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Masum Ibn Musa via Wikimedia Commons // CC BY-SA 4.0

The Devious Strategy of the Mind-Controlling Cat-Poop Parasite

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Masum Ibn Musa via Wikimedia Commons // CC BY-SA 4.0

Toxoplasma gondii, a parasitic protozoan, infects more than 50 percent of people on Earth and millions of cats and other animals, yet the secrets to its success have largely remained a mystery—until now. A new study published in the journal Structure concludes that the parasite can hack into and rewire its host’s immune system to suit its own purposes.

You may not recognize this parasite by name, but you’ve probably heard it mentioned. T. gondii infection, better known as toxoplasmosis, has the power to produce strange changes in its hosts. The parasite can only reproduce within a cat’s body, and scientists believe that it can manipulate other animals to make that happen. Mice with toxoplasmosis lose their healthy fear of cats and will stroll right up to their predators, essentially delivering their parasitic passengers directly into the mouth of the beast.

Some scientists believe that toxoplasmosis can also influence human behavior, and studies have linked infection to symptoms of schizophrenia, bipolar disorder, and intermittent explosive disorder. Other researchers say these findings are overhyped, overblown, and impossible to reproduce.

Whether or not T. gondii can change our minds, it’s definitely changing our bodies. Toxoplasmosis can be dangerous for pregnant women and people with compromised immune systems, but most people never even know they’re sick—which is not how our bodies are supposed to work. Our immune systems are supposed to protect us from parasites like T. gondii, or, if they can’t, at least alert us by getting riled up and inflamed.

But somehow, this intruder found a way to override our personal security systems. The first clue to its strategy came last year, when scientists at the Institute for Advanced Biosciences discovered that T. gondii makes a protein called GRA24 that in turn convinces the body to make an inflammatory protein called p38α.

This raised a new question, one which became the focus of the new study: Why would a parasite ever want to trigger inflammation?

The researchers cultured human cells in the laboratory, then gave them toxoplasmosis and monitored the molecular-level interactions between the two proteins. They discovered that GRA24 can essentially hot-wire the security system and bypass multiple steps of the immune response process. By making its own p38α, T. gondii can control the flow and extent of inflammation. It doesn’t shut down the immune system; doing so could make its host sick and jeopardize the parasite’s new, cushy existence. Instead, it muffles the system just enough to keep itself safe and undetectable.

Watch your back, T. gondii. We're on to you.

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Medicine
New Technique Can Spot a Heart Attack in the Making Long Before It Happens
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Cardiology experts have developed a noninvasive way of measuring the fat around a person's blood vessels, which could help determine their risk for dangerous cardiac events. The researchers described their technique today in the journal Science Translational Medicine.

Heart attacks are incredibly common, affecting around 750,000 Americans every year. Heart disease is the number one cause of mortality in the U.S., responsible for one out of every four deaths. There are many reasons for this. Among them is the difficulty of identifying at-risk patients before it's too late.

Cardiologists' current method of choice uses a metric called coronary calcification score (CCS) to measure the hardening of a patient's arteries. CCS is a reliable way to predict future heart problems, paper co-author Charalambos Antoniades said in a statement, but it has its limitations.

"When coronary calcification is detected," he said, "it is already too late, as the calcification is not reversible."

And so, rather than measuring calcification, many researchers have begun looking for a way to measure blood vessel inflammation, which is usually a pretty good—and early—predictor of heart disease.

The inflammation itself can be hard to see without entering a patient's body. But recent studies have shown that it rarely travels alone: Blood vessels that are inflamed are also often wrapped in larger fat cells than healthy vessels. 

With this link in mind, Antoniades and his colleagues decided to try measuring the fat cells instead. They reviewed computed tomography scans from 453 patients about to undergo heart surgery, and used these data to create what they call the fat attenuation index (FAI). The higher a patient's FAI, the more inflammation they had, and the more advanced or severe their heart disease. 

The researchers then compared the FAI of 40 additional patients with the results of invasive scans of the inflammation in their hearts. Sure enough, each patient's FAI matched the swelling onscreen.

There are many benefits to using FAI, the authors say. Not only is it noninvasive and accurate, but it can be used in tandem with CCS and other methods for an even more complete picture. The next step will be validating the test's safety and accuracy in clinical trials.

FAI scans "could help direct these new types of treatments to the appropriate subgroups of patients at greatest risk," Antoniades says, "reducing costs and targeting more powerful drugs to the patients who will benefit most."

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Health
Don't Panic About the Plague
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If reports of measles and whooping cough making a reappearance aren't alarming enough, the news that three people in New Mexico have contracted plague this year might have you on edge. But these aren't the only recent cases of plague in the state—the disease appeared in both 2016 and 2015, causing one death—or even in the U.S.

In 2015, a child contracted the plague in Yosemite National Park, and so did a tourist from Georgia; park officials closed a campground where they discovered two dead squirrels infected with the disease. That same year in Colorado, a pitbull infected four humans with pneumonic plague before being put down, and two other Colorado residents died from plague, including a 16-year-old boy.

It all seems very scary, but don't go sealing yourself in protective gear yet. There's less to fear about plague than you may think. While the public is prone to panic that a medieval illness, which wiped out a quarter of Europe in the Middle Ages during the Black Death, has suddenly arisen from obscurity, the truth is: Plague never left.

Though we haven't seen a widespread epidemic of plague since the early 20th century, thanks to advances in sanitation and medicine, and there hