A comparative serologic and virologic study was performed in pigs from 5 herds with postweaning multisystemic wasting syndrome (PMWS) and 2 herds without PMWS in Quebec. In each herd, 60 blood samples were collected at 4-wk intervals from pigs from 3 to 23 wk of age. The serum was evaluated for the presence of antibodies to porcine circovirus type 2 (PCV2) and porcine reproductive and respiratory syndrome virus (PRRSV), as well as for the presence of nucleic acid of PCV2, PRRSV, and porcine parvovirus (PPV), by means of the polymerase chain reaction (PCR). Serologic profiles for PCV2 were very similar in 6 of the 7 herds, including the 2 without PMWS, and were characterized by a gradual decrease in antibody titres from 3 until 11 wk of age, followed by seroconversion at 15 wk, and high PCV2 antibody titres thereafter in all pigs. Only starting at 11 to 15 wk of age could PCV2 viremia be detected, except in 1 herd, in which clinical signs were observed at 6 to 7 wk of age. A PCV2 viremia could be detected within the same pigs for a minimum of 8 wk, and the virus could still be detected in 41% of the serum samples obtained at 23 wk of age. The antibody level did not appear to influence the occurrence of disease, since titres were similar in pigs in the herds with or without PMWS. Infection with PRRSV, as demonstrated by PCR and seroconversion, preceded that of PCV2 by at least 1 mo in both types of herd. Both PRRSV and PCV2 were detected in some pigs in 5 of the 7 herds, including 1 herd without PMWS. Porcine parvovirus could be detected in serum by PCR in 2 herds with PMWS after the onset of clinical signs and also in 1 herd without PMWS. Genomic analysis of PCV2 strains identified in the herds without PMWS indicated complete or very high homology (99.4% to 100%) with the PCV2 strains identified in 4 herds with PMWS. In our field study, the triggering of PMWS in the herds could not be linked to coinfection with either PRRSV or PPV or to the use of a specific immunostimulant, such as vaccines, or to particular genomic differences between the PCV2 strains identified.

Cross-reactivity indices (CRIs) of 28 isolates of Moraxella bovis recovered from outbreaks of infectious bovine keratoconjunctivitis in Argentina (A, 11 isolates), Brazil (B, 7), and Uruguay (U, 10) between 1983 and 2000 were estimated. Hyperimmune sera were produced in rabbits and antibody titres determined with each isolate. Isolates showing CRIs3 70 were placed in the same group. Group I had 13 isolates (A, 1; B, 6; U, 6); group II had 6 isolates (A, 4; U, 2); groups III, IV, and V had 2 isolates each, recovered in Argentina; group VI had 2 isolates, from Uruguay; and group VII had 1 isolate, from Brazil. The CRIs3 70 between vaccine strains and isolates recovered before and after 1990 were 58% and 42%, 50% and 50%, and 33% and 67% with vaccine strains 2419, 2358, and 2439, respectively. Isolate 273, from Uruguay, showed CRIs > 70 with 78% of the isolates and is recommended as the vaccine strain.

Objective-To determine whether passively acquired antibodies prevent development of a protective immune response to live virus in calves. Procedures-18 calves. Procedure-Calves were caught immediately after birth and tested free of bovine viral diarrhea virus (BVDV) and serum antibodies against BVDV. Within 48 hours, 12 calves were fed colostrum that contained antibodies against BVDV and 6 calves received BVDV antibody free milk replacer. Three milk replacer fed and 6 colostrum fed calves were exposed to virulent BVDV2-1373 at 2 to 5 weeks of life when passively acquired serum antibody titers were high. After serum antibody titers against BVDV had decayed to undetectable concentrations (at 7 to 9 months of age), the 3 remaining milk replacer fed calves, 6 colostrum fed calves previously exposed to BVDV2-1373, and 6 colostrum fed calves that had not been exposed to the virus were inoculated with BVDV2-1373. Results-Passively acquired antibodies prevented clinical disease in inoculated colostrum fed calves at 2 to 5 weeks of life. Serum antibody titers did not increase in these calves following virus inoculation, and serum antibody titers decayed at the same rate as in noninoculated colostrum fed calves. Inoculated colostrum fed calves were still protected from clinical disease after serum antibody titers had decayed to nondetectable concentrations. Same age colostrum fed calves that had not been previously exposed to the virus were not protected. Conclusion and Clinical Relevance-A protective immune response was mounted in calves with passive immunity, but was not reflected by serum antibodies titers. This finding has implications for evaluating vaccine efficacy and immune status.

Two studies were performed in order to test the relative ability of different strains of porcine reproductive and respiratory syndrome virus (PRRSV) to replicate and cross the placental barrier in pregnant gilts. Study 1 comprised 6 nonvaccinated gilts. Study 2 comprised 8 nonvaccinated gilts and 12 gilts that were vaccinated twice before conception. On, or about, gestation day 90 all gilts were simultaneously exposed to 20 field strains of PRRSV (all strains were distinguishable by restriction fragment length polymorphism (RFLP) patterns). Gilts of study 1 were euthanized on day 7 postpartum. Gilts of study 2 were euthanized on, or about, gestation day 111. All gilts, pigs, and fetuses were tested for the presence and type of strain of PRRSV. Of 128 samples shown to contain PRRSV, 118 contained a single strain, 4 contained 2 strains, and 2 contained a strain or strains for which the RFLP pattern was undecipherable. Only 8 of the 20 strains were isolated from nonvaccinated gilts and their litters. And only 2 of the 20 strains (notably 2 of the same strains isolated from nonvaccinated gilts and their litters), were isolated from vaccinated gilts and their litters. Moreover, 1 of the 2 strains accounted for most (31 of 37; 84%) of the isolates from the vaccinated group. Collectively these results indicate that strains differ in their ability to replicate in pregnant gilts and cross the placental barrier. And they suggest that maternal immunity, although sometimes insufficient to prevent transplacental infection, can exert additional selective pressure.