The term enzootic pneumonia has commonly been used when referring to a syndrome observed in growing pigs that was characterized by cough, mild-to-moderate loss of appetite, uneven growth rates and a low number of pigs with active signs of pneumonia.
The primary cause of these conditions is Mycoplasmal pneumonia, with secondary bacteria including Pasteurella multocida playing a significant role. A large number of secondary bacteria have been associated with enzootic pneumonia.
Pneumonia Patterns Changed
In recent years, the pattern of respiratory disease in growing pigs has changed in many hog operations. This change coincides with the emergence of new viral diseases such as porcine reproductive and respiratory syndrome (PRRS) virus, porcine circovirus type 2 (PCV) and the new H3N2 strain of swine influenza virus (SIV). Well-known viral infections such as H1N1 SIV and pseudorabies (PRV) remain a problem, when present.
The emergence of viruses plays a role in changing the pattern of respiratory disease. Management practices also have had an impact. Those practices include increasing herd sizes, large numbers of pigs housed in the same air space and the resulting variation in immune status of the pigs.
With the involvement of viruses, the resulting respiratory syndrome is more severe than the disease induced by enzootic pneumonia and has been designated the porcine respiratory disease complex (PRDC).
PRDC, characterized by labored breathing, cough, fever, lethargy, depressed appetite and decreased rate of gain and feed efficiency, is a significant economic problem affecting pork production worldwide.
Many pathogens have been isolated from pigs with PRDC, including SIV, PRRS, PRV, Pasteurella multocida, Actinobacillus suis, Streptococcus suis, Actinobacillus pleuropneumonia, Haemophilus parasuis and mycoplasma. The most common PRDC pathogens isolated from pigs at the Iowa State Diagnostic Laboratory are mycoplasma, PRRS and SIV.
Infection with only mycoplasma induces a mild chronic pneumonia consisting of well-defined, dark-red (acute) to tan-grey (chronic) areas of consolidation in certain regions of the lung. Live pigs infected with mycoplasma exhibit a sporadic cough with little effect on growth performance.
Pasteurella is generally considered an opportunistic bacterial pathogen. It rarely causes pneumonia by itself.
There are three serotypes of pasteurella that are important in pigs.
Dermonecrotic, toxin-producing strains are responsible for atrophic rhinitis, but less is known about strains involved with pneumonia.
Non-toxigenic strains of pasteurella are the most common secondary pathogen isolated from the respiratory tract of pigs with enzootic pneumonia. Pneumonia associated with pasteurellosis typically consists of red-grey cranioventral pneumonia with exudates (oozing materials) in the airways. Pleuritis is occasionally observed.
Growth of pasteurella in the respiratory tract may affect the cilia similar to the impact produced by mycoplasma. This further decreases the ability of the cells to clear bacteria and debris from the airways.
Studies have revealed a significant interaction between mycoplasma and pasteurella. One study determined that mycoplasma predisposed pigs to infection with pasteurella. Pigs infected with both organisms demonstrated increased severity of coughing and had difficulty breathing. No lesions were observed in the lungs of pigs infected with only pasteurella, in contrast to the severe pneumonia observed in pigs infected with both pathogens.
Likewise, the ability to isolate pasteurella changes when pigs are infected with mycoplasma. In one study, pasteurella was not isolated from experimentally infected pigs with the organism at two weeks following inoculation.
In contrast, pasteurella was isolated from three of four pigs infected with both pasteurella and mycoplasma. Similar findings were observed by Purdue University's Sandy Amass, DVM, et al., (1994), where pigs infected with both mycoplasma and pasteurella had significantly more pneumonia and respiratory disease problems than pigs experimentally inoculated with either pathogen alone.
Impact on Viral Disease
Mycoplasma's ability to increase the severity of respiratory disease is not limited to bacterial infections. In a study in our laboratory, mycoplasma increased the duration and severity of pneumonia induced by PRRS virus. Shibata, et al (1998) found that the presence of mycoplasma made pneumonia in pigs co-infected with PRV more severe.
The degree that mycoplasma influences the respiratory disease caused by other organisms varies. A study in our laboratory found that the pneumonia in pigs infected with mycoplasma and SIV was more additive in nature. While disease and pneumonia were more severe and lasted longer when the two were together, the pneumonia did not last as long as observed with joint PRRS and mycoplasma infections.
