Felipe Fernández-Cuenca

Hospital Universitario Virgen del Rocío, Hispalis, Andalusia, Spain

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Publications (59)172.23 Total impact

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    ABSTRACT: Acinetobacter baumannii is one of the most important antibiotic-resistant nosocomial bacteria. We investigated changes in the clinical and molecular epidemiology of A. baumannii over a 10-year period. We compared the data from 2 prospective multicenter cohort studies in Spain, one performed in 2000 (183 patients) and one in 2010 (246 patients), which included consecutive patients infected or colonized by A. baumannii. Molecular typing was performed by repetitive extragenic palindromic polymerase chain reaction (REP-PCR), pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST).The incidence density of A. baumannii colonization or infection increased significantly from 0.14 in 2000 to 0.52 in 2010 in medical services (p < 0.001). The number of non-nosocomial health care-associated cases increased from 1.2% to 14.2%, respectively (p < 0.001). Previous exposure to carbapenems increased in 2010 (16.9% in 2000 vs 27.3% in 2010, p = 0.03). The drugs most frequently used for definitive treatment of patients with infections were carbapenems in 2000 (45%) and colistin in 2010 (50.3%). There was molecular-typing evidence of an increase in the frequency of A. baumannii acquisition in non-intensive care unit wards in 2010 (7.6% in 2000 vs 19.2% in 2010, p = 0.01). By MSLT, the ST2 clonal group predominated and increased in 2010. This epidemic clonal group was more frequently resistant to imipenem and was associated with an increased risk of sepsis, although not with severe sepsis or mortality.Some significant changes were noted in the epidemiology of A. baumannii, which is increasingly affecting patients admitted to conventional wards and is also the cause of non-nosocomial health care-associated infections. Epidemic clones seem to combine antimicrobial resistance and the ability to spread, while maintaining their clinical virulence.
    Medicine. 07/2014; 93(5):202-210.
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    ABSTRACT: Introduction. Acinetobacter baumannii is one of the most important antibiotic-resistant, nosocomial bacteria. We investigated changes in the clinical and molecular epidemiology of A. baumannii over a 10 year period. Methods. We compared the data from two prospective multicenter cohort studies performed in 2000 (183 patients) and 2010 (246 patients) in Spain, which included consecutive patients infected or colonized by A. baumannii. Molecular typing was performed by REP-PCR, PFGE and MSLT. Results. The incidence density of A. baumannii colonization or infection increased significantly from 0.14 to 0.52 in medical services (p<0.001). The number of non-nosocomial healthcare-associated cases increased from 1.2% to 14.2% (p<0.001). Previous exposure to carbapenems increased in 2010 (16.9 vs 27.3%, p=0.03). The drugs most frequently used for definitive treatment of patients with infections were carbapenems in 2000 (45%) and colistin in 2010 (50.3%). There was molecular-typing evidence of an increase in the frequency of A. baumannii acquisition in non-intensive care unit (ICU) wards in 2010 (7.6% vs 19.2%, p=0.01). By MSLT, the ST2 clonal group predominated and increased in 2010. This epidemic clonal group was more frequently resistant to imipenem and was associated with an increased risk of sepsis, although not with severe sepsis or mortality. Conclusions. Some significant changes were noted in the epidemiology of A. baumannii, which is increasingly affecting patients admitted to conventional wards and is also the cause of non-nosocomial healthcare-associated infections. Epidemic clones seem to combine antimicrobial resistance and the ability to spread, while maintaining their clinical virulence.
