Infectious myositis is an acute, subacute, or chronic infection of skeletal muscle. Once considered a tropical disease, it is now seen in temperate climates as well, particularly with the emergence of HIV infection.[1, 2] In addition to HIV, other viruses, bacteria (including mycobacteria), fungi, and parasites can cause myositis. For a detailed discussion of HIV-associated myopathies, refer to HIV-1 Associated Myopathies.
Single or multiple muscle groups in the limbs can be involved, a notable exception being trichinosis, which commonly involves orbital muscles. In most instances, involvement of proximal muscles is predominant. Characteristic myopathic features and findings of polymyositis, including inflammatory infiltrates, may be seen.
Viruses: Viruses implicated in the pathogenesis of myositis include HIV-1, human T lymphotrophic virus 1 (HTLV-1), influenza, coxsackieviruses, and echoviruses. As in the non–HIV-infected population, HIV-associated polymyositis is most likely autoimmune in origin. Influenza myositis could be due to direct viral invasion or autoimmune response.
Pyomyositis: The pathogenesis is unclear, but trauma, viral infection, and malnutrition have been implicated. Although most cases of pyomyositis occur in healthy individuals, other pathogenetic factors include nutritional deficiency and associated parasitic infection in tropical climates. In the temperate climates, pyomyositis is seen most commonly in patients with diabetes, HIV infection, and malignancy.
Lyme borreliosis: Musculoskeletal manifestations are noted frequently in Lyme borreliosis. The disease is transmitted by the bites of ticks of the Ixodes genus that carry the spirochete (see image below). The animal reservoirs are the white-footed mouse in the Eastern United States and the wood rat in California. Human infection results from the bite of infected ticks in the late spring and early summer. Lyme myositis may result from direct invasion of muscle by the spirochete Borrelia burgdorferi or by autoimmune mechanisms.
Ixodes scapularis (dammini), tick vector for Lyme disease. Courtesy of Centers for Disease Control and Prevention.
American trypanosomiasis: The causative organism is a protozoan, Trypanosoma cruzi. The insect vectors are reduviid bugs such as Rhodnius prolixus ("vinchuca"), Triatoma infestans, and Panstrongylus megistus. The insect defecates on the host's skin as it feeds, contaminating the bite wound with feces containing the parasites. T cruzi occurs in 2 forms in humans, the intracellular amastigote and the trypomastigote form in blood, which is ingested by the insects (see image below). The parasite reproduces asexually and migrates to the hindgut. In humans, the parasite loses its flagellum and transforms into the amastigote form, which may enter muscle and multiply, resulting in myositis.
Trypanosoma cruzi in blood smear. Courtesy of Centers for Disease Control and Prevention.
Cysticercosis: Myositis also can occur in cysticercosis, which represents an infection by the larval stage of the intestinal tapeworm Taenia solium. Human infection results from ingestion of raw or incompletely cooked pork. Another mode of infection is by contamination of food and water by feces containing the eggs of the tapeworm. The larvae migrate throughout the body and may form fluid-filled cysts in a variety of tissues, including muscle.
Pyomyositis: Approximately 676 cases have been reported in the US literature since 1971.
Lyme disease: Endemic areas include the Northeast, mainly Connecticut, Massachusetts, Maryland, and New York; the North-Central region, mainly Wisconsin and Minnesota; and the West Coast, especially Northern California.
In eastern Uganda, 400-900 cases of tropical myositis occur per year; it is rare in western Kenya.
Cysticercosis is most prevalent in India, Eastern Europe, Central America, and Mexico.
In endemic areas of Latin America, 8% of the population is seropositive for American trypanosomiasis.
A potentially life-threatening complication of pyomyositis is toxic shock syndrome.
Rhabdomyolysis can complicate influenza and, rarely, coxsackievirus myositis.
In Hawaii, muscle abscesses were noted to be confined to the Polynesians.
In the French Pacific islands, the disease is not seen in the French settlers.
Infectious myositis has a male predominance.
Infectious myositis typically is seen in young adults.
Parasitic -T gondii, Trichinella spiralis, Trichinella nativa (from eating bear meat), T nelsoni, T britovi, T pseudospiralis, Echinococcus granulosus, T solium, T cruzi, microsporidia
Fungal -Cryptococcus neoformans, Candida species (especially Candida tropicalis, Candida krusei, Candida albicans) , Histoplasma capsulatum, Coccidioides species , Aspergillus species , Pneumocystis jiroveci, Fusarium species, and Actinomyces species; less common are mucormycosis, Sporothrix schenckii, and Blastomyces dermatitidis
MRI is the imaging modality of choice for the diagnosis of pyomyositis. MRI is helpful in differentiating pyomyositis from osteomyelitis. It is especially useful in differentiating early muscle inflammation from abscess formation. MRI is also the best imaging modality for evaluation of pelvic infections.
CT scanning may show hypertrophy of involved muscle groups and effacement of the fat planes. Contrast enhancement may indicate abscess formation. CT is also useful for distinguishing tumors and hematomas from abscess.
Ultrasound or MRI also may be used to localize involved muscle.
Gallium scan is useful for localization in the early stages of illness.
MRI: Findings are consistent with an abscess (ie, low signal intensity on T1-weighted images and high signal intensity on T2-weighted images of affected muscles).
Following gadolinium infusion, peripheral rim enhancement is noted. This is indicated by subtle hyperintensity on T1-weighted images and hypointensity on T2-weighted images.
Cysticercosis with orbital involvement: Multiplanar imaging with MRI may be obtained to identify a cyst with a mural nodule. With gadolinium, a nodule shows intense enhancement.
Imaging of soft tissue or muscles may demonstrate the calcified lesions with classic "puffed rice" or "spindle-shaped" radiographic appearance.
MRI, CT, and ultrasonography may show a clear cyst with a scolex.
MRI is superior at demonstrating the cysts in the soft tissues.
Muscle biopsy is required to confirm diagnosis. Findings in the acute stage of larval invasion of the muscles include segmental necrosis and interstitial infiltrates composed mainly of eosinophils. The Trichinella species larvae sometimes can be seen in the muscle biopsy. However, encapsulated cysts (without larvae), granulomas, and focal calcification are more likely to be encountered.
Widespread necrosis of muscle fibers, perimysium, and blood vessels is noted. Pleomorphic inflammatory response consisting of both neutrophils and lymphocytes is noted.
The viable larvae produce little or no tissue reaction. However, rupture or death of a cysticercus (mature larva) evokes an acute inflammatory response with a pleomorphic exudate composed of neutrophils and eosinophils. Over time, fibrous tissue encapsulates the cysts. A chronic granulomatous response may surround the cysts.
Muscle biopsy shows atrophic fibers and an infiltrate consisting of lymphocytes, plasma cells, and macrophages. Borrelia burgdorferi can be detected in muscle fibers by the modified Dieterle silver stain method.
Histopathology: Borrelia burgdorferi spirochetes in Lyme disease, with Dieterle silver stain. Courtesy of Centers for Disease Control and Prevention a....
Sections of infected tissues may reveal clusters of amastigotes in muscle cells surrounded by acute or chronic inflammation.
Muscle fiber necrosis without inflammatory change is observed. Influenza viral particles have been identified in muscle fibers under electron microscopy. Muscle fiber regeneration is seen in some, with an inflammatory response consisting of mononuclear and polymorphonuclear leukocytes.
Muscle biopsy is needed to confirm diagnosis. Budding yeast and pseudohyphae may be seen.
All medical care should be provided in conjunction with an infectious disease specialist and the primary care physician.
HIV polymyositis: Corticosteroids remain the mainstay of treatment of polymyositis.
Thiabendazole is effective if administered within 24 hours of infection. It has minimal effect in established infection.
Optimal dosage has not been established.
It can be combined with prednisone 40-60 mg/day in patients with severe pain and weakness.
Benznidazole is a trypanocidal drug that is quite effective in the acute phase of the illness.
It reduces cardiac complications and parasitemia and has been found to be beneficial in the early chronic phase.
Successful treatment is evinced by serological tests remaining negative for at least 1 year after conclusion of treatment.
Treatment comprises bed rest, intravenous fluids, and symptomatic management with antipyretics and analgesics.
Antiviral agents such as amantadine could be considered in adults.
Tuberculous and toxoplasmal myositis, cysticercosis: Please refer to the following articles: HIV-1 Associated Myopathies, Neurocysticercosis, and Neuroimaging in Neurocysticercosis.
Promptly administer systemic antibiotics. This could eliminate the need for surgical drainage in selected cases.
The choice of antibiotic is determined by identification of the causative organism.
Antibiotics initially are given intravenously until clinical improvement is noted, followed by oral antibiotics for a total course of 3 weeks (eg, cefazolin or ceftriaxone IV followed by cephalexin PO).
Fungal myositis: Use an antifungal agent such as amphotericin B or an echinocandin such as caspofungin.
Treats trichinosis infections; inhibits helminth-specific mitochondrial fumarate reductase; alleviates symptoms of trichinosis during invasive phase. Little value in disease that spreads beyond lumen of intestines; absorption from GI tract is poor.
May be useful in early stages of trichinosis. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.
For treatment of Lyme myositis. Treats gram-positive and gram-negative organisms as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).
Drug of choice for most neurologic manifestations of Lyme disease; third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to penicillin-binding proteins.
Can be used for treatment of pyomyositis. Semisynthetic cephalosporin effective against: S aureus (including penicillinase-producing strains), Staphylococcus epidermidis, group A beta-hemolytic streptococci, and other strains of streptococci.
For treatment of severe infections caused by methicillin-resistant (beta-lactam-resistant) staphylococci; and for treatment of staphylococcal infection in individuals allergic to penicillin or cephalosporins.
Prevent trichinosis and cysticercosis by adequately processing pork.
When traveling in endemic areas of Latin America, apply insect repellents such as N -diethyl-meta-toluamide (DEET) to avoid American trypanosomiasis. Pyrethrin insecticides also may be used to kill insect vectors. Using bed nets to keep away insects is advisable.
Mohammed J Zafar, MD, FAAN, Associate Clinical Professor of Medicine, Kalamazoo Center for Medical Studies, Michigan State University College of Human Medicine; Neurologist, Clinical Neurophysiologist and Neuroimager, Kalamazoo Nerve Center, PLLC
Disclosure: Nothing to disclose.
Roberta J Seidman, MD, Associate Professor of Clinical Pathology, Stony Brook University; Director of Neuropathology, Department of Pathology, Stony Brook University Medical Center
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Florian P Thomas, MD, MA, PhD, Drmed, Director, Regional MS Center of Excellence, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Director, Neuropathy Association Center of Excellence, Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine
Disclosure: Nothing to disclose.
Karen L Roos, MD, John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine