European Congress of Clinical Microbiology &amp; Infectious Diseases 2021
Authors: Priya Venkatesan
Journal: The Lancet Microbe (2021)

WHO panel discussion on antimicrobial resistanceA collective response and collaborative efforts between policymakers and researchers are urgently needed to combat the growing threat of antimicrobial resistance.A panel co-organised by WHO discussed the scale of the threat of antimicrobial resistance, and ways to address the gaps between policy and research. Antimicrobial resistance is one of the top ten global threats facing human beings and threatens to undo more than 100 years of progress in medicine, according to keynote speaker Zsuzsanna Jakab (WHO, Geneva, Switzerland). The drivers of resistance are complex and cross-sectional, including overuse, misuse, and inadequate infection control, highlighting that efforts to combat resistance and develop both new antimicrobials and effective alternatives can only be achieved through a collaborative multisectoral approach. Awareness must be raised so that individuals take action to prevent misuse and the rise of resistance; as Jeffrey Scott Weese (University of Guelph, Guelph, ON, Canada) highlighted, prevention of resistance and reducing use of antimicrobials (including disinfectants, antifungals, etc) is key. Sally Davies (Trinity College, Cambridge University, Cambridge, UK) discussed the need for behavioural and economic research as the basis for setting national targets. Evidence must underpin everything, and information should be communicated in an accessible way from researchers to policymakers. Global manufacturers, including those in the food industry also have a role to play; Robert Baker (Mars, McLean, VA, USA) commented that although antimicrobial resistance is not typically perceived as a food safety issue, resistance is linked to antimicrobials used in the food supply chain and in the home; some are becoming less effective in treating infections and there is evidence linking resistance with hypervariability in pathogens creating so-called superbugs. One idea for preventing resistance would be to safely reduce chemical-dependent food production. Maggie De Block (Ministry of Public Health & Social Affairs, Brussels, Belgium) commented on the need to share research with all policymakers, to update government administration on the latest research, and to invite all stakeholders in health to discuss research, so that policymakers can direct policy accordingly. Cost was raised as a major barrier to overcoming resistance as the WHO 2020 report on new antimicrobials in the pipeline showed that private investment has decreased and public investment cannot compensate; adequate funding combined with political will are important to the collaborative approach.Dissemination of a carbapenem-resistant plasmid in a hospitalWithin-patient transfer of a high-risk carbapenemase-encoding plasmid occurs via the gut microbiota of colonised patients in hospital and contributes to the overall dissemination of carbapenem resistance in the clinical setting.Plasmids and other mobile genetic elements carry antimicrobial resistance and virulence genes and can increase the emergence of pathogenic Gram-negative enterobacterial lineages. Carbapenemase-producing enterobacteria, especially those carrying high-risk carbapenemase-encoding plasmids such as pOXA-48 (which successfully survives even in hostile conditions) pose a substantial threat to patients in hospital and are associated with an increased mortality risk. In a 2-year epidemiological study, Álvaro San Millán (Centro de Nacional de Biotecnología, Madrid, Spain) and colleagues used mechanistic models to analyse data from swab samples of 9275 patients admitted to the gastroenterology, pneumology, neurosurgery, and urology wards in Ramón y Cajal hospital (Madrid, Spain) between March, 2014, and March, 2016. 105 patients (1·13%) tested positive for pOXA-48-carrying enterobacteria, and 250 isolates were recovered from these patients. 218 (87%) of the 250 isolates contained more than 90% of the genetic sequence of the pOXA-48 plasmid, and 140 (56%) of the isolates were of Klebsiella pneumoniae. The spread of K pneumoniae sequence type (ST) 11 was the most pervasive in all wards (between-patient transfer) and was highest in the neurosurgery ward and in some individual rooms that acted as hotspots for infection. High-resolution plasmid sequence analysis showed that pervasive within-patient transfer of pOXA-48 also occurred, potentially through horizontal transmission via the gut microbiota, raising the possibility that these patients could become long-term pOXA-48 carriers. Within-patient transfer should be considered in hospital strategies for controlling the spread of carbapenemase-producing enterobacteria.Mobile genetic elements as transmission vehicles of MDR in Escherichia coliIn a sequencing study, multidrug resistance (MDR) was noted in around a fifth of E coli ST95 clones that carry plasmids involved in the transmission of extraintestinal E coli diseases.E coli