Objective-To develop a spatial epidemic model to simulate intraherd and interherd transmission of footand- mouth disease (FMD) virus. Sample Population-2,238 herds, representing beef, dairy, swine, goats, and sheep, and 5 sale yards located in Fresno, Kings, and Tulare counties of California. Procedure-Using Monte-Carlo simulations, a spatial stochastic epidemic simulation model was developed to identify new herds that would acquire FMD following random selection of an index herd and to assess progression of an epidemic after implementation of mandatory control strategies. Results-The model included species-specific transition periods for FMD infection, locations of herds, rates of direct and indirect contacts among herds, and probability distributions derived from expert opinions on probabilities of transmission by direct and indirect contact, as well as reduction in contact following implementation of restrictions on movements in designated infected areas and surveillance zones. Models of supplemental control programs included slaughter of all animals within a specified distance of infected herds, slaughter of only high-risk animals identified by use of a model simulation, and vaccination of all animals within a 5- to 50-km radius of infected herds.

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.

In order to examine an association between porcine circovirus type-2 (PCV2) infection and reproductive failure in pigs, sera (n = 171) from stillborn fetuses were collected from 3 different farms with prolonged histories of reproductive problems. These sera were tested for the presence of antibodies to PCV2 using an immunoperoxidase monolayer assay. Of the 171 sera tested, 28 had PCV2 antibody titers of ≥ 1:16. When these 28 samples were tested by a polymerase chain reaction assay, 13 were found to contain PCV2 viral DNA. Of these 13 samples containing both PCV2 antibodies and viral DNA, 9 yielded PCV2 on virus isolation. Amino acid sequences comprising open reading frame 2 of PCV2 from 2 of these isolates were compared to PCV2 isolates from cases of post-weaning multi-systemic wasting syndrome (PMWS). The amino acid sequences of the 2 isolates from stillborn pigs were shown to be nearly identical to each other, as well as to other PCV2 isolates associated with reproductive failure. When compared with PMWS isolates, the isolates from the stillborn fetuses showed differences of at least 2 amino acids. These results confirm previous findings that transplacental infection of PCV2 occurs in the field and that stillbirths in pigs may be associated with PCV2 infections. At present, the significance of minor differences in amino acid sequences is not known.

Multiplex nested polymerase chain reactions (PCRs) were developed for the simultaneous detection and differentiation of genomic material of porcine circovirus 1 (PCV1), porcine circovirus 2 (PCV2), and porcine parvovirus (PPV) in formalin-fixed, paraffin-embedded tissues. Multiplex conventional and nested PCR and in situ hybridization were compared for their ability to detect the 3 viruses in such tissues. Xylene deparaffinization followed by proteinase K digestion yielded DNA of sufficient quality for reliable and consistent PCR analyses. The DNA from PCV1, PCV2, and PPV was detected by both multiplex nested PCR and in situ hybridization in lymph-node tissue from 12 pigs experimentally co-infected with the 3 viruses, as well as in formalin-fixed, paraffin-embedded lymph-node tissue from 30 pigs with naturally occurring postweaning multisystemic wasting syndrome; the agreement rates for the 2 methods were 100% in both groups of pigs. Thus, multiplex nested PCR could be applied successfully to formalin-fixed, paraffin-embedded tissues for simultaneous detection of these 3 porcine viruses.

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.

The objectives of the study were to determine the duration of porcine reproductive and respiratory syndrome virus (PRRSV) survival in houseflies (Musca domestica Linnaeus) following feeding on an infected pig, and to determine whether the virus was present on the exterior surface or within the internal viscera of the fly. A total of 210 laboratory-colonized houseflies were allowed to feed to repletion on a pig, experimentally infected with PRRSV on day 7 postinoculation, and then maintained alive under laboratory conditions (27°C). Two subsets (A and B) of 30 flies were collected at each of the following sampling points; 0, 6, and 12 hours post feeding (pf). Subset A contained an extra group of 30 flies collected at 24 hours pf due to the availability of extra flies. Flies in subset A were processed as whole fly homogenates, while the exterior surface washes and digestive organs were collected from flies in subset B. Whole fly homogenates, collected at 0, 6, and 12 hours pf, were positive by both polymerase chain reaction (PCR) and swine bioassay. Digestive organs, collected at 0 and 12 hours pf, were positive by PCR and swine bioassay. The PRRSV RNA was detected by PCR from the exterior surface wash of subset B flies collected at 0, 6, and 12 hours pf; however, only the subset collected at 0 hour pf was swine bioassay-positive. This study indicates that infectious PRRSV can survive within the intestinal tract of houseflies for up to 12 hours following feeding on an infected pig, but only for a short period on the exterior surface of the flies.