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Biomedical subjects

M Worley

Publications and source records attributed to M Worley.

8 recordsLinked to original sources
PubMed1998

Primary Mycobacterium avium complex infections correlate with lowered cellular immune reactivity in Matschie's tree kangaroos (Dendrolagus matschiei).

The National Zoological Park has maintained a breeding colony of Matschie's tree kangaroos (Dendrolagus matschiei) since 1975 with a documented history and continued prevalence of Mycobacterium avium complex (MAC) infections. No evidence of immunosuppressive retrovirus infections or loss of heterozygosity that may have led to an immune dysfunction in these animals was found. Isolates of MAC organisms from affected tree kangaroos and from their environment had no common restriction fragment DNA types. Cellular immune reactivity in apparently healthy tree kangaroos was 3- to 6-fold lower than in humans and other marsupial and eutherian mammals, as determined by lymphocyte proliferative assays. Thus, while MAC infections are typically opportunistic in humans and other mammals, tree kangaroos commonly develop primary progressive disease with MAC from random sources. Comparative information derived from this study should benefit both the endangered tree kangaroo and humans with immunosuppressive disorders that lead to mycobacterial infections.

Animals↗
PubMed1994

Human microvascular endothelial cell toxicity caused by Brazilian purpuric fever-associated strains of Haemophilus influenzae biogroup aegyptius.

An in vitro cytotoxicity model that uses an immortalized human microvascular endothelial cell line (HMEC-1) differentiates Brazilian purpuric fever (BPF)-associated Haemophilus influenzae biogroup aegyptius (HAE) strains from non-BPF-associated HAE strains. Toxic strains produced a characteristic HMEC-1 phenotype at an MOI of < 1 bacterium/1000 tissue culture cells (TCC). Nontoxic strains required MOIs of > 1000 bacteria/TCC to produce an observable effect. The cytotoxic phenotype was characterized by the presence of large clumps of HMEC-1 cells, which detached from the monolayer within 48 h of inoculation by HAE cells. The cytotoxic phenotype was observed with 100% of BPF-associated HAE (40/40) and 14% of non-BPF-associated HAE (8/57; P < .001). The ability to study a BPF-associated phenotype in vitro using human microvascular cells should enhance our knowledge of BPF pathogenesis.

Cell Line↗
PubMed1992

Comparative study of antipneumocystis agents in rats by using a Pneumocystis carinii-specific DNA probe to quantitate infection.

A repetitive genomic DNA clone (B12-2) that specifically hybridizes to Pneumocystis carinii DNA has been identified. No cross-hybridization to genomic DNA prepared from bacteria, other fungi, protozoa, or mammals was observed. Clone B12-2 is multiply represented in the P. carinii genome. By direct hybridization to DNA prepared from the lungs of immunosuppressed rats, the probe can detect the equivalent of fewer than 1,000 P. carinii organisms. A hybridization assay employing clone B12-2 has been developed to quantitate organism load in the rat model for P. carinii. Application of the assay to track the accumulation of organisms during the immunosuppression regimen as well as to monitor the efficacy of two drug therapies used clinically for the treatment of P. carinii pneumonia is described here. The clone B12-2 hybridization assay for the determination of P. carinii organism load possesses several advantageous features and thus should serve to complement conventional staining and immunohistochemical methods.

Animals↗
PubMed1991

In vitro mitogen responses and lymphocyte subpopulations in cheetahs.

Lack of genetic variability and apparent susceptibility of cheetahs (Acinonyx jubatus jubatus) to coronavirus infection has lead to speculation that this species may have immune system deficits. To establish a foundation for evaluation of the immune function, cheetah peripheral blood mononuclear cells (PBM) were stimulated by a panel of six mitogens, and responses compared with those of domestic cat PBM. Individual responses in both species were variable, but evenly distributed throughout the range of stimulation for each mitogen. Proliferation by PBM from domestic cats occurred within the same range as that of the cheetahs. However, a significantly lower response to peanut agglutinin (PNA) was observed with domestic cat PBM. Although responses varied between animals, certain individual cheetahs were consistent low responders. The decreased values could not be explained by lack of IL-2 responsiveness since exogenous IL-2 significantly enhanced mitogen-stimulated proliferation in 11 of 12 cheetahs tested. The phenotypic distribution of domestic cat and cheetah lymphocyte subpopulations was similar as assessed by immunofluorescence staining for surface immunoglobulin (sIg) and cytotoxic T (Tc) cells (using a specific monoclonal antibody, FT2). Values for B cells (31.2% sIg+) and Tc (28.7% FT2+) were slightly higher in domestic cats as compared with cheetah PBM (13.3% sIg+; 19.0% FT2+). Even though no species-specific deficits were detected, a significant negative correlation between PHA-stimulated proliferation and percent FT2+ (Tc) cheetah cells was observed. This indicates that proliferation can be used indirectly to assess relative numbers of functional T helper cells in cheetahs. Our studies suggest that these aspects of the cheetah's immune system are comparable with the domestic cat, and establish a basis for in vitro assays evaluating antigen-specific responses.

Acinonyx↗
PubMed1989

A new transmissible viral hepatitis of marmosets and tamarins.

Callitrichid hepatitis (CH) is a newly recognized, acute, fatal, epizootic disease of New World primates in the family Callitrichidae. Since 1980, 12 outbreaks of CH have occurred in US zoos, involving several callitrichid species including the endangered golden lion tamarin (Leontopithecus rosalia). CH was experimentally transmitted to common marmosets via a bacteria-free filtrate of liver from a naturally infected tamarin. All three inoculated marmosets developed an acute fatal disease with the characteristic clinical and histopathologic findings of CH. Human hepatotropic viruses that can infect the livers of callitrichids were not detected serologically in any of the experimentally infected marmosets. Enveloped viruslike particles 85-105 nm in diameter were observed in the rough endoplasmic reticulum and Golgi complex of hepatocytes from both naturally infected and experimentally inoculated animals. An immunoblot assay was developed using sera from tamarins exposed to natural outbreaks of CH and liver extracts from experimentally infected or control marmosets. A new CH-specific antigen was detected in the livers of naturally infected and experimentally inoculated marmosets but not controls. These results suggest that the etiologic agent of callitrichid hepatitis is a new primate hepatitis virus.

Animals↗
PubMed1977

Chemoimmunotherapy for canine lymphosarcoma.

A total of 157 dogs with lymphosarcoma were available for study; 67 were treated. All of the treated dogs were given 4 drug combinations and 20 of them also were given autogenous vaccine. Sixty (90%) of the dogs treated with multiple drugs improved clinically. Of the dogs with clinical improvement, 48 (80%) had either complete or partial remission; of these, 32 (67%) had complete remission. Clinical staging proved useful in increasing the accuracy of prognosis, whereby dogs in less advanced stages of disease responded better to therapy, with a higher percentage of complete clinical remissions and longer survival. The mean survival time of the 47 dogs treated with drugs alone was 138 days, which compared with a mean survival time of 30 days for 34 nontreated dogs. Dogs subjected to chemotherapy and immunotherapy had a mean survival time of 341 days. Dogs in complete remission at time of vaccination survived significantly (P less than 0.01) longer than did dogs treated with drugs and vaccinated while not incomplete remission.

Animals↗
PubMedDate not supplied

The hHFE gene of browsing and grazing rhinoceroses: a possible site of adaptation to a low-iron diet.

When rhinoceros species that are browsers in the wild are fed in captivity they become iron overloaded. Presumably, their iron-absorptive mechanisms have evolved to become highly efficient. In humans, mutations of the HFE gene cause increased iron absorption. To determine whether the HFE gene of rhinoceroses has undergone mutation as an adaptive mechanism to improve iron absorption from iron-poor diets, we have sequenced the entire coding region of the HFE genes of four species of rhinoceros. Two of these were browsing species and two were grazing species. Although the HFE gene has been well preserved across species, numerous nucleotide differences were found between rhinoceros and human or mouse, some of which changed deduced amino acids. Of these mutations, only one found in the black rhinoceros appears to be a viable candidate mutation that might adversely affect HFE function. This mutation, S88T, is in a highly conserved region that is involved in the interaction between transferrin receptor and HFE.

Adaptation, Physiological↗