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Fig. 6.18 A, B. The formation of microabscesses in the subperiosteum in fungal infection. A The microabscesses develop when there is a subperiosteal fungal colony which drains externally, giving rise to a periosteal reaction. As the abscesses drain, the periosteum is lifted and punctured, and the sinus forms. B When the fungal colonies and the granuloma enter a bone from the adjacent soft tissue, they "lyse" the cortex. As the microabscesses coalesce, they produce a different lucent defect radiographically. (Courtesy of Dr. Sudarisanam, Velore, India). C-E There are major differences between pyogenic, fungal, and nocardial osteomyelitis. C Pyogenic osteomyelitis is nearly always a hematogenous infection, so that the infective foci spread from within outwards, through cancellous bone to cortex and up to the soft tissues. Pyogenic infections form pus, but the periosteum is intact and forms a barrier, which is elevated by the pus and stripped off the cortex. This cuts off the vascular supply to the cortex and results in sequestration and devitalization. D In fungal osteomyelitis the infection is usually from the outside spreading inwards; the periosteum does not form a barrier and is easily perforated. This permits the visual impression of periosteum with multiple holes in the cortex. Fungal infection is much less purulent and the cortex is not devitalized. Radiologically there will be spicules of periosteal reaction where the bone is invaded, but no sequestrum. This is seen in mycetomas due to eumycetes and the streptomycetes group of schizomycetes. When there is hematogenous spread of the infection, the periosteum is easily perforated and decompression occurs without devitalization of the cortex, in such cases spreading from within outwards. E Nocardial osteomyelitis is a more purulent type of infection, but the fungus still easily perforates the cortex and periosteum, effectively allowing periosteal decompression in spite of the diffuse periosteal reaction. The process is the same whether the infection is hematogenous or there is local invasion from the outside into the bone. There is no sequestration in either. A similar pattern is sometimes seen in systemic hematogenous spread from other fungal groups, but for all the periosteum does not form a barrier and is easily punctured and decompressed, so that there is no cortical devitalization. (Drawings in C-E courtesy of Dr. A. C. Johnson, from the first edition)

 

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Clinical Characteristics

Almost all mycetomas start as a localized nodule or, less commonly, an abscess: all have a long history, often many months or even years. Progress is very slow, but eventually multiple abscesses and sinus tracts develop (Fig. 6.20 A-C). The initial mycetoma usually starts in one foot (or one other localized site) and the whole foot will eventually become swollen. Pain is not significant, and the patient walks on the infected foot, which can carry the full weight of the body. The skin surface will be discolored and as the sinuses start to form, there will also be atrophic scars: the discharge is odorless. There is often secondary bacterial infection, which causes local ulceration and an unpleasant odor.

The sinuses develop in the center of the multiple nodules and are lined by red granulation tissue. The discharge from the sinuses is serosanguinous and purulent with creamy yellowish pus and multiple grains of different colors and sizes. Neither the color nor the size of the grains can be used to recognize the organism, because large, medium, or small grains can come from the same infection. Some grains are soft, others are hard.

The whole infectious process of swelling, nodulation, and sinus formation spreads locally for months and years, usually tracking along some cutaneous fascial planes and causing marked induration. The speed at which the sinuses develop varies greatly: they are seldom apparent in less than 3 months, but by the end of the first 12 months, almost every mycetoma will have discharging sinuses. Once drainage has started, it may continue for a long time, or close spontaneously. The number of sinuses and the amount of swelling provide an indication of the extent but not the duration of the infection.

When bone becomes infected, there is little pain on weight bearing until late in the disease. This lack of pain is probably because the organisms which cause mycetoma penetrate the periosteum and there is no increase in subperiosteal pressure. Tendons, nerves, and muscles are not usually involved so that the movement of the foot (or arm) is often little affected until the infection has spread extensively. There is very little systemic reaction: there is seldom any fever, anemia, weight loss, or other sign of systemic ill health.

Spread along a limb is usually through lymphatics; regional lymph nodes become enlarged, but seldom contain the causative organism. In one series of 949 mycetomas, the typical grains were only found in the regional nodes of 13 patients. Hematogenous spread is very uncommon, so that it is rare to have mycetoma in multiple sites. (This is not true in fungal pulmonary infections.)

If untreated, mycetomas continue to spread for many years, the outcome depending on the organism concerned. The actinomycetes infections often progress more rapidly than infection caused by eumycetes (true fungi).

The clinical differential diagnosis is very dependent on the long history, and the discharging sinuses. The embedded foreign body, if found, provides further evidence. Early lesions have been mistaken to pyogenic granulomas or, in some countries, tuberculosis: some resemble Kaposi sarcoma. If the surface of the skin is unbroken and if bones are not involved, the initial swelling be mistaken for a lipoma. As soon as there are sinuses, and grains are recognized, and particularly when there is bone destruction, the diagnosis of mycetoma is straightforward: defining the causative organism may be more difficult.

 

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