Contents Definitions Incidence and epidemiology Pathogenesis Clinical manifestations Diagnosis Antimicrobial therapy Bladder infection Kidney infection Bactreremia, sepsis and septic shock Catheter associated UTI UTI in spinal injury Pt
Definitions UTI : An inflammatory response of the urothelium to bacterial invasion that is usually associated with bacteriuria and pyuria. Bacteriuria : The presence of bacteria in the urine, which is normally free of bacteria. Pyuria: The presence of white blood cells (WBCs) in the urine, is generally indicative of infection and an inflammatory response of the urothelium to the bacterium.
Bacteriuria without pyuria bacterial colonization Pyuria without bacteriuria tuberculosis stones cancer
Infections defined by their site of origin Cystitis A clinical syndrome of dysuria, frequency, urgency, and occasionally suprapubic pain. Acute pyelonephritis An acute bacterial infection of the kidney. Chronic pyelonephritis Describes a shrunken, scarred kidney, diagnosed by morphologic, radiologic, or functional evidence of renal disease that may be postinfectious
UTIs definition in terms of functional status of the urinary tract and the health of the host. Uncomplicated UTI : An infection in a healthy patient with a structurally and functionally normal urinary tract. A complicated infection Associated with factors that increase the chance of acquiring bacteria and decrease the efficacy of therapy
Functional or anatomic abnormality of urinary tract Male gender Pregnancy Elderly Diabetes Immunosuppression Childhood UTI Recent antimicrobial agent use Indwelling urinary catheter Urinary tract instrumentation Symptoms for more than 7 days at presentation
UTIs defined by their relationship to other UTIs. : First or isolated infection An individual who has never had a UTI or has one remote from a previous UTI. :Unresolved infection One that has not responded to antimicrobial therapy. :Recurrent infection One that occurs after successful resolution of an antecedent infection. Reinfection : Describes a new event associated with reintroduction of bacteria into the urinary tract from outside.
INCIDENCE AND EPIDEMIOLOGY
Account for: >7 million visits to physicians' offices >1 million complicate office visits 1 million emergency department visit 100,000 hospitalizations annually 1.2% of all office visits by women 0.6% of all office visits by men Surveys screening for bacteriuria in female : 1% of schoolgirls have bacteriuria 4% by young adulthood 1% to 2% per decade of age
The prevalence of bacteriuria in women has been estimated at 3.5%, and increasing with age in a linear trend 30% of 24 y women with symptomatic UTI requiring antimicrobial therapy Half of all women will experience a UTI during their lifetime. Bacteriuria in young women is 30 times >men. with increasing age, the ratio of women to men progressively decreases. 20% of women and 10% of men older than 65 years have bacteriuria
UTIs are a result of interactions between the uropathogen and the host. Successful infection of the urinary tract is determined by The virulence factors of the bacteria, The inoculum size The host defense mechanisms.
Routes of Infection : Ascending Route: Bowel reservoir Adherence to the introital and urothelial mucosa Hematogenous Route: Uncommon Secondarily infected in patients Lymphatic Route: Occur in unusual circumstances, such as: Severe bowel infection Retroperitoneal abscesses..
Urinary Pathogens community-acquired infections : E. coli accounting for 85% gram-negative Enterobacteriaceae,(Proteus and Klebsiella,) gram-positive (E. faecalis and S. saprophyticus) Nosocomial infections E. coli, accounting for 50% Klebsiella, Enterobacter, Citrobacter, Serratia, Pseudomonas aeruginosa, Providencia, E. faecalis, and S. epidermidis Gardnerella vaginalis, Mycoplasma species, and Ureaplasma urealyticum may infect patients with intermittent or indwelling catheters
Anaerobes in the Urinary Tract The distal urethra, perineum, and vagina are normally colonized by anaerobes. Anaerobic organisms are frequently found in suppurative infections of the genitourinary tract. Bacteroides species, including B. fragilis, Fusobacterium species, anaerobic cocci, and Clostridium perfringens Mycobacterium tuberculosis and Other Non- Tuberculous Mycobacteria Chlamydia
Bacterial Virulence Factors play a role in determining the ability of an organism to invade the urinary tract and level of infection within the urinary tract. uropathogenic E. coli (UPEC), can infect the urinary tract by the expression of virulence factors that enable them to adhere to and colonize the perineum and urethra and migrate to the urinary tract where they establish an inflammatory response in the urothelium. A recent genomic analysis of a UPEC strain revealed the presence of genes for putative chaperone-usher that may function as adhesins, toxins, proteases, invasins, serum resistance factors, or motility mediators
Early Events in UPEC Pathogenesis Bacterial Adherence Bacterial adherence is a specific interaction that plays a role in determining the organism, the host, and the site of infection. This interaction is influenced by: The adhesive characteristics of the bacteria, The receptive characteristics of the epithelial surface The fluid bathing both surfaces.
UPEC expresses a number of adhesins that allow it to attach to urinary tract tissues classified as either fimbrial or afimbrial, A typical piliated cell may contain 100 to 400 pili. The pilus is usually 5 to 10 nm in diameter, is up to 2 μm long, Pili are defined functionally by their ability to mediate hemagglutination of specific types of erythrocytes. The most well-described pili are types 1, P and S.
Type 1 (Mannose Sensitive) Pili: Expressed on both nonpathogenic and pathogenic E. coli Facilitate bacterial colonization of the vaginal mucosa and bladder. These pili mediate hemagglutination of guinea pig erythrocytes The reaction is inhibited by the addition of (mannoseMSHA) Consist of a helical rod composed of repeating FimA subunits joined to a 3-nm wide distal tip structure containing the adhesin FimH
Binding of the FimH adhesin to mannosylated host receptors on the uroepithelium colonization of E. coli in the vaginal introitus, urethra, and bladder and cause cystitis The luminal surface of the bladder is lined by umbrella cells. appear as a quasi-crystalline array of hexagonal complexes composed of four integral membrane proteins known as uroplakins Two of the uroplakins, UPIa and UPIb, can specifically bind UPEC expressing type 1 pili.
P (Mannose Resistant) Pili: Found in most pyelonephritogenic strains of UPEC Mediate hemagglutination of human erythrocytes that is not altered by mannose (MRHA) The adhesin PapG, at the tip of the pilus, recognizes the α-d- galactopyranosyl-(1-4)-β-d-galactopyranoside moiety present in the globoseries of glycolipids which are found on P-blood group antigens and on uroepithelium. Other Adhesins: S pili: which bind to sialic acid residues via the SfaS adhesin, It is associated with both bladder and kidney infection F1C pili: bind to glycosphingolipids in renal epithelial cells and induce an interleukin-8 inflammatory response
Epithelial Cell Receptivity Vaginal Cells: E. coli strains that cause cystitis adhere more to epithelial cells from susceptible women The increased bacterial adherence was also characteristic of buccal epithelial cells. A small variation in both vaginal cell and buccal cell receptivity from day to day premenopausal women susceptible at certain times during the menstrual cycle and early pregnancy Uropathogens attached in larger numbers to uroepithelial cells from women > 65 years
Blood group antigens are important part of the uroepithelial cell membrane. women with Lewis blood group Le(ab) and Le(a+b) (nonsecretor) phenotypes have higher incidence of recurrent UTIs than women with Le(ab+) phenotype The protective effect in women with the Le(a-b+) phenotype may be due to fucosylated structures at the vaginal cell surface or in the overlying mucus which decreases availability of putative receptors for E. coli
Bladder Cells the initial step in the intricate cascade of events leading to UTIs is fimH-mediated binding to the bladder epithelium FimH binds mannosylated residues on the uroplakin molecules covering bladder superficial epithelial cells.
UPEC Persistence in the Bladder: After attachment to the epithelium, UPEC is quickly internalized into the bladder superficial cells establish a new niche to protect itself from the host innate immune response Once intracellular, the UPEC organisms rapidly grow and divide within the cell cytosol small clusters of bacteria(early intracellular bacterial communities IBCs ) As they grow, the bacteria maintain their typical rod shape of 3 μm and form a loosely organized cluster, with microorganisms randomly oriented in the cell cytoplasm. Between 6 to 8 hours after inoculation, early IBCs show a drop in bacterial growth rate doubling times greater than 60 minutes, a significant shortening of the bacterial morphology to of 0.7 μm, a biofilm-like community
Biofilms shield bacteria from antimicrobial agents and the host immune response by: Slower growth rate of the bacteria Expression of factors that inhibit antimicrobial activity, Inability of the antimicrobial agent to penetrate the biofilm Protects the bacteria from neutrophils because they are unable to effectively penetrate the IBC and engulf the bacteria. Bacteria on the edge of IBCs eventually detach then escape the host cell into the bladder lumen (fluxing) to readhere and reinvade superficial cells second IBC formation.
Natural Defenses of the Urinary Tract Periurethral and Urethral Region: The normal flora usually contain microorganisms such as lactobacilli, coagulase-negative staphylococci, corynebacteria, and streptococci that form a barrier against uropathogenic colonization. Changes in the vaginal environment related to estrogen, cervical IgA, and low vaginal pH may alter the ability of bacteria to colonize.
Urine The most inhibitory factors : - Flow of urine and voiding #1 defense - High osmolality with a low pH inhibitory to bacterial growth - High urea and organic acid content can reduce survival of bacteria within the urinary tract - Uromodulin (Tamm-Horsfall protein), saturating all the mannose-binding sites of the type 1 pili, blocking bacterial binding to the uroplakin receptors of the urothelium - Lactoferrin within urine: can scavenge essential iron away from bacteria Bladder Factors responsible for defense : - The ability of the bladder to empty - Innate and adaptive immunity - Exfoliation of epithelial cells.
Immune Response: mediated by a series of pathogen-associated molecular pattern receptors (PAMPs), Toll-like receptors (TLRs) : provide the link between recognition of invading organisms and development of the innate immune response. TLRs are conserved among many species of pathogens, such as (LPS) and peptidoglycan (PG), activate signaling pathways that initiate immune and inflammatory responses to kill pathogens. TLR4 expressed on Superficial bladder epithelial cells with CD14 recognize LPS from the bacteria and the innate immune response TLR11 expressed on uroepithelial cells recognizes UPEC and protects the kidneys from ascending infection cells
Alterations in Host Defense Mechanisms Obstruction Vesicoureteral Reflux Underlying Disease Diabetes Mellitus Renal Papillary Necrosis Human Immunodeficiency Virus Pregnancy Spinal Cord Injury with High-Pressure Bladders
Symptoms and Signs
Diagnosis Urine Collection: Voided and Catheterized Specimens Men: Circumcised menno preparation. Not circumcised, the foreskin should be retracted and the glans penis washed with soap and then rinsed with water before specimen collection. Women: contamination with introital bacteria and WBCs is common, The first 10 mL of urine: urethra Midstream specimen bladder Prostatic fluid First 10 mL after massage catheteraization Suprapubic Aspiration
Urinalysis Sediment from an approximately 5- to 10-mL specimen obtained by centrifugation for 5 minutes at 2000 rpm is analyzed. Bacteriuria, Pyuria, and Hematuria
Bacteriuria: Microscopic bacteriuria 10 5 colony-forming units (cfu) per milliliter of urine The bacterial count must be approximately 30,000/mL before bacteria can be found in the sediment, stained or unstained, spun or unspun False-negative : Early infection due to low no of bacteria and WBCs Diluted samples False-positive: Contamination of the urine specimen collection.
Pyuria : Examining the centrifuged sediment or using a hemocytometer to count the number of WBCs in the unspun urine. 1 to 2 WBCs per high-power field (HPF) in sediment from a centrifuged specimen = 10 WBCs/mm 3 in an unspun specimen. > 2 WBCs per HPF in a centrifuged specimen or 10 WBCs/mm 3 of urine correlates well with the presence of bacteriuria and is rarely seen in nonbacteriuric patients Hematuria : Microscopic hematuria is found in 40% to 60% of cases of cystitis and is uncommon in other dysuric syndromes Nitrites: formed when bacteria reduce the nitrate present in urine Leukocyte esterase : sensitivity of 75% to 96% in detecting pyuria associated with infection
Urine Culture: Two techniques: A: Direct surface plating of urine on split-agar disposable plates. - Blood agar G+tive – G-tive bacteria - Desoxycholate or eosin–methylene blue (EMB) G-tive 0.1 mL of urine onto each half of the plate. Overnight incubation, The number of colonies multiplied by 10 to report the number of cfu per milliliter of urine. Urine must be refrigerated immediately on collection and should be cultured within 24 hours of refrigeration.
B: The dip slides Soy agar (a general nutrient agar to grow all bacteria) on one side and EMB or MacConkeys agar on other. A slide is dipped into urine, the excess is allowed to drain off, and the slide is replaced in its plastic bottle and incubated. The volume of urine that attaches to the slide is between 1/100 mL and 1/200 mL. the colony count is 100 to 200 times the number of colonies that become visible with incubation.
