Lecture 2

Urinary Tract Infection

Name of Prof

GENITO-URINARY INFECTIONS
These include infections caused by different pathogens and microbial agents. The latter include:
1- Bacteria that underlie:
- Non-specific infection: Such bacteria include (bacilli & cocci), (gram -ve & gram +ve) and
(aerobes & anaerobes).
These bacteria can be grown on ordinary culture media within 2 – 3 days. They cause non-specific
infection since with such type of infection symptoms, signs, pathologic effects and treatment are
similar, in common and not peculiar to the causative agent.
The most common of these bacteria are:

* Bacilli (mainly gram negative): E. coli is the most common pathogen and represents > 80% of
all UTI. Others include klebsiella and proteus and pseudomonas aeruginosa.
* Cocci: e.g. streptococci and staphylococci (gram positive) and gonococci (gram negative).

- Specific infection: Here, the symptoms, signs, pathologic effects and treatment are peculiar to
that infection. A good example of this type of infection is tuberculosis (acid-fast bacilli). Culture
of such organism requires several weeks on specific culture media and the micro-organism does
not respond to ordinary antibiotics, rather requires specific agents and again for several weeks.
2- Non- bacterial agents e.g.:
• Chlamydia trachomatis & Ureaplasma urealyticum that cause urethritis
• Fungi e.g. candida albicans
• Viruses e.g. mumps virus that causes mumps orchitis
• Parasites e.g. schistosoma hematobium and trichomonas vaginalis

Non-specific Genito-Urinary infections

Definitions:
 Urinary tract infection (UTI) is an inflammatory response of the urinary tract to
microbial invasion.
It may be complicated or uncomplicated UTI.
 o Uncomplicated (simple) UTI is infection that occurs in a patient with a
structurally and functionally normal urinary tract. It responds quickly to a short
courseof antibiotics.

o Complicated UTI
 Is one occurring in the presence of an underlying anatomical or functional abnormality
(e.g. incomplete bladder emptying due to BPH).
 It takes longer time to respond to antibiotic treatment with increased risk of recurrence.

 Bacteriuria is the presence of bacteria in urine, either asymptomatic or symptomatic.

 Pyuria is the presence of white blood cells (pus cells) in urine (detected by dipstick
test) or more than 10 WBCs / HPF in sediment of centrifuged urine.
- Pyuria is mainly caused by bacterial infection.
- Bacteriuria without pyuria indicates the presence of bacterial colonization of
the urine, rather than the presence of active infection.
- Pyuria without bacteriuria (sterile pyuria) may occur with urinary stones,
carcinoma in situ of the bladder and urinary TB infection.

Routes of entry:
1. Ascending: it is the most common route for UTI e.g. renal infection due to
reflux of infected urine.
2. Other routes include: hematogenous (from a septic focus), lymphatic and
direct spread (from neighboring organs).

Natural defense mechanisms against UTI include:

- complete periodic emptying of the urinary bladder.
-Antegrade ureteral peristalsis
- non refluxing vesico-ureteral junction
- acidic pH of urine.

Risk factors for UTI:

1. Urinary tract obstruction (urinary stasis) e.g. by stones, strictures, BPH.
2. Foreign bodies e.g. indwelling catheters, urinary stents and stones.
3. Vesico-ureteral reflux.
4. Urinary diversion e.g. ureterosigmoidostomy
5. Neuropathic bladder.
6. Gender: Females are more liable essentially due to short straight urethra.
7. Systemic factors e.g. DM, renal failure and immuno-suppression.
8. Organism factors including its virulence and number.

The diagnosis of UTI is based on symptomatology, urinalysis, and urine culture findings.
Urine culture is the gold standard for the diagnosis of bacterial UTI.
Treatment is usually indicated if >105 colony forming unit/mL in a patient with symptomatic
UTI, particularly with associated pyuriua
High grade fever, recurrent UTI, pregnancy and systemically ill patients are some
indications that require further investigations e.g. total leukocytic count (leukocytosis),
abdominal U/S, KUB film, abdominal CT, assessment of post void residual urine, voiding
cystourethrography and urodynamic studies

1) 1) Acute pyelonephritis
It is a clinically diagnosed disease due to acute inflammation and infection process of
the pelvicalyceal system and renal parenchyma.

Clinical diagnosis:
1. High grade fever with acute onset and associated with rigors.
2. Severe flank pain and tenderness.
3. Other symptoms as malaise, vomiting, irritative LUTS and turbid urine.

