Urinary tract infection (UTI)

Urinary tract infection (UTI) is common in women, uncommon in men and of special importance in children. Recurrent infection causes considerable morbidity; if complicated, it can cause severe renal disease including end-stage renal failure. It is also a common source of life-threatening Gram-negative septicaemia.

Pathogenesis of Urinary tract infection

Infection is most often due to bacteria from the patient's own bowel flora. Transfer to the urinary tract may be via the bloodstream, the lymphatics or by direct extension (e.g. from a vesicocolic fistula), but is most often via the ascending transurethral route. For the latter route, three important steps are involved.

First, the lower vagina and periurethral area is heavily colonized by uropathogenic bacteria. This is facilitated by the adhesion of bacteria to uroepithelial surfaces by pili or fimbriae present on the bacterial cell surface. Previous UTIs may also predispose to further colonization which may not be eliminated by treatment of the infection, initiating a vicious circle.

Important factors contributing to colonization include use of a diaphragm and spermicidal jelly, hormone-deficient vaginal atrophy, and systemic antibiotic treatment for non-urinary tract infections. There is little evidence that personal hygiene affects colonization, but the use of bubble baths may be a contributory factor.

Second, bacteria are transferred along the urethra to the bladder. This step is facilitated by sexual intercourse or catheterization. Spontaneous transfer along the short female urethra is easy, while the longer male urethra protects against transfer of bacteria to the bladder; in addition, prostatic fluid has defensive bactericidal properties.

The third is the establishment and multiplication of bacteria within the bladder. Bladder urine is normally sterile, owing to defence mechanisms within the bladder. These include hydrokinetic and bladder mucosal factors and constituents of urine. A low flow rate and infrequent and poor bladder emptying predispose to infection.

Mucosal defence mechanisms are poorly understood. The establishment of infection may be facilitated by fimbriated bacteria adhering to the bladder uroepithelium or previous damage to this epithelium. A thin layer of mucopolysaccharide coats the transitional epithelial cells and prevents adhesion of bacteria. Loss or depletion of this layer because of previous infection, bladder trauma from catheterization or vigorous intercourse may predispose to infection.

The first phase in the development of UTI is the entry and establishment of bacteria within the bladder. Extension of infection up the ureters to the kidneys is relatively easy and is facilitated by vesicoureteric reflux and dilated hypotonic ureters. Once infection is established it can pass up or down the system quite readily.

UTI is commonly an isolated, rather than a repeated event.

Signs and symptoms of Urinary tract infection (UTI)

The most typical symptoms of UTI are:

• frequency of micturition by day and night
• painful voiding (dysuria)
• suprapubic pain and tenderness
• haematuria
• smelly urine.

These symptoms relate to bladder and urethral inflammation, commonly called 'cystitis', and suggest lower urinary tract infection. Loin pain and tenderness, with fever and systemic upset, suggest extension of the infection to the pelvis and kidney, known as pyelitis or pyelonephritis. However, localization of the site of infection on the basis of symptoms alone is unreliable.

UTI may also be present with minimal or no symptoms or may be associated with atypical symptoms such as abdominal pain, fever or haematuria in the absence of frequency or dysuria.

In small children, who cannot complain of dysuria, symptoms are often 'atypical'. The possibility of UTI must always be considered in the fretful, febrile sick child who fails to thrive.

Acute Pyelonephritis, Chronic Pyelonephritis, Dysuria Urethral Syndrome, Chronic Bacterial Prostatitis, Acute Bacterial Prostatitis, Retroperitoneal Fibrosis, Benign Prostatic Hypertrophy