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      Infección nosocomial II: Resistencia a ß-lactámicos y aminoglucósidos en Pseudomonas aeruginosa en centros médicos de Venezuela durante el año 2000 Translated title: Nosocomial infection II: Resistance to ß-lactams and aminoglycosides in Pseudomonas aeruginosa at the Venezuelan medical centres (2000)

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          Abstract

          Entre el 5 y el 10% de los pacientes que ingresan a hospitales de EE UU adquieren una o mas infecciones dentro del hospital. Una cuarta parte de esas infecciones nosocomiales están representadas por infecciones de la Unidad de Cuidados Intensivos (UCI). De estas últimas, el 70% son producidas por microorganismos resistentes a antimicrobianos; constituyendo este último, un problema de salud global por sí solo. El alto grado de resistencia por parte de estos microorganismos es una de las razones más relevantes que contribuyen a incrementar el número de muertes en los casos de infección nosocomial. Los bacilos Gram-negativos son los primeros responsables de infección nosocomial, y entre ellos P. aeruginosa es la primera en frecuencia. La división entre diferentes ecosistemas en el hospital refleja diferentes poblaciones con diferentes características. En este estudio presentamos comparaciones de los porcentajes de resistencia ante ß-lactámicos y aminoglicósidos en P. aeruginosa nosocomial (UCI y cirugía) y comunitaria (COM), en centros médicos de Venezuela, diferenciando los públicos (Hpu) de los privados (Hpri), para el año 2000. Se usó el método de difusión de disco, de acuerdo al NCCLS [National Committe for Clinical Laboratories Standards (Comité Nacional de Estándares para Laboratorios Clínicos)]. Se siguió el programa software WHONET (World Health Organization Net). Se incluyeron todas las cepas reportadas en los diferentes servicios. Se realizó la evaluación estadística por prueba Z (p≤ 0,05). 1. Se muestran diferencias significativas en la frecuencia de resistencia (fr) en P. aeruginosa nosocomial entre UCI/COM en Hpu (mayores diferencias: piperacilina, 44/8% y gentamicina, 39/10%), entre UCI/CI (la mayor ≠ piperac, 44/23% y la menor cefepime, 10/8%). 2. Hay diferencias significativas entre la frb de CI de Hpu/Hpri, siendo las mayores ≠ : piper, 23/15%; piper-tazob, 11/2%; tobra, 25/2%; netilm, 25/8%; genta, 37/22%. No se observaron diferencias significativas entre UCI de Hpu/Hpri. 3. No hubo diferencias en la frb ante Amg para P. aeruginosa entre UCI/Ci de Hpu, pero sí de Hpri (mayores ≠ : tobra, 40/1 y netilm, 40/9). 4. Tiene relevancia las diferencias observadas ante ß-L entre UCI/CI y entre éstos y la comunidad, tanto en Hpu como en Hpri. Estas observaciones ponen en evidencia la importancia del medio ambiente en la dinámica de la resistencia, y por tanto la necesidad de poner en práctica, y de rutina, medidas especiales de asepsia y antisepsia. Por otra parte, y debido a la gravedad y frecuencia tanto de las infecciones como de la resistencia producidas por P. aeruginosa en este medio ambiente, se impone el uso en estos pacientes de medidas farmacológicas especiales, para asegurar el éxito de la terapia antimicrobiana, tanto para curar la infección como para prevenir la aparición de cepas resistentes.

