The Microbiological Profiles of Infected Prosthetic Implants with an Emphasis on the Organisms which Form Biofilms

Fernandes, Anisha

doi:10.7860/jcdr/2013/4533.2732

Cited by 60 publications

(77 citation statements)

References 11 publications

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“…From our study it was found that the most common organism causing orthopedic implant site infection is Staphylococcus aureus which correlates with most of the other similar studies like Anisha Fernandez et al, [2] Khosravi et al [4] and Vishwajith et al [1] The second most common organism isolated was CONS and Eschericia coli. CONS is a normal skin commensal which could have reached the surgical site due to improper disinfection of the skin during surgery or it might be due to improper collection of sample for the diagnosis.…”

Section: Discussionsupporting

confidence: 76%

“…[11] It is said that with sonication the culture positivity rate can be increased from 84.2% to 94.7%. In our study the culture positivity was found to be 73.01% which is less when compared to other studies where Anisha Fernandez et al [2] reported 84% and Khosravi et al, [4] Vishwajith et al [1] reported the culture positivity of 93.9% and 94.89% respectively. However Gomez et al [12] reported even lesser positivity of 60%.…”

Section: Discussioncontrasting

confidence: 52%

“…[1] Though the incidence of orthopedic implant related infection has been reduced to less than 1%, it remains a diagnostic, therapeutic and cost related problem. [2] It is said that overall 5% of internal fixation devices get infected, where the incidence of infection after internal fixation of closed fractures is generally lower (0.5-1%), whereas for internal fixation of open fractures, the incidence is still higher and may exceed 30%. [3] Major risk factor for development of orthopedic implant site infection depends upon the extent of damage which has occurred to the soft tissues and periosteum following fracture, because devascularised bone and necrotic tissue are ideal for multiplication of bacteria as there is no access for the immune host defenses to reach the infection site, since there is damage to the periosteal blood supply and lack of perfusion of the soft tissues.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Characterisation of Aerobic Bacteriological Isolates From Orthopedic Implant Site Infections With Special Reference to Biofilm Formation in a Teritiary Care Hospital

S¹,

Prathab²

2015

jemds

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Section: Discussionsupporting

confidence: 76%

Section: Discussioncontrasting

confidence: 52%

Section: Introductionmentioning

confidence: 99%

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Characterisation of Aerobic Bacteriological Isolates From Orthopedic Implant Site Infections With Special Reference to Biofilm Formation in a Teritiary Care Hospital

S¹,

Prathab²

2015

jemds

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“…Klebsiella pneumoniae is a Gram-negative, opportunistic pathogen that is frequently associated with nosocomial infections such as pneumonia, urinary tract infections, and septicemia (1). An important clinical pathogenic mechanism of K. pneumoniae is its ability to form biofilms on inert surfaces such as medical devices, which can lead to rapid microbial colonization on host tissues (2)(3)(4)(5)(6).…”

mentioning

confidence: 99%

Positive Autoregulation ofmrkHIby the Cyclic Di-GMP-Dependent MrkH Protein in the Biofilm Regulatory Circuit of Klebsiella pneumoniae

