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Urinary tract infection (UTI) is defined by ≥ 5 × 104 colonies/mL in a catheterized urine specimen or, in older children, by repeated voided specimens with ≥ 105 colonies/mL. In younger children, UTIs are frequently caused by anatomic abnormalities. UTI may cause fever, failure to thrive, flank pain, and signs of sepsis, especially in young children. Treatment is with antibiotics. Follow-up imaging studies of the urinary tract are done.
UTI may involve the kidneys, bladder, or both. Sexually transmitted infections of the urethra (eg, gonococcal or chlamydial urethritis), although involving the urinary tract, are not typically termed UTI.
Mechanisms that maintain the normal sterility of the urinary tract include urine acidity and free flow, a normal emptying mechanism, intact ureterovesical and urethral sphincters, and immunologic and mucosal barriers. Abnormality of any of these mechanisms predisposes to UTI.
Etiology
By age 6 yr, 3 to 7% of girls and 1 to 2% of boys have had a UTI. The peak age of UTI is bimodal, with one peak in infancy and the other peak between ages 2 to 4 yr (at the time of toilet training for many children). The female:male ratio ranges from 1:1 to 1:4 in the first 2 mo of life (estimates vary, likely because of different proportions of uncircumcised males in study groups and the exclusion of infants with urologic anomalies now more commonly diagnosed in utero by prenatal ultrasonography). The female:male ratio quickly rises with age, being about 2:1 between 2 mo to 1 yr, 4:1 during the 2nd yr, and > 5:1 after 4 yr. In girls, infections usually are ascending and less often cause bacteremia. The marked female preponderance beyond infancy is attributed both to the shorter female urethra and male circumcision.
Predisposing factors include malformations and obstructions of the urinary tract, prematurity, indwelling catheters, and lack of circumcision. Other predisposing factors in younger children include constipation and Hirschsprung's disease. Risk factors in older children include diabetes, trauma, and, in adolescent females, sexual intercourse.
Urinary tract abnormalities:
UTIs in children are a marker of possible urinary tract abnormalities (eg, obstruction, neurogenic bladder, ureteral duplication); these abnormalities are particularly likely to result in infection if vesicoureteral reflux (VUR—see also Congenital Renal and Genitourinary Anomalies: Vesicoureteral Reflux) is present. The likelihood of VUR varies inversely with age at the first UTI. About 30 to 40% of infants and toddlers with UTI have VUR. Severity of reflux may determine the probability of subsequent hypertension and renal failure (caused by repeated infection and chronic pyelonephritis), but proof is lacking (see Miscellaneous Infections in Infants and Children: Vesicoureteral reflux). VUR is classified by grade (see Table 1: Miscellaneous Infections in Infants and Children: Grades of Vesicoureteral Reflux* ).
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Table 1
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| Grades of Vesicoureteral Reflux* |
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Grade
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Characteristics
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I
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Only the ureters are involved, but not the renal pelvis.
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II
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Reflux reaches the renal pelvis, but the calyces are not dilated.
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III
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The ureter and renal pelvis are dilated, with minimal or no blunting of calyces.
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IV
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Dilation increases, and the sharp angle of the calyceal fornices is obliterated.
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V
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The ureter, pelvis, and calices are grossly dilated.
Papillary impressions frequently are absent.
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*As defined by the International Reflux Study Committee.
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Organisms:
Many organisms cause infection in anatomically abnormal urinary tracts.
In relatively normal urinary tracts, the most common pathogens are strains of Escherichia coli with specific attachment factors for transitional epithelium of the bladder and ureters. E. coli causes > 75% of UTIs in all pediatric age groups. The remaining causes are other gram-negative enterobacteria, especially Klebsiella, Proteus mirabilis, and Pseudomonas aeruginosa. Enterococci (group D streptococci) and coagulase-negative staphylococci (eg, Staphylococcus saprophyticus) are the most frequently implicated gram-positive organisms. Fungi and mycobacteria are rare causes, mainly in immunocompromised hosts. Adenoviruses rarely cause UTIs, and when they do, the disorder is predominantly hemorrhagic cystitis.
