Actinobacillus pleuropneumoniae (APP)

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This organism causes severe pleuropneumonia which is a highly contagious disease of swine often characterized by sudden onset, short clinical course, high morbidity, and high mortality.


Porcine pleuropneumonia (PPN; currently referred to as APP) is widely distributed throughout major swine-raising countries. It has been a major problem in many European countries and is relatively common in the United States, Canada and Asia. APP is restricted to swine. In naïve herds, APP occurs in all age groups but usually is seen in 6-20 week old pigs. Actinobacillus suis can cause similar disease and lesions but is not as contagious as Actinobacillus pleuropneumoniae (APP).

Historical information

In the United States, APP was first reported in 1957. It was reported frequently in the 1960s and 1970s. Frequency of outbreaks increased with the industrialization of swine production. Research has been greatly facilitated by use of infected seeder pigs to reproduce APP under experimental conditions. Because of the economic consequences of disease, most producers strive to eliminate infection from herds.


The etiologic agent of APP is Actinobacillus (previously Haemophilus) pleuropneumoniae. The organism is a hemolytic, Gram-negative, capsulated, coccobacillary rod, highly host-specific for swine. Strains vary in virulence and pathogenicity. There are two biotypes distinguished by their dependency for NAD (nicotinamide adenine dinucleotide) in culture. Within the two biotypes, at least 15 serotypes are commonly recognized; four (1, 3, 5, 7) are most common in North America. The organism does not persist for any significant time in the environment.

The APP organism secretes 4 exotoxins, ApxI, ApxII, ApxIII and ApxIV, together called RTX toxins, and produces abundant endotoxin. The RTX toxins are cytotoxic and/or hemolytic. The toxins produced vary among the 15 serotypes. Antibodies to the exotoxins probably are important in protective immunity.

Actinobacillus suis is closely related to A. pleuropneumoniae and some strains produce one or more of the RTX toxins. The two organisms may cross react on some serologic tests.


Swine that survive acute APP often remain carriers. Swine can also be subclinically infected carriers with only occasional disease outbreaks. Most transmission is by direct contact of APP via nasal secretions but transmission may be via aerosol, at least for short distances. Overstocking, inadequate ventilation, coinfection with other respiratory pathogens, or unusual stress may facilitate transmission or precipitate outbreaks. Fomites, including boots and coveralls, can spread the organism but are infectious for only a short time.


Hemolysin and other toxins produced by APP are active against endothelial cells and pulmonary alveolar macrophages. Presumably, they also cause a vasculitis in the lungs and at other sites. Vasculitis precedes thrombosis and is followed by infarction and sequestration of infarcts in the lungs. Sudden deaths may be caused by endotoxic shock.

Pathogenesis probably involves both variable host resistance and various degrees of virulence among serotypes. Generally, serotypes 1 and 5 are considered more virulent than 7 or 3 but all can cause significant disease and any of these may be present subclinically in populations of pigs.

Other pathogens or environmental factors that affect the lung may influence onset and course of the disease. Colostral immunity in young pigs confers some resistance to infection and permits gradual development of active immunity in many exposed, growing pigs. Naïve pigs suddenly exposed to APP are more likely to develop fulminating clinical signs.

Clinical signs

Signs vary considerably between acute and chronic forms of APP. In acute outbreaks, sudden deaths are common. The early signs include sudden onset of prostration, high temperatures, apathy, anorexia, stiffness, and perhaps vomiting and diarrhea. A shallow, nonproductive cough is occasionally present. As disease progresses, there is marked dyspnea with mouth breathing and, perhaps, a foamy, bloody discharge from the mouth and nose. There is early peripheral cyanosis of extremities. As circulation fails, generalized cyanosis follows. Morbidity and mortality in growing swine varies but can become high. Peak mortality usually occurs in pigs 10-16 weeks old. Mortality can reach 20-80% in fattening pigs. Abortions may occur in acutely infected pregnant females.

Chronic cases may become apparent following an acute outbreak. Chronic cough and slow growth then are the usual signs due to the presence of pleural adhesions and abscesses that form in recovered lungs.


Lesions of APP are usually restricted to the respiratory tract; characteristic lesions include necro-hemorrhagic areas of consolidation in the lung accompanied by fibrinous pleuritis. The thoracic cavity often contains blood-tinged fluid. The classic lesion is hemorrhage and necrosis in the dorsal portion of one or both diaphragmatic lobes. Lesions in the lungs are dark red to black, firm, and develop as areas of infarction. Bloody froth often fills larger airways and there may be interlobular edema. Fibrinous pleuritis almost always overlays pneumonic areas and extends to adjacent costal pleura. There may be serofibrinous pericarditis. Pharyngitis, sometimes necrotic and ulcerative, may be present. Occasionally there is polyarthritis.

