Use of metronidazole in horses.
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Biomedical subjects
Publications and source records attributed to J M Rutter.
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The Pig Health Control Association launched a health scheme for atrophic rhinitis in 1978. For several years pig herds were monitored by scoring the degree of turbinate damage and by clinical inspections. When laboratory facilities became available for detecting toxigenic Pasteurella multocida, nasal swabs were taken from pigs in Association herds during 1988 and 1989 to determine whether the organism was present. Sows were screened routinely and in the worst affected herds, sucklers and weaners were also swabbed. In 12 of 19 herds with consistently low snout scores toxigenic P multocida were not isolated, and in 15 herds which developed higher snout scores with time toxigenic P multocida were also not found. Eleven herds had never been listed by the Association, either because their snout scores were consistently high or because they had received importations of stock from herds with high snout scores; of six of these herds with the most persistently high snout scores five showed varying degrees of the clinical signs of atrophic rhinitis, but none of the six showed evidence of infection with toxigenic P multocida, and the organism was not found in the other five herds in the group. There seems to be an overlap between the clinical and gross pathological signs of atrophic rhinitis seen in some herds not infected with toxigenic P multocida and the mild and spasmodic signs of atrophic rhinitis seen in some herds which are substantially infected with the organism.
Four herds of pigs were selected which had different degrees of clinical atrophic rhinitis and used different specific counter-measures. In two of them, the clinical signs occurred spasmodically and were slight. The sows, suckling pigs and growing pigs in all the herds were sampled for toxigenic Pasteurella multocida. In one of the slightly affected herds (herd D), the weaners were moved to a second farm for finishing. No toxigenic P multocida were found at the breeding farm, but 50 per cent of the large growing pigs were positive. It seemed that the organism had entered only at the finishing farm and that the mild clinical signs were due to the infection starting in older pigs than usual. In the second mildly affected herd, 47 per cent of the sows and 42 per cent of the growers were infected. Three toxigenic isolates from this herd produced as severe turbinate damage experimentally in specific-pathogen-free pigs as a stock pathogenic strain. Except in herd D, toxigenic P multocida were found in all the age groups of pigs sampled. However, the pattern of distribution of the organism within the herds was not obviously correlated with the severity of the disease. In a fifth herd there were obvious cases of clinical atrophic rhinitis, with marked turbinate atrophy, from which toxi-genic P multocida were recovered in abundance. Subsequently, the clinical disease disappeared and, despite extensive and repeated sampling, the organism was not found again.
Gnotobiotic pig antisera to purified toxoid from a capsule type A or D strain of Pasteurella multocida contained large quantities of antitoxin but comparatively little antibody to a crude lysate of P. multocida. These sera given intraperitoneally to further pigs were almost completely protective against turbinate atrophy after intranasal inoculation of dilute acetic acid and infection with type D toxigenic P. multocida. In contrast, antisera to a crude lysate or bacterin of toxigenic P. multocida which contained large titres of antibody to P. multocida lysate, but no detectable antitoxin, were not protective. Colonisation by toxigenic P. multocida was significantly reduced in protected pigs and was similar to colonisation by nontoxigenic P. multocida in pigs untreated or treated with dilute acetic acid. These results indicated (1) that antitoxin was protective and cross protective between toxins from different capsule types; and (2) that the toxin was the main colonisation factor produced by toxigenic bacteria in the acetic acid model of infection and that immunity to it did not eliminate infection.
An in vitro assay was developed using calf corneal cells to assess the importance of fimbriae in the colonisation of the bovine ocular surface by Moraxella bovis, and the role of fimbrial antibodies in the bovine immune response and resistance to infectious bovine keratoconjunctivitis (IBK). Fimbriae promoted adherence of M. bovis to calf corneal cells in culture; 15 fimbriate isolates, representative of 6 fimbrial serogroups of M. bovis, adhered to the cells whereas 4 non-fimbriate isolates failed to do so. Fimbrial antibodies in hyperimmune rabbit serum inhibited attachment of all fimbriate strains of the homologous fimbrial serogroup but not those of 5 heterologous serogroups. The relevance of these results to the use of a polyvalent fimbrial vaccine in the control of IBK is discussed.
The efficacy of detecting toxigenic Pasteurella multocida from nasal swabs of slaughtered and live pigs was assessed. The isolation of toxigenic P multocida from nasal cavities of slaughtered bacon pigs from two herds with atrophic rhinitis was reduced by immersion in the hot water tank by 25 per cent and 75 per cent. Individual sows from one of the infected herds were repeatedly swabbed to find the best method of isolating toxigenic P multocida. Toxigenic P multocida were isolated from 50 per cent of cotton swabs inoculated on to selective medium the same day. After 24 hours in the post, 45 per cent of cotton swabs placed in transport medium, 38 per cent of alginate swabs dissolved in transport medium and inoculated into mice, and 36 per cent of the dissolved swabs inoculated directly on to selective medium yielded toxigenic P multocida. These bacteria were isolated from only 25 per cent of cotton swabs held in transport medium at 10 degrees C for 48 hours to simulate prolonged postage times; from slaughtered pigs a similar reduction in isolation was seen with swabs kept for 24 or 48 hours. The reduced isolation caused by a delay before culture was associated with an overgrowth of other flora. The development of this flora was prevented by storage of swabs at 4 degrees C in the laboratory or by the use of cool boxes for postage.