Venugopal, Anilrudh A. MD*; Johnson, Leonard B. MD*†; Pawlak, Joan BS*; Fozo, Paul K. MD*; Saravolatz, Louis D. MD*†
*St John Hospital and Medical Center and †Wayne State University School of Medicine, Detroit, MI.
Alternate Contact: Anilrudh Venugopal, MD, Mack Office Building, 19251 Mack Avenue, Suite 335, Grosse Pointe Woods, MI 48236. Email: email@example.com.
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An injection drug user presenting with respiratory complaints was diagnosed with an empyema secondary to a psoas abscess. Methicillin-resistant Staphylococcus aureus was cultured from both the empyema and psoas abscess. The isolate was found to carry the staphylococcal cassette chromosome mec type IV and Panton-Valentine leukocidin genes.
In recent years, infections due to community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) have been reported in the Detroit area.1 The typical infections due to CA-MRSA are skin and soft tissue infections and less commonly necrotizing pneumonias.2,3 Community-associated strains appear to be unique from hospital associated, both genetically and clinically.3 Most CA-MRSA strains carry the staphylococcal cassette chromosome (SCC) mec type IV gene and the genes for Panton-Valentine leukocidin (PVL), a cytotoxin, which is a virulence factor for primary skin infections and pneumonia.4,5
Psoas abscesses are generally the result of either hematogenous spread from another source or direct extension from a local source.6 S. aureus is the most frequently identified pathogen associated with psoas abscess due to hematogenous seeding.6 Methicillin-resistant S. aureus (MRSA) had been reported in several case series of psoas abscess7,8 and has also been associated with a "community-acquired" case after trauma.9 We report a case of psoas abscess caused by a recognized strain of CA-MRSA that presented with respiratory symptoms due to a secondary empyema.
A 46-year-old woman with a history of injection drug use presented with a cough for 1 week and a history of chills, yellow sputum, and difficulty in breathing. She also complained of pain in the right forearm where she injects heroin. The patient had a medical history of chronic hepatitis C virus infection. Her only recent hospitalization was at another facility approximately 1 month before she was treated for anemia, and she had not recently received antibiotic therapy. On examination, the patient was cachectic appearing and in no acute distress. Her vital signs were a temperature of 100.5°F, heart rate of 96/min, blood pressure of 114/70 mm Hg, and O2 saturation of 99% on room air. Examination of the lungs found reduced breath sounds at the right lung base extending half way up with dullness to percussion. The abdominal examination was negative and examination of the right forearm showed an area of erythema over the antecubital fossa with no fluctuance. The chest radiograph revealed a large right pleural effusion. The baseline laboratory testing included a hemoglobin of 11.6 gm/dL, platelet count of 579,000 cells/mm3, and white blood cell count of 30,200 cells/ mm3 with 91% neutrophils. Ultrasound of the forearm was negative for deep venous thrombosis or abscess but did show the presence of a superficial thrombophlebitis in a branch of the right antecubital vein. Blood cultures were drawn, and the patient was initiated on empirical treatment for community-acquired pneumonia with ceftriaxone and azithromycin.
A computerized tomography (CT) scan of the chest was performed and showed the presence of a large right-sided pleural effusion with loculation (Fig. 1A). In addition, the upper portion of the abdomen was imaged and demonstrated the presence of a multiloculated right psoas fluid collection (Fig. 1B). A chest tube was placed with resultant drainage of 1400 cc of cloudy pleural fluid. The fluid analysis revealed an LDH of 2554 U/L, glucose of 7 mg/dL, protein of 5.2 g/dL, RBC of 3117 cells/mm3, total WBC of 397/mm3 with 99% polymorphonuclear cells. Repeat imaging after the chest tube was placed showed atelectasis but no underlying pneumonia in the right lung. The psoas fluid collection was drained using CT guidance, and a drain was left in place after draining nearly 100 mL of frank purulent material. The pleural and psoas fluid cultures grew MRSA that was susceptible to vancomycin, trimethoprim-sulfamethoxazole, clindamycin, levofloxacin, and tetracycline but resistant to erythromycin. Therapy was changed to intravenous vancomycin. The patient's vancomycin dose was 750 mg intravenously every 12 hours with goal trough levels of 5 to 10 μg/mL. Her serum levels ranged from 6.5 to 9.1 μg/mL. Her human immunodeficiency virus test was nonreactive, and a transthoracic echocardiogram showed no evidence of endocarditis. The patient had a video-assisted thoracoscopy procedure to remove the adhesions and fibropurulent material in the pleural cavity. The patient was later transferred to an extended care facility to complete a 6-week course of vancomycin. The patient was discharged clinically improved but failed to return for follow-up evaluation.
