Asymptomatic carriage of Neisseria meningitidis and Neisseria lactamica was studied in a total of 2,969 healthy infants and children in Danbury, Conn., between October 1971 and June 1975. The prevalence of N. meningitidis averaged 0.71% during the first four years of life and increased to 5.4% by 14--17 years. Rates of carriage of N. lactamica increased from 3.8% in three-month-old infants to a peak of 21.0% at 18 months and then declined to 1.8% by 14--17 years of age. Of the children who acquired N. lactamica, 66% developed fourfold or greater rises in titers of IgG antibody to groups A, B, and/or C meningococci as determined by immunofluorescence compared with only 5% of control children. Of new carriers of N. lactamica, 40% developed increased titers of bactericidal antibody to groups A, B, and/or C meningococci as compared with 7% of noncarriers. Carriage of N. lactamica may assist in the development of natural immunity to N. meningitidis by induction of cross-reactive antibodies.

A B S T R A C T GroupApproximately 90% of 3-mo-old and 100% of 7-and 12-mlo-old infants had detectable antibody responses to primary immunization with C vaccine. The 100-iug dose appeared to be optimal, resulting in geometric mean anti-C concentrations of 0.49, 1.55, and 2.64 Mug/iln in 3-, 7-, and 12-mo-old infants, respectively. Significalnt booster responses were not observed with C vaccine. Indeed, except for the 10-,ug dose, booster injections of C vaccine in 7-and 12-mo-old ilnfants resulted in lower anti-C concentrations than did primary immunizations.

Mixed infections with seasonal influenza A virus strains are a common occurrence and an important source of genetic diversity. Prolonged viral shedding, as observed in immunocompromised individuals, can lead to mutational accumulation over extended periods. Recently, drug resistance was reported in immunosuppressed patients infected with the 2009 pandemic influenza A (H1N1) virus within a few days after oseltamivir treatment was initiated. To better understand the evolution and emergence of drug resistance in these circumstances, we used a deep sequencing approach to survey the viral population from an immunosuppressed patient infected with H1N1/2009 influenza and treated with neuraminidase inhibitors. This patient harbored 3 genetic variants from 2 phylogenetically distinct viral clades of pandemic H1N1/2009, strongly suggestive of mixed infection. Strikingly, one of these variants also developed drug resistance de novo in response to oseltamivir treatment. Immunocompromised individuals may, therefore, constitute an important source of genetic and phenotypic diversity, both through mixed infection and de novo mutation.

RSVIG infusions seemed safe and generally well tolerated. Although some beneficial effect trends were seen for those with more severe disease who were treated there was no evidence that treatment with RSVIG resulted in reduced hospitalization and reduced ICU stays in all children with RSV disease.

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RSVIG treatment was safe but not efficacious in the treatment of children with bronchopulmonary dysplasia, congenital heart disease, or premature gestation who were hospitalized with RSV LRI.

A cohort of infants, previously immunized once or twice between three and 12 months of age with vaccines containing polysaccharide of groups A and C Neisseria meningitidis, received boosters at two and five and one-half years of age with bivalent A/C vaccine. Antibody concentrations were measured by a radioactive antigen-binding assay. Concentrations of antibody to groups A and C N. meningitidis were 5.59 and 2.86 microgram/ml, respectively, by four years of age. After booster immunization at five and one-half years of age, concentrations of antibody to groups A and C N. meningitidis increased to 15.67 and 7.59 microgram/ml, respectively. Protective levels of antibody to group A meningococci may be achievable throughout early childhood by routine immunization with the A vaccine. Although the group C vaccine is effective in control of epidemics, the rapid decline in the concentration of antibody to group C meningococci following immunization of young children suggests that protection may not be long-lasting.

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