Actinobacillus suis

Also known as: A.suis, Actinobacillosis, A. equuli in swine, Actinobacillus suis septicaemia in horses, Actinobacillus suis septicaemia in pigs, Acute haemorhagic pulmonary infarction and necrotizing pneumonia in horses, Otitis media, externa, interna, middle and inner ear infections.

Scientific Classification
Kingdom	Bacteria
Phylum	Proteobacteria
Class	Zymobacteria
Sub-class	Alphaproteobacteria
Order	Pasteurellales
Family	Pasteurellaceae
Genus	Actinobacillus
Species	Actinobacillus suis

Introduction

A.suis is a beta-haemolytic Gram-negative bacterium. Strains of A.Suis vary due to differences in their lipopolysaccharides (LPS), which is known as the 'O' antigen and is referred to as O1,O2 and O3 and capsules (CPS), called 'K' antigen with variants described as K1, K2 and K3. In piglets aged 1 to 8 weeks old the organism causes acute and rapidly fatal septicaemia, and localized infections such as endocarditis, polyarthritis, and respiratory distress may also been seen with additional neurological signs. Adult pigs can suffer pneumonia like symptoms, see clinical signs for more details. Although A.suis mainly affects pigs it has also been linked to septicaemia, acute haemorrhagic pulmonary infarction and necrotizing pneumonia in horses, airsaculitis in waterfowl, neonatal calf pneumonia and localised infections and polyarthritis in alpacas. It is not considered a zoonosis but there has been a report of human infection after a pig bite A.suis have genes that encode toxins similar to apxI and apxII of A. pleuropneumoniae, but are less virulent as they produce less Apx toxins than A. pleuropneumoniae. Once an animal is infected with A.suis it can provide partial cross protection against A. pleuropneumoniae.

Signalment

A.Suis can be found worldwide in both healthy and diseased animals which are genetically and biochemically similar. Wild hosts include anatidae (ducks, geese and swans) and Coypu but A.suis can also affect domestic species including dogs, cats, horses, cattle, pigs, sheep, goats, alpacas and zebu. High health status herds with lower immune challenges are more at risk then conventional herds. Piglets from high health status herds can suddenly die without any premonitory signs. Excessive temperature fluctuation, high humidity, mixing of pigs of different ages and overcrowding may also have an important role in the development of disease.

Clinical Signs

Clinical signs vary from fever, lethargy, depression, erysipelas-like lesions, abscesses, haemorrhage, vomiting/regurgitation and lameness and multiple joint swelling. More serious cases progress to pneumonia (clinical signs similar to A. pleuropneumoniae) and sudden death. Cardiorespiratory signs include tachycardia, heart murmurs, purulent or serous occulonasal discharges, sneezing, coughing, abnormal lung sounds, dyspnoea, changes in heart rate and open mouthed breathing. Aural purulent mucoid discharge and increased amounts of wax are present along with a foul odour. Pigs can become deaf and are often found rubbing and scratching their ears. Affected animals are in a lot of pain and discomfort and which manifests as dysphagia lymphadenopathy , anorexia, and unthriftiness. Pregnant sows can suffer from agalactia, mastitis, abortions, still births or weak piglets. Neurological signs include head tilt, circling, temors, nystagmus, strabismus, decreased or absent menace response, ptosis, miosis or meiosis, photophobia, headshaking, opisthotonus, facial paralysis, paraparesis and ataxia.

Diagnosis

Diagnosis can be difficult as it shares clinical signs with pathogens, such as Streptococcus suis and Haemophilus parasuis, both being able to induce a septicemic infection with sudden death. Infection can be confirmed by the isolation of A. suis, from culturing different tissues of affected organs on post mortem. Differential diagnosis include A. pleuropneumoniae, erysipelas, Glasser’s disease, streptococcus suis, and mulberry heart disease. On post-mortem serous or fibrinous exudates can be found in the thorax and pericardium and ecchymotic haemorrhages can be seen in kidneys, lungs, liver, spleen and other organisms.

Treatment

A.suis has good sensitivity to ceftioufur, gentamicin and trimethoprim/sulfadiazine, and moderate sensitivity to ampicillin, neomycin, sulfadimethoxine and tiamulin. Culture and sensitivity is recommended.

Control

Routine biosecurity and disinfection should be followed and maintained. At present there is no commercial vaccine for A. suis Radostitis et al, 2007 but there is evidence that autogenous vaccines in a herd could help stabilize antibody levels in the whole population Lapointe et al., 2001.