This is a brief content about Fish poisoning

1. Fish Poisoning
Poisoning resulting from fish and other marine creatures is referred to as
ichthyism, which may result either from envenomation by stinging or biting, or
from ingestion of toxic or decomposing fish.
Poisonous fish are subdivided into:
Ichthyosarcotoxic fish: - which contain a toxin within their flesh
Ichthyohaemotoxic fish: - which have poisonous blood and
Ichthyo-otoxic fish: - which contain a toxin mainly in their gonads
Based on the nature of toxin, there are 5 types of seafood poisoning:
scombroid, ciguatera, tetrodotoxic, paralytic shellfish, neurotoxic shellfish, and
amnesic shellfish poisoning.
Scombroid poisoning: (Histamine fish poisoning)
Source:
Tuna, bonito, escolar, skipjack, mackerel, needlefish, saurie, kingfish, wahoo,
albacore, amberjack, blue fish, dolphin, mahi mahi, marlin, anchovy, herring,
swordfish, Australian ocean salmon, Bombay duck (a kind of dried fish)
Toxin:
Scombroid poisoning is a form of ichthyosarcotoxicosis (the toxin is contained
within the flesh of the fish).
Poisoning occurs from consumption of improperly preserved fish in which the
endogenous histidine has been broken down by bacteria into high levels of
histamine and saurine.
Unfortunately, tainted fish may look and smell normal. Rarely, there is a “sharp”
or “peppery” taste. To add insult to injury, even if such contaminated fish is
subsequently cooked well or smoked, the toxins are not destroyed.
Incubation Period:
Few minutes to few hours: Symptoms may develop as early as 5 to 10 minutes
after eating the fish, or be delayed up to 1 to 2 hours.

2. Clinical features:
1. Manifestations are mostly histamine-mediated, and comprise erythema of
face, urticaria, pruritis, dermal flushing, diaphoresis, burning sensation of the
mouth, dizziness, throbbing headache, vomiting, diarrhoea, and abdominal
cramps.
2. Palpitations are frequently described.
3. Diarrhoea and vomiting are also common findings after scombroid poisoning.
4. Tachycardia/bradycardia and hypotension have been described.
5. Conjunctival irritation, and angioneurotic facial oedema may develop.
6. In severe cases there may be bronchospasm and respiratory distress.
Symptoms usually subside on their own in 6 to 12 hours.
Diagnosis:
1. Diagnosis of scombrotoxicosis:
a. Clinical picture
b. Histamine levels of serum and urine will be greatly elevated.
c. Detection and quantitation of histamine in implicated fish flesh is more
important. Normal fish has less than 1 mg of histamine per 100 gm of flesh.
Illness is usually associated with more than 100 mg of histamine per 100 gm of
flesh (though illness can result from much less concentrations).
Antihistamines- Cimetidine

3. Ciguatera poisoning:
Source:
Ciguatera poisoning is the commonest form of seafood poisoning, accounting
for more than 50% of the cases.
Barracuda, sea bass, parrot fish, red snapper, grouper, amberjack, kingfish,
sturgeon, and many other large-sized fish are the main culprits
Toxin (Ciguatoxin) ispresentindinoflagellates→ small herbivorousfish→ largercarnivorous fish→ Humans
(Dinoflagellates are microscopic, single-celled, photosynthetic, often
bioluminescent algae with two flagellae)
Toxin:
The toxins are mainly contained in the muscle, skin and mucosa of the fish, with
the highest concentration present in the viscera (liver, intestines, gonads).
Incubation period:
About 2 to 6 hours, (range 2 to 24 hours).
Clinical features:
1.Sudden onset of sweating, abdominal cramps, nausea, vomiting, profuse
watery diarrhoea, dysuria, tingling and numbness of lips, tongue, and throat,
metallic taste, paraesthesias, dysaesthesias, chills, headache, myalgia, arthralgia,
tremor, ataxia, vertigo, blurred vision, and convulsions. Profound weakness may
occur. Patients may be unable to rise or move. Paralysis of limbs and facial
muscles may develop in severe cases. Death may result.
2. Pruritus is frequently reported, and may be mild to severe. It may persist for
weeks after an exposure.

