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Non-Tuberculous Environmental Mycobacterial Infections (Ref. P. McKee)

INTRODUCTION

Non-tuberculous mycobacteria, which are usually non-pathogenic, are widespread in varied sites throughout the world. They inhabit vegetation and water (stagnant, fresh or salty), and are saprophytic in soil, on animals and within animal faeces. They can be subdivided according to their growth rate on culture media and by their ability to produce a yellow pigment in culture with and without exposure to light.

There are therefore four categories :

Group I are photochromogens, which produce pigment after exposure to light (e.g. Mycobacterium marinum and Mycobacterium kansasii).

Group II organisms are the scotochromogens, which produce pigmented colonies whether light is present or not (e.g. Mycobacterium scrofulaceum and Mycobacterium szulgai).

Group III organisms are consistently non-pigmented and include Mycobacterium avium and Mycobacterium intracellulare.

Group IV are the fast growers and include Mycobacterium chelonei and Mycobacterium fortuitum.

The environmental mycobacterial infections are becoming of increasing importance in the immunocompromised patients, particularly in those with AIDS. Cutaneous infection with these organisms in the immunocompent patient usually follows an episode of trauma and gives rise to a localised lesion often clinically resembling panniculitis. In the immunosuppressed, a history of trauma is usually lacking and patients tend to present with multiple subcutaneous nodules. Systemic spread is obviously of particular importance in this latter group. As the features may be atypical diagnosis is facilitated by a healthy index of suspicion.

CLINICAL FEATURES MYCOBACTERIUM MARINUM

M. marinum (balnei) is a slow-growing photochromogen, which is associated with injuries in aquatic environments or by fish or equipment, usually under water. Infections have been contracted most often in swimming pools, usually on the elbows and knees of children, or from aquaria, usually on the hands. The lesions usually present 1 week to 2 months (average 2 weeks) after superficial injury and are typically painless inflammatory nodules. They may ulcerate and discharge yellow fluid and older lesions can be warty. Occasionally abscesses are seen. Quite often there is extension along lymphatics, with the development of secondary nodules in a pattern comparable to sporotrichosis. Penetrating injures sometimes result in tenosynovitis. Infection in immunodeficient individuals produces a deeply undermined ulcer; otherwise lesions usually resolve within a few months.

Infection with Mycobacterium Marinum (Ref. Lever)

Infections with M. marinum, formerly referred to also as M. balnei, can take place through minor abrasions incurred while bathing in swimming pools (Hellerstrm) or in ocean or lake water (Zeligman; Even-Paz et al; Izumi et al) or while cleaning home aquariums (Adams et al; Mansson et al; Marsch et al). Infected swimming pools have caused epidemics, the largest of which affected 290 persons (Philpott et al). The period of incubation usually is about 3 weeks but may be longer.

Clinically, most of the lesions caused by M. marinum are solitary and consist of indolent, dusky red, hyperkeratotic, papillomatous papules, nodules, or plaques. Superficial ulceration is seen occasionally. The fingers, knees, elbows, and feet are most commonly affected. In some instances, satellite papules arise (Even-Paz et al). Quite commonly, multiple intracutaneous or subcutaneous nodules arise in a linear arrangement, as seen in sporotrichosis, several weeks affer the appearance of the primary lesion at the periphery of an extremity (Dickey; Adams et al; Marsch et al). Lesions may form at different sites in the case of multiple injuries (Jolly and Seabury). Although spontaneous heafing usually takes place within a year, the lesions persist in some patients for many years (Zeligman; Izun-d et al).

Histopathology. Early lesions no more than 2 or 3 months old show a nonspecific infiammatory infiltrate composed of neutrophils, monocytes, and macrophages. In lesions about 4 months old, a few multinucleated giant cells and a few small epithelioid cell granulomas usually are present, and in lesions 6 months old or older, typical tubercles or tuberculoid structures may be seen (Mansson et al). Areas of necrosis are only occasionally present in the center of the granulomas. The epidermis often shows papillomatosis and hyperkeratosis, and there may be central ulceration.
Acid-fast organisms usually can be identified in histologic sections of early lesions that show a nonspecific inflammatory infiltrate (Adams et al). In contrast, tuberculoid granulomas generally no longer show acid-fast organisms, unless areas of central necrosis are present (Scholz-Jordan et al).
In histologic sections, the atypical mycobacteria appear slightly larger than M. tuberculosis and show transverse striation (Philpott et al). If acidfast bacilli cannot be detected in histologic sections, they can be identified by culture or by animal inoculation, except in heafing lesions.
Although primary lesions usually require a few months for the formation of tuberculoid granulomas, the sporotrichoid nodules that arise later show tuberculoid granulomas and a lack of acidfast bacilfi even when they have been present for only a few weeks (Dickey; Marsch et al).

Histogenesis. In some instances in which M. marinum is not demonstrable in biopsy specimens, it may be seen in smears of exudates (Even-Paz et al). When tissue homogenates are cultured on standard mycobacterial culture media, M. marinum shows optimal growth at 30'C to 33'C, and does not grow at 37C, as do most other atypical mycobacteria and M. tuberculosis. M. marinum is not pathogenic to guinea pigs, but it is pathogenic to mice if inoculated into their footpads (Cott et al).

Differential Diagnosis. The granulomatous reaction produced by M. marinum often is very similar to that seen in tuberculosis verrucosa cutis or lupus vulgaris, so that cultures and animal inoculations are necessary for their differentiation.