Ranking the big three in Porcine Respiratory Disease Complex (PRDC) has been easy: PRRS (Porcine Reproductive and Respiratory Syndrome), mycoplasmal pneumonia and swine influenza virus (SIV).
That ranking has been virtually undisputed since PRDC was identified a few years ago as the cause of grow-finish respiratory stall-out, some refer to as the "18- to 20-week wall."
Now comes new evidence which seems to indicate mycoplasmal pneumonia is the chief agitator in PRDC, not PRRS.
The Surprise Leader It's no secret that PRRS and mycoplasma add up to a serious dual infection in pigs. The assumption is PRRS virus always comes first, stirring things up, leaving the pig's immune system open to secondary bacteria, led by mycoplasmal pneumonia. Often coming next is SIV, followed by a large cast of minor diseases.
Surprisingly, however, the order of the top two in importance may be reversed.
"Classically, we were taught that viruses cause immune suppression and then the bacteria are secondary invaders," says Eileen Thacker, DVM, associate scientist at Iowa State University's (ISU) Veterinary Medical Research Institute (VMRI).
"But what our trials are showing is that it was the mycoplasma that was making the viral condition worse," she says. That is, mycoplasma causes PRRS-induced pneumonia to worsen.
Thacker says this revelation suggests the control of mycoplasma infection may be important in decreasing the impact of PRRS virus-induced pneumonia and, ultimately, PRDC.
In a study reported at the International Pig Veterinary Society annual meeting in Birmingham, England, Thacker compared seven groups of 20, two-week-old pigs. Groups were infected with mycoplasma 21 days prior to, concurrent with, or 10 days following administration of PRRS virus. Control groups received one or the other of the organisms or nothing. Pigs were then necropsied, 3, 10 and 28 days after they were experimentally infected to check the lungs for infection and lesions from mycoplasma and PRRS.
Without exception, Thacker reports that all pigs infected with PRRS and mycoplasma experienced more severe clinical respiratory disease than those pigs only infected with one or the other of the respiratory organisms.
At necropsy, PRRS-induced pneumonia showed up in PRRS-infected pigs three days after infection. Mycoplasma-induced pneumonia was evident 10 days after infection. At 28 days post-infection, all of the dual-infected pigs continued to show signs of PRRS-induced pneumonia. Only two of eight pigs given PRRS virus alone showed signs of PRRS-induced pneumonia at 28 days post-infection, says Thacker. Mycoplasma-induced pneumonia was similar in all age groups of pigs infected with mycoplasma alone, regardless of the PRRS virus infection status.
At 10 days post-infection, microscopic lesions in the lung indicative of mycoplasma were more severe in the dual-infected group. By 28 days after experimental infection, lesions from both mycoplasma and PRRS were more severe in the jointly infected pigs, compared to pigs given a single organism.
According to Thacker, mycoplasma increased the severity of PRRS-induced pneumonia regardless of the order of infection, whether mycoplasma or PRRS was given first to the pigs.
Also, PRRS-linked pneumonia increased in severity even when the mycoplasma infection was very mild, Thacker points out.
"This experimental challenge model demonstrates that mycoplasma acts as a co-factor in potentiating or augmenting PRRS-induced pneumonia," she states. The fact that mycoplasma made PRRS pneumonia worse was documented clinically, macroscopically and microscopically.
Most telling is that all pigs in all of the groups infected with both mycoplasma and PRRS experienced more severe pneumonic lesions caused by PRRS.
Because there wasn't an increase in levels of either mycoplasma or PRRS virus levels in the dual-infected pigs, it suggests that the increased severity and duration of PRRS-induced pneumonia may not be due to an increase in either of the pathogens, according to ISU's Thacker.
"Rather, we propose that the chronic inflammatory response induced by mycoplasma may be important in the potentiation of PRRS-induced pneumonia," declares Thacker.
Mycoplasma Is Elusive PRRS is a tough organism to control because it mutates so easily. But mycoplasmal pneumonia is tough from several aspects.
It is tough to see in the live pig because the infection takes weeks to develop and provides few signs of infection other than a nagging cough. On slaughter check, most if not all of the lung lesions may have resolved.
The bacteria is extremely tough to grow in culture in the laboratory, and by the time you have cultured them, they may well have changed and lost some of their virulence, explains Thacker. Also, the mechanism by which mycoplasmal pneumonia produces an infection in the pig is unknown. A laboratory study is being developed to mimic infection by growing cells in culture and adding mycoplasma to them, she points out.
