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Biomedical subjects

M J Appel

Publications and source records attributed to M J Appel.

At least 55 records · Page 3Linked to original sources
PubMed1994

Serologic survey of giant pandas (Ailuropoda melanoleuca), and domestic dogs and cats in the Wolong Reserve, China.

Sera from captive and recently rescued giant pandas (Ailuropoda melanoleuca) in the Wolong Reserve, China, were examined by serum neutralization or hemagglutination inhibition for antibodies to canine distemper virus (CDV), canine coronavirus (CCV), canine herpesvirus (CHV), pseudorabies virus (PRV), canine adenovirus type 2 (CAV), and canine parvovirus (CPV). Serum samples from village domestic dogs and cats, which run free throughout the reserve also were examined. Antibodies against CPV were detected in six of eight giant pandas and all dogs and cats tested. The origin of the virus was not determined. Two of eight giant pandas and two of seven dogs had CDV antibody titers. Three of eight pandas and three of seven dogs had CCV antibody titers. Four of eight pandas and two of seven dogs had CAV titers; the titers in dogs were very high. No pandas or dogs had evidence of exposure to CHV or PRV.

Adenoviruses, Canine↗
PubMed1994

African wild dogs (Lycaon pictus) endangered by a canine distemper epizootic among domestic dogs near the Masai Mara National Reserve, Kenya.

A longitudinal study of canine distemper (CD) among domestic dogs on Malsai communal land to the north of the Masai Mara National Reserve in Kenya was conducted from 1989 to 1991. Prevalence of antibodies to CD was very low among domestic dogs in 1989 and 1990 (4%, n = 49; and 1%, n = 119, respectively) and no African wild dogs (Lycaon pictus; n = 16) collected simultaneously from the same area had detectable antibodies. Among 51 domestic dogs sampled in 1991, however, prevalence of CD antibodies rose significantly (P < 0.01) to 76%. Disease-related mortality rates among domestic dogs were estimated from 1990 to 1992; they rose significantly (P < 0.01) from 21% in 1990 to 50% in 1991 and then decreased significantly (P < 0.01) to 38% in 1992. The 1992 mortality rate remained significantly (P < 0.01) higher than that of 1990. Signs observed in clinically ill domestic dogs were consistent with CD and included listlessness, decreased appetite, bilateral serous to mucopurulent oculonasal discharge, and diarrhea. No carcasses could be retrieved for virus isolation and postmortem examination. Concurrent with this CD epizootic in domestic dogs, the known African wild dog packs in this region disappeared.

Animals↗
PubMed1993

Expression and secretion of outer surface protein (OSP-A) of Borrelia burgdorferi from Escherichia coli.

Outer surface protein A (OspA) is encoded by the ospA gene from Borrelia burgdorferi. This protein induces immunity against infection in mice. The cloning and expression of OspA in Escherichia coli have been previously described, but the secretion of OspA into culture media in E. coli has not yet been reported. In this report we demonstrate that a chimeric OspA protein was secreted into culture media by E. coli when it also harbors the hemolysin secretion genes hlyBD. The OspA fusion protein was also overexpressed from a T7 promoter and purified by immobilized metal ion chromatography. This was possible because the fusion protein contains six histidyl residues in its N-terminus.

Antigens, Surface↗
PubMed1993

Cross-reactivity between B. burgdorferi and other spirochetes affects specificity of serotests for detection of antibodies to the Lyme disease agent in dogs.

Western immunoblots, the kinetics-based enzyme-linked immunosorbent assay (KELA), and the microagglutination test were used to evaluate cross-reactivity among antibodies to serovars of Leptospira interrogans (leptospiral serovars), and B. burgdorferi from naturally infected dogs, and to Serpulina (Treponema) hyodysenteriae from vaccinated rabbits. Whole-cell lysates from Borrelia spp., leptospiral serovars, and Serpulina spp. were used for SDS-PAGE, western blots, and KELA. Crossreactivity occurred between the antibodies to B. burgdorferi and leptospiral serovars when tested on the heterologous antigens. Antibodies to leptospiral serovars tended to cross-react more strongly with antigens of B. burgdorferi spp. than did antibodies to B. burgdorferi when tested against antigens of leptospiral serovars. The antibodies against B. burgdorferi showed a lesser degree of cross-reactivity to the antigens of S. hyodysenteriae and S. innocens than they did to leptospiral serovars. We conclude that cross-reactivity occurs between B. burgdorferi and leptospiral serovars. Validation and interpretation of ELISA tests for detection of antibody activity to whole cell lysates of the Lyme agent must take this cross-reactivity into consideration. Conversely, dogs infected with the Lyme agent do not show significant cross-reactivity in the microagglutination test for antibody to the leptospiral serovars.

Agglutination Tests↗
PubMed1993

Experimental Lyme disease in dogs produces arthritis and persistent infection.

Lyme disease was reproduced in specific pathogen-free beagle dogs by exposure to Borrelia burgdorferi-infected ticks (Ixodes dammini). Seroconversion and disease frequency were higher after exposure to infected adult ticks than to infected nymphs. Young pups developed clinical disease more readily than older dogs. The incubation period lasted 2-5 months. Acute recurrent lameness with fibrinopurulent arthritis was the dominant clinical sign. Dogs recovered but developed persistent mild polyarthritis. B. burgdorferi persisted in recovered dogs for at least 1 year. Isolation of B. burgdorferi and detection by polymerase chain reaction was most successful from skin biopsies at the site of the tick bite. Antibody to B. burgdorferi antigens was first detected by ELISA and Western blots by 4-6 weeks after exposure. High serum levels persisted during 17 months of observation. In contrast to infection from ticks, inoculation of dogs with cultured B. burgdorferi resulted in seroconversion with a shorter duration of antibody persistence and no clinical disease.

Age Factors↗
PubMed1992

Role of cholecystokinin in dietary fat-promoted azaserine-induced pancreatic carcinogenesis in rats.

The role of cholecystokinin in dietary fat-promoted pancreatic carcinogenesis was investigated in azaserine-treated rats, using lorglumide, a highly specific cholecystokinin-receptor antagonist. The animals were killed 8 months after the start of treatment. Cholecystokinin, but not dietary unsaturated fat, increased pancreatic weight. Rats treated with cholecystokinin developed more acidophilic atypical acinar cell nodules, adenomas and adenocarcinomas than control animals. Rats maintained on the high-fat diet developed significantly more adenomas and adenocarcinomas than controls given a diet low in unsaturated fat. Lorglumide largely inhibited the enhancing effect of cholecystokinin, but not of dietary fat, on pancreatic carcinogenesis indicating that it is unlikely that the promoting effect of dietary unsaturated fat on pancreatic carcinogenesis is mediated via cholecystokinin.

Animals↗
PubMed1992

Effects of cholecystokinin and bombesin on development of azaserine-induced pancreatic tumours in rats: modulation by the cholecystokinin receptor antagonist lorglumide.

Cholecystokinin and bombesin have been shown to promote pancreatic growth and development of azaserine-induced acidophilic atypical acinar cell nodules in rat pancreas after treatment for 16 weeks. Lorglumide, a specific cholecystokinin receptor antagonist, inhibited the stimulating effect of cholecystokinin, but not of bombesin. The present study was carried out to determine effects of cholecystokinin and bombesin, alone and in combination with lorglumide, on pancreatic growth and carcinogenesis after chronic treatment. The animals were killed 8 months after the start of treatment. Growth of the pancreas and the development of acidophilic atypical acinar cell nodules in exocrine pancreas was enhanced significantly by both cholecystokinin and bombesin, but the number of carcinomas was increased only by bombesin. Lorglumide inhibited the effects of cholecystokinin on both pancreatic growth and on the development of acidophilic nodules. The effects of bombesin on pancreatic growth and development of pancreatic lesions, except for adenomas, were not inhibited by lorglumide.

Animals↗
PubMed1992

Dog lymphocyte cultures facilitate the isolation and growth of virulent canine distemper virus.

Optimal conditions for the isolation and growth of virulent canine distemper virus (CDV) in canine thymic and peripheral blood lymphocyte cultures were determined. Peak virus titers were seen from 3 to 6 days postinoculation of lymphocytes and depended on the multiplicity of infection. Dog lymphocytes were at least as susceptible as canine macrophages to infection with virulent CDV. Virus replication in lymphocytes resulted in higher virus titers than in dog lung macrophages. Peripheral blood lymphocytes (PBL) from CDV-immune dogs were as susceptible to CDV as were PBL from susceptible dogs.

Animals↗
PubMed1992

Diseases and parasites of red foxes, gray foxes, and coyotes from commercial sources selling to fox-chasing enclosures.

Fifty-six red foxes (Vulpes vulpes), 18 gray foxes (Urocyon cinereoargenteus), and 13 coyotes (Canis latrans) obtained by the South Carolina Wildlife and Marine Resources Department during an investigation of suspected illegal wildlife translocation were examined for diseases and parasites. Red foxes and coyotes were confiscated from an animal dealer based in Ohio (USA), and gray foxes were purchased from an animal dealer in Indiana (USA). Emphasis was placed on detection of pathogens representing potential health risks to native wildlife, domestic animals, or humans. All animals were negative for rabies; however, 15 gray foxes were incubating canine distemper at necropsy. Serologic tests disclosed antibodies to canine parvovirus, canine distemper virus, canine adenovirus, canine coronavirus, canine herpesvirus, and canine parainfluenza virus in one or more host species. Twenty-three species of parasites (two protozoans, three trematodes, four cestodes, eleven nematodes, and three arthropods) were found, including species with substantial pathogenic capabilities. Echinococcus multilocularis, a recognized human pathogen not enzootic in the southeastern United States, was found in red foxes. Based on this information, we conclude that the increasingly common practice of wild canid translocation for stocking fox-chasing enclosures poses potential health risks to indigenous wildlife, domestic animals, and humans and, therefore, is biologically hazardous.

Animals↗
PubMed1991

Virulent and attenuated canine distemper virus infects multiple dog brain cell types in vitro.

Canine Distemper Virus (CDV) produces an encephalitis in dogs that varies with viral strain. We have studied the cell tropisms of two virulent strains (CDV-SH and CDV A75-17) and an attenuated strain, Rockborn (CDV-RO), in cultured canine brain cells. Infected cell types were identified by double immunofluorescent labeling of specific cell markers and viral antigens. All viral strains studied produced infection in astrocytes, fibroblasts, and macrophages. Neurons were not infected by CDV A75-17 but were rapidly infected by CDV-SH and CDV-RO. Multipolar oligodendrocytes were very rarely infected by any of the virus strains. In contrast, a morphologically distinct subset of bipolar oligodendrocytes were commonly infected by CDV-SH and CDV-RO. The kinetics of infection in the astrocytes, oligodendrocytes, neurons, and macrophages varied between strains. Both CDV-SH and CDV-RO rapidly infected bipolar oligodendrocytes, astrocytes, neurons, and macrophages by 14 days post infection while infection by CDV A75-17 was delayed until after 28-35 days post infection. The differences in the growth kinetics and cell tropisms for some brain cells, exhibited by the three viral strains examined in this in vitro study, may relate to the different CNS symptoms that these strains produce in vivo.

Animals↗
PubMed1991

Canine distemper virus infection and encephalitis in javelinas (collared peccaries).

Canine distemper virus has been isolated in dog lymphocyte cultures from the brains of three javelinas that became moribund with signs of encephalitis. Canine distemper viral antigen was demonstrated predominantly in neurons and morbillivirus-like structures were seen by electron microscopy in brains of diseased animals. Serological studies suggest that CDV infection may be common in javelinas.

Animals↗
PubMed1991

Correlation between humoral immune responses and presence of virus in the CNS in dogs experimentally infected with canine distemper virus.

The role of the humoral immune response in clearance or prevention of canine distemper viral encephalitis of dogs infected with a virulent strain of canine distemper virus has been evaluated. Dogs that have demyelinating lesions, CDV proteins and infectious virus in their brains demonstrate an impaired humoral immune response. In dogs that recover from infection and contain no demyelinating lesions, viral proteins or infectious virus in the brain, antibodies to the internal proteins of CDV are observed early after infection. Later antibodies to primarily the H protein are detectable in sera of these dogs and the appearance of antibodies against the surface glycoprotein (H) correlates with the absence of lesions, CDV antigen and infectious virus in the brains of these dogs. Very late after infection immunoprecipitating antibody to all CDV antigens diminished rapidly so that at about ten weeks post infection antibodies that precipitate CDV antigens are barely detectable.

Animals↗
PubMed1991

Viral expression in experimental canine distemper demyelinating encephalitis.

We have characterized the relationship between the expression of canine distemper virus (CDV) and demyelinating lesions in the white matter of the cerebellum of experimentally infected dogs. In animals which had demyelinating lesions, CDV proteins (N, P, F and H) were expressed and infectious virus could be recovered from brain tissue. Viral proteins (N, P, F and H) were detected by monoclonal antibodies and immunocytochemistry within demyelinating lesions as well as in scattered glial cells in areas of the white matter which lacked detectable lesions. Many cell types, including astrocytes, neurons, ependymal cells, choroid plexus cells, meningeal cells and perivascular inflammatory cells were labelled for viral antigen. We conclude from our results that the mechanism of demyelination in canine distemper virus-induced encephalitis involves expression of viral gene products at the lesion site.

Animals↗
PubMed1991

Inhibitory effects of micronutrients on pancreatic carcinogenesis in azaserine-treated rats.

A study was made on the effects of long-term dietary administration of beta-carotene, vitamin C, vitamin E and selenium, either alone or in combination, on azaserine-induced pancreatic carcinogenesis in rats. Male Wistar rats were given two i.p. injections of 30 mg azaserine per kg body weight at 19 and 26 days of age. The rats were allocated to eight groups of 40 animals each and were fed an AIN-76 diet rich in saturated fat (20% lard), either as such or after supplementation with beta-carotene, vitamin C, beta-carotene + vitamin C, vitamin E, selenium, vitamin E + selenium, or the combination of all micronutrients investigated. Fifteen months after the last treatment with azaserine the survivors were killed. The pancreata were examined for the number and size of advanced putative preneoplastic lesions and the number of neoplasms as well. Rats maintained on a diet high in either beta-carotene, vitamin C or selenium developed significantly less atypical acinar cells nodules, adenomas and carcinomas as compared to controls. The number of tumour-bearing animals was significantly lower in the groups fed the diet high in beta-carotene or selenium. In animals of the group given a diet high in all micronutrients investigated, both the number and incidence of pancreatic tumours was lower than in all other groups. It was concluded that selenium, beta-carotene and vitamin C, alone as well as in combination, have an inhibitory effect on pancreatic carcinogenesis induced in rats by azaserine.

Animals↗
PubMed1991

Detection of IgM antibodies against canine distemper virus in dog and mink sera employing enzyme-linked immunosorbent assay (ELISA).

An enzyme-linked immunosorbent assay (ELISA) for the detection of IgM antibodies against canine distemper virus (CDV) in canine and mink serum is described. The diagnostic potential of this technique was evaluated by analyzing sera from natural or experimental infections in dog and mink and negative control sera. These results were compared with results obtained in the developed CDV IgG ELISA and in the virus neutralization test. The IgM test, which requires only a single serum specimen, is a useful method for diagnosing current or recent CDV infections in dog and mink.

Animals↗
PubMed1990

Azaserine-induced pancreatic carcinogenesis in rats: promotion by a diet rich in saturated fat and inhibition by a standard laboratory chow.

Dietary fat has been shown to enhance pancreatic carcinogenesis. Uncertainty still exists whether the amount of linoleic acid or the amount of fat is the main determining factor. In the present study the effects of a high lard, a low lard, a linoleic acid supplemented low lard and a laboratory chow diet were investigated on the development of (pre)neoplastic pancreatic lesions in rats treated with azaserine. The rats were killed 15 months after carcinogen treatment and the pancreata were examined for the number and size of putative preneoplastic lesions and for the occurrence of neoplasms. The linoleic acid supplemented low lard group showed a significantly increased number of basophilic foci as compared to the low lard group. Rats maintained on the linoleic acid supplemented diet or the laboratory chow developed significantly less atypical acinar cell nodules larger than 1.0 mm in diameter and adenocarcinomas as compared to the high lard group. Animals maintained on the low lard diet developed significantly less adenocarcinomas than rats on the high lard diet did. Overall, the number of benign and malignant pancreatic tumours was consistently higher in the high lard group and consistently lower in the linoleic acid supplemented low lard group than the number of these types of tumours in the low lard group, with the exception of the number of carcinomas in situ, which was lower in the high lard group. The laboratory chow group showed a significant lower number of atypical acinar cell nodules with a diameter over 1.0 mm and a lower number of adenocarcinomas as compared to both the high lard and the low lard group. It is concluded that a diet high in saturated fat has a promoting and that laboratory chow has an inhibitory effect on pancreatic carcinogenesis in azaserine-treated rats.

Animals↗
PubMed1990

Growth of canine distemper virus in cultured astrocytes: relationship to in vivo persistence and disease.

Canine distemper virus (CDV) causes an encephalomyelitis in dogs which varies with the viral strain. The CDV Cornell A75-17 strain produces a delayed, subacute to chronic, demyelinating CNS disease. In contrast, the Snyder Hill (CDV-SH) strain-associated neurological disease is more acute in onset, is usually non-demyelinating and primarily produces lesions in the gray matter. In these studies we describe the effects of these two virulent and one avirulent CDV strain, Rockborn (CDV-RO), on astrocytes in dissociated canine brain cell cultures. In multiple replicate experiments, astrocytes were infected most rapidly by CDV-RO [100% of astrocytes were infected by 14 days post-inoculation (p.i.)]. This strain caused severe cytopathic effect (CPE) and cytolysis. CDV-SH similarly produced a rapid infection of the astrocytes. In contrast, CDV A75-17 infected less than 25% of the astrocyte population during the first 28 days p.i. (+/- 7 days); after 28 days p.i., a rapid rise in astrocyte infection occurred. Both virulent viruses caused astrocytic syncytial formation but did not cause cytolysis of the astrocyte population as was observed with the attenuated virus. Titers of infectious virus, released into the supernatant fluid, reflected the degree of astrocyte infection. Virus released by the cultures late in CDV A75-17 infection showed enhanced ability to infect newly derived astrocytes; in contrast, brain cell passaged CDV-SH did not show increased growth in these cells. These results show that (1) there is a difference in growth rate, CPE and capacity for adaptation of three different CDV strains in astrocytes in vitro, and (2) some aspects of the disease (such as persistence in white matter) produced by the virulent strains in vivo may be related to the course of astrocyte infection observed in vitro.

Animals↗