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Abstract

Objectives

To determine whether intrauterine inoculation of porcine reproductive and respiratory syndrome virus (PRRSV) interferes with conception and whether exposure to one strain of PRRSV provides protection against challenge-exposure (CE) with homologous or heterologous strains of PRRSV.

Animals

40 gilts.

Procedure

Gilts were inoculated by intrauterine administration of a PRRSV isolate (nadc-8) at breeding. Inoculated and noninoculated gilts were exposed oronasally to homologous (nadc-8) or heterologous (European isolate) PRRSV during late gestation. Specimens from gilts and fetuses were tested against CE virus. Lack of virus in gilts indicated protective immunity for the dam, in fetuses indicated protection of gilt from reproductive losses, and in both groups indicated complete protection.

Results

In the homologous CE group, interval from inoculation to CE ranged from 90 to 205 days, and protection was complete. In the heterologous CE group, interval from inoculation to CE ranged from 90 to 170 days, and protection was incomplete. The CE virus was detected in gilts necropsied 134 to 170 days after CE and in a litter necropsied 170 days after CE.

Conclusions

Homologous protection can be induced in gilts by exposure to live PRRSV. Heterologous protection from reproductive losses can be induced in gilts by exposure to live PRRSV; however, this protection is incomplete and may have a shorter duration than homologous protection.

Clinical Relevance

Exposure of swine to enzootic PRRSV will provide protection against homologous PRRSV-induced reproductive losses. Extent and duration of protection against heterologous PRRSV may be variable and dependent on antigenic relatedness of the virus strains used for inoculation and CE. (Am J Vet Res 1999;60:1022-1027)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To compare the virulence of selected strains of porcine reproductive and respiratory syndrome virus (PRRSV) relative to reproductive performance of pregnant gilts.

Design

16 pregnant gilts (principals) were exposed oronasally to 4 strains (vaccine strain RespPRRS, field strains VR-2385, VR-2431, and NADC-8, 4 gilts/strain) of PRRSV on or about day 90 of gestation. 4 pregnant gilts (controls) were kept under similar conditions, except for exposure to PRRSV. Samples and specimens obtained from gilts, pigs (before ingestion of colostrum), and fetuses were tested for PRRSV and homologous antibody.

Animals

20 pregnant gilts.

Procedure

The virulence of each strain of PRRSV was evaluated mainly on the clinical status of the corresponding litters at farrowing.

Results

Most gilts remained clinically normal throughout the study and farrowed normally at or near the expected farrowing time. All virus strains crossed the placenta of principal gilts to infect fetuses in utero. The number of late-term dead fetuses (which appeared to be the best measure of relative virulence) ranged from 0 for litters of control gilts and gilts exposed to strain RespPRRS, to 38 for gilts exposed to strain NADC-8. All principal gilts became viremic and developed antibody against PRRSV. All strains persisted in alveolar macrophages of at least some principal gilts for at least 7 weeks after exposure.

Conclusion

Strains of PRRSV vary in virulence.

Clinical Relevance

The effects of PRRSV on reproductive performance are strain dependent and this should be considered in making a tentative diagnosis on the basis of clinical observations. (Am J Vet Res 1996;57:834–839)

Free access
in American Journal of Veterinary Research

Summary

Various procedures of vaccination for Pseudorabies were compared for their effects on shedding, latency, and reactivation of attenuated and virulent Pseudorabies virus. The study included 6 groups: group 1 (10 swine neither vaccinated nor challenge-exposed), group 2 (20 swine not vaccinated, but challenge-exposed), and groups 3 through 6 (10 swine/group, all vaccinated and challenge-exposed). Swine were vaccinated with killed virus im (group 3) or intranasally (group 4), or with live virus im (group 5) or intranasally (group 6). The chronologic order of treatments was as follows: vaccination (week 0), challenge of immunity by oronasal exposure to virulent virus (week 4), biopsy of tonsillar tissue (week 12), treatment with dexamethasone in an attempt to reactivate latent virus (week 15), and necropsy (week 21).

Vaccination im with killed or live virus and vaccination intranasally with live virus mitigated clinical signs and markedly reduced the magnitude and duration of virus shedding after challenge exposure. Abatement of signs and shedding was most pronounced for swine that had been vaccinated intranasally with live virus. All swine, except 4 from group 2 and 1 from group 4, survived challenge exposure. Only vaccination intranasally with live virus was effective in reducing the magnitude and duration of virus shedding after virus reactivation. Vaccination intranasally with killed virus was without measurable effect on immunity.

Of the 55 swine that survived challenge exposure, 54 were shown subsequently to have latent infections by use of dexamethasone-induced virus reactivation, and 53 were shown to have latent infections by use of polymerase chain reaction (pcr) with trigeminal ganglia specimens collected at necropsy. Fewer swine were identified by pcr as having latent infections when other tissues were examined; 20 were identified by testing specimens of olfactory bulbs, 4 by testing tonsil specimens collected at necropsy, and 4 by testing tonsillar biopsy specimens. Eighteen of the 20 specimens of olfactory bulbs and 3 of the 4 tonsil specimens collected at necropsy in which virus was detected by pcr were from swine without detectable virus-neutralizing antibody at the time of challenge exposure. One pig that had been vaccinated intranasally with live virus shed vaccine virus from the nose and virulent virus from the pharynx concurrently after dexamethasone treatment. Evaluation of both viral populations for unique strain characteristics failed to provide evidence of virus recombination.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To examine effects of co-infection with porcine reproductive and respiratory syndrome virus (PRRSV) and Bordetella bronchiseptica in pigs.

Animals—Forty 3-week-old pigs.

Procedure—30 pigs (10 pigs/group) were inoculated with PRRSV, B bronchiseptica, or both. Ten noninoculated pigs were control animals.

Results—Clinical signs, febrile response, and decreased weight gain were most severe in the group inoculated with both organisms. The PRRSV was isolated from all pigs in both groups inoculated with virus. All pigs in both groups that received PRRSV had gross and microscopic lesions consistent with interstitial pneumonia. Bordetella bronchiseptica was cultured from all pigs in both groups inoculated with that bacterium. Colonization of anatomic sites by B bronchiseptica was comparable between both groups. Pigs in the group that received only B bronchiseptica lacked gross or microscopic lung lesions, and B bronchiseptica was not isolated from lung tissue. In the group inoculated with B bronchiseptica and PRRSV, 3 of 5 pigs 10 days after inoculation and 5 of 5 pigs 21 days after inoculation had gross and microscopic lesions consistent with bacterial bronchopneumonia, and B bronchiseptica was isolated from the lungs of 7 of those 10 pigs.

Conclusions and Clinical Relevance—Clinical disease was exacerbated in co-infected pigs, including an increased febrile response, decreased weight gain, and B bronchiseptica-induced pneumonia. Bordetella bronchiseptica and PRRSV may circulate in a herd and cause subclinical infections. Therefore, co-infection with these organisms may cause clinical respiratory tract disease and leave pigs more susceptible to subsequent infection with opportunistic bacteria. (Am J Vet Res 2000;61:892–899)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine effects of intranasal inoculation with porcine reproductive and respiratory syndrome virus (PRRSV) or Bordetella bronchiseptica on challenge with nontoxigenic Pasteurella multocida in pigs.

Animals—Seventy 3-week-old pigs.

Procedure—In experiment 1, pigs were not inoculated (n= 10) or were inoculated with PRRSV (10), P multocida (10), or PRRSV followed by challenge with P multocida (10). In experiment 2, pigs were not inoculated (n = 10) or were inoculated with B bronchiseptica (10) or PRRSV and B bronchiseptica (10); all pigs were challenged with P multocida. Five pigs from each group were necropsied 14 and 21 days after initial inoculations.

ResultsPasteurella multocida was not isolated from tissue specimens of pigs challenged with P multocida alone or after inoculation with PRRSV. However, in pigs challenged after inoculation with B bronchiseptica, P multocida was isolated from specimens of the nasal cavity and tonsil of the soft palate. Number of bacteria isolated increased in pigs challenged after coinoculation with PRRSV and B bronchiseptica, and all 3 agents were isolated from pneumonic lesions in these pigs.

Conclusion and Clinical Relevance—Infection of pigs with B bronchiseptica but not PRRSV prior to challenge with P multocida resulted in colonization of the upper respiratory tract and tonsil of the soft palate with P multocida. Coinfection with PRRSV and B bronchiseptica predisposed pigs to infection of the upper respiratory tract and lung with P multocida. Porcine reproductive and respiratory syndrome virus and B bronchiseptica may interact to adversely affect respiratory tract defense mechanisms, leaving pigs especially vulnerable to infection with secondary agents such as P multocida. (Am J Vet Res 2001; 62:521–525)

Full access
in American Journal of Veterinary Research