title: Porcine reproductive and respiratory syndrome: NEB-1 PRRSV infection did not potentiate bacterial pathogens.
abstract: A 2-phase study was conducted to evaluate the ability of the NEB-1 strain of porcine reproductive and respiratory syndrome virus (PRRSV) to potentiate common bacterial pathogens of swine. In phase I, 25 of 50 4-5-week-old specific-pathogen-free (SPF) pigs were exposed to NEB-1 PRRSV (day 0). Seven days after virus inoculation, 8 groups received 1 of 4 bacterial pathogens: Haemophilus parasuis, Streptococcus suis, Salmonella cholerasuis, and Pasteurella multocida. The ability of NEB-1 PRRSV to produce clinical disease, viremia, neutralizing antibody, gross and microscopic lesions and to potentiate bacterial pathogens was assessed. Response to NEB-1 PRRSV was similar among inoculated pigs; prolonged hyperthermia, lethargy, mild to moderate dyspnea, and cutaneous erythema were consistent clinical signs. No clinical differences were observed in groups after bacterial challenge. Virus was isolated from serum at weekly intervals through the end of the study, and all PRRSV-inoculated pigs had seroconverted by study termination. Two of 5 pigs died in non-PRRSV-inoculated groups challenged with H. parasuis and Streptococcus suis. Mortality in PRRSV-infected pigs was limited to 1 of 5 pigs from the Salmonella cholerasuis-challenged group. Gross lesions were seen in pigs dying after inoculation in H. parasuis- and Streptococcus suis-inoculated groups, in Salmonella cholerasuis- and P. multocida-challenged pigs, and in 1 non-PRRSV-inoculated control pig. Microscopic lesions consisted of mild to moderate proliferative interstitial pneumonia, nonsuppurative myocarditis, lymphoid hyperplasia, and nonsuppurative encephalitis in PRRSV-inoculated pigs. Findings in phase I indicated that NEB-1 PRRSV does not potentiate bacterial disease while inducing consistent clinical signs, viremia, seroconversion, and microscopic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Veterinary Diagnostic Center, University of Nebraska, Lincoln 68583-0907, USA.
authors.forename: V L
authors.initials: VL
authors.lastname: Cooper
authors.forename: A R
authors.initials: AR
authors.lastname: Doster
authors.forename: R A
authors.initials: RA
authors.lastname: Hesse
authors.forename: N B
authors.initials: NB
authors.lastname: Harris
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000150:complications / Q000662:veterinary*; D005260:Female; D005831:Genital Diseases, Female / Q000150:complications / Q000662:veterinary* / Q000821:virology; D005832:Genital Diseases, Male / Q000150:complications / Q000662:veterinary / Q000821:virology; D006192:Haemophilus Infections / Q000150:complications / Q000662:veterinary; D008297:Male; D010326:Pasteurella Infections / Q000150:complications / Q000662:veterinary; D016979:Pasteurella multocida; D012141:Respiratory Tract Infections / Q000150:complications / Q000662:veterinary* / Q000821:virology; D012481:Salmonella Infections, Animal / Q000150:complications; D013290:Streptococcal Infections / Q000150:complications / Q000662:veterinary; D017011:Streptococcus suis; D013552:Swine; D013553:Swine Diseases; D013577:Syndrome; D014035:Togaviridae / Q000472:pathogenicity*; D014036:Togaviridae Infections / Q000150:complications / Q000662:veterinary*