Actinobacillus pleuropneumoniae - Molecular diagnosis (PCR).


Actinobacillus pleuropneumoniae (Haemophilus pleuropneumoniae previously), is a Gram - negative coccobacillus, capped, still facultative anaerobe, respiratory pathogen for pigs. Structurally, in the outer membrane, it has the lipopolysaccharide (LPS) and different types of proteins of interest. The capsule is also a structure of great importance is related to the pathogenesis and is very useful in classifying. In recent isolates it described the presence of fimbriae.


Described 15 different serotypes of Actinobacillus pleuropneumoniae according to different capsular polysaccharides exposed. There are two different biotypes, biovar 1 including 13 different serotypes and biovar 2 which includes two serovars. Differences in virulence, immunogenicity and geographical distribution worldwide contribute to the diversity of the serotypes of A. pleuropneumoniae. 15 serotypes may lead to the disease, with one serotype generally predominates in a particular herd. The main difference between serotypes is the expression of Apx toxins and other virulence factors.


This bacterium causes porcine pleuropneumonia, a highly contagious respiratory disease that mainly affects young pigs, usually less than 6 months. Porcine pleuropneumonia is one of the most important bacterial diseases affecting the respiratory tract few of the pigs. All signs and symptoms of swine pleuropneumonia can be attributed to the virulence factors of this bacterium. The incubation period may vary depending on the animal's age, immune status, environmental conditions and the degree of exposure to infectious agent, having been described experimental cases since some hours to several days post - inoculation.

Actinobacillus pleuropneumoniae infection occurs by aerosol or direct contact between infected animals and healthy animals. It has been shown that A. pleuropneumoniae colonizes the tonsil and alveolar epithelium. In the lung the microorganism is phagocytosed by alveolar macrophages rapidly due to the production of ApxI, ApxII and ApxIII toxins which are highly toxic effect for alveolar macrophages, phagocytosis so does not act properly. In addition, toxins also affect the endothelial cells of alveolar capillaries and their effects are responsible for the typical lesions of the disease. The bacterium colonizes the host quickly and binds to epithelial cells of the tonsils, moving down the respiratory tract using type IV fimbriae. As the bacteria divide, they release cytotoxins (in the form of toxins APX), hemolysin and LPS of their outer membranes. Subsequent lysis of macrophages causes the release of lysozyme, which in turn causes tissue damage as observed in swine pleuropneumonia. In particular, A. pleuropneumoniae activates the release of various cytokines such as interleukin 1? (IL-1?), IL-8 and tumor necrosis factor alpha (TNF-?). Several virulence factors account for the remarkable pathogenicity of A. pleuropneumoniae. The most important include the production and release of the APX toxins, the ability to produce a biofilm, the component of LPS, capsule polysaccharides, and their ability to survive in an environment of limited iron. Of these, the most important are its capsule and producing Apx toxins.


The symptoms of swine pleuropneumonia include respiratory distress, blood - stained exudate, usually frothy mouth, fever, anorexia, mild diarrhea, cyanosis, lethargy, and spontaneous abortion in sows. Specifically, A. pleuropneumoniae can cause arthritis, endocarditis , and abscesses in various locations in some animals. For pig farmers, the most common sign is the sudden death of several pigs in a short period of time. In this regard, the peak mortality is usually achieved when pigs are approximately 10 to 16 weeks of age. Pigs that survive the disease remain carriers and spread the bacteria to other pigs. One of the most frequent complications of swine pleuropneumonia is the serofibrinous pericarditis with further development of adhesions and fibrous thickening. Although in most cases the lesions are limited to the thoracic cavity, sometimes it can be observed also fibrinous peritonitis, purulent meningoencephalitis, endocarditis colitis, arthritis and osteomyelitis.


The clinical course of the disease can take three different ways: hyperacute, acute or chronic. Hyperacute and acute picture is typical of farms free agent, while the chronic condition is more related to areas where the disease has endemic.


      • Hyperacute box. This table is characterized by the sudden appearance of some very sick animals with hyperthermia (41.5 - 42 ° C), anorexia and apathy. There may be brief periods of vomiting, mild diarrhea, cough, and epistaxis. Furthermore, an increased pulse, heart failure and respiratory may occur, and cyanosis of skin of the nose, ears, legs , and finally the whole organism. Terminally severe dyspnea appears with mouth breathing, sudden decrease in the rectal temperature and abundant, and blood - tinged frothy through the nostrils and mouth secretion before death. In general, the affected animal dies within 24 to 36 hours of development of clinical symptoms. In young animals death can occur so rapidly that the above symptoms reach not observed.
      • Sharp picture. This picture is characterized by the occurrence of severe respiratory symptoms: cough, dyspnoea and occasionally mouth breathing. In addition, hyperthermia, cardiac and circulatory failure with limb edema occurs. The course of the disease differs from one animal to another, depending on the extent of lung lesions and time of initiation of treatment. In individuals with an acute, death is due to a combination of heart failure and toxins produced by the organism. It is possible to observe any kind of evolution: from the death of animals in a few days to progression to chronic form after a few days of onset of the disease.
      • Chronic condition. This dialog box appears after acute or simultaneously. There is no fever and variable and intermittent cough is observed. Other signs and symptoms include decreased appetite, exercise intolerance (these affected animals are the last to rise when it comes into operation) and pneumonia characterized by abdominal breathing due to a very painful pleuritis. Affected pigs may carry the organism for long periods of time and therefore represent a potential risk for younger pigs.

The typical presentation of A. pleuropneumoniae in pigs are characteristic lesions limited media, cranial and caudal lobes of the lung. Severe pneumonic areas are dark and consolidated growth. In the case of chronically infected pigs, they are frequently pleural adhesions and abscesses. Histological studies of infected lung tissue , usually show pulmonary necrosis, neutrophil infiltration, activation of macrophages and platelets, and exudate. In addition, intense bleeding or hemolysis is also present.


The post - mortem findings confirmed the diagnosis. Injuries are caused largely by the toxins produced. These include; Hemorrhagic consolidation near the main bronchus or lung lobe diaphragmatic, usually located. It may also be visible necrosis and fibrinous pleuritis. In animals recovered, it may have developed lung scarring and pleural adhesions.


Tests in IVAMI:


  • Molecular diagnosis (PCR), to detect DNA of Actinobacillus pleuropneumoniae.

Recommended sample:


  • Swab with respiratory exudate.

Preservation and shipment of sample:


  • Refrigerated (preferred) for less than 2 days.
  • Frozen: over 2 days.

Delivery term:

  • Molecular diagnosis (PCR): 24 to 48 hours.

Cost of tests:

  • Consult to