Urology infectionUrology infection

Edmond Wong

Outline• Definition• Bacteriology• Cystitis & urethritis• Recurrent UTI• Pyelonephritis, EPN & XGP• General principles of antibiotic and prophylaxis• Mx of septicaemia• TB urinary tract • Prostatitis• Epididymal orchitis• Viral disease of Genital tract (condylomata, AIDS, Herpes)• Schistosomiasis• Radiation cystitis• Chemical cystitis and mx• Antibiotic prophylaxis in uro procedure

Definition

• Bacteriuria: Presence of bacteria in urine• Pyuria: presence of WBC in urine• Sterile Pyuria: Pyuria without bacteriuria

1. Incomplete antimicrobial treatment of UTI2. Infections caused by Mycobacterium tuberculosis

and other fastidious bacteria, e.g. Chlamydia trachomatis

3. Urolithiasis and foreign bodies4. CIS5. Interstitial cystitis6. schistosomiasis

Definition

• Cystitis: – Clinical syndrome of dysuria, frequency & urgency +/-

Bladder pain

• Acute pyelonephritis: – Syndrome of Fever, Chills & rigor, flank pain ,

bacteriuria + pyuria

• Chronic pyelonephritis: – Radiological diagnosis– Scarred , shrunkened kidney (may or maynot result

from recurrence infection)

What is the definition of UTI?

• UTI – Inflammatory response of urothelium to microorganism invasion, commonly bacteria , associated with pyuria and bacteriuria

• Opportunistic infection : infection caused by non-pathogens (commensals) due to weakened host defence mechanisms

Definition of UTI

• Isolated UTI: – Occur at least 6m after the previous UTI

• Recurrent UTI : >=2 UTI in 6m / >=3 UTIs in 1yr– Bacterial persistence: UTI by same organism

• Nidus (stone, bladder/urethral diverticulum, chronic prostatitis, colo-vesical fistula)

– Reinfection: by different organisms each time• Increased susceptibility to UTI, e.g. poor hygiene, sexual

intercourse, post menopause• > 95% female recurrent UTI is reinfection

Definitions of UTI

• Unresolved infection: not response to txn1. Bacterial resistence to antibiotic

2. Development of resistance in a previously susceptible organism

3. Multiple organism

4. Rapid re-infection & overwhelming pathogens

5. Subtherapeutic level of antimicrobial

6. Non-compliance with treatment

Definition of UTI:

• Complicated UTI– Structurally and functionally abnormal urinary tract– Underlying disease prone to complicated UTI

1. Male gender , elderly2. Pregnancy3. Catheter or stent or instrumentation4. immunocompromised, DM, hospital acquired infection

• uncomplicated UTI– No structurally and functionally abnormal urinary

tract– No underlying disease prone to acquire UTI

How does the urinary dipstick – How does the urinary dipstick – (blood) work?(blood) work?

• Chromogen indicator : orthotolidine is a peroxidase substrate• Haemoglobin has peroxidase activity• Oxidation process take place• Positive result : BLUE• False positive (oxidasing agent):

1. Povidone iodine2. Hypochlorite (bleach)3. Menstrual blood4. Dehydration, exercise and myoglobin

• False negative (reducing agent):– Vitamin C– Poorly mixed urine

• Dipstick positive but microscopy negative – dilute urine

How does the urinary dipstick – How does the urinary dipstick – (WBC) work?(WBC) work?

• Neutrophils produce leucocyte esterase • Catalyzes the hydrolysis of a indoxyl carbonic acid ester

to indoxyl • Idoxyl oxidise the diazonium salt chromogen to produce

blue colour • False positive : vaginal discharge or formalin• False negative (reducing agent)

1. Vitamin C2. Dehydration3. Glycosuria, urobilinogen4. Test is read too fast (< 2min) or too long (lysis of WBC)

• 30% of infection with negative leucocyte esterase ( = 70% sensitivity)

How does the urinary dipstick – How does the urinary dipstick – (nitrites) work?(nitrites) work?

• Gram negative bacteria convert nitrates to nitrites (not usually in urine)

• Nitrite react with the aromatic amine to form diazonium salt • Which react with hydroxybenzoquinolone to form pink colour

(Griess reaction) – 4 hours processing• High specificity but low sensitivity – means +ve UTI, negative

cannot rule out UTI• When negative for both nitrites and leukocytes 90% of MSU will

be negative for significant bacteriuria• When positive for both nitrites and leucocytes, 80% will have

positive cultures on MSU– More specific but less sensitive to either test alone

• False positive – contamination • False negative – gram positive bacteria, pseudomonas, ascorbic

acid, and dilute urine, urine in bladder < 4 hours (so only early morning urine is reliable)

Why is urine pH important?

• Normal urinary pH: 5.5- 6.5• pH> 7.5 possibility of stone• Urea splitting organism produce urease: (PKS, PPS)

1. Proteus2. Klebsiella3. Staphylococcus4. Pseudomonas5. Providencia6. Serratia

• Induce following reaction: – Urea CO2 + NH3 (ammonia) – NH3 raise pH – Precipitation of magnesium ammonium phosphate to form

staghorn stone

BacteriuriaBacteriuria

What are the definitions of significant bacteriuria?

• Kass first introduced quantitative microbiology in diagnosis UTI– Significant bacteriuria ≥ 105 cfu/mL of pure growth – However, miss 1/3 symptomatic UTI with growth ≥ 103

cfu/mLof pure growth• > 103 : uncomplicated cystitis in women• > 104 : uncomplicated pyelonephrisitis in women,

catheter urine in women, men

• Asymptomatic bacteriuria should be treated in children, pregnant female and immunocompromized patents, prior to an invasive genitourinary procedure for which there is a risk of mucosal bleeding, but not DM or elderly patient (Canada’s study)

What is the implication of bacteriuria?

• A single in/out uretheral catheterization may be complicated by bacteriuria in 5% of cases

• Bacteriuria is almost universal when the catheter is left in situ for longer than 3 days

• 10-20% of patients with pyelonephritis have bacteriuria

• Bacteriuria without pyuria may be found– bacterial contamination– Colonization (asymptomatic bacteriuria)

• Absence of pyuria may cause doubt on the diagnosis of UTI

Risk factor for bacteriuria

1. Female2. Low oestrogen state (menopause) 3. Pregnancy 4. Age5. Institutional state in elderly 6. Indwelling catheters7. Previous UTI8. DM9. Stone disease10.GU malformation & voiding dysfunction (including

obstruction)

How would you instruct the pt for MSU?

• Women: – Spread the labia– Wash and cleanse the periurethral area with moist gauze from back to

front– Void first 100-150ml , collect next 10-15ml

• Men: – Circumcised: no special preparation– Uncircumcised:

• Retract foreskin , wash glans with soap and rinse with water• Keep foreskin retracted: collect 10-15ml

• Handling of MSU:– Culture with hours or refrigerated immediately & culture within 24hr– Microscopy: 5-10ml urine centrifuge for 5min (2000rpm) – Culture: 0.1ml urine of split-agar plate

• Blood agar gram +ve culture• Eosinmethylene blue (EMB) gram –ve culture• Estimate CFU after overnight incubation

What is the gram’s stain?

• Bacterial smear is stained with crystal violet for 1-2min then pour off

• Then Gram’s iodine for 1-2min then pour off• Decolorized by acetone• Washed with water and counterstained with safranin

for 2 mins• Gram +ve: cell wall that retain the crystal violet dye

– MRSA is a gram +ve coccus. It is present on the skin of about 40% of people. Over 90% of isolates produce the penicillin binding protein which makes the strain resistant to penicillin base antibiotics

• G-ve – pink safranin

Pathogenesis of UTI

Why patient will have UTI?

