Porcine Respiratory Disease Complex

The vast majority of respiratory problems in grow-finish swine are due to a combination of disease pathogens, hence the name “PRDC” or porcine respiratory disease complex. Some of the more common viral components include Porcine Reproductive and Respiratory Syndrome virus (PRRS), swine influenza virus (SIV), pseudorabies virus (PRV), porcine cirovirus type 2 (PCV II), and porcine respiratory corona virus (PRCV). We can say with confidence PRRS, SIV, and PRV can be major players in swine respiratory disease outbreaks. The rest of the list seems to change as new technologies and better methods of diagnosing disease pathogens become available.

The list of bacterial infections involved in PRDC is quite long. Mycoplasma hyopneumoniae, Pasteurella multocida, Streptococcus suis, Haemophilus parasuis, Actinobacillus pleuropneumoniae, Actinobacillus suis, and Salmonella choleraesuis are some of the more common and all too familiar to some of us. Interestingly enough, most of these bacterial infections, by themselves are not that difficult to treat or even prevent. Put a combination together in an intense management system, and you have a real challenge.

The clinical signs of swine respiratory disease may include: coughing, sneezing, nasal discharge, tear stains under the eyes, lethargic pigs that are often off-feed, have elevated rectal temperatures, and labored breathing. In severe cases cyanosis is seen. This is purple discoloration of the skin due to a lack of oxygen. The tips of the ears, and underline are most commonly affected.

Porcine Reproductive and Respiratory Syndrome

PRRS is caused by an Arterivirus and was first diagnosed in 1987. It has since become a focal point for swine researchers, practitioners and just about everyone involved in pork production. It has forced us to rethink our way of doing things (McRebel) or reconsider old ideas (all-in-all-out, depopulation- repopulation) that were once considered too costly. It has been a real thorn in our side, and in some cases an excuse for things gone wrong. There are considerable differences in virulence between PRRS virus isolates. Some infected herds are devastated while others exhibit minimal clinical signs. The characteristic PRRS virus induced lung lesion is a tan-red mottled (patchy) colored lung that fails to collapse due to interstitial pneumonia. In cases of PRDC, PRRS virus causes damage to the pulmonary macrophages. Macrophages are cell in the bodies immune system that engulf foreign material, break it down, process it, and present it to the immune system so it can further fight off the invasion. Damage and dysfunction of macrophages impairs the pig’s ability to fight off other infections, and increases their susceptibility to diseases caused by secondary bacterial invaders. PRRS virus infections can impair the pig’s ability to respond to vaccines and antibiotics, thus reducing their effectiveness.

Swine Influenza

Swine Influenza is caused by an Orthomyxovirus. There are two primary subtypes in the United States. H1N1 has been in the USA since the 1930’s. In 1998 a second subtype was identified in North Carolina, H3N2. More recently there have been reports of a third subtype made of a combination of the two, H1N2. SIV causes damage to the respiratory epithelium lining the airways. This is why one of the most noticeable clinical signs is a harsh, barking cough. Clinical signs vary depending on the immune status of the affected pigs (maternal immunity or vaccination), and the subtype involved. Acute outbreaks of SIV are characterized by a sudden onset were 80-90% of the pigs have a barking cough, nasal and ocular discharge, high rectal temperatures (105° or higher), labored breathing, are off-feed, and reluctant to move. In most cases, these clinical signs subside in 10 days to 2 weeks. Typically, the percent of unthrifty or cull pigs has increased in that time period. Grossly lungs are wet, heavy, have plum-colored areas of consolidation, and fail to collapse. When you cut through the lung tissue excessive mucus or pus can be seen in the airways. Passive antibody from the sow’s colostrum is generally protective up to 8 to 12 weeks of age. Loss of passive immunity in the absence of piglet vaccine explains why SIV induced disease is most common in pigs 12 to 24 weeks of age.

