Background Staphylococcus aureus is a common nasal colonizer in 20–30% of the general population. When mucosal and cutaneous barriers are disrupted, S. aureus can cause severe infections. While MRSA nasal carriers have an increased risk of infections when compared to non-carriers, prolonged exposure to the hospital environment may cause an increase in carriage of MRSA. Materials and methods A survey questionnaire was filled for analyzing risk factors of colonization. Swab isolates were identified as S. aureus by traditional microbiological assays. Antibiotic susceptibility profiles were performed following the CLSI standard guidelines. Multiplex PCR was conducted to determine the presence of genes mecA and lukS-PV/lukF-PV . Chi-squared, univariate, and multivariate logistic regressions were applied to find statistically significant associations between risk factors and the presence of S. aureus and MRSA. Results One hundred and eighty-six isolates were identified as S. aureus . The strains showed high resistance to penicillin, oxacillin, azithromycin, erythromycin, clindamycin (inducible), and tetracycline. The overall prevalence of MRSA in medical students was 45.9% [40.4–51.6] 95% CI. PCR showed a prevalence of mecA gene in MRSA isolates of 6.1% while lukS-PV/lukF-PV gene was present in 3.2% [1.2–6.9] 95% CI of the S. aureus samples. The risk factors frequency of antibiotic intake and repeated visits to hospitals demonstrated statistical significance. Conclusion S. aureus and MRSA isolates have a high prevalence of colonization, and antibiotic resistance in the population studied. MRSA resistance was not related to the presence of the mecA gene. The prevalence of PVL genes was low, but it could represent a risk because they are circulating in the community.

In tropical areas, the predominant cause of fever has historically been malaria. However by 2011, among febrile patients in northwestern Ecuador, dengue was identified in 42% and malaria in none. This finding suggests a transition in the cause of fever from malaria to other illnesses, such as dengue.

Dengue is a major vector-borne infection causing large outbreaks in urban communities in tropical regions. During the period 2010- 2014; 434 serum samples from febrile patients were collected from a  semi-rural community hospital located in the norwestern region of Ecuador. Dengue virus (DENV) was investigated by reverse transcriptase PCR; a total of 48 samples were positive for dengue. During our study we detected  DENV-2 and DENV-3 from 2010 to 2013 and the four  DENV  serotypes during the period 2013-2014.  Surprisingly, our results contrasted with surveys carried out in urban centers throughout the  Ecuadorian Coast in which  DENV-1, DENV-2 and DENV-4 were prevalent during years 2010-2013 and only 2 serotypes  (DENV-1 and DENV-2) in 2014.These results suggest  that dengue viruses in semi-rural communities didn’t  originate in the Ecuadorian cities.

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Background:The gut microbiota is a significant reservoir of antimicrobial resistance genes (ARGs). The use and misuse of antimicrobials can select multi-resistant bacteria and modify the repertoire of ARGs in the gut. Developing effective interventions to manipulate the intestinal resistome would allow us to modify the antimicrobial resistance risk. Materials and Methods:Applying shotgun metagenomics, we compared the composition of fecal resistome from individuals treated with triple therapy for Helicobacter pylori plus Saccharomyces boulardii CNCM-I 745 (Sb) versus triple antibiotherapy without S. boulardii (control) before, after, and one month after treatments. DNA samples were sequenced on an Illumina NovaSeq 6000 platform. Reads were trimmed and filtered for quality, and the reads classified as host genome were removed from further analysis. We used the ResFinder database for resistome analysis and the web-based tool ResistoXplorer and RStudio for graphical representation and statistical analysis. Results:We identified 641 unique ARGs in all fecal samples, conferring resistance to 18 classes of antibiotics. The most prevalent ARGs found in at least 90% of the samples before the treatments were against tetracyclines, MLS-B (macrolide, lincosamide, and streptogramin B), beta-lactams, and aminoglycosides. Differential abundance analysis allowed the identification of ARGs significantly different between treatment groups. Thus, immediately after the treatments, the abundance of ARGs that confer resistance to lincosamides, tetracyclines, MLS-B, and two genes in the beta-lactam class (cfxA2 and cfxA3) was significantly lower in the group that received Sb than in the control group (edgeR, FDR <0.05). Conclusion:Our study demonstrated that the addition of S. boulardii CNCM-I 745 to the conventional antibiotic eradication therapy for H. pylori reduced the abundance of ARGs, particularly those genes that confer resistance to lincosamides, tetracyclines, MLS-B, and a few genes in the beta-lactams class.

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type; QACs, quaternary 28 ammonium compounds; KL, K-locus; ybt, yersiniabactin; clb, colibactin; ICEKp, integrative conjugative 29 element K. pneumoniae; pLVPK, large virulence plasmid of K. pneumoniae; CPS, capsular 30 polysaccharides; MLST, multilocus sequence typing; YbSTs, yersiniabactin sequence types; CbSTs, 31 colibactin sequence types; CR-Kp, carbapenem-resistant K. pneumoniae; MIC, minimum inhibitory 32 concentration; ESBL, extended-spectrum beta-lactamase; HM, heavy metal; ML, maximum likelihood; 33 MDR, multidrug resistance; PDR, pandrug resistance; Inc, incompatibility; IS, insertion sequence; KPZM, 34 Zn2+/Mn2+metabolism module; QRDR, quinolone-resistance determining region; PMQR, plasmid-35 mediated quinolone resistance.36 2 Abstract 37 The emergence and dissemination of carbapenem-resistant hypervirulent Klebsiella 38 pneumoniae (CR-hvKp) is a worrisome public health issue compromising the treatment and 39 outcome of infections caused by this pathogen. We performed a detailed virulome and 40 resistome analysis of representative KPC-and/or CTX-M-producing K. pneumoniae 41 belonging to clonal group (CG) 258 (sequence types ST11, ST258, ST340, ST437), 42 circulating in Argentina, Brazil, Chile, Colombia and Peru; with further evaluation of the 43 virulence behavior using the Galleria mellonella infection model. Genomic analysis of K. 44 pneumoniae strains recovered from the human-animal-environment interface revealed a wide 45 resistome characterized by the presence of genes and mutations conferring resistance to 46 human and veterinary antibiotics, quaternary ammonium compounds (QACs) and heavy 47 metals. Plasmid Inc typing revealed the presence of a wide diversity of replicon types with 48 IncF, IncN, IncR and Col-like being frequently detected. Moreover, KPC-2-producing K. 49 pneumoniae belonging to ST11 (KL-64 andKL-105) and ST340 (KL-15) carried multiple 50 variants of distinct yersiniabactin siderophore (ybt) and/or genotoxic colibactin (clb) genes. In 51 this regard, ICEKp3, ICEKp4 and ICEKp12 were identified in strains belonging to ST11 and 52 ST340, recovered from Argentina, Brazil, Chile and Colombia; whereas ybt 17 and a novel 53 ybt sequence type (YbST346) were identified together with clb in ICEKp10 structures from 54 ST11 and ST258, from Brazil and Colombia, respectively. K. pneumoniae ST11 55 (ICEKp10/YbST346 and ICEKp4/ybt 10) strains killed 100% of wax moth larvae, in a similar 56 way to hypervirulent K1/ST23 strain (ybt-and clb-negative) carrying the pLVPK-like 57 plasmid, indicating enhanced virulence. In summary, our results indicate that yersiniabactin, 58 colibactin and an expanded resistome have contributed to enhanced virulence and persistence 59 of KPC-2-producing K. pneumoniae CG258 in South America. Therefore, active surveillance 60 of hospital-associated lineages of K. pneumoniae should not only focus on clonal origin and 61 antimicrobial resistance, but also on the virulence factors ybt and clb. 62 3 INTRODUCTION 63