is one of the most common Gram-negative pathogens in humans, and extraintestinal pathogenic E coli strains are responsible for many human extraintestinal diseases including urinary tract infections, ventilator-associated pneumonia, and neonatal meningitis. Some of these strains are becoming increasingly resistant to multiple antimicrobials; this resistance might be linked to two major virulence plasmids, CoIV and pUTI89, which play a major role in extraintestinal E coli disease. Using an extensive genome sequencing database, Steven Djordjevic (University of Technology Sydney, Sydney, NSW, Australia) and colleagues examined the genomes of 34 175 E coli strains comprising 2570 sequence types for the carriage of the CoIV and pUTI89 plasmids. They observed MDR in 148 (22%) of 668 E coli ST95 clones—the leading cause of many urinary tract infections, bloodstream infections, and bacterial meningitis, especially in neonates. Most prevalent were genes associated with resistance to β-lactams, aminoglycosides, and fluoroquinolones.Immune response to SARS-CoV-2 variants of concernThe second dose of the Pfizer–BioNTech BNT-162b2 vaccine is important for acquiring high concentrations of neutralising antibodies against SARS-CoV-2. However, neutralisation is substantially reduced for the beta variant (lineage B.1.351), highlighting the importance of targeting new variants in future vaccines.SARS-CoV-2 is continually mutating and has produced several variants of concern with increased risks of transmission and reduced neutralisation susceptibility. Nicole Schneiderhan-Marra (Natural and Medical Sciences Institute, University of Tübingen, Reutlingen, Germany) and colleagues assessed the humoral immune response towards SARS-CoV-2 variants of concern (B.1.1.7 [alpha], B.1.351, cluster 5, and B1.429) compared with the original wild-type strain in serum and saliva samples from 23 health-care workers vaccinated with the BNT-162b2 vaccine. Samples were obtained around 17 days after the first dose and around 12 days after the second dose; controls were individuals who had been previously infected and recovered (but had not received a vaccination; n=27) and samples from donors that were taken before the pandemic (n=49).All vaccinated individuals showed an enhanced antibody response with increasing time after the first dose with a further substantial boost after the second dose. In saliva samples, previously infected individuals had significantly higher concentrations of IgA than pre-pandemic samples (p=0·0008) or vaccinated individuals (p=0·03), with no difference between vaccinated and pre-pandemic samples (p=0·23). However, there was significantly more spike-reactive IgG in the saliva of vaccinated individuals (p<0·0001). When assessing RBD-binding antibodies against the variants, for the B.1.1.7 variant the antibody response was similar for vaccinated and infected individuals compared with the wild-type variant (Kendall's t=0·965). By contrast, for B.1.351 the immune RBD response was varied and reduced (t=0·844). The response against cluster 5 and B1.429 variants was similar to that against the wild-type variant. Additionally, there were minimal to no changes in neutralisation for B.1.1.7, cluster 5, and B1.429 variants versus the wild type; however, neutralisation capacity against B.1.351 was substantially decreased. The findings highlight the need to update vaccines accordingly, and future studies should assess the longevity of the vaccination response.Impact of SARS-CoV-2 variants on mRNA vaccinesIn vaccinated serum samples, neutralising activity of the BNT162b2 vaccine was reduced against the variant viruses B.1.617.1 (kappa), B.1.617.2 (delta), B.1.618, and B.1.525 (eta) but all were neutralised at titres of at least 1:40, supporting the strategy of mass immunisation.Pei-Yong Shi (University of Texas Medical Branch, Galveston, TX, USA) and colleagues used a reverse genetic system to swap the complete spike gene from the B.1.617.1, B.1.617.2, B.1.618, and B.1.525 variants into an original wild-type isolate. The investigators then used a classic plaque neutralisation assay (50% plaque reduction neutralisation test [PRNT50]) to compare the susceptibility of the variants to neutralisation using 20 serum samples obtained from volunteers around 2–4 weeks after their second dose of immunisation with the BNT162b2 vaccine. Neutralisation of all variants, except the B.1.617.1 variant, was only modestly reduced compared with neutralisation of the original wild-type virus (geometric mean neutralising titres were 502 PRNT50 against the wild-type, 320–355 PRNT50 against the B.1.617.2, B.1.618, and B.1.525 variants, and 157 PRNT50 against B.1.617.1). However, all the samples neutralised the wild-type and all mutant viruses with titres of 1:40 or higher. The findings did not suggest that these virus variants have escaped BNT162b2-mediated protection from COVID-19, thus mass vaccination remains a key strategy to ending the COVID-19 pandemic.The European Congress of Clinical Microbiology & Infectious Diseases 