The myopathy, which occurs with variable fever, lymphopenia, and failure of other organs, consists of weakness, wasting, myalgia, and elevated CK levels. Presumably, the immunocompromised patient is unable to respond to protozoan infections, allowing latent infections to be reactivated. Sulfadiazine in combination with pyrimethamine or trisulfapyrimidine, which acts synergistically against the toxoplasmic trophozoites, improves the muscle symptoms and reduces serum CK. Folic acid is given in addition.
Other Parasitic and Fungal Infections of Muscle
Echinococcosis, cysticercosis, trypanosomiasis (Chagas disease), sparganosis, toxocariasis, and actinomycosis have all been known to affect skeletal muscle on occasion, but the major symptoms relate more to involvement of other organs. Only cysticercosis may first claim the attention of the clinical myologist because of a dramatic pseudohypertrophy of thigh and calf muscles. Hydatids infest the paravertebral and lumbar girdle muscles in 5 percent of cases and may lead to their enlargement. Coenurosis and sparganosis are causes of movable lumps in the rectus abdominis, thigh, calf, and pectoralis muscles. Protozoan infections of muscle—microsporidiosis,
African and American trypanosomiasis—which occurred only rarely until a few decades ago, are now being observed in immunodeficient (HIV-infected) individuals in endemic areas. The reader who seeks more details may refer to the chapter on parasitic myositis by Banker (2004).
Viral Infections of Muscle
HIV and human T-lymphotropic (or leukemia) virus type I (HTLV-I) are increasingly common causes of viral myositis (Engel and Emslie-Smith). Moreover, as discussed further on, zidovudine (ZVD), a drug included in many regimens to treat HIV infections, may itself induce a myopathy with myalgia and weakness that is, at times, indistinguishable from HIV myopathy (Dalakas et al).
An inflammatory, and presumed infectious, myopathy may develop early in the course of HIV infection but is rarely the initial manifestation. The pattern is like that of idiopathic polymyositis with painless weakness of the girdle and proximal limb muscles. Reflexes are diminished in most cases, but this is difficult to interpret in view of the high incidence of concomitant polyneuropathy. Serum CK is elevated, and the EMG shows an active myopathy with fibrillations, brief polyphasic motor units, and complex repetitive discharges.
The myopathologic changes in AIDS are also like those of idiopathic polymyositis described further on. Additionally, in some cases electron microscopy discloses the presence of nemaline (rod) bodies within type 1 fibers, similar to those observed in the congenital form of nemaline myopathy discussed further on. As implied earlier, the pathogenesis of the HIV myopathy has not been firmly established as there is scant evidence of a direct viral infection of the muscle fibers. An immune basis has been suggested in view of a response to corticosteroids, plasma exchange, and gamma globulin, comparable to the beneficial effects in the idiopathic variety of polymyositis. Corticosteroids in doses similar to those used in the treatment of idiopathic polymyositis are effective in ameliorating the weakness, but they entail special risks in immunocompromised patients.