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Primary pyomyositis

Primary pyomyositis
Literature review current through: Jan 2024.
This topic last updated: Feb 27, 2023.

INTRODUCTION — Primary pyomyositis is a purulent infection of skeletal muscle that arises from presumed or confirmed hematogenous infection, whereas secondary pyomyositis occurs from localized penetrating trauma or contiguous spread to the muscle [1]. Primary infections usually have a subacute onset and most commonly affect the extremities or muscles of the hip and pelvis.

The clinical approach to primary pyomyositis will be reviewed here, except for psoas abscess, which is discussed elsewhere (see "Psoas abscess"). Secondary pyomyositis and other soft tissue infections, such as clostridial myonecrosis and necrotizing fasciitis, are discussed elsewhere. (See "Clostridial myonecrosis" and "Necrotizing soft tissue infections".)

DEFINITIONS — Pyomyositis is a purulent infection of skeletal muscle, often with abscess formation [1]. It is classified as either primary or secondary:

Primary pyomyositis – Pyomyositis is classified as primary if it is presumed to have occurred via hematogenous spread from prior transient bacteremia or concurrent bacteremia [2]. The bacteremia may be idiopathic or secondary to a remote site of infection.

Traditionally, primary pyomyositis was termed "tropical myositis" or "tropical pyomyositis" because it was reported most frequently in tropical regions of the world. However, new terminology has emerged because the disease can occur in any climate [3-10]. The following terms are now used interchangeably: primary pyomyositis, tropical pyomyositis, tropical myositis, infectious pyomyositis, pyogenic myositis, suppurative myositis, myositis purulenta tropica, myositis tropicans, epidemic abscess, pyomyositis, and bacterial pyomyositis.

For the purposes of this topic, we utilize the term "primary pyomyositis," regardless of geography. The only differences between tropical pyomyositis and nontropical pyomyositis are the geography and risk factors for infection.

Secondary pyomyositis – Secondary pyomyositis is due to localized penetrating trauma (eg, puncture wound) or contiguous spread to muscle from an adjacent infection (eg, appendicitis). Secondary pyomyositis is discussed in separate topics. (See "Infectious complications of puncture wounds", section on 'Evaluation'.)

EPIDEMIOLOGY

Geographic prevalence — Traditionally, primary pyomyositis was mostly reported in the tropical regions of Asia, Africa, Oceania, and the Caribbean islands [2,10,11]. Data suggest that it is responsible for 1 to 4 percent of all surgical admissions in some tropical countries [5,12-14].

Observational data suggest an increasing prevalence in temperate climates, and primary pyomyositis is estimated to account for up to 0.1 percent of pediatric admissions in these regions [7,8,15-18]. Most cases in temperate locales occur during warmer months or rainy seasons, and countries with tropical and temperate regions have higher rates of infection in the tropical regions [5,15,19-21].

Risk factors

Young age — Healthy children older than two years of age and young adults compose the majority of cases in tropical regions [2,5,10-14]. In the United States, the highest incidence of hospitalization for primary pyomyositis occurs in children, especially those between the ages of 5 and 9 years [3,8,14,17].

Exercise or muscle trauma — In case series, 20 to 60 percent of individuals with primary pyomyositis report prior vigorous exercise or nonpenetrating muscle trauma, such as a bruise or strain [5,8,10,14,15,17,19,22-32].

Immunocompromising condition — Patients with primary pyomyositis often have an underlying immunocompromising condition.

HIV infection – Human immunodeficiency virus (HIV) is a particularly important risk factor [3,6,8,14,33-39]. In a systematic review and meta-analysis of 12 studies involving over 500 individuals with pyomyositis in Africa, the only risk factors identified were HIV infection (odds ratio [OR] 4.8; 95% CI, 1.7-13.9) and acquired immunodeficiency syndrome (AIDS) (OR 6.1; 95% CI, 2.8-13.2) [39]. In a review of all pyomyositis hospitalizations in the United States between 2002 and 2014, HIV infection was the strongest risk factor identified (OR, 4.8; 95% CI, 4.3-5.4) [8].

Other immunocompromising conditions – Numerous other conditions with some level of immunocompromise have been identified in case series, including diabetes mellitus, injection drug use disorder, pregnancy, hematologic malignancy, rheumatologic conditions (eg, Felty syndrome, systemic lupus erythematosus), solid organ transplant, biologic therapies (eg, obinutuzumab, certolizumab), malnutrition, cirrhosis, and renal disease [2,3,15,22,30,32,33,40-69].

Recent infection — Recent bloodstream infection and concurrent infections (eg, pneumonia, toxocariasis, varicella, tuberculosis) have been associated with pyomyositis [17,32,39,40].

MICROBIOLOGY — The most common cause of primary pyomyositis is Staphylococcus aureus (S. aureus), including methicillin-resistant S. aureus (MRSA). S. aureus causes approximately 90 percent of tropical cases and 75 percent of cases in temperate regions [2,3,5,8,10,22,39,41-43,70-74].

Group A Streptococcus (GAS; ie, S. pyogenes) is more common in healthy children and young adults than in other patient populations; observational data suggest that 20 to 25 percent of infections in children are due to GAS [3,8,14,15,62].

Other less common microbial causes include non-GAS streptococci, gram-negative bacilli (eg, Escherichia coli, Klebsiella spp, Pseudomonas spp), and anaerobes [2-4,14,22,43,45,46,57,62,63,75-79]. Reports suggest that these pathogens occur more frequently in individuals who have serious comorbidities, such as an immunocompromising condition or injection drug use disorder. Polymicrobial infections have been reported as well.

Rarely, pyomyositis may be caused by atypical pathogens such as Neisseria gonorrhoeae, Neisseria meningitidis, mycobacteria, and Candida spp [3,14,55,58,61,77,80-86].

CLINICAL MANIFESTATIONS — Patients with pyomyositis typically present with fever and pain localized to a single muscle, although multifocal infection occasionally occurs.

Course of illness — Onset of symptoms is typically gradual, beginning with dull localized pain that becomes more severe over one to two weeks.

The illness has been described as evolving over three stages that represent progression of disease from diffuse inflammation to focal abscess to sepsis; over 95 percent of patients present with stage 2 or 3 disease [2,15,70]:

Stage 1 – Patients in stage 1 experience insidious onset of dull, crampy, localized muscle pain and swelling. Low-grade fever and mild leukocytosis may be present. Palpation may reveal induration or a "woody" texture of the affected muscle, but fluctuance is not present.

Stage 2 – Ten to 21 days after the initial onset of symptoms, stage 2 begins. Patients with stage 2 disease have fever (>100.5°F/38°C), a tender muscle mass often described as either fluctuant or firm and woody, and mildly erythematous and edematous overlying skin. Marked leukocytosis is usually present. More than 90 percent of patients with primary pyomyositis present at this stage.

Stage 3 – This stage is characterized by systemic toxicity with high fever (eg, temperature >101.3°F/38.5°C, hypotension, tachycardia) and an exquisitely tender and fluctuant muscle mass with erythema and edema.

In clinical practice, the stages may overlap, particularly for pyomyositis of the hip and pelvis [17,21,87].

