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Urinary tract infection pathogens

Gordon KA, Jones RN, et al. Susceptibility patterns of orally administered antimicrobials among urinary tract infections pathogens from hospitalized patients in North America Comparison report to Europe and Latin America. Results from the SENTRY Antimicrobial Surveillance Program (2000). Diagn Microbiol Infect Dis 2003 45 295-301. [Pg.2095]

Urinary tract infection (UTI) is an infection caused by pathogenic microorganisms of one or more structures of the urinary tract. The most common structure affected is the bladder, with the urethra, prostate, and kidney also affected (see Pig. 47-1). Display 47-1 identifies the disorder most frequently associated with each of these structures within the urinary system. Clinical manifestations of a UTI of the bladder (cystitis) include urgency, frequency, burning and pain on urination, and pain caused by spasm in the region of the bladder and the suprapubic area. [Pg.456]

Table 6.3 Urinary tract infection—distribution of pathogenic bacteria in the community and hospitalized patients... Table 6.3 Urinary tract infection—distribution of pathogenic bacteria in the community and hospitalized patients...
Ronald A. The etiology of urinary tract infection traditional and emerging pathogens. Am J Med 2002 113(Suppl 1A) 14S-19S. [Pg.1158]

For infections frequently encountered outside hospitals, e.g. uncomplicated urinary tract infection in young women, surveillance of resistance data of the most likely pathogens Escherichia coli) allows physicians to prescribe empiric therapy without performing cultures in the individual patient. However, in severely ill hospitalised patients, it is necessary to take samples for culture before starting empiric therapy. Microscopy of the Gram stained smear can help fine-tune empiric therapy at an early stage. Whether the infection is community-acquired or hospital-acquired, and whether the patient has been exposed to previous antimicrobial therapy should also be taken into account when choosing empiric therapy. [Pg.521]

Acute uncomplicated urinary tract infections caused by E. coli and other pathogens generally respond promptly to one of the short-acting sulfonamides. Recurrent urinary tract infections (UTIs), when related to some structural abnormality in the tract, are frequently caused by sulfonamide-resistant bacteria. [Pg.517]

A combination of trimethoprim-sulfamethoxazole is effective treatment for a wide variety of infections including P jiroveci pneumonia, shigellosis, systemic salmonella infections, urinary tract infections, prostatitis, and some nontuberculous mycobacterial infections. It is active against most Staphylococcus aureus strains, both methicillin-susceptible and methicillin-resistant, and against respiratory tract pathogens such as the pneumococcus, Haemophilus sp, Moraxella catarrhalis, and Klebsiella pneumoniae (but not Mycoplasma pneumoniae). However, the increasing prevalence of strains of E coli (up to 30% or more) and pneumococci that are resistant to trimethoprim-sulfamethoxazole must be considered before using this combination for empirical therapy of upper urinary tract infections or pneumonia. [Pg.1035]

Inflammation is a common component associated with sepsis, meningitis, as well as respiratory tract, urinary tract, viral, and bacterial infections (Table 1). Bik is elevated during bacterial or viral infection. The presence of urinary Bik correlates well with standard urinalysis tests for urinary tract infections [20]. Endotoxins released from infectious pathogens induce inflammation and immune cell activation. Macrophages release interleukins and cytokines (IL-1, IL-6, IL-12, IL-15, IL-18, TNF-a) on exposure to lipo-polysaccharide (LPS) and lipoteichoic acid (LTA) endotoxins. These cytokines act as a chemotactic factors causing immune cell migration to the site of the infection followed by activation and release of proteases. Cytokines also induce increased vascular permeability in the endothelial. Bik suppresses further cytokine release by protease and intern additional migration and activation of immune cells. Additionally, a stabilization of the immune cell membrane prevents further release of proteases [4]. [Pg.235]

Knowledge of the likely pathogens (and their current local susceptibility rates to antimicrobials) in the clinical situation. Thus cephalexin may be a reasonable first choice for lower urinary tract infection (coliform organisms — depending on the prevalence of resistance locally), and benzylpenicillin for meningitis in the adult (meningococcal or pneumococcal). [Pg.205]

Others. Leoofloxacin (t) 7h) has greater activity against Streptococcus pneumoniae than ciprofloxacin and is used for respiratory and urinary tract infection. Moxifloxacin (t) 12 h) has strong anti-Gram-positive activity, and may prove useful for respiratory tract infections including those caused by atypical pathogens and penicillin-resistant Streptococcus pneumoniae. [Pg.233]

Uropathogenic E. coli cause 90% of the urinary tract infections. The bacteria colonize from the feces or perineal region and ascend the urinary tract to the bladder. With the aid of specific adhesins (pyelonephritis-associated pili) they are able to colonize the bladder. Another factor involved in the pathogenicity of the uropathogenic strains of E. coli is their resistance to complement-dependent bactericidal effect of serum. This phenomenon is associated with the presence of a capsule, which decrease the ability of antibodies and/or complement to bind to the bacterial surface, which in turn prevents the phagocytes from recognizing and engulfing the bacterial cells. [Pg.926]

Uncomplicated urinary tract infection" Eradication of bacterial pathogen... [Pg.43]

This observation has an analogy in the world of microbes, which need to adhere effectively to the surface of their host cells to escape the shear forces of body fluids. Bacteria utilize both protein-protein and carbohydrate-protein interactions for adhesion. Pathogenic Escherichia coli (E. coli) bacteria, for example, responsible for more than 80% of urinary tract infections [2], possess thin hair-like structures on their surfaces, called pili and the shorter fimbriae. Fimbriae specifically recognize carbohydrates. Type 1 fimbriae of E. coli, for example, can, via their FimH lectin domain [3], bind a-D-mannopyranosides. Lectins, e.g. [4-7] named after the Latin word legere to pick out or choose [8] are carbohydrate recognizing proteins found everywhere in nature, e.g. [9-13] and are intensively studied structures. [Pg.19]


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See also in sourсe #XX -- [ Pg.119 , Pg.120 , Pg.159 ]




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Urinary infections

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