Mycoplasmal Pneumonia (Enzootic Pneumonia)

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A widespread, chronic respiratory disease of swine characterized by coughing, growth retardation and reduced feed efficiency.


Mycoplasmal pneumonia of swine (MPS, also referred to as “enzootic pneumonia,” EP) is a common, widely distributed disease that occurs throughout the year. It is restricted to swine and occurs in all major swine-raising countries. MPS often is more apparent in chronic form on premises where there is continuous flow production and management, and where husbandry and environmental conditions are poor. MPS may cause fairly acute and severe disease in immunologically naïve pigs in age-segregated systems. It may affect pigs early after weaning, when passive immunity has waned, but more commonly occurs in grower and finisher (80-200 lbs) stages. Mycoplasmal pneumonia often interacts with and contributes to other respiratory diseases and is considered to have a central role in porcine respiratory disease complex (PRDC). Secondary bacterial infections are common.

Historical information

Chronic pneumonia in swine, part of which probably was MPS, has been recognized for about a century. MPS was once believed to be caused by a virus and was misnamed “virus pig pneumonia.” Clear separation of MPS from swine influenza and recognition of it as a specific disease began in 1948. MPS was first reproduced experimentally in the United States and England in 1965. Subsequently, it was reported in most major swine-raising countries. MPS is now recognized as a very costly, widespread disease of swine, largely because of its negative effects on growth rate and feed efficiency, and its role in PRDC.


Mycoplasma hyopneumoniae, the etiologic agent, is difficult to isolate and grows slowly in the laboratory. It is small, filterable, survives only a short time in swine housing environments and can be destroyed by most disinfectants. Mycoplasma hyopneumoniae is frequently found in association with other respiratory pathogens, including viruses and bacteria, and is then sometimes termed “porcine respiratory disease complex” (PRDC). In pigs with pneumonia, it may be difficult to determine which agent is the primary pathogen. Evidence suggests that M. hyopneumoniae increases the severity of several other infections, including porcine reproductive and respiratory syndrome (PRRS) and influenza, and is capable of acting as a significant primary pathogen on its own.

Two other pathogenic mycoplasmas are recognized in swine. Mycoplasma hyosynoviae is a sporadic cause of epidemic synovitis in growing swine. Mycoplasma hyorhinis infection is common in swine and it is reported to cause fibrinous polyserositis in young pigs but actual disease attributable to this agent is sporadic.


Carrier swine are the most common source of infection. Since M. hyopneumoniae does not survive for long in the environment, carriers are essential for its maintenance in populations. The organism persists for months in the lungs of infected pigs, including young breeding stock. There is no evidence to implicate infection or carriage in other species. Pigs are infected by M. hyopneumoniae transmitted from dams, cohorts, or exposure to other, usually older, pigs. The organism can be frequently isolated from nasal secretions so transmission by nose-to-nose contact and coughing are likely. The organisms also appears to be transmitted by aerosol; empirical evidence suggests that aerosol spread can occur over several miles. A mycoplasma-free status of a herd can be difficult to maintain.


Mycoplasma hyopneumoniae can be observed microscopically on ciliary epithelium of trachea, bronchi and bronchioles. Distribution of pulmonary lesions suggests bronchogenic distribution with settling of exudate cranioventrally because of compromised mucociliary apparatus. Virulence factors derived from M. hyopneumoniae outer membrane proteins damage several respiratory defense mechanisms and facilitate infection. The cell membrane presents a mosaic of epitopes that camouflage protective antigens, rendering immune response inefficient. Poor air quality (dust or noxious gases) can irritate airways and increase susceptibility.

The initial lesions are bronchitis and bronchiolitis. There is hyperplasia of mucus secreting cells in the mucosa and a loss of cilia from many epithelial cells of airways. The inflammatory reaction spreads into surrounding alveoli causing alveolitis, pneumonia, airway obstruction, and atelectasis. Over time there is a marked hyperplasia of lymphoid tissue around airways and adjacent blood vessels. Increased mucus in airways, ciliostasis, and pressure of surrounding lymphoid tissue interfere with the lung clearance of mucus and exudate. Secondary bacterial infections contribute substantially and are the usual cause of severe pneumonia and deaths.

Clinical signs

The principal clinical sign is chronic, persistent, nonproductive cough. Onset often occurs about two to three weeks after exposure and usually is gradual in a herd. Coughing may persist for weeks to months. Excessive dust, irritating gases, or concurrent infections result in more severe coughing. As pneumonia develops in some pigs, dyspnea becomes more marked. Growth is retarded and feed efficiency decreases in the face of near-normal appetites. Morbidity is high and mortality is low.


In affected pigs, pneumonic lesions are predominantly well demarcated and cranioventral, involving apical, intermediate, and cardiac lobes but extend into diaphragmatic lobes in severe cases. Chronic lesions usually are reduced in volume (atelectic) and dark gray. More recent lesions tend to be reddish brown or a lighter gray, with edema, mucus, and inflammatory cells apparent in the airways. Raised areas adjacent to pneumonic areas often are emphysematous and lighter pink than normal lung. On cut surface of pneumonic areas, mucopurulent exudate often can be squeezed from airways. Secondary infection with other respiratory pathogens is common and may modify the appearance of mycoplasma-initiated lesions.