IMAGING TECHNIQUES Plain Film of the Abdomen Radiopaque calculi Gas patterns Absent psoas or abnormal renal contour, perirenal or renal abscess Plain Film Renal Tomograms Small or poorly calcified stones despite overlying gas Struvite and uric acid stones that contain small amounts of calcium may be seen
Excretory Urogram Useful to determine the exact site and extent of urinary tract obstruction Not the best screening test for hydronephrosis, pyonephrosis, or renal abscess Unnecessary for routine evaluation Voiding Cystourethrogram Neuropathic bladders Female patient who has a urethral diverticulum causing her persistent infections VUR
Ultrasonography Useful in r/o hydronephrosis associated with UTI, pyonephrosis, and perirenal abscesses No radiation or contrast agent risk CT and MRI Best antomic detail More sensitive than IVP or U/S for acute focal bacterial nephritis and renal and perirenal abscesses MR: advantages in delineating extrarenal extension of inflammation
Radionuclide Studies Gallium-67 used to distinguish some upper tract from lower tract infections possible mechanisms: –concentration within labeled PMNs –leakage of protein- bound gallium through capillaries –increased vascularity of the lesion can see focal bacterial nephritis and infected renal cysts Indium Indium 111–labeled WBC accumulate only in sites of inflammation and not in normal kidneys or tumors - highly specific for inflammation
PRINCIPLES OF ANTIMICROBIAL THERAPY
Efficacy of the antimicrobial therapy is critically dependent on: - The antimicrobial levels in the urine - The duration that this level remains above the minimal inhibitory concentration of the infecting organism Resolution of infection is closely associated with the susceptibility of the bacteria to the concentration of the antimicrobial agent achieved in the urine The concentration of the antimicrobial agent achieved in blood is not important in treatment of uncomplicated UTIs.
In renal insufficiency, dosage modifications are necessary for agents that are cleared primarily by the kidneys In renal failure, the kidneys may not be able to concentrate an antimicrobial agent in the urine; difficulty in eradicating bacteria may occur. A decision regarding the antimicrobial selection and the duration of therapy must consider: - The spectrum of activity of the drug against the pathogen - Uncomplicated or complicated, - Potential adverse effect - Cost.
Bacterial Resistance Inherited chromosomal resistance Exists in a bacterial species because of the absence of the proper mechanism on which the antimicrobial agent can act. Proteus and Pseudomonas species are always resistant to nitrofurantoin.
Acquired chromosomal resistance Selection of resistant mutants within the urinary tract during therapy Resistant organism (clone) was present before, but only in one per 10 5 to organisms The remainder of the bacteria, which are susceptible to the administered antimicrobial agent, will be eradicated by therapy, but within 24 to 48 hours a repeat urine culture will show high bacterial counts of the resistant mutant. This phenomenon is most likely to occur when the antimicrobial level in the urine is close to or below the minimal inhibitory concentration of the drug
Extrachromosomal-mediated resistance Acquired and transferable via plasmids, which contain the genetic material for the resistance, called R-factor resistance Much more common Produces multiply resistant strains, making therapy more difficult Occurs only in the fecal flora, never within the urinary tract Patients previously exposed to β-lactams, aminoglycosides, sulfonamides, TMP, and tetracycline will often have R-factor resistance to both the antimicrobial agent to which the bacteria were exposed and also to other antimicrobial agents.
Mechanisms of Drug ResistanceMechanism of ActionDrug or Drug Class Production of β-lactamase- - Alteration in binding site of penicillin-binding protein - Changes in cell wall porin size (decrease penetration) Inhibition of bacterial cell wall synthesis β-Lactams penicillins, cephalosporins, aztreonam - Mutation in DNA gyrase- binding site - Changes in cell wall porin size (decrease penetration) Active efflux Inhibition of bacterial DNA gyrase Quinolones - Downregulation of drug uptake into bacteria - Bacterial production of aminoglycoside-modifying enzymes Inhibition of ribosomal protein synthesis Aminoglycosides - Not fully elucidated-develops slowly with prolonged exposure Inhibition of several bacterial enzyme systems Nitrofurantoin Draws folate from environment (enterococci) Antagonism of bacterial folate metabolism Trimethoprim- sulfamethoxazole Enzymatic alteration of peptidoglycan target Inhibition of bacterial cell wall synthesis (at different point than β-lactams) Vancomycin
Antimicrobial Formulary Gram-Negative PathogensGram-Positive PathogensAntimicrobial Agent or Class Escherichia coli Proteus mirabilis Streptococcus Enterococci Amoxicillin Amoxicillin or ampicillinampicillin P. mirabilisHaemophilus influenzae, Klebsiella species Staphylococcus (not MRSAEnterococci) Amoxicillin Amoxicillin with clavulanate E. Coli P. Mirabilis Klebsiella species Streptococcus Staphylococcus (not MRSA) First-generation cephalosporins E. coli, P. mirabilisStreptococcusSecond-generation cephalosporins (cefamandole, cefuroxime, cefaclor )cefuroxime cefaclor Most, excluding P. aeruginosaStreptococcus Staphylococcus (not MRSA) Third-generation cephalosporins (ceftriaxone) Most, including P. aeruginosaStreptococcusThird-generation cephalosporins (ceftazidime )ceftazidime Reliable Coverage of Antimicrobials Used in the Treatment of UTIs of Commonly Encountered Pathogens :
Gram-Negative PathogensGram-Positive PathogensAntimicrobial Agent or Class Most, including P. aeruginosaStaphylococcus (urine)Aminoglycosides Most, including P. aeruginosaStreptococcus*Fluoroquinolones Many Enterobacteriaceae (not Providencia, Serratia, Acinetobacter) Klebsiella species Staphylococcus (not MRSA) Enterococci Nitrofurantoin Most Enterobacteriaceae (not P. aeruginosa) Streptococcus Staphylococcus Trimethoprim-sulfamethoxazole None All, including MRSA Vancomycin
ANTIMICROBIAL PROPHYLAXIS FOR COMMON UROLOGIC PROCEDURES
Host Factors That Increase the Risk of Infection Advanced age Anatomic anomalies Poor nutritional status Smoking Chronic corticosteroid use Immunodeficiency Chronic indwelling hardware Infected endogenous/exogenous material Distant coexistent infection Prolonged hospitalization
Urethral Catheterization and Removal The risk of infection after one-time urethral catheterization is 1% to 2% in healthy domiciliary women Prolonged use of an indwelling urethral catheter in hospitalized patients risk of bacterial colonization - 3% to 10% incidence of bacteriuria per catheter day - 100% incidence of bacteriuria with long-term (>30 days) Prophylactic administration of antimicrobial agents during catheterization is not generally recommended because of bacterial resistance
Special Considerations Patients with Risk of Endocarditis The urinary tract is the second most common site of entry of organisms that cause endocarditis. The risk of endocarditis after urologic procedures is low Enterococcus faecalis (enterococci) is the most common organism causing endocarditis after urologic procedures Prophylaxis is recommended for both high- and moderate-risk patients.
Prophylaxis should be initiated for urologic procedures, including - obstructed urinary tract - prostatic surgery - urinary reconstruction with intestine - percutaneous renal surgery - cystoscopy, and urethral dilation
Moderate-risk patients include other congenital malformations
Patients with Indwelling Orthopedic Hardware
Uncomplicated Cystitis Risk Factors for UTIs urethral stricture, foreign body (calculus) Reduced Urine Flow Neurogenic bladder Outflow obstruction, prostatic hyperplasia, prostatic carcinoma, Promote Colonization Inadequate fluid uptake (dehydration) Spermicide-increased binding Sexual activity-increased inoculation Antimicrobial agents-decreased indigenous flora Estrogen depletion-increased binding Facilitate Ascent Catheterization Residual urine with ischemia of bladder wall Urinary and Fecal incontinence
Clinical Presentation Dysuria, frequency or urgency, and suprapubic pain Hematuria or foul-smelling urine may develop. Fever, chills, and other signs of dissemination are not present. (superficial infection of bladder mucosa), suprapubic tenderness causative organism : 75% to 90% E. coli 10% to 20% S. saprophyticus,
Laboratory Diagnosis pyuria : sensitivity 95% and specificity 70%. bacturia : sensitivity 40-70% and specificity %, Dipsticks: nitrite or leukocyte esterase Urine culture -/+
Management Antimicrobial Selection Duration (days) Frequency per dose Dosage (mg) DrugRoute Circumstanc es Women 3BID QD BID 500 mg 1 double- strength tablet ( mg) 400 mg Ciprofloxacin Levofl oxacin TMP-SMX Norfloxacin Oral Healthy 7As above TMP-SMX or Fluoroquinolo ne Symptoms for >7 days, recent UTI, age >65 yr, diabetes, diaphragm use 7TID QID As above 250 mg 500 mg As above Amoxicillin Cephalexin Nitrofurantoin Nitrofurantoin macrocrystals TMP-SMX* Pregnancy Men 77As above TMP-SMX Fluoroquinolone Oral Healthy and age <50 yr
Follow-Up young asymptomatic no Follow-up. older women or men urinalysis, and urine culture
Asymptomatic Bacteriuria Women : Two consecutive voided urine specimens with isolation of the same bacterial strain in quantitative counts of 10 5 cfu/mL Men: A single clean-catch voided specimen with similar counts is adequate. Catheter : A single catheterized urine specimen with a solitary isolate with a quantitative count of 10 2 cfu/mL identifies bacteriuria in women or men
Prevalence, %Population Healthy, premenopausal women Pregnant women Postmenopausal women aged years Diabetic patients Women Men Elderly persons in the community Women Men 28Patients undergoing hemodialysis Prevalence, %Population Elderly persons in a long-term care facility Women Men Patients with spinal cord injuries Intermittent catheter use 57 Sphincterotomy and condom catheter in place Patients with indwelling catheter use 9-23 Short-term 100 Long-term Prevalence of Asymptomatic Bacteriuria in Selected Populations
Management : Observation Screening for and Treatment of Asymptomatic Bacteriuria Not recommendedPremenopausal nonpregnant women RecommendedPregnant women Not recommendedDiabetic women Not recommendedOlder persons residing in the community Not recommendedElderly institutionalized subjects Not recommendedSubjects with spinal cord injuries Not recommendedPatients with indwelling urethral catheters RecommendedUrologic interventions Not recommendedImmunocompromised patients and transplant patients
Complicated Cystitis infection in a compromised urinary tract or caused very resistant pathogen. Complicating Host Factors Functional/structural abnormalities of urinary tract Recent urinary tract instrumentation Recent antimicrobial agent use Diabetes mellitus Immunosuppression Pregnancy Hospital-acquired infection
Treatment of Complicated UTIs Recommended Empirical TreatmentMitigating Circumstances Common Pathogens Oral* norfloxacin, ciprofloxacin, or ofloxacin for daysnorfloxacin ofloxacin Mild-to-moderate illness, no nausea or vomiting-outpatient therapy E. coli, Proteus species, Klebsiella species, Pseudomonas species, Serratia species, enterococci, staphylococci Parenteral ampicillin and gentamicin, ciprofloxacin, levofloxacin, ceftriaxone, aztreonam, ticarcillin-clavulanate or imipenem-cilastin until fever gone; then oral* trimethoprim- sulfamethoxazole, norfloxacin, ciprofloxacin, or levofloxacin for daysampicillin levofloxacin aztreonam norfloxacin levofloxacin Severe illness or possible urosepsis- hospitalization required
Unresolved UTIs inadequate initial therapy eliminate symptoms and/or bacterial growth in the urinary tract. Causes of Unresolved Bacteriuria, in Descending Order of Importance Bacterial resistance to the drug selected for treatment Development of resistance from initially susceptible bacteria Bacteriuria caused by two different bacterial species with mutually exclusive susceptibilities Rapid reinfection with a new, resistant species during initial therapy for the original susceptible organism Azotemia Papillary necrosis from analgesic abuse Giant staghorn calculi in which the "critical mass" of susceptible bacteria is too great for antimicrobial inhibition Self-inflicted infections or deception in taking antimicrobial drugs (a variant of Munchausen's syndrome) Body_ID: HC Initial empirical antimicrobial agent different from the original agent Fluoroquinolones for 7 days.
Recurrent UTIs Reemergence of bacteria from a site within the urinary tract (bacterial persistence) or new infections from bacteria outside the urinary tract (reinfection). Bacterial persistence : Caused by the same organism Close intervals Cured by identification, removal or correction of the focus
Correctable Urologic Abnormalities That Cause Bacterial Persistence Unilateral medullary sponge kidneysInfection stones Nonrefluxing, normal-appearing, infected ureteral stumps after nephrectomy Chronic bacterial prostatitis Infected urachal cystsUnilateral infected atrophic kidneys Infected communicating cysts of the renal calycesUreteral duplication and ectopic ureters Papillary necrosisForeign bodies Perivesical abscess with fistula to bladderUrethral diverticula and infected periurethral glands
Reinfections : Caused by different species. Long intervals No an alterable urologic abnormality medical management. women and girls : ascending from the bowel flora. Men: associated with a urinary tract abnormality. Risk factors Fistula,Evidence of upper tract infections Analgesic abuseHistory of unexplained hematuria, Severe diseaseObstructive symptoms, Diaphragm-spermicideNeurogenic bladder dysfunction, Postmenopausal women,Renal calculi,
Antimicrobial management : Indicated in women 2 UTIs over 6-month or 3 UTIs within a 12- month involves: Low-dose continuous prophylaxis, Self-start intermittent therapy Postintercourse prophylaxis.
Low-Dose Continuous Prophylaxis: Oral antimicrobial agents with minimal adverse effects on the bowel and vaginal flora and do not cause bacterial resistance (1) Nitrofurantoin, 50 to 100 mg half-strength (HS) (2) TMP-SMX, 40 to 200 mg (3) TMP, 50 mg (4) Keflex, 250 mg Monitoring for infections every 1 to 3 months, even in asymptomatic patients. Breakthrough infections usually respond to full-dose therapy with the drug used for prophylaxis
Self-Start Intermittent Therapy The patient is given a dip slide device to culture the urine and is instructed to perform a urine culture when symptoms of UTI occur A broad spectrum antibiotics with minimal or no side effects on the bowel flora. Fluoroquinolones are ideal Post-intercourse Prophylaxis Nitrofurantoin, Cephalexin, TMP-SMX, or a fluoroquinolone taken as a single dose, will effectively reduce the incidence of reinfection
Acute Pyelonephritis Clinical Presentation: Abrupt onset of chills, fever (100° F or greater) unilateral or bilateral flank Accompanied by dysuria, increased urinary frequency, and urgency. Laboratory Diagnosis: Blood tests: leukocytosis with a predominance of neutrophils, ESR C-reactive protein levels elevated creatinine creatinine clearance may be decreased. Blood cultures may be positive.( 25% uncomplicated )
Urinalysis usually : The presence of large amounts of granular or leukocyte casts in the urinary sediment is suggestive of acute pyelonephritis. Bacteriology: - E. coli 80% of cases. - Proteus, Klebsiella, Pseudomonas, Serratia, Enterobacter, or Citrobacter should be suspected in patients with recurrent UTIs, are hospitalized, or have indwelling catheters, as well as in those who required recent urinary tract instrumentation - Gram-positive bacteria rarely cause pyelonephritis. Brightfield micrograph of a mixed bacterial leukocyte cast from patient with acute pyelonephritis. Only the bacteria and the nucleus of a leukocyte stain strongly. Many bacteria are clearly demonstrated by through-focusing (toluidine blue O stain, magnification ×640). (From Lindner LE, Jones RN, Haber MH: A specific urinary cast in acute pyelonephritis. Am J Clin Pathol 1980;73: )
Radiologic Findings: Excretory Urogram: Renal enlargement, (most common) An overall length of 15 cm or a length 1.5 cm greater than the unaffected side has been established as a criterion for the diagnosis of renal enlargement in acute pyelonephritis The calyces have an attenuated or spidery appearance. Calyceal and ureteral dilation (the bacte-rial endotoxins that impair ureteral peristalsis). A, Excretory urogram. Ten-minute film demonstrates enlarged right kidney with minimum function. Findings are consistent with edema. B, Ultrasound of the right kidney demonstrates renal enlargement, hypoechoic parenchyma, and compressed central collecting complex (arrows). (From Schaeffer AJ: Urinary tract infections. In Gillenwater JY, et al [eds]: Adult and Pediatric Urology. Philadelphia, Lippincott William & Wilkins, 2002, pp )
Renal Ultrasonography and Computed Tomography: used : Complicated UTIs Not respond after 72 hours of therapy Renal enlargement, Hypoechoic or attenuated parenchyma and a compressed collecting system.
Pathology : The parenchyma shows a focal, patchy infiltrate of neutrophils. Bacteria are often in the infiltrate. Early: limited to the interstitium Later: linear bands extend from the papillae to the cortex Abscesses may cause tubular destruction; The glomeruli are usually spared.
Management: Initial Management. Subdivided into : (1) Uncomplicated infection : Not warrant hospitalization (2) Uncomplicated infection : Ill patient with normal urinary tracts warrant hospitalization (3) Complicated infection : Associated with hospitalization, catheterization, urologic surgery, or urinary tract abnormalities
Risk factors associated with increased risk of death or hospitalization: Advanced age, Septic shock, Bedridden status, Immunosuppression, Recent antibiotic use, Diabetes mellitus, Long-term urinary catheterization A change in initial antimicrobial therapy
Duration (days) Frequency per DoseDosageDrugRouteCircumstances 10-14BID160 to 800 mg TMP-SMX Oral Outpatient- moderately ill, no nausea or vomiting 7 BID 500 mg Ciprofloxacin QD500 mg Levofloxacin BID 400 mg Norfloxacin 14 BID160 to 800 mg TMP-SMX Parenteral Inpatient-severely ill, possible sepsis QD TID 1 g 1.5 mg/kg Ampicillin Ampicillin and gentamicin BID 400 mg Ciprofloxacin QD 500 mg Levofloxacin QD 1 to 2 g Ceftriaxone Take until afebrile, then take oral TMP-SMX or fluoroquinolone 14 QD 1 to 2 g Ceftriaxone Parenteral Pregnant QD 1 g Ampicillin Ampicillin and gentamicin 1 g Aztreonam TID-QID Take until afebrile, then take: BID 500 mg Cephalexin Oral
Acute Focal or Multifocal Bacterial Nephritis An uncommon, severe form of acute renal infection in which a heavy leukocyte infiltrate is confined to a single renal lobe (focal) or multiple lobes (multifocal). Clinical Presentation: Similar but more severe. 50% of the patients are bacteremic
Radiologic Findings: IVP : Poorly marginated mass The mass has slightly less nephrographic density than the surrounding normal renal parenchyma. Ultrasonography : poorly marginated sonolucent with low- amplitude echoes that disrupt the cortical medullary junction CT contrast : Wedge-shaped areas of decreased enhancement Acute focal bacterial nephritis. A, Excretory urogram. Five-minute tomogram demonstrates normally functioning upper and lower poles and a poorly marginated midrenal mass with poor function and absent collecting system visualization. B, Ultrasound; longitudinal view of the left kidney demonstrates spleen (S) and left kidney (arrows). Note irregular midpole mass (M) of slightly higher echo texture than surrounding normal renal parenchyma. C, Contrast medium-enhanced CT scan demonstrates a wedge-shaped area of low density (arrows) in the middle portion of the left kidney. The findings resolved after antimicrobial therapy.
Management: Hydration and IV antimicrobial agents for at least 7 days, followed by 7 days of oral antimicrobial therapy. Follow-up studies will show resolution of the wedge-shaped zones of diminished attenuation. Failure to respond to antimicrobial therapy : Rule out obstructive uropathy, Renal or perirenal abscess, Renal carcinoma Acute renal vein thrombosis.
