METHODS: A systematic search of relevant cohort studies from three electronic databases to identify all relevant studies published up to 7 November 2022. The review was conducted in accordance with PRISMA guidelines. Estimates were pooled using random-effects meta-analyses.

RESULTS: A total of 54 articles with 355 787 matched pairs of parturient women and neonates from 30 countries were included in the analysis. The pooled prevalence of GBS colonisation was 17.1% among the pregnant women and 1.0% among neonates. The pooled prevalence of vertical transmission of GBS was 4.5% and the pooled relative risk of GBS colonisation of neonates born to mothers with GBS was 9.9.

OBJECTIVE: To describe the pathological changes, identification and distribution of B. melitensis in foetuses of experimentally infected does.

METHODS: Twelve female goats of approximately 90 days pregnant were divided into 4 groups. Group 1 was exposed intra-conjunctival to 100 µL of sterile PBS while goats of Groups 2, 3 and 4 were similarly exposed to 100 µL of an inoculum containing 109 CFU/mL of live B. melitensis. Goats of these groups were killed at 15, 30 and 60 days post-inoculation, respectively. Foetal fluid and tissues were collected for bacterial identification (using direct bacterial culture, PCR and immuno-peroxidase staining) and histopathological examination.

RESULTS: Bilateral intra-conjunctival exposure of pregnant does resulted in in-utero infection of the foetuses. All full-term foetuses of group 4 were either aborted or stillborn, showing petechiations of the skin or absence of hair coat with subcutaneous oedema. The internal organs showed most severe lesions. Immune-peroxidase staining revealed antigen distribution in all organs that became most extensive in group 4. Brucella melitensis was successfully isolated from the stomach content, foetal fluid and various other organs.

METHODS: Data on children with perinatally acquired HIV aged <18 years on first-line, non-nucleoside reverse transcriptase inhibitor-based cART with viral suppression (two consecutive pVL <400 copies/mL over a six-month period) were included from a regional cohort study; those exposed to prior mono- or dual antiretroviral treatment were excluded. Frequency of pVL monitoring was determined at the site-level based on the median rate of pVL measurement: annual 0.75 to 1.5, and semi-annual >1.5 tests/patient/year. Treatment failure was defined as virologic failure (two consecutive pVL >1000 copies/mL), change of antiretroviral drug class, or death. Baseline was the date of the second consecutive pVL <400 copies/mL. Competing risk regression models were used to identify predictors of treatment failure.

RESULTS: During January 2008 to March 2015, there were 1220 eligible children from 10 sites that performed at least annual pVL monitoring, 1042 (85%) and 178 (15%) were from sites performing annual (n = 6) and semi-annual pVL monitoring (n = 4) respectively. Pre-cART, 675 children (55%) had World Health Organization clinical stage 3 or 4, the median nadir CD4 percentage was 9%, and the median pVL was 5.2 log10 copies/mL. At baseline, the median age was 9.2 years, 64% were on nevirapine-based regimens, the median cART duration was 1.6 years, and the median CD4 percentage was 26%. Over the follow-up period, 258 (25%) CLWH with annual and 40 (23%) with semi-annual pVL monitoring developed treatment failure, corresponding to incidence rates of 5.4 (95% CI: 4.8 to 6.1) and 4.3 (95% CI: 3.1 to 5.8) per 100 patient-years of follow-up respectively (p = 0.27). In multivariable analyses, the frequency of pVL monitoring was not associated with treatment failure (adjusted hazard ratio: 1.12; 95% CI: 0.80 to 1.59).