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We report the case of a 14-week fetus who developed a generalized vaccinia virus infection after primary vaccination of the mother in the 10th week of pregnancy. Special emphasis is given to the skeletal lesions, which have not been previously reported in prenatal vaccinial infection.

Multiformal abnormal configurations of virus particles and virus factories were observed in pig skin inoculated with vaccinia, cowpox and monkeypox viruses. The discussion is based on the data of multiplication of the viruses and production of circulating antibody.

Two cases of human infection caused by vaccinia virus were recorded in the Rzeszów province (Poland), this infection being absent both in this province and in the whole country for many years. The diagnosis was based on the investigation of isolated samples (from one female patient) and the identification of the causative agent by its biological properties and the results of the analysis of its genome, made with the use of restrictases, as well as on the results of the serological investigation. Of the two female patients, one suffered from a prolonged and severe infection in her eye, the other had a lesion on the backside of her hand. Apart from local lesions, systemic phenomena (fever, malaise, headache) were observed in both patients. The authors state that, most likely, rodents were the source of infection in these two cases. This is confirmed by the fact that wild rodents (rats, mice) caught in the focus of infection show the presence of antibodies to orthopoxviruses.

Scanning electron microscopy (SEM) has been used during the past few years to determine surface alterations of cells infected with a variety of RNA and DNA viruses. Infection of different cultured cells by RNA and DNA viruses usually revealed dramatic shape changes with surface alterations. The most frequent changes seen were "rounding up" of cells and the development of surface microprojections such as ruffles and microvilli. In the light of available knowledge, suggestions are made in this review for future SEM studies in this field with more sensitive methodologies, which will enable even better characterization of virus-induced cell surface changes.

The Brighton Red (BR) strain of cowpox virus induces a flat, bright red pock on the chorioallantoic membrane (CAM) of the 12-day-old chick embryo. In contrast, mutants with a deleted 38K gene (which is located 31 to 32 kb from the right-hand end of the virus genome) induced a raised, white, and opaque pock. During the first 24-hr p.i., both CPV-BR and the 38K deletion mutants replicated similarly in the CAM of the chick embryo, as indicated by immunocytochemical detection of similar amounts of virus antigen. By 48 hr p.i., the pocks induced by the mutant and CPV-BR are strikingly different. The pocks induced by the 38K deletion mutants were infiltrated by large numbers of heterophils and macrophages, which correlated with a reduction in the levels of virus antigen and virus infectivity. The CPV-BR pock had an absence of inflammatory cells and increased levels of virus antigen and infectivity. By 72 hr p.i., many of the pocks induced by the mutant were undergoing resolution of the virus infection, as indicated by further decrease of virus antigen and visible signs of healing, whereas CPV-BR pocks continued to be a site of active viral replication. These data are consistent with a model where this 38-kDa protein directly or indirectly inhibits the generation of chemotactic molecules which are elicited during virus replication in the CAM or, alternatively, blocks the interaction of these molecules with cells of the host inflammatory response.

Newborn hamsters and kittens infected with vaccinia virus developed communicating hydrocephalus without fibrotic changes in the meninges. Following intracerebral viral inoculation, a transient inflammation of the meninges, ependyma, and choroid plexus was found. One month later, 70% of hamsters infected with the WR strain of vaccinia virus and 35% infected with the vaccine strain developed hydrocephalus. The mechanism of hydrocephalus production is unclear, but differs from other models in which it is associated with stenosis of the aqueduct of Sylvius or fibrosis of the subarachnoid space.

A case of progressive vaccinia complicating chronic lymphocytic leukaemia is reported. At necropsy a vaccinial pneumonia, focal pancreatitis, and evidence of disseminated intravascular coagulation were found. Epithelial proliferation was noted in sweat glands, bronchi, and pancreatic ducts associated with lesions in these sites. The significance of these findings is discussed.