Lábrea fever

Lábrea fever, also known as Lábrea's black fever and Lábrea hepatitis, is a lethal tropical viral infection discovered in the 1950s in the city of Lábrea, in the Brazilian Amazon basin, where it occurs mostly in the area south of the Amazon River, in the states of Acre, Amazonas and Rondônia . The disease has also been diagnosed in Colombia and Peru. The similar form in Colombia has been named Santa Marta fever.

Its main manifestation is a fulminant hepatitis which may kill in less than a week, and which characteristically affects children and young adults, and more males than females. It is accompanied also by an encephalitis in many cases. The disease is highly lethal: in a study carried out in 1986 at Boca do Acre, also in the Amazon, 39 patients out of 44 died in the acute phase of the disease.^[1] Survivors may develop chronic disease.

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Symptoms and signs

Lábrea fever has a sudden onset, with jaundice (bilious color of the skin), anorexia (lack of appetite), hematemesis (blood vomits), headache, fever and severe prostration. Death occurs by acute liver failure (ALF). In the last phase, neurological symptoms such as agitation, delirium, convulsions and hemorrhagic coma commonly appear.

Etiology

Lábrea fever is a coinfection or superinfection of hepatitis D or delta virus and hepatitis B (HBV).^[1] The infection by delta virus may occur in a patient who already has the HBV, or both viruses may infect at the same time a previously uninfected patient. Delta virus can only multiply in the presence of HBV, therefore vaccination against HBV prevents infection. Thus, American and Brazilian scientists have determined that the delta virusa, virus, which is a small circular RNA virus, is normally unable to cause illness by itself, due to a defect. When it is combined with HBV, Lábrea hepatitis may ensue. The main discovery of delta virus and HBV association was done by Dr. Gilberta Bensabath, a leading tropical virologist of the Instituto Evandro Chagas, of Belém, state of Pará, and her collaborators.

Infected patients show extensive destruction of liver tissue, with steatosis of a particular type (microsteatosis, characterized by small fat droplets inside the cells), and infiltration of large numbers of inflammatory cells called morula cells, comprised mainly by macrophages containing delta virus antigens.

In the 1987 Boca do Acre study, scientists did an epidemiological survey and reported delta virus infection in 24% of asymptomatic HBV carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. The delta virus seems to be endemic in the Amazon region.

Treatment and prevention

Treatment is similar to hepatitis B, but due to its high lethality, more aggressive therapeutic approaches are recommended in the acute phase. In absence of a specific vaccine against delta virus, the vaccine against HBV must be given soon after birth in risk groups.

References

1. ^ ^{a b} Bensabath G, Hadler SC, Soares MC, Fields H, Dias LB, Popper H, Maynard JE (1987). "Hepatitis delta virus infection and Labrea hepatitis. Prevalence and role in fulminant hepatitis in the Amazon Basin". JAMA 258 (4): 479-83. PMID 3599343.

• Specter SC (Ed.). (1999). Viral Hepatitis: Diagnosis, Therapy, and Prevention. Humana Press. ISBN 0896034240. 
• da Fonseca JC (2004). "[Hepatitis fulminant in Brazilian Amazon]". Rev Soc Bras Med Trop 37 Suppl 2: 93-5. PMID 15586904.
• Bensabath G, Soares Mdo C (2004). "[The evolution of knowledge about viral hepatitis in Amazon region: from epidemiology and etiology to the prophilaxy]". Rev Soc Bras Med Trop 37 Suppl 2: 14-26. PMID 15586892.
• Fonseca JC, Souza RA, Brasil LM, Araujo JR, Ferreira LC (2004). "Fulminant hepatic failure in children and adolescents in Northern Brazil". Rev Soc Bras Med Trop 37 (1): 67-9. PMID 15042190.