ABSTRACT
Nosocomial severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections have severely affected bed capacity and patient flow. We utilized whole-genome sequencing (WGS) to identify outbreaks and focus infection control resources and intervention during the United Kingdom's second pandemic wave in late 2020. Phylogenetic analysis of WGS and epidemiological data pinpointed an initial transmission event to an admission ward, with immediate prior community infection linkage documented. High incidence of asymptomatic staff infection with genetically identical viral sequences was also observed, which may have contributed to the propagation of the outbreak. WGS allowed timely nosocomial transmission intervention measures, including admissions ward point-of-care testing and introduction of portable HEPA14 filters. Conversely, WGS excluded nosocomial transmission in 2 instances with temporospatial linkage, conserving time and resources. In summary, WGS significantly enhanced understanding of SARS-CoV-2 clusters in a hospital setting, both identifying high-risk areas and conversely validating existing control measures in other units, maintaining clinical service overall.
Subject(s)
COVID-19 , Cross Infection , Disease Outbreaks/prevention & control , Reverse Transcriptase Polymerase Chain Reaction/methods , Whole Genome Sequencing , Asymptomatic Infections , Cross Infection/epidemiology , Delivery of Health Care , Health Personnel , Humans , Personal Protective Equipment , Phylogeny , SARS-CoV-2ABSTRACT
[This corrects the article DOI: 10.1016/j.infpip.2021.100125.].
ABSTRACT
BACKGROUND: Carbapenemase Producing Enterobacterales (CPE) are a global health concern. Nosocomial outbreaks have been reported globally with patient-to-patient transmission felt to be the most frequent route of cross-transmission. AIM: To describe the investigation and control of an outbreak of healthcare-associated New Delhi Metallo-beta-lactamase (NDM) CPE on a haematology ward, over 2 months. METHODS: Four patients acquired CPE; all had gastrointestinal tract colonisation with two subsequently developing bacteraemias. The outbreak team performed a retrospective review, prospective case finding and environmental sampling using swabs, settle plates, air and water sampling. Immediate control measures were implemented including appropriate isolation of cases and additional ward cleaning with chlorine disinfectant, ultra-violet light decontamination and hydrogen peroxide. FINDINGS: Following two cases of nosocomial acquired CPE prospective case finding identified two further cases. 4.6% of the initial environmental samples were positive for CPE including from waste water sites, the ward sluice and the ward kitchen. Three of the four CPE isolates were identical on pulse field gel electrophoresis (PFGE) typing. Detection of the CPE from the ward kitchen environmental samples suggests a possible role for cross transmission. CONCLUSION: This is the first CPE outbreak report to highlight the role of a ward kitchen as a possible source of cross-transmission. In view of this we suggest ward kitchens are reviewed and investigated in nosocomial CPE outbreaks.
ABSTRACT
OBJECTIVES: To determine the presence and genotypic macrolide susceptibility of Mycoplasma amphoriforme, and the presence of Ureaplasma spp. and Mycoplasma fermentans among clinical samples from England previously investigated for Mycoplasma pneumoniae. METHODS: Quantitative and conventional PCR methods were used to retrospectively screen a collection of 160 clinical samples previously submitted to Public Health England (PHE) for the detection of M. pneumoniae between October 2016 and December 2017. Samples which were positive for M. amphoriforme DNA were further investigated for mutations associated with genotypic macrolide resistance by sequencing domain V of the 23s rRNA. RESULTS: M. amphoriforme was detected in 10/160 samples (6.3%), Ureaplasma parvum was detected in 4/160 samples (2.5%), and M. fermentans was not detected in any samples (0/160). Of the nine individuals (two samples were from the same patient) in which M. amphoriforme was detected, eight were male (age range 10-60 years) and one was female (age range 30-40 years). One individual with cystic fibrosis was positive for both M. amphoriforme and U. parvum. All M. amphoriforme DNA was genotypically susceptible to macrolides. CONCLUSIONS: Mycoplasma amphoriforme was found in clinical samples, including lower respiratory tract samples of patients with pneumonia. In the absence of other respiratory pathogens, these data suggest a potential role for this organism in human disease, with no evidence of acquired macrolide resistance. Ureaplasma parvum was detected in cerebrospinal fluid and respiratory tract samples. These data suggest that there is a need to consider these atypical respiratory pathogens in future diagnostic investigations.