Infectious Myositis

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Background

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.

Pathophysiology

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.[3]


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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.


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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.

Epidemiology

Frequency

United States

International

Mortality/Morbidity

Race

Sex

Infectious myositis has a male predominance.

Age

Infectious myositis typically is seen in young adults.

History

Physical

Causes

Known pathogens include the following:

Laboratory Studies

Imaging Studies

Other Tests

Trichinosis: Skin test with trichinellar antigen is unreliable.

Procedures

Histologic Findings

Trichinosis

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.

Pyomyositis

Widespread necrosis of muscle fibers, perimysium, and blood vessels is noted. Pleomorphic inflammatory response consisting of both neutrophils and lymphocytes is noted.

Cysticercosis

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.

Lyme myositis

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.


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Histopathology: Borrelia burgdorferi spirochetes in Lyme disease, with Dieterle silver stain. Courtesy of Centers for Disease Control and Prevention a....

Trypanosomiasis

Sections of infected tissues may reveal clusters of amastigotes in muscle cells surrounded by acute or chronic inflammation.

Influenza myositis

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.

Fungal myositis

Muscle biopsy is needed to confirm diagnosis. Budding yeast and pseudohyphae may be seen.

Medical Care

All medical care should be provided in conjunction with an infectious disease specialist and the primary care physician.

Surgical Care

Pyomyositis: During the suppurative phase, abscess aspiration under ultrasonic or CT guidance may be required. Surgical drainage is especially necessary for large abscesses.

Fungal myositis: Focal fungal abscesses may require surgical drainage/debridement.

Consultations

Medication Summary

Treat the underlying cause of infectious myositis. Use appropriate antibiotics for pyomyositis. Prednisone may be effective to treat HIV-1–associated polymyositis.[7]

Prednisone (Sterapred)

Clinical Context:  Can be used for HIV-1–associated polymyositis. Use in combination with thiabendazole for trichinosis.

Class Summary

These agents decrease inflammatory reactions by reversing increased capillary permeability and suppressing PMN activity.

Thiabendazole (Mintezol)

Clinical Context:  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.

Mebendazole (Vermox)

Clinical Context:  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.

Class Summary

Parasite biochemical pathways are sufficiently different from those of the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Tetracycline (Sumycin)

Clinical Context:  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).

Ceftriaxone (Rocephin)

Clinical Context:  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.

Cefazolin (Ancef)

Clinical Context:  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.

Cephalexin (Keflex, Biocef)

Clinical Context:  Indicated for treatment of infections by S aureus (including penicillinase-producing strains) and streptococci

Vancomycin (Vancocin)

Clinical Context:  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.

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Further Inpatient Care

Pyomyositis: Hospitalize for systemic antibiotics.

Deterrence/Prevention

Complications

Prognosis

Author

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.

Specialty Editors

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.

Chief Editor

Karen L Roos, MD, John and Nancy Nelson Professor of Neurology, Professor of Neurological Surgery, Department of Neurology, Indiana University School of Medicine

Disclosure: Nothing to disclose.

References

  1. O'Neill DS, Baquis G, Moral L. Infectious myositis. A tropical disease steals out of its zone. Postgrad Med. Aug 1996;100(2):193-4, 199-200. [View Abstract]
  2. Crum NF. Bacterial pyomyositis in the United States. Am J Med. Sep 15 2004;117(6):420-8. [View Abstract]
  3. Reimers CD, de Koning J, Neubert U, et al. Borrelia burgdorferi myositis: report of eight patients. J Neurol. May 1993;240(5):278-83. [View Abstract]
  4. Costa RM, Dumitrascu OM, Gordon LK. Orbital myositis: diagnosis and management. Curr Allergy Asthma Rep. Jul 2009;9(4):316-23. [View Abstract]
  5. Wong SL, Anthony EY, Shetty AK. Pyomyositis due to Streptococcus pneumoniae. Am J Emerg Med. Jun 2009;27(5):633.e1-3. [View Abstract]
  6. Trusen A, Beissert M, Schultz G, et al. Ultrasound and MRI features of pyomyositis in children. Eur Radiol. May 2003;13(5):1050-5. [View Abstract]
  7. Simpson DM, Citak KA, Godfrey E, et al. Myopathies associated with human immunodeficiency virus and zidovudine: can their effects be distinguished?. Neurology. May 1993;43(5):971-6. [View Abstract]
  8. Belman AL, Preston T, Milazzo M. Human immunodeficiency virus and acquired immunodeficiency syndrome. In: Goetz, Pappert, eds. Textbook of Clinical Neurology;1999:898-900.
  9. Crum-Cianflone NF. Bacterial, fungal, parasitic, and viral myositis. Clin Microbiol Rev. Jul 2008;21(3):473-94. [View Abstract]
  10. Crum-Cianflone NF. Nonbacterial myositis. Curr Infect Dis Rep. Sep 2010;12(5):374-82. [View Abstract]
  11. Hays AP, Gamboa ET. Acute viral myositis. In: Engel, Franzini-Armstrong, eds. Myology: Basic and Clinical. 2nd ed. 1994:1399-409.
  12. Kim JY, Park YH, Choi KH, et al. MRI of tuberculous pyomyositis. J Comput Assist Tomogr. May-Jun 1999;23(3):454-7. [View Abstract]
  13. Patel SR, Olenginski TP, Perruquet JL, Harrington TM. Pyomyositis: clinical features and predisposing conditions. J Rheumatol. Sep 1997;24(9):1734-8. [View Abstract]
  14. Tulio AM et al. Strickland TG. American trypanosomiasis. 7th ed. Hunter's Tropical Medicine; 1991:628-37.

Ixodes scapularis (dammini), tick vector for Lyme disease. Courtesy of Centers for Disease Control and Prevention.

Trypanosoma cruzi in blood smear. Courtesy of Centers for Disease Control and Prevention.

A patient with trichinosis and ocular involvement. Courtesy of Centers for Disease Control and Prevention and Dr. Thomas F. Sellers, Jr.

Histopathology: Borrelia burgdorferi spirochetes in Lyme disease, with Dieterle silver stain. Courtesy of Centers for Disease Control and Prevention and Dr Edwin P. Ewing, Jr.

Ixodes scapularis (dammini), tick vector for Lyme disease. Courtesy of Centers for Disease Control and Prevention.

Trypanosoma cruzi in blood smear. Courtesy of Centers for Disease Control and Prevention.

A patient with trichinosis and ocular involvement. Courtesy of Centers for Disease Control and Prevention and Dr. Thomas F. Sellers, Jr.

Histopathology: Borrelia burgdorferi spirochetes in Lyme disease, with Dieterle silver stain. Courtesy of Centers for Disease Control and Prevention and Dr Edwin P. Ewing, Jr.