• An interaction of susceptibility of host & virulence of organism

• Pathogenicity: ability of an organsim to cause disease

• Virulence: degree of pathogenicity– Characteristics of uropathogens to colonised

and flourish within the host

Bacterial virulence factors?

• Directed against external agents (i.e antimicrobial resistence) – Inherited chromosomally (intrinsic resistance of

proteus to nitrofurnatoin)• Enzyme inactivation: beta-lactamase which hydrolyses the

beta-lactam bone within penicillin gp of antibiotic • Secrete by S. aureus , gonorrhoea & enterobacteria

– Acquired chromosomally (mutations)• Alter the antibiotic target & receptor activity

– Acquire extra-chromosomally (plasmids)

Direct against host: 1. General: extracellular capsule prevent phagocytosis (E coli)2. Toxin, e.g. haemolysin3. Enzyme, e.g. urease4. Antihumoral factors, e.g. IgA inactiviting protein by gonorrhoea and

Proteus5. Adherence mechanism – afimbrial or fimbrial types (E.coli)

– Afimbrial adhesin – Dr adhesins (UTI in children and pregnancy) – Fimbriase: 100 pili, 5nm diameter , 2um long– Type P fimbriae (mannose resistant) have adhesions that bind to renal

urothelium and are associated with >90% of pyelonephritis– Type P fimbriae are more virulent and more adhesive than type 1 fimbriae– Type 1 fimbriae (mannose sensitive) binds to elements of bladder urothelium

and are associated with cystitis– Type 1 fimbriae are also referred to as mannose sensitive. This means that

fimbriae have the ability to adhere to and agglutinate guinea pig erythrocytes. Such an event is inhibited by mannose

– S pili – both bladder and kidney infection 6. Others

– Penetration of host by schistosoma apine– Intrinsic resistance of Proteus to nitrofurantoin

What are normal host defence mechanisms against UTI?

1. Normal commersal flora of vaginal introitus and periurethral area– Lactobacilli reduced uropathogens to colonise by lowering pH

as a result of converting glycogen to lactic acid (lower pH)2. Vaginal oestrogen and IgA3. Normal antegrade flow of urine 4. Characteristic of urine (high osmolality, low pH, Urea , etc)5. Mechnical integrity of mucous membrane6. Normal exfoliation of urothelial cells7. Tamm-horsfall protein by ascending limb of loop of Henle –

bind type 1 pili & prevent attachment8. GAG (Glycosiaminoglycan) layer

Route of infection

• Ascending infection (majority)– Bacteria colonize perineum, vagina & distal urethra– Ascend to bladder (cystitis)– Ascend to kidney (pyelonephritis), encourage by

reflux

• Hematogenous (uncommon):– Staph aureus, candida, fungaemia & TB

• Via lymphatics: – Inflammatory bowel disease– Retroperitoneal abscess

Mx of UTI

Anbitiotic Formulary

• TMP-SMX—inhibits dihydrofolic acid reductase– Enterococcus and Pseudomonas are resistant

• Nitrofurantoin—mechanism unknown– Pseudomonas and Proteus resistant, not useful in upper tract infections,

development of resistance very low

• Cephalosporins—1st to 3rd generation increases Gram negative and anaerobic coverage

• Aminopenicillins—effective enterococcus, 30% resistance development in common uropathogen isolates.

• Aminoglycoside—combined with ampicillin 1st line therapy for urosepsis, nephrotoxic

• Flouroquinolone—DNA gyrase inhibitor, enterococcus resistant, damages cartilage in animal studies

Cystitis & urethritis

Uncomplicated Cystitis

• Absence of physiologic or anatomic abnormalities & no recent urologic surgery

• 30% of women between age 20-40 have had a UTI– 80% E. coli– 15% S. Saprophyticus

• Rarely occurs in men– Uncircumcised– HIV

Uncomplicated Cystitis

• Microscopic analysis is more sensitive than dip-stick testing– Bacteriuria– Pyuria– Hematuria

Symptoms:– Dysuria, frequency,

urgency, small urine volumes, suprapubic pain

• Differential Diagnosis:– Vaginitis– Urethral infection /

urethritis– STD

Uncomplicated Cystitis

• Pretherapy urine Cx only for the following:

– Dx in doubt– Symptoms longer than

7 days– Older than age 65– DM– Pregnancy

– All males

• Treatment (3-days):– TMP-SMX– TMP alone– Nitrofurantoin– Fluoroquinolones (use

for patients with allergy to less costly drugs or with high risk of infection with resistant organism)

– Amoxicillin-Clavulanate during pregnancy

Urethritis• Inflammation of urethra• Men: STD with dysuria + urethral discharge• Gonococcal urethritis (GU)

– gram-negative diplococcus Neisseria gonorrhoea (incubation 10 day)– concomitant infection with Chlamydia trachomatis– Investigation: urethral swab for C/ST– Treatment:

• ceftriaxone 125 mg IM in a single dose• cefixime 400 mg orally in a single dose• plus treatment for chlamydia• Quionolone is not recommended

• Non gonococcal urethritis (NGU)– Chlamydia trachomatis (incubation 1–5 weeks)– Azithromycin, 1 g as a single oral dose– Doxycycline, 100 mg orally twice a day for 7 days– Transmission to females results in increased risk of pelvic inflammatory

disease, abdominal pain, ectopic pregnancy, infertility, and perinatal infection

• Gonococci located intracellularly as Gram-negative diplococci

• Ciprofloxacin (gonococci) and doxycycline (chlamydial) for 2 weeks if young epididymoorchitis

• Fluoroquinolones are contraindicated in adolescents (< 18 years) and pregnant women

Recurrent UTI in Recurrent UTI in femalefemale

Female refer for recurrent UTI , what is your approach?

• History: – Age– Isolated or recurrent UTI?– Trace all previous MSU result– Re-infection or persistence? – Number of confirmed UTI in

one year– Cystitis or pyelonephritis?– Complicated or uncomplicated

infection?– Hematuria (CIS)

• PMH: – Marital and obs hx– OCP– STD – DM– TB– Stone– Constipation– Neurological illness– Previous UTI in childhood

• Family hx of UTI– ABO bld gp Ag non-secretors– Lewis non-secretor– P bld gp secretors

PE

• Abd: – Palpable kidney– Palpable bladder– Loin pain

• Vaginal examine: – State of oestrogenisation– Genital prolapse– Urethral diverticulum

• Focused neurological examination

Ix of post-menopausal

Despite all investigation, no cause of infection identify, what

can you explain to her ?

Why do women increase risk of recurrent infection?

Susceptibility to infections 1. Increased number of receptors sites for

uropathogen2. Shorter urethra3. Close proximity to anus4. Asymptomatic bacteriuria in pregnant women5. Large PVR in older women6. Genital prolapse7. P blood group secretor / ABO blood group non-

secretor / Lewis non-secretor8. HLA-A3 phenotype

What are the risk factors of What are the risk factors of recurrent UTI?recurrent UTI?

