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.
Race-, sex-, and age-related demographics
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 and is typically seen in young adults.
Risk factors for Staphylococcus aureus pyomyositis - Strenuous activity, muscle trauma, skin infections, infected insect bites, illicit drug injections, connective tissue disorders, and diabetes
Consumption of poorly cooked meats (especially pork products in the case of trichinosis or cysticercosis)
Psoas abscess - Subtle symptoms such as fever and flank and hip pain; may manifest as pyrexia of unknown origin; may be primary (no identifiable source of infection/from occult hematogenous spread) or secondary (spread from infection in the vicinity)
Occur mostly in the immunocompromised
Fever and malaise
Most common form is group A streptococci (GAS) necrotizing myositis/streptococcal myonecrosis
Usually seen in the men and young adults
Spontaneous occurrence (no history of penetrating trauma) or in the immunocompromised
Cardinal features - Myalgia, periorbital swelling, and fever (see following image)
A patient with trichinosis and ocular involvement. Courtesy of Centers for Disease Control and Prevention and Dr. Thomas F. Sellers, Jr.
Depending on site of involvement - Diplopia, dysarthria, dysphagia, dyspnea
Pain and weakness of the proximal muscle groups
Symptoms in the vicinity of skin lesions or in limb muscles
Cysticercosis with myositis - Fever, myalgias
Trypanosomiasis with myositis
May be asymptomatic or characterized by fever
Myositis occurring in the early stage of infection - Symptoms such as muscle weakness and myalgias mimicking those of polymyositis
Chronic stage - Myalgias
Toxoplasma myositis - Fever, myalgias, and muscle weakness
Influenza myositis - Childhood and adult forms recognized
Fever, malaise, and rhinorrhea followed 1-7 days later by severe pain, especially in the calves
Muscle pain worse with movement, especially with walking
Symptoms of myositis - Generally last 1-7 days
Fever, myalgias, generalized weakness
Muscle swelling in some patients
Acute coxsackievirus myositis
Group A virus infection - Myalgias, weakness
Group B virus infection - Causes epidemic pleurodynia (Bornholm disease or epidemic myalgia), which is considered a form of myositis
This is an acute, febrile disorder with abrupt onset of pain in the abdomen or lower thoracic region.
Pain can be referred to the back and shoulders.
Pain is worse with movement, breathing, or coughing.
Most often seen in severely immunosuppressed patients
Clinical presentation is similar to pyomyositis
Rare cause of myositis
Most involve immunocompromised patients.
Symptoms overlap those of bacterial myositis.
Often present with lower extremity pain and swelling
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.
Streptococcal myositis - CT scan helpful in assessing extent of muscle involvement and necrosis
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.
Muscle necrosis and gram-positive bacteria in chains 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).
High-dose penicillin G (4 million units) and clindamycin (800-900mg) IV
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, FACP, Associate Clinical Professor of Medicine, West Michigan University School of Medicine; Neurologist, Clinical Neurophysiologist and Neuroimager, Kalamazoo Nerve Center, PLLC
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: Received salary from Medscape for employment. for: Medscape.
Florian P Thomas, MD, PhD, Drmed, MA, MS, Director, National MS Society Multiple Sclerosis Center; Professor and Director, Clinical Research Unit, Department of Neurology, Adjunct Professor of Physical Therapy, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine
Disclosure: Nothing to disclose.
Niranjan N Singh, MD, DM, Associate Professor of Neurology, University of Missouri-Columbia School of Medicine
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