OVERVIEW: What every practitioner needs to know about myositis
Are you sure your patient has myositis? What should you expect to find?
Infectious myositis is uncommon, and may be due to a wide variety of pathogens, ranging from viruses to invasive microorganisms, such as bacteria, mycobacteria, fungi, and even parasites. In some cases, particularly viral infections, myositis accompanies systemic viral infection and is managed supportively. In the case of invasive bacterial and fungal infections, myositis can be a progressive and life-threatening illness requiring early diagnosis and aggressive management. Most cases of bacterial myositis are due to Staphylococcus aureus and recognized as pyomyositis. However, additional distinct rapidly necrotizing myositis syndromes, such as streptococcal myositis and clostridial myonecrosis, may be recognized by their dramatic clinical presentations, which promote early diagnosis and therapy. Since localized or generalized pain is a prominent and often nonspecific feature of infectious myositis, early diagnosis can be challenging.
Pyomyositis evolves through three clinical stages.
Symptoms of pyomyositis
Invasive stage: subacute development of pain, fever, and minimal tenderness at site of infection
Suppurative stage: follows 10 to 21 days later, with increased local pain, fever, and tenderness
Sepsis stage: spread of infection systemically, with systemic symptoms and signs of sepsis
Signs of pyomyositis
Invasive stage: variable fever, localized swelling and induration (± erythema), and minimal tenderness
Suppurative stage: progressive fever, localized muscle tenderness, swelling, with or without fluctuance, and successful aspiration of purulent fluid if attemptedSepsis stage: marked local findings of erythema, fluctuance, exquisite tenderness, and signs of sepsis (i.e., hypotension, shock, etc.)
How did the patient develop pyomyositis?
In most cases, initially asymptomatic transient bacteremia presumably leads to localized muscle infection. Primary dermatitis or superficial skin infection may increase the risk of transient bacteremia, and prior blunt trauma or vigorous exercise predisposes some individuals to develop myositis at the site of damaged muscle tissue.
Pyomyositis occurs most commonly in tropical climates, where it accounted for 1 to 4% of hospital admissions several decades ago. In temperate climates, pyomyositis remains very uncommon; about 15 cases are recorded annually in the United States, although it is likely significantly underreported, and has an incidence of 0.5 cases per 100,000 population annually in Australia. It can develop in individuals of all ages, including children and the elderly.
Which individuals are of greater risk of developing pyomyositis?
Roughly 40% of individuals have no underlying systemic risk factors, but a wide variety of underlying illnesses and/or high risk behaviors (particularly intravenous drug abuse) appear to increase the risk of developing pyomyositis. These include common disorders, such as diabetes mellitus and alcoholic liver disease, and classic disorders of immunosuppression, including human immunodeficiency virus (HIV) infection. Immunosuppressive medications, including corticosteroid therapy are also important risk factors. A variety of less common conditions (hematologic malignancies [i.e., leukemia, lymphoma, multiple myeloma]; other hematologic disorders [i.e., myelodysplasia, sickle cell disease, Felty syndrome, cyclic neutropenia]; rheumatologic disorders, especially rheumatoid arthritis and systemic lupus erythematosus; and postpartum and postoperative states) confer an increased risk of pyomyositis.
In almost all cases, these underlying processes are clinically prominent by history and routine clinical evaluation at the time myositis develops.
Beware: there are other diseases that can mimic pyomyositis:
The subacute nature of pyomyositis and paucity of initial findings makes prompt diagnosis challenging.
In the absence of fever, muscle strain, contusion, and even muscle infarction or rupture may be suspected.
An enlarging soft tissue mass may be mistaken for a solid tumor, such as a sarcoma.
When fever accompanies focal pain, possible osteomyelitis or septic arthritis is often considered.
Rupture of an intramuscular abscess with overlying skin erythema mimics cellulitis.
Pelvic muscle involvement, including iliopsoas infection, may mimic appendicitis or diverticulitis, and pyriformis involvement may be mistaken for an epidural abscess.
Occasionally, nonclostridial myositis (e.g., anerobic streptococcal myonecrosis) can resemble pyomyositis, although it usually has a more accelerated tempo of illness.
