Methicillin-Resistant Staphylococcus aureus Prevalence among Captive Chimpanzees,Texas, USA, 2012

Methicillin-resistant Staphylococcus aureus (MRSA) infection in humans and animals is concerning. In 2012, our evaluation of a captive chimpanzee colony in Texas revealed MRSA prevalence of 69%. Animal care staff should be aware of possible zoonotic MRSA transmission resulting from high prevalence among captive chimpanzees.     

Relationship between quinolone use and resistance of Staphylococcus epidermidis in patients with acne vulgaris

Staphylococcus epidermidis is a bacterium known to inhabit the skin. In treatment of acne vulgaris, the cutaneous milieu is exposed to oral or topical antimicrobials. We previously reported that the antimicrobial resistance of Cutibacterium acnes isolated from acne patients is affected by antimicrobial use. The aim of this study was to investigate the relationship between quinolone use and resistance in skin bacteria, particularly S. epidermidis, from acne patients. A total of 92 and 87 S. epidermidis strains isolated from clinic patients and hospital outpatients with acne vulgaris, respectively, were tested. No significant difference was found between the prevalence of methicillin‐resistant S. epidermidis (MRSE) strains from clinic patients (37.0%) and hospital outpatients (39.1%). The MRSE strains (20.6%, 14/68 strains) showed a significantly higher ratio of high‐level levofloxacin resistance (minimum inhibitory concentrations were 64 to ≥256 μg/mL) compared with methicillin‐susceptible S. epidermidis strains (2.7%, 3/111 strains) (P < 0.01). The rate of levofloxacin resistance in C. acnes strains, which were isolated from the same samples of acne patients, showed a strong positive correlation with that in S. epidermidis strains (r = 0.93, P < 0.01). The high‐level levofloxacin‐resistant strains were frequently found in patients with history of quinolone use compared with those without (P < 0.01). Our data showed for the first time that antimicrobial administration for acne treatment affects the antimicrobial resistance in not only C. acnes but also S. epidermidis. Thus, caution should be exercised in antimicrobial use for acne treatment to prevent increasing antimicrobial resistance in these species.     

Two arginine residues in the COOH‐terminal of human β‐defensin‐3 constitute an essential motif for antimicrobial activity and IL‐6 production

Human β‐defensin‐3 (HBD‐3) possesses antimicrobial activities and the potential to induce proinflammatory cytokines. HBD‐3 contains a unique motif of two arginine residues (Arg or R) in the COOH‐terminal region. To understand the bioactive properties of the Arg residues of HBD‐3, we examined antimicrobial activities against Staphylococcus aureus and Pseudomonas aeruginosa using synthetic HBD‐2, HBD‐3 and two variant peptides of HBD‐3: the Arg‐truncated variant designated desR HBD‐3 and NRR HBD‐3, in which both Arg residues were shifted to the N‐terminal region. IL‐6 production from keratinocytes was studied using the peptides. HBD‐3 possessed approximately five‐fold more potent antimicrobial activities, evaluated as the minimum inhibitory concentration (MIC), against S. aureus compared with desR and NRR HBD‐3, while no significant activity was observed in HBD‐2. The antimicrobial activity of HBD‐3 against S. aureus was well preserved even at high sodium chloride concentrations, but was attenuated in desR and NRR HBD‐3. All the peptides exhibited similar antimicrobial activities against P. aeruginosa, but HBD‐2 and desR HBD‐3 showed diminished antimicrobial activities against P. aeruginosa at high salt concentrations. IL‐6 production was significantly induced in keratinocytes with HBD‐3, but not remarkably with stimulation by other peptide. These Arg residues are essential for the antimicrobial and biological properties of HBD‐3.     

Human skin engages different epidermal layers to provide distinct innate defense mechanisms

Keratinocytes are able to sense bacteria or bacterial products leading to a rapid defense reaction by the increased expression of antimicrobial peptides and cytokines. Recent data by Percoco and collaborators published in Experimental Dermatology indicate that bacteria colonizing the skin surface induce a differential spatial expression pattern of antimicrobial peptides and cytokines. Using laser capture microdissection followed by real‐time PCR as well as immunohistochemistry and transmission electron microscopy, the authors provide evidence that antimicrobial peptides such as human beta‐defensin (hBD)‐2 and ‐3 were more strongly induced in the uppermost epidermal layers, whereas the main induction of cytokines such as IL‐1beta and IL‐6 occurred in the lower parts of the epidermis.     

New definitions of extended‐spectrum β‐lactamase conferring worldwide emerging antibiotic resistance

Although there is no consensus of the precise definition of ESBL, three kinds of ESBL definitions have been proposed. First, the classical definition includes variants derived from TEM‐1, TEM‐2, or SHV‐1; K1 (KOXY) of Klebsiella oxytoca. Second, the broadened definition has stretched the classical definition of ESBL to include: (1) β‐lactamases (CTX‐M‐ESBLs, GES‐ESBLs, and VEB‐ESBLs), with spectra similar to those of TEM and SHV variants (designated as TEM‐ and SHV‐ESBLs, respectively) but derived from other sources; (2) TEM and SHV variants with borderline ESBL activity; e.g., TEM‐12; and (3) various β‐lactamases conferring wider resistance than their parent types but not meeting the definition for group 2be; e.g., OXA‐types (OXA‐ESBLs) and mutant AmpC‐types (AmpC‐ESBLs), with increased activity against oxyimino‐cephalosporins and with resistance to clavulanic acid. Third, the all‐inclusive definition includes: (1) ESBL_A (named for class A ESBLs); (2) ESBL_M (miscellaneous ESBLs), which has been subdivided into ESBL_M‐C (class C; plasmid‐mediated AmpC) and ESBL_M‐D (class D); and (3) ESBL_CARBA (ESBLs with hydrolytic activity against carbapenems), which has been subdivided into ESBL_CARBA‐A (class A carbapenemases), ESBL_CARBA‐B (class B carbapenemases), and ESBL_CARBA‐D (class D carbapenemases). The consensus view about the ESBL definition is that the classical ESBL definition must be expanded to class A non‐TEM‐ and non‐SHV‐ESBLs (CTX‐M‐, GES‐, VEB‐ESBLs, etc.). However, these three definitions evoke rational debate on the question “Which would be included in the category of ESBLs among AmpC‐ESBLs, OXA‐ESBLs, and/or carbapenemases?” Therefore, there is a great need for consensus in the precise definition of ESBL. © 2010 Wiley Periodicals, Inc. Med Res Rev 32:216‐232, 2012