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National Hog Farmer

Mycoplasma Vaccine Failures Suspected

Mycoplasma Vaccine Failures Suspected
Infection of the pig by the tiny bacteria, Mycoplasma pneumonia, has been a problem for years. The bacteria teams up with other pathogens, especially porcine reproductive and respiratory syndrome (PRRS) virus or swine influenza virus (SIV), to wreak havoc in the lungs of pigs.

Infection of the pig by the tiny bacteria, Mycoplasma pneumonia, has been a problem for years. The bacteria teams up with other pathogens, especially porcine reproductive and respiratory syndrome (PRRS) virus or swine influenza virus (SIV), to wreak havoc in the lungs of pigs.

We have successfully created and maintained myco­plasma-negative herds, but this status is difficult to retain in commercial production, especially in pig-dense areas.

In our practice, I would estimate over 90% of commercial production to be infected with mycoplasma. Advancements in vaccine technology and elimination or control of other pathogens have allowed mycoplasma control to be a reality.

However, I have recently struggled with cases of apparent mycoplasma vaccine failure in late finishing.

Case Study No. 1

A 5,000-sow unit weans 2,400 pigs/week into multiple nursery-finish sites. The herd is positive for PRRS and mycoplasma. Piglets are vaccinated for circovirus and mycoplasma at 2 weeks of age and again at 5 weeks of age. Normally, the herd experiences mild respiratory signs when the pigs are 100-120 lb. in early finishing attributed to mycoplasma.

Early this summer, pigs had respiratory distress with a slight increase in mortality in late finishing (within 30 days of marketing). Diagnostics revealed mycoplasma and PRRS virus. Finishing mortality increased, growth rate declined and market weights dropped precipitously.

Case Study No. 2

A producer receives 750 weaned, single-source pigs every eight weeks. The sow herd is PRRS-negative, but positive for mycoplasma. Piglets weigh 15-16 lb. at weaning and nursery mortality is less than 2%. Piglets are vaccinated for circovirus, erysipelas and mycoplasma at 2 and 5 weeks of age.

Prior to this summer, finishing mortality was less than 3%, and pigs finished out in a 24-week turn averaging more than 280 lb. The last two turns saw coughing in late finishing and lighter market weights. Diagnostic sampling revealed the pigs were still PRRS-negative and SIV-negative, but had mycoplasma lesions.

In both case studies, a clinical diagnosis of mycoplasma infection was made by gross lesions on postmortem, histopathology and testing by polymerase chain reaction (PCR). Vaccination protocols were reviewed. Vaccine usage and inventories were checked to be sure vaccines were actually given. To the best of our knowledge, the pigs were vaccinated according to protocol.

Both producers were frustrated because they felt that Mycoplasma pneumonia should not be an issue with vaccinated pigs, especially when given two doses. We felt that the protocols were appropriate as the piglets should be immunocompetent by 2 weeks of age.

Research data suggests that vaccinating a 2-week-old piglet should work and not be blocked by maternal immunity from the sow. The flip side is whether piglets were being exposed to the pathogen before they had time to develop immunity for the vaccine.

In both cases, we felt that the pigs were not being challenged with mycoplasma in the nursery and should respond to the vaccine before exposure in the finisher.

The operation in the first case study has the distinct disadvantage of having a PRRS-infected herd. It is well documented that PRRS virus interferes with the pig’s ability to not only defend itself in the face of infection but also respond to an intended infection, such as the ones we purposely introduce in the form of vaccine.

We wondered if the PRRS virus was interfering with the pig’s ability to mount an immune response to the mycoplasma vaccine in the nursery phase. The piglets were known to be infected with PRRS virus in the nursery. Did the pigs never respond to the mycoplasma vaccine in the first place, or was the PRRS virus infection just allowing the late-finishing mycoplasma to cause more of a clinical problem than usual?

The second case study counters the theory that PRRS virus might be the culprit because this system is PRRS negative. It appears there is vaccine failure or a vaccine duration of immunity (DOI) issue.


The outcome of these clinical cases is still pending. In the current pig market, we must put a pencil to all options:

  • Add a mycoplasma vaccine booster to increase DOI for protection all the way to market. This adds significant costs.
  • Medicate pigs to prevent losses at the time of clinical infection. However, these infections are occurring during late finishing, not a time to treat pigs, given cost and withdrawal considerations.
  • Try different vaccines to see if another one works better in that particular herd.
  • Depopulate/repopulate the herd to eliminate both PRRS and mycoplasma.
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