PubMed · 7797309
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A K Hati. Plague.. https://pubmed.ncbi.nlm.nih.gov/7797309/
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INTRODUCTION: Outbreaks of healthcare-associated infections (HAI) result in substantial patient morbidity and mortality; mitigation efforts by infection prevention teams have the potential to curb outbreaks and prevent transmission to additional patients. The incorporation of whole genome sequencing (WGS) surveillance of suspected high-risk pathogens often identifies outbreaks that are not detected by traditional infection prevention methods and provides evidence for transmission. Our approach to real-time WGS surveillance, the Enhanced Detection System for Healthcare-Associated Transmission (EDS-HAT), has 1) identified serious outbreaks that were otherwise undetected and 2) shown the potential to be cost saving. METHODS: We describe our cost-efficient methods to perform WGS surveillance and data analysis of pathogens for institutions that are interested in expanding infection prevention surveillance. We provide an overview of the weekly workflow of EDS-HAT during two distinct phases over three years. RESULTS: In an average week at our tertiary healthcare system, we sequenced 60 samples at a cost of less than $100 each during Phase 1, and 80 samples for less than $70 each in Phase 2, inclusive of laboratory reagents and staff salaries. The average turnaround time, from sample collection to reporting data to infection prevention, was nine days. CONCLUSIONS: Performing EDS-HAT in real-time can be both feasible and time-efficient. Providing such timely information to aid in outbreak detection could identify transmission events sooner and thus could increase patient safety.
In late 2024, an outbreak of over 400 cases of undiagnosed febrile illness, predominantly presenting as fever and cough, was reported in Panzi Health Zone, southwestern Democratic Republic of the Congo. Here we conducted an epidemiological and laboratory investigation to determine the etiology of the outbreak. Clinical data and specimens were prospectively collected from 108 individuals, of whom 59/108 (54.6%) were female. Children aged <5 years were the most affected (47/108, 43.5%); 14/32 (43.7%) were malnourished. Oro/nasopharyngeal swabs from 96/108 individuals were PCR tested; 26 blood samples were sequenced. Plasmodium falciparum was detected in 56/108 (51.8%) individuals. Co-infections were also detected, with influenza A(H1N1)pdm09 virus in 16/56 (28.6%) and severe acute respiratory syndrome coronavirus 2 in 10/56 (17.9%) individuals. No novel pathogens were detected via metagenomics. Our findings suggest that the outbreak was primarily associated with a surge in malaria cases, with concurrent viral respiratory infections. Increasing decentralized laboratory capacity and strengthening broader health systems remain crucial for faster outbreak detection and investigation.
The 1997/'98 influenza season in the Netherlands was marked by influenza A/H3N2 activity which never reached a true epidemic level. There was no real peak activity either but a prolonged period of increased activity of approximately eight weeks with a maximum in week 13, when sentinel physicians reported 16.6 cases of influenza-like illness per 10,000 inhabitants. It was not until week 18 of 1998 that the influenza activity declined to baseline levels. During the season, almost exclusively influenza A/H3N2 viruses were isolated, of which the majority resembled the new strain influenza A/Sydney/5/97 (H3N2). Further analysis of these variant viruses revealed that, although there was some cross-reactivity with the vaccine strain (A/Nanchang/933/95), no optimal protection could be expected to be induced by the vaccine. Antigenic characterisation of the sporadic influenza A/H1N1 and influenza B viruses showed that these were related to the vaccine strains. As a result of these findings, the World Health Organization (WHO) recommended to change the H3N2 strain in the influenza vaccine for the season 1998/'99 to an influenza A/Sydney/5/97(H3N2)-like strain. Based on epidemiological data from other countries, it was also decided to change the influenza A/H1N1 component to an influenza A/Beijing/262/95 (H1N1)-like strain.