Emphysematous Pyelonephritis An acute necrotizing parenchymal and perirenal infection caused by gas-forming uropathogens. Considered a complication of severe pyelonephritis rather than a distinct entity. Pathogenesis: Usually occurs in diabetic patients, High tissue glucose levels provide the substrate for microorganisms such as E. coli, which are able to produce carbon dioxide by the fermentation of sugar. Impaired host response caused by local factors, such as obstruction, or a systemic condition, such as diabetes, allows organisms producing carbon dioxide to use necrotic tissue to generate gas
Clinical Presentation: Severe, acute pyelonephritis A chronic infection precedes the acute attack. Some time Classic triad: Fever Vomiting Flank pain Pneumaturia is absent unless the infection involves the collecting system.
Radiologic Findings: The diagnosis is established radiographically. KUB: A crescentic collection of gas over the upper pole of the kidney Gas extends to the perinephric space and retroperitoneum. (progression) Emphysematous pyelitis Vs pyelonephritis Air is in the collecting system Secondary to a gas-forming bacterial UTI, Nondiabetic patients plain film. Extensive perinephric (long arrows) and intraparenchymal (short arrows) gas secondary to acute bacterial pyelonephritis. (From Schaeffer AJ: Urinary tract infections
Excretory urography Not recommended (abnormal renal function) Ultrasonography Focal echoes suggesting the presence of intraparenchymal gas CT scan: Define the extent of the emphysematous process and guiding management A nuclear renal scan Assess the degree of renal function impairment A, CT scan of the right kidney shows complete destruction with gas (arrowheads) extending beyond the renal fascia. B, CT scan with a modified lung window display shows the characteristic streaky gas in the completely destroyed kidney. The patient died on arrival in the emergency department.
Management : Emphysematous pyelonephritis is a surgical emergency. Most patients are septic Fluid resuscitation and broad-spectrum antimicrobial therapy Functioning kidney: Medical therapy can be considered. Nephrectomy if not improve after a few days of therapy Nonfunctioning kidney: Not obstructed nephrectomy. Obstructed catheter drainage If improved nephrectomy may be deferred
Renal Abscess A collection of purulent material confined to the renal parenchyma. Hematogenous gram-positive abscess (past) Gram-negative organisms (majority) Ascending infection associated with tubular obstruction from prior infections or calculi appears to be the primary pathway predisposing factors: Complicated UTIs associated with stasis, calculi, pregnancy, neurogenic bladder, and diabetes mellitus Clinical Presentation fever, chills, abdominal or flank pain, and occasionally weight loss and malaise.
Radiologic Findings : Ultrasonography : low-echodensity space-occupying lesion with increased transmission Acute renal abscess. Transverse ultrasonographic scan of the right kidney demonstrates a poorly marginated rounded focal hypoechoic mass (arrows) in the anterior portion of the kidney
CT contrast scan: Initially : - Renal enlargement and focal, rounded areas of decreased attenuation Later : - A thick fibrotic wall begins to form around the abscess. Acute renal abscess. Nonenhanced CT scan through the mid pole of the right kidney demonstrates right renal enlargement and an area of decreased attenuation (arrows). After antimicrobial therapy, a follow- up scan showed complete regression of these findings.
Chronic: - Obliteration of adjacent tissue planes - Thickening of Gerota's fascia - A round or oval parenchymal mass of low attenuation - The ring sign is caused by the increased vascularity of the abscess wall Chronic renal abscess. A, Enhanced CT scan shows an irregular septated low-density mass (M) extensively involving the left kidney. Note thickening of perinephric fascia (arrowheads) and extensive compression of the renal collecting system. Findings are typical of renal abscess. B, Ultrasound longitudinal scan demonstrates a septated hypoechoic mass (M) occupying much of the renal parenchymal volume
Management : The classic treatment for an abscess has been percutaneous or open incision and drainage (>5 cm) Evidence that the intravenous use of antimicrobial agents and careful observation of a small abscess less than 3 cm in diameter CT- guided needle aspiration may be necessary to differentiate an abscess from a hypervascular tumor. Empirical antimicrobial therapy
Hematogenous: penicillin, cephalosporin or vancomycin. Gram-negative Third-generation cephalosporins, antipseudomonal penicillins, or aminoglycosides 5 cm in immunocompromised hosts or those that do not respond to antimicrobial therapy should be drained percutaneously
Infected Hydronephrosis and Pyonephrosis Infected hydronephosis : Bacterial infection in a hydronephrotic kidney. pyonephrosis : Infected hydronephrosis associated with suppurative destruction of the parenchyma of the kidney with loss of renal function Clinical Presentation : Very ill ppatient, High fever, chills, flank pain, and tenderness. History of urinary tract calculi, infection, or surgery is common. Pyonephrosis-gross specimen. The kidney shows marked thinning of the renal cortex and medulla, suppurative destruction of the parenchyma (arrows), and distention of the pelvis and calyces. Previous incision released a large quantity of purulent material. The ureter showed obstruction distal to the point of section
Radiologic Findings U/S : Infected hydronephrosis: internal echoes within the dependent portion of a dilated pyelocalyceal system. pyonephrosis : Focal areas of decreased echogenicity are seen within the hydronephrotic parenchyma. Pyonephrosis. A, Longitudinal ultrasound scan of the right kidney demonstrates echogenic central collecting complex (C) with radiating echogenic septa (arrows) and thinned hypoechoic parenchyma. Multiple dilated calyces (o) with diffuse low-level echoes are seen.
Management : Antimicrobial drugs and drainage of the infected pelvis. A ureteral catheter to drain the kidney Percutaneous nephrostomy tube insertion.
Perinephric Abscess Route : Rupture of an acute cortical abscess into the perinephric space Hematogenous seeding from sites of infection. Bowel perforation, Crohn's disease Spread of osteomyelitis from the thoracolumbar spine E. coli, Proteus, and S. aureus account for most infections
paranephric abscess: A perinephric infection ruptures through Gerota's fascia into the pararenal space Left, Normal anatomic relationships of structures surrounding the kidney. Right, Anatomic differences seen in subcapsular (A) and perirenal (B) processes. In perirenal abscesses, the abscess fluid extends outside the renal capsule, thus causing the capsular artery and renal fascia to deviate away from the kidney. These findings may be seen in radiologic studies.
