Insusceptible Strains Research Articles

Intrinsic resistance of Enterococcus faecalis strains to ΦEf11 phage endolysin is associated with the presence of ΦEf11 prophage.

The use of bacteriophage-encoded murein hydrolases (endolysins) is being actively explored as a means of controlling multidrug-resistant pathogens. Previously, we isolated and characterized one such enzyme, the phage ΦEf11 ORF28 lysin, which demonstrated profound antimicrobial activity against many strains of Enterococcus faecalis. Although the lysin is eminently active against manyvancomycin-resistant enterococal (VRE) strains, and displays lower minimum inhibitory concentrations than vancomycin against vancomycin-sensitive strains, there is a subset of E. faecalis strains that is not affected by the lysin. Currently, there is no explanation for the disparate sensitivity to ORF28 lysin among E. faecalis strains. In the present investigation, we show that the intrinsic insensitivity of the insusceptible strains to the lysin is associated with the presence of a ΦEf11 prophage. Of the strains harboring phage ΦEf11 genes (N = 28), 68% were insensitive to the lysin, whereas 91% of the strains (N = 75) lacking detectable ΦEf11 genes demonstrated lysin sensitivity. Furthermore, curing a lysin-resistant, lysogenic E. faecalis strain resulted in a lysin-sensitive derivative, whereas lysogenizing a wild-type non-lysogenic strain converted it from lysin sensitivity to lysin resistance. Our results suggest that lysin resistance comes about through lysogenic conversion of non-lysogenic, lysin-sensitive strains.

Propionibacterium acnes is developing gradual increase in resistance to oral tetracyclines.

Propionibacterium acnes is an anaerobic bacterium that causes deep infection in organs and prosthetic joints, in addition to acne vulgaris. Many tetracycline-resistant P. acnes strains have been isolated because oral tetracyclines are frequently used as an acne treatment against P. acnes. In this study, we found a novel tetracycline resistance mechanism in P. acnes. Three doxycycline-resistant (MIC: 16 µg ml-1) strains were isolated from 69 strains in acne patients in Japan between 2010 and 2011. Additionally, six insusceptible strains (MIC: 1-2 µg ml-1) that had reduced susceptibility compared to susceptible strains (MIC: ≤0.5 µg ml-1) were identified. All doxycycline-resistant strains had a G1036C mutation in the 16S rRNA gene in addition to an amino acid substitution in the ribosomal S10 protein encoded by rpsJ. By contrast, insusceptible strains had an amino acid substitution in the S10 protein but no mutation in the 16S rRNA. When the mutant with decreased susceptibility to doxycycline was obtained in vitro, only the mutated S10 protein was found (MIC: 4 µg ml-1), not the mutated 16S rRNA gene. This result shows that the S10 protein amino acid substitution contributes to reduced doxycycline susceptibility in P. acnes and suggests that tetracycline resistance is acquired through a 16S rRNA mutation after the S10 protein amino acid substitution causes reduced susceptibility.

In vitro antifungal activity of phenothiazines and their combination with amphotericin B against different Candida species

Candidiosis is a mycosis that is currently increasingly affecting the population in consequence of its frequency and the severity of its complications, especially among immunocompromised hosts. In this work, the in vitro anticandidal activities of two phenothiazines (PTZs), chlorpromazine (CPZ) and trifluoperazine (TFP), and their combinations with amphotericin B (AMB) were tested against 12 different Candida strains representing 12 species (Candida albicans, Candida glabrata, Candida guillermondii, Candida inconspicua, Candida krusei, Candida lusitaniae, Candida lypolitica, Candida norvegica, Candida parapsilosis, Candida pulcherrima, Candida tropicalis and Candida zeylanoides). When used alone, both tested PTZs exerted antifungal effects against these strains. In their combinations, these PTZs and AMB mainly acted antagonistically at higher concentrations, but additively and synergistically at lower concentrations as concerns the clinically most important species (C. albicans and C. parapsilosis). For C. albicans, only synergistic interactions were revealed between CPZ and AMB. Synergistic, additive or no interactions were demonstrated between the investigated compounds for the most PTZ-susceptible (C. glabrata to TFP and C. krusei to CPZ) and insusceptible strains (C. glabrata to CPZ and C. lypolitica to TFP).

Activity ofCorynebacterium jeikeiumBacteriocinIn Vivo

Strains of Corynebacterium jeikeium which produce a bacteriocin-like-substance in vitro are shown to outgrow susceptible. but not insusceptible strains when placed in mixed culture on the skin of the hairless-obese mouse under occlusion for 24 h. Keywords: Corynebacterium ; Bacteriocin; Mouse model; Skin surface.

Short Communications: Activity of CorynebacteriumjeikeiumBacteriocin inVivo

Strains of Corynebacterium jeikeium which produce abacteriocin-like-substance in vitro are shown to outgrow susceplcible, but not insusceptible strains when placed in mixed culture on the skin of the hairless-obese mouse under occlusion for 24 h.

The autologous mixed lymphocyte reaction is decreased in Freund's adjuvant-injected rats of arthritis-susceptible and -insusceptible strains.

We examined the T-non-T cell autologous mixed lymphocyte reaction (AMLR) of spleen cells from rats with arthritis induced by Freund's complete adjuvant in an effort to establish an animal model for the study of the relationship between the AMLR and autoimmune disease. We found that the splenic T-non-T AMLR was markedly decreased in rats with adjuvant-induced arthritis and that this decrease was mediated by suppressor cells within the nylon-wool-adherent stimulator cell population. However, we also found a similar decrease in the AMLR of arthritis-resistant Fisher 344 rats that received Freund's complete adjuvant but did not develop arthritis. Control animals with local inflammation induced by turpentine, a non-arthritogenic inflammatory substance, had normal AMLR, whereas other controls given Freund's incomplete adjuvant, also a non-arthritogenic substance, had a modest responder cell-mediated decrease in AMLR. These studies help to clarify the relationship between the decreased AMLR and the pathogenesis of adjuvant-induced arthritis by demonstrating that: 1) the acute-phase inflammatory response does not reduce the AMLR; and 2) the decreased AMLR can occur in the absence of overt autoimmune disease. This latter observation calls into question the proposed pathogenetic relationship between the AMLR and autoimmune disease states.