\r\n\tRecent advances in gene-editing research and technologies have enabled the CRISPR Cas9 system to become a popular tool for sequence specific gene editing to correct and modify eukaryotic systems. The technology allows targeted knock-ins and knocks-outs of any gene within the genome. DNA mutations ranging from a single base pair to large deletions in both in vitro and in vivo model systems have been accomplished, thereby, revolutionizing the molecular biology world of science. \r\n\tCurrently, most research on genome editing is conducted to understand diseases using cells and animal models, making it a promising therapeutic tool to treat and prevent complex diseases, such as cancer, heart disease and neurological disorders. \r\n\tIn this book we will focus on the mechanisms, applications, regulations (their pros and cons); and various ways in which the CRIPSR technology has stimulated the genome editing revolution.
",isbn:null,printIsbn:null,pdfIsbn:null,doi:null,price:0,priceEur:null,priceUsd:null,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"48b8714f62093216c058c5a7e801fb94",bookSignature:"Dr. Aditi Singh and Dr. Mohammad W. Khan",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/7051.jpg",keywords:"Genome Editing, Knock-Out, Knock-in, CRISPR, Cas9 Nuclease , Cell Engineering, Genomic Deletion, Homology Directed Repair (HDR), Guide RNA, Tracer RNA, CRISPR RNA, PAM Motif , Transgenic Animals",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:0,numberOfDimensionsCitations:0,numberOfTotalCitations:0,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"April 11th 2018",dateEndSecondStepPublish:"May 2nd 2018",dateEndThirdStepPublish:"July 1st 2018",dateEndFourthStepPublish:"September 19th 2018",dateEndFifthStepPublish:"November 18th 2018",remainingDaysToSecondStep:"3 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"240724",title:"Dr.",name:"Aditi",middleName:null,surname:"Singh",slug:"aditi-singh",fullName:"Aditi Singh",profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:"Aditi Singh is a Research Enthusiast, working as an Application Scientist in a Biotechnology company. She has a PhD degree in Molecular-Cell Biology from University of Heidelberg in Germany; and worked as a Post-Doctoral Scholar at University of California San Diego, USA. Aditi has more than 10 years of experience in Molecular and Cell Biology area where she has been involved in various R&D projects and Technical Support. Her Research Interests are RNA Biology, Gene Editing, and Infectious Diseases.",institutionString:"Independent scientist",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],coeditorOne:{id:"243898",title:"Dr.",name:"Mohammad W.",middleName:null,surname:"Khan",slug:"mohammad-w.-khan",fullName:"Mohammad W. Khan",profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:"Mohammad Khan is a research enthusiast, working as an Application Scientist in a Biotechnology company. He has a Ph.D. degree from the University of Heidelberg in Germany and a DVM degree from India. He also worked as a Post-Doctoral scholar at San Diego State University , USA.\n\nDr. Khan has more than 15 years of experience in Molecular and Cell Biology area where he has been involved in various R&D projects and Technical Support. He has authored and reviewed several research articles and has also served as guest editor for few high impact journals.\n\nHis Research Interests are RNA biology, cancer research, immunology, genomics, gene editing, and infectious diseases.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"6",title:"Biochemistry, Genetics and Molecular Biology",slug:"biochemistry-genetics-and-molecular-biology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"184402",firstName:"Romina",lastName:"Rovan",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/184402/images/4747_n.jpg",email:"romina.r@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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\n\t\t\t
1. Introduction
\n\t\t\t
Urinary tract infections (UTIs) are among the most common conditions requiring medical treatment with 6-10% of all young females demonstrating bacteriuria (Raz 2001). The incidence of UTIs increases with age and 25-50% of females aged 80 or more have bacteriuria (Abrutyn et al. 1988). UTIs occur as a result of interactions between the uropathogen and host and their pathogenesis involves several processes. Initially the uropathogen attaches to the epithelial surface; it subsequently colonises and disseminates throughout the mucosa causing tissue damage. After the initial colonisation period, pathogens can ascend into the urinary bladder resulting in symptomatic or asymptomatic bacteriuria. Further progression may lead to pyelonephritis and renal impairment. Specific virulence factors residing on the uropathogen’s membrane are responsible for bacterial resistance to the normally effective defence mechanisms of the host. Recently, bacterial adhesins and their associated epithelial binding sites have been identified and natural anti-adherence mechanisms are currently under investigation.
\n\t\t\t
An understanding of pathogenic and anti-adherence mechanisms may allow physicians to develop appropriate strategies for UTI prevention and adequate management protocols. In the present chapter we discuss current concepts on the pathogenesis of UTIs with particular emphasis on pathogenic bacteria, virulence factors, predisposing factors, natural defences within genitourinary tract and consequences when these defence mechanisms are altered.
\n\t\t
\n\t\t
\n\t\t\t
2. Routes of infection
\n\t\t\t
In healthy patients most uropathogens originate from rectal flora and enter the urinary tract via the urethra into the bladder (Handley et al. 2002). This is known as the ascending route and uropathogens initially adhere to and colonise urothelium of the distal urethra (Fig.1). Enhancement of this route is exacerbated in patients with soiling around the perineum, in patients with urinary catheters and in females that use spermicidal agents (Foxman 2002). In patients with established cystitis up to 50% of infections may ascend into the upper urinary tracts and most episodes of pyelonephritis are caused by ascension of bacteria from the bladder through the ureter and into the renal pelvis (Busch and Huland 1984). Bacterial ascent is aided by conditions such as pregnancy and ureteral obstruction as these conditions inhibit ureteral peristalsis. Bacteria that reach the renal pelvis can penetrate the renal parenchyma through the collecting ducts and disrupt the renal tubules.
\n\t\t\t
In healthy individuals infection of the kidney through the haematogenous route is uncommon. Occasionally, the renal parenchyma may be breeched in patients with Staphylococcus aureus bacteraemia or Candida fungaemia that originate from oral sources in immunosuppressed patients (Smellie et al. 1975). On rare occasions bacteria from adjacent organs may penetrate the urinary tract via the lymphatics. Conditions associated with the lymphatic route are retroperitoneal abscesses and severe bowel infections.
\n\t\t\t
Figure 1.
Urinary tract infections may arise from ascending, haematogenous or lymphatic routes. Ascending routes of infection are most common among patients with an established UTI.
\n\t\t
\n\t\t
\n\t\t\t
3. Urinary pathogens
\n\t\t\t
\n\t\t\t\t
3.1. Pathogenic bacteria
\n\t\t\t\t
E. coli accounts for 85% of community acquired and 50% of hospital acquired urinary tract infections. Within the E.coli species a number of subgroups (O1, O2, O4, O6, O7, O8, O18, O25, O68 and O75) are frequently isolated from patients with UTI (Brooks et al. 1981, Gruneberg 1969, Roberts and Phillips 1979, Vosti et al. 1964). Gram negative bacteria such as Klebsiella and Proteus; and Gram positive Enterococcus faecalis and Staphylococcus saprophiticus are causative agents for the remainder of community acquired infections (Kennedy et al. 1965). The remainder of hospital acquired infections usually occur after colonisation with Klebsiella, Enterobacter, Citrobacter, Serratia, Pseudomonas aeruginosa, Providencia, E. faecalis, or S. epidermidis (Kennedy et al. 1965). Notably, the patient’s age may influence they type of infective organism present with Staphylococcus saprophiticus now accounting for 10% of UTIs in young females compared to less than 1% in elderly female patients.
\n\t\t\t
\n\t\t\t
\n\t\t\t\t
3.2. Uncomplicated UTIs
\n\t\t\t\t
UTIs can be classified as either complicated or uncomplicated depending on underlying host factors and on underlying uropathogens as illustrated in table 1. The aetiology of uncomplicated UTIs has remained constant over the last 2 to 3 decades with E. coli accounting for the vast majority of cases. Previously, female patients with uncomplicated UTIs generally remained sensitive to a trimethoprim-sulfamethoxazole combination and the traditional approach to therapy had been an empirical short-course treatment with this antibiotic regimen (Hooton and Stamm 1997, Stamm and Hooton 1993). Unfortunately, a number of more recent studies have demonstrated increasing antimicrobial resistance among uropathogens causing uncomplicated cystitis and traditional antibiotic regimens have been questioned (Gupta et al. 1999). One study investigated antimicrobial resistance among 4000 female petients with UTI isolates over a 5 year experimental time period. Results from this study demonstrated an increase in antimicrobial (E. coli) resistance from 9% to 18% in patients treated with trimethoprim-sulfamethoxazole (Gupta et al. 1999). In addition, resistance to cephalothin (a first generation cephalosporin) increased from 20% to 28% and resistance to ampicillin increased from 26% to 34%. Notably, resistance to nitrofrantoin and ciprofloxacin remained <1% after the 5 year period. This increase in bacterial resistance has been attributed to recent administration of trimethoprim-sulfamethoxazole, diabetes mellitus, recent hospitalisation and recent administration of any other antibiotic (Wright et al. 1999).
\n\t\t\t\t
Clinical implications for increasing resistance trends include a potential alteration to antibiotic regimens commonly administered for treating uncomplicated UTIs. One study demonstrated a greater cure rate after a 7-day course of ciprofloxacin compared to a 14-day course of trimethprim-sulfamethoxazole in premenopausal females with uncomplicated pyelonephritis (Talan et al. 2000). In this study it is also notable that E. coli resistance to trimethoprim-sulfamethoxazole was significantly greater (18%) compared to ciprofloxacin (0%). Lower cure rates for uncomplicated UTIs in females treated with trimethoprim-sulfamethoxazole have also been demonstrated in another study where failure rates increased from 3% to 13% in sensitive E.coli strains and from 27% to 40% in resistant strains (McCarty et al. 1999). Based on these studies antimicrobial treatment with either a fluoroquinolone, nitrofurantoin or fosfomycin are currently recommended for uncomplicated UTIs. Importantly, clincians should also be aware of the antimicrobial spectrum for these agents prior to administration as nitrofurantoin is not effective for treating uncomplicated pyelonephritis but highly effective for treating acute cystitis. Recurrent uncomplicated UTIs occur after 3 to 6 months in 25% to 35% of patients after their initial UTI. The second strain is caused by an identical strain to the first UTI in up to 60% of patients with recurrent UTI (Ronald 2003).
\n\t\t\t
\n\t\t\t
\n\t\t\t\t
3.3. Complicated UTIs
\n\t\t\t\t
Underlying host factors such as age, catheterisation, diabetes mellitus and spinal cord injury predispose to complicated UTIs (Fig. 2). In complicated UTIs less virulent uropathogens (that rarely cause disease in a normal urinary tract) can cause significant damage to an abnormal urinary tract. Studies have demonstrated associations between Group B streptococcal bacteraemia, Candida and Enterococci with complicated UTIs in the elderly population (Khan and Ahmed 2001, Munoz et al. 1997).
\n\t\t\t\t
Figure 2.
Predisposing factors for complicated UTIs.
\n\t\t\t\t
Children with comorbidities are more likely to develop complicated UTIs and Staphylococcus aureus is the most frequently isolated micro-organism in paediatric patients with indwelling catheters (Schlager 2001). Candida and coagulase-negative staphylococci are associated with complicated UTIs after instrumentation of the paediatric urinary tract. Of note, enterobacteriaceae are the most frequently isolated uropathogen in children with uncomplicated UTIs (Schlager 2001).
\n\t\t\t\t
UTIs are among the top 10 complicating illnesses in patients with diabetes mellitus with E. coli, Klebsiella, Group B Streptococci and Enterococcus among the common uropathogens (Ronald and Ludwig 2001). In fact, Group B Streptococcus and Klebsiella are 2-3 times more common in patients with diabetes mellitus than in patients without the condition (Ronald and Ludwig 2001). However, E. coli remains the most causative uropathogen for UTIs in patients with diabetes as demonstrated in one prospective study where E. coli was isolated in 56.1% of diabetic patients with a UTI (Bonadio et al. 1999). There is a higher rate of bladder catheterisation in patients with diabetes and this factor may partially account for the higher incidence in this patient cohort (Ronald 2003).
\n\t\t\t\t
Common uropathogens causing complicated UTIs among patients with spinal cord injuries and indwelling catheters include E. coli, Pseudomonas and Proteus mirabilis (Mobley et al. 1994). The latter is particularly associated with complicated UTIs as it possesses unique virulence factors that enhance its invasive potential (Coker et al. 2000). One study demonstrated a significant increase in nosocomial UTIs from 2.63 of 1000 patient days to 4.35 of 1000 patient days over a 9 year period (p<0.003). Notably, 88% of nosocomial UTIs in this study were catheter related (Bronsema et al. 1993).
