Mycobacterial Skin Infections

It is important to consider mycobacteria infection in any stubborn and atypical skin problem in immunocompromised individuals. Mycobacteria cause slowly developing chronic skin infections. Mycobacterial infection is increasing, partly due to emerging drug resistance and the HIV epidemic.¹

Lupus vulgaris

• Commonest form of cutaneous tuberculosis, occurring after primary infection in individuals with good natural resistance.
• Females are more often affected and it is also more common in children.
• Most commonly affects the face and neck and is seen initially as firm, translucent, brown nodules.
• Without treatment, the lesions slowly spread laterally, leading to disfiguring scarring. Malignant change has been reported in these scars.
• Diagnosis is confirmed by biopsy and culture. Patients should receive full anti-tuberculous therapy for at least one year.

Scrofuloderma

• Scrofuloderma results from breakdown of skin overlying a tuberculous focus, usually at a lymph node but also at the skin over infected bones or joints.
• Lesions present as firm, painless, subcutaneous nodules that gradually enlarge and suppurate, then form ulcers and sinus tracts in overlying skin. Typical ulcers have undermined edges and a floor of granulation tissue. Causes fistulae and scarring.
• M. tuberculosis can be identified both in the nodes and in the material draining on to the skin surface.
• Full anti-tuberculous therapy and surgical excision is required.

Warty tuberculosis

• Commonest form of cutaneous tuberculosis in developing countries but rare in western countries.
• Occurs with infection in someone who has immunity from previous infection.
• Causes a warty plaque, often on the hands, knees or buttocks.

Tuberculides

• Skin reactions to systemic tuberculosis, e.g. erythema nodosum, erythema induratum.

• Leprosy is a disease of overcrowding, poor hygiene and poverty.
• Hypopigmented anaesthetic macules, plaques, papules, or annular lesions (with raised erythematous rims).
• There are many lesions in lepromatous leprosy but just a few asymmetrical, hypopigmented lesions in tuberculoid leprosy.
• Areas of anaesthesia may occur, along with damage to autonomic fibres, causing loss of sweating within that area.
• Patients with leprosy often suffer skin damage, e.g. burns, because of anaesthesia caused by nerve damage due to the primary infection.

Tuberculoid leprosy

• Cutaneous manifestation likely to be single macule or plaque, which is erythematous or purple (depigmentation often seen on coloured skin) and has a raised edge sloping towards a flattened hypopigmented centre.
• The surface is anaesthetised, dry, and hairless.
• The depigmented areas may resemble vitiligo.
• No M. leprae are found in skin smears.
• Good prognosis and many infections resolve without treatment; peripheral nerve damage is limited.
• In borderline cases the lesions are similar but more numerous.

Lepromatous leprosy

• Hypopigmented or erythematous macules, papules, nodules and ulceration develop at sites of low temperature, e.g. nostrils (may lead to septal perforation and collapse of the nasal bones).
• Generalised thickening of involved facial tissues causes leonine facies.
• Loss of hair and sweating and progressive glove and stocking sensory loss.
• Damage to peripheral nerves is symmetrical and occurs late in disease.
• Bone involvement is common.

Erythema nodosum leprosum

• Occurs in lepromatous disease, especially during the first year of treatment.
• Painful red nodules on the face and extensor surfaces.
• Fever and malaise may be accompanied by uveitis, arthritis, neuritis, lymphadenitis, and orchitis.
• The use of clofazimine in multidrug therapy has reduced the risk from 50% to 15%.
• Attacks are acute and may recur over several years.

Diagnosis

• Full-thickness skin biopsy, skin snips, a peripheral nerve biopsy and lepromin test.
• Does not grow in artificial culture but it can be maintained in the laboratory in the footpad of immunosuppressed mice.

Treatment

• Is based on systemic sulphones, rifampicin and clofazimine (latter now only available from WHO/Novartis for leprosy treatment).
• Resistance is becoming a problem and reactions may occur in the initial stages.
• Tuberculoid variety should be treated for 1-2 years after disease activity has ceased but treatment for lepromatous leprosy should continue for life.
• Children who are household contacts should be followed up as they can harbour the organism for many years and develop disease in adult life.
• Adult contacts rarely become infected.

