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At least 1,099 records · Page 61Linked to original sources
PubMed2006

Full genome sequence and some biological properties of reticuloendotheliosis virus strain APC-566 isolated from endangered Attwater's prairie chickens.

Reticuloendotheliosis virus (REV) causes runting, high mortality, immunosuppression, and chronic neoplasia associated with T and/or B cell lymphomas in a variety of domestic and wild birds, including Attwater's prairie chickens (APC) (Tympanuchus cupido attwateri). The complete proviral sequence of a recent REV isolate from APC (REV APC-566) was determined. This virus was isolated from an APC maintained in captivity in a reproduction program intended to avoid its extinction. REV APC-566 was determined to be oncogenic in Japanese quail (Coturnix coturnix japonica), chickens (Gallus gallus) and turkeys (Meleagris gallopavo). Immune responses against bacteria and viruses were significantly reduced in turkeys infected with REV APC-566. The proviral genome is 8286 nucleotides in length and exhibits a genetic organization characteristic of replication-competent gammaretroviruses. The REV APC-566 provirus contains two identical long terminal repeats (LTR) and a complete set of genes including gag, gag-pol and env. As previously reported, alignments with other REV sequences showed high similarity with sequences found in the gag and pol genes from other REVs. The REV APC-566 env gene showed high nucleotide sequence homology with REV sequences inserted in fowl poxvirus (99.8%), and with spleen necrosis virus (SNV) (95.1%). Sequences coding for a previously reported immunosuppressive peptide contained in the transmembrane region of the env gene are well conserved among all REV sequences analyzed. The LTR was the most divergent region, exhibiting various deletions and insertions. REV APC-566 has a unique insertion of 23 bp in U3 and shares deletions of 19 and 5 bp with chicken syncytial virus and REV inserts in fowlpox virus.

Amino Acid Sequence↗
PubMed1988

The possible involvement of immunosuppression caused by a lentivirus in the aetiology of jaagsiekte and pasteurellosis in sheep.

A South African isolate of ovine lentivirus was shown to cause a mild immunosuppression in sheep, reflected by a reduced delayed hypersensitivity reaction. This effect, measured in terms of skin swelling after intradermal inoculation with tuberculin, showed a positive linear relationship with the latency period before the appearance of jaagsiekte symptoms in animals co-infected with JSRV, as well as with the activity of monocytes. In a parallel study, increased susceptibility of lentivirus-infected sheep to infection with Pasteurella haemolytica was demonstrated. It is concluded that the lentivirus may play an enhancing role in both viral and bacterial infections of sheep by compromising the host's cellular immune response.

Animals↗
PubMed1998

Sepsis puerperalis caused by a genotypically proven cat-derived Pasteurella multocida strain.

We report a disseminated intrauterine Pasteurella multocida infection in a puerperal woman who could not remember any traumatic exposure to her cat. An oral swab taken from the cat, just 2 days after the patient's admission, grew Pasteurella multocida, with an PCR-fingerprinting pattern identical to the patient's isolate. Hand-washing after every contact with cats and dogs and if feasible separation of in-house pets from mother and infant should be applied to prevent this uncommon but serious occurrence of post-partum infections. To our knowledge this is the first case of Pasteurella multocida 'child-bed fever', with a genotypically identical strain isolated from the in-house cat.

Adult↗
PubMed1950

A quantitative antibody response of man to infection or vaccination with Pasteurella tularensis.

A polysaccharide antigen, prepared from a virulent strain of Past. tularensis by phenol extraction, was employed in assaying the antibody in sera from persons recovered from infection with, or vaccinated with Past. tularensis, using the serological technique of quantitative precipitation. Antibody levels in sera of individuals vaccinated with or recovered from infection with Past. tularensis were found to resemble those observed in similar studies by other investigators, such as the antibody response to pneumococcal antigen, meningococcal polysaccharide, and blood group substances. It is suggested that the value of actively or of passively acquired antibody to an individual exposed to tularemia is dependent not on the amount of antibody alone, but also on the amount of antigen with which the antibody is capable of combining.

Antibody Formation↗
PubMed1973

Synergistic effect in viral-bacterial infection: combined infection of the murine respiratory tract with Sendai virus and Pasteurella pneumotropica.

Synergism was demonstrated between Sendai virus and Pasteurella pneumotropica in the respiratory tract of mice showing no evidence of previous infection with either agent. Mice aerosol challenged with P. pneumotropica invariably eliminated the viable organism from their lungs within 72 h. In contrast, intrapulmonary killing was delayed in animals previously infected with Sendai virus. Maximum synergism was observed when virus infection preceded bacterial challenge by 6 days. At this time, a mortality rate of 37% was observed as compared with 0, 10, 20, and 10%, respectively, in those animals in which the virus infection preceded bacterial challenge by 1, 3, 9, and 12 days. Previous immunization with Sendai virus completely prevented virus infection and thus the synergistic effect. Synergism with endogenous flora was also noted. Six days after virus infection an endogenous Pasteurella sp. began to proliferate in the bronchopulmonary tissues. Up to 10(4) colony-forming units per lung were recovered but no animals died of the endogenous Pasteurella infection.

Aerosols↗