Anatomic sites of infection — Primary pyomyositis can occur in any skeletal muscle. Careful clinical history and physical examination are necessary to localize symptoms and signs to the involved muscle(s), particularly for infections in young children or involving nonextremity muscles.

Most patients have only a single muscle or muscle group involved. Multifocal infection has been reported in up to 20 percent of cases [3,15,88].

Extremity muscles — Patients with pyomyositis of an extremity typically present with pain and tenderness at the site of the affected muscle group, and they may or may not have focal signs of inflammation (eg, induration, fluctuance) (picture 1).

In adults, an extremity is the most common site of infection. The lower extremity is affected more often than the upper, and hands and feet are rarely involved [3,4,14,15,64]. An understanding of the anatomy of the extremity muscles can help to localize the site of infection (figure 1 and figure 2 and figure 3 and figure 4 and figure 5).

In patients without signs of inflammation (ie, stage 1), the infection can be easily confused with more benign conditions, such as muscle strain. As the infection progresses, symptoms and signs of infection become more obvious.

Muscles of the hip and pelvis — The muscles of the hip and pelvis are commonly reported sites of infection, especially in children [2-4,7,14,15,17,21,64-69,87]. A notable exception is the muscles of the pelvic floor which seem to be spared.

Psoas and iliacus muscles (ie, iliopsoas muscles) – Patients with iliopsoas infection present with subacute onset of back, flank, or lower abdominal pain that worsens with passive extension of the hip (ie, the "psoas sign") and improves with hip flexion. Most patients prefer to lie still with their hip flexed. The muscle itself is rarely palpable on exam.

Most patients with iliopsoas infection have concomitant vertebral osteomyelitis and/or discitis. It is often unclear whether the iliopsoas or the vertebral infection came first [4,15,64,89,90].

The iliopsoas muscles are among the most common sites of primary pyomyositis. Further detail regarding psoas abscesses is found elsewhere, and the anatomy of the iliopsoas muscles is depicted in the figures (figure 1 and figure 3 and figure 6). (See "Psoas abscess".)

Gluteus muscles – Patients with infections of the gluteus muscles have localized tenderness of the buttocks on palpation. During stage 1 of infection, misdiagnosis as muscle strain or bruising is common, but induration and/or fluctuance are palpable in stages 2 and 3.

The anatomy of the gluteal muscles can be seen in the figures (figure 2 and figure 4 and figure 7).

Deep muscles of the hip and pelvis – The small, deep muscles of the hip and pelvis (eg, piriformis, obturators, quadratus femoris) are commonly reported sites of infection, especially in children [2,3,17,64-69,87,90,91]. The pelvic floor muscles are typically spared.

Adult patients typically complain of hip or groin pain with movement. The type of movement (eg, flexion, extension, abduction, adduction) that elicits pain depends on the specific muscle involved; this finding is in contrast to septic arthritis of the hip which causes pain with any movement of the joint [87]. Deep palpation of the hip and buttocks may reveal tenderness. In some cases, rectal examination may reveal tenderness on palpation of the involved muscle.

Young children with pelvic pyomyositis often cannot verbalize the location of their pain and often present with irritability. Examination of children often reveals a limp or inability to bear weight as well as decreased range of motion of the hip joint [17,87]. The correct diagnosis is often delayed in children; case series suggest that the correct diagnosis is made on admission in zero to 25 percent of childhood cases [15,17,92].

Pregnant individuals are particularly prone to infection of the pyriformis muscle. The primary complaint in such patients is low back pain with or without unilateral leg pain [64-69]. The diagnosis is often delayed due to the increased frequency of noninfectious causes of musculoskeletal pain during pregnancy, as discussed elsewhere. (See "Maternal adaptations to pregnancy: Musculoskeletal changes and pain".)

The anatomy of deep hip and pelvis muscles is depicted in the figure (figure 8).

Other sites of infection — Less common anatomic sites of infection include the shoulder, abdominal wall, latissimus dorsi, and sternocleidomastoid muscles [4,21,64,93-95].

Laboratory findings — Laboratory findings are nonspecific.

Leukocytosis with a left shift is common, especially in advanced stages of infection. Inflammatory markers (eg, erythrocyte sedimentation rate [ESR], C-reactive protein [CRP]) are often elevated; in one series of 47 children with hip or pelvic pyomyositis, over 90 percent of tested patients had elevated ESR and CRP with a mean ESR of 68 mm/hour (normal ≤31 mm/hour) and CRP of 103 mg/L (normal <10 mg/L) [17]. Procalcitonin has also been reported to be elevated in case series.

Counterintuitively, serum creatine kinase levels are usually normal in all stages of illness, but elevations occasionally occur in the late stages [3,4,15,17].

SPECIAL POPULATIONS — While pyomyositis can occur in any individual, children and individuals who are pregnant appear to be particularly prone.

Children — Children older than two years of age have higher rates of pyomyositis than adults. Presentations are often different in children because children often can't localize their pain and because the muscles of the deep pelvis are disproportionately affected in children, as discussed above. (See 'Extremity muscles' above and 'Muscles of the hip and pelvis' above.)

Pyomyositis symptoms in children have been incorrectly attributed to multiple conditions, including muscle strain, septic arthritis, appendicitis, and hip pathology, as discussed elsewhere. (See 'Differential diagnosis' below.)

Pregnant individuals — Pyomyositis has been reported in pregnant individuals, and the pyriformis muscle is particularly affected in this population. The presentation is often nonspecific, and the diagnosis is often delayed due to the many causes of localized back and buttock pain during pregnancy, as discussed above. (See 'Muscles of the hip and pelvis' above.)

COMPLICATIONS — Most cases of primary pyomyositis are isolated only to the muscle. However, certain complications have been described:

Toxic shock syndrome – In patients with pyomyositis due to group A Streptococcus (GAS; ie, S. pyogenes) and other beta-hemolytic streptococci, toxic shock syndrome (TSS) can occur and is associated with poorer outcomes [14,32,96,97]. Reports of TSS due to staphylococcal pyomyositis are scarce. Diagnosis of TSS includes refractory hypotension and multiorgan system involvement and is described in detail elsewhere. (See "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical features' and "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis", section on 'Diagnostic criteria'.)

Septic arthritis and osteomyelitis – The most frequently reported complication of primary pyomyositis is septic arthritis or osteomyelitis from contiguous spread of infection to an adjacent joint or bone. These complications are particularly common in individuals with pyomyositis of the hip and pelvis [2,11,17,21,36].

Joint or bone pain is the primary complaint in these patients, but their pain may be difficult to differentiate from pain caused by the adjacent muscle infection. These conditions are discussed in detail elsewhere. (See 'Additional tests' below and "Septic arthritis in adults", section on 'Diagnosis' and "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

Compartment syndrome – Patients with pyomyositis of the extremities may develop compartment syndrome, a surgical emergency [2,7,17,81,98-100]. This condition should be suspected in patients whose pain suddenly worsens or extends circumferentially. Compartment syndrome is discussed in detail elsewhere. (See "Acute compartment syndrome of the extremities".)

Septic pulmonary emboli – Several reports of septic pulmonary emboli suggest that primary pyomyositis due to S. aureus may cause embolic events even in the absence of infective endocarditis or appreciable venous thrombosis on imaging [101-107]. Most reports describe the presence of concomitant staphylococcal bacteremia. Symptoms of septic pulmonary emboli include cough, shortness of breath, and pleuritic chest pain. Further discussion of septic pulmonary emboli is found elsewhere. (See "Right-sided native valve infective endocarditis", section on 'Clinical manifestations'.)

DIAGNOSIS

When to suspect pyomyositis — The diagnosis of primary pyomyositis should be suspected in adults and children with pain that localizes to a specific muscle, most often in an extremity. It should also be considered in patients with hip or low back pain that steadily worsens over several days, especially if they are a child or are pregnant or have a fever or leukocytosis.

Diagnosis of primary pyomyositis is often delayed due to the nonspecific nature of muscle pain, especially in children. A careful physical examination, frequent follow-up, and a low threshold for further workup may help to prevent delays in therapy and consequent complications.

Diagnostic evaluation — The diagnosis of pyomyositis is confirmed by aspiration of pus or identification of an organism from specimens collected from the involved muscle. A presumptive diagnosis is based on specific radiographic and physical exam findings, especially when blood cultures are positive.

When pyomyositis is suspected, we perform the following tests:

Physical examination to localize the site of disease. (See 'Anatomic sites of infection' above.)

Blood tests for complete blood count with differential, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and procalcitonin.

Two sets of blood cultures drawn from separate peripheral venous sites.

Magnetic resonance imaging (MRI) with gadolinium (preferred). If MRI is not an option, ultrasound or computed tomography (CT) with intravenous contrast of the involved area can be helpful. (See 'Radiographic imaging' below.)

Gram stain and culture of fluid or tissue from the involved muscle.

Additional testing if complications are suspected, as described elsewhere. (See 'Additional tests' below.)

Radiographic imaging — Radiographic imaging is the most useful tool for defining the site(s) and extent of infection and for ruling out other conditions.

Magnetic resonance imaging – MRI with gadolinium is the preferred imaging technique [1,17,30,41,87,92,108-111]. It is highly sensitive for abscess, muscle inflammation, and infection of adjacent structures (image 1 and image 2 and image 3).

Ultrasound – Ultrasonography is less sensitive than MRI, especially for muscle inflammation in the absence of an abscess or for pelvic abscesses. It can be helpful for ultrasonographic-guided sampling and drainage of purulent material (image 4 and image 3 and image 5) [2,15,17,92,112-115].

Computed tomography – CT with intravenous contrast can detect muscle swelling and abscess but it is often unable to define the full extent of muscle involvement and is sometimes unable to distinguish abscess from hematoma (image 6) [17,92,114,116]. Like ultrasound, it is helpful for guided drainage of purulent material (image 7 and image 8).

Other imaging tests – Nuclear medicine scans, such as gallium or positron-emission tomography (PET/CT) scans, are generally unnecessary but can demonstrate locations of multifocal pyomyositis [15,17,21]. Plain radiographs (x-rays) and bone scans are not helpful. (See "Imaging techniques for evaluation of the painful joint", section on 'Nuclear medicine' and "Fever of unknown origin in adults: Evaluation and management", section on 'Whole-body imaging'.)

Microbiologic tests — Microbiologic findings are necessary to confirm the diagnosis of pyomyositis. In clinically stable patients, we obtain samples prior to administration of antibiotics to optimize yield from culture.

Abscess or muscle specimens – Samples should be obtained via ultrasound-guided abscess aspiration, muscle biopsy, or a surgical procedure and should be sent for Gram stain and culture (aerobic and anaerobic). A positive Gram stain or culture from the involved muscle confirms the diagnosis [1].

Blood cultures – Positive blood cultures are highly suggestive of the diagnosis in patients with consistent clinical and imaging findings. Based on available data, blood cultures are positive in 10 to 53 percent of cases [1-3,5,7,10,21,32].

Additional tests — In certain situations, additional testing may be indicated to evaluate for complications or concomitant conditions.

We perform the following tests, based on the clinical scenario:

Echocardiography in patients with S. aureus bacteremia – All patients with confirmed S. aureus bacteremia should undergo evaluation for endocarditis, including echocardiogram, as described elsewhere [47]. In patients with S. aureus pyomyositis whose blood cultures are negative but were drawn after administration of antibiotics, we also obtain echocardiography. (See "Clinical approach to Staphylococcus aureus bacteremia in adults", section on 'Clinical approach'.)

Arthrocentesis or bone biopsy – For patients with clinical findings or radiographic imaging consistent with concomitant septic arthritis or osteomyelitis, arthrocentesis or bone biopsy can confirm the diagnosis. To avoid contamination of the sample, joint, or bone, we utilize ultrasound to avoid passing the needle though the infected muscle. For patients undergoing surgical drainage for pyomyositis, sampling and pre-emptive joint or bone debridement can be performed during surgery.

In some situations (eg, suspected infection of pelvic joints or bones), bone or joint fluid sampling may be deferred due to anatomic risks associated with obtaining the sample. In this situation, empiric treatment for septic arthritis or osteomyelitis may be warranted based on imaging. Further discussion of septic arthritis and osteomyelitis are found elsewhere. (See "Septic arthritis in adults" and "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

Measurement of compartment pressures – When compartment syndrome is suspected, measurement of compartment pressures can be confirmatory. Further information regarding compartment syndrome is found elsewhere. (See "Acute compartment syndrome of the extremities", section on 'Clinical features' and "Acute compartment syndrome of the extremities", section on 'Measurement of compartment pressures'.)

Chest imaging – Patients with symptoms of pulmonary infection (eg, cough, shortness of breath, chest pain) should undergo chest imaging (eg, CT scan without contrast) to rule out septic pulmonary emboli.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis for primary pyomyositis is broad and primarily involves conditions that cause focal muscle pain.

In children who present with a limp and are unable to verbalize pain, the differential is even broader and is discussed in detail elsewhere. (See "Overview of the causes of limp in children".)

Patients with focal muscle pain and no signs of infection (eg, no fever, leukocytosis) – Because the early stage of primary pyomyositis often has no associated signs of infection, misdiagnosis as a noninfectious syndrome is common.

Muscle strain, tear, contusion, or hematoma – Patients with these conditions usually report sudden motion just prior to onset of symptoms. These conditions steadily improve without antibiotics, whereas pyomyositis worsens without antibiotics. (See "Quadriceps muscle and tendon injuries", section on 'Quadriceps strain' and "Quadriceps muscle and tendon injuries", section on 'Quadriceps and patellar tendon tears' and "Hamstring muscle and tendon injuries", section on 'Clinical presentation and examination' and "Calf injuries not involving the Achilles tendon", section on 'Diagnosis' and "Approach to acute knee pain and injury in children and skeletally immature adolescents", section on 'Muscle strain or tear'.)

Diabetic muscle infarction (ie, spontaneous diabetic myonecrosis) – This syndrome presents with pain, swelling, and tenderness in a thigh or calf that can be acute or evolve over days or weeks without a history of preceding trauma. Imaging usually shows edema and muscle destruction without abscess, which can be difficult to distinguish from the early stages of pyomyositis. Unlike pyomyositis, diabetic muscle infarction gradually improves without antibiotic therapy. (See "Diabetic muscle infarction".)

Deep vein thrombosis (DVT) – Calf pain, tenderness, and erythema is frequently due to DVT and can be easily diagnosed by ultrasound confirming the presence of venous clot. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

Compartment syndrome – Compartment syndrome presents with deep diffuse severe pain and tenseness in the entire muscle compartment of an extremity. The rapidity and severity of progression help to differentiate it from early pyomyositis. Neurologic and vascular symptoms (eg, paresthesias, pallor) indicate advanced disease. (See "Acute compartment syndrome of the extremities", section on 'Clinical features'.)

Sarcoma – Soft tissue sarcomas present as slow-growing painless muscle masses, features which help to differentiate them from pyomyositis. (See "Clinical presentation, histopathology, diagnostic evaluation, and staging of soft tissue sarcoma", section on 'Clinical presentation'.)

Patients with signs of infection – The presence of focal muscle pain with fever, leukocytosis, or systemic toxicity (hypotension, tachycardia) may suggest any of the following etiologies:

Septic arthritis – In the extremities, differentiating joint infection from pyomyositis is straightforward because pain, tenderness, and edema localize to the site of infection. When infection involves the hip, pelvis, or shoulder, the correct diagnosis requires careful musculoskeletal exam; any movement of the joint elicits pain in septic arthritis, whereas pyomyositis may only elicit pain when the direction of movement affects the involved muscle. Imaging and arthrocentesis are often necessary to differentiate these conditions [30]. (See "Septic arthritis in adults".)

Osteomyelitis – Osteomyelitis typically has deeper and less severe tenderness than pyomyositis. However, psoas abscess can be challenging to differentiate from vertebral osteomyelitis based on exam alone, and MRI is often necessary. (See "Psoas abscess" and "Vertebral osteomyelitis and discitis in adults", section on 'Clinical features' and "Vertebral osteomyelitis and discitis in adults", section on 'Suggested clinical approach'.)

Clostridial myonecrosis (gas gangrene) – This condition is usually caused by direct penetrating trauma. The overlying skin is discolored, tense, and exquisitely tender, and patients have systemic toxicity, crepitus on exam, and gas in the soft tissue on imaging (table 1) (See "Clostridial myonecrosis", section on 'Clostridial myonecrosis'.)

Necrotizing myositis due to beta-hemolytic Streptococcus (eg, group A Streptococcus [GAS]) – Fulminant gangrenous muscle destruction with systemic toxicity characterize this rare condition which may or may not have overlying skin changes. (See "Necrotizing soft tissue infections", section on 'Necrotizing myositis'.)

Cellulitis and necrotizing fasciitis – Both of these conditions involve erythema and other skin changes (eg, bullae, ecchymosis) that are not seen in pyomyositis. Compared with pyomyositis, necrotizing fasciitis progresses more rapidly and has firm and indurated skin that often disallows delineation of the underlying muscle on exam (table 1). (See "Necrotizing soft tissue infections", section on 'Clinical manifestations' and "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Appendicitis – Pyomyositis of the right hip and pelvis muscles has been confused with appendicitis, especially in children. In some cases, patients have undergone unnecessary surgery for appendectomy due to nonspecific findings on CT scan [2,17,21]. Signs that may help to differentiate appendicitis include antecedent periumbilical pain, anorexia, vomiting, pain in the right lower quadrant with palpation on the left side (ie, Rovsing sign), and rebound tenderness. (See "Acute appendicitis in children: Clinical manifestations and diagnosis", section on 'Common signs and symptoms' and "Acute appendicitis in adults: Clinical manifestations and differential diagnosis", section on 'Clinical manifestations'.)

TREATMENT — The cornerstones of treatment of pyomyositis are abscess drainage and antibiotic therapy.

Drainage — Surgical or image-guided percutaneous drainage is indicated for patients who have an abscess [1,111].

Often, image-guided percutaneous drainage is performed at the time of diagnostic sampling of the abscess. If percutaneous drainage does not completely empty the abscess, surgical debridement is indicated. Other indications for immediate surgical drainage include extensive muscle involvement, complex loculated abscesses, toxic shock syndrome (TSS), and suspected compartment syndrome.

There are no data comparing percutaneous drainage to surgical drainage for pyomyositis. For psoas abscess, drainage procedures are discussed elsewhere. (See "Psoas abscess", section on 'Drainage'.)

Antibiotic therapy

Initial antibiotic selection — Initial selection of antibiotics is based on the suspected bacterial etiology as well as the patient's severity of illness and underlying medical conditions. Prior to selecting empiric antibiotics, any prior culture results from recent infections should be reviewed to help guide therapy.

We administer intravenous antibiotic formulations as initial therapy, in accordance with expert guidelines (algorithm 1) [1,111].

Immunocompetent patients without sepsis – These patients, especially those who are young and healthy, can be treated with monotherapy with an agent that covers S. aureus (including methicillin-resistant S. aureus [MRSA]) and group A Streptococcus (GAS) [1].

We suggest one of the following regimens (dosages are listed in the algorithm (algorithm 1)):

Intravenous vancomycin (preferred). Dosages for adults and children are found in the tables (table 2 and table 3).

Daptomycin (alternative).

Alternative agents that should be restricted and only used when vancomycin and daptomycin are not options are listed in the table (only adult dosing is listed (table 4)).

Once a pathogen is identified, therapy should be tailored to target the organism, as described elsewhere. (See 'Directed therapy' below.)

Patients with sepsis or an immunocompromising condition – For these patients, we administer broad-spectrum antibiotics that cover S. aureus (including MRSA), GAS, gram-negative bacilli, and anaerobes [1,111].

We suggest one of the following regimens (dosages are listed in the algorithm (algorithm 1)):

Intravenous vancomycin (dosages for adults and children are found in the tables and algorithm (table 2 and table 3 and algorithm 1))

PLUS

Piperacillin-tazobactam, or meropenem, or combination therapy with cefepime and intravenous metronidazole.

If septic shock is present, we add intravenous clindamycin to the above regimen until streptococcal TSS is ruled out (algorithm 1). Diagnosis and treatment of streptococcal TSS are discussed elsewhere. (See "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis", section on 'Toxic shock syndrome' and "Invasive group A streptococcal infection and toxic shock syndrome: Treatment and prevention", section on 'Treatment'.)

For patients who have an immediate immunoglobulin (Ig)E-mediated beta-lactam allergy, we suggest a regimen of vancomycin plus intravenous ciprofloxacin plus intravenous metronidazole (algorithm 1). Although many patients have reported beta-lactam allergies, most do not have allergies that would prohibit the use of beta-lactams. In particular, many with penicillin allergies can still take a cephalosporin or carbapenem. Evaluation and management of reported penicillin allergies are discussed in detail elsewhere. (See "Choice of antibiotics in penicillin-allergic hospitalized patients" and "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics".)

There is spectrum of immunocompromising conditions that predispose to atypical pathogens in patients with pyomyositis (see 'Immunocompromising condition' above). Ultimately, the decision to use a broader spectrum regimen requires clinical judgement.

Directed therapy — Once an organism is identified, the antibiotic regimen should be narrowed to target the causative organism.

A transition to oral therapy can occur after the patient has clinically improved, bloodstream infection has cleared (if initially detected), and there is no residual abscess or evidence of endocarditis; we generally continue intravenous therapy for at least 48 hours [1,111]. Of note, patients who have certain complications, such as S. aureus bacteremia, are managed with prolonged antibiotics [1,111]. (See 'Duration of therapy' below and "Clinical approach to Staphylococcus aureus bacteremia in adults" and "Staphylococcus aureus bacteremia in children: Management and outcome", section on 'Management'.)

Example regimens for the three most common pathogens include the following:

Methicillin-sensitive S. aureus (MSSA) – For MSSA infections, we treat with cefazolin, nafcillin, oxacillin, or intravenous flucloxacillin. For oral therapy, we switch to dicloxacillin, flucloxacillin, cephalexin, or cefadroxil. Oral options for patients with serious beta-lactam allergy include doxycycline, trimethoprim-sulfamethoxazole, and linezolid. We generally avoid clindamycin due to its risk for causing Clostridium difficile infection.

Methicillin-resistant S. aureus (MRSA) – For MRSA infections, we continue treatment with parenteral vancomycin or daptomycin. For oral therapy, options include trimethoprim-sulfamethoxazole, doxycycline, and linezolid. We generally avoid clindamycin due to its risk for causing C. difficile infection.

Group A Streptococcus (GAS) – For infections due to GAS (ie, Streptococcus pyogenes), we change to parenteral penicillin G, ceftriaxone, or cefazolin. If TSS is present, we add or continue parenteral clindamycin and consider administration of intervenous immune globulin. Treatment of streptococcal TSS is discussed in detail elsewhere. (See "Invasive group A streptococcal infection and toxic shock syndrome: Treatment and prevention", section on 'Treatment'.)

For patients infected with other pathogens, antibiotic selection should be based on the organism's susceptibility profile and patient tolerance.

Duration of therapy — Duration of therapy should be individualized based on clinical response. Most patients require a total of two to four weeks of antibiotic therapy, although patients with extensive, multifocal, or poorly drained infection may warrant longer courses [1,111].

Patients who have complications, such as S. aureus bacteremia, septic arthritis, or osteomyelitis, generally require prolonged courses of intravenous antibiotics, as described elsewhere. (See "Clinical approach to Staphylococcus aureus bacteremia in adults" and "Staphylococcus aureus bacteremia in children: Management and outcome", section on 'Management' and "Septic arthritis in adults", section on 'Antibiotic therapy' and "Nonvertebral osteomyelitis in adults: Treatment", section on 'Antibiotic therapy'.)

MONITORING RESPONSE TO THERAPY — Patients should be closely monitored during therapy to ensure steady improvement of symptoms, exam findings, and lab tests (eg, white blood cell, C-reactive protein [CRP]). Follow-up imaging is typically unnecessary in patients who respond well to therapy.

REFRACTORY OR RECURRENT INFECTION — Failure to respond after drainage and 24 to 48 hours of appropriate antibiotic therapy should prompt further assessment. A common reason for failure is inadequate drainage of an initial abscess or development of a new abscess; available data suggest that 10 to 25 percent of infected individuals require multiple drainage procedures [7,117]. Radiographic imaging can help to detect residual abscess.

In refractory cases, complications such as compartment syndrome or septic arthritis should also be considered. Additionally, culture results and antibiotic dosing should be reviewed; broadening the antibiotic regimen may be appropriate in culture-negative cases. In these cases, molecular techniques may be needed to define a pathogen. (See 'Complications' above.)

Recurrences after complete resolution of infection are rare [3,17].

OUTCOMES — The overall mortality from primary pyomyositis is undefined; in case studies and systematic reviews, mortality has ranged from zero to 10 percent [3,7,32,39,118].

Long-term sequelae appear to be uncommon, although residual weakness and disfigurement at the site of infection have been reported [7,15,119].

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

Geographic prevalence – Primary pyomyositis is a purulent infection of skeletal muscle that arises from hematogenous spread, often with abscess formation. It is classically an infection of the tropics, although it has been recognized in temperate climates with increasing frequency. (See 'Geographic prevalence' above.)

Risk factors – Risk factors associated with pyomyositis include young age, prior vigorous exercise or nonpenetrating muscle trauma, immunocompromising conditions (particularly HIV infection), pregnancy, and injection drug use disorders. (See 'Risk factors' above.)

MicrobiologyStaphylococcus aureus (including methicillin-resistant strains) is the most common cause of pyomyositis; it causes up to 90 percent of tropical cases and up to 75 percent of temperate cases. Group A Streptococcus (GAS) is also a common cause, especially in children. (See 'Microbiology' above.)

Clinical manifestations – Pyomyositis presents with fever and pain localized to a single muscle group. It develops most often in the lower extremity, but any muscle group can be involved, including the iliopsoas and muscles of the hip and pelvis. (See 'Clinical manifestations' above.)

Diagnosis – Aspiration of pus or detection of an organism from specimens of involved muscle confirms the diagnosis. (See 'Diagnostic evaluation' above.)

Radiographic imaging – MRI is the most useful radiographic tool to diagnosis pyomyositis, define the extent of infection, and rule out other entities. (See 'Radiographic imaging' above.)

Microbiologic tests – Bacteriologic diagnosis is secured by Gram stain and culture of drainage specimens and/or blood cultures. (See 'Microbiologic tests' above.)

Differential diagnosis – The differential diagnosis is broad and includes noninfectious and infectious conditions. In the early stages of illness, it is commonly misdiagnosed as muscle strain, especially if fever is absent. (See 'Differential diagnosis' above.)

Treatment – In the absence of an abscess, pyomyositis can be treated with antibiotics alone. Abscesses require drainage and antibiotic therapy. (See 'Treatment' above.)

For initial therapy for immunocompetent individuals without sepsis, we suggest an intravenous antibiotic directed against staphylococci and beta-hemolytic streptococci (Grade 2C). For patients with sepsis or an immunocompromising condition, we suggest broadened antibiotic coverage that covers gram-positive, gram-negative, and anaerobic organisms (Grade 2C). Antibiotic regimens are outlined in the algorithm (algorithm 1).