Symptoms and Signs
In neonates, symptoms and signs are nonspecific and include poor feeding, diarrhea, failure to thrive, vomiting, mild jaundice, lethargy, fever, and hypothermia. Neonatal sepsis (see Infections in Neonates: Neonatal Sepsis) may develop.
Infants and toddlers may also present with poorly localizing signs, such as fever, GI symptoms (eg, vomiting, diarrhea, abdominal pain), or foul-smelling urine.
In children > 2 yr, the more classic picture of cystitis or pyelonephritis can occur. Symptoms of cystitis include dysuria, frequency, hematuria, urinary retention, suprapubic pain, urgency, pruritus, incontinence, foul-smelling urine, and enuresis. Symptoms of pyelonephritis include high fever, chills, and costovertebral pain and tenderness.
Physical findings suggesting associated urinary tract abnormalities include abdominal masses, enlarged kidneys, abnormality of the urethral orifice, and signs of lower spinal malformations. Diminished force of the urinary stream may be the only clue to obstruction or neurogenic bladder.
Diagnosis
Urine tests:
Diagnosis requires culture showing significant bacteriuria in properly collected urine. Most clinicians obtain urine by transurethral catheterization in infants and young children, reserving suprapubic aspiration of the bladder for boys with moderate to severe phimosis. Both procedures require technical expertise, but catheterization is less invasive, slightly safer, and has sensitivity of 95% and specificity of 99% compared with suprapubic aspiration. Bagged specimens are unreliable and should not be used for diagnosis.
If urine is obtained by suprapubic aspiration, the presence of any bacteria is significant. In a catheterized specimen, ≥ 5 × 104 colonies/mL commonly defines UTI. Clean-catch, midstream-voided specimens are significant when colony counts of a single pathogen (ie, not the total count of mixed flora) are ≥ 105 colonies/mL. However, at times symptomatic children may have UTI despite lower colony counts on urine cultures. Urine should be examined and cultured as soon as possible or stored at 4° C if a delay of > 10 min is expected. Occasionally, UTI may be present despite colony counts lower than the described guidelines, possibly because of prior antibiotic therapy, very dilute urine (sp gr < 1.003), or obstruction to the flow of grossly infected urine. Sterile cultures generally rule out UTI unless the child is receiving antibiotics or the urine is contaminated with antibacterial skin-cleaning agents.
Microscopic examination of urine is useful but not definitive. Pyuria (> 5 to 10 WBCs/high-power field in spun urine sediment) is about 70% sensitive for UTI. A WBC count (using a hemocytometer) > 10/μL in unspun urine has greater sensitivity (90%) but is not used by many laboratories. Presence of bacteria on Gram stain of spun or unspun urine is about 80% sensitive. Specificity of microscopy also is about 80%.
Dipstick tests on urine to detect bacteria (nitrite test) or leukocytes (leukocyte esterase test) are typically done; if either is positive, the diagnostic sensitivity for UTI is about 93%. The specificity of the nitrite test is quite high; a positive result on a freshly voided specimen is highly predictive of UTI. Specificity of leukocyte esterase is much lower.
Differentiating an upper UTI from a lower UTI can be difficult. High fever, costovertebral angle tenderness, and gross pyuria with casts indicate pyelonephritis. However, many children without these symptoms and signs have an upper UTI. Tests to distinguish upper infection from lower infection are not indicated in most clinical settings, because treatment is not altered.
Blood tests:
A CBC and tests for inflammation (eg, ESR, C-reactive protein) may help diagnose infection in children with borderline urine findings. Some authorities measure serum BUN and creatinine during a first UTI. Blood cultures are appropriate for infants with UTIs and for children > 1 to 2 yr who appear toxic.
Urinary tract imaging:
Many major renal or urologic anomalies now are diagnosed in utero by routine prenatal ultrasonography. However, the high incidence of anatomic anomalies still warrants imaging the urinary tracts of all children 2 mo to 2 yr of age after a first UTI. If a first UTI occurs at ≥ 2 yr, most authorities recommend imaging; however, some physicians postpone imaging until after a second UTI in girls > 2 yr. Options include voiding cystourethrogram (VCUG), radionuclide cystogram (RNC) with technetium-99m pertechnetate, and ultrasonography.