4. 3. Paraesthesias are the hallmark of ciguatera poisoning, and may also persist for
weeks. A characteristic feature is reversal of temperature discrimination; i.e. cold
substances feel hot. But this is not a true sensory switch; it can be described as
the sensation one gets when gripping something very cold (e.g. ice), and the
resultant sensation of a “burning” feeling. These sensations are usually localised
to palms, soles, lips and mouth. This phenomenon is said to be due to abnormal
bursts of discharges occurring specifically in the peripheral C-polymodal
nociceptor fibres (cutaneous afferent unmyelinated fibres). These fibres are not
spontaneously active at normal temperature in undamaged skin, but have a heat
threshold above 40°C, and cold threshold below 23°C. However, contact with
heat generally does not produce the reverse effect.
4. Other sensory effects include a metallic taste, and a “carbonated” sensation
when food or drink is consumed. Teeth may appear loose and painful.
5. Bradycardia and orthostatic hypotension have also been reported. Transient T
wave inversion has been described. Extrasystoles may occur, probably because
of noradrenergic myocardial stimulation.
6. Respiratory depression, dyspnoea, and bronchospasm may also occur.
7. Neurological manifestations tend to linger for a long time even in patients
who have fully recovered.
8. Ocular effects include blurred vision, photophobia, visual loss (usually
temporary), mydriasis and lacrimation.
9. Painful ejaculation and dyspareunia in the unaffected partner have been
reported occasionally.
10. Symptoms of ciguatera poisoning are exacerbated by ethanol and stress
(physical and/or emotional).
11. Foetal distress has occurred after ingestion of ciguatera contaminated fish by
the pregnant mother. Premature labour and spontaneous abortion have been
reported. Infants exposed to ciguatoxin in late pregnancy have been noted to
have abnormal prenatal movement and temporary cranial nerve deficits. Several
cases of ciguatera poisoning in breastfeeding infants whose mothers were
poisoned have also been reported

5. Diagnosis:
ELISA test for ciguatoxin.
HPLC.
A rapid test (dipstick immunobead assay) is being developed to test suspect fish
for the presence of toxin.
Treatment:
1.Decontamination (activated charcoal, catharsis) may be of benefit if the
patient is seen within 2 hours of ingestion.
2. The primary treatment is the use of antihistamines; cold showers can also be
helpful. Cyproheptadine may be of benefit.
3. Myalgias usually respond to NSAIDs or other analgesics.
4. Monitor fluid and electrolytes. Monitor vital signs and ECG.
5. Administration of IV fluids, electrolytes.
6. IV mannitol is said to be useful in the management of neurological and
muscular manifestations. The recommended dose is 0.5 to 1 gm/kg of 20%
solution, administered over 30 to 45 minutes. Hypotension may occur, and must
be anticipated whenever mannitol is given. Some investigators are of the opinion
that mannitol is not effective in the management of neurological manifestations
of ciguatera poisoning.
7. Atropine has been of some use in treating bradycardia and hypotension.
8. Dopamine, plasma expanders, and calcium gluconate may be useful for shock.
9. Chronic neurologic symptoms may resolve with tocainide, mexiletine, or
amitryptiline.
10. Avoidance of alcohol and exercise (which can exacerbate symptoms), is
recommended.
Tetrodotoxic poisoning:
Source:
Puffer fish, Newts, Salamanders, Blue-ringed octopus, Snails, Horseshoe crab
eggs.

6. Toxin:
Tetrodotoxin (TTX) is a potent, heat-stable, water soluble, non-protein
aminoperhydroquanizole neurotoxin concentrated mainly in the skin, liver,
ovary, and intestine of the fish. The highest concentration is found in the
ovaries, and hence the female is most poisonous, especially if eaten during the
spawning season.
Mode of action:
Tetrodotoxin affects myelinated nerve fibres throughout the entire length of the
axon by lowering the conduction of sodium currents at nodes of Ranvier. It is a
selective and potent sodium channel blocker.
Incubation period:
Onset is usually within 4 to 6 hours, but may be delayed. Oral paraesthesia is
usually the initial symptom of puffer fish poisoning. Death may occur within the
first 6 to 24 hours.
Clinical features:
Poisoning is caused by ingestion of the flesh, viscera, ovaries, or skin containing
tetrodotoxin (TTX). The highest concentration is in the viscera. Body musculature
is usually free of poison.
Main features of poisoning include headache, sweating, dysaesthesias, and
paraesthesias of lips, tongue, mouth, face, fingers, and toes. Circumoral tingling
may include the tongue and inner surface of the mouth, and generally occurs
within 10 to 45 minutes of ingestion.
Later, the following are seen: salivation, dysphagia, dysarthria, nausea, vomiting,
abdominal pain, ataxia, weakness, fasciculations, and ascending paralysis in 4 to
24 hours.
Blurred vision, aphonia, and dysphagia may be seen as muscle paralysis
progresses. Miosis is an early effect of TTX poisoning, but later there is mydriasis.
Hypotension, bradycardia, and fixed and dilated pupils indicate severe poisoning.
Mortality may approach 50%. Death is usually due to respiratory depression and
respiratory muscle paralysis.