1. Reduce antegrade flow of urine (low fluid intake, BOO, neurogenic bladder) 2. Sexual intercourse3. Use of spermicides4. Urinary and fecal incontinence5. Atrophic vaginitis

• Raz (NEJM 1993) published a small randomized trial of 93 post menopausal female with recurrent urinary tract infections and reported a significant reduction in the frequency of UTI’s in ladies treated with topical estriol

6. History of UTI7. Immumocompromised, e.g. DM / HIV

Mx of recurrent UTI : general measure

Aim: control symptom & reduce frequency of infection• High fluid intake• Void before and after sexual intercourse (vigorous

activity may “milk” the bacteria to the bladder)• Avoid using detergents in her bath• Avoid using spermicidal contraceptive• Apply lactobacilli to vagina to keep her urine acidic• Apply oestrogen to atrophic vagina to restore normal

vaginal environment and recolonisation with lactobacilli• Cranberry juice (proanthocyanidin) – block bacterial

adherence to urothelium, 20% reduction risk of infection

Treatment strategies

• < 3 UTI / year: patient initiated therpay

• > 3 UTI/ year: prophylaxis for 6/12

• Post-coital single dose therapy

Mx: Antibiotic3 regimens available:• Low dose long-term continuous antibiotics:

– Eliminate introitoal and enteric reservoir, does not cause resistant– Trimethoprim (100mg) , cephalexin (250mg) ,nitrofurantoin(50mg) QD– Break thru infection txn with course of A/B, then restart prophylaxis– 6-12 months, 95% reduction of recurrence, but 60% reinfected after

stopping the antibiotics• Postcoital antimicrobial prophylaxis

– Ciprofloxacin 125 mg once daily– Nitrofurantoin 50 mg once daily – lower systemic absorption and less

microbial resistance, but avoided in pyelonephritis as tissue level in kidney is low

– Avoid amoxicillin and cephalosporin which change fecal flora• Intermittency self-start therapy:

– Recurrent uncomplicated cystitis– 3-day course regimen of an antimicrobial with MSU beforehand– If failed > send MSU for proper culture– 1 week course if symptom persist or for men

• Trimethoprim: – Eradicate gram –ve aerobic from gut and vaginal fluid (eradicate

source) – Batericidal concentration in urine– Adverse: GI disturbance, mylotoxicity, erythema multiforme,

TEN, photosensitivity– Cautions in renal impairment

• Nitrofurantonin: – No effect on gut flora– High concentration in urine elimination of bacteria– Would not induce bacterial resistance– Adverse: Pulmonary fibrosis , peripheral neruopathy,

agranulocytosis , liver damage• Cefalexin:

– Would not induce resistance– Adverse: GI upset , allergic rxn

• Fluoroguinolones :– Short course eradicate enterobacteria from faecal & vaginal flora– Adverse reaction: tendon rupture in 48 hour (esp with

concomittent use of steriod) , GI , Steven-Johnson syndrome

Mx if bacterial persistent

• Identify potential cause: – KUB (stone)– Renal USG (hydronephrosis, stone)– FR + RU– IVU or CTU– FC (bladder stone, Ca bladder, urethral or

BNS , fistula)

• Txn: treat underlying cause

Acute and chronic Acute and chronic pyelonephritispyelonephritis

Acute pyelonephritis• Inflammation of the kidney and renal pelvis• Presentation:

– Fever, chills rigor– Flank pain and tenderness– Lower UTI symptom– Unilateral or bilateral

• Ddx: cholecystitis, pancreatitis, diverticulitis, apendicitis• Risk factor:

– Female– VUR, Urinary tract obstruction or Neuopathetic bladder– DM, immunocompromised state– Congenital malformation– Pregnancy – Catheter and instrumentation

Acute pyelonephritis

• Pathology: – Patchy infiltration of neutrophil & bacteria in

parenchyma– Inflammatory band extending to cortex– Small cortical abscess (80%)

• Organism: E.coli , enterococci, klebsiella , proteus, pseudomonas

• Investigation: – Bld– KUB– MSU– USG if derange RFT

Radiologic Findings

• Generalized renal enlargement– Overall length of 15cm– 1.5cm greater length on the the affected side

• Focal renal enlargement– Renal mass

• Cortical striations during the nephrogram phase of the urogram (perinephric stranding)

• Dilatation of ureter/pelvis

Treatment

• Not systemically unwell : oral cirprofloxacin 500mg BD for 10 days

• Systemically unwell:– IVF– IV antibiotic (quinolone +/- gentamicin)

• Change to oral antibiotic after afebrile

• Complete antitbiotic for 14 days intotal

Is it necessary to perform upper tract imaging?

• If the patients remain febrile after 72 h of treatment

• Evaluation of the upper urinary tract with ultrasound should be performed to rule out abscess, urinary obstruction

• CTU: pyonephrosis, perinephric abscess , emphysematous pyelonephritis, Stone

• Chronic pyelonephritis – scarred shrunken kidney

What is the antibiotic of choice?

• Augmentin is not recommended as a drug of first choice for empirical oral therapy of acute pyelonephritis. It is recommended when susceptibility testing shows a susceptible Gram-positive organism

• In communities with high rates of fluoroquinolone-resistant and extended-spectrum β-lactamase (ESBL)-producing E. coli, initial empirical therapy with an aminoglycoside or carbapenem has to be considered until susceptibility testing demonstrates that oral drugs can also be used

Chronic Pyelonephritis

• Dx: Radiologic, Pathologic– Radiographically scarred & shrunken

• Often no history of UTI– Bacterial antigens detectable in renal tissue

• Unpredictable association between infection and renal scarring

• Early antimicrobial treatment decreases scarring

Chronic Pyelonephritis

• Associated with reflux nephropathy– Scarring associated with reflux of infected urine– No scarring with reflux of sterile urine

• 55 Adults with reflux nephropathy– UTI diagnostic event in 80%– 20% with enuresis– 50% with elevated serum creatinine– 38% had hypertension– 35% had proteinuria

Chronic Pyelonephritis - Diagnosis

• Often discovered incidentally

• Azotemia, hypertension, fatigue

• UA: WBC, proteinuria

• Decreased ability to concentrate urine

Chronic Pyelonephritis

• IVU– Small, atrophic kidney– Scarring with calyx

clubbing

• VCUG in children

Renal Abscess - Etiology

• Majority are secondary to ascending gram-negative infection– Associated tubular obstruction (due to prior

infection or calculi)

• Skin carbuncles or IVDU may lead to gram-positive abscess formation

• Complicated UTI with associated stasis due to calculi or neurogenic bladder.

Renal Abscess – Clinical Sx / Labs

• Symptom:– Fever , chill , pain – weight loss, malaise

• Lab: Marked leukocytosis

• UA may be normal, unless there is communication between abscess and collecting system

Renal Abscess – Radiologic findings

• CT of early abscess:– Renal enlargement

• CT of late abscess:– Fibrotic wall– Obliteration of

adjacent tissue planes– Ring-enhancing

• U/S shows hypoechoic mass

Renal Abscess - Treatment

< 3 cm: IV ABx & observation- Serial exam with U/S or CT until resolution

3-5 cm: Percutaneously drain

>5 cm: Surgical I&D

Pyonephrosis

Infected hydronephrosis associated with suppurative destruction of the kidney parenchyma & in which there is total or nearly total loss of renal function.

Pyonephrosis - Diagnosis

• F/C/Pain

• Lack of bacteriuria indicates complete ureteral obstruction

• Urographic findings – obstruction

• Infected hydronephrosis always shows good ultrasonic transmission; pyonephrosis shows persistent echoes or a fluid-debris level

Pyonephrosis - Treatment

• Antimicrobial drugs

• Drainage of the infected pelvis (ureteral cath or perc drain)

• Identify & treat source of infection after patient becomes hemodynamically stable

Perinephric Abscess

• Located within Gerota’s fascia• 56% mortality rate

– Delay in Dx (misdiagnosed as acute pyelo)

• Due to hematogenous seeding or from renal extension of ascending UTI– Use of antimicrobial therapy has decreased

the chance of hematogenous seeding from wound and skin infections.

Perinephric Abscess - Diagnosis

• No pathognomonic abnormalities on any radiologic examination.

