Risk assessment and quantitative measurement along with monitoring of Legionella in hospital water sources.

Legionella spp. as a causative agent of Legionnaires' disease (LD) and an opportunistic pathogen creates a public health problem. Isolation and quantification of this bacteria from clinic water sources are essential for hazard appraisal and sickness avoidance. This study aimed at risk assessment and quantitative measurement along with Legionella monitoring in educational hospital water sources in Tehran, Iran. A cross-sectional study was carried out in 1 year. The conventional culture method was used in this study to isolate Legionella from water samples. The polymerase chain reaction (PCR) technique was used to confirm the identity of the isolates and ensure that they were all Legionella. Quantitative PCR (qPCR) was used to determine the count of bacteria, and HeLa cell culture was used to determine the invasion of isolates. A total of 100 water samples were collected and inoculated on GVPC (glycine, vancomycin, polymyxin, and cycloheximide) agar; 12 (12%) and 42 (42%) cases were culture and PCR positive, respectively. Percentage of Legionella presence in PCR-positive samples by the qPCR method in <103 GU/L, in about 103 and lower than 104 GU/L, and in 104 GU/L was 40.47 (17 cases), 4.76% (two cases), and 54.76% (23 cases), respectively. Invasion analysis revealed that five and four isolates had invaded HeLa cells more than twice and equally, respectively, and the others had a lower invasion than the reference strain. The findings revealed that the spread of LD in hospitals was linked to the water system. Given the importance of nosocomial infections in the medical community, establishing a hospital water monitoring system is the most effective way to control these infections, particularly Legionella infections.

Urinary excretion of glucagon-like peptide 1 (GLP-1) 7-36 amide in human type 2 (non-insulin-dependent) diabetes mellitus.

The urinary excretion of insulinotropic glucagon-like peptide 1 (GLP-1) was investigated as an indicator of renal tubular integrity in 10 healthy subjects and in 3 groups of type 2 diabetic patients with different degrees of urinary albumin excretion rate. No significant difference emerged between the groups with respect to age of the patients, known duration of diabetes, metabolic control, BMI, or residual beta-cell pancreatic function. Endogenous creatinine clearance was significantly reduced under conditions of overt diabetic nephropathy, compared with normo and microalbuminuric patients (p < 0.01). Urinary excretion of GLP-1 was significantly higher in normoalbuminuric patients compared to controls (490.4 +/- 211.5 vs. 275.5 +/- 132.1 pg/min; p < 0.05), with further increase under incipient diabetic nephropathy conditions (648.6 +/- 305 pg/min; p < 0.01). No significant difference resulted, in contrast, between macroproteinuric patients and non-diabetic subjects. Taking all patients examined into account, a significant positive relationship emerged between urinary GLP-1 and creatinine clearance (p = 0.004). In conclusion, an early tubular impairment in type 2 diabetes would occur before the onset of glomerular permeability alterations. The tubular dysfunction seems to evolve with the development of persistent microalbuminuria. Finally, the advanced tubular involvement, in terms of urinary GLP1 excretion, under overt diabetic nephropathy conditions would be masked by severe concomitant glomerular damage with the coexistence of both alterations resulting in a peptide excretion similar to control subjects.

Effect of nutrient ingestion on glucagon-like peptide 1 (7-36 amide) secretion in human type 1 and type 2 diabetes.

Exogenous glucagon-like peptide 1(GLP-1) bioactivity is preserved in type 2 diabetic patients, resulting the peptide administration in a near-normalization of plasma glucose mainly through its insulinotropic effect. GLP-1 also reduces meal-related insulin requirement in type 1 diabetic patients, suggesting an impairment of the entero-insular axis in both diabetic conditions. To investigate this metabolic dysfunction, we evaluated endogenous GLP-1 concentrations, both at fasting and in response to nutrient ingestion, in 16 type 1 diabetic patients (age = 40.5 +/- 14yr, HbA1C = 7.8 +/- 1.5%), 14 type 2 diabetics (age = 56.5 +/- 13yr, HbA1C = 8.1 +/- 1.8%), and 10 matched controls. In postabsorptive state, a mixed breakfast (230 KCal) was administered to all subjects and blood samples were collected for plasma glucose, insulin, C-peptide and GLP-1 determination during the following 3 hours. In normal subjects, the test meal induced a significant increase of GLP-1 (30', 60': p < 0.01), returning the peptide values towards basal concentrations. In type 2 diabetic patients, fasting plasma GLP-1 was similar to controls (102.1 +/- 1.9 vs. 97.3 +/- 4.01 pg/ml), but nutrient ingestion failed to increase plasma peptide levels, which even decreased during the test (p < 0.01). Similarly, no increase in postprandial GLP-1 occurred in type 1 diabetics, in spite of maintained basal peptide secretion (106.5 +/- 1.5 pg/ml). With respect to controls, the test meal induced in both diabetic groups a significant increase in plasma glucagon levels at 60' (p < 0.01). In conclusion, either in condition of insulin resistance or insulin deficiency chronic hyperglycemia, which is a common feature of both metabolic disorders, could induce a progressive desensitization of intestinal L-cells with consequent peptide failure response to specific stimulation.