Zootoxins - Scorpion, Spider, Toads and Fish Toxins by Dr. Mohan B R

ZOOTOXINS – SCORPION, SPIDER,
TOAD AND FISH TOXIN
2/22/2023 10:34:49 AM 1

CONTENTS
 What is Poison???
 What is Toxicant???
 What is Toxin???
 What is Venom???
 What is Zootoxin???
 Scorpion Toxins.
 Spider Toxins.
 Toad Toxins.
 Fish Toxins.
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WHAT IS POISON????
 Any substance or matter which when applied either externally or internally
produces ill effects on health or entirely destroys the life.
What is Toxicant????
 It is a synonym of poison and is a more professional term.
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WHAT IS TOXIN????
 Special types of poison that are produced by living organisms in small
quantities.
 Classified as biotoxins.
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WHAT IS VENOM????
 It is a toxicant synthesized in a specialized gland and ejected by the process
of biting or stinging.
 It is also a zootoxin but is transmitted by the process of biting or stinging.
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WHAT IS ZOOTOXIN????
 Toxins produced by the lower animals.
 These toxins may have genus name as prefix.
 E.g.: Bufotoxin from the toxic toad.
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SCORPION
 Order: Scorpionida.
 Family: Buthide.
 Genera: Buthus, Parabuthus, Mesobuthus, Tityus, Leiurus, Androctonus
and Centruroides.
 Black Bark Scorpion (Centruroides exilicauda) – Mexico and South west
America.
 Leiurus quinquestriatus (Deathstalker) – Asia and Africa.
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CHARACTERISTICS
 Eight legged arthropods.
 Hard exoskeleton and 3 body parts – cephalothorax, abdomen and tail
(stinging apparatus).
 Regulate the amount of venom to be injected through striated muscles –
usual amount is 0.1 – 0.6mg.
 Nocturnal and take shelter during day under rocks, piles of debris or may
hide inside house in clothing and shoes.
 Habitat: Desert and semi arid regions
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CHARACTERISTICS
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TOXIC COMPONENTS
 Heterogenous mixture.
 Composed of various concentration of – Neurotoxin, Cardiotoxin,
Nephrotoxin, Hemolysin, Agglutinins, Coagulins, Phosphodiesterases,
Phospholipases, Hyaluronidases, Glycosaminoglycans, Histamine,
Serotonin, Tryptophan, and Cytokine releasers.
 Most potent – Neurotoxin.
 Long and Short chain polypeptides.
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TOXICITY
 Amount, Species, and Site of injection.
 Leiurus quinquestriatus – potent venom.
 S/C LD value in mice: 0.16 – 0.50 mg/kg.
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MECHANISM OF ACTION
 Long chain polypeptide – voltage dependent sodium channel = stabilize it in
open position – firing of somatic, sympathetic and parasympathetic neurons.
 Excess release of NT – Ach, Noradrenaline and Adrenaline.
 Cause autonomic and neuromuscular over-excitation signs.
 Over-excitation followed by inhibition of normal nerve impulse
transmission.
 Short chain polypeptide – block Potassium channel – Over excitation.
 Binding to the target sites is reversible, but different neurotoxins has different
affinities.
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CLINICAL SIGNS
 Local pain, numbness, hyperesthesia, skin discoloration, salivation,
agitation, wheezing, tachycardia, hypertension and muscle spasm.
 Cranial nerves and somatic motor abnormalities – eye movement disorder,
blurred vision, tongue fasciculation, convulsions, impaired pharyngeal
muscle control and jerking of extremities.
 Death – Respiratory and Cardiac failure.
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NECROPSY FINDINGS
 Toxic myocarditis
 DIC
 Acute Pancreatitis, and
 Pulmonary edema.
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TREATMENT
 Specific Therapy: Antivenom therapy – its safety, efficacy and specificity is
not clear.
 Cold Compress – Pain and Inflammation.
 Atropine Sulphate – control excess parasympathetic manifestations.
 Propranolol – Beta adrenoceptor blocker.
 Calcium gluconate – IV – Muscle spasm.
 First aid – Wound Cleaning and TT injection.
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CONTRAINDICATIONS
 Morphine and Meperidine HCl – worsen the respiratory depression.
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THERAPEUTIC USE OF VENOM
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EXAMPLES
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SPIDER
 Order: Arachnidae.
 Family: Theridiidae.
 Black widow spider, Brown recluse spider, red widow spider, red-legged
spider, desert violin spider and Cobweb spider – Human bites.
 Black widow spider (Lactrodectus mactans) – Most toxic.
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CHARACTERISTICS
 Black widow spider – Eastern and South-western US.
 Female spiders – 1-1.5 inch in size, shiny black in color – red hourglass mark
on the abdomen.
 Male spiders – 0.5 inch in size and no hourglass mark on abdomen.
 After mating female eats male – Name “Widow”.
 Claw like hallow fangs – connected to 2 venom glands in cephalothorax.
 Brown recluse spider – Fiddle or violin marking on its back.
 Back and belly – Brown.
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TOXIC COMPONENTS
 Black widow spider venom – α- lactrotoxin / α- latrotoxin – potent
neurotoxin.
 Isoleucin and leucin, lipoproteins and hyaluronidase.
 Brown recluse spider venom – Hyaluronidase, proteases, sphingomyelinase
D, esterases and haemolysin.
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TOXICITY
 Both male and female black widow spider are toxic. But female is large
enough to envenomate an animal.
 Venom gland – less than 0.2 mg of venom.
 𝐿𝐷50 = 0.005 – 1.0 mg/kg B.wt.
 Cause systemic reaction.
 Brown recluse spider – necrotic local lesion at the site of bite and also cause
DIC.
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MECHANISM OF ACTION
Black Widow Spider:
 α- lactrotoxin – acts at NMJ – release of Ach from pre-synaptic nerve fiber.
 Ach release continues – complete depletion of NT.
 Ach release – severe painful cramping.
 Neurotoxins binds to glycoproteins or gangliosides on neuromuscular
synaptic membranes and allow opening of cationic channels.
 𝑪𝒂𝟐+
channel binding – Increase membrane permeability to calcium and
enhances depolarization.
 Enhanced calcium influx cause – calcium dependent release of NT.
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 Solid Black Line – Casual
Findings.
 Solid Grey Line – Interaction
of Unknown Findings.
 Dotted Arrow – Respective
Phenomena.
 α LTX – Latrotoxin.
 PTP-σ – Protein Tyrosine
Phosphate.