2021 was held online between July 9, and July 12, 2021. https://www.eccmid.org/ WHO panel discussion on antimicrobial resistanceA collective response and collaborative efforts between policymakers and researchers are urgently needed to combat the growing threat of antimicrobial resistance.A panel co-organised by WHO discussed the scale of the threat of antimicrobial resistance, and ways to address the gaps between policy and research. Antimicrobial resistance is one of the top ten global threats facing human beings and threatens to undo more than 100 years of progress in medicine, according to keynote speaker Zsuzsanna Jakab (WHO, Geneva, Switzerland). The drivers of resistance are complex and cross-sectional, including overuse, misuse, and inadequate infection control, highlighting that efforts to combat resistance and develop both new antimicrobials and effective alternatives can only be achieved through a collaborative multisectoral approach. Awareness must be raised so that individuals take action to prevent misuse and the rise of resistance; as Jeffrey Scott Weese (University of Guelph, Guelph, ON, Canada) highlighted, prevention of resistance and reducing use of antimicrobials (including disinfectants, antifungals, etc) is key. Sally Davies (Trinity College, Cambridge University, Cambridge, UK) discussed the need for behavioural and economic research as the basis for setting national targets. Evidence must underpin everything, and information should be communicated in an accessible way from researchers to policymakers. Global manufacturers, including those in the food industry also have a role to play; Robert Baker (Mars, McLean, VA, USA) commented that although antimicrobial resistance is not typically perceived as a food safety issue, resistance is linked to antimicrobials used in the food supply chain and in the home; some are becoming less effective in treating infections and there is evidence linking resistance with hypervariability in pathogens creating so-called superbugs. One idea for preventing resistance would be to safely reduce chemical-dependent food production. Maggie De Block (Ministry of Public Health & Social Affairs, Brussels, Belgium) commented on the need to share research with all policymakers, to update government administration on the latest research, and to invite all stakeholders in health to discuss research, so that policymakers can direct policy accordingly. Cost was raised as a major barrier to overcoming resistance as the WHO 2020 report on new antimicrobials in the pipeline showed that private investment has decreased and public investment cannot compensate; adequate funding combined with political will are important to the collaborative approach. A collective response and collaborative efforts between policymakers and researchers are urgently needed to combat the growing threat of antimicrobial resistance. A panel co-organised by WHO discussed the scale of the threat of antimicrobial resistance, and ways to address the gaps between policy and research. Antimicrobial resistance is one of the top ten global threats facing human beings and threatens to undo more than 100 years of progress in medicine, according to keynote speaker Zsuzsanna Jakab (WHO, Geneva, Switzerland). The drivers of resistance are complex and cross-sectional, including overuse, misuse, and inadequate infection control, highlighting that efforts to combat resistance and develop both new antimicrobials and effective alternatives can only be achieved through a collaborative multisectoral approach. Awareness must be raised so that individuals take action to prevent misuse and the rise of resistance; as Jeffrey Scott Weese (University of Guelph, Guelph, ON, Canada) highlighted, prevention of resistance and reducing use of antimicrobials (including disinfectants, antifungals, etc) is key. Sally Davies (Trinity College, Cambridge University, Cambridge, UK) discussed the need for behavioural and economic research as the basis for setting national targets. Evidence must underpin everything, and information should be communicated in an accessible way from researchers to policymakers. Global manufacturers, including those in the food industry also have a role to play; Robert Baker (Mars, McLean, VA, USA) commented that although antimicrobial resistance is not typically perceived as a food safety issue, resistance is linked to antimicrobials used in the food supply chain and in the home; some are becoming less effective in treating infections and there is evidence linking resistance with hypervariability in pathogens creating so-called superbugs. One idea for preventing resistance would be to safely reduce chemical-dependent food production. Maggie De Block (Ministry of Public Health & Social Affairs, Brussels, Belgium) commented on the need to share research with all policymakers, to update government administration on the latest research, and to invite all stakeholders in health to discuss research, so that policymakers can direct policy accordingly. Cost was raised as a major barrier