Hepatic Necrosis in Disseminated Herpes

Infection with herpes simplex virus is extremely common and the primary infection is frequently asymptomatic, as is shown by the high proportion of the adult population who possess herpes antibody but yet give no history of the clinical disease. In the symptomatic form, characterized by the appearance of a vesicular eruption on the skin or mucous membranes, considerable variation is seen both in the site and extent of the eruption, as well as in the severity of the accompanying constitutional reaction. Typically the infection is self-limiting and, even in the more extensive forms, recovery is usually complete in two or three weeks with the development of active immunity. In generalized herpes simplex secondary lesions appear on the skin or mucosal surfaces as the result of dissemination of virus from the initial site of infection. In addition to direct spread on the surface which accounts for some of these lesions, particularly in eczematous patients, there is potent clinical evidence to support the view of spread by the blood stream. Laboratory evidence of viraemia, on the other hand, is fragmentary as the virus has only rarely been recovered from the blood stream (Ruchman and Dodd, 1950; Dudgeon, 1952; McNair Scott, Coriell, Blank and Burgoon, 1952). There seems little doubt, however, that haematogenotis spread is primarily responsible for an atypical form of disseminated herpes that has recently been reported from the United States by Zuelzer and Stulberg (1952). Their eight fatal cases fall into two groups; five newborn infants who were found to have widespread herpetic lesions in the viscera, and three older infants with less extensive visceral involvement. In both groups focal necrotic lesions were a prominent feature in the affected viscera and were invariably found in the liver. Essentially similar hepatic lesions in premature infants were described by Hass (1935), who suggested