OBJECTIVES: The pathogens that cause bacterial meningitis in infants and their antimicrobial susceptibilities may have changed in this era of increasing antimicrobial resistance, use of conjugated vaccines, and maternal antibiotic prophylaxis for group B Streptococcus (GBS). The objective was to determine the optimal empirical antibiotics for bacterial meningitis in early infancy. METHODS: This was a cohort study of infants <90 days of age with bacterial meningitis at 7 pediatric tertiary care hospitals across Canada in 2013 and 2014. RESULTS: There were 113 patients diagnosed with proven meningitis (n = 63) or suspected meningitis (n = 50) presented at median 19 days of age, with 63 patients (56%) presenting a diagnosis from home. Predominant pathogens were Escherichia coli (n = 37; 33%) and GBS (n = 35; 31%). Two of 15 patients presenting meningitis on day 0 to 6 had isolates resistant to both ampicillin and gentamicin (E coli and Haemophilus influenzae type B). Six of 60 infants presenting a diagnosis of meningitis from home from day 7 to 90 had isolates, for which cefotaxime would be a poor choice (Listeria monocytogenes [n = 3], Enterobacter cloacae, Cronobacter sakazakii, and Pseudomonas stutzeri). Sequelae were documented in 84 infants (74%), including 8 deaths (7%). CONCLUSIONS: E coli and GBS remain the most common causes of bacterial meningitis in the first 90 days of life. For empirical therapy of suspected bacterial meningitis, one should consider a third-generation cephalosporin (plus ampicillin for at least the first month), potentially substituting a carbapenem for the cephalosporin if there is evidence for Gram-negative meningitis.

We studied a cohort of children initiated on treatment doses of combination antiretroviral therapy within 72 hours of birth. In children who achieved sustained virologic suppression, measures of HIV-1 reservoir size in peripheral blood were very low. Background. A human immunodeficiency virus type 1 (HIV-1)–infected infant started on combination antiretroviral therapy (cART) at 30 hours of life was recently reported to have no detectable plasma viremia after discontinuing cART. The current study investigated the impact of early cART initiation on measures of HIV-1 reservoir size in HIV-1–infected children with sustained virologic suppression. Methods. Children born to HIV-1–infected mothers and started on cART within 72 hours of birth at 3 Canadian centers were assessed. HIV serology, HIV-1–specific cell-mediated immune responses, plasma viremia, cell-associated HIV-1 DNA and RNA, presence of replication-competent HIV-1, and HLA genotype were determined for HIV-1–infected children with sustained virologic suppression. Results. Of 136 cART-treated children, 12 were vertically infected (8.8%). In the 4 who achieved sustained virologic suppression, HIV serology, HIV-1–specific cell-mediated immune responses (Gag, Nef), and ultrasensitive viral load were negative. HIV-1 DNA was not detected in enriched CD4⁺ T cells of the 4 children (<2.6 copies/10⁶ CD4⁺ T cells), whereas HIV-1 RNA was detected (19.5–130 copies/1.5 µg RNA). No virion-associated HIV-1 RNA was detected following mitogenic stimulation of peripheral blood CD4⁺ T cells (5.4–8.0 million CD4⁺ T cells) in these 4 children, but replication competent virus was detected by quantitative co-culture involving a higher number of cells in 1 of 2 children tested (0.1 infectious units/10⁶ CD4⁺ T cells). Conclusions. In perinatally HIV-1–infected newborns, initiation of cART within 72 hours of birth may significantly reduce the size of the HIV-1 reservoirs. Cessation of cART may be necessary to determine whether functional HIV cure can be achieved in such children.

We describe a case of blastomycosis in an 8-year-old boy with Blastomyces-associated osteomyelitis and possible pulmonary involvement. We also identify 309 cases of blastomycosis in Ontario that were seen during a 10-year period, 57% of which occurred from 2001 to 2003. The overall incidence during the study period was 0.30 cases per 100,000 population. Most patients were from north Ontario (n = 188), where the incidence was 2.44 cases per 100,000. The incidence in the Toronto region was 0.29 per 100,000. Thirteen percent of cases occurred in children <19 years of age. These findings substantially increase the number of known cases in Ontario and Canada. Clinicians may encounter persons infected with Blastomyces dermatitidis and must be familiar with its signs and symptoms and be aware of locations, such as northwestern Ontario, where disease is endemic or hyperendemic. We advocate resuming blastomycosis as a reportable disease in Ontario to facilitate tracking cases.

We describe the presenting features and long-term outcome of an unusual cluster of pediatric acute flaccid paralysis cases that occurred in Canada during the 2014 enterovirus D68 outbreak. Children (n = 25; median age 7.8 years) presenting to Canadian centers between July 1 and October 31, 2014, and who met diagnostic criteria for acute flaccid paralysis were evaluated retrospectively. The predominant presenting features included prodromal respiratory illness (n = 22), cerebrospinal fluid lymphocytic pleocytosis (n = 18), pain in neck/back (n = 14) and extremities (n = 10), bowel/bladder dysfunction (n = 9), focal central gray matter lesions found in all regions of the spinal cord within the cohort (n = 16), brain stem lesions (n = 8), and bulbar symptoms (n = 5). Enterovirus D68 was detectable in nasopharyngeal specimens (n = 7) but not in cerebrospinal fluid. Acute therapies (corticosteroids, intravenous immunoglobulins, plasmapheresis) were well tolerated with few side effects. Fourteen of 16 patients who were followed beyond 12 months post onset had neurologic deficits but showed ongoing clinical improvement and motor recovery.