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Biomedical subjects

J M Rutter

Publications and source records attributed to J M Rutter.

At least 37 records · Page 2Linked to original sources
PubMed1989

Interactions between Bordetella bronchiseptica and toxigenic Pasteurella multocida in atrophic rhinitis of pigs.

Three strains of Bordetella bronchiseptica were compared for their ability to assist colonisation of the nasal cavity of gnotobiotic pigs by toxigenic Pasteurella multocida. Toxigenic P multocida (counted in nasal washings) colonised the cavity in large numbers in pigs previously infected with a cytotoxic phase I strain of B bronchiseptica (B58), whereas it colonised only in small numbers in those previously infected with B65, a phenotypic phase III variant of B58. Toxigenic P multocida colonised pigs infected with a non-cytotoxic phase I strain of B bronchiseptica (PV6) in fewer numbers than were seen in pigs infected with the cytotoxic phase I strain but in greater numbers than in pigs infected with the phase III strain. The turbinates of pigs infected with the cytotoxic phase I strain of B bronchiseptica and toxigenic P multocida were most severely affected and those in pigs infected with the non-cytotoxic phase I strain and toxigenic P multocida were moderately reduced in size. The turbinates of pigs infected with the phase III strain and toxigenic P multocida were slightly reduced in size except for one piglet whose turbinates were severely affected. Pigs infected with the non-cytotoxic phase I strain of B bronchiseptica alone showed no signs of atrophy and their turbinates were used to calculate reductions (per cent) in those infected with P multocida. The reduction (per cent) in size of turbinates and total numbers of P multocida isolated from the nasal washings of each pig were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The pathogenesis of turbinate atrophy in pigs caused by Bordetella bronchiseptica.

The pathogenicity of 3 strains of Bordetella bronchiseptica designated B58, PV6 and B65 was compared by intranasal infection of gnotobiotic piglets. Strain B58 was a phase 1 isolate that produced haemolysin, an adhesin for calf erythrocytes, adenylate cyclase, mouse lethal factor, dermonecrotic factor and cytotoxin. B65 was a variant of B58 that produced no detectable haemolysin, adhesin or adenylate cyclase and 10-fold smaller amounts than B58 of mouse lethal factor, dermonecrotic factor and cytotoxin. Strain PV6 was a phase 1 isolate that produced only haemolysin, adhesin and adenylate cyclase. After nasal infection of gnotobiotic pigs, 10(3.2)-10(6.2) colony forming units ml-1 (cfu ml-1) of strains B58 and PV6 were cultured from nasal washings during the next 25 days. In contrast, only 10(1.0)-10(2.8) cfu ml-1 of strain B65 were recovered during the same period. Only pigs infected with strain B58 had turbinate atrophy when they were slaughtered 25 days after infection and neutralising antibody to cytotoxin was detected only in these pigs. These results suggested that the cytotoxin, which may be the same as the mouse lethal and dermonecrotic factors, was the cause of turbinate atrophy. They also support the view that the adhesin for calf erythrocytes is required for colonisation of the nasal cavity in vivo.

Animals↗
PubMed1987

Antigenic analysis of fimbrial proteins from Moraxella bovis.

Fimbrial proteins were extracted from 15 isolates of Moraxella bovis, and antisera to each of the preparations were raised in rabbits. The antigenic relationships of the fimbriae were investigated by an enzyme-linked immunosorbent assay, tandem crossed immunoelectrophoresis, and a slide agglutination test. With all three methods there was a similar pattern of antigenic cross-reactivity among the fimbriae. The 15 isolates, together with 23 additional isolates, could be grouped into seven fimbrial serogroups.

Agglutination Tests↗
PubMed1986

Partial purification of an osteolytic toxin from Pasteurella multocida.

A protein toxin apparently composed of one polypeptide with an estimated Mr of 155,000 was purified from sonicated cells of a type D strain of Pasteurella multocida (LFB3) by preparative polyacrylamide gel electrophoresis (PAGE) and DEAE-Sephadex A50 chromatography. Its specific activity was 150-fold greater than that of the crude extract. The partially purified protein was cytotoxic for embryonic bovine lung cells, lethal for mice and caused turbinate atrophy in gnotobiotic pigs; a single intraperitoneal injection of approximately 360 ng kg-1 caused 50% turbinate atrophy. Reversal of the two-step purification procedure using DEAE-Sephacel chromatography followed by preparative PAGE increased the yield of toxin 30-fold; the specific activity of the partially purified toxin was 1970-fold greater than that of the crude extract.

Bacterial Toxins↗
PubMed1985

Virulence of Bordetella bronchiseptica in the porcine respiratory tract.

