● Bacterial virulence: pili/fimbriae help adhesion.
UTI
● Vesicoureteral reflux: reflux of urine → kidney.
● Genetic factors: urothelial receptors aiding bacterial adhesion.
Urinary Tract Infection (UTI) – Exam Notes
Definition Etiology
● UTI = microbial invasion of urinary tract, extending from renal cortex → urethral meatus. ● E. coli (uropathogenic strain) → most common (≈70% all cases).
● 2nd most common community infection (after RTI). ● Other Enterobacteriaceae: Klebsiella, Proteus, Enterococci.
● Most common hospital-acquired infection (≈35% of HAIs). ● Hospital-acquired: often multidrug-resistant → Staphylococci, Pseudomonas,
Acinetobacter.
Classification ● Rare: Viruses, fungi, parasites.
1. By anatomical site
○ Lower UTI: Urethritis, Cystitis, Prostatitis Pathogenesis
○ Upper UTI: Pyelonephritis, Perinephric abscess Two routes:
2. By source 1. Ascending route (most common)
○ Community-acquired ○ Endogenous enteric bacteria enter via urethra.
○ Healthcare-associated → especially Catheter-associated UTI (CAUTI) ○ Steps:
1. Colonization → adhesion to urethral epithelium (pili, fimbriae in E. coli).
Catheter-associated UTI (CAUTI) 2. Ascension → to bladder → cystitis.
● Most common HAI. 3. Further ascension → via ureters (esp. if reflux present) → pyelonephritis.
● Indwelling catheter = single most important risk factor. 4. Complication: Acute tubular injury → interstitial nephritis.
● Accounts for ~50% nosocomial UTIs. 2. Descending route (hematogenous spread)
○ From bacteremia → renal parenchyma. (~5% cases).
Normal Commensals ○ Organisms: S. aureus, Salmonella, M. tuberculosis, Leptospira.
● Healthy urinary tract = sterile, except distal urethra.
● Flora: Lactobacilli, diphtheroids, coagulase-negative staphylococci, anaerobes. Host Defense Mechanisms
● Potential pathogens present: Enterobacteriaceae, Candida spp. 1. Urine-related factors
○ High osmolality, low pH, urea concentration → inhibit bacteria.
Predisposing Factors ○ Unidirectional flow of urine prevents colonization.
● 2. Mucosal immunity
Prevalence: ~10% of people get UTI sometime in life.
○ TLRs & cytokine activation by uropathogens.
● Gender: Females > males (short urethra + proximity to anus).
○ Local immune response (neutrophils, IgA).
● Age:
○ Females: incidence ↑ with age (10–20% adults).
○ Males: ↑ risk in infancy & old age (prostate enlargement).
● Pregnancy: Anatomical + hormonal changes → asymptomatic bacteriuria common.
● Obstruction: Clinical Manifestations of UTI
○ Structural → stones, prostate enlargement. Types of Presentation
○ Functional → neurogenic bladder.
● Lower UTI:
● Catheterization: most important hospital risk factor.
○ Asymptomatic bacteriuria
○ Cystitis 3. Acute Urethral Syndrome
○ Urethritis ● Seen in young sexually active females.
○ Acute urethral syndrome ● Features:
● Upper UTI: ○ Classical cystitis symptoms (dysuria, frequency, urgency).
○ Pyelonephritis ○ Low bacterial count (10²–10⁵ CFU/mL).
○ Ureteritis ○ Pyuria present.
○ Perinephric abscess ● Causative agents:
○ Renal abscess ○ Usual UTI organisms (E. coli, Enterococci, etc.)
○ Renal tuberculosis ○ Sometimes Neisseria gonorrhoeae, Chlamydia trachomatis, HSV.
● Immunological sequelae: Post-streptococcal glomerulonephritis (PSGN)
Upper UTI
Lower UTI Pyelonephritis
1. Asymptomatic Bacteriuria ● Inflammation of renal parenchyma, calyces, pelvis.
● Definition: Isolation of significant bacteria from properly collected urine sample without ● Systemic features:
any UTI symptoms. ○ Fever
● Epidemiology: ○ Flank pain
○ More common in females. ○ Vomiting
○ Incidence ↑ with age (1% school girls → >20% elderly). ● Associated lower tract symptoms:
● Clinical significance: ○ Dysuria, frequency, urgency.
○ Important & needs treatment in: ● May progress to abscess or chronic renal damage if untreated.
◆ Pregnant women (risk to mother + fetus).
◆ Patients undergoing prostatic/urologic surgery (risk of complications/
bleeding).
