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Biomedical subjects

J H Gillespie

Publications and source records attributed to J H Gillespie.

At least 73 records · Page 4Linked to original sources

Intracellular and extracellular mineral crystal formation induced by viral infection of cell cultures.

Intracellular mineral crystals were observed in cell cultures infected with one or more feline viruses. One was a feline syncytium-forming virus, and the other was a new feline virus which produced intranuclear inclusions in cell cultures. Crystals were noted both in autogenous cell cultures from trypsinization of kidneys and urinary bladders of infected cats (three passages) and in subcultures of culture fluids from these, made in a stable feline kidney cell line. Free mineral crystals were also noted in the fluids of the cell cultures. In two bladder and two kidney infected autogenous cultures, structures resembling the urinary calculi observed in obstructed cats were seen. These consisted of mineral crystals in a matrix of cellular debris.

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Pathogenesis of feline panleukopenia virus in susceptible newborn kittens I. Clinical signs, hematology, serology, and virology.

Inoculation of susceptible newborn kittens with a large dose of panleukopenia virus caused subclinical infection in 19 of 23 cases. All infected kittens developed severe and prolonged leukopenia. Cell-free virus was present in the blood from 1 to 7 postinoculation days. The virus spread to all organs, regardless of the route of inoculation. The thymus, spleen, mesenteric lymph nodes, and the cerebellum were the most severely infected organs. Kittens responded to virus infection by production of specific antibodies, first detectable in the circulatory system 6 to 8 days after infection. Antibody production preceded recovery from leukopenia by 3 days.

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Pathogenesis of Feline Panleukopenia Virus in Susceptible Newborn Kittens II. Pathology and Immunofluorescence.

Twenty-three susceptible newborn kittens were inoculated with feline panleukopenia virus on the day of birth and were sacrificed from 18 hr to 43 days postinoculation (DPI). Macroscopic lesions included thymic atrophy in animals examined at 4 to 14 DPI and cerebellar hypoplasia and degeneration in animals examined at 22 to 43 DPI. Clinical signs of ataxia were not observed in the four kittens with cerebellar lesions sacrificed at 22 to 43 days of age. Intranuclear inclusions were present in a variety of cell types in the organs examined from kittens that died or were sacrificed at 4 to 14 DPI. The most severely infected and depleted tissues were the thymus, spleen, mesenteric lymph nodes, and the cerebellum, whereas the bladder, testes, ovaries, and uterus were the least susceptible to panleukopenia virus infection. Specific fluorescence was demonstrated with panleukopenia antiglobulin conjugate in various cell types in tissues from 2 to 22 DPI and only in cerebellar Purkinje cells of kittens sacrificed at 29, 36, and 43 DPI. The virus replicated in the cells of all layers of blood vessels (endothelial, muscular, and connective tissue cells), suggesting that this is the route of dissemination of the agent throughout the body.

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