) ; A= Anti tetanus (TT)
If snake has not been identified, give polyvalent antivenin
intravenously and also infiltrate the antivenin locally around the
site of bite.(????)
Polyvalent antisnake venom IV@ 10-20 ml per animal depending on
the weight of the animal,
Managing shock and cardio-pulmonary disturbances by
administering corticosteroids.
Potential side effects of antivenom (anaphylaxis, serum sickness)





Polyvalent ASV : contain antibody against Cobra, Russells viper,
common krait and saw-scaled viper.
In India ASV is manufactured by Bengal Chemicals & Pharmaceuticals,
Kolkata; Bharat Serums, Mumbai; Biological Evans, Hyderabad; Central
Research Institute, Kausali; Haffkins Pharmaceuticals, Mumbai; King
Institute of preventive medicine, Chennai; Serum Institute, Pune and
Vins bio-products, Hyderabad.
ASV is produced in both liquid and lyophilised forms.
No evidence to suggest which form is more effective and many doctors
prefer one or the other based purely on personal choice.
Liquid ASV requires a reliable cold chain and refrigeration and has a 2
years shelf life.
Lyophilised ASV, in powder form, requires only to be kept cool and
hence, is useful in remote areas where power supply is inconsistent

TREATMENT
ELAPIDAE
Polyvalent snake anti-venin
(PVSAV) I/V
@ 20 ml/12 kg in calves and
dogs (Another
recommendation) 50 ml in
cattle and 100 ml in dog Along
with epinepherine 1:1000 (0.5
1 ml S/C) to avoid shock
Analgesic
Corticosteroids
Fluid therapy
Neostigmine @ 5-7.5 mg/kg.
I/V along with PVA SVS @ 10
ml / 12 kg. (Neostigmine is
synergistic with PVASVS, binds
ChEs present in venom).


VIPERIDAE
Polyvalent snake anti-venin
(PVSAV) I/V @ 20 ml/12 kg in
calves and dogs(Another
recommendation) 50 ml in
cattle and 100 ml in dog Along
with epinepherine 1:1000 (0.5
1 ml S/C) to avoid shock.
Supportive: Cortisone 50 mg
I/M / animal and subsequently
25 mg at 8 hourly interval

Vitamin K
1
/Heparin Na

Calcium gluconate
Corticosteroids
Blood transfusion
Peritoneal dialysis
Local adm. of antivenin





In Humans
Antivenom therapy
Total amount of venom injected by snakes-
cobra 120 mg, Russells viper 150 mg, krait 60 mg and Echis carinatus 80
mg.

Amount of venom neutralized by one ml of polyvalant ASV-
Cobra 0.6mg, Russells viper 0.6mg, krait 0.45 and Echis carinatus 0.45
mg.

COMPLICATIONS OF ANTIVENOM THERAPY
Acute adverse reactions- Anaphylaxis and related early reactions, Rash.
Febrile reactions (usually related to toxin contamination).
Serum sickness., Failure of efficacy.
Incorrect antivenom, Inadequate dose.
Inappropriate route of administration (IM or local when IV was required).
Therapy commenced too late.
Out of date antivenom or poorly stored antivenom (ie refrigerated
antivenom that has been exposed to prolonged heat).
Poor quality antivenom.


METHODS(CONTROVERSIAL.??) EMPLOYED TO MINIMISE THE
CHANCE OF ADVERSE EFFECTS FROM ANTIVENOM THERAPY.
1. Skin sensitivity testing prior to administration
May delay treatment, fail to reliably predict major
adverse reactions (eg anaphylaxis), potentially
sensitise the patient to antivenom should it be
required in the future and may precipitate an
anaphylactic reaction.
For these reasons skin sensitivity testing is not
recommended, even though it is advised by a
number of antivenom producers and is routinely
used in some countries (eg USA).
Methods(Controversial.??) employed to minimise the
chance of adverse effects from antivenom
therapycontd

2. Premedication prior to antivenom therapy.
This is controversial and is not widely accepted or used.
Antihistamines and steroids have been shown to have no real
benefit in preventing acute antivenom reactions.
In addition, antihistamines may induce drowsiness or
occasionally, hyperexcitability, both potentially dangerous in
major envenoming.
Epinephrine (adrenaline) has been shown to reduce the
likelihood of adverse reactions for certain high risk antivenoms
This is particularly true if the envenoming causes increased
bleeding, as seen with many snakebites.
Premedication is not currently recommended by antivenom
producers.
Future studies may better define its role, if any.

Methods(Controversial.??) employed to minimise the chance of adverse effects from
antivenom therapycontd

3. Use of diluted antivenom infusions.
Most antivenoms should be given IV.
Many recommend dilution of the antivenom up to 1:10 in a suitable diluent for IV
use, such as normal saline or Hartmans solution.
The degree of dilution will be limited by the volume of antivenom and the size of the
patient.
While this technique may be useful, it is not strictly necessary, as studies have shown
that IV push neat antivenom does not carry a higher incidence of acute adverse
effects.
In addition, the latter technique requires the doctor to stay with the patient
throughout the antivenom infusion, which increases the chances of rapidly and
effectively responding to acute adverse events.

