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Abstract

Introduction: Late onset group B streptococcal (LOGBS) infection has an estimated 5% case fatality rate in term and even higher in preterm infants. It usually manifests as occult bacteremia or meningitis but also as a focal infection like pneumonia, septic arthritis, osteomyelitis, and cellulitis-adenitis syndrome. LOGBS infection in twins has been reported mainly as bacteremia and/or meningitis. We report LOGBS cellulitis-adenitis syndrome in twins caused by the same GBS strain. To our knowledge, this is the first such report in twins with cellulitis-adenitis syndrome. Twin A: A 2- month old, 26 weeks gestation male, presented with fussiness and fever for one day. He was the first born of a twin pregnancy by c-section. Mother's GBS screen was negative. Neonatal course was complicated by respiratory distress syndrome, apnea of prematurity and grade 1 intracranial hemorrhage. He was discharged at six weeks of age. At presentation, he was irritable, afebrile with heart rate(HR) 214 /min, respiratory rate(RR) 40/min and was hypoxic. CBG showed pH 7.0, PCO2 71, PO2 93, HCO3 17, base deficit -14 and lactate 9. He received 60 ml/kg of fluid bolus. His perfusion worsened, HR decreased to 70/min and was intubated. WBC was 4500/mm3, hemoglobin 6.6 gm/dl and platelets 298,000/mm3. Blood and urine cultures were obtained, IV cefotaxime and vancomycin were started. CSF analysis was normal. He received packed red blood cell transfusion. Following 12 hours of aggressive fluid resuscitation and antibiotic treatment, lactic acidosis persisted. On reevaluation he was noted to have a firm, warm and erythematous right submandibular swelling. Ultrasound (US) of the neck revealed cellulitis and enlarged submandibular lymph nodes. Blood culture grew GBS. CSF culture was negative. Antibiotics were changed to IV ampicillin. Lactic acidosis resolved within 30 hours, the submandibular swelling improved, infant was extubated on day 7 and received 10 days of antibiotic treatment. Twin B: Five days after twin A's admission, his sister twin B presented with poor feeding for 1 day but no associated fever or fussiness. Neonatal course was complicated by respiratory distress syndrome, apnea and anemia of prematurity and Enterococcus bacteremia. She was afebrile, HR 168/min, RR 40/min, blood pressure 91/50. She had an erythematous, firm, tender right submandibular swelling. WBC was 6900/mm3, hemoglobin 8.5 gm/dl and platelets 358000/mm3. Urine, blood and CSF cultures were obtained; ampicillin and cefotaxime were started. US of the neck revealed multiple swollen lymph nodes. Blood culture grew GBS. CSF and urine cultures were negative. Ampicillin alone was continued. The cervical swelling resolved after 10 days of ampicillin treatment. The GBS isolates from both patients were sent to the Michigan Department of Community Health Bureau of Laboratories for pulsed field gel electrophoresis (PFGE). The electrophoresis patterns were produced by using restriction enzyme sma-l. The PFGE patterns of both isolates were indistinguishable suggesting a common source of exposure in the twins. Discussion: Our twin infants presented five day apart with cellulitis-adenitis syndrome caused by the same GBS strain. The co-twin of an index case with GBS infection has been shown to be at exceptionally higher risk (25-fold) of GBS infection. The American Academy of Pediatrics recommends that "the sibling of a multiple birth index case with early- or late-onset GBS disease should be observed carefully and evaluated and treated empirically for suspected systemic infection if any signs of illness occur." However, such conservative approach of observation and no treatment of the asymptomatic twin may still result in invasive disease. In our report the co-twin became symptomatic due to GBS disease 5 days after the onset of symptoms in the index case. Earlier evaluation and empiric treatment of the asymptomatic co-twin may have prevented the development of invasive GBS disease.