Laboratory Diagnosis of UTI
○ Not significant → no need of screening/treatment in:
1. Specimen Collection
◆ Non-pregnant, premenopausal women.
● Wide-mouth, sterile container.
◆ Elderly.
● Methods:
◆ Catheterized patients.
○ Clean voided midstream urine → most common.
◆ Spinal injury patients.
○ Suprapubic aspiration → most ideal (infants, unconscious patients).
○ Catheterized patients → collect from catheter tube (after clamping & disinfecting),
2. Cystitis (Bladder infection)
not from urobag.
● Symptoms:
○ Dysuria (painful micturition)
2. Transport
○ Frequency & urgency
● Process urine immediately.
○ Suprapubic pain/tenderness
● If delay >1–2 hrs → refrigerate or add boric acid (preserves up to 24 hrs).
● Urine changes:
○ Cloudy urine, bad odor
○ 3. Direct Examination
May be gross hematuria
● ● Wet mount → >8 pus cells/mm³ = significant pyuria.
Systemic features absent (distinguishes from pyelonephritis).
● Leukocyte esterase test → detects enzymes of pus cells (cheap, rapid).
● Leukocyte esterase test → detects enzymes of pus cells (cheap, rapid).
● Nitrate reduction test (Griess test) → nitrate-reducing bacteria (e.g. E. coli) give positive ● Purpose: Differentiate upper vs lower UTI.
result. ● Upper UTI: bacteria coated with specific antibody (hematogenous spread) → detected by
● Gram stain: immunofluorescence.
○ Not reliable (low bacterial count, pus cells deteriorate). ● Lower UTI: bacteria never antibody-coated.
○ Used mainly in pyelonephritis/invasive UTI.
○ ≥1 bacteria/oil immersion field = significant. Treatment of UTI
General principle: Always base treatment on AST report.
4. Culture
● First-line drugs (community-acquired, uncomplicated UTI):
● Media: ○ Quinolones (e.g. Norfloxacin)
○ CLED agar (preferred for heavy load labs). ○ Nitrofurantoin
○ Or MacConkey agar + Blood agar. ○ Cephalosporins
● Kass concept of Significant Bacteriuria: ○ Aminoglycosides
○ ≥10⁵ CFU/mL = significant (infection). ● For multidrug-resistant, hospital-acquired UTI:
○ 10⁴–10⁵ CFU/mL = doubtful → correlate clinically. ○ Carbapenems (Meropenem)
○ <10⁴ CFU/mL = contamination (commensals). ○ β-lactam/β-lactamase inhibitor combinations (Piperacillin–tazobactam)
● Exceptions: Low count may still be significant in: ○ Fosfomycin
○ Patients on antibiotics/diuretics.
○ Gram-positive infections (S. aureus).
Etiological Agents of UTI
○ Pyelonephritis / acute urethral syndrome.
○ Suprapubic aspiration samples. 1. Enterobacteriaceae
○ Catheterized patients (≥10³ CFU/mL if symptomatic). (a) Escherichia coli (UPEC)
Quantitative Culture Methods:
● Most common: 70–75% of UTIs.
● Semi-quantitative: Standardized loop technique. ● Serotypes: O1, O2, O4, O6, O7, O75.
● Quantitative: Pour plate method. ● Virulence factors:
Colony appearance: ○ Cytotoxins → CNF1, SAT
● Lactose fermenters (E. coli, Klebsiella) → pink (MacConkey), yellow (CLED). ○ Hemolysins
● Non-lactose fermenters (Proteus, Pseudomonas, Acinetobacter) → pale colonies. ○ Fimbriae (P fimbriae) → lower UTI
Identification: ○ Capsular K antigen → upper UTI
● Automated → MALDI-TOF, VITEK. ● Other diseases: diarrhea, meningitis, pyogenic infections.
● Conventional → biochemical tests. (b) Klebsiella pneumoniae
● Commensal in intestine.
5. Antimicrobial Susceptibility Testing (AST) ● Causes: UTI, neonatal meningitis, septicemia, abscesses, wound infections.
● Essential to guide therapy.
(c) Enterobacter spp.
● Methods:
● Opportunistic & nosocomial.
○ Disk diffusion test (Mueller-Hinton agar).
● Infections: wound, UTI, pneumonia.
○ Automated MIC-based (e.g. VITEK).
(d) Citrobacter (C. freundii, C. koseri)
6. Antibody-Coated Bacteria Test ● Environmental contaminants.
● Cause: UTI, gallbladder infection, otitis media, neonatal meningitis.
● Purpose: Differentiate upper vs lower UTI.
● Most isolates MDR → treated like E. coli. ○ Surgical site & neonatal infections.
Laboratory diagnosis
2. Tribe Proteeae (Proteus, Morganella, Providencia) ● Gram+ cocci in pairs (“spectacle shape”).
● Culture:
(a) Proteus (P. mirabilis, P. vulgaris)
○ Blood agar → non-hemolytic.
● Features: ○ MacConkey → tiny pink colonies.
○ Pleomorphic, swarming colonies on agar. ● Bile esculin +; grow in 6.5% NaCl, bile, extreme pH/temp.
○ Strong odor (“fishy”). ● Differentiation: Arabinose fermentation (faecalis vs faecium).
● Pathogenesis: ● Automated: VITEK, MALDI-TOF.
○ Urease → ↑ pH → struvite stones in bladder.
Treatment
○ Opportunistic → UTI, wound, septicemia.
● UTI: ampicillin, nitrofurantoin, fosfomycin.
● Weil–Felix reaction: Proteus OX strains cross-react with Rickettsia.
● Severe infections: penicillin/ampicillin + gentamicin (synergy).
● Biochemical ID: Indole (P. vulgaris +), urease +, H₂S +, catalase +, oxidase –.
● Alternatives: vancomycin, linezolid, daptomycin.
● Treatment: often MDR; resistant to many β-lactams & nitrofurantoin.
VRE (Vancomycin-Resistant Enterococci)
○ Drugs: aminoglycosides, cefepime, carbapenems.
● Mechanism: van genes (A/B) → D-Ala-D-Lac substitution → ↓ binding.
(b) Morganella morganii
● Prevalence:
● Found in feces. ○ US: 35%
● Causes rare UTI, pneumonia, wound infections (mostly nosocomial). ○ Europe: 4%
(c) Providencia spp. (P. stuartii, P. rettgeri, etc.) ○ Asia: 10–15%
● Nosocomial UTI, wound & burn infections. ○ India: ~9.7% (higher in E. faecium).
● Management: infection control, not decolonization.
● Drugs: linezolid, daptomycin, streptogramins (for E. faecium).
3. Non-Fermenters
● Pseudomonas, Acinetobacter
● Important causes of healthcare-associated UTIs, pneumonia, wound infections.
Other Causes of Urinary Tract Infections
Although Escherichia coli remains the most frequent cause of UTIs, several Gram-positive
4. Enterococci (Gram-positive cocci) cocci, Mycobacteria, viruses, parasites, and fungi may also infect the urinary tract. Each has
● its own epidemiological importance, clinical spectrum, and diagnostic considerations.
Most common Gram+ cocci causing UTI.
● Normal flora → intestine, biliary tract, vagina, urethra.
● Virulence factors: 1. Gram-Positive Cocci
○ Aggregation substance (plasmid exchange).
Staphylococcus aureus
○ ESP (adhesion to bladder mucosa).
● While S. aureus is best known for causing skin and soft tissue infections, it can also
○ Group D antigen (induces TNF-α).
cause urinary tract infections.
● Species:
● In most cases, S. aureus bacteriuria suggests either:
○ E. faecalis → common, less resistant.
○ Hematogenous spread (e.g., from bacteremia or endocarditis)
○ E. faecium → less common, more resistant.
○ Secondary colonization in catheterized patients
● Clinical manifestations:
○ Catheter-associated UTI (cystitis).
Staphylococcus saprophyticus
○ Pyelonephritis, prostatitis, bacteremia, endocarditis. ● A well-recognized cause of UTI in sexually active young women.
● Pathogenicity is due to expression of a 160 kDa hemagglutinin/adhesin protein, which Diagnosis:
facilitates strong adherence to urothelial cells. ● Elevated anti-DNase B (70%), anti-hyaluronidase (40%), and sometimes ASO (30%)
● Differentiation from other Staphylococcus species: ● Anti-DNase B > 300–350 units/mL is highly suggestive
○ It is resistant to novobiocin (5 µg disk test), unlike S. epidermidis.
Streptococcus agalactiae (Group B Streptococcus, GBS) 4. Perinephric and Renal Abscesses
● Can cause cystitis and asymptomatic bacteriuria, particularly in pregnant women. ● Usually occur as a complication of UTI → cystitis → pyelonephritis → renal parenchymal
● Frequently colonizes the female genital tract, hence peripartum transmission is common. abscess → perinephric spread.
● Also associated with postpartum infections, neonatal sepsis, and soft tissue infections. ● Risk factor: renal stones causing obstruction.
● Pathogens: E. coli, Proteus, Klebsiella.
2. Other Bacterial Infections ● Treatment: Drainage of pus + antibiotics targeted to recovered organisms.
Renal Tuberculosis (Genitourinary TB)
● Accounts for 10–15% of all extrapulmonary TB.
