Infection, bacterial adherence

O For infective endocarditis to develop, the occurrence of several factors is required. These factors involve alterations to the endocardial surface that allow for bacterial adherence and eventual infection. 

Rosenberg, E., Gottlieb, A. and Rosenberg, M. (1983). Inhibition of bacterial adherence to hydocarbons and epithelial cells by emulsan, Infect. Immun., 39, 1024-1028. 

Enteric bacterial pathogens must maneuver through a lengthy stretch of hazardous terrain before they reach their intended target or infection site within a host. Initially, they must tolerate salivary enzymes having various hydrolytic activities in the mouth, followed by exposure to shedded epithelial cells in the esophagus that may prevent local bacterial adherence (Pearson and Brownlee, 2005). In the stomach, bacteria must endure another severe environment created by the secretion of digestive enzymes and hydrochloric acid (up to 0.1 M concentration and a pH as low as 1.0). Once bacteria reach the intestines, they then encoimter mechanical. 

Aronson, M., Medalia, O., Schori, L., Mirelman, D., Sharon, N., and Ofek, I. (1979). Prevention of colonization of the urinary tract of mice with Escherichia coli by blocking bacterial adherence with methyl alpha-mannopyranoside. /. Infect. Dis. 139, 329-332. 

Sobota AE. Inhibition of bacterial adherence by cranberry juice potential use for the treatment of urinary tract infections. JUrol 1984 131 1013-6. 

In summary, bacterial adherence is not just mediated by one bacterial surface structure interacting with one host receptor. Rather, adherence is a process involving several bacterial and host cell components which interact in a temporal and special order. Interference with these processes in order to block infection will not be an easy task [68],... 

Often, less intense reactions are encountered. The epidermolytic, exfoliative toxins A and B attack the epidermidis causing epidermal necrosis (e.g., Sap/tytococcMX-scalded skin syndrome) [9]. Membrane-damaging toxins at infection sites (e.g., a-toxin, a-hemolysin) are a major factor in tissue damage after bacterial adherence has occurred. Other exoproteins, such as proteases, collage-nase, hyaluronidase, and lipase, act as virulence enhancers but do not actively destroy host tissues. 

Bach A. Clinical studies on the use of antibiotic- and antiseptic-bonded catheters to prevent catheter-related infection. Zentralbl Bakteriol December 1995 283(2) 208-14. Greenfeld JI, Sampath L, Popilskis SJ, et al. Decreased bacterial adherence and biofilm formation on chlorhexidine and silver sulfadiazine-impregnated central venous catheters implanted in swine. Crit Care Med May 1995 23(5) 894-900. 

Finally, it is known that HA as glycosaminoglycan and chondroitin sulphate (CS) protect the urothelium but a damage to the urothelium may increase bacterial adherence and cause infection risk. For this a meta-analysis was carried out in order to evaluate the effect of intravesical HA and HA and CS (HA-CS) combination therapy in recurrent bacterial cystitis in adult women. A systematic literature search was performed. Primary outcomes were urinary tract infection (UTI) rate per patient-year, and UTI recurrence time (days). Secondary outcomes were 3-day voids and pelvic pain and urgency/frequency (PUF) symptom scale total score [35. ... 

Reynolds HY. Bacterial adherence to respiratory tract mucosa a dynamic interaction leading to colonization. Semin Respir Infect 1987 2 8-19. 

Svensson, M., Lindstedt, R., Radin, N. S. and Svanborg, C., Epithelial glycosphingolipid expression as a determinant of bacterial adherence and cytokine production. Infect Immun, 1994, 62 4404-4410. 

Altered mucociliary clearance Epithelial injury Increased bacterial adherence Altered alveolar macrophage function Reflex bronchoconstriction Increased airway inflammation Increased particle deposition Increased susceptibility to viral infection... 

In the very early phases of the acute inflammatory response most of the cells invading the damaged area are polymorphonuclear neutrophils, also denoted as PMNs, which serve as initial line of defense and source of proinflammatory cytokines. These cells, which usually live for 4-5 days, circulate in the blood until they are attracted by chemokines into injured tissues. Whereas physical injury does not recruit many neutrophils, infections with bacteria or fungi elicit a striking neutrophil response. The characteristic pus of a bacterial abscess is composed mainly of apoptotic (apoptosis) and necrotic PMNs. Emigration of neutrophils from the blood starts with a process denoted as margination where neutrophils come to lie at the periphery of flowing blood cells and adhere to endothelial cells (Fig. 1). L-Selectin is expressed... 

This chapter will provide an overview of the research on anti-adhesion agents. Particular attention will be devoted to the anti-adherence agents derived from or foimd naturally in foods. In addition, the pathogen infection process, the architecture of host epithelial cell surfaces, and the chemistry and mechanisms involved in bacterial interactions with host cell surfaces will also be reviewed. 

The initial adherence of pathogens to host cell surfaces is considered an essential step in colonization and infection (Savage, 1977, 1984). Therefore, identifying the bacterial molecules that mediate adherence has been a major area of research, especially since these molecules may serve as targets for anfi-adherence strategies. As discussed previously (Section VI), the detailed interactions between a pathogen and a host cell are often mediated by proteinaceous surface structures on the bacterial surface. These bacterial proteins are referred to as adhesins (Finlay and Falkow, 1989), and are most often foimd on the tips of bacterial fimbriae or pili (fimbrial adhesins), but may also be anchored in the bacterial membrane so that it can be presented on the bacterial outer membrane (afimbrial adhesins) (Sharon and Ofek, 1986). Models of fimbrial and afimbrial adhesins of some human pathogens are discussed here. 

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