Background
Prevalence and epidemiology
Urinary tract infection (UTI) is one of the most common bacterial infections of childhood. Among febrile infants, unwell children in general practice and older children with urinary symptoms, 6%–8% will have a UTI.1 2 Prevalence varies with age, peaking in young infants, toddlers and older adolescents. UTI is more common in female and uncircumcised male infants,1 understandable given bacterial skin flora concentration under the nappy in infancy, shorter female urethral distance and foreskin surface area in uncircumcised males. During toddler years, toilet training can lead to volitional holding and bladder stasis, promoting UTIs.3 Prevalence peaks again in adolescent females when sexual activity disrupts bacteria near the urethral orifice.1
Conditions that impair urinary flow increase susceptibility to UTI. Voiding flushes bacteria out of the urinary system.3 Impaired urine flow leads to urinary stasis, giving bacteria an increased reservoir and more time to establish infection. Causes of disordered voiding can be structural (urogenital anomalies) or functional (neurogenic bladder, constipation and behavioural withholding). Altered immune function can increase the risk of uncommon viral and fungal causes of UTI.
Over 30% of children with UTI will have recurrent UTI.4 Common risk factors for recurrence include vesicoureteric reflux (VUR) and bladder–bowel dysfunction.4 Older non-continent children (eg, developmental delay) also have more recurrent UTIs.
Being such a common infection, UTI contributes a significant economic burden to the healthcare system. Use of evidence-based management has the potential for significant cost savings.5
Aetiology
Most paediatric UTIs are caused by Gram negative coliform bacteria arising from faecal flora colonising the perineum, which enter and ascend the urinary tract.3Escherichiacoli (E.coli) is the most common uropathogen, responsible for approximately 80% of paediatric UTIs.6 Uropathogenic E.coli strains possess specific properties, such as fimbriae to attach to the uroepithelial cell surface, to allow them to overcome host defences (figure 1).3 Other common uropathogens include Klebsiella, Proteus, Enterobacter and Enterococcus species.6 7
Upper versus lower tract UTI
UTI can be categorised anatomically into upper tract and lower tract infection.8 Upper tract UTI involves infection and inflammation in the kidneys (pyelonephritis) and ureters (figure 2). This typically leads to abdominal pain and loin tenderness, with systemic features such as fever, anorexia, vomiting, lethargy and malaise. Lower tract UTI involves infection within the bladder (cystitis) and urethra, with localised symptoms such as lower abdominal or suprapubic pain, dysuria, urinary frequency and urgency. Older children may present with signs and symptoms suggesting the site of infection. In younger patients, these classical signs are often absent, and differentiating between upper and lower UTI is less obvious.
Morbidity
Acute UTI encompasses the full spectrum of severity from mild dysuria in an otherwise well child to life-threatening urosepsis. While serious infections are less common, they can and do occur, particularly in neonates.9 Since routine immunisation for Haemophilus influenzae type B and Streptococcus pneumoniae, UTI has become a more common cause of occult and serious bacterial infection in infants.8
Short-term morbidity can arise from infection within the renal system. This includes systemic features including poor oral intake and dehydration, and uncommon local complications including perinephric abscess formation. Short-term morbidity also arises from haematogenous uropathogen spread. Bactaraemic UTI has been best studied in infants, as this population is most likely to have blood cultures collected during febrile illnesses. Approximately 5% of infants <12 months with UTI have bacteraemia identified,10 depending on study setting. Bacteraemia can then lead to urosepsis. Meningitis can also occur with haematogenous spread to the cerebrospinal fluid (CSF). The risk of coexisting meningitis and UTI is 1% in the neonatal period,11 suggesting a low threshold to perform lumbar puncture in this age group. Beyond 1 month, the risk is smaller.11 Typical empirical UTI antibiotics have poor CSF penetration and inadequate duration to treat bacterial meningitis.
Long-term morbidity follows renal injury and scarring from upper tract UTI. Around 15% of children with first UTI who have follow-up scanning will have evidence of renal scarring.12 This scarring would be clinically important if it led to renal dysfunction, hypertension and chronic kidney disease (CKD). Historical thinking suggested these sequalae were common, leading to aggressive imaging guidelines to identify children at risk of CKD. Recent data suggest the risks are much lower. A 2011 systematic review of 1576 cases found no cases where childhood UTI was the main cause of subsequent CKD.13 Of a further 366 local CKD patients in the same study, 13 (3%) had a history of UTI in childhood but all had renal abnormalities evident on renal ultrasound, and recurrent UTI was possibly the cause of CKD in only one case (0.3%).13 Therefore, in the absence of structural renal anomalies or recurrent UTI, the risk of CKD appears minimal. Debate about the significance of post-UTI renal scarring continues.