Deborah S. Asnis
Albert Einstein College of Medicine
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Clinical Infectious Diseases | 2000
Deborah S. Asnis; Rick Conetta; Alex A. Teixeira; Glenn Waldman; Barbara A. Sampson
West Nile Virus (WNV) is a mosquito-borne flavivirus, which has been known to cause human infection in Africa, the Middle East, and southwestern Asia. It has also been isolated in Australia and sporadically in Europe but never in the Americas. Clinical features include acute fever, severe myalgias, headache, conjunctivitis, lymphadenopathy, and a roseolar rash. Rarely is encephalitis or meningitis seen. During the month of August 1999, a cluster of 5 patients with fever, confusion, and weakness were admitted to the intensive care unit of the same hospital in New York City. Ultimately 4 of the 5 developed flaccid paralysis and required ventilatory support. Three patients with less-severe cases presented shortly thereafter. With the assistance of the New York City and New York State health departments and the Centers for Disease Control and Prevention, these were documented as the first cases of WNV infection on this continent.
Annals of the New York Academy of Sciences | 2006
Deborah S. Asnis; Rick Conetta; Glenn Waldman; Alex A. Teixeira
Abstract: Viruses cause most forms of encephalitis. The two main types responsible for epidemic encephalitis are enteroviruses and arboviruses. The City of New York reports about 10 cases of encephalitis yearly. Establishing a diagnosis is often difficult. In August 1999, a cluster of five patients with fever, confusion, and weakness were admitted to a community hospital in Flushing, New York. Flaccid paralysis developed in four of the five patients, and they required ventilatory support. Three, less severe, cases presented later in the same month. An investigation was conducted by the New York City (NYC) and New York State (NYS) health departments and the national Centers for Disease Control and Prevention (CDC). The West Nile virus (WNV) was identified as the etiologic agent. WNV is an arthropod‐borne flavivirus, with a geographic distribution in Africa, the Middle East, and southwestern Asia. It has also been isolated in Australia and sporadically in Europe but never in the Americas. The majority of people infected have no symptoms. Fever, severe myalgias, headache, conjunctivitis, lymphadenopathy, and a roseolar rash can occur. Rarely, encephalitis or meningitis is seen. The NYC outbreak resulted in the first cases of WNV infection in the Western Hemisphere and the first arboviral infection in NYC since yellow fever in the nineteenth century. The WNV is now a public health concern in the United States.
The Joint Commission Journal on Quality and Patient Safety | 2010
Robert S. Crupi; David Di John; Peter Michael Mangubat; Deborah S. Asnis; Jaime Devera; Paul Maguire; Sheila L. Palevsky
Article-at-a-Glance Background Health care workers (HCWs) can acquire and transmit influenza to their patients and coworkers, even while asymptomatic. The U.S. Healthy People 2010 initiative set a national goal of 60% coverage for HCW influenza vaccination by 2010. Yet vaccination rates remain low. In the 2008–2009 influenza season, Flushing Hospital Medical Center (FHMC; New York) adopted a “push/pull” point-of-dispensing (POD) vaccination model that was derived from emergency preparedness planning for mass vaccination and/or prophylaxis to respond to an infectious disease outbreak, whether occurring naturally or due to bioterrorism. Launch of the HCW Vaccination Program In mid-September 2008, a two-week HCW vaccination program was launched using a sequential POD approach. In Push POD, teams assigned to specific patient units educated all HCWs about influenza vaccination and offered on-site vaccination; vaccinated HCWs received a 2009 identification (ID) validation sticker. In Pull POD, HCWs could enter the hospital only through one entrance; all other employee entrances were “locked down.” A 2009 ID validation sticker was required for entry and to punch in for duty. Employees without the new validation sticker were directed to a nearby vaccination team. After the Push/Pull POD was completed, the employee vaccination drive at FHMC was continued for the remainder of the influenza season by the Employee Health Service. Results Using this model, in two days 72% of the employees were reached, with 54% of those reached accepting vaccination. Conclusions This model provides a novel approach for institutions to improve their HCW influenza vaccination rates within a limited period through exercising emergency preparedness plans for infectious disease outbreaks.
Clinical Pulmonary Medicine | 2005
Vladimir Sabayev; Richard H. Savel; Angela Schiteanu; Deborah S. Asnis; Alice Veloudios
We report the case of a 43-year-old HIV-positive male who developed a pulmonary artery pseudoaneurysm as a complication of invasive aspergillosis. The patient was treated with amphotericin B with clinical improvement, and was discharged to a nursing home on voriconazole. He died of unrelated complications of his end-stage HIV 4 months later. Invasive pulmonary aspergillosis is a recognized complication in immunocompromised patients. Pulmonary artery pseudoaneurysm in the setting of invasive aspergillosis has not been described in patients with AIDS. Hemoptysis in these settings is usually a preterminal event. In our case, the management was conservative with clinical improvement.
Clinical Microbiology Newsletter | 1996
Deborah S. Asnis; Joaquin Tavares
2. Butler, T. 1983. Plague and other Yersinia infections. Plenum Press, New York. 3. Solomon, T. 1995. Alexandre Yersin and the plague baciUus. J. Trop. IVied. Hyg. 98:2129-212. 4. Gross, L 1995. How the plague bacillus and its transmission through fleas were discovered: reminiscences from my years at the Pasteur Institute in Paris. Prec. Natl. Acad. Sci. U.S.A. 92:7609--7611. 5. Bmbaker, R.R. 1979. Expression of virulence in yersiniae. In D. Schlessingur (ed.), Microbiology. 1979. American Society for Microbiology. Washington, D.C. 6. Une, T., and R.R. Brubaker. 1984. In vivo comparison of avirulent Vwa and Pgmor Pst r phenotypes of yersiniae. Infect. Immun. 43:95--900. 7. Lindier, L.E., M.S. Klernpner, and S.C. Straley. 1990. Yersiniapestis pH6 antigen, genetic, biochemical and virulence characterization of a protein involved in the pathogenesis of bubonic plague. Infect. Immun. 58:2569-2577. 8. McDonough, K.A., and S. Falkow. 1989. A Yersinia pestis-specific DNA fragment encodes temperature-dependent coagulase and fibrinolysin-associated phenotypes. Mol. Microbiol. 3:767-775. 9. Straley, S.C., et al. 1993. Yops of Yersinia spp. pathogenic for humans. Infect. Inamun. 61:3105-3110. 10. Butler, T. 1995. Yersinia species (including plague), p. 2070-2078. In G.L. Mandell, J.E. Bennett, and R. Dolin (ed.), Principles and pr~,ctice of infectious diseases. 4th ed. Churchill Livingstone, New York. 11. Centers for Disease Control and Prevention. 1994. Human plague---United States, 1993-1994. Morbidity Mortality Weekly Report 43:243-246. 12. Doll, J.M., et al. 1994. Cat-transmitted fatal pneumonic plague in a person who traveled from Colorado to Arizona. Am. J. Trop. Med. Hyg. 51:109-114. 13. Dar, L., R. Thak-ur, and W.S. Dar. 1994. India: is it plague? Lancet 344:1359. 14. Jayaraman, K.S. 1994. Indian plague poses enigma to investigators. Nature 371:547.
American Journal of Clinical Pathology | 1996
Tsieh Sun; Carl F. Ilardi; Deborah S. Asnis; Alfred R. Bresciani; Steven Goldenberg; Beth Roberts; Saul Teichberg
Clinical Infectious Diseases | 1998
Chi Go; Deborah S. Asnis; Herbert P. Saltzman
American Journal of Emergency Medicine | 2003
Robert S. Crupi; Deborah S. Asnis; Christopher C. Lee; Thomas Santucci; Mark J. Marino; Bruce J. Flanz
Clinical Infectious Diseases | 1997
Deborah S. Asnis; Anna Niegowska
Clinical Infectious Diseases | 1994
Deborah S. Asnis; Gunwant S. Dhaliwal
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