Wireless electroceutical dressing (WED) fabric kills bacteria and disrupts bacterial biofilm. This work tested, comparing with standard of care topical antibiotic ketoconazole, whether the weak electric field generated by WED is effective to manage infection caused by ketoconazole-resistant yeast Candida albicans. WED inhibited Candida albicans biofilm formation and planktonic growth. Unlike ketoconazole, WED inhibited yeast to hyphal transition and downregulated EAP1 curbing cell attachment. In response to WED-dependent down-regulation of biofilm-forming BRG1 and ROB1, BCR1 expression was markedly induced in what seems to be a futile compensatory response. WED induced NRG1 and TUP1, negative regulators of filamentation; it down-regulated EFG1, a positive regulator of hyphal pathway. Consistent with the anti-hyphal properties of WED, the expression of ALS3 and HWP1 were diminished. Ketoconazole failed to reproduce the effects of WED on NRG1, TUP1 and EFG1. WED blunted efflux pump activity; this effect was in direct contrast to that of ketoconazole. WED exposure compromised cellular metabolism. In the presence of ketoconazole, the effect was synergistic. Unlike ketoconazole, WED caused membrane depolarization, changes in cell wall composition and loss of membrane integrity. This work presents first evidence that weak electric field is useful in managing pathogens which are otherwise known to be antibiotic resistant.

无线电敷料 (WED) 织物可杀死细菌并破坏细菌生物膜。这项工作测试了与标准护理局部抗生素酮康唑相比，WED 产生的弱电场是否能有效控制酮康唑耐药酵母白色念珠菌引起的感染。WED 抑制白色念珠菌生物膜形成和浮游生长。与酮康唑不同，WED 抑制酵母菌向菌丝的转变，并下调EAP1抑制细胞附着。为了响应 WED 依赖性生物膜形成BRG1和ROB1的下调，BCR1表达被显着诱导，这似乎是一种无效的补偿反应。WED 诱导NRG1和TUP1，丝状形成的负调节因子；它下调了菌丝途径的正调节因子EFG1 。与 WED 的抗菌丝特性一致，ALS3和HWP1的表达减少。酮康唑未能重现 WED 对NRG1、TUP1和EFG1的影响。WED 外排泵活动减弱；这种作用与酮康唑的作用形成鲜明对比。WED 暴露会损害细胞代谢。在酮康唑存在下，该作用具有协同作用。与酮康唑不同，WED 会导致膜去极化、细胞壁组成发生变化以及膜完整性丧失。这项工作提供了第一个证据，表明弱电场可用于控制已知具有抗生素抗性的病原体。