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UTIs

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Question
Answer
uncomplicated urethritis or cystitis   painful urination  
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some cases of pyelonephritis   fever, sepsis, decreased kidney function  
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Etiologic agents of urinary tract infections   90% caused by E. coli; others include: enterobacteriaceae family, pseudomonads, enterococci, yeast (candida)  
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Increased risk or UTI in sexually active women a/w:   use of diaphragm with spermicide d/t inc colonization of vagina w/uropathogens; Spermicide inc adherence of E. coli to vaginal epithelial cells  
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Cystitis   infxn of bladder wall; freq/urgent urination & dysuria (pain); Tender suprapubic area; Bacteria & WBCs common in urine (50% have blood); malodorous  
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Pyelonephritis   infxn of kidney & renal pelvis; mc follows bladder infxn; Acute can lead to chronic  
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Acute pyelonephritis   presence of WBCs, cellular casts, bacteria and protein in urine  
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Chronic pyelonephritis   gradual nephron loss and renal failure  
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Urethritis   inflam of urethra usu caused by bacteria  
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Glomeruloneprhitis   inflam of glomeruli in nephrons; glomerular capillary network becomes leaky allowing plasma ptn & RBCs to be excreted in urine  
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Bugs a/w Cystitis   **E. coli**, Klebsiella, Proteus, Staphylococcus saprophyticus, Serratia marcescens, Pseudomonas aeruginosa, Enterococcus faecalis; mc in women d/t proximity of short urethra to fecal contamination  
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Prostatitis   inflam of prostate gland; acute infxn is often an extension of a bladder or uretha; follows catheterization  
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Virulence Factors a/w UTIs   adherence to vaginal wall and uroepithelial cells; Cytotoxic necrotizing factors; Hemolysin; Genes are linked together as multigene segments called "Pathogenicity Islands" that are abscent in normal fecal coliforms  
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Pathogenicity Islands   mobile genetic elements (in addition to virulence plasmids) that encode secreted virulence protein components of: Fimbriae, Pili, Outer membrane ptns; all surface components mediating colonization, attachment & location of infxn  
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Adhesive capacities   E. coli pyelonephritis isolates adhere better than E. coli cystitis isolates; urinary isolates adhere to uroepithelial cells more strongly than fecal isolates  
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Escherichia coli   G(-) rods; facultative anaerobes; mc source of urinary tract infxn d/t fecal contamination of genital area; Adheres to mucosa w/pili causing tissue damage; Endotoxin (LPS) causes inflam; Treat w/PCN or Ciprofloxacin  
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Col V plasmid - codes for Siderophores   captures Fe and brings it in for E. coli to grow  
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Hemolysin   damages host cells; releases Fe from RBCs  
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Enterochelin   chelates Fe for bacterial uptake  
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K1 antigen   impedes phagocytosis, blocks binding of C3b opsonin  
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P-pili   allows bacterial to bind to P blood group antigens on urinary tract cells (esp in kidneys)  
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Type 1 Pili   allows bacteria to bind to bladder epithelium, Tamm-Horsfall glycoprotein & D-mannose residues on variety of cells  
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Proteus sp (vulgaris, mirabilis, etc)   G(-) rods, facultative anaerobes; Opportunistic (catheters); Enteric bacteria (same as E. coli, salmonella, shigella, enterobacter, serratia); *Urease Positive --> converts urea to ammonia raising pH*; highly motile; swarms agar  
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Proteus mirabilis   2nd to E. coli in causing UTIs; commonly infects kidneys (>E.coli); Non-traditional infxs occuring in individuals w/abnormalities in UT & elderly w/long-term catheters  
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Proteus mirabilis pathogenicity   invades & attaches to host epithelial cells; resists host defenses by producing: Pore-forming hemolysins, Endotoxin (bc G-), Urease, Adhesins, Polysaccharide capsule, Pili, fimbrae, flagella, Biofilms  
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Proteus mirabilis: Urease activity   hydrolyzes urea; produces ammonia and CO2; raises pH; precipitates nml soluble ions to form stones (calculi) --> Mg-ammonium-phosphate (struvite) & Calcium-phosphate (apatite)  
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Proteus mirabilis: Swarming ability   critical to the virulence of the sp.; expression of virulence determinants (protease, hemolysin) specific to swarmer bacteria  
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Proteus mirabilis: treatment   PNPG (anti-swarm agent inhibits hemolysins, proteases, flagella; may prevent invasion of urothelial cells); Broad spectrum PCNs & Cephalosporins (not nitrofurantoin or tetracycline); Inc resistance to: Ampicillin, Ciprofloxin, Trimethoprim  
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Staphylococcus saprophyticus   G+ cocci; Nitrite neg, non(gamma)-hemolytic; Catalase +, Coagulase neg; Resistant to Novobiocin; UTI common in sexually active women (5-15% of UTIs) "honeymoon cystitis"  
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Serratia marcescens   G(-) bacilli; facultative anaerobes; Enterobacteriaceae family; Positive for (DNAse, Gelatinase, Lipase, Citrate utilization); Opportunistic pneumonia & UTI agent (used in army experiment)  
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Enterococcus faecalis   aka: (Grp D streptococci, Streptococcus faecalis); GI tract normal flora, causative agent for: (endocarditis, cystitis, wound infections); Blood agar (gamma/some alpha-hemolysis); Bile-esculin agar (black color); also gros on 6.5% NaCl; *Catalase negative  
