Pediatric Urinary Tract Infection 

Urinary tract infection (UTI) is one of the most common infections of childhood. It distresses the child, concerns the parents, and may cause permanent kidney damage.

The 2 broad clinical categories of UTI are pyelonephritis (upper UTI) and cystitis (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, has pyelonephritis (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 38°C.

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.

Go to Urinary Tract Infection in Males and Urinary Tract Infection in Females for complete information on these topics.

Almost all urinary tract infections (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).

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.)

Most episodes of UTI during the first year of life are pyelonephritis.

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 coli being 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 of 14 genes investigated in humans may be associated with susceptibility to recurrent UTIs; the genes that are possibly responsible include HSPA1B, CXCR1, CXCR2, TLR2, TLR4, and TGFβ1.

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. 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).

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.

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.

The incidence of urinary tract infections (UTIs) varies based on age, sex, and gender.

US and international incidence

Overall, UTIs are estimated to affect 2.4-2.8% of all children every year in the United States. The international incidence of UTI is difficult to accurately assess, especially in developing countries, but is assumed to be similar to that in the United States.

Age predilection

Occurrences of a first-time symptomatic UTI are highest in boys and girls during the first year of life and markedly decrease after that. The minimum cumulative incidence in boys and girls aged 2 years is slightly over 2%.

As many as 5% of children below age 2 years who present to the emergency department with fever have a UTI.

Sex predilection

During the first few months of life, the incidence of UTI in boys exceeds that in girls. By the end of the first year and thereafter, first-time and recurrent UTIs are most common in girls. The prevalence of UTI in girls aged between 1 and 2 years is 8.1%; in boys, it is 1.9%. Studies from Sweden have indicated that at least 3% of girls and 1% of boys have a symptomatic UTI by age 11 years.

Other data, however, has suggested that 8% of girls have a symptomatic UTI during childhood and that the incidence of a first-time UTI in boys older than 2 years is probably less than 0.5%.

In sexually active teenaged females, the incidence of UTIs approaches 10%.

Race predilection

In studies by Hoberman et al, the prevalence of a febrile UTI in white infants exceeded that of black infants.^[2] These investigators found that 17% of white female infants younger than 1 year with a temperature of 39°C or more seen in an emergency department had UTI.

Mortality related to urinary tract infection (UTI) is exceedingly rare in otherwise healthy children in developed countries.

Morbidity associated with pyelonephritis is characterized by systemic symptoms, such as fever, abdominal pain, vomiting, and dehydration. Bacteremia and clinical sepsis may occur. Children with pyelonephritis also may have cystitis.

Long-term complications of pyelonephritis are hypertension, impaired kidney function, end-stage renal disease (ESRD), and complications of pregnancy (eg, UTI, pregnancy-related hypertension, low-birth-weight neonates).

Long-term complications of UTI are caused by renal damage secondary to pyelonephritis.

Cystitis may cause voiding symptoms and require antibiotics, but it is not associated with long-term deleterious kidney damage. The voiding symptoms are usually transient, clearing within 24-48 hours of effective treatment.

In developed countries, kidney damage with long-term complications as a consequence of UTI per se is currently less common than it was in the early 20th century, when pyelonephritis was a frequent cause of hypertension and ESRD in young women. This change is probably a result of improved overall healthcare and close follow-up of children after an episode of pyelonephritis.

In countries with high-quality healthcare, hypertension, impaired renal function, and ESRD are now most commonly encountered in infants with intrauterine renal damage.

For patient education information, see the Kidneys and Urinary System Center, as well as Urinary Tract Infections and Bladder Control Problems.