Investigations:
1. Abdominal U/S: mostly within normal but it may show mildly enlarged edematous
kidney and renal stones.
2. Urine analysis shows microscopic pyuria and bacteriuria.
1. Urine culture & sensitivity specifies the infecting organism and the appropriate antimicrobial
therapy. However its result takes 3-5 days.

Complications:
 Septicemia up to septic shock
 Chronic pyelonephritis.
 renal or perinephric abscess.

Treatment:
a. Drug treatment: prompt treatment is essential to prevent complications.
1. Antimicrobials: empiric broad spectrum parenteral antibiotic therapy (e.g. ceftriaxone) is
started until the result of culture and sensitivity tests is obtained. Oral antimicrobials are used
and continued thereafter.
2. Symptomatic treatment e.g. anti-pyretics, analgesics and anti-emetics.
3. Intra-venous fluids: if there is vomiting or hypotension.
b. Hospitalization is indicated in pregnancy, solitary kidney and immune-compromised patients.
Obstructive pyelonephritis requires ureteric stenting.
2) 2) Chronic pyelonephritis
It is a radiologic and pathologic disease due to chronic corticomedullary inflammation and
scarring (fibrosis) of the kidney.
1. The presentation may be asymptomatic, mild renal pain or by complication(s).
2. Abdominal U/S shows smaller sized kidney, irregular outline, increased echogenicity
and irregular calyceal dilatation with non-dilated pelvis.
3. Urine analysis may show proteinuria, pyuria and bacteriuria.

Complications:
1. Renal hypertension.
2. Renal stones. Sonographic appearance of
3. Renal function loss that may lead to chronic renal failure if chronic pyelonephritis

bilateral or in a solitary kidney.

Treatment:
• Pathogen specific antibiotic.
• Chronic suppressive therapy (long term use of a low-dose regimen of antimicrobials).
• Nephrectomy may be carried out for unilateral poorly functioning kidney complicated
by hypertension, persistent renal pain or persistent pyuria.

3) 3) PYONEPHROSIS:
It may result from chronic kidney infection (which was not promptly treated) with
concomitant obstruction of the infected kidney:
- The kidney is enlarged and tender but less than the case of infected hydronphrosis.
- Fever is also lower and not of high grade.
- Infection may extend to the perinephric fat and result in perinephric abscess.
- The renal tissue is destroyed leading to loss of renal function and ultimately, it may
indicate nephrectomy.
- If bilateral, it leads to chronic renal impairment and failur

4) 4) Renal & peri-nephric abscessv

5)
Etiology: The organism that underlies such condition may come from:
• Urinary tract (gram negative bacilli) in most cases.
• Blood (staphylococcus organism) from a distant site.

Clinical picture:
• Fever (high grade) and rigors.
• Throbbing renal pain and severe renal tenderness with reflex rigidity.
• Peri-nephric abscess may be additionally associated with:
 - Bulging of the renal angle when it extends posteriorly.
- Reflex muscle spasm leading to scoliosis (concavity toward the affected side)
and flexion of the ipsilateral thigh (psoas spasm).

Investigations:
• Abdominal U/S shows the collected pus, its amount and condition of the kidney(s). It
is beneficial to follow up and evaluate the response of medical treatment.
• KUB may show scoliosis, renal stone(s) and ipsilateral pleural effusion.
• CT. scan is indicated if medical treatment fails.
• Laboratory investigations include:
urine analysis (pyuria, bacteriuria) and blood count (leukocytosis). Culture of urine,
blood and drained pus reveals the causative organism and its antimicrobial
susceptibility.

Treatment:
1. Hospitalization.
2. Medical treatment by broad spectrum IV antibiotics, IV fluids together with
symptomatic treatment e.g. anti-pyretics and analgesics.
3. Follow up for fever, pain and abscess size.
4. Drainage is indicated in large abscesses or after failure of medical treatment.

6) 5) Cystitis
 Acute bacterial cystitis is due to ascending infection especially in women (e.g. honey-
moon cystitis) and girls.
 Symptoms: irritative LUTS (frequent voiding of small volumes, dysuria & urgency)
and suprapubic pain. Gross hematuria and fever are infrequent.
 Signs are non specific.
 Investigations
- Urinalysis: pyuria and bacteriuria ± microscopic hematuria.
- Additional imaging (e.g. abdominal U/S) and urine culture are indicated in febrile patients,
when symptoms persist or renal pain co-exits.
 Treatment:
unless complicated, trimethoprim-sulphamethoxasole or quinolones for 3-5 days is sufficient.
 Cystitis persists in the presence of bladder outlet obstruction, neuropathic bladder, bladder stone,
bladder diverticulum or infection with(atypical or specific microorganism).

