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Pitfalls in Screening for Ebola Virus Disease: The Variable Febrile and Human Subjective Response

Authors:
  • Hale O'mana'o Biomedical Research

Abstract

ABSTRACT The Ebolavirus outbreak of 2014 in West Africa is unprecedented. As of the most recent situation report from the World Health Organization on November 11, 2014, there have been 14,098 suspected, probable and confirmed cases with 5160 deaths reported globally in this Public Health Emergency of International Concern. 5 cases outside the continent of Africa have been reported. Entry and exit screening for EVD (Ebola Virus Disease) of individuals originating from known outbreak regions currently include the presence of fever or additional symptoms consistent with EVD. Despite these efforts, the rate of transmission [R(t)] remains at 1.4 to 1.7, transnational cases are increasing, and a resurgence of the outbreak in Mali has recently been reported. This perspective article discusses the pitfalls associated with the determination of fever in the screening process as well as the difficulties with individual, subjective self-reporting of symptoms. Keywords EVD Screening Ebolavirus Ebola Virus Disease EVD Ebola fever Ebola Hemorrhagic Fever Ebola outbreak 2014 Screening for EVD EVD Exit Screening EVD Entry Screening Asymptomatic EVD Denial of Disease in EVD Fever determination in EVD
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Outbreak of Marburg virus disease in Johannesburg
  • Js Gear
  • Ga Cassel
  • Gear
  • Aj
Gear JS, Cassel GA, Gear AJ, et al. Outbreak of Marburg virus disease in Johannesburg. Br Med J 1975;4:489-!
Harrison's Principles of Internal Medicine, 18e; Chapter 16 Fever and Hyperthermia
  • Ca L Dan
  • Longo
  • Editor
  • S Anthony
  • Fauci
  • Editor
  • L Dennis
  • Kasper
  • Editor
  • Stephen
Harrison's Principles of Internal Medicine, 18e; Chapter 16 Fever and Hyperthermia. Dinarello CA; Dan L. Longo, Editor, Anthony S. Fauci, Editor, Dennis L. Kasper, Editor, Stephen L. Hauser, Editor, J. Larry Jameson, Editor, Joseph Loscalzo!