7. A rare “locked-in” syndrome has been described with tetrodotoxic poisoning, in
which the patient appears completely flaccid, but remains conscious.
Diagnosis:
Mouse bioassay: Laboratory determination of tetrodotoxin (TTX) is not
commonly available. Potency of TTX must be done by bioassay; identification may
be done with thin layer chromatography.
Fluorescent spectrometry.
Use of electrophoresis, HPLC, LC/MS, etc., have also been reported by various
investigators
Treatment:
Because of the differences in susceptibility, and unpredictability of an individual’s
course, at least 24 hours of observation is recommended in every patient.
1. Decontamination: Activated charcoal may be useful.
2. IV edrophonium (10 mg) or IM neostigmine (0.5 mg) may be effective in
restoring motor strength.
3. Artificial ventilation should be implemented if necessary. Assisted ventilation
may be necessary for 4 to 6 hours, and in some cases up to 12 hours.
4. Haemodialysis may be effective in the treatment of tetrodotoxin poisoning,
because the toxin has low molecular weight, is water soluble, and is not
significantly bound to protein.
Shellfish poisoning:
Source:
Shellfish (especially oysters, clams, mussels, and scallops) contaminated by
dinoflagellates.
Other sources include univalve mollusks, starfish, limpets, sand crabs, whelks,
turban shells, top shells, xanthid crabs and various fish

8. Paralytic Shellfish Poisoning:
Toxin:
PSP toxins are a group of 21 structurally related neurotoxins, and are among the
most common and deadly phycotoxins. The main toxin is saxitoxin which is
produced by the following dinoflagellates (unicellular algae): Pyrodinium,
Gymnodinium and Alexandrium.
Mode of action:
These toxins affect the central nervous system and can produce muscular nerve
block and paralysis
(Note: Paralytic shellfish poisoning is often associated with “red tide” blooms, but
may occur with or without the red tide. These are natural phenomena triggered
by a series of events, which can include human pollution. Over 300 phytoplankton
species can produce red tides, but only 60 to 70 species are actually harmful.
Swimming in the “red tide” may produce pruritus and skin irritation.)
Incubation period:
The incubation period is usually 30 minutes (occasionally can extend to 3 hours).
Clinical features:
Mild: Tingling and numbness of the tongue and lips, that soon spreads to the face,
neck, arms, fingers and toes; headache and nausea. Diarrhoea may also occur.
Moderate: Limb weakness, ataxia, incoherent speech, difficulty breathing,
hypersalivation, and sweating. Giddiness, rash, fever, tachycardia, hypertension,
and dyspnoea can occur. Temporary blindness has been reported.
Severe: Muscle paralysis, “choking” sensation, severe respiratory difficulty, and
respiratory failure.
Diagnosis:
Mouse bioassay or enzyme immunoassay, HPLC, liquid chromatography-mass
spectrometry (LC-MS), immunoaffnity chromatography (IAC), and capillary
electrophoresis.

9. Treatment:
 In symptomatic patients, the following should be monitored closely:
haemodynamic status, acid-base, serum electrolytes, BUN, creatinine,
calcium, magnesium, phosphorous, urine output, CPK, ECG, pulse oximetry,
and cardiac rhythm.
 Decontamination: Activated charcoal.
 Since saxitoxin is excreted mainly via urine, diuresis can enhance renal
excretion
 Supportive measures: Most patients recover with supportive care alone.
Monitor for respiratory depression. Patients with significant neurotoxicity
may need endotracheal intubation and mechanical ventilation.
 Because saxitoxin acts by blocking sodium channels, sodium bicarbonate
may be effective in reversing ventricular conduction delays and
arrhythmias, though this has not been proved: administer 1 to 2 mEq/kg
sodium bicarbonate as a bolus, and repeat as necessary