    Medicine 02/2014; · 4.35 Impact Factor
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    ABSTRACT: We investigated the mechanisms of resistance to carbapenems, aminoglycosides, glycylcyclines, tetracyclines, and quinolones in 90 multiresistant clinical strains of Acinetobacter baumannii isolated from two genetically unrelated A. baumannii clones: clone PFGE-ROC-1 (53 strains producing the OXA-58 β-lactamase enzyme and 18 strains with the OXA-24 β-lactamase) and clone PFGE-HUI-1 (19 strains susceptible to carbapenems). We used real-time reverse transcriptase PCR to correlate antimicrobial resistance (MICs) with expression of genes encoding chromosomal β-lactamases (AmpC and OXA-51), porins (OmpA, CarO, Omp33, Dcap-like, OprB, Omp25, OprC, OprD, and OmpW), and proteins integral to six efflux systems (AdeABC, AdeIJK, AdeFGH, CraA, AbeM, and AmvA). Overexpression of the AdeABC system (level of expression relative to that by A. baumannii ATCC 17978, 30- to 45-fold) was significantly associated with resistance to tigecycline, minocycline, and gentamicin and other biological functions. However, hyperexpression of the AdeIJK efflux pump (level of expression relative to that by A. baumannii ATCC 17978, 8- to 10-fold) was significantly associated only with resistance to tigecycline and minocycline (to which the TetB efflux system also contributed). TetB and TetA(39) efflux pumps were detected in clinical strains and were associated with resistance to tetracyclines and doxycycline. The absence of the AdeABC system and the lack of expression of other mechanisms suggest that tigecycline-resistant strains of the PFGE-HUI-1 clone may be associated with a novel resistance-nodulation-cell efflux pump (decreased MICs in the presence of the inhibitor Phe-Arg β-naphthylamide dihydrochloride) and the TetA(39) system.
    Antimicrobial Agents and Chemotherapy 08/2013; 57(11):5247-57. · 4.57 Impact Factor
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    ABSTRACT: The fitness and virulence costs associated with the clinical acquisition of colistin resistance by Acinetobacter baumannii were evaluated. The growth of strain CR17 (colistin-resistant) was lower than the strain CS01 (colistin-susceptible) when grown in competition (72h competition index, 0.008). In a murine sepsis model, CS01 and CR17 reached spleen concentrations when co-infecting of 9.31 and 6.97 log10CFU/g, respectively, with an in vivo competition index of 0.016. Moreover, CS01 was more virulent than CR17 with respect to mortality and time to death.
    Antimicrobial Agents and Chemotherapy 07/2013; · 4.57 Impact Factor
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    Enfermedades Infecciosas y Microbiología Clínica 05/2013; 31(5):353. · 1.48 Impact Factor
  • Lorena López-Cerero, Felipe Fernández-Cuenca, Alvaro Pascual
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    ABSTRACT: The most relevant activities of clinical microbiologist and the laboratory in the surveillance and the control of nosocomial infections (NI) are mainly focused on the collection, analysis and management of the information obtained in the Microbiology Laboratory; the design, development and validation of microbiological techniques, particularly rapid tests for the early detection of nosocomial pathogens, especially those multi-drug resistant ones, and the study of the genetic relationship between them. It also assists in the design of specific programs for the prevention of the NI, and the evaluation of their impact, as well as taking part in educational and training programs on topics related to NI. The management of laboratory resources, and communications with hospital information systems is also important.The most suitable tools for the control of NI include the correct identification at the species level of relevant nosocomial pathogens, analysis of the evolution of resistance to antimicrobials, monitoring sentinel organisms, active surveillance of carriers, and molecular epidemiology studies (genotyping). Prospectively typing of these pathogens, which has been achieved through advances in technology, and dissemination of molecular techniques, have a direct impact on the design of prevention and control interventions. To achieve the maximum performance with all these tools, it is essential to have a good communication strategy and an effective alert system.
    Enfermedades Infecciosas y Microbiología Clínica 01/2013; 31(1):44–51. · 1.48 Impact Factor
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    ABSTRACT: Objectives To determine the prevalence of resistance to antimicrobials in Acinetobacter baumannii (A. baumannii) from Spain and to compare it with those obtained in the first national study (GEIH-Ab project 2000).MethodsA total of 446 isolates of A. baumannii obtained from 43 Spanish hospitals during February-March 2010 were studied. Identification of A. baumannii was confirmed by ARDRA and MALDI-TOF. Susceptibility to 18 antimicrobial agents was determined by microdilution (Clinical and Laboratory Standards Institute, CLSI). The CLSI break-points were used, except for doripenem, rifampin, sulbactam (Societé Française de Microbiologie [SFM] break-points) and tigecycline (European Committee on Antimicrobial Susceptibility Testing [EUCAST] break-points for Enterobacteriaceae).ResultsThe percentage of resistant isolates (intermediate susceptible plus resistant) was: > 94% (ceftazidime, piperacillin and ciprofloxacin), 82-86% (carbapenems, tetracycline), 60-70% (tobramycin, sulbactam, gentamicin, doxycycline), 49% (amikacin), 30% (minocycline, rifampin), 24% (tigecycline), and 3% (colistin). These isolates were, in comparison with those of the first study, more resistant (P < .01) to ceftazidime (99% vs 83%), carbapenems (82-86% vs 43-48%), sulbactam (65% vs 53%) and colistin (3% vs 0%), but more susceptible to aminoglycosides (particularly gentamicin: 70% vs 96% of resistant isolates), tetracycline (83% vs 91%) and rifampicin (30% vs 51%).Conclusion There is a high prevalence of A. baumannii resistant to antimicrobials, particularly to carbapenems. The resistance to carbapenems, ceftazidime and sulbactam was significantly higher than that observed for isolates from the GEIH-Ab project 2000. The resistance to aminoglycosides, tetracycline and rifampin, however, was significantly decreased.
    Enfermedades Infecciosas y Microbiología Clínica 01/2013; 31(1):4–9. · 1.48 Impact Factor
  • Lorena López-Cerero, Felipe Fernández-Cuenca, Alvaro Pascual
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    ABSTRACT: The most relevant activities of clinical microbiologist and the laboratory in the surveillance and the control of nosocomial infections (NI) are mainly focused on the collection, analysis and management of the information obtained in the Microbiology Laboratory; the design, development and validation of microbiological techniques, particularly rapid tests for the early detection of nosocomial pathogens, especially those multi-drug resistant ones, and the study of the genetic relationship between them. It also assists in the design of specific programs for the prevention of the NI, and the evaluation of their impact, as well as taking part in educational and training programs on topics related to NI. The management of laboratory resources, and communications with hospital information systems is also important. The most suitable tools for the control of NI include the correct identification at the species level of relevant nosocomial pathogens, analysis of the evolution of resistance to antimicrobials, monitoring sentinel organisms, active surveillance of carriers, and molecular epidemiology studies (genotyping). Prospectively typing of these pathogens, which has been achieved through advances in technology, and dissemination of molecular techniques, have a direct impact on the design of prevention and control interventions. To achieve the maximum performance with all these tools, it is essential to have a good communication strategy and an effective alert system.
    Enfermedades Infecciosas y Microbiología Clínica 12/2012; · 1.48 Impact Factor
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    ABSTRACT: BACKGROUND: To describe the long term outcome of patients who interrupted highly active antiretroviral therapy (HAART) once, identify the variables associated with earlier need to re-start HAART, and the response when therapy was resumed. A retrospective observational cohort of 66 adult patients with HIV-1 infection who interrupted HAART with a CD4+cell count >=350 cells/muL and undetectable viral load (VL) was performed. The pre-established CD4+ cell count for restarting therapy was 300cells/muL. Cox regression was used to analyse the variables associated with earlier HAART reinitiation. RESULTS: The median follow-up was 209 weeks (range, 64--395). Rates of HIV-related or possible HIV-related events were 0.37 (one case of acute retroviral syndrome) and 1.49 per 100 patient-years, respectively. Two patients died after re-starting therapy and having reached undetectable VL. Three patients suffered a sexually transmitted disease while off therapy. Fifty patients (76%) resumed therapy after a median of 97 weeks (range, 17--267). Age, a nadir of CD4+ <250 cells/muL, and a mean VL during interruption of >10,000 copies/ml were independent predictors for earlier re-start. The intention-to-treat success rate of the first HAART resumed regimen was 85.4%. There were no differences by regimen used, nor between regimens that were the same as or different from the one that had been interrupted. CONCLUSIONS: Our data suggest that the highly active antiretroviral therapy may be interrupted in selected patients. Because in these patients, when the HAART is restarted, the viral and clinical response may be achieved.
    BMC Research Notes 10/2012; 5(1):578.
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    ABSTRACT: A carbapenem-resistant Acinetobacter baumannii clinical isolate belonging to the European clone II and ST2 was recovered from a patient in the Son Espases hospital in Mallorca, Spain. Genetic analysis showed the presence of the bla(OXA-23) gene in association with the widely disseminated transposon Tn2006. This is the first reported identification of A. baumannii carrying bla(OXA-23) in Spain.
    Antimicrobial Agents and Chemotherapy 10/2012; · 4.57 Impact Factor
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    ABSTRACT: OBJECTIVES: The aims of this study were to analyse the presence of oqxA and oqxB genes in a collection of extended-spectrum β-lactamase (ESBL)-producing Klebsiella pneumoniae strains, to determine their chromosomal and/or plasmidic locations and to analyse expression levels in relation to susceptibility or resistance to quinolones. METHODS: A collection of 114 non-repetitive isolates of ESBL-producing K. pneumoniae was used. K. pneumoniae ATCC 27799 and K. pneumoniae ATCC 700603 were also included. Detection of oqxA and oqxB genes was performed by PCR. Testing for chromosomal and/or plasmidic location was carried out using plasmid DNA and subsequent hybridization. oqxA gene expression was analysed using real-time RT-PCR. Transfer of the plasmid-encoded OqxAB was evaluated. RESULTS: The prevalence of both oqxA and oqxB detected in K. pneumoniae was high: 76% and 75%, respectively. Hybridization assays showed that oqxA (16%) and oqxB (13%) were simultaneously present in locations on the chromosome and on large plasmids. The plasmids were transferable by transformation into K. pneumoniae. RT-PCR assays showed higher expression (4-fold) in strains with reduced susceptibility to quinolones than in susceptible strains. Interestingly, K. pneumoniae ATCC 700603 showed an 18-fold higher expression than K. pneumoniae ATCC 27799. These differences were in accordance with quinolone susceptibility. CONCLUSIONS: The prevalence of the OqxAB efflux pump (both chromosomal and plasmid encoded) in ESBL-producing K. pneumoniae is high in Spain and represents a potential reservoir for the spread of these genes. High expression of this pump contributes to reduced susceptibility to quinolones in clinical isolates of ESBL-producing K. pneumoniae.
    Journal of Antimicrobial Chemotherapy 09/2012; · 5.34 Impact Factor
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    ABSTRACT: OBJECTIVES: To determine the prevalence of resistance to antimicrobials in Acinetobacter baumannii (A. baumannii) from Spain and to compare it with those obtained in the first national study (GEIH-Ab project 2000). METHODS: A total of 446 isolates of A. baumannii obtained from 43 Spanish hospitals during February-March 2010 were studied. Identification of A. baumannii was confirmed by ARDRA and MALDI-TOF. Susceptibility to 18 antimicrobial agents was determined by microdilution (Clinical and Laboratory Standards Institute, CLSI). The CLSI break-points were used, except for doripenem, rifampin, sulbactam (Societé Française de Microbiologie [SFM] break-points) and tigecycline (European Committee on Antimicrobial Susceptibility Testing [EUCAST] break-points for Enterobacteriaceae). RESULTS: The percentage of resistant isolates (intermediate susceptible plus resistant) was: > 94% (ceftazidime, piperacillin and ciprofloxacin), 82-86% (carbapenems, tetracycline), 60-70% (tobramycin, sulbactam, gentamicin, doxycycline), 49% (amikacin), 30% (minocycline, rifampin), 24% (tigecycline), and 3% (colistin). These isolates were, in comparison with those of the first study, more resistant (P < .01) to ceftazidime (99% vs 83%), carbapenems (82-86% vs 43-48%), sulbactam (65% vs 53%) and colistin (3% vs 0%), but more susceptible to aminoglycosides (particularly gentamicin: 70% vs 96% of resistant isolates), tetracycline (83% vs 91%) and rifampicin (30% vs 51%). CONCLUSION: There is a high prevalence of A. baumannii resistant to antimicrobials, particularly to carbapenems. The resistance to carbapenems, ceftazidime and sulbactam was significantly higher than that observed for isolates from the GEIH-Ab project 2000. The resistance to aminoglycosides, tetracycline and rifampin, however, was significantly decreased.
