45,000 snakebites in the US annually, 78000 are from venomous species which result in 10 deaths' 255

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• 45,000 snakebites in the US annually, 7-8000 are
  from venomous species which result in 10 deaths.
  25-50 of bites are dry (bite, no venom). 120
  snake species indigenous to US only 26 are
  venomous only two families of snakes native to
  the US are venomous Elapidae (coral snakes) and
  Crotalinae (pit vipers). Pit vipers account for
  95 of envenomations. Exotic venomous snakes are
  also a source of envenomations.

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• Pit Vipers (Crotalinae) Heat sensitive pit
  between eyes and nostrils, elliptical pupil and
  triangular head.
• Rattlesnakes, cottonmouths water moccasins
• Mojave rattlesnakes are the only pit viper with a
  neurotoxic venom
• Coral Snakes (Elapidae) Shy, reclusive, must be
  provoked
• Eastern coral snake (AR, NC, SC, FL, LA, GA, MS,
  TX)
• Western coral snake (AZ, NM)

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• Toxicity
• Pit Vipers
• Multiple toxins (local damage)
• Proteolytic enzymes
• Anti-coagulants
• Mojave Rattlesnake toxins
• A neurotoxin (blocks Ca2 channels)
• B hemotoxin cytotoxin (found in Phoenix)
• Coral Snakes
• Neurotoxin Potent toxin causes paresthesias,
  weakness, CN dysfunction, confusion,
  fasiculations and lethargy.
• a-neurotoxin postsynaptic Ach receptor
  antagonist causes a nondepolarizing NM blockade.
• ß-neurotoxin increases the release of Ach then
  inhibits the release of Ach.

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• Clinical Presentation
• Coral snakes
• Often mild local findings
• Symptoms may be delayed 8-12 hours
• Nausea, vomiting and salivation are common
• Potent neurotoxin causes paresthesias, weakness,
  CN dysfunction, confusion, fasiculations and
  lethargy. Diplopia dysarthria are common early
  symptoms.
• Fatalities are due to respiratory paralysis which
  may develop rapidly

Ptosis indicates significant venom load
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• Clinical Presentation
• Vipers
• Edema usually lt 1 hour, can be pronounced and
  spreads over 8-24 hours
• Ecchymosis, petechiae and hemorrhagic bullae
  often develop.
• Pain is immediate severe
• Systemic effects nausea, vomiting, paresthesias,
  dizziness, diaphoresis. Hypotension,
  rhabdomyolysis, renal failure, respiratory
  distress
• Coagulopathy which can progress to DIC
• Head trunk bites are usually more severe
• Dose of venom/ body weight determines severity,
  children are at higher risk.

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• Treatment
• Pit Vipers
• Immobilize the bite site below just below heart
  level
• Minimize physical activity
• Do not incise the bite marks
• Tourniquets to localize toxins increase local
  tissue damage.
• Antivenoms for Pit vipers
• Polyvalent antivenom made from horse serum, there
  is a risk of anaphylaxis and other reactions,
  pre- or co-administer antihistamines and
  steroids.
• CroFab polyvalent immune Fab, sheep derived Fab
  fragments that bind and neutralize venom. Risk of
  anaphylaxis and other allergic reactions is
  slightly lower.
• Elapidae
• Intubation for any evidence of respiratory or
  cranial nerve dysfunction
• Antivenom for Eastern coral snake bites (none for
  Western). As above there is significant risk for
  anaphylaxis and other allergic reactions.

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• Special Notes
• Dead snakes or heads can still contain venom
• Many bites from pet snakes occur when one of
  the pair is intoxicated.
• Systemic effects of venom takes time, minor
  symptoms may progress.

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• Spiders
• There are 30,000 species of spiders in the world
  , all are venomous but most are harmless to
  humans because they are unable to penetrate human
  skin with their fangs. Only 50 species have
  produced significant envenomations in the US and
  the vast majority of theses result in local pain
  and pruritis. Only two species present
  significant risk in the US.

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• Loxosceles Brown recluse
• Brown, 8-15 mm legs
• Dark violin-shaped mark on cephalothorax
• Nocturnal, prefer dry indoor areas with little
  large animal traffic5 species associated with
  toxicity L. recluse, L. refuscens, L. Arizona,
  L. unicolor, L. laeta.
• The recluse is unable to penetrate human skin
  with its fangs, envenomation requires the spider
  be smashed into the body to inject sufficient
  toxin.
• Latrodectus Black widow
• Common worldwide, 5 species in the US mainly in
  western and southern states
• L.mactans mactans black widow
• Black, shiny, 2-2.5 cm body with long legs
• Female is venomous, male is harmless
• Found in basements, woodpiles and garages

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• Toxicity
• Loxosceles Digestion externale then the spider
  sucks up the juice.
• Severe cutaneous reaction infrequently can cause
  systemic reaction with coagulopathy, hemolysis,
  renal failure, death.
• The vemon is hemolytic and cytotoxic, it contains
  sphingomyelinase D a potent cytotoxin which
  causes WBC aggregation and platelet thrombosis of
  arterioles and venules leading to tissue
  necrosis.
• Latrodectus Potent neurotoxin
• Causes severe muscle spasm, the venom
  (a-latrotoxin) causes neurotoxicity by releasing
  Ach and NE at synaptic junctions. The toxin
  inserts into the presynaptic nerve membrane
  creating an unregulated Ca2 channel resulting in
  massive neurotransmitter release.

