The diagnosis of the different types of shellfish poisoning is based on anamnestic and clinical criteria, as there is still no clinical diagnostic test available. The clinical diagnosis may be indirectly supported by the detection of shellfish toxins in the shellfish meat or stock left over from a meal.

There are four main groups of shellfish poisoning:

1. Paralytic shellfish poisoning (PSP) (saxitoxin and gonyautoxins),
2. Neurotoxic shellfish poisoning (NSP) (brevetoxins) including inhalation of toxins,
3. Amnesic shellfish poisoning (ASP) (domoic acid),
4. Diarrhoetic shellfish poisoning (DSP) (okadaic acid, among others).

There are great differences in the clinical course of poisoning between the four groups, in particular with regard to morbidity and mortality.

NSP represents a milder form of PSP, to date has only been observed in a geographically limited area and, curiously, its clinical symptoms overlap with those of ciguatera poisoning (reversal of temperature perception). Mortality due to PSP was high in several outbreaks; in contrast, there have been no reported fatalities due to NSP.

Among the neurotoxic forms of shellfish poisoning, ASP is rare; in contrast to the other forms, it is accompanied by permanent CNS damage and to date has been limited to a small geographical area.

DSP is substantially different from the other 3 types of shellfish poisoning, in that it is the only one that shows no neurological components, but rather, as seen from its name, causes disturbances in the gastrointestinal tract.

It is difficult to make any detailed comment on the variability of the clinical picture within the individual groups, as PSP is the only group for which there are a larger number of documented cases. Variability is probably primarily determined by a dose-effect relationship. There is evidence that children are more susceptible to saxitoxin than adults (Rodrigue et al. 1990). Differences in the design of the available studies make it even more difficult to characterise the different types of shellfish poisoning.

 

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Paralytic shellfish poisoning (PSP)

Studies

N: documented number of sick people in an outbreak ("epidemic").

n: number of sick people who were included in the documentation of the symptoms of poisoning.

 

Great Britain

• McCollum et al. 1968: retrospective study. N = 78, n = 58. Toxin determination: mouse assay.

Switzerland (origin of the shellfish: Spain)

• Zwahlen et al. 1977: N = ca. 120, n = 23. Retrospective study.

Germany (origin of the shellfish: Spain)

• Simon et al. 1977: N = ca. 120, n = 19. Retrospective study. Identification of saxitoxin in shellfish samples (6,228–20,000 MU/100 g shellfish meat).

USA (Massachusetts)

• MMWR 1991: n = 6. Identification of saxitoxin in shellfish that had not been eaten: 24,400 µg/100 g raw shellfish, 4,280 µg/100 g cooked shellfish (maximum concentration considered harmless: 80 µg/100 g).

Guatemala

• Rodrigue et al. 1990: N = 187, n = 81–83. Retrospective study and case-control study. Inclusion criteria for determination of the size and characteristics of the outbreak: acute onset of illness with at least 2 symptoms (1 sensory, 1 non-sensory), occurring between 23 July and 7 August 1987. Inclusion criteria for the case-control study for the identification of risk factors: acute onset of illness, characterised by headache, hypaesthesia of 2 or more body regions and 2 or more of the following symptoms: vertigo, dysarthria, difficulty in standing from a lying or sitting position, dyspnoea. Toxin detection: mouse assay, saxitoxin identification in shellfish and in cooking stock (HPLC).

 

South Africa

• Popkiss et al. 1979: n = 17. Toxin determination in shellfish samples (mouse assay).

Taiwan

• Cheng et al. 1991: N = 116, n = 5. Toxin determination in shellfish samples (gonyautoxins).