Brown Recluse Spider:
 Primarily cytotoxic to endothelial cells.
 Venom – DIC and microthrombi formation within capillaries.
 Capillary occlusion, hemorrhage and necrosis.
 Polymononuclear leucocytes and complement – potentiating the response to
envenomation.
 Bite is slow to heal.
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CLINICAL SIGNS
Black Widow Spider:
 Dull-numbing pain, which gradually spreads from the region of bite to the
muscles of the entire body.
 Restlessness, Vomiting, Anxiety or apprehension, Muscle cramps, and rapid,
shallow and irregular respiration.
 Later stages – abdominal rigidity and tenderness, muscle fasciculation,
tonic-clonic convulsions, sweating, hypersalivation, flaccid paralysis and
shock.
 Death – Respiratory or cardiovascular failure.
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Brown Recluse Spider:
 Two forms – Cutaneous and Viscerocutaneous forms.
 Cutaneous form – Pain and edema at bite site and progress to ulcerated
wound.
 Viserocutaneous form – More severe form.
 Hemolytic anemia, Hemoglobinuria, Jaundice and Hyperthermia.
 Complications – Intravascular hemolysis – Kidney damage.
 Skin lesions resolve in 1 – 3 weeks.
 Some lesions are permanent and may need skin grafting.
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CUTANEOUS FORM
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NECROPSY FINDINGS
 Only venous congestion.
Diagnosis:
 Based on Clinical signs.
 No laboratory analysis is useful.
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TREATMENT
 Most spider envenomation are self limiting and clinical signs resolve within
few hours.
 Specific therapy – Antivenin (Black widow spider) – IV.
 Muscle relaxants – methocarbamol; analgesics – Meperidine; Sedatives –
Diazepam = control muscle spasm and pain.
 Atropine Sulphate – Reduce salivation.
 Therapy for shock – Corticosteroids and Fluids.
 Antihistamines and Respiratory stimulants.
 Brown recluse spider envenomation – Hemolytic anemia – Blood transfusion.
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PROGNOSIS
 Black Widow Spider: Dogs – Good; Cats – Guarded.
 Prolonged recovery.
 Weakness and paralysis persist for several days.
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TOADS
 Family: Bufonidae.
 Genus: Bufo.
 Not present in Australia and Antarctica.
 Toxic toads – Bufo marinus (Marine toad, Giant toad), Bufo alvarius (River
toad) and Bufo vulgaris (Common toad).
 Two lumps on either side of the back of their head – parotid glands – produce
venom – warding off intruders and predators.
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CHARACTERISTICS
 Marine toad – large and lethargic – South and Central America.
 Grow 9 inches in length and about 1 Kg in weight.
 Prefer developed areas – man made canals, and ponds for spawning and
collect under electric lights to feed on insects.
 Venom – thick, creamy-white, highly irritating substance secreted by glands
located dorsal and posterior to eyes and other dermal structures including
warts.
 Expelled – contraction of peri-glandular muscles in the skin.
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TOXIC COMPONENTS
 Mixture of different classes of toxic chemicals.
First Class: Cardiac glycosides – Bufodienolides.
 2 subgroups – Bufogenins and their derivative bufotoxin.
 Affect cardiovascular system – Heart and Blood vessels.
Second Class: Phenethylamines and their derivatives.
 Catecholamines – Dopamine, Noradrenaline and Adrenaline.
 Not prominent as bufodienolides in producing the quick adverse effects.
 Contribute to vasoconstriction. 2/22/2023 10:34:49 AM 54

2/22/2023 10:34:49 AM 55
Third Class: Tryptamines and their derivatives.
 Serotonin and 5- hydroxy dimethyltryptamine (5-hydroxy DMT,
bufotenine).
 Oxytocic action and frequently a marked pressor effect.
 5-MeO-DMT trptaminergic derivative – Bufo alvarius – hallucinating and
psychoactive effect.
Fourth Class: Non-cardiac sterols.
 Cholesterol, Provitamin D, Ergosterol and Gamma sitosterol.

TOXICITY
 Venom potency varies from species to species.
 Bufo vulgaris – least toxic and Bufo marinus – most toxic.
 Commonly occurs in dogs, cats and children.
 Dogs, severity – size of the dog and amount of toxin absorbed into the blood
stream.
 Susceptibility – Puppies and small breeds – Dachshunds, Mini-Pins, Jack
Russel Terries and miniature Schnauzers.
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TOXICITY
 Bufo toads are more active in spring and summer months – warm and moist
environment.
 Also Nocturnal – most of the poisoning in evening, late-night or early
morning hours.
 A dog will die after exposure to B. marinus toxin.
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MECHANISM OF ACTION
 Ingestion – Absorption across the mucous membranes.
 Bufodienolides bind to a specific receptor site on cardiac cell membrane –
Inhibit 𝑵𝒂+/𝑲+ ATPase pump.
 Normally, 𝑁𝑎+/𝐾+ ATPase pump 𝑁𝑎+into the cell and 𝐾+ out of the cell.
 When this pump is inhibited it depends on the 𝑵𝒂+/𝑪𝒂𝟐+ pump – maintain
𝑁𝑎+
gradient.
 Increase intracellular calcium concentration in cardiac cells – excess cardiac
stimulation and ventricular fibrillation.
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MECHANISM OF ACTION
 Failure of 𝑵𝒂+
/𝑲+
ATPase pump – Increase the extracellular potassium –
hyperkalemia.
 Death – Heart failure.
 Bufodienolides – similar effects to that of digitalis.
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CLINICAL SIGNS
 Variable and ranges from local to systemic effects.
 Local effects – Profuse or sometimes frothy salivation.
 Vigorous head shaking, pawing at mouth and retching – extreme irritant
nature of venom.
 More severe intoxication – Cardiac arrhythmias, dyspnea, diarrhea,
incoordination or stiff gait, cyanosis, apparent blindness, convulsions,
prostration and collapse.
 High morbidity.
 Death – Ventricular fibrillation leads to cardiac failure.
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NECROPSY FINDINGS
 No distinct lesions.
Diagnosis:
 Oral examination.
 Toad pieces in the vomitus.
 Circumstantial evidences and clinical signs.
 Hematological chemistry – Polycythemia, Hyperglycemia, Hyperkalemia,
Hypercalcemia, and Uremia.
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TREATMENT
 No specific antidote for bufotoxin.
 Thoroughly clean the oral cavity of the animal using water. Sometimes it
needs rubbing of the mucus membrane since the toxin is sticky.
 Detoxification – Activated charcoal and Osmotic cathartic.
 Large dose of Propranolol (up to 2mg/kg) – Cardiac arrhythmia and
potential fibrillation.
 Atropine Sulphate – Salivation and Bronchoconstriction.
 Sedatives – Phenobarbitone or Diazepam – CNS excitation.
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FISH
 Produce poisoning – Attacking and biting (Shark); Injecting through stings
(Stingrays); and eating fish whose flesh is toxic (Puffer fish).
 Injected venom through spines – intense pain and potentially fatal.
1. Tetrodotoxic Fish / Pufferfish Poisoning.
2. Ciguatera.
3. Scombroid Fish / Scombroid Poisoning.
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TETRADOTOXIC FISH
 Potent marine neurotoxin – Tetrodotoxin (TTX).
 Syndrome – Tetrodotoxication.
 Order: Tetraodontiformes.
 Family: Tetrodontidae.
 Genera: Tetraodon, Fugu and Takifugu.
 Species: T. fahaka, T. miurus and T. mbu; F. flavidus, F. poecilonotus and F. niphobles;
AND T. rubripes.
 Other marine and terrestrial animals store TTX – Starfish, Toads, Crabs, Mollusca,
Salamanders and algae.
 Susceptible: Pets and Humans consume toxic fishes. 2/22/2023 10:34:49 AM 69

