In Europe, fetal loss due to Parvovirus B19 (B19V) is under-reported and a poorly addressed occupational risk to pregnant women. This is exemplified internationally, where it was unmentioned in the last two European Centre for Disease Prevention and Control (ECDC) annual surveillance reports or its 2009 special report on infections in pregnancy. To assess this potential for underestimating B19V fetal loss in pregnancy, we undertook a systematic review of practice in Northern Ireland in the management and reporting of B19V infections over a 12-month period of heightened transmission, one of six observed in a span of 9 years. Pregnant and non-pregnant women presented with symptomatic infection in 24 and 93 % of confirmed B19V infections, respectively, with no difference in viral loads. There was underinvestigation of viral causes of fetal loss, with only 143/2739 (5 %) tested for B19V, and a failure to follow up most non-immune women tested following rash contact. Occupational exposure was recorded in 31/60 (51.6 %) of pregnancies audited following rash exposure, the majority teachers or day care workers. Against a background seroprevalence of 66.5 % immunity in women of child-bearing years, two patterns of infection were identified. Firstly, pregnant women investigated for a rash or exposure to slapped cheek syndrome, where an infection incidence of 18 % was observed, resulted in 42 confirmed infections, all proceeding to healthy term deliveries. Secondly, pregnant women with unsuspected infection had six cases of confirmed B19V fetal loss, including four of 22 (18 %) diagnosed at autopsy, of which three were non-hydropic. While many studies have reported B19V fetal loss in pregnancy, there are no robust public health surveillance figures to draw on. That all six confirmed fetal losses came from the small number of miscarriages/stillbirths investigated, 143 out of 2739, suggests inadequate follow-up of those pregnancies where B19V-related fetal loss may be most common, and supports the need for enhanced surveillance pilots to address this significant gap in public health knowledge.

Summary Objective: To understand the transmission dynamics of SARS-CoV-2 in a hospital outbreak to inform infection control actions. Design: Retrospective cohort study. Setting: General medical and elderly inpatient wards in a hospital in England. Methods: COVID-19 patients were classified as community or healthcare-associated by time from admission to onset/positivity using European Centre for Disease Prevention and Control definitions. COVID-19 symptoms were classified as asymptomatic, non-respiratory or respiratory. Infectiousness was calculated from 2 days prior to 14 days post symptom onset or positive test. Cases were defined as healthcare-associated COVID-19 patients where infection was acquired from the wards under investigation. COVID-19 exposures were calculated based on symptoms and bed proximity to an infectious patient. Risk ratios and adjusted odds ratios (aOR) were calculated from univariable and multivariable logistic regression. Results: Of 153 patients: 65 were COVID-19 patients (45 healthcare-associated). Exposure to a COVID-19 patient with respiratory symptoms was associated with healthcare-associated infection irrespective of proximity (aOR 3.81; 95%CI 1.6.3-8.87), non-respiratory exposure was only significant within 2.5m (aOR 5.21; 95%CI 1.15-23.48). A small increase in risk ratio was observed for exposure to a respiratory patient for >1 day compared to 1 day from 2.04 (95%CI 0.99-4.22) to 2.36 (95%CI 1.44-3.88) Discussion: Respiratory exposure anywhere within a 4-bedded bay was a risk whereas non-respiratory exposure required bed distance ≤2.5m. Standard Infection control measures required beds to be >2m apart; our study suggests this may be insufficient to stop SARS-CoV-2 spread. We recommend improving cohorting and further studies into bed distance and transmission factors.

High-throughput sequencing (HTS) has successfully identified novel resistance genes in enterococci and determined clonal relatedness in outbreak analysis. We report the use of HTS to investigate two concurrent outbreaks of glycopeptide-resistant Enterococcus faecium (GRE) with an uncharacterised resistance mechanism to quinupristin-dalfopristin (QD). Seven QD-resistant and five QD-susceptible GRE isolates from a two-centre outbreak were studied. HTS was performed to identify genes or predicted proteins that were associated with the QD-resistant phenotype. MLST and SNP typing on HTS data was used to determine clonal relatedness. Comparative genomic analysis confirmed this GRE outbreak involved two distinct clones (ST80 and ST192). HTS confirmed the absence of known QD resistance genes, suggesting a novel mechanism was conferring resistance. Genomic analysis identified two significant genetic determinants with explanatory power for the high level of QD resistance in the ST80 QD-resistant clone: an additional 56aa leader sequence at the N-terminus of the lsaE gene and a transposon containing seven genes encoding proteins with possible drug or drug-target modification activities. However, HTS was unable to conclusively determine the QD resistance mechanism and did not reveal any genetic basis for QD resistance in the ST192 clone. This study highlights the usefulness of HTS in deciphering the degree of relatedness in two concurrent GRE outbreaks. Although HTS was able to reveal some genetic candidates for uncharacterised QD resistance, this study demonstrates the limitations of HTS as a tool for identifying putative determinants of resistance to QD.

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