CLOSE
Original image

Being Infected With Malaria Helped Ebola Victims to Survive

Original image
Ebola survivor James Harris, 29, stands for a portrait before a shift as a nurse's assistant at the Doctors Without Borders (MSF), Ebola treatment center on October 12, 2014 in Paynesville, Liberia. Image credit: John Moore/Getty Images

 
A recent study revealed a surprising finding: Of those infected in the West African Ebola epidemic in 2014, patients who had an active malaria parasite infection were actually more likely to survive the Ebola virus, and by a significant degree. While just over half (52 percent) of Ebola patients not infected with malaria survived, those co-infected with malaria had a survival rate of 72 to 83 percent, depending on their ages and the amount of Ebola virus in their blood.

What gives? Shouldn’t having a second, potentially deadly infection make you more likely to die of Ebola? 

Maybe not. Though researchers aren’t yet sure of the mechanism by which malaria co-infection in Ebola patients might be protective, they have some ideas. The prevailing thought is that malaria is somehow modifying the immune response to Ebola, making it less deadly than in people who aren’t co-infected with the malaria parasite.

The authors of the study, published in the journal Clinical Infectious Diseases, note that malaria can make other infections less deadly. For example, in a group of children from Tanzania, those who had respiratory infections along with malaria were less likely to have those infections develop into pneumonia than kids who had respiratory infections without it.

It may be that malaria is able to tone down a phenomenon called the “cytokine storm”—the body’s own response to an Ebola infection that inadvertently kills the host while attempting to eliminate the pathogen. If malaria can turn this host response down, patients may have a better chance of surviving the virus’s assault.

This wouldn’t be the first time that malaria infection has been hailed as a hero, rather than an enemy. In 1927, the Nobel Prize in Physiology or Medicine was awarded to Julius Wagner-Jauregg “for his discovery of the therapeutic value of malaria inoculation in the treatment of dementia paralytica.” Wagner-Juaregg and others had observed that sometimes syphilis seemed to be cured following “febrile infectious diseases” as far back as 1887. He also noted in his Nobel speech that he had “singled out as a particular advantage of malaria that there is the possibility of interrupting the disease at will by the use of quinine, but I did not then anticipate to what degree these expectations from induced malaria would be fulfilled.” While there was no “cure” for syphilis at the time, and no cure for the other infection he had considered (erysipelas, usually caused by the same bacterium that causes strep throat and scarlet fever), malaria could be treated with quinine, a compound that we still use today.

Before Wagner-Juaregg’s “malariotherapy,” treatments for syphilis included mercury, Salvarsan (an arsenic-containing drug), and bismuth—all of which had serious side effects, including death. Wagner-Juaregg’s methods seemed to have no more risks than the conventional treatments of the era, and in 1917, he injected nine individuals suffering from advanced syphilis with malaria parasites. He reported three of them to be cured, and three more to have “extensive remission.” Soon, malariotherapy spread across the U.S. and into Europe, with tens of thousands of syphilis patients treated with the malaria parasite.

However, the degree to which malariotherapy worked is still a matter of controversy. And it was not without its own serious side effects, with death resulting in up to 15 percent of those treated. With the introduction of penicillin as a treatment for syphilis in the 1940s, malariotherapy was replaced, but the decades of use of malaria as a treatment significantly advanced our knowledge of the malaria parasite.

Today, scientists may be able to use this natural experiment to create drugs that could mimic malaria’s effect without actively infecting individuals. (Malaria is a devastating disease, causing hundreds of thousands of deaths every year, primarily in Africa.) Animal models could potentially be used to tease apart the host’s response to Ebola infection and determine how malaria alters the usual response to the Ebola virus to make it less deadly. These alterations could be used to create new drugs or other interventions to treat Ebola infection.