 

Table 4.2 Signs and symptoms of PSP, NSP, DSP, ASP: comparison of various studies

Country/region	Study		N/n	1	2	3	4	5	6	7	8	9	10	11	12	13	14	15	16	17	18	19	20
Great Britain Mytilis edulis	PSP	McCollum et al. 1968	78/58
Switzerland Mytilis edulis (Spain, Oct. 1976)	PSP	Zwahlen et al. 1977	120/23
Germany Mytilis edulis (Spain, Oct. 1976)	PSP	Simon et al. 1977	120/19
USA (Massachusetts) Mytilis edulis	PSP	MMWR 1991	6
Guatemala Amphichaena kindermani	PSP	Rodrigue et al. 1990	187/ 81–83																				26
South Africa Choromytilus meridionalis	PSP	Popkiss et al. 1979	17
Taiwan Sanguinolaria rostrata	PSP	Cheng et al. 1991	116/5																				2
USA (North Carolina) Oysters, shellfish	NSP	Morris et al. 1991	48
Japan Mytilus edulis?, Patinopecten, Chlamys	DSP	Yasumoto et al. 1978	164
Canada Mytilus edulis	ASP	Pearl et al. 1990	107/99																				3

 

1	Nausea	11	Vertigo
2	Vomiting	12	Ataxia
3	Diarrhoea	13	Cerebral seizures
4	Abdominal pain	14	Coma
5	Dyspnoea/respiratory failure	15	Mutism
6	Paraesthesias/hypaesthesias (perioral)	16	Short-term memory loss
7	Paraesthesias/hypaesthesias (extremities)	17	Headache
8	Burning/painful sensation of the skin upon contact with cold objects	18	Unstable blood pressure/arrhythmias
9	Dysarthria	19	Myalgias
10	Pareses/muscle weakness (extremities)	20	Fatalities

 

	<10%	N: documented number of sick people in an outbreak ("epidemic")    n: number of sick people who were included in documentation of the symptoms of poisoning
	10–25%
	26–50%
	51–75%
	76–90%
	>90%
	not mentioned

Further studies and epidemiological investigations

Papua New Guinea
Rhodes et al. 1975

Thailand
Kodama et al. 1988

Case reports

Long et al. 1990

Signs & symptoms

Local effects

Nausea, vomiting, diarrhoea, abdominal pain (Table 4.2). Time between ingestion and onset of symptoms: 2 h (median, range 30 min–8 h) (Rodrigue et al. 1990).

Neurological effects

Paraesthesias/hypaesthesias (perioral), paraesthesias/hypaesthesias (extremities), double images, dysarthria, paralysis of the skeletal musculature, including the respiratory musculature with respiratory insufficiency and respiratory failure, vertigo, ataxia, headache, temporary blindness, myalgias (muscle spasms?) (Table 4.2).

Time between ingestion and onset of symptoms: 2 h (median, range 30 min–8 h) (Rodrigue et al. 1990).

Muscular effects

Myalgias (direct muscular effect of the poison? muscle spasms? hypoxic muscle damage?) (Table 4.2).

Time between ingestion and onset of symptoms: 2 h (median, range 30 min–hours) (Rodrigue et al. 1990).

Other signs & symptoms

Chills, sensation of heat.

Differential diagnosis

Paralytic shellfish poisoning has a significantly more severe course than the neurotoxic form of shellfish poisoning.

Morbidity

If a patient survives the first 12–18 h, the prognosis is good (Eastaugh and Shepherd 1989). Muscle weakness can persist for days to weeks.

Case fatality rate

Mortality may be considerable in individual outbreaks and is primarily dependent on the availability and success of symptomatic treatments. The cause of death is almost exclusively respiratory failure, which generally occurs 1–12 h after ingestion of the poison (Eastaugh and Shepherd 1989).

In an epidemic in Guatemala, the mortality rate was 26/187, whereby children <6 years had a mortality rate of 50% and adults >18 years of 7% (Rodrigue et al. 1990).

Between 1927 and 1985, 505 PSP cases were recorded in California, of which 32 ended fatally (MMWR 1983). In contrast, in 10 PSP epidemics in the USA between 1971 and 1977, there were no recorded fatalities (Hughes 1979).

2/116 died in an epidemic in Taiwan (Cheng et al. 1991).

Laboratory and physical investigations

1. Detection of poison

Detection of shellfish toxins with the aid of thin-layer or high-performance liquid chromatography (Luckas et al. 1990).

2. CK
Increased (McCollum et al. 1968, Cheng et al. 1991).

3. Electrophysiological investigations

Electrophysiological findings, which can be explained by incomplete blockade of sodium channels, distinguish PSP from most other acute-onset paralytic illnesses. Complete return to normal within 5 days (Long et al. 1990). Only cases of poisoning due to tetrodotoxin, a sodium channel blocker similar to saxitoxin, present an identical picture (Oda et al. 1989).

First aid

Gastric lavage, instillation of activated charcoal and laxatives are recommended; however, their value has not yet been documented in a controlled clinical trial.

Treatment (symptomatic)

Endotracheal intubation and artificial respiration (may be necessary for a period of several days).

Treatment (specific)

No specific treatment exists. The use of monoclonal neutralising antibodies has been proposed.

 

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Neurotoxic shellfish poisoning (NSP)

Studies

Morris et al. 1991: retrospective cohort study. n = 48. Inclusion criteria: subjects were included in the study if, after consuming toxic shellfish, they developed one of the neurological symptoms that have previously been reported in connection with NSP (paraesthesia, reversal of temperature perception, myalgia, vertigo, ataxia) within 24 h after consuming the shellfish and for a duration of at least 1 h. Shellfish was considered toxic if it caused at least one case of poisoning according to the above-mentioned criteria and came from an area known to be a "red tide" region (>5,000 P. brevis organisms/litre water).

Detection of P. brevis neurotoxins in shellfish samples.

Signs & symptoms

Where relevant, the figures shown after the symptoms are the median time (in hours; range in parentheses) between ingestion and appearance of the symptom and the median duration of the symptom (in hours; range in parentheses).

Local effects

Gastrointestinal tract: nausea: 3 (0.5–18), 18 (1–48); vomiting: 3 (1–15), 8 (0.5–48); diarrhoea: 10 (1–18), 17 (2–48); abdominal pain: 5 (1–18), 17 (1–48) (Morris et al. 1991) (Table 4.2).

Respiratory tract and conjunctivae: rhinorrhoea, cough, conjunctivitis in non-asthmatics. Induces asthma attacks in asthmatics (Asai et al. 1982, Pierce 1986).

Neurological effects

Paraesthesias: 4 (0.25–15), 8 (0.5–51); burning/painful sensation of the skin upon contact with cold objects (temperature reversal): 7 (0.25–16), 8 (1–26); pareses/muscle weakness: 3 (0.25–17), 24 (0.5–51); vertigo: 3 (0.25–17), 16 (0.5–72); ataxia: 3 (0.25–14), 7 (0.5–40); myalgias: 6 (0.5–13), 7 (2–24); headache: 2 (0.5–12), 7 (2–24); chills: 2 (2–8), 11 (2–48) (Morris et al. 1991) (Table 4.2).

Muscular effects

Myalgias (see Neurological effects; aetiology?).

Differential diagnosis

Has a milder course than paralytic shellfish poisoning. Likewise in comparison to ciguatera poisoning, which shows similarities with regard to symptoms. The patient history with regard to the type of seafood consumed and the self-limiting and short-lived course of the illness are important distinguishing features.

Morbidity

The illness is self-limiting and resolves within several days with no lasting effects.

Case fatality rate

No known fatalities to date.

Laboratory and physical investigations

Detection of poison: detection of brevetoxin in shellfish tissue: radioimmunoassay (RIA), enzyme-linked immunosorbent assay (ELISA) (Hokama 1992).

First aid

No proven methods known.

Treatment (symptomatic)

1. Rehydration,
2. in the case of inhalation: treatment of asthma attacks.

Treatment (specific)

None available.

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Diarrhoetic shellfish poisoning (DSP)

Studies

Yasumoto et al. 1978: n = 164. Retrospective study (first documented DSP epidemic). Toxicity investigations in a mouse assay. Toxin that causes DSP not yet isolated.

Signs & symptoms

Local effects

Nausea, vomiting, diarrhoea, abdominal pain (Table 4.2). Time between ingestion and onset of symptoms: 30 min – several hours (rarely >12 h) (Yasumoto et al. 1978).

Differential diagnosis

In contrast to the other forms of shellfish poisoning, no neurological signs or symptoms occur.

Morbidity

Self-limiting illness that resolves within several days with no lasting effects.

Case fatality rate

No known fatalities to date.

Laboratory and physical investigations

Detection of poison: detection of okadaic acid in shellfish tissue: HPLC-fluorometry, enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA) (Hokama 1992).

First aid

No proven methods known.

Treatment (symptomatic)

Rehydration.

Treatment (specific)

None available.

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Amnesic or central nervous form of shellfish poisoning (ASP)

Studies

Perl et al. 1990: retrospective study. N = 197, n = 99. Inclusion criteria: occurrence of one or several gastrointestinal symptoms (vomiting, diarrhoea, abdominal cramps) within 24 h after the consumption of shellfish from King Edward Island on 1 November or later – or at least one of the following neurological symptoms within 48 h after the consumption of shellfish: confusion, amnesia, disorientation or other serious signs and symptoms, such as seizures or coma. Identification of the toxin responsible for the poisoning (domoic acid).

Problems with the study: the documented 107 cases are probably an underestimation of the actual number of persons affected, with the most under-represented being those with solely gastrointestinal symptoms. The study was based on a questionnaire, and thus the range of symptoms included was limited by the questions asked.

Signs & symptoms

The acute phase of illness is characterised by a neuronal "hyperexcitation" syndrome that is most probably due to stimulation of central and possibly also peripheral neurons. In the chronic phase of illness there is degeneration of neuronal structures in the hippocampus and the anterior horn cells of the spinal cord (Teitelbaum et al. 1990).

Local effects

Nausea, vomiting, diarrhoea, abdominal cramps (Table 4.2).
Time between ingestion and onset of symptoms (all symptoms): 15 min–38 h (median 5.5 h) (Perl et al. 1990).

Neurological effects

Coma, cerebral seizures, mutism, involuntary chewing and grimacing, emotional instability (uncontrolled screaming and aggression), headache, short-term memory loss (positively associated with male gender, advanced age and dose of domoic acid), increased bronchial secretion (Table 4.2).

Time between ingestion and onset of symptoms (all symptoms): 15 min–38 h (median 5.5 h) (Perl et al. 1990).

Cardiac effects

Unstable blood pressure, cardiac arrhythmias (Table 4.2).
Time between ingestion and onset of symptoms (all symptoms): 15 min–38 h (median 5.5 h) (Perl et al. 1990).

Differential diagnosis

Severe persistent central nervous disorders distinguish ASP from other forms of shellfish poisoning with neurological disturbances.

Morbidity

18% of patients were hospitalised for 4–101 days (median 37.5 days). The reason for hospitalisation was almost exclusively neurological disorders (Perl et al. 1990).

Persistence of neurological disorders: chronic residual memory deficit, motor neuronopathy and axonopathy (Teitelbaum et al. 1990).

Case fatality rate

3/107 (Perl et al. 1990).

Laboratory and physical investigations

Detection of poison

• Detection of domoic acid in shellfish tissue (Lawrence et al. 1989, Quilliam and Wright 1989, Quilliam et al. 1989, Pocklington et al. 1990).
• Detection of domoic acid in blood, serum or CSF of patients with ASP not yet successful, probably due to too long a time interval between ingestion and investigation (Perl et al. 1990).
• Detection of domoic acid in serum with high-performance liquid chromatography (HPLC) (Blanchard and Tasker 1990).

First aid

No proven methods known.

Treatment (symptomatic)

1. Rehydration.
2. Endotracheal intubation due to bronchial hypersecretion (Perl et al. 1990), possibly artificial respiration.
3. Unstable blood pressure: vasopressors, antihypertensives (Perl et al. 1990).
4. Cardiac dysrhythmias: antiarrhythmics (Perl et al. 1990).

Treatment (specific)

There are efforts to develop antagonists (Glavin et al. 1990).