This type of infection may occur in moist wounds such as leg ulcers treated with occlusive bandages or dressings. Pseudomonas aeruginosa is the most frequent contaminant of such wounds. Astringent solutions such as acetic acid 1-2% will often dry the skin sufficiently to discourage the growth of Gram-negative organisms. Potassium permanganate 0.01% can be used as an alternative for bathing the limb or may be applied as a compress. Debilitated or immunocompromised patients may rarely develop necrotic skin lesions (from which Pseudomonas may be isolated) when local vasculitis follows Ps. aeruginosa septicaemia (ecthyma gangrenosum).
Chronic, localized, pigmented, scaled lesions of the skin occur over skin flexures such as the axillae, groin, toewebs and beneath the breasts.
The organism isolated from such sites is often a normal commensal of the skin, Corynebacterium minutissimum. It is not clear therefore why some adults are especially prone to the disease. Excessive sweating and poor hygiene are frequent accompanying features. Examination by Wood’s light causes the organism to fluoresce, producing a pink-red colour.
Oral erythromycin will eradicate extensive disease, and the drying of macerated skin with imidazole powders or topical fucidic acid cream will clear more limited infection.
Cutaneous disease can be due to Mycobacterium tuberculosis or M. leprae. It is uncommon in the Western Hemisphere. It is also associated with atypical mycobacteria, including M. ulcerans, which causes tropical Buruli ulcer, and M. marinum, which causes fish tank or swimming pool granuloma.
This condition is the most common form of skin disease associated with tuberculosis. Two forms are recognized:
1 Haematogenous spread from a reactivated primary lesion
2 More rarely, following scrofuloderma, which occurs when the skin is ulcerated by the spread of infection from an adjacent infected lymph gland or bone
Histologically, the cutaneous lesions show granulomas with central caseation. It is usual to be able to demonstrate the organism from the skin lesions.
Sites of involvement are usually on cooler areas of the skin, with the face being most frequently involved. Erythema, scaling and scarring plaques.
In severe intractable disease subcutaneous tissues appear ‘gnawed’ and hence the term ‘lupus’ (meaning ‘wolf).
Tuberculosis verrucosa cutis
Primary inoculation of the skin with M. tuberculosis may give rise to warty lesions on the skin of young children who come into contact with infected sputum or on the fingers of surgeons or pathologists who handle infected tissue.
Secondary inoculation of the skin occurs from endogenous sources, e.g. at the side of the mouth from
infected sputum (tuberculosis orificalis cutis); it appears as a plaque or papule.
Tuberculides form a group of poorly defined eruptions and knowledge of their pathogeneses is incomplete. It is probable that they represent a reaction in the skin to the haematogenous spread of M. tuberculosis. They have declined in parallel with pulmonary tuberculosis. Inc- luded under this general heading are papulonecrotic tuberculide, lichen scrofulosorum and erythema induratum or Bazin’s disease.
Lupus vulgaris and other forms of tuberculosis of the skin should be treated with standard chemotherapy for 6-9 months (see p. 686). Tuberculides such as erythema induratum will clear on the same regimen.
Atypical mycobacterial infections
Skin granulomas develop where the skin is traumatized against the rough surface of the lining or surround of a swimming pool, or over a digit, hand or forearm abraded against the side of an aquarium during cleaning. The latter is more common nowadays, when the patient presents with a chronic papular lesion on the finger, usually with scaling and less frequently with atrophic changes. On occasions more than one lesion may be seen following spread along cutaneous lymphatics. The organism causing this infection is M. marinum.
Lesions may clear over the course of months and routine antituberculous treatment is ineffective. Minocycline in doses of up to 100 mg twice daily for 6-8 weeks may hasten resolution of the lesions.
M. leprae infection of the skin gives rise to leprosy. However, in order to lessen the stigma associated with the disease, the term Hansen’s disease is preferred.
The organism may be confined to the primary site of involvement in neural tissue from where it spreads to the skin. Lesions are few and typically there are plaques with an elevated rim, dusky red in colour and with some central pallor. The surface of the skin is often dry over the lesion, hairless and insensitive. Local peripheral nerves may be enlarged.
Biopsy shows tuberculoid granulomas but no bacilli.
Evidence of nerve involvement in the skin is often lacking and presenting signs may be in the respiratory system with nasal congestion. The plaques, nodules, macules and papules that occur are usually erythematous and multiple and have no appreciable loss of sensation. With untreated disease, the facial skin may become thickened and the remainder of the integument is often scaly and dry.
Increasing nerve damage leads to loss of sensation, ulceration of limbs, loss of digits and muscle wasting. Diagnosis and treatment are discussed.