Gram-positive cocci: 5000 CFU/mL (or 5 × 106/L) Source: Reproduced with permission from Reference 47.
N.B. CFU/mL = colony-forming units per mL (or organisms/mL).

Bacteria grow rapidly, so specimens containing few introduced bacteria left at room temperature or greater for more than an hour can yield false-positive urine cultures.

10.1.2 Method of urine collection

Catheter urine collection is less painful and more likely to succeed than suprapubic aspirate3-5 (see Section 4.1.4).

10.2 Pathogenesis

In neonates, it is not known whether kidney infection is primary with secondary spread to the bloodstream and even the meninges or occurs embolically secondary to septicaemia. The primary site of infection might be different in early-onset and late-onset UTI, with bacteraemic spread more likely in early sepsis and ascending infection from the urethra more likely in late UTI.

Urine cultures are sometimes positive in early-onset septicaemia and/or meningitis. In one study, 9 of 188 infants investigated for early-onset sepsis had bacteraemia and 1 also had a positive urine culture (with GBS).6 Two babies had positive urine cultures with negative blood cultures. One grew Escherichia coli and was treated for UTI. The other baby grew Staphylococcus epidermidis from an SPA and recovered untreated, showing that SPA urines are not immune to contamination.

In the same study, 1 of 189 infants with suspected late-onset sepsis had Klebsiella grown from both blood and urine. Ten other babies had positive blood but negative urine cultures and 13 babies had positive urine cultures but negative blood cultures.6

Anatomic abnormalities of the urinary tract, particularly obstructive abnormalities such as posterior urethral valves, vesico-ureteric and pelvi-ureteric junction stenosis are associated with UTI. Reports suggest that 5–20% of neonates with UTI have an obstructive uropathy,7 while half of all infants with an obstructive uropathy will present with UTI.8

The incidence of UTI increases with decreasing gestational age and birth weight. Fungal UTIs occur almost exclusively in babies <;1500 g. Mature babies who develop fungal UTI are usually receiving parenteral nutrition for major congenital malformations, for example, gastrointestinal disease, or prolonged broad-spectrum antibiotics (see Chapter 16).9

In the first year of life, boys have double the incidence of UTI than girls,10,11 whereas girls predominate after the age of one. The reported incidence of UTI in retrospective studies was 0.1–0.2% for circumcised male infants, 0.4–0.6% for female infants, but 1.1–4.1% for uncircumcised male infants. Circumcision is protective against UTI in males (Section 10.6). Within 2 weeks of birth the prepuce is heavily colonized with E. coli.12 Circumcision is associated with a reduction in peri-urethral carriage of E. coli and Proteus.13,14 These data support the theory that the prepuce is an important source of the uropathogens that cause UTI in boys.

While the above data suggest that host factors are a major determinant of susceptibility to UTI, organism factors are also important. There are many strains of E. coli in faeces, yet the strains that cause UTI are very different from diarrhoeal and non-pathogenic strains. Uropathogenic strains of E. coli have been extensively studied and carry genes for various virulence factors including adhesins such as P-fimbriae that facilitate adherence to uroepithelium, iron uptake systems and cytotoxins.15-17

Vesico-ureteric reflux (VUR) has been associated with UTI, but it remains controversial whether babies are born with VUR which predisposes to UTI or whether UTI can cause transient reflux and to what extent babies with UTI should be investigated for reflux7 (Section 10.5).

10.3 Clinical

The clinical presentation of UTI is non-specific. In a US study, the symptoms of infants with bacteraemia did not differentiate them from those with bacteriuria.6 Most of the data on the clinical presentation of neonatal UTI come from studies in the 1970s of relatively mature preterm and full-term infants.7 In these studies, half the infants had an insidious presentation with failure to thrive with or without low-grade fever, feeding problems, vomiting, irritability, lethargy and jaundice.

Infants with UTI can also present acutely with signs of sepsis including fever, meningismus, abdominal distension and hepatosplenomegaly. Jaundice occurs in about 20% of patients with UTI but is an unreliable indicator of UTI (see Chapter 3).

10.4 Laboratory

10.4.1 Microscopy

10.4.2 Urinalysis

10.4.3 Urine culture

Urine obtained by catheter or SPA should be cultured for bacteria and yeasts. The microbiology of UTI has changed with advances in neonatal intensive care. E. coli continues to be by far the most important cause of community-acquired UTI in most countries, although neonatal Klebsiella UTI is increasing in some developing countries (Table 10.2). The major shift, however, has been in neonatal intensive care units (NICUs), where CoNS have become responsible for up to 30% of UTIs7,23 In addition, yeasts are a major cause of UTI in high-risk infants (see Chapter 16).

Table 10.2 Important causes of neonatal urinary tract infections.

There are increasing reports of UTI caused by multi-resistant Gram-negative bacilli from many countries, including resource-rich and developing countries.24-29 These include increasing reports of infections with Gram-negative bacilli producing extended-spectrum β-lactamases (ESBL).24-29

10.4.4 Blood culture

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