Characterization of genes encoding type 1 fimbriae of Klebsiella pneumoniae, Salmonella typhimurium, and Serratia marcescens.

Background: Extended-spectrum β-lactamases (ESBLs) are enzymes capable of hydrolyzing oxyimino-β-lactams and inducing resistance to third generation cephalosporins. The genes encoding ESBLs are widespread and generally located on highly transmissible resistance plasmids. We aimed to investigate the complement of ESBL genes in E. coli and Klebsiella pneumoniae causing nosocomial infections in hospitals in Ho Chi Minh City, Vietnam. Methodology: Thirty-two non-duplicate isolates of E. coli and Klebsiella pneumoniae causing nosocomial infections, isolated between March and June 2010, were subjected to antimicrobial susceptibility testing. All isolates were PCR-amplified to detect the blaSHV, blaTEM and blaCTX-M ESBL genes and subjected to plasmid analysis. Results: We found that co-resistance to multiple antimicrobials was highly prevalent, and we report the predominance of the blaCTX-M-15 and blaCTX-M-27 genes, located on highly transmissible plasmids ranging from 50 to 170 kb in size. Conclusions: Our study represents a snap shot of ESBL-producing enteric bacteria causing nosocomial infections in this setting. We suggest that antimicrobial resistance in nosocomial E. coli and Klebsiella pneumoniae is rampant in Vietnam and ESBL organisms are widespread. In view of these data and the dramatic levels of antimicrobial resistance reported in Vietnam we advocate an urgent review of antimicrobial use in the Vietnamese healthcare system.

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Decreased Expression of Type 1 Fimbriae by apstMutant of Uropathogenic Escherichia coli Reduces Urinary Tract Infection

Infection and Immunity ◽

10.1128/iai.00162-12 ◽

2012 ◽

Vol 80 (8) ◽

pp. 2802-2815 ◽

Cited By ~ 34

Author(s):

Sébastien Crépin ◽

Sébastien Houle ◽

Marie-Ève Charbonneau ◽

Michaël Mourez ◽

Josée Harel ◽

...

Keyword(s):

Escherichia Coli ◽

Urinary Tract ◽

Bacterial Virulence ◽

Pho Regulon ◽

Upec Strain ◽

Content Type ◽

Type 1 Fimbriae ◽

Genes Encoding ◽

Tract Infections

ABSTRACTThepstSCAB-phoUoperon encodes the phosphate-specific transport system (Pst). Loss of Pst constitutively activates the Pho regulon and decreases bacterial virulence. However, specific mechanisms underlying decreased bacterial virulence through inactivation of Pst are poorly understood. In uropathogenicEscherichia coli(UPEC) strain CFT073, inactivation ofpstdecreased urinary tract colonization in CBA/J mice. Thepstmutant was deficient in production of type 1 fimbriae and showed decreased expression of thefimAstructural gene which correlated with differential expression of thefimB,fimE,ipuA, andipbAgenes, encoding recombinases, mediating inversion of thefimpromoter. The role offimdownregulation in attenuation of thepstmutant was confirmed using afimphase-locked-on derivative, which demonstrated a significant gain in virulence. In addition, thepstmutant was less able to invade human bladder epithelial cells. Since type 1 fimbriae contribute to UPEC virulence by promoting colonization and invasion of bladder cells, the reduced bladder colonization by thepstmutant is predominantly attributed to downregulation of these fimbriae. Elucidation of mechanisms mediating the control of type 1 fimbriae through activation of the Pho regulon in UPEC may open new avenues for therapeutics or prophylactics against urinary tract infections.

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Capsule and Fimbria Interaction in Klebsiella pneumoniae

Infection and Immunity ◽

10.1128/iai.73.8.4626-4633.2005 ◽

2005 ◽

Vol 73 (8) ◽

pp. 4626-4633 ◽

Cited By ~ 86

Author(s):

Mark A. Schembri ◽

Jens Blom ◽

Karen A. Krogfelt ◽

Per Klemm

Keyword(s):

Klebsiella Pneumoniae ◽

Defense Mechanisms ◽

Capsular Polysaccharide ◽

Phase Variation ◽

Cell Agglutination ◽

Type 1 Fimbriae ◽

Entire Cell ◽

Major Surface ◽

Two Parameters

ABSTRACT The capsular polysaccharide and type 1 fimbriae are two of the major surface-located virulence properties associated with the pathogenesis of Klebsiella pneumoniae. The capsule is an elaborate polysaccharide matrix that encases the entire cell surface and provides resistance against many host defense mechanisms. In contrast, type 1 fimbriae are thin adhesive thread-like surface organelles that can extend beyond the capsular matrix and mediate d-mannose-sensitive adhesion to host epithelial cells. These fimbriae are archetypical and consist of a major building block protein (FimA) that comprises the bulk of the organelle and a tip-located adhesin (FimH). It is assumed that the extended major-subunit protein structure permits the FimH adhesin to function independently of the presence of a capsule. In this study, we have employed a defined set of K. pneumoniae capsulated and noncapsulated strains to show that the function of type 1 fimbriae is actually impeded by the concomitant expression of a polysaccharide capsule. Capsule expression had significant effects on two parameters commonly used to define FimH function, namely, yeast cell agglutination and biofilm formation. Our data suggest that this effect is not due to transcriptional/translational changes in fimbrial gene/protein expression but rather the result of direct physical interference. This was further demonstrated by the fact that we could restore fimbrial function by inhibiting capsule synthesis. It remains to be determined whether the expression of these very different surface components occurs simply via random events of phase variation or in a coordinated manner in response to specific environmental cues.

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