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Biomedical subjects

M J Appel

Publications and source records attributed to M J Appel.

107 records · Page 6Linked to original sources
PubMed1979

Early events in canine distemper demyelinating encephalomyelitis.

The early neuropathological development of demyelinating Canine Distemper Encephalomyelitis (CDE) was studied in SPF dogs. Neural tissues were examined up to 30 days post infection (PI). Three phases of activity were observed. The primary event (first observed 8 days PI) was a nonsuppurative encephalomyelitis associated with the initiation of central nervous system (CNS) infection by virus-laden lymphocytes. At 24 days PI noninflammatory demyelination occurred in well defined, subependymal foci. Cell fusion and syncytia formation accompanied this early demyelination. The third phase, found at day 30 PI in one dog showing signs of recovery, was a second wave of nonsuppurative inflammation. The initial encephalomyelitis was widely disseminated throughout the CNS but subsequent demyelination appeared to be initiated from within the ventricular system. Myelin was phagocytosed by endogeneous CNS macrophages often infected with Canine Distemper Virus (CDV). The possible importance of viral induced cell fusion as well as immune factors in the mechanism of demyelination are discussed.

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PubMed1979

Canine viral enteritis. I. Status report on corona- and parvo-like viral enteritides.

This report attempts to provide the most recent information on salient features of two newly recognized viral enteritides of dogs. The viruses, a corona-like virus and canine parvo-like virus, are distinct but the disease manifestations in a particular outbreak often are similar. Laboratory study is therefore required. The parvoviral infection generally is more severe, with leukopenia (relative lymphopenia) a most prominent feature. Knowledge of the pathogenesis, epizootiology and the host's immune response is fragmentary at the present time, but research now in progress will doubtless expand knowledge of both diseases and of the viruses that cause them.

Animals↗
PubMed1979

Interferon induction in dogs.

A synthetic complex of poly (I)-poly (C) with poly-L-lysine and carboxymethyl cellulose (poly ICLC), as well as UV-inactivated Newcastle disease virus, B-1 strain, was used to induce interferon production in dogs. Several criteria were used for interferon specificity. The interferon response depended on dosage and route of inoculation. Serum interferon concentrations usually reached a peak by 8 hours after inoculation (AI), rapidly declined thereafter, and were nondetectable in most instances at 24 hours AI. Dogs responded less to interferon inducers when reinoculated 2 days after primary induction. The interferon response was biphasic (2 and 8 hours AI) when reinoculated 1 week after primary inoculation. Reinoculation 2 weeks after primary inoculation simulated the first response. Although both inducers caused severe lymphopenia in dogs, the toxic side effects would limit clinical use (in dogs) of poly ICLC, but not of UV-inactivated Newcastle disease virus.

Animals↗
PubMed1978

Possible initiation of viral encephalomyelitis in dogs by migrating lymphocytes infected with distemper virus.

The principal pathways by which viruses spread to the central nervous system (C.N.S.) are considered to be direct invasion along peripheral nerves or the haematogenous route. The latter is thought to involve passive transfer or active replication of virus in C.N.S. endothelial cells. In this study histological evidence of mild perivascular encephalomyelitis was found 8-10 days after infection of dogs with canine distemper virus (C.D.V.). C.D.V. antigen and viral nucleocapsids were detectable in the mononuclear cells infiltrating nervous tissue and C.D.V. was isolated from lymphoid tissue and buffy-coat cells. C.N.S. infection may thus be initiated by migrating virus-infected lymphocytes and this pathway may operate in other viral disorders of the C.N.S.

Animals↗
PubMed1977

Pathogenesis of canine bordetellosis.

Bordetella bronchiseptica produced tracheobronchitis when administered in aerosol to specific pathogen-free dogs. Clinical signs appeared to be directly related to numbers of bacteria in the trachea. Electron microscopic examination revealed that each bacterium was close to one or more tracheal cilia and that a fibrillar material was radiating from the bacterial cell wall. B. bronchiseptica required 14 weeks to be cleared from the tracheas of infected dogs; in contrast, other organisms commonly isolated from the respiratory tracts of dogs were cleared within one to three days. Strains of high and low in vitro passage and strains representing three different morphotypes were of equal pathogenicity. Local immunity was observed after infection and appeared to be of primary importance in recovery from the infection. Presumably this response involves prevention of bacterial attachment and reattachment to cilia.

