Buscar en
Enfermedades Infecciosas y Microbiología Clínica
Toda la web
Inicio Enfermedades Infecciosas y Microbiología Clínica Lectura interpretada del antibiograma de bacilos gramnegativos no fermentadores
Journal Information
Vol. 20. Issue 6.
Pages 304-312 (June 2002)
Share
Share
Download PDF
More article options
Vol. 20. Issue 6.
Pages 304-312 (June 2002)
Full text access
Lectura interpretada del antibiograma de bacilos gramnegativos no fermentadores
Interpretative reading of the non-fermenting Gram-negative bacilli antibiogram
Visits
12570
Jordi Vila1
Corresponding author
jvilaestape@yahoo.com

Dr. J. Vila. Servicio de Microbiología. Institut d’Infeccions i Immunologia. Hospital Clínic i Provincial. Barcelona. España. Villarroel, 187. 0000 Barcelona. España.
, Francesc Marco
Servicio de Microbiología. Institut d’Infeccions i Immunologia. Hospital Clínic i Provincial. Barcelona. España
This item has received
Article information

Las tres especies de bacilos gramnegativos no fermentadores más relevantes clínicamente, Pseudomonas aeruginosa, Acinetobacter baumannii y Stenotrophomonas maltophilia son, frecuentemente, multirresistentes. La resistencia de P. aeruginosa a los betalactámicos depende de la producción de betalactamasa cromosómica, de betalactamasas plasmídicas, de alteraciones de la permeabilidad (pérdida de la porina OprD, relacionada con la resistencia a carbapenemas), y de bombas de expulsión activa, en especial MexAB-OprM. En las cepas resistentes a aminoglucósidos, la principal causa es la producción de enzimas inactivantes; también está implicada la bomba de expulsión MexXY-OprM. La resistencia a quinolonas en P. aeruginosa se relaciona con alteraciones de las topoisomerasas, alteraciones de las porinas y bombas de expulsión activa. Los mecanismos de resistencia de A. baumannii no se conocen adecuadamente, lo que dificulta la lectura interpretada del antibiograma en esta especie. La resistencia a betalactámicos se relaciona con la producción de betalactamasas y con alteraciones en proteínas fijadoras de penicilinas. La resistencia a aminoglucósidos se ha relacionado con enzimas modificantes y la resistencia a quinolonas con alteraciones de las dianas. S. maltophilia presenta resistencia natural a carbapenemas y otros betalactámicos por producción de dos betalactamasas (L-1 y L-2). También en esta especie se han descrito enzimas modificantes de aminoglucósidos. A diferencia de lo observado en otros muchos organismos, la resistencia de S. maltophilia a quinolonas se relaciona más con bombas de expulsión que con alteraciones de la diana.

Palabras clave:
Pseudomonas aeruginosa
Acinetobacter baumannii
Stenotrophomonas maltophilia
Determinación de la sensibilidad
Resistencia

Among non-fermenting Gram-negative rods, the most clinically important species are Pseudomonas aeruginosa, Acinetobacter baumannii, and Stenotrophomonas maltophilia, which are frequently multiresistant. P. aeruginosa resistance to beta-lactams depends on the production of chromosomal and plasmid-mediated beta-lactamases, altered permeability (loss of OprD porin is related to carbapenem-resistance) and active efflux pumps, particularly MexAB-OprM. In aminoglycoside-resistant strains the main mechanism of resistance is the production of inactivating enzymes; the efflux pump MexXY-OprM is also involved. Quinolone-resistance in P. aeruginosa is related to changes in topoisomerases, altered permeability and efflux pumps. The mechanisms of resistance of A. baumannii have not been well characterized, which makes interpretative reading of the antibiogram in this organism difficult. Resistance to beta-lactams is associated with the production of beta-lactamases and altered penicillin-binding proteins. Resistance to aminoglycosides has been related to modifying enzymes and resistance to quinolones to altered targets. S. maltophilia is resistant to carbapenems and other beta-lactams because of the production of two beta-lactamases (L-1 and L-2). Aminoglycoside-modifying enzymes have also been described in this species. In contrast to what is observed in other organisms, S. maltophilia resistance to quinolones has been mainly related to active efflux, rather than to target alterations.