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• Clinical Presentation
• Loxosceles
• Local symptoms are immediate with pain and
  pruritis.
• The bite becomes red edematous with the
  development of a purple/black central necrotic
  area. Hemorrhagic bullae may form over 1-3 days
  (indicates large amount of venom).
• Eschar forms then sloughs away to reveal an
  slow/non healing ulcer.
• Systemic involvement is uncommon (most often in
  children) nausea, vomiting, hemolysis, fever,
  thrombocytopenia, renal failure. Deaths are
  rare.
• Intermediate age wound can be confused with 3rd
  degree burn, decubitus ulcer or herpes simplex
  lesion.

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• Latrodectus
• Initial bite may be painful but often is
  overlooked, local reaction is often trivial
  (small papule or punctum), significant swelling
  mitigates against Black widow bite.
• Progression to neuromuscular symptoms may be
  rapid (30-60 min) but usually develop over 6
  hours.
• Spasms, cramps and rigidity begin in the area of
  the bite then spread. Pain is severe associated
  with fasiculations, weakness, vomiting, priapism,
  and rarely rhabdomyolysis. Involvement of the
  abdominal muscles may mimic peritonitis.
• Hypertension with or with out seizures
• Symptoms usually subside over hours may recur for
  up to 7 days.

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• Treatment
• Loxosceles
• Treatment involves local care for swelling, wound
  care to prevent infection if systemic effects
  are noted monitor for hemolysis and renal
  failure.
• Latrodectus
• Local wound care
• Spasms require BZDs, pain meds
• Hypertension requires IV agents as it tends to be
  labile and transient.
• An antivenom (from horse) is indicated for
  significant venom exposure (respiratory arrest,
  seizures, uncontrolled hypertension).

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• Ciguatera Fish Poisoning (Ciguatera toxin)
• The most common nonbacterial fish-borne
  poisoning Gambierdiscus toxicus is the
  dynoflagellate responsible for producing
  ciguatera toxin.
• Sources
• Amberjack, barracuda, dolphin fish, grouper, sea
  bass, sturgeon fish, eel, red snapper, Spanish
  mackerel.
• Toxicity This toxin is heat stable and
  unaffected by cooking temperature or stomach
  acid. It is lipid soluble and does not affect
  taste, color or odor of the fish. Larger fish
  tend to have larger toxin loads.
• Presentation
• Onset of symptoms 1 hour -3 days after ingestion,
  neurologic symptoms may persist for months.

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Ciguatera toxin
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• Common symptoms
• Salivation, chills, pruritis, dyspnea, neck
  stiffness, nausea, vomiting, diarrhea, abdominal
  pain, myalgias arhtralgias, dysuria, urethitis,
  
• Neurologic symptoms include headache, weakness,
  vertigo, ataxia, CN palsy, visual hallucinations,
  seizures and coma in serious cases.
• Paradoxical temperature reversal (cold feels hot,
  hot feels cold)can occur.
• Tooth pain and the sensation of having a loose
  tooth.
• CV symptoms bradycardia, hypotension,
  arrhythmias
• Respiratory bronchospasm, respiratory depression
  and failure
• There is a specific ELISA test for this toxin to
  confirm diagnosis. The differential diagnosis
  includes other fish toxins, snake bite, Hg or As
  toxicity, drug toxicity (beta-blockers, Ca2
  channel blockers, et al).

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• Tetrodotoxin
• Poisonings primarily occur in Japan where the
  consumption of Puffer fish is a delicacy. The
  toxin is present in the skin, viscera and gonads.
  A mortality rate of 50 is reported. This is a
  potential WMD as it is stable in drinking water
  but inactivated by 0.5ppm chlorine
• Sources
• Puffer, balloon, blow, swell, toad and glove
  fishes
• Some salamanders newts
• Blue-ringed octopus
• Frogs, gastropods, crabs and starfish

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• Toxicity Directly impairs Na channel involved
  in nerve muscle excitability, acts directly on
  both central and peripheral synapses. Onset of
  symptoms is 15 minutes to several hours. LD50
  is 8µg/kg. Death can occur within 4-6 hours
• Presentation
• Perioral, tongue, facial and extremity
  paresthesias.
• Blurred vision, dysarthria, salivation, nausea,
  vomiting are usually present
• Hypo- and hyper tension
• Paralysis can occur and is often rapid in onset
• Seizures and coma can occur
• Death is due to respiratory failure
• Differential DX
• Other fish toxins
• Guillain-Barre syndrome
• Octopus envenomation
• Botulism
• Gastroenteritis
• There is no antidote

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• To serve fugu one must be a trained and licensed
  fugu chef licensure requires years of
  apprenticeship, a rigorous written examination
  and chefs are required to demonstrate correct
  preparation of this delicacy for a panel of
  experts they are required to eat their final
  exam (I suppose its pass/fail).

