Sera and tracheal washings (TW) were used to identify antigens of Bordetella avium recognized during experimentally induced bordetellosis in young turkeys. Pooled sera and TW were examined for antibody by a microtitration agglutination test and by western immunoblotting. In addition, comparable samples collected from 1-day-old turkeys and uninoculated control turkeys also were examined. At least 8 outer membrane proteins of B avium were recognized in immunoblots of sera and TW from infected turkeys. Reactivity of TW in immunoblots was qualitatively similar but less intense, compared with reactivity of corresponding sera collected on postinoculation (PI) weeks 2, 3, and 4. Molecular weights of the major outer membrane proteins of B avium recognized by sera and TW at PI week 4 were 100,000, 97,000, 36,000, 31,000, 21,000, 18,000, 14,000, and < 14,000. A protein with a molecular weight of 55,000 reacted nonspecifically in all samples tested. Antibody, detectable by microtitration agglutination, was in sera of 1-day-old turkeys and in sera and TW of B avium-infected turkeys during PI weeks 2 to 4.

The in vitro antimicrobial activities of aditoprim (AP), a new dihydrofolate reductase (DHFR) inhibitor, trimethoprim (TMP), sulfadimethoxine (SDM), sulfamethoxazole (SMX), and combinations of these drugs against some porcine respiratory tract pathogens were determined by use of an agar dilution method. The minimal inhibitory concentrations (MIC) of these agents were determined twice against Bordetella bronchiseptica (n = 10), Pasteurella multocida (n = 10), and Actinobacillus pleuropneumoniae (n = 20) strains isolated from pigs suffering from atrophic rhinitis or pleuropneumonia. All B bronchiseptica strains were resistant to AP and TMP. The MIC50 values of AP and TMP for P multocida were 0.25 and 0.06 microgram/ml, respectively, and for A pleuropneumoniae, 1 and 0.25 microgram/ml, respectively. The MIC50, values of SDM and SDM for B bronchiseptica were 4 and 1 microgram/ml, respectively; for P multocida, 16 and 8 microgram/ml, respectively; and for A pleuropneumoniae, 16 and 8 microgram/ml, respectively. The investigated combinations of the DHFR inhibitors and the selected sulfonamides had synergism for the A pleuropneumoniae strains; the MIC90 values of the combinations were less than or equal to 0.06 microgram/ml. Potentiation was not observed for the B bronchiseptica and the P multocida isolates. The MIC of the combinations against B bronchiseptica and P multocida corresponded respectively to the concentrations of the sulfonamides and the DHFR inhibitors in the combinations. For A pleuropneumoniae, 2 types of strains were used (25% of serotype 2 and 75% of serotype 9). Type-2 strains had lower susceptibility than type-9 strains to AP and TMP as well as to SDM and SMX (at least a fourfold difference in MIC between the 2 types of strains). The MIC of the combinations were similar for the 2 types of strains.