Group A streptococcal necrotizing myositis
In addition to the slowly progressive pyomyositis syndrome more typically associated with S. aureus, group A streptococcal infection may also cause an extreme rapidly progressive illness evolving more than 24 to 48 hours frequently accompanied by features of streptococcal toxic shock syndrome.
In contrast to staphylococcal pyomyositis, which often develops in truncal or pelvic musculature, group A streptococcal necrotizing myositis most commonly arises in an extremity.
Severe and rapidly progressive pain, with marked local swelling accompanied by fever and progressive systemic toxicity, often with features of toxic shock syndrome, are clues to its early diagnosis. As with pyomyositis, a compartment syndrome further threatening muscle viability may develop. Prior streptococcal pharyngitis is uncommon.
Roughly one-half of all cases of invasive group A streptococcal disease occur in previously healthy individuals. Invasive disease results from the integrated expression of proteases and other virulence factors, coupled with a lack of prior immunity and protective antibody expression in infected individuals (i.e., both pathogen and host factors contribute to the development of this life-threatening infection).
The dramatic and fulminant presentation of group A streptococcal necrotizing myositis has few clinical mimics. Clostridial myonecrosis, bacterial myositis (due to group A streptococci, S. aureus, or less commonly other bacterial pathogens) with evolution of a compartment syndrome or staphylococcal toxic shock syndrome and group A streptococcal necrotizing fasciitis may all resemble group A streptococcal necrotizing myositis. Skin necrosis and tense bullae are more common with streptococcal necrotizing fasciitis, although both fasciitis and necrotizing myositis develop in concert in some patients.
Clostridial myonecrosis ("gas gangrene")
Clostridial myonecrosis develops following local contamination of injured muscle by clostridia (typically Clostridium perfringens) following penetrating trauma or surgery or as the result of hematogenous seeding in the absence of trauma, primarily by C. septicum. This is usually associated with occult compromise of the colonic mucosal integrity by a previously unrecognized adenocarcinoma or as a complication of neutropenic colitis.
Clostridia perfringens is part of the normal colonic flora and may naturally contaminate skin surfaces, especially of the perineum and lower extremities. Thus, any local trauma can predispose injured muscle to secondary clostridial invasion.
Although dramatic injuries, such as penetrating war wounds or severe civilian injuries, especially with open fractures, may precede the development of clostridial myonecrosis, less prominent prior processes, including intra-abdominal surgery, septic abortion, and parenteral injections (even subcutaneous injections), have been reported, and even chronic arterial insufficiency without additional trauma has been reported as a risk factor for clostridial myonecrosis.
Devitalized tissue and contaminated foreign bodies are major risk factors for the development of gas gangrene; prompt debridement of wounds and delaying wound closure have played major roles in reducing the incidence of these infections.
Spontaneous nontraumatic disease due primarily to hematogenous seeding by C. septicum does not require significant prior local tissue injury. Occult adenocarcinoma is the major risk factor for the development of this condition, but other bowel lesions, including diverticulitis, bowel infarction, and necrotizing enterocolitis, may trigger this process. Compromise of the colonic mucosa in the setting of neutropenia, seen in leukemic patients receiving cytotoxic chemotherapy, and diabetes are additional risk factors.
Clostridial myonecrosis should be suspected by its rapid clinical evolution, with progression of severe pain over 6 to 48 hours disproportionate to clinical findings, particularly when risk factors of recent trauma or surgery are present. Local tenderness and swelling are the initial findings, with the expression of a thin malodorous serosanguinous fluid from open wounds. Crepitus in the affected tissue can often be appreciated, and bullae containing similar thin serosanguinous fluid arising from tensely edematous discolored tissue may precede the development of cutaneous necrosis. Acute illness with clinical toxicity, pallor, diaphoresis, followed rapidly by hypotension and tachycardia culminating in shock and renal failure, are present. Interestingly, low grade fever (or even hypothermia) is the rule. The course of illness is rapidly progressive, with visible skin changes advancing and evolving hour by hour in the emergency ward or intensive care unit (ICU).
Beware: there are other diseases that can mimic clostridial myonecrosis:
Several distinct soft tissue and muscle infections associated with gas formation may mimic clostridial myonecrosis (clostridial and nonclostridial anerobic [crepitant] cellulitis, nonclostridial crepitant myositis or cellulitis).
