Staphylococcus aureus resistente a la meticilina y a descolonizadores habituales con reservorio en un trabajador sanitario en un hospital de tercer nivel / Staphylococcus aureus resistant to methicillin and usual decolonizers with a reservoir in a health worker in a tertiary hospital

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Staphylococcus aureus resistente a la meticilina y a descolonizadores habituales con reservorio en un trabajador sanitario en un hospital de tercer nivel / Antibiotic ointments and methicillin-resistant Staphylococcus aureus with a reservoir in a healthcare worker in a tertiary hospital

INTRODUCCIÓN: Staphylococcus aureus resistente a la meticilina (SARM) es un patógeno nosocomial, con reservorio en portadores o infectados y que tiene como principal mecanismo de transmisión el contacto con las manos del personal. Métodos Se puso en marcha una investigación epidemiológica y se realizaron determinaciones de laboratorio para abordar el estudio de la situación provocada por la aparición de nuevos casos de SARM resistente a los descolonizadores habituales. Resultados Desde septiembre de 2010 a febrero de 2012, en nuestro centro, 16 pacientes y una trabajadora tuvieron un aislamiento de SARM resistente a los descolonizadores habituales (mupirocina y ácido fusídico). Se detectaron casos esporádicos no relacionados, y a su vez brotes epidémicos relacionados con la ubicación de la actividad del personal sanitario portador de SARM. El análisis mediante electroforesis en campo pulsado de las muestras de pacientes y de la trabajadora puso de manifiesto la clonalidad de las cepas, lo que sugiere que el reservorio pudiera ser la trabajadora afectada. La descontaminación con antibióticos sistémicos no tuvo éxito y la trabajadora fue adscrita a otro puesto de trabajo sin contacto directo con pacientes, con lo que se consiguió que no aparecieran más casos hasta el momento actual (septiembre de 2012). Conclusiones Este trabajo ilustra el riesgo de transmisión nosocomial relacionada con la atención prestada por los trabajadores sanitarios

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) has become an important hospital acquired pathogen, with transfer of the organism from a carrier or infected patient to uninfected patients by the hands or clothing of staff as the main mode of transmission. METHODS: Investigation of a cluster of new cases of MRSA resistant to mupirocin and fusidic acid, using epidemiological and microbiological resources. RESULTS: From September 2010 to February 2012, sixteen patients had at least one culture positive for MRSA resistant to mupirocin and fusidic acid. Some not apparently related cases and outbreaks appeared. By analysing cultures taken from patients and staff using pulsed-field. CONCLUSION: This report illustrates the risk of nosocomial transmission linked to care delivered by healthcare workers

Outbreak of Pseudomonas aeruginosa infections in a neonatal care unit associated with feeding bottles heaters.

This report describes an outbreak caused by Pseudomonas aeruginosa in a neonatal care unit possibly linked to feeding bottles heaters. Infection control measures were undertaken such as reinforcement of contact isolation precautions, environmental microbiologic sampling, educational sessions on hand hygiene, and use of sterilized water to refill feeding bottles heaters. The sustained eradication of P aeruginosa isolates after implementing control measures on feeding bottles heaters strongly suggests those as the source of the outbreak.

[Antibiotic ointments and methicillin-resistant Staphylococcus aureus with a reservoir in a healthcare worker in a tertiary hospital]. / Staphylococcus aureus resistente a la meticilina y a descolonizadores habituales con reservorio en un trabajador sanitario en un hospital de tercer nivel.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) has become an important hospital-acquired pathogen, with transfer of the organism from a carrier or infected patient to uninfected patients by the hands or clothing of staff as the main mode of transmission. METHODS: Investigation of a cluster of new cases of MRSA resistant to mupirocin and fusidic acid, using epidemiological and microbiological resources. RESULTS: From September 2010 to February 2012, sixteen patients had at least one culture positive for MRSA resistant to mupirocin and fusidic acid. Some not apparently related cases and outbreaks appeared. By analysing cultures taken from patients and staff using pulsed-field gel electrophoresis, it was demonstrated that most likely this situation was started by an auxiliary nurse who was a carrier of the MRSA. Healthcare worker decontamination using oral antibiotic therapy was unsuccessful. Eventually, the situation was controlled by placing the carrier in a different job, with no further cases to date (September, 2012). CONCLUSION: This report illustrates the risk of nosocomial transmission linked to care delivered by healthcare workers.

Effect of fixed-dose ACE-inhibitor/calcium channel blocker combination therapy vs. ACE-inhibitor monotherapy on arterial compliance in hypertensive patients with type 2 diabetes.

Assessment of vascular compliance may be a useful measurement of the clinical effects of antihypertensive treatment. Both angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers are known to improve vascular elasticity. A study was performed to test the hypothesis that combined therapy with an ACE inhibitor and a calcium channel blocker would have additive benefits on vascular compliance at similar levels of blood pressure (BP), as compared with monotherapy with an ACE inhibitor. This 12-week, double-blind study was a substudy of a larger clinical hypertension study conducted in patients with hypertension and type 2 diabetes. Subjects (N = 20) were randomized to either a fixed-dose combination of amlodipine besylate/benazepril HCl or to enalapril monotherapy. BP, heart rate, large- and small-vessel compliance, systemic vascular resistance, and urinary microalbumin excretion were assessed at baseline and after treatment. Both treatments were similarly effective in lowering BP, reducing systemic vascular resistance, and decreasing urinary microalbumin excretion. Improvement in large-vessel compliance was significantly greater among subjects who received ACE-inhibitor/calcium channel blocker combination therapy (52%) as compared with those who received ACE-inhibitor monotherapy (32%; p < 0.05). No significant change in small-vessel compliance was observed with either treatment. Greater improvement in large-vessel compliance with combination therapy was independent of BP lowering.

Impact of obesity and the metabolic syndrome on risk factors in African American stroke survivors: a report from the AAASPS.

BACKGROUND: The rates of obesity and the metabolic syndrome and the impact on traditional vascular risk factors in African American stroke survivors are unknown. OBJECTIVE: To describe the relationships between body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters) and hypertension, dyslipidemia, and diabetes mellitus. DESIGN: We classified 1711 subjects as underweight (BMI, <18.5), normal (BMI, 18.5-24.9), overweight (BMI, 25.0-29.9), or obesity class 1 (BMI, 30.0-34.9), 2 (BMI, 35.0-39.9), or 3 (BMI, >40.0). We compared the proportions with hypertension, dyslipidemia, and diabetes mellitus and control of these factors by clinical history and results of physical examination and laboratory analysis across BMI groups. SETTING: Multicentered clinical trial. PATIENTS: African American subjects with previous ischemic stroke. MAIN OUTCOME MEASURES: Rates of obesity and the metabolic syndrome, odds ratios (ORs) of associated vascular risk factors at baseline, and relationship to longitudinal risk factor control. RESULTS: Overall, 76% were overweight or obese (70% of men and 81% of women). Hypertension, dyslipidemia, and diabetes mellitus were all present in 43.3% of men and 29.1% of women with obesity class 3. The ORs for having the metabolic syndrome were 2.14 (95% confidence interval [CI], 1.52-3.01) for class 1, 1.92 (95% CI, 1.26-2.91) for class 2, and 1.98 (95% CI, 1.27-3.09) for class 3 obesity. In addition, increasing BMI was negatively associated with systolic (P<.001) and diastolic (P<.001) blood pressure and glycemic control (P<.001). CONCLUSION: Our analysis of the data from the African American Antiplatelet Stroke Prevention Study supports the association of increasing risk factor profiles with increasing weight in African American stroke survivors.

Relationship between bridging with ventricular assist device on rejection after heart transplantation.