\n\t\t\t\t
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\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tPathogens in uncomplicated UTIs\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tPathogens in complicated UTIs\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Escherichia coli
\n\t\t\t\t\t\t\t
Escherichia coli
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Staphylococcus saprophyticus
\n\t\t\t\t\t\t\t
Kelbsiella
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Kelbsiella
\n\t\t\t\t\t\t\t
Enetrobacter cloacae
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Enterococcus faecalis
\n\t\t\t\t\t\t\t
Serratia marcescens
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Proteus mirabilis
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Pseudomonas aeruginosa
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Enterococcus faecalis
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Group B streptococci
\n\t\t\t\t\t\t
\n\t\t\t\t\t
Table 1.
Underlying uropathogens commonly isoloated in complicated and uncomplicated urinary tract infection (UTI) (Ronald 2003).
\n\t\t\t
\n\t\t
\n\t\t
\n\t\t\t
4. Bacterial adherence mechanisms
\n\t\t\t
\n\t\t\t\t
4.1. Virulence factors
\n\t\t\t\t
Bacterial virulence factors play a significant role in determining whether an organism will invade the urinary tract and the level of infection acquired. Uropathogenic E. coli (UPEC) is present within bowel flora and pathogenic strains of this microorganism can infect the urinary tract by expressing specific virulence factors that permit adherence and colonisation of the lower urinary tract (Schlager et al. 2002, Yamamoto et al. 1997). Adherence of the micro-organism is dependent on 3 important environmental characteristics; firstly the bacteria’s own adhesive characteristics, secondly the receptive features of the urothelium and finally the fluid that is present between both surfaces (Schaeffer et al. 1981). Bacteria will migrate proximally and precipitate a host derived inflammatory response after adhering to the mucosal surface.
\n\t\t\t\t
Adhesins found on the surface of the bacterial membrane are responsible for initial attachment onto urinary tract tissues (Mulvey 2002) (Fig. 3).
\n\t\t\t\t
Figure 3.
Adhesins on the uropathogen are responsible for attachment of the bacteria to the uroepithelial cell membrane of the host.
\n\t\t\t\t
Adhesins are classified as fimbrial or afimbrial, depending on whether the adhesin is displayed as part of a rigid fimbria or pilus. Fimbriae and pili are surface glycoproteins that function as ligands for glycolipid and glycoprotein receptors on uroepithelial cells. Bacteria may produce 100-400 pili on the same cell and other cells can produce the same pilus type. Each pilus is 5-10 μm in diameter and up to 2 μm in length (Klemm 1985). A pilus is composed of subunits referred to as pilin and they are classified as either mannose sensitive or mannose resistant, based on their ability to mediate haemagglutination of erythrocytes. The most common types of pili are types 1, P and S. Assemblance of pili within the urinary tract is mediated by the ‘chaperone/ usher pathway’ where periplasmic chaperones such as P pilus chaperone ‘PapD’ and type 1 pilus chaperone ‘FimC’ possess two immunoglobulin (Ig)-like domains that are oriented to form a boomerang like shape (Kau et al. 2005, Kuehn et al. 1993, Lau et al. 2005). These chaperones are important for binding with pilus subunits to form stable complexes. The FimC chaperone accelerates the folding of type 1 pilus subunits to strengthen its binding process after its initial attachment process (Vetsch et al. 2004).
\n\t\t\t
\n\t\t\t
\n\t\t\t\t
4.2. Type 1 pili
\n\t\t\t\t
Type 1 pili are also referred to as mannose sensitive pili and they are commonly expressed in pathogenic and non pathogenic strains of E. coli. They are termed mannose sensitive as haemagglutination of erythrocytes is inhibited in the presence of mannose (Reid and Sobel 1987). Type 1 pili are composed of a helical rod with repeating Fim A subunits that are bound to a distal tip structure containing the Fim H adhesin (Jones et al. 1995). During the colonisation process Fim H adhesins bind to mannosylated receptors that are found on the host’s uroepithelium. An inflammatory process occurs shortly after this binding process has been initiated. A number of studies have demonstrated that interactions between the Fim H adhesin and epithelial cells on the bladder’s surface are essential for colonisation and infection of bladder epithelium with strains of uropathogenic E. coli (Sun 1996, Wu et al. 1996). This specific ‘adhesin-epithelial cell’ binding process occurs when type 1 pili bind to uroplakin 1a (UP1a) and uroplakin 1b (UP1b) (Malaviya and Abraham 1998). (Fig. 4) Uroplakins are membrane proteins that are found on umbrella cells which line the luminal surface of the urinary bladder. Initially adhesin binding mechanisms were investigated in a mouse cystitis model where numerous bacteria attached to the urothelial surface of the mouse urinary tract shortly after an inoculation period. Scanning electron microscopy of the urothelial layers demonstrated that Fim H containing pili bound to the central cavity of uroplakin hexameric rings and this binding process is responsible for the initial steps leading to active UTI (Mulvey et al. 1998).
\n\t\t\t\t
Figure 4.
During the colonisation period FimH adhesins bind to umbrella cells via uroplakin 1a and uroplakin 1b membrane receptors.
\n\t\t\t\t
After binding to the epithelial surface the activated Fim H adhesins migrate towards deeper urothelial layers and penetrate the cell membrane (Mulvey et al. 2000). Once the uropathogen is intracellular the invasive process continues as bacteria proliferate within the cytosol to form clusters (Anderson et al. 2004b). Eight hours after inoculation the phenotypic appearance of the bacteria changes to an engulfing ‘biofilm’ like structure that protects against the host’s immune response and shields the uropathogen from its surrounding environment (Justice et al. 2004) (Fig. 5). A decrease in the rate of bacterial proliferation will allow for effective production of a ‘biofilm matrix’. This matrix can prevent the host’s neutrophils from penetrating its surface. The ‘biofilm’ concept stems from the idea that bacteria co-operate with one another to remain viable and proliferate after attaching to a suitable substrate. Previously, it has been demonstrated that biofilms play an important role in a number of disease processes (Kau et al. 2005, Parsek and Singh 2003). Bacterial biofilms can form within infected urinary tract calculi, during Pseudomonas infections in patients with cystic fibrosis and in infective endocarditis. During the disease process biofilms form irreversible associations with their host by forming extracellular polysaccharides that have specialised functions (Justice et al. 2004).
\n\t\t\t\t
Biofilms can form on many different types of bacteria however the sequence of events during the ‘formation process’ remains similar in all bacteria. Firstly, bacteria express extracellular polymeric substances that are initially reversible and subsequently become irreversible. Bacteria that have irreversibly attached to a surface will serve as a nidus for continued replication and recruitment of other bacteria. Irreversible attachment is usually established after 24 hours where the bacteria will develop into a complicated ‘tower’ like structure and become filamentous (up to 70 µm in length). Morphological changes allow the uropathogen to evade the host’s immune response (Justice et al. 2004). Bacteria that have clustered will eventually detach from their group, become motile and flee the host cell. Bacterial adherence and replication will recur after the uropathogen escapes its intracellular environment and this effective replication process will allow bacterial invasion to persist (Anderson et al. 2004a) (Fig. 5).
\n\t\t\t\t
Figure 5.
After attaching to the epithelial surface the uropathogen will enter the cytosol (A). Intracellular bacteria rapidly proliferate within the first 24 hours (B). Subsequently, proliferation rate decreases and a protective biofilm matrix forms (C). Morphological changes allow the uropathogen to evade the host’s immune response. Uropathogens that have clustered become motile and detach from the biofilm to disperse (D).
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\n\t\t\t
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4.3. P Fimbriated pili
\n\t\t\t\t
P fimbriated pili or mannose resistant strains of E. coli are associated with uncomplicated pyelonephritis as the receptor for P fimbriae is the major glycolipid component present on renal cell membranes (Mulvey 2002). They are termed mannose resistant as they are not affected by mannose during the haemagglutination process for human erythrocytes (Vaisanen et al. 1981). PapG is an adhesin found at the tip of the pilus and it recognizes the α-d-galctopyranosyl-(1-4)-β-d-galctopyranoside receptor which is found on P-blood group antigens on the host’s uroepithelium (Kallenius et al. 1981) (Fig. 6). Mannose resistant adhesins that do not demonstrate digalactoside-binding affinity are referred to as ‘X’ adhesins. A correlation between severe UTIs and bacterial adherence was first identified in 1976 (Eden et al. 1976). Strains of uropathogenic E. coli in girls with established pyelonephritis had an adhesive ability of 70-80% compared to 10% in strains that caused asymptomatic bacteriuria. P pili were present in 91% of strains that caused pyelonephritis compared to a prevalence of 7% in bowel isolates from healthy children (Eden et al. 1976). Although mannose resistant haemagglutinins (MRHA) are associated with pyelonephritis it is important to note that no link exists between MRHA and renal scarring.
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4.4. Phase variation
\n\t\t\t\t
Interestingly, in vivo studies have shown that environmental factors are responsible for rapid changes in pili in E. coli isolates. This transformation process is known as known as
\n\t\t\t\t
Figure 6.
P fimbiae bind to the α-d-galctopyranosyl-(1-4)-β-d-galctopyranoside receptor on the host’s renal epithelial cell via the PapG adhesin.
\n\t\t\t\t
phase variation and it involves alternating periods of piliated and nonpiliated adhesins during in vivo E. coli infection (Hultgren et al. 1986, Schaeffer et al. 1987). One study showed phase variation of pili using indirect immunofluorescense assays of voided urine in human patients. Analysis of the urine samples showed type 1 pili in 31 of 41 samples and P pili in 6 of 18 samples with piliation status varying from predominantly piliated to nonpiliated cells (Kisielius et al. 1989). These results demonstrated that type 1 and P pili are expressed and subject to phase variation in vivo during acute UTIs. The process of phase variation among adhesins has notable clinical implications. Importantly, the presence of type 1 pili may facilitate adherence and colonisation of the host’s mucosa in the lower urinary tract. However, P pili may predominate as the infective process progresses and ascends. This transformation process occurs because primary mediators for the attachment of P pili to their glycolipid receptors are found within the kidney (Mulvey et al. 1998).
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4.5. Cell receptivity
\n\t\t\t\t
Epithelial cell receptivity also plays an important pathogenic role in female patients that are susceptible to recurrent UTI. The receptivity concept was established after vaginal epithelial cells were collected from patients susceptible to recurrent UTI with E. coli and compared with control samples that were resistant to UTI (Fowler and Stamey 1977). Results from this study demonstrated that strains of E. coli associated with cystitis ardently adhered to vaginal epithelial cells of susceptible females. Notably, buccal cell receptivity is also increased for different strains of E. coli in females with increased vaginal cell receptivity. These findings indicate a genotypic trait as the increase in receptor sites for strains of E. coli is not confined to the vagina in females with recurrent UTIs. Further analysis of this genetic concept by assessing human leukocyte antigens (HLAs) in females with recurrent UTIs has demonstrated that HLA-A3 may be a contributing factor. It has also been shown that a greater number of uropathogens attach to epithelial cell surface in females that are greater than 65 years of age compared to premenopausal females (i.e. age 18-40) (Schaeffer et al. 1983).
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5. Predisposing factors for pathogenic adherence
\n\t\t\t
\n\t\t\t\t
5.1. Alterations to the host’s natural defence mechanisms
\n\t\t\t\t
Normal flora around the vaginal introitus, periurethral region and urethra include microorganisms such as lactobacilli, coagulase negative staphylococci and streptococci that form a barrier against pathogenic colonisation. Alterations in the vaginal mucosa and decreases in its pH are thought to play an important role for with coliforms (Hooton et al. 1996a). Acute disruptions to this mucosal barrier are frequently attributed to spermicidal and antimicrobial agents that alter normal flora and induce increased receptivity for uropathogens (Hooton et al. 1996a). Host factors that contribute to the disruption of this mucosal barrier are illustrated in table 2.
