INTRODUCTION — Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation [1]. The clinical approach to pyomyositis will be reviewed here. Other soft tissue infections such as clostridial myonecrosis and necrotizing fasciitis are discussed separately. (See "Clostridial myonecrosis" and "Necrotizing soft tissue infections".)
EPIDEMIOLOGY — Pyomyositis is classically an infection of the tropics, although it has been recognized in temperate climates with increasing frequency [2-7]. Tropical pyomyositis primarily occurs in two age groups: children (ages 2 to 5) and adults (ages 20 to 45), while the majority of temperate pyomyositis cases occurs in adults. Males appear to be more commonly affected than females. Most patients with tropical pyomyositis are otherwise healthy without underlying comorbidities, while most patients in temperate regions are immunocompromised or have other serious underlying conditions.
Predisposing factors — Predisposing factors associated with pyomyositis include immunodeficiency, trauma, injection drug use, concurrent infection, and malnutrition [2,8-12].
Immunodeficiency — Immunodeficiency has been implicated in the development of pyomyositis in both temperate and tropical climates. Forms of immunodeficiency associated with pyomyositis include HIV infection, diabetes mellitus, malignancy, cirrhosis, renal insufficiency, organ transplantation, and administration of immunosuppressive agents [2,13].
HIV infection is a particularly important risk factor [2,5,11,14-18]. A case-control series in Uganda demonstrated a significant association between pyomyositis and HIV infection [5]. In a review of 98 cases in North America, about half of pyomyositis patients with underlying medical conditions were seropositive for HIV. The mechanism of HIV infection in the predisposition to pyomyositis is unclear; factors may include immune compromise, primary HIV myopathy, antiretroviral therapy, and increased rates of staphylococcal carriage [2,5,17,18].
Trauma — Trauma has been postulated as a predisposing factor for pyomyositis; about 25 to 50 percent of patients with pyomyositis report a history of trauma. In addition, pyomyositis has been described in temperate regions among athletes performing vigorous exercise, suggesting the potential role of minor muscle damage in the pathogenesis of the disease [19-25]. Development of infection may be related to hematoma formation or increased muscle perfusion due to trauma, providing additional iron to the muscle bed for favorable bacterial growth conditions [4,7].
Injection drug use — Injection drug use, which has been a major complication of the opioid epidemic in the United States, has been associated with pyomyositis-induced bacteremia. Local injection site infection and abscess extension into muscle tissue should not be confused with true pyomyositis caused by hematogenous seeding of muscle groups distant from injection sites [26-29].
Concurrent infection — Toxocariasis has been associated with the subsequent development of pyomyositis, perhaps because of predisposing muscle damage and impaired local immunity [30]. Underlying skin conditions predisposing to secondary bacteremia, such as varicella infection, have also been described [2,31].
MICROBIOLOGY — Staphylococcus aureus is the most common cause of pyomyositis; it causes up to 90 percent of tropical cases and up to 75 percent of temperate cases [2,4,8-10,12,32]. Methicillin-resistant S. aureus (MRSA), including community-acquired strains, is also an increasingly important pathogen [33-36]. In a retrospective review of 29 adults with pyomyositis, MRSA comprised 25 percent of cases due to S. aureus [35]. Group A beta-hemolytic streptococcus is the second most common pathogen.
Less common causes include non-group A, beta-hemolytic streptococci, pneumococci, and gram-negative enteric bacilli [2,3,9,12,26,37-39]. Escherichia coli pyomyositis is an emerging infection among patients with hematologic malignancy [40]. It is usually caused by members of E. coli ST131, a cause of fluoroquinolone-resistant, extended-spectrum beta-lactamase-positive E. coli infection worldwide. Meningococcal pyomyositis has been described in a case report [41].
Mycobacterial pyomyositis has also been reported [39,42-46]. Pyomyositis can also be polymicrobial, particularly in diabetic patients [2].
CLINICAL MANIFESTATIONS — Pyomyositis presents with fever and pain with cramping localized to a single muscle group. The disease occurs most often in the lower extremity (sites include the thigh, calf, and gluteal muscles), but any muscle group can be involved, including the iliopsoas, pelvic, trunk, paraspinal, and upper extremity muscles [2,47]. Multifocal infection with involvement of more than one muscle group may be observed in up to 20 percent of cases [2,48].
