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Subsequent investigations have failed to uphold the association between bridging necrosis and such a poor prognosis in patients with acute hepatitis. In massive hepatic necrosis (fulminant hepatitis, "acute yellow atrophy"), the striking feature at postmortem examination is the finding of a small, shrunken, soft liver. Histologic examination reveals massive necrosis and dropout of liver cells of most lobules with extensive collapse and condensation of the reticulin framework. When histologic documentation is required in the management of fulminant or very severe hepatitis, a biopsy can be done by the angiographically guided transjugular route, which permits the performance of this invasive procedure in the presence of severe coagulopathy. Modes of transmission overlap, however, and a clear distinction among the different types of viral hepatitis cannot be made solely on the basis of clinical or epidemiologic features (Table 92-2). In the 1970s, serologic evidence of prior hepatitis A infection occurred in ~40% of urban populations in the United States, most of whose members never recalled having had a symptomatic case of hepatitis. Travel to endemic areas is a common source of infection for adults from nonendemic areas. Although hepatitis A is rarely bloodborne, several outbreaks have been recognized in recipients of clotting factor concentrates. We now recognize that many cases of hepatitis B result from less obvious modes of nonpercutaneous or covert percutaneous transmission. In Sub-Saharan Africa, intimate contact among toddlers is considered instrumental in contributing to the maintenance of the high frequency of hepatitis B in the population. Although the precise mode of perinatal transmission is unknown, and although ~10% of infections may be acquired in utero, epidemiologic evidence suggests that most infections occur approximately at the time of delivery and are not related to breast feeding. In the Far East and Africa, hepatitis B, a disease of the newborn and young children, is perpetuated by a cycle of maternalneonatal spread. In North America and western Europe, hepatitis B is primarily a disease of adolescence and early adulthood, the time of life when intimate sexual contact as well as recreational and occupational percutaneous exposures tend to occur. Occasionally, the migrating epidemiology of hepatitis D is expressed in explosive outbreaks of severe hepatitis, such as those that have occurred in remote South American villages as well as in urban centers in the United States. A prospective analysis of transfusion-associated hepatitis conducted between 1986 and 1990 showed that the incidence of transfusion-associated hepatitis at one urban university hospital fell from a baseline of 3. In addition, this virus can be transmitted by occupational exposure to blood, and the likelihood of infection is increased in hemodialysis units. Although the frequency of transfusion-associated hepatitis C fell as a result of blood donor screening, the overall frequency of hepatitis C remained the same until the early 1990s, when the overall frequency fell by 80%, in parallel with a reduction in the number of new cases in injection drug users. The high frequency in Egypt is attributable to contaminated equipment used for medical procedures and unsafe injection practices. Genotype 4 predominates in Egypt; genotype 5 is localized to South Africa and genotype 6 to Hong Kong. Although new acute cases of hepatitis C are rare, newly diagnosed cases are common among otherwise healthy persons who experimented briefly with injection drugs, as noted above, two or three decades earlier.
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However, active prospective surveillance has demonstrated an incidence as high as 414 cases per 100,000 population in some regions of the United States. Tick bites and exposures are reported by patients, frequently in rural areas and especially in May through July. Clinical manifestations are undifferentiated and include fever (97% of cases), headache (80%), myalgia (57%), and malaise (82%). Despite low blood cell counts, the bone marrow is hypercellular, and noncaseating granulomas may be present. This diagnosis is suggested by fever with a known tick exposure during the preceding 3 weeks, thrombocytopenia and/or leukopenia, and increased serum aminotransferase activities. Most patients develop thrombocytopenia (71%) and/or leukopenia (49%) with increased serum hepatic aminotransferase activities (71%). Although co-infections with Borrelia burgdorferi and Babesia microti [transmitted by the same tick vector(s)] occur, there is little evidence of comorbidity or persistence. In regions where seroprevalence is high, a single acute-phase titer may be misleading. The use of protective clothing and tick repellents, careful postexposure tick searches, and prompt removal of attached ticks markedly diminish infection risk. White-footed mice and white-tailed deer in the United States and red deer in Europe are natural reservoirs for A. Clinical Manifestations Seroprevalence rates are high in endemic regions; thus it seems likely that most individuals develop subclinical infections. Coxiella 686 escapes intracellular killing in macrophages by inhibiting the final phagosome maturation step (cathepsin fusion) and adapts to the acidic phagolysosome. Very few organisms and a strong cellular response are observed in patients with acute Q fever, whereas many organisms and a moderate cellular response are seen in chronic Q fever. Persons at risk for Q fever include abattoir workers, veterinarians, and other individuals who have contact with infected animals, particularly newborn animals or products of conception. The ingestion of contaminated milk in some geographic areas probably represents a major route of transmission to humans, although the experimental evidence on this point is contradictory.