These processes all require surgical exploration and debridement in addition to appropriate antibiotic therapy. Gas production in clostridial anerobic cellulitis typically exceeds that seen with myonecrosis, and the tempo of illness with anerobic cellulitis is typically somewhat slower and associated with less toxicity than in cases of clostridial myonecrosis.
Since clostridial myonecrosis is the most acutely tissue- and life-threatening gas-producing infection, all patients presenting with crepitant soft tissue infections should be approached aggressively with emergent exploration and intensive support. Broad spectrum antibiotic therapy is appropriate until initial Gram stain and culture data define the etiologic agent or agents and enable more targeted antibiotic therapy.
Other forms of crepitant myositis
Anerobic streptococcal myonecrosis
This mixed infection of gram-positive pathogens mimics clostridial myonecrosis in many ways, although its tempo is somewhat slower. A few days following penetrating trauma, patients present with swelling, erythema, seropurulent wound drainage, and progressive pain at the site of injury. There is gas present in the muscles and fascial planes. Gram stain of the drainage fluid and operative specimens shows an inflammatory reaction with polymorphonuclear leukocytes, and evidence of a mixed infection, including streptococci. Wound culture usually recovers both anerobic streptococci (e.g., peptostreptococci) and group A streptococci or S. aureus.
Synergistic nonclostridial anerobic myonecrosis
A mixture of anerobic and facultative organisms can cause rapidly invasive soft tissue infection in diabetic individuals and in neutropenic patients. The infection typically begins following minor superficial injury but progressively spreads to deeper structures, including subcutaneous tissue, fascia, and muscle. This is a rapidly progressing infection requiring emergency exploration and debridement and initial empiric broad-spectrum antibiotic therapy.
Aeromonas hydrophila myonecrosis
Individuals who sustain penetrating injuries in freshwater settings (e.g., after boating or swimming accidents) or associated with fish or other water-based wildlife may develop a fulminant myonecrosis syndrome, often with gas production and pain, swelling, bullae formation, and marked systemic toxicity that resembles clostridial myonecrosis. The history of freshwater exposure is key for early diagnosis. As with clostridial myonecrosis, emergent surgical debridement and antibiotic therapy is crucial. Aeromonas hydrophila is present in wound drainage and surgical excised tissue and is frequently present in blood cultures obtained on presentation.
Infected vascular grafts
Devitalized tissue due to arterial insufficiency/graft thrombosis is the focus of this infection. It occurs in patients with failed vascular grafts, especially in diabetic patients. Unlike the rapidly progressive crepitant myositis syndromes, these infections remain largely localized to the area of vascular insufficiency. The responsible pathogens typically include a mixture of facultative gram-negative rods, such as Proteus species, anerobic streptococci, and anerobic gram-negative rods, such as Bacteroides species.
What laboratory studies should you order and what should you expect to find?
Results consistent with the diagnosis
Routine clinical laboratory screening studies, including peripheral white blood cell (WBC) with differential, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures, should be obtained in all patients. Assessment of liver and kidney function tests are important to screen for underlying metabolic disorders, as well as to guide appropriate antibiotic therapy. If pustules, infected traumatic lesions, bullae, or other concerning skin lesions are present, these should be unroofed and sent for routine culture in otherwise normal individuals, and for broader culture, including fungal cultures in compromised hosts and HIV-infected individuals. If a fluctuant soft tissue collection is appreciated or documented by preliminary imaging, this can be aspirated for Gram stain and culture, which should include primary anaerobic culture.
Patients with truncal or pelvic pain should have urinalysis and urine culture performed as well. Leukocytosis is generally present in almost all forms of bacterial myositis. Evolving leukopenia may be present with delayed or fulminant presentations, particularly in the presence of toxic and/or septic shock.
A low hematocrit is commonly present in clostridial myonecrosis due to toxin-mediated hemolysis.
Muscle enzymes (e.g., CPK) are variably elevated and, in fact, often normal in bacterial pyomyositis, but are commonly quite markedly elevated in patients with streptococcal necrotizing myositis.