to overcoming resistance as the WHO 2020 report on new antimicrobials in the pipeline showed that private investment has decreased and public investment cannot compensate; adequate funding combined with political will are important to the collaborative approach. Dissemination of a carbapenem-resistant plasmid in a hospitalWithin-patient transfer of a high-risk carbapenemase-encoding plasmid occurs via the gut microbiota of colonised patients in hospital and contributes to the overall dissemination of carbapenem resistance in the clinical setting.Plasmids and other mobile genetic elements carry antimicrobial resistance and virulence genes and can increase the emergence of pathogenic Gram-negative enterobacterial lineages. Carbapenemase-producing enterobacteria, especially those carrying high-risk carbapenemase-encoding plasmids such as pOXA-48 (which successfully survives even in hostile conditions) pose a substantial threat to patients in hospital and are associated with an increased mortality risk. In a 2-year epidemiological study, Álvaro San Millán (Centro de Nacional de Biotecnología, Madrid, Spain) and colleagues used mechanistic models to analyse data from swab samples of 9275 patients admitted to the gastroenterology, pneumology, neurosurgery, and urology wards in Ramón y Cajal hospital (Madrid, Spain) between March, 2014, and March, 2016. 105 patients (1·13%) tested positive for pOXA-48-carrying enterobacteria, and 250 isolates were recovered from these patients. 218 (87%) of the 250 isolates contained more than 90% of the genetic sequence of the pOXA-48 plasmid, and 140 (56%) of the isolates were of Klebsiella pneumoniae. The spread of K pneumoniae sequence type (ST) 11 was the most pervasive in all wards (between-patient transfer) and was highest in the neurosurgery ward and in some individual rooms that acted as hotspots for infection. High-resolution plasmid sequence analysis showed that pervasive within-patient transfer of pOXA-48 also occurred, potentially through horizontal transmission via the gut microbiota, raising the possibility that these patients could become long-term pOXA-48 carriers. Within-patient transfer should be considered in hospital strategies for controlling the spread of carbapenemase-producing enterobacteria. Within-patient transfer of a high-risk carbapenemase-encoding plasmid occurs via the gut microbiota of colonised patients in hospital and contributes to the overall dissemination of carbapenem resistance in the clinical setting. Plasmids and other mobile genetic elements carry antimicrobial resistance and virulence genes and can increase the emergence of pathogenic Gram-negative enterobacterial lineages. Carbapenemase-producing enterobacteria, especially those carrying high-risk carbapenemase-encoding plasmids such as pOXA-48 (which successfully survives even in hostile conditions) pose a substantial threat to patients in hospital and are associated with an increased mortality risk. In a 2-year epidemiological study, Álvaro San Millán (Centro de Nacional de Biotecnología, Madrid, Spain) and colleagues used mechanistic models to analyse data from swab samples of 9275 patients admitted to the gastroenterology, pneumology, neurosurgery, and urology wards in Ramón y Cajal hospital (Madrid, Spain) between March, 2014, and March, 2016. 105 patients (1·13%) tested positive for pOXA-48-carrying enterobacteria, and 250 isolates were recovered from these patients. 218 (87%) of the 250 isolates contained more than 90% of the genetic sequence of the pOXA-48 plasmid, and 140 (56%) of the isolates were of Klebsiella pneumoniae. The spread of K pneumoniae sequence type (ST) 11 was the most pervasive in all wards (between-patient transfer) and was highest in the neurosurgery ward and in some individual rooms that acted as hotspots for infection. High-resolution plasmid sequence analysis showed that pervasive within-patient transfer of pOXA-48 also occurred, potentially through horizontal transmission via the gut microbiota, raising the possibility that these patients could become long-term pOXA-48 carriers. Within-patient transfer should be considered in hospital strategies for controlling the spread of carbapenemase-producing enterobacteria. Mobile genetic elements as transmission vehicles of MDR in Escherichia coliIn a sequencing study, multidrug resistance (MDR) was noted in around a fifth of E coli ST95 clones that carry plasmids involved in the transmission of extraintestinal E coli diseases.E coli is one of the most common Gram-negative pathogens in humans, and extraintestinal pathogenic E coli strains are responsible for many human extraintestinal diseases including urinary tract infections, ventilator-associated pneumonia, and neonatal meningitis. Some of these strains are becoming increasingly resistant to multiple antimicrobials; this resistance might be linked to two major virulence plasmids, CoIV and pUTI89, which play a major role in extraintestinal E coli disease. Using an extensive genome sequencing database, Steven Djordjevic (University