Key Messages

• In-vivo studies were conducted in piglets infected with PRRSv and/or Mycoplasma hyopneumoniae at different times. Clinical and pathological effects were compared.
• This paper demonstrates a potentiating (in vivo) effect of a viral and mycoplasma infection in pigs.
• Pigs infected with M. hyopneumoniae and PRRSV had more severe clinical disease than the one infected with only one agent.

Article Brief

One hundred forty PRRSV- and Mycoplasma-free piglets were selected, and around six weeks of age were inoculated with the two agents at the same time or one before the other. Also, three groups of piglets were only infected with PRRS, Mycoplasma or left as uninfected controls.

Also, three groups of piglets were only infected with PRRS, Mycoplasma or left as uninfected controls.

Clinical signs in piglets were daily evaluated: appetite, cough, respiration rate, or behavioural changes. And piglets were necropsied on days 3, 10 or 28.

Pigs infected with PRRSV showed pneumonia on day 3 post-infection, but it was well developed when had been infected with PRRSV 13 days before necropsy.

The group that was inoculated with M. hyopneumoniae 21 days prior to PRRSV inoculation developed more severe respiratory disease as well as more severe PRRSV interstitial pneumonia than any other group only infected with PRRSV.

Even when M. hyopneumoniae did not induce observable lesions, the viral pneumonia was potentiated. Specifically, pigs, which had received M. hyopneumoniae 21 days before PRRSV inoculation, had a low level of mycoplasmal pneumonia but their PRRSV lesions lasted for four weeks after inoculation. On the other hand, PRRSV lesions resolved by four weeks post-inoculation in the group only infected with PRRSV.

The presence of PRRSV early in infection with M. hyopneumoniae increases the rate of mycoplasmal pneumonia and the damage induced at cellular level but does not increase the percentage of macroscopic pneumonia. Piglets infected with both M. hyopneumoniae and PRRSV had higher percentages of pneumonic lung lesions due to M. hyopneumoniae and more severe microscopic lesions consistent with M. hyopneumoniae than in M. hyopneumoniae-only group.

It is suggested that the increased severity and duration of pneumonia is not due to increased PRRSV or M. hyopneumoniae replication however, the specific cellular and subcellular mechanisms by which M. hyopneumoniae potentiates PRRSV are currently unknown.

The most commonly proposed hypothesis is that PRRSV is the primary pathogen and bacteria are secondarily involved in the pathogenesis of PRDC. Moreover, in the study reported here, also the infection with M. hyopneumoniae potentiates and prolongs PRRSV pneumonia clinically, macroscopically and microscopically.

Clinical scores

Macroscopic pneumonia lesions

Microscopic lesion scores

Reference

Thacker, E.L., P.G. Halbur, R.F. Ross, R. Thanawongnuwech and B.J. Thacker. 1999. Mycoplasma hyopneumoniae potentiation of porcine peproductive and respiratory syndrome virus-induced pneumonia. J. Clin. Microbiol. 37:620–627.

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July 2015