Powassan virus: What is the risk to the blood supply?

Powassan virus (POWV) is an emerging tick-borne arbovirus that is found widely in Canada, the Northeastern and Northcentral United States, and the Russian Far East. While still rare, there has been an increase in reported cases of POWV disease over the last decade; most (>90%) cases have been neuroinvasive and the associated fatality rate is high (>10%). Transfusion-associated risk of POWV remains uncertain; while no intervention is likely indicated, one probable case of transfusion-transmitted POWV in the context of an increase in the incidence of POWV and other tick-borne infections, merits vigilance.     

The epidemic of West Nile virus in the United States, 2002

Since 1999, health officials have documented the spread of West Nile virus across the eastern and southern states and into the central United States. In 2002, a large, multi-state, epidemic of neuroinvasive West Nile illness occurred. Using standardized guidelines, health departments conducted surveillance for West Nile virus illness in humans, and West Nile virus infection and illness in non-human species. Illnesses were reported to the Centers for Disease Control and Prevention (CDC) through the ArboNET system. In 2002, 39 states and the District of Columbia reported 4,156 human West Nile virus illness cases. Of these, 2,942 (71%) were neuroinvasive illnesses (i.e., meningitis, encephalitis, or meningoencephalitis) with onset dates from May 19 through December 14; 1,157 (28%) were uncomplicated West Nile fever cases, and 47 (1%) were clinically unspecified. Over 80% of neuroinvasive illnesses occurred in the central United States. Among meningitis cases, median age was 46 years (range, 3 months to 91 years), and the fatality-to-case ratio was 2%; for encephalitis cases (with or without meningitis), median age was 64 years (range, 1 month to 99 years) and the fatality-to-case ratio was 12%. Neuroinvasive illness incidence and mortality, respectively, were significantly associated with advanced age (p = 0.02; p = 0.01) and being male (p < 0.001; p = 0.002). In 89% of counties reporting neuroinvasive human illnesses, West Nile virus infections were first noted in non-human species, but no human illnesses were reported from 77% of counties in which non-human infections were detected. In 2002, West Nile virus caused the largest recognized epidemic of neuroinvasive arboviral illness in the Western Hemisphere and the largest epidemic of neuroinvasive West Nile virus ever recorded. It is unknown why males appeared to have higher risk of severe illness and death, but possibilities include higher prevalence of co-morbid conditions or behavioral factors leading to increased infection rates. Several observations, including major, multi-state West Nile virus epidemics in 2002 and 2003, suggest that major epidemics may annually reoccur in the United States. Non-human surveillance can warn of early West Nile virus activity and needs continued emphasis, along with control of Culex mosquitoes.     

Tympanic temperature measurements: are they reliable in the critically ill? A clinical study of measures of agreement

OBJECTIVE: Accurate measurement of temperature is vital in the intensive care setting. A prospective trial was performed to compare the accuracy of tympanic, urinary, and axillary temperatures with that of pulmonary artery (PA) core temperature measurements. DESIGN: A total of 110 patients were enrolled in a prospective observational cohort study. SETTING: Multidisciplinary intensive care unit of a university teaching hospital. PATIENTS: The cohort was (mean +/- sd) 65 +/- 16 yrs of age, Acute Physiology and Chronic Health Evaluation (APACHE) II score was 25 +/- 9, 58% of the patients were men, and 76% were mechanically ventilated. The accuracy of tympanic (averaged over both ears), axillary (averaged over both sides), and urinary temperatures was referenced (as mean difference, Delta degrees centigrade) to PA temperatures as standard in 6,703 recordings. Lin concordance correlation (pc) and Bland-Altman 95% limits of agreement (degrees centigrade) described the relationship between paired measurements. Regression analysis (linear mixed model) assessed covariate confounding with respect to temperature modes and reliability formulated as an intraclass correlation coefficient. MEASUREMENTS AND MAIN RESULTS: Concordance of PA temperatures with tympanic, urinary, and axillary was 0.77, 0.92, and 0.83, respectively. Compared with PA temperatures, Delta (limits of agreement) were 0.36 degrees C (-0.56 degrees C, 1.28 degrees C), -0.05 degrees C (-0.69 degrees C, 0.59 degrees C), and 0.30 degrees C (-0.42 degrees C, 1.01 degrees C) for tympanic, urinary, and axillary temperatures, respectively. Temperature measurement mode effect, estimated via regression analysis, was consistent with concordance and Delta (PA vs. urinary, p = .98). Patient age (p = .03), sedation score (p = .0001), and dialysis (p = .0001) had modest negative relations with temperature; quadratic relationships were identified with adrenaline and dobutamine. No interactions with particular temperature modes were identified (p > or = .12 for all comparisons) and no relationship was identified with either mean arterial pressure or APACHE II score (p > or = .64). The average temperature mode intraclass correlation coefficient for test-retest reliability was 0.72. CONCLUSION: Agreement of tympanic with pulmonary temperature was inferior to that of urinary temperature, which, on overall assessment, seemed more likely to reflect PA core temperature.     

