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Late-onset group B streptococcal meningitis: still dangerous

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January 1999

A 5-week-old African American boy was born July 2, 1998, by normal vaginal delivery at term to a 23-year-old multiparous mother. The prenatal history was remarkable only for a vaginal culture positive for group B streptococcus. No antibiotic prophylaxis was given during delivery. The patient had a normal postnatal course and was seen for his second well-child care follow up on Aug. 4. At 11 p.m., Aug. 4, he fed well but at 2 a.m. did not awake for his feeding. The mother woke the infant who was irritable, took some water then fell asleep. At 6:00 a.m. the infant did not wake for feeding, was lethargic, and had tactile temperature. At 7:00 am on August 6, 1998, the mother brought the baby to the emergency department at Boston Medical Center.

The examination was remarkable for a very ill-appearing infant, a flat fontanella, lethargy, grunting, nasal flaring. T 103.8°F, P 200 bpm, RR 50/minute, BP 68 mmHg/palpable.

Laboratory studies revealed a total white blood cell count of 1,800/mm³ with a differential of 35% segmented neutrophils, 58% lymphocytes; hematocrit: 31%; platelet count 103,000; arterial blood gases 7.31/27.4/13.5/207. A lumbar puncture revealed cerebrospinal fluid (CSF) glucose of 0 mg/dL, protein of 1,360 mg/dL, and a CSF count of 227 (74% of poly, 18% of lymph) white blood cells/ mm³ and 16 red blood cells. Gram stain of the CSF revealed Gram-positive cocci in pairs. Group B streptococci were isolated from CSF culture. The chest X-ray showed slight hyperinflation without infiltrate. Blood culture was drawn and did not growth GBS.

The patient initially received ampicillin and ceftriaxone in the emergency department for presumed bacterial meningitis but therapy was changed to ampicillin and gentamicin once the CSF culture result was available. On the fourth hospital day, a second lumbar puncture revealed CSF glucose of 10 mg/dL, protein of 537 mg/dL, and a CSF count of 1,480 (21% of poly, 74% of lymph) white blood cells/mm³ and 3,670 red blood cells. Gram stain of the CSF did not reveal organisms. On the sixth hospital day, gentamicin was discontinued and ampicillin changed to penicillin G.

A CT scan of the head done 24 hours after admission revealed diffuse meningeal enhancement, right temporal lobe infarct, left parietal hematoma, and bilateral extra-axial frontal effusions. A follow-up study done three days later showed diffuse cerebral edema, compression on the ventricular system, and evolution of left frontal and right temporoparietal infarcts. An MRI of the head done on the eighth hospital day revealed subdural collections in the frontal regions, infarct in the right frontal area and right posterior parietal area.

Seizure activity began 24 hours after admission; multiple anticonvulsants were given but persistent, intermittent seizures occurred over the next five days. Seizures were finally controlled with phenobarbital and phenytoin.

On the eighth day of hospitalization, the patient became more alert. He completed a 21-day course of antibiotics and was discharged.

Points of interest

• Intrapartum antibiotic prophylaxis has been documented to decrease the incidence of neonatal colonization and early-onset infection with GBS. However, intrapartum chemoprophylaxis has no efficacy in prevention of late-onset infant infection.
• Late-onset GBS diseases may occur suddenly in a patient who was previously entirely well. This baby was well during the day of Aug. 5, but likely had GBS bacteremia during the evening to early morning hours of Aug. 6, progressing to meningitis soon after; a clinical course from onset of bacteremia to meningitis of less than 12 hours. Late-onset GBS diseases presents as bacteremia without focus (40% to 50%), meningitis (30% to 40%), and osteoarthritis (5% to 10%). The serotype 3 strain is the most commonly isolated (90%).
• Late-onset GBS may be accompanied by severe sequelae even if treated at the earliest possible time. The complications of GBS meningitis are Subdural effusions which are found in up to 20% of patients with late-onset meningitis, SIADH, and Seizures. A substantial number of survivors (25% to 50%) had permanent neurologic sequelae of varying severity. The mortality rate of GBS meningitis is 26%.
• The source of infection of the infant with late-onset GBS is uncertain. Colonization of the maternal genital tract by GBS - for reasons unknown - may persist for months. Alternatively, the mother may infect the child after birth. It is unclear why some colonized infants never develop disease while others progress to invasive infection.

For your information:

• Marisol Figueira, MD,and Megan T. Sandel, MD, are from the Boston Combined Residency Program, Boston Medical Center/Children's Hospital and the Division of Pediatric Infectious Diseases, Boston Medical Center.

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Copyright 2000, SLACK Incorporated. Revised 15 September 2000.