GC210 Urinary Tract Infection
A urinary tract infection is an infection of any part of the urinary system—including the urethra, bladder, ureters, or kidneys—most commonly caused by gram-negative bacteria such as *Escherichia coli*, presenting with dysuria, frequency, urgency, and sometimes systemic signs.
Urinary Tract Infection (UTI)
This lecture (GC 210) is one of the most high-yield surgical urology lectures for the Fourth Summative. It covers the entire spectrum of UTI: from definitions and host-pathogen interactions, through diagnosis (urinalysis, dipstick, culture), to management of uncomplicated/complicated UTI, asymptomatic bacteriuria, recurrent UTI, catheter-related UTI, emphysematous pyelonephritis (EPN), emphysematous cystitis (EC), xanthogranulomatous pyelonephritis (XGP), biofilm, and genitourinary tuberculosis (GUTB). It also covers UTI in special populations (pregnancy, children, males, renal impairment, diabetes). The lecture deliberately includes several embedded exam-style questions (Q21, Q68) that have been tested in past papers.
Learning Objectives [1]:
- Diagnose and treat UTI
- Microbiological basis of UTI diagnosis and treatment
- How to manage asymptomatic bacteriuria
- How to manage recurrent UTI
- Basic understanding of urinary tuberculosis
UTI is the inflammatory response of the urothelium to invasion by bacteria or other pathogens, usually associated with bacteriuria and pyuria. [1]
This definition is critical because it separates genuine UTI from mere bacteriuria or pyuria, which are not synonymous with infection.
| Term | Definition | Key Points |
|---|---|---|
| Bacteriuria | Presence of bacteria in urine | Does NOT equate infection. DDx: colonisation, contamination |
| Pyuria | Presence of WBCs in urine (≥10 WBC/mm³) | Does NOT equate infection. DDx: urolithiasis, malignancy, TB, interstitial cystitis, ketamine cystitis |
| Sterile pyuria | Pyuria WITHOUT bacteriuria | DDx: TB, Chlamydia, bladder CIS (carcinoma-in-situ), stones, schistosomiasis, foreign body in bladder, partially treated/residual UTI, interstitial cystitis, ketamine cystitis, leukoplakia [1] |
Why does this matter?
Examiners love asking "Does bacteriuria = UTI?" The answer is no. You must have the combination of symptoms + pyuria + significant bacteriuria to diagnose UTI. This distinction is especially important in catheterised patients and asymptomatic bacteriuria.
UTI is one of the commonest bacterial infections. One-third of women have one UTI by age 24; more than half will have at least one UTI in their lifetime. [1]
- A large number of urology SOPD referrals are for "recurrent UTI" / "persistent dysuria" [1]
- Overlap in symptomatology with CPPS (chronic pelvic pain syndrome), OAB, interstitial cystitis, BPH/LUTS [1] — this is a common exam trap: not all "dysuria" is UTI.
- Demographics: F >>> M (except neonates where M > F, and elderly men with BPH) [2]
3. Pathogenesis: Host vs Pathogen
UTI is the result of the interaction between the host and the uropathogens. [1]
Understanding these defences explains why UTI occurs when they fail:
| Defence Layer | Mechanism | Why It Works |
|---|---|---|
| 1. Normal flora | Lactobacilli convert glycogen → lactic acid → low vaginal pH; cervical IgA | Acidic environment suppresses Enterobacteriaceae colonisation. Altered by: hypo-oestrogen states, spermicides, antibiotics |
| 2. Urine properties | Antegrade flow, normal pH (5.5–6.5), high osmolality, Tamm-Horsfall protein | THP saturates mannose-binding sites on Type 1 pili, preventing E. coli adhesion. THP is produced by tubular cells of the ascending limb of the Loop of Henle. [1] Flow physically washes bacteria out. Altered by: obstruction |
| 3. Bladder | Normal emptying, exfoliation of urothelial cells, LPS receptors → innate immunity (PMN, macrophages) | Regular voiding prevents bacterial multiplication. Urothelial shedding removes adherent bacteria. Altered by: BOO, neurogenic bladder, catheter, VUR, bladder diverticulum |
| 4. GAG layer | Glycosaminoglycan coating of bladder mucosa | Physical barrier against bacterial adhesion |
Bacterial virulence = degree of pathogenicity = ability to colonise and invade the urinary tract. [1]
| Factor | Details |
|---|---|
| Fimbrial adhesins (pili) | Type 1 (mannose-sensitive): FimH, FimA → binds bladder urothelium → majority of acute cystitis isolates. Type P (mannose-resistant): PapG → binds upper tract urothelium → found in 80% of acute pyelonephritis isolates. Type P fimbriae are more virulent and more adhesive than Type 1. Type S: both bladder and kidney |
| Afimbrial adhesins | Dr adhesins family |
| Toxins | Haemolysin HlyA → pore formation in host cell membranes, RBC lysis |
| Urease | Breaks urea → ammonia → raises pH → facilitates struvite stone formation |
| Others | IgA inactivating protein; phasic variation (switch fimbriae on/off to evade phagocytosis); antimicrobial resistance |
Vaginal cells' susceptibility to bacterial adherence is genetically determined and directly affects rates of recurrent UTI. [1]
- Lewis blood group determines ability of cellular fucosylation → affects bacterial adherence:
- Le(a−b−) and Le(a+b−) → higher incidence of recurrent UTI
- Non-secretor status (Le b−) → associated with premenopausal acute pyelonephritis [1]
- HLA-A3 phenotype → associated with increased susceptibility [1]
- P blood group secretor / ABO non-secretor status [1]
| Setting | Predominant Organism | Other Organisms |
|---|---|---|
| Community-acquired | E. coli (85%) | Proteus, Klebsiella, Enterococcus, S. saprophyticus (10% of acute cystitis in young sexually active females) |
| Nosocomial | E. coli (50%); can be polymicrobial | Pseudomonas, Citrobacter, Providencia, Serratia, Enterobacter, coagulase-negative Staph |
| Anaerobes | Suppurative infections | ~80% of scrotal, prostatic and perinephric abscesses |
The ascending route is the commonest. [1]
| Route | Mechanism | Examples |
|---|---|---|
| Ascending | Rectum → urethra → bladder (± kidney) | Facilitated by catheter, VUR, ureteral obstruction |
| Haematogenous | Extrarenal bacteraemia → kidney (uncommon in normal individuals) | Renal abscess from septic emboli (S. aureus), genitourinary TB |
| Direct extension | From neighbouring suppurative infection | Unusual |
Pathogenesis steps: 1. Bacterial adherence → 2. Colonisation / ascension → 3. Invasion and clinical UTI [1]
6. Classification of UTI
| Feature | Uncomplicated UTI | Complicated UTI |
|---|---|---|
| Definition | Anatomically/physiologically normal tract, normal host defence | Neuropathic bladder, obstruction, stones, diverticulum, catheter |
| Organisms | "Usual" (E. coli 70–95%) | Broader spectrum, often resistant |
| Treatment duration | Shorter | Longer |
| Setting | Outpatient | May need admission |
| Cure | Complete cure very likely | True cure not possible unless complicating features eradicated |
Special groups: pregnancy and children are considered complicated. [1]
| Category | Description | Clinical features | Lab (slide thresholds) |
|---|---|---|---|
| 1 | Acute uncomplicated UTI / cystitis in women | Dysuria, urgency, frequency, suprapubic pain; no UTI symptoms in prior 4 weeks | ≥ 10 WBC/mm³; ≥ 10³ cfu/mL |
| 2 | Acute uncomplicated pyelonephritis | Fever, chills, flank pain; no urological abnormality | ≥ 10 WBC/mm³; ≥ 10⁴ cfu/mL |
| 3 | Complicated UTI | Features of 1 and/or 2 + ≥1 complicating factor | ≥ 10 WBC/mm³; ≥ 10⁵ cfu/mL (women) or ≥ 10⁴ (men / catheter specimen) |
| 4 | Asymptomatic bacteriuria | No urinary symptoms | ≥ 10⁵ cfu/mL in two consecutive MSUs ≥ 24 h apart |
| 5 | Recurrent UTI (prophylaxis context) | ≥ 3 culture-documented uncomplicated episodes in 12 months (women; no structural/functional abnormality) | < 10³ cfu/mL between episodes (as shown) |
- Acute: cystitis, pyelonephritis, pyonephrosis/renal abscess, prostatitis, epididymo-orchitis, urethritis/STD
- Others: Mycobacterial, parasitic, fungal [1]
7. Workup of Suspected UTI
Key history points [1]:
- Associated gross haematuria?
- Previous antibiotic treatment
- Presence of "complicated" features (neuropathic bladder, stones, previous urinary surgery)
- Recurrent attacks?
- Social & drug history: ?ketamine use
Components [1]:
| Test | What It Detects | Normal/Significance |
|---|---|---|
| pH | Normal 5.5–6.5. pH > 7.5 suggests urease-producing organism (Proteus, Klebsiella, Pseudomonas) | Urease converts urea → ammonia → raises pH → facilitates struvite (MgNH₄PO₄) stone formation |
| Specific gravity | Concentration of urine | Affects sensitivity of dipstick tests |
| Leukocyte esterase (LE) | Enzyme from neutrophils → suggests pyuria | Sensitivity 70–95% |
| Nitrites | GNB convert nitrates → nitrites → suggests bacteriuria | Sensitivity 35–85%; Specificity 92–100% |
| Microscopy: Pyuria | ≥10 WBC/mm³ | Important to differentiate contamination from true infection |
| Microscopy: RBC, casts, dysmorphic cells | Haematuria, pyelonephritis (WBC casts), glomerular disease | WBC casts are pathognomonic of pyelonephritis |
Dipstick Details (HIGH YIELD)
Leukocyte esterase [1]:
- Mechanism: Neutrophil enzyme hydrolyses indoxyl carbonic acid ester → indoxyl → oxidises diazonium salt → colour change (orange to pink)
- False positive: vaginal discharge contamination, formalin
- False negative: high SG, dehydration, glycosuria, urobilinogen, large amount of Vitamin C, test read too soon ( < 2 min) or too late (WBC lysis)
Nitrites [1]:
- Mechanism: Nitrates in urine → nitrites by GNB (Griess test, takes 4 hours in bladder)
- False positive: vaginal flora contamination
- False negative: non-nitrate-reductase producers (Pseudomonas, Gram-positive organisms), dilute urine, absent dietary nitrates, urine in bladder < 4 hours
- Clinical pearl: When BOTH nitrites and LE are negative → 90% of MSU will be negative for significant bacteriuria. When BOTH positive → 80% will have positive cultures. [1]
Blood (haemoglobin) dipstick [1]:
- Mechanism: Haemoglobin (peroxidase activity) → oxidises chromogen orthotolidine → yellow to blue/green
- False positive: iodine, hypochlorite (bleach), menstrual blood, dehydration, exercise, myoglobin
- False negative: reducing agents, Vitamin C (ascorbic acid)
- Microscopic haematuria defined as ≥3 RBC/HPF or > 5 RBC/mL (AUA) [1]
Vitamin C Trap
Vitamin C (ascorbic acid) causes false negatives for BOTH blood AND leukocyte esterase on dipstick. This is a favourite MCQ distractor.
Traditionally ≥10⁵ CFU was the definition (Kass 1960), but generally lower cut-offs used for symptomatic patients [1]:
| Setting | Threshold (IDSA/ESCMID) |
|---|---|
| Uncomplicated cystitis | ≥10³ CFU (or even ≥10² per Stamm et al.) |
| Uncomplicated pyelonephritis | ≥10⁴ CFU |
| Asymptomatic bacteriuria (women) | ≥10⁵ CFU |
| Asymptomatic bacteriuria (men) | ≥10³ CFU |
MSU Collection Instructions [1]:
- Female: Spread labia → cleanse periurethral area with moist gauze front to back → void initial 100–150 mL → collect 10–15 mL mid-stream
- Male (uncircumcised): Retract foreskin → wash glans → keep retracted → collect mid-stream
Up to 1/3 of MSU specimens from female patients are contaminated. [1]
| Feature | Genuine UTI/Bacteriuria | Contamination |
|---|---|---|
| LE | Positive | Negative |
| Nitrites | Positive | Negative |
| Pyuria | > 10/mm³ | Absent |
| Haematuria | ±present | Absent |
| Culture | Positive, pure growth | Positive / polymicrobial |
| Squamous epithelial cells | Absent | Present |
Squamous Cells = Contamination
The presence of squamous epithelial cells on microscopy strongly suggests the specimen is contaminated (skin/vaginal cells). This is a crucial discriminator the examiner expects you to mention.
Uncomplicated cystitis in women: NO role for imaging [1]
Uncomplicated pyelonephritis: USG to rule out stones/obstruction. Further imaging (CT) if symptoms not improving at 72 hours [1]
UTI in men: urologic evaluation including imaging indicated for febrile UTI, pyelonephritis, recurrent infection, or suspected complicated UTI [1]
| Condition | Duration | Notes |
|---|---|---|
| Uncomplicated cystitis | 3 days (except nitrofurantoin → 7 days) | Outpatient |
| Uncomplicated pyelonephritis | 10–14 days | Admission may be needed for severe cases |
| UTI in males | Minimum 7 days; if prostatic involvement → minimum 2 weeks, preferably fluoroquinolone |
Augmentin is NOT recommended as first-line empirical oral therapy for acute pyelonephritis — only use when susceptibility shows a susceptible Gram-positive organism. [1]
In areas with high ESBL/FQ-resistant E. coli rates → initial empirical therapy with aminoglycoside or carbapenem until susceptibility available. [1]
Nitrofurantoin should be avoided in pyelonephritis as tissue level in the kidney is low — it concentrates only in urine, not renal parenchyma. [1]
9. Asymptomatic Bacteriuria (ASB)
Definition: ≥10⁵ CFU (women) or ≥10³ CFU (men) in MSU, WITHOUT symptoms. [1]
Occurs in 4–7% of women. Pyuria in the absence of symptoms does NOT equate clinical UTI. [1]
Screening and treatment NOT indicated in: [1]
- Premenopausal non-pregnant women
- Postmenopausal women
- Men
- Patients on indwelling catheters
- Patients on nephrostomy tubes / ureteric stents
- Patients with spinal cord injury
Screening and treatment IS recommended in: [1]
- Pregnant patients
- Patients about to undergo invasive genitourinary procedure with risk of mucosal bleeding
Why pregnancy?
- Incidence of ASB similar (4–7%), BUT physiological changes (↑GFR, hydronephrosis, hydroureter from progesterone effect) make progression to upper tract infection likely (up to 25–40%) [1]
- Upper tract infection in pregnancy → prematurity, low birth weight
- Therefore routine screening and treatment is standard of care
ASB in DM: Very common (26% in diabetic women), but a landmark RCT (Harding et al, NEJM 2002) showed that treatment of ASB does NOT reduce complications in DM patients → screening/treatment NOT clinically indicated [1]
High-Yield Exam Distinction
The two indications to treat ASB are: (1) pregnancy and (2) pre-invasive GU procedure. Everything else = do NOT treat. This is one of the most commonly tested points.
10. Recurrent UTI
| Bacterial Persistence/Relapse | Bacterial Reinfection | |
|---|---|---|
| Organism | Same organism, same strain | Different organism (or same organism with documented negative cultures in between) |
| Source | Focus within urinary tract (stones, urethral diverticulum) | Fecal flora reservoir |
| Proportion | < 5% | > 95% of recurrent UTI |
| Implication | Potentially correctable by removing the focus | Indicates underlying genetic susceptibility |
| Premenopausal Women | Postmenopausal Women |
|---|---|
| Sexual intercourse (frequency, new partner) | Oestrogen deficiency |
| Use of spermicide and diaphragm | Urinary incontinence |
| Pelvic anatomy (urethra-to-anus distance) | Presence of cystocele |
| Age of first UTI | Large post-void residual |
| Family history / genetic factors | Hx of UTI before menopause |
| Prior antimicrobial use | Genetic factors |
Why are women at increased risk? [1]
- More receptor sites for uropathogens on vaginal cells
- Shorter urethra
- Close proximity to anus
- Blood group genetics (P group secretor, ABO non-secretor, Lewis non-secretor, HLA-A3)
History [1]: Pre/postmenopausal state, sexual history, spermicide/diaphragm use, upper tract involvement (loin pain, fever), frequency of episodes, relationship with coitus, previous cultures and antibiotic treatment, possible factors for relapse (urologic surgery, stones).
Examination [1]:
- Ballottable kidney (hydronephrosis)
- Palpable bladder (voiding dysfunction)
- Degree of oestrogenisation of introitus/vagina
- Cystocele / uterine prolapse
- Periurethral fullness/mass (urethral diverticulum)
- Focused neurological exam (DRE)
Investigations [1]:
- Urinalysis and culture — confirm UTI, determine persistence vs reinfection
- Imaging NOT routinely recommended in women with recurrent UTI (low diagnostic yield)
- Further workup indicated if: gross haematuria, persistent microhaematuria between UTIs, evidence of bacterial persistence, suspicion of complicated UTI, urease-splitting organisms, symptoms/signs of obstruction
1. "Recurrent UTI" with gross haematuria or persistent microscopic haematuria → formal urologist referral to rule out malignancy (requires cystoscopy) [1]
2. Recurrent bacterial persistence with urease-producing organisms → may indicate underlying urolithiasis [1]
3. Recurrent UTI with pyuria but no growth → send EMU for TB, rule out stones, consider ketamine cystitis [1]
Prevention and Management of Recurrent UTI
The following have NEVER been shown in case-controlled studies to reduce recurrent UTI (i.e. NOT evidence-based): [1]
- Personal hygiene
- Post-coital voiding
- Hydration to maintain adequate urine output
Evidence-based measures: [1]
- Avoid spermicides / diaphragms
- Topical vaginal oestrogen (postmenopausal)
Three types [1]:
| Type | Description | Details |
|---|---|---|
| Continuous prophylaxis | 6–12 months nightly low-dose | 95% reduction in recurrences; 60% reinfected after stopping. Agents: Septrin 480mg, nitrofurantoin 50mg, trimethoprim 100mg, cephalexin 250mg. Breakthrough infections (~5%) treated with full-course full-dose antibiotics |
| Post-coital prophylaxis | Single dose after coitus | For recurrent UTI temporally related to intercourse. Less antibiotic consumption. Agents: Septrin 480mg, Ciproxin 125mg |
| Self-start therapy | Patient starts 3-day course when symptoms appear | For motivated patients; 86% symptomatic episodes culture-positive, 92% achieved symptomatic relief |
Nitrofurantoin 50mg OD is preferred for continuous prophylaxis — lower systemic absorption and less microbial resistance, but avoided in pyelonephritis due to low renal tissue levels. [1]
Avoid amoxicillin and cephalosporin for prophylaxis as they change faecal flora. [1]
Table: Continuous antimicrobial prophylaxis — expected UTIs per year [1]
| Regimen | Expected UTIs/year |
|---|---|
| TMP-SMX 40/200 mg once daily | 0–0.2 |
| TMP-SMX 40/200 mg three times weekly | 0.1 |
| Trimethoprim 100 mg once daily | 0–1.5* |
| Nitrofurantoin 50 mg once daily | 0–0.6 |
| Nitrofurantoin 100 mg once daily | 0–0.7 |
| Cefaclor 250 mg once daily | 0.0 |
| Cephalexin 125 mg once daily | 0.1 |
| Cephalexin 250 mg once daily | 0.2 |
| Norfloxacin 200 mg once daily | 0.0 |
| Ciprofloxacin 125 mg once daily | 0.0 |
| Fosfomycin 3 g every 10 days | 0.14 |
*High recurrence rates observed when trimethoprim resistance is present.
Table: Post-coital antimicrobial prophylaxis — expected UTIs per year [1]
| Regimen | Expected UTIs/year |
|---|---|
| TMP-SMX 40/200 mg | 0.30 |
| TMP-SMX 80/400 mg | 0.00 |
| Nitrofurantoin 50 or 100 mg | 0.10 |
| Cephalexin 250 mg | 0.03 |
| Ciprofloxacin 125 mg | 0.00 |
| Norfloxacin 200 mg | 0.00 |
| Ofloxacin 100 mg | 0.06 |
Cranberry juice (Proanthocyanidin 36 mg/day) — blocks bacterial adherence to urothelium, 20% reduction in risk. [1]
11. UTI in Special Populations
Very few UTI in men aged 15–50 are uncomplicated. [1] Most men with febrile UTI have concomitant prostatitis. [1] Minimum 7-day antibiotic regimen; if prostatic involvement → minimum 2 weeks, preferably fluoroquinolone. [1] Prophylactic antibiotics reduce bacteriuria and septicaemia by 65% and 75% respectively after TURP. [1]
Risk factors [1]:
- Age (neonates/infants: immature immunity, increased periurethral colonisation)
- VUR
- GU abnormalities (PUJ obstruction, VUJ obstruction, ureterocele, posterior urethral valves)
- Voiding dysfunction
- Uncircumcised boys: 10-fold higher UTI risk in first year (bacterial colonisation of glans/foreskin)
- Constipation
- Girls 5%, Boys 1% overall, but males more common in first year
Urine collection methods [1]:
- Suprapubic aspiration (most sensitive/accurate)
- Bladder catheterisation (sensitive, but risk of nosocomial introduction)
- Clean-catch
- MSU
- Plastic bag on genitalia (screening only; never send bag urine for culture → too contaminated [4])
Criteria [1]:
- Pyuria ( > 10 WBC/HPF) + bacteriuria in fresh sample reinforces diagnosis
- Epithelial cells strongly suggest contamination
- WBC casts pathognomonic of pyelonephritis
Urine culture thresholds by specimen type (paediatric) [1]:
| Specimen Type | Culture Criterion |
|---|---|
| Suprapubic bladder puncture | Any CFU/mL (at least 10 identical colonies) |
| Bladder catheterisation | ≥1,000–50,000 CFU/mL |
| Mid-stream void | ≥10⁴ CFU/mL with symptoms; ≥10⁵ CFU/mL without symptoms |
Types (NICE) [1]:
- Simple: no fever, responds within 48 hours, E. coli
- Atypical: seriously ill, poor urine flow, abdominal/bladder mass, raised creatinine, septicaemia, failure to respond to antibiotics in 48 hours, non-E. coli
DMSA scan [1]: For atypical and recurrent UTI
- Binds to basement membrane of proximal tubular cells
- Star-shaped defect → acute pyelonephritis
- Focal cortical defect → chronic scar ("renal scar")
- Defect persisting at 6 months = renal scarring
Antibiotics in children [1]:
- AVOID: chloramphenicol, sulphonamides, tetracyclines (teeth staining), rifampicin, amphotericin B, quinolones
- AVOID ceftriaxone (Rocephin): undesired side effect of jaundice (displaces bilirubin from albumin in neonates)
- Aminoglycosides if necessary → monitor serum levels
- Most antibiotics have a wide therapeutic index; no dose adjustment necessary until GFR < 20 mL/min, except for nephrotoxic agents (e.g. aminoglycosides) [1]
- Drugs removed by dialysis should be administered after dialysis treatment [1]
- Combination of loop diuretics (e.g. furosemide) and a cephalosporin is nephrotoxic [1]
- Nitrofurantoin and tetracyclines are contraindicated in renal impairment, but doxycycline is NOT contraindicated [1]
12. Catheter-Related UTI
Biofilm = accumulation of microorganisms and their extracellular products forming a structured community on a surface. [1]
Biofilm Structure [1]:
- Linking film layer (bottom): attaches to the surface of the device
- Base film layer: compact layer of microorganisms
- Surface layer: outer layer from which planktonic bacteria can arise and spread
Steps of Formation [1]:
- Mucopolysaccharide layer adsorbs onto device → conditioning film
- Microorganisms attach
- Upregulation of surface adhesins → "cementing"
- Colony formation → basic biofilm community (10–20% bacteria, 80–90% mucopolysaccharide matrix)
Why biofilms resist treatment [1]:
- Glycocalyx restricts antibiotic diffusion → extrinsic resistance
- Slow bacterial growth inside biofilm → less susceptible to antibiotics
- Phenotypically different bacteria (intrinsic resistance), possibly from genetic change
- Exchange of resistance genes (plasmids) within biofilm
- Bacteria survive 1000× higher antibiotic concentrations than planktonic bacteria
Management [1]:
- Antimicrobials useful only in young biofilm ( < 24 hours)
- For older biofilms → device must be removed
Prevention [1]:
- Device: controlled-release antibiotics, antiadhesive surface, silver alloy coating (delays biofilm by ~1 week), JNC spray
- Meticulous tissue handling, aseptic prosthesis handling
- Eradicate other foci of infection before insertion
- Minimise OT traffic
- Silicon Foley preferred
- Indwelling catheter should be introduced under aseptic conditions
- Minimise urethral trauma: use adequate lubricant and the smallest possible catheter calibre
- Antibiotic-impregnated catheters: may decrease asymptomatic bacteriuria within 1 week, but no evidence they decrease symptomatic infection → cannot be recommended routinely
- Silver alloy catheters: significantly reduce asymptomatic bacteriuria for < 1 week only; some evidence of reduced symptomatic UTI → may be useful in selected settings
- If symptomatic CAUTI and catheter in place > 7 days → replace or remove catheter before starting antimicrobials
- Empirical therapy: broad-spectrum antibiotics based on local susceptibility patterns; adjust once culture and sensitivity results available
- Candiduria with urinary symptoms or signs of systemic infection → systemic antifungal therapy indicated
- Patients with urethral catheters in place for ≥ 10 years → screen for bladder cancer [1]
Clinical examples of biofilm-related infections [1]:
- Prosthesis infections (AUS, penile prosthesis)
- Ureteral stent infections
- Chronic prostatitis
- Infectious stones
13. Sepsis from UTI (Urosepsis)
| Term | Definition |
|---|---|
| Infection | Presence of organisms in a normally sterile site, usually but not necessarily accompanied by an inflammatory host response |
| Bacteraemia | Bacteria present in blood as confirmed by culture; may be transient |
| SIRS | Response to clinical insults (infectious or non-infectious, e.g. burns, pancreatitis) manifested by ≥2 of: Temp > 38°C or < 36°C; HR > 90; RR > 20 or PaCO₂ < 32 mmHg; WBC > 12,000 or < 4,000 or > 10% bands |
| Sepsis | Activation of the inflammatory process due to infection |
| Severe sepsis | Sepsis + organ dysfunction, hypoperfusion, or hypotension (lactic acidosis, oliguria, altered mental status) |
| Septic shock | Sepsis + hypotension (SBP < 90 or drop > 40 from baseline) despite adequate fluid resuscitation, with perfusion abnormalities |
| Refractory septic shock | Septic shock lasting > 1 hour not responding to fluids or pharmacological intervention |
Heat-stable endotoxin of Gram-negative bacteria (lipo-polysaccharide) → triggers mediator release (cytokines) → activates kinin, complement, fibrinolytic systems → WBC/macrophage activation → widespread microvascular injury → tissue ischaemia
14. Emphysematous Pyelonephritis (EPN)
EPN is an acute severe necrotising infection of the renal parenchyma and surrounding tissues with gas in the renal parenchyma, collecting system, or perinephric tissue. [1]
| Feature | Details |
|---|---|
| Pathogens | E. coli, Klebsiella (most common); also Proteus, Streptococcus, Pseudomonas |
| Predisposing factors | DM (single most common), female > male, urinary tract obstruction (stones), immunocompromised |
| Pathogenesis | High glucose + gas-forming microbes + impaired blood supply + reduced immunity + obstruction → G−ve anaerobes ferment glucose → N₂, O₂, CO₂, H₂ accumulate |
| Histopath | Abscess formation, micro/macro-infarction, vascular thrombosis, gas-filled spaces, necrosis with acute/chronic inflammatory cells (septic infarction) |
| Diagnosis | Gold standard: CT (more sensitive, defines extent). KUB: abnormal gas shadow in renal bed |
Wan classification (prognostic) [1]:
- Type I: Parenchymal destruction with streaky/mottled gas, no/minimal fluid → mortality ~60%
- Type II: Renal/perinephric fluid with bubbly/loculated gas or gas in collecting system → mortality ~20%
Michaeli classification (based on plain radiograph and IVP) [1]:
- Class I: Gas in renal parenchyma or perinephric tissue
- Class II: Gas in the kidney and its surroundings
- Class III: Extension of gas through fascia, or bilateral disease
Huang & Tseng classification (guides management) [1]:
| Class | Description | Management |
|---|---|---|
| 1 | Gas in collecting system only | PCD + MM |
| 2 | Parenchymal gas only | PCD + MM |
| 3A/3B | Perinephric / pararenal gas | Depends on risk factors (DM, thrombocytopenia, ARF, altered consciousness, shock): 0–1 RF → PCD+MM (85% survival); ≥2 RF → nephrectomy (90% failure with PCD) |
| 4 | Solitary kidney / bilateral EPN | PCD + MM → if failed → nephrectomy + ICU + renal support |
- High index of suspicion when patient fails medical Rx for acute pyelonephritis
- Active resuscitation (ABC)
- Medical management: O₂, IVF, acid-base balance, antibiotics, good glycaemic control, keep SBP > 100
- Empirical antibiotics: aminoglycoside, β-lactamase inhibitor, cephalosporin, quinolones → adjust with culture
- Renal support if ARF
- ICU if multiorgan support needed
- Percutaneous catheter drainage (PCD) ± nephrectomy based on classification
Necklace appearance of gas beads in bladder wall on KUB = diagnostic of emphysematous cystitis. [1]
| Feature | Details |
|---|---|
| Demographics | Middle-aged diabetic women (M:F = 1:6) |
| Predisposing factors | DM (66%), chronic UTI, indwelling catheter, urinary stasis (BOO), neurogenic bladder |
| Pathogens | Same as EPN (E. coli, Klebsiella) |
| Pathogenesis | Like EPN (glucose fermentation); in non-diabetics → urinary albumin as substrate |
| DDx of air in bladder | Instrumentation, fistula to hollow viscus, tissue infarct/necrosis, infection |
| Presentation | Variable: asymptomatic, pneumaturia, irritative voiding, acute abdomen, severe sepsis |
| Diagnosis | KUB: curvilinear radiolucency in bladder wall ± intraluminal air. CT: more sensitive, defines extent |
| Histopath | Bladder wall thickening with vesicles; microscopy: gas-filled vesicles in mucosa lined by flattened fibrocytes and multinucleated giant cells |
| Management | Antibiotics + bladder drainage + DM control. If failed/severe necrosis (10%) → partial cystectomy/cystectomy/debridement |
| Mortality | EC alone: 7%; EC + EPN: 14% |
CT "bear's paw" appearance + renal stones + ballottable mass = XGP [1]
- KUB shows multiple renal stones
- CT shows classic "bear's paw" pattern (dilated calyces with stones)
- Histology: lipid-laden macrophages (xanthoma cells) [1]
- Typically presents with vague flank pain and large renal mass
- Treatment: nephrectomy
TB is the most common cause of infection-related death globally. 5–45% have extrapulmonary manifestations; 30–40% of extrapulmonary cases involve the urogenital tract. [1]
| Feature | Details |
|---|---|
| Pathogenesis | Haematogenous spread during initial infection → bacilli remain dormant → reactivate with immunosuppression (risk up to 15%) |
| Latency | 5–40 years after pulmonary TB |
| Other routes | Lymphatic spread, sexual transmission |
| Risk factors for reactivation | DM, advancing age, low BMI, concurrent cancer, immunosuppression, kidney failure |
| Organs affected | Both sexes: urethra, bladder, ureters, kidneys. Male: scrotum, penis, testes, epididymis, vas deferens. Female: vulva, vagina, cervix, uterus, ovaries, fallopian tubes |
| Complications | Ureteric/urethral strictures, renal failure, infertility (often diagnosed late) |
| Diagnosis | Sterile pyuria → send EMU for TB (3 consecutive early morning urines) [5]; culture on Löwenstein-Jensen medium |
Treatment of GUTB [1]
Medical: Standard 4-drug anti-TB regimen × 6 months:
- 2 months: rifampicin + isoniazid + pyrazinamide + ethambutol
- 4 months: rifampicin + isoniazid
- Longer treatment needed for: HIV co-infection, renal abscess, bone infiltration
- MDR-TB: MDR regimens for up to 18–24 months
Surgical [1]:
- Ureteric stricture with hydronephrosis → early stenting or percutaneous nephrostomy
- Nephrectomy: non-functioning kidney, co-existing RCC, extensive whole-kidney involvement
The lecture includes a clinical photo of an elderly woman with sudden severe cystitis symptoms + vesicular rash → herpes zoster [1].
- Typical cystoscopic appearance: hemitrigonal vesicles [1]
- The sacral dermatome involvement of VZV can cause a neuropathic bladder (S2-S4 involvement) along with haemorrhagic cystitis from the virus itself.
Exam Intelligence
| Trap | Correct Answer |
|---|---|
| "Bacteriuria = UTI" | No. Bacteriuria can be colonisation or contamination |
| "Pyuria = UTI" | No. Pyuria can be from stones, TB, CIS, IC, ketamine |
| "Treat ASB in catheterised patients" | No — do NOT screen or treat |
| "Treat ASB in DM" | No — Harding et al RCT showed no benefit |
| "Personal hygiene/post-coital voiding reduces recurrent UTI" | NOT evidence-based in case-controlled studies |
| "Nitrofurantoin for pyelonephritis" | No — poor renal tissue penetration |
| "Augmentin as first-line empirical for acute pyelonephritis" | No — not recommended for empirical use |
| "Proteus susceptible to nitrofurantoin" | No — Proteus has intrinsic resistance |
| "Type 1 pili → pyelonephritis" | No. Type 1 → cystitis. Type P → pyelonephritis |
| "Nitrites negative → no UTI" | Not necessarily — Pseudomonas and Gram-positives don't produce nitrites |
| "Bag urine for culture in children" | Never — contamination risk too high; use SPA/catheter/clean-catch |
- S. saprophyticus vs S. epidermidis: S. saprophyticus causes community-acquired UTI in young sexually active women; S. epidermidis causes prosthetic/catheter infections
- EPN Type I (streaky gas, parenchymal destruction) → 60% mortality vs Type II (bubbly gas, fluid) → 20% mortality
- Struvite stones = infection stones = urease-producing organisms (Proteus, Klebsiella, Pseudomonas) → alkaline pH > 7.5 → MgNH₄PO₄
- DMSA scan: star-shaped defect = acute pyelonephritis; focal cortical defect at 6 months = renal scarring
High Yield Summary
-
UTI = urothelial inflammation from bacterial invasion + bacteriuria + pyuria
- ; bacteriuria and pyuria alone ≠ UTI
-
E. coli
- causes 85% community-acquired, 50% nosocomial UTI; S. saprophyticus in young sexually active females
-
Type 1 pili → cystitis; Type P pili → pyelonephritis
- (80% of isolates)
-
Natural defences
- lactobacilli/low pH, antegrade flow, Tamm-Horsfall protein, urothelial exfoliation, bladder emptying
-
Uncomplicated cystitis
- 3 days Abx (nitrofurantoin 7 days); pyelonephritis: 10–14 days; males: min 7 days (2 weeks if prostate)
-
ASB
- treat ONLY in pregnancy and pre-invasive GU procedure; do NOT treat in DM, catheterised patients, or spinal cord injury
-
Recurrent UTI
- ≥2/6mo or ≥3/12mo; > 95% are reinfection; evidence-based prevention = topical oestrogen + antibiotic prophylaxis; hygiene/hydration/post-coital voiding NOT evidence-based
-
EPN
- gas in renal bed in DM patient failing medical Rx → CT gold standard → Wan classification (I vs II) → PCD ± nephrectomy
-
Sterile pyuria DDx
- TB, CIS, stones, schistosomiasis, partially treated UTI, IC, ketamine cystitis → send EMU for TB
-
Biofilm
- device removal needed for mature biofilm; antibiotics ineffective (1000× resistance); silver coating delays formation by ~1 week
- GUTB
- haematogenous spread, 5–40 year latency, standard 6-month anti-TB regimen, surgery for strictures/non-functioning kidney
Active Recall - Urinary Tract Infection
[1] Lecture slides: GC 210. Urinary tract infection.pdf [2] Senior notes: Ryan Ho Urogenital.pdf (Ch 6.2) [3] Senior notes: Gen Clerk Anaes + Microbiology Summary.pdf (p.20) [4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.394) [5] Lecture slides: GC 101. Diagnosis of infections [Handouts].pdf (Section X - Urine) [6] Lecture slides: GC 106. Practical issues in antibiotic use.pdf (p.10) [7] Lecture slides: CFB WCS27_Surgical Infection.pdf (p.37) [8] Senior notes: Adrian Lui Pediatrics Notes.pdf (p.340-342) [9] Senior notes: Maksim Medicine Notes.pdf (p.192) [10] Senior notes: Block A - Nephrotology Teaching Clinic RTD.pdf (p.13)
GC209 Urinary Incontinence And Overactive Bladder
Urinary incontinence is the involuntary loss of urine, while overactive bladder is a syndrome characterized by urgency, with or without urge incontinence, usually accompanied by frequency and nocturia, resulting from detrusor muscle overactivity or other lower urinary tract dysfunction.
GC212 Weight Loss And Vomiting Gastric Cancer; Abdominal Imaging
Gastric cancer presenting with weight loss and vomiting due to gastric outlet obstruction or advanced disease, evaluated with abdominal imaging such as CT to assess tumor extent, local invasion, and metastatic spread.