Mycoplasma Pneumonia

Mycoplasma pneumonia (MPS) or enzootic pneumonia. is caused by a very slow growing bacterium called Mycoplasma hyopneumoniae. It is the most economically significant swine respiratory pathogen (1). This organism adheres to the cilia that line the tracheal and bronchial epthielium. Cilia are microscopic finger like projections that move in a wave-like fashion to help remove dust, debris, and bacteria from the lungs. After adhering, Mycoplasma hyopneumoniae causes the cilia to clump together and eventually fall off. This compromises the ciliary clearance and predisposes the pig’s lung to secondary bacterial infections. MPS by itself produces a mild chronic pneumonia. Affected pigs have a non-productive hacking cough. The cough is most noticeable when you first enter the building and get the pigs up. Mortality is usually low if uncomplicated by other infectious agents, but morbidity can be quite high. “Thumping” respiration is seen only when lung damage is severe or other secondary infections are involved. The characteristic lung lesions associated with MPS are purple to gray areas of consolidation on the cranial (near the trachea) and ventral (lower portions) of the lung lobes. Often the damaged lung has a meaty appearance and is atelectic or collapsed. Atelectic lung looks indented or depressed relative to the adjacent normal lung tissue. The major source of Mycoplasma hyopneumoniae infections comes from carrier pigs. The organism can be isolated from the nasal passage of infected swine, and is spread from pig-to-pig by direct contact with their respiratory secretions. The disease is much more severe when younger pigs are housed in contact with older pigs as occurs in continuous flow systems (2). Virtually all naturally occurring cases of MPS are mixed infections. The secondary bacterial infection most often isolated is Pasteurella multocida.

Pasteurella Pneumonia

Pasteurella pneumonia is caused by Pasteurella multocida a gram-negative bacterium. It can be isolated from the nasal passage of almost any hog (healthy or sick). Experimental infections are very difficult to establish, as healthy pigs tolerate large doses and can effectively clear it from their lungs. This pathogen is not a primary agent of swine pneumonia, yet it is the most common bacteria isolated from pneumonic lungs of slaughter weight swine (3). If diagnostic laboratory reports identifying Pasteurella multocida as the bacteria isolated from lung tissue, understand that another disease agent (although it may be unidentified) is involved. Most likely, that disease agent is Mycoplasma hyopneumoniae.

Conclusion

Hopefully this presentation and accompanying paper has given you a better understanding of the major pathogens currently involved in grow-finish swine respiratory disease in North Carolina. The important thing to remember is that it is in fact a disease complex. Multiple pathogens are involved challenging the pigs ability to fight off any given disease agent.

The real question is “What can we do about it”? In my mind that is a six-step process. The first step is to identify the pathogens or diseases involved. This is accomplished by a combination of history, clinical signs, and laboratory diagnostics. There are several diagnostic tools available. Consult your veterinarian or the laboratory that you will be submitting samples to insure that you: select the right pigs, collect the correct samples, preserve and submit samples so you can get the most for your money.

Step two – Consider how the disease is transmitted. Are there biosecurity measures you can take to reduce the spread of disease? Are you increasing the viral or bacterial load with high stocking densities, humidity, poor air quality, sanitation, or excessive fluctuations in environmental temperatures?

Step three – Develop a plan of action. There are several things to consider in this process. Before implementing a vaccine program, you need to determine the level of maternal antibody. When do maternal antibodies decline to a low enough level for vaccines to be affective? What is the PRRS status of these pigs? Dr. Eileen Thacker has shown that vaccination with a modified live vaccine or infection with PRRS virus during or following vaccination with a mycoplasma vaccine appears to decrease mycoplasma vaccine efficacy (4). When is the timing of infection? Do pigs have sufficient time to respond to vaccine before being challenged? What is the duration of immunity? Will one or two doses of vaccine protect pigs all the way to market? Are preventative antibiotics given at the time of disease transmission a better alternative?

Step four – Implement your plan in such a way that the results can be measured. This sounds easy, but in fact can be quite difficult to accomplish. Most systems have are plagued with a high degree of normal variation. Statistical analysis and multiple replications will be necessary to determine true change.

Step five – Monitor results. Charting performance trends and statistical process control are useful tools for monitoring change over time.