Background The aim of this study was to investigate the risk factors for acquisition of extended spectrum β‐lactamase (ESBL)‐producing bacteria in community‐acquired urinary tract infection (UTI) and to evaluate their antimicrobial resistance. Methods The medical records of hospitalized children were retrospectively evaluated. Children with ESBL‐producing bacteria UTI were matched with controls with non‐ESBL‐producing bacteria UTI of the same age and gender. Results A total of 243 patients with community‐acquired UTI in a 5 year period were evaluated, of whom 46% had UTI caused by ESBL bacteria. Seventy‐seven cases were matched with 77 controls. There were no significant differences in the clinical presentation between the two groups apart from a longer hospital stay in the ESBL group (9.1 ± 5.5 days vs 8.0 ± 4.4 days, P = 0.013). Significant potential risk factors for ESBL‐UTI were previous use of antibiotics in the last 3 months, previous hospitalization in the last 3 months, history of recurrent UTI, and presence of renal anomalies. On logistic regression analysis, history of previous hospitalization in the last 3 months (OR, 3.83; 95%CI: 1.49–9.84) was identified as an independent significant risk factor for ESBL‐UTI. There was a significantly higher resistance to amoxicillin‐clavulanate, amikacin, gentamycin and quinolones in the ESBL group compared with the control group. Conclusion Recognizing the risk factors for ESBL‐UTI helps to identify the high‐risk cases and enables proper management.

BackgroundThere is evidence that Candida colonization contributes to increasing invasion of candidiasis in hospitalized neonates. Few studies investigated the epidemiology and risk factors of Candida colonization among hospitalized and non-hospitalized infants. This prospective study investigated the major epidemiological characteristics of Candida species colonizing oral and rectal sites of Jordanian infants.MethodsInfants aged one year or less who were examined at the pediatrics outpatient clinic or hospitalized at the Jordan University Hospital, Amman, Jordan, were included in this study. Culture swabs were collected from oral and rectal sites and inoculated on Sabouraud dextrose agar. All Candida isolates were confirmed by the Remel RapID yeast plus system, and further investigated for specific virulence factors and antifungal susceptibility MIC using E-test. Genotyping of C. albicans isolates was determined using random amplified polymorphic DNA (RAPD) analysis method.ResultsA total of 61/492 (12.4%) infants were colonized with Candida species by either their oral/rectal sites or both. Rectal colonization was significantly more detected than oral colonization (64.6% verses 35.4%), particularly among hospitalized infants aged more than one month. The pattern and rates of colonization were as follows: C. albicans was the commonest species isolated from both sites and accounted for 67.1% of all isolates, followed by C.kefyr (11.4%), each C. tropicalis and C. glabrata (8.9%) and C. parapsilosis (3.8%).A various rates of Candida isolates proved to secrete putative virulence factors in vitro; asparatyl proteinase, phospholipase and hemolysin. C. albicans were associated significantly (P < 0.05) with these enzymes than other Candida species. All Candida isolates were susceptible to amphotericin B and caspofungin, whereas 97% of Candida species isolates were susceptible to fluconazole using E-test.The genetic similarity of 53 C. albicans isolates as demonstrated by dendrogram revealed the presence of 29 genotypes, and of these one genotype accounted for 22% of the isolates.ConclusionThis study presents important epidemiological features of Candida colonization of Jordanian infants.

Sanjad Sakati syndrome is a rare autosomal recessive disorder that has been described in Arabs. We report 8 patients from 7 Jordanian families, 6 of whom underwent genetic testing and were found to have a 12 bp (155-166 del) deletion within the tubulin-specific chaperone E (TBCE gene) in exon 3 at 1q42-43. All patients had severe growth retardation, distinct phenotypic features and hypoparathyroidism. Parental consanguinity was recorded in all families. This is the first genetically proven case series of Sanjad Sakati syndrome in Jordan.

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This is a retrospective study of 40 patients admitted to Hamad General Hospital in the state of Qatar between January 1983 and December 1987 with the diagnosis of Henoch-Schöenlein syndrome. Of the 40 patients, 25 were boys and 15 were girls, with a ratio of 1.6:1. Ages ranged from 2 years 3 months to 13 years, with a mean of 6 years. There were six episodes of recurrence in four patients. There was a clustering of cases in late summer and early winter. About half of the patients had a history of preceding upper respiratory infection. All of them had the typical skin rash. The percentages of joint, gastro-intestinal and renal manifestations were 80%, 65% and 17.39%, respectively. One patient had penile swelling which has not been reported before. Steroid therapy seemed to enhance early resolution of abdominal pain but did not affect the course of the syndrome. Sixty-seven per cent of the patients were followed up for from 4 weeks to 5 years, with a mean of 8 months. Only one patient with renal involvement continued to have proteinuria with microscopic haematuria and hypertension. The rest were normal within about 2 months. The remarkably low incidence of renal involvement in our study may be related to local variations in causative factors. Henoch-Schöenlein syndrome is a milder disease in Qatar than in other countries.