    Enfermedades Infecciosas y Microbiología Clínica 08/2012; · 1.48 Impact Factor
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    ABSTRACT: The objective of this study was to identify risk factors for the acquisition of Acinetobacter baumannii with phenotypic heterogeneous resistance (PHR) to carbapenems and to determine whether these factors are similar to those associated with A. baumannii not showing this phenotype. Microbiological and clinical data from 211 patients included in the GEIH-Ab 2000 project were used. Isolates of A. baumannii were studied for their susceptibility to imipenem (IPM) by microdilution and for PHR to IPM as determined by the presence of colonies growing within the inhibition zone of IPM disks. Isolates were divided into three groups: (i) IPM-PHR isolates, i.e. susceptible and non-susceptible A. baumannii displaying PHR to IPM; (ii) non-IPM-PHR isolates, i.e. susceptible A. baumannii showing an inhibition halo but no colonies growing within it; and (iii) IPM-FR isolates, i.e. fully resistant A. baumannii displaying no halo of inhibition. IPM-PHR isolates of A. baumannii were more commonly isolated from respiratory tract samples and less commonly from urine, and were more frequently causes of infection than were IPM-FR isolates. Independent risk factors identified in patients with IPM-PHR isolates were Intensive Care Unit admission, surgery, and previous use of piperacillin/tazobactam or carbapenems, whilst risk factors for IPM-FR and IPM-PHR were previous use of cephalosporins and isolation from a urine sample. In conclusion, risk factors associated with colonisation/infection by isolates of A. baumannii with PHR to carbapenems are similar to those previously described for isolates resistant to carbapenems.
    International journal of antimicrobial agents 07/2012; 40(3):235-8. · 3.03 Impact Factor
  • International journal of antimicrobial agents 01/2012; 39(1):93-4. · 3.03 Impact Factor
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    ABSTRACT: Extended-spectrum AmpC cephalosporinases (ESACs) have been reported in Enterobacteriaceae, Pseudomonas aeruginosa and Acinetobacter baumannii. Here, we characterize a new AmpC variant presenting a broadened substrate activity towards fourth-generation cephalosporins, selected in vivo following cefepime treatment for Enterobacter aerogenes. Two consecutive clonally related isolates of E. aerogenes were evaluated. Screening for ESAC production was performed using plates containing 200 mg/L cloxacillin. MICs were determined by microdilution (CLSI guidelines). bla(AmpC) genes were cloned into a pCR-Blunt II-TOPO vector and expressed in Escherichia coli. The ampC genes were cloned into vector pGEX-6P-1 for protein purification. Isolate Ea595 was resistant to two fourth-generation cephalosporins, cefepime and cefpirome; using plates containing cloxacillin, susceptibility to ceftazidime and cefepime was restored, suggesting overproduction of the ESAC β-lactamase. Sequencing identified a new AmpC β-lactamase variant presenting one amino acid substitution, Val291Gly, inside the H-10 helix. Recombinant plasmids harbouring this ESAC β-lactamase conferred a broadened resistance profile to cefepime and cefpirome, with resistance levels increasing from 16- to 32-fold in E. coli. AmpC-Ea595 hydrolysed ceftazidime, cefepime and cefpirome at high levels, presenting a lower K(m) and enabling us to classify the enzyme as an ESAC. Homology modelling suggested that the size of the active site could have increased. We characterized an ESAC β-lactamase selected in vivo and conferring a high level of resistance to fourth-generation cephalosporins in E. aerogenes. The broadened spectrum was caused by a new modification to the H-10 helix, which modified the active site.
    Journal of Antimicrobial Chemotherapy 01/2012; 67(1):64-8. · 5.34 Impact Factor
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    ABSTRACT: Optimizing treatment for patients with persistent low-level viremia is complicated because most genotyping tests are validated for viral loads >1000 copies per milliliter. In this study, genotypes of 92 treatment-experienced patients with persistent low-level viremia were determined using an in-house assay. Based on the resistance profiles obtained from genotyping and patient pharmacologic history, patients were either maintained on their antiviral regimen (n = 51) or received an optimized regimen (n = 41). In the group receiving optimized treatment, undetectable viral loads were achieved in 73.2% at 6 months and at 90.2% at 1 year, indicating that treatment guided by genotyping of patients with low-level viremia is effective in achieving viral suppression.
    JAIDS Journal of Acquired Immune Deficiency Syndromes 09/2011; 58(5):446-9. · 4.65 Impact Factor
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    ABSTRACT: There is limited information on the role of penicillin-binding proteins (PBPs) in the resistance of Acinetobacter baumannii to β-lactams. This study presents an analysis of the allelic variations of PBP genes in A. baumannii isolates. Twenty-six A. baumannii clinical isolates (susceptible or resistant to carbapenems) from three teaching hospitals in Spain were included. The antimicrobial susceptibility profile, clonal pattern, and genomic species identification were also evaluated. Based on the six complete genomes of A. baumannii, the PBP genes were identified, and primers were designed for each gene. The nucleotide sequences of the genes identified that encode PBPs and the corresponding amino acid sequences were compared with those of ATCC 17978. Seven PBP genes and one monofunctional transglycosylase (MGT) gene were identified in the six genomes, encoding (i) four high-molecular-mass proteins (two of class A, PBP1a [ponA] and PBP1b [mrcB], and two of class B, PBP2 [pbpA or mrdA] and PBP3 [ftsI]), (ii) three low-molecular-mass proteins (two of type 5, PBP5/6 [dacC] and PBP6b [dacD], and one of type 7 (PBP7/8 [pbpG]), and (iii) a monofunctional enzyme (MtgA [mtgA]). Hot spot mutation regions were observed, although most of the allelic changes found translated into silent mutations. The amino acid consensus sequences corresponding to the PBP genes in the genomes and the clinical isolates were highly conserved. The changes found in amino acid sequences were associated with concrete clonal patterns but were not directly related to susceptibility or resistance to β-lactams. An insertion sequence disrupting the gene encoding PBP6b was identified in an endemic carbapenem-resistant clone in one of the participant hospitals.
    Antimicrobial Agents and Chemotherapy 09/2011; 55(12):5907-13. · 4.57 Impact Factor
  • International journal of antimicrobial agents 09/2011; 38(6):548-9. · 3.03 Impact Factor
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    ABSTRACT: Most of the non-B HIV-1 subtypes are predominant in Sub-Saharan Africa and India although they have been found worldwide. In the last decade, immigration from these areas has increased considerably in Spain. The objective of this study was to evaluate the prevalence of non-B subtypes circulating in a cohort of HIV-1-infected immigrants in Seville, Southern Spain and to identify drug resistance-associated mutations. Complete protease and first 220 codons of the reverse transcriptase coding regions were amplified and sequenced by population sequencing. HIV-1 subtypes were determined using Stanford University Drug Resistance Database, and phylogenetic analysis was performed comparing multiple reported sequences. Drug resistance mutations were defined according to the International AIDS Society-USA. From 2000 to 2010 a total of 1,089 newly diagnosed HIV-1-infected patients were enrolled in our cohort. Of these, 121 were immigrants, of which 98 had ethical approval and informed consent to include in our study. Twenty-nine immigrants (29/98, 29.6%) were infected with non-B subtypes, of which 15/29 (51.7%) were CRF02-AG, mostly from Sub-Saharan Africa, and 2/29 (6.9%) were CRF01-AE from Eastern Europe. A, C, F, J and G subtypes from Eastern Europe, Central-South America and Sub-Saharan Africa were also present. Some others harboured recombinant forms CRF02-AG/CRF01-AE, CRF2-AG/G and F/B, B/C, and K/G, in PR and RT-coding regions. Patients infected with non-B subtypes showed a high frequency of minor protease inhibitor resistance mutations, M36I, L63P, and K20R/I. Only one patient, CRF02_AG, showed major resistance mutation L90M. Major RT inhibitor resistance mutations K70R and A98G were present in one patient with subtype G, L100I in one patient with CRF01_AE, and K103N in another patient with CRF01_AE. Three patients had other mutations such as V118I, E138A and V90I. The circulation of non-B subtypes has significantly increased in Southern Spain during the last decade, with 29.6% prevalence, in association with demographic changes among immigrants. This could be an issue in the treatment and management of these patients. Resistance mutations have been detected in these patients with a prevalence of 7% among treatment-naïve patients compared with the 21% detected among patients under HAART or during treatment interruption.
    Virology Journal 08/2011; 8:416. · 2.09 Impact Factor
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    ABSTRACT: Detecting resistance in gram-negative microorganisms has a strong clinical and epidemiological impact, but there is still a great deal of debate about the most sensitive phenotypic method and whether in vitro susceptibility results should be interpreted. The present work reviews the phenotypes and mechanisms of resistance to beta-lactams, quinolones and aminoglycosides in gram-negative bacilli and also revises the different phenotypic methods used for their detection. A clinical interpretation of in vitro susceptibility results is also discussed. Extended-spectrum and inhibitor resistant beta-lactamases, AmpC type beta-lactamases and carbapenemases are thoroughly reviewed. As regards quinolones, the resistance mediated both by plasmids and by mutations in the DNA gyrase and the topoisomerase IV genes is also reviewed. This report includes resistance patterns to aminoglycosides caused by modifying enzymes. Phenotypic detection of beta-lactam resistance in Neisseria spp. and Haemophilus influenzae is also reviewed in a separate section.
    Enfermedades Infecciosas y Microbiología Clínica 06/2011; 29(7):524-34. · 1.48 Impact Factor

Publication Stats

615 Citations
172.23 Total Impact Points

Institutions

  • 2010–2013
    • Hospital Universitario Virgen del Rocío
      • • Infectious Diseases Service
      • • Servicio de Enfermedades Infecciosas
      Hispalis, Andalusia, Spain
  • 2004–2013
    • Universidad de Sevilla
      • • Departamento de Microbiología
      • • Departamento de Medicina
      Hispalis, Andalusia, Spain
    • Hospital Universitario Virgen Macarena
      Hispalis, Andalusia, Spain
  • 2004–2012
    • Hospital Clínic de Barcelona
      • Servicio de Microbiología
      Barcino, Catalonia, Spain
  • 2011
    • Centro De Biología Molecular Severo Ochoa
      Madrid, Madrid, Spain
    • Universidad de Cantabria
      • Department of Molecular Biology
      Santander, Cantabria, Spain
  • 2006
    • University of Barcelona
      • Departament de Microbiologia
      Barcelona, Catalonia, Spain
    • Leiden University Medical Centre
      • Department of Infectious Diseases
      Leyden, South Holland, Netherlands