of Technology Sydney, Sydney, NSW, Australia) and colleagues examined the genomes of 34 175 E coli strains comprising 2570 sequence types for the carriage of the CoIV and pUTI89 plasmids. They observed MDR in 148 (22%) of 668 E coli ST95 clones—the leading cause of many urinary tract infections, bloodstream infections, and bacterial meningitis, especially in neonates. Most prevalent were genes associated with resistance to β-lactams, aminoglycosides, and fluoroquinolones. In a sequencing study, multidrug resistance (MDR) was noted in around a fifth of E coli ST95 clones that carry plasmids involved in the transmission of extraintestinal E coli diseases. E coli is one of the most common Gram-negative pathogens in humans, and extraintestinal pathogenic E coli strains are responsible for many human extraintestinal diseases including urinary tract infections, ventilator-associated pneumonia, and neonatal meningitis. Some of these strains are becoming increasingly resistant to multiple antimicrobials; this resistance might be linked to two major virulence plasmids, CoIV and pUTI89, which play a major role in extraintestinal E coli disease. Using an extensive genome sequencing database, Steven Djordjevic (University of Technology Sydney, Sydney, NSW, Australia) and colleagues examined the genomes of 34 175 E coli strains comprising 2570 sequence types for the carriage of the CoIV and pUTI89 plasmids. They observed MDR in 148 (22%) of 668 E coli ST95 clones—the leading cause of many urinary tract infections, bloodstream infections, and bacterial meningitis, especially in neonates. Most prevalent were genes associated with resistance to β-lactams, aminoglycosides, and fluoroquinolones. Immune response to SARS-CoV-2 variants of concernThe second dose of the Pfizer–BioNTech BNT-162b2 vaccine is important for acquiring high concentrations of neutralising antibodies against SARS-CoV-2. However, neutralisation is substantially reduced for the beta variant (lineage B.1.351), highlighting the importance of targeting new variants in future vaccines.SARS-CoV-2 is continually mutating and has produced several variants of concern with increased risks of transmission and reduced neutralisation susceptibility. Nicole Schneiderhan-Marra (Natural and Medical Sciences Institute, University of Tübingen, Reutlingen, Germany) and colleagues assessed the humoral immune response towards SARS-CoV-2 variants of concern (B.1.1.7 [alpha], B.1.351, cluster 5, and B1.429) compared with the original wild-type strain in serum and saliva samples from 23 health-care workers vaccinated with the BNT-162b2 vaccine. Samples were obtained around 17 days after the first dose and around 12 days after the second dose; controls were individuals who had been previously infected and recovered (but had not received a vaccination; n=27) and samples from donors that were taken before the pandemic (n=49).All vaccinated individuals showed an enhanced antibody response with increasing time after the first dose with a further substantial boost after the second dose. In saliva samples, previously infected individuals had significantly higher concentrations of IgA than pre-pandemic samples (p=0·0008) or vaccinated individuals (p=0·03), with no difference between vaccinated and pre-pandemic samples (p=0·23). However, there was significantly more spike-reactive IgG in the saliva of vaccinated individuals (p<0·0001). When assessing RBD-binding antibodies against the variants, for the B.1.1.7 variant the antibody response was similar for vaccinated and infected individuals compared with the wild-type variant (Kendall's t=0·965). By contrast, for B.1.351 the immune RBD response was varied and reduced (t=0·844). The response against cluster 5 and B1.429 variants was similar to that against the wild-type variant. Additionally, there were minimal to no changes in neutralisation for B.1.1.7, cluster 5, and B1.429 variants versus the wild type; however, neutralisation capacity against B.1.351 was substantially decreased. The findings highlight the need to update vaccines accordingly, and future studies should assess the longevity of the vaccination response. The second dose of the Pfizer–BioNTech BNT-162b2 vaccine is important for acquiring high concentrations of neutralising antibodies against SARS-CoV-2. However, neutralisation is substantially reduced for the beta variant (lineage B.1.351), highlighting the importance of targeting new variants in future vaccines. SARS-CoV-2 is continually mutating and has produced several variants of concern with increased risks of transmission and reduced neutralisation susceptibility. Nicole Schneiderhan-Marra (Natural and Medical Sciences Institute, University of Tübingen, Reutlingen, Germany) and colleagues assessed the humoral immune response towards SARS-CoV-2 variants of concern (B.1.1.7 [alpha], B.1.351, cluster 5, and B1.429) compared with the original wild-type strain in serum and saliva samples from 23 health-care workers vaccinated with the BNT-162b2 vaccine. Samples were obtained around 17 days