PPB 532

VENOMS
❑ Are complex organic substances

❑Contain: components e.g.

✓Anticoagulants

✓Glycosides

✓Formic acid

✓Tetrodotoxin in octopuses and pufferfish: neurotoxic; a

sodium channel inhibitor; causes gastrointestinal, neurologic &

cardiac symptoms ; no known antidote

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 ✓Hyaluronidase: enables other components of toxins to

penetrate
✓Phospholipase A2 stimulants e.g melittin leads to increased

presence and activity of PLA2 resulting from a snake or insect

bite, arachidonic acid is released from the phospholipid
membrane disproportionately. There is inflammation and pain
occur at the site; also hemolysis

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BEES AND WASPS
❑Wasp venom: acetylcholine, serotonin, histamine releasers,

hyaluronidase
✓Wasps can sting severally

❑Bee's venom: melittin (promotes inflammation), histamine

releasers, hyaluronidase
✓A bee stings once but produces pheromones that attract other

bees to sting

✓Produce: local swelling, anaphylaxis, death

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❑Treatment

✓O2 therapy in respiratory depression

✓Adrenaline 0.2-0.5mg IM every 15 m; 3doses

✓If wheezing : β2 agonists

✓Remove spines ( for bees)

✓Chlorpheniramine 10mg IV stat, then IM/SC/oral TDS × 3/7

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SPIDERS
❖Toxic: Black widow & black recluse spiders

❑Black widow spider

➢Neurotoxic: produces latrotoxin which stimulates

neurotransmitter release from neurons in the presence or absence

of extracellular Ca2+
✓ Causes ascending motor paralysis ; localized pain; paresthesia;

muscle rigidity, spasms &weakness; headache, eyelid oedema;

rash; salivation; resp paralysis; coma; death
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❑Black recluse spider

➢They contain hyaluronidase, esterases, lipases, alkaline

phosphatase, 5-ribonucleotide phosphohydrolase &

sphingomyelinase D
➢Venom also inactivates serum hemolytic complement, leading

to intravascular coagulation, occlusion of small capillaries,

and tissue necrosis, systemic depletion of clotting factorsVII, IX,
XI & XII

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 ✓Lipases can cause free lipids in the blood that may act as

inflammatory mediators and/or cause embolization

✓Ulcerating wound takes long to heal; mostly affected are the

young; elderly and those of low immune status

➢Venom is hemotoxic and necrotizing

✓Fever; malaise; nausea; vomiting; rash; muscle & joint pain;

hemolytic anaemia, DIC; thrombocytopenia

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 ❑Treatment
✓T.T
✓Monitor vital signs
✓IV Antivenin over 15 mins
✓Muscle pain/spasm: Methocarbamol 10 mls IV
✓Pain: Morphine; tramadol
✓Salivation: atropine
✓Antihistamines
✓Wound: cleaning, dressing;
✓Antibiotics in presence of infection
✓Rest

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 SCORPIONS
➢Have sting apparatus on the tail

➢The venom contains mucopolysaccharides, hyaluronidase,

phospholipase, acetylcholinesterase, serotonin, histamine,

protease inhibitors, histamine releasers, neurotoxins
➢Serotonin mediates most of the immediate pain experienced

after an envenomation

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 ➢Venom: simulates strychnine (a spinal convulsant)

➢Acts on smooth and striate muscles

➢Produces: localized swelling; excitability; muscle contractions;

trembling; paralysis; oedema; fever; respiratory distress

➢Improvement in 15-20 hrs.; death may occur

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❑Treatment

✓Assisted ventilation

✓Appropriate antivenin

✓Muscle relaxants

✓Sedatives

✓Atropine to counter sympathetic action

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 SNAKES
❖Poisonous species

➢Elapidae: cobras, coral snakes; are relatively long, thin, usually

uniformly-coloured snakes with large smooth symmetrical

scales on the top of the head.
✓Cobras, raise the front part of their body off the ground and

spread a hood
➢Hydroptidsae snakes; have flattened paddle-like tails

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➢Viperidae: vipers and puff adders; divided into typical vipers

(Viperinae) and pit-vipers (Crotalinae)

✓Relatively short, thick-bodied, short-tailed snakes with many

small rough scales on the top of the head and characteristic

patterns of coloured markings on their backs.
✓The include Russell’s vipers (Daboia), saw-scaled vipers