BACKGROUND: Ventricular assist devices (VADs) are commonly used to bridge patients to heart transplantation. Recipients of VADs may develop anti-human histocompatibility leukocyte antigen antibodies, as reflected by elevated panel-reactive antibodies (PRA). The purpose of this study was to evaluate the relationship between bridging with VAD before heart transplantation and development of cellular rejection, humoral rejection, and allograft vasculopathy after transplantation. METHODS: Data on all patients who underwent cardiac transplantation between July 1994 and February 2001 at Rush Presbyterian St Luke's Medical Center were retrospectively reviewed. Data collected included sex, age, etiology of cardiomyopathy, percentage panel reactive antibodies (by cytotoxic method), type and duration of mechanical circulatory support, transfusion history, rejection history (both cellular and humoral) after cardiac transplantation, and development of allograft vasculopathy. Cellular rejection was treated when International Society of Heart and Lung and Transplantation Grade 2 or greater in the first 12 months after transplant and Grade 3 or greater after 12 months and treated with intensification of immunosuppression. Humoral rejection was defined clinically as allograft dysfunction by echocardiography without evidence of cellular rejection on endomyocardial biopsy or allograft vasculopathy. Allograft vasculopathy was defined by presence of any degree of luminal narrowing or pruning of distal vessels by coronary arteriography. Statistical analyses were performed by chi-square test, Fisher's exact test, and Wilcoxon rank sum test, as appropriate. RESULTS: Ninety-eight patients underwent cardiac transplantation during the study period (87 men, mean age 49 years, 46 ischemic etiology). Of these, 48 were bridged with HeartMate VAD (20 patients received vented electric device, 28 received pneumatic device). Nineteen percent of VAD patients had a peak pretransplant PRA > or =10% vs 2% of patients without VAD (p = 0.014). PRA > or =10%, use of VAD, or duration of VAD support did not predict development of humoral rejection. Use of VAD did not predict development of cellular rejection or allograft vasculopathy. VAD use was not associated with sudden death after heart transplantation. In the entire group of 98 patients, neither humoral nor cellular rejection predicted development of allograft vasculopathy. Longer ischemic time correlated with increased cellular rejection and humoral rejection after transplantation (p = 0.01). CONCLUSIONS: Some patients bridged to cardiac transplantation with VADs have increased PRA before heart transplantation, but this does not appear to translate into increased risk of either humoral or cellular rejection after transplantation or development of allograft vasculopathy as detected by coronary angiography.

Effects of COX inhibition on blood pressure and kidney function in ACE inhibitor-treated blacks and hispanics.

Cyclo-oxygenase (COX) inhibitors attenuate the antihypertensive effects of angiotensin-converting enzyme (ACE) inhibitors and reduce kidney function. The study tests the hypothesis that these two classes of drugs have similar effects on glomerular filtration rate (GFR) and 24-hour blood pressure. The primary endpoint was change in 24-hour systolic blood pressure. Using a randomized crossover design, 25 black and Hispanic hypertensive participants (mean age 58+/-3 years) with osteoarthritis were studied. All participants received an ACE inhibitor at baseline. Once systolic blood pressure was <140 mm Hg, either celecoxib 200 mg/d or diclofenac 75 mg twice daily for 4 weeks was started. After measurements were obtained, all participants underwent a 2-week washout period and crossed over to the other drug for 4 weeks. A significant difference in mean 24-hour systolic blood pressure was noted between groups at 4 weeks (+4.1+/-1.1 mm Hg diclofenac versus +0.6+/-0.6 mm Hg celecoxib; P=0.01). However, because celecoxib has duration of action shorter than 24 hours, we compared ambulatory values at celecoxib trough and peak activities. At peak, no difference in systolic blood pressure was noted between agents (+3.6+/-0.04 mm Hg diclofenac versus +4.2+/-1.9 mm Hg celecoxib; P=0.67). GFR was also differentially affected at 24 hours (-9.9+/-2.4 mL/min diclofenac versus -0.4+/-1.2 mL/min celecoxib; P=0.01). We conclude that diclofenac and celecoxib increase systolic blood pressure at peak levels; however, these agents differ in their 24-hour effects. Differences observed in blood pressure response between COX inhibitors may not be related in their sensitivity but rather their dosing frequency.

