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The 13-valent pneumococcal conjugate vaccine (PCV13) was introduced for routine administration to infants and children in 2010 in the United States. We have monitored clinical and microbiologic features of invasive pneumococcal infections among children before and after PCV13 use.

Introduction of the heptavalent conjugate vaccine for Streptococcus pneumoniae(PCV7) has led to a dramatic decline in meningitis by PCV7 serotypes, raising the possibility of similar trends by PCV7-related serogroups through cross-protection. A present concern, however, is of serotype replacement by pneumococci not related to PCV7 serogroups. If this occurs, there are currently few data to predict whether clinical outcomes will change substantially.

Recurrent systemic pneumococcal infection usually occurs in immunocompromised patients and patients with underlying conditions.

Increasing macrolide resistance among middle ear isolates complicates treatment of otitis media in children. When macrolide resistance is mediated via an efflux pump (M phenotype), the MICs of erythromycin, clarithromycin and azithromycin are usually below 32 g/ml, and the pneumococcus remains susceptible to clindamycin. The association of prior specific macrolide therapy with the isolation of a macrolide resistant strain has not been reported.

To determine the outcome of children treated primarily with beta-lactam antibiotics for a systemic infection outside the central nervous system (CNS) caused by isolates of Streptococcus pneumoniaenonsusceptible to ceftriaxone (MIC ≥ 1.0 g/ml).

To determine patterns of resistance for isolates of Streptococcus pneumoniaerecovered from middle ear fluids of children from eight children’s hospitals between September, 1994, and August, 1997.

Fifty children with bacterial meningitis were prospectively evaluated in a randomized comparative trial of twice daily ceftriaxone with conventional ampicillin and chloramphenicol therapy. The groups were comparable in age, sex, days of illness before admission, severity of illness at admission, etiology and admission cerebrospinal fluid (CSF) parameters and bacterial colony counts. The pathogens were Haemophilus influenzaetype b (34 beta-Iactamasenegative, 8 beta-lactamase-positive); Streptococcus pneumoniae(4); Neisseria meningitidis(3); and Streptococcus agalactiae(1). Initial CSF colony counts ranged from 2.5 x 102to 1 x 1010colony-forming units/ml. In 44 children a lumbar puncture was repeated 10.5 to 18 hours after starting treatment; 16 to 21 (67) ceftriaxone patients and 12 of 20 (60) conventional therapy patients had sterile cultures. The reduction in the CSF bacterial colony counts (6.3 log10colony-forming units/ml) was similar in both groups. Ceftriaxone CSF levels ranged from 1.0 to 8.0 $mU/ml, representing a mean CSF penetration of 11.3 (range, 3.0 to 24.5) of the simultaneous serum concentration. The median ceftriaxone bactericidal titer in CSF was 1:1024 compared with 1:4 achieved with conventional therapy. There were no significant differences in clinical responses or in frequency of complications, except for diarrhea which occurred in 59 of the ceftriaxone group and in 22 of the other (P< 0.01). Despite one H. influenzaetype b relapse occurring in the ceftriaxone group, ceftriaxone appears to be safe and as effective as conventional therapy for bacterial meningitis in children older than 2 months of age.

Cat scratch disease is generally characterized by a self-limited chronic regional lymphadenopathy, but numerous other clinical manifestations involving a variety of organ systems have been reported. Cardiac involvement is unusual and when reported, it has been associated with culture-negative endocarditis in adults. We present the case of an adolescent male with typical cat scratch disease and associated myopericarditis.

Invasive meningococcal infections can be devastating. Substantial endotoxemia releases mature and immature neutrophils. Endothelial margination of mature neutrophils may increase the immature-to-total neutrophil ratio (ITR). These changes have not been previously well-described in invasive meningococcal disease.