Transmission of swine dysentery with Treponema hyodysenteriae and Vibrio coli.
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The immune status of 29 pigs recovered from swine dysentery (SD) was evaluated after reexposure to Treponema hyodysenteriae. Pigs which had recovered from SD and remained asymptomatic for 4 to 6, 9 to 13, and 16 to 17 weeks after initial inoculation were reexposed to 1.5 X 10(9) viable cells of T hyodysenteriae per pig. Pigs which had recovered from SD were not shedding T hyodysenteriae, as determined by selective cultural examination of feces, before they were reexposed. Of 29 pigs reexposed to T hyodysenteriae, 27 were resistant to SD. In contrast, 23 of 28 control pigs developed signs of SD when exposed to T hyodysenteriae for the first time. Significant differences in immunity were not observed between pigs from the three convalescent periods. Serum agglutinins to T hyodysenteriae were present in recovered pigs for approximately 8 weeks after inoculation.
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A method was designed to evaluate and compare the microtitration agglutination test (MAT) and the enzyme-linked immunosorbent assay (ELISA) to detect antibodies in swine sera to Treponema hyodysenteriae and thereby establish a method for determining the prevalence of swine dysentery (SD) in herds. According to sampling criteria based on the hypergeometric distribution, sera were collected from 3 age groups of swine from farms having a history of SD on the premises (SD+) recently or being free of the disease (SD-). The highest degree of test sensitivity was obtained when sera from market age swine were evaluated with the ELISA. Of 14 SD+ herds from which sera were obtained from market-age swine, 13 were positive with the ELISA (93%); none of the 8 SD- herds was positive. The detection rates of individual swine in the SD+ herds for the 2 tests by age group were as follows: MAT--adult swine 1.4%, market-age swine 6%, and weaned pigs 0.8%; ELISA--adult swine 16%, market swine 31%, and weaned pigs 0.5%.
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Groups of five pigs were vaccinated at three to four weeks old with either formolised Treponema hyodysenteriae in oil adjuvant alone, formolised T hyodysenteriae in oil adjuvant plus formolised Campylobacter coli in oil adjuvant, or sterile medium in oil adjuvant (as a control). Each group was challenged four weeks after vaccination by oral dosing on two consecutive occasions with pure cultures of the homologous strain of T hyodysenteriae plus direct contact with two pigs exhibiting severe swine dysentery. The disease was observed in two of five pigs immunised with T hyodysenteriae alone, three of five pigs immunised with T hyodysenteriae plus C coli and all five controls; haemorrhagic diarrhoea was exhibited only by the control group. Each pig immunised with T hyodysenteriae (alone or with C coli) recovered spontaneously, whereas four controls died. Vaccination with T hyodysenteriae also markedly reduced the severity and duration of clinical signs and of weight loss. No differences were observed in response to challenge between pigs immunised with T hyodysenteriae alone and pigs immunised with T hyodysenteriae plus C coli.
Swine dysentery (SD) was transmitted to healthy pigs by contact with experimentally-induced carrier pigs. Carrier pigs were produced by exposure of specific pathogen-free (SPF) swine to swine acutely affected with SD. When carrier pigs became acutely affected with SD, they were allowed to recover naturally or were treated with dimetridazole or ronidazole. Recovery was based on disappearance of clinical signs of SD. At a given time after recovery, normal SPF swine were housed with the carriers in a disinfected isolation unit to determine the ability of carriers to transmit SD. In each of 3 experiments, carriers that had recovered and remained asymptomatic for 11 to 25 days transmitted SD to contacts in 14 to 51 days. In 2 experiments, pathogenic Treponema hyodysenteriae was isolated from carriers 12 days before clinical SD was observed in contacts. Carriers which had recovered and remained asymptomatic for 70 and 90 days transmitted SD to contacts in 1 of 3 experiments. Treponema hyodysenteriae was isolated only from contacts with clinical signs of SD. In 4 experiments, carriers that had been treated with nitroimidazole compounds and subsequently recovered for 19 to 44 days failed to transmit SD. Culture of fecal samples on trypticase soy agar with 5% bovine blood and 400 microgram of spectinomycin/ml was helpful in predicting the carrier state, but phase contact contact microscopy of wet fecal smears was not.
Agglutinin-absorption and precipitin-absorption studies demonstrated that three strains of weak beta-hemolytic treponeme isolated from cases of diarrhea of swine and from a clinically normal dog were antigenically different from each other.
Multiple, ligated loops of swine colon were used as an in vivo model in which to test enteropathogenicity of isolates of Treponema hyodysenteriae. Gross and microscopic lesions observed in 21 of 22 colonic loops in pigs killed 48 to 72 hours after inoculation with isolates known to be enteropathogenic were characteristic of swine dysentery. These lesions were not observed in 12 loops exposed to uninoculated media or in 12 loops inoculated with nonpathogenic isolates of T hyodysenteriae. The swine-loop technique provides a relatively rapid, economical, reliable model in which to test enteropathogenicity of T hyodysenteriae isolates.
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