Context During the 2007-2008 influenza season, oseltamivir resistance among influenza A(H1N1) viruses increased significantly for the first time worldwide. Early surveillance data suggest that the prevalence of oseltamivir resistance among A(H1N1) viruses will most likely be higher during the 2008-2009 season. Objectives To describe patients infected with oseltamivir-resistant influenza A(H1N1) virus and to determine whether there were any differences between these patients and patients infected with oseltamivir-susceptible A(H1N1) virus in demographic or epidemiological characteristics, clinical symptoms, severity of illness, or clinical outcomes. Design, Setting, and Patients Influenza A(H1N1) viruses that were identified and submitted to the Centers for Disease Control and Prevention by US public health labo

[1] Ice sheets in the North American Arctic and, to a lesser extent, those in northern Eurasia calved large quantities of icebergs that drifted through Fram Strait into the Greenland Sea several times during the late Pleistocene. These icebergs deposited Fe oxide grains (45-250 mm) and coarse lithic clasts >250 mm matched to specific circum-Arctic sources. Four massive Arctic iceberg export events are identified from the Laurentide and the Innuitian ice sheets, between 14 and 34 ka (calendar years) in a sediment core from Fram Strait. These relatively short duration (<1-4 kyr) events contain 3-5 times the background levels of Fe oxide grains. They began suddenly, as indicated by a steep rise in the number of grains matched to an ice sheet source, suggesting rapid purges of ice through Fram Strait, due perhaps to collapse of ice sheets. The larger events from the northwestern Laurentide ice sheet are preceded by events from the Innuitian ice sheet. Despite the chronological uncertainties, the Arctic export events appear to occur prior to Heinrich events.

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The recommended breakpoints for the cefoxitin disk diffusion test for Staphylococcus aureus were recently modified. In this large-sample study, cefoxitin sensitivity and specificity compared to those of oxacillin were 97.3% and 100%, respectively. This study validated the new cefoxitin breakpoints for the detection of mecAmediated resistance in S. aureus.Staphylococcus aureus is a serious current health care concern. Both community-associated methicillin-resistant S. aureus (MRSA) and health care-associated MRSA are growing threats to the immunocompromised, as well as to the general public. Accurate detection of methicillin resistance in S. aureus is of the utmost importance to ensure effective treatment for the affected patient and to prevent further transmission.The mecA gene confers resistance to methicillin in S. aureus. The gene is located on the staphylococcal chromosome cassette mec and encodes penicillin binding protein 2a (PBP2a). PBP2a is located in the bacterial cell wall and has a low binding affinity for ␤-lactams (1, 2). This study evaluated the new Clinical Laboratory Standards Institute (CLSI) breakpoints for the cefoxitin disk test for determining mecA-mediated resistance in S. aureus (4).CLSI recommends usage of cefoxitin instead of oxacillin when using the disk diffusion method to determine resistance against methicillin for S. aureus (4). Cefoxitin results are easier to interpret and are thus more sensitive for the detection of mecA-mediated resistance than oxacillin results (5, 6, 7, 9-11). The recommended resistance and susceptibility breakpoints for the 30-g cefoxitin disk test used to detect mecA-mediated resistance in S. aureus were changed in January 2007 by CLSI from Յ19 mm and Ն20 mm to Յ21 mm and Ն22 mm, respectively. This study sampled a large number of recent S. aureus isolates to compare the performance of the cefoxitin disk test at the new breakpoints to that of the 1-g oxacillin disk test.Between August and September 2007, a total of 1,611 nonduplicate S. aureus isolates were collected by 53 Wisconsin clinical laboratories (up to 20 consecutive MRSA and methicillin-susceptible S. aureus isolates per laboratory) and submitted to the Wisconsin State Laboratory of Hygiene. Species identification was confirmed by colony morphology, coagulase slide test, subsequent tube test, and biochemicals. The isolation sites of the S. aureus isolates collected were as follows: skin and soft tissue (1,159 isolates; 71.9%), urine (136 isolates; 8.4%), respiratory tract (130 isolates; 8.1%), bloodstream (65 isolates; 4.0%), and other (121 isolates; 7.5%).Susceptibility to antimicrobial agents for confirmed S. aureus isolates was evaluated by the CLSI disk diffusion method on Mueller-Hinton agar (3). All agar plates and antibiotic disks were obtained from Remel (Lenexa, KS). A direct colony suspension of each S. aureus isolate was prepared to a 0.5 McFarland standard and plated on Mueller-Hinton agar. The zones of inhibition were measured using the Biomic V 3 system

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.