(Echis), Malayan pit viper (Calloselasma), mamushis

(Gloydius), hump-nosed pit- vipers (Hypnale), Chinese habu
(Protobothrops mucrosquamatus), and green pit vipers
14 (Trimeresurus) 7/1/2023
 ❖Clinical presentations of snake bites

❑Cytotoxic bites: puff adders; cobras

✓Swelling; watery blood leak; pain; shock; discolouration

❑Neurotoxic bites: mambas; cobras

✓Swelling; cold/clammy sweat; mydriasis, joint aches, salivation,

lymphadenopathy, breathing difficulties

❑Haemotoxic bites: saw scaled viper; boomslang

✓Bloody gums, nose, eye corners; bleeding from scratches and

previous scars/old wounds

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Components of snake venom
❑Proteases: elapids, pit vipers, sea snakes; digest tissue proteins

❑Acetylcholine: mambas – acts on the heart and neuromuscular

muscular junction
❑Phospholipase A2: damage mitochondria, red blood cells,
leucocytes, platelets, peripheral nerve endings, skeletal muscle,
vascular endothelium;
✓Produces presynaptic neurotoxic activity, cardiotoxicity,
myotoxicity, necrosis, hypotension, haemolysis, anti-coagulation,
haemorrhage, plasma leakage (oedema formation) and auto
pharmacological release of histamine and other autacoids
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❑ Cholinesterase: elapids – muscle blockade

❑Snake venom metalloproteases (SVMPs) damage basement

membranes, causing endothelial cell damage and spontaneous

systemic bleeding.

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18 7/1/2023
 Summary of snake envenomation
Snake venoms
❖Several snake venoms block nicotinic acetylcholine receptors at the
NMJ resulting in muscular weakness and paralysis
❖Muscarinic toxins from mamba snakes inhibit the binding of
quinuclidinyl benzilate to muscarinic acetylcholine receptors
❖ Mamba fasciculins inhibit acetylcholinesterase, thus enhancing the
action of acetylcholine
❖ Phospholipases A2: elapids , hydrophids , viperids & crotalid
venoms
19 01/07/2023 16:50
❖Phospholipases A2 and proteases can cause a cascade effect at

various levels of blood coagulation causing bleeding diathesis

❖Metalloproteases can cause cytoskeleton destruction, disrupting

cellular adhesion, cell damage and apoptosis

❖Other venoms have pre-synaptic action through inhibition of

neurotransmitter release from the nerve ending

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❑Snake envenomation also has elevations of serum TNFα, IL-1,
IL-6, IL-10, IFN-γ , NO & vasoactive mediators e.g
catecholamines, dopamine, thromboxanes, angiotensin II,
endothelins and prostaglandins, free radicals and adhesion
molecules
❑Involvement of cytokines and vasoactive mediators in snake
envenoming is therefore similar to that observed in sepsis
❑Bothrops jararaca venom inhibits angiotensin converting
enzyme & decreases blood pressure
❑Habu snake venom has a direct effect on the mesangial cells &
vascular endothelial cells by decreasing the cell viability and
increasing the number of apoptotic cells

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 ❑Snake poisoning also causes hemodynamic changes such as

hypotension ,transient hypertension, intravascular haemolysis,

haemorrhage, disseminated intravascular coagulation
❑Myonecrosis, complement activation and free radicals further

contribute to hemodynamic changes

❑ Sarafotoxin from burrow or mole vipers has direct vascular

effects similar to endothelin

❑Snake bite cause neuromuscular symptoms through both action

on ion channels and muscle cell membrane by phospholipase A2

22
causing rhabdomyolysis 7/1/2023
❑Snake venom enzymes affect blood coagulation cascade,

platelets & vascular endothelium causing haemorrhagic diathesis

& disseminated intravascular coagulation
❑Procoagulant enzymes are thrombin-like, splitting fibrinogen,

or activators of factors V, X, prothrombin and other clotting

factors, causing DIC, consumption coagulopathy and
incoagulable blood

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❑Pulmonary haemorrhage due to pulmonary capillary injury caused

by metalloproteases & coagulopathy as seen with envenomation by

viperid or crotalid snakes
❑Hypersensitivity to venoms can play some role in interstitial

nephritis. Nephrotic syndrome has been described in snake bite

❑DDX

✓Bruises; hematomas; infections of the head; cellulitis; allergic

reactions; arthritis; photosensitivity

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 Management and Treatment
Within 1 hr
✓Reassurance/Remain calm

