Other Forms of Acute Hepatitis

Clinical hepatitis due to cytomegalovirus occurs mainly in immunocompromised patients, in whom the disease may be severe or even fatal. It is clinically indistinguishable from HBV hepatitis, but the histopathological picture is distinctive because of the intranuclear inclusions in giant cells produced by coalescence of proliferating bile duct epithelium, and infiltration of mononuclear cells . Virus and antigens can be identified by culture or by immunofluorescent staining in blood and liver , and in other body fluids and tissues.

A mild, self-limited hepatitis, manifested by elevation of hepatocellular enzymes in the serum, occurs in 80-90% of patients with infectious mononucleosis due to the Epstein-Barr virus . Occasionally severe hepatitis with jaundice is observed. Progression to chronic hepatitis or cirrhosis occurs rarely, if ever.

Yellow fever is an acute viral illness caused by a group B arbovirus transmitted by the mosquito Aedes aegypti. The virus is viscerotropic and produces damage in the liver, kidney, heart and gastrointestinal tract. The name `yellow fever' refers to the jaundice which is present in severe infections. After an incubation period of a few days the illness begins abruptly with fever and chills, headache, myalgias, nausea and vomiting and leucopenia. After a few days the patient appears to improve, but the illness returns with fever, jaundice, haemorrhages, albuminuria and renal failure. Death often occurs in 7-10 days, following a terminal stage characterized by agitation, delirium, shock and coma.

The hepatic lesion consists of acute coagulative necrosis of the midzonal portion of the lobule . Intracellular hyaline deposits (Councilman bodies) and intranuclear eosinophilic inclusions (Torres bodies) may be seen. Even in severe cases there is a conspicuous absence of infiltration by inflammatory cells. Yellow fever formerly occurred throughout much of the world (except Asia), but is now found only in tropical America and Africa. Control of yellow fever has been achieved primarily by elimination of the insect vector from much of its former range, and the live attenuated 17D vaccine provides essentially life-long protection from infection.

In immunocompromised individuals with herpes simplex infection or varicella (chickenpox), the virus may disseminate to visceral organs, including the liver. The characteristic hepatic lesion is focal coagulative necrosis with little surrounding inflammation .

In Q fever, a rickettsial disease, there may be hepatic necrosis and lipogranulomatous lesions with eosinophilic material surrounding the central vacuole .

In congenital syphilis , there is a hepatitis characterized by fibrosis around individual hepatocytes , and there are abundant spirochaetes in the liver. In tertiary syphilis the typical lesion is the gumma, a necrotic nodule surrounded by granulation tissue , which produces deep scars (hepar lobatum) as it heals by fibrosis.

Most infections with Leptospira are either asymptomatic or result in mild anicteric infections without evidence of significant hepatic involvement. In severe cases of leptospirosis (Weil's disease), jaundice and impaired liver function are characteristically present. The jaundice is usually not associated with hepatocellular necrosis and leptospires are rarely seen in the liver . After recovery, hepatic function returns to normal.

Jaundice is a well-recognized complication of severe bacterial infection in newborns, but this syndrome occurs rarely in adults. Occasionally in severe bacteraemic infections, especially those due to Escherichia coli and related members of the family Enterobacteriaceae, cholestatic jaundice is observed. Serum bilirubin and alkaline phosphatase levels are elevated, but transaminases are usually normal or elevated only slightly. Histopathological examination reveals intrahepatic cholestasis with little or no hepatocellular necrosis.

Reye's syndrome is a syndrome of unknown aetiology seen primarily in children following influenza B (less commonly influenza A), varicella and a number of other viral infections. The incidence appears to be increased in children who have received aspirin. Involvement of the central nervous system is the most serious aspect of Reye's syndrome, and most deaths are due to cerebral oedema. In the liver the predominant findings are fatty infiltration of hepatocytes, with multiple small droplets of lipids uniformly distributed throughout the cells and . Swelling and pleomorphism of hepatic mitochondria are seen using electron microscopy. Inflammatory changes are absent, and there is little or no hepatocellular necrosis.