5. Viral Infections of Urinary System
● May involve any part of the genitourinary tract. Although rare, a few viruses can infect the urinary tract.
● In up to 75% of cases, chest X-ray shows signs of past or active pulmonary TB. BK Virus
Clinical Features: ● A polyomavirus with dsDNA, named after the initials of the first patient described.
● Urinary frequency, dysuria, nocturia, hematuria, flank or abdominal pain ● Mainly causes problems in immunocompromised patients:
● Sterile pyuria (pus cells in urine but negative standard bacterial culture) is a classic clue ○ Nephropathy in kidney transplant recipients
Diagnosis: ○ Hemorrhagic cystitis in stem cell transplant recipients
● Urine culture for TB: Three consecutive early morning specimens; culture in MGIT or LJ ● Usually asymptomatic in immunocompetent hosts.
medium (90% sensitivity). Diagnosis:
● Imaging (CT/MRI): Detects strictures, calcification, hydronephrosis, and renal damage. ● Renal biopsy (histopathology + immunohistochemistry)
Treatment: Responds well to standard antitubercular therapy (ATT). ● PCR for BK viremia
● BK viruria is less specific
3. Immunological Sequelae of Bacterial Infections Treatment: No specific drug; Cidofovir may be used in refractory cases.
Post-streptococcal Glomerulonephritis (PSGN) Adenovirus Cystitis
● A non-suppurative sequela of Group A Streptococcus infection. ● Serotypes 11 and 21 can cause acute hemorrhagic cystitis in children, especially boys.
● Occurs due to immune complex deposition on the glomerular basement membrane → Others
complement activation → inflammation. ● CMV and HSV can be detected in urine but usually do not cause UTIs.
● The nephritogenic antigen is often streptococcal pyogenic exotoxin-B (SPE-B). ● HSV may cause urinary retention due to autonomic dysfunction.
Epidemiology:
● Follows streptococcal skin infection (pyoderma) (M serotypes 47, 49, 55, 57, 60) → 2–6 6. Parasitic Infections of Urinary System
weeks later.
Urinary Schistosomiasis (Schistosoma haematobium)
● Or after streptococcal pharyngitis (M serotypes 1–4, 12, 25) → 1–3 weeks later.
● Common in children (2–14 years), generally good prognosis. ● Endemic in Africa, Middle East, Indian Ocean islands.
Clinical Manifestations: ● Rare in India, except a small endemic focus in Maharashtra.
● Life cycle involves freshwater snails as intermediate hosts; humans get infected by skin
● Edema, hypertension, hematuria, oliguria, proteinuria
● penetration of cercariae.
May cause acute renal insufficiency
Clinical Manifestations: ● Resistant strains → Flucytosine ± Amphotericin B.
● Acute phase: Cercarial dermatitis
● Chronic phase: Egg deposition → granulomas →
○ Dysuria, hematuria
○ Obstructive uropathy (hydroureter, hydronephrosis)
○ Bladder squamous cell carcinoma
Diagnosis:
● Microscopy: Urine examination for eggs (oval, elongated, terminal spine)
● Antigen detection (CCA/CAA assays) for recent infection
● Antibody detection (HAMA-ELISA/EITB) for epidemiology, not acute diagnosis
Treatment:
● Praziquantel (20 mg/kg × 2 doses in one day) – drug of choice
● Metrifonate (alternative, less preferred due to multiple doses)
● Prevention: sanitation, snail control, treatment of cases
Dioctophyme renale (Giant Kidney Worm)
● Rare zoonotic nematode infection in humans (23 reported cases).
● Acquired by eating undercooked fish containing larvae.
● Worms invade kidneys (commonly right kidney).
Clinical features: Hematuria, renal colic, progressive renal parenchymal destruction.
Diagnosis: Detection of large eggs with thick, sculptured shell in urine.
Treatment: No standard therapy; prevention by properly cooking fish.
Trichomonas vaginalis
● Primarily a cause of sexually transmitted urethritis.
● May be detected in urine sediment as motile trophozoites.
7. Fungal Infections of Urinary System
Candiduria (Candida species)
● Very common finding; may represent contamination, colonization, or true infection.
● Risk groups: catheterized patients, immunosuppressed, neonates, critically ill.
When to treat?
● Asymptomatic → usually no treatment (except in high-risk cases: immunosuppressed,
neonates, pre-urologic surgery).
● Symptomatic cystitis/pyelonephritis → treat.
Treatment:
● Fluconazole (14 days) → first choice (excellent urine penetration).
