Porcine pleuropneumonia (PPP) caused by Actinobacillus pleuropneumoniae (App)

*Updated September 2021


Porcine pleuropneumonia (PPP) is an infectious respiratory disease of swine caused by the bacteria Actinobacillus pleuropneumoniae (APP). The disease occurs throughout the world and results in significant economic losses due to mortality, growth retardation, veterinary costs and slaughter condemnations. It is rather well controlled in North America, but PPP remains a major concern in Latin-American, Australasian and most European countries.



  • Explain how APP serotype differences can result in a wide range of clinical signs
  • Provide additional factors that may influence APP infections
  • Describe the transmission, lung lesions and diagnosis of APP
  • Discuss various treatment, control and prevention strategies


Cause and Distribution

APP has different serotypes and not all are equally dangerous.

APP is a bacterial organism that can be grown via laboratory culture. After culturing the organism, a single colony or isolate can be further characterized. APP isolates belong to one of 18 variations of the bacteria, called serotypes. Serotypes are determined by the isolated bacteria’s capsule (protector shields that surrounds the bacteria). The bacterium has another important structural component called lipopolysaccharides (LPS). Some serotypes have the same LPS components.  For example, serotypes 1, 9 and 11, 3, 6, 8 and 15 and 4 and 7, share similar LPS components. Since the LPS is used in some blood tests, cross-reactions may occur due to these serotype similarities. Composition of the capsule and LPS of serotypes 16, 17 and 18 (recently described) are still poorly known.


The virulence (ability to cause disease) of APP isolates varies greatly and is usually related to the serotype involved. This variation results in a large spectrum of clinical situations from absence of clinical signs to acute and chronic infections. The basis for APP virulence is not completely understood. To cause disease, the bacteria secrete toxins that lead to severe lung damage and destruction of the host’s defense cells. These toxins are called Apx and there are four types: ApxI, ApxII, ApxIII and ApxIV. The first three are extremely harmful to pigs and some serotypes produce combinations of these three toxins. The ApxIV toxin is produced by all serotypes and is used for diagnostic testing. Presence of antibodies (immune response) against this toxin in the blood of an animal means that it has been infected by APP. The role of ApxIV in causing disease is still unknown.


In North America, serotypes 1, 5 and 7 are the most virulent. However, serotype 1 has been nearly completely eradicated during recent years. Serotypes 12, 6, 8, 13, 15 and 17 are considered to have intermediate virulence, causing clinical disease mainly in high health status herds or when other cofactors are involved. Serotypes 2, 3, 4 and 10 are rarely recovered from diseased pigs and serotypes 9, 11, 14, 16 and 18 have never been reported in North America.


Transmission of APP between herds occurs mainly through the introduction of healthy appearing animals carrying the bacteria. The main route of spread is by direct contact from pig to pig or by air droplets transmitted over short distances. In sudden outbreaks, sick animals will secrete large amounts of pathogenic bacteria; therefore, APP also has the potential to be transmitted several hundred meters by air. Other animal species have not been shown to carry or spread the bacteria to pigs. APP survival in the environment is usually of short duration. However, when protected with organic matter, such as feces, it can survive for several days. This may explain why fomites and people are occasionally involved in the transmission of APP.


The cycle of infection usually starts with chronically infected sows who transmit the bacteria to their offspring. Only a few piglets become infected from their mother during lactation. Antibodies provided by the mother through the milk may reduce and/or prevent the bacterial colonization of piglets. The later the age of weaning, the greater the chance piglets could be infected. Infected piglets spread the bacteria to other pigs after weaning as immunity from their mother declines. The presence of antibodies from the mother may last 2 to 10 weeks, depending on their initial level of antibodies in the sow and the amount of colostrum consumed by the pigs.


Presence of APP in a herd does not automatically mean presence of clinical signs and death.

Most herds are infected by one or more low or mildly virulent serotype(s) without clinical signs or clear lung lesions at slaughter. Some herds may even be infected with virulent serotypes without causing death, clinical signs or even lung lesions. However, many of these herds will experience occasional clinical outbreaks when cofactors help APP cause disease. Examples of these cofactors are (Figure 1):

  • Co-infections with Mycoplasma hyopneumoniae, swine influenza virus, and/or virulent Pasteurella multocida. A possible synergism between APP and the Porcine reproductive and respiratory syndrome virus (PRRSV) has yet to be scientifically confirmed
  • Environmental stressors such as overcrowding, poor ventilation, rapid temperature changes and/or high humidity
  • Management-related factors such as mixing pigs from different sources, continuous flow production and/or weaning piglets >21 days of age
  • Immunity status of the animals i.e. presence or absence of antibodies (vaccinated animals would have more protection, while animals from herds free of all APP serotypes would be more susceptible to infection)

Figure 1: Interactions between the APP isolate, environmental and management factors, immunological status of the host and co-infections may influence the appearance of disease.