CHARACTERISTICS
 Habitat – Coastal areas, Oceans and live in deep sea.
 Ability to inflate themselves – by swallowing water or air.
 Four large teeth – beak like structure – crush the shells of mullscans and
crustaceans.
 Neurotoxin – internal organs (Defense chemical).
 Found in Ovaries and Liver.
 In Japan and Korea – meat of pufferfish is delicacy.
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TOXIC COMPONENTS
 Toxin – Tetrodotoxin = anhydro tetrodotoxin 4-epitetrodotoxin, tetrodonic
acid.
 Molecular formula - 𝑪𝟏𝟏𝑯𝟏𝟕𝑶𝟖𝑵𝟑.
 Oxygen link between 𝑪𝟓 and 𝑪𝟏𝟎 − cause toxicity.
 Produced by the bacteria – Pseudoalteromonas tetraodonis and some species
of Pseudomonas and Vibrio acquired through food.
 Saxitoxin – PSP.
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CHEMICAL STRUCTURE OF TOXIN
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TOXICITY
 Accidental consumption of fish or meat tainted with pufferfish.
 Weigh for weight – ten times as deadly as the venom of many snakes.
 10 to 100 times as lethal as black widow spider.
 >1200 times deadlier than cyanide.
 𝐿𝐷50 = 10 mcg/kg IV in mice (same as saxitoxin).
 Absorption better than saxitoxin.
 More toxic during winter.
 Single pufferfish – kill 30 adult humans. 2/22/2023 10:34:49 AM 76

MIGRATION OF TETRODOTOXIN
2/22/2023 10:34:49 AM 77

MECHANISM OF ACTION
 Neurotoxin – Blocking neurotransmission in CNS and PNS.
 Reaches the voltage-gated 𝑵𝒂+
channels – surface of nerve membrane and
bind to pore opening of the channel.
 Binding – Interaction of positively charged guanidino carboxylate groups on
the side chains in the mouth of channel.
 Binding – blocks the 𝑵𝒂+ channels – 𝑁𝑎+ movement stops – Action potential
along the nerve membrane stops.
 Blocks 𝑵𝒂+
current in myocytes, inhibit their contraction.
 Immunity to the poison due to mutation in protein sequence of 𝑁𝑎+
channel
pump on cell membrane. 2/22/2023 10:34:49 AM 78

CLINICAL SIGNS
 Appear between 20 minutes to 3 hours.
 Numbness of lips, tongue and fingers.
 Nausea, vomiting, epigastric pain, muscular paralysis of extremities, ataxia
and respiratory distress.
 Speech is affected – dyspnea, cyanosis and hypotension.
 Paralysis, convulsions, mental impairment, cardiac arrhythmia and
unconsciousness.
 Death – 4 to 6 hours – Respiratory paralysis.
2/22/2023 10:34:49 AM 81

NECROPSY FINDINGS
 No specific lesions.
Diagnosis:
 History of eating fish.
 Circumstantial evidences.
 Clinical signs.
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TREATMENT
 It is not antigenic – No antiserum is available.
 Intestinal detoxification with gastric lavage and activated charcoal.
 Supportive care – Artificial respiration.
 Anticholinergics – Edrophonium.
 Prognosis – Grave.
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CIGUATERA
 Ingesting certain marine fish – bioaccumulate a toxin – Ciguatoxin (CTX).
 Synthesis – Micro-algae Gambierdiscus toxicus – tropical water.
 Species of reef fish – warm tropical waters.
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TOXICITY
 Lipid soluble and a very heat resistant toxin – not destroyed by temperature,
gastric acid or cooking method.
 Toxin – won’t affect odor, color or taste of the fish.
 𝐿𝐷50 = 0.45 mcg/kg IP in mice.
 0.1 mcg PO – illness in humans.
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CHEMICAL STRUCTURE
2/22/2023 10:34:49 AM 90