Clinical Presentation : Similar to that of pyelonephritis One third of patients may be afebrile. An abdominal or flank mass. Should be suspected in a patient with UTI and abdominal or flank mass or persistent fever after 4 days of antimicrobial therapy. Laboratory features : Leukocytosis, creatinine,. Urine cultures Blood culture
Radiologic Findings : Nonenhanced CT scan through the lower pole of the right kidney (previous left nephrectomy) shows extensive perinephric abscess. Extensive abscess (A) distorts and enlarges the renal contour, infiltrates perinephric fat (straight arrows), and also extends into the psoas muscle (asterisk) and the soft tissues of the flank (curved arrow). Also note that normal renal collecting system fat has been obliterated by the process. Perinephric abscess involving the right adrenal gland. CT scan shows large right pararenal mass (arrows) with multiple low-density areas within. At surgery, a large pararenal abscess with extensive involvement of the right adrenal was found.
Management : The primary treatment for perinephric abscess is drainage Vs nephrectomy Percutaneous drainage contraindicated in large abscess cavities filled with thick, purulent fluid. Antimicrobial therapy. An aminoglycoside together with an antistaphylococcal agent
Chronic Pyelonephritis Clinical Presentation : No symptoms until renal insufficiency, Symptoms of chronic renal failure. History of recurrent of acute pyelonephritis, Intermittent symptoms of fever, flank pain, and dysuria may be elicited.
Radiologic Findings : pyelographic findings Asymmetry and irregularity of the kidney outlines, Blunting and dilation of calyces Cortical scars In advanced pyelonephritis, Calyceal distortion and irregularity together with cortical scars complete the picture. Chronic pyelonephritis. Ten-minute excretory urogram demonstrates irregular renal outline with upper pole parenchymal atrophy. Note significant loss of renal cortical thickness over blunted and dilated calyces. Lower pole mass (M) is a simple cyst. (From Schaeffer AJ: Urinary tract infections.
Pathology : Gross: kidney is often diffusely contracted, Y-shaped scar, and pitted. The parenchyma is thin, and the corticomedullary demarcation is lost. Histology: An interstitial infiltrate of lymphocytes, plasma cells, and occasional polymorphonuclear cells. Portions of the parenchyma replaced by fibrosis, Periglomerular fibrosis Atrophied tubules with Leukocyte and hyaline casts
Management : Treating infection, if present; ( prolonged AB) Preventing future infections; and Monitoring and preserving renal function. Antimicrobial prolonged Underlying renal Nephrologic and urologic evaluation
Xanthogranulomatous Pyelonephritis A rare, severe, chronic renal infection typically resulting in diffuse renal destruction. Unilateral nonfunctioning, enlarged kidney associated with obstructive uropathy secondary to nephrolithiasis. Characterized by accumulation of lipid-laden foamy macrophages It begins within the pelvis and calyces and subsequently extends into and destroys renal parenchymal and adjacent tissues. It has been known to imitate virtually every other inflammatory disease of the kidney, as well as renal cell carcinoma, on radiographic examination
Pathogenesis : Nephrolithiasis(1ry factor) obstruction + infection tissue destruction and collections of lipid material by macrophages. These macrophages (xanthoma cells) are distributed in sheets around parenchymal abscesses and calyces and are intermixed with lymphocytes, giant cells, and plasma cells. Other possible interrelated factors include: Venous occlusion and hemorrhage, Abnormal lipid metabolism, Lymphatic blockage, Failure of antimicrobial therapy in UTI, Altered immunologic competence, Renal ischemia
Histology : The parenchyma contains dark sheets of lipid-laden macrophages (foamy histiocytes with small, dark nuclei and clear cytoplasm) intermixed with lymphocytes, giant cells, and plasma cells Xanthogranulomatous pyelonephritis. A, Gross specimen. Kidney is massively enlarged, measuring 23 × 12 cm; the normal architecture is replaced by a shaggy yellow upper pole mass corresponding to xanthogranulomatous inflammation and numerous distorted and dilated calyces. B, Microscopically, the shaggy yellow tissue is composed primarily of lipid-laden histiocytes mixed with other inflammatory cells. (From Schaeffer AJ: Urinary tract infections.
Clinical Presentation : Flank pain (69%), Fever and chills (69%), Persistent bacteriuria (46%) Flank mass (62%) Classic triad : Unilateral renal enlargement Poor function A large calculus in the renal pelvis Bacteriology and Laboratory Diagnosis Proteus is the most common organism Azotemia or frank renal failure is uncommon
Radiologic Findings : CT scan: (most useful) A large, reniform mass with the renal pelvis tightly surrounding a central calcification but without pelvic dilatation 99m Tc-DMSA : confirm and quantify the differential lack of function in the involved kidney Xanthogranulomatous pyelonephritis. Enhanced CT scan shows collecting system and parenchymal calculi (straight arrows) with lower pole pyonephrosis (curved arrow) and an irregular, predominantly low- density perinephric abscess (A) extending into the soft tissues of the flank
Management : Primary obstacle to treatment of XGP is incorrect diagnosis XGP + hydronephrosis looks just like pyonephrosis Usually post-operative diagnosis RCC is usual pre-op diagnosis, so nephrectomy performed - If localized, may be amenable to partial nephrectomy. Xanthoma cells resemble clear cell adenocarcinoma difficult to distinguish on frozen section Do nephrectomy if can't exclude malignancy
Antibiotics may be necessary to stabilize the patient preop If diffuse and extensive disease goes to retroperitoneum, must remove of the kidney and perinephric fat - Dissection of granulomatous tissue from the diaphragm, great vessels, and bowel - Remove entire mass, as tissue infected in ¾ of pts if I&D alone, illness may persist, or develop reno-cutaneous fistula
BACTEREMIA, SEPSIS AND SEPTIC SHOCK
Bacteremia: The presence of viable bacteria in the blood. Systemic inflammatory response syndrome (SIRS): Extremes of body temperature, heart rate, ventilation, and immune response. SIRS can occur in response to multiple insults including systemic infection, trauma, thermal injury or a sterile inflammation.
Sepsis: A clinical syndrome characterized by extremes of body temperature, heart rate, respiratory rate, and WBC count that occurs in response to an infection. Sepsis occurs when a local infectious process becomes an uncontrolled systemic bloodborne inflammatory response resulting in damage to tissues or organs remote from the initial site of infection or injury Septic shock: An extreme form of sepsis complicated by organ dysfunction and persistent circulatory failure despite fluid and pharmacologic resuscitation.
Pathophysiology: Bacterial Cell Wall Components in Septic Shock The exotoxins (P. aeruginosa) Bacterial cell wall components innate immunologic pathways (macrophages, neutrophils, and dendritic cells and the complement system). The endotoxin (G – tive) : An LPS component the coagulation, complement, and fibrinolytic systems release of small molecules that cause vasodilation and endothelial permeability
Cytokine Network : Monocytic cells have a role in mediation of the biologic effects of SIRS and septic shock. Monocytes can remove and detoxify LPS However, LPS-stimulated monocytes produce cytokines such as tumor necrosis factor (TNF) and interleukin (IL)-1. The intravascular activation of inflammatory systems involved in septic shock is mainly the consequence of an overproduction of these and other cytokines.