Aerosols↗
PubMed1977

Bacteriological variation among Bordetella bronchiseptica isolates from dogs and other species.

Bacteriological properties of 50 isolates of Bordetella bronchiseptica were compared. Phase variation, which involved colonial morphology and its associated characters of hemagglutination, hemolysis, acriflavine agglutination; crystal violet staining, flagellation, and fimbriation, occurred among these isolates. Organisms representing the three observed morphotypes did not have different growth rates, nor were any differences in their bacteriological characteristics observed after repeated subculture on agar. There were also variations in antimicrobial drug susceptibility, especially to sulfonamide-trimethoprim, and in nitrate reduction. The relationships among these variable parameters were not apparent. None of the observed variations could be attributed to differences in the species of origin.

Animals↗
PubMed1977

Naturally occurring respiratory disease in a kennel caused by Bordetella bronchiseptica.

The role of Bordetella bronchiseptica as a primary pathogen in nautrally occurring respiratory disease of dogs has been in question since its original isolation in 1911. A study to determine the incidence of B. bronchiseptica in a closed breeding kennel has revealed that the frequency of such isolations is closely associated with mild respiratory disease characterized by a moist, sometimes productive, cough. Infection with B. bronchiseptica usually occurred shortly after weaning and produced illness which lasted for one to two weeks. The organisms, however, continued to be shed for two to three months, and important factor in maintaining the infection in this kennel. Adult dogs sampled at frequent intervals did not harbor B. bronchiseptica in spite of their almost constant exposure to heavily infected pups; immunity to reinfection, therefore, appeared to develop. The involvement of several known canine respiratory viral agents was excluded by virus isolation and serological techniques. It therefore was concluded that B. bronchiseptica was the primary cause of respiratory disease in this large breeding kennel.

Animals↗
PubMed1976

Vaccine-induced canine distemper in a lesser panda.

A fatal disease occurred in a lesser panda (Ailurus fulgens) 2 weeks after vaccination with modified live distemper vaccine. The disease clinically resembled canine distemper. Pathologically there was giant cell pneumonia, with canine distemper viral inclusion bodies in pulmonary and digestive tract epithelium. Viral isolates were indicative of an attenuated strain rather than virulent types.

Animals↗
PubMed1976

Fatal vaccine-induced canine distemper virus infection in black-footed ferrets.

Four black-footed ferrets that were live-trapped in South Dakota and transported to the Patuxent Wildlife Research Center died within 21 days after vaccination with modified live canine distemper virus. Immunofluorescence, European ferret inoculation, virus isolation attempts, and serum-neutralization tests indicated insufficient attenuation of the vaccine for this species.

Animals↗
PubMedDate not supplied

Modulation of pancreatic carcinogenesis by antioxidants.

Previously performed short-term (4-month) studies demonstrated that vitamins C and E, beta-carotene and selenium modulate growth of early putative preneoplastic acinar lesions induced in rat pancreas by azaserine. The present paper summarizes the results of long-term studies performed with azaserine-treated rats maintained on diets high in either beta-carotene, vitamins C and E or selenium. It appeared that rats given a diet high in beta-carotene, vitamin C or selenium, but not vitamin E, developed fewer pancreatic tumours than controls. The chemopreventive effects of these micronutrients were most pronounced when beta-carotene and/or selenium were given during the promotion phase of the carcinogenic process. Surprisingly, cell proliferation in azaserine-induced preneoplastic acinar lesions was higher in rats given beta-carotene and/or selenium via the diet in comparison to controls. It is considered unlikely that any antioxidant alone can be associated with protection against cancer. It is concluded that dietary supplementation of combinations of antioxidants may have practical application in chemoprevention of cancer.

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