Biologic behavior of canine mammary neoplasms based on a histogenetic classification.
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Biomedical subjects
Publications and source records attributed to A Koestner.
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Thirty-four gnotobiotic dogs were used to study the effects of R252 canine distemper virus (CDV) infection on the lymphoid system. Twenty-one dogs were inoculated parenterally, and 6 dogs were infected by contact exposure to inoculated littermates. Seven littermate dogs were maintained as uninfected controls. The means of the absolute lymphocyte counts of dogs infected with R252 CDV were significantly decreased for 7 weeks after infection. The lymphocyte counts failed to return to normal in 7 dogs which became moribund with neurologic signs and were sacrificed 27 to 47 days after infection (group I). The 19 dogs which survived the 12-week observation period had normal lymphocyte counts by 8 weeks after infection. Five of these dogs (group II) were subsequently found to have demyelination of the central nervous system (CNS), while no CNS lesions were demonstrated in the remaining 14 infected dogs (group III). The thymuses of dogs of group I were atrophic and their lymph nodes were depleted in lymphoid cells. In addition, the number of Hassall's corpuscles per thymic lobule were decreased in dogs of group I. Viral nucleoprotein was demonstrated in thymus and lymph node cells by electron microscopy. No lymphoid lesions were found in the dogs of group II. Some of the thymuses of dogs of group III were significantly larger than those of uninfected controls, and they contained increased numbers of Hassall's corpuscles per thymic lobule. Further, germinal centers were found in two thymuses of dogs of group III.
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Sera from dogs with spontaneously occurring and experimentally produced canine distemper virus-associated demyelinating encephalitis were examined for antibodies to central nervous system myelin by the complement fixation and indirect immunofluorescent methods. Complement-fixing immunoglobulin M antibodies and non-complement-fixing immunoglobulin G antibodies were found in 97% of the spontaneous cases. In comparison, only 28% of control sera contained these antibodies; furthermore, mean antibody titers in the control groups were significantly lower (P < 0.005) when compared to the distemper group. Complement-fixing antimyelin antibodies were also demonstrated in gnotobiotic dogs with experimentally induced distemper virus-associated demyelination. The antibody response could be correlated with clinicopathological features of the disease produced. Results of this study indicate that demyelination in canine distemper may proceed by immune mechanisms.
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