Evidence of another anthropic impact on iguana delicatissima from the lesser Antilles: the presence of antibiotic resistant enterobacteria

The improper use of antibiotics by humans may promote the dissemination of resistance in wildlife. The persistence and spread of acquired antibiotic resistance and human-associated bacteria in the environment, while representing a threat to wildlife, can also be exploited as a tool to monitor the extent of human impact, particularly on endangered animal species. Hence, we investigated both the associated enterobacterial species and the presence of acquired resistance traits in the cloacal microbiota of the critically endangered lesser Antillean iguana (Iguana delicatissima), by comparing two separate populations living in similar climatic conditions but exposed to different anthropic pressures. A combination of techniques, including direct plating, DNA sequencing and antimicrobial susceptibility testing allowed us to characterize the dominant enterobacterial populations, the an- tibiotic resistant strains and their profiles. A higher frequency of Escherichia coli was found in the samples from the more anthropized site, where multi-drug resistant strains were also isolated. These results confirm how human-associated bacteria as well as their antibiotic-resistance determinants may be transferred to wildlife, which, in turn, may act as a reservoir of antibiotic resistance

Antimicrobial susceptibility and emerging resistance determinants (blaCTX-M, rmtB, fosA3) in clinical isolates from urinary tract infections in the Bolivian Chaco

Summary Background Bolivia is among the lowest-resourced South American countries, with very few data available on antibiotic resistance in bacterial pathogens. The phenotypic and molecular characterization of bacterial isolates responsible for urinary tract infections (UTIs) in the Bolivian Chaco are reported here. Methods All clinical isolates from UTIs collected in the Hospital Basico Villa Montes between June 2010 and January 2014 were analyzed ( N =213). Characterization included susceptibility testing, extended-spectrum beta-lactamase (ESBL) detection, identification of relevant resistance determinants (e.g., CTX-M-type ESBLs, 16S rRNA methyltransferases, glutathione S-transferases), and genotyping of CTX-M producers. Results Very high resistance rates were observed. Overall, the lowest susceptibility was observed for trimethoprim–sulphamethoxazole, tetracycline, nalidixic acid, amoxicillin–clavulanic acid, ciprofloxacin, and gentamicin. Of E. coli and K. pneumoniae , 11.6% were ESBL producers. Resistance to nitrofurantoin, amikacin, and fosfomycin remained low, and susceptibility to carbapenems was fully preserved. CTX-M-15 was the dominant CTX-M variant. Four E. coli ST131 (two being H30-Rx) were identified. Of note, isolates harbouring rmtB and fosA3 were detected. Conclusions Bolivia is not an exception to the very high resistance burden affecting many South American countries. Optimization of alternative approaches to monitor local antibiotic resistance trends in resource-limited settings is strongly encouraged to support the implementation of effective empiric treatment guidelines

In vitro time-kill kinetics of dalbavancin against Staphylococcus spp. biofilms over prolonged exposure times

Abstract Staphylococcus aureus and Staphylococcus epidermidis are leading pathogens of biofilm-related infections and represent the most common cause of osteomyelitis and biomedical implants infections. Biofilm-related infections usually require long-term antibiotic treatment, often associated to surgical interventions. Dalbavancin is a newer lipoglycopeptide approved for the treatment of acute skin and skin-structure infections caused by Gram-positive pathogens. In addition, dalbavancin has recently been considered as a potential option for the treatment of staphylococcal osteomyelitis and orthopedic implant infections. In this study, time-kill kinetics of dalbavancin against S. aureus and S. epidermidis biofilms were determined over prolonged exposure times (up to 7 days), using both a standardized biofilm susceptibility model and biofilms grown onto relevant orthopedic biomaterials (i.e. titanium and cobalt-chrome disks). Dalbavancin (at concentrations achievable in bone and articular tissue) showed a potent activity against established staphylococcal biofilms in both tested models, and was overall superior to the comparator vancomycin

Methicillin-resistant Staphylococcus aureus in hospitalized patients from the Bolivian Chaco

Summary Objectives Information is lacking on the methicillin-resistant Staphylococcus aureus (MRSA) clonal lineages circulating in Bolivia. We investigated the prevalence and molecular epidemiology of S. aureus colonization in hospitalized patients from the Bolivian Chaco, and compared their features with those of the few clinical isolates available from that setting. Methods S. aureus nasal/inguinal colonization was investigated in 280 inpatients from eight hospitals in two point prevalence surveys (2012, n =90; 2013, n =190). Molecular characterization included genotyping ( spa typing, multilocus sequence typing, and pulsed-field gel electrophoresis), detection of virulence genes, and SCC mec typing. Results Forty-one inpatients (14.6%) were S. aureus nasal/inguinal carriers, of whom five were colonized by MRSA (1.8%). MRSA isolates mostly belonged to spa- type t701, harboured SCC mec IVc, and were negative for Panton–Valentine leukocidin (PVL) genes. However, a USA300-related isolate was also detected, which showed the characteristics of the USA300 Latin American variant (USA300-LV; i.e., ST8, spa- type t008, SCC mec IVc, presence of PVL genes, absence of arc A). Notably, all the available MRSA clinical isolates ( n =5, collected during 2011–2013) were also identified as USA300-LV. Conclusions Overall, MRSA colonization in inpatients from the Bolivian Chaco was low. However, USA300-LV-related isolates were detected in colonization and infections, emphasizing the importance of implementing control measures to limit their further dissemination in this resource-limited area

Synergistic activity profile of an antimicrobial peptide against multidrug-resistant and extensively drug-resistant strains of Gram-negative bacterial pathogens

7noreservedInfection sustained by multidrug-resistant and extensively drug-resistant bacterial pathogens is often untreatable with the standard of care antibiotics, and the combination of anti-infective compounds often represents the only therapeutic strategy to face this major clinical treat. SET-M33 is a novel antimicrobial peptide (AMP) that has demonstrated in vitro and in vivo antimicrobial activity against Gram-negative bacteria and has shown interesting features in preclinical evaluations. Particularly, it showed efficacy against a number of multidrug-resistant and extensively drug-resistant clinical strains of Gram-negative pathogens, in in vitro and in vivo assessments. Here, we explored the potential synergistic activity of SET-M33 in combination with different standard of care antibiotics by the checkerboard method against a panel of six strains of Gram-negative pathogens including multidrug-resistant and extensively drug-resistant Klebsiella pneumoniae, Pseudomonas aeruginosa, and Acinetobacter baumannii. SET-M33 showed synergistic activity with antibiotics of different families against these clinically relevant strains. A synergistic effect was observed for SET-M33 in combination with rifampin, meropenem, aztreonam, and tobramycin mostly on K. pneumoniae and A. baumannii strains, while the SET-M33 plus ciprofloxacin combination was additive with all tested strains. Synergy was not apparently linked to the bacterial species or phenotype but was rather strain-specific, highlighting the need for individual strain testing for synergistic antimicrobial combinations. These findings extend current knowledge on synergistic activity of AMPs in combination with conventional agents and support the potential role of SET-M33 as a novel therapeutic agent against antibiotic-resistant Gram-negative pathogens.mixedPollini, Simona; Brunetti, Jlenia; Sennati, Samanta; Rossolini, Gian Maria; Bracci, Luisa; Pini, Alessandro; Falciani, ChiaraPollini, Simona; Brunetti, Jlenia; Sennati, Samanta; Rossolini, Gian Maria; Bracci, Luisa; Pini, Alessandro; Falciani, Chiar