Genetic Basis of Biofilm Formation and Spread of Nosocomial Infections

Author(s):  
Snehashis Koley ◽  
Mandira Mukherjee
2019 ◽  
pp. 1180-1187
Author(s):  
Mahmood Abd AL- Razzaq Hassan AL-Sheikhly ◽  
Laith N. Musleh ◽  
Harith J. F. Al-Mathkhury

Owing to high antibacterial resistance of Pseudomonas aeruginosa, it could be considered as the main reason behind the nosocomial infections. P. aeruginosa has a well-known biofilm forming ability. The expression of polysaccharide encoding locus (pelA gene) by P. aeruginosa is essential for this ability. The purpose of the current research was to determine the biofilm formation in P. aeruginosa isolated from clinical samples and to evaluate the role of the selected PelA gene in biofilm formation using PCR method in Iraqi patients. Results revealed that 24 (96%) isolates were found to have the ability to form biofilm that was remarkably related to gentamicin resistance. Moreover, the pelA gene was found in all biofilm-producers. In conclusion, the results of the current study revealed that the P. aeruginosa biofilm-producer isolates were resistant to the antibiotics in question. Likewise, because of wide spreading, it appears that the pelA gene is related to biofilm formation.


Author(s):  
Naveen Kumar Devanga Ragupathi ◽  
Dhiviya Prabaa Muthuirulandi Sethuvel ◽  
Hariharan Triplicane Dwarakanathan ◽  
Dhivya Murugan ◽  
Yamini Umashankar ◽  
...  

AbstractKlebsiella pneumoniae is one of the leading causes of nosocomial infections. Carbapenem-resistant (CR) K. pneumoniae are on the rise in India. The biofilm forming ability of K. pneumoniae further complicates patient management. There is still a knowledge gap on the association of biofilm formation with patient outcome and carbapenem susceptibility, which is investigated in the present study.K. pneumoniae isolates from patients admitted in critical care units with catheters and ventilators were included. K. pneumoniae (n = 72) were tested for antimicrobial susceptibility as recommended by CLSI 2019 and subjected to 96-well microtitre plate biofilm formation assay. Based on optical density at 570 nm isolates were graded as strong, moderate and weak biofilm formers. Subset of strong biofilm formers were subjected to whole genome sequencing and a core genome phylogenetic analysis in comparison with global isolates were performed. Biofilm formation was compared for an association with the carbapenem susceptibility and with patient outcome. Statistical significance, correlations and graphical representation were performed using SPSS v23.0.Phenotypic analyses showed a positive correlation between biofilm formation and carbapenem resistance. Planktonic cells observed to be susceptible in vitro exhibited higher MICs in biofilm structure. The biofilm forming ability had a significant association with the morbidity/mortality. Infections by stronger biofilm forming pathogens significantly (P<0.05) resulted in fewer ‘average days alive’ for the patient (3.33) in comparison to those negative for biofilms (11.33). Phylogenetic analysis including global isolates revealed the clear association of sequence types with genes for biofilm mechanism and carbapenem resistance. Carbapenemase genes were found specific to each clade. The known hypervirulent clone-ST23 with wcaG, magA, rmpA, rmpA2 and wzc with a lack of mutation for hyper-capsulation might be poor biofilm formers. Interestingly, ST15, ST16, ST307 and ST258 – reported global high-risk clones were wcaJ negative indicating the high potential of biofilm forming capacity. Genes wabG and treC for CPS, bcsA and pgaC for adhesins, luxS for quorum sensing were common in all clades in addition to genes for aerobactin (iutA), allantoin (allS), type I and III fimbriae (fimA, fimH, mrkD) and pili (pilQ, ecpA).This study is the first of its kind to compare genetic features of antimicrobial resistance with a spectrum covering most of the genetic factors for K. pneumoniae biofilm. These results highlight the importance of biofilm screening to effectively manage nosocomial infections by K. pneumoniae. Further, data obtained on epidemiology and associations of biofilm and antimicrobial resistance genetic factors will serve to enhance our understanding on biofilm mechanisms in K. pneumoniae.


2017 ◽  
Author(s):  
M. Lisandra Zepeda Mendoza ◽  
Gary R. Graves ◽  
Michael Roggenbuck ◽  
Karla Manzano Vargas ◽  
Lars Hestbjerg Hansen ◽  
...  

AbstractBackgroundVultures have adapted the remarkable ability to feed on carcasses that may contain microorganisms that would be pathogenic to most other animals. The holobiont concept suggests that the genetic basis of such adaptation may not only lie within their genomes, but additionally in their associated microbes. To explore this, we generated shotgun DNA sequencing datasets of the facial and gut microbiomes from the black and turkey vultures. We characterizedi) the functional potential and taxonomic diversity of their microbiomes,ii) the potential pathogenic challenges they face, and iii) elements in the microbiome that could play a protective role to the vulture’s face and gut.ResultsWe found elements involved in diseases, such as periodontitis and pneumonia (more abundant in the face), and gas gangrene and food poisoning (more abundant in the gut). Interestingly, we found taxa and functions with potential for playing health beneficial roles, such as antilisterial bacteria in the gut, and genes for the production of antiparasites and antiinsectisides in the face. Based on the identified phages, we suggest that phages aid in the control, and possibly elimination as in phage therapy, of microbes reported as pathogenic to a variety of species. Interestingly, we also identifiedAdineta vagain the gut, an invertebrate that feeds on dead bacteria and protozoans, suggesting a defensive predatory mechanism. Finally, we suggest a colonization resistance role though biofilm formation played byFusobacteriaandClostridiain the gut.ConclusionsOur results highlight the importance of complementing genomic analyses with metagenomics in order to obtain a clearer understanding of the host-microbial alliance and show the importance of microbiome-mediated health protection for adaptation to extreme diets, such as scavenging.