The virulence of Bordetella bronchiseptica in gnotobiotic piglets was studied by intranasal infection with 11 cultures derived from eight strains isolated from pigs (4), dogs (2), a human subject and a monkey. Six of the cultures contained organisms in phase I and five contained phenotypically different phase-III or -IV organisms. Of the phase-III and -IV cultures, four were derived from strains that had been isolated in phase I. Colonisation of the nasal cavity was investigated by counting bacteria in nasal swabs and washings. The toxigenicity of cell extracts from each strain and variant was determined by tests of lethality in mice or of cytopathogenicity in cell cultures. The results showed that two phase-I cultures from pigs colonised the nasal cavity and respiratory tract of gnotobiotic piglets better than did four phase-I cultures from other species. Phase-I organisms invariably produced capsules, fimbriae and mannose-resistant haemagglutination of guinea-pig erythrocytes. Four of five cultures in phases III and IV consisted of organisms that did not produce capsules, fimbriae or haemagglutination and colonised the nasal cavity poorly. Phase variation from I to III occurred in culture and in vivo, but variation from III to I occurred in vivo only and was accompanied by enhanced colonisation. Gnotobiotic piglets infected with porcine phase-I organisms exhibited atrophy of the nasal turbinate bones after 28 days; these organisms produced significantly more toxin than did bacteria in phase I from other species, or those in phases III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Epidemiological study of Pasteurella multocida and Bordetella bronchiseptica in atrophic rhinitis.

An epidemiological study of atrophic rhinitis was carried out in four pig herds. Observations were made of (i) infection with Bordetella bronchiseptica and Pasteurella multocida, (ii) the presence of brachygnathia superior (BS score), (iii) the extent (grade) of turbinate atrophy and pneumonia at slaughter and (iv) growth rates from two to 16 weeks of age and average daily weight gains to slaughter. In two of the herds with no history of atrophic rhinitis, B bronchiseptica and non-toxigenic strains of P multocida were isolated; only one of 47 pigs (2 per cent) had a BS score greater than +10 mm and the most severe turbinate atrophy observed in 21 pigs at slaughter was grade 3. In contrast, from two herds with atrophic rhinitis, toxigenic strains of P multocida were isolated as well as B bronchiseptica and non-toxigenic P multocida. BS scores of greater than +10 mm were present in six of 47 pigs (13 per cent) of which five were infected with toxigenic P multocida and had severe turbinate atrophy of grade 4 or 5. There was no significant reduction in growth rates in the affected compared with the unaffected herds nor in the affected compared with the unaffected pigs in the same herd. Neither was there a correlation between progressive disease and the extent of pneumonia found at slaughter. It was concluded that in field cases of the disease, high BS scores plus severe turbinate atrophy were associated with infection by toxigenic type-D strains of P multocida.

Animals↗
PubMed1984

Cell culture assay for toxigenic Pasteurella multocida from atrophic rhinitis of pigs.

A toxin produced by strains of Pasteurella multocida isolated from pigs with atrophic rhinitis caused a cytopathic effect in cell cultures derived from embryonic bovine lung. The toxin was produced during the late logarithmic phase of bacterial growth and inactivated by heating for 30 minutes at 56 degrees C. The cell culture assay was reproducible and 10(3) to 10(4) times more sensitive than a lethal assay in BALB/c mice. There was complete agreement between results in the two tests with 76 isolates of P multocida. Neutralising activity was demonstrated in both assays with sera from infected gnotobiotic piglets. It was concluded that embryonic bovine lung cell cultures provided a sensitive in vitro test for the differentiation of toxigenic from non toxigenic isolates of P multocida. The assay could be used in diagnostic laboratories and for characterisation of the toxin.

Animals↗
PubMed1983

Virulence of Pasteurella multocida in atrophic rhinitis of gnotobiotic pigs infected with Bordetella bronchiseptica.