Clinical Signs and Lesions

In the peracute or extremely sudden form, it is common to find one or more animals dead without observing clinical signs and with a characteristic foamy blood tinged nasal discharge. In the acute or sudden form, usually many pigs are sick with elevated body temperatures of 105–106˚F (40.5–41˚C). Animals are depressed and reluctant to rise, eat and/or drink. They may show difficulty breathing, coughing, blood from the nose, and sometimes open mouth breathing. The course of the disease differs from animal to animal, depending on the extent of the lung lesions and the time of initial treatment. In the subacute or not sudden form, animals have mild to no fever and cough with variable (usually low) intensity and duration; these signs are not easily distinguished from respiratory disease caused by other pathogens. Appetite may be reduced or intermittent, which is hard to appreciate where ad-lib feeding systems are in use, and this may contribute to decreased rate of weight gain. In the chronic form, there is little to no fever, and a spontaneous or irregular cough of varying intensity develops. Feed consumption may be reduced, and affected animals may not tolerate exercise. When forced to move they remain behind the group and struggle minimally when restrained. Mortality is seldom a feature of this form of infection, although an increase in cull pigs many be seen.


Lung inflammation (pneumonia) may be in one or both lungs, with major involvement of the top of the lung(s) near the diaphragm. There are usually areas of lung consolidation that are firm to the touch and are colored dark red to black (necrotic and easy to break apart), the lungs will also accumulate fluid (interlobular edema), and fibrin deposits will be present on the lung surface (fibrinous pleuritis) (Image 1). The chest cavity usually contains a blood-tinged fluid. In healthy appearing animals with chronic disease, the dark red or black color of the early lung lesion becomes lighter in color and remains firm in the worst affected areas of the lung. In many cases, the lung lesion resolves, and only an area of thickened scar tissue (fibrous adhesion) remains. A high occurrence of membrane inflammation (pleuritis) at slaughter is strongly suggestive of PPP. These lesions may result in slaughter condemnations or trimming of affected tissue.

Image 1: Typical lung lesions in pigs with acute APP infection: dark areas of firm consolidation, fluid accumulation (interlobular edema or oedema), and fibrin deposits on the lung surface (fibrinous pleuritis). Source: Dr. Robert Desrosiers.



Even if lung lesions are suggestive of PPP, it is recommended to confirm the diagnosis through culture of the organism. Bacterial colony growth from pigs with sudden pneumonia is usually easy, except if the animal has been recently treated with antibiotics. Identification of the serotype is recommended for surveillance when vaccination is being considered. Serotyping should be conducted in appropriate diagnostic laboratories to prevent misidentification. Antimicrobial susceptibility testing is also available to support veterinarian’s antibiotic selection.


Chronic PPP infections are more difficult to diagnose since it is usually hard to grow APP from chronic lung lesions, such as those observed at slaughter. Recently, a new bacterium (Glaesserella australis) has been isolated in Australia and France from lung lesions similar to those caused by APP. Detection of APP from tonsils in healthy animals carrying the bacteria is even more difficult and should be attempted only in certain cases by highly experienced diagnostic laboratories.


Detection of antibodies in blood samples is the most powerful tool for the diagnosis of later staged infections; presence of antibodies shows that animals have been or still are infected with APP. Many blood tests have been developed, but only two major categories of tests are currently used: a) tests that will identify the serotype/serogroup and b) a test that is specific for APP (all serotypes). The most useful tests able to identify serotypes/serogroups are based on the LPS and they will give a clear answer of which serotypes/serogroups are present (remember that some serotypes are more virulent than others). These tests can identify serogroups/serotypes as follows: 1, 9 and 11 (serotypes 9 and 11 are absent in the U.S.); 2; 3, 6 and 8; 4 and 7; 5 and 10; and 12. Commercial kits based on these antigens are available and used in several diagnostic laboratories. The second type of test, which is also commercially available, detects antibodies against the ApxIV toxin, which is produced by all isolates of APP. The test only detects APP antibodies; it cannot differentiate serotypes. Moreover, field data suggests that it is less likely to identify animals with APP than LPS-based tests. The test may be useful for the routine surveillance of herds believed to be free of all serotypes. However, its use in typical herds is questionable. Indeed, most herds are infected with one or more APP serotype(s) of low to mild virulence and many positive results are expected with this test. Interestingly, in an infected herd, the percentage or prevalence of infected animals depends on the serotype. Indeed, some serotypes are highly contagious, but poorly virulent and will not cause clinical disease (e.g., serotypes 6, 8, 12 and 15) whereas the opposite is true for others which infect less animals, but cause disease (e.g., serotypes 1 and 5). This should be taken into consideration when selecting pigs for blood testing.