Impact of a negative prior stress test on emergency physician disposition decision in ED patients with chest pain syndromes

OBJECTIVE: Many emergency department (ED) patients with potential acute coronary syndromes (ACS) have prior visits and prior cardiac testing; however, the effect of knowledge of prior testing on the emergency physician disposition decision making is not known. We studied the impact of prior noninvasive testing (ie, stress testing) for myocardial ischemia on disposition decision making in ED patients with potential ACS. METHODS: We performed a prospective cohort study of ED patients with chest pain who received an electrocardiogram for potential ACS. Data included demographics, medical history, stress test history, and TIMI risk score. Patients were followed in-house; 30-day telephone interviews were performed for follow-up. Main outcomes were ED disposition (admit/discharge) and a composite of 30-day death, acute myocardial infarction, and revascularization stratified on the basis of prior stress testing known at the time of presentation. Standard statistical techniques were used with 95% confidence intervals (CI). RESULTS: There were 1853 patients enrolled and 97% had follow-up. Patients had a mean age of 53 +/- 14 years; 60% were women, 67% were black. There were 1491 (79%) patients without a prior stress test, 291 (16%) had a normal prior stress test result, and 89 (5%) had an abnormal prior stress test result. Admission rates were 92% (95% CI, 87%-98%) for patients with a prior abnormal stress test, 73% (95% CI, 67%-78%) for patients with a normal prior stress test, and 70% (95% CI, 67%-72%) for patients without a prior stress test. Adverse outcomes were the highest among patients with prior abnormal stress test but did not differ significantly between patients with no prior stress test and patients with prior normal stress test (10.1% [95% CI, 3.6-16.7%] vs 5.2% [95% CI, 4.1-6.4%] vs 4.8% [95% CI, 2.4-7.3%]). CONCLUSION: Patients without prior stress tests and patients with prior normal stress tests were admitted for potential ACS at the same rate and had the same 30-day cardiovascular event rates. This suggests that prior stress testing does not affect subsequent disposition decisions. Perhaps cardiac catheterization or computed tomography coronary angiograms would have more of an impact on subsequent visits, making them potentially more cost-effective in the low-risk patient.     

Measurement of Novel Biomarkers to Predict Chronic Heart Failure Outcomes and Left Ventricular Remodeling

Myocardial remodeling is pivotal in the progression and complication of chronic heart failure (HF). We assessed serial measurement of five biomarkers with biologic links to remodeling (biglycan, secreted frizzled-related protein 3, endostatin, insulin-like growth factor binding protein 7 [IGFBP7], mimecan) in 142 patients with HF followed through 882 office visits. IGFBP7 and mimecan were most associated with events; in fully adjusted models, lower IGFBP7 concentrations across visits independently predicted fewer events (odds ratio [OR]?=?0.83; 95 % confidence interval [CI]?=?0.73–0.95, p?=?0.01). Subjects with rising mimecan had greater decrease in left ventricular end diastolic (p?=?0.07) and systolic (p?=?0.01) volumes, greater increase in ejection fraction (p?=?0.02), and had lowest event rates. Statistical models suggested several HF medications might lead to changes in both IGFBP7 and mimecan values. The results suggest serial measurement of IGFBP7 provides prognostic information, while changes in mimecan provide unique information regarding myocardial remodeling.     

Bcl-2-related protein A1 is an endogenous and cytokine-stimulated mediator of cytoprotection in hyperoxic acute lung injury

Hyperoxic acute lung injury (HALI) is characterized by a cell death response with features of apoptosis and necrosis that is inhibited by IL-11 and other interventions. We hypothesized that Bfl-1/A1, an antiapoptotic Bcl-2 protein, is a critical regulator of HALI and a mediator of IL-11-induced cytoprotection. To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci. In WT mice, 100% O(2) caused TUNEL(+) cell death, induction and activation of intrinsic and mitochondrial-death pathways, and alveolar protein leak. Bcl-2 and Bcl-xl were also induced as an apparent protective response. A1 was induced in hyperoxia, and in A1-null mice, the toxic effects of hyperoxia were exaggerated, Bcl-2 and Bcl-xl were not induced, and premature death was seen. In contrast, IL-11 stimulated A1, diminished the toxic effects of hyperoxia, stimulated Bcl-2 and Bcl-xl, and enhanced murine survival in 100% O(2). In A1-null mice, IL-11-induced protection, survival advantage, and Bcl-2 and Bcl-xl induction were significantly decreased. VEGF also conferred protection via an A1-dependent mechanism. In vitro hyperoxia also stimulated A1, and A1 overexpression inhibited oxidant-induced epithelial cell apoptosis and necrosis. A1 is an important regulator of oxidant-induced lung injury, apoptosis, necrosis, and Bcl-2 and Bcl-xl gene expression and a critical mediator of IL-11- and VEGF-induced cytoprotection.