Chronic cases often have large, sequestered or encapsulated nodules of necrosis in the lungs that incompletely resolve as abscesses. Lung lesions often are attached to the rib cage by fibrous adhesions which lead to condemnations at slaughter.

Accurate differentiation of APP and Actinobacillus suis on the basis of lesions is difficult, perhaps impossible.

A. suis infection more often is accompanied by bacteremia with involvement of other organs making bacterial culture an important tool in establishing a diagnosis. Disease caused by A. suis tends to be more sporadic and less severe but this organism can cause substantial disease in naïve or “high health” populations. Also in finishers and older animals, cutaneous lesions that resemble those of acute erysipelas are reported with A. suis.


The sudden onset of an acute, rapidly-spreading, respiratory disease causing high morbidity and mortality is suggestive of APP. Dark red infarcts in the lungs of acutely affected cases, sequestered nodules in lungs of chronic cases and a high incidence of pleuritis in the herd also are suggestive. Virulent serotypes exist within both biotype I (NAD dependent) and biotype II (NAD independent). Isolation and identification of APP is confirmatory. A culture technique using immunomagnetic separation has been described for isolating the organism from mixed bacterial populations. Polymerase chain reaction (PCR) techniques targeting the RTX toxin genes are also available and can facilitate differentiation from A. suis infection.

Despite limitations of specificity, the complement fixation (CF), enzyme-linked immunosorbent assay (ELISA), or hemolysin neutralization serology tests also are useful for diagnosis of APP on a herd basis. They help in identifying infected herds and serotypes in a locality. Low antibody titers to APP in only a few pigs may have little diagnostic significance.

Acute outbreaks of APP must be differentiated from other respiratory diseases, especially A. suis infection, pneumonic pasteurellosis, pneumonic salmonellosis, influenza and mycoplasmal pneumonia.


Herds on premises free of APP should be managed as closed herds since introduced swine may be carriers. Swine necessarily introduced should be from APP-free herds. They should be introduced only after testing before and following a quarantine period of at least 30 days.

Management factors of importance in prevention include all in/all out production with careful cleaning and disinfection between farrowings, avoidance of overstocking, proper ventilation, and elimination or control of predisposing diseases.

A new generation of vaccines, cross protective for all serotypes, has been developed. They are subunit vaccines based on the use of purified and, in some instances, outer membrane proteins. They should not interfere with the serologic tests that use capsular or lipopolysaccharides (LPS) or polysaccharides.

The older type vaccines are serotype specific. They often are used to increase immunity in the sow herd but routine practice of sow herd vaccination remains controversial. Vaccination of piglets should be delayed until piglets are 5-7 weeks old and maternally derived antibodies are depleted. Some autogenous bacterins contain stabilized hemolysin and may be of benefit.

A novel vaccination approach based on intranasal inoculation of baby piglets has recently been developed in Australia. Results of early work with the product look promising but only limited experimental work has been presented to support its distribution to a world-wide market.

Usually, control of APP in endemically infected herds requires combinations of vaccination, medications and improved husbandry. In some cases, the best efforts fail to control disease effectively. Often, the cost of long-term control is unacceptably high.

If APP is endemic in a sow farm, depopulation can be a cost-effective approach to eradication of the disease. Depopulation should be followed by thorough cleaning and disinfection of the buildings and leaving them vacant for a few weeks; restocking can then follow using APP-free swine. As possible alternatives, APP may be controlled in the offspring by early weaning or medicated early weaning at no more than 17 days of age. Important caveats include first boosting immunity in the sows using serotype-specific antigens, assuring that piglets received adequate amounts of their colostrum, weaning to a clean site, and good biosecurity.

Acute outbreaks demand immediate parenteral antimicrobial treatment of affected animals and those in adjacent pens. This, combined with the addition of antibiotics in feed or water for a few weeks, can reduce mortality. Commonly used agents used for prevention and/or treatment include tiamulin, tulathromycin, chlortetracycline, ceftiofur, tilmicosin, florfenicol, enrofloxacin and procaine penicillin G. Many strains are resistant to tetracyclines. Chronic cases usually are unresponsive to treatment.