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Biomedical subjects

B McCullough

Publications and source records attributed to B McCullough.

46 records · Page 3Linked to original sources
PubMed1974

Experimental canine distemper virus-induced lymphoid depletion.

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.

Animals↗
PubMed1973

Myelin-specific autoantibodies associated with central nervous system demyelination in canine distemper virus infection.

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.

Absorption↗
PubMedDate not supplied

Infection and disease induced in chimpanzees with 6/94, a parainfluenza type 1 virus isolated from human multiple sclerosis brain.

A parainfluenza type 1 virus (6/94) recovered from brain cell cultures of two patients with multiple sclerosis (MS) was inoculated into newborn chimpanzees by the intranasal (IN) or intracerebral (IC) routes. Four of the five animals receiving the virus IN developed clinical signs ranging from mild fever, with or without rhinorrhea, to severe respiratory disease. Two of the chimpanzees died as a result of pneumonia. Virus could be recovered from respiratory tracts for as long as 9 days after exposure and was followed by development of specific neutralizing antibody to the 6/94 virus but not to the HA2 strain of parainfluenza type 1. Brain examination showed astrocytosis, especially of posterior fossa structures, activation of microgliacytes and, in one animal, round cell infiltration of leptomeninges. Of thse three animals receiving virus IC, two developed recurrent seizures beginning 14 months after inoculation. One of these was sacrificed at 23 months of age after progressive neurologic disease, with electroencephalographic abnormalities, developed. The third animal died at 3 months of age of intercurrent pneumonia. No virus was recovered from these animals, although all showed antibody conversion to 6/94 but not HA2 virus. A variety of pathologic lesions were seen in the brains of both animals coming to necropsy particularly in the sacrificed chimpanzee. These included subacute encephalitis, extensive cortical and subcortical degeneration, vascular sclerosis, white matter gliosis and axonal dystrophy.

Animals↗
PubMedDate not supplied

Platelet kinetics in dogs treated with a glycoprotein IIb/IIIa peptide antagonist.

Platelet glycoprotein IIb/IIIa (GPIIb/IIIa) receptor antagonists have been highly effective inhibitors of platelet aggregation in preclinical studies and in clinical trials. However, decreased platelet counts have been documented in preclinical studies and in some patients receiving GPIIb/IIIa antagonists. We evaluated changes in platelet kinetics and fate in dogs receiving the GPIIb/IIIa receptor antagonist RPR 109891 orally for 4 days. Dogs receiving RPR 109891 had a 22-52% decrease in platelet count with the nadirs at 3-5 days after initiation of treatment. Platelet survival time was reduced by 19%, and platelet half-life was reduced by 63%. Indium-111-labeled platelets were rapidly cleared from the blood within 1 hour after administration of RPR 109891 on treatment days 1 and 2. This clearing was associated with a sharp increase in radioactivity in spleen but not in liver or lung. Platelet clearance was markedly attenuated on treatment days 3 and 4. Platelet counts returned to baseline within 1 week after discontinuation of treatment. These data indicate that RPR 109891 causes rapid and selective sequestration of platelets in the spleen.

Administration, Oral↗