Search

Three trials were conducted to establish if young primary specific pathogen free (SPF) pigs could be protected from Glasser's disease by vaccination. Three age groups of cesarean-derived isolator-reared gnotobiotic pigs were vaccinated twice at 4 and 6, 3 and 5, and 2 and 4 wk of age respectively with a formalin killed aluminum hydroxide adsorbed bacterin prepared from three strains of Haemophilus parasuis isolated from Ontario pigs affected with Glasser's disease. When challenged two weeks later with the homologous strains of virulent bacteria, all the vaccinated pigs remained healthy, while 17/18 nonvaccinated pigs became severely sick or died between three and seven days postchallenge. The one surviving nonimmunized pig was retarded in growth. All of the nonimmunized pigs had visible lesions of polyserositis, the most common being polyarthritis (14/18). Other lesions were fibrinous meningitis, pericarditis, pleurisy and/or peritonitis. Two of the pigs died with a septicemia. Haemophilus parasuis was isolated from 15/18 nonimmunized pigs, usually from several of the affected sites. The organisms were not isolated from the immunized pigs, nor from the surviving nonimmunized pig. Attempts to detect the presence of specific antibodies against the H. parasuis strains in the sera of the immunized or exposed pigs by the passive hemagglutination test or by enzyme linked immunoassay were unsuccessful. The results of this work indicate that primary SPF pigs can be protected from Glasser's disease by vaccination as early as 2 and 4 wk of age. The nature of this protective mechanism was not established in this study.

Sixty-six male pigs were allotted at random at birth to six castration treatments: partial castration at 6 and 26 days according to the Baiburtcjan method and complete castration at 6, 26, and 76 days and at 68 kg liveweight. No meaningful treatment differences were detected in growth rate or in carcass measurements (length, backfat thickness, loin eye area, percent lean in the ham face and percent ham of the side). The overall environment of the experiment limited growth rate of normal castrates to approximately 0.45 kg per day. The possibility of the environment dampening the expression of treatment effects cannot be precluded. The method of partial castration used was difficult to perform and more time-consuming than complete castration. It reduced testicular development bur did not eliminate it. Many of the partial castrates molested pen mates and sonic mated with gilts. Of 22 carcasses from partial castrates, 15 were detected as having odor.

Campylobacter jejuni of human and canine origin was inoculated orally into six gnotobiotically reared Beagle puppies and reactions were compared with two controls. Inoculated dogs developed transient lassitude, inappetence, mild diarrhea and tenesmus during the period 36-72 hours after inoculation. Pairs of dogs killed 43 hours, and five and seven days after inoculation had lesions limited to typhlitis and colitis. Congestion of colonic mucosa, associated loss of goblet cells, attenuation and exfoliation of surface epithelium with microerosions, hypertrophy of glands and neutrophil infiltration of lamina propria were seen during the acute phase. Less severe surface and inflammatory lesions were evident at five and seven days, with hyperplasia of the proliferative compartment in mucosal glands. Campylobacter established at over 10(10) organisms per gram of colonic content but did not invade the mucosa. It was concluded that the gnotobiotic dog may be a suitable model for investigation of the pathogenesis of Campylobacter colitis.

A whole cell formalin killed trivalent Haemophilus parasuis bacterin was tested for efficacy in four week old, weaned specific pathogen free pigs challenged under laboratory conditions. The vaccine contained three field strains of H. parasuis selected from confirmed cases of Glasser's disease. Two different formulations were evaluated in separate trials. In trial 1, ten pigs received 5 mL of bacterin subcutaneously in the neck, followed by a second 5 mL dose two weeks later. Another ten pigs served as nonvaccinated controls. One week after the second dose, all pigs were subjected to an aerosol challenge containing the strains of H. parasuis present in the vaccine. In trial 2, a broth rather than a saline based vaccine was prepared, and tested as in trial 1. In both trials, the vaccinated pigs remained healthy postchallenge, while eight of nine (Trial 1) and eight of ten (Trial 2) nonvaccinated pigs succumbed to Glasser's disease.

