Fulminant hepatic failure in northern Brazil: morphological, immunohistochemical and pathogenic aspects of Lábrea hepatitis and yellow fever.

A morphological evaluation of histopathological liver samples from 42 fulminant hepatic failure cases from the Amazon Basin was undertaken in order to differentiate yellow fever (YF) from Lábrea hepatitis (LH) and other entities. The pattern and distribution of liver cell death as well as ballooning degeneration and midzonal apoptotic bodies were the most distinctive features of YF, whereas morula cells were the major finding for LH. Nineteen well characterised cases were further submitted to immunohistochemical studies for expression of YF antigen, hepatitis B surface antigen (HBsAg) and delta virus antigen. In both diseases, but particularly in LH, portal vein branch phlebitis was evident and might have played a role in the pathogenesis of hepatic injury, leading to hepatic extinction and portal tract approximation. The regeneration pattern was remarkable: a high proliferative index was detected in YF, whereas in LH multinucleation and pseudoacinar transformation, associated with portal type I collagen deposition and portal elastic fibre proliferation, was seen. In conclusion, midzonal apoptosis, portal phlebitis and a high proliferative index in patients without evidence of previous liver injury was the dominant picture in YF. On the other hand, LH cases showed extensive, predominantly lytic hepatocytic necrosis, portal and hepatic vein phlebitis and morula cells in patients with a morphological background of chronic liver disease.

Experimental yellow fever virus infection in the Golden Hamster (Mesocricetus auratus). I. Virologic, biochemical, and immunologic studies.

This report describes the clinical laboratory findings in golden hamsters experimentally infected with yellow fever (YF) virus. An accompanying paper describes the pathologic findings. Following intraperitoneal inoculation of a virulent strain of YF virus, hamsters developed a high-titered viremia (up to 109/mL) lasting 5--6 days and abnormal liver function tests. YF hemagglutination-inhibiting antibodies appeared 4 or 5 days after infection, often while viremia was still present. The mortality rate in YF-infected hamsters was variable, depending on the virus strain and the age of the animals. Clinical and pathologic changes in the infected hamsters were very similar to those described in experimentally infected macaques and in fatal human cases of YF, which indicates that the golden hamster may be an excellent alternative animal model, in place of nonhuman primates, for research on the pathogenesis and treatment of YF and other viscerotropic flavivirus diseases.

[Giant left atrial myxoma]. / Mixoma gigante de átrio esquerdo.

A 65 year-old man with dilated cardiomyopathy and long history of high blood pressure and a previous cerebral vascular accident had a giant left atrial myxoma as an echocardiographic finding.

Hepatitis delta virus infection and Labrea hepatitis. Prevalence and role in fulminant hepatitis in the Amazon Basin.

To define more exactly the epidemiology of delta virus infection and confirm its role in causing fulminant Labrea hepatitis in the Amazon Basin, we studied the prevalence of delta virus infection among persons with acute and chronic hepatitis B virus infection in the Boca do Acre district of the southern Amazon Basin. Delta virus infection was found in 24% of asymptomatic hepatitis B virus carriers, 29% of acute nonfulminant hepatitis B cases, 74% of fulminant hepatitis B cases, and 100% of chronic hepatitis B cases. Chronic delta virus infection occurred primarily in older children and adults, while acute and fulminant delta virus infection occurred in young children as well. In fulminant hepatitis cases, delta virus superinfection of hepatitis B virus carriers was the most common serological pattern; histopathologic examination showed features identical to those described in fulminant hepatitis cases of similar etiology in Colombia and Venezuela. Delta virus infection is highly endemic in the southern Amazon Basin and is the principal cause of Labrea hepatitis.