ABSTRACT
Streptococcus pneumoniae and Staphylococcus aureus cause significant morbidity and mortality worldwide. We investigated both the colonization and co-colonization characteristics for these pathogens among 250 healthy children from 2 to 5 years of age in Merida, Venezuela, in 2007. The prevalence of S. pneumoniae colonization, S. aureus colonization, and S. pneumoniae-S. aureus co-colonization was 28%, 56%, and 16%, respectively. Pneumococcal serotypes 6B (14%), 19F (12%), 23F (12%), 15 (9%), 6A (8%), 11 (8%), 23A (6%), and 34 (6%) were the most prevalent. Non-respiratory atopy was a risk factor for S. aureus colonization (p = 0.017). Vaccine serotypes were negatively associated with preceding respiratory infection (p = 0.02) and with S. aureus colonization (p = 0.03). We observed a high prevalence of pneumococcal resistance against trimethoprim-sulfamethoxazole (40%), erythromycin (38%), and penicillin (14%). Semi-quantitative measurement of pneumococcal colonization density showed that children with young siblings and low socioeconomic status were more densely colonized (p = 0.02 and p = 0.02, respectively). In contrast, trimethoprim-sulfamethoxazole- and multidrug-resistant-pneumococci colonized children sparsely (p = 0.03 and p = 0.01, respectively). Our data form an important basis to monitor the future impact of pneumococcal vaccination on bacterial colonization, as well as to recommend a rationalized and restrictive antimicrobial use in our community.
Subject(s)
Carrier State/epidemiology , Pneumococcal Infections/epidemiology , Staphylococcal Infections/epidemiology , Staphylococcus aureus/isolation & purification , Streptococcus pneumoniae/isolation & purification , Anti-Bacterial Agents/pharmacology , Bacterial Typing Techniques , Child, Preschool , Drug Resistance, Bacterial , Family Health , Female , Humans , Male , Microbial Sensitivity Tests , Prevalence , Risk Factors , Serotyping , Socioeconomic Factors , Venezuela/epidemiologyABSTRACT
La queratinolisis por hongos, un proceso enzimático, puede ser evidenciada "in vitro" a través de la colonización de sustratos queratináceos. Las observaciones microscópicas de pelo humano atacado por especies y/o cepas de aspergillus, chaetomium, chrysosporium, curvularia, dreschlera, fusarium, penicillium y trichoderma, aislada mediante el método de "cebo de pelo", en una tenería y un matadero de Maracaibo- Venezuela, manifestaron la producción de estructuras fúngicas especializadas típicas, más un "desfibrilamiento" del sustrato causado por algunos aislamientos. Se presenta una revisión de literatura referida al análisis de la expresión morfológica de la queratinolisis
Subject(s)
Animals , Arthrodermataceae , Ascomycota , Mitosporic Fungi , VenezuelaABSTRACT
As implemented in their program MINMOD, some of the parameters and variables of the equations representing Bergman and coworkers' minimal model of glucose metabolism have no simple rational relationship with the kinetic constants and constants of proportionality of the minimal model as such. In this work we implemented the original version of the minimal model, which does not suffer from this problem, and used it to investigate the source of insulin resistance among obese but otherwise healthy subjects. A fasting sampled intravenous glucose tolerance (FSIGT) test was performed in 38 healthy subjects of varying degrees of obesity (standard FSIGT test in 21 and tolbutamide FSIGT test in 17 subjects) in order to compare MINMOD and 'modified' equations (MI). Insulin sensitivity index (SI) in obese subjects was significantly lower than in lean subjects (4.58 +/- 3.5 vs. 11.7 +/- 4.3. 10(-5) min-1 (pmol.l-1)-1, P < 0.0001). The lower SI in obese subjects was a consequence P3 parameter (0.178 +/- 0.08 vs. 0.440 +/- 0.26.10(-5) min-2 (pmol.l-1)-1, P < 0.01), being p2 similar between obese and lean subjects (0.389 +/- 0.19 vs. 0.376 +/- 0.19.10(-1) min-1, NS). SI index correlated with p3 (r = 0.73, P < 0.0001), but not with p2 (r = 0.01, NS). Using these results and assuming that interstitial insulin is higher in obese subjects than in lean subjects, we have demonstrated that the proportionality constants of the model (k4 and k6) were lower in obese subjects than in lean subjects, but not the rate constant for insulin transfer across capillaries, k2. Our results suggest that the modified equations are a better theoretical approach to the minimal model method; and that low insulin sensitivity in obese subjects is due to receptor and/or post-receptor events rather than to slow transfer of insulin across capillary endothelium into the interstitial space.
