Papanin Putsathit1, Stacey Hong2,3, Narelle George4, Christine Hemphill5, Peter G Huntington6, Tony M Korman7, Despina Kotsanas7, Monica Lahra8, Rodney McDougall9, Andrew McGlinchey5, Casey V Moore10, Graeme R Nimmo4, Louise Prendergast5, Jennifer Robson9, Lynette Waring5, Michael C Wehrhahn11, Gerhard F Weldhagen10, Richard M Wilson12, Thomas V Riley1,2,3,13, Daniel R Knight2,3. 1. School of Medical and Health Sciences, Edith Cowan University, Joondalup 6027, WA, Australia. 2. Marshall Centre for Infectious Diseases Research and Training, School of Biomedical Sciences, The University of Western Australia, Queen Elizabeth II Medical Centre, Nedlands 6009, WA, Australia. 3. Medical, Molecular and Forensic Sciences, Murdoch University, Murdoch 6150, WA, Australia. 4. Pathology Queensland, Royal Brisbane and Women's Hospital, Herston 4029, QLD, Australia. 5. Melbourne Pathology, Collingwood 3066, VIC, Australia. 6. Department of Microbiology, NSW Health Pathology, Royal North Shore Hospital, St Leonards, 2065, NSW, Australia. 7. Monash Infectious Diseases, Monash Health, Monash Medical Centre, Clayton 3168, VIC, Australia. 8. Department of Microbiology, The Prince of Wales Hospital, Randwick 2031, NSW, Australia. 9. Sullivan Nicolaides Pathology, Taringa 4068, QLD, Australia. 10. Microbiology and Infectious Diseases Laboratories, SA Pathology, Adelaide 5000, SA, Australia. 11. Douglass Hanly Moir Pathology, Macquarie Park 2113, NSW, Australia. 12. Australian Clinical Labs, Microbiology Department, Wayville 5034, SA, Australia. 13. Department of Microbiology, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Nedlands 6009, WA, Australia.
Abstract
BACKGROUND: Clostridioides difficile was listed as an urgent antimicrobial resistance (AMR) threat in a report by the CDC in 2019. AMR drives the evolution of C. difficile and facilitates its emergence and spread. The C. difficile Antimicrobial Resistance Surveillance (CDARS) study is nationwide longitudinal surveillance of C. difficile infection (CDI) in Australia. OBJECTIVES: To determine the antimicrobial susceptibility of C. difficile isolated in Australia between 2015 and 2018. METHODS: A total of 1091 strains of C. difficile were collected over a 3 year period by a network of 10 diagnostic microbiology laboratories in five Australian states. These strains were tested for their susceptibility to nine antimicrobials using the CLSI agar incorporation method. RESULTS: All strains were susceptible to metronidazole, fidaxomicin, rifaximin and amoxicillin/clavulanate and low numbers of resistant strains were observed for meropenem (0.1%; 1/1091), moxifloxacin (3.5%; 38/1091) and vancomycin (5.7%; 62/1091). Resistance to clindamycin was common (85.2%; 929/1091), followed by resistance to ceftriaxone (18.8%; 205/1091). The in vitro activity of fidaxomicin [geometric mean MIC (GM) = 0.101 mg/L] was superior to that of vancomycin (1.700 mg/L) and metronidazole (0.229 mg/L). The prevalence of MDR C. difficile, as defined by resistance to ≥3 antimicrobial classes, was low (1.7%; 19/1091). CONCLUSIONS: The majority of C. difficile isolated in Australia did not show reduced susceptibility to antimicrobials recommended for treatment of CDI (vancomycin, metronidazole and fidaxomicin). Resistance to carbapenems and fluoroquinolones was low and MDR was uncommon; however, clindamycin resistance was frequent. One fluoroquinolone-resistant ribotype 027 strain was detected.
BACKGROUND:Clostridioides difficile was listed as an urgent antimicrobial resistance (AMR) threat in a report by the CDC in 2019. AMR drives the evolution of C. difficile and facilitates its emergence and spread. The C. difficile Antimicrobial Resistance Surveillance (CDARS) study is nationwide longitudinal surveillance of C. difficileinfection (CDI) in Australia. OBJECTIVES: To determine the antimicrobial susceptibility of C. difficile isolated in Australia between 2015 and 2018. METHODS: A total of 1091 strains of C. difficile were collected over a 3 year period by a network of 10 diagnostic microbiology laboratories in five Australian states. These strains were tested for their susceptibility to nine antimicrobials using the CLSI agar incorporation method. RESULTS: All strains were susceptible to metronidazole, fidaxomicin, rifaximin and amoxicillin/clavulanate and low numbers of resistant strains were observed for meropenem (0.1%; 1/1091), moxifloxacin (3.5%; 38/1091) and vancomycin (5.7%; 62/1091). Resistance to clindamycin was common (85.2%; 929/1091), followed by resistance to ceftriaxone (18.8%; 205/1091). The in vitro activity of fidaxomicin [geometric mean MIC (GM) = 0.101 mg/L] was superior to that of vancomycin (1.700 mg/L) and metronidazole (0.229 mg/L). The prevalence of MDR C. difficile, as defined by resistance to ≥3 antimicrobial classes, was low (1.7%; 19/1091). CONCLUSIONS: The majority of C. difficile isolated in Australia did not show reduced susceptibility to antimicrobials recommended for treatment of CDI (vancomycin, metronidazole and fidaxomicin). Resistance to carbapenems and fluoroquinolones was low and MDR was uncommon; however, clindamycin resistance was frequent. One fluoroquinolone-resistant ribotype 027 strain was detected.