\n\t\t\t\t
Comorbidities such as diabetes mellitus, sickle cell disease, hyperphosphataemia, gout and analgesics are also associated with altering the host’s natural defence mechanisms (Freedman 1975). The incidence of pyelonephritis is up to fivefold higher in diabetics compared to non diabetic patients (Nicolle et al. 1996). Furthermore, female patients with diabetes mellitus are 3 times more likely to develop pyelonephritis compared to male patients with the condition (Nicolle et al. 1996). Diabetes also predisposes patients to more complicated UTIs with an inflammatory urothelial response occurring in the upper tracts of up to 80% of diabetic patients with UTIs (Forland et al. 1977, Stapleton 2002). In addition, UTIs in this patient cohort are often caused by atypical organisms and complications may progress to include papillary necrosis, perinephric abscesses or multisystemic infections (Stapleton 2002).
\n\t\t\t\t
Urinary tract obstruction and stasis of urine flow can significantly alter the host’s defence mechanisms and both factors strongly predispose to complicated UTIs (Hooton 2000). During the obstructive process local mucosal defence mechanisms are disturbed as the epithelial lining over-distends and pooled urine functions as a mean for bacterial growth and proliferation (Hooton et al. 2000). Urinary catheters, particularly in patients with high residual volumes, are also ideal media for uropathogens to colonise the urinary tract. Finally, fistulae can facilitate direct access into the genoitourinary tract via the gastrointestinal system.
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\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tGenetic\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tBiological\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tBehavioural\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t\tOthers\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Blood group antigen
\n\t\t\t\t\t\t\t
Congenital abnormalities
\n\t\t\t\t\t\t\t
Sexual intercourse
\n\t\t\t\t\t\t\t
Decreased mental status
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Non-secretor status
\n\t\t\t\t\t\t\t
Urinary obstruction
\n\t\t\t\t\t\t\t
Use of diaphragm
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Increased density of adhesion receptors
\n\t\t\t\t\t\t\t
Calculi
\n\t\t\t\t\t\t\t
Use of spermicides
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\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Diabetes mellitus
\n\t\t\t\t\t\t\t
Antimicrobial use
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Anatomical
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Residual urine
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Atrophic vaginitis
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Urinary incontinence
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Prior history of UTI
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Maternal history of UTI
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Urinary catheters
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Stents
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Immunological deficiency (HIV)
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t\t
Renal transplant
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\n\t\t\t\t\t\t\t
\n\t\t\t\t\t\t
\n\t\t\t\t\t
Table 2.
Host factors that contribute to the pathogenesis of UTIs in female patients.
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5.2. Anatomical and physiological factors
\n\t\t\t\t
It is widely acknowledged that a number of factors contribute to a greater prevalence in UTIs in females compared to males. In particular, female pelvic anatomy plays an important predisposing role for recurrent UTIs in female patients. One study investigated differences in perineal anatomical measurements and voiding characteristics in 100 females with a history of recurrent UTIs and in 113 females with no prior history of UTIs. Analysis of the results demonstrated that the urethra and anus were significantly closer together in cases of UTI (4.8 ± 0.6cm) compared to controls (5.0 ± 0.7cm, p= 0.03) (Hooton 2000). Other important physiological and anatomical factors that predispose to bacterial adherence in females (compared to males) include a drier urethral meatus, a shorter urethra and the absence of antibacterial properties provided by prostatic fluid (Lipsky 1989).
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5.3. Spermicidal compounds
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Nonoxynol-9 is a non-ionic surfactant that is the most active ingredient found in spermicidal compounds in the USA. Results from in vitro studies have shown that it is less active against uropathogenic bacteria compared to Lactobacillus (Hooton et al. 1991a, McGroarty et al. 1990) with hydrogen peroxide-producing strains being particularly susceptible (Hooton et al. 1991a). Therefore, it appears that vaginal colonisation with hydrogen peroxide vaginal strains of lactobacilli may play an important role in bacterial resistance (Eschenbach et al. 1989). This hypothesis has been tested in other studies where hydrogen peroxide-producing lactobacilli had a protective effect against bacterial vaginosis, symptomatic candidosis and vaginal colonisation with genital pathogens (Hawes et al. 1996, Hillier et al. 1992). In support of this hypothesis one case-control study has also demonstrated that vaginal colonisation with E. coli occurs more frequently in females without hydrogen peroxide-producing lactobacilli compared to females with these strains (odds ratio 4.0; p=0.01) (Gupta et al. 1998). In this study, spermicidal use among females correlated with an increased risk of vaginal colonisation with E. coli (odds ratio 12.5; p<0.001) and with the absence of hydrogen peroxide-producing lactobacilli. Another study also showed decreased vaginal lactobacilli and an increase in vaginal coliforms after nonoxynol-9 instillation in the absence of sexual activity and diaphragm use (Rosenstein et al. 1998).
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Based on these studies, it seems likely that the antimicrobial activity of spermicides alters the vaginal ecosystem and provides a suitable environment for growth and proliferation of uropathogens. It is interesting to note that small amounts of nonoxynol-9 on condoms can increase the risk of UTI in females in the absence of sexual intercourse (Fihn et al. 1998, Fihn et al. 1996).
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\n\t\t\t
\n\t\t\t\t
5.4. Premenopausal females
\n\t\t\t\t
In premenopausal healthy females sexual intercourse and spermicide use are the most important factors predisposing to UTIs. One study demonstrated a 2.6 fold increased risk of UTI in females (age 24) that have sexual intercourse 3 times a week compared to females that do not have intercourse (Hooton et al. 1996a). It is hypothesised that an increased risk of UTI from sexual intercourse occurs from trauma at the introitus (Foxman et al. 1997, Hooton et al. 1991b) or through mechanical introduction of the uropathogen into the bladder (Hooton et al. 1991b). Other predisposing factors to UTI in premenopausal patients are a new sexual partner during the last year, having a first UTI less than 15 years of age and having a mother with a history of UTIs (Hooton et al. 1996a). Interestingly, the latter two are associated with a two- to four- fold increase in risk compared to normal females, perhaps suggesting a genetic predisposition. Finally, a previous history of UTI is a strong predictor of having a subsequent UTI. This may be attributable to a host’s biological or behavioural features or from persistent colonisation of a particular bacterial strain.
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\n\t\t\t\t
5.5. Oestrogen
\n\t\t\t\t
The role of oestrogen in the pathogenesis of UTIs is controversial. In vitro studies have demonstrated that oestrogen permits adherence of uropthogens to vaginal epithelial cells (Hooton et al. 1996b). However, other studies also suggest that oestrogen deficiency in postmenopausal females may increase the risk of UTI (Haspels et al. 1981, Thomas et al. 1980). In fact, one study showed that half of females aged 61 or older had genitourinary symptoms and 29% of this cohort also complained of urinary incontinence (Iosif and Bekassy 1984). Furthermore, the risk of UTI in postmenopausal females is decreased by topical application of oestrogen creams as demonstrated in one double-blinded-placebo controlled study (Raz and Stamm 1993). In this study results showed that vaginal colonization with E. coli was halved and lactobacillus colonization was re-established after topical application of oestrogen in postmenopausal females (Fig. 7). As a result vaginal pH was decreased along with colonisation with Enterobacteriaceae.
\n\t\t\t\t
Figure 7.
Proposed pathophysiology of UTIs in patients with oestrogen deficiency (Raz 2001).
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\n\t\t\t
\n\t\t\t\t
5.6. Genetic susceptibility
\n\t\t\t\t
Interleukin-8 is an inflammatory cytokine that promotes neutrophil migration across infected urothelial cells (Godaly et al. 1998, Godaly et al. 1997). Absence of its receptor CXCR1 has recently been shown to promote bacteraemia within the urinary tract as demonstrated in one study in knockout mice that lacked CXCR1 (Frendeus et al. 2001). A genetic predisposition to UTIs has been suggested in paediatric patients where children with recurrent pyelonephritis demonstrated a defect in the CXCR1 receptor (Frendeus et al. 2000).
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\n\t\t\t
\n\t\t\t\t
5.7. Antimicrobial agents
\n\t\t\t\t
Animal and human studies suggest that antimicrobial agents predispose females to UTIs by altering their host’s vaginal ecology (Herthelius-Elman et al. 1992, Winberg et al. 1993). Colonisation with E. coli is increased after administering β-lactam antimicrobial agents in monkeys (Herthelius-Elman et al. 1992). Notably, trimethoprim and nirofuarantoin do not enhance vaginal colonisation with E.coli in similar trials on monkeys and these findings suggest that β-lactam antibiotics may be responsible for altering the genital flora of female patients. Less vaginal colonisation with uropathogens occurs after a course of co-trimoxazole or fluoroquinolones when compared to β-lactam antimicrobials. Finally, the timing of antimicrobial agents also appears to play a role for increasing the risk of UTI. One prospective study on premenopausal females demonstrated an increased risk for UTI in females that had been prescribed antimicrobial therapy during the preceding 15-28 days compared to the previous 3-14 days (Smith et al. 1997).
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5.8. Urological factors
\n\t\t\t\t
Several urological factors are associated with a predisposition to UTIs in female patients. Cystocele, high post-void residual volume and urinary incontinence are strongly associated with recurrent UTIs as demonstrated in one case control study (Raz et al. 2000). In addition, surgery of the genitourinary tract often precedes the onset of a UTI and urological surgery itself is also an independent risk factor for recurrent UTI (Raz et al. 2000).
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\n\t\t
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6. Host response to pathogenic adherence
\n\t\t\t
A series of defence pathways are activated by the host after the uropathogen adheres to the mucosal surface. Epithelial cells exfoliate within hours of the initial infection and infected urothelial cells are shed during this process (Mysorekar et al. 2002). Secretion and excretion of the infected urothelial cells is mediated by type 1 piliated bacteriae that induce cell apoptosis (Mulvey et al. 1998). In healthy patients the epithelium lining the surface of the bladder is quiescent as the umbrella cell layer is renewed every few months. However these normally repressed proliferation and differentiation cascades are rapidly activated after the infective process in the murine cystitis model. These proliferation cascades have the potential to induce effective regeneration of an umbrella cell layer within 24 hours of the exfoliation process (Fig. 8) Another study in mice has demonstrated that exfoliation of urothelial cells prevents uropathogenic E. coli from forming clusters (Anderson et al. 2004b). Notably, mice that elicited a mild exfoliation process in response to the uropathogen were more likely to form biofilms that migrated into deeper layers.
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The host’s innate immune response is primarily responsible for providing resistance to the invading uropathogen. Numerous cell types such as neutrophils, macrophages, eosinophils and natural killer cells are activated as the uropathogen invades. In addition, polymorphonuclear leukocytes synthesise nitric oxide by increasing the transcription of nitric oxide synthase and this process has a toxic effect on the invading pathogen (Poljakovic and Persson 2003, Poljakovic et al. 2001). During the initial inflammatory response period it is important to note that neutrophils play a key role as they migrate towards the infected site. The migratory process is mediated by pathogen-associated molecular pattern receptors (PAMPs) and Toll-like receptors (TLRs) (Anderson et al. 2004b). After lipopolysaccharides (LPS), peptidoglycans (PG) and other bacterial products are recognised TLRs activate signalling pathways that initiate immune and inflammatory responses to kill pathogens (Anderson et al. 2004a). TLR4 and its co-receptors (CD14 and MD2) recognise Gram-negative bacterial LPS and activate the innate immune response (Haraoka et al. 1999). In addition, TLR11 is released from the kidney and activated to prevent the infection from ascending towards the renal parenchyma (Zhang et al. 2004). Notably, more recent studies have demonstrated that uropathogens can suppress NFĸB and consequentially decrease the host’s inflammatory response. This tactic allows the uropathogen to invade into deeper tissues (Klumpp et al. 2001). After 7-10 days the adaptive immune response is activated where specific uropathogens are recognised by B and T lymphocytes with high affinity antibodies.
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Figure 8.
In healthy patients the umbrella cell layer lining the lumen of the urinary bladder is renewed every few months (A). However, epithelial cells exfoliate within 6 hours after infection with an invasive uropathogen (B). This excretory process allows for effective excretion of infected urothelial cells. Within 24 hours of exfoliation proliferation cascades induce effective regeneration of a new umbrella cell layer.
\n\t\t\t
Apart from triggering the initial inflammatory response, recruited neutrophils are also important for providing resistance to UTIs as demonstrated in one study on mice (Haraoka et al. 1999). Results from this study showed that UTIs are persistent in mice with specific genetic backgrounds and that UTIs will resolve spontaneously in mice with normal backgrounds. These findings suggest that specific host genes may be important for effective resolution of the UTI as demonstrated in another study on mice where TLR11 recognised uropathogenic E. coli and prevented its ascension into the kidneys (Hopkins et al. 1998). Interestingly, TLR11 is truncated in humans and susceptibility for pyelonephritis is increased. Furthermore, a study by Mysorekar et al demonstrated that females with recurrent UTIs had reduced levels of CD16 which led to decreased bacterial phagocytosis (Mysorekar et al. 2002).