The mechanism, by which mycoplasma increases the severity of disease, in conjunction with other pathogens, currently is unknown. But, mycoplasma has been shown to have a negative effect on the immune system and causes chronic, long-term pneumonia.
Mycoplasma causes pneumonia by direct damage to the cells of the respiratory system. In addition, it appears to misdirect the responses of the host's immune system. Direct damage to the cells of the respiratory tract occurs when mycoplasma attaches to the cilia of the airway epithelial cells. This results in clumping and loss of cilia. The tiny, hair-like cilia in the respiratory tract work to clear organisms and debris from the lungs and airways. The loss of function of these cilia is thought to be a major contributor to the increased incidence of disease associated with secondary infections, especially pasteurella.
In addition, indirect changes to the immune system of the respiratory tract are a major part of mycoplasma infection. Mycoplasma diminishes the ability of the immune system of the respiratory tract to work efficiently and effectively. When mycoplasma causes chronic inflammation in the lungs, tissue damage occurs, which in turn increases the ability of opportunistic secondary bacteria such as pasteurella to develop and reproduce in the respiratory tract.
Mycoplasma also lessens the ability of white blood cells to clear debris and bacteria from the lungs, further increasing the damage caused by secondary bacterial infections.
While many questions remain about how mycoplasma causes pneumonia, even less is known about how the non-toxigenic strains of pasteurella induce disease.
An additional factor that may be involved in disease induced by pasteurella is lipopolysaccharide (LPS), an endotoxin, that is a component of the bacterial cell wall. LPS may also be an important factor in pasteurella's ability to induce damage by inflammation and disease in the lungs.
Diagnosis of pneumonia caused by either pasteurella or mycoplasma remains challenging. The pneumonic lesions observed with either or both organisms can't be differentiated from most other bacterial pneumonias.
Diagnosis of pneumonia due to pasteurella infection is based on isolation of the organism from affected lung tissues or airways. Antibiotic sensitivity testing is recommended for selection of the appropriate treatment.
Diagnosis of mycoplasma is often based on observation of characteristic lesions and examination of lung tissue. A precise diagnosis with only observable or microscopic examination may be difficult as a number of other pathogens, including SIV, induce similar lesions.
Further testing is commonly undertaken to confirm mycoplasma infection. Culture and isolation of mycoplasma is difficult, labor intensive and takes weeks to complete.
Isolation of mycoplasma is also difficult as other, non-pathogenic mycoplasmas and bacteria commonly overgrow the cultures, further complicating the diagnosis. All of these problems make culture of mycoplasma impractical.
Polymerase chain reaction (PCR) assays are becoming increasingly popular for detection of mycoplasma and are frequently used to aid in strategically placing medication and vaccination programs. Serology is also widely used, although vaccination and the length of time (usually 3-6 weeks) for pigs to seroconvert to mycoplasma often makes it hard to determine the timing of infection.
Control of the respiratory disease induced by mycoplasma and pasteurella is similar to that for all pathogens associated with PRDC. Proper management of production inputs, including environment, nutrition, biosecurity, weaning practices and all-in, all-out pig flow, have proven to be effective if protocols are followed diligently.
Antibiotic therapy also can be used for control of the pneumonia associated with pasteurella. A number of antibiotics are approved for use in the treatment of pasteurella, although antibiotic sensitivity testing is recommended to ensure that the appropriate therapy is used.
Various medication strategies are used to treat mycoplasma with varying degrees of success. There are few antibiotics that are effective against mycoplasma.
Vaccination is a common control method for mycoplasma. Amass, et al. (1994) demonstrated that mycoplasma vaccination decreased the severity of pneumonia in pigs infected with both mycoplasma and pasteurella. Mycoplasma vaccines have been shown to decrease the onset of PRRS-induced pneumonia caused by mycoplasma.
However, vaccination with a modified live virus PRRS vaccine and/or infection with PRRS during and after mycoplasma vaccination greatly reduced the efficacy of the mycoplasma vaccine with respect to mycoplasma-induced lesions. This suggests that vaccine effectiveness can be reduced by the presence of other diseases at the time of vaccination.
Vaccination for pneumonic pasteurellosis is not commonly practiced in the United States, although several products were commonly used from 15 to 25 years ago.
Mycoplasma and pasteurella are important pathogens associated with PRDC. While neither organism is very pathogenic alone, in combination, they increase the severity of pneumonia. Proper management and strategic timing of antibiotic therapy and vaccination are required to control the pneumonia these organisms induce, as well as the other pathogens associated with PRDC.