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Interesting facts about Enterococcus faecalis   25% of genome is exogenously acquired DNA (lateral gene transfer btw genus & species; Virulece factors from Staph and Strep); leading cause of nosocomial infxns; Pathogenicity island codes for toxins that form holes in cell wall & allow adherence  
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Enterococcus faecalis: Virulence and Treatment   development of Abx resistance (d/t ability to acquire mobile gene elements); Tx (amoxicillin, ampicillin, vancomycin-some resistant strains exist)  
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Klebsiella sp   G(-), non-motile, rod, aerobic, endotoxin & enterotoxin activity; Ubiquitous (may colonize skin, pharynx, GI tract); Large mucoid colonies w/large mucoid polysaccharide capsule "K antigen" that protects against phagocytosis & aids in adherence  
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Klebsiella pneumoniae, Klebsiella oxytoca   opportunistic pathogens; found in environment/mucosal surfaces; passed by hands in hospital; Common infxns: UTI, lower resp tract (red current jelly sputum/hemoptysis), biliary tract, surgical wounds  
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Klebsiella sp Clinical Syndromes & Treatmtent   UTIs; Primary pneumonia; wound infxns, bacteremia, meningitis, diarrhea by enterotoxigenic strains; Cephalosporins  
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Candida sp.   normal urogenital tract flora in 20-50% of healthy women; Inc risk of infection with: (broad-spectrum Abx, pregnancy, diabetes, AIDS, surgery, in-dwelling catheters); Treat topically with Nystatin or Clotrimazole  
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Candida Germ Tube Formation   triggered by environmental cues (pH, temp, chemicals); adherence/virulence factor; induced by serum at 37*C; 1st step in transition from yeast to hyphae; D-glucose (active component in serum for induction; can be inhibited by glucose oxidase at pH 7-8)  
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Catheter-associated UTIs (CAUTI)   UT is mc site of nosocomial infxns (40%); 66-86% of nosocomial UTIs follow catheterization (duration inc incidence)  
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Pathogens a/w CAUTIs   **Pseudomonas cepacia, Serratia marcescens (neither are normal flora)**; E. coli, Klebsiella, Proteus, Enterococcus, Enterobacter, Candida; biofilms assist in stickiness to plastic  
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Extraluminal CAUTI   early (occurs at insertion site); Late (occurs by capillary action)  
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Intraluminal CAUTI   Intraluminal (break in closed drainage; contamination of collection bag urine)  
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Catheter colonization by Proteus mirabilis   leads to precipitation of phosphatic salts, stone formation and blockage  
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Schistosoma haemotobium: Urinary Tract schistosomiasis   can lead to renal failure d/t obstructive uropathy, pyeloneprhitis, bladder carcinoma  
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Schistosoma haemotobium: Female genital schistosomiasis   causes lesions in lower female genital tract; may facilitate spread of STDs such as HIV and HPV  
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Urinary Schistosomiasis: Clinical manifestations and Lab studies   dysuria, urinary frequency, terminal hematuria; ID and speciate eggs in urine; urinary excretion of eggs is not uniform throughout day (more likely btw 10am and 2pm; quantify with 24hr collection)  
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Urinary Schistosomiasis: Diagnostics   UA (culture for associated infections); UTI caused by Salmonella is suspicion for this infection (esp if blood cultures show Salmonella); Blood chemistries (renal panel); CBC (check for anemia and eosinophilia)  
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Urinary Schistosomiasis: Treatment   Antihelmintics (Praziquantil damages tegument membrane, exposing worm to immune defenses); Test effectiveness of treatment with "egg viability test  
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Routine Urinalysis: Chemical Testing - Nitrite   detects bacteriuria (some convert nitrate to nitrite; usu G(-)s); dipstic method forms diazonium salt forming a pink azodye; False positives if contaminated or if stored improperly  
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Routine Urinalysis: Chemical Testing - Leukocytes   dipstick detects leukocyte esterase activity in WBCs (granulocytic cells); detects lysed and intact; indixylcarbonic acid ester reacts w/diazonium salt to form purple azodye  
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Routine Urinalysis: Chemical Testing - Hemoglobin (blood)   in renal dx or trauma, RBCs enter urine & become hemolyzed; Hemolytic anemia (Hb is filtered into urine from transfusion rxns, severe burns, infxns, strenuous exercise); Dipstick orthotoluidine reacts w/Hb & organic peroxide to turn blue  
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UTI: Treatment   most treated with: Trimethoprim-sulfamethoxazole (amoxicillin) or Fluoroquinolones (Levaquin); Those caused by Chlamydia trachomatis or Mycoplasma hominis may require *tetracycline or doxycycline*  
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Recurrent UTIs   20% of women suffer >1; bacterial strains will differ; Related to "nonsecretors" for certain blood group antigens (cells lining urethra/vagina are more susceptible to bacterial attachment)  
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Recurrent UTIs: Secretors vs Nonsecretors   80% of population secrete A, B, & H antigens into body fluid w/same specificity as Ag on RBC membrane; trait is a/w Se gene which is inherited independently from other blood Ags; H-gene is precursor for ABO (all secretors secrete H gene)  
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ABO Blood Group System Biochemistry   Oligosaccharide chain precursor: H-gene produces enzyme that puts on L-fucose; A-gene produced enzyme that puts on A-antigen; B-gene produces enzyme that puts on B-antigen  
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Recurrent UTIs: Secretor Testing   useful in determining blood group types on individuals whose RBC antigens are poorly developed or missing (also determining blood grps in forensic medicine)  
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Recurrent UTIs: Nonsecretors   20% of population; homozygous for Se gene and do not secrete ABH antigens; All bombay individuals are nonsecretors since they don't produce H, A, or B antigens  
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