Genetic heterogeneity and predominance of blaCTX-M -15 in cefotaxime-resistant Enterobacteriaceae isolates colonizing hospitalized children in Tunisia.

Extended-spectrum ß-lactamase (ESBL)-producing Enterobacteriaceae have emerged as important nosocomial pathogens. Community infections by these organisms have been also reported and were associated with previous intestinal colonization. We aimed to characterize cefotaxime-resistant Enterobacteriaceae (CTX-R-En) isolated from hospitalized children in a Tunisian paediatric ward. Seventy CTX-R-En isolates were collected from 227 rectal swabs from hospitalized children in a paediatric ward. Antimicrobial susceptibility testing was determined according to the EUCAST guidelines. Isolates were characterized by polymerase chain reaction (PCR, genes encoding: ESBLs, pAmpC, carbapenemases, plasmid-mediated quinolone resistance, virulence factors in Escherichia coli and Klebsiella pneumoniae isolates, occurrence of classes 1 and 2 integrons, phylogenetic groups of E. coli isolates, ERIC-PCR and PCR-based replicon typing) and conjugal transfer experiments. In total, 65 out of 227 (28·6%) hospitalized children were colonized with CTX-M-R-En, and 70 isolates were identified. Isolates were 59 ESBL-, 7 plasmidic-AmpC (pAmpC)-, 3 ESBL+pAmpC-, and one ESBL+carbapenemase producers. The following bla genes were identified: blaCTX-M-15 (n = 54), blaCTX-M-1 (n = 5), blaCTX-M-9 (n = 2), blaCTX-M-13 (n = 1) and blaCTX-M-14 (n = 1), blaCMY-2 (n = 5), blaCMY-4 (n = 4), blaACC-1 (n = 1) and blaOXA-48 (n = 1). Our results showed that hospitalized children were colonized with various CTX-R-En-producing several beta-lactamase enzymes.

[Biochemical and molecular diagnosis of primary hyperoxaluria type 1: Tunisian study about 15 cases]. / Diagnostic biochimique et moléculaire de l'hyperoxalurie primaire de type 1: étude tunisienne à propos de 15 cas.

BACKGROUND: The primary type 1 hyperoxaluria (HP1) is the most frequent and severe form of the primary hyperoxaluriae. It is related to an enzymatic deficit in alanine glyoxylate aminotransferase (AGT). It is a recessive autosomic disease. Rare in Europe, it is responsible for 13% of the end stage renal failure in the Tunisian child. AIM: The aim of this work is to evaluate the biological and molecular examinations contributing with the early diagnosis and the follow-up of the HP1 patients and to test their response to pyridoxin. PATIENTS AND METHODS: A prospective study of 15 children who have oxaluria lower than 500 µmol/l and normal renal function is carried out. The cristalluria study, oxaluria and the glycolate-glycerate urinary ratio were carried out on all the patients. The so-called mutation maghrebean T853 (Ile244 Thr) was detected by direct sequencing of the exon 7 gene AGXT. The response to pyridoxin was tested among 13 patients. RESULTS: The oxaluria concentration was greater or equal to 1000 µmol/l in nine cases (60%) and ranging between 600 and 1000 µmol/l in the remaining cases. The oxaluria flow was significantly high depending on the age. The glycolaturia was high among eight patients (57%). In 61,5% of the cases, the most frequent crystalline species was whewellite (C1). The "maghrebin" mutation was identified in nine patients at the heterozygous state, showing 25% allelic frequency. The response to pyridoxin was observed in the 13 tested cases. CONCLUSION: The HP1 is frequent in our country from where the need for an early diagnosis. The use of simple biochemical tools such as the study of the cristalluria, the morphological analysis of stones and the oxaluria allow to direct the diagnosis towards a HP1, confirmed by the glycolaturia determination. The molecular biology is required in the atypical forms.

Nephrolithiasis-induced end stage renal disease.

INTRODUCTION: Nephrolithiasis still remains a too frequent and underappreciated cause of end stage renal disease (ESRD). METHODS AND PATIENTS: Of the entire cohort of 7128 consecutive patients who started maintenance dialysis in our nephrology department between January 1992 and December 2006, a total of 45 patients (26 women, 19 men) had renal stone disease as the cause of ESRD. The type of nephrolithiasis was determined in 45 cases and etiology in 42. The treatment and evolution of stone disease and patient's survival were studied. RESULTS: The overall proportion of nephrolithiasis related ESRD was 0.63%. The mean age was 48.4 years. Infection stones (struvite) accounted for 40%, calcium stones, 26.67% (primary hyperparathyroidism:15.56%; familial hypercalciuria: 4.44%, unknown etiology: 6.66%), primary hyperoxaluria type 1, 17.78% and uric acid lithiasis in 15.56% of cases. The mean delay of the evolution of the stone renal disease to chronic renal failure was 85.8 months. The feminine gender, obesity and elevated alkaline phosphatases >128 IU/L were significantly correlated with fast evolution of ESRD. The median evolution to ESRD was 12 months. The normal body mass index (BMI), medical treatment of stone and primary hyperoxaluria type 1 were correlated with fast evolution to ESRD. All patients were treated by hemodialysis during a mean evolution of 60 months. Sixteen patients died. The patient's survival rate at 1, 3 and 5 years was 97.6, 92.8 and 69% respectively. Hypocalcemia, cardiopathy and normal calcium-phosphate product were significantly correlated with lower survival rate. CONCLUSION: Severe forms of nephrolithiasis remain an underestimated cause of ESRD. These findings highlight the crucial importance of accurate stone analysis and metabolic evaluation to provide early diagnosis and efficient treatment for conditions leading to ESRD.