Actinobacillus suis

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An infectious disease characterized by hemorrhages and embolic lesions at multiple sites, more obviously in the lungs, and often by serous or serofibrinous exudates in the thorax and abdomen.


Outbreaks occur predominantly in immunologically naïve populations. These include primary and secondary specific pathogen free (SPF) pigs or in segregated early weaned (SEW) pigs. Most outbreaks are in recently weaned pigs and in grow/finish pigs derived from an SEW system. Outbreaks occur in both younger and older swine and, less often, in conventionally raised pigs.

Historical information

There have been reports of the disease since 1962. In the 1980s, after management techniques were introduced that minimized exposure of neonates to many endemic pathogens, the incidence of Actinobacillus suis infections appeared to increase in the US industry. Misdiagnosis of the disease as Actinobacillus pleuropneumoniae (APP) infection or other septicemias likely contributes to under-reporting of the true prevalence of the disease.


The etiologic agent, Actinobacillus suis, is only now being studied in detail. It is a Gram-negative, nicotinamide adenine dinucleotide (NAD)-independent, non-motile coccobacillus. It is aerobic and facultatively anaerobic. All isolates appear to be of a single serotype. Strains from swine appear to be clearly different from those isolated from horses.

Thus far there is no serologic test to reliably identify infected swine and establish A. suis-free herds. Antibodies to A. suis and A. pleuropneumoniae may cross-react with some serologic tests.


The epidemiology is not completely understood but carrier pigs probably introduce A. suisinto herds. It can be isolated from the nasal cavity and tonsils of many healthy pigs and has been found in the reproductive tract of healthy sows. It is believed to be an “early colonizer” of neonates. Less than optimal environmental conditions or concurrent diseases may increase the ability of A. suis to cause disease.


Invasion probably occurs through the tonsil and spreads through the bloodstream. This is suggested by the presence of the organism in emboli in the vasculature at many lesion sites. The agent’s pathogenic effect is probably a result of production of hemolysin and other toxins similar to those produced by A. pleuropneumoniae.

Clinical signs

The first signs of an outbreak may include sudden death of young pigs with lesions attributed to a bacterial septicemia. Sick piglets are febrile, breathe rapidly, and may have congested or cyanotic extremities. Cyanosis, arthritis, enteritis, and rarely necrosis of the feet, tail and ears have been reported and are similar to other causes (streptococcal, erysipelas, salmonella) of bacterial septicemia. Occasionally, infected pigs may show central nervous system (CNS) signs including tremors, shaking or paddling. Mortality within affected litters can be high, up to 50%.

Older growing pigs and adults can have similar signs but may also have signs of acute respiratory distress. Lethargy or depression, anorexia, and rarely irregular reddened skin lesions that resemble those of erysipelas may be observed. Pregnant sows may abort.


Lesions are similar in pigs of all age groups. They include petechial and ecchymotic hemorrhages in many organs. Frequently, lesions are present in the lungs as disseminated foci of hemorrhagic to necrotizing pneumonia, the latter more marked in older piglets and growers. A consistent lesion in all age groups is serous or serofibrinous exudate in the abdominal and thoracic cavities. Polyarthritis may occur in grow/finish pigs.

Microscopic lesions occur in many major organs. These develop around small colonies of A. suis within the vascular emboli or thrombi. Occasionally there are eosinophilic clubs surrounding the colony. Both gross and microscopic lesions are typical of embolic, bacterial septicemias.


History, signs and lesions are suggestive of the diagnosis but it should be confirmed by culture of A. suis from multiple organs. Serologic diagnosis is unreliable because antibodies to A. suis and APP may cross react.


Autogenous vaccines have been used but have not been evaluated critically. Because there are multiple types of lipopolysaccharides (LPS) in A. suis, the LPS profile of the vaccine strain must match that of the pathogen. Although unproven, vaccines against APP may offer some cross-protection.

Actinobacillus suis is sensitive to many antibiotics including ampicillin, amoxicillin, oxytetracycline and others. Sick pigs should be treated parenterally as soon as possible. The exposed group can be treated by medicating the water.