Key words:
Pseudomonas aeruginosa
Acinetobacter baumannii
Stenotrophomonas maltophilia
Susceptibility testing
Resistance
Full text is only aviable in PDF
Bibliografía
[1.]
K. Poole.
Multidrug efflux pumps and antimicrobial resistance in Pseudomonas aeruginosa and related organisms.
J Mol Microbiol Biotechnol, 3 (2001), pp. 255-264
[2.]
D.M. Livermore.
β-lactamases in laboratory and clinical resistance.
Clin Microbiol Rev, 8 (1995), pp. 557-584
[3.]
H. Vahaboglu, R. Ozturk, G. Aygun.
Widespread detection of PER-1-type extended-spectrum β-lactamases among nosocomial Acinetobacter and Pseudomonas aeruginosa isolates in Turkey: A nationwide multicenter study.
Antimicrob Agents Chemother, 41 (1997), pp. 2265-2269
[4.]
T. Naas, P. Nordmann.
OXA-type β-lactamases.
Curr Pharm Des, 5 (1999), pp. 865-889
[5.]
K. Senda, Y. Arakawa, K. Nakashima.
Multifocal outbreaks of metallo-β-lactamases-producing Pseudomonas aeruginosa resistant to broad-spectrum β-lactams, including carbapenems.
Antimicrob Agents Chemother, 40 (1996), pp. 349-353
[6.]
A.P. Gibb, C. Tribuddharat, R.C. Moore.
Nosocomial outbreaks of carbapenem- resistant Pseudomonas aeruginosa with a new blaIMP allele, blaIMP-7.
Antimicrob Agents Chemother, 46 (2002), pp. 255-258
[7.]
L. Lauretti, M.L. Riccio, A. Mazzariol.
Cloning and characterization of blaVIM, a new integrin-borne metallo-β-lactamase gene from a Pseudomonas aeruginosa clinical isolate.
Antimicrob Agents Chemother, 43 (1999), pp. 1584-1590
[8.]
D.M. Livermore, N. Woodford.
Carbapenemases: A problem in waiting?.
Curr Opin Microbiol, 3 (2000), pp. 489-495
[9.]
G. Prats, E. Miró, B. Mirelis, L. Poirel, S. Bellais, P. Nordmann.
First isolation of a carbapenem-hydrolyzing β-lactamase in Pseudomonas aeruginosa in Spain.
Antimicrob Agents Chemother, 46 (2002), pp. 932-933
[10.]
A.E. Studemeister, J.P. Quinn.
Selective imipenem resistance in Pseudomonas aeruginosa associated with diminished outer membrane permebility.
Antimicrob Agents Chemother, 32 (1988), pp. 1267-1268
[11.]
N. Msuda, E. Sakagawa, S. Ohya, N. Gotoh, H. Tsujimoto, T. Nishino.
Substrate specifities of MexAB-OprM, MexCD-OprJ, and MexXY-OprM efflux pumps in Pseudomonas aeruginosa.
Antimicrob Agents Chemother, 44 (2000), pp. 3322-3327
[12.]
M.M. Ochs, M.P. McCusker, M. Bains, R.E. Hancock.
Negative regulation of the Pseudomonas aeruginosa outer membrane porin OprD selective for imipenem and basic aminoacids.
Antimicrob Agents Chemother, 43 (1999), pp. 1085-1090
[13.]
G.H. Miller, F.J. Sabatelli, R.S. Hare.
The most frequent aminoglycoside resistance mechanisms changes with time and geographic area: A reflection of aminoglycoside usage patterns?.
Clin Infect Dis, 24 (1997), pp. 46-62
[14.]
M. Nakano, T. Deguchi, T. Kavamura.
Mutations in the gyrA and parC genes in fluoroquinolone-resistant clinically isolates of Pseudomonas aeruginosa.
Antimicrob Agents Chemother, 41 (1997), pp. 2289-2291
[15.]
S. Jalal, B. Wretlind.
Mechanisms of quinolone resistance in clinical strains of Pseudomonas aeruginosa.
Microb Drug Resist, 4 (1998), pp. 257-261
[16.]
J. Vila.
Mechanisms of antimicrobial resistance in Acinetobacter baumannii.
Rev Med Microbiol, 9 (1998), pp. 87-97
[17.]
J. Vila, A. Ribera, F. Marco, J. Ruiz, J. Mensa, J. Chaves, G. Hernandez, M.T. Jimenez de Anta.
Activity of clinafloxacin, compared with six other quinolones, against Acinetobacter baumannii clinical isolates.
J Antimicrob Chemother, 49 (2002), pp. 471-477
[18.]
A. Ribera, J. Ruiz, M.T. Jimenez de Anta, J. Vila.
Effect of an efflux pump inhibitor on the MIC of nalidixic acid for Acinetobacter baumannii and Stenotrophomonas maltophilia clinical isolates.
J Antimicrob Chemother, 49 (2002), pp. 697-702
[19.]
G. Bou, J. Martinez-Beltrán.
Cloning, nucleotide sequencing and analysis of the gene encoding an AmpC beta-lactamase in Acinetobacter baumannii.
Antimicrob Agents Chemother, 44 (2000), pp. 428-432
[20.]
Danes C, Navia MM, Ruiz J, Marco F, Jurado A, Jimenez de Anta MT, Vila J. Distribution of beta-lactamases in Acinetobacter baumannii clinical isolates and the effect of Syn 2190 (AmpC inhibitor) in the MICs of different beta-lactam antibiotics [en prensa]. J Antimicrob Chemother 2002.