✓Patient not to move bitten part

✓Lower bitten part below heart level

✓Remove constrictions on bitten area

✓Light tourniquet above bite area

✓Incise fang marks and suction within 1 hr

✓Specific antivenin 10 ml IV stat

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 ✓Pain: analgesics e.g paracetamol

✓Allergies/coma: adrenaline 0.5 mg adults/ 0.2mg children;

corticosteroids
✓Eyes spat on: wash with water; adrenaline eye drops

✓Muscle spasms: Calcium gluconate

✓Convulsions: diazepam

✓Hemorrhage: transfuse; fluid and electrolyte therapy

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 RABID ANIMALS
➢Rabies virus is a lyssavirus

➢Infects CNS affecting brain and causing death

➢Sources: bite from infected animal; contaminated mucous

membranes; aerosol transmission; organ transplants

➢Incubation is long: 2-8 wks.

➢Early symptoms: fever; headache; weakness; itching &

paresthesia at site of bite

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➢Later: insomnia; anxiety; confusion; partial or ascending
paralysis, excitation; hallucinations; salivation; hydrophobia;
difficulty in swallowing; encephalitis; death

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 MANAGEMENT
❑Wound:

✓Irrigate with saline solution; clean with soapy water; povidone

of iodine
✓Infiltrate wound with rabies immunoglobulin

❑T.T

❑Antibiotics eg amoxicillin + metronidazole or flucloxacillin

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 ❑Antirabies vaccine
➢IM 1 ml ( 1 dose) at days 0,3,7,14,28
OR
➢Intradermal 0.1 ml at 2 sites @ upper arm or forearm at days
0,3,7 and 1 dose at 1 site at 30,90

❑Pre exposure prophylaxis

➢Lab staff, animal handlers, wildlife officers
✓3 doses: 0,3,7
✓Previous exposures: 2 booster doses @ 0,3

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 Centipede and Millipede Bites
❑Centipede's venom produces burning pain, swelling, erythema ,
lymphangitis, Dizziness, nausea, and anxiety, rhabdomyolysis ,renal
failure
❑Treatment
✓Washing of the site
✓Application of cold dressings
✓T.T
✓Narcotic analgesics
31 ✓Local lidocaine infiltration 7/1/2023
❑Millipedes do not bite but secrete defensive fluids that burn and

discolor human skin.

➢ Affected skin may blister and exfoliate. If secretions enter in the

eye, they cause pain , inflammation ,corneal ulceration &

blindness.
❑Management

 Irrigation with water/N/S ; use of analgesics & care of affected

skin

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MARINE INVERTEBRATES ANDVERTEBRATES
❑Sea anemones; jelly fish; octopus; sting ray possess specialized
living stinging cells (cnidocytes) , which encapsulate
intracytoplasmic stinging organelles (cnidae)
❑Symptoms:
prickling; burning; pruritus; paresthesia; anaphylaxis, painful
throbbing with radiation ; skin is reddened, darkened, edematous
and/ or blistered
❑Management

✓T.T

✓Pain relief: immerse in warm water immediately; morphine, fentanyl,

pethidine
✓Bleeding: apply pressure
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 ✓Decontaminate the skin area with 5% acetic acid : it inactivates
the nematocysts should be applied immediately and then for
10–30 min tds/ qid.
✓Shaving the skin helps remove remaining nematocysts

✓Topical local anaesthesia ointment eg lidocaine;

✓Remove spines: resist the urge to scratch, scratching fractures
retrievable spines;
✓Rubbing the skin leads to further stinging by adherent
nematocysts

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 ✓Granulomas : excise; administer intralesional triamcinolone
(5mg/mL).
✓Wound: Explore ,debride wound, Irrigate with sterile
water/NS/ povidone, leave them open
✓Severe vesiculation : systemic glucocorticoids
✓Allergies/pruritus: antihistamines; corticosteroids
✓Muscle spasm: 10% calcium gluconate (5–10 mL)
✓Convulsions: diazepam 5-10 mg
✓Antibiotics : serious wounds & immunocompromised ptns

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