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Background: Infections caused by extended-spectrum β-lactamase-producing Enterobacterales (ESBL-E) among hospitalized neonates in sub-Saharan Africa pose significant clinical challenges. Data on prevalence and acquisition of ESBL-E carriage among hospitalized neonates in the region are few, and risk factors for transmission are not clearly defined., Methods: In a cohort study of consecutive neonatal admissions to Kilifi County Hospital from July 2013 through August 2014, we estimated ESBL-E carriage prevalence on admission using rectal swab cultures and identified risk factors using logistic regression. Using twice-weekly follow-up swabs, we estimated the incidence and identified risk factors for ESBL-E acquisition in hospital using Poisson regression., Results: The prevalence of ESBL-E carriage at admission was 10% (59/569). Cesarean delivery, older neonatal age, and smaller household size were significant risk factors. Of the 510 infants admitted without ESBL-E carriage, 238 (55%) acquired carriage during their hospital stay. The incidence of acquisition was 21.4% (95% confidence interval, 19.0%-24.0%) per day. The rate was positively associated with the number of known neonatal ESBL-E carriers and with the total number of neonates on the same ward., Conclusions: Carriage of ESBL-E was common among neonates on admission, and in-hospital acquisition was rapid. The dissemination and selection of ESBL-E appears to be driven by hospital exposures, operative delivery, and neonatal ward patient density. Further attention to infection control, patient crowding, and carriage surveillance is warranted., (© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.)

Streptococcus agalactiae (group B streptococcus, GBS) causes neonatal disease and stillbirth, but its burden in sub-Saharan Africa is uncertain. We assessed maternal recto-vaginal GBS colonization (7,967 women), stillbirth and neonatal disease. Whole-genome sequencing was used to determine serotypes, sequence types and phylogeny. We found low maternal GBS colonization prevalence (934/7,967, 12%), but comparatively high incidence of GBS-associated stillbirth and early onset neonatal disease (EOD) in hospital (0.91 (0.25-2.3)/1,000 births and 0.76 (0.25-1.77)/1,000 live births, respectively). However, using a population denominator, EOD incidence was considerably reduced (0.13 (0.07-0.21)/1,000 live births). Treated cases of EOD had very high case fatality (17/36, 47%), especially within 24 h of birth, making under-ascertainment of community-born cases highly likely, both here and in similar facility-based studies. Maternal GBS colonization was less common in women with low socio-economic status, HIV infection and undernutrition, but when GBS-colonized, they were more probably colonized by the most virulent clone, CC17. CC17 accounted for 267/915 (29%) of maternal colonizing (265/267 (99%) serotype III; 2/267 (0.7%) serotype IV) and 51/73 (70%) of neonatal disease cases (all serotype III). Trivalent (Ia/II/III) and pentavalent (Ia/Ib/II/III/V) vaccines would cover 71/73 (97%) and 72/73 (99%) of disease-causing serotypes, respectively. Serotype IV should be considered for inclusion, with evidence of capsular switching in CC17 strains., Competing Interests: We declare no competing interests.

To determine the extent of group A Streptococcus (GAS) infections in sub-Saharan Africa and the serotypes that cause disease, we analyzed surveillance data for 64,741 hospital admissions in Kilifi, Kenya, during 1998-2011. We evaluated incidence, clinical presentations, and emm types that cause invasive GAS infection. We detected 370 cases; of the 369 for which we had data, most were skin and soft tissue infections (70%), severe pneumonia (23%), and primary bacteremia (14%). Overall case-fatality risk was 12%. Incidence of invasive GAS infection was 0.6 cases/1,000 live births among neonates, 101/100,000 person-years among children <1 year of age, and 35/100,000 among children <5 years of age. Genome sequencing identified 88 emm types. GAS causes serious disease in children in rural Kenya, especially neonates, and the causative organisms have considerable genotypic diversity. Benefit from the most advanced GAS type-specific vaccines may be limited, and efforts must be directed to protect against disease in regions of high incidence.