Urinary Tract Infections

Physiology of UT

The passing of urine from the kidney to the bladder is by peristalsis. The angle at which the ureter enters the bladder forms a physiological valve such that urinary reflux is prevented. The bladder has muscle called Detrusor. When this contracts, it opens the neck of bladder so that urinary flow is allowed. The bladder must empty its entire volume, because if it doesn’t – then there is opportunity for normal flora to multiply.

The urinary system remains healthy ONLY IF the flow is normal. If the flow is DISTURBED, it will cause an UTI.

Aetiology & Pathogenesis of UTI (Robbins pp 972, )

Aetiology: The dominant aetiological agents of UTI are: Escherichia Coli, Proteus mirabilis, Klebsiella pneumoniae, Enterococci. Others such as: Staph aureus, Strep faecalis also are involved.

Pathogenesis: There are two routes by which bacteria can cause a UTI/kidney infection: 1) ascending infection (E coli, Klebsiella, Proteus), 2) haematogenous (Staph aureus, S. typhi, Candida, TB). About 80% of UTIs are ascending infections. The urine in the ureters and bladder are sterile, so how do bacteria get in?

The following is a brief explanation of the steps involved in the development of an UTI:

• Gaining entrance: How do they gain entrance? Instrumentation (catheters etc), shorter urethra in females, prostatic fluid in males have antibacterial properties.

• Multiplication: How do they multiply? Normally, the bladder empties regularly therefore flushing out any growing organisms. But if there is an obstruction or neurological defect affecting the emptying process, the organisms can multiply. Obstruction can be caused by: calculi, tumours, prostate hypertrophy etc.

• Vesicoureteral reflux: The angle at which the ureters enter the bladder provide for a physiological valve (i.e.: ureters go through muscular wall of bladder such that when muscles contract, they close off the ureter entrance). What if this valve does not work because there is something inherently wrong with the anatomy? Residual volume of urine is still present even after voiding, so organisms can multiply (see above).

Complicated vs Uncomplicated UTIs

Just remember that complicated UTIs occur in patients with some sort of abnormality (i.e.: anatomical / functional) in their UT system. They represent seriousness, and are difficult to treat.

UNCOMPLICATED UTI

Uncomplicated UTI is when the UTI occurs “as part of life” and passes by without causing any major problems. These UTI commonly occur in females. Organisms responsible are: E. coli (80%), Proteus mirabilis, Klebsiella pneumoniae, Staph saprophyticus (occurs in sexually active young women), enterococcus. Treatment: antibiotics (gram –ve) + ↑ fluids.

COMPLICATED UTI

Complicated UTIs occur when there is an abnormality in the urinary tract. These abnormalities can be anatomical or functional.

Anatomical: cysts in kidney can obstruct urinary outflow, prostrate hypertrophy/vaginal prolapse will cause obstruction, strictures along ureter (stones etc).

Functional: vesicoureteral reflux, diabetes (neuropathy causes impaired bladder emptying + glucose is recipe for bacterial growth), MS, spinal injury**.

The moral of the story is, cure the anomaly first before treating UTI. Otherwise, recurrent infections are inevitable. Organisms responsible are: E. coli, Proteus mirabilis, Klebsiella pneumoniae, Enterobacter, Entercocci, Staph aureus.

SYMPTOMS OF UTI: Triad: dysuria, frequent toilet trips, lower abdominal pain.

DX OF UTI: 1) look at urine sample, 2) 10⁵⁰ WCC is normal, anything> = abnormal, 3) urine culture.

COMPLICATED UTIs  What are some of the disease associations? (Robbins 974)

Cystitis: This is caused by organisms such as: E coli, Proteus, Klebsiella, Enterobacter, enterococci. The reasons for colonisation of these bacteria have been given: attachment, multiplication, reflux. The triad of symptoms is present. Usually, cystitits is caused by some preceding problem such as: prostatic hypertrophy, calculi, tumour, diabetes etc.

Ureteritis: When there is reflux the organisms will move retrograde to the ureters. Here they will cause inflammatory changes.

Pyelonephritis: 2 varieties exist: 1) acute, 2) chronic

• Acute pyelonephritis: This is the suppurative inflammation of the kidney mostly due to an ascending infection. Morphology: Initially the inflammation is in the interstitial tissue, and then extends into the tubules. Here it destroys the tubular  tubular necrosis. Later on, scar tissue laid down. Complications: 1) papillary necrosis: papillary areas necrosed, 2) pyonephrosis: exudates fills proximally to renal pelvis, 3) perinephric abscess: inflammation goes through renal capsule. Clinical features: triad of symptoms, pain in costovertebral angle, systemic symptoms of infection: pyrexia, chills, rigors, diaphoresis.

• Chronic pyelonephritis: This is pretty much the same as the acute type, but there is involvement of the calyces and renal pelvis. Glomeruli tend to be preserved. Two types: 1) chronic obstructive (i.e.: calculi, ureteric anomalies), 2) reflux nephropathy. The latter is the most common cause of chronic pyelonephritis. Morphology: Macroscopically corticomedullary scar overlying blunted calyx. Microscopically: thyroidisation of tubules.

Category: Pathology Notes