Pyomyositis

Pyomyositis is a pyogenic infection that leads to abscess formation deep within skeletal muscle. The disease was first described in 1855 in Japan. What may have been the first recorded case in North America occurred in 1971.[1] However, an earlier report of pyomyositis in 1892 in the United States is credited to Osler.[2] Although pyomyositis was previously rare in North America, it is now becoming more common, especially in persons with human immunodeficiency virus (HIV) infection and other immunocompromising conditions.[1,3] We report a case of pyomyositis in a man with newly diagnosed insulin-dependent diabetes mellitus. As demonstrated in the illustrative case, pyomyositis is a serious infection that may easily be mistaken in its early stages as musculoskeletal aches of a benign nature.

Illustrative Case

A 50-year-old man presented to the emergency department with generalized muscle pain and cramping in the lower extremities. The patient's blood glucose level was incidentally found to be 521 mg per dL (28.7 mmol per L), and diabetes mellitus was diagnosed. The patient had been seen in the emergency department on three previous occasions. At the first visit, 11 days before the current admission, incision and drainage of a sebaceous cyst on his left cheek was performed. He reported that he had plucked an ingrown hair from his cheek a few days earlier, and he subsequently noticed progressive swelling of the area. Three days before the current admission, he presented to the emergency department with acute muscle pain and cramping of the lower extremities. Since no obvious abnormalities were noted, the patient was discharged with instructions to take ibuprofen and use heat pads to relieve the pain.

The patient denied injection drug use, homosexuality, trauma or recent international travel, but he admitted to moderate alcohol intake every night and polyphagia in recent weeks. He also reported polyuria with bloody color.

Physical examination revealed a thin, middle-aged man in moderate pain who exhibited rigidity of the lower extremities. Vital signs were stable. Both knees were swollen, and both thighs were tender to palpation. Other findings included induration of the lower medial portion of the left thigh, and sebaceous cysts of the left cheek and the right deltoid.

The white blood cell count was 13,900 per [mm.sup.3] (13.9 x [10.sup.9] per L), with segmented neutrophils, 78 percent; band neutrophils, 7 percent; lymphocytes, 6 percent; monocytes, 7 percent, and eosinophils, 2 percent. Hemoglobin and hematocrit levels were unremarkable, and the platelet count was 112,000 per [mm.sup.3] (112 x [10.sup.9] per L). Blood urea nitrogen (BUN) was 21 mg per dL (7.5 mmol per L); creatinine, 1.2 mg per dL (110 [mu]mol per L); albumin, 2.2 g per dL (22 g per L); total bilirubin, 3.2 mg per dL (54 [mu]mol per L); alkaline phosphatase, 225 U per L; aspartate transaminase, 70 U per L, and gamma-glutamyltransferase, 2,400 U per L. Prothrombin time and partial thromboplastin time were normal. Nonfasting blood glucose level was 512 mg per dL (28.2 mmol per L), and hemoglobin [A.sub.1c] was 12.5 percent.

Two blood cultures were negative. A culture of the cysts on the patient's right deltoid and left cheek grew Staphylococcus aureus. Urine culture showed 50,000 to 100,000 colony-forming units per mL, with S. aureus as the pathogen. Results of a rapid plasma reagin test were negative. Serologic testing for hepatitis A and B were negative, but a test for hepatitis C was positive. Results of an HIV antibody test were negative.

Radiographs of the lower extremities revealed normal bone structure, and findings of a Duplex ultrasound scan were negative for deep venous thrombosis. A computed tomographic (CT) scan of the abdomen showed a normal liver and spleen but revealed cholelithiasis, which was confirmed by an ultrasonographic study of the right upper quadrant. Findings of a two-dimensional echocardiogram were essentially normal. Magnetic resonance imaging studies of the lower extremities showed multiple micronbscesses widely distributed within the muscle mass and between the muscle fascial planes, with the largest lesions in the quadriceps and adductor muscle groups of the lower portion of the left thigh (Figures 1a and 1b). Ultrasonography was also helpful in demonstrating the pyogenic foci (Figure 2).

After the patient was admitted to the hospital, nafcillin was chosen to treat the presumptive S. aureus infection that was shown on the culture of the right deltoid and left cheek. Antibiotic treatment was later changed to cefazolin after the development of azotemia, which was thought to be secondary to the nafcillin. Incision and drainage of the left thigh abscess was performed. Significant bleeding complicated this procedure, and the patient received two units of packed red blood cells. Culture of the pus drained from the left thigh grew S. aureus. Diet and insulin therapy resulted in good control of blood glucose levels. Before discharge, antibiotic therapy was switched to oral cephalexin.

