Perinephric Abscess Caused by Community-Acquired Methicillin Resistant Staphylococcus aureus

Abstract

To the Editors: As presented by Zaoutis et al,1 there has been a steady increase in the proportion of community acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates recovered from skin and soft tissue infections in the pediatric population. Invasive infections with CA-MRSA are also on the rise, and are reportedly associated with a longer duration of bacteremia, more febrile days, and more inpatient hospital days than invasive infections with CA-MRSA.2 We report a complicated perinephric abscess caused by CA-MRSA in a toddler with a history of recent blunt abdominal trauma. A 13-month old boy was admitted to the pediatric ICU with a 3-day history of fever, vomiting, decreased activity, and abdominal distention. He was febrile to 38.3°F with a markedly tender and distended abdomen (girth 54 cm). A computed tomography scan with contrast demonstrated a subcapsular hematoma around the left kidney; thickening of the descending colon, a peri-colonic hematoma, and moderate hemoperitoneum. Ampicillin, gentamicin, and metronidazole were initiated. An exploratory laparotomy yielded 100 mL of purulent fluid from the peritoneum. A perforation measuring 5 cm in length was seen in the descending colon, and a small perforation was also noted in the Gerota fascia, actively draining purulent fluid. Six centimeters of the colon was resected at the site of perforation, and a Jackson-Pratt drain was left draining the Gerota's capsule. Antibiotics were changed to vancomycin, gentamicin, and metronidazole. Peritoneal and perinephric abscess cultures grew MRSA, which was susceptible to vancomycin, clindamycin, gentamicin, levofloxacin, linezolid, and trimethoprim-sulfamethoxazole; and resistant to ampicllin/sulbactam, cefazolin, erythromycin, oxacillin, and penicillin. He recovered after 2 weeks of parenteral therapy with vancomycin, gentamicin, and metronidazole, and 2 additional weeks of oral trimethoprim-sulfamethoxazole. The most probable mechanism for development of this abscess was blunt trauma to the abdomen resulting in renal laceration and bleeding around the kidney, followed by seeding with CA-MRSA during an episode of transient bacteremia. The delay in seeking medical care likely allowed the abscess to extend beyond the perinephric space into the peritoneum, with subsequent peritonitis and rupture of the descending colon. The CA-MRSA strain from our patient carried genes for Panton-Valentine leukocidin (PVL), a potent cytotoxin that mediates tissue necrosis and destruction of leukocytes by creating pores in leukocyte cell membranes. PVL is found in up to 72% of CA-MRSA isolates in the community,3 and may have accounted for the rapid progression of infection seen in our patient. In a recent study from Texas,4 children with osteomyelitis caused by PVL-positive isolates of CA-MRSA were more likely to have severe infection than osteomyelitis caused by CA-MRSA isolates lacking PVL genes. Zainab A. Malik, MD Nathan Litman, MD Department of Pediatrics, Division of Infectious Diseases Children's Hospital at Montefiore Bronx, NY E-mail: [email protected].