7) 6) Urethritis
 It is mainly a sexually transmitted disease.
 It is either acute or chronic & gonococcal or non-gonococcal. The causative organism is
 revealed by examination of the urethral discharge. If the discharge is scanty, use a
urethral swap.
 The presentation includes urethral pain, dysuria, urethral discharge and painful ejaculation.

Complications:
-Acute (acute urinary retention & acute prostatitis and epididymo-orchitis).
-Chronic (urethral stricture & infertility due to obstruction of the ejaculatory ducts).

Treatment:
Treatment should be started immediately covering both gonococcal and non-gonococcal types (dual
therapy).
-Sexual partner should be simultaneously treated.
-Sexual abstinence is highly recommended till cure.
-Urethral catheterization and instrumentation are contraindicated.
-Acute retention of urine - if occurred- requires insertion of a suprapubic percutaneous cystostomy
tube.

The following table summarizes the main differences between:

Gonococcal and non- gonococcal urethritis

7) Acute epididymo-orchitis
 It is commonly due to infection spreading through the lumen of the vas secondary to
urethritis, cystitis, urethral catheterization or instrumentation. It affects the
epididymis firstly then it may progress to the testis. Orchitis may be caused
specifically by mumps (viral infection).
Diagnosis:
 Acute severe scrotal pain associated with tender swelling
 History pointing to the source of infection e.g. urethral discharge and irritative LUTS.
 Constitutional symptoms e.g. fever, rigors, malaise….etc.
 The epididymis and the testis are swollen, tender and lately appear as one inflamed structurewith
redness and edema of the overlying scrotal skin.
 It should be differentiated from other causes of acute scrotum, mainly testicular
 torsion.

Complications: abscess formation, recurrence & chronicity and testicular atrophy.(especially with
mumps orchitis) that may risk fertility.

Treatment:
•Antibiotics for two weeks e.g. quinolones or ceftriaxone.
•Bed rest, testicular support, ice packs, anti-inflammatory, antipyretic and analgesic drugs.
•Any form of urethral instrumentation should be avoided

Genito-urinary tuberculosis (TB).

It is usually secondary to extra-urologic primary tuberculous focus e.g. lungs or GIT. The
causative organism is mycobacterium tuberculosis an acid fast bacillus. It is usually caught
by inhalation and spreads hematogenously to the urinary tract with a latent period of 7-15
years. However, in rare cases, acute diffuse systemic dissemination of tuberculous bacilli can
result in fatal miliary TB.

Renal tuberculosis
 Hematogenous spread causes granuloma formation in the renal cortex, associated with
caseous necrosis of the renal papillae. Spillage of this caseous material into the
pelvicalyceal system releases bacilli (bacilliuria) into urine and leaves cavitations
leading to deformity of the calyces.
 Rupture of caseous lesions outside the kidney causes perinerphric cold abscess.
 This is followed by healing, fibrosis and calcification, which causes destruction of renal
architecture, uretero-pelvic junction (UPJ) obstruction and autonephrectomy.

Ureteral TB
is an extension of the disease from the kidney.
 TB affects all layers of the ureter which becomes thick walled, slightly dilated
and non-tortuous (pipe stem ureter).
 Stricture occurs at UPJ, middle ureter and sometimes the whole ureter becomes
strictured with subsequent hydronephrosis.

TB of the urinary bladder

is secondary to renal tuberculosis starting at the ureteral orifices.
 Bladder mucosa shows TB ulcers (rare, superficial with irregular outline).
 Fibrosis around the ureteral orifices may cause vesico-ureteral reflux (VUR).
 When the disease spreads to the muscle, fibrosis results in contracted bladder.
Male genital TB
• Genital TB is more common than urinary TB. It is common in the third and fourth decades.
• Hematogenous spread (from a primary focus in the gastro-intestinal tract or the lungs) affects the
epididymis and the prostate.
• Subsequently the epididymis infects the vas deferens and the testis causing indurated swollen
epididymis, thickened beaded vas and secondary vaginal hydrocele. In neglected cases, posterior
scrotal epididymal sinus may develop.
• Likewise, the prostate infects the seminal vesicles. Prostatic nodule/s, hemospermia, ejaculatory
duct obstruction and low ejaculate volume are some of the sequels.