Tan¹,

Wilksch²,

Hocking³

et al. 2015

J. Bacteriol.

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Klebsiella pneumoniae is an important cause of nosocomial infections, primarily through the formation of surface-associated biofilms to promote microbial colonization on host tissues. Expression of type 3 fimbriae by K. pneumoniae facilitates surface adherence, a process strongly activated by the cyclic di-GMP (c-di-GMP)-dependent transcriptional activator MrkH. In this study, we demonstrated the critical importance of MrkH in facilitating K. pneumoniae attachment on a variety of medically relevant materials and demonstrated the mechanism by which bacteria activate expression of type 3 fimbriae to colonize these materials. Sequence analysis revealed a putative MrkH recognition DNA sequence ("MrkH box"; TATCAA) located in the regulatory region of the mrkHI operon. Mutational analysis, electrophoretic mobility shift assay, and quantitative PCR experiments demonstrated that MrkH binds to the cognate DNA sequence to autoregulate mrkHI expression in a c-di-GMP-dependent manner. A half-turn deletion, but not a full-turn deletion, between the MrkH box and the ؊35 promoter element rendered MrkH ineffective in activating mrkHI expression, implying that a direct interaction between MrkH and RNA polymerase exists. In vivo analyses showed that residues L260, R265, N268, C269, E273, and I275 in the C-terminal domain of the RNA polymerase ␣ subunit are involved in the positive control of mrkHI expression by MrkH and revealed the regions of MrkH required for DNA binding and transcriptional activation. Taken together, the data suggest a model whereby c-di-GMP-dependent MrkH recruits RNA polymerase to the mrkHI promoter to autoactivate mrkH expression. Increased MrkH production subsequently drives mrkABCDF expression when activated by c-di-GMP, leading to biosynthesis of type 3 fimbriae and biofilm formation. IMPORTANCEBacterial biofilms can cause persistent infections that are refractory to antimicrobial treatments. This study investigated how a commonly encountered hospital-acquired pathogen, Klebsiella pneumoniae, controls the expression of MrkH, the principal regulator of type 3 fimbriae and biofilm formation. We discovered a regulatory circuit whereby MrkH acts as a c-di-GMP-dependent transcriptional activator of both the gene cluster of type 3 fimbriae and the mrkHI operon. In this positive-feedback loop, whereby MrkH activates its own production, K. pneumoniae has evolved a mechanism to ensure rapid MrkH production, expression of type 3 fimbriae, and subsequent biofilm formation under favorable conditions. Deciphering the molecular mechanisms of biofilm formation by bacterial pathogens is important for the development of innovative treatment strategies for biofilm infections. Biofilm-related infections substantially contribute to patient morbidity and place a significant burden on health care systems. The evolution of high-technology medicine such as intensive and invasive hospital care practices and immunosuppressive therapy and the emergence of multiply antibiotic-resistant organisms have contributed to the rise...

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“…The pathogenicity of K. pneumonia is associated with its ability to form biofilms, which are largely recalcitrant to treatment (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). Key to K. pneumonia biofilm development are mannose-resistant Klebsiella-like (Mrk) hemagglutinins or Mrk proteins, which are encoded by the mrkABCDF operon (7)(8)(9)(10)(11)(12)(13)(14).…”

mentioning

confidence: 99%

Structures of the activator of K. pneumonia biofilm formation, MrkH, indicates PilZ domains involved in c-di-GMP and DNA binding

Schumacher

Zhang

2016

Proc. Natl. Acad. Sci. U.S.A.

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The pathogenesis of Klebsiella pneumonia is linked to the bacteria’s ability to form biofilms. Mannose-resistant Klebsiella-like (Mrk) hemagglutinins are critical for K. pneumonia biofilm development, and the expression of the genes encoding these proteins is activated by a 3′,5′-cyclic diguanylic acid (c-di-GMP)–regulated transcription factor, MrkH. To gain insight into MrkH function, we performed structural and biochemical analyses. Data revealed MrkH to be a monomer with a two-domain architecture consisting of a PilZ C-domain connected to an N domain that unexpectedly also harbors a PilZ-like fold. Comparison of apo- and c-di-GMP–bound MrkH structures reveals a large 138° interdomain rotation that is induced by binding an intercalated c-di-GMP dimer. c-di-GMP interacts with PilZ C-domain motifs 1 and 2 (RxxxR and D/NxSxxG) and a newly described c-di-GMP–binding motif in the MrkH N domain. Strikingly, these c-di-GMP–binding motifs also stabilize an open state conformation in apo MrkH via contacts from the PilZ motif 1 to residues in the C-domain motif 2 and the c-di-GMP–binding N-domain motif. Use of the same regions in apo structure stabilization and c-di-GMP interaction allows distinction between the states. Indeed, domain reorientation by c-di-GMP complexation with MrkH, which leads to a highly compacted structure, suggests a mechanism by which the protein is activated to bind DNA. To our knowledge, MrkH represents the first instance of specific DNA binding mediated by PilZ domains. The MrkH structures also pave the way for the rational design of inhibitors that target K. pneumonia biofilm formation.

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The Microbiological Profiles of Infected Prosthetic Implants with an Emphasis on the Organisms which Form Biofilms

Cited by 60 publications

References 11 publications

Characterisation of Aerobic Bacteriological Isolates From Orthopedic Implant Site Infections With Special Reference to Biofilm Formation in a Teritiary Care Hospital

Characterisation of Aerobic Bacteriological Isolates From Orthopedic Implant Site Infections With Special Reference to Biofilm Formation in a Teritiary Care Hospital

Positive Autoregulation ofmrkHIby the Cyclic Di-GMP-Dependent MrkH Protein in the Biofilm Regulatory Circuit of Klebsiella pneumoniae

Structures of the activator of K. pneumonia biofilm formation, MrkH, indicates PilZ domains involved in c-di-GMP and DNA binding

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