Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CATTLE DISEASES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

Electron microscopic studies of bovine viral diarrhea virus in tissues of diseased calves and in cell cultures.

Pathomorphological studies by electron microscopy (EM) were carried out on the intestines and lymphoid tissues, the buffy coat cells and cultured lymphocytes from calves suffering from mucosal disease (MD). This led to the detection of particles, 45--55 nm in diameter, within characteristic vesicular structures. As these findings coincided with the isolation of bovine viral diarrhea virus (BVDV) from the same tissues and demonstration of BVDV-antigen by immunocytochemical techniques in corresponding samples, the particles were tentatively identified as the BVDV. A detailed study of in vitro infected bovine cell cultures corroborated this supposition and contributed to a conjectural evaluation of the viral morphogenesis. It revealed a difference from the morphogenesis of most other togaviruses, as the presumed virions were assembled within smooth-membraned vesicles, formed during the infection. Thus, in the material examined, a budding process was not involved in the development of BVDV.

Animals↗

Clinical observations on bovine parasitic otitis in Tanzania.

Between January 1982 and December 1989 more than 5,000 clinical cases of bovine parasitic otitis were examined. Clinical signs were mild in early cases and were characterised by dullness, anorexia and occasional head shaking, but were severe in long standing cases where the major presenting clinical signs were dark brown aural discharges which soiled the hair below and in front of the ear, emaciation, central nervous signs, recumbency and death.

Animals↗

A 45-nucleotide insertion in the NS2 gene is responsible for the cytopathogenicity of a bovine viral diarrhoea virus strain.

Cytopathogenicity (cp) markers have recently been investigated in the genomes of field isolates of bovine viral diarrhoea virus (BVDV). Most of the isolates originated from mucosal disease (MD) cases observed after vaccination with a live attenuated vaccine, termed here BVDV-X. The NS2-3 genes of these isolates and of the vaccine proved to be identical, including a 45-nucleotide (nt) viral insertion at nt position 4355. The insertion originated from the NS4B/5A junction region of the BVDV genome. Interestingly, in BVDV strain CP7 a 27-nt insertion originating from the NS2 is located exactly at the same position. Complete genome analysis of BVDV-X did not reveal further potential cp markers. Furthermore, expression studies indicated that the insertion promotes NS2-3 cleavage. In order to examine the possible role of the 45-nt insertion in viral cytopathogenicity in details, a full-length infectious cDNA clone of BVDV-X was generated, and bovine turbinate (BT) cells were transfected with RNA transcribed from the clone. The recovered virus, termed BVDV-XR, showed slight retardation in growth in comparison with the original BVDV-X, and induced cytopathogenic effect (CPE). Since the natural non-cytopathogenic (ncp) counterpart of the vaccine virus was not available, an insertion-negative mutant cDNA clone was generated from BVDV-XR by PCR-directed mutagenesis. The recovered virus, termed BVDV-XR-INS-, showed the same growth characteristics as its cp counterpart BVDV-XR, but caused no CPE. These findings provide a direct proof that the 45-nt insertion at position 4355 has a basic role in the cytopathogenic character of this BVDV strain.

Animals↗

Occurrence of 14 cases of bovine spongiform encephalopathy in a closed dairy herd.

Fourteen cases of bovine spongiform encephalopathy (BSE) were diagnosed on the basis of clinical examination in a closed herd of British Friesian cows during a 9-month period from October 1987 until June 1988. The diagnosis was confirmed on histopathological examination of brain tissue from five of the six samples submitted. The main presenting clinical signs were of altered behaviour: apprehension, anxiety and hyperaesthesia. One cow was euthanized after a short period of recumbency; the remaining 13 cows were slaughtered on humane or economic grounds. No protein of animal origin had been fed to either heifers or cows in this herd during the past 5 years and there had been no direct contact with sheep. The epidemiology of BSE in this report suggests that, if the postulate of Morgan (1988) is correct, infection is ingested within the first 6 months of life and there then follows a 4-5-year period before clinical signs appear.

Animals↗

Propagation of bovine rotavirus by young dogs.

Ten young dogs were experimentally infected twice with different isolates of bovine rotavirus and 2 uninfected dogs were kept in contact with them. None of the animals developed diarrhoea, but all of them excreted rotavirus in their faeces over a period of up to 10 days after each inoculation, as shown by counterimmunoelectro-osmophoresis and virus isolation. Dogs may thus play a role in the epizootiology of rotavirus diarrhoea in calves. Seroconversion occurred in 6 of the 10 infected dogs but in neither of the 2 contact controls.

Animals↗

Neutralization kinetics of bovine viral diarrhea virus by hyperimmune serum: one or multi-hit mechanism.

The kinetics of bovine viral diarrhea (BVD) virus neutralization (VN) by hyperimmune serum followed first order kinetics at low dilutions (1:8 and 1:16) of hyperimmune bovine serum. A lag phase in the VN curve occurred when the serum was further diluted. Addition of rabbit anti-bovine IgG, but not anti-IgM, significantly increased the degree of VN after BVD virus was reacted with further diluted (1:256 dilution) anti-BVD bovine hyperimmune serum. Incubation of virus-hyperimmune serum (1:64 dilution) at 4 degrees C for 0 to 60 min, followed by incubation at 37 degrees C indicated VN occurred as a two-stage process: a binding (temperature-independent) phase that was followed by a triggering (temperature-dependent) phase. The data favor the thesis that neutralization of BVD virus occurs by a multi-hit mechanism and requires combination of at least two molecules of antibody with each virus.

Animals↗