The 2014-2016 Ebola virus disease (Ebola) epidemic in West Africa underscores the need for health care infection prevention and control (IPC) practices to be implemented properly and consistently to interrupt transmission of pathogens in health care settings to patients and health care workers. Training and assessing IPC practices in general health care facilities not designated as Ebola treatment units or centers became a priority for CDC as the number of Ebola virus transmissions among health care workers in West Africa began to affect the West African health care system and increasingly more persons became infected. CDC and partners developed policies, procedures, and training materials tailored to the affected countries. Safety training courses were also provided to U.S. health care workers intending to work with Ebola patients in West Africa. As the Ebola epidemic continued in West Africa, the possibility that patients with Ebola could be identified and treated in the United States became more realistic. In response, CDC, other federal components (e.g., Office of the Assistant Secretary for Preparedness and Response) and public health partners focused on health care worker training and preparedness for U.S. health care facilities. CDC used the input from these partners to develop guidelines on IPC for hospitalized patients with known or suspected Ebola, which was updated based on feedback from partners who provided care for Ebola patients in the United States. Strengthening and sustaining IPC helps health care systems be better prepared to prevent and respond to current and future infectious disease threats. The activities summarized in this report would not have been possible without collaboration with many U.S. and international partners (http://www.cdc.gov/vhf/ebola/outbreaks/2014-west-africa/partners.html).

Of the 9 vancomycin-resistant Staphylococcus aureus (VRSA) cases reported to date in the literature, 7 occurred in Michigan (MI). In 5 out of 7 of the Michigan VRSA cases, an Inc18-like vanA plasmid was identified in the VRSA isolate and/or an associated vancomycin-resistant Enterococcus (VRE) isolate from the same patient. This plasmid may play a critical role in the emergence of VRSA and analysis of the geographical distribution of VRE containing this plasmid may explain the observed prevalence of VRSA in MI. A total of 1,641 VRE from three separate collections were tested for the Inc18-like vanA plasmid by PCR for traA, repR, and vanA. All VRE from 2 MI institutions (N= 386), and between 60 to 70 VRE (N=883) from 17 institutions in 13 other states were tested. Fifteen isolates (3.9%) from MI were positive for an Inc18-like vanA plasmid (9 E. faecalis [12.5%], 3 E. faecium [1.0%], 2 E. avium, and 1 E. raffinosus). Six isolates (0.6%) from outside of MI were positive (3 E. faecalis [2.7%] and 3 E. faecium [0.4%]). Fourteen of the 15 plasmid-positive isolates from MI had the same Tn1546 insertion site location as those of the VRSA-associated Inc18 plasmid whereas 5 out of 6 plasmid-positive isolates from outside of MI differed in this characteristic. The one exception was an E. faecium isolate with a pulsed-field gel electrophoresis (PFGE) pattern that was indistinguishable from a plasmid-positive isolate from MI. Most plasmid-positive E. faecalis demonstrated diverse patterns by PFGE, with the exception of three pairs with indistinguishable patterns, suggesting the plasmid is mobile. Although VRE with the VRSA-associated Inc18-like vanA plasmid were more common in MI, they remain rare. Periodic surveillance of VRE for the plasmid may be useful in predicting occurrence of VRSA.