Introduction Scombroid fish poisoning Vibrio vulnificus infection due to seafood ingestion Mercury poisoning due to fish ingestion Acute vitamin A toxicity due to ingestion of fish
Various syndromes that may affect the skin have been described after ingestion of fish or fish products. These include:
A combination of the above can occur in the same patient. It can be difficult to differentiate the cause as symptoms may appear similar.
Scombroid fish poisoning is caused by eating decomposing scombroid fish (eg, kahawai, mackerel, and tuna). Bacteria in the decomposing fish produce various by-products including scombrotoxin, which contains histamine.
The clinical features of scombroid fish poisoning include:
Scombroid fish poisoning resolves without complications. In severe cases, symptoms may persist for several days.
Scombroid fish poisoning is usually diagnosed from a clear history of the onset of symptoms within 1 hour of eating a particular fish.
The main differential diagnosis for scombroid fish poisoning is type 1 allergic reaction including anaphylaxis.
Scombroid fish poisoning tends to take minutes to induce a reaction. Other reactions due to fish ingestion tend to progress more slowly, over hours, days, or weeks.
The treatment for scombroid fish poisoning is rapid-acting oral antihistamines, which may resolve the symptoms within minutes.
The decomposing fish responsible for the reaction should be discarded.
Scombroid fish poisoning rapidly resolves. Patients can eat the same species of fish again, as long as it has been stored in cold conditions to prevent bacterial decomposition.
V. vulnificus infection can follow the consumption of contaminated raw seafood (eg, raw oysters). The organism is killed by cooking the fish. This infection may also contaminate open wounds exposed to warm seawater.
The clinical features of a V. vulnificus infection from eating contaminated seafood include:
V. vulnificus can also cause a primary necrotising wound infection if an open wound is in contact with contaminated seawater or brackish water. Signs are:
Patients with V. vulnificus infection may become very unwell and require hospitalisation. It is often fatal, especially if treatment is delayed beyond 2 or 3 days.
Infection with V. vulnificus can be suspected in unwell patients if they have a history of eating contaminated seafood or have bathed or splashed in seawater.
The bacteria can be isolated from blood, stool, and/or wound cultures using a special medium.
The differential diagnosis for V. vulnificus infection includes:
V. vulnificus infection is treated with antibiotics (eg, doxycycline or a third-generation cephalosporin).
The outcome of V. vulnificus infection is usually good with prompt treatment. However, the infection may be fatal in up to 50% of patients with pre-existing liver disease and septic shock. It has been recommended that patients with liver disease do not eat raw shellfish.
Mercury poisoning is due to the ingestion of mercury, including mercury in fish. In New Zealand, high mercury levels are found in the following species of fish:
The clinical features of mercury poisoning tend to occur weeks to months after acute ingestion. Symptoms may include:
Skin signs may include colour changes in the hands and feet, with associated pain and itch. Hair loss and nail loss has been described. Excessive sweating and inflammation of the gums may also occur.
Complications from mercury poisoning include pain and colour change in the extremities and permanent loss of teeth resulting from gum inflammation. Hair and nail loss may be slow to resolve.
If the mercury poisoning is severe, patients may develop acute renal failure.
Mercury poisoning can be diagnosed from measuring levels of mercury in the blood.
The differential diagnosis for mercury poisoning is broad, as symptoms may be nonspecific. It may include:
The treatment of mercury poisoning includes supportive care, such as correcting any fluid and electrolyte imbalances. Chelation with meso 2,3-dimercaptosuccinic acid may be used to prevent methylmercury uptake by erythrocytes (red blood cells) and hepatocytes (liver cells).
It is essential to avoid further exposure to mercury. Avoid eating the fish species mentioned above. Be aware that various herbal and traditional remedies may also contain mercury.
The signs and symptoms of mercury poisoning gradually disappear once treatment is started, providing there is no further ingestion.
Acute vitamin A toxicity is caused by the ingestion of too much vitamin A. There are high levels of vitamin A in the liver of various fish species, including:
Vitamin A toxicity can also result from the ingestion of:
Acute vitamin A toxicity results in redness of the skin, followed by desquamation, dryness, peeling of the lips, and dry eyes. Hair loss and nail thinning or loss may become apparent after some weeks.
Other features of vitamin A toxicity include a headache, abdominal pain, nausea, and vomiting.
A severe overdose of vitamin A can lead to death. The intake of high levels of vitamin A or other retinoids during pregnancy has been associated with birth defects.
The diagnosis of vitamin A toxicity is based on the patient’s signs and symptoms, and a history of the ingestion of vitamin A or a retinoid. There is a poor correlation between toxicity and serum retinol levels, as vitamin A is rapidly metabolised to retinoic acid. Blood samples must be stored in the dark before analysis.
The differential diagnosis for vitamin A toxicity is broad, as symptoms may be nonspecific. When symptoms are associated with the ingestion of fish, consider:
The source of the vitamin A toxicity should be avoided, including fish and various supplements, and herbal or traditional remedies containing vitamin A.
Vitamin A will be processed by the body over time. Fluid and electrolyte abnormalities due to vomiting should be corrected.
The outcome of vitamin A toxicity is good. Skin peeling settles over a few weeks as new skin cells are generated.
