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• W1967428863 abstract "Enterococcal meningitis in children is unusual and occurs most commonly in the setting of nosocomial sepsis.1, 2 Enterococci also cause meningitis in children as a complication of cerebrospinal fluid (CSF) shunts, neurosurgical procedures and head trauma. Abnormal fistulous communications between the gastrointestinal tract and the spinal cord occasionally have been associated with enterococcal meningitis.3, 4 Congenital cutis aplasia (CCA) is a rare hereditary anomaly characterized by defects in the scalp, calvaria and dura.5 Children with CCA are thought to be at increased risk for development of meningitis; however, reports of infectious complications of CCA are scant. Here we report a case of enterococcal meningitis complicating CCA in an infant. Case report. A 9-week-old male infant delivered at term was admitted to Vanderbilt Children's Hospital with a 1-day history of fever of 102°F, irritability, vomiting, decreased oral intake and a bulging anterior fontanel. There was no diarrhea or seizures. He was born with CCA and had been treated with dressing changes and topical antibiotics. The defect was closing well. His family history was significant for cutis aplasia in the father and a paternal aunt. On physical examination he had an 8- by 10-cm scalp defect. There were areas of scar tissue and eschar formation. There was no oozing. The anterior fontanel was full. His neck was stiff. The skin had a marbled appearance with extensive cutis marmorata. The white blood cell count was 14 500/μl, with a differential of 70% neutrophils and 23% lymphocytes, the hematocrit 32% and the platelet count 537 000/μl. The CSF was cloudy with 1010 white blood cells/μl (73% neutrophils and 27% lymphocytes); the CSF protein was 119 mg/dl, and the CSF glucose was 63 mg/dl. Cultures of blood and CSF grew Enterococcus faecalis, which was susceptible to ampicillin, gentamicin and vancomycin. Cultures of the scalp wound were sterile. Abdominal ultrasound examination and transthoracic echocardiography were normal. A three dimensional head computerized tomography showed osseous aplasia of the parietal bones with abnormal thinning of the existing calvaria (Fig. 1) and absence of overlying scalp and dura.Fig. 1: Three dimensional computerized tomography scan of the head of an infant with congenital cutis aplasia complicated by enterococcal meningitis. Note the absence of the scalp, parietal bones and dura with thinning of the existing skull bones.The patient received a 14-day course of ampicillin (100 mg/kg/dose every 6 h) and gentamicin (2.5 mg/kg/dose every 8 h). He was discharged home without antibiotics afebrile and feeding normally. An auditory evaluation was normal. Two days after discharge he was readmitted to the hospital with fever and fussiness for 6 h. The white blood cell count was 19 900/μl, with a differential of 48% neutrophils and 41% lymphocytes. The CSF was cloudy with a white blood cell count of 475/μl (41% neutrophils and 55% lymphocytes). Blood and CSF cultures were sterile. He completed an additional 3-week course of intravenous ampicillin and gentamicin. He remains in good health 9 months after the second course of antibiotics, and the scalp defect continues to heal. Discussion. Enterococcal bacteremia and meningitis complicating CCA have not been previously reported. Congenital absence of the scalp, calvaria and dura in our patient likely led to enterococcal infection as a consequence of local wound contamination during dressing changes. It is also possible that enterococcal infection occurred in this child as a consequence of direct invasion of the meninges through the defect in the scalp and calvaria. Fistulous connection between the gastrointestinal tract and the spinal cord as a source of infection was excluded by radiologic evaluation. There are few reports of infectious complications of CCA. Cutaneous herpes simplex virus type 2 without CNS involvement was reported in a full-term male infant with congenital absence of the scalp.6 He was born by vertex delivery. Herpes simplex virus type 2 was isolated from a maternal cervical smear. Recurrent shunt infection was reported in a 9-month-old child with CCA after cranioplasty.7 He had a lumboperitoneal shunt placed as a result of herniation of brain through the scalp defect and development of hydrocephalus. The causative organism was not described. Using MEDLINE to search the English language literature from 1966 to 1999 for articles containing one or more of the key words congenital cutis aplasia, scalp defect, infection, complication, meningitis, bacteremia and enterococcus we did not find reports of bacteremia or meningitis in children with CCA. The rapid recurrence of meningitis in this child after 2 weeks of appropriate parenteral antibiotic therapy suggests relapse rather than reinfection, although the causative organism in the second episode was not isolated. Antibiotic courses of 2 to 3 weeks have been recommended for the treatment enterococcal meningitis.4 Our experience with this patient suggests that antibiotics for enterococcal meningitis should be administered for 3 to 4 weeks, especially when there is a predisposing condition such as CCA. Repeat CSF examinations may serve to guide decisions about the duration of antimicrobial therapy." @default.
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• W1967428863 date "2000-07-01" @default.
• W1967428863 modified "2023-10-06" @default.
• W1967428863 title "ENTEROCOCCAL MENINGITIS IN AN INFANT COMPLICATING CONGENITAL CUTIS APLASIA" @default.
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• W1967428863 doi "https://doi.org/10.1097/00006454-200007000-00023" @default.
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