What we do know about Ebola

Ebola

Ebola is a simple virus. It consists of seven genes that are wrapped in two layers of protein. This is packaged with a polymerase (enzyme) and wrapped in a membrane studded with glycoproteins (proteins with sugar attached). When Ebola gets inside a cell, the enzyme makes copies of the Ebola genes and tricks the host cell into using them to make the proteins Ebola needs. Two of the proteins are sneaky. VP35 stops interferons from being made. Interferons alert the immune system that an invader is present. So, VP35 knocks out some sites of the immune system radar. VP24 works acts like a stealth bomber and makes the remaining immune system radar less effective. Ebola then attacks immune system cells and spreads via the liver, spleen and lymph nodes. This eventually results in a cytokine storm which initiates the pathologic response, in which a patient can lose 10 liters of fluid a day.

Ebola is the name of a river near the town of Yambuku. In September of 1976, a thermos containing two blood samples from a dying nun were sent to Antwerp. One of the vials in the thermos broke. The other was scooped out of the bloody, icy water and analyzed. The scientists determined they had a new and deadly virus. They called it by the name of the river so the town would not be stigmatized. Between 1976 and 2012 there were 20 Ebola epidemics in central Africa. Each subsided after claiming fewer than 300 lives. The current epidemic is of much greater magnitude. The World Health Organization (WHO) has described it as “the most acute severe public health emergency in modern times.” The WHO estimates by December there could be 10,000 new victims a week and 70% of them could die. Dead bodies have their largest viral load and are most infectious. Reports from Africa have shown there have been times when bodies have waited a week for disposal. We don’t need to be reminded that Africa is much closer. It is practically our next door neighbor. How do we answer the questions we asked before we described Ebola? We must develop risk literacy.

In 2011, Nathan Wolfe, a microbiologist, wrote “The Viral Storm, The Dawn of a New Pandemic Age”. He defined risk literacy as “the ability to distinguish between different levels of risk severity.” Wolfe declared “the constant barrage of threats articulated by the media has led to chronic risk habituation.” How do epidemiologists look at how easily a disease is transmitted? The use a concept called the Ro, the basic reproduction number. The higher the Ro, the easier it is for  disease to be transmitted. For example, the Ro for measles is 18. The Ro for Ebola is between 1.5 and 2.2. Ro is not a constant. It is dependent on the biology of the virus, the setting of its spread, and the behavior of people. For Ebola, the game plan is to identify cases quickly, isolate patients, trace their contacts, and change behavior to reduce transmission rates.

There is no need for panic. We need to stay informed, act on the information, and engage in protective, not paranoid, behaviors. Apply the same level of situational awareness to all of your patient encounters that you would use at a potential hazardous materials event. Assess the patient from a safe distance and take appropriate precautions. My approach is simple. I never get a patient’s blood, body fluids or other potentially infectious materials on me or in me. I never assume that my skin is intact. There are plenty of infections that can kill us besides Ebola. An infection can kill us or make us sick without being obvious or dramatic.

Ebola
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