Two indirect ELISA containing outer membrane protein (OMP) and lipopolysaccharide (LPS) antigens from a field isolate of Salmonella choleraesuis var kunzendorf were developed and evaluated in experimentally infected and uninfected control pigs. Experimentally induced infection with S choleraesuis was successfully established in 10 pigs by oral inoculation with 10(8) organisms, and 3 pigs died of clinical salmonellosis at postinoculation (PI) weeks 1, 2, and 4. Swab specimens from tonsils, nostrils, and rectum of pigs were obtained for culture, and sera were evaluated at weekly intervals for 9 weeks after inoculation. The ELISA containing OMP and LPS antigens with either anti-swine IgG or protein albumin-to-globulin ratio (antiglobulin) conjugates were standardized for serologic evaluation. All 4 ELISA (2 OMP and 2 LPS) detected seroconversion by PI week 3 and had sensitivities and specificities of 97.8 and 88.8, 100 and 100, 95.6 and 88.8, and 93.3 and 72.5%, at their ideal cutoff points (negative mean optical density + 2 SD). There was excellent agreement between all 4 ELISA systems as determined by kappa values. Cultures of fecal, tonsil, and nasal swab specimens were positive for S choleraesuis until the fourth week of infection. Fecal swab specimens from 1 pig were positive for S choleraesuis until PI week 7. Persistent infection after antemortem culture results were negative was detected by all 4 ELISA, which indicated consistently high titers until the end of PI week 9. Conventional bacteriologic examination of intestines, mesenteric lymph nodes, bone marrow, lung, liver, spleen, and bile yielded positive results for S choleraesuis in the 3 pigs that died of clinical infection, whereas results were negative in the other 7 pigs infected by the end of PI week 9. Histologic examination of lung, liver, spleen, intestines, and mesenteric lymph nodes from the 3 pigs that died of S choleraesuis infection revealed severe ulceration and inflammatory cell infiltration.

A challenge-exposure model was developed for dose-dependent induction of subclinical (moderate) atrophic rhinitis (AR) in conventionally raised Dutch Landrace and Large White pigs, about 4 weeks old. Under favorable climatic and housing conditions, pigs were intranasally challenge-exposed with Pasteurella multocida-derived toxin (Pm-T) 3 days after pretreatment by inoculation with 1% acetic acid. Pigs were challenge-exposed with 1 of the following Pm-T doses: 0 (control), 5, 13, 20, or 40 microgram of Pm-T/ml of phosphate-buffered saline solution (PBSS), 0.5 ml/ nostril/d on 3 consecutive days. Five weeks after challenge exposure, subclinical moderate) AR status was defined as intermediate conchal atrophy (grade 2 for ventral conchae on a 0 to 4 scale and grade 1 or 2 for dorsal conchae on a 0 to 3 scale, respectively) and perceptible difference in change in brachygnathia superior (CBS) between control and challenge-exposed pigs between the beginning and end of the study. All Pm-T-exposed pigs had nasal damage that was dose-dependent. The higher Pm-T doses resulted in higher ventral conchae atrophy and dorsal conchae atrophy scores. The CBS increased with applied Pm-T dose, resulting in significant (P < 0.05) differences between controls (3.88 mm) and the 13-, 20-, and 40-microgram Pm-T-treated groups (7.77, 6.58, and 7.98 mm, respectively). In response to the applied dose, weight gain per week for Pm-T-exposed pigs was lower than that of controls after week 3 (P < 0.01). Difference from controls was 32, 54, 52, and 96 g/d/pig for 5-, 13-, 20-, and 40-microgram Pm-T-treated groups respectively, in the last 2 weeks. For Dutch Landrace and Large White pigs, intranasally administered Pm-T mimicked the pathogenic effect of in vivo infection with toxigenic Pm strains. The optimal model to induce subclinical AR appeared to be 13 microgram of Pm-T/ml (0.5 ml/nostril/d) on 3 consecutive days.

An ELISA was developed and tested to detect antibodies to Eperythrozoon suis in swine. Results were compare with those of the indirect hemagglutination (IHA) test. Antigen isolated from swine heavily infected with E suis was used for both tests. Comparison of the ELISA with the IHA test revealed a significant (P < 0.001) correlation between results. Of 114 samples obtained from 9 swine infected with E suis, 8 7.7% were seropositive (titer greater than or equal to 200) via the ELISA, and 80.7% were seropositive (titer greater than or equal to 20) via the IHA test. The sensitivity of the ELISA was greater than that of the IHA test. All blood samples obtained from specific-pathogen-free swine tested negative for E suis antibody. Cross-reactions were not observed between E suis antigen and antisera against various swine and cattle disease agents using ELISA. We concluded that the ELISA may be used for rapid and effective diagnosis of infection with E suis in swine.

Three-week-old weaned and colostrum-deprived neonatal (< 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs < 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.