Prevalence and Etiology

Urinary tract infections (UTIs) occur in 1-3% of girls and 1% of boys. In girls, the first UTI usually occurs by the age of 5 yr, with peaks during infancy and toilet training. In boys, most UTIs occur during the 1st yr of life; UTIs are much more common in uncircumcised boys, especially in the 1st year of life. The prevalence of UTIs varies with age. During the 1st yr of life, the male : female ratio is 2.8-5.4 : 1. Beyond 1-2 yr, there is a female preponderance, with a male : female ratio of 1 : 10.

UTIs are caused mainly by colonic bacteria. In girls, 75-90% of all infections are caused by Escherichia coli (Chapter 192), followed by Klebsiella spp and Proteus spp. Some series report that in boys >1 yr of age, Proteus is as common a cause as E. coli; others report a preponderance of gram-positive organisms in boys. Staphylococcus saprophyticus and enterococcus are pathogens in both sexes. Adenovirus and other viral infections also can occur, especially as a cause of cystitis.

Historically, UTIs have been considered a risk factor for the development of renal insufficiency or end-stage renal disease in children. Some researchers have questioned the importance of UTI as a risk factor, because only 2% of children with renal insufficiency report a history of UTI. This paradox may be secondary to better recognition of the risks of UTI and prompt diagnosis and therapy. Furthermore, many children receive antibiotics for fever without a focus (such as treating a questionable otitis media) resulting in a partially treated UTI.

Clinical Manifestations and Classification

The 3 basic forms of UTI are pyelonephritis, cystitis, and asymptomatic bacteriuria. Focal pyelonephritis (nephronia) and renal abscesses are less common.

Clinical Pyelonephritis

Clinical pyelonephritis is characterized by any or all of the following: abdominal, back, or flank pain; fever; malaise; nausea; vomiting; and, occasionally, diarrhea. Fever may be the only manifestation. Newborns can show nonspecific symptoms such as poor feeding, irritability, jaundice, and weight loss. Pyelonephritis is the most common serious bacterial infection in infants <24 mo of age who have fever without an obvious focus (Chapter 170). These symptoms are an indication that there is bacterial involvement of the upper urinary tract. Involvement of the renal parenchyma is termed acute pyelonephritis, whereas if there is no parenchymal involvement, the condition may be termed pyelitis. Acute pyelonephritis can result in renal injury, termed pyelonephritic scarring.

Acute lobar nephronia (acute lobar nephritis) is a renal mass caused by acute focal infection without liquefaction. It may be an early stage in the development of a renal abscess. Manifestations are identical to pyelonephritis; renal imaging demonstrates the abnormality (Fig. 532-1). Renal abscess can occur following a pyelonephritic infection due to the usual uropathogens or may be secondary to a primary bacteremia (S. aureus). Perinephric abscess (see Fig. 532-4) can occur secondary to contiguous infection in the perirenal area (e.g., vertebral osteomyelitis, psoas abscess) or pyelonephritis that dissects to the renal capsule.

Figure 532-1 Characteristic precontrast (A) and contrast-enhanced (B) CT scans for an 8 mo old patient who had acute lobar nephronia and presented with severe bilateral nephromegaly but without a focal mass sonographically. No attenuation area is seen in the kidney before enhancement.

(From Cheng CH, Tsau YK, Lin TY: Effective duration of antimicrobial therapy for the treatment of acute lobar nephronia, Pediatrics 117:e84–e89, 2006.)

Xanthogranulomatous pyelonephritis is a rare type of renal infection characterized by granulomatous inflammation with giant cells and foamy histiocytes. It can manifest clinically as a renal mass or an acute or chronic infection. Renal calculi, obstruction, and infection with Proteus spp or E. coli contribute to the development of this lesion, which usually requires total or partial nephrectomy.

Pathogenesis and Pathology

Most UTIs are ascending infections. The bacteria arise from the fecal flora, colonize the perineum, and enter the bladder via the urethra. In uncircumcised boys, the bacterial pathogens arise from the flora beneath the prepuce. In some cases, the bacteria causing cystitis ascend to the kidney to cause pyelonephritis. Rarely, renal infection occurs by hematogenous spread, as in endocarditis or in some neonates.

If bacteria ascend from the bladder to the kidney, acute pyelonephritis can occur. Normally the simple and compound papillae in the kidney have an antireflux mechanism that prevents urine in the renal pelvis from entering the collecting tubules. However, some compound papillae, typically in the upper and lower poles of the kidney, allow intrarenal reflux. Infected urine then stimulates an immunologic and inflammatory response. The result can cause renal injury and scarring (Figs. 532-2 and 532-3). Children of any age with a febrile UTI can have acute pyelonephritis and subsequent renal scarring, but the risk is highest in those <2 years of age.

Figure 532-2 Scarred kidney from recurrent pyelonephritis.

Figure 532-3 CT scan showing an area of parenchymal thinning corresponding to an underlying calyx, characteristic of pyelonephritic scarring or reflux nephropathy.

Host risk factors for UTI are listed in Table 532-1. Vesicoureteral reflux is discussed in Chapter 533. If there is grade III, IV, or V vesicoureteral reflux and a febrile UTI, 90% have evidence of acute pyelonephritis on renal scintigraphy or other imaging studies. In girls, UTIs often occur at the onset of toilet training because of voiding dysfunction that occurs at that age. The child is trying to retain urine to stay dry, yet the bladder may have uninhibited contractions forcing urine out. The result may be high-pressure, turbulent urine flow or incomplete bladder emptying, both of which increase the likelihood of bacteriuria. Voiding dysfunction can occur in the toilet-trained child who voids infrequently. Similar problems can arise in school-age children who refuse to use the school bathroom. Obstructive uropathy resulting in hydronephrosis increases the risk of UTI because of urinary stasis. Urethral catheterization for urine output monitoring or during a voiding cystourethrogram or nonsterile catheterization can infect the bladder with a pathogen. Constipation with fecal impaction can increase the risk of UTI because it can cause voiding dysfunction.

The pathogenesis of UTI is based in part on the presence of bacterial pili or fimbriae on the bacterial surface. There are two types of fimbriae, type I and type II. Type I fimbriae are found on most strains of E. coli. Because attachment to target cells can be blocked by D-mannose, these fimbriae are referred to as mannose-sensitive. They have no role in pyelonephritis. The attachment of type II fimbriae is not inhibited by mannose, and these are known as mannose-resistant. These fimbriae are expressed by only certain strains of E. coli. The receptor for type II fimbriae is a glycosphingolipid that is present on both the uroepithelial cell membrane and red blood cells. The Gal 1-4 Gal oligosaccharide fraction is the specific receptor. Because these fimbriae can agglutinate by P blood group erythrocytes, they are known as P fimbriae. Bacteria with P fimbriae are more likely to cause pyelonephritis. Between 76-94% of pyelonephritogenic strains of E. coli have P fimbriae, compared with 19-23% of cystitis strains.