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Biomedical subjects

D A Harbour

Publications and source records attributed to D A Harbour.

At least 73 records · Page 4Linked to original sources
PubMed1990

Persistent excretion of rotavirus by pregnant cows.

In a study of the epizootiology and prevalence of enteropathogens which may be involved in neonatal calf diarrhoea, 10 in-calf cows from a herd with a history of rotavirus-induced calf diarrhoea were monitored over a period of six to seven months. All the cows excreted rotavirus intermittently without showing any clinical signs, and 21.8 per cent of faecal samples contained rotavirus. Reoviruses were isolated from 87 per cent of the samples from the cows, and from all the 10 calves born to them. However, rotavirus was detected in only one calf, and diarrhoea developed only in this calf even though the calves were housed in communal pens. Campylobacter jejuni was isolated from six of the 10 dams and from five of the 10 calves, not including the calf with diarrhoea. Other potential enteropathogens such as cryptosporidium, salmonella, Clostridium difficile, coronavirus and other viruses were not found, but two cows and two calves shed enterotoxigenic Escherichia coli.

Animals↗
PubMed1990

Concurrent cryptosporidium and coronavirus infections in an Arabian foal with combined immunodeficiency syndrome.

Combined immunodeficiency syndrome is an inherited disorder of the Arabian breed of horses. Affected foals usually die of infectious disease within the first few months of life, and the respiratory tract is the commonest site of infection. This report describes the clinical and pathological features of a case which showed signs of alimentary and respiratory infections. Intestinal infection by coronavirus (not previously recorded in cases of the syndrome) and cryptosporidia was identified. Histopathological evidence also suggested the presence of an adenovirus infection.

Animals↗
PubMed1990

Immunogenicity of recombinant feline infectious peritonitis virus spike protein in mice and kittens.

The gene encoding the fusogenic spike protein of the coronavirus causing feline infectious peritonitis (FIPV) was recombined into the genome of vaccinia virus, strain WR. The recombinant induced spike protein specific, in vitro neutralizing antibodies in mice. When kittens were immunized with the recombinant, low titers of neutralizing antibodies were obtained. After challenge with FIPV, these animals succumbed earlier than the vWR-immunized control group ("early death syndrome").

Animals↗
PubMed1990

Early death after feline infectious peritonitis virus challenge due to recombinant vaccinia virus immunization.

The gene encoding the fusogenic spike protein of the coronavirus causing feline infectious peritonitis was recombined into the genome of vaccinia virus. The recombinant induced spike-protein-specific, in vitro neutralizing antibodies in mice. When kittens were immunized with the recombinant, low titers of neutralizing antibodies were obtained. After challenge with feline infectious peritonitis virus, these animals succumbed earlier than did the control group immunized with wild-type vaccinia virus (early death syndrome).

Animals↗
PubMed1990

Restriction endonuclease analysis of DNA from isolates of feline herpesvirus type 1.

DNAs prepared from whole feline embryo cells infected with a standard laboratory strain of FHV-1, B927, and 50 wild type isolates were digested with a variety of restriction endonucleases. The resulting fragments were separated on agarose gels and Southern blotting performed. To visualize the fragments, B927 DNA was purified by pulsed field gel electrophoresis, labelled with alpha 32P and used as a hybridization probe. With most enzymes a large number of the isolates displayed altered mobilities of several fragments with some fuzzy band heterogeneity. A few isolates gave distinct cleavage patterns, in particular using the enzymes Bam HI, Cla I and Sac I. It is suggested that different strains of FHV-1 exist but that changes in the viral genome occur only sporadically and thus may not be readily detected.

Animals↗
PubMed1989

Clinical and laboratory findings in cats infected with feline immunodeficiency virus.

