What is atypical mycobacterial infection?

Atypical mycobacterial infections are infections caused by a species of mycobacterium other than Mycobacterium tuberculosis, the causative bacteria of pulmonary TB and extrapulmonary TB including cutaneous TB; and Mycobacterium leprae, the cause of leprosy.

Atypical mycobacteria may cause many different types of infections, which are divided into the following four clinical syndromes:

Pulmonary disease
Lymphadenitis
Skin and soft tissue disease
Disseminated disease

Skin infection tends to result in crusted nodules and plaques. Abscesses may develop in skin and bone infection.

What causes atypical mycobacterial infection?

There are many different species of mycobacterium. To date at least 30 species of mycobacteria that do not cause tuberculosis or leprosy have been identified.

How is atypical mycobacterial infection diagnosed?

Atypical mycobacteria are diagnosed on culture of tissue. Specific conditions are required, such as cool temperature, so the laboratory must be informed of the clinician's suspicion of this diagnosis. The infections have specific pathological features on skin biopsy.
Other diagnostic tools used include radiographic imaging studies and more recently, polymerase chain reaction (PCR) testing on swabs of ulcers or tissue biopsies.

What is the treatment of atypical mycobacterial infection?

Treatment of atypical mycobacterial infections depends upon the infecting organism and the severity of the infection. In most cases a course of antibiotics is necessary. These include rifampicin, ethambutol, isoniazid, minocycline, ciprofloxacin, clarithromycin, azithromycin and cotrimoxazole. Usually treatment consists of a combination of drugs.

Consider the following points when treating atypical mycobacterial infections with antibiotics:

Mycobacterium marinum species are often resistant to isoniazid, streptomycin, pyrazinamide, and para-aminosalicylic acid. Effective antimicrobials include tetracyclines, fluoroquinolones, macrolides, and sulfonamides. Treatment should be for at least 4 to 6 weeks, and sometimes up to two months.

Mycobacterium kansasii should be treated with at least 3 drugs for 12 to 18 months. One of the drugs must be rifampicin, which is still the cornerstone of treatment for these infections.

Mycobacterium chelonae is best treated with clarithromycin or azithromycin in localised infections, particularly if used with surgical debridement. Disseminated infections require combination treatment, usually a macrolide and an aminoglycoside.

Treatment of Mycobacterium ulcerans is most successful if treatment is started in lesions less than 6 months old with a diameter less than 10 cm. Rifampicin and streptomycin are the current recommended antibiotics.

Surgery is used as an adjunct to antibiotic treatment in patients with severe infection. Most lesions eventually spontaneously heal after 6 to 9 months but may leave behind extensive scarring and disfigurement.

AIDS patients on HIV protease inhibitor drugs cannot be treated with rifampicin because rifampicin significantly increases the breakdown of these drugs. Rifabutin is a suitable alternative.

Surgical removal of infected lymph nodes and aggressive debridement of infected skin lesions is sometimes necessary. In severe cases, skin grafts may be necessary to repair the surgical wound.
Adopted from www.dermnetnz.org