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At least 343 records · Page 19Linked to original sources
PubMed1999

Evidence for immunosuppression associated with Jembrana disease virus infection of cattle.

Jembrana disease virus (JDV) is a newly recognised bovine lentivirus causing an acute disease syndrome in Bali cattle (Bos javanicus) in Indonesia. We evaluated the effect of JDV infection on the antibody response to chicken ovalbumin (cOVA) and Brucella abortus Strain 19 in Bali cattle. In infected cattle the IgG and IgM response to cOVA was suppressed and delayed and the IgG response to B. abortus Strain 19 was delayed. The results indicate that the humoral immune response is suppressed and delayed in JDV infected cattle.

Animals↗
PubMed1999

[Borna disease in cattle (consensus report)].

Short survey on definition, occurrence, cause, importance, pathogenesis, clinical findings, course, postmortal lesions, treatment, prevention and eradication of Borna disease in cattle.

Animals↗
PubMed1990

The diagnosis of bovine virus diarrhoea-mucosal disease in cattle.

Laboratory diagnostic procedures for bovine virus diarrhoea and mucosal disease are reviewed. For serology, emphasis is placed on the virus neutralisation test and enzyme immunoassays. The techniques and the pitfalls which may be encountered in culture procedures for isolation of the virus are described, with special reference to the use of immunofluorescence and immunoperoxidase methods for the detection of non-cytopathogenic virus strains. Viral antigen may also be detected directly in clinical or pathological samples. Monoclonal antibodies are expected to play an increasing role in diagnostic tests, and the application of gene probes for virus detection is anticipated in future years. In the interpretation of diagnostic laboratory test results, the importance is stressed of reviewing them in the context of the herd disease and breeding history, and relating them to current understanding of the pathogenesis and epidemiology of the disease.

Animals↗
PubMed1995

Experimental mucosal disease in cattle: changes of lymphocyte subpopulations in Peyer's patches and in lymphoid nodules of large intestine.

Changes in the number and distribution of lymphocyte subtypes were investigated in Peyer's patches in the jejunum and ileum, and mucosa-associated lymphoid nodules in the proximal colon and rectum of cattle with end-stage mucosal disease. Mucosal disease had been induced experimentally in seven of 13 animals by inoculation with cytopathogenic bovine viral diarrhea virus (cp BVD-virus). For comparison, six clinically healthy, persistently viremic cattle were used. IgM+, IgA+, BoCD4+, BoCD8+ and gamma delta TCR+lymphocytes, and the cp BVD-viral antigen were visualized in tissue sections by immunohistochemistry. In cattle with mucosal disease, the size of lymphoid follicles was significantly decreased in all localizations resulting in decreased numbers of B-lymphocytes per average follicular area. In most animals domes were missing and epithelium was invaginated into the lymphoid follicles. Numbers of BoCD4+ and BoCD8 + T-lymphocytes were increased per mm2 of lymphoid follicle. Conversion of these counts into number of cells per average follicular area revealed, however, that the absolute number of BoCD4 + T-lymphocytes had decreased within lymphoid follicles and there was no distinct change of BoCD8 + T-lymphocytes in comparison to the controls. Interfollicular areas were less densely populated due to reduced numbers of BoCD4 + and BoCD8 + T-lymphocytes. cp BVD-viral antigen was detected predominantly in epithelial cells and in cells with dendritic morphology within lymphoid follicles. This may indicate that the severe depletion of B-lymphocytes in the lymphoid follicles is due to alterations of the microenvironment. The decrease of BoCD4 + and BoCD8 + T-lymphocytes does not support the hypothesis of T-cell-mediated tissue damage. Destruction of mucosa-associated lymphoid nodules does not only lead to local disruption of the gastrointestinal barrier, but will reduce the seeding of effector cells to the mucosa and therefore impair the defense mechanisms of the gastrointestinal barrier.

Animals↗
PubMed1999

[Foot-and-mouth disease of cattle is not a zoonosis].

In 1997 there was an outbreak of foot-and-mouth disease (FMD) among cattle in Turkey. People visiting that country were warned against importing animal products into the Netherlands. This had nothing to do with hazards to human health, as FMD virus is not a zoonotic virus, but with the risk of spread of the disease to livestock in the Netherlands, notably to cattle and pigs. A disease with similar clinical symptoms in pigs is swine vesicular disease (SVD), which is not a zoonosis either. FMD virus is an aphtovirus, SVD virus is an enterovirus. Hand-foot-and-mouth disease in humans is caused by other enteroviruses, i.e. Coxsackie virus and enterovirus 71.

Animals↗
PubMed1990

Spontaneous mutations leading to antigenic variations in the glycoproteins of vesicular stomatitis virus field isolates.

