Urinary tract infection (UTI) is one of the most common pediatric infections.

It distresses the child, concerns the parents, and may cause permanent kidney damage. The 2 broad clinical categories of UTI are pyelonephritis (upper UTI) andcystitis (lower UTI). The most common causative organisms are bowel flora, typically gram-negative rods. Escherichia coli is the most commonly isolated organism from pediatric patients with UTIs. However, any organism that gains access to the urinary tract system may cause infection, including fungi (Candida species) and viruses. In some instances, UTI results in recognition of an important underlying structural or neurogenic abnormality of the urinary tract. The febrile infant or child with clinically significant bacteriuria and no other site of infection to explain the fever, even in the absence of systemic symptoms, haspyelonephritis (ie, upper UTI). Most episodes of UTI during the first year of life are pyelonephritis. Febrile infants younger than 3 months are an important subset of children who may present with fever without a localizing source. Workup of fever in these infants should always include evaluation for UTI. The chart below details a treatment approach for febrile infants younger than 3 months with a temperature of more than 38C.

Application of low-risk criteria and approach for the febrile infant. A reasonable approach for treating febrile infants younger than 3 months who have a temperature of greater than 38C.

Children with UTIs who have voiding symptoms or dysuria, little or no fever, and no systemic symptoms, have lower cystitis. After age 2 years, UTI manifesting as cystitis is common among girls. The site of infection is often unclear when a child with pyuria and clinically significant bacteriuria has another potential source of fever (eg, otitis media,pharyngitis). Clinically significant urinary tract abnormalities are frequently identified using intrauterine ultrasonography. After birth, these children may incur additional kidney damage as a result of postnatal infection, but UTI is not the major cause of the kidney impairment. The major causes of impaired kidney function are developmental abnormalities. See Urinary Tract Infection in Males and Urinary Tract Infection in Females for complete information on these topics.

Patient education
For patient education information, see Urinary Tract Infections and Bladder Control Problems.

Etiology
Almost all UTIs are ascending in origin. Most infections begin in the bladder; from there, pathogens can spread up the urinary tract to the kidneys (pyelonephritis) and possibly to the bloodstream (bacteremia). Most episodes of UTI during the first year of life are pyelonephritis. Pyelonephritis may lead to renal scarring and long-term complications, such as hypertension and chronic renal failure. (Approximately 10-30% of children with UTI develop renal scarring.) Simple cystitis may progress to pyelonephritis. Predicting which patients will develop pyelonephritis is difficult, although evidence suggests that genetics may play a role. Bacterial infections are the most common cause of UTI, with E colibeing the most frequent pathogen, causing 75-90% of UTIs. Other bacterial sources of UTI include the following: Klebsiella species Proteus species Enterococcus species Staphylococcus saprophyticus - Especially among female adolescents and sexually active females Streptococcus group B - Especially among neonates Pseudomonas aeruginosa Fungi (Candida species) - Especially after instrumentation of the urinary tract

Adenovirus - Rare After birth, the periurethral area, including the distal urethra, becomes colonized with aerobic and anaerobic microorganisms that appear to function as a defense barrier against colonization by uropathogens. In early childhood, enterobacteria and enterococci are part of the normal periurethral flora. Escherichia coli is the dominant gram-negative species in young girls, whereas E coli and Proteus species predominate in boys. Studies of girls and women prone to UTI showed that periurethral colonization occurs with the specific bacterium that causes the next infection.

Infection routes and spread of pathogens

Children up to approximately age 5 years are predisposed to UTIs, partly because of periurethral colonization by E coli, enterococci, and Proteus species. These potential uropathogens usually diminish in the first year of life and are rarely found in children older than 5 years. Urine in the proximal urethra, urinary bladder, and other proximal sites in the urinary tract is normally sterile. Because normal voiding usually results in an essentially complete washout of contaminating bacteria, successful pathogenic colonization of the urinary bladder is unlikely unless bladder defense mechanisms are impaired. Therefore, disturbance of the normal periurethral flora predisposes a person to UTI. Entry of bacteria into the urinary bladder can result from turbulent flow during normal voiding, voiding dysfunction, or catheterization. In addition, sexual intercourse or genital manipulation may foster the entry of bacteria into the urinary bladder. More rarely, the urinary tract may be colonized during systemic bacteremia (sepsis); this usually happens in infancy. Pathogens can also infect the urinary tract through direct spread via the fecal-perineal-urethral route.

Genetic factors
Deregulation of candidate genes in humans may predispose patients to recurrent UTIs. The identification of a genetic component may allow the identification of at-risk individuals and, therefore, prediction of genetic recurrences in their offspring.[1]Thus far, 6 genes investigated in humans may be associated with susceptibility to recurrent UTIs; these are HSPA1B, CXCR1, CXCR2, TLR2, TLR4, and TGF1. As previously mentioned, evidence suggests that genetics may play a role in the progression of simple cystitis to pyelonephritis.

Risk factors
When UTI is diagnosed in a child, an attempt should be made to identify any risk factors for the UTI (eg, anatomic anomaly, voiding dysfunction, constipation). Children who receive broad-spectrum antibiotics (eg, amoxicillin, cephalexin) that are likely to alter gastrointestinal (GI) and periurethral flora are at increased risk for UTI, because these drugs disturb the urinary tract's natural defense against colonization by pathogenic bacteria. Prolonged incubation of bacteria in bladder urine due to incomplete bladder emptying or infrequent voiding compromises an important bladder defense against infection. Uninhibited detrusor contractions Symptoms of voiding dysfunction, such as urgency, frequency, hesitancy, dribbling, or incontinence, may occur in the absence of infection or local irritation, because of uninhibited detrusor contractions. Consequently, the child may attempt to prevent incontinence during a detrusor contraction by voluntarily increasing outlet resistance. This may be achieved by using various posturing maneuvers, such as tightening of the pelvic-floor muscles, applying direct pressure to the urethra with the hands, or performing the Vincent curtsy, which consists squatting on the floor and pressing the heel of one foot against the urethra. As a result, bacteria-laden urine in the distal urethra may be milked back into the urinary bladder (urethrovesical reflux). Neurogenic and anatomic abnormalities Voiding dysfunction is not usually encountered in a child without neurogenic or anatomic abnormality of the bladder until the child is in the process of achieving daytime urinary control. Constipation, with the rectum chronically dilated by feces, is an important cause of voiding dysfunction. Neurogenic or anatomic abnormalities of the urinary bladder may also cause voiding dysfunction.

Risk reduction after circumcision Neonatal circumcision decreases the risk of UTI by about 90% in male infants during the first year of life. The risk of UTI in a circumcised infant is about 1 in 1000 during the first year, whereas an uncircumcised male infant has a 1 in 100 risk of developing a UTI. Overall, the rate of UTIs in circumcised boys has been estimated at 0.2-0.4%, with the rate in uncircumcised boys being 5-20 times higher than in circumcised boys.

http://emedicine.medscape.com/article/969643-overview#a0156