Environmental Mycobacterial Infections (Ref. P. McKee)
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
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
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.
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
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).
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.