Sally P. Bauer

Viral pancreatitis: Ultrastructural pathological effects of coxsackievirus B3 infection in newborn mouse pancreas

Abstract An electron microscopic study of Coxsackievirus B3-infected newborn mice revealed pathological changes in both the endocrine and exocrine portions of the pancreas. Damage ranged from a focal degeneration in which small areas of individual cells were affected to a widespread necrosis and inflammation in which entire acini and islets were so changed that identification of individual cell types was difficult. Compound membrane-vesicle complexes typical of picornavirus infection and virus particles in various arrays were observed in the acinar cells and macrophages. Fibrosis of the islets and a thickening of the basal laminae of associated capillaries were noted also. Comparisons were made to the pancreatitis caused by this and other group B Coxsackieviruses in both human and experimental animals.

Lymphocytic choriomeningitis: Ultrastructural pathology☆

Abstract The pathogenesis of lymphocytic choriomeningitis (LCM) virus infection was studied in mice by associating the development of ultrastructural changes with parallel light microscopic alterations and the build-up of viral antigen as detected by immunofluorescence. From early in the course of the disease, viral antigen was localized in the choroid plexus and ependymal epithelium and the arachnoid cells of the meninges. Typical LCM virus particles were found enmeshed in the microvillous border of the choroid plexus and ependyma as a result of budding from plasma membranes and entrapment beneath overlying macrophages and epithelial projections. These virus particles and nascent budding particles were considered the target of the terminal cell-mediated immune (CMI) response. Arenavirus inclusions were observed in the cytoplasm of the same epithelia throughout the late stages of infection, but such antigen masses were effectively sequestered. On the day before death (day 6 postinoculation), mononuclear cells invaded the choroid plexus by extravasation through the central capillary endothelium and basement lamina, and then via emperipolesis and intercellular migration through the epithelium into the cerebrospinal fluid of the ventricles. The most common invading cell type was considered a medium or large lymphocyte, but monocytes and macrophages were also present. Similar cell types invaded the ependyma and the subarachnoid space of the meninges. No cytopathology was associated with the viral infection of the choroid plexus, ependyma, or meninges, nor with the mononuclear cell influx of the CMI reaction to infection. The parenchyma of the brain remained normal throughout infection; there was no evidence of infection, inflammation, or edema. Because correspondence of the immunopathologic target site and the anatomic location of the blood-cerebrospinal fluid barrier occurred only in the choroid plexus, this organ was considered to have the central role in LCM pathogenesis. Its functional breakdown must be the proximate cause of the convulsive diatheses characteristic of the disease.

A bat rabies isolate with an unusually short incubation period.

Abstract Rabies viruses from two types of bats were inoculated intracerebrally into laboratory mice. The reactions of the mice differed markedly. Those inoculated with virus from a Mexican freetail bat, Tadarida brasiliensis mexicana , died a violent death after an incubation of 4 to 5 days. The pathology was marked, with much neuronal destruction noted. Those mice inoculated with virus from a vampire bat, Desmodus rotundus , died after incubation periods similar to those noted after inoculation of common “street” viruses, i.e., 7 days or more. The pathology corresponded to the limited amount usually seen after death from “street” virus.

Myocardial and pancreatic necrosis induced by rocio virus, a new flavivirus

Abstract Rocio virus, the etiologic agent of an epidemic of human encephalitis in Sao Paulo State, Brazil, produced a severe, generalized infection in suckling hamsters. Of the non-neural organs, heart and pancreas were most severely affected. Focal necrosis was apparent in the heart 48 hr after intracerebral inoculation, and by 72 hr it was widespread. Virus particles were seen within cisternae in both the myocardial fibers and the smooth musculature of small blood vessels. The pancreas exhibited minimal changes at 48 hr but within 72 hr there was extensive necrosis, with both exocrine and endocrine portions of the organ severely affected. Virus particles were found mostly within the acinar cells where frequently they were sequestered in the zymogen granules, and within the beta cells in the islets. They were also seen in vacuoles in unmyelinated nerve fibers supplying the pancreas.

Enteric inoculation with ERA rabies virus: evaluation of a candidate wildlife vaccine in laboratory rodents.

SummaryA series of experiments on the safety and efficacy of enteric vaccination was carried out in laboratory rodents using the ERA strain of rabies virus both live and inactivated. In the first and second experiments in white Norway rats, several methods of inoculation were compared for the development of rabies neutralizing antibody. In later experiments, the potential for disease transmission through salivary excretion of the ERA strain, or through scavenging, or cannibalism were evaluated. Enteric inoculation of rats with high doses of live ERA virus often failed to give an antibody response yet would occasionally kill adult animals. Rabies antigen was demonstrable in the trigeminal ganglion and tongue of one of these rats, and 14 of 65 (21.5 percent) adult mice died from rabies after eating infants infected with the ERA strain.

Experimental vesicular stomatitis virus infection: Ultrastructural pathology

Abstract Vesicular stomatitis virus infection in mice and hamsters was rapidly lethal, but primary target organs and pathogenesis varied with the route of inoculation. Ultrastructural observations of brain tissue after intracerebral inoculation indicated widespread neuronal infection with viral maturation upon plasma membranes. This was associated with the development of interstitial edema and necrosis. When virus was inoculated intramuscularly, the most important target organs were liver and kidney. Focal necrosis of tubular epithelium of the kidney was prominent, and in the liver a clear progression of infection through Kupffer cells and into parenchyma was extremely destructive. Virus particle production from liver littoral cells appeared to be a major potential source of virus for spread to other organs, but the peracute course of disease in these rodents precluded development of other lesions or an inflammatory response.