Ron Dagan1, Shalom Ben-Shimol1,2, Rachel Benisty1,2, Gili Regev-Yochay3,4, Stephanie W Lo5, Stephen D Bentley5,6,7, Paulina A Hawkins8, Lesley McGee9, Merav Ron10, Noga Givon-Lavi1,2, Lea Valinsky10, Assaf Rokney10. 1. Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel. 2. Pediatric Infectious Disease Unit, Soroka University Medical Center, Beer Sheva, Israel. 3. Infectious Prevention & Control Unit, Sheba Medical Center, Ramat-Gan, Israel. 4. Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel. 5. Parasites and Microbes Programme, Wellcome Sanger Institute, Wellcome Genome Campus, University of Cambridge, Cambridge, United Kingdom. 6. Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom. 7. Department of Pathology, University of Cambridge, Cambridge, United Kingdom. 8. Rollins School of Public Health, Emory University, Atlanta, Georgia, USA. 9. Respiratory Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia, USA. 10. Government Central Laboratories, Ministry of Health, Jerusalem, Israel.
Abstract
BACKGROUND: Invasive pneumococcal disease (IPD) caused by Streptococcus pneumoniae serotype 2 (Sp2) is infrequent. Large-scale outbreaks were not been reported following pneumococcal conjugate vaccine (PCV) implementation. We describe a Sp2 IPD outbreak in Israel, in the PCV13 era, with focus on Sp2 population structure and evolutionary dynamics. METHODS: The data were derived from a population-based, nationwide active surveillance of IPD since 2009. PCV7/PCV13 vaccines were introduced in July 2009 and November 2010, respectively. Sp2 isolates were tested for antimicrobial susceptibility, multilocus sequence typing, and whole-genome sequencing (WGS) analysis. RESULTS: Overall, 170 Sp2 IPD cases were identified during 2009-2019; Sp2 increased in 2015 and caused 6% of IPD during 2015-2019, a 7-fold increase compared with 2009-2014. The outbreak was caused by a previously unreported molecular type (ST-13578), initially observed in Israel in 2014. This clone caused 88% of Sp2 during 2015-2019. ST-13578 is a single-locus variant of ST-1504, previously reported globally including in Israel. WGS analysis confirmed clonality among the ST-13578 population. Single-nucleotide polymorphism-dense regions support a hypothesis that the ST-13578 outbreak clone evolved from ST-1504 by recombination. All tested strains were penicillin-susceptible (minimum inhibitory concentration <0.06 μg/mL). The ST-13578 clone was identified almost exclusively (99%) in the Jewish population and was mainly distributed in 3 of 7 Israeli districts. The outbreak is still ongoing, although it began declining in 2017. CONCLUSIONS: To the best of our knowledge, this is the first widespread Sp2 outbreak since PCV13 introduction worldwide, caused by the emerging ST-13578 clone.
BACKGROUND: Invasive pneumococcal disease (IPD) caused by Streptococcus pneumoniae serotype 2 (Sp2) is infrequent. Large-scale outbreaks were not been reported following pneumococcal conjugate vaccine (PCV) implementation. We describe a Sp2 IPD outbreak in Israel, in the PCV13 era, with focus on Sp2 population structure and evolutionary dynamics. METHODS: The data were derived from a population-based, nationwide active surveillance of IPD since 2009. PCV7/PCV13 vaccines were introduced in July 2009 and November 2010, respectively. Sp2 isolates were tested for antimicrobial susceptibility, multilocus sequence typing, and whole-genome sequencing (WGS) analysis. RESULTS: Overall, 170 Sp2 IPD cases were identified during 2009-2019; Sp2 increased in 2015 and caused 6% of IPD during 2015-2019, a 7-fold increase compared with 2009-2014. The outbreak was caused by a previously unreported molecular type (ST-13578), initially observed in Israel in 2014. This clone caused 88% of Sp2 during 2015-2019. ST-13578 is a single-locus variant of ST-1504, previously reported globally including in Israel. WGS analysis confirmed clonality among the ST-13578 population. Single-nucleotide polymorphism-dense regions support a hypothesis that the ST-13578 outbreak clone evolved from ST-1504 by recombination. All tested strains were penicillin-susceptible (minimum inhibitory concentration <0.06 μg/mL). The ST-13578 clone was identified almost exclusively (99%) in the Jewish population and was mainly distributed in 3 of 7 Israeli districts. The outbreak is still ongoing, although it began declining in 2017. CONCLUSIONS: To the best of our knowledge, this is the first widespread Sp2 outbreak since PCV13 introduction worldwide, caused by the emerging ST-13578 clone.
Authors: Geetha Nagaraj; Vandana Govindan; Feroze Ganaie; V T Venkatesha; Paulina A Hawkins; Rebecca A Gladstone; Lesley McGee; Robert F Breiman; Stephen D Bentley; Keith P Klugman; Stephanie W Lo; K L Ravikumar Journal: Microb Genom Date: 2021-09
Authors: Kate C Mellor; Stephanie Lo; Mition Yoannes; Audrey Michael; Tilda Orami; Andrew R Greenhill; Robert F Breiman; Paulina Hawkins; Lesley McGee; Stephen D Bentley; Rebecca L Ford; Deborah Lehmann Journal: Microb Genom Date: 2022-07