Thirty-two cats referred to the Feline Studies Centre between June 1987 and October 1988, and 14 in-contact cats, were found to be infected with feline immunodeficiency virus. Most of the 46 cats were non-pedigree and free ranging; 27 were male (19 neutered) and 19 were female (18 neutered). Their ages ranged from one to 17 years and the average age was 5.8 years. The most common clinical signs were lethargy, inappetence, weight loss, pyrexia and lymphadenopathy; most cases had multiple abnormalities. Other common signs were gingivitis, diarrhoea, rhinitis and ocular discharge. Eight cats had neoplasia. The commonest haematological abnormalities were anaemia, neutropenia, lymphopenia and monocytosis. Eight cats had lymphocytosis; seven of these were in a single house-hold. Several cats had high serum globulin levels and half of those tested had high IgG levels. Seven cats had no detectable antibody to feline immunodeficiency virus even though the virus was cultured from the peripheral blood lymphocytes. During follow-up for up to 60 weeks one cat died and 23 were destroyed on humane grounds.

Age Factors↗
PubMed1988

Virus shedding and immune responses in cats inoculated with cell culture-adapted feline infectious peritonitis virus.

Eight specific pathogen-free cats were inoculated orally or parenterally with a cell culture-adapted strain of feline infectious peritonitis virus (FIPV). Faeces and oropharyngeal swabs were monitored daily for infectious virus by inoculation of feline embryo lung cells. Virus was recovered from both sites for approximately 2 weeks after inoculation, before clinical signs of disease developed. Peripheral blood lymphocytes collected from these cats were tested in an in-vitro blastogenic assay using concanavalin A (con A) and FIPV antigen. All cats showed a profound suppression of the response to con A which only recovered to pre-inoculation levels in 2 cats, one of which survived. These 2 cats also responded to FIPV antigen on the 21st day after infection, the greater response being in the survivor. The other cats, surviving 16-18 days, developed no response to FIPV antigen. Antibody titres, measured by immunofluorescence and by virus neutralization, rose rapidly to very high levels in all cats, regardless of the route of inoculation.

Animals↗
PubMed1988

The sites of early viral replication in feline infectious peritonitis.

The sites of early replication of feline infectious peritonitis virus were studied following oral inoculation of specific-pathogen-free (SPF) cats with virus grown in cell cultures. Viral antigen was first detected by immunofluorescence in the tonsils and small intestine within 24 h of inoculation, and was later found in caecum, colon, mesenteric lymph nodes and liver. However, histological changes in the gut did not appear until relatively late in the course of infection. Virus was recovered from the oropharynx and the faeces from as early as the second or third day after inoculation, and shedding continued until euthanasia.

Animals↗
PubMed1987

Restriction endonuclease analysis of herpes simplex virus from recrudescent lesions, from latent infection and during passage in the skin and nervous system of mice.

The stability of the restriction endonuclease profile of herpes simplex virus type 1 strain SC16 in mice was studied. Virus isolated from skin during acute infection was compared with that from latently infected ganglia and with that from recrudescent lesions induced by trauma. In another experiment virus serially passaged only in skin was compared with virus that had also replicated in the nervous system. The loss or gain of specific restriction sites was not observed but in some cases the mobility of certain fragments decreased.

Animals↗
PubMed1986

Responses of cats to nasal vaccination with a live, modified feline herpesvirus type 1.

Intranasal vaccination with a cold-adapted strain of feline herpesvirus type 1 (FHV-1) two days before challenge gave partial protection, and four days before challenge gave complete protection, against feline viral rhinotracheitis. Protection at this time appeared to be specific since vaccination with FHV-1 did not affect the disease caused by the unrelated feline calicivirus. The time course of onset of protection also confirmed that the protective mechanism was likely to be specific. However, six days after vaccination only low levels of FHV-specific IgA and IgM antibody and of interferon were found in serum and nasal washings. In lymphocyte transformation assays neither peripheral blood lymphocytes nor tonsil lymphocytes gave a significant proliferative response in the presence of FHV antigen. Pathogenesis experiments demonstrated that the tonsil and nasal turbinates were the most important sites of virulent FHV-1 replication. Vaccination significantly reduced levels of infectious virus found in both sites. The results provide evidence that no one mechanism is responsible for protection following vaccination but local specific responses are more likely to be involved.

Administration, Intranasal↗