More importantly, further study of the phenomenon of malaria co-infection with other pathogens could lead to changes in patient care. The current standard operating procedure is to treat malaria infection when it is found in an Ebola case. But might it actually improve a patient's outcome to delay treatment for malaria? The authors of the current study note that a mouse model of malaria-Ebola co-infection found that treatment for malaria led to death from Ebola infection in all animals. And yet during the 2014 Ebola outbreak, work carried out at one Ebola treatment center in Liberia showed that Ebola fatality rates decreased with effective malaria treatment. Complicating the matter, the malarial drug used in that case (artesunate-amodiaquine, or ASAQ) may have been responsible for the anti-Ebola activity.

While it’s unlikely that a malaria treatment for Ebola would be as popular (or legal or ethical) as the “malariotherapy” of the early 1900s, it’s certainly worth closely examining the clues this co-infection has provided scientists about the nature of both Ebola and malaria infections—and how we could harness them to fight against one of nature’s most frightening diseases.

Original image
iStock
arrow
Medicine
Why Haven't We Cured Cancer Yet?
Original image
iStock

Walkathons, fundraisers, and ribbon-shaped bumper stickers raise research dollars and boost spirits, but cancer—the dreaded disease that affects more than 14 million people and their families at any given time—still remains bereft of a cure.

Why? For starters, cancer isn't just one disease—it's more than 100 of them, with different causes. This makes it impossible to treat each one using a one-size-fits-all method. Secondly, scientists use lab-grown cell lines cultivated from human tumors to develop cancer therapies. Living masses are far more complex, so potential treatments that show promise in lab experiments often don't work on cancer patients. As for the tumors themselves, they're prone to tiny genetic mutations, so just one growth might contain multiple types of cancer cells, and even unique sub-clones of tumors. These distinct entities might not respond the same way, or at all, to the same drug.

These are just a few of the challenges that cancer researchers face—but the good news is that they're working to beat all of them, as this TED-Ed video explains below.

Original image
iStock
arrow
Health
Skipping Breakfast Could Be Bad for Your Heart
Original image
iStock

There are mountains of evidence supporting the claim that breakfast really is the most important meal of the day. Getting something in your stomach in the first hours of the morning can regulate your glucose levels, improve your cognition, and keep your hunger in check. Now new research published in the Journal of the American College of Cardiology points to another reason not to wait until lunchtime to break last night’s fast. As TIME reports, people who skip breakfast are at an increased risk for atherosclerosis, a disease caused by plaque buildup in the arteries.

Researchers surveyed over 4000 men and women between the ages of 40 and 54 living in Spain. After looking at the dietary habits of each participant, they broke them into three groups: people who consumed more than 20 percent of their daily calories in the morning; those who got 5 to 20 percent; and those who ate less than 5 percent.

The subjects who ate very little in the a.m. hours or skipped breakfast all together were 2.5 more likely to have generalized atherosclerosis. This meant that plaque was starting to collect on the walls of their arteries, hardening and narrowing them and increasing the risk for heart attack or stroke. People who fell into the 5 to 20 percent calorie category were also more likely to show early signs of the disease, while those who ate the most calories in the morning were the healthiest.

These results aren’t entirely surprising. Previous studies have shown a connection between skipping breakfast and health problems like high blood pressure, high cholesterol, diabetes, and unwanted weight gain. A possible explanation for this trend could be that waiting several hours after waking up to eat your first meal of the day could trigger hormonal imbalances. The time between getting into and out of bed is the longest most of us go without eating, and our bodies expect us to consume some calories to help kickstart our energy for the day (drinking straight coffee doesn’t cut it). Another theory is that people who don’t eat in the morning are so hungry by the time lunch rolls around that they overcompensate for those missing calories, which is why skipping breakfast doesn’t make sense as a diet strategy.

But of course there are many breakfast skippers who aren’t motivated by health reasons either way: They just don’t think they have the time or energy to feed themselves in the morning before walking out the door. If this describes you, here are some simple, protein-packed meals you can prepare the night before.

[h/t TIME]

SECTIONS

arrow
LIVE SMARTER
More from mental floss studios