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Klaus Hummeler, M.D.; Daniel Kirk, M.D.; Mykola Ostapiak
JAMA. 1954;156(7):676-679. doi:10.1001/jama.1954.02950070004002.
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The numerous strains of Coxsackie viruses that have been isolated and described since Dalldorf and Sickles first directed attention to these agents1 are grouped together mainly because they produce characteristic lesions in the suckling mouse or hamster. They were further segregated into two groups (A and B) according to the distinct pathological differences that they produce in the suckling mouse. Group A viruses produce typical lesions in the striated muscle, resembling Zenker's hyaline degeneration, and hardly any other recognizable pathological changes. The group B viruses, on the other hand, while producing only moderate muscle lesions also cause a characteristic encephalopathy and panniculitis. Furthermore, the group B viruses cause an extensive pancreatitis in adult mice. The viruses have a wide distribution in the world, and from the first isolation in 1948 considerable effort has been spent to relate the isolation of any of the Coxsackie viruses to a particular clinical


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