Haffkines - Snake Polyvalent Anti Venin Serum I.P.(ASVS)

A freeze-dried -a powder form it can be stored at comparatively
high room temperature.
On reconstitution, it is a solution of purified antibodies prepared
from equine blood.
Available in vials, along with water for injection, to reconstitute
10ml.
Reconstituted Qty. 10 ml.
1ml of the reconstituted serum neutralises
0.6 mg of dried Indian Cobra (Naja naja) venom.
0.45 mg of dried Common krait (Bungarus caeruleus) venom.
0.6 mg of dried Russell's viper (Vipera russell's) venom.
0.45 mg of dried saw scaled viper (Echis carinatus) venom.


Role of snake venom in medical and
biological research

Therapeutic removal of thrombus
Fibrinolytic enzymes isolated from venom can
directly break down a fibrin clot. Current medical
research seeks to find such an enzyme to remove
clots causing heart attacks and strokes.
Disintegrins - prevent tumor cell growth through
inhibition of angiogenesis, prevent tumor metastasis
through inhibition of cellular adhesion and inhibit platelet
aggregation.
Hemostatic effect:
Analgesia:-pain caused by advanced cancer.
Manufacture of anti-venom serum:







TOADS
Dogs and cats 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 and catecholamines.
Bufogenins are cardiotoxic glycosides and have effect
on the heart and other smooth muscles.
The toxins differ amongst different species of toads.
Some of the poisonous/toxic species of toads are Bufo
vulgaris (common toad), Bufo marinus, Bufo regularis
and Bufo alvarius;
B. alvarius (river toad) and Bufo marinus (marine toad)
are the most toxic ones.



Clinical signs of toad poisoning are
hypersalivation (some times foamy), vomiting
and pawing at the mouth, cardiac
irregularities such as cyanosis, weakness,
pulmonary oedema, convulsions, prostration
and collapse.
In case of B. marinus, death occurs within 15
minutes while in B. regularis poisoning there
is 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 and
bronchoconstriction.
Give antihistaminics, sedatives or tranquilizers,
Administer corticosteroids,
Give large doses of propranolol (0.2 mg/kg) to
control cardiac arrythmias and myocardial
fibrillation;


SPIDERS
Species of spiders implicated in bites of human beings &
animals.
Black widow spider, brown widow spider, red legged
spiders, brown recluse spider, desert violin spider, Arizona
violin spider, cobweb spiders, jumping spiders, running
spiders etc.
Black widow spider (Latroclectus maclans)-dogs and cats.
Venom - Alpha latrotoxin, is a potent and labile neurotoxin
which affects neuromuscular junctions and also binds to
calcium channels and increases the membranes
permeability to calcium ions and enhances depolarization.
Has a 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.
On pressing, jelly like oedematous swelling around the bite,
Whole integument is painful and hypersensitive to pressure,
Cramping spasms of abdominal muscles,
Nervous 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.
The venom of brown recluse spider {Loxosceles reclusa) is
rich in hyaluronidase, proteases and other spreading factors
and haemolysins.
The toxin damages endothelial cell membranes
The toxin is known to cause local swelling, vascular
thrombosis and necrosis.



Treatment:

No specific treatment is available, however, if
available, specific antivenin may be injected,
Symptomatic treatment needs to be given,
Give calcium gluconate, sodium
pentobarbitone and muscle relaxants
intravenously,
Administer antihistaminics, intravenous
fluids, respiratory stimulants, corticosteroids
and atropine sulfate.

TICKS (TICK TOXINS)/TICK PARALYSIS
Vectors of many diseases
Tick paralytic disease is common in man, cattle, sheep and bison.
Dermacentor andersonii (wood ticks) if attached to skin, produce
paralytic symptoms which disappear when ticks are removed.
May result in death of animals if ticks are not removed.
Symptoms of toxicity are due to a neuroparalytic toxin of ticks.
Ixodes holocyclus - causes tick paralysis in sheep and cattle.
Cats are comparatively more resistant.
Amblyomma sp. and Ornithodorus sp. also cause tick paralysis.
Symptoms - violent itching, anorexia, lethargy, drooling of saliva,
muscle weakness, incoordination, extensive dehydration and complete
ascending flaccid paralysis.
The sequence of paralysis is : hind limbs, fore limbs, chest muscles;

Treatment:
No specific treatment or the antidote
Administer hyperimmune serum in dogs.
Remove the ticks either manually or by
making use of acaricides.
Control :
Eradicate the ticks from the animals and the
premises by periodic use of effective
acaricides.


FISH (ICHTHYOTOXINS)

Fish is the principle source of proteins for inhabitants of
the coastal areas and also the animals and birds in the
form of fish meal in their feed.

Worldover about 125 people are estimated to die of
puffer fish poisoning per annum,

However, fish poisoning is not common in animals,
though dogs and certain animals and birds being fed fish
or fish meal in their feed, respectively, may at times be
poisoned.


toxin MOA Clinical signs
Saxitoxin
(Shell fish)
Inhibits inward current of Na"
across the axonal membrane.
Burning sensation in lips and gums, tongue,
face and numbness of these parts, pain in
joints, difficulty in movement, thirst,
progressive generalized paralysis and death
due to respiratory failure.