\n\t\t\t
The urinary tract is a component of the secretory immune system as it is the first defence system encountered by invading uropathogens. Infections of the kidneys are associated with serum and kidney immunoglobulin synthesis and type specific antibodies have been detected in the host’s urine. Serum antibodies targeting type 1 and P pili have been detected after episodes of pyelonephritis with IgG and SIgA antibodies also detected in the urine (Rene et al. 1982). Synthesis of these specific antibodies occurs locally to enhance the opsonisation process in infected patients and to reduce adherence of E. coli (de Ree and van den Bosch 1987). The potential for modifying these immunological factors to decrease the incidence of UTIs in susceptible patients has been explored through immunisation techniques in animal models. Vaccination with P fimbria has been shown to decrease adherence of P-fimbriated E. coli to uroepithelial cells and prevent pyelonephritis in monkeys (Roberts and Phillips 1979). In addition, vaccination with FimH adhesin has been shown to prevent cystitis in mice (Langermann et al. 1997). It is therefore plausible that vaccination techniques may reduce colonisation and ascending infections in susceptible female patients (Uehling et al. 1994a, Uehling et al. 1994b).
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\n\t\t
\n\t\t\t
7. Conclusions
\n\t\t\t
A renewed interest in the pathogenesis of UTIs has developed over recent years. Pathogenic mechanisms are complicated and influenced by the biological and behavioural features of the host as well as adhesins from the invading uropathogen. Advances at a molecular level have led to a greater understanding in adherence mechanisms between bacterial virulence factors and the host’s uroepithelial receptors. An improved understanding of these pathogenic mechanisms and associated host risk factors is important for developing novel strategies for the treatment and prevention of UTIs.
\n\t\t
\n\t\n',keywords:null,chapterPDFUrl:"https://cdn.intechopen.com/pdfs/19318.pdf",chapterXML:"https://mts.intechopen.com/source/xml/19318.xml",downloadPdfUrl:"/chapter/pdf-download/19318",previewPdfUrl:"/chapter/pdf-preview/19318",totalDownloads:12304,totalViews:4210,totalCrossrefCites:1,totalDimensionsCites:9,hasAltmetrics:0,dateSubmitted:"November 18th 2010",dateReviewed:"April 20th 2011",datePrePublished:null,datePublished:"September 6th 2011",dateFinished:null,readingETA:"0",abstract:null,reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/19318",risUrl:"/chapter/ris/19318",book:{slug:"clinical-management-of-complicated-urinary-tract-infection"},signatures:"Niall F. Davis and Hugh D. Flood",authors:[{id:"47196",title:"Mr",name:"Niall",middleName:null,surname:"Davis",fullName:"Niall Davis",slug:"niall-davis",email:"nialldavis2001@yahoo.com",position:null,institution:null},{id:"94837",title:"Mr.",name:"Hugh",middleName:null,surname:"Flood",fullName:"Hugh Flood",slug:"hugh-flood",email:"hugh.flood@hse.ie",position:null,institution:{name:"Mid-Western Regional Hospital",institutionURL:null,country:{name:"Ireland"}}}],sections:[{id:"sec_1",title:"1. Introduction ",level:"1"},{id:"sec_2",title:"2. Routes of infection",level:"1"},{id:"sec_3",title:"3. Urinary pathogens",level:"1"},{id:"sec_3_2",title:"3.1. Pathogenic bacteria ",level:"2"},{id:"sec_4_2",title:"3.2. Uncomplicated UTIs ",level:"2"},{id:"sec_5_2",title:"3.3. Complicated UTIs ",level:"2"},{id:"sec_7",title:"4. Bacterial adherence mechanisms",level:"1"},{id:"sec_7_2",title:"4.1. Virulence factors ",level:"2"},{id:"sec_8_2",title:"4.2. Type 1 pili ",level:"2"},{id:"sec_9_2",title:"4.3. P Fimbriated pili ",level:"2"},{id:"sec_10_2",title:"4.4. Phase variation ",level:"2"},{id:"sec_11_2",title:"4.5. Cell receptivity ",level:"2"},{id:"sec_13",title:"5. Predisposing factors for pathogenic adherence",level:"1"},{id:"sec_13_2",title:"5.1. Alterations to the host’s natural defence mechanisms ",level:"2"},{id:"sec_14_2",title:"5.2. Anatomical and physiological factors ",level:"2"},{id:"sec_15_2",title:"5.3. Spermicidal compounds ",level:"2"},{id:"sec_16_2",title:"5.4. Premenopausal females ",level:"2"},{id:"sec_17_2",title:"5.5. Oestrogen ",level:"2"},{id:"sec_18_2",title:"5.6. Genetic susceptibility ",level:"2"},{id:"sec_19_2",title:"5.7. Antimicrobial agents ",level:"2"},{id:"sec_20_2",title:"5.8. Urological factors ",level:"2"},{id:"sec_22",title:"6. Host response to pathogenic adherence",level:"1"},{id:"sec_23",title:"7. Conclusions ",level:"1"}],chapterReferences:[{id:"B1",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAbrutyn\n\t\t\t\t\t\t\tE.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBoscia\n\t\t\t\t\t\t\tJ. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKaye\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1988\n\t\t\t\t\tThe treatment of asymptomatic bacteriuria in the elderly’\n\t\t\t\t\tJ Am Geriatr Soc, 36(5), 473 EOF\n\t\t\t\t\t5 EOF\n\t\t\t\t\n\t\t\t'},{id:"B2",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAnderson\n\t\t\t\t\t\t\tG. G.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDodson\n\t\t\t\t\t\t\tK. W.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultgren\n\t\t\t\t\t\t\tS. 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R.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPallares\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWenzel\n\t\t\t\t\t\t\tR. P.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1993\n\t\t\t\t\tSecular trends in rates and etiology of nosocomial urinary tract infections at a university hospital’\n\t\t\t\t\tJ Urol, 150(2 Pt 1), 414 EOF\n\t\t\t\t\t6 EOF\n\t\t\t\t\n\t\t\t'},{id:"B6",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBrooks\n\t\t\t\t\t\t\tH. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBenseman\n\t\t\t\t\t\t\tB. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPeck\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBettelheim\n\t\t\t\t\t\t\tK. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1981\n\t\t\t\t\tCorrelation between uropathogenic properties of Escherichia coli from urinary tract infections and the antibody-coated bacteria test and comparison with faecal strains’\n\t\t\t\t\tJ Hyg (Lond), 87(1), 53-61.\n\t\t\t'},{id:"B7",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBusch\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHuland\n\t\t\t\t\t\t\tH.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1984\n\t\t\t\t\tCorrelation of symptoms and results of direct bacterial localization in patients with urinary tract infections’\n\t\t\t\t\tJ Urol, 132(2), 282 EOF\n\t\t\t\t\t5 EOF\n\t\t\t\t\n\t\t\t'},{id:"B8",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tCoker\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPoore\n\t\t\t\t\t\t\tC. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tLi\n\t\t\t\t\t\t\tX.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMobley\n\t\t\t\t\t\t\tH. 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The role of bacterial adherence’, J Urol, 117(4), 472\n\t\t\t\t6 .'},{id:"B16",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFoxman\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2002\n\t\t\t\t\tEpidemiology of urinary tract infections: incidence, morbidity, and economic costs’\n\t\t\t\t\tAm J Med, 113 Suppl 1A, 5S EOF\n\t\t\t\t\t13S EOF\n\t\t\t\t\n\t\t\t'},{id:"B17",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFoxman\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMarsh\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGillespie\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRubin\n\t\t\t\t\t\t\tN.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKoopman\n\t\t\t\t\t\t\tJ. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSpear\n\t\t\t\t\t\t\tS.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1997Condom use and first-time urinary tract infection’, Epidemiology, 8(6), 637-41.\n\t\t\t'},{id:"B18",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFreedman\n\t\t\t\t\t\t\tL. R.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1975\n\t\t\t\t\tNatural history of urinary infection in adults’\n\t\t\t\t\tKidney Int Suppl, 4, S96\n\t\t\t\t\t100\n\t\t\t\t\n\t\t\t'},{id:"B19",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFrendeus\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGodaly\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHang\n\t\t\t\t\t\t\tL.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKarpman\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tLundstedt\n\t\t\t\t\t\t\tA. C.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvanborg\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2000\n\t\t\t\t\tInterleukin 8 receptor deficiency confers susceptibility to acute experimental pyelonephritis and may have a human counterpart\n\t\t\t\t\tJ Exp Med, 192(6), 881-90.\n\t\t\t'},{id:"B20",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFrendeus\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGodaly\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHang\n\t\t\t\t\t\t\tL.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKarpman\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvanborg\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2001\n\t\t\t\t\tInterleukin-8 receptor deficiency confers susceptibility to acute pyelonephritis’\n\t\t\t\t\tJ Infect Dis, 183 Suppl 1, S56\n\t\t\t\t\t60\n\t\t\t\t\n\t\t\t'},{id:"B21",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGodaly\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFrendeus\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tProudfoot\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvensson\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKlemm\n\t\t\t\t\t\t\tP.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvanborg\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1998\n\t\t\t\t\tRole of fimbriae-mediated adherence for neutrophil migration across Escherichia coli-infected epithelial cell layers’\n\t\t\t\t\tMol Microbiol, 30(4), 725 EOF\n\t\t\t\t\t35 EOF\n\t\t\t\t\n\t\t\t'},{id:"B22",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGodaly\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tProudfoot\n\t\t\t\t\t\t\tA. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tOfford\n\t\t\t\t\t\t\tR. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvanborg\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAgace\n\t\t\t\t\t\t\tW. W.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1997\n\t\t\t\t\tRole of epithelial interleukin-8 (IL-8) and neutrophil IL-8 receptor A in Escherichia coli-induced transuroepithelial neutrophil migration’\n\t\t\t\t\tInfect Immun, 65(8), 3451 EOF\n\t\t\t\t\t6 EOF\n\t\t\t\t\n\t\t\t'},{id:"B23",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGruneberg\n\t\t\t\t\t\t\tR. N.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1969\n\t\t\t\t\tRelationship of infecting urinary organism to the faecal flora in patients with symptomatic urinary infection’\n\t\t\t\t\tLancet\n\t\t\t\t\t766 EOF\n\t\t\t\t\t8 EOF\n\t\t\t\t\n\t\t\t'},{id:"B24",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGupta\n\t\t\t\t\t\t\tK.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tScholes\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1999\n\t\t\t\t\tIncreasing prevalence of antimicrobial resistance among uropathogens causing acute uncomplicated cystitis in women’\n\t\t\t\t\tJAMA, 281(8), 736 EOF\n\t\t\t\t\t8 EOF\n\t\t\t\t\n\t\t\t'},{id:"B25",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGupta\n\t\t\t\t\t\t\tK.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStapleton\n\t\t\t\t\t\t\tA. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tP. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFennell\n\t\t\t\t\t\t\tC. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1998\n\t\t\t\t\tInverse association of H2O2 -producing lactobacilli and vaginal Escherichia coli colonization in women with recurrent urinary tract infections’\n\t\t\t\t\tJ Infect Dis, 178(2), 446-50.\n\t\t\t'},{id:"B26",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHandley\n\t\t\t\t\t\t\tM. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tReingold\n\t\t\t\t\t\t\tA. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tShiboski\n\t\t\t\t\t\t\tS.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPadian\n\t\t\t\t\t\t\tN. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2002\n\t\t\t\t\tIncidence of acute urinary tract infection in young women and use of male condoms with and without nonoxynol-9 spermicides\n\t\t\t\t\tEpidemiology\n\t\t\t\t\t431 EOF\n\t\t\t\t\n\t\t\t'},{id:"B27",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHaraoka\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHang\n\t\t\t\t\t\t\tL.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFrendeus\n\t\t\t\t\t\t\tB.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGodaly\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBurdick\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStrieter\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvanborg\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1999Neutrophil recruitment and resistance to urinary tract infection’, J Infect Dis, 180(4), 1220-9.\n\t\t\t'},{id:"B28",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHaspels\n\t\t\t\t\t\t\tA. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tLuisi\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKicovic\n\t\t\t\t\t\t\tP. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1981\n\t\t\t\t\tEndocrinological and clinical investigations in post-menopausal women following administration of vaginal cream containing oestriol’\n\t\t\t\t\tMaturitas\n\t\t\t\t\t321 EOF\n\t\t\t\t\t7 EOF\n\t\t\t\t\n\t\t\t'},{id:"B29",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHawes\n\t\t\t\t\t\t\tS. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHillier\n\t\t\t\t\t\t\tS. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBenedetti\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStevens\n\t\t\t\t\t\t\tC. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKoutsky\n\t\t\t\t\t\t\tL. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWolner-Hanssen\n\t\t\t\t\t\t\tP.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHolmes\n\t\t\t\t\t\t\tK. K.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1996Hydrogen peroxide-producing lactobacilli and acquisition of vaginal infections’, J Infect Dis, 174(5), 1058-63.\n\t\t\t'},{id:"B30",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHerthelius-Elman\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMollby\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tNord\n\t\t\t\t\t\t\tC. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWinberg\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1992\n\t\t\t\t\tThe effect of amoxycillin on vaginal colonization resistance and normal vaginal flora in monkeys’\n\t\t\t\t\tJ Antimicrob Chemother, 29(3), 329 EOF\n\t\t\t\t\t40 EOF\n\t\t\t\t\n\t\t\t'},{id:"B31",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHillier\n\t\t\t\t\t\t\tS. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKrohn\n\t\t\t\t\t\t\tM. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKlebanoff\n\t\t\t\t\t\t\tS. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tEschenbach\n\t\t\t\t\t\t\tD. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1992\n\t\t\t\t\tThe relationship of hydrogen peroxide-producing lactobacilli to bacterial vaginosis and genital microflora in pregnant women’\n\t\t\t\t\tObstet Gynecol, 79(3), 369 EOF\n\t\t\t\t\t73 EOF\n\t\t\t\t\n\t\t\t'},{id:"B32",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2000\n\t\t\t\t\tPathogenesis of urinary tract infections: an update’\n\t\t\t\t\tJ Antimicrob Chemother, 46 Suppl A, 1\n\t\t\t\t\t7\n\t\t\t\t\n\t\t\t'},{id:"B33",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFennell\n\t\t\t\t\t\t\tC. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tClark\n\t\t\t\t\t\t\tA. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1991a\n\t\t\t\t\tNonoxynol-9: differential antibacterial activity and enhancement of bacterial adherence to vaginal epithelial cells’\n\t\t\t\t\tJ Infect Dis, 164(6), 1216 EOF\n\t\t\t\t\t9 EOF\n\t\t\t\t\n\t\t\t'},{id:"B34",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHillier\n\t\t\t\t\t\t\tS.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tJohnson\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tP. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1991bEscherichia coli bacteriuria and contraceptive method’, JAMA, 265(1), 64-9.\n\t\t\t'},{id:"B35",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tScholes\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHughes\n\t\t\t\t\t\t\tJ. P.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWinter\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tP. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStapleton\n\t\t\t\t\t\t\tA. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStergachis\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1996aA prospective study of risk factors for symptomatic urinary tract infection in young women’, N Engl J Med, 335(7), 468-74.\n\t\t\t'},{id:"B36",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tScholes\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStapleton\n\t\t\t\t\t\t\tA. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tP. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWinter\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGupta\n\t\t\t\t\t\t\tK.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSamadpour\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2000A prospective study of asymptomatic bacteriuria in sexually active young women’, N Engl J Med, 343(14), 992-7.\n\t\t\t'},{id:"B37",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1997\n\t\t\t\t\tDiagnosis and treatment of uncomplicated urinary tract infection’\n\t\t\t\t\tInfect Dis Clin North Am, 11(3), 551 EOF\n\t\t\t\t\t81 EOF\n\t\t\t\t\n\t\t\t'},{id:"B38",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWinter\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tTiu\n\t\t\t\t\t\t\tF.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1996b\n\t\t\t\t\tAssociation of acute cystitis with the stage of the menstrual cycle in young women’\n\t\t\t\t\tClin Infect Dis, 23(3), 635 EOF\n\t\t\t\t\t6 EOF\n\t\t\t\t\n\t\t\t'},{id:"B39",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHopkins\n\t\t\t\t\t\t\tW. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGendron-Fitzpatrick\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBalish\n\t\t\t\t\t\t\tE.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tUehling\n\t\t\t\t\t\t\tD. T.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1998\n\t\t\t\t\tTime course and host responses to Escherichia coli urinary tract infection in genetically distinct mouse strains\n\t\t\t\t\tInfect Immun, 66(6), 2798-802.\n\t\t\t'},{id:"B40",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultgren\n\t\t\t\t\t\t\tS. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchwan\n\t\t\t\t\t\t\tW. R.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchaeffer\n\t\t\t\t\t\t\tA. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDuncan\n\t\t\t\t\t\t\tJ. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1986\n\t\t\t\t\tRegulation of production of type 1 pili among urinary tract isolates of Escherichia coli’\n\t\t\t\t\tInfect Immun, 54(3), 613-20.\n\t\t\t'},{id:"B41",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tIosif\n\t\t\t\t\t\t\tC. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBekassy\n\t\t\t\t\t\t\tZ.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1984\n\t\t\t\t\tPrevalence of genito-urinary symptoms in the late menopause’\n\t\t\t\t\tActa Obstet Gynecol Scand, 63(3), 257 EOF\n\t\t\t\t\t60 EOF\n\t\t\t\t\n\t\t\t'},{id:"B42",body:'\n\t\t\t\tJones, C. H., Pinkner, J. S., Roth, R., Heuser, J., Nicholes, A. V., Abraham, S. N. and Hultgren, S. J. (1995) ‘FimH adhesin of type 1 pili is assembled into a fibrillar tip structure in the Enterobacteriaceae’, Proc Natl Acad Sci U S A, 92(6), 2081-5.\n\t\t\t'},{id:"B43",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tJustice\n\t\t\t\t\t\t\tS. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHung\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tTheriot\n\t\t\t\t\t\t\tJ. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFletcher\n\t\t\t\t\t\t\tD. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAnderson\n\t\t\t\t\t\t\tG. G.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tFooter\n\t\t\t\t\t\t\tM. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultgren\n\t\t\t\t\t\t\tS. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2004\n\t\t\t\t\tDifferentiation and developmental pathways of uropathogenic Escherichia coli in urinary tract pathogenesis\n\t\t\t\t\tProc Natl Acad Sci U S A, 101(5), 1333-8.\n\t\t\t'},{id:"B44",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKallenius\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMollby\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSvenson\n\t\t\t\t\t\t\tS. B.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWinberg\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1981Microbial adhesion and the urinary tract’, Lancet, 2(8251), 866.\n\t\t\t'},{id:"B45",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKau\n\t\t\t\t\t\t\tA. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHunstad\n\t\t\t\t\t\t\tD. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultgren\n\t\t\t\t\t\t\tS. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2005\n\t\t\t\t\tInteraction of uropathogenic Escherichia coli with host uroepithelium’\n\t\t\t\t\tCurr Opin Microbiol, 8(1), 54 EOF\n\t\t\t\t\t9 EOF\n\t\t\t\t\n\t\t\t'},{id:"B46",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKennedy\n\t\t\t\t\t\t\tR. P.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPlorde\n\t\t\t\t\t\t\tJ. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPetersdorf\n\t\t\t\t\t\t\tR. G.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1965\n\t\t\t\t\tStudies on the Epidemiology of Escherichia Coli Infections. Iv. Evidence for a Nosocomial Flora’\n\t\t\t\t\tJ Clin Invest,\n\t\t\t\t\t44\n\t\t\t\t\t193\n\t\t\t\t\t201\n\t\t\t\t\n\t\t\t'},{id:"B47",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKhan\n\t\t\t\t\t\t\tS. W.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAhmed\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2001\n\t\t\t\t\tUropathogens and their susceptibility pattern: a retrospective analysis’\n\t\t\t\t\tJ Pak Med Assoc, 51(2), 98 EOF\n\t\t\t\t\t100 EOF\n\t\t\t\t\n\t\t\t'},{id:"B48",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKisielius\n\t\t\t\t\t\t\tP. V.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchwan\n\t\t\t\t\t\t\tW. R.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tAmundsen\n\t\t\t\t\t\t\tS. K.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDuncan\n\t\t\t\t\t\t\tJ. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchaeffer\n\t\t\t\t\t\t\tA. 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E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2000Recurrent urinary tract infections in postmenopausal women’, Clin Infect Dis, 30(1), 152-6.\n\t\t\t'},{id:"B70",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRaz\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1993\n\t\t\t\t\tA controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections’\n\t\t\t\t\tN Engl J Med, 329(11), 753 EOF\n\t\t\t\t\t6 EOF\n\t\t\t\t\n\t\t\t'},{id:"B71",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tReid\n\t\t\t\t\t\t\tG.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSobel\n\t\t\t\t\t\t\tJ. D.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1987\n\t\t\t\t\tBacterial adherence in the pathogenesis of urinary tract infection: a review\n\t\t\t\t\tRev Infect Dis, 9(3), 470 EOF\n\t\t\t\t\n\t\t\t'},{id:"B72",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRene\n\t\t\t\t\t\t\tP.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDinolfo\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSilverblatt\n\t\t\t\t\t\t\tF. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1982\n\t\t\t\t\tSerum and urogenital antibody responses to Escherichia coli pili in cystitis’\n\t\t\t\t\tInfect Immun, 38(2), 542-7.\n\t\t\t'},{id:"B73",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tA. P.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPhillips\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1979\n\t\t\t\t\tBacteria causing symptomatic urinary tract infection or asymptomatic bacteriuria’\n\t\t\t\t\tJ Clin Pathol, 32(5), 492-6.\n\t\t\t'},{id:"B74",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRonald\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2003\n\t\t\t\t\tThe etiology of urinary tract infection: traditional and emerging pathogens’\n\t\t\t\t\tDis Mon, 49(2), 71-82.\n\t\t\t'},{id:"B75",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRonald\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tLudwig\n\t\t\t\t\t\t\tE.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2001\n\t\t\t\t\tUrinary tract infections in adults with diabetes’\n\t\t\t\t\tInt J Antimicrob Agents, 17(4), 287 EOF\n\t\t\t\t\t92 EOF\n\t\t\t\t\n\t\t\t'},{id:"B76",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRosenstein\n\t\t\t\t\t\t\tI. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStafford\n\t\t\t\t\t\t\tM. K.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKitchen\n\t\t\t\t\t\t\tV. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWard\n\t\t\t\t\t\t\tH.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWeber\n\t\t\t\t\t\t\tJ. N.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tTaylor-Robinson\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1998\n\t\t\t\t\tEffect on normal vaginal flora of three intravaginal microbicidal agents potentially active against human immunodeficiency virus type 1’\n\t\t\t\t\tJ Infect Dis, 177(5), 1386 EOF\n\t\t\t\t\t90 EOF\n\t\t\t\t\n\t\t\t'},{id:"B77",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchaeffer\n\t\t\t\t\t\t\tA. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tJones\n\t\t\t\t\t\t\tJ. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDunn\n\t\t\t\t\t\t\tJ. K.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1981\n\t\t\t\t\tAssociation of vitro Escherichia coli adherence to vaginal and buccal epithelial cells with susceptibility of women to recurrent urinary-tract infections’\n\t\t\t\t\tN Engl J Med, 304(18), 1062 EOF\n\t\t\t\t\t6 EOF\n\t\t\t\t\n\t\t\t'},{id:"B78",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchaeffer\n\t\t\t\t\t\t\tA. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRadvany\n\t\t\t\t\t\t\tR. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tChmiel\n\t\t\t\t\t\t\tJ. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1983\n\t\t\t\t\tHuman leukocyte antigens in women with recurrent urinary tract infections’\n\t\t\t\t\tJ Infect Dis, 148(3), 604 EOF\n\t\t\t\t\n\t\t\t'},{id:"B79",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchaeffer\n\t\t\t\t\t\t\tA. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchwan\n\t\t\t\t\t\t\tW. R.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultgren\n\t\t\t\t\t\t\tS. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tDuncan\n\t\t\t\t\t\t\tJ. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1987\n\t\t\t\t\tRelationship of type 1 pilus expression in Escherichia coli to ascending urinary tract infections in mice’\n\t\t\t\t\tInfect Immun, 55(2), 373-80.\n\t\t\t'},{id:"B80",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchlager\n\t\t\t\t\t\t\tT. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2001\n\t\t\t\t\tUrinary tract infections in children younger than 5 years of age: epidemiology, diagnosis, treatment, outcomes and prevention\n\t\t\t\t\tPaediatr Drugs, 3(3), 219 EOF\n\t\t\t\t\t227 EOF\n\t\t\t\t\n\t\t\t'},{id:"B81",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSchlager\n\t\t\t\t\t\t\tT. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHendley\n\t\t\t\t\t\t\tJ. O.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBell\n\t\t\t\t\t\t\tA. L.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWhittam\n\t\t\t\t\t\t\tT. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2002\n\t\t\t\t\tClonal diversity of Escherichia coli colonizing stools and urinary tracts of young girls\n\t\t\t\t\tInfect Immun, 70(3), 1225-9.\n\t\t\t'},{id:"B82",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSmellie\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tEdwards\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHunter\n\t\t\t\t\t\t\tN.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tNormand\n\t\t\t\t\t\t\tI. C.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPrescod\n\t\t\t\t\t\t\tN.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1975Vesico-ureteric reflux and renal scarring’, Kidney Int Suppl, 4, S65\n\t\t\t\t\t72\n\t\t\t\t\n\t\t\t'},{id:"B83",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSmith\n\t\t\t\t\t\t\tH. S.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHughes\n\t\t\t\t\t\t\tJ. P.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tRoberts\n\t\t\t\t\t\t\tP.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tScholes\n\t\t\t\t\t\t\tD.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStergachis\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStapleton\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1997Antecedent antimicrobial use increases the risk of uncomplicated cystitis in young women’, Clin Infect Dis, 25(1), 63-8.\n\t\t\t'},{id:"B84",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1993Management of urinary tract infections in adults’, N Engl J Med, 329(18), 1328-34.\n\t\t\t'},{id:"B85",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStapleton\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2002\n\t\t\t\t\tUrinary tract infections in patients with diabetes’\n\t\t\t\t\tAm J Med, 113 Suppl 1A, 80S EOF\n\t\t\t\t\t84S EOF\n\t\t\t\t\n\t\t\t'},{id:"B86",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSun\n\t\t\t\t\t\t\tT. T.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1 EOF\n\t\t\t\t\t2 EOF\n\t\t\t\t\n\t\t\t'},{id:"B87",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tTalan\n\t\t\t\t\t\t\tD. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tStamm\n\t\t\t\t\t\t\tW. E.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHooton\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMoran\n\t\t\t\t\t\t\tG. J.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBurke\n\t\t\t\t\t\t\tT.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tIravani\n\t\t\t\t\t\t\tA.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tReuning-Scherer\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tChurch\n\t\t\t\t\t\t\tD. A.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2000\n\t\t\t\t\tComparison of ciprofloxacin (7 days) and trimethoprim-sulfamethoxazole (14 days) for acute uncomplicated pyelonephritis pyelonephritis in women: a randomized trial’\n\t\t\t\t\tJAMA, 283(12), 1583 EOF\n\t\t\t\t\t90 EOF\n\t\t\t\t\n\t\t\t'},{id:"B88",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tThomas\n\t\t\t\t\t\t\tT. M.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPlymat\n\t\t\t\t\t\t\tK. R.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tBlannin\n\t\t\t\t\t\t\tJ.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tMeade\n\t\t\t\t\t\t\tT. 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B.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tHultberg\n\t\t\t\t\t\t\tH.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tKorhonen\n\t\t\t\t\t\t\tT.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t1981Mannose-resistant haemagglutination and P antigen recognition are characteristic of Escherichia coli causing primary pyelonephritis’, Lancet, 2(8260-61), 1366-9.\n\t\t\t'},{id:"B92",body:'\n\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tVetsch\n\t\t\t\t\t\t\tM.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tPuorger\n\t\t\t\t\t\t\tC.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tSpirig\n\t\t\t\t\t\t\tT.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGrauschopf\n\t\t\t\t\t\t\tU.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tWeber-Ban\n\t\t\t\t\t\t\tE. U.\n\t\t\t\t\t\t\n\t\t\t\t\t\t\n\t\t\t\t\t\t\tGlockshuber\n\t\t\t\t\t\t\tR.\n\t\t\t\t\t\t\n\t\t\t\t\t\n\t\t\t\t\t2004Pilus chaperones represent a new type of protein-folding catalyst’, Nature, 431(7006), 329-33.\n\t\t\t'},{id:"B93",body:'\n\t\t\t\tVosti, K. 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Department of Urology, Mid-Western Regional Hospital, Dooradoyle, Co. Limerick, Ireland
'},{corresp:null,contributorFullName:"Hugh D. Flood",address:null,affiliation:'
Department of Urology, Mid-Western Regional Hospital, Dooradoyle, Co. Limerick, Ireland
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Flood",authors:[{id:"47196",title:"Mr",name:"Niall",middleName:null,surname:"Davis",fullName:"Niall Davis",slug:"niall-davis"},{id:"94837",title:"Mr.",name:"Hugh",middleName:null,surname:"Flood",fullName:"Hugh Flood",slug:"hugh-flood"}]},{id:"19319",title:"Urinary Tract Immunology",slug:"urinary-tract-immunology",totalDownloads:6328,totalCrossrefCites:0,signatures:"Kelesidis Theodoros",authors:[{id:"45494",title:"Dr.",name:"Theodoros",middleName:null,surname:"Kelesidis",fullName:"Theodoros Kelesidis",slug:"theodoros-kelesidis"}]},{id:"19320",title:"Biofilm and Urogenital Infections",slug:"biofilm-and-urogenital-infections",totalDownloads:4023,totalCrossrefCites:1,signatures:"Peter Tenke, Bela Koves, Karoly Nagy, Shinya Uehara, Hiromi Kumon, Scott J. 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1. Introduction
For millennia the Bengal delta has been home to dynamic interplay of sediment, water, and land. The southwestern region of Bangladesh, comprised mainly of the Khulna, Jessore, Satkhira, and Bagerghat (shown in Figure 1), is characterized by an agro-economical system with numerous morphologically active tidal rivers and brackish water regime. Before the lowlands were enclosed by earthen embankments, that keep the main tidal channels outside the polder, the tidal river would inundate vast tract of lowland two times in a day. In addition, there were less population pressure and lower level of agricultural production. In the past Zamindars (landlords) were managing the water resources in an open-wetland ecosystem of southwestern delta. They used low earthen embankments during eight dry months of the year (commonly known as “ostomasi bundh” in local Bengali language) for prevention of tidal intrusion and protection of agricultural lands. After the harvest, the embankments were dismantled or swept away by natural river flood during monsoon [2]. The flood water during the monsoon enabled the deposition of sediment, nutrients in the form of over land irrigation, and soil nourishment and also allowed for seasonal fishing [3].
Figure 1.
Map showing prevailing waterlogging in the coastal polders across the southwestern (SW) region of Bangladesh. A representative photo [1] shows permanent waterlogging in Tala, Satkhira in august 2011.
After the abolition of Zamindari system (land holding by Zamindars), the maintenance became disrupted. In addition, there were disastrous floods in 1954, 1955 and 1956 which caused large-scale damage to human lives and food crop [4]. In order to meet the food demand of rapidly increasing population there was a need of all-round the year cultivation which requires a proper flood control [5]. In the 1960s, the Coastal Embankment Project (CEP) constructed 123 polders in southwestern coastal region of Bangladesh. Polders were constructed to protect land and livelihood from floods, salinity intrusion and to facilitate increased agricultural production. Daily tidal intrusions became a thing of past [6] and with two-three harvests annually the agriculture-based economy gained significantly for 10–15 years.
At the same time, coastal embankments denied the entry of the tides into the polders and gradually prevented the slow process of land formation on flood plains. As a result, unintended heavy loads of riverbed siltation [7] altered the natural river flow seriously and tidal rivers lost their navigability. Several rivers completely dried within a few years to few decades. The floodplains inside the polders gradually lowered than riverbed outside the polders and closed the exits of the sluiced gates. Adding to the problem, the Farakka Barrage across the Ganges River reduced the freshwater flow since 1976. In the southwestern region of Bangladesh, the Matabhanga and Gorai Rivers (shown in Figure 1) are the main distributaries of the Padma River for freshwater upland flow. Moreover, due to the heavy siltation at the rivers’ mouth, their distributaries virtually gets no water from upstream in dry season. These tidal rivers could not effectively drain the nearby beels (low lying land or natural depression) inside polders anymore, which results in serious waterlogging (shown in a representative photo in Figure 1). There is water everywhere but not drinking water.
2. Emergence of de-poldering
Since the 1980s, vast tracts of land went under water semi-permanently; the rainwater in the region could not drain resulting to a long-standing waterlogging problem (for more than 6 months in a year). Major flood events in 1987, and 1988 triggered large-scale long-standing waterlogging problems. In an apparent move to address waterlogging especially in the beel Dakatia, the largest beel in southwestern region of Bangladesh (shown in Figure 2), the Khulna Coastal Embankment Rehabilitation Project (KCERP) was introduced in the late 80s with support from Asian Development Bank (ADB). There was lack of consultation with local concerned people and their needs were hardly reflected in the project design. The waterlogging problem further deteriorated leading to widespread public protest [5].
Figure 2.
Location of Beel Dakatia, beel Kedaria, beel Kapalia, east beel Khuksia, and beel Bhaina in Hari- Mukteswari River system. Note: Other beels (unnamed) are visible in shape and locations (adapted from Talchabhadel et al. [8]).
The project was ultimately suspended as local people cut the embankment at four places during a mahashamabesh (mass community mobilization) with the intention of draining away water from the beel in September 1990. They believed the tidal flow could be restored through breaching, the land would rise through the accumulation of silt and the stored water coming out could push through the narrow river [4]. The restored open connection with the river immediately initiated tidal dynamics and sedimentation processes within the beel. Approx. 1000 ha of high land had been gained in the beel Dakatia via public cuts (i.e. without any technical studies on design of de-poldering).
To solve drainage congestion issue, enhance flooding protection (both tidal and seasonal), and rehabilitate existing drainage infrastructure the Khulna-Jessore Drainage and Rehabilitation Project (KJDRP) started in 1993. For Bangladesh Water Development Board (BWDB), the public cutting of embankments was unacceptable because it went against the law. The cuts were closed in beel Dakatia by BWDB in 1994; the land level was elevated substantially. The beel Dakatia public cutting enhanced the tidal free flow and restored the navigability of the river by increasing both depth and width within a short span of time. But then, the river largely died when the cut points were filled up.
The river was almost rescued by local people through their intuitive knowledge but ultimately it died. The dry river bed is covered by paddy field and homesteads. Although international consultants had incorporated plans for controlled tidal flooding in the early 1990s, BWDB did not include the practice in the KJDRP, arguing that it misrepresented the real problem and that it was not scientifically grounded [3]. The waterlogging scenario in southwestern region was intensified in 1997 flood (monsoon) season. The water could not be drained away overland, nor could it be discharged. In post flood season, local people had cut the embankment of beel Bhaina for quicker drainage needed for Boro-rice cultivation on their land. Although rapid drainage and recession of water occurred from beel Bhaina due to high magnitude of head difference the beel could not be brought under Boro-rice cultivation by closing the cut-point. It became gradually wider and deeper and went beyond the capacity of the local people to close. But at the end of the dry season, they observed that land level of beel Bhaina was raised, on the other hand, depth of Hari River increased significantly. The temporary restoration of tidal flooding by de-poldering came to be known conceptually as TRM. The basic idea in this process is to allow high tides bringing muddy water flow with a thick concentration of sediment into designated tidal basin and releasing the tidal flow back into the river during the low tides. During the repetitive process of such tidal restoration, a large chunk of sediment deposits on the tidal basin which otherwise would deposit in the river channel if there were no de-poldering. In addition, during low tides the flow even washes away sediment from river bed making the river congestion free and more navigable.