MECHANISM OF ACTION
 Opening of voltage dependent 𝑵𝒂+
channels – cell membranes – membrane
depolarization.
2/22/2023 10:34:49 AM 91

CLINICAL SIGNS
 GI distress – Nausea, Vomiting and Diarrhea.
 Neurological signs – Headache, muscle ache, numbness, ataxia and
hallucination.
 Hot-cold sensation reversal.
 Signs lost for weeks to months also for many years.
 Excreted in milk and transmitted sexually.
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DIAGNOSIS
2/22/2023 10:34:49 AM 94

TREATMENT
 Gut emptying.
 Decontamination – charcoal in acute cases – prevent severe ongoing
vomiting and diarrhea.
 Vitamins, Antihistamines, Anticholinesterases, Steroids and Tricyclic
antidepressants – Limited results.
 Mannitol – 1g/kg IV – administered within 72 hours – effective.
 Control – Avoid consumption of reef fish.
2/22/2023 10:34:49 AM 95

SCOMBROID FISH
 Consumption of scombroid and scombroid like marine fish species.
 Family: Scombridae (Tunas and Mackerels).
 Poison causing fish – Scombridae family and non-Scombridae fish (Bluefish,
Dolphin or Mahi-mahi, and Amberjack).
2/22/2023 10:34:49 AM 99

 It is attributed to the histamine produced by bacterial decarboxylation of
amino acid histidine – High concentration in fish.
 Histamine concentration reach up-to 5mg/kg in fish.
 Histamine – destroyed in GIT (Humans and Animals).
 Putrescine and cadaverine – trigger the toxicity of histamine.
2/22/2023 10:34:49 AM 102

CHEMICAL STRUCTURE
2/22/2023 10:34:49 AM 103

MECHANISM OF ACTION
2/22/2023 10:34:49 AM 104

CLINICAL SIGNS
 Few minutes to two hours.
 Allergic reaction – Histamine.
 Initially – Nausea, Vomiting, Diarrhea, Dizziness and Abdominal pain.
 Advanced – Skin rashes, hives, edema, urticaria, tachycardia, hypotension
and respiratory stress.
 Poisoning – within 16 hours with no lasting ill effects.
 Fatality – Rare.
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URTICARIA IN CANINES
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TREATMENT
 No specific therapy is present.
Supportive Therapy:
 IV Fluids.
 Oxygen.
 𝑯𝟏 𝒂𝒏𝒅 𝑯𝟐 receptor antagonist – some success.
2/22/2023 10:34:49 AM 107

REFERENCE
 Barsoum, G.S., Nabawy, M. and Salama, S., 1954. Scorpion Poisoning-its
Signs, Symptoms and Treatment. Journal of the Egyptian Medical Association,
37(8), pp.857-94.m.
 Freire-Maia, L. and Campos, J.A., 1989. Pathophysiology and treatment of
scorpion poisoning. In Natural toxins (pp. 139-159). Pergamon.
 Garg, S.K., 2011. Veterinary toxicology. CBS Publishers & Distributors.
 Gawade, S.P., 2007. Therapeutic alternatives from venoms and toxins. Indian
Journal of Pharmacology, 39(6), p.260.
2/22/2023 10:34:49 AM 109

110
 Haddad Junior, V. and Haddad Junior, V., 2021. Ingestion of Venomous Aquatic
Animals: Toxinology, Clinical Aspects, and Treatment. Medical Emergencies Caused by
Aquatic Animals: A Biological and Clinical Guide to Trauma and Envenomation Cases,
pp.301-334.
 Herms, W.B., Bailey, S.F. and McIvor, B., 1935. The black widow spider. Bulletin of the
California Agricultural Experiment Station, (591).
 Isoardi, K.Z. and Isbister, G.K., 2020. Poisoning by venomous animals. Medicine,
48(3), pp.220-223.
 Mailho‐Fontana, P.L., Titon Jr, B., Antoniazzi, M.M., Gomes, F.R. and Jared, C., 2022.
Skin and poison glands in toads (Rhinella) and their role in defence and water
balance. Acta Zoologica, 103(1), pp.112-128.
 Sandhu, H.S. and Brar, R.S., 2008. Textbook of veterinary toxicology. Kalyani publishers.
 Trakulsrichai, S., Chumvanichaya, K., Sriapha, C., Tongpoo, A. and Wananukul, W.,
2020. Toad poisoning: clinical characteristics and outcomes. Therapeutics and clinical
risk management, pp.1235-1241.

Zootoxins - Scorpion, Spider, Toads and Fish Toxins by Dr. Mohan B R

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