Ng Jamie May Ling, Ngeow Yun Fong, Saw Seow Hoon, Ng Hien Fuh, Zin Thaw
Centre for Research on Communicable Diseases, Faculty of Medicine and Health Sciences, Universiti Tunku Abdul Rahman, Jalan Sungai Long, Bandar Sungai Long, 43000 Kajang, Selangor, Malaysia.
Department of Allied Health Sciences, Faculty of Science, Universiti Tunku Abdul Rahman, 31900 Kampar, Perak, Malaysia.
J Med Microbiol. 2022 Dec;71(12). doi: 10.1099/jmm.0.001618.
Listeriosis, a foodborne infection caused by , could lead to febrile listerial gastroenteritis and a more invasive form which is often associated with a high mortality and hospitalisation rate. Gentamicin, used as an adjunct therapy with ampicillin, remains the treatment of choice for this life-threatening and invasive infection. Nevertheless, there is little data on gentamicin resistance determinants in . In this study, we selected and characterised B2b, a gentamicin-resistant mutant derived from ATCC 19115 to determine the target(s) of resistance in after exposure to gentamicin. Whole-genome sequencing was carried out to identify the mutation site(s) and possible mechanism(s) of resistance. The mutant was characterised using antimicrobial susceptibility testing and PCR. For biological verifications, complementation and allelic exchange mutagenesis were carried out. We found that the gentamicin resistance in B2b was caused by a 10 bp deletion in which encodes a gamma subunit of the ATP synthase in . Using PCR, various other mutations were identified in other gentamicin resistant mutants derived from ATCC 19115. In addition, the mutation from B2b, when introduced into , also caused gentamicin resistance in this species. Hence, mutations appear to be important determinants of gentamicin resistance not only in but possibly also in other species.
李斯特菌病是一种由[未提及具体病原体]引起的食源性感染，可导致发热性李斯特菌性肠胃炎以及一种更具侵袭性的形式，后者通常与高死亡率和住院率相关。庆大霉素与氨苄西林联合用作辅助治疗，仍然是这种危及生命的侵袭性感染的首选治疗方法。然而，关于[未提及具体病原体]中庆大霉素耐药决定因素的数据很少。在本研究中，我们选择并鉴定了B2b，它是一种源自[未提及具体菌株]ATCC 19115的庆大霉素耐药突变体，以确定[未提及具体病原体]在接触庆大霉素后的耐药靶点。进行全基因组测序以确定突变位点和可能的耐药机制。使用抗菌药敏试验和PCR对该突变体进行鉴定。为了进行生物学验证，进行了互补和等位基因交换诱变。我们发现B2b中的庆大霉素耐药性是由[未提及具体基因]中的10 bp缺失引起的，该基因编码[未提及具体病原体]中ATP合酶的γ亚基。使用[未提及具体方法]PCR，在源自ATCC 19115的其他庆大霉素耐药突变体中鉴定出各种其他突变。此外，将来自B2b的突变引入[未提及具体菌株]时，也导致该[未提及具体菌株]物种产生庆大霉素耐药性。因此，[未提及具体基因]突变似乎不仅是[未提及具体病原体]中庆大霉素耐药的重要决定因素，而且可能也是其他[未提及具体菌株]物种中的重要决定因素。