Complications of genito-urinary TB on the:

1- whole urinary tract: secondary bacterial infection, urolithiasis and urinary fistula.
2- kidney/s: UPJ obstruction, ureteric stricture & VUR (all can cause hydronephrosis and
pyonephrosis), renal hypertension and renal function loss up to chronic renal failure.
3- bladder: chronic bladder ulceration, hematuria and contracted bladder
4- male genital system: genital sinus (spontaneous or after surgical intervention) & male
subfertility

Clinical presentation of genito-urinary TB:

• Symptoms are generally chronic, intermittent and non-specific.
• Complications represent the usual form of presentation.
• Clinically genito-urinary TB should be suspected in the following situations:
- History of any extra-urologic TB e.g. pulmonary TB.
- Chronically toxic patient (anorexia, pallor, loss of weight, night sweating).
- Afebrile renal or perinephric abscess as fever is rare in GU tuberculosis.
- Sterile pyuria with highly acidic urine.
- UTI treatment failure with the current broad spectrum antibiotics.
- The characteristic thickened beaded vas and posterior scrotal sinus.
- Genital sinus and urinary fistula after surgical intervention.

Investigations may be in the form of:

I- Laboratory investigations that include:
A- Tuberculin test: It is a good negative test.
B- Ziehl-Neelsen staining of 3-5 early morning urine samples to detect acid-fast bacilli. Although
it has low sensitivity, it is very specific and good positive test.
C- Culture of urine, semen or any discharge on Lowenstein-Jensen or Dorset-egg
media which takes more than 4 weeks.
D- Polymerase Chain Reaction (PCR) for blood, urine, semen or sinus discharge. It is highly
sensitive, specific and rapid.

II- Radiological imaging that include:

• Abdominal ultrasonography: may reveal cavitary lesions, cortical abscesses, hydronephrosis or
lately (cortical scarring, perinephric abscess and urinary stones).
• KUB film may show mottled renal calcification (pathognomonic) and calcified bladder.
• IVU or CT with contrast may show:
- Renal cavitary lesions, irregular calyces (moth-eaten kidney) or localized hydrocalycosis (due to
infundibular stenosis).
- Hydronephrosis due to UPJ obstruction, ureteric stricture or VUR.
- Non-excreting kidney.
- Pipe-stem ureter(mildly dilated, stretched, non-tortuous ureter/s). It is a pathognomonic sign.
- Contracted bladder suggests extensive TB involvement of the bladder.

III- Cystoscopy in case of TB may show:

* Hyperemic bladder mucosa with tubercles & ulcers * Gapping (golf-hole) ureteral orifice/s.
* Low bladder capacity (contracted bladder) * Biopsy can be taken from bladder lesions.

Treatment
aims to make the patient non-infectious, preserve the renal function and manage any comorbid
condition. Treatment includes:
I- Medical treatment (anti-tuberculous drugs):
• Chemotherapy for 4-6 months is the mainstay of treatment. It includes a combination of isoniazid
(INH), rifampicin and pyrazinamide.
In resistant cases drug sensitivity testing is mandated.
Ethambutol and streptomycin are two other optional anti-tuberculous drugs.
• The patient should be monitored during treatment. Anti-tuberculous drugs must be started once the
diagnosis is confirmed and should continue for at least 4-6 weeks before surgical intervention.

II- Surgical treatment: Drainage of any perinephric collection or abscess with concomitant
drainage of the kidney (by JJ ureteral stent) may be indicated. Other definitive maneuvers include:
A- Reconstructive surgery e.g.
- pyeloplasty for UPJ obstruction
 - ureteric re-implantation with an anti-reflux technique for VUR
- endoscopic dilatation or uretero-neocystostomy for ureteral stricture:
- augmentation cystoplasty e.g. ileo-cystoplasty for contracted bladder
- assisted reproductive techniques for male sub-fertility

B- Ablative surgery e.g. nephro-ureterectomy (for symptomatic non-functioning) kidney,

epididymectomy for persistent epididymal sinus + orchidectomy if the testis is also involved

Schistosomiasis of the urinary tract

Urinary schistosomiasis (bilharziasis) is a parasitic infestation caused by Schistosoma

haematobium. The disease has two stages:
- active with actively laying eggs that can cross from veins to the lumen
- inactive when the adult worms die and there is a host reaction to the submucosal
entrapped eggs.
Ova which pass with urine continue the life cycle of the parasite and leave microscopic abrasions in
the mucosal layer causing hematuria
Tissue reaction includes granuloma formation (hypertrophic lesions), fibrosis (atrophic lesions),
egg calcification (dystrophic calcification) and metaplasia (precancerous lesions).

