Diagnosis Clinically, one should suspect the disease in a patient who presents with a puffy face and tender muscles. Eosinophilia is practically always present in the peripheral blood (>700 cells/mm3), although the sedimentation rate is often normal. The CK level is moderately elevated. A skin test using Trichinella antigen is available, but it is unreliable. The enzyme-linked immunosorbent assay (ELISA) blood test is more accurate, but it becomes positive only after 1 or 2 weeks of illness. Biopsy of almost any muscle (usually the deltoid or gastrocnemius), regardless of whether it is painful or tender, is probably the most reliable confirmatory test. More than 500 mg of muscle may be required to demonstrate larvae, but smaller specimens will almost invariably show an inflammatory myopathy. Muscle fibers undergo segmental necrosis, and the interstitial inflammatory infiltrates contain a predominance of eosinophils. This accounts for the edema, pain, and tenderness of heavily infested muscles. The capsules of the larvae gradually thicken in the first month of the infection and then calcify. The EMG may exhibit profuse fibrillation potentials, a phenomenon attributed on theoretical grounds to the disconnection of segments of muscle fibers from their motor endplates (Gross and Ochoa).
Treatment No treatment is required in most cases. In patients with severe weakness and pain, a combination of thiabendazole, 25 to 50 mg/kg daily in divided doses for 5 to 10 days, and prednisone, 40 to 60 mg/d, is recommended. Albendazole, in a single oral dose of 400 mg daily, or mebendazole are equally effective but are quite expensive in the United States. Recovery, as mentioned, is complete as a rule, except in rare patients with cerebral infarcts. Other aspects of this parasitic infestation are discussed in Chap. 31.
This is an acute or subacute systemic infection caused by the encephalitozoon Toxoplasma gondii. Most Toxoplasma infections in immunocompetent patients, which occur in up to 10 to 30 percent of the population, are asymptomatic, but there may be fever and varying degrees of involvement of the skin, lymph nodes, retina, myocardium, liver, brain, and muscle. In one such case studied by our colleagues, Toxoplasma organisms and pseudocysts were detected in skeletal muscle (Kass et al); wherever a parasitic pseudocyst had ruptured, there was focal inflammation. Some muscle fibers had undergone segmental necrosis, but this was not prominent (one contained the organism), accounting for the relative paucity of muscle symptoms. With the emergence of HIV, many more toxoplasmic infections of the brain, but also including those of skeletal muscle, were seen (Gherardi et al). However, physicians who see many cases of HIV have indicated to us that a primary HIV myopathy and treatment-related muscle diseases are more common (see later under “HIV and Human T-Lymphotropic Virus Type I Myositis”). Again, in this population, brain infestation with Toxoplasma is many times more common than is myositis. The subject of HIV is discussed in Chap. 31 and toxoplasmic infection is discussed in greater detail in Chap. 32.