Antibiotic treatment is effective in clinically affected animals only in the initial phase of disease. The antibiotic selected should be based on research evidence, veterinary experience, clinical response and laboratory antimicrobial susceptibility testing. APP isolates are naturally resistant or may become resistant to certain antibiotics. Antimicrobials should be given by injection as affected animals often do not eat or drink normally. The success of treatment depends mainly on prompt treatment following the early detection of clinical signs. Medicated water or feed may be used to treat affected groups of pigs if food and water intake have not decreased significantly.


Feed and water medication can also be used in anticipation of acute outbreaks if the disease is recurrent. However, other measures should be implemented to control the disease and reduce the use of antibiotics and the antimicrobial susceptibility of the organism should be monitored as resistance may develop. Strategic medication should be targeted at periods of high risk, which can be identified through clinical examinations, post-mortem examinations, and blood sampling. Antibiotic treatments alone may control clinical signs but will not eliminate the bacteria.



When stocking a new farm, it is strongly recommended to choose breeding stock free of all or at least the most virulent APP serotypes. This requires that the supplier has implemented a health program that includes regular blood testing and necropsies, as well as an effective biosecurity program. Open communication between the veterinarians of the supplier and the buyer is also essential to ensure that all health requirements are addressed. By contrast, introduction of naïve animals (free of all APP serotypes) into an infected herd is also dangerous and measures such as vaccination should be considered and applied to avoid clinical disease.


In herds facing clinical signs, the priority must be to control economic losses. Vaccination may be effective to reduce disease, death, antibiotic treatments, carcass condemnations and improve overall growth performance. The decision to vaccinate should be carefully evaluated. It is recommended that animals should not receive the primary vaccination before 8 weeks of age to avoid interference with antibodies from the mother. Gilts and sows can be vaccinated during pregnancy to improve passive immunity in piglets, although higher levels of antibodies may increase the risk of interference with piglet vaccination. Replacement animals can be vaccinated before their introduction into an infected herd.


APP vaccines fall into two main categories: those based on killed organisms (called “bacterins”) and the subunit toxin-based vaccines. All commercial vaccines are currently available in the U.S., along with mechanisms to create autogenous vaccines. Autogenous vaccines are created from cultures of organisms collected from a herd. These bacteria are then used to make a vaccine to be used in the same herd. Under experimental conditions, vaccination with bacterins only protects against the serotype(s) in the vaccine (serotype specific). Proof of autogenous vaccine effectiveness under field conditions is still lacking. Subunit vaccines composed mainly of the three major toxins (ApxI, ApxII and ApxIII) as well as toxin-bacterin combination vaccines also exist. Contrary to bacterins, these vaccines are supposed to provide protection against most serotypes due to the immune response against the toxins. Overall, vaccination of animals does not prevent infection and live bacteria may remain in the tonsils despite high levels of protective antibodies.



Eradication of the organism may be attempted in infected herds. Several successful eradication procedures have been reported, but a careful economic evaluation is recommended before starting an eradication program. Depopulation and restocking with pigs from certified APP-free herds is probably the most effective means. This method is usually implemented in commercial herds that are facing severe PPP problems as well as other health issues (e.g., PRRSV, Mycoplasma hyopneumoniae, etc.). Nucleus breeding herds must use other methods to preserve their bloodlines. One approach that has succeeded in the past is medicated early weaning (MEW).



Even if PPP is generally well controlled in North America, it remains a concern for some producers. Losses result from increased mortality, reduced growth, veterinary costs and slaughter condemnations. Knowledge of the disease has greatly improved in the last 20 years and more efficient tools to diagnose and control the infection are now available. New herds should preferably be stocked with pigs from sources certified free of all or at least the most virulent APP serotypes. In infected herds, the disease can be partially prevented by vaccination or controlled by medication. Effective control of infectious (such as Mycoplasma hyopneumoniae) and non-infectious cofactors (such as overcrowding) is also extremely important.


Additional Resources

  1. Gottschalk, M. 2015. The challenge of detecting herds sub-clinically infected with Actinobacillus pleuropneumoniae, Vet. J. 206:30–38.
  2. Gottschalk, M., A. Broes. 2019. Actinobacillosis, in: Zimmerman JJ, Karriker LA, Ramirez A, Schwartz KJ, Stevenson GW, Zhang J, eds., Diseases of Swine, 11th ed., Hoboken, NJ: Wiley-Blackwell, pp. 749–766.
  3. Loera-Muro A, C. Angulo. 2018. New trends in innovative vaccine development against Actinobacillus pleuropneumoniae. Vet. Microbiol. 217:66–75.
  4. Sassu, E.L., J.T. Bossé, T.J. Tobias, M. Gottschalk, P.R. Langford PR, I. Hennig-Pauka. 2018. Update on Actinobacillus pleuropneumoniae-knowledge, gaps and challenges. Transb. Emerg. Dis. 65 (Suppl. 1):72–90.


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