Epidemiology of 2009 pandemic influenza A (H1N1) deaths in the United States, April-July 2009.

During the spring of 2009, pandemic influenza A (H1N1) virus (pH1N1) was recognized and rapidly spread worldwide. To describe the geographic distribution and patient characteristics of pH1N1-associated deaths in the United States, the Centers for Disease Control and Prevention requested information from health departments on all laboratory-confirmed pH1N1 deaths reported from 17 April through 23 July 2009. Data were collected using medical charts, medical examiner reports, and death certificates. A total of 377 pH1N1-associated deaths were identified, for a mortality rate of .12 deaths per 100,000 population. Activity was geographically localized, with the highest mortality rates in Hawaii, New York, and Utah. Seventy-six percent of deaths occurred in persons aged 18-65 years, and 9% occurred in persons aged ≥ 65 years. Underlying medical conditions were reported for 78% of deaths: chronic lung disease among adults (39%) and neurologic disease among children (54%). Overall mortality associated with pH1N1 was low; however, the majority of deaths occurred in persons aged <65 years with underlying medical conditions.

Characteristics of patients with oseltamivir-resistant pandemic (H1N1) 2009, United States.

During April 2009-June 2010, thirty-seven (0.5%) of 6,740 pandemic (H1N1) 2009 viruses submitted to a US surveillance system were oseltamivir resistant. Most patients with oseltamivir-resistant infections were severely immunocompromised (76%) and had received oseltamivir before specimen collection (89%). No evidence was found for community circulation of resistant viruses; only 4 (unlinked) patients had no oseltamivir exposure.

The assessment of data sources for influenza virologic surveillance in New York State.

BACKGROUND: Following the 2013 USA release of the Influenza Virologic Surveillance Right Size Roadmap, the New York State Department of Health (NYSDOH) embarked on an evaluation of data sources for influenza virologic surveillance. OBJECTIVE: To assess NYS data sources, additional to data generated by the state public health laboratory (PHL), which could enhance influenza surveillance at the state and national level. METHODS: Potential sources of laboratory test data for influenza were analyzed for quantity and quality. Computer models, designed to assess sample sizes and the confidence of data for statistical representation of influenza activity, were used to compare PHL test data to results from clinical and commercial laboratories, reported between June 8, 2013 and May 31, 2014. RESULTS: Sample sizes tested for influenza at the state PHL were sufficient for situational awareness surveillance with optimal confidence levels, only during peak weeks of the influenza season. Influenza data pooled from NYS PHLs and clinical laboratories generated optimal confidence levels for situational awareness throughout the influenza season. For novel influenza virus detection in NYS, combined real-time (rt) RT-PCR data from state and regional PHLs achieved ≥85% confidence during peak influenza activity, and ≥95% confidence for most of low season and all of off-season. CONCLUSIONS: In NYS, combined data from clinical, commercial, and public health laboratories generated optimal influenza surveillance for situational awareness throughout the season. Statistical confidence for novel virus detection, which is reliant on only PHL data, was achieved for most of the year.

Effects of delayed administration of low-dose lidocaine on transient focal cerebral ischemia in rats.

BACKGROUND: The authors' previous study demonstrated that a clinical antiarrhythmic dose of lidocaine, when given before ischemia, is neuroprotective in a rat model of transient focal cerebral ischemia. In this study, the authors investigated whether the administration of this dose of lidocaine, when delayed until 45 min after the onset of ischemia, also reduces ischemic brain injury. METHODS: Lidocaine was administered as an intravenous bolus (1.5 mg/kg) followed by an intravenous infusion (2 mg. kg(-1).h(-1)) for 165 min, beginning 45 min after the onset of a 90-min period of transient focal cerebral ischemia. Control animals were given the same volume of saline. Focal cerebral ischemia was induced by occluding the right middle cerebral artery using an intraluminal suture. Neurologic outcome and body weight loss were quantified 7 days later. The brain was fixed 7 days after ischemia and brain sections were stained with hematoxylin and eosin for assessment of infarct size and the number of intact neurons. In separate experiments, local cerebral blood flow and the electroencephalogram were measured during ischemia and 180 min into the reperfusion period. Infarct size was assessed after 24 h. RESULTS: Infarct size, at either 24 h or 7 days after ischemia, was not significantly reduced in the lidocaine group. However, the number of intact neurons was significantly increased in both the ischemic penumbra and core of the lidocaine group 7 days after ischemia, compared with the vehicle group. Rats treated with lidocaine demonstrated better neurologic outcome and less weight loss (P < 0.05). Lidocaine treatment had no significant influence on local cerebral blood flow and electroencephalogram during ischemia and reperfusion. CONCLUSIONS: Administration of a clinical antiarrhythmic dose of lidocaine, beginning 45 min after the onset of ischemia, reduces ischemic brain injury after transient focal cerebral ischemia in the rat. This indicates that delayed administration of neuroprotective agents may reduce brain damage resulting from ischemia.