2015 ◽  
Vol 81 (10) ◽  
pp. 3306-3315 ◽  
Author(s):  
Sara Remuzgo-Martínez ◽  
María Lázaro-Díez ◽  
Celia Mayer ◽  
Maitane Aranzamendi-Zaldumbide ◽  
Daniel Padilla ◽  
...  

ABSTRACTSerratiaspp. are opportunistic human pathogens responsible for an increasing number of nosocomial infections. However, little is known about the virulence factors and regulatory circuits that may enhance the establishment and long-term survival ofSerratia liquefaciensin the hospital environment. In this study, two reporter strains,Chromobacterium violaceumCV026 and VIR24, and high-resolution triple-quadrupole liquid chromatography–mass spectrometry (LC-MS) were used to detect and to quantifyN-acyl-homoserine lactone (AHL) quorum-sensing signals in 20S. liquefaciensstrains isolated from clinical samples. Only four of the strains produced sufficient amounts of AHLs to activate the sensors. Investigation of two of the positive strains by high-performance liquid chromatography (HPLC)-MS confirmed the presence of significant amounts of short-acyl-chain AHLs (N-butyryl-l-homoserine lactone [C4-HSL] andN-hexanoyl-l-homoserine lactone [C6-HSL]) in both strains, which exhibited a complex and strain-specific signal profile that included minor amounts of other short-acyl-chain AHLs (N-octanoyl-l-homoserine lactone [C8-HSL] andN-3-oxohexanoyl-l-homoserine lactone [OC6-HSL]) and long-acyl-chain (C10, C12, and C14) AHLs. No correlation between biofilm formation and the production of large amounts of AHLs could be established. Fimbria-like structures were observed by transmission electron microscopy, and the presence of the type 1 fimbrial adhesin genefimHin all strains was confirmed by PCR. The ability ofS. liquefaciensto adhere to abiotic surfaces and to form biofilms likely contributes to its persistence in the hospital environment, increasing the probability of causing nosocomial infections. Therefore, a better understanding of the adherence properties of this species will provide greater insights into the diseases it causes.


2017 ◽  
Vol 5 (39) ◽  
Author(s):  
Deeksha Shetty ◽  
Alexander A. Grigoryan ◽  
Sahar Alshalchi ◽  
Niradha Withana Gamage ◽  
Julie Roy ◽  
...  

ABSTRACT The genetic basis for biofilm formation among nontyphoidal salmonellae (NTS) remains poorly understood. This draft genome submission provides initial insights on the genetic differences between biofilm-forming and non-biofilm-forming clinical and environmental NTS serovars.


2012 ◽  
Vol 22 (9) ◽  
pp. 3089-3094 ◽  
Author(s):  
Dhamodharan Bakkiyaraj ◽  
Chandran Sivasankar ◽  
Shunmugiah Karutha Pandian

Author(s):  
Nisha Mahey ◽  
Rushikesh Tambat ◽  
Nishtha Chandal ◽  
Dipesh Kumar Verma ◽  
Krishan Gopal Thakur ◽  
...  

Staphylococcus aureus is a frequent pathogen bacterium and the predominant cause of worsened nosocomial infections. Efflux pumps contribute to drug efflux and are reportedly associated with biofilm formation, thereby promoting difficult-to-treat biofilm-associated S. aureus infections.


2018 ◽  
Author(s):  
Shi-qi An ◽  
Ji-liang Tang

AbstractStenotrophomonas maltophilia is a Gram-negative bacterium commonly isolated from nosocomial infections. Analysis of the genome of the clinical Stenotrophomonas maltophilia isolate K279a indicates that it encodes a diffusible signal factor (DSF)-dependent cell-cell signaling mechanism that is highly similar to the system previously described in phytopathogens from the genera Xanthomonas and Xylella. Here we demonstrate that in S. maltophilia strain K279a, DSF signaling regulates factors contributing to virulence, biofilm formation and motility of this important opportunistic pathogen.


1999 ◽  
Vol 181 (11) ◽  
pp. 3606-3609 ◽  
Author(s):  
Paula I. Watnick ◽  
Karla Jean Fullner ◽  
Roberto Kolter

ABSTRACT While much has been learned regarding the genetic basis of host-pathogen interactions, less is known about the molecular basis of a pathogen’s survival in the environment. Biofilm formation on abiotic surfaces represents a survival strategy utilized by many microbes. Here it is shown that Vibrio cholerae El Tor does not use the virulence-associated toxin-coregulated pilus to form biofilms on borosilicate but rather uses the mannose-sensitive hemagglutinin (MSHA) pilus, which plays no role in pathogenicity. In contrast, attachment ofV. cholerae to chitin is shown to be independent of the MSHA pilus, suggesting divergent pathways for biofilm formation on nutritive and nonnutritive abiotic surfaces.


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