          Translated abstract

          Currently, between 5 and 10 percent of patients admitted to acute care hospitals acquire one or more infections in the hospital. A quarter of these nosocomial infections are originated in the intensive care unity (ICU), 20% of these are produced by antimicrobial agents resistant microorganisms; which is a global health problem by it self. This high degree of resistance is one of the reasons which contribute to increases the numbers of death by nosocomial infections. Gram-negative bacilli are the principals responsible of nosocomial infections, and among them, the first in frequency is P. aeruginosa. We compare the percentages of resistance to either ß-lactams or aminoglycosides in nosocomial (ICU and surgery=SU) and communitarian (Com) P. aeruginosa, at the Venezuelan Medical Centres, evaluating the differences between public (puC) and privates centres (priC) for the year 2000. It was used diffusion disk, according NCCLS. The software program WHONET was used. Statistical significance (p≤0,05-0,01) was determined by "Z". 1. We show significant differences in the frequency of resistance to ß-lactams (frb) in nosocomial P. aeruginosa from puC, between ICU/Com (major differences: piperacillin 44/ 8% and genta 39/ 10%), and between ICU/ Su (the major ≠ piperacillin 44/23%, and the minor ≠ cefepime 10/8%). 2. We observe a significant difference in frb, between puC and priC, in infections of patients from Su (majors ≠ : piper 23/15%, piper-tazob 11/2%, tobra 25/2%, netilm 25/8%, genta 37/22%, but not in those from ICU. 3. We did not found any difference in the P. aeruginosa resistant isolated to aminoglycosides between ICU and Su at the puC, but at the priC majors ≠ : tobra 40/1% and netilm 40/9%. 4. The differences in the fr to ß-lactams showed by P. aeruginosa infection are noteworthy between ICU and Su and between these and Com, either for puC or for priC. These observations support the implication of the environment, and specially the hospital environment in the dynamic of bacterial resistance, and then the necessity to take in account specials routine habit of asepsis and antisepsis measures. Moreover and due to the seriousness and high frequency, either for the infections or for the resistance produced by P. aeruginosa in this environment, demand the use in these patients, of specials pharmacological strategies; in order to ensure the success of the antimicrobial therapy, either to cure the infection or to prevent resistance

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          Most cited references55

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          Inactivation of antibiotics and the dissemination of resistance genes.

          J. Davies (1994)
          The emergence of multidrug-resistant bacteria is a phenomenon of concern to the clinician and the pharmaceutical industry, as it is the major cause of failure in the treatment of infectious diseases. The most common mechanism of resistance in pathogenic bacteria to antibiotics of the aminoglycoside, beta-lactam (penicillins and cephalosporins), and chloramphenicol types involves the enzymic inactivation of the antibiotic by hydrolysis or by formation of inactive derivatives. Such resistance determinants most probably were acquired by pathogenic bacteria from a pool of resistance genes in other microbial genera, including antibiotic-producing organisms. The resistance gene sequences were subsequently integrated by site-specific recombination into several classes of naturally occurring gene expression cassettes (typically "integrons") and disseminated within the microbial population by a variety of gene transfer mechanisms. Although bacterial conjugation once was believed to be restricted in host range, it now appears that this mechanism of transfer permits genetic exchange between many different bacterial genera in nature.
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            In the last several years, the frequency and spectrum of antimicrobial-resistant infections have increased in both the hospital and the community. Certain infections that are essentially untreatable have begun to occur as epidemics both in the developing world and in institutional settings in the United States. The increasing frequency of drug resistance has been attributed to combinations of microbial characteristics, selective pressures of antimicrobial use, and societal and technologic changes that enhance the transmission of drug-resistant organisms. Antimicrobial resistance is resulting in increased morbidity, mortality, and health-care costs. Prevention and control of these infections will require new antimicrobial agents, prudent use of existing agents, new vaccines, and enhanced public health efforts to reduce transmission.
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                Author and article information

                Journal
                rsvm
                Revista de la Sociedad Venezolana de Microbiología
                Rev. Soc. Ven. Microbiol.
                Organo Oficial de la Sociedad Venezolana de Microbiología. (Caracas, DF, Venezuela )
                1315-2556
                July 2003
                : 23
                : 2
                : 183-189
                Affiliations
                [02] Caracas orgnameUniversidad Central de Venezuela orgdiv1Escuela de Medicina J M Vargas Facultad de Medicina orgdiv2Catedra de Microbiologia Venezuela
                [01] Caracas orgnameUniversidad Central de Venezuela orgdiv1Escuela de Medicina J M Vargas Facultad de Medicina orgdiv2Catedra de Farmacologia Venezuela
                [03] Caracas orgnameUniversidad Central de Venezuela orgdiv1Servicio de Enfermedades Infecciosas y Microbiologia del Hospital J M Vargas Venezuela
                Article
                S1315-25562003000200016 S1315-2556(03)02300216
                5bfa77a1-a9fb-4037-8e76-d52321191edd

                http://creativecommons.org/licenses/by/4.0/

                History
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 39, Pages: 7
                Product

                SciELO Venezuela

                Categories
                Resistencia Bacteriana en Venezuela

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