It brought the attention of the donor agency to apply these phenomena in all the beels adjacent to Hari River sequentially as a tool to remove waterlogging from the inundated beels. A socio-environmental impact study carried out by research institute EGIS (now Center for Environmental and Geographic Information System - CEGIS) in 1998 was crucial in the debate of open and closed approaches of flood/sediment management: the study supported closed and embanked approach (i.e. polder), but it equally argued for the inclusion of a TRM (de-polder) [9].
An iconic public embankment cutting in beel Dakatia proved to be the centerpiece of the discussion on open (de-polder and temporary water retention) versus closed (embanked and detached catchment) approaches. With beel Dakatia and beel Bhaina together, there was a decade of local people driven TRM. The attention to environmental issues and an emphasis on social participation have (forcefully) created some space for de-polder in the domain of embanked flood management. Since the beel Bhaina was taken up by KJDRP, it is considered as the first TRM officially. In 2002, BWDB incorporated TRM in beel Kedaria, then in east beel Khuksia in 2006. It showed that, over time, a dominant paradigm suggesting poldering was supplemented by some incidental occasions of de-poldering. The description of operated TRMs are summarized in Table 1.
Technical Context
Informal - Local people proactive
Formal
Beel Dakatia
Beel Bhaina
Beel Kedaria
East Beel Khuksia
11000 ha
600 ha
600 ha
800 ha
(1990–1994)
(1997–2001)
(2002–2005)
(2006–2012)
Strategy
No technical planning
No technical planning, started by local people and undertaken by BWDB later
Planned and approved by BWDB
Planned and approved by BWDB
Embankment Opening
Public Cut in 4 places
Public Cut and continuous operation
No breaching of embankment, operated through 21 vent Bhabodah regulator (6 months per year)
Formal De-poldering and continuous operation
Peripheral Embankment
No
No
Yes
Yes
Land Heightening
Not measured exactly; Around 10% of such a large area significantly land heightened
Around 60% uniformly silted; Average of 0.8 m land heightening (1.5–2.0 m at cut point and 0.2 m in the far end); Net silt deposition = 6.48 million m3
Insignificant Siltation; Net silt deposition = 0.5 million m3
Around 50% uniformly silted; Average of 1.2 meter land heightening (1.5–2.0 m at cut point and 0.5 m in the far end)
Compensation
No
No
No
Yes (not easy to get)
Stakeholder Participation
Local Communities and NGOs, Social and political activists
Local Communities and NGOs, Social and political activists
Local Communities and NGOs, Social and political activists, Government institutions, research organizations, donors and so on
Local Communities and NGOs, Social and political activists, Government institutions, research organizations, donors and so on
Conflicts
Local conflicts were resolved
Conflicts exist among local stakeholders (shrimp-field owners, local farmers, landless people, daily-wage workers, NGOs, civil society organizations) as well as between local stakeholders and government institutions (local government, Union Parishad, Upazilla, district administrative, BWDB,)
Table 1.
Summary of description of operated TRMs (both informal and formal) [2, 4, 10, 11].
3. Shifting of Tidal River Management
The people of beel Kedaria were very much in favor of TRM to raise their land, but it did not meet their expectation. Although there was no waterlogging in the area during the operation the landowners lost their interest to operate TRM by submerging their land without any yield and compensation for three years. This created a negative impact on TRM and ultimately BWDB could not find any beels to operate TRM in the year 2005. The riverbed silted up immediately after stopping the operation of TRM shown in Figure 3. After the termination of TRM, the riverbed rose almost by 4–6 meters due to reduced tidal prism. It clearly indicates the area will remain inundated if TRM is not operated in any of the beels. To solve the problems in the long run, TRM operations are to be shifted/rotated effectively in different beels. It is reported that the shifting of TRMs from downstream to upstream yields larger sediment deposition than from shifting TRMs from upstream to downstream [6].
Figure 3.
Impact on Hari River morphology at Ranai after termination of Tidal River Management operation in beel Kedaria (source: IWM [12]).
The challenges of operation are social and institutional. People are unwilling to provide their land since they cannot do economic activities like agriculture or fisheries. To overcome this challenge a compensation mechanism for crop and fisheries has been established then after. During the operation of TRM in east beel Khuksia, compensation mechanism was developed.
The plan of shifting of TRMs has been included in long-term policy for the southwestern region. Planned large-scale rotational TRMs were then developed in major river systems. Such as Hari-Mukteswari river system: East Khuksia, Kapalia, Baruna, Payra, West Khuksia and Singha by 2047 [12]; Kobadak river system: Pakhimara, Hariharnagar, Raruli, Rajapur Harinkhola, Delua and Jalalpur by 2045 [13].
In Hari-Mukteswari river system, beel Kapalia was planned to be operated as TRM from 2012 onwards for a period of 5 years, but violent protests prevented this. Some of the major reasons are compensation mechanism and lack of trust in government. East beel Khuksia was operated for 7 years but the initial plan was to only operate for 4 years. BWDB is currently bringing back the planned operation of TRM in Hari-Mukteswari river system (including beel Kedaria) by addressing pertinent social, economic, technical, and political problems. Meanwhile, BWDB is replicating the TRM concept in other receptive river system such as Kobadak river system. Beel Pakhimara is at present operational since 2015.
4. Tidal River Management for flood/sediment management
Dredging and excavation are costly and are not eco-friendly. They are again more time consuming to manage huge drainage congestion. In addition, the deposited sediments by excavating again fall into the river through runoff in a rainy season. De-poldering and then controlled flooding (during TRM process) in a particular beel is not a new way of sediment management. However, the method involves taking full advantages of the natural tide movement with little human interventions. This concept involves temporary de-poldering to allow jowar-bhata khelano (free play of tidal flow) in selected beel through a link canal shown in Figure 4a. At high tide, muddy water enters with a thick concentration of sediment and deposits large chunks of sediment on the selected beel. At low tide, relatively clearer water erodes the river bed, increasing the depth of the river. This process is a participatory approach where the people of the identified tidal basin have to provide their land remain flooded for an intended period (about 5 years depending on tidal prism and area of the beel). Figures 4a–c and 5 show that TRM reclaims land from waterlogging and inundation, increases the river navigability by increasing river depth and width, and provides solution of drainage congestion of southwestern region.
Figure 4.
(a) Tidal basin concept: Free play of tidal flow in selected beel, (b) land reclamation in Arua village in between 2005 and 2011 [11], and (c) revival of Hari River near Bhabodah regulator in between 2006 and 2011 [14] (adapted from Talchabhadel et al., [8]).
Figure 5.
Comparison of inundation area with and without operation of TRM (adapted from Talchabhadel et al., [8]).
This concept is technically feasible, environmentally friendly and socially acceptable [11, 15]. The experiences of TRM operated so far, exhibited that there was no drainage congestion and waterlogging problem throughout in the river system and the selected beels were heightened significantly. Though the TRM operated beel is not suitable for practicing any agriculture, about 20–25 surrounding beels located upstream could have favorable ecological conditions for better agricultural production. And, TRM can increase drainage capacity to a long distance up to 20 km of the lower stream at a single intervention from the place of TRM implementation [16].
Several studies have been conducted qualitative/quantitative analyses of TRM and its relation to disaster, ecosystem, environment, agriculture and suggested the appropriate design of TRM. Some studies [17, 18, 19] have analyzed the effectiveness with different interventions like crossing dam, dredging, and compartmentalization. Some [20, 21, 22] have suggested optimum opening sizes of link canals connecting the tidal basin and tidal river. The TRM is effective when there is no upland flow or the upland flow is reduced, therefore, crossing dam at upstream of cut point is recommended during the operation of TRM. There have been still issues related to non-uniform sediment deposition across the selected beel despite of several studies based on experimental and numerical simulation. Higher sedimentation occurs close to the opening and decreases gradually to the further end of the beel [23]. To solve this issue, one option could be construction of embankment on both sides of main channel inside tidal basin and allowing siltation from most remote areas and cutting embankment part by part from remote end to link canal or introduce compartmentalization [18]. Also, the alignment of link canal controls the area of high shear stress [22]. A relationship between the tidal prism and minimum area for a tidal equilibrium can be established using historical data of nearby tidal rivers while designing the link canal [17, 21].
A combination of TRM with some degree of dredging/excavation could serve effective drainage and sediment management. Most importantly, the operation of TRM should be continuous. In the absence of sequential or shifting of TRMs, the acquired benefits might be wasted due to repetitive heavy siltation. Therefore, there should not be any time gaps between closing of one beel and operation of successive TRM beel [24]. Effective operation of TRMs could contribute to flood alleviation in southwestern Bangladesh and more than 100 beels are suitable of operation of TRM process [7]. However, during the operation of TRM agriculture is affected for a few years in operated beel. A systematic program of TRM is therefore necessary in order to increase overall agricultural production by reducing flood susceptibility and managing sediments. A manageable size of the tidal basin at one intervention is around 1000–2000 ha.
5. Toward sustainable solution
TRM evolved into an environmentally accepted flood/sediment management practice based on indigenous knowledge and it contributes to land heightening, flood resistance, and food security. However, the socio-political use of TRM complicates its implementation and there have been well-documented failures of TRM implementation. The effectiveness of TRM has not matched the expectation of majority of stakeholders. The challenges include engineering, socio-political, and institutional. Overall, a key barrier to the successful implementation is a proper management of compensation. Though the compensation mechanism started in east beel Khuksia, there were conflicts among different stakeholders (farmers, landless people, daily-wage workers, shrimp-field owners, NGOs, local organizations) and between these stakeholders and government bodies (BWDB, local government, district administrative) are prevalent [6]. The conflicts are related to compensation amount, procedure of compensation, land use practices, employment, shifting of TRMs and overall coordination.
Generally, the landless farmers and poor fishermen are the main sufferers of TRM implementation. Because they worked under landowners and they would not get the land compensation [25]. It is a high time to identify programs addressing their needs, for instance, provision for the cooperative fish culture. Shrimp farmers, who did not want to lose their leased land under any circumstances are against the TRM [4].
BWDB officials being primarily engineers and hydrologists, they may lack the skills and expertise to facilitate stakeholder [26]. The river channels should be kept open as far as possible. Unplanned drainage obstacles like ghers (shrimp aquaculture ponds) should be removed and appropriate policy should be developed to stop misuse of khals (drainage canals). Sediment management for uniform distribution is required to improve TRM practices. Highly saline zones are unsuitable for the TRM sites as high saline sediment precludes agriculture. A temporary cross dam should be constructed in the dry season. If possible, the river should be re-excavated before the monsoon and the crossing dam should be made open during the monsoon. Peripheral embankment should enclose the selected beel. A simple mechanism of distributing the crop compensation has to be established. There is a strong need of an open, transparent and inclusive planning, implementation, and operation-maintenance of TRM.
The evolution of social learning, and participation of different stakeholders clear indicate a need for an approach that considers multi-dimensional (social, economic and environmental) consequences [4]. Also, bringing together people from different backgrounds, perspectives, values does not automatically lead to effective management. It requires a multi-loop process in improving a multiple-actor-based management practice [2]. Key criteria for successful TRM implementation are:
Intensive consultation with concerned communities, and affected landowners
Collaborative working (conflict resolution among different land-use groups, working agencies, and government institutions)
Strengthening of local institutions
Regular supervision by government institutions
Continuous information and motivational campaign
Interdisciplinary research (technical and socio-economic research for proper selection of beels, their operation, and compensation distribution)
Iterative learning (evaluation of success and failure to guide for the effective operation in next beel)
Sequential implementation of TRM (no stoppage of operation at any cost)
A long-term strategy of Bangladesh Delta Plan (up to 2100) has highly acknowledged the TRM concept for solving waterlogging problems and making river alive. Restoration of tidal plain allowing tidal inundation is an effective measure for increasing the tidal prism, raising the low lying land (sediment-starved flood plain), and ultimately solving waterlogging issues with sustainable sediment management. In order to obtain faster drainage, pumping might be required in addition to gravity drainage of polders. The iterative learning in coming days will surely move toward the sustainable solutions. Although an embankment along the coast is required, sediment management is also essential for sustainability. The concept of TRM, evolved from indigenous knowledge and blended with scientific understanding, should go hand in hand with other water/sediment-related interventions.
6. Conclusion
Unlike excavating, TRM is eco-friendly, cost-effective (no need of large-scale engineering), and time-efficient (maximum utilization of natural tidal flow). It simply allows beneficial flood in raising low-lying land, scouring silted river, and improving drainage congestion. The TRM process restores the tidal prism and provides sufficient space for the river. However, internal roads, cultivation, and economic activities are hampered during the TRM operation period. The TRM concept is one of the effective measures of managing flood/sediment problems in tide-dominated river system.
