Doctor who survived Ebola received experimental drug treatment

On 28 September, 2014, a 38-year old doctor, who was in charge of an Ebola virus treatment unit in Lakka, Sierra Leone, developed a fever and diarrhea. He tested positive for the virus on the same day. He was placed on a ventilator and on kidney dialysis, and was given antibiotics together with a 3-day course of an experimental drug called FX06 -- a fibrin-derived peptide that has been shown to reduce vascular leakage and its complications in mice with Dengue hemorrhagic shock. Credit: © nito / Fotolia

On 28 September, 2014, the 38-year old doctor, who was in charge of an Ebola virus treatment unit in Lakka, Sierra Leone, developed a fever and diarrhea. He tested positive for the virus on the same day. The doctor was airlifted to Frankfurt University Hospital on the 5th day of his illness and admitted to a specialized isolation unit.

Within 72 hours of admission he developed signs of vascular leakage and severe multi-organ failure, including the lungs, kidneys, and gastrointestinal tract. He was placed on a ventilator and on kidney dialysis, and was given antibiotics together with a 3-day course of an experimental drug called FX06 -- a fibrin-derived peptide that has been shown to reduce vascular leakage and its complications in mice with Dengue hemorrhagic shock.

A marked improvement in vascular and respiratory function was seen under the combined measures of intensive care and drug treatment. After a 30-day observation period, no Ebola virus genetic material was detected in the patient's blood plasma. The patient was released from hospital and is now with his family.
"Even though the patient was critically ill, we were able to support him long enough for his body to start antibody production and for the virus to be cleared by his body's defenses," explains Dr Wolf.

"In terms of improving treatment for Ebola patients, we have shown how intensive care medicine can successfully be applied under strict isolation conditions," adds senior author Professor Zacharowski, head of the Department of Anaesthetics and Intensive Care Medicine at Frankfurt University Hospital."
The authors conclude by calling for FX06 to be evaluated in clinical trials.

Source: The Lancet

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What bank voles can teach us about prion disease transmission and neurodegeneration

This image shows accumulation of misfolded, toxic prion protein (brown staining) in the brain of a transgenic mouse expressing bank vole PrP and challenged with human variant Creutzfeldt-Jakob disease (vCJD) prions. Credit: Image courtesy of Dr. Joel Watts

When cannibals ate brains of people who died from prion disease, many of them fell ill with the fatal neurodegenerative disease as well. Likewise, when cows were fed protein contaminated with bovine prions, many of them developed mad cow disease. On the other hand, transmission of prions between species, for example from cows, sheep, or deer to humans, is -- fortunately -- inefficient, and only a small proportion of exposed recipients become sick within their lifetimes.

A study published on April 3rd in PLOS Pathogens takes a close look at one exception to this rule: bank voles appear to lack a species barrier for prion transmission, and their universal susceptibility turns out to be both informative and useful for the development of strategies to prevent prion transmission.
Prions are misfolded, toxic versions of a protein called PrP, which in its normal form is present in all mammalian species that have been examined. Toxic prions are "infectious"; they can induce existing, properly folded PrP proteins to convert into the disease-associated prion form. Prion diseases are rare, but they share features with more common neurodegenerative diseases like Alzheimer's disease.

Trying to understand the unusual susceptibility of bank voles to prions from other species, Stanley Prusiner, Joel Watts, Kurt Giles and colleagues, from the University of California in San Francisco, USA, first tested whether the susceptibility is an intrinsic property of the voles' PrP, or whether other factors present in these rodents make them vulnerable.

The scientists introduced into mice the gene that codes for the normal bank vole prion protein, thereby generating mice that express bank vole PrP, but not mouse PrP. When these mice get older, some of them spontaneously develop neurologic illness, but in the younger ones the bank vole PrP is in its normal, benign folded state. The scientists then exposed young mice to toxic misfolded prions from 8 different species, including human, cattle, elk, sheep, and hamster.