Pure cultures of Treponema hyodysenteriae given orally to conventional pigs resulted in the development of swine dysentery, whereas identical cultures given to gnotobiotic pigs did not produce the disease. Oral inoculation of gnotobiotic pigs with Vibrio coli and/or a peptostreptococcus in addition to T. hyodysenteriae did not result in dysentery. Neutralization of gastric secretions with NaHCO3 immediately prior to inoculation with T. hyodysenteriae increased the period during which treponemes were evident in the feces, as did the inoculation of this organism via the intracecal route. None of the gnotobiotic pigs with a persistent fecal Treponema population developed signs of dysentery. Factors other than those investigated in this work must play a part in the etiology of swine dysentery.

Glasser's disease accounted for less than 1% of total swine mortalities in an 11 year retrospective postmortem survey of swine submissions at three provincial government diagnostic laboratories in southern Ontario. However, Glasser's disease was suspected in 17 of 83 boar mortalities at the Record of Production Boar Test Station between 1983 and 1985 and was much more common in specific-pathogen-free (SPF) boars than in conventional boars. The prevalence of the causative organism, Haemophilus parasuis, was determined for 19 SPF herds in Ontario classified as "Excellent" under the Ontario Swine Herd Health Policy. Nasal swabs from two-month-old pigs were cultured on chocolate agar containing 1.5 mug/mL lincomycin, 5 mug/mL bacitracin, and 0.1 mug/mL crystal violet. Three herds were negative for H. parasuis infection; 16 herds contained clinically healthy carrier pigs.

To study the occurrence and distribution of various strains of Haemophilus parasuis in southern Ontario swine, organisms isolated from healthy swine, from specific pathogen-free and conventional herds, and from disease cases were examined using restriction endonuclease fingerprinting analysis. In most herds, several strains of H. parasuis could be detected although one or two strains usually predominated. Individual animals were colonized by a single or limited number of strains. In several cases, the same strains were isolated from more than one specific pathogen-free herd. Conventional herds carried a more heterogeneous population of H. parasuis. Only one strain was isolated which was common to more than one conventional herd. No strains were isolated which were common to both specific pathogen-free and conventional herds. None of the strains isolated from disease cases were found in healthy conventional or specific pathogen-free swine examined in this study.

The significance of enterotoxin production and proliferative ability of Escherichia coli in the intestinal tract as related to porcine enteric colibacillosis was studied in 68 gnotobiotic pigs. The animals were monocontaminated at seven to ten days of age with eight selected strains of E. coli. The strains were two naturally occurring porcine enteropathogens - P155 (0149:K91;K88a,c:H10) and P307 (08:K87;K88a,b:H19), two nonenteropathogenic strains - P104 (0139:K82:H1) and F11 (018-ab:K?:H14), and four enterotoxigenic derivatives of the above strains - P104(P155), P104(P307), F11(P155) and F11(P307). The response of the animals was evaluated on the basis of clinical observations and necropsy lesions 22 hours after exposure to the organisms. E.coli counts were determined at seven different levels of the intestinal tract. Cell free extracts of the intestinal contents were examined for enterotoxic activity by the ligated pig intestine loop test. All of the strains possessing the enterotoxin plasmid produced enterotoxin in the pig's intestine and were capable of causing diarrhea. The nonenteropathogenic E. coli failed to do so. The strains possessing the P155 enterotoxin plasmid were more virulent than the corresponding derivatives with the P307 enterotoxin plasmid. Strains P155, P307 and P104(P155) proliferated in the upper small intestine at a greater rate and were more virulent than the other strains. The numbers attained in the upper small intestine by the other enterotoxigenic derivatives were comparable to those of their nonenteropathogenic parent strains. It was considered that enterotoxin produced by E. coli was the essential factor for causing a diarrheic response in gnotobiotic pigs. The virulence of each of the tested strains appeared to be governed by the degree of enterotoxicity associated with a particular enterotoxin plasmid, the numbers attained by these organisms in the upper small intestine, (but not in the lower small intestine or in the colon), and by other undetermined factors.