Results that confirm the diagnosis
Gram staining of fluid or excised necrotic tissue provides presumptive identification of causative pathogens, and culture of abscess fluid confirms the diagnosis of pyomyositis and the various forms of necrotizing muscle infection and guides specific antibiotic therapy. Patients often undergo definitive drainage of established muscle abscesses after receiving initial (preprocedural) empiric antibiotic therapy, thus, cultures may be unrevealing. In these cases, pretreatment cultures of blood and/or infected skin sites may help to identify the causative pathogen.
What imaging studies will be helpful in making or excluding the diagnosis?
Imaging plays an essential role in the assessment of patients with focal soft tissue pain and fever to establish the presumptive diagnosis of myositis and guide urgent surgical exploration.
Plain films may reveal focal soft tissue swelling, the presence of soft tissue gas at the painful site, and possible relevant associated skeletal abnormalities, such as osteomyelitis or a primary bone tumor. $
Ultrasonography is readily available and can demonstrate focal muscle enlargement in early stage disease, and complex hypoechoic areas in the suppurative stage of disease, reflecting abscess formation. It is also valuable for the prompt assessment of patients with possible gas-forming infections in the emergency ward. $
Magnetic resonance imaging (MRI) is the most informative single imaging modality, because it identifies focal muscle edema and localized abscess formation with great precision, particularly with gadolinium administration. In patients with rapidly progressive disease, surgical exploration should not be delayed to obtain an MRI study. Gadolinium administration is contraindicated in the setting of renal insufficiency, a complication frequently present in patients with rapidly progressive necrotizing muscle infection. $$$$
Computed tomography (CT) scanning is generally readily available and rapidly performed. It can demonstrate muscle edema, focal low density (necrotic) muscle abnormalities suggestive of evolving infection, as well as well-established fluid collections often accompanied by ring enhancement. CT scans readily detect the presence of gas in the tissues in patients with clostridial myonecrosis, and contrast-enhanced studies demonstrate the extent of muscle infarction. As with MRI, surgical exploration should not be delayed while awaiting urgent CT imaging, and contrast administration is contraindicated in the setting of renal insufficiency. $$$
($ = 60–125, $$ 125–500, $$$ 500–1,000, $$$$ >1000)
What consult service or services would be helpful for making the diagnosis and assisting with treatment?
If you decide the patient has pyomyositis or necrotizing muscle infection, what therapies should you initiate immediately?
General Surgery or Orthopedic Surgery and Infectious Diseases should be consulted.
In addition to the initiation of appropriate antibiotic therapy, urgent drainage of established abscesses and surgical debridement of necrotizing disease in patients with bacterial myositis is critical. In the case of pyomyositis, the selection of open surgical drainage, typically by orthopedic or general surgeons, or percutaneous drainage via ultrasound or CT guidance by interventional radiologists depends on the abscess location, size, complexity, and institutional expertise. Patients with streptococcal necrotizing myonecrosis, clostridial myonecrosis, or other necrotizing crepitant infections should have emergency open exploration to achieve aggressive debridement of necrotic muscle until viable tissue is found.
Empiric antibiotic therapy for pyomyositis must target the preponderant pathogen S. aureus and should include vancomycin. Additional broad-spectrum coverage against gram-negative pathogens and anerobes should include a beta-lactam/beta lactamase inhibitor combination, such as piperacillin-tazobactam, or a carbapenem agent, such as imipenem, as part of the initial empiric coverage, especially in immunocompromised hosts. Formal Infectious Disease consultation should be obtained when possible to optimize empiric antibiotic selection, refining therapy as the microbiological data becomes available.
In patients with suspected streptococcal or clostridial myonecrosis, an inhibitor of protein synthesis, such as clindamycin should be added to initial broad spectrum therapy to reduce the production of bacterial exotoxins. Since penicillin is the agent of choice in these fulminant infections, the combination of penicillin, clindamycin, together with empiric coverage for possible mixed infection with a fluoroquinolone, such as ciprofloxacin, or an advanced cephalosporin (e.g., cefepime) is appropriate.
Appropriate ICU supportive care is necessary in patients with streptococcal or clostridial infection, as well as patients with toxic shock syndrome due to S. aureus pyomyositis, since they require hemodynamic and ventilatory support and blood product replacement therapy.