  1. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis 2014; 59:147.
  2. Taksande A, Vilhekar K, Gupta S. Primary pyomyositis in a child. Int J Infect Dis 2009; 13:e149.
  3. Crum NF. Bacterial pyomyositis in the United States. Am J Med 2004; 117:420.
  4. Bickels J, Ben-Sira L, Kessler A, Wientroub S. Primary pyomyositis. J Bone Joint Surg Am 2002; 84-A:2277.
  5. Chauhan S, Jain S, Varma S, Chauhan SS. Tropical pyomyositis (myositis tropicans): current perspective. Postgrad Med J 2004; 80:267.
  6. Horn CV, Master S. Pyomyositis tropicans in Uganda. East Afr Med J 1968; 45:463.
  7. Moriarty P, Leung C, Walsh M, Nourse C. Increasing pyomyositis presentations among children in Queensland, Australia. Pediatr Infect Dis J 2015; 34:1.
  8. Maravelas R, Melgar TA, Vos D, et al. Pyomyositis in the United States 2002-2014. J Infect 2020; 80:497.
  9. Comegna L, Guidone PI, Prezioso G, et al. Pyomyositis is not only a tropical pathology: a case series. J Med Case Rep 2016; 10:372.
  10. Evans JA, Ewald MB. Pyomyositis: a fatal case in a healthy teenager. Pediatr Emerg Care 2005; 21:375.
  11. Elzohairy MM. Primary pyomyositis in children. Orthop Traumatol Surg Res 2018; 104:397.
  12. Levin MJ, Gardner P, Waldvogel FA. “Tropical” pyomyositis. An unusual infection due to staphylococcus aureus. N Engl J Med 1971; 284:196.
  13. Verma S. Pyomyositis in Children. Curr Infect Dis Rep 2016; 18:12.
  14. Christin L, Sarosi GA. Pyomyositis in North America: case reports and review. Clin Infect Dis 1992; 15:668.
  15. Gubbay AJ, Isaacs D. Pyomyositis in children. Pediatr Infect Dis J 2000; 19:1009.
  16. Unnikrishnan PN, Perry DC, George H, et al. Tropical primary pyomyositis in children of the UK: an emerging medical challenge. Int Orthop 2010; 34:109.
  17. Abbati G, Abu Rumeileh S, Perrone A, et al. Pelvic Pyomyositis in Childhood: Clinical and Radiological Findings in a Tertiary Pediatric Center. Children (Basel) 2022; 9.
  18. Kiran M, Mohamed S, Newton A, et al. Pelvic pyomyositis in children: changing trends in occurrence and management. Int Orthop 2018; 42:1143.
  19. Verma S, Singhi SC, Marwaha RK, et al. Tropical pyomyositis in children: 10 years experience of a tertiary care hospital in northern India. J Trop Pediatr 2013; 59:243.
  20. Kerrigan KR, Nelson SJ. Tropical pyomyositis in eastern Ecuador. Trans R Soc Trop Med Hyg 1992; 86:90.
  21. Spiegel DA, Meyer JS, Dormans JP, et al. Pyomyositis in children and adolescents: report of 12 cases and review of the literature. J Pediatr Orthop 1999; 19:143.
  22. Widrow CA, Kellie SM, Saltzman BR, Mathur-Wagh U. Pyomyositis in patients with the human immunodeficiency virus: an unusual form of disseminated bacterial infection. Am J Med 1991; 91:129.
  23. Burkhart BG, Hamson KR. Pyomyositis in a 69-year-old tennis player. Am J Orthop (Belle Mead NJ) 2003; 32:562.
  24. Chusid MJ, Hill WC, Bevan JA, Sty JR. Proteus pyomyositis of the piriformis muscle in a swimmer. Clin Infect Dis 1998; 26:194.
  25. Jayoussi R, Bialik V, Eyal A, et al. Pyomyositis caused by vigorous exercise in a boy. Acta Paediatr 1995; 84:226.
  26. King RJ, Laugharne D, Kerslake RW, Holdsworth BJ. Primary obturator pyomyositis: a diagnostic challenge. J Bone Joint Surg Br 2003; 85:895.
  27. Koutures CG, Savoia M, Pedowitz RA. Staphylococcus aureus thigh pyomyositis in a collegiate swimmer. Clin J Sport Med 2000; 10:297.
  28. Meehan J, Grose C, Soper RT, Kimura K. Pyomyositis in an adolescent female athlete. J Pediatr Surg 1995; 30:127.
  29. Viani RM, Bromberg K, Bradley JS. Obturator internus muscle abscess in children: report of seven cases and review. Clin Infect Dis 1999; 28:117.
  30. Karmazyn B, Kleiman MB, Buckwalter K, et al. Acute pyomyositis of the pelvis: the spectrum of clinical presentations and MR findings. Pediatr Radiol 2006; 36:338.
  31. Amoozgar B, Kaushal V, Garsondiya B. Primary Pyomyositis: Contact Sports as the Rare Risk Factors. Case Rep Infect Dis 2019; 2019:5739714.
  32. Stevens D, Bryant A. Group A streptococcal and staphylococcal infections. In: Tropical infections diseases: Principles, pathogens, and practice, 3, Guerrant R, Walker D, Weller P (Eds), Elsevier Saunders, Edinburgh 2011. p.209.
  33. Rodgers WB, Yodlowski ML, Mintzer CM. Pyomyositis in patients who have the human immunodeficiency virus. Case report and review of the literature. J Bone Joint Surg Am 1993; 75:588.
  34. Ansalonl L, Acaye GL, Re MC. High HIV seroprevalence among patients with pyomyositis in northern Uganda. Trop Med Int Health 1996; 1:210.
  35. Blumberg HM, Stephens DS. Pyomyositis and human immunodeficiency virus infection. South Med J 1990; 83:1092.
  36. Jellis JE. Viral infections: musculoskeletal infection in the human immunodeficiency virus (HIV) infected patient. Baillieres Clin Rheumatol 1995; 9:121.
  37. Holbrook KA, Klein RS, Hartel D, et al. Staphylococcus aureus nasal colonization in HIV-seropositive and HIV-seronegative drug users. J Acquir Immune Defic Syndr Hum Retrovirol 1997; 16:301.
  38. Miller M, Cespedes C, Vavagiakis P, et al. Staphylococcus aureus colonization in a community sample of HIV-infected and HIV-uninfected drug users. Eur J Clin Microbiol Infect Dis 2003; 22:463.
  39. Ngor C, Hall L, Dean JA, Gilks CF. Factors associated with pyomyositis: A systematic review and meta-analysis. Trop Med Int Health 2021; 26:1210.
  40. Coombs S, Bui A, Mirzan HS, et al. Pyomyositis presenting as myonecrosis secondary to methicillin-resistant Staphylococcus aureus bacteremia in chronic lymphocytic leukemia. Proc (Bayl Univ Med Cent) 2022; 35:665.
  41. Small LN, Ross JJ. Tropical and temperate pyomyositis. Infect Dis Clin North Am 2005; 19:981.
  42. Schwartzman WA, Lambertus MW, Kennedy CA, Goetz MB. Staphylococcal pyomyositis in patients infected by the human immunodeficiency virus. Am J Med 1991; 90:595.
  43. Gomez-Reino JJ, Aznar JJ, Pablos JL, et al. Nontropical pyomyositis in adults. Semin Arthritis Rheum 1994; 23:396.