• Decreased renal mobility is the most specific finding – (Insp/Expir films).

• U/S or CT Scan – Dx &/or Treat

• Treatment: Drainage (surgical vs. perc)

Perinephric Abscess vs. Acute Pyelo

• >5 days of symptoms prior to hospitalization

• Fevers persist beyond 4 days

• <5 days of symptoms prior to hospitalization

• No fevers beyond 4 days after appropriate antibiotics started

SepsisSepsis

What are the definitions of infection?

What is Systemic inflammatory response syndrome (SIRS) ?

• Response to infection (sepsis) or non-infection (burn, pancreatitis)• 2 of the criteria require

What is the pathogenesis of sepsis?

• Endotoxin release by G-ve bacteria• Trigger release of mediators, like cytokine,

activation of kinin system, complement system and fibrinolytic system

• Activation of white cell and macrophages• Widespread microvascular injury, tissue

ischemia & clinical manifestation

Pt is very unwell , what to do?

• ICU

• Consideration of vasopressor, inotropes, steriod

• Radiological investigation to identified source and complication

Emphysematous Emphysematous pyelonephritispyelonephritis

Case• F/40• Good PH• HPI:

– Acute left loin pain– Low grade fever– Vomiting (secondary to paralytic ileus)

• PE: – BP 120/60, p 110, temp 37.8– Abd soft, left loin mild tenderness, no mass,

• KUB: no stone• Urine stix: nitrate+, WBC+, RBC + • Bedside USG: no hydronephrosis/stone• CBC: WCC 14, Hb 12• RFT Cr 100, CaPO4, urate normal

Case

• Imp: Acute pyelonephritis

• IV zinacef

• Progress– Low grade fever and tachycardia– Left loin pain slightly improved– Not septic looking

• DDx?

• Ix?

KUB

CT

EPN causes and pathogenesis

• Acute necrotizing infection of the renal parenchyma and its surrounding tissues by gas forming organism

• Presence of gas in the renal parenchyma, collecting system or perinephric tissue

• Most common: Escherichia coli in 70% and Klebsiella• Others:

– Proteus mirabilis, Group D Steptococcus and CNS– Anaerobic and rare: Clostridium septicum, Candida albicans,

Cryptococcus neoformans and Pneumocystis jiroveci• Bacteriaemia: found in 50% EPN, same species as

urine/pus• Severe, acute pyelo that fails to improve during the initial

3 days of treatment

EPN pathogenesis

• Female: Male = 6:1• Factors

– High glucose level (DM)– Gas-forming microbes– Impaired vascular blood supply– Reduced host immunity– Urinary tract obstruction (stone)

• Mechanism– G-ve facultative anaerobes e.g. E coli produce gas via

fermentation of glucose high levels of nitrogen, oxygen, CO2 and H2 accumulating at inflammatory site gas may extended the inflammatory site to subcapsular, perinephric and pararenal spaces

EPN histopathology

• Abscess formation• Foci of micro and

macro-infarction• Vascular thrombosis• Numerous gas-filled

spaces• Area of necrosis

surrounded by acute and chronic inflammatory cells implying septic infarction

EPN presentation

• Age: 40-50• S/s = pyelonephritis

– dysuria, fever/rigors, nause, vomiting, flank pain

• Impaired consciousness• Septic shock• PE:

– Loin tenderness (most common)

– Crepitus around renal area or scrotum

• NOT respond to pyelonephritis Tx

• Ix:

– Leucocytosis (70-80% reported case)

– Thrombocytopenia (15-20%)

– Acute renal dysfunction

– Acid-base disturbance

– Hyperglycaemia

– Microscopic / gross haematuria

– Severe proteinuria

EPN diagnosis

• Radiological Dx– Gold standard: CT

• CT: more sensitive and define extent of EPN by identifying features of parenchymal destruction

• USG accuracy 69%, KUB 65%

– KUB: abnormal gas shadow in renal bed

EPN classification• Base on CT feature• Wan: used in 2 meta-analysis, prognostic value,

type 1 > 60% mortality, type2 > 20% mortality• Huang and Tseng: for Mx• One classification proposed by Wan et al

– Type I : parenchymal destruction with either an absence of fluid collection or presence of streaky or mottled gas (mortality 60%)

– Type II : renal or perinephric fluid collection with bubbly or located gas or gas in the collecting system (mortality 20%)

EPN prognostic factors

• Falagas et al J Uro 2007

• Poor PF:1. SBP <90

2. Impaired consciousness

3. Increase serum Cr

4. Thrombocytopenia

5. Bil EPN

6. Medical Mx with Abx alone

7. Wan’s Type I (air only, no fluid)

• Factors NOT increased mortality– DM

– Stone

– E. coli

– K. pneumaiae

– Age >50

– Female

– Hx of UTI

– Alcoholism

EPN management

• High index of suspicion in pt fail medical treatment for acute pyelonephritis

• Active resuscitation• Medical Mx (MM)

– O2, IVF, Acid base balance, Abx, good glycaemic control

– Keep SBP >100 with IVF +/- inotropes– Empirical Abx: AG, b-lactamase inhibitor, CS,

quinolones, till c/st a/v– Renal support if ARF– ICU care if multiorgan support need

EPN Management

• Percutaneous drainage PCD + MM– 1st shown in Hudson et al. J Urol 1986– Meta-analysis (Somani BK et al. J Urol 2008):

• PCD + MM as most successful Mx (30-100%) with lowest mortality 13.5%, subsequent nephrectomy mortality 6.6%

– Significant reduction in mortality (nephrectomy mortality 40-50%)– Preserve function of affected kidney in ~70% cases– For pt with localized areas of gas + functioning renal tissue– Multiple catheters for loculated/multiple abscess– Tube can be flushed with Abx solutions

EPN: PCD + MM

• Huang and Tseng classification– Class 1 (gas in collecting system only): PCD + MM– Class 2 (parenchymal gas only): PCD +MM– Class 3 (3A peripheric gas, 3B pararenal gas):

• Depend on risk factors:– diabetes, thrombocytopenia, acute renal failure, altered

level of consciousness, shock• 0-1 risk factor: PCD+MM survival rate 85%• >=2 risk factors: failure 90% nephrectomy

– Class 4 (soliatory kidney/Bil EPN): • PCD + MM

– If failed to respond: Nephrectomy + ICU + renal support

Huang and Tseng classification

Class 1 Pelvicalyceal gas only

Class 2 Parenchymal gas only

Class 3A Perinephric gas

Class 3B Pararenal gas

Class 4 Solitary kidney/Bil EPN

Risk factors:1.DM2.PLT3.ARF4.GCS5.Shock

Xanthogranulomatous Xanthogranulomatous pyelonephritispyelonephritis

Q68

• KUB and CT scan of a patient with vague R flank pain and ballottable mass

• What is the diagnosis? (3)

• Under microscopy, what is a characteristic feature in this condition? (2)

• KUB : multiple renal stones in R kidney

• CT : classic “bear’s paw” appearance, lower cut showing stones inside dilated calyces

• Dx : Right xanthogranulomatous pyelonephritis (3)

• Lipid-laden macrophages (Xanthoma cells) (2)

Xanthogranulomatous Xanthogranulomatous PyelonephritisPyelonephritis

• Chronic renal infection that results in local or diffuse (2 types) renal destruction.