Staphylococcus aureus was recovered from the pleural fluid, and identification was determined by catalase production and Staphaurex latex agglutination test (Remel, Lenexa, Kans). Susceptibility testing was done on the Vitek 2 (BioMerieux, Hazelwood, Mo) and methicillin resistance confirmed by growth on Mueller Hinton agar containing 6 μg/mL oxacillin. The MRSA isolate from the pleural fluid was analyzed using pulsed field gel electrophoresis (PFGE). The DNA sample was digested with SmaI restriction endonuclease (Invitrogen Corp, Carlsbad, Calif). PFGE was performed on the CHEF-DR III (Bio-Rad Laboratories, Hercules, Calif) with switch times of 5 to 40 seconds, at 6 V/cm for 21 hours. Gel was stained with ethidium bromide, destained in water, and photographed on the ChemiImager 4000 (Alpha Innotech, San Leandro, Calif). The SCC mec types were determined by a previously described polymerase chain reaction-based multiplex assay.10 PCR amplification of the cassette chromosome recombinase gene was performed using the primers described by Okuma et al.11 Positive controls for each assay included S. aureus HPV 107/ATCC BAA-44 (type I), NYBK 2464/ATCC BAA-41 (type II), HUSA 304/ATCC BAA-39 (type III), and HDE 288/ATCC BAA-42 (type IV). The mec A gene served as an internal control for the multiplex assay. Polymerase chain amplification of the genes encoding PVL lukS- V and lukF-PV was performed using primers described elsewhere.12 The positive control for the PVL assay was ATCC 49775, and sterile water served as the negative control.
The patient isolate carries the SCC mec type IV and PVL genes. The PFGE pattern of our patient isolate is identical to the strain of CA-MRSA causing skin and soft tissue infections in our community.1 This strain is identical to clone USA 300, a frequently identified strain among community-associated outbreaks.13
We describe a patient with a history of injection drug use that presented with a concomitant empyema and psoas abscess due to a strain of MRSA that is identical to USA 300 and carries the PVL genes. The most likely source of the psoas infection was hematogenous seeding from the superficial thrombophlebitis that was present on the right arm. The patient did not have the typical symptoms from her psoas infection and presented after the development of her empyema. Although most patients with psoas abscess present with pain or fluctuant mass, a small number may present with other findings including constitutional symptoms. In one series that reviewed the clinical presentation of 17 patients with psoas abscess, only 11/17 (64%) had flank, hip, or abdominal pain, whereas one patient had only constitutional complaints.7
This case is unique in several aspects. Empyemas and complicated parapneumonic effusions due to CA-MRSA have been reported as a complication of pneumonia and not due to contiguous muscle abscess.14-16 The development of empyema and effusions due to psoas abscess is infrequently reported and has not been reported with S. aureus infection.17,18 Although the patient's initial symptoms were suggestive of pneumonia, follow-up imaging after drainage of the pleural effusion showed no underlying iniltrate. In addition, CT images showed contiguous spread from the psoas muscle into the pleural space. It is unlikely that the psoas abscess was secondary to a primary empyema because secondary extension of empyema to a subdiaphragmatic structure is rare. This case demonstrates the importance for clinicians to consider subdiaphragmatic processes when evaluating pleural effusions and empyemas. Failure to appropriately diagnose and treat primary subdiaphragmatic infections such as psoas abscess is likely to result in recurrence of infection.
Most of the infections reported due to CA-MRSA are skin and soft tissue infections and pneumonias. One series of 4 pyomyositis cases due to CA-MRSA has been reported.19 However, in all patients, the infected muscles were located in the thigh. The only other reported case of psoas abscess due to community-acquired MRSA occurred in a patient with chronic vertebral osteomyelitis and discitis who developed secondary psoas infection.9 There was no information on the patient's substance abuse or hospitalization history, and the MRSA isolate was not tested for SCC mec type or PVL genes. Our case adds to the growing list of clinical manifestations associated with strains of CA-MRSA. The patient responded well to therapeutic drainage of empyema and the psoas abscess as well as prolonged therapy with vancomycin.
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