Evolved from traditional wisdom, the TRM process is blended with scientific knowledge and it proves to be a sustainable way forward for effective flood/sediment management. However, a key barrier to the successful implementation is compensation. The landless farmers and poor fishermen are the main sufferers of TRM implementation. Programs focused for main sufferers are equally needed along with a simple mechanism of distribution of the compensation to land owners.
Since the TRM is a participatory approach, all the organizations and stakeholders connected with the different stages of the development process of TRM should be responsible for promoting the entire process. Multiple-stakeholders-based inclusive planning, operation-management practice with iterative learnings are necessary for successful implementation of TRM concept. With time we need to rethink and recalibrate the roles of stakeholders in order to manage possible conflicts and maintain impulsive monitoring and evaluation of all groups involved from local communities to government bodies. Therefore, the process need continuous updating based on the monitoring results.
Acknowledgments
The research was supported by JST/JICA SATREPS program on disaster prevention/mitigation measures against floods and storm surges in Bangladesh (PI: Dr. Hajime Nakagawa). The first author was supported by a Monbukagakusho (MEXT) scholarship during his Ph.D. (2014 – 2017) and the Japan Society for the Promotion of Sciences (JSPS) Postdoctoral Fellowship Program, 2019 – 2020, (grant in aid P19052; Host: Dr. Kenji Kawaike).
Conflict of interest
No conflict of interest.
\n',keywords:"beel, de-polder, polder, siltation, Tidal River Management (TRM), waterlogging",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/74917.pdf",chapterXML:"https://mts.intechopen.com/source/xml/74917.xml",downloadPdfUrl:"/chapter/pdf-download/74917",previewPdfUrl:"/chapter/pdf-preview/74917",totalDownloads:56,totalViews:0,totalCrossrefCites:0,dateSubmitted:"July 13th 2020",dateReviewed:"November 27th 2020",datePrePublished:"February 15th 2021",datePublished:null,dateFinished:"January 23rd 2021",readingETA:"0",abstract:"Southwestern Bangladesh has been seriously affected by perennial waterlogging over the last few decades. It is primarily due to excessive riverbed siltation outside the polders after the construction of embankments along both sides of the tidal rivers. These embankments de-linked the huge natural floodplains and restricted a gradual process of natural deposition inside the polders. An introduction of the tidal basin concept by temporary de-poldering (embankment cut) at some designated locations has substantially solved the issues. The current chapter looks at the historical practice of flood/sediment management, the evolution of embankments and their de-poldering, inclusion of Tidal River Management (TRM) in long term flood/sediment management, and discusses a technical aspect of flood/sediment dynamics across the tidal river system. The process of restoring beneficial tidal flooding by cutting embankment at certain locations, commonly known as TRM, is not a novel method. The TRM has started from age-old practice and proves technically one of the effective methods of sustainable flood/sediment management in the tide-dominated river system. It is an example of building with nature, where little human interventions are needed, and a resilient measure for waterlogging, drainage-congestion, and river-siltation.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/74917",risUrl:"/chapter/ris/74917",signatures:"Rocky Talchabhadel, Kenji Kawaike and Hajime Nakagawa",book:{id:"10405",title:"River Basin Management - Sustainability Issues and Planning Strategies",subtitle:null,fullTitle:"River Basin Management - Sustainability Issues and Planning Strategies",slug:null,publishedDate:null,bookSignature:"Prof. José Simão Antunes Do Carmo",coverURL:"https://cdn.intechopen.com/books/images_new/10405.jpg",licenceType:"CC BY 3.0",editedByType:null,editors:[{id:"67904",title:"Prof.",name:"José Simão",middleName:null,surname:"Antunes Do Carmo",slug:"jose-simao-antunes-do-carmo",fullName:"José Simão Antunes Do Carmo"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Emergence of de-poldering",level:"1"},{id:"sec_3",title:"3. Shifting of Tidal River Management",level:"1"},{id:"sec_4",title:"4. Tidal River Management for flood/sediment management",level:"1"},{id:"sec_5",title:"5. Toward sustainable solution",level:"1"},{id:"sec_6",title:"6. Conclusion",level:"1"},{id:"sec_7",title:"Acknowledgments",level:"1"},{id:"sec_10",title:"Conflict of interest",level:"1"}],chapterReferences:[{id:"B1",body:'Awal MA. Water logging in south-western coastal region of Bangladesh: local adaptation and policy options. Sci Postprint. 2014;1(1):1-13'},{id:"B2",body:'Mutahara M, Warner JF, Wals AEJ, Khan MSA, Wester P. Social learning for adaptive delta management: Tidal River Management in the Bangladesh Delta. Int J Water Resour Dev. 2018;34(6):923-943'},{id:"B3",body:'Staveren MF Van, Warner JF, Khan MSA. Bringing in the tides. From closing down to opening up delta polders via Tidal River Management in the southwest delta of Bangladesh. Water Policy. 2017;19:147-164'},{id:"B4",body:'Gain AK, Benson D, Rahman R, Datta DK, Rouillard JJ. Tidal river management in the south west Ganges-Brahmaputra delta in Bangladesh: Moving towards a transdisciplinary approach? Environ Sci Policy. 2017;75(May):111-120'},{id:"B5",body:'Haque KNH, Chowdhury FA, Khatun KR. Participatory environmental governance and climate change adaptation: mainstreaming of tidal river management in south-west Bangladesh. In: Ha H, editor. Land and Disaster Management Strategies in Asia. 2015. p. 189-208'},{id:"B6",body:'Talchabhadel R, Nakagawa H, Kawaike K. Selection of Appropriate Shifting of Tidal River Management. In: Water, Flood Management and Water Security Under a Changing Climate. Cham: Springer International Publishing; 2020. p. 283-299'},{id:"B7",body:'Adnan MSG, Talchabhadel R, Nakagawa H, Hall JW. The potential of Tidal River Management for flood alleviation in South Western Bangladesh. Sci Total Environ. 2020 Aug;731:138747'},{id:"B8",body:'Talchabhadel R, Nakagawa H, Kawaike K, Sadik MS. Polder to De-polder: an Innovative Sediment Management in Tidal Basin in the Southwestern Bangladesh. Annu Disaster Prev Res Inst. 2018 Feb;(61B):623-630'},{id:"B9",body:'EGIS. Environmental and Social Impact Assessment of the Khulna-Jessore Drainage Rehabilitation Project, BWDB. Dhaka, Bangladesh; 1998'},{id:"B10",body:'Leendert Ferdinand de D. Tidal River Management Temporary depoldering to mitigate drainage congestion in the southwest delta of Bangladesh. Wageningen University; 2013'},{id:"B11",body:'Rezaie AM, Islam T, Rouf T. Limitations of institutional management and socio-economic barriers of Tidal River Management, a semi-natural process to save bhabodaho from water-logging problem. Fukuoka S, Nakagawa H, Sumi T, Zhang H, editors. Adv River Sediment Res. 2013;2173-2183'},{id:"B12",body:'IWM. Feasibility Study and Detailed Engineering Design for Long Term Solution of Drainage Problems in the Bhabodah Area. Dhaka, Bangladesh; 2010'},{id:"B13",body:'IWM. Feasibility Study for Sustainable Drainage and Flood Management of Kobadak River Basin under Jessore and Satkhira Districts. 2010'},{id:"B14",body:'Paul A, Nath B, Abbas MR. Tidal River Management (TRM) and its implication in disaster management : A geospatial study on Hari-Teka river basin, Jessore,. Int J Geomatics Geosci. 2013;4(1):125-135'},{id:"B15",body:'Rezaie AM, Naveram UK. Tidal river management : An innovative approach for terminating drainage congestion and raising land through sedimentation in the Bhabodaho area, Bangladesh. Fukuoka S, Nakagawa H, Sumi T, Zhang H, editors. Adv River Sediment Res. 2013;1363-75'},{id:"B16",body:'Al M, Naher N, Azadi H, Passel S Van. Sustainability impacts of tidal river management : Towards a conceptual framework. Ecol Indic [Internet]. 2018;85(November 2017):451-67. Available from: https://doi.org/10.1016/j.ecolind.2017.10.022'},{id:"B17",body:'Shampa, Pramanik MIM. Tidal River Management (TRM) for Selected Coastal Area of Bangladesh to Mitigate Drainage Congestion. Int J Sci Technol Res. 2012;1(5):1-6'},{id:"B18",body:'Ibne Amir MSI, Khan MSA, Kamal Khan MM, Golam Rasul M, Akram F. Tidal river sediment management - a case study in southwestern Bangladesh. Int J Civil, Archit Struct Constr Eng. 2013;7(3):183-193'},{id:"B19",body:'Rahman MZ, Islam MS, Khan ZH. Tidal River Management (TRM)-An Innovative Scientific Approach for Sustainable Sediment Management. In: international Conference on Recent Innovation in Civil Engineering for Sustainable Development (IICSD-2015). 2015. p. 954-959'},{id:"B20",body:'Stive MJF, Rakhorst RD. Review of empirical relationships between inlet cross-section and tidal prism. J Water Resour Environ Eng. 2008;23(23):89-95'},{id:"B21",body:'Talchabhadel R, Nakagawa H, Kawaike K, Hashimoto M, Sahboun N. Experimental investigation on opening size of tidal basin management : A case study in southwestern Bangladesh. J Japan Soc Civ Eng Ser B1 Hydraulic Eng. 2017;73(4):I_781-I_786'},{id:"B22",body:'Talchabhadel R, Ota K, Nakagawa H, Kawaike K. Three-dimensional simulation of flow and sediment transport processes in tidal basin. J Japanese Soc Civ Eng Ser B1 Hydraulic Eng. 2018;74(4):I_955-I_960'},{id:"B23",body:'Talchabhadel R, Nakagawa H, Kawaike K. Sediment management in tidal river : A case study of East Beel Khuksia, Bangladesh. In: RiverFlow 2018. 2018. p. 1-10'},{id:"B24",body:'Ullah MW, Mahmud S. Appropriate planning, design and implementation modalities for successful application of Tidal River Management (TRM) in coastal delta. In: 6th International Conference on Flood Management (ICWFM-2017). 2017. p. 133-140'},{id:"B25",body:'Talchabhadel R, Nakagawa H, Kawaike K. Tidal River Management (TRM) and Tidal Basin Management (TBM): A case study on Bangladesh. Lang M, Klijn F, Samuels P, editors. E3S Web Conf. 2016 Oct 20;7:12009'},{id:"B26",body:'Gain AK, Schwab M. An assessment of water governance trends: The case of Bangladesh. Water Policy. 2012;14(5):821-840'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Rocky Talchabhadel",address:"rocky.ioe@gmail.com",affiliation:'
Texas A&M AgriLife Research, Texas A&M University, USA
Disaster Prevention Research Institute, Kyoto University, Japan
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Integrity - We are consistent and dependable, always striving for precision and accuracy in the true spirit of science.
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Openness - We communicate honestly and transparently. We are open to constructive criticism and committed to learning from it.
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Disruptiveness - We are eager for discovery, for new ideas and for progression. We approach our work with creativity and determination, with a clear vision that drives us forward. We look beyond today and strive for a better tomorrow.
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What makes IntechOpen a great place to work?
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IntechOpen is a dynamic, vibrant company, where exceptional people are achieving great things. We offer a creative, dedicated, committed, and passionate environment but never lose sight of the fact that science and discovery is exciting and rewarding. We constantly strive to ensure that members of our community can work, travel, meet world-renowned researchers and grow their own career and develop their own experiences.
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His research mainly\nfocuses on the development of optical\nand electronics systems for spectroscopy\napplication in environmental monitoring,\nagriculture and dermatology. He has\nmore than 10 years of teaching\nexperience in subjects related to\nelectronics, mathematics and applied optics for\nuniversity students and industrial engineers.",institutionString:null,institution:{name:"Universiti Sains Malaysia",country:{name:"Malaysia"}}},{id:"191072",title:"Prof.",name:"A. K. M. Aminul",middleName:null,surname:"Islam",slug:"a.-k.-m.-aminul-islam",fullName:"A. K. M. Aminul Islam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191072/images/system/191072.jpg",biography:"Prof. Dr. A. K. M. Aminul Islam received both of his bachelor and Master’s degree from Bangladesh Agricultural University. 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