  44. Belsky DS, Teates CD, Hartman ML. Case report: diabetes mellitus as a predisposing factor in the development of pyomyositis. Am J Med Sci 1994; 308:251.
  45. Hsueh PR, Hsiue TR, Hsieh WC. Pyomyositis in intravenous drug abusers: report of a unique case and review of the literature. Clin Infect Dis 1996; 22:858.
  46. Ebright JR, Pieper B. Skin and soft tissue infections in injection drug users. Infect Dis Clin North Am 2002; 16:697.
  47. Lo TS, Mooers MG, Wright LJ. Pyomyositis complicating acute bacterial endocarditis in an intravenous drug user. N Engl J Med 2000; 342:1614.
  48. Crossley M. Temperate pyomyositis in an injecting drug misuser. A difficult diagnosis in a difficult patient. Emerg Med J 2003; 20:299.
  49. Rayes AA, Nobre V, Teixeira DM, et al. Tropical pyomyositis and human toxocariasis: a clinical and experimental study. Am J Med 2000; 109:422.
  50. Hossain A, Reis ED, Soundararajan K, et al. Nontropical pyomyositis: analysis of eight patients in an urban center. Am Surg 2000; 66:1064.
  51. Montazeri N, Athale UH, Fulford M, Tarnopolsky MA. Pyomyositis Causing Temporary Quadriparesis During Induction Therapy for Acute Lymphoblastic Leukemia: Case Report and Review of the Literature. J Pediatr Hematol Oncol 2015; 37:223.
  52. Fukushima T, Iwao H, Nakazima A, et al. MRSA-pyomyositis in a patient with acute myelogenous leukemia after intensive chemotherapy. Anticancer Res 2009; 29:3361.
  53. Singh P, Chan W, Blomfield P, McIntosh R. Pyomyositis after chemotherapy for endometrial cancer. Int J Gynecol Cancer 2010; 20:1256.
  54. Falagas ME, Rafailidis PI, Kapaskelis A, Peppas G. Pyomyositis associated with hematological malignancy: case report and review of the literature. Int J Infect Dis 2008; 12:120.
  55. Kompa KG, Trottier CA, Hyman CL, Kohli R. Disseminated Mycobacterium avium Complex Myositis in a Patient With Graft-Versus-Host Disease. Open Forum Infect Dis 2022; 9:ofac385.
  56. Kalra S, Damle NA, Gupta SD, et al. Polymicrobial Pyomyositis in a Patient with Suspected Myeloma on 18F-FDG PET-CT. Indian J Nucl Med 2022; 37:192.
  57. Migliarino V, Naviglio S, Barbi E, Rabusin M. Pseudomonas aeruginosa Pyomyositis in a Child With Acute Lymphoblastic Leukemia: A Case Report and Review of Literature. J Pediatr Hematol Oncol 2021; 43:e795.
  58. Yang HW, Wu UI, Hsieh JH, Tai HC. How long should we treat Candida albicans pyomyositis? Insight from a cured case. J Microbiol Immunol Infect 2020; 53:665.
  59. Xipell M, Ventura-Aguiar P, Revuelta I, et al. Pyomyositis in a Patient with IgA Nephropathy and Kidney Transplant. Case Rep Transplant 2019; 2019:7305683.
  60. Wig S, McCabe PS, Swamy S, et al. Pyomyositis: an unusual cause of hip pain in a patient on certolizumab pegol and leflunomide. Rheumatology (Oxford) 2018; 57:1685.
  61. Chen YH, Lu CC, Chen HC. Candida albicans Pyomyositis in a Patient with Systemic Lupus Erythematosus. J Rheumatol 2018; 45:286.
  62. Minami K, Kenzaka T, Kumabe A, Matsumura M. Thigh pyomyositis caused by group A streptococcus in an immunocompetent adult without any cause. BMC Res Notes 2017; 10:33.
  63. Vigil KJ, Johnson JR, Johnston BD, et al. Escherichia coli Pyomyositis: an emerging infectious disease among patients with hematologic malignancies. Clin Infect Dis 2010; 50:374.
  64. Colmegna I, Justiniano M, Espinoza LR, Gimenez CR. Piriformis pyomyositis with sciatica: an unrecognized complication of "unsafe" abortions. J Clin Rheumatol 2007; 13:87.
  65. Kennedy B, Botros K, Rashid H, Bermingham J. Unprovoked piriformis myositis presenting in a pregnant patient. BMJ Case Rep 2022; 15.
  66. Kinahan AM, Douglas MJ. Piriformis pyomyositis mimicking epidural abscess in a parturient. Can J Anaesth 1995; 42:240.
  67. Wong CH, Choi SH, Wong KY. Piriformis pyomyositis: a report of three cases. J Orthop Surg (Hong Kong) 2008; 16:389.
  68. Wong LF, Mullers S, McGuinness E, et al. Piriformis pyomyositis, an unusual presentation of leg pain post partum--case report and review of literature. J Matern Fetal Neonatal Med 2012; 25:1505.
  69. Siddiq MAB, Rasker JJ. Piriformis pyomyositis, a cause of piriformis syndrome-a systematic search and review. Clin Rheumatol 2019; 38:1811.
  70. Chiedozi LC. Pyomyositis. Review of 205 cases in 112 patients. Am J Surg 1979; 137:255.
  71. Martínez-Aguilar G, Avalos-Mishaan A, Hulten K, et al. Community-acquired, methicillin-resistant and methicillin-susceptible Staphylococcus aureus musculoskeletal infections in children. Pediatr Infect Dis J 2004; 23:701.
  72. Ruiz ME, Yohannes S, Wladyka CG. Pyomyositis caused by methicillin-resistant Staphylococcus aureus. N Engl J Med 2005; 352:1488.
  73. Zalavras CG, Rigopoulos N, Poultsides L, Patzakis MJ. Increased oxacillin resistance in thigh pyomyositis in diabetic patients. Clin Orthop Relat Res 2008; 466:1405.
  74. Fowler A, Mackay A. Community-acquired methicillin-resistant Staphylococcus aureus pyomyositis in an intravenous drug user. J Med Microbiol 2006; 55:123.
  75. Wang TK, Wong SS, Woo PC. Two cases of pyomyositis caused by Klebsiella pneumoniae and review of the literature. Eur J Clin Microbiol Infect Dis 2001; 20:576.
  76. Falasca GF, Reginato AJ. The spectrum of myositis and rhabdomyolysis associated with bacterial infection. J Rheumatol 1994; 21:1932.
  77. Lawn SD, Bicanic TA, Macallan DC. Pyomyositis and cutaneous abscesses due to Mycobacterium avium: an immune reconstitution manifestation in a patient with AIDS. Clin Infect Dis 2004; 38:461.
  78. Knees M, Ayub MT, Manikkan A. Gram-Negative Pyomyositis in an Immunocompetent Patient. Cureus 2018; 10:e2453.
  79. Whittier WL. Percutaneous kidney biopsy: "the needle and the damage done"? Am J Kidney Dis 2011; 57:808.
  80. Barakat MT, Gajurel K, Fischer K, et al. A Case of Meningococcal Pyomyositis in an Otherwise Healthy Adult. Open Forum Infect Dis 2016.
  81. Jensen M. Neisseria gonorrhoeae pyomyositis complicated by compartment syndrome: A rare manifestation of disseminated gonococcal infection. IDCases 2021; 23:e00985.