Strains of vesicular stomatitis virus, New Jersey serotype (VSV-NJ), isolated from diseased cattle or swine were examined by genomic RNA sequencing for genetic diversity potentially leading to antigenic variations in their type-specific glycoproteins as determined by reactivity with epitope-specific monoclonal antibodies (MAbs). Seven field isolates recovered in Colorado, New Mexico, Georgia, and Mexico during the widespread 1982-1985 epizootic in the western United States resembled the prototypic 1952 Hazelhurst subtype by partial sequence homology, but amino acid reversions to the 1949 Ogden subtype occurred frequently. When studies were performed with MAbs directed to the Ogden subtype glycoprotein, relatively limited antigenic variation, and only in neutralization epitope VIII, was noted among two of five epizootic isolates from Colorado and New Mexico. However, amino acid differences in the glycoprotein of a 1983 isolate from an enzootic region of Georgia resulted in major antigenic deficiencies in epitopes V, VI, and VII as determined by Western blotting and neutralization of infectivity with epitope-specific MAbs. Quite a few genetic but no antigenic differences were noted in an enzootic 1984 isolate from Mexico, a potential origin of the United States epizootic. Marked or complete loss of epitopes VII, VI, VIII, and V can be traced to spontaneous mutations leading to amino acid substitutions at glycoprotein positions 199, 263, 275, and 317, respectively, in the enzootic Georgia isolate 07/83-GA-P and the epizootic New Mexico isolate 06/85-NM-B. By comparison, closely adjacent amino acid substitutions at glycoprotein positions 210, 268, 277, and 364 occurred in epitope-deficient mutants selected for resistance to neutralization by MAbs specific for epitopes VII, VI, VIII, and V, respectively. Two neutralization epitopes designated X and XI were found to be unique for the G protein of the 1952 Hazelhurst isolate..../52-GA-P. The epitope X-specific MAb H21, in particular, failed to neutralize the infectivity not only of the Ogden subtype..../49-UT-B but also was ineffective against all the 1982-1985 field isolates. The classical 1952 Hazelhurst strain of VSV-NJ is genetically and antigenically quite different from those viruses isolated during the 1982-1985 epizootic.

Amino Acid Sequence↗
PubMed2000

Serotyping of Mannheimia (Pasteurella) haemolytica isolates from the upper Midwest United States.

Mannheimia (Pasteurella) haemolytica biotype A serotype1 (A1) is the primary bacterial agent responsible for the clinical signs and pathophysiologic events in bovine pneumonic pasteurellosis. The goal of this study was to determine the prevalence of other serotypes of M. haemolytica biotype A organisms obtained from the upper Midwest diagnostic laboratories. A total of 147 M. haemolytica isolates were collected from Minnesota, South Dakota, and Michigan. Isolates were tested against M. haemolytica antisera obtained from the National Animal Disease Center, Ames, Iowa. Results indicated that M. haemolytica serotype 1 represented approximately 60%, serotype 6 represented 26%, and serotype 2 represented 7% of the total examined isolates. In addition, 7% of the isolates were serotype 9, 11, or untypable. This finding suggests that M. haemolytica serotypes other than serotype 1 can be isolated from the lung lesions of diseased cattle and seem to be capable of causing the pathologic changes observed in the lung with pneumonic pasteurellosis.

Animals↗
PubMed1990

An outbreak of bovine ephemeral fever in Nagasaki Prefecture in 1988.

In October, 1988, bovine ephemeral fever (BEF) occurred in Nagasaki Prefecture and throughout Kyushu island, with the exception Miyazaki Prefecture. The first outbreak occurred in Hirado-shi on October 17. The total number of diseased cattle was 24 in 24 farms in Nagasaki Prefecture. The clinical findings were mainly sudden fever, anorexia, and instability in standing. The serum neutralizing antibodies against BEF virus (BEFV) rose in all infected cattle. Twelve strains of the virus were isolated in HmLu-1 cell cultures made directly from the heparinized blood of 17 infected cattle. The buffy coat was mainly collected from the samples and washed three times with phosphate buffered saline. These isolates were all neutralized by an antiserum against BEFV (Yamaguchi strain). With the aid of an electron microscope, a representative of isolates named Hirado-9 with a length of 150 nm was seen in the sample of infected HmLu-1 cell cultures. Both Hirado-9 and Yamaguchi strains reacted with antisera. The outbreak of BEF in 1988 was the first since 1971 in Nagasaki Prefecture. The result proved that BEFV can be easily isolated in HmLu-1 cell culture from the washed blood cells of infected cattle.

Animals↗
PubMed2004

Escherichia coli O157:H7 in a cohort of weaned, preconditioned range beef calves.

Escherichia coli O157:H7 (EC O157) is an important cause of foodborne disease. Cattle are reservoirs for the bacteria and are implicated in transmission to humans. Prevalence data in prefeedlot calves are limited. With the use of sensitive methods, a cohort of weaned beef calves (n = 408) was sampled before and after preconditioning to estimate fecal point prevalence and describe changes in EC O157 fecal shedding. EC O157 isolates were confirmed and characterized by PCR and pulsed-field gel electrophoresis. Calves from 29 cow-calf farms were commingled at three preconditioning sites and placed on a transition ration containing oxytetracycline (200 g/ton) for 45 days. Initial animal-level fecal point prevalence was 2.5% (95% confidence interval, 1 to 5) with a herd-level prevalence of 17.2% (95% confidence interval, 6 to 36). Point prevalence following the preconditioning feeding period was 0%. An unexpected finding in our study was EC O157 isolates that were Shiga toxin-deficient. Pulsed-field gel electrophoresis subtypes of EC O157 were unique in epidemiologically unlinked herds, except one herd that had two unique subtypes. We expected, but observed, neither increased fecal shedding in the cohort nor horizontal transmission of unique EC O157 subtypes. The absence of fecal shedding following the 45-day feeding period might be attributable to seasonal influences, inhibitory concentrations of oxytetracycline in the transition ration, or transient colonization that ended before sampling. EC O157 is apparently widely dispersed at low prevalence in U.S. prefeedlot, weaned calves.

Animals↗
PubMed1985

[Laboratory diagnosis of respiratory diseases of cattle].

The authors describe the procedure of laboratory diagnosis for bovine respiratory diseases: direct diagnosis by isolation and for identification of bacteria or viruses and indirect diagnosis by serological methods. They specify the restraints and limits of this diagnosis and the significance results which are obtained and connected with knowledge of anamnestic information.

Animals↗