The bacterial genus Actinobacillus belongs to the Proteobacteria division and the Pasteurellaceae family. There is a name relationship with actinomycetes because the genus is often involved in actinomycosis as an opportunistic pathogen.
What is actinobacillus?
Bacterial species of the genus Actinobacillus have a slender and sometimes oval shape. They do not have flagella and are immobile. Gram staining is negative, so Actinobacilli have only a murein envelope with an overlying lipid layer. Bacteria of this genus are facultatively anaerobic and can thus survive very well in oxygen-deficient to oxygen-less environments. Actinobacilli are not spore-formers and degrade carbohydrates without gas production.
Occurrence, distribution, and characteristics
Bacteria of the genus Actinobacillus specialize in a parasitic lifestyle. They can parasitize mammals, birds, and reptiles. A detailed analysis of Actinobacillus actinomycetemcomitans revealed a monophyletic conspecific relationship to Haemophilus aphrophilus and Haemophilus segnis. A reclassification of the above species into the new genus Aggregatibacter (“aggregare” in the sense of “to combine, to unite”) is discussed.
Diseases and ailments
Germs from the genus Actinobacillus are concomitant germs in actinomycosis. Actinomycosis is a mixed infection caused by bacteria of the Actinomyzetaceae family. Pathogens of the genus Actinobacillus are not causative, but form part of the mixed infection as opportunistic pathogens. The disease actinomycosis is called “ray fungus” in German, because the focus of infection was initially explained by fungal colonization. It is true that actinomycosis can also involve fungal colonization, but since this is not to be regarded as causative, the German designation “ray fungus” is misleading. Actinomycosis is triggered by lesions of the mucous membranes. Resident actinomycetes of the normal germ flora penetrate through these injuries into deeper tissue layers and trigger purulent inflammations here. Furthermore, granulation tissue and widely ramified fistulas are formed. Fistula formation is considered to be the main complication of the infection, as pathogens can penetrate through it into the bloodstream and trigger a systemic infection. Once at the point of systemic infection, the prognosis for the sufferer is not good, as systemic inflammation makes a high recurrence (relapse) very likely, even after apparent recovery. Chronic disease cannot be ruled out even with timely antibiotic therapy. Furthermore, actinomycetes need several days of cultivation to be identified (about 14 days). PCRs also have difficulty in identifying the causative pathogen in mixed infections. Antibiotic administration may ultimately result in elimination of the causative pathogen, but other pathogens with existing resistance may continue to drive actinomycosis. Given the described complications and mechanisms of this mixed infection, it is not surprising that antibiotic therapy can last for a full year and beyond. Cervicofacial actinomycosis, which is the name given to actinomycosis of the mouth, neck, and facial area, is the most common. Other forms of actinomycosis that extend into deeper layers of the skin or into the CNS are less commonly described. In principle, the possibility of actinomycosis is present in all positions of the body. Thus, actinomycosis has also been observed in the genital area and on the mammary gland. An exact diagnosis of the pathogen including existing resistances takes place via the sputum. Alternatively, lung biopsies are also possible. The collection of tissue samples for direct detection of the pathogen is not promising. Analysis of the sputum by PCR is the best solution to date for identifying the pathogen. Antibiotic therapy can be started intravenously with aminopenicillin during the first three months. Tetracycline or cephalosporin can also be used. Chronic infection with recurrent symptoms cannot be ruled out despite several months of antibiotic administration. Bacteria of the genus Actinobacillus are still considered to cause wound infections, endocarditis and bacteremia. A fatal course of infection may occur especially in immunocompromised individuals. Here the mortality rate is about 30%.The wound infections caused spread only slowly and are usually localized. Lymphadenitis can often be observed as an accompanying symptom. Secondary infections, which can occur even after successful treatment and healing of the acute infection, also play a role. Severe late complications can be caused here, especially in the central nervous system and the inner lining of the heart. The germs Actinobacillus hominis and Actinobacillus urea play a special role for humans. Although the germs can also be found in the respiratory tract of healthy people, an involvement in the development of sinusitis, bronchopneumonia as well as meningitis is still controversially discussed. Actinobacillus actinomycetemcomitans can also be found in the normal oral flora and is suspected to be responsible for endocarditis together with other anaerobic organisms. To date, the germs of the genus Actinobacillus have no pronounced resistance. Therefore, penicillin is resorted to by default. Benzylpenicillins in particular show good results in the treatment of Actinobacillus infections. The efficacy of benzylpenicillins (penicllin G) against gram-negative rod bacteria is unusual. However, the germs of the genus Actinobacillus are an exception, which is useful for successful antibiotic therapy. In the case of resistant germs, antibiotic treatment can be continued with ampicillin, tetracycline and cephalosporins. Identification of the causative pathogen is particularly important for effective treatment of present infections. Infections with strains of the Actinobacillus species can always be mixed infections, and thus there is a risk that partially resistant germs are present.
