The bacterial genus Actinobacillus belongs to the Department of Proteobacteria and the family of Pasteurellaceae. There is a name affinity with the actinomycetes, since the genus is often involved as an opportunistic pathogen in actinomycoses.

What is Actinobacillus?

Bacterial species of the genus Actinobacillus have a slender and partially oval shape. They have no flagella and are immobile. The Gram stain is negative, so Actinobacilli have only one Mureinhülle with superimposed lipid layer.

Bacteria of this genus are facultatively anaerobic and can thus survive very well in oxygen-depleted to oxygen-free areas. Actinobacilli are not spore formers and degrade carbohydrates without gas production.

Occurrence, distribution & characteristics

Bacteria of the genus Actinobacillus have specialized in a parasitic lifestyle. They can parasitize in mammals, birds and reptiles.

A detailed analysis of Actinobacillus actinomycetemcomitans revealed a monophyletic relationship to Haemophilus aphrophilus and Haemophilus segnis. A reclassification of the named species into the new genus Aggregatibacter ("aggregate" in the sense of "summarize, combine") is discussed.

Diseases & complaints

Germs of the genus Actinobacillus are accompanying germs in actinomycoses. Actinomycosis is a mixed infection caused by bacteria of the family Actinomyzetaceae. Pathogens of the genus Actinobacillus are not causative, but as opportunistic pathogens form part of the mixed infection.

The disease actinomycosis is referred to in German as a "ray fungus", since the infection was initially explained by a fungal colonization. Although actinomycoses may also involve fungal colonization, as these are not to be regarded as causal, the German name "ray fungus" is misleading.

Actinomycosis is triggered by injuries of the mucous membranes. Resident actinomycetes of the normal germ flora penetrate through these injuries into deeper tissue layers and trigger purulent inflammations. Furthermore, it comes to the formation of granulation tissue and widely branched fistulas.

Fistula formation is considered to be the major complication of the infection as pathogens can enter the bloodstream and cause systemic infection. Arriving at the point of systemic infection, the prognosis for the patient is not good, because the systemic inflammation a high recidivism (recurrence) is very likely even after apparent recovery. A chronic disease can not be ruled out even with timely antibiotic therapy.

A further complicating factor is that actinomycetes require several days of cultivation in order to be identified (about 14 days). PCRs also have a hard time finding the causative agent in mixed infections.

The administration of antibiotics may ultimately result in the elimination of the causative agent, but other germs with existing resistance will continue to drive actinomycosis. With the described complications and mechanisms of this mixed infection, it is not surprising that the antibiotic therapy can last for a whole year and beyond.

Cervicofacial actinomycosis, which is the name for actinomycosis in the mouth, neck, and facial area, is most common. Other forms of actinomycosis, which extend into deeper layers of the skin or into the CNS, are described less frequently. Basically, the possibility of actinomycosis is present at all positions of the body. Actinomycoses were also observed in the genital and mammary glands.

An exact diagnosis of the pathogen together with existing resistance takes place via the ejection. As an alternative, lung biopsies are also possible. The removal of tissue samples for the direct detection of the pathogen is not promising.

An analysis of the ejection via the PCR method is the best solution for the identification of the pathogen so far. Antibiotic therapy can be started intravenously with aminopenicillin in the first three months. Tetracycline or cephalosporin are also suitable. A chronic infection with recurrent complaints can not be excluded despite several months of antibiotics.

Actinobacillus bacteria continue to cause wound infections, endocarditis and bacteremia. A fatal course of the infection can occur especially in immunocompromised persons. Here, the mortality rate is around 30%. The wound infections caused only widen slowly and are usually localized. Often a lymphadenitis can be observed as a concomitant.

Another secondary role play secondary infections, which can occur even after the successful treatment and cure of the acute infection. Severe late complications can be caused mainly in the central nervous system and in the heart.

The germs Actinobacillus hominis and Actinobacillus urea play a special role in humans. Although the germs can also be found in the airways of healthy people, a involvement in the development of sinusitis, bronchopneumonia and meningitis is still a controversial topic.

The Actinobacillus actinomycetemcomitans can also be found in the normal oral flora and is suspected to be responsible for endocarditis along with other anaerobic organisms.

The germs of the genus Actinobacillus have so far no pronounced resistance. Therefore penicillin is used by default. In particular, the benzylpenicillins show good results in the treatment of Actinobacillus infections. The efficacy of benzylpenicillins (penicillin G) against Gram-negative rod bacteria is unusual. However, the bacteria of the genus Actinobacillus are an exception, which is useful for successful antibiotic therapy.

For resistant bacteria, antibiotic treatment with ampicillin, tetracycline and cephalosporins can be continued. Especially important for an effective treatment of existing infections is an identification of the causative agent. Infections with strains of the Actinobacillus species can always be mixed infections and thus there is a risk of the partially resistant germs being present.

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