They found that all of these foreign-species prions can cause prion disease in the transgenic mice, and that the disease develops often more rapidly than it does in bank voles. The latter is likely because the transgenic mice express higher levels of bank vole PrP than are naturally present in the voles.

The results show that the universal susceptibility of bank voles to cross-species prion transmission is an intrinsic property of bank vole PrP. Because the transgenic mice develop prion disease rapidly, the scientists propose that the mice will be useful tools in studying the processes by which toxic prions "convert" healthy PrP and thereby destroy the brain. And because that process is similar across many neurodegenerative diseases, better understanding prion disease development might have broader implications.

Source:  PLOS

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Mapping bats could help stop Ebola's spread

Fruit bats (Pteropodidae) are considered the likely host of the Ebola virus. Credit: Satit Srihin

In the fight against Ebola, mapping fruit bat habitats could be one important step, says a geoinformatics researcher at Sweden's Royal Institute of Technology.

Like the Black Death that ravaged medieval Europe, the Ebola virus' progress through remote areas of West Africa is enabled by lack of understanding about the disease, including its causes and transmission.

Mapping technology however will give responders to the crisis in Africa the upper hand in stopping the spread of the deadly disease, says Skog, a researcher in geoinformatics at Sweden's KTH Royal Institute of Technology.

Skog's research has produced a method that medical professionals can use to visualise the geographical distribution of a disease over time. In his research, Skog has explored the relationship between geography and disease distribution in major epidemics of the past, including the Black Death, the Russian Flu pandemic of 1889, the Asiatic Influenza of 1957 and the swine flu. He says the historical data provides a basis for predicting the course of future epidemics and pandemics.

"My research and method can also be used to report the current state of a pandemic, or predict how extensive the spread will be. And where the disease will strike next," Skog says.

In fact, the way in which Black Death spread during the mid 14th, century bears a no small resemblance to today's Ebola epidemic, he says. Both diseases were hosted by small mammals -- black rats and fruit bats, respectively. But ultimately it was humans that enabled its spread.

"The Black Death was very much depending on total lack of knowledge regarding the etiology of the disease and how to avoid further transmission," Skog says. "That is also the case for the mainly remote locations where Ebola now is spread."

Fruit bats are believed to be the natural hosts of Ebola. These bats are among the creatures that residents of rural West Africa hunt for "bush meat." The disease is also spread by the droppings of the bat, and it is believed to have spread to other types of bush meat, as well as monkeys and pigs that are raised for slaughter.

"The local population is getting part of their nourishment from bush hunting, leading to contact with the virus that is transmitted via body fluids," Skog says, suggesting that closer study of the fruit bat could provide vital answers.

"A guess of mine is that the number of infected fruit bats is a determining factor for an Ebola outbreak," he says. "Are there any known factors that may have changed the ecosystem in favor of the bats? Are the bats affected by the virus too? Do fruit bats always carry the Ebola virus or is the virus fatal to them as well? If so the percentage of infected bats will vary over the years also depending on the immunology of the species."

There are a number of geoinformation technology options available to public health organizations that have sent field crews to respond to the crisis. These, Skog says, including equipping field workers with hand-held GPS devices that feed a central database with data and findings regarding locations of bodies, possible infections and diagnosed cases personnel.

"The data can easily be centrally monitored and used for decisions and policies to mitigate the spread," he says. "Using satellite imagery, population centers can be localized. Collected disease data can also be compared and analysed with environmental and climatologic data to support other efforts to control the spread."

For instance, assuming that fruit bats are the reservoir for the ebola virus, Skog says it would be of interest to find out if the first detected cases in an outbreak are located in or close to a fruit bat habitat. "If the environmental and climatologic parameters for fruit bat habitats can be defined, there is a chance these habitats could be mapped using existing map data and satellite or airborne imagery," he says.

"Then risk areas could be monitored and preventive measures could be performed by health authorities. If the natural reservoir is in fact some other animal, positioning the first cases in each outbreak would still give a clue about what to look for."

Source: KTH The Royal Institute of Technology

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