For Thacker's trials at VMRI's research facilities at Ames, IA, specific-pathogen-free pigs are purchased and then are experimentally infected. In the fie ld, the dual infection of mycoplasma and PRRS doesn't produce dramatic outward results, but drags down performance and drags out the infection because protective antibodies wane at different times, leaving different groups of pigs susceptible at different periods of time.
The most noticeable signs of the dual infection in Thacker's research groups include that of poor-doing pigs that are gaunt, have great difficulty breathing and don't eat much. Stress them or attempt to move them and breathing becomes very labored.
Of course, points out Thacker, most commercial grow-finish hogs carry around more than just those two organisms. They become infected with a host of viral and bacterial infections that interact, which have been known to kill 100-lb. pigs. Those that survive perform very poorly.
Thacker suggests that this deadly interaction is the result of the development of the PRRS virus, increased concentration of pork production and poor environment as hog buildings in the industry age.
But Thacker's research suggests the key ingredient in the PRDC mix may be mycoplasma.
If your grow-finish herd is performing poorly and you'd like to have it checked, select a group of 120-pounders and deliver them live to a diagnostic laboratory. She stresses the hogs must arrive alive in order to culture them for mycoplasma.
Vaccination Precautions Mycoplasmal pneumonia vaccines don't protect herds from infection, just the expression of clinical signs; they often help restore grow-finish performance, says Thacker, an immunologist.
However, vaccination failure in the field is frequently observed even though studies conducted at ISU by Thacker have found vaccines to be very effective against experimental challenge.
Most commercial mycoplasma vaccines are labeled for administration at 1 and 3 weeks of age in piglets. The problem is that research has shown that the presence of passive immunity at those recommended times of vaccination can reduce vaccine effectiveness, according to co-investigator Brad Thacker, DVM, also of ISU's VMRI. Pat Halbur, DVM, ISU Diagnostic Laboratory collaborated.
In a presentation at the IPVS meeting in England, Brad Thacker explained that his research protocol for the vaccination trial consisted of vaccinating sows twice, at 5 and 2 weeks before farrowing. Pigs from those litters were allotted to three groups. Group 1 was vaccinated at 11-15 and 25-29 days of age. Group 2 was vaccinated at 25-29 days and 39-43 days of age. Group 3 pigs were not vaccinated and served as controls.
It appears that the amount of antibody produced by vaccination was reduced when pigs had passive immunity at the time of vaccination, he concludes. These results have been confirmed in a follow-up study.
Some producers are compensating for this dilemma by changing the times they vaccinate their pigs for mycoplasma, says Eileen Thacker. There are many time options, but she says a number of producers she has consulted with are switching to vaccination of pigs when they leave the nursery and giving the second shot when they leave the grower.
To determine the best time to vaccinate, producers should blood-test their pigs. Because the duration of maternal antibodies varies from farm to farm, she recommends producers bleed a group of 30, 2-4-week-old piglets from across several parities of sows to find out what kind of passive immunity there is in your individual herd.
If producers keep in tune with industry trends and turn over their sow herd at a clip of 40% or more, their sow herd will be very young. This means that maternal antibody levels will be much higher because the females are closer to vaccination and closer to infection.
Old sows, on the other hand, will actually go seronegative. "They still have the mycoplasma, it's just that the protective levels of antibodies are virtually gone, so their pigs may not have any maternal antibodies, or they will be very low," observes Eileen Thacker.
A herd profile helps make an educated guess of what would probably be the best time to vaccinate pigs for mycoplasma. She advises the first vaccination should probably be given just before maternal antibodies wane and the second given 2-4 weeks later.
Because of the rise in severity of mycoplasmal pneumonia, she theorizes that the industry will need to develop better vaccines that more directly target the local site of infection in lung tissues.
"But I have the feeling that in order to manage mycoplasmal pneumonia, ultimately, it will probably take both vaccine and antibiotic therapies, strategically placed," she comments.
Current injectable vaccines for mycoplasma are bacterins, developed by killing the organism and reformulating it into a product that can be administered either subcutaneously or intramuscularly, says Eileen Thacker.
What's needed is the development of a vaccine that can protect against the stronger challenge presented by today's mycoplasma, while not overwhelming the pig, she asserts.
But even before that is achieved, Eileen Thacker is already planning to do research on the other important co-infection pair in PRDC - mycoplasma and SIV.