VCUG and RNC are better than ultrasonography for detecting VUR and anatomic abnormalities. RNC delivers about 1% of the gonadal radiation of VCUG; it is sensitive in detecting VUR, and some recommend it as the initial test. However, most authorities prefer the better anatomic definition of contrast VCUG as the initial test, using RNC in follow up to determine when VUR has resolved. Low-dose x-ray equipment has narrowed the gap in radiation between the contrast VCUG and RNC. These tests are recommended at the earliest convenient time after clinical response, typically toward the end of therapy, when bladder reactivity has resolved and urine sterility has been regained. If imaging is not scheduled until after therapy is due to be completed, the child should continue antibiotics at prophylactic doses until VUR is excluded.
Ultrasonography helps exclude obstruction and hydronephrosis and is typically done within a week of diagnosing UTI in infants, especially if they do not respond quickly to antimicrobials. Otherwise, ultrasonography can be delayed until VCUG is done.
Prognosis
Properly managed children rarely progress to renal failure unless they have uncorrectable urinary tract abnormalities. However, repeated infection, particularly in the presence of VUR, is thought (but not proved) to cause renal scarring, which may lead to hypertension and end-stage renal disease. In children with high-grade VUR, long-term scarring is detected at a 4- to 6-fold greater rate than in children with low-grade VUR and at an 8- to 10-fold greater rate than in children without VUR.
Treatment
Treatment aims to eliminate the acute infection, prevent urosepsis, and preserve renal parenchymal function. Antibiotics are begun presumptively in all toxic-appearing children and in nontoxic children with likely UTI (positive leukocyte esterase or nitrite test or microscopy showing pyuria or bacteriuria). Others can await culture results.
In infants 2 mo to 2 yr with toxicity, dehydration, or inability to retain oral intake, parenteral antibiotics are used, typically a 3rd-generation cephalosporin (eg, ceftriaxone 75 mg/kg IV/IM q 24 h, cefotaxime 50 mg/kg IV q 6 h). A 1st-generation cephalosporin (eg, cefazolin) may be used if typical local pathogens are known to be sensitive. Aminoglycosides (eg, gentamicin), although potentially nephrotoxic, are useful in complex UTIs (eg, urinary tract abnormalities, presence of indwelling catheters, recurrent UTIs) to treat potentially resistant gram-negative bacilli such as Pseudomonas. If blood cultures are negative and clinical response is good, an appropriate oral antibiotic (eg, a cephalosporin, trimethoprim/sulfamethoxazole [TMP/SMX], amoxicillin, or, for selected children such as those > 1 yr with complicated UTI caused by multidrug-resistant E. coli, P. aeruginosa, or other gram-negative bacteria, a fluoroquinolone) selected on the basis of antimicrobial sensitivities can be used to complete a 10- to 14-day course. A poor clinical response suggests a resistant organism or an obstructive lesion and warrants urgent evaluation with ultrasonography and repeat urine culture.
In nontoxic, nondehydrated infants and children who are able to retain oral intake, oral antibiotics may be given initially. The drug of choice is TMP/SMX 5 to 6 mg/kg (of TMP component) bid. Alternatives include cephalosporins such as cefixime 4 mg/kg bid or cephalexin 25 mg/kg qid. Therapy is changed based on the results of cultures and antimicrobial sensitivities. Treatment is generally for > 10 days, although many older children with uncomplicated UTI can be treated for 7 days. Urine culture is repeated 2 to 3 days after therapy starts if efficacy is not clinically apparent.
Vesicoureteral reflux:
It is generally thought that antibiotic prophylaxis reduces UTI recurrences and prevents kidney damage. However, few long-term data are available on the actual risks of renal scarring and the effectiveness of antimicrobial prophylaxis or operative repair in preventing end-stage renal disease. An ongoing clinical trial is attempting to address these questions, but until results are available, most clinicians provide long-term antimicrobial prophylaxis to children with VUR, especially those with grades II through V. For those with grade IV or grade V VUR, open repair or endoscopic injection of polymeric bulking agents is usually recommended.
Drugs for prophylaxis include nitrofurantoin 2 mg/kg po once/day or TMP/SMX 3 mg/kg po (of TMP component) once/day, usually given at bedtime.
Last full review/revision March 2010 by Geoffrey A. Weinberg, MD
Content last modified February 2012
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