Tetrodotoxin
.
(Puffer fish)

Alters neuronal membrane
permeability to Na" and K\
Rapid onset of weakness, dizziness,
paresthesia around lips, tongue and throat,
increased salivation, diaphoresis,
hypotension, bradycardia, intense cyanosis,
dyspnoea, epigastric pain, ataxia and flaccid
paralysis
Ciguatoxin
(Gambierdisc
us toxicus)

Increases neuronal membrane
permeability to Na" and causing
depolarization of nerves. It also
has anticholinesterase activity.


Tingling of lips, tongue and throat, numbness
of these parts, nausea, vomition, abdominal
pain, diarrhoea, pruritis, bradycardia, pain in
joints and muscles, paresis and temporary
blindness.


Stingrays

Stingrays are cartilagenous fish (like sharks) with a unique body
shape, including a long tail, equipped with a venom gland
ensheathed spine.
Stingray injuries are common in seaside regions and consist of 2
components; the mechanical trauma of the sting, plus the venom
effects.
It is the former which is generally most important. The injury occurs
when a human comes too close to a stingray, which whips its tail
around in defense.
This most often is the result of the victim running into shallow,
sandy bottomed seawater, or stepping out of a small boat into
similar water; the stingray, resting or hiding on the sandy bottom is
surprised and reacts .
The spine is driven at speed and with great force into the victim,
sometimes resulting in deep or lengthy laceration, which may
extend into deep structures.
This may result in damage to nerves, tendons, muscle or
blood vessels.
Death has occurred from exsanguination after severing a
major vessel.
There are rare cases of puncture of the abdomen or
thorax, with potentially catastrophic consequences,
including a case of direct heart puncture.
Treatment
Control of mechanical injury, with stemming of blood loss.
Tthe wound should be left open and allowed to close by
secondary intention.
Infection may be common in stingray injuries, so antibiotic
therapy is often indicated.
Immersion in hot water, as for fish stings, is often helpful in
relieving pain, at least in less severe injuries
Sever or persistent pain- Systemic analgesia or regional
nerve block.

SCORPION
About 650 spp distributed world wide
Amount of venom produced b/w 0.1-0.6mg
Venom is heterogenous mixture of neurotoxin
cardiotoxins ,nephrotoxins , hemolysins
agglutinins , coagulins, enzymes such as
phospholipase A and B, hyaluronidase, formic
acid and biologically active amines, such as
histamine
Leiurus quinquestriatus is most toxic with LD50
0.16-0.5 mg/kg s/c in rat
Toxicity is due to neurotoxins
Acts on voltage dependant Na channels leads to
over excitation by release of ach , epi , nor epi
Sign local pain , numbness , hyperesthesia , skin
discoloration , salivation , tachycardia , muscle
spasms , convulsions , death due respiratory
failure.

Treatment ;-antitoxin
Cold compress to relieve pain ,atropine
sulphate to control parasympathetic action
Beta blockers used to supress adrenergic
symptoms
Ca gluconate to relieve muscle spasm
Should not use morphine bcz it aggravate
respiratory depression

Honey Bees(Apis mellifera )

Venom of bees is complex mixture of peptides,
nonenzymatic proteins such as apamin, melittin or
kinins, enzymes such as phospholipase A and B,
hyaluronidase, formic acid and biologically active
amines, such as histamine and 5-HT etc.
Apamin is a toxin that disrupts neurological function. It
binds itself to the calcium and potassium channels
located in the brain and spinal cord and inhibits their
activity.
Melittin is a protein mainly found in honey bees and
is antigenic in nature and produces allergic reactions
mainly in human beings and horses.

Following insect bite, there is extreme serous
exudation leads to moderate inflammation and
painful swelling is observed.
Anaphylaxis and death from a single sting occurs
in hypersensitive animals.
In severe cases in horses, there may be diarrhoea,
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 be 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 functions and
management of anaphylaxis.


CHEMICAL WARFARE AGENTS
Chemical warfare is the use of the toxic properties of chemical
substances to kill, injure or incapacitate an enemy in warfare
and associated military operations. ( terrorism?)
A chemical substance intended for such use in military
operations is defined as a chemical warfare agent (CWA).
Chemical agents have been used in war since times
immemorial.
North Atlantic Treaty Organization (NATO) has
classified agents of chemical terrorism as
Blister agents- Sulfur mustard, Nitrogen mustard, Lewisite
Nerve agents- Tabun, Sarin, Soman
Asphyxiants - Cyanogen chloride, Hydrogen cyanide, Arsine
Choking Agents-Chlorine, Chloropicrin, Phosgene
Incapacitating/behavior altering agents-Lysergic acid
diethylamide (LSD-25),ketamine, fentanyl, carfentanil and several glycolate
anticholinergic.- 3-quinuclidinyl benzilate,