PubMed Health⌕ Search

PubMed · 15630321

Urinary tract infection: the urological perspective.

Abstract

Urinary tract infection in babies often presents with non specific symptoms and signs. It must be considered in the differential diagnosis of a febrile sick baby or any baby with failure to thrive. In a significant proportion of babies with recurrent urinary tract infection, urological abnormality is demonstrable. The diagnosis of urinary tract infection is confirmed by the presence of pus cells and growth of microorganism in a fresh urine specimen. The voidoing history and detailed ultrasound examination in the baby including a post void evaluation of the upper and lower urinary tract can lead to the possible diagnosis in the majority. Antibiotic therapy for urinary tract infection should be followed by consideration about the need for urinary drainage at the appropriate level, particularly in cases where resolution is delayed despite antibiotics. There is a role for prophylactic antibiotics after the resolution of acute infection, at least until detailed evaluation several weeks after the acute episode, has excluded any abnormality. Micturating cytourethrogram is usually done under antibiotic cover and better done in centres with facility for fluoroscopic examination. Isotope studies have to be evaluated in the light of inherent limitations. Transient urodynamic abnormality of the urinary bladder in infancy is being increasingly recognized and should be the subject of evaluation in specific circumstances. A multidisciplinary team improves the quality of investigations, subsequent interpretation and long term care of these children. A large majority of urological abnormality in infancy and early childhood can be effectively managed by endocopic procedures. Temporary urinary diversion may be required in a small proportion. Urological reconstruction should be approached with caution, after a detailed analysis of the evolving urological tract in a baby. An aggressive approach to early diagnosis and appropriate treatment of urinary tract infection and any underlying abnormality, has been shown to significantly reduce the incidence of chronic renal failure in long term longitudinal studies in children.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S K Chowdhary, M Kolar, C K Yeung. 2004. Urinary tract infection: the urological perspective.. https://doi.org/10.1007/bf02829827

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