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Volume 12, Number 1—January 2006


Community Case of Methicillin-resistant Staphylococcus aureus Infection

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EID Nelson L, Cockram CS, Lui G, Lam R, Lam E, Lai R, et al. Community Case of Methicillin-resistant Staphylococcus aureus Infection. Emerg Infect Dis. 2006;12(1):172-174.
AMA Nelson L, Cockram CS, Lui G, et al. Community Case of Methicillin-resistant Staphylococcus aureus Infection. Emerging Infectious Diseases. 2006;12(1):172-174. doi:10.3201/eid1201.050279.
APA Nelson, L., Cockram, C. S., Lui, G., Lam, R., Lam, E., Lai, R....Ip, M. (2006). Community Case of Methicillin-resistant Staphylococcus aureus Infection. Emerging Infectious Diseases, 12(1), 172-174.

To the Editor: Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging infectious disease worldwide and is increasingly reported in Asia (1). We describe a community case of invasive MRSA infection, which appeared as bacteremia and pneumonia; CA-MRSA was initially suspected, and eventually the patient was treated successfully with ampicillin/sulbactam.

A 52-year-old man with chronic eczema was admitted to the Prince of Wales Hospital, Hong Kong, with fever and chills. Before admission, he had been treated for infected eczematous lesions for several weeks with oral ampicillin, cloxacillin, and cefazolin. He had no history of hospitalization in the past 10 years, and none of his family members were healthcare workers. Examination showed an oral temperature of 40°C, blood pressure 95/55 mm Hg, and no audible murmur. Cellulitis in the left leg complicated his eczematous skin lesions. Chest radiograph showed right-middle-zone pneumonia. Neutrophilia (leukocytes 15.5 × 109/L, neutrophils 86%), thrombocytopenia (platelets 55 × 109/L), prolonged activated partial thromboplastin time (43.6 s), and elevated bilirubin level (31 μmol/L) were observed. Two initial blood cultures grew gram-positive cocci in clusters, identified as S. aureus by positive results for catalase and slide/tube coagulase and a negative result for ornithine decarboxylase. Intravenous cloxacillin (2 g every 6 h) was given on days 2–5. Antimicrobial drug susceptibility testing was performed by the disk-diffusion method (1 μg oxacillin/disk, Mueller-Hinton agar, 2% NaCl), followed by MIC determination with the agar dilution method in accordance with NCCLS (former National Committee for Clinical Laboratory Standards, now Clinical and Laboratory Standards Institute) recommendations (2). One blood isolate was identified as methicillin-resistant S. aureus (MRSA), with an oxacillin MIC 4 μg/mL. The other isolate was identified as methicillin-sensitive S. aureus (MSSA), with an oxacillin MIC of 0.5 μg/mL. In view of a possible CA-MRSA infection (which could have been β-lactam–resistant), cloxacillin was substituted with intravenous vancomycin plus rifampin on day 5.

However, the patient's condition progressively deteriorated from day 2 to day 10 with persistent fever, chills, hypotension, and hemoptysis. A repeated chest radiograph showed small lung cavities with fluid, and a thoracic computed tomographic scan confirmed multiple lung abscesses. Results of an initial transthoracic echocardiograph were normal, but a subsequent transesophageal echocardiograph demonstrated tricuspid valve vegetation.

The MRSA isolate was susceptible to gentamicin, cotrimoxazole, erythromycin, ciprofloxacin, clindamycin, fusidic acid, tetracycline, chloramphenicol, vancomycin, and rifampin; a different pattern of multidrug-resistant MRSA isolates from that usually found in our facility (2,3). The isolate was also susceptible to ampicillin/sulbactam, with an equivalent breakpoint MIC <8/4 μg/mL by disk testing (2). Latex detection for PBP2a (Slidex MRSA-Detection, bioMérieux, Marcy l'Etoile, France) and polymerase chain reaction (PCR) detection for mecA were both negative, predicting nonresistance to oxacillin (25). A nitrocefin-disk test was positive for β-lactamases, and a 4-fold reduction in MIC was demonstrated in the presence of sulbactam (6). Panton-Valentine leukocidin (PVL) gene locus was not detected (1). Community-acquired BORSA (borderline oxacillin-resistant S. aureus), infective endocarditis, and lung abscesses were diagnosed. Intravenous ampicillin/sulbactam (3 g every 6 h) was given on day 10 with rifampin; vancomycin treatment was stopped. Defervescence occurred 3 days later, subsequent blood cultures became sterile, and radiographic changes gradually resolved. Ampicillin/sulbactam was given for 6 weeks without complication.