  82. Chu CK, Yang TL, Tan CT. Tuberculous pyomyositis of the temporal muscle in a nonimmunocompromised woman: diagnosis by sonography. J Laryngol Otol 2004; 118:59.
  83. Wang JY, Lee LN, Hsueh PR, et al. Tuberculous myositis: a rare but existing clinical entity. Rheumatology (Oxford) 2003; 42:836.
  84. Ahmed J, Homans J. Tuberculosis pyomyosits of the soleus muscle in a fifteen-year-old boy. Pediatr Infect Dis J 2002; 21:1169.
  85. Johnson DW, Herzig KA. Isolated tuberculous pyomyositis in a renal transplant patient. Nephrol Dial Transplant 2000; 15:743.
  86. Shih JY, Hsueh PR, Chang YL, et al. Pyomyositis due to Mycobacterium haemophilum in a patient with polymyositis and long-term steroid use. Clin Infect Dis 1998; 26:505.
  87. Bertrand SL, Lincoln ED, Prohaska MG. Primary pyomyositis of the pelvis in children: a retrospective review of 8 cases. Orthopedics 2011; 34:e832.
  88. Niamane R, Jalal O, El Ghazi M, et al. Multifocal pyomyositis in an immunocompetent patient. Joint Bone Spine 2004; 71:595.
  89. Peckett WR, Butler-Manuel A, Apthorp LA. Pyomyositis of the iliacus muscle in a child. J Bone Joint Surg Br 2001; 83:103.
  90. Vij N, Ranade AS, Kang P, Belthur MV. Primary Bacterial Pyomyositis in Children: A Systematic Review. J Pediatr Orthop 2021; 41:e849.
  91. Shepherd JJ. Tropical myositis: is it an entity and what is its cause? Lancet 1983; 2:1240.
  92. Gonzalez Moran G, Garcia Duran C, Albiñana J. Imaging on pelvic pyomyositis in children related to pathogenesis. J Child Orthop 2009; 3:479.
  93. Meena AK, Rajashekar S, Reddy JJ, et al. Pyomyositis - clinical and MRI characteristics report of three cases. Neurol India 1999; 47:324.
  94. Pannaraj PS, Hulten KG, Gonzalez BE, et al. Infective pyomyositis and myositis in children in the era of community-acquired, methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis 2006; 43:953.
  95. Fountoukis T, Tsatsanidis N, Tilkeridou M, et al. Abdominal rectus muscle pyomyositis: Report of a case and review of the literature. Infect Dis Rep 2018; 10:7522.
  96. Watkins R, Vyas H. Toxic shock syndrome and streptococcal myositis: three case reports. Eur J Pediatr 2002; 161:497.
  97. Feigenberg T, Sela HY, Applbaum YH, Mankuta D. Puerperal widespread pyomyositis after group A streptococcal toxic shock syndrome. Isr Med Assoc J 2008; 10:483.
  98. Harrington P, Scott B, Chetcuti P. Multifocal streptococcal pyomyositis complicated by acute compartment syndrome: case report. J Pediatr Orthop B 2001; 10:120.
  99. Aynaci O, Onder C, Kalaycioglu A. Anterior tibial compartment syndrome due to the pyomyositis in a patient with rheumatoid arthritis. A case report. Joint Bone Spine 2003; 70:77.
  100. Cone LA, Lamb RB, Graff-Radford A, et al. Pyomyositis of the anterior tibial compartment. Clin Infect Dis 1997; 25:146.
  101. Lin MY, Rezai K, Schwartz DN. Septic pulmonary emboli and bacteremia associated with deep tissue infections caused by community-acquired methicillin-resistant Staphylococcus aureus. J Clin Microbiol 2008; 46:1553.
  102. Mantilla-Flórez YF, Echeverry-Díaz T, de la Espriella LD, Tuta-Quintero EA. Septic emboli from pyomyositis. Trop Doct 2020; 50:375.
  103. Yuksel H, Yilmaz O, Orguc S, et al. A pediatric case of pyomyositis presenting with septic pulmonary emboli. Joint Bone Spine 2007; 74:491.
  104. Chaudhary D, Aggarwal T, Pannu AK. Staphylococcus aureus pyomyositis and septic lung emboli. CMAJ 2022; 194:E126.
  105. Chowdhury J, Sheth V, Patel K, et al. 1757: Pyomyositis resulting in septic pulmonary emboli: a rare presentation. Crit Care Med 2016; 44 (12): 514.
  106. Savvidou S, Kalogiannis E, Tsakiri K, et al. Primary pyomyositis and disseminated septic pulmonary emboli: a reactivated staphylococcal infection? Braz J Infect Dis 2014; 18:457.
  107. Wang S, Yeh T, Chang S, et al. Pelvic primary pyomyositis complicated by septic pulmonary embolism and shock in a young adult. J Med Sciences 2014; 34 (2): 88-90.
  108. Theodorou SJ, Theodorou DJ, Resnick D. MR imaging findings of pyogenic bacterial myositis (pyomyositis) in patients with local muscle trauma: illustrative cases. Emerg Radiol 2007; 14:89.
  109. Mitsionis GI, Manoudis GN, Lykissas MG, et al. Pyomyositis in children: early diagnosis and treatment. J Pediatr Surg 2009; 44:2173.
  110. Soler R, Rodríguez E, Aguilera C, Fernández R. Magnetic resonance imaging of pyomyositis in 43 cases. Eur J Radiol 2000; 35:59.
  111. Kwak YG, Choi SH, Kim T, et al. Clinical Guidelines for the Antibiotic Treatment for Community-Acquired Skin and Soft Tissue Infection. Infect Chemother 2017; 49:301.
  112. Quillin SP, McAlister WH. Rapidly progressive pyomyositis. Diagnosis by repeat sonography. J Ultrasound Med 1991; 10:181.
  113. Tichter A, Riley DC. Emergency department diagnosis of a quadriceps intramuscular loculated abscess/pyomyositis using dynamic compression bedside ultrasonography. Crit Ultrasound J 2013; 5:3.
  114. Agarwal V, Chauhan S, Gupta RK. Pyomyositis. Neuroimaging Clin N Am 2011; 21:975.
  115. Levitt DL, Byer R, Miller AF. Point-of-Care Ultrasound to Diagnose Pyomyositis in a Child. Pediatr Emerg Care 2019; 35:69.
  116. Struk DW, Munk PL, Lee MJ, et al. Imaging of soft tissue infections. Radiol Clin North Am 2001; 39:277.
  117. Radcliffe C, Gisriel S, Niu YS, et al. Pyomyositis and Infectious Myositis: A Comprehensive, Single-Center Retrospective Study. Open Forum Infect Dis 2021; 8:ofab098.
  118. Sharma A, Kumar S, Wanchu A, et al. Clinical characteristics and predictors of mortality in 67 patients with primary pyomyositis: a study from North India. Clin Rheumatol 2010; 29:45.
  119. Hall RL, Callaghan JJ, Moloney E, et al. Pyomyositis in a temperate climate. Presentation, diagnosis, and treatment. J Bone Joint Surg Am 1990; 72:1240.
Topic 7669 Version 27.0

References

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