• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • br We have concerns about both the accuracy


    We have concerns about both the accuracy and underlying rationale of Eugene Richardson and colleagues\' Comment about the “Ebola suspect\'s dilemma”. The authors quote a nosocomial infection rate of “around 25%” for individuals admitted to Ebola treatment facilities without Ebola virus disease. However, two previous papers document rates of 3% and 7%. In our previous study of over 1000 children admitted to Ebola treatment facilities with suspected Ebola virus disease, only three (0·5%) of 630 children who tested negative were subsequently readmitted with a positive test, all of whom had lost a parent to Ebola virus disease before their first admission; therefore, they were more likely to have acquired Ebola virus disease in the community than nosocomially. Furthermore, the case:fatality ratio of children who were admitted to hospital and were Ebola virus disease-negative was 9% (95% CI 8–12; 66 of 697), similar to previous inpatient mortality rates of children who were negative for Ebola virus disease at Ola During Children\'s Hospital in Freetown from 2013-2014, prior to the Ebola virus disease outbreak. By framing the outbreak within the trope of African subjugation or passivity in the face of international colonialists (humanitarian or otherwise), the agency is removed and the sacrifice belittled of the west African health-care workers, such as those who ran the Sierra Leonean Ministry of Health and military facilities in which our study was based. For example, far from “offering little in the way of intravenous resuscitation”, the Republic of Sierra Leone Armed Forces provided aggressive parenteral fluid resuscitation from their opening in September, 2014, several months before this protocol was scaled up in internationally run facilities. Nosocomial transmission rates and mortality rates for children who were Ebola virus disease-negative appear to have been lower than those estimated by Richardson and colleagues, which is testament to the leadership of these Sierra Leonean health-care workers and their commitment to patient care and infection control. By misrepresenting the outcomes achieved by efforts of these west African health-care workers, Richardson and colleagues seem to only bolster the faah inhibitors structural determinants that they denigrate.
    We thank Thomas Mayrhofer and colleagues for offering their threshold model as an explanation for patients\' aversion to accessing Ebola facilities during the recent Ebola outbreak in west Africa. We agree that this threshold model provides a rational and more elegant explanation of patients\' avoidance of ill-equipped and poorly sanitised holding centres; however, such an explanation was not the goal of our Comment. Instead, we aimed to produce a reductio ad absurdum of rationalist approaches to understanding behaviour during faah inhibitors the Ebola outbreak. Our argument was that these approaches reproduce an ideology of individualism that maps poorly onto our understanding of care seeking during the outbreak. By hypostasising individual autonomy and assuming perfect information, rationalist paradigms perniciously normalise the perception that clinical outcomes are a result of patient choice, rather than a result of intentional underdevelopment of health systems coupled with the historical prioritisation by colonial medicine and its legacies (including contemporary humanitarian aid) of containment by isolation. Hence the absurdity of our suggestion that a rational decision for patients with Ebola virus disease might be to deliberately infect themselves with malaria, which Robert Colebunders and colleagues correctly recognise as facetious. Furthermore, our ironic reflections on terms such as “rational” and “superspreader” are a call to recognise and interrogate the categories of thought that are instilled by our training as scientists, clinicians, and public health professionals. Colebunders and Felicity Fitzgerald and their colleagues also question whether we overestimate the potential for nosocomial Ebola virus transmission. In contrast with the low nosocomial transmission ates that they cite in Freetown, our experience in rural areas—which are so much more poorly resourced than the capital that they are deemed internal colonies—revealed, at times, much less effective infection prevention and control than in the metropole. For example, upon arrival at a rural district hospital in November, 2014, we entered wards crowded with corpses, pools of infectious vomit and excreta, and large amounts of contaminated personal protective equipment. Patients with suspected Ebola virus disease were admitted on clinical grounds because samples, if they were taken, took several days until results were attained; nine (100%) of nine nurses working there contracted Ebola virus disease. Additionally, it was not uncommon for several patients with suspected Ebola virus disease who were vomiting and had diarrhoea to be transported over great distances in a single ambulance. Thus, for the absurdist exercise presented in our Comment, we did not feel that it was far-fetched to posit that a quarter of negative individuals exposed to a similar field of risk could have become infected.