Genus Characteristics

The genus Actinobacillus is within the Pasteurellaceae family, along with genera such as Pasteurella, Haemophilus, Histophilus and Mannheimia. The genus consists of many species that are commensals, some are pathogens of animals and more rarely humans. The Actinobacillus species are facultatively anaerobic fastidious Gram-negative, medium-sized rods (0.3–0.5 × 0.6–1.4 µm) that can produce coccal forms on routine solid media but longer forms in serum or sugar broths. Organisms may exhibit bipolar staining. Distinguishing features of the genus Actinobacillus from other Gram-negative rods can be found in Table 20.1. They are non-motile, non-spore-forming, non-acid-fast, indole-negative, usually oxidase-positive, reduce nitrates and produce beta-galactosidase. Actinobacillus species ferment carbohydrates within 24 hours without the production of gas. Most species grow on MacConkey agar as tiny lactose-fermenting colonies and produce urease. The reaction in the catalase test is variable. Actinobacillus species have a limited viability on solid media (seven to 10 days) and most have complex nutritional requirements. Growth is usually improved by a 5 to 10% CO₂ atmosphere.

Natural Habitat

The natural habitat for actinobacilli is primarily the mucous membranes of the upper respiratory tract and oral cavity of their hosts. They do not survive well in the environment. Some species are commensals while others are responsible for several distinct diseases of animals. The geographical distribution of the various Actinobacillus species is typically worldwide.

Pathogenesis and Pathogenicity

Actinobacillus species are responsible for several distinct diseases of animals (Rycroft & Garside 2000). The major pathogenic Actinobacillus species in veterinary medicine are presented in Table 20.2. Actinobacilli are usually transmitted via the aerosol route or by close contact. The organisms can also gain entry through breaks in the skin. Actinobacillus pleuropneumoniae, A. suis, A. equuli and A. lignieresii are the most significant veterinary pathogens. Actinobacillus pleuropneumoniae is the aetiological agent of porcine pleuropneumonia, a highly contagious and often fatal disease. The organism can also colonize the upper respiratory tract of healthy pigs; no other natural host has been described to date. The disease can be peracute, acute or chronic. The peracute and acute forms are characterized by a necrotizing, fibrinohaemorrhagic pneumonia with pleurisy. Haemorrhage and severe congestion are seen in the lungs with serosanguinous exudate in the pulmonary cavity. This form has high morbidity and mortality. The chronic form of the disease can be seen in animals that survive infection, characteristic lung lesions include focal necrotic abscesses with layers of fibrous tissue that result in scarring of the lung. A review of the pathogenesis of A. pleuropneumoniae has been published by Bosse et al. (2002). Virulence factors such as adhesins, iron-acquisition factors, capsule, lipopolysaccharide (LPS), RTX (Repeat in Toxins) cytotoxins are all important with regard to colonization, avoidance of host clearance mechanisms and damage of host tissues. A summary of the principal virulence factors of A. pleuropneumoniae can be found in Table 20.3.

Actinobacillus suis colonizes the upper respiratory tract and vagina of healthy pigs. It is an opportunistic pathogen that is more common in high-health status (or start-up) herds. Disease is sporadic and is characterized by an acute septicaemia in piglets that may be accompanied by neurological signs and arthritis. In grower-finisher pigs, the disease can resemble the pleuropneumonia associated with A. pleuropneumoniae infection. Meningitis, abortion, myocarditis (mulberry heart disease), metritis and skin lesions (resembling erysipelas) have been reported in adult pigs. Virulence factors similar to those documented for A. pleuropneumoniae have been reported including transferring-binding proteins (TbpA and TbpB), urease, capsule, LPS and RTX toxins (except ApxIV). However, A. suis shares only 50% DNA-DNA homology with A. pleuropneumoniae and distinct virulence factors presumably exist.

Actinobacillus equuli subsp. equuli is the agent of the sleepy foal disease, a frequently fatal septicaemia of neonatal foals. Infection of the foal is thought to occur via the upper respiratory tract or the umbilicus soon after birth. The chronic form of the disease is characterized by purulent arthritis (joint ill) and suppurative multifocal nephritis. Actinobacillus equuli subsp. equuli is also considered an opportunistic pathogen of pigs capable of causing septicaemia. Actinobacillus equuli subsp. haemolyticus is an opportunistic pathogen of the horse and can cause various infections such as metritis, abortion, pneumonia and meningitis. Little is known about the virulence factors of A. equuli. Haemolytic isolates seem to produce a RTX toxin, the AqxA protein, encoded by the aqxA gene of the aqxCABD operon.

Actinobacillus lignieresii is the cause of actinobacillosis, wooden (timber) tongue, in cattle and less commonly in sheep. It is a sporadic, insidious, granulomatous infection. The organism appears to be a commensal of the upper respiratory tract of ruminants, causing disease after inoculation into mucous membranes during abrasion by rough feed. The lesions, numerous small abscesses, are usually limited to the soft tissues of the jaw, throat and tongue. Ulcers filled with pus can be seen on the tongue. The granulomatous lesions can also involve the skin and underlying tissues of the head, neck and limbs. Spread of infection by the lymphatics can occur occasionally to affect the lungs and other internal organs. The pyogranulomatous lesions formed by A. lignieresii resemble those of Actinomyces bovis (actinomycosis). Small, greyish-white granules (about 1 mm in diameter) are present in exudates from lesions of A. lignieresii. If these granules are crushed on a slide and stained, club colonies are seen consisting of club-like processes of calcium phosphate with the Gram-negative rods of A. lignieresii in the centre. Clinically, it can be difficult to distinguish a granulomatous lesion of A. lignieresii in the soft tissues of the jaw area from lumpy jaw (A. bovis). Table 20.4 summarizes the differential features of the two conditions. Virulence factors of A. lignieresii are still unknown.