Community-Associated MRSA Infection in Remote Amazon Basin Area, Peru.

To the Editor: Two predominant community-associated methicillin-resistant Staphylococcus aureus (CAMRSA) clones have been reported in South America: 1) sequence type 30 staphylococcal cassette chromosome mec IV (ST30-SCCmec IV) (USA 1100), first found in Uruguay (2002) and later in Brazil and Argentina (2005); and 2) ST8SCCmec IVc/E (USA300–Latin American variant), found predominantly in Ecuador and Colombia (2006–2008) (1). In hospitals in Colombia, USA300–Latin American variant has replaced the most common hospital-associated lineage, known as the Cordobes/Chilean clone (MRSA ST5-SCCmec I) (2). In Peru, a limited number of imported cases of CA-MRSA have been reported (3). We describe a case of CA-MRSA infection in a patient living in a remote area of the Amazon Basin of Peru. The patient was a 58-year-old woman who was hospitalized in June 2014 for a skin ulcer. She had been well until 10 days before admission, when she noticed a papule on her right arm, followed the next day by localized swelling and redness. Three days later, spontaneous secretion of a purulent material was noted. At the time of admission, the patient had no fever or constitutional symptoms; the ulcer was deep with irregular borders (≈10 × 4 cm) and active purulent secretion (Figure, panel A). Other physical examination findings were unremarkable. For the past 2 years, the patient had lived in a remote, rural, jungle village in Peru. She was a housewife but also farmed in nearby areas. There were ducks, chickens, and guinea pigs on the farm where she lived. Her village had neither running water nor roads and almost no access to healthcare (reaching the nearest healthcare center required a 36-hour boat trip). She previously experienced several episodes of malaria (most recently in February 2014), for which she received antimalarial medication provided by a Brazilian military post at the border of Peru. She had never taken antimicrobial drugs and had not traveled in the past 2 years. She first noticed the skin lesion on the first day of an 8-day boat trip from her home village to Iquitos, the largest city in the Peruvian Amazon Basin. Cultures from wound exudate and skin biopsy samples yielded S. aureus resistant to oxacillin, tetracycline, and erythromycin and susceptible to ciprofloxacin, gentamicin, rifampin, and trimethoprim/sulfamethoxazole (susceptibility testing performed by an agar dilution method). D test showed inducible resistance to clindamycin. The presence of mecA and the genes (lukS-PV, lukF-PV) encoding Panton-Valentine leucocidin (PVL) were confirmed by PCR. The isolate was characterized as MRSA ST6-t701SCCmecV. Whole-genome sequence analyses identified a predicted protein with 100% aa identity (98% coverage) to the truncated b-hemolysin of the reference genome of S. aureus USA300_FPR3757 (GenBank accession no. gb|ABD20946.1|) and the prophage groups 1, 2, and 3. Pulsed-field gel electrophoresis (PFGE) exhibited a pulsotype different from other typical CA-MRSA PFGE patterns found in MRSA from Latin America, labeled as CAMRSA 120 (online Technical Appendix, http://wwwnc. cdc.gov/EID/article/22/5/15-1881-Techapp1.pdf). Intravenous clindamycin (600 mg every 8 hours for 5 days) was empirically prescribed, after which treatment was switched to vancomycin (1 g every 12 hours for 1 week). Subsequently, the patient received trimethoprim/sulfamethoxazole (160/800 mg every 12 hours for 1 week). The clinical evolution was satisfactory, and the infection resolved (Figure, panel B). This case of a skin and soft tissue infection caused by a CA-MRSA ST6-t701-SCCmec V PVL-producing organism is notable for several reasons. First, infection occurred in a remote rural jungle area of Peru at the border with Brazil