Mycoplasmal pneumonia is a chronic, clinically mild, infectious pneumonia of pigs, characterized by its ability to become endemic in a herd and to produce a persistent dry cough, retarded growth rate, sporadic “flare-ups” of overt respiratory distress, and a high incidence of lung lesions in slaughter pigs. It occurs worldwide.
Clinical outbreaks of mycoplasmal pneumonia may impair growth rate and feed conversion. This effect is enhanced when large numbers of pigs are closely confined in poorly ventilated buildings under poor husbandry conditions. The effects of the disease are uneven and unpredictable and place limits on the efficiency and flexibility of large production units. However, in swine units with good disease control measures, mycoplasmal pneumonia may remain largely subclinical and is of little economic importance.
Etiology and Epidemiology
The terms “viral pneumonia” and “enzootic pneumonia” are frequently used to describe a characteristic disease syndrome now known to be caused primarily by Mycoplasma hyopneumoniae. The pleomorphic organism is fastidious, smaller than most bacteria, and difficult to see clearly under ordinary light microscopes. It can be cultured in specially prepared media, but isolation from field cases is difficult. It is rapidly inactivated in the environment and by disinfectants, but it may survive longer in cold weather. It appears to be host-specific.
Mycoplasmal pneumonia is also frequently complicated by other mycoplasmas, bacteria, and viruses, which affect the severity of the disease. Certain strains of M hyorhinis, and perhaps some viruses, may themselves act as primary agents to produce a syndrome resembling the pneumonia caused by M hyopneumoniae.
In most countries that use modern pig-farming methods, the lungs of 30–80% of the pigs slaughtered show pneumonic lesions of the type associated with mycoplasmal infection. Pigs of all ages are susceptible, but within a herd, pigs become infected in the first few weeks of life either by their dam or by other young pigs after mixing. Transmission to lactating piglets can occur from sows of all parities but is most prevalent in first-parity (gilt) litters. In addition, with the adaptation of segregated (multisite) production, the onset of the disease has been delayed and may be most evident in the finishing stage at ~18–20 wk of age. The incidence of lung lesions is highest in pigs 3–5 mo old. Immunity develops slowly, followed by regression of the lung lesions. Older growing and mature pigs may recover completely.
In herds in which the disease is endemic, morbidity is high, but clinical signs may be minimal and mortality is low. Coughing is the most common sign and is most obvious when pigs are roused. Individual pigs or groups sporadically develop severe pneumonia. A common predisposing factor is a change of weather, but other stresses (eg, transient viral infections, parasitic migration, and mixing pigs) may also cause outbreaks. The disease is usually more severe when it first enters a naive herd.
Affected lungs are gray or purple, most commonly in the apical and cardiac lobes. Old lesions become clearly demarcated. The associated lymph nodes may be enlarged. Histologically, inflammatory cells are present in the bronchioles; there is perivascular and peribronchiolar cuffing and extensive lymphoid hyperplasia.
Clinical, pathologic, and epidemiologic findings are usually adequate for diagnosis. M hyopneumoniae can be demonstrated in impression smears of the cut surface of the affected lung, identified by fluorescent antibody technique, and sometimes isolated and identified in culture. Serologic tests, principally the complement fixation test, and ELISA are occasionally used on a herd basis, but results may be difficult to interpret. Recently, a PCR test for the detection of M hyopneumoniae from nasal swabs has been developed and appears to be very sensitive and specific.
When the disease first enters a herd, mass treatment with antibiotics (eg, tylosin, lincomycin, tiamulin, or a tetracycline) helps to control the severity of signs. When disease increases in endemic herds, treatment of individual pigs with antibiotics usually results in remission, presumably by controlling secondary bacteria.
Inactivated mycoplasmal cultures have been developed as bacterins and consist of whole-cell preparations as well as new subunit bacterins. These induce excellent protection against the development of gross lesions and significantly reduce clinical signs (coughing) in growing pigs. Recent data indicate that prefarrowing vaccination of sows with M hyopneumoniae vaccines significantly reduces colonization of suckling piglets.
The economic effects of the disease can be reduced, and sometimes eliminated, by improvements in housing and husbandry, particularly ventilation and overcrowding, along with medication and vaccination. “All-in/all-out” management of pigs from birth to market is extremely effective at reducing negative effects of disease; following this practice improves growth performance and reduces lung lesions.
In large intensive units, starting with foundation stock free of mycoplasmal pneumonia and adopting strict precautions against direct and indirect contact with pigs from other herds is advisable. Unfortunately, many herds set up in this way do not remain free of mycoplasmas for very long, particularly in areas with a high density of pigs. Field observations suggest that infection can be windborne for at least a mile between large herds in cold, wet weather.
In the USA and parts of Europe, most herds free of mycoplasmal pneumonia were established by the pig repopulation technique. More recently, some have been established by segregated early weaning. The biggest problems with these herd programs are the breakdown rate and the difficulty of monitoring herds that claim to be free of mycoplasmal pneumonia. Current hypotheses for these outbreaks suggest that the organism may never have been successfully eliminated in certain herds; rather, it coexisted within the population at an undetectable level for extended periods. Use of nasal swab PCR technology has demonstrated the presence of the organism in pigs free of clinical signs, lesions, and antibodies. Analysis of tracheal sections from these pigs by electron microscopy has indicated the presence of the organism on the cilia.
Last full review/revision March 2012 by Scott A. Dee, DVM, MS, PhD, DACVM