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• Scombroid Fish Poisoning (Scombrotoxin) the
  second most common fish poisoning
• Sources
• Dark-meat fish tuna, mackerel, bonito, marlin
  Mahi-mahi, sardine, yellowtail, herring,
  bluefish
• Toxicity
• Histidine decarboxylase produced by normal
  bactrial flora that have grown due to improper
  storage.Decarboxylation of histidine (normally in
  high concentration in these fishes) to histamine.
  
• Presentation
• Onset of symptoms is usually with in 10-60
  minutes of consumption often the fish has a
  bitter or peppery taste. Symptoms usually last
  3-36 hours Flushing, angioedema of skin and
  face, tachycardia, palpitations, asthma-like
  symptoms, headache, anxiety, dizziness weakness,
  nausea, vomiting diarrhea.

The eruption started 1 hour after eating a tuna
dish. One hour after presentation with no
treatment the eruption resolved. Two additional
cases presenting a similar clinical picture and
having eaten tuna from the same restaurant were
observed during the following days.
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• Test the fish Histamine levels in the fish
  (normally 1mg/100g) are usually at least
  100mg/100g (as little as 20mg/100 g can produce
  symptoms in some individuals).
• Treatment
• Supportive treatment is usually all that is
  indicated
• Antihistamines are commonly used occasionally
  subQ epinephrine is indicated for asthma
  symptoms.

Some reports have been linked to canned tuna,
histamine is relatively heat stable.
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Shellfish Toxicity

• Shellfish toxicity results form the consumption
  of filter feeding mollusks (clams, mussels,
  oysters and scallops) which accumulate toxins
  from dynoflagellates. All shellfish are
  potentially toxic, out breaks are associated with
  algae blooms called red tides which usually occur
  in warmer months.

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• Paralytic Shellfish Poisoning Saxitoxin
• Saxitoxin a selective axonal sodium channel
  blocker
• Paresthesias of the lips, tongue and gingival are
  common headache, ataxia, muscle weakness,
  paralysis and CN dysfunction can occur. Patients
  denote a sensation of floating. Nausea,
  vomiting and diarrhea can occur. Death is due to
  respiratory paralysis. Symptoms may present from
  3 days to weeks post-consumption.

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Brevotoxin 10 types with slightly different R1
R2

• Neurologic Shellfish Poisoning Brevotoxin
• Brevotoxin Brevetoxins bind with high affinity
  to the voltage-gated sodium channels and induce a
  channel mediated Na ion influx. Neuro-excitation
  results from the nerve membrane depolarization
  and spontaneous firing. In some cases only the
  nerve is depolarized, but both nerve and muscle
  depolarization have been noted.
• Similar to ciguatera toxin with reversal of
  hot/cold sensation. Paresthesias of the face and
  extremities are common, nausea, vomiting, ataxia,
  vertigo, tremors, diarrhea are reported.
  Symptomatic bradycardia may occur. Symptoms abate
  over 2-3 days, no deaths have been reported.
  Allergic response to brevotoxin may develop in
  near shore dwellers duet to aerosolization of
  toxin this presents with asthma-like symptoms.

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Okadaic acid

• Diarrheal Shellfish Poisoning Okadaic acid
• Okadaic acid a potent inhibitor of protein
  phosphorylase phosphatase 1 and 2A in the cytosol
  of the mammalian cells that dephosphorylate
  serine and threonine. It probably causes diarrhea
  by stimulating the phosphorylation that controls
  sodium secretion by intestinal cells resulting in
  a secretory diarrhia (like cholera).
• Primarily nausea, vomiting and diarrhea lasting
  1-2 days this is most common is Europe and Japan.

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• Amnestic Shellfish Poisoning Domoic acid
• Domoic acid damages the hippocampus and
  amygdaloid nucleus. It damages the neurons by
  activating glutamate receptors, causing an influx
  of calcium, uncontrolled increase of calcium
  causes the cell to degenerate.
• Rare, presents with nausea, vomiting, diarrhea
  and short-term memory loss. Seizures,
  hemiparesis, ophthalmoplegia and coma are
  associated with severe exposures. Long term
  memory deficits may persist. The mortality rate
  is 3.
• Differential Dx
• Botulism, ciguatera scombroid toxins
• Tetrodotoxin
• OP insecticides

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Seafood Products Most Often Associated with
Dynoflagellate Induced Poisoning
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• Red Tide
• Saxitoxin

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Domoic acid
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Okadaic acid
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Source of saxitoxin