Prevalence and risk factors of extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella pneumoniae in an Israeli long-term care facility.

The purpose of this study was to ascertain the prevalence of extended-spectrum beta-lactamases (ESBLs) among Escherichia coli and Klebsiella pneumoniae strains obtained from urine samples of residents of a long-term care facility and to determine the risk factors for acquisition of ESBL-producing strains. All urine samples collected from January 2003 to October 2003 that were positive for E. coli or K. pneumoniae were tested for the presence of ESBL. Records of patients with ESBL-positive (ESBL-P) samples were analyzed for clinical and demographic data. The records of a matched control group of patients whose urine samples were positive for E. coli or K. pneumoniae but were ESBL-negative (ESBL-N) were also analyzed. The overall rate of ESBLs among the E. coli and K. pneumoniae samples was 25.6%. Of 350 urine samples that grew E. coli, 77 (22%) were positive for ESBL; 34 of 84 (40.5%) samples that grew K. pneumoniae were ESBL-P. Male sex, treatment in the subacute care unit, recent antimicrobial treatment, pressure sores, (percutaneous endoscopic gastrostomy) PEG tube, anemia, hypoalbuminemia, permanent urinary catheter, and any recent invasive procedure were all associated with ESBL-P bacteria in the univariate analysis. The multivariate analysis revealed three independent risk factors for the presence of an ESBL-producing strain: anemia, permanent urinary catheter, and previous antibiotic use. Fluoroquinolones were most strongly associated with the development of ESBL-producing bacteria. The prevalence of ESBL-producing E. coli and K. pneumoniae in the long-term care facility investigated was unexpectedly high and corroborates the notion that long-term care facilities could be important reservoirs of resistant bacteria. Identification of the risk factors for ESBLs is the first step in formulating an effective strategy to curtail the spread of ESBL resistance in long-term care facilities.

Penetrance and phenotypic expression of a mutation linked to Creutzfeldt-Jakob disease in the elderly.

We have previously reported several carriers of the PRNP E200K point mutation among subjects aged over 65 years. In order to examine the prevalence of this mutation among demented subjects of Libyan and Tunisian origin and the clinical characteristics associated with it, we screened 58 elderly subjects belonging to this ethnic group. Five mutation carriers were identified, all of whom had cognitive deterioration consistent with primary degenerative dementia. All had low Hachinski ischemic scores (0.8 +/- 0.8, mean +/- SD) as compared with noncarriers (6.7 +/- 3.0; p = 0.011, Wilcoxon rank sum test). In addition to the cognitive decline, 4 carriers had additional cerebellar, pyramidal, or extrapyramidal findings compatible with the diagnosis of possible or probable Creutzfeldt-Jakob disease.

The risk of developing Creutzfeldt-Jakob disease in subjects with the PRNP gene codon 200 point mutation.

We determined the penetrance of the PRNP 200Lys mutation in the large cluster of Creutzfeldt-Jakob disease (CJD) cases among Jews of Libyan-Tunisian origin living in Israel, utilizing data from 52 carriers with definite or probable CJD and 34 unaffected mutation carriers. A life table analysis was carried out with development of CJD as the end point. The probability of developing CJD rose with age, fitting a second-order regression curve (R = 0.97, p < 0.001). The cumulative penetrance reached 50% at the age of 60 and 80% at 80 years. Including seven elderly possible CJD patients in the analysis made the penetrance approach 100% by age eighty. The penetrance of the mutation is high, and although age is a predominant influencing factor, other factors, such as gender, may also play a role.

Sheehan's syndrome with diabetes insipidus. A case study.

A case of a woman in whom Sheehan's syndrome and diabetes insipidus were found is presented. This association is very uncommon, but well-documented cases have been reported. Controversial opinions about the primary lesion still exist. To find out whether the pituitary gland responds to hypothalamic releasing factors, three kinds of test were performed. The failure of the pituitary to respond suggested pituitary damage. Because diabetes insipidus was present, presumably the hypothalamus was also damaged. A review of the literature and different opinions about the primary anatomic lesions in this syndrome are discussed.