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 such as cutaneous TB.

Atypical mycobacteria may cause many different types of infections such as septic arthritis, abscesses and skin and bone infection. They may also affect the lungs, gastrointestinal tract, lymphatic system and other parts of the body.

Skin infection tends to result in crusted nodules.

What causes atypical mycobacterial infection?

There are many different species of mycobacterium. Those that cause atypical mycobacterial infections include:

Mycobacterium avium-intracellulare
Mycobacterium kansasii
Mycobacterium marinum
Mycobacterium ulcerans
Mycobacterium chelonae

Mycobacterium avium-intracellulare and Mycobacterium kansasii primarily cause lung disease similar to pulmonary TB, whilst Mycobacterium marinum, Mycobacterium ulcerans and Mycobacterium chelonae cause skin infections.

What are the clinical features of atypical mycobacterial infection?

The clinical features of atypical mycobacterial infection depend on the infecting mycobacteria.

Mycobacteria	Clinical features
Mycobacterium avium-intracellulare	Also known as MAC (Mycobacterium avium complex) Most common non-tuberculous mycobacterial infection associated with AIDS Symptoms include fever, swollen lymph nodes, diarrhoea, fatigue, weight loss and shortness of breath May develop into pulmonary MAC
Mycobacterium kansasii	May cause a chronic infection of the lungs similar to pulmonary TB Second most common non-tuberculous mycobacterial infection associated with AIDS Symptoms include fever, swollen lymph nodes and lung crackles and wheezing Skin lesions may occur either alone or as part of a more widespread disease
Mycobacterium marinum	Also known as fishtank granulomas Uncommon infection that occurs most often in people with recreational or occupational exposure to contaminated freshwater or saltwater Usually a single lump or pustule that breaks down to form a crusty sore or abscess Other lumps may occur around the initial lesion, particularly along the lines of lymphatic drainage (sporotrichoid forms) Most often affects elbows, knees, feet, knuckles or fingers Multiple lesions and widespread disease may occur in immunocompromised patients Rarely causes red, swollen and tender joints
Mycobacterium ulcerans	Also known as Buruli ulcers Infection most common in Central and West Africa around areas of lush vegetation and swamps but may also occur in Australia Solitary, painless and sometimes itchy nodule of 1-2 cm develops about 7-14 days after infection through broken skin Over one to two months the nodule may break down to form a shallow ulcer that spreads rapidly and may involve up to 15% of the patient's skin surface Severe infections may destroy blood vessels, nerves, and invade bone
Mycobacterium chelonae	Worldwide distribution: found in tap water and other water sources May cause lung disease, joint infection, eye disease and other organ infections May result in non-healing wound, subcutaneous nodule or abscess Immunosuppression may cause disseminated lesions throughout the body

*Mycobacterium marinum* infection

		Image provided by Alastair Hazell

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. Some points to consider when treating atypical mycobacterial infections:

Mycobacterium marinum species are often resistant to isoniazid. Treatment with other antibiotics should be for at least two months.

Mycobacterium kansasii should be treated for at least 18 months.

Mycobacterium chelonae is best treated by clarithromycin in combination with another agent, Sometimes surgical excision is the best approach.

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. Antibiotics are usually ineffective in treating large skin lesions caused by Mycobacterium ulcerans. Rifampicin may promote healing of pre-ulcerative lesions. Most lesions eventually spontaneously heal after 6-9 months but may leave behind extensive scarring and disfigurement.

Surgical removal of infected lymph nodes and skin lesions is sometimes necessary. In severe cases, skin grafts may be necessary to repair the surgical wound.

Related information

References:

Textbook of Dermatology. Ed Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL. Fourth edition. Blackwell Scientific Publications.

On DermNet NZ:

Other websites:

Mycobacterium ulcerations World Health Organization (WHO)
emedicine, the online textbook

Books about skin diseases:

See the DermNet NZ bookstore

Author: Vanessa Ngan, staff writer