Bladder bilharziasis
 The urinary bladder is the most common urinary organ to be involved and heaviest to
be affected.
 Hypertrophic bladder lesions: early foreign body reaction leads to increase vascular
supply resulting in nodules, polyps, von Brunn’s nests and granulomata.
 Atrophic bladder lesions: Healing by fibrosis hinders the blood supply resulting in
ischemic changes that include:
- Mucosa: sandy patches, ground glass mucosa, calcific plaques and chronic bladder
ulcer/s.
- Bladder neck contracture (bladder neck obstruction due to extensive fibrosis at
the submucosa and musculosa)
- Contracted bladder (marked reduction of bladder capacity due to heavy ova
deposition that extends to the perivesical fat) with subsequent VUR.
 Metaplastic lesions (precancerous):
- Squamous metaplasia (leukoplakia) may progress tosquamous cell carcinoma.
- Glandular metaplasia (cystitis glandularis) may progress to adenocarcinoma.

Ureteral bilharziasis
 The lower third is the most commonly affected site.
  Healing by fibrosis and calcification of submucosal ova leads to ureteric stricture
and subsequent hydroureter (dilated & tortuous) and hydronephrosis.
 Secondary infection and ureteric stone formation may take place.
 Bilateral affection may eventually produce chronic renal impairment.

Other sites of bilharziasis are rare including the prostate (nodules), seminal vesicles (calcification),
and perineal urethra (mass or water-cane fistula).

Clinical picture includes:

 Schistosomal dermatitis (swimmer’s itch) is the first clinical sign due to cercarial
skin penetration
 Acute (active) schistosomiasis is concomitant with the onset of ova deposition.
producing several manifestations mainly terminal hematuria, painful micturition and
increased urinary frequency. Other rare manifestations may be diarrhea, abdominal
pain, cardiac disturbances and mental weakness.

 Chronic schistosomiasis (inactive stage = stage of complications) can produce:

o Irritative LUTS from e.g. bladder ulcer, secondary infection, contracted bladder or even
bladder cancer.
o Obstructive LUTS from e.g. bladder neck contracture polyps or cancer.
o Post-voiding pain and suprapubic dull aching pain signify constant bladder wall
pathology (chronic ulcer or cancer).
o Hematuria (terminal or total) from e.g. ureteric stones, bladder ulcer or cancer.
o Renal pain, swelling and/or uremic manifestations due to ureteric stricture
stone/s or VUR.
o Examination may reveal different signs e.g. renal swelling, suprapubic
tenderness, bladder base tenderness or mass, prostatic nodule/s and palpable
seminal vesicles.

Investigations for Schistosomiasis and its complications:

1. Urine analysis: Detection of ova with terminal spines is diagnostic of active
infestation. Microscopic hematuria is usually evident.

2. Serologic tests can aid in the diagnosis of infection especially In chronic

inactive cases where egg excretion is uncommon.

3. Radiological investigations: mainly for the diagnosis of complications.

a- Abdominal ultrasonography for the detection of:
- Echogenic bladder growth/s
- Hydronephrosis and hydroureter.
 b- KUB film can shaw
- Bilharzial calcifications of the bladder & ureter/s (linear) and the seminal
vesicles (honey-comb appearance).
- Secondary stones: radio-opaque ureteric or bladder stones.
c- Intravenous urography or CT with contrast
- Hydronephrosis and hydroureters due to ureteral strictures, ureteral stones,
vesico-ureteral reflux or basal bladder cancer.
- Filling defects on cystography in hypertrophic or malignant lesions.
- Contracted bladder.
d- Voiding cysto-urethrography to detect contracted bladder and VUR.

4. Cystoscopy:
- Sandy patches and ground glass mucosa have characteristic cystoscopic pictures.
- Bladder nodules, polyps, granulomata, ulcers, leukoplakia and bladder cancer may be detected
and indicate trans-urethral resection (TUR) biopsy.
- Bladder neck obstruction may cause bladder wall trabeculations, diverticula and secondary
stones.

Treatment:
I- Medical: oral treatment in the active stage:
• Praziquantel is the current drug of choice in a single dose of 40 mg/kg. It is active
against all schistosomal species.
• Alternatively, Mirazid can be used in a dose of 600 mg daily for six days.

II- Endoscopic:
• TUR and biopsy for any bladder growth, ulcers or leukoplakia. Leukoplakia
mandates follow up as it is a precancerous condition.
• Bladder neck incision for bladder neck contracture
• Endoscopic ureteric dilation for ureteric stricture
• Endoscopic treatment of bladder or ureteric stones.

III- Surgical:
• Ureteric reimplantation or Boari bladder flap for complicated ureteric stricture.
• Augmentation cystoplasty for contracted bladder.
• Radical cystectomy for bladder cancer with appropriate urinary diversio