The clinical features of putative ZVD-induced myopathy are much the same as those of HIV myopathy except that moderate pain is said to be characteristic of the drug-induced variety. The myopathy has been attributed to the mitochondrial toxicity of the drug, which may account for the presence of “ragged red” fibers in biopsy specimens. The onset of symptoms appears to be related to the sustained administration of high doses of the drug (1,200 mg daily for a year or longer). Cessation or reduction in dosage of the drug diminishes the muscular discomfort within weeks, but strength recovers more slowly.
Distinguished from the HIVand ZVD-related inflammatory myopathies is the severe generalized muscle wasting that characterizes advanced, cachectic AIDS. Muscle enzymes are normal and strength is affected little, especially considering the loss of muscle bulk. Histologically, there is atrophy of type 2 fibers. The pathogenesis of this cachectic syndrome is uncertain; it has been attributed to a multiplicity of systemic factors, including circulating catabolic cytokines, just as in other wasting syndromes such as cancer.
A myopathy caused by HTLV-I infection also simulates polymyositis in its clinical and histologic features. The illness occurs most often in endemic areas but is less common than the myelopathy that is associated with the virus.
In most patients with pleurodynia (epidemic myalgia, Bornholm disease), muscle biopsies disclose no abnormalities and there is no clear explanation of the pain. However, group B Coxsackie virus has been isolated from striated muscle of a few patients with this disorder. A necrotizing myositis has been suspected in a number of patients with influenza; under the electron microscope, some muscle fibers contain structures with the features of influenza virions. Malaise, myalgia, and slight weakness and stiffness were the clinical manifestations. Because of the myalgia, it is difficult to know how much of the weakness is only apparent. Recovery has been complete within a few weeks. In 1 patient with generalized myalgia and myoglobinuria, the influenza virus was isolated from muscle (Gamboa et al). These observations suggest that the intense muscle pain in certain viral illnesses might be the result of a direct viral infection of muscle. However, there are many cases of influenzal myalgia, mainly of the calves and thighs, such as those reported by Lundberg and by Antony and coworkers, in which it was not possible to establish that there was a muscular disorder at all. In the condition described as epidemic neuromyasthenia (benign myalgic encephalomyelitis, Icelandic disease), in which influenza-like symptoms were combined with severe pain and weakness of muscles, a viral cause was postulated, but an organism was never isolated. The illness has been absorbed into the large and indistinct category of chronic fatigue syndrome (discussed in Chap. 23).
Despite these ambiguities, viral myositis is an established entity in myopathology. Echo 9, adenovirus 21, herpes simplex, Epstein-Barr virus, coxsackievirus, and Mycoplasma pneumoniae have all been cited by Mastaglia and Ojeda and by others as causes of sporadic myositis with rhabdomyolysis. In these infections the nonmyopathic aspects of the disease usually predominate; in some of them, the evidence of invasion of muscle has not been fully substantiated, as in many instances a nonspecific (Zenker-type) degeneration could have explained the muscle findings. The existence of a postinfectious type of polymyositis is also unsettled.