Carvacrol and eugenol were encapsulated in micellar nonionic surfactant solutions to increase active component concentrations in the aqueous phase and used to treat two strains of Listeria monocytogenes (Scott A and 101) and two strains of Escherichia coli O157:H7 (4388 and 43895) grown as biofilms in a Centers for Disease Control and Prevention reactor. L. monocytogenes biofilms were grown in two different growth media, 1:20 TSB and Modified Welshimer's broth (MWB), while E. coli O157:H7 was grown in M9. In general, L. monocytogenes strains were more resistant to both micelle-encapsulated antimicrobials than E. coli O157:H7 strains. The two antimicrobials were equally effective against both strains of E. coli O157:H7, decreasing viable counts by 3.5 to 4.8 log CFU/cm(2) within 20 min. For both bacteria, most of the bactericidal activity took place in the first 10 min of antimicrobial exposure. Biofilm morphology and viability were assessed by the BacLight RedoxSensor CTC Vitality kit and confocal scanning laser microscopy, revealing an increasing number of dead cells when biofilms were treated with sufficiently high concentrations of carvacrol- or eugenol-loaded micelles. This study demonstrates the effectiveness of the application of surfactant-encapsulated essential oil components on two pathogen biofilm formers such as E. coli O157:H7 and L. monocytogenes grown on stainless steel coupons.

Cross-resistance (CR) between voriconazole and fluconazole for non-albicans Candida (NAC) species is not uncommon, but little is known about the risk factors and clinical consequences associated with this resistance phenotype. A case-case-control study was performed at a university-affiliated hospital in China between November 2012 and April 2016. The two case groups respectively comprised patients with a mono-resistance (MR) NAC infection (fluconazole or voriconazole resistance) and patients with a CR NAC infection (fluconazole and voriconazole resistance). Patients with a no-resistance (NR) NAC infection were included as the control group. Models were adjusted for demographic and clinical risk factors, and the risk of resistance associated with exposure to specific antibiotics or non-antibiotics were assessed. Of 259 episodes, 33 (12.7%) and 27 (10.4%) were identified as MR and CR NAC infections, respectively. The broad use of azoles was strongly associated with the emergence of MR and CR NAC infections (adjusted odds ratio [95% confidence interval] = 2.69 [1.10-6.58] and 2.53 [1.02-6.28], respectively). The time at risk (1.02 [1.00-1.03]) with 12 days as a breakpoint was also an independent risk factor for CR NAC infection. The number of species associated with a high minimum inhibitory concentration (≥128 μg/mL) of fluconazole was higher for CR NAC infections than for MR NAC infections. Different resistance phenotypes (CR vs. MR vs. NR) were associated with all-cause mortality rates. These findings indicate a worrisome propensity of CR NAC infections and emphasize the need for strict antifungal stewardship.