Significant laboratory values at discharge were white blood cells, 5,400 per [mm.sup.3] (5.4 x [10.sup.9] per L); hemoglobin, 11.7 g per dL (117 g per L); hematocrit, 33.8 percent, and platelets, 162,000 per [mm.sup.3] (162 x 109 per L). Sodium was 133 mEq per L (133 mmol per L); BUN, 31 mg per dL (11.05 mmol per L); creatinine, 1.3 mg per dL (110 [mu]mol per L), and alkaline phosphatase, 228 U per L. Occult blood studies of the stool were negative. Carcinoembryonic antigen was 3.9 U per L (3.9 [mu]g per L). Blood, sputum, urine and fungal cultures were all negative. As of the date of reporting, the patient had received a total of 52 days of antibiotic therapy and was making gradual but definite progress.

Etiology and Pathogenesis

The pathogen most commonly involved in pyomyositis is S. aureus (95 percent of cases). More rarely encountered infectious agents include Streptococcus pyogenes, Streptococcus pneumoniae (pneumococci), Streptococcus groups B, C and G, Escherichia coli, Mycobacterium avium and even gram-negative organisms. Very rarely, Clostridia species have also been reported to disseminate from intestinal sources to muscle in patients with bacteremia.[2] Infection caused by S. pyogenes, S. pneumoniae, E. cold and other organisms rarely involved in pyomyositis is not limited to the immunocompromised patient. However, defects in host immunity implicated in the pathogenesis of the disease render such individuals more susceptible to these less commonly encountered organisms.[2] HIV-associated pyomyositis appears to be a recognized entity,[4-6] and necrotizing pyomyositis caused by Mycobacterium avium complex has been described in patients with acquired immunodefiency syndrome.[7]

Pyomyositis may develop by local spread from adjacent bone or soft tissue infection, via lymphatics from infected skin, or by hematogenous spread to susceptible muscle tissue during a period of transient bacteremia.[3] Susceptibility is increased by muscle damage from local mechanical trauma or exercise. Pyomyositis is much more prevalent in the tropics, where children are more commonly affected than adults, particularly in the presence of malnutrition. Pyomyositis has been associated with scurvy and thiamine deficiency in humans, and with selenium and vitamin E deficiency in cattle. In patients who are HIV-positive, underlying abnormalities of host defense, muscle damage from HIV-associated myopathy, and myositis from parasitic infection or disseminated mycobacterial infection are all predisposing factors to pyomyositis.[5-9] Large muscles are more frequently involved, including the quadriceps, gluteus, shoulder and upper arm muscles. Pyomyositis usually has a solitary focus, but it involves multiple sites in up to 40 percent of cases.

In the tropics, pyomyositis has been associated with parasitic infestation, including migration of the guinea worm, Dracunculus medinensis, in the deep connective tissues of the lower extremities. Malaria, filariasis, arbovirus infection and bacterial infection such as leptospirosis have also been reported to predispose to the development of pyomyositis. However, the theory of parasitic infestation as a significant predisposing factor for pyomyositis, at least in North America, has been disputed.[8] Outside the tropics, several other underlying conditions have been reported in pyomyositis, including HIV infection[4] and AIDS, intravenous drug abuse, diabetes mellitus,[3] leukemia, asplenia, lupus erythematosus, Felty's syndrome,[2] herpes zoster, measles, picornavirus, coxsackievirus, arenavirus, sickle cell anemia, and chemotherapy for malignant neoplasms.

Stages of Pyomyositis

Pyomyositis has been categorized into three stages: the invasive stage, the purulent stage and the late or septic stage.

INVASIVE STAGE

The invasive stage of pyomyositis is associated with cramping pain, edema in the affected muscle group, increasing discomfort and fever. At this stage when tenderness may be minimal, indurated muscle has been described as "woody" on palpation.

PURULENT STAGE

During the purulent stage of pyomyositis, the patient may complain of fever with chills. Edema is more noticeable, with fluctuation, and tenderness is more definite. The overlying skin is mildly erythematous. Leukocytosis is present, with an elevated erythrocyte sedimentation rate, and needle aspiration yields thick purulent fluid from which S. aureus is most often cultured. Noninvasive demonstration of abscesses is best accomplished by ultrasonography, magnetic resonance imaging or CT scanning.

