Dr. Health: Infectious hepatitis has been shown in recent years to be a viral disease. For despite the fact that the virus has never been isolated or visualized, despite the fact that characteristic lesions have never been produced in the chick embryo or the virus grown in tissue culture, despite the failure to demonstrate inclusion bodies in infected material and despite the failure to find a susceptible laboratory animal, the work of Neefe and others using human volunteers has conclusively shown that an agent can be isolated from human cases of infectious hepatitis which will reproduce the disease when administered to other human beings. This infectious agent passes bacteria-retaining filters, is not destroyed by ordinary bacterial disinfectants, survives 56 °c. for one hour and remains infectious under a wide range of conditions. On the other hand, it may be inactivated in plasma on exposure to ultraviolet light and under certain conditions may be destroyed when subjected to 60 °c. for several hours. So far, at least two distinct varieties of hepatitis-producing agents have been identified, the IH and SH strains. The former, isolated from cases of epidemic infectious hepatitis, would appear to be the more widespread and common agent. After inoculation it produces symptoms, often with fever, in twelve to forty-two days although the incidence of takes is considerably higher (80 per cent) when the material is given orally than when injected parenterally. The resulting disease cannot be distinguished either pathologically or in its clinical course from that due to SH virus, except that gamma globulin when given during the incubation period protects against or modifies the IH disease, but so far has not been shown to be active against the SH disease. SH virus can be inoculated successfully (75 per cent) only by the parenteral route and then exhibits a prolonged incubation period of 60 to 300 days, during which time the virus is present in the blood. The thymol turbidity test may be negative in SH hepatitis. During the period of active jaundice viremia is common to both diseases and presumably the virus may be found in the stool in each case (though demonstrated only in IH), but how long either of these phenomena persists after recovery is not known. Each virus infection is followed by the development of long-term specific immunity, presumably permanent, but there is no cross-immunity. How infectious hepatitis is transmitted is not entirely clear. A certain number of cases due to IH virus apparently follow the ingestion of infected material. But accidental transmission of both IH and SH virus may follow upon improper handling of needles and syringes so that adequate heat sterilization of these implements and avoidance of the “multiple dose—single syringe” technic seems essential. Sterilization of feces, urine, bedside utensils, bed linen and blankets is also recommended. When these measures have been carried out, accidental transmission of either virus has not been a problem. The hepatic lesion in virus hepatitis may have three components: 1. 1. Parenchymal damage is associated with a positive cephalin flocculation test; elevation of the direct serum bilirubin and impaired liver function as measured by galactose tolerance and cholesterol esterification. 2. 2. Involvement of the reticuloendothelial system, i.e., the Kupffer cells and the sinusoidal lining, leads to hyperglobulinemia and portal obstruction as evidenced by splenomegaly, ascites and elevation of indirect serum bilirubin and serum alkaline phosphatase. 3. 3. Periportal inflammation may produce abnormalities of both types noted above. Some 60 per cent of patients following recovery from acute hepatitis may have symptoms such as fatigue, drowsiness, fatty food and alcohol intolerance, in addition to physical findings such as liver tenderness, without any detectable abnormality in liver function tests. In the 15 per cent with definite relapse the laboratory findings are usually limited to bromsulfalein retention and positive flocculation tests, although in instances of severe relapse, jaundice may recur with alteration in other tests as well. Therapy of the acute disease is limited chiefly to bed rest and dietary measures. The former should be complete and prolonged until the bromsulfalein retention is normal since too early activity may be responsible for relapse. A high caloric diet with high protein and, after the first few days of anorexia and fatty food intolerance, high fat content seems most desirable at the present time. Liver extract intravenously may stimulate the appetite, especially in chronic cases, but it should be emphasized that ordinary liver extract prepared for intramuscular injection cannot be so used. Finally, in patients with edema and ascites on the basis of hypoalbuminemia, the administration of plasma or human albumin may be temporarily beneficial.
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Jul 1, 2004
A Margerit + 3
Open Access