Mycoplasma hyopneumoniae potentiation of porcine reproductive and respiratory syndrome virus-induced pneumonia

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.

FIG. 1

(a) Normal lungs from an uninfected pig. (b) Lungs from a pig infected 10 days previously with PRRSV. The lungs fail to collapse and are diffusely mottled and tan in appearance. (c) Lungs from a pig infected 28 days previously with M. hyopneumoniae. Lungs have multiple well-demarcated, dark-red areas of pneumonia in the cranioventral region. (d) Lungs from a pig dually infected 28 days previously with PRRSV and M. hyopneumoniae, exhibiting both the characteristic failure to collapse and mottled tan appearance of PRRSV and the well-demarcated, dark-red consolidated areas typical of M. hyopneumoniae.

FIG. 2

(a) Microscopic section of a normal lung from a pig. (b) Microscopic section of a lung from a pig infected 10 days previously with PRRSV. There is moderate diffuse interstitial pneumonia characterized by accumulation of necrotic debris and inflammatory cells in alveolar spaces, septal infiltration by mononuclear cells, and type 2 pneumocyte hypertrophy and hyperplasia. (c) Microscopic section of a lung from a pig infected 28 days previously with M. hyopneumoniae. There is peribronchiolar and perivascular lymphoid hyperplasia characteristic of M. hyopneumoniae infection. (d) Microscopic section of a lung from a pig infected 28 days previously with PRRSV and M. hyopneumoniae. Lesions characteristic of both M. hyopneumoniae- and PRRSV-induced pneumonia are present.