• Almost all cases are unilateral • A nonfunctioning, enlarged kidney associated with

obstructive uropathy secondary to nephrolithiasis• Female in their 5th to 7th decade• 75% have positive urine cultures and 90% have

positive tissue culture• The commonest organisms isolated are Proteus or

E.coli• 83% of patients have associated nephrolithiasis • 50% such stones are of staghorn stones

Xanthogranulomatous PyelonephritisXanthogranulomatous Pyelonephritis

• Presentation: 70% flank pain, 70% fever/chills, 60% flank mass• Histologically

– Accumulation of lipid-laden foamy macrophages (xanthoma cells)

– Inflammatory process begins within the pelvis and calyces & subsequently extends into and destroys renal parenchymal and adjacent tissues.

– Can be confused with RCC even on frozen section• Treatment :

– if malignancy suspected / kidney diffusely destroyed – open nephrectomy

– very stuck and high risk of vessels and visceral injury• Imaging triad (seen in 50-80%) :

– Unilateral renal enlargement– no / poor function– A large calculus in the renal pelvis

• Classic “Bear’s paw sign” on CT

Urinary TBUrinary TB

How to diagnosis urinary TB?How to diagnosis urinary TB?

• Presentation: – Previous TB exposure– Loss of appetite– Fever, night sweat– Loin pain , hematuria and suprapubic pain

• Physical examination: – Temp , LN– Chest , abdomen , genital (bead like cord)

• Bld , EMU, CXR, KUB, USG + RU

• EMU – more concentrated as TB is secreted intermittently

1. Ziehl-Neelsen stain to look for acid fast bacilli1. Bacterial smear is stained with carbol fuchsin for 2 minutes,

then decolorised with HCL and ethanol which then restained with crystal violet view under oil immersion

2. Acid-fast bacilli pink, non acid fast bacilli purple3. Not suitable for gram stain as high lipid content of cell wall

2. Lowenstein-Jensen is an egg based solid culture medium used to identify TB

3. Culture in a liquid medium takes 2-3 days whereas in a solid medium takes 6-8 weeks

4. PCR to amplify the specific DNA by in-vitro enzymatic replication

• Pathogensis – caseating granuloma (Langhan’s giant cells surrounded by lymphocytes and fibroblast) fibrosis + calcification autonephrectomy

• TB epididymis is likely from hematogenous spread as it is usually isolated finding

How to diagnosis urinary TB?How to diagnosis urinary TB?• Tuberculin: purified protein deverivative to prove TB status.

– Positive confirmed exposure to TB– Negative exclude the diagnosis

• CXR: lung primary focus in 50% of cases with urogenital TB• KUB shows calcification in 50% of cases• CT or IVU is abnormal in 60-90% of cases

1. Small shrunken kidneys (autonephrectomy)2. Infundibular stricture (pathognomonic)3. Calyceal distortion + calcification4. Papillary necorisis5. Multiple ureteric stricture : commonly at lower third of ureter 6. Distortion of ureteric orifice – VUR (Golf-Hole app)7. Contracted calcified bladder: Bullous edema , ulcearation and

hemorrhage (Thimble bladder) 8. Calcified vas (beaded), seminal vesicle or prostate

What is the treatment of TB?

• Isoniazid, rifampicin, ethambutol and pyrazinamide for 2 months

• Isoniazid and rifampicin for 4 months• Steroid for ureteric stricture that do not respond

to anti-TB drugs

• Cycloserine is used to inhibit the growth of BCG sepsis within 24 hours– But if will lower seizure threshoid

What is the complication of the drugs?

ProstatitisProstatitis

Acute bacterial prostatitis• Infection of the prostate asso with LUT infection & generalized

sepsis• Risk factor:

– UTI– Acute epididymitis– Catheter , post TURP– Intraprostatic ductal relfux– Phimosis– Prostate stone

• Presentation: – Systemic illness– Preineal and SP pain– Irritative LUTS– AROU– Prostate is exteremely tender

• Investigation: – Bld + c/st– MSU

• Txn: – Antibiotic: Cirpo 500mg BD for 2-4 week– Pain relief– Catheter– Prostate abscess: dx by TRUS or CT– Drainage: percutaneous or TUR

Men present with recurrent UTI• History:

– Associate LUTS– Stone disease– Diverticulum +/- fistula: pneumaturia, recurrent diarrhoea ,

rectal bleeding , fecaluria– Chronic prostatitis : Dysuria, hematuria, Perineal/suprapubic

discomfort, Ejaculatory problems• PE:

– Abd + kidney– Suprapubic region– External genitalia and prostate

• Investigation: – MSU– KUB– USG – FR + RU– Specific test : Stemey + NIH-CPSI

UTI in men

• Men should receive, as minimum therapy, a 7-day antibiotic regimen

• Minimum treatment duration of 2 weeks is recommended, preferably with a fluoroquinolone if prostatic involvement

• Prophylactic antibiotics reduce the risk of bacteriuria and septicemia by 70% and 80% respectively after TURP– Berry: Prophylactic antibiotics in TURP J Urol

2002

Prostatitis• Definition: Infection or inflammation of prostate• Chronic prostatitis:

– Clinical syndrome characterize by pain in perineum, pelvis, suprapubic area or external genitalia

– Variable degree of voiding or ejaculatory disturbance• Dx of exclusion : to rule out BPH , stricture, UTI• Pathophysiology poorly understood:

1. Infection2. Chemical irritation3. Dysfunctional high-pressure voiding4. Intraductal reflux5. Altered immunity

– Proposed inflammatory process cause tissue edema & intraprostatic pressure local hypoxia mediator induced tissue damage altered neurotransmission in sensory nerve pain and other symptom

What is the definition of What is the definition of prostatitis?prostatitis?

>10 WBC /HPF

Prostadynia – pain without positive culture or inflammatory component

What is stamey test?What is stamey test?

Meares and Stamey

• Drink 400ml of water 30min before the test• 4 sterile specimen container: VB1, VB2, EPS, VB3• Expose glans penis and retract foreskin • Cleanse the glans with soap• 1st 10-15ml urine: VB1• Pass next 100-200ml into toliet• 2nd 10-15ml urine: VB2• Patient bend forward & hold container marked EPS near

urethral meatus• Massage prostate until few drops of prostatic secretion

are collected : EPS• Void and collect the 10-15ml urine: VB3

Interpretation of Stamey test

• +ve VB1: Urethritis• +ve VB2: Cystitis• Chronic prostatitis

– II: +ve c/st in EPS & VB3– IIIa: -ve c/st in EPS & VB3, +ve WBC– IIIb : -ve c/st in EPS & VB3 , -ve WBC

• Modification of Stamey test: – Pre & post-message test (PPMT) [Nickel]– +ve post-message c/st chronic prostatitis

Prostatitis Prostatitis • NIH – CPSI (National Institutes of Health- Chronic Prostatitis

Sympotm Index) – Measure the severity of chronic prostatitis– 9 item questionnaire with 3 main domains (pain, urinary symptoms and

QOL)– Pain (location, frequency , severity) – Voiding (obstructive and irritative) – QOL – For assess need of treatment and monitor response

• MTOPS study suggests that prostatitis may be a predictor of BPH progression

• Nickel and coworker report a 2% incidence of bladder CIS in patients with clinical prostatitis and they therefore recommend urine cytology when investigating men with suspected prostatitis

Management

• According to predominant symptom & QOL• Discuss about benign nature of the condition• Lock of evidence in favour of any treatment• Goal should be symptom control rather than

eradication• Conner stone:

– Antibiotic– Anti-inflammatory– Alpha-blockers

Chronic bacterial prostatitis RxChronic bacterial prostatitis Rx• NSAID/Antibiotics at least 6 weeks - empirical treatment

suggested by European consensus group• E Coli positive in prostate massage in asymptomatic patient

should be treated• Quinolone and tetracycline – good penetration• Moxifoxacin – good in G+ve• Macrolide – good for chlamydia• Tetracyclin for sub-clinical infection : Chlamydia & ureaplasma • Nitrofurantoin and penicillin – poor penetration