Clinical Presentation and Diagnosis: Early signs of the sirs include: - Temperature extremes (>38° C [100.4° F] or <36° C [96.8 ° F]), - Tachycardia (heart rate > 90 beats per minute), - Tachypnea - Altered mental status.
Characteristics of Sepsis Fever (core temperature >38.3° C) Hypothermia ( core temperature <36) Heart rate > 90, 1or 2 SD above the normal value for age. Tachypnea Altered mental state Significant edema or positive fluid balance (20mg\kg over 24h) Hyperglycemia plasma sugar >120mg\dl or 7.7 mol\l in absence of diabetes General Leukocytosis (WBC count >12,000/μL) Leukopenia ( WBC count < 4000/µL) Normal WBC count with >10% immature forms inflammatory Arterial hypoxemia (PaO2/FIO2 >300) Acute oligouria (urine output 0.5 Ml\kg in 1hr for at least 2 hrs) Creatinine increase 0.5mg\dl Coagulation abnormalities ( INR 1.5 or aptt >60 sec) Illus absent bowel sound Thrombocytopenia ( platelets <100,000µL) Hyperbilirubinemia ( plasma bilirubin >4mgdl or 70 mmol/L) Organ dysfunction Hyperlactatemia (>1 mmol/L) Decreased capillary refill or mottling Tissue perfusion
The classic findings of septic shock : - Peripheral vasodilation, and SVR - A warm patient, - Brisk capillary refill - A bounding pulse - Hypotension, oliguria, or ileus - WBC, hyperbilirubinemia, hyperlactatemia, hyperglycemia, coagulation abnormalities, and elevated C reactive protein and respiratory alkalosis due to hyperventilation. Bacteriology : Gram-negative 30% to 80% of cases mainly E.coli Gram-positive 5% to 24% of cases
Management : Resuscitation, vasoactive(phenylephrine) Supportive care, monitoring, Administration of broad-spectrum antimicrobial agents (aminoglycoside+/-) Antimicrobial treatment should be continued until the patient has been afebrile for 3 to 4 days and is clinically stable. Human activated protein C (Drotrecogin alfa) It reduces mortality in sepsis An inhibitor of multiple inflammatory and coagulation pathway components: The inhibition of the coagulation factors Va and VIIIa, Inhibition of macrophage production of TNF, limitation of thrombin-induced inflammation inhibition of plasminogen activator inhibitor
The most common hospital-acquired infection Accounting for up to 40% and 1 million per year The incidence of bacteriuria : 10% per day of indwelling catheterization. 1% in healthy individuals and 15% in elderly hospitalized patients for Intermittent catheterization
risk factors : Duration of catheterization, Female gender, Absence of systemic antimicrobial agents, Catheter-care violations
Clinical Presentation : A symptomatic. Symptomatic. Suprapubic discomfort,fever, chills, or flank pain Laboratory Diagnosis Significant bacteriuria if >100 cfu/mL
Management : Careful aseptic insertion of the catheter and maintenance of a closed dependent drainage system are essential to minimize development of bacteriuria. The catheter-meatal junction should be cleaned daily with water Incorporation of silver oxide or silver alloy into the catheter and hydrogen peroxide into the drainage bag has been reported to decrease the incidence of bacteriuria in some studies but not in other populations.
Patients with indwelling catheters should only be treated if they become symptomatic (e.g., febrile). Urine cultures should be performed before initiating antimicrobial therapy. Empirical antimicrobial therapy such as TMP-SMX or a fluoroquinolone before de-catheterization for 2 days. A post-therapy Culture should be obtained 7 to 10 days later to confirm the eradication of the bacteriuria.
MANAGEMENT OF UTI IN PATIENTS WITH SPINAL CORD INJURY
Epidemiology : UTIs are among the most common urologic complications of spinal cord injury. 33% of spinal cord-injured patients have bacteriuria at any time. patients on CIC or condom catheterization: 18 episodes of bacteriuria per person per year 1.8 per person per year of febrile UTIs
risk factors impaired voiding, overdistention of the bladder, elevated intravesical pressure, increased risk of urinary obstruction, vesicoureteral reflux, instrumentation increased incidence of stones. decreased fluid intake poor hygiene, perineal colonization, local tissue trauma reduced host defense associated with chronic illness
Clinical Presentation : The majority of patients are asymptomatic UTI is the most common cause of fever in spinal cord-injured Flank, back, or abdominal discomfort, leakage between catheterizations, increased spasticity, malaise, lethargy, and/or cloudy, malodorous urine. Bacteriology and Laboratory Diagnosis Urinalysis : bacteriuria and pyuria. E. coli is isolated in approximately 20% of patients. Enterococci, P. mirabilis, and Pseudomonas are more common among spinal cord-injured patients than patients with intact spinal cords. Other common organisms are Klebsiella species, Serratia species, Staphylococcus, and Candida species.
Management : urine culture must be obtained before initiating empirical therapy. (diverse flora + resistance)
UTI in Pt with spinal cor injury Febrile UTI admitted and treated with a parenteral aminoglycoside and a penicillin or a third- generation cephalosporin for24-48 h No clinical improvement - reculture and adjustment of antimicrobial therapy - imaging - urodynamic clinical improvementAfebrile UTI - oral fluoroquinolone - β-Lactams, TMP-SMX, and nitrofurantoin are not recommended because of bacterial resistance An indwelling catheter should be change
The virulence factor that is most important for adherence is : A- hemolysin B- K antigin C- pilli D- colicin production E- O serogroupe
The most accurate test for evaluation of infection in the kidney is : A- the fairly bladder washout test B- ureteral catheterization C- gallium scanning D- CT E- the Antibody-coated bacteria test
The most common bacterial cause of xanthogranulomaous pyelonephritis is : A- Echerichia coli. B- Pseudomonas. C- Klebsiella. D- Proteus mirabillis. E- Staphylococcus.
Antimicrobial prophylaxis for transurethral resection of prostate is not indicated in patients with : A- valvular heart disease. B- prosthetic valves. C- unknown urine culture. D- sterile urine. E- indwelling catheter.
The optimal duration of antimicrobial therapy for symptomatic acute uncomplicated cystitis in women is : A- 1 day. B- 3 days. C- 7 days. D- 14 days. E- 21 days.
The drug thought to be safe in any phase of pregnancy is : A- a fluoroquinolone. B- nitrofurantoin. C- a sulfonamide. D- penicillin. E- tetracycline.