Article

Urinary tract infections caused by Pseudomonas aeruginosa: A minireview

Division of Infectious Diseases, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA.
Journal of infection and public health 01/2009; 2(3):101-11. DOI: 10.1016/j.jiph.2009.08.003
Source: PubMed

ABSTRACT

Urinary tract infections (UTIs) are a serious health problem affecting millions of people each year. Infections of the urinary tract are the second most common type of infection in the body. Catheterization of the urinary tract is the most common factor, which predisposes the host to these infections. Catheter-associated UTI (CAUTI) is responsible for 40% of nosocomial infections, making it the most common cause of nosocomial infection. CAUTI accounts for more than 1 million cases in hospitals and nursing homes annually and often involve uropathogens other than Escherichia coli. While the epidemiology and pathogenic mechanisms of uropathogenic Escherichia coli have been extensively studied, little is known about the pathogenesis of UTIs caused by other organisms like Pseudomonas aeruginosa. Scanty available information regarding pathogenesis of UTIs caused by P. aeruginosa is an important bottleneck in developing effective preventive approaches. The aim of this review is to summarize some of the advances made in the field of P. aeruginosa induced UTIs and draws attention of the workers that more basic research at the level of pathogenesis is needed so that novel strategies can be designed.

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Available from: Rahul Mittal
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    • "Pseudomonas aeruginosa is a common opportunistic pathogen capable of infecting both humans and animals. It causes various nosocomial diseases such as pneumonia, respiratory infection (Pereira and Cardoso, 2014), festering wounds (Altoparlak et al., 2005), urinary tract (Mittal et al., 2009), bacteremia (Al-Hasan et al., 2008), and keratitis (Hazlett, 2004). Pulmonary colonizationwith P. aeruginosa is considered a major cause of morbidity and mortality in patients with cystic fibrosis (Davies, 2002). "
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    ABSTRACT: Pseudomonas aeruginosa is a major opportunistic pathogen in hospital-acquired infections and exhibits increasing antibiotic resistance. A rapid and sensitive molecular method for its detection in clinical samples is needed to guide therapeutic treatment and to control P. aeruginosa outbreaks. In this study, we established a polymerase spiral reaction (PSR) method for rapid detection of P. aeruginosa by targeting the toxA gene, which regulates exotoxin A synthesis. Real-time turbidity monitoring and a chromogenic visualization using hydroxynaphthol blue were used to assess the reaction. All 17 non- P. aeruginosa strains tested negative, indicating the high specificity of the PSR primers. The detection limit was 2.3 pg/μl within 60 min at isothermal temperature (65°C), 10-fold more sensitive than conventional PCR. Then, the PSR assay was applied to a clinical surveillance of P. aeruginosa in three top hospitals in Beijing, China. Of the 130 sputum samples collected from ICU patients with suspected multi-resistant infections, 37 P. aeruginosa isolates were identified from the positive samples. All clinical strains belonged to 10 different P. aeruginosa multilocus sequence typing groups and exhibited high resistance to carbapenems, cephalosporins, and aminoglycosides. Interestingly, of the 33 imipenem-resistant isolates, 30 (90.9%) had lost the outer membrane porin oprD gene. Moreover, isolate SY-95, containing multiple antibiotic resistance genes, possessed the ability to hydrolyze all antibiotics used in clinic and was susceptible only to polymyxin B. Our study showed the high level of antibiotic resistance and co-occurrence of resistance genes in the clinical strains, indicating a rapid and continuing evolution of P. aeruginosa. In conclusion, we developed a P. aeruginosa PSR assay, which could be a useful tool for clinical screening, especially in case of poor resources, or for point-of-care testing.
    Full-text · Article · Oct 2015 · Frontiers in Microbiology
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    • "Reports on Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, Bacillus subtilis and Enterococcus faecalis infections and antibacterial resistance reveal the need for a constant search of new drugs against these organisms (Gupta et al., 2001; Tamma et al., 2012). E. coli is a major cause of travellers' diarrhoea, one of the most common forms of diarrhoea worldwide (Mittal et al., 2009; Canizalez-Roman et al., 2013). Both E. coli and P. aeruginosa are also major causes of urinary tract infections while S. aureus and E. faecalis are common causes of nosocomial infections (Sood et al., 2008; Oli et al., 2012). "

    Preview · Article · Oct 2014 · African journal of microbiology research
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    • "The ubiquitous Gram-negative bacterium Pseudomonas aeruginosa is an opportunistic human pathogen, which is a frequent cause of hospital-acquired infections, including ventilator-associated pneumonia and catheter infections in immunocompromised patients (1). Furthermore, P. aeruginosa is an etiologic agent of ear (2) and urinary tract infections (3) and causes infections in severely burned individuals (4) as well as in patients who suffer from cystic fibrosis (5). The establishment of P. aeruginosa infection is accompanied by the synthesis of several extracellular and cell-associated virulence factors, among which is exotoxin A, encoded by the toxA gene (6,7). "
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    ABSTRACT: In the human pathogen Pseudomonas aeruginosa, the GltR regulator is required for glucose transport, whereas GtrS is a sensor kinase that plays a key role in mediating bacteria–host interaction and pathogen dissemination in the host. We show that GtrS and GltR form a two-component system that regulates the expression from the promoters Pedd/gap-1, PoprB and Pglk, which control the expression of genes involved in glucose metabolism and transport. In addition, the GtrS/GltR pair regulates the expression of toxA that encodes exotoxin A, the primary virulence factor. Microcalorimetry-based ligand screening of the recombinant GtrS ligand-binding domain revealed specific binding of 2-ketogluconate (2-KG) (KD = 5 μM) and 6-phosphogluconate (KD = 98 μM). These effectors accelerate GtrS autophosphorylation, with concomitant transphosphorylation of GltR leading to a three-fold increase in transcription. Surprisingly, in vivo a similar increase in expression from the above promoters was observed for the mutant deficient in GltR regardless of the presence of effectors. The GltR operator site was found to contain the consensus sequence 5′-tgGTTTTTc-3′. We propose that 2-KG is a key metabolite in the stringent transcriptional control of genes involved in virulence and glucose metabolism. We show that GltR is a transcriptional repressor that is released from DNA upon phosphorylation.
    Full-text · Article · Jun 2014 · Nucleic Acids Research
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