Despite the relative increase in invasive disease caused by group A beta-hemolytic streptococcal (GABHS) infection in the recent past1 and the increased risk for bacterial infections in HIV-infected children,2 there has been little recognition of invasive GABHS disease in HIV-infected children. We report a case of primary peritonitis caused by GABHS in an HIV-infected adolescent.
Case report. A 15-year-old HIV-infected African-American female patient presented with a 3-day history of abdominal pain, nausea, vomiting and watery diarrhea and a 2-day history of mild rhinitis and sore throat. Her last menstrual period had ended the day before onset of symptoms.
HIV infection was documented at 5 years of age and was presumed to be perinatally acquired. She had been in good health and had never been on antiretroviral therapy, persistently refusing treatment from its first offering during her preadolescent years. The most recent CD4 lymphocyte count was 400 cells/mm3 at 10 years of age. On admission temperature was 102.3°(39.1°C), heart rate was 146 beats/min and blood pressure was 110/46 mm Hg. The abdomen was mildly distended and diffusely tender. No rebound tenderness was present. The bowel sounds were diminished. Pelvic examination revealed only minimal adnexal tenderness. The white blood cell count was 27 900 cells/mm3 with a differential of 80% neutrophils, 14% band forms, 3% lymphocytes and 3% monocytes. CD4 lymphocyte count was 60 cells/mm3 (14% of total T lymphocytes), hemoglobin was 10.5 mg/dl and platelets were 152 000/mm3. Computed tomographic scan of the abdomen with intravenous contrast revealed thickened walls of the small bowel and ascending colon with a small amount of free fluid in the pelvis. Sigmoidoscopy revealed normal colonic mucosa. Laparoscopy was converted to laparotomy when a diffuse, purulent peritoneal exudate was seen. No focal process was evident on examination of abdominal and pelvic organs. The appendix appeared injected but not indurated or perforated, and subsequent histopathology was normal. Gram-positive cocci and white blood cell count were seen on Gram stain of the peritoneal exudate, and cultures grew group A beta-hemolytic Streptococcus. A blood culture was negative. The patient received 12 days of intravenous clindamycin and was discharged home. One year later she remained well with stable HIV infection status [CDC Clinical Category A2 (CD4 lymphocyte count of 400 cells/mm3, apparently reflecting a return to her preperitonitis immunologic state and without the use of antiretroviral therapy)].
Discussion. To the best of our knowledge this is the third report of invasive GABHS disease in an HIV-infected child. A 7-month-old infant with CDC Category B (P2D3) HIV infection who had fatal GABHS sepsis and pneumonia was reported in 1990.3 A 12-year-old HIV-infected boy (CDC Category A2, CD4 count of 285 cells/mm3) with GABHS meningitis and bacteremia who survived was reported in 1991.4
Invasive GABHS has been described in HIV-infected adults. Six (14%) of 44 episodes of community-acquired bacteremia among 38 patients with AIDS hospitalized at San Francisco General Hospital between August, 1986, and December, 1987, were caused by GABHS.5 All 6 patients recovered. Group A Streptococcus was the third most common isolate in this series after Staphylococcus aureus and Streptococcus pneumoniae. Nine HIV-infected adults with invasive GABHS in New Jersey were reported in 1994 (7 were intravenous drug abusers).6 Bacteremia was present in 7, 5 of whom also had pneumonia. Three had skin and soft tissue infection. Two of the 9 died as a result of GABHS infection.
In Ontario, Canada, during the 24 months of 1992 and 1993, 4 of 97 adults who had GABHS bacteremia and whose underlying disease status was known were HIV-positive.7 The relative risk of invasive GABHS disease in HIV-infected adults compared with those without underlying diseases was 9.4 (95% confidence interval, 3.5 to 25; P = 0.001). In New York City from April, 1995, through March, 1996, 15 of 159 persons with invasive GABHS disease were HIV-positive.8 Among those patients HIV was the second most common underlying disease present (9% of cases) after diabetes (25% of cases).
Primary bacterial peritonitis in children has declined in frequency during the antibiotic era and now occurs most often in children with nephrotic syndrome and postnecrotic cirrhosis.9 This decline has been attributed to the widespread use of oral antibiotics for minor upper respiratory tract infections. In the preantibiotic era hemolytic streptococci (presumably GABHS in the majority of cases) rivaled the pneumococcus as the most common cause of bacterial peritonitis in children.10 Pneumococci remain a common etiology of primary peritonitis in children, especially among those with nephrotic syndrome.11 However, the historically prominent GABHS has been an uncommon cause of primary peritonitis in childhood for the past 40 years. The relative proportion of cases caused by Escherichia coli and other Gram-negative enteric bacilli has increased during this time, especially among patients with cirrhosis.9, 11
Two HIV-infected men with GABHS peritonitis have been reported. A 40-year-old man with phlegmonous gastritis and peritonitis caused by GABHS was reported in 1992.12 He seroconverted to HIV-positive during hospitalization for this infection. A 70-year-old HIV-positive man who developed GABHS peritonitis while receiving continuous peritoneal dialysis for diabetic nephropathy was reported in 1995.13 Both recovered.
HIV infection appears to be a risk factor for invasive GABHS disease in adults. This may reflect in part the frequent occurrence of intravenous drug abuse, itself a risk factor for invasive GABHS disease,14 in this population. The current case confirms earlier reports of the occurrence of serious GABHS infections in HIV-infected children. However, it remains unclear whether HIV infection is a risk factor for invasive GABHS disease in children.
Acknowledgments. We thank Dr. Allen Chauvenet for help with translation of French medical literature and Dr. Laurence Givner for helpful comments and review of the manuscript.
Charles R. Woods, M.D.
Cate Shappley Mason, M.D.
Department of Pediatrics; Bowman Gray School of Medicine; Wake Forest University; Winston-Salem, NC
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