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This is caused in part by the infection and in part by the inflammatory processes. The consequence is a decline in the lung function, which is the primary cause of death in CF patients. So, because of the organization of the bacteria as biofilm in the lungs of the infected patients it becomes incurable, resulting in death of the cystic fibrosis patients. The severe consequences of the patients chronically infected with biofilm bacteria particularly patients with cystic fibrosis, resulted in a focused, multidisciplinary effort to delineate the role of biofilm in the infection and disease process and design of appropriate therapy 5, 23, Safadi et al 27 showed that correlation exists between in vivo biofilm formation and virulence gene expression in E.

Biofilm formation helps V. Biofilm formation also helps to protect the pathogen during passage through the stomach and enhance its infectivity upon oral ingestion. Biofilm V. Biofilms exhibit an inherent resistance to all classes of antimicrobial agents such as antibiotics, disinfectants and germicides.

Bacterial biofilm formation on implantable devices and approaches to its treatment and prevention

EPS, which encases the biofilm, functions as a diffusional barrier to antimicrobial agents 1, The nutrient availability gradually decreases in the depth of biofilm as the EPS interferes with flow of nutrients, just the way it does with the diffusion of antibiotics. The result is the existence of slow growing or starvation state of bacteria in biofilm. Most antimicrobials require at least some degree of cellular activity to be effective; since their mechanism of action usually relies on disrupting different microbial metabolic processes.

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So, existence in biofilm of bacterial population in a wide variety of metabolic states and the fact that slow growing and non-growing cells are less susceptible to antibiotics in comparison to actively growing cells, contributes significantly to resistance of biofilm bacteria to antibiotics 21, Biofilm bacteria in general exhibit higher levels of resistance to all classes of antibiotics 29, In comparison to their non-attached, individual planktonic counterparts, biofilm bacteria are in the range of times more resistant 29, Multiple mechanisms are involved in resistance of bacteria in biofilm to antimicrobial agents.

First, depending of the type of biofilm and the poor penetration of biofilm by antimicrobial agents as the EPS which constitute the biofilm retard the diffusion of the antibiotics and the drugs cannot penetrate the full depths of the biofilm matrix 31, Rate of penetration also varies with the nature of the drug and structure of the biofilm. Antibiotic ciprofloxacin required 21 minutes versus 4 sec to reach a surface when the surface was coated with a P. Comparative analysis of susceptibility to antibiotic tobramycin revealed that biofilm cells were 15 times more resistant to the drug than their isogenic, planktonic counterparts Another factor that also contributes to resistance is the gene expression profile of bacteria in biofilm.

A large number of genes are modulated as bacteria transit from free floating state to biofilm state and also gene expression of bacteria in different region of biofilm is different 2, 6. This differential gene expression leads to modulation of a wide range of phenotypic characteristics including susceptibility to antibiotics. In addition, development of persistors and the biologically programmed response to growth on a surface are also considered to add to enhanced resistance of biofilm bacteria to antimicrobial agents 19, Biofilm poses a great challenge as bacteria in biofilm exhibit varied protein expression profile as they are morphologically, physiologically and genetically heterogeneous 9, To make things more complicated with regard to the action of antibiotics, it has been found that certain antibiotics such as aminoglycosides induce biofilm formation at sub-inhibitory concentration 5, In a recent study Cook and Dunny 37 showed that biofilm growth increases plasmid copy number and expression of antibiotic resistance genes in Enterococcus faecalis.

Alternative Approaches to Combat Medicinally Important Biofilm-Forming Pathogens

The plasmid copy number and the expression of resistance gene levels reverted to pre-biofilm formation state, once the bacteria were grown as planktonic culture. These findings further highlight the complexity and diversity that bacteria in biofilm life style acquire as the transit from planktonic state, which may interfere with effective drug development. In addition to attempts to develop anti-biofilm therapeutic agents, two approaches are now in active perusal attempting to resolve chronic infection; modulating the host immune response and use of genomic and proteomic techniques to identify vaccine candidates 3, 6.

As the antimicrobial resistance of biofilm is higher, use of antibiotic at recommended dose is often unable to eradicate biofilm infection.


Challenging biofilm with such sub-lethal dose often leads to partial disruption of biofilm, facilitating repopulation and formation of biofilm at newer locations As bacteria from a biofilm have enhanced potential to form new biofilm in comparison to their isogenic, planktonic counterparts 20 , the eradication of the newer biofilms thus formed may be more difficult.

Biofilm can be made up of single species or multiple species of microorganisms. For example biofilm in the lung of patients with cystic fibrosis, P. On the other hand dental biofilm may contain more than species of bacteria Biofilm formation on medical devices is considered as a virulence factor and they pose a challenge in clinical settings as biofilm protect bacteria from antibiotics and host immune system. Various approaches are at different investigational stages for development of methodology for prevention or reduction of biofilm formation on medical devices in clinical settings.

These include coating implantable medical devices with trimethylsaline TMS which has been found to markedly reduce biofilm formation Biofilms of potable water distribution systems have the potential to harbor enteric pathogens, L. Host Immune Response to Biofilm: Numerous in vitro and in vivo studies unraveled multitude of mechanisms of host immune response to infecting bacterial pathogens; however, in vast majority of cases the infectious bacteria used was planktonic bacteria.

As majority of infections are caused by bacteria in biofilm stage, the real scenario of host pathogen interaction remains largely unknown. Many host defense strategies which are highly lethal against single, planktonic bacteria are not effective gains biofilm bacteria leading chronic infections which are difficult to treat 3, 6, 8.

To formulate better antimicrobial strategies to eradicate biofilm bacteria from chronic infection settings, it is essential to understand the extremely complex and varied interactions between host defense systems and biofilms. It is now apparent that our standing of host-pathogen interactions needs to be re-evaluated with biofilm bacteria as most of the studies which cumulatively formed our understanding of antibiotic resistance and virulence of a pathogen came from studies with planktonic bacteria. The bacteria embedded within clinically-relevant biofilms use quorum sensing based cell-cell communication system and often express new, more virulent phenotypes The structure of biofilms is such that host immune responses may be directed only at those antigens found on the outer surface of the biofilm In addition, bacteria have evolved and adopted numerous strategies to counteract the action of both innate and adaptive arms of the immune system.

To make the scenario more complicated serum and salivary antimicrobial factors such as complement proteins, lysozymes are rendered ineffective as they fail to penetrate the biofilm 35, Studies have shown that interaction of neutrophils with biofilm is varied and complex. Intense accumulation of neutrophils at the site of biofilms has been demonstrated recently in biopsies from chronic wounds In addition, induction of biofilm formation was observed during the interaction between normal human neutrophils and P.

Studies directed towards understanding of the correlation between biofilm formation and virulence of pathogens and how the immune system reacts to bacteria in biofilm revealed important finding and identification of putative drug targets for development of potential therapeutic strategies to control and eradicate such microbial communities Extensive research is being carried out to determine the mechanistic detail of persistent infections caused by pathogens.

Recently, it has been found that S. Biofilm Eradication and Preventions presents the basics of biofilm formation on medical devices, diseases related to this formation, and approaches pharmaceutical researchers need to take to limit this problem. In the second section, the author discusses biofilm-mediated chronic infections occurred in various organs eyes, mouth, wounds and pharmaceutical and drug delivery knowledge gained from research in these area Questions as to why biofilms form over medical device surfaces and what triggers biofilm formation are addressed Split into three parts, the first deals with the development and characterization of biofilm on the surfaces of implanted or inserted medical devices The third part explores pharmaceutical approaches like lipid-and polymer-based drug delivery carriers for eradicating biofilm on device-related infections.

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