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Open AccessJournal ArticleDOI

Mycoplasma hyopneumoniae Potentiation of Porcine Reproductive and Respiratory Syndrome Virus-Induced Pneumonia

TLDR
Results indicate that M. hyopneumoniae infection potentiates PRRSV-induced disease and lesions, which is important with respect to the control of respiratory disease in pigs and has implications in elucidating the potential contribution of mycoplasmas in the pathogenesis of viral infections of other species, including humans.
Abstract
An experimental model that demonstrates a mycoplasma species acting to potentiate a viral pneumonia was developed. Mycoplasma hyopneumoniae, which produces a chronic, lymphohistiocytic bronchopneumonia in pigs, was found to potentiate the severity and the duration of a virus-induced pneumonia in pigs. Pigs were inoculated with M. hyopneumoniae 21 days prior to, simultaneously with, or 10 days after inoculation with porcine reproductive and respiratory syndrome virus (PRRSV), which induces an acute interstitial pneumonia in pigs. PRRSV-induced clinical respiratory disease and macroscopic and microscopic pneumonic lesions were more severe and persistent in M. hyopneumoniae-infected pigs. At 28 or 38 days after PRRSV inoculation, M. hyopneumoniae-infected pigs still exhibited lesions typical of PRRSV-induced pneumonia, whereas the lungs of pigs which had received only PRRSV were essentially normal. On the basis of macroscopic lung lesions, it appears that PRRSV infection did not influence the severity of M. hyopneumoniae infection, although microscopic lesions typical of M. hyopneumoniae were more severe in PRRSV-infected pigs. These results indicate that M. hyopneumoniae infection potentiates PRRSV-induced disease and lesions. Most importantly, M. hyopneumoniae-infected pigs with minimal to nondetectable mycoplasmal pneumonia lesions manifested significantly increased PRRSV-induced pneumonia lesions compared to pigs infected with PRRSV only. This discovery is important with respect to the control of respiratory disease in pigs and has implications in elucidating the potential contribution of mycoplasmas in the pathogenesis of viral infections of other species, including humans.

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Citations
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Journal ArticleDOI

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV): Pathogenesis and Interaction with the Immune System.

TL;DR: This review addresses important issues of porcine reproductive and respiratory syndrome virus infection, immunity, pathogenesis, and control, with a special focus on immune factors that modulate PRRSV infections during the acute and chronic/persistent disease phases.
Journal ArticleDOI

Control of Mycoplasma hyopneumoniae infections in pigs.

TL;DR: The main effects of vaccination include less clinical symptoms, lung lesions and medication use, and improved performance, however, bacterins provide only partial protection and do not prevent colonization of the organism.
Journal ArticleDOI

Experimental reproduction of postweaning multisystemic wasting syndrome in pigs by dual infection with Mycoplasma hyopneumoniae and porcine circovirus type 2.

TL;DR: This study indicates that M. hyopneumoniae potentiates the severity of PCV2-associated lung and lymphoid lesions, increases the amount and prolongs the presence of PCv2-antigen, and increases the incidence of PMWS in pigs.
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Polymicrobial respiratory disease in pigs

TL;DR: This review discusses the latest findings on polymicrobial respiratory disease in pigs and recommends best practices for control of swine respiratory disease outbreaks caused by concurrent infection of two or more pathogens.
Journal ArticleDOI

The Genome Sequence of Mycoplasma hyopneumoniae Strain 232, the Agent of Swine Mycoplasmosis

TL;DR: The complete genome sequence of Mycoplasma hyopneumoniae, an important member of the porcine respiratory disease complex, is presented, finding few genes with tandem repeat sequences that could be involved in phase switching or antigenic variation and it is not clear how M. hyop pneumoniae evades the immune response and establishes a chronic infection.
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Journal ArticleDOI

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