Typical microscopic lesions, although not pathognomonic, reveal lymphohistiocytic peribronchiolar cuffing, mucocellular exudates, and atelectasis.

Neither gross nor microscopic lesions are pathognomonic for M. hyopneumoniae. Cranioventral or bronchogenic, clearly demarcated consolidation of lungs is a characteristic of bacterial bronchopneumonia and is not always associated with the presence of M. hyopneumoniae.


History, signs, gross and microscopic lesions are suggestive of M. hyopneumoniae but laboratory assistance is needed for accurate diagnostic confirmation. Isolation is slow, laborious, difficult and generally not routinely available. Identification of the agent in lung samples taken at necropsy is possible using fluorescent antibody, immunohistochemical, or polymerase chain reaction (PCR) techniques. Serologic tests including complement fixation and enzyme-linked immunosorbent assay (ELISA) tests can be useful on a herd basis but interpretation must be made with care and knowledge of the herd, individuals sampled, and vaccination status.

Tests on individual animals have little value because many pigs without active disease have antibodies to M. hyopneumoniae or other cross-reacting mycoplasmas. Antibody levels develop slowly in many infected animals. A recently developed, nested PCR test on nasal or lung swabs collected from live pigs permits earlier, more accurate diagnosis of infection. Detection of the organism by PCR confirms the presence of the organism but does not confirm its role in disease.

A careful study of lung lesions at slaughter by one familiar with gross lesions of MPS can be of value in determining prevalence and evaluating progress toward control. However, many gross lesions heal by the time that pigs reach market weight and other bacterial pneumonias may mimic the gross lesions of M. hyopneumoniae. For differential diagnosis, see the table, Respiratory Diseases.


Many methods of control are in use and many herds supplying genetic stock are maintained negative for M. hyopneumoniae. Such herds obviously must have scrupulous isolation, acclimatization, testing, and biosecurity protocols in place to assure the organism is not introduced with breeding stock.

Most negative herds are the result of depopulation and repopulation with negative breeding stock. In some cases, herds have become negative through strict medicated or segregated early weaning, and other minimal disease programs. Specific pathogen free (SPF) herds are derived from pigs taken via hysterectomy or cesarean section and raised on colostrum-free diets. They are then used to repopulate clean, swine-raising facilities. Maintaining commercial herds free of M. hyopneumoniae infection when located in swine-dense regions has not been successful long term. A control strategy developed in Europe and referred to as “Swiss depopulation” has gained favor in recent years. The technique is based on a hypothesis that most adult swine raised on an endemically infected farm are exposed to M. hyopneumoniae early in life with subsequent recovery (and presumably robust immunity with limited carrier status) by 10 months of age. Swiss depopulation involves a period of intensive vaccination of all breeding animals on a farm followed by removal of all animals less than 10 months of age. For a period of approximately three-weeks following this, on-site farrowing is stopped. During the stand-down period, all animals remaining on the farm are intensively treated with antibiotics aimed at elimination of any M. hyopneumoniae organisms that may be residing in carrier animals. Removal of all susceptible swine combined with vaccination/medication programs generally results in a significant decrease in effect from the disease for up to two years with eradication of the organism reported in some instances.

Other measures to aid in control but not elimination include early weaning, medicated early weaning (MEW) or modifications of MEW. Piglets are weaned before 21 days of age. Early weaning may prevent transmission of M. hyopneumoniae (and other organisms) from dams to piglets before they are weaned and moved to a separate, clean nursery or grow/finish facility. Age segregated rearing and the all in/all out system of management with cleaning and disinfection of facilities between batches of pigs is widely used and believed to be one of the more practical and useful measures.

Despite methods to eliminate or control M. hyopneumoniae, it remains a significant economic problem, particularly when PRRS virus or swine influenza virus (SIV) is endemic. Vaccines are generally thought to be efficacious and can be effective in mitigating losses due to M. hyopneumoniae infection. Vaccines reduce lung lesions and improve growth performance. In some systems, sows are vaccinated once or twice several weeks before farrowing but most programs rely on vaccination of piglets. In most herds, maternal antibodies do not seem to interfere with piglet vaccination. Piglets are usually vaccinated before weaning and again two to three weeks later.

Antibiotics may augment management and vaccination techniques and can be given in feed, water, or by injection. Many antibiotics and chemotherapeutic agents have been used in feed or water for prevention or treatment, often with inconsistent results. Efficacy of antimicrobials in controlling M. hyopneumoniae losses may be related either to antimycoplasmal activity or suppression of other infections. Those reported efficacious specifically for M. hyopneumoniae include lincomycin, tiamulin, tetracyclines, tylosin, tilmicosin, tulathromycin, enrofloxacin and perhaps others.