Aspirin and ticlopidine for prevention of recurrent stroke in black patients: a randomized trial.

CONTEXT: Blacks are disproportionately affected by stroke, and they are about 2 times more likely than most other individuals in the United States to die of or experience stroke. OBJECTIVE: To determine the efficacy and safety of aspirin and ticlopidine to prevent recurrent stroke in black patients. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind, investigator-initiated, multicenter trial of 1809 black men and women who recently had a noncardioembolic ischemic stroke and who were recruited between December 1992 and October 2001 from 62 academic and community hospitals in the United States and followed up for up to 2 years. INTERVENTION: A total of 902 patients received 500 mg/d of ticlopidine and 907 received 650 mg/d of aspirin. MAIN OUTCOME MEASURES: Recurrent stroke, myocardial infarction, or vascular death was the composite primary end point (according to intention-to-treat analysis). The secondary outcome was fatal or nonfatal stroke. RESULTS: The blinded phase of the study was halted after about 6.5 years when futility analyses revealed a less than 1% probability of ticlopidine being shown superior to aspirin in the prevention of the primary outcome end point. The primary outcome of recurrent stroke, myocardial infarction, or vascular death was reached by 133 (14.7%) of 902 patients assigned to ticlopidine and 112 (12.3%) of 907 patients assigned to aspirin (hazard ratio, 1.22; 95% confidence interval, 0.94-1.57). Kaplan-Meier curves for time to event for the primary outcome did not differ significantly (P =.12 by log-rank test). Kaplan-Meier curves for time to the secondary outcome of fatal or nonfatal stroke approached a statistically significant reduction favoring aspirin over ticlopidine (P =.08 by log-rank test). The frequency of laboratory-determined serious neutropenia was 3.4% for patients receiving ticlopdine vs 2.2% for patients receiving aspirin (P =.12) and 0.3% vs 0.2% for thrombocytopenia, respectively (P =.69). One ticlopidine-treated patient developed thrombocytopenia, which was thought to be a case of possible thrombotic thrombocytopenia purpura, and recovered after therapy with plasmapheresis. CONCLUSIONS: During a 2-year follow-up, we found no statistically significant difference between ticlopidine and aspirin in the prevention of recurrent stroke, myocardial infarction, or vascular death. However, there was a nonsignificant trend for reduction of fatal or nonfatal stroke among those in the aspirin group. Based on these data and the risk of serious adverse events with ticlopidine, we regard aspirin as a better treatment for aspirin-tolerant black patients with noncardioembolic ischemic stroke.

Stroke risk factor profiles in African American women: an interim report from the African-American Antiplatelet Stroke Prevention Study.

BACKGROUND AND PURPOSE: If sex differences in stroke risk factor profiles exist among African Americans in the United States, prevention strategies will need to reflect those differences. African Americans and women have been underrepresented in stroke prevention studies. The purpose of this study was to determine whether medical and lifestyle factors differ among women and men who have enrolled in the African-American Antiplatelet Stroke Prevention Study (AAASPS). METHODS: We performed a planned exploratory analysis of differences in baseline characteristics and risk factors between women and men enrolled in AAASPS, a double-blind, randomized, multicenter, controlled trial. Frequencies of vascular risk factors and related conditions, medical therapies, stroke subtypes, and vascular territories were compared between women and men by 1-way ANOVA and Fisher's exact test where appropriate. RESULTS: A total of 1087 African American patients (574 women, 513 men) enrolled between December 1995 and June 1999. Women had higher rates of hypertension, diabetes, family history of stroke, and no reported leisure exercise. Men had higher rates of smoking and heavy alcohol use. Few differences were noted in proportions of stroke subtype or proportions receiving preventive therapy. CONCLUSIONS: AAASPS represents the largest enrollment of African American women in a recurrent stroke prevention study. Our data suggest that African American women in a clinical trial differ from men in the frequency of key vascular risk factors. Although limited, these data provide an important first characterization of sex differences in African Americans with stroke.