after the first dose and around 12 days after the second dose; controls were individuals who had been previously infected and recovered (but had not received a vaccination; n=27) and samples from donors that were taken before the pandemic (n=49). All vaccinated individuals showed an enhanced antibody response with increasing time after the first dose with a further substantial boost after the second dose. In saliva samples, previously infected individuals had significantly higher concentrations of IgA than pre-pandemic samples (p=0·0008) or vaccinated individuals (p=0·03), with no difference between vaccinated and pre-pandemic samples (p=0·23). However, there was significantly more spike-reactive IgG in the saliva of vaccinated individuals (p<0·0001). When assessing RBD-binding antibodies against the variants, for the B.1.1.7 variant the antibody response was similar for vaccinated and infected individuals compared with the wild-type variant (Kendall's t=0·965). By contrast, for B.1.351 the immune RBD response was varied and reduced (t=0·844). The response against cluster 5 and B1.429 variants was similar to that against the wild-type variant. Additionally, there were minimal to no changes in neutralisation for B.1.1.7, cluster 5, and B1.429 variants versus the wild type; however, neutralisation capacity against B.1.351 was substantially decreased. The findings highlight the need to update vaccines accordingly, and future studies should assess the longevity of the vaccination response. Impact of SARS-CoV-2 variants on mRNA vaccinesIn vaccinated serum samples, neutralising activity of the BNT162b2 vaccine was reduced against the variant viruses B.1.617.1 (kappa), B.1.617.2 (delta), B.1.618, and B.1.525 (eta) but all were neutralised at titres of at least 1:40, supporting the strategy of mass immunisation.Pei-Yong Shi (University of Texas Medical Branch, Galveston, TX, USA) and colleagues used a reverse genetic system to swap the complete spike gene from the B.1.617.1, B.1.617.2, B.1.618, and B.1.525 variants into an original wild-type isolate. The investigators then used a classic plaque neutralisation assay (50% plaque reduction neutralisation test [PRNT50]) to compare the susceptibility of the variants to neutralisation using 20 serum samples obtained from volunteers around 2–4 weeks after their second dose of immunisation with the BNT162b2 vaccine. Neutralisation of all variants, except the B.1.617.1 variant, was only modestly reduced compared with neutralisation of the original wild-type virus (geometric mean neutralising titres were 502 PRNT50 against the wild-type, 320–355 PRNT50 against the B.1.617.2, B.1.618, and B.1.525 variants, and 157 PRNT50 against B.1.617.1). However, all the samples neutralised the wild-type and all mutant viruses with titres of 1:40 or higher. The findings did not suggest that these virus variants have escaped BNT162b2-mediated protection from COVID-19, thus mass vaccination remains a key strategy to ending the COVID-19 pandemic.The European Congress of Clinical Microbiology & Infectious Diseases 2021 was held online between July 9, and July 12, 2021. https://www.eccmid.org/ In vaccinated serum samples, neutralising activity of the BNT162b2 vaccine was reduced against the variant viruses B.1.617.1 (kappa), B.1.617.2 (delta), B.1.618, and B.1.525 (eta) but all were neutralised at titres of at least 1:40, supporting the strategy of mass immunisation. Pei-Yong Shi (University of Texas Medical Branch, Galveston, TX, USA) and colleagues used a reverse genetic system to swap the complete spike gene from the B.1.617.1, B.1.617.2, B.1.618, and B.1.525 variants into an original wild-type isolate. The investigators then used a classic plaque neutralisation assay (50% plaque reduction neutralisation test [PRNT50]) to compare the susceptibility of the variants to neutralisation using 20 serum samples obtained from volunteers around 2–4 weeks after their second dose of immunisation with the BNT162b2 vaccine. Neutralisation of all variants, except the B.1.617.1 variant, was only modestly reduced compared with neutralisation of the original wild-type virus (geometric mean neutralising titres were 502 PRNT50 against the wild-type, 320–355 PRNT50 against the B.1.617.2, B.1.618, and B.1.525 variants, and 157 PRNT50 against B.1.617.1). However, all the samples neutralised the wild-type and all mutant viruses with titres of 1:40 or higher. The findings did not suggest that these virus variants have escaped BNT162b2-mediated protection from COVID-19, thus mass vaccination remains a key strategy to ending the COVID-19 pandemic. The European Congress of Clinical Microbiology & Infectious Diseases 2021 was held online between July 9, and July 12, 2021. https://www.eccmid.org/ The European Congress of Clinical Microbiology & Infectious Diseases 2021 was held online between July 9, and July 12, 2021. https://www.eccmid.org/ The European Congress of Clinical Microbiology & Infectious Diseases 2021 was held online between July 9, and July 12, 2021. https://www.eccmid.org/