1. Anti-infective agents
If I am not sure what pathogen is causing the infection what anti-infective should I order?
Empiric therapy for pyomyositis should target gram-positive pathogens, including S. aureus (both methicillin-sensitive and methicillin-resistant isolates), as well as potential gram-negative pathogens, particularly in compromised hosts. Vancomycin together with a broad-spectrum beta lactam/beta-lactamase inhibitor (e.g., piperacillin-tazobactam) or a carbapenem, such as imipenem, is appropriate initial empiric coverage pending Gram stain and culture of abscess material. In the rare setting in which presumed staphyloccal pyomyositis is complicated by features of toxic shock syndrome, clindamycin should be added, as well as an inhibitor of toxin production.
Streptococcal necrotizing myonecrosis and clostridial myonecrosis, and the related necrotizing soft tissue syndromes outlined above, are presumptively confirmed at the time of surgical debridement or Gram stain and culture of bulla fluid. The initial broad spectrum antibiotic regimens listed above may be initiated at presentation, with inclusion of clindamycin, until preliminary etiologic confirmation has been achieved. Myonecrosis due to group A streptococci or clostridia should be treated with high dose penicillin and clindamycin parenterally once confirmed.
For treatment of specific pathogens, see Table I.
|S. aureus (MRSA or unknown susceptibility)||Vancomycin||2–4g/day (divided every 6 to 12 hours) with trough target >15mcg/mL||linezolid (600mg every 12 hours)|
|S. aureus (MSSA)||Nafcillin||12 g/d (divided Q4-6 H)||Oxacillin (see nafcillin)Cefazolin 4–6g/day (divided every 8 hours)Vancomycin 2–4g/day (divided every 6 to 12 hours) with trough target >15mcg/mL|
|Group A streptococci (S. pyogenes)||Penicillin||24 million units/day(divided every 4 hours)||Ceftriaxone (2g every 12 hours)|
|Clostridia species(perfringens, septicum)||Penicillin||24 million units/day(divided every 4 hours)||Clindamycin (600mg every 6 to 8 hours)Imipenem (1g every 6 hours) [limited experience]Metronidazole (500mg every 6 hours) [limited experience]|
|Peptostreptococci and other anerobic streptococci||Penicillin||24 million units/day(divided every 4 hours)||Vancomycin (2–4g/day (divided every 6 to 12 hours) with trough target >15mcg/mL|
|Aeromonas hydrophila||Ciprofloxacin||500–750mg every 12 hours||Gentamicin (80mg every 8 hours, adjusted by peak >4, trough <2) imipenem 1g every 6 to 8 hours|
MRSA, methicillin-resistant S. aureus; MSSA, methicillin-sensitive S. aureus.
2 Other key therapeutic modalities.
Intravenous immunoglobulin G (IVIG) administration is often administered as adjunctive therapy to patients with streptococcal necrotizing myonecrosis and toxic shock in an attempt to neutralize streptococcal exotoxins and possibly as an immunomodulatory agent based on limited clinical data.
Hyperbaric oxygen remains a controversial adjunctive modality in the management of patients with clostridial myonecrosis. Aggressive surgical debridement should never be delayed by hyperbaric oxygen therapy, particularly in view of its limited availability and uncertain efficacy. It may be considered in patients with truncal myonecrosis where debriding surgery is particularly mutilating or anatomically impractical.
What complications could arise as a consequence of myositis or myonecrosis?
What should you tell the family about the patient's prognosis?
The inexorable progression of untreated pyomyositis makes prompt diagnosis and early definitive drainage the foundations of management. Patients and their families must understand these considerations and cooperate with intensive diagnostic studies and invasive therapeutic procedures. In most cases, the prognosis following satisfactory drainage is excellent, with little long-term morbidity.
Ongoing fever or progressive local pain suggests inadequate therapeutic drainage (particularly after percutaneous drainage procedures) or the presence of additional undrained suppurative foci.
Pyomyositis may be complicated by the development of a compartment syndrome, particularly when infection develops in the anterior tibial compartment, and fasciotomies may be necessary in addition to surgical drainage and debridement, leading to compromised functional status of the affected limb.
