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Several careful bacteriological studies have shown that in 90% of patients Staphylococcus aureus predominates. Not surprisingly, other organisms have been found, such as Escherichia coli, hemolytic streptococci, and S. albus, but contamination cannot be excluded. Phage typing in Uganda suggests that S. aureus type II and predominantly single phage 3a, 3b, 3c, and 55/71 are responsible, but typing from other series is not so detailed and the Uganda results may not be applicable elsewhere. The abscesses are almost always confined to muscles and do not involve perifascial connective tissues or surrounding structures (Fig. 30.2 A). Progress to pus formation is often quite rapid.

The majority of patients come late for treatment, with a fully developed abscess or abscesses, but in those who undergo surgery at a stage when no pus is found, the muscles are pale and edematous. Histologically there is loss of muscle striations and marked cellular infiltration, predominantly lymphocytic (Fig. 30.2 B, C). Necropsy reports on 19 patients who died from pyomyositis revealed edema along the major axis of muscles between the myofibrils, which may be widely displaced. There is cytolysis, coagulative necrosis, and degeneration, with the same lymphocytic and plasma cell infiltration (Taylor, Kampala).

Fig. 30.2. A An in-depth section of the skin and underlying tissue, fascia, and muscle from a patient in Zaire with a tropical pyomyositis abscess. There is a draining sinus on the left side and a track (central, dark, wedge-shaped area) extending into the subcutaneous area. B The cavity of an abscess containing fragments of degenerating skeletal muscle. H&E, x250. C The lining of the abscess is necrotic: there are cocci (arrow) in a degenerating phagocyte. Giemsa, x 1000. (Constructed by Dr. Daniel H. Connor).

Two theories recur in the literature to explain the etiology. One supposes that these histological findings result from a viral infection, particularly the Coxsackie-B virus (which is common in the tropics and can produce muscle necrosis), and subsequent infection by Staphylococcus. This theory is tempting but unproven. In Thailand there were a cluster of 17 patients, which tends to support the possibility of a mosquito-borne viral infection, so far unrecognized. The other theory blames chronic vitamin C deficiency (latent scurvy), the result of the common diet in many areas where pyomyositis is frequent. This alternative was investigated in Nigeria, but the plasma vitamin C levels of patients with myositis were, if anything, higher than a matched control group (Idoko et al. 1990). Neither in Papua New Guinea nor Swaziland was there any evidence of scurvy and in one unpublished series of southern African mine employees there was no evidence of any nutritional deficiency. There is no consistent history of prior local injury in any series.

A third more recent explanation suggests that pyomyositis is always associated with an IgM antibody deficiency or with defective phagocytosis. Lowering of general cell-mediated immunity is known to occur in West African children following measles infection (but not in those who have been vaccinated against measles). Being immunodeficient is likely to increase the risk of infections such as pyomyositis, as is shown by its considerably increased frequency in HIV+ individuals. Nevertheless, so far no one has completely unraveled the cause of tropical pyomyositis.

Laboratory Diagnosis

Apart from the bacteriology of the infecting organism, laboratory tests do not provide any specific information. Some patients are anemic, but not more so than the rest of the local population. The erythrocyte sedimentation rate is raised, but there is often very little cellular response. The white cell count is normal or mildly increased; the differential cell count is normal. There is no eosinophilia and no parasites have been identified. Considering that there may be several hundred milliliters of pus, these negative results are unexpected.

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