The Pathology of Epidemic Hepatitis

Mallory, Tracy B.

doi:10.1001/jama.1947.02880250003002

Cited by 109 publications

(22 citation statements)

References 8 publications

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“…The extent of involvement was increased with more severe disease. Similar findings were observed in large series reported over the ensuing 30 years (127,158,195,225). All agreed that the cardinal features of acute hepatitis were the presence of hepatocellular degeneration, characterized as either ballooning or acidophilic (apoptotic) change, together with various degrees of portal and lobular inflammation and hepatocyte regeneration.…”

Section: Percutaneous Liver Biopsysupporting

confidence: 90%

Hepatitis A: Old and New

2001

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The hepatitis A virus (HAV), a picornavirus, is a common cause of hepatitis worldwide. Spread of infection is generally person to person or by oral intake after fecal contamination of skin or mucous membranes; less commonly, there is fecal contamination of food or water. Hepatitis A is endemic in developing countries, and most residents are exposed in childhood. In contrast, the adult population in developed countries demonstrates falling rates of exposure with improvements in hygiene and sanitation. The export of food that cannot be sterilized, from countries of high endemicity to areas with low rates of infection, is a potentially important source of infection. After ingestion and uptake from the gastrointestinal tract, the virus replicates in the liver and is excreted into the bile. Cellular immune responses to the virus lead to destruction of infected hepatocytes with consequent development of symptoms and signs of disease. Humoral immune responses are the basis for diagnostic serologic assays. Acute HAV infection is clinically indistinguishable from other causes of acute viral hepatitis. In young children the disease is often asymptomatic, whereas in older children and adults there may be a range of clinical manifestations from mild, anicteric infection to fulminant hepatic failure. Clinical variants include prolonged, relapsing, and cholestatic forms. Management of the acute illness is supportive, and complete recovery without sequelae is the usual outcome. Research efforts during World War II led to the development of passive immunoprophylaxis. Pooled immune serum globulin is efficacious in the prevention and attenuation of disease in exposed individuals. More recently, active immunoprophylaxis by vaccination has been accomplished. Future eradication of this disease can now be contemplated

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Section: Percutaneous Liver Biopsysupporting

confidence: 90%

Hepatitis A: Old and New

2001

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“…The Councilman-like bodies were also found in the Kupffer cells . Concerning the origin of the Cuncilman-like body, there have been the following three different reports: It is originally produced in (1) the Kupffer cell (Ruebner and Miyai 1962; Smetana 1962), (2) the hepatocyte (Mallory 1947;Klion and Schaffner 1966), and (3) both the Kupffer cell and the hepatocyte (Ruebner et al . 1967).…”

Section: Resultsmentioning

confidence: 99%

A scanning electron microscopic study on hepatic changes induced by mouse hepatitis virus-2.

Oikawa

1979

Tohoku J. Exp. Med.

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A Scanning Electron Microscopic Study on Hepatic Changes Induced by Mouse HepatitisVirus-2. Tohoku J. exp. Med., 1979, 129 (4), 389-404 -No significant changes in the structure of the liver were seen until 9 hr after the inoculation of mouse hepatitis virus-2 (MHV-2) into mice. At the 24 hr stage, distinct swelling of hepatocytes and narrowing of sinusoidal lumina were observed from the middle to the central area of the hepatic lobules. Most of the Kupffer cells were swollen. Their villous projections were decreased in number, and the remaining projections became like blebs.Virus particles appeared from this stage in the hepatocytes, the Kupffer cells and the space of Disse. At the 48 hr stage, parenchymal necrotic foci were present in the central and the middle area of the lobules. The necrotic change was increased from 72 hr after inoculation, and was followed by submassive or massive necrosis. It is suggested that hepatic necrosis in both the central and the middle area, or in either area, of the lobules was advanced by aggravation of the sinusoidal microcirculation, as a result of the swelling of the hepatocytes and the Kupffer cells in addition to the direct affection by virus. Fine granulation was observed on the surface of most of the central flagella of the bile duct. Some flagella were degenerated, and came in part to be a fibrillar net.

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“…Out of 40 patients in whom Mallory performed liver biopsy because of persistence of symptoms following hepatitis, 15 were normal, 10 were doubtful and 15 showed changes similar to a normal convalescent group; that is, histological evidence of periportal and interlobular inflammation and focal hyalin necrosis (32). From these studies it is clear that liver disease can be demonstrated by biopsy when histological change is present, but it seems possible that minimal physiological impairment may not always be manifested by structural change.…”

Section: Discussionmentioning

confidence: 98%