The prognosis following definitive therapy for pyomyositis is more guarded if:
the diagnosis is delayed and recognized at the (late) sepsis stage, or
the episode of pyomyositis is due to a toxin-producing strain of S. aureus or group A streptococci with resultant toxic shock syndrome
In these circumstances, patients are at increased risk for the development of multiorgan system failure and death.
The treatment of clostridial myonecrosis requires aggressive surgical debridement back to viable tissue. This often requires debilitating and mutilating surgery culminating in amputation of an extremity or excision of wide areas of truncal soft tissue. The postoperative course is typically stormy, with a frequent need for repeat surgical exploration to insure the adequacy of debridement and with multisystem failure requiring intensive care, mechanical ventilation, pressor support for shock, and renal replacement therapy. Although the prognosis of C. septicum myonecrosis remains guarded, most patients with other forms of crepitant myonecrosis will survive following aggressive combined surgical and medical therapy.
Muscle involvement in viral diseases
Muscle pain (myalgia) commonly accompanies many febrile illnesses. Certain viral illnesses, such as dengue and influenza, are frequently associated with diffuse muscle pain and tenderness. There is no associated weakness, and muscle-specific enzyme measures (creatine phosphokinase, aldolase) are variably and minimally elevated.
Rhabdomyolysis, associated with marked pain and severe objective weakness and accompanied by extreme elevations of muscle enzymes, is a rare complication of influenza A infection. The rapid course of illness, accompanied by fever and typical respiratory manifestations of influenza, make the diagnosis rather straightforward.
Acute trichinosis may have a comparably acute course but is accompanied by marked eosinophilia. The myositis associated with toxoplasmosis is nearly always restricted to individuals with profound immunosuppression. Autoimmune myositis is generally more insidious in onset with a gradually progressive course.
Muscle involvement in parasitic diseases
Trichinella spiralis is the parasite best known for producing symptomatic muscle disease. Following ingestion of infective larvae through the consumption of undercooked carnivore or omnivore meat (most commonly pork, but may follow game ingestion as well, especially bear meat), an initial gastroenteritis syndrome with nausea, vomiting, and diarrhea develops as larvae excyst, mature, reproduce, and progeny larvae invade the intestinal mucosa. The larvae are hematogenously disseminated and invade skeletal muscle but can also invade extraocular muscles, myocardium, and, rarely, the lungs and/or central nervous system.
A few weeks following ingestion a systemic illness with fever, prominent generalized myalgia and muscle swelling, and edema (periorbital and possibly acral as well) develops. Laboratory evaluation is notable for the presence of striking eosinophilia and elevated muscle enzyme levels. Diagnosis can be made by serologic testing at least 3 weeks following larval ingestion; muscle biopsy of tender muscle can be performed in selected cases.
Following the ingestion of Taenia solium (pork tapeworm) eggs, larvae invade the bowel wall to disseminate widely and encyst in host structures. Neurocysticercosis is most commonly diagnosed following the onset of seizures or as an incidental finding following cranial imaging for another indication. Similarly, cysticercosis may be an incidental finding following radiologic studies that include skeletal muscle, where longstanding encysted larvae may be recognized by scattered focal calcifications. Muscle symptoms are uncommon, unless there is significant egg ingestion with widespread inflammation associated with larval encystation. Fever and eosinophilia in this setting may mimic trichinosis.
Toxoplamosis is acquired following the ingestion of oocysts (typically from cat excreta) or ingestion of tissue cysts from undercooked meat. Infection can be transmitted vertically during pregnancy, resulting in congenital toxoplasmosis, or rarely through human tissues (organ transplantation, blood transfusion). Oocyst ingestion results in intestinal mucosal invasion and systemic dissemination of the parasite’s trophozoite form.
Most individuals with toxoplasmosis are asymptomatic, although a mononucleosis-like syndrome following acute infection, as well as reactivation of toxoplasma retinitis, can occur in immunologically normal individuals.