LATE OR SEPTIC STAGE

The late or septic stage of pyomyositis is characterized by high fever or septic shock. Overlying skin is erythematous and indurated, and tenderness is exquisite.

The patient in the illustrative case was admitted to the hospital during the purulent stage of pyomyositis but may have initially presented, albeit unrecognized, to the emergency department at the invasive stage. He remained afebrile throughout the illness, despite widespread subcutaneous, subdermal and intramuscular abscesses. Newly diagnosed diabetes mellitus and alcohol use were predisposing factors in this case and may have slowed the patient's recovery. With such widespread involvement, bacterial endocarditis was considered possible, but findings on echocardiography were completely normal. Transient S. aureus bacteremia from a septic focus on the face, with hematogenous dissemination to distant areas, remains the plausible source in this case. No other solid organ involvement seemed to have occurred.

Clinical Management

Pyomyositis may be readily recognized in the tropics, but in temperate climates the diagnosis is sometimes missed at the invasive stage. For reasons that are still not clear, pyomyositis occurs less commonly in temperate climates. The diagnosis is clinical, making a high index of suspicion important. The presence of persistent localized muscle pain, tenderness and induration accompanied by mild fever, leukocytosis and an elevated erythrocyte sedimentation rate in a person with diabetes mellitus or another immunocompromising condition should put pyomyositis high on the list of possible diagnoses.

A penicillinase-resistant penicillin is the empiric antibiotic therapy of choice. Once suppuration has occurred, surgical drainage with debridement of necrotic tissue is mandatory. Septic shock necessitates intensive care. Modifications of antibiotic choice are based on results of Gram's stain, culture and sensitivity testing, and the clinical progress of the patient. Long-term antibiotic therapy for up to six weeks is recommended.

[Figure 1 to 2 ILLUSTRATION OMITTED]

REFERENCES

[1.] Nielsen EJ. Tropical pyomyositis in a temperate climate in an immunocompetent adult. Ann Emerg Med 1992;21:880-2. [2.] Strickland GT, ed. Hunter's Tropical medicine. 7th ed. Philadelphia: Saunders, 1991:454-5. [3.] Walling DM, Kaelin WG Jr. Pyomyositis in patients with diabetes mellitus. Rev Infect Dis 1991;13:797-802. [4.] Schwartzman WA, Lambertus MW, Kennedy CA Goerz MB. Staphylococcal pyomyositis in patients infected by the human immunodeficiency virus. Am J Med 1991;90:595-600. [5.] Watts RA, Hoffbrand BI, Paton DF, Davis JC. Pyomyositis associated with human immunodeficiency virus infection. Br Med J [Clin Res] 1987;294:1524-5. [6.] 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;91:129-36. [7.] Diego Miralles G, Bregman Z. Necrotizing pyomyositis caused by Mycobacterium avium complex in a patient with AIDS [Letter]. Clin Infect Dis 1994;18:833-4. [8.] Christin L, Sarosi GA. Pyomyositis in North America: case reports and review. Clin Infect Dis 1992;15:668-77. [9.] Nitta AT, Kuritzkes DR. Pyomyositis due to group C streptococci in a patient with AIDS [Letter]. Rev Infect Dis 1991;13:1254-5.

The Authors

GARY R. DUNKERLEY, M.D. is director of the St. Clare's Hospital Family Practice Residency Program in Schenectady, N.Y. He earned a medical degree from Hahnemann Medical College, Philadelphia, where he also completed a residency in family practice.

JON OLDER is a fourth-year medical student at the University of New England College of Osteopathic Medicine, Biddeford, Maine.

BENJAMIN ONWOCHEI, M.D. is a research fellow at the St. Clare's Hospital Residency Program, where he also completed a residency in family practice. Dr. Onwochei earned a medical degree from the University of Nigeria Medical School, Enugu, Nigeria.

JOSEPH PAZIENZA, M.D. is an associate radiologist at St. Clare's Hospital. He earned a medical degree from Albany (N.Y.) Medical College, where he also completed a residency in radiology.

Address correspondence to Gary R. Dunkerley, M.D., Family Practice Residency, St. Clare's Hospital, 600 McClellan St., Schenectady, NY 12304.

COPYRIGHT 1996 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group