Bordetella bronchiseptica and Pasteurella multocida have been impLicated in the aetiology of atrophic rhinitis of pigs but the precise cause and pathogenesis of field outbreaks have still to be clarified. The virulence of 11 strains of P multocida was investigated by intraperitoneal injection of culture filtrates in BALB/C mice, or by infection of gnotobiotic piglets given B bronchiseptica five days previously. Three of four type D strains of P multocida were lethal for mice and caused severe turbinate lesions and shortening of the snout with B bronchiseptica in gnotobiotic pigs; large numbers of P multocida and B bronchiseptica persisted for 64 days in the nasal cavity of these pigs. The fourth strain caused moderately severe turbinate lesions in gnotobiotic pigs infected with B bronchiseptica; small numbers of P multocida were found in these pigs and the lesions were attributed mainly to B bronchiseptica. Filtrates from seven strains of P multocida (four type A and three type D) were not lethal for mice and these strains with B bronchiseptica caused moderately severe turbinate lesions in gnotobiotic pigs; five of them colonised the nasal cavity reasonably well for 35 days but the lesions were attributed mainly to B bronchiseptica. The turbinate bones had regenerated by 64 days in pigs given type A strains of P multocida whereas the lesions persisted in pigs given type D strains. Antibodies to P multocida were detected in sera from infected gnotobiotic pigs by acid agglutination but not by indirect haemagglutination tests; neutralising activity to the mouse lethal toxin was detected in serum from one of five piglets at 64 days. The lethal toxin was inactivated at 56 degrees C for 30 minutes, by incubation with protease K for two hours and by 0.2 per cent formalin for 18 hours at 37 degrees C but not by trypsin; it was precipitated by 30 to 40 per cent saturation with ammonium sulphate and remained in the supernatant after centrifugation at 150,000 g. It was concluded that infection with virulent, type D strains of P multocida and B bronchiseptica could explain severe outbreaks of atrophic rhinitis; large numbers of both organisms persisted in the nasal cavity of gnotobiotic pigs with severe lesions; and that a soluble, heat-labile toxin may be an important virulence determinant in the type D strains of P multocida that cause severe atrophic rhinitis.

Animals↗
PubMed1982

Virulence of Bordetella bronchiseptica from pigs with or without atrophic rhinitis.

The virulence of 17 isolates of Bordetella bronchiseptica from 13 pig herds was compared by intranasal infection of gnotobiotic piglets and LD50 tests on mice. Of 59 piglets given 8.1-10-5 log 10 colony-forming units (cfu) of isolates from two herds with atrophic rhinitis (AR isolates) or isolates from six unaffected herds (non-AR isolates), 16 died of acute pneumonia; the survivors developed non-progressive turbinate hypoplasia and chronic pneumonia. Infection of 11 piglets with c. 3.0 log to cfu of three AR isolates or three non-AR isolates caused turbinate hypoplasia, but only slight pneumonia and no deaths. There were no significant differences between the virulence of AR and non-AR isolates in piglets. In LD50 tests in mice, there were no significant differences between the results from six AR isolates and six non-AR isolates, or from toxin prepared from two AR isolates and one non-AR isolates was fairly uniform, and that other factors must be responsible for the occurrence of progressive lesions of atrophic rhinitis in some but not all infected herds.

Animals↗
PubMed1981

Quantitative observations on Bordetella bronchiseptica infection in atrophic rhinitis of pigs.

Clinical atrophic rhinitis in seven pig herds could not be associated with the infection rate or higher numbers of B bronchiseptica in nasal swabs when compared with unaffected herds. B bronchiseptica isolates from herds with atrophic rhinitis and receiving sulphonamide medication were resistant to sulphonamides in vitro and there was a beneficial clinical response after changing to oxytetracycline medication. In an unaffected herd three piglets naturally infected with B bronchiseptica but possessing low levels of passive antibody showed marked turbinate hypoplasia when killed at seven weeks, the lesions had resolved in four of six litter mates by 21 weeks and did not occur in another litter of nine piglets which had a high level of passive antibody. The results indicate that although B bronchiseptica can produce non-progressive turbinate changes in pigs that have inadequate antibody protection, the relationship between these lesions and the chronic progressive field disease needs further investigation.

Animals↗
PubMed1976

Antibacterial activity in colostrum and milk associated with protection of piglets against enteric disease caused by K88-positive Escherichia coli.

Piglets suckled by dams that had been vaccinated with K88 antigen were significantly more resistant to deaths caused by neonatal diarrhea after challenge with a large dose of a K88-positive enteropathogenic strain of Escherichia coli than piglets suckled by control dams. The factors most likely to be involved in protection of the piglets were investigated by comparing the antibacterial activities of serum and mammary secretions from the two groups of dams. Vaccination stimulated the production of K88 antibodies, which were associated with anti-adhesive activity directed against the adhesive properties of the K88 antigen, and of O8 antibodies; the latter antibodies were attributed to traces of O8 antigen in the vaccine. Neutralizing activity against heat-labile enterotoxin was present in several dams before vaccination but was not stimulated by bacteriostatic activities were similar in serum and mammary secretions from both groups of dams and appeared to play no significant role in the protective after parturition were atrributed to exposure of the dams to the challenge strain excreted by the piglets. It was concluded that neutralization of the adhesive properties of K88 antigen by K88 antibodies in colostrum and in milk contributed significantly to the protection of piglets from vaccinated dams. However, the contribution of antibacterial activities associated with the greater levels of O8 antibodies in colstrum from the vaccinated group cannot be entirely excluded.

Agglutinins↗