• Cutaneous infections with atypical mycobacterium are much more common in immunosuppressed patients, especially those with HIV infection, leukaemia or those undergoing immunosuppressive therapy.
• Atypical mycobacterium infections are also more common in the elderly.
• The environmental mycobacteria cause two named diseases with characteristic features:
  • Swimming pool (or fish tank) granuloma caused by M. marinum.
  • Buruli ulcer caused by M. ulcerans infection.
• The other mycobacterioses are much less specific, often resembling tuberculosis.

Buruli ulcer

• Buruli ulcer is also known as Bairnsdale ulcer or Searles' ulcer, (Australia), and Kakerifu ulcer or Toro ulcer (Congo).
• Is a re-emerging infection and is now the third most prevalent mycobacterial disease worldwide, behind tuberculosis and leprosy.²
• Due to infection by M. ulcerans in tropical zones.
• Acquired from vegetation or water after trauma.
• Initially a painless erythematous nodule, usually on the leg or forearm, becomes necrotic and ulcerates.
• Treatment is usually by wide surgical excision.
• Antimicrobial therapy with rifampicin and clarithromycin is recommended before and after surgery.
• BCG gives short term prevention.

Fish tank granuloma (or swimming pool granuloma)

• Caused by M. marinum infection, which infects fish and is also found in swimming pools.
• Typically causes a reddish, slightly scaly plaque on the hand or arm of someone who keeps tropical fish.
• M. marinum is sensitive to minocycline, clarithromycin, amikacin, rifampicin, ethambutol and doxycycline.³

Other environmental mycobacteria

• M. kansasii:
  • Most patients who present with localised primary cutaneous M. kansasii infection are immunocompetent, whereas most patients with disseminated or pulmonary infection are immunocompromised.
  • It may resemble cellulitis or sporotrichosis.
  • May also present with tenosynovitis, cutaneous lymphadenitis; the clinical presentation similar to that expected in lupus profundus and with ulcerative perineal lesions.
• M. malmoense: cervical lymphadenitis in preschool-aged children. It has also been associated with cutaneous nodules on the hands.
• M. szulgai: cellulitis, nodules and plaques.
• A case of disseminated M simiae infection with blood, pulmonary, and cutaneous localisation has been reported.
• M. gordonae: granulomatous synovitis and bursitis. It is sometimes called tap water scotochromogen. It has also caused granulomatous nodules on the back of the hand.
• M. haemophilum: multiple, tender, cutaneous nodules, which may develop into ulcers or abscesses. They are often situated over limb joints. May lead to muscle wasting, tenosynovitis, and joint effusions.

• Mainly affects otherwise healthy children under 5 years old.
• Usually affects the cervical lymph nodes, often just a single node.
• Is caused by many mycobacterial species, most often M. avium complex and M. scrofulaceum.
• Infection in older children and more diffuse involvement is often associated with HIV infection.
• Surgical excision is curative.

• The optimal way to make the diagnosis is by performing a culture of tissue. Most mycobacteria require special culture conditions, which if not specifically requested, are frequently not used.⁴
• The development of DNA fingerprinting technology, especially pulsed-field gel electrophoresis, has been suggested as a diagnostic tool.
• Polymerase chain reaction has been used to aid diagnosis.
• Chest x-ray: associated pulmonary disease.
• The purified protein derivative test (antigen skin test used to aid the diagnosis of tuberculosis) result is usually negative in infections with atypical mycobacteria.

• Effective treatment depends on precise diagnosis and identification of the underlying organism. Treatment will also be governed by results of culture and sensitivity.
• Treatment of atypical mycobacteria skin infections is often difficult because many atypical mycobacteria are resistant to common antibiotics.⁵
• A combined therapeutic approach, including surgical drainage, debridement, and prolonged treatment with combined antimicrobial agents has been used in some cases of atypical mycobacteria.
• In some cases (especially fast-growing environmental mycobacteria), successful treatment requires aggressive debridement of all infected subcutaneous tissues and skin.

• Scarring and nerve damage can occur from long-standing untreated infections.

• The prognosis is good with proper medical and surgical treatment.
• However many patients are often not properly treated because of insufficient health resources in developing countries or treatment may be difficult because of underlying immunosuppression and consequent diffuse infection.

• Avoidance of contaminant material.
• BCG gives variable degree and duration of protection.