• Add alpha blocker for 3m if no response by 6week• Finasteride can cause a 50% improvement in the symptoms

of about 50% of patients with type 3 prostititis• Muscle relaxant – diazepam or baclofen• Tricyclic antidepressant: Amitriptyline • Prostatic message if not responsive

– Expression of prostatic secretion, relief of pelvic muscle spasm, physical disruption of protective biofilm and improve circulation

– Some symptomatic relief in ~1/4 to 1/3 patients

Epididymitis & Orchitis

Scrotal pain and fever• Ddx: Trauma , testicular torsion , epididymo-orchitis• History

– Trauma– < 35 yo STD: Chlamydial or gonococcal– In old: UTI cause by E coli– UTI : dysuria, frequency , urgency , SP pain – Systemic illness– Long term use of amiodarone (chemical epididymitis)

• P/E:– Cannot diff from torsion– Scrotal pain radiate to groin– Erythema or scrotal skin– Thickening of spermatic cord, reactive hydrocele– Urethral discharge– Elevation of scrotum relieved pain in epididymo-orchitis (Prehn’s

sign)

• Investigation: – MSU– Gram staining and C/st of urethral swab (Gram –ve intracellular

diplococci)– Chlamydia: detect DNA by PCR on first void urine– Basic blood test

• Treatment: – Bed rest, scrotal suppor– Analgesic– Antibiotic: Cipro 500mg BD (cover gonococccal) + Doxycycline

100mg BD (cover Chlamydia) x 2 weeks– If allergic to doxycycline azithromycin 1g x1– If elderly likely E coli : Ciprofloxacin only– Order USG if not resolved (abscess)– FR + RU exclude underlying LUTS

• Complication: – Abscess, infarction , chronic pain , infertility

• Mumps orchitis: 30% post-pubertal male, 3 day after parotitis, 30% bilateral , result in testicular atrophy and infertility

BiofilmBiofilm

What is the biofilm?What is the biofilm?

• Complex aggregation of organisms on solid substrate, protected by extracellular mucopolysaccharide matrix in an aqueous environment

• Or , structured community of micro-organisms and their extracellular products form on the surface of any biomaterial

UTI in pregnancyUTI in pregnancy

Anatomic & Physiologic Changes

• 1cm increase in renal length

• Smooth muscle atony of collecting system– Progesterone & Uterus size

• Bladder displaced superior & anterior

• 30-50% increase in GFR– Evaluate renal Fx if Cr >0.8 or BUN >13– Normal to have proteinuria up to 300mg/24

hours

UTI

• Incidence of male UTI - 1%• Incidence of female UTI – 5%• Incidence of female UTI after

menopause – 20%• High fluid intake/voiding every 4 hrs/

post-coital voiding/perineal hygiene• -ve urine c/st to confirm eradication of

bacteria

Asymptomatic Bacteriauria

• All women should be screen at week16• Definition:

– Asymptomatic + 10 5 (CFU) of a single pathogen / ml of urine 

– But 102 CFU can also be counted as significant

• Asymptomatic bacteriuria in pregnancy – ~5%• Risk of acute pyelonephritis: in 3rd trimester

– 1-4% in all pregnant women– 20-40% in untreated bacteriuria

• Treatment is necessary 1% if treated

• 3-day course of therapy• Reculture urine 1-2 days after treatment• Use parenteral agents to treat acute pyelonephritis

AntibioticsSafe: • Penicillin: OK • Cephalosporin: OK• Marcolide - Erythromycin (bacteriostatic): OK

Use with cautions: • Nitrofurantoin: avoid in third trimester

– Fetal hemolytic anemia in G6PD deficiency mother– hepatotoxicity, lung toxicity, inadequate urine concentration if GFR<60

• Aminoglycoside (bacteriostatic): CI in 2nd and 3rd trimesters– can cross placental barrier: fetal ototoxicity & nephrotoxicity– Used only for short periods for severe acute pyelonephritis threatening

materal-fetal prognosis

• Sulphonamide : contraindicated in third trimester– Risk of neual tube defect in 1st trimester due to anti-folate mechanism– Risk of fetal anemia in G6PD def mother

• Triamethoprim : contraindicated in first trimester

Contraindicated: • Fluoroquinolone (bacteriostatic):

contraindicated as toxicity to fetal cartilage and joints, tendon damage

• Chloramphenicol: contraindicated in third trimester as “grey-baby” syndrome

• Tetracycline (bacteriostatic): contraindicated as hepatotoxicity, deposit in teeth and bone

• Recurrent UTI in pregnancy – cephalexin 125mg daily

Acute pyelonephritis

• USG findings: focal or diffuse hyperechogenicity, thickening of renal pelvis and ureteral dilation

• Higher risk if asymptomatic bacteriuria / VUR (correction of VUR cannot prevent UTI during pregnandy) / history of renal scarring

• Complications associated with bacteria during pregnancy– Prematurity, low birth weight, prenatal mortality– Maternal anemia

• Hospitalization and parental antibiotics

Pregnancy and VUR

• Higher chance of pyelonephritis if previous VUR or history of renal scarring

• History of renal scarring– Higher chance of HT (3.3 fold)– Pre-eclampsia (7.6 fold)– Obstetric intervention

• Higher chance of pre-eclampsia if bilateral scarring or impaired creatinine level

• Despite previous reimplantation in childhood, still higher risk of UTI, but not miscarrage

(Spontaneous renal rupture)

• No cause vs upper tract obstruction vs tumour like AML

• Lumbar or abdominal pain / shock

• US : retroperitoneal hematoma

• JJ / PCN if obstruction

• Unstable hemodynamically: nephrectomy

Before having babies…

• Consider stone treatment before pregnancy

• Consider AML treatment

Gentamicin Gentamicin

How to use gentamicin?• Bactericidal – inhibit ribosomal protein synthesis• 3-7mg/Kg• Check level after the 3rd dose• <1mg/l give the same dose• 1-2mg/l reduce the dose by 25% and check the level before

next dose• 2mg/l omit one dose and check the level• Bad with Frusemide (increase nehrotoxicity)• Good for pseudomonas, enterococcus and staphylococcus• Daily dose is usually used • Can be used in patient with renal impairment with dose modification• Ototoxicity cause more commonly vestibular damage than

deafness, 2/3 patients present as tinnitus• Nephrotoxicity and impaired neuromuscular transmission

UTI in renal UTI in renal impairmentimpairment

What is the antibiotic in renal impairment?

Catheter related UTICatheter related UTI

• Up to 25% of hospitalized patients undergo urinary catheterization.• indwelling urinary catheters are a leading cause of nosocomial

infection and have been associated with both morbidity and mortality.

• Up to 30% of catheterized patients can have genitourinary or systemic symptoms related to catheter-associated UTI (CAUTI)

• Up to 4% may develop catheter-related bacteraemia• Once the catheter has been removed some patients with

asymptomatic CAUTI continue to have bacteriuria or become symptomatic

• To prevent or reduce this type of catheter-related morbidity, many clinicians have a policy of administering a short course of prophylactic antibiotics on catheter withdrawal for all or selected groups of patients.

• Currently, the most appropriate agents for the empirical management of CAUTIs seem to be co-amoxiclav, ciprofloxacin and nitrofurantoin.

What is the recommendation of catheter insertion and choice of

catheter?

How to prevent catheter related UTI?

What is the treatment of catheter related UTI?

Patient with dysuria, KUB

SPINAL CORD INJURY & UTI

Spinal cord injury patients

• 33% have bacteriuria• UTI is the most common urologic complication &

the most common cause of fever in these patients

• Risk factors:– Bladder overdistention– Elevated intravesical pressure– VUR– Impaired voiding– Instrumentation

Clinical presentation & Bacteriology

• Majority are asymptomatic

• Symptoms:– Abdominal discomfort– Urinary leakage– Lethargy / Malaise– Cloudy, malodorous urine

• E. coli isolated in only ~20%

• Enterococci, P. mirabilis, Pseudomonas

Management

• SP cath delay onset of bacteriuria, when compared with indwelling urethral cath

• CIC allows for lowest risk of complications

• Urine culture prior to therapy

• Oral fluoroquinolone is 1st line

Emphysematous cystitis

• Necklace appearance of gas beads in bladder wall diagnostic of emphysematous cystitis

• due to infection by gas forming organisms (commonest E Coli) in an immunocompromised patient (usually DM)

Emphysematous Cystitis

EC• DDx:

– Instrumentation– Fistula to hollow viscus– Tissue infarct with necrosis– Infection

• EC more common in– Middle aged diabetic women

(M: F = 1:6)• Predisposing factors

– DM (66%), Chronic UTI, indwelling urethral catheter, urinary stasis due to BOO, neurogenic bladder

• Various s/s– Asymptomatic, pneumaturia,

irritative voiding, acute abdomen to severe sepsis

• Pathogens:– E. coli (58%)– Others: K. pneumoniae, P.

aeruginosa, Proteus mirabilis, Candida albicans and C. tropicalis, Aspergillus fumigatus, Staphylococcus aureus, Group D Streptococcus, Enterococcus faecalis, Enterobacter aerogenes and Clostridium perfringens and Cl. welchii.

• Pathogenesis: – like EPN,– non-diabietic: urinary albumin as

substrate

EC

• Radiological Dx– KUB: curvilinear area of

radiolucency delineating the bladder wall with or without intraluminal air

– CT: more sensitive, define extent and severity, differentiate vesicoenteric fistula, intraabdominal abscess, adjacent neoplastic disease, EPN

• Histopathology– Gross:

• Bladder wall thickening with vesicles of varying size

– Microscopic: • multiple gas-filled

vesicles predominantly within the bladder mucosa, lined by flattened fibrocytes and multinucleated giant cells

EC management

• MM:– Abx, bladder drainage, DM control, correct

underlying comorbidities

• If fail to respond/severe necrotizing infection (10%)– Consider partial cystectomy, cystectomy or

surgical debridement– EC alone Mortality 7%– EC + EPN Mortality 14%

Endotoxin Endotoxin

What is endotoxin?What is endotoxin?

• Lipopolysaccharide complex related to the outer membrane of gram negative bacteria

• Gram negative sepsis• Their lipid component is the toxic one (Lipid A)

and the polysaccharide element is the immunogenic one (O-antigen)

• Endotoxins are heat stable to boiling point

Papillary necrosisPapillary necrosis

What is papillary necrosis?What is papillary necrosis?

• Possible causes of papillary necrosis is POSTCARD

• Pyelonephritis, Obstruction. Sickle cell, Tuberculosis, Cirrhosis, Analgesic, Renal vein thrombosis, Diabetes

HIV in urology

Viral disease of the genital tract

Painful ulcer Diagnosis? (1) Chancroid Causative agent? (1) Haemophilus ducreyi

Q3

ChancroidChancroid

• Presentation: painful nonindurated ulcer + tender unilateral inguinal adenopathy

• Characteristic suppurative inguinal adenopathy • Haemophilus ducreyi :

– fastidious (difficult to culture)– short, fine, gram-negative streptobacilli – FDA approved: PCR assays

• Treatment: – Ciprofloxacin, (500 mg orally BD for 3 days) – Erythromycin , (500 mg orally TID for 7 days)– Azithromycin, (1 g as a single oral dose )– Ceftriaxone, (250 mg as a single intramuscular dose )– Tetracycline

Male 30 with painless ulcer over coronal sulcus

Genital

• What is the diagnosis?– Chancre, ulcer typically painless, indurated and with

raised border. Regional lymphadenopathy appear in one week.

• What is the causative agent?– Treponema pallidum (spirochetes), confirmed by dark

field examination

• What is the treatment?– Penicillin – good prognosis if treated. If not treated >

neurosyphillis/dementia/gumma

Male 25 with lesion over glans. Biopsy done.

Genital

• What is the diagnosis?– Condyloma acuminatum

• What is the causative agent?– Human papillomavirus types 6,11. – Dysplastic types are caused by type 16, 18.

(premalignant)

• What is the treatment?– Podophyllin, cautery after biopsy or surgical excision

or CO2 laser

Condyloma acuminatum of scrotum

25 year old man with ulcer over glans.

Genital

• What is the diagnosis?– Granuloma inguinale - Irregular painful ulcer with

purulent base. No inguinal lymphadenopathy, but subcutaneous granulomatous process

– Dx: identification of “Donovan Body” on stained smear

• What is the cause?– Calymmatobacterium granulomatis

• What is the treatment?– Tetracycline/ampicillin , septrin or erythromycin

25 year old man with painful lesions over penile skin

Genital

• What is the diagnosis?– Genital herpes.

• What is the cause?– Usually herpes simplex virus type 2 infection

• What is the treatment?– Acyclovir, long term suppression may be

required if recurrence. Prevent transmission with barrier contraception

Male 25, itchy lesion over penile skin. Biopsy done

Genital• What is the diagnosis?

– Molluscum contagiosum – small papules, may express cheesy-like material

• What are the diagnostic features on histology exam?– Molluscum bodies in cells (Basophilic inclusion filled

with the virus) in biopsy• What is the cause?

– Viral infection by poxvirus, transmitted by sexual contact

• What is the treatment?– Self limited. Healed without scars. Podophyllin or

cauterisation

Schistosomiasis

Schitosomiasis (Biharzia)

• Cause: trematode called Schitosoma haematobium

• Endemic : Africa , Egypt, middle east• Pathology :

– Fresh water snails release infective form of the parasite (cercariae)

– Penetrate skin and migrate to live (schitosomules) where they mature

– Adult form migrate to vesical vein – Lay egg (containing miracidian larvae) leave body

by pentrating the bladder and enter urine

• 2 phase: – Active: where adult worm laying eggs– Inactive: when adult die and reaction to remaining egg

• Clinical presentation: 1. “Swimmer’s itch” : local inflammation by cercarial penetration

(24hr)2. Katayama fever (acute schistosomiasis):

• Egg lying : induce fever, urticaria, LN, Hepatosplenomegaly

3. Acute inflammation phase: egg penetrate & excreted in urine : hematuria, frequency and terminal dysuria

4. Chronic active phase: • Low egg laying• Nephritic syndrome by deposition of IG complex in glomeruli

5. Chronic inactive phase: no viable egg• Symptom of obstructive uropathy

Diagnosis + MxDiagnosis + MxDiagnosis: 1. Midday urine: continue egg2. Bladder and rectal biopsy : identify egg3. Serology test: ELISA4. Cystoscopy: identifies egg in trigone (Sandy Patches)5. CT or IVU: calcified , contracted bladder with obstrucitve uropathy6. USS: hydronephrosis and thicken bladder wallTreatment is pharmacological with praziquental• 20 mg/kg in 2 divided does 4-6 hours apart on the same day• Single dose of praziquental may be effective• Praziquental is effective against all species of schistosoma and all

stages of the disease. It will cure 85-100% of cases. When it fails to cure the disease a second course of praziquental could be tried

• Complications - Bladder contracture, ureteric obstruction, squamous cell ca bladder

These are the eggs of 3 species of Schistosoma Which of the above species is related to bladder cancer?

(1) In what form does this species infect human in water? (1)

A B C

• A : Schistosoma japonicum• B : Schistosoma haematobium• C : Schistosoma mansoni

• B (1)• Cercariae (1)

– The flatworm cercaria is found in river water and will penetrate unbroken human skin, typically through the web between toes, to enter the peripheral systemic vein

– The eggs will penetrate through the bladder wall and will be found in the urine

Urinary schistosomiasisUrinary schistosomiasis

• Urinary schistosomiasis is most commonly caused by schistosoma hematobium. This is endemic in Africa and middle east. It produces the characteristic end spined eggs but this is not the only species with end spined eggs

• Schistosoma japonicum is endemic in the far east

• Schistosoma Mansoni in Latin America

What is the diagnosis? (1) What is the acute phase of this disease called? (2)

• Characteristic egg-shell calcification outlining urinary bladder

• Dx : Schistosomiasis (1), DDX: TB

• Katayama fever (2)– Coincides with egg laying – Active phase is characterized by urinary symptoms such as

hematuria and terminal dysuria. Cystoscopically there may be inflammatory polypoid lesions in the bladder and eggs in the urine

– The chronic inactive phase,although asymptomatic, will slowly progress into obstructive uropathy and may be complicated by bladder cancer

Hydatid diseaseHydatid disease

Hydatid diseaseHydatid disease• Also known as echinococcus, is a tapeworm parasite infection• The intermediate host is the sheep and the final host is the dog. • Kidneys can be affected in about 5% of cases• The disease is bilateral in 6% of cases • In the kidney the upper and lower poles of the kidneys are more

commonly affected (80%) than the midpole of the kidney• The renal cysts are not symptomatic until late in the disease• Common symptoms are flank pain (80%) and flank mass (40-75%)• USG and CT scans show thick wall multiloculated cysts• KUB shows calcifications in 30% of cases• Bld: peripheral eosinophilia & +ve hydatid complement fixation test

• Medical: Albendazole • The mainstay of treatment is surgical excision of he cysts with 1st

sterilized with formalin or alcohol

• Diagnosis ? (1)• Is this premalignant? (1)

Q11

• Angiokeratoma of Fordyce (1)

• No malignant potential (1)

Angiokeratoma of Fordyce

• Vascular ectasias of dermal blood vessels • Visible on the penis and scrotum of adult men• 1- to 2-mm red or purple papules with associated generalized

scrotal redness • Benign condition without systemic manifestations• Rare cause of troublesome scrotal bleeding Can be seen in

patients with Fabry's disease : rare glycogen storage deficiency

• Treatment : – Usually unnecessary – Success achieved using YAG, KTP/ argon laser photocoagulation

in select cases

Physical findings of a sexually inactive 20-yr-old male Diagnosis ? (2) Is it associated with HPV infection? (1)

• Pearly penile papules (PPP) (2)

• No relationship with HPV. Benign lesion (1)

PPP

• White, dome-shaped, closely spaced small papules at glans penis

• Arranged circumferentially at corona• Histology : angiofibromas similar to lesion TS• 14-48% of young adults (uncircumcised)• NO association with HPV infection/ cervical CIN• Mx: Reassurance• Local destruction: CO2 laser, cryotherapy

These ulcers in a sexually-inactive 20-yr-old man are painful and recurrent.

Diagnosis ? (3)

Q29

• Pictures showing multiple scrotal, perianal ulcers as well as oral aphthous ulcers

• Behçet’s disease (3)

Behçet’s disease

• Classified as a form of vasculitis• Initially found along Silk Road, now found everywhere in the world• No gender difference in epidemiology, mean age of onset ~30yrs• Clinical manifestation:

– Mucous membrane manifestation• Oral aphthosis (nearly in every patient)• Genital aphthosis (60-100% of patients) : Scrotal and vulval ulceration,

sometimes on shafts of penis– Skin manifestation

• Skin aphthosis / pustulosis • Pathergy phenomenon (skin hypersensitivity to trauma, considered a

diagnostic test)– Ocular manifestation

• Anterior and posterior uveitis, retinal vasculitis– Arthritis, Meningoencephalitis, Vascular involvement (DVT), gastrointestinal

aphthosis• Diagnostic criteria: International Criteria for Behçet’s disease (ICBD)• Genetic background: HLA-B51 may be associated• Treatment: Colchicine 1mg daily is 1st line

This is the result of a chronic infective process Name three possible micro-organisms responsible. (3) Name one vector of transmission of the above micro-

organisms (1)

Q30

• Picture showing penoscrotal elephantiasis

1. Wucheraria Bancrofti (1)2. Brugia Malayi (1)3. Onchocerca volvulus (1)

4. Vectors • (W. bancrofit, B. malayi) Mosquito eg. Culex spp• (O. volvulus) Black fly of Simulium spp

• Dx: Thick film , serology or biopsy• Presentation:

– Funiculoepididymitits, orchititis– Hydrocele– Scroal and penile elephantitis

• Treatment: – Medical: Diethylcarbamazine– Surgerical excision of fibrotic & edematous tissue

This is an STD What is the diagnosis? (1) What is the causative organism? (1) Name two other diseases this organism is

responsible for (0.5 each)

Q47

• Lymphogranuloma venereum (LGV) (1)

• Chlamydia trachomatis (serotype L1, L2, L3) (1)

1. Trachoma (serotype A, B, Ba, C) (0.5)

2. Non-gonococcal urethritis (serotype D to K) (0.5)

Lymphogranuloma VenereumLymphogranuloma Venereum

• STD caused by Chlamydia trachomatis types L1, L2 & L3• Transient painless ulcer on the penis, anus or vulvovaginal area that

goes unnoticed painful unilateral suppurative inguinal adenopathy and constitutional symptoms that occur 2-6wks after resolution of the ulcer

• Groove sign: large inguinal and femoral LN separated by inguinal ligament. Secondary LN lesions in lymphogranuloma venereum

• Mainly clinical diagnosis• Culture positive <50% cases• Can be diagnosed using antibody titre• Tx: Doxycycline 100mg BD or erythromycin 500mg QID for three weeks

at least

Photo

• This elderly woman complained of severe symptoms of cystitis of sudden onset.

Q

• A. What abnormality is shown?– herpes zoster (1/2)

• B. What are the typical cystoscopic appearances?– hemitrigonal vesicles (1/2)

Q. CT

• These are CT and ultrasound scans of a 74 year old man with urinary retention and fever of 38.6

Q

• A. What is the diagnosis?– prostatic abscess (1)

• B. How should his retention be managed?– suprapubic catheterisation and drainage of

abscess (1)

Antibiotic prophylaxis in urology

• Brief course of antibiotic administer before or at the start of an intervention

• To minimize the infectious complications of the procedure

• Possible side effect & microbial resistance patterns are potential risk

• Yes with high level of evidence: – TURP (decrease bacteriuria & infectious complication) – Prostate biopsy (reduce bacteriuria but no conclusive evidence

on reducing symptomatic UTI or other infectious complication)

• Yes with moderate to low evidence: – Cystoscopy (not require in the absence of risk factor) – Therapeutic URS– Open /lap uro intervention (clean-contaminated & contaminated)

• Not required in: – Urodynamic study (except with increase risk e.g neurogenic

bladder, transplant patient, immunocompromised , VUR) – TURBT– ESWL (in uncomplicated case & pre-op –ve c/st)– URS (diagnostic)– PCNL (when pre-op –ve c/st)– Open /lap uro intervention (clear surgery)