As this case suggests, BORSA can sometimes be confused with CA-MRSA because of similar clinical signs and symptoms and overlapping oxacillin MICs (2–8 μg/mL and 4–64 μg/mL, respectively) (1,4,6). Both pathogens can appear as community-acquired infections and may be related to previous antimicrobial drug usage (6,7). Although CA-MRSA has been associated with soft tissue infections and necrotizing pneumonia (7,8), MSSA or BORSA strains can also cause these diseases. Thus, in view of potentially different treatment options, when MRSA isolates (e.g., oxacillin MICs >4–8 μg/mL) are associated with community-acquired, serious infections (e.g., blood isolates) and are not multidrug resistant, one can consider mecA (or PBP2a) testing to delineate the resistance mechanism (Table). If mecA is present, further testing for PVL gene locus with or without staphylococcal chromosomal cassette mec (SCCmec) type IV can be performed to diagnose CA-MRSA; if mecA is not detected, further testing for BORSA may be indicated, and β-lactam therapy should be evaluated individually. If these pathogens are not differentiated and all are treated as CA-MRSA, a non–β-lactam antimicrobial drug, such as vancomycin, will be used (1,4,7,8). However, for serious and deep-seated S. aureus infections (e.g., bacteremia, endocarditis), vancomycin is inferior to β-lactam antimicrobial drugs, even when in vitro testing indicates susceptibility. Treatment failures have been encountered (4). Linezolid is a good alternative but limited by availability and cost, and clindamycin therapy can be associated with inducible resistance. For BORSA-associated infections, β-lactam antimicrobial drugs, including high-dose penicillinase-resistant penicillins (PRPs) (e.g., cloxacillin) or β-lactam/β-lactamase–inhibitor combinations (e.g., ampicillin/sulbactam) are regarded as treatments of choice (4,6,9).

BORSA initially described nonheteroresistant strains of S. aureus with oxacillin MIC <2 mg/L, which produce ample β-lactamases and are rendered fully susceptible to PRP by β-lactamase-inhibitors (4,6). Subsequent BORSA strains described have had higher oxacillin MICs (4–8 mg/L) (4). The proportion of BORSA among clinical isolates of S. aureus varies (1.4%–12.5%) but is usually ≈5% (4,10). A BORSA infection outbreak among dermatology patients with severe skin diseases has also been reported (10). Postulated resistance mechanisms include overproduction of conventional penicillinases, production of an inducible, plasmid-mediated, membrane-bound methicillinase, and in some cases, point mutations of penicillin-binding-proteins (4). The clinical importance of BORSA is unknown since early clinical/animal data suggest treatment efficacy of PRP (against strains with MIC <2 mg/L) (4,6,9). Whether BORSA with higher oxacillin MICs (4–8 mg/L) will respond equally well to PRP is less clear. Further studies into the treatment of BORSA, including pharmacokinetic considerations, are needed (4). However, high-dose β-lactam/β-lactamase inhibitor combinations (e.g., ampicillin/sulbactam), as shown in animal models, are at least as effective as PRP (9). In conclusion, our report suggests that mecA (or PBP2a) detection may help manage serious, community-acquired, non–multidrug-resistant MRSA infections because of the potential confusion between BORSA and CA-MRSA.

Lee Nelson*, Clive S. Cockram*, Grace Lui*, Rebecca Lam*, Edman Lam*, Raymond Lai*, and Margaret Ip*Comments to Author 

Author affiliations: *Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China


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Cite This Article

DOI: 10.3201/eid1201.050279

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Table of Contents – Volume 12, Number 1—January 2006


Please use the form below to submit correspondence to the authors or contact them at the following address:

Margaret Ip, Department of Microbiology, Prince of Wales Hospital, Chinese University of Hong Kong, Ngan Shing St, Hong Kong SAR, People’s Republic of China; fax: 852-2647-3227

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