Influenza B virus encephalitis.

Acute encephalitis and postinfectious encephalopathy have been reported infrequently in association with influenza A and B virus infections. We report herein a case of a 6-year-old girl with acute influenza B virus encephalitis resulting in neurological sequelae. The diagnosis was made by isolation of influenza B virus from the nasopharynx, seroconversion to influenza B, and reverse transcription polymerase chain reaction (RT-PCR) identification of the virus from the patient's cerebrospinal fluid. Direct sequencing of viral RNA from the patient's nasopharynx and cerebrospinal fluid revealed identical nucleotide sequences in the HA1 region of the hemagglutinin gene. This is the first report of influenza B virus encephalitis diagnosed by use of RT-PCR and illustrates the need for increased awareness of influenza virus as a cause of acute encephalitis. PCR may be a useful tool for diagnosing future cases.

Nasopharyngeal carriage of penicillin-resistant Streptococcus pneumoniae in children with sickle cell disease.

OBJECTIVE: We studied the prevalence of nasopharyngeal (NP) carriage, antimicrobial susceptibilities, and serotypes of Streptococcus pneumoniae (SP) in children with sickle cell disease (SCD) in the Mid-South. In addition, we examined risk factors for NP carriage of penicillin-resistant SP (PRSP). STUDY DESIGN: Between July 1994 and December 1995, we obtained NP cultures from 312 children with SCD followed at the Mid-South Sickle Cell Center, 208 (67%) of whom were receiving penicillin prophylaxis. RESULTS: Among the 312 patients, colonization with SP occurred in 42 (13%), 30 (71%) of whom were receiving penicillin prophylaxis. Twenty-three of the 42 SP isolates (55%) were resistant to penicillin; 5 of the 23 (22%) were highly resistant. PRSP organisms were also resistant to cefotaxime (43%), trimethoprim-sulfamethoxazole (57%), and erythromycin (22%). Serotypes 6A, 6B, 14, 19A, and 23F accounted for 19 (90%) of 21 resistant strains. Children who were treated with antibiotics during the preceding month were more likely to carry PRSP than children who were not treated. CONCLUSIONS: There is a high prevalence of NP carriage of PRSP in children with SCD in the Mid-South, which raises concerns regarding the continued effectiveness of penicillin prophylaxis in these children. Further studies on the antimicrobial susceptibilities of resistant organisms and the relationship between NP carriage of SP and invasive disease are needed before developing new recommendations for prophylaxis and treatment.

Penicillin- and cephalosporin-resistant strains of Streptococcus pneumoniae causing sepsis and meningitis in children with sickle cell disease.

OBJECTIVE: We investigated the possibility that antimicrobial-resistant pneumococci were causing invasive disease in children with sickle-cell disease (SCD). STUDY DESIGN: Records of all children with SCD observed at the Mid-South Sickle Cell Center (MSSCC) at LeBonheur Children's Medical Center were reviewed from January 1990 to June 1994. Children with SCD and pneumococcal sepsis were identified. The Streptococcus pneumoniae isolates from these children were examined for serotype and antimicrobial susceptibilities. Two additional children not observed in the MSSCC had pneumococcal sepsis caused by penicillin-resistant isolates and were also included. RESULTS: Antimicrobial susceptibility testing of the six penicillin-resistant isolates revealed that four were resistant to trimethoprim-sulfamethoxazole, two to erythromycin, and one to clindamycin. The two isolates that were resistant to ceftriaxone also were multiply resistant. From the MSSCC, 26 children had pneumococcal sepsis during the 4 1/2-year period studied. Five of these children (19%) died. Four (15%), including one who died, were infected with penicillin-resistant strains. CONCLUSION: Pneumococcal sepsis, meningitis, and infections of other foci in children with SCD may be caused by S. pneumoniae that is resistant to one or more antimicrobial agents, including penicillin. The addition of vancomycin to the antibiotics currently used for initial management should be considered in areas where the antibiotic resistance of S. pneumoniae is prevalent.

Staphylococcus aureus cellulitis: an unusual presentation.

Staphylococcus aureus has long been known as one of the most virulent microbes, with capabilities that make it threatening in both nosocomial and community-acquired infections. It remains the most frequent cause of skin-structure and traumatic infections in the community. S. aureus infections in the maxillofacial region are likely to be associated with a known portal of entry, but this is not always the case. Once invasion occurs, the organism may produce virulent enzymes including coagulase, hyaluronidase, proteases, DNA-ase, lipases, hemolysins, and lysozyme as well as exotoxins. Markel et al point out that cellulitis associated with coagulase-positive staphylococci will often resolve without abscess formation. Hence, there is often no site from which to obtain specimens, making this infection a diagnostic and therapeutic challenge. This report describes an infection in which the etiologic organism was identified as S. aureus. The source of the infection, however, remained unclear.

A randomized study of outpatient treatment with ceftriaxone for selected febrile children with sickle cell disease.

BACKGROUND: Because of their susceptibility to pneumococcal sepsis, children with sickle cell disease and fever are usually hospitalized for antibiotic therapy. Outpatient treatment may be a safe and less expensive alternative for selected patients. METHODS: After evaluation in the emergency room, children ranging from 6 months to 12 years of age who had sickle hemoglobinopathies and temperatures exceeding 38.5 degrees C were randomly assigned to treatment as either inpatients or outpatients. We excluded from randomization children at higher risk of sepsis (as defined by specific criteria, including temperature above 40 degrees C, white-cell count below 5000 per cubic millimeter or above 30,000 per cubic millimeter, and the presence of pulmonary infiltrates) or with complications of sickle cell disease (such as a hemoglobin level below 5 g per deciliter, dehydration, or severe pain); these children were treated as inpatients. All patients received an initial intravenous dose of ceftriaxone (50 mg per kilogram of body weight). Those treated as outpatients returned 24 hours later for a second dose of ceftriaxone, whereas the in patients were treated as directed by their physicians. RESULTS: None of the 86 patients (with a total of 98 febrile episodes) in the randomized groups had sepsis, as compared with 6 of the 70 patients (7 of 86 episodes) excluded because of higher risk (P = 0.004). Among the 44 children (50 episodes) assigned to outpatient treatment, there were 11 hospitalizations (22 percent of episodes) within two weeks after treatment (95 percent confidence interval, 12 to 36 percent), whereas after inpatient care only a single patient (2 percent of episodes) was rehospitalized. When the randomized groups were compared, outpatient treatment saved a mean of $1,195 per febrile episode. The median hospital stay was 3 days (range, 1 to 6) for the children randomly assigned to inpatient care and 4 days (range, 1 to 18) for the higher-risk children treated as inpatients (P < 0.001). CONCLUSIONS: With the use of conservative eligibility criteria, at least half the febrile episodes in children with sickle cell disease can be treated safely on an outpatient basis, with substantial reductions in cost.

Detection of a second widespread strain of Epstein-Barr virus.

The prevalence of Epstein-Barr virus (EBV) type B, which was previously found mainly in equatorial Africa, was investigated with the polymerase chain reaction in a population of healthy adults in Memphis, Tennessee. EBV was detected in the throat washings of 34 (22%) of 157 randomly selected donors, 14 (41%) of whom had type B virus and 17 (50%) type A; 3 donors (9%) had both strains. 18 additional adults with human immunodeficiency virus (HIV-1) infection and 6 severely immunocompromised children were also investigated. Results indicated that type B EBV is widespread in nature and may be reactivated by immunodeficiency.