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Name- Jitendra Chandra Devrari
Reg. no- 155/Jan 2015
Gist of the articles:
1. María D. Alcántar-Curiel et. al. Multi-functional analysis of Klebsiella pneumonia
fimbrial types in adherence and biofilm formation. Landes Bioscience, 2013, virulence 4:2,
p.129–138.
Klebsiella pneumonia is one of the emerging opportunistic pathogen which is responsible for the
most common hospital acquired infection. The Type 1 and type 3 fimbriae which are encoded by
the fimA and mrkA gene respectively mediates the host cell adherence and biofilm formation of
klebsiella pneumonia. among E. coli patho groups and adhesive structure that is e coli common
pilus (ECP) is being produced however a homolog of the ecpABCDE operon is present in the
klebsiella pneumonia genome.
The prevalence of mrkA, fimA, ECP fimbrial genes were
determine among the clinical and environmental klebsiella pneumonia and correlation was
stablished with fimbrial production during cell adherence and biofilm formation. ECP is reqired
both in vitro and in vivo for expression of these fimbrial subunits. therefore ecp produced by
Klebsiella pnumoniae strain represents a new important adhesive structure of this organism.
2.
Magesh
H
et.
al.
Identification
of
plasmid-mediated
quinolone
resistance
genes qnrA1, qnrB1 and aac(6')-1b-cr in a multiple drug-resistant isolate of Klebsiella
pneumoniae from Chennai, Indian J Med Microbiol, 2011, vol. 29, p.262-268.
Fluoroquinolones were the commonly prescribed antimicrobial for gram positive as well as gram
negative microorganism before the emergence of resistance to these antimicrobials. The
determinants of PMQR in the clinical isolates were identified in this study. The qnrA and qnrB
are the gens which mediates the PMQR in MDR Klebsiella pneuoniae isolates. However high
ciprofloxacin rersistance was conferred by the MDR plasmid which was found to carry another
mutant gene that is aac(6’)-lb-cr which is another type of PMQR gene. This was the first report
submitted from the India.
3. Yamane Kunikazu et. al. New Plasmid-Mediated Fluoroquinolone Efflux Pump, QepA
Found in an Escherichia coli Clinical Isolate. Antimicrobial agents and chemotherapy,
2007,vol. 51 (9), p. 3354–3360.
A new molecular mechanism responsible for fluoroquinolone resistance have been identified by
plasmid mediated qnr and aac(6’)-lb-cr gene. A PCR detection was failed for the detection qnr
genes for fluoroquinolones resistance in a variant of E. coli thus suggesting that the novel
mechanism for PMQR. However another novel qepA gene was identified for PMQR in E coli
C316. Under the AcrB- TolC-deficient conditions and the presence of qep gene in e coli C316
significantly raises the resistance levels of norfloxacin, ciprofloxacin and enrofloxcin. Thus to
stop the dissemination of plasmid dependent fluoroquinolone resistance among pathogenic
microbe it is important to check periodically qepA harboring clinical isolates.
4. Bendaoud Meriem et. al. Broad-Spectrum Biofilm Inhibition by Kingella kingae
Exopolysaccharide. Journal of bacteriology, 2011, p. 3879–3886.
Extracted exopolysacharide from the Kingella kingae which inhibited the biofilm formation of
Aggregatibacter actinomycetemcomitans, Klebsiella pneumoniae, S. aureus, S. epidermidis, C.
albicans and K. kingae. Exopolysaccharide will inhibit the biofilm formation of bacteria due to
the certain changes in the chemical structure of the cell wall, matrix and its substrate. Extracted
polysaccharide is belonging to the two important polysaccharide which is the major role in
inhibition of bifilm formation. One was the linear polysaccharide that is 6α-D-GlcNAcp-(1-5)-βD-OclAp-2 extracted from the Actinobacillus pleuropneumoniae and other was the novel linear
PAM galactan. In e.coli for the synthesis of PAM galactan, clusters of 3 genes were used from
K. kingae. PAM galactan acts as antibiofilm agent, which inhbits the biofilm production in
bacteria.
5. Struve Carsten et. al. Characterization of Klebsiella pneumoniae Type 1 Fimbriae by
Detection of Phase Variation during Colonization and Infection and Impact on Virulence.
INFECTION AND IMMUNITY, 2008, Vol. 76(9), p. 4055–4065.
Klebsiella pneumoniae is one of the most common hospital acquired pathogen, which is also
producing the disease in immunocompromised patients. The type 1 fimbrial gene cluster of
k.pneumoniae was examined which was not identical to the gene cluster of e.coli although their
structural resemblance was quite high. The fimbrial gene in Klebsiella species was named as
fimk gene, which belongs to the EAL domain in gene cluster, having main role in the regulation
and adhesion property to the host cell. Expression of Type 1 fimbriae of Klebsiella pneumoniae
has a significant role in UTIs in comparison with the colonization in the intestine or infection in
the lungs. With the help of molecular techniques like PCR, the expression of switching on or off
of fimK gene during infections of urinary tract, intestine and lung was determined. It has been
found that all the expressions of fimK gene while UTIs were found to be “switched on”, while it
was all “switched off” during the infection of intestine and lungs. Therefore the expression of
type1 fimbrie of K.pneumoniae in the colonization and infection is dependent on the host
environment.
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