[21.]
Navia MM, Ruiz J, Vila J. Characterization of an integron carrying a new class D -lactamase (OXA-37) in Acinetobacter baumannii [en prensa]. Microb Drug Resist 2002.
[22.]
H.M. Donald, W. Scaife, S.G.B. Amyes, H.K. Young.
Sequence analysis of ARI-1, a novel OXA β -lactamase, responsible for imipenem resistance in Acinetobacter baumannii 6B92.
Anrimicrob Agents Chemother, 44 (2000), pp. 196-199
[23.]
G. Bou, A. Oliver, J. Martínez-Beltran.
A novel class D β-lactamase (OXA-24) with carbapenemase activity in an Acinetobacter baumannii clinical strain.
Antimicrob Agents Chemother, 44 (2000), pp. 1556-1561
[24.]
M. Afzal-Shah, N. Woodford, D.M. Livermore.
Characterization of OXA-25, OXA-26 and OXA-27, molecular class D β -lactamases associated with carbapenem resistance in clinical isolates of Acinetobacter baumannii.
Antimicrob Agents Chemother, 45 (2000), pp. 583-588
[25.]
M.L. Riccio, N. Franceschini, L. Boschi, B. Carravelli, G. Cornaglia, R. Fontana.
Characterization of the metallo-β -lactamase determinant of Acinetobacter baumannii AC-54/97 reveals the existence of blaIMP allelic variants carried by gene cassettes of different phylogeny.
Antimicrob Agents Chemother, 44 (2000), pp. 1229-1235
[26.]
Y.W. Chu, M. Afzal-Shah, E.T. Houang, M.F. Palepou, D.J. Lyon, N. Woodford.
IMP-4, a novel metallo-β-lactamase from nosocomial Acinetobacter spp. collected in Hong Kong between 1994 and 1998.
Antimicrob Agents Chemother, 45 (2001), pp. 710-714
[27.]
Fernández-Cuenca F. Mecanismos de resistencia a carbapenemas en cepas clínicas de Acinetobacter baumannii [tesis]. Universidad de Sevilla 2001.
[28.]
J. Vila, J. Ruiz, M.M. Navia.
Spread of amikacin resistance in Acinetobacter baumannii strains isolated in Spain due to an epidemic strain.
J Clin Microbiol, 37 (1999), pp. 758-761
[29.]
S. Magnet, P. Courvalin, T. Lambert.
Resistance-Nodulation-Cell Division-type efflux pump involved in aminoglycoside resistance in Acinetobacter baumannii strain BM4454.
Antimicrob Agents Chemother, 45 (2001), pp. 3375-3380
[30.]
J. Vila, J. Ruiz, P. Goñi, M.T. Jimenez de Anta.
Mutation in the gyrA gene of quinolone-resistant clinical isolates of Acinetobacter baumannii.
Antimicrob Agents Chemother, 39 (1995), pp. 1201-1203
[31.]
J. Vila, J. Ruiz, P. Goñi, M.T. Jimenez de Anta.
Quinolone resistance in the topoisomerase IV parC gene of Acinetobacter baumannii.
J Antimicrob Chemother, 39 (1997), pp. 757-762
[32.]
M. Denton, K.G. Kerr.
Microbiological and clinical aspects of infection associated with Stenotrophomonas maltophilia.
Clin Microb Rev, 11 (1998), pp. 57-80
[33.]
L. Zhang, X.Z. Li, K. Poole.
Multiple antibiotic resistance in Stenotrophomonas maltophilia: Involvement of a multidrug efflux system.
Antimicrob Agents Chemother, 44 (2000), pp. 287-293
[34.]
Ribera A, Domenech-Sánchez A, Ruiz J, Benedí VJ, Jimenez de Anta MT, Vila J. Mutations in gyrA and parC QRDRs are not relevant for quinolone resistance in epdiemiological unrelated Stenotrophomonas maltophilia clinical isolates [en prensa]. Microbial Drug Resistance 2002.
[35.]
S. Valdezate, A. Vindel, A. Echeita, F. Baquero, R. Cantón.
Topoisomerase II and IV quinolone resistance-determining regions in Stenotrophomonas maltophilia clinical isolates with different levels of quinolone susceptibility.
Antimicrob Agents Chemother, 46 (2002), pp. 665-671
[36.]
A. Ribera, A. Jurado, J. Ruiz, F. Marco, O. Del Valle, J. Mensa.
In vitro activity of clinafloxacin in comparison with other quinolones against Stenotrophomonas maltophilia clinical isolates in the presence and abscence of reserpine.
Diag Microbiol Infect Dis, 42 (2002), pp. 123-128
[37.]
S. Valdezate, A. Vindel, E. Loza, F. Baquero, R. Cantón.
Antimicrobial susceptibilities of unique Stenotrophomonas maltophilia clinical strains.
Antimicrob Agents Chemother, 45 (2001), pp. 1581-1584
Copyright © 2002. Elsevier España, S.L.. Todos los derechos reservados
Article options
Tools
es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos