Group A streptococcal primary peritonitis in a healthy girl

We report the case of a previously healthy 10-year-old girl admitted to hospital in a state of septic shock. Three days prior to admission she developed abdominal pain and diarrhoea, along with fever, sore throat and vomiting. There were no sick contacts in her immediate entourage (including family members). At initial presentation she was tachycardic, with a blood pressure of 80/40 mmHg. Physical exam revealed an erythematous rash on the face and trunk, non-necrotic small petechiae on her legs and an abdomen that was tense and guarded. Neutrophil count was 8.6 · 109/L, C reactive protein (CRP) 327 mg/L and lactate 2.6 mmol/L. Blood capillary gas and coagulation studies were normal. She required IV fluid resuscitation, after which she was started on norepinephrine, cefazolin, cefotaxime and clindamycin, and transferred to the Intensive Care Unit. Abdominal ultrasound showed a large quantity of free peritoneal fluid. She underwent laparoscopic surgery which revealed a large volume of pus, but no stool, in the abdominal cavity. There were no signs of bowel perforation or appendicitis. A diagnosis of primary peritonitis and toxic shock syndrome (TSS) was made. Antibiotics were changed to piperacillin-tazobactam and clindamycin. Cultures from blood, urine, throat and vaginal secretions were negative. Gram stain of the peritoneal fluid revealed Gram-positive cocci in pairs, however the culture did not grow. Polymerase chain reaction (PCR) of the liquid was positive for Group A Streptococcus (GAS) (confirmed by the 16S rDNA PCR) and for virulence genes speA, speB and smeZ, while negative for speC, ssa and sic.1 The strain was emm 3.1 (serotype M3). Over the next 72 h the patient did well, with resolution of her skin rash and abdominal tenderness, and a decrease in CRP to 128 mg/L. Intravenous clindamycin was stopped on day five, and the patient was discharged from hospital on day 10 with oral amoxicillin for additional 4 days. Primary peritonitis in a previously healthy child is rare. Gram negative bacilli, Streptococcus pneumoniae and Staphylococcus aureus are the main causal pathogens. However, several cases of GAS primary peritonitis have been reported recently, in which patients present with clinical signs of TSS, as did our case.2 A recent nation-wide survey in Finland identified primary peritonitis as the focus of GAS invasive infections in 5% of children.3 The pathogenesis of GAS primary peritonitis remains unclear. The source of infection could be the respiratory tract or the skin (through hematogenous spread), the female genital tract (ascending contamination) or the gastro-intestinal tract, although GAS is not considered part of the normal bowel flora. Our patient had negative cultures from both the throat and vagina. The serotype identified in our patient (M3) is frequently associated with TSS and scarlet fever.4 In summary, we describe a previously healthy 10-year-old girl hospitalised with GAS primary peritonitis and TSS. Our report highlights the potential benefit of bacterial PCR in detecting the causative agent of a primary peritonitis when antibiotics are given prior to surgery. Emm typing can also be performed even when the bacteria fails to thrive on culture. Finally, our report reminds clinicians to be aware of this unusual presentation of GAS infection, which, while uncommon, may be on the rise.

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