Gentamicin-resistantPseudomonas aeruginosa: Concepts regarding their evolution and attenuated virulence
J M Janda1, D J Sheehan, A Das
1Department of Microbiology, The Mount Sinai Hospital, One Gustave L. Levy Place, 10029, New York, New York, USA.
Abstract:
Pseudomonas aeruginosa, a free-living bacterial species, is a major nosocomial pathogen, especially of compromised patients within medical facilities. Numerous factors contribute to the ecological selection of this bacterial species within the hospital environment, among which the expression of newly acquired or quiescent enzymatic capability seems par-amount. The emergence of pathogenic strains ofP. aeruginosa appears to be gradual, embodying a transition of strains from their natural aquatic environment, to establishing inanimate (hospital) and animate (human) reservoirs. In this stepwise transition, subsets ofP. aeruginosa may evolve which express a survival trait, for example, gentamicin resistance, but concomitantly suffer a loss of invasive potential. In this study,P. aeruginosa strains from natural [22], hospital [11], and stool [17] sources were evaluated for their physiological and exoenzymatic activity and compared with gentamicin-resistantP. aeruginosa (GRPA) strains [49] of clinical origin. As a whole, environmental and hospital isolates showed reduced enzymatic potential, for example, frequency of production of elastase, lipase, deoxyribonuclease, and pyocyanin production. Human fecal isolates most closely resembled the prototype of human invasiveP. aeruginosa in their gentamicin susceptibility (95%) and increased frequencies of exoenzymes, including elastase production. On the other hand, GRPA were frequently apyocyanogenic (9/49), lacked extracellular enzymes correlated with pathogenicity, and were rarely isolated from systemic sites. When encountered, these strains appeared to represent colonization of a body site rather than incitants of overt infection. As a "subset" ofP. aeruginosa, gentamicin resistance was seen predominantly among serotype 11 strains, and encountered most frequently from patients with localized urinary tract infections.
Insights
Gentamicin-resistant Pseudomonas aeruginosa strains often lose key enzymes, reducing their ability to cause severe infections. These strains primarily colonize, rather than infect, and are common in urinary tract infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Pseudomonas aeruginosa is a significant nosocomial pathogen, particularly in immunocompromised patients.
- Environmental and hospital strains may evolve distinct traits, influencing their pathogenicity.
- The transition from environmental to clinical settings involves adaptation and potential loss of virulence factors.
Purpose of the Study:
- To compare the physiological and exoenzymatic activity of Pseudomonas aeruginosa strains from various sources.
- To investigate the characteristics of gentamicin-resistant Pseudomonas aeruginosa (GRPA) strains.
- To understand the ecological selection and evolution of pathogenic Pseudomonas aeruginosa.
Main Methods:
- Evaluation of physiological and exoenzymatic activity (elastase, lipase, deoxyribonuclease, pyocyanin) of bacterial strains.
- Comparison of strains from natural, hospital, and human stool sources.
- Analysis of gentamicin resistance and serotype distribution in clinical isolates.
Main Results:
- Environmental and hospital isolates exhibited reduced enzymatic potential compared to invasive strains.
- Human fecal isolates showed high gentamicin susceptibility and increased exoenzyme production.
- Gentamicin-resistant Pseudomonas aeruginosa strains often lacked key virulence enzymes and were associated with colonization, particularly in urinary tract infections (UTIs).
Conclusions:
- Gentamicin resistance in Pseudomonas aeruginosa may be linked to a decrease in virulence and invasive potential.
- Human fecal isolates represent a closer phenotype to invasive strains.
- Gentamicin-resistant strains, often serotype 11, are primarily associated with colonization and localized UTIs.
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