Pyomyositis can be divided into three clinical stages [32]:
●Stage 1 is characterized by crampy local muscle pain, swelling, and low-grade fever. Mild leukocytosis and induration of the affected muscle may be present. A deep abscess may not be discretely palpable, but the muscle may have a "woody" texture on palpation. Fluctuation is not present, and aspiration of the muscle will not yield purulent material. Only 2 percent of patients present at this stage.
●Stage 2 occurs 10 to 21 days after the initial onset of symptoms and is characterized by fever, exquisite muscle tenderness, and edema. A frank abscess may be clinically apparent, and aspiration of the affected muscle typically yields pus [49]. Marked leukocytosis is usually present. More than 90 percent of the patients present at this suppurative stage.
●Stage 3 is characterized by systemic toxicity. The affected muscle is fluctuant. Complications of S. aureus bacteremia such as septic shock, endocarditis, septic emboli, pneumonia, pericarditis, septic arthritis, brain abscess, and acute renal failure can occur [50,51]. Rhabdomyolysis has also been described [38].
The course of pyomyositis is variable. Although most patients present with stage 2 or 3 disease, some experience a more indolent course; a delay in diagnosis in such cases may result in involvement of multiple muscle groups, requiring prolonged therapy. Recurrent infection is rare but has been described in immunocompromised individuals [2]. Mortality due to pyomyositis was reported to be as high as 10 percent in one retrospective cohort study [52].
DIFFERENTIAL DIAGNOSIS — Pyomyositis may be confused with muscle strain, contusion, hematoma, cellulitis, deep vein thrombosis, osteomyelitis, septic arthritis, or neoplasm. It must also be distinguished from clostridial myonecrosis, necrotizing fasciitis, spontaneous gangrenous myositis, diabetic muscle infarction, septic arthritis, and other forms of myositis (table 1). (See "Clostridial myonecrosis" and "Necrotizing soft tissue infections" and "Diabetic muscle infarction".)
DIAGNOSIS — Tools for diagnosis of pyomyositis include radiography, cultures, and laboratory data.
Radiography — Radiographic imaging is the most useful tool for diagnosing pyomyositis, defining the site(s) of infection, and for ruling out other entities, and magnetic resonance imaging (MRI) is the optimal imaging technique [1,53]. It is highly sensitive for muscle inflammation, even prior to the formation of a frank abscess, and can demonstrate the extent of involvement. MRI findings include diffuse muscle enlargement with an increase in signal intensity on T2-weighted images and intermediate signal on T1-weighted images as well as single or multiple intramuscular abscesses with peripheral enhancement [8,53-55].
If MRI is not available, computed tomography is helpful for detecting muscle swelling and well-delineated areas of fluid attenuation that display rim enhancement with contrast, as well as for radiographic-guided drainage of purulent material [56]. Ultrasonography is also a potentially useful diagnostic and therapeutic tool, particularly during the purulent stage of infection when it may reveal diffuse muscle hyperechogenicity with or without localized hypoechogenicity and diffuse hyperemia (image 1) [57,58].
Cultures — Bacteriologic diagnosis can be made by cultures of drainage specimens. Diagnostic aspiration and/or drainage prior to antibiotic therapy is critical in identification of a pathogen, particularly in cases where blood cultures are negative, with susceptibility testing to direct specific therapy.
Blood cultures are positive in up to 10 percent of tropical cases and 35 percent of temperate cases [1,2,4]. Given that the pathogenesis of pyomyositis likely involves bloodstream infection, patients with pyomyositis should be evaluated for the presence of additional complications of bacteremia. Rarely, pyomyositis has been described in association with endocarditis [28,59]. In the setting of systemic toxicity, at least two sets of blood cultures should be obtained prior to initiation of antimicrobial therapy; presence of bacteremia should prompt a careful clinical assessment for signs and symptoms of infective endocarditis. (See "Clinical approach to Staphylococcus aureus bacteremia in adults".)
Laboratory data — Nonspecific laboratory findings include leukocytosis with left shift and elevated inflammatory markers (erythrocyte sedimentation rate and C-reactive protein). Eosinophilia should raise suspicion for a concomitant parasitic infection [60]. Counterintuitively, creatine kinase levels are often normal [2,3].
TREATMENT — Although stage 1 pyomyositis can be treated with antibiotics alone, most patients present with stage 2 or 3 disease and therefore require both antibiotics and drainage for definitive management [32].
Drainage — Image-guided percutaneous drainage is an option for many patients and can be useful both to secure a microbiologic diagnosis early in patient evaluation and as a therapeutic measure when combined with antimicrobial therapy. Percutaneous drainage is often computed tomography guided, but, in selected patients, an ultrasound (US)-guided procedure is an option. In the setting of deep infection or extensive muscle involvement with significant necrosis, however, surgical intervention may be required. Regardless of the type of drainage procedure done, antimicrobial therapy should be initiated without delay in patients who present with systemic toxicity.
Antibiotics — For immunocompetent individuals, initial empiric parenteral antibiotic therapy should be directed against staphylococci, including methicillin-resistant S. aureus (MRSA) and beta-hemolytic streptococci [1]. Parenteral agents for treatment are outlined in the table (table 2). (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology", section on 'Risk factors' and "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Treatment of bacteremia".)
For immunocompromised individuals, broad antibiotic coverage for gram-positive, gram-negative, and anaerobic organisms should be administered. In such circumstances, vancomycin may be combined with a broad-spectrum regimen that has activity against gram negatives and anaerobes (table 3).
Clindamycin is sometimes included in the antibiotic regimen for severe infections due to S. aureus or beta-hemolytic streptococci because it has several unique characteristics. It suppresses synthesis of bacterial toxins and penicillin-binding proteins, which are involved in cell wall synthesis and degradation, it has a longer post-antibiotic effect compared with beta-lactams, and it is not affected by bacterial inoculum size or stage of growth. It is not known whether the addition of clindamycin as adjunctive therapy can reduce morbidity and mortality rates in severely ill patients with pyomyositis due to these organisms. We do not routinely use it for this purpose in the absence of necrotizing infection or toxic shock syndrome. (See "Staphylococcal toxic shock syndrome", section on 'Antibiotic therapy' and "Necrotizing soft tissue infections", section on 'Antibiotic therapy'.)
The duration of antimicrobial therapy should be tailored to clinical and radiographic improvement. Three to four weeks of parenteral therapy is usually sufficient, although patients with extensive, multifocal, or poorly drained infection may warrant longer courses of therapy [2]. The course of therapy for patients with other sequelae of bacteremia (such as endocarditis or osteomyelitis) should be adjusted based on the nature of infection at these other sites [4]. In rare cases of infections caused by mycobacteria, the nature and duration of treatment should be tailored to the species identified.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Skin and soft tissue infections".)
SUMMARY AND RECOMMENDATIONS
●Pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, usually with abscess formation. It is classically an infection of the tropics, although it has been recognized in temperate climates with increasing frequency. (See 'Epidemiology' above.)
●Risk factors for pyomyositis include immunodeficiency (particularly HIV infection), trauma, injection drug use, concurrent infection, and malnutrition. (See 'Predisposing factors' above.)
●Staphylococcus aureus is the most common cause of pyomyositis; it causes up to 90 percent of tropical cases and up to 75 percent of temperate cases. Methicillin-resistant S. aureus, including community-acquired strains, is also an increasingly important pathogen. (See 'Microbiology' above.)
●Pyomyositis presents with fever and pain with cramping localized to a single muscle group. It develops most often in the lower extremity (sites include the thigh, calf, and gluteal muscles), but any muscle group can be involved, including the iliopsoas, pelvic, trunk, paraspinal, and upper extremity muscles. The clinical stages of pyomyositis are outlined above. (See 'Clinical manifestations' above.)
●Radiographic imaging with magnetic resonance imaging is the most useful tool for diagnosing pyomyositis, defining the site(s) of infection, and for ruling out other entities. Bacteriologic diagnosis can be made by cultures of drainage specimens and/or blood. Nonspecific laboratory findings include leukocytosis and elevated inflammatory markers; creatine kinase levels are often normal [2,3]. (See 'Diagnosis' above.)
●Although stage 1 pyomyositis can be treated with antibiotics alone, most patients present with stage 2 or 3 disease and therefore require both antibiotics and drainage for definitive management. (See 'Treatment' above.)
●For immunocompetent individuals, initial empiric parenteral antibiotic therapy should be directed against staphylococci and beta-hemolytic streptococci. For immunocompromised individuals, broad antibiotic coverage for gram-positive, gram-negative, and anaerobic organisms should be considered. Reasonable antibiotic regimens are outlined in the tables (table 2 and table 3). (See 'Antibiotics' above.)