Myositis and myocarditis (typically reactivation disease) can develop with some frequency in immunocompromised individuals, including patients with advanced HIV infection, as well as patients receiving immunosuppressive therapy following organ transplantation or anti-tumor necrosis factor biologicals for inflammatory disorders. Patients develop myalgias, tenderness, swelling, and weakness, mimicking autoimmune polymyositis. Serologic diagnosis is generally effective, although, in severely immunocompromised patients, muscle biopsy may be required.
Psoas abscess: a site of myositis arising from local spread or hematogenous seeding
Bacterial infection of the psoas muscle may occur following hematogenous seeding, similar to the process involving other sites of pyomyositis, and is most commonly associated with S. aureus infection (“primary psoas pyomyositis”).
More commonly, psoas muscle infections initially arise in adjacent structures and spread to the psoas muscle (“secondary psoas pyomyositis”).
Adjacent foci of infection may include the vertebrae (vertebral osteomyelitis), primary intra-abdominal infection (appendicitis, diverticulitis, Crohn disease), or perinephric abscess.
Since a variety of pathogens may be implicated in adjacent primary infections, there is a broad spectrum of potential pathogens involved in psoas abscesses:
Enterobacteriaceae (from gastrointestinal [GI] or genitourinary [GU] sources)
facultative and anerobic streptococci (from GI sources)
anerobic gram-negative rods (from GI sources)
M. tuberculosis (from vertebral osteomyelitis [Pott disease])
Management involves initial broad spectrum therapy, adequate drainage by interventional radiological or open surgical approaches, and subsequent targeted antibiotic therapy, as with primary pyomyositis. It is important in cases of psoas abscess to assess the need for additional surgical or drainage procedures from an adjacent feeding focus of infection (e.g., perinephric or intra-abdominal abscess).
What pathogens are responsible for pyomyositis?
The following pathogens are responsible for pyomyositis:
S. aureus (both methicillin-sensitive and methicillin-resistant) is the most common etiology
group A streptococcus
other streptococci (e.g., Group B, C, or G)
S. pneumoniae (rarely)
gram-negative Rods (rarely)
anerobic bacteria (rarely)
What pathogens are responsible for gas gangrene?
The following pathogens are responsible for gas gangrene:
Clostridium perfringens (predominant)
C. septicum and other histotoxic clostridia (occasionally)
What pathogens are responsible for nonclostridial crepitant myositis?
The following pathogens are responsible for nonclostridial crepitant myositis:
anerobic streptococcal gangrene: Peptostreptococcus (+group A streptococci and/or S. aureus)
synergistic nonclostridial anerobic myonecrosis: mixed infections due to:
Bacteroides (and other anerobic non-spore forming gram-negative bacilli)
Peptostreptococcus and other streptococci
enteric gram-negative bacilli: E. coli, Klebsiella, Enterobacter
infected vascular graft (mixed infections, similar to synergistic nonclostridial anerobic myonecrosis)
may also be associated with Bacillus cereus or Proteus species
Aeromonas hydrophila myonecrosis: Aeromonas hydrophila
What pathogens are responsible for psoas abscess?
The following pathogens are responsible for psoas abscess:
hematogenous source: S. aureus predominant (primary or complicating vertebral osteomyelitis)
perinephric source: urinary pathogens (gram-negative bacilli)
intestinal/intra-abdominal source: enteric gram-negative rods, streptococci, anerobes (mixed infection)
tuberculous (M. tuberculosis), often complicating tuberculous vertebral osteomyelitis
How can myositis and myonecrosis be prevented?
There are no prophylactic regimens or vaccines available to prevent the development of myositis or myonecrosis.
WHAT'S THE EVIDENCE for specific management and treatment recommendations?
Bickels, J, Ben-Sira, L, Kessler, A, Wientroub, S. “Primary pyomyositis”. J Bone Joint Surg Am. vol. 84. 2002. pp. 2277-86.
Caplan, ES, Kluge, RM. “Gas gangrene: review of 34 cases”. Arch Intern Med. vol. 136. 1976. pp. 788-91.
Capo, V, Despommier, DD. “Clinical aspects of infection with spp”. Clin Microbiol Rev. vol. 9. 1996. pp. 47-54.
Chambers, CH, Bond, GF, Morris, JH. “Syngeristic necrotizing myositis complicating vascular injury”. J Trauma. vol. 14. 1974. pp. 980-4.
Crum, NF. “Bacterial pyomyositis in the Unites States”. Am J Med. vol. 117. 2004. pp. 420-8.
Crum-Cianflone, NF. “Bacterial, fungal, parasitic, and viral myositis”. Clin Microbiol Rev. vol. 21. 2008. pp. 474-94.
Darenberg, J, Ihendyane, N, Sjolin, J. “Intravenous immunoglobulin G therapy in streptococcal toxic shock syndrome: a European randomized, double-blind, placebo-controlled trial”. Clin Infect Dis. vol. 37. 2003. pp. 333-40.
Davis, WA, Kane, JG, Garagusi, VR. “Human infections: a review of the literature and case report of endocarditis”. Medicine. vol. 57. 1978. pp. 267-77.
Flier, S, Dolgin, SE, Saphir, RL. “A case confirming the progressive stages of pyomyositis”. J Pediatr Surg. vol. 38. 2003. pp. 1551-3.
Gordon, BA, Martinez, S, Collins, AJ. “Pyomyositis: characteristics at CT and MRI imaging”. Radiology. vol. 197. 1995. pp. 279-86.
Hsueh, P-R, Hsiue, TR, Hsieh, W-C. “Pyomyositis in intravenous drug abusers: report of a unique case and review of the literature”. Clin Infect Dis. vol. 22. 1996. pp. 858-60.
Stevens, DL. “Streptococcal toxic shock syndrome associated with necrotizing fasciitis”. Ann Rev Med. vol. 51. 2000. pp. 271-88.
Severns, DL, Bryant, AE. “The role of clostridial toxins in the pathogenesis of gas gangrene”. Clin Infect Dis. vol. 35. 2002. pp. S93-100.
Stevens, DL, Musher, DM, Watson, DA. “Spontaneous, nontraumatic gangrene due to “. Rev Infect Dis. vol. 12. 1990. pp. 286-96.
Vassilopulos, D, Chalasani, P, Jurado, RL. “Musculoskeletal infections in patients with human immunodeficiency virus infection”. Medicine (Baltimore). vol. 76. 1997. pp. 284-94.
Wang, C, Schwaitzberg, S, Berliner, E. “Hyperbaric oxygen for treating wounds: a systematic review of the literature”. Arch Surg. vol. 138. 2003. pp. 272-9.
Wolfe, MW, Bennett, JT. “Pyomyositis with toxic shock syndrome presenting as back pain and fever: a case report and literature review”. Am J Orthop. vol. 26. 1997. pp. 135-37.
Ytterberg, SR. “The relationship of infectious agents to inflammatory myositis”. Rheum Dis Clin North Am. vol. 20. 1994. pp. 995-1015.
Zissin, R, Gayer, G, Kots, E. “Iliopsoas abscess: a report of 24 patients diagnosed by CT”. Abdom Imaging. vol. 26. 2001. pp. 533-9.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- OVERVIEW: What every practitioner needs to know about myositis
- Are you sure your patient has myositis? What should you expect to find?
- How did the patient develop pyomyositis?
- Which individuals are of greater risk of developing pyomyositis?
- Beware: there are other diseases that can mimic pyomyositis:
- Group A streptococcal necrotizing myositis
- Clostridial myonecrosis ("gas gangrene")
- Other forms of crepitant myositis
- What laboratory studies should you order and what should you expect to find?
- What imaging studies will be helpful in making or excluding the diagnosis?
- What consult service or services would be helpful for making the diagnosis and assisting with treatment?
- If I am not sure what pathogen is causing the infection what anti-infective should I order?
- What complications could arise as a consequence of myositis or myonecrosis?
- What should you tell the family about the patient's prognosis?
- Muscle involvement in viral diseases
- Muscle involvement in parasitic diseases
- Psoas abscess: a site of myositis arising from local spread or hematogenous seeding
- What pathogens are responsible for pyomyositis?
- What pathogens are responsible for gas gangrene?
- What pathogens are responsible for nonclostridial crepitant myositis?
- What pathogens are responsible for psoas abscess?
- How can myositis and myonecrosis be prevented?
- WHAT'S THE EVIDENCE for specific management and treatment recommendations?