Diagnosis & Treatment — General practitioner / health post
At particular risk are children, elderly people and patients with pre-existing conditions, such as coronary heart disease, arterial hypertension, lung disease, kidney disease, allergies (sensitisation) and patients taking particular drugs, such as beta-blockers. In one outbreak of the central nervous form of shellfish poisoning (ASP), all patients who had a severe course of poisoning had a pre-existing condition (e.g. diabetes mellitus, renal insufficiency) and all were >65 years old (Pearl et al. 1990).
Is it likely that poisoning caused by a poisonous animal is present?
Patient history: consumption of a meal containing potentially poisonous animal foodstuffs in the last few hours? (see Biomedical database entries)
Gastrointestinal symptoms: nausea, vomiting, diarrhoea, abdominal pain within hours after such a meal
Systemic signs and symptoms consistent with poisoning caused by a poisonous animal.
The following forms of poisoning due to poisonous animals are described:
- Ciguatera, scombroid and tetrodotoxin poisoning and the 4 different forms of shellfish poisoning,
- paralytic shellfish poisoning = PSP,
- neurotoxic shellfish poisoning = NSP,
- the central nervous form of shellfish poisoning (amnesic shellfish poisoning) = ASP,
- the gastrointestinal form of shellfish poisoning (diarrhoetic shellfish poisoning) = DSP;
- allergic reactions to fish, shellfish and crabs.
All other forms of poisoning due to poisonous animals are dealt with in the relevant Biomedical database entries.
From a differential diagnostic perspective with regard to poisoning due to poisonous animals, only scombroid (histamine) poisoning and ciguatera need to be positively identified. All other forms of poisoning caused by poisonous animals are treated solely symptomatically.
The following complaints, which can also be caused by the consumption of seafood, including those animals that are poisonous, need to be delineated for the purposes of differential diagnosis (Eastaugh and Shepherd 1989, Liston 1990, Noble 1990, Scoging 1991):
1. Infectious gastroenteritis
Norwalk virus (Norovirus): source of infection: shellfish, incubation period 24–48 h. Symptoms: nausea, vomiting, cramping abdominal pain, diarrhoea, (headache, myalgia, weakness), duration 1–2 days (Benenson 1990, Morse et al. 1986).
Vibrio sp. (Vibrio cholerae, V. parahaemolyticus among others): source of infection: usually shellfish and crabs, incubation period a few hours–5 days. Signs and symptoms: large loss of plasma isotonic fluid (secretory enteritis) with rapid dehydration, acidosis and circulatory failure, occasionally vomiting, generally no fever (Benenson 1990).
Type E botulism (Clostridium botulinum): source of infection: incorrectly processed fish and fish eggs, incubation period: 12–36 h. Symptoms: nausea and vomiting with neurological symptoms (cerebral nerve deficits, descending paralysis) that occur concurrently or after a delay of some days (Schaffner 1990, Telzak et al. 1990).
Other bacteria: Campylobacter, Salmonella, Shigella, E. coli: in rare cases carried by seafood.
Hepatitis A, helminthiasis: due to the long incubation period alone, these conditions do not represent a differential diagnostic problem with regard to poisoning due to poisonous animals.
Other food allergies need to be distinguished from toxin-induced fish and shellfish poisoning (ciguatera, scombroid poisoning, PSP, NSP etc.) and fish, shellfish and crab allergies (Taylor and Bush 1988). They can either be caused by food that is eaten at the same time as seafood (peanuts, walnuts, eggs etc.) or by additives to seafood or other foods consumed together with seafood (monosodium glutamate, preservatives such as sulfites, food colouring such as tartrazine) (Cochran and Cochran 1984, Settipane 1986, Twarog and Leung 1982, Vitoria et al. 1982). An essential characteristic that distinguishes these food allergies from toxin-induced fish and shellfish poisoning is the fact that the latter nearly always affect several people at the same time, whereas allergies only affect individuals with the relevant predisposition.
3. Other contaminants
Contamination of foodstuffs by organophosphates (insecticides) produces gastrointestinal-neurological symptoms that are similar to those of fish and shellfish poisoning. Moreover, this type of poisoning also occurs in the form of small epidemics.
4. Psychogenic hyperventilation
When coinciding with gastrointestinal symptoms, the acroparaesthesias and perioral paraesthesias caused by this condition can mimic the clinical picture of fish or shellfish toxin-induced poisoning.
Differential diagnosis of poisoning caused by poisonous animals
It is nearly always possible to determine whether the cause of poisoning was shellfish, fish, crabs or mammals on the basis of the patient history. This allows an initial delimitation of the possible clinical characteristics.
Further taxonomic differentiation requires the necessary knowledge on the patient's part or that the animal be available for identification.
With regard to treatment of poisoning caused by poisonous animals, a more precise level of differentiation is not actually necessary as, with the exception of scombroid (histamine) poisoning and ciguatera, treatment is only symptomatic anyway whereby specific treatment of ciguatera with manitol is, however, no longer convincing.
If the poisoning is caused by consumption of fish, the following associations can generally be relied on:
However, these associations are not unequivocal, as different toxins that determine the symptoms of distinct poisoning syndromes may be present in the same fish (e.g. ciguatoxin and its derivatives and scombrotoxin) (Table 4.1). Likewise, poisoning that is actually known as a form of fish poisoning, e.g. tetrodotoxin poisoning, may occasionally also be caused by a number of other invertebrates.
It is not surprising that the ability to differentiate between different forms of marine poisoning is limited, as the accumulation of toxins via food or the food chain is evidently not particularly species specific.
The same is true for the taxonomic differentiation of the different forms of shellfish poisoning (PSP, NSP, ASP, DSP). The form of envenoming caused depends on the type of dinoflagellates ingested by the shellfish and not on the species of shellfish itself. In certain cases, the origin of the shellfish makes it possible to narrow down the cause, as it is now known that the distribution of certain species of dinoflagellates is geographically confined, and thus also the occurrence of certain forms of shellfish poisoning.
It is important to find out if internal organs were consumed, as these may accumulate high doses of toxins or because sometimes they are the only part of the animal that is actually poisonous.
The broth in which the poisonous shellfish or crustaceans are cooked is especially high in toxins.
Once the cause of the poisoning has been narrowed down as far as possible by taxonomic differentiation, further differentiation is based on clinical features (see below).
2. Clinical differentiation
Patient history: time between ingestion and the onset of symptoms:
- Fish, shellfish and crab allergies: minutes.
- Ciguatera: on average 5.7 h (1–48 h) (Frenette et al. 1988). A few minutes to up to 30 h, <24 h (96%), <12 h (77%), <6 h (52%) (Bagnis and Legrand 1987).
- Scombroid (histamine) poisoning: 10 min–2 h (Bartholomew et al. 1987).
- Tetrodotoxin poisoning: usually within 10–45 min, but also up to a few hours (Bower et al. 1981).
- Paralytic shellfish poisoning (PSP): on average 2 h (30 min–8 h) (Rodrigue et al. 1990).
- Neurotoxic shellfish poisoning (NSP): 15 min–many hours (Morris et al. 1991).
- Gastrointestinal form of shellfish poisoning (DSP): 30 min–several hours, rarely >12 h (Yasumoto et al. 1978).
- Central nervous form of shellfish poisoning (ASP): on average 5.5 h (15 min–38 h) (Perl et al. 1990).
Symptoms of envenoming (short descriptions):
- Fish, shellfish and crab allergies: systemic anaphylactic reaction:
- skin symptoms (urticaria, "flushing", angio-oedema, pruritus),
- respiratory disturbances (dyspnoea, rhonchi),
- cardiovascular disturbances (arterial hypotension, syncope, arrhythmias),
- gastrointestinal disturbances (cramping abdominal pain, nausea, vomiting, diarrhoea).
- impairment of sensitivity, especially to cold,
- in the majority of cases concurrent or preceding gastrointestinal symptoms (primarily nausea and diarrhoea).
- Scombroid (histamine) poisoning:
- skin symptoms (erythema, "flushing", burning sensation in the mouth),
- short incubation period (10 min–2 h),
- in approximately 1/3 of cases gastrointestinal symptoms as well (nausea, vomiting, diarrhoea).
- Tetrodotoxin poisoning:
- autonomic nervous system disturbances,
- rapid onset of symptoms of poisoning,
- respiratory and cardiovascular failure (arterial hypotension, bradycardia),
- high mortality rate (approx. 40%).
- Paralytic shellfish poisoning (PSP):
- acroparaesthesias without impairment of sensitivity to cold,
- marked paralysis of the skeletal musculature in the majority of cases,
- in severe cases of poisoning the respiratory musculature is also affected,
- respiratory failure is the cause of death in fatal cases,
- gastrointestinal symptoms are not very pronounced.
- Neurotoxic shellfish poisoning (NSP):
- the clinical picture is comparable to that of PSP, but the course is milder (to date no reports of fatalities),
- reversal of temperature perception, similar to ciguatera.
- Gastrointestinal form of shellfish poisoning (DSP):
- nausea, vomiting, diarrhoea and abdominal cramps,
- no neurological symptoms,
- benign course,
- in the absence of laboratory investigations it cannot be distinguished from infectious gastrointestinal disorders.
- Amnesic or central nervous form of shellfish poisoning (ASP):
- nausea, vomiting, diarrhoea, abdominal cramps,
- confusion, lethargy, seizures, coma, loss of short-term memory,
- high risk of death.
The short descriptions above are simplified representations of the most important forms of poisoning caused by poisonous marine animals, although it must be noted that there is great variability in the signs and symptoms within the individual types of poisoning and there is a high degree of overlap between them (Tables 4.2, 4.3 and 4.5)
Purely clinical differentiation of most forms of poisoning caused by poisonous marine animals is thus very limited due to the low specificity and/or sensitivity of the signs and symptoms that are caused.
Moreover, the time periods between ingestion and onset of the first symptoms of poisoning overlap to a high degree in almost all the types of poisoning.
On the other hand, it is easy to distinguish fish, shellfish and crab allergies, as they affect individuals with an allergic predisposition, which may already be known.
Ciguatera, tetrodotoxin poisoning and the paralytic form of shellfish poisoning (PSP) all have neurological as well as gastrointestinal components. It is thus difficult or even impossible to distinguish between them on the basis of clinical criteria alone. It has been suggested that these 3 types of poisoning be combined under the term "pelagic paralysis" for practical/clinical purposes (Mills and Passmore 1988).
In all forms of poisoning due to poisonous animals, with the exception of scombroid poisoning, treatment is symptomatic. The use of antihistamines in the treatment of histamine (scombroid) poisoning is an antidote in the most literal sense.
Among the different types of fish poisoning, paraesthesias upon contact with cold are a symptom with high sensitivity and specificity for ciguatera: sensitivity 0.78, specificity 1.00 (Frenette et al. 1988). With regard to differential diagnosis, NSP can be excluded (shellfish!). One problem, however, with the symptom of paraesthesias upon contact with cold in fulminant cases of poisoning is that it may not actually be practicable, as cardiovascular complications completely dominate the course of poisoning even before the paraesthesias occur (Bagnis and Legrand 1987, Lawrence et al. 1980).
DSP differs from all other forms of poisoning due to poisonous animals in that the symptoms are exclusively gastrointestinal. However, this makes it all the harder to distinguish it from infectious diseases caused by the consumption of seafood.
ASP does have highly specific characteristics, such as short-term memory loss and destructive processes in the central nervous system; however, these features have markedly low sensitivity.
Immunological and chemical methods complement differentiation on the basis of biological (taxonomic) and clinical criteria (see below).
3. Immunological-chemical differentiation
Detection of poison
Immunological methods (Hokama 1991, 1992) to detect:
- ciguatoxin and related polyethers in fish tissue → ciguatera poisoning,
- palytoxin → ciguatera poisoning,
- brevetoxin → neurotoxic shellfish poisoning (NSP),
- okadaic acid → gastrointestinal form of shellfish poisoning (DSP).
Chemical methods to detect:
- histamine in fish tissue → scombroid poisoning,
- increased urinary excretion of histamine and its metabolite N-methylhistamine in the presence of normal PGD-M levels → scombroid poisoning,
- shellfish toxins in shellfish tissue and broth → paralytic shellfish poisoning,
- tetrodotoxin (TTX) in fish tissue, vomit or serum → tetrodotoxin poisoning.
At present there is no clinical-diagnostic test to confirm an anamnestic-clinical diagnosis of poisoning due to consumption of poisonous animals. There are, however, immunological and chemical tests that can indirectly contribute to substantiation of the diagnosis, as long as remains of the consumed fish or shellfish are still available for examination. These tests were primarily developed with the aim of identifying toxic fish and muscles and thus preventing them from being consumed. As the essential characteristics of such test systems for this purpose are ease of use and high sensitivity and specificity, their development focused on immunological methods (Hokama 1991, 1992).
Toxicity tests in animals are problematic and unsatisfactory for various reasons. A large number of animals are required, some of which suffer an agonising death. The interpretation of such tests is subjective, and they are not specific, i.e. they do not enable differentiation of different toxins.
Emergency medical treatment according to symptom complexes
- Poisoning with neurological, cardiovascular and gastrointestinal components,
- poisoning with acute gastrointestinal symptoms alone.
If it is certain that poisoning caused by a poisonous animal is present, emergency medical treatment according to symptom complexes will cover the great majority of therapeutic possibilities, as very few specific treatments are available. This will also cover symptoms of acute gastrointestinal infections.
1. Poisoning due to poisonous marine animals with neurological, cardiovascular and gastrointestinal components
- State of consciousness,
- respiratory rate, blood gases,
- blood pressure, pulse,
- urinary output,
- intensive medical observation.
- Endotracheal intubation and artificial respiration,
This group comprises the following types of poisoning: ciguatera, tetrodotoxin poisoning, PSP, NSP, ASP, type E botulism. From the perspective of emergency medical treatment, only 1 condition from this group needs to be diagnosed definitively, so that the specific treatment can be administered
- type E botulism
- for ciguatera poisoning (manitol) evidence for a specific treatment effect is no longer convincing
2. Poisoning due to poisonous marine animals with anaphylactic symptoms, including fish, shellfish and crab allergies
- State of consciousness,
- respiratory rate, blood gases,
- blood pressure, pulse,
- urinary output,
- intensive medical observation.
Treatment of anaphylactic reactions.
Scombroid (histamine) poisoning and IgE-mediated fish, shellfish and crab allergies do not differ clinically, as histamine effects are equally at the basis of both. Treatment is identical.
3. Poisoning due to poisonous marine animals with acute gastrointestinal symptoms alone
- Blood pressure, pulse,
- state of hydration,
- urinary output,
- possibly blood cultures.
DSP, the only form of poisoning caused by poisonous marine animals that always has only acute gastrointestinal symptoms, does not differ clinically from acute gastrointestinal infections. Treatment is identical, i.e. oral or parenteral rehydration.
Specific treatment for type E botulism
Nausea and vomiting with neurological symptoms, such as cerebral nerve deficits and descending paralysis, that occur concurrently or after a delay of some days.
Trivalent ABE antitoxin.