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Cutaneous toxicity from fish ingestion

Author: Dr Lydia Chan, Dermatology Registrar, Dermatology Department, Auckland District Health Board, Auckland, New Zealand. DermNet NZ Editor-in-Chief: Adjunct A/Prof Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Maria McGivern/Gus Mitchell. September 2017.


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What skin signs can be seen as a result of fish ingestion?

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.

Skin peeling due to fish poisoning

Scombroid fish poisoning

What causes scombroid fish poisoning?

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.

What are the clinical features of scombroid fish poisoning?

The clinical features of scombroid fish poisoning include:

What are the complications of scombroid fish poisoning?

Scombroid fish poisoning resolves without complications. In severe cases, symptoms may persist for several days.

How is scombroid fish poisoning diagnosed?

Scombroid fish poisoning is usually diagnosed from a clear history of the onset of symptoms within 1 hour of eating a particular fish.

What is the differential diagnosis for scombroid fish poisoning?

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.

What is the treatment for scombroid fish poisoning?

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.

What is the outcome of scombroid fish poisoning?

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.

Vibrio vulnificus infection due to seafood ingestion

What causes Vibrio vulnificus infection?

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.

What are the clinical features of Vibrio vulnificus infection?

The clinical features of a V. vulnificus infection from eating contaminated seafood include:

  • Fever
  • Chills
  • Decreased blood pressure (septic shock)
  • Nausea
  • Diarrhoea
  • Painful, rapidly spreading haemorrhagic bullae on the trunk and lower limbs causing necrotising fasciitis in multiple sites.

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:

  • Rapidly progressive cellulitis around the wound
  • Localised, painful necrotising ulceration
  • Ecchymoses and haemorrhagic bullae
  • Subsequent sepsis.

What are the complications of Vibrio vulnificus infection?

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.

How is Vibrio vulnificus infection diagnosed?

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.

What is the differential diagnosis for Vibrio vulnificus infection?

The differential diagnosis for V. vulnificus infection includes:

  • Another form of systemic or local bacterial infection, (eg, Pseudomonas infection)
  • Anaphylaxis (allergic reaction) to seafood  
  • Gastroenteritis due to seafood contaminants  
  • Norovirus (norwalk virus)
  • Ciguatera
  • Infection with other Vibrio species (eg, V. cholera).

What is the treatment for Vibrio vulnificus infection?

V. vulnificus infection is treated with antibiotics (eg, doxycycline or a third-generation cephalosporin).  

What is the outcome of Vibrio vulnificus infection?

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 due to fish ingestion

What causes mercury poisoning?

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:

  • Cardinalfish
  • Dogfish (excluding rig shark)
  • Lake Rotomahana trout
  • Lake trout from geothermal regions
  • School shark (greyboy or tope)
  • Striped marlin
  • Southern bluefin tuna
  • Swordfish.

What are the clinical features of mercury poisoning?

The clinical features of mercury poisoning tend to occur weeks to months after acute ingestion. Symptoms may include:

  • Tiredness
  • Loss of appetite
  • Light sensitivity
  • Generalised weakness
  • Painful extremities
  • Tremor
  • Changes in mood.

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.

What are the complications of mercury poisoning?

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.

How is mercury poisoning diagnosed?

Mercury poisoning can be diagnosed from measuring levels of mercury in the blood.

What is the differential diagnosis for mercury poisoning?

The differential diagnosis for mercury poisoning is broad, as symptoms may be nonspecific. It may include:

  • Vitamin A toxicity, which may present with hair loss and nail loss
  • Arsenic toxicity, which may present with changes to the hands and feet (eg, blackfoot disease from peripheral vessel occlusion)
  • Scurvy from vitamin C deficiency, which may present with an unusual rash and inflammation of the gums
  • Various psychiatric illnesses, (eg, depression with low mood and poor appetite).

What is the treatment for mercury poisoning?

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.

What is the outcome of mercury poisoning?

The signs and symptoms of mercury poisoning gradually disappear once treatment is started, providing there is no further ingestion.

Acute vitamin A toxicity due to ingestion of fish

What causes acute vitamin A toxicity?

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:

  • Ocean perch
  • Reef or tropical fish in Bermuda (these may not be carnivorous species)
  • Mediterranean greater amberjack
  • Lutjanidae (snappers or Etelis carbunculus)
  • Grouper fish (Cephalopholis boenak)
  • Hapuka (Polyprion oxygeneios)
  • Shark
  • Tuna
  • Seabass.

Vitamin A toxicity can also result from the ingestion of:

  • Meat or organs (especially liver) from mammals (eg, whales, seals, and polar bear) 
  • Fish liver oil capsules.
  • Vitamin A analogues (oral retinoids, such as isotretinoin and acitretin).

What are the clinical features of acute vitamin A toxicity?

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.

What are the complications of vitamin A toxicity?

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.

How is vitamin A toxicity diagnosed?

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.

What is the differential diagnosis of vitamin A toxicity?

The differential diagnosis for vitamin A toxicity is broad, as symptoms may be nonspecific. When symptoms are associated with the ingestion of fish, consider:

  • Mercury poisoning
  • Scombroid fish poisoning (if the onset of symptoms is acute).

What is the treatment for vitamin A toxicity?

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.

What is the outcome of vitamin A toxicity?

The outcome of vitamin A toxicity is good. Skin peeling settles over a few weeks as new skin cells are generated.

 

References

  • Ardigier G, Drouet G, de Haro L. Poisoning after ingestion of Mediterranean greater amberjack liver: Hypervitaminosis A clinical feature [French]. Presse Med 2010 Jul-Aug; 39: 833–4. DOI: 10.1016/j.lpm.2010.03.016. PubMed
  • Chiu YK, Lai MS, Ho JC, Chen JB. Acute fish liver intoxication: report of three cases. Changgeng Yi Xue Za Zhi. 1999; 22: 468–73. PubMed
  • Clarkson TW, Magos L, Myers GJ.  The toxicology of mercury—current exposures and clinical manifestations.  N Engl J Med 2003; Oct 30: 349: 1731–7. DOI: 10.1056/NEJMra022471. Journal
  • Dewailly E, Rouja P, Schultz E, Julien P, Tucker T. Vitamin A intoxication from reef fish liver consumption in Bermuda. J Food Prot 2011; 74: 1581–3. DOI: 10.4315/0362-028X.JFP-10-566. Journal
  • Eastaugh J, Shepherd S. Infectious and toxic syndromes from fish and shellfish consumption. A review. Arch Intern Med. 1989; 149: 1735–40. PubMed
  • Grubb BP. Hypervitaminosis A following long-term use of high-dose fish oil supplements. Chest. 1990 May; 97: 1260. PubMed
  • Hayman RM, Dalziel SR. Acute vitamin A toxicity: a report of three paediatric cases. J Paediatr Child Health. 2012 Mar; 48: E98–100. DOI: 10.1111/j.1440-1754.2011.02122.x. PubMed
  • Homma Y, Otani N, Ishimatsu S. A Case Report of Acute Vitamin A Intoxication due to Ocean Perch Liver Ingestion. J Emerg Med. 2015; 49: 15–7. DOI: 10.1016/j.jemermed.2014.12.056. PubMed
  • Hwang DF, Lu CH, Lin WF. Species identification and vitamin A level in lutjanid fish implicated in vitamin A poisoning. J Food Prot. 2010; 73: 769–73. PubMed
  • New Zealand Ministry for Primary Industries. Mercury in fish. January 2016. Available at: www.mpi.govt.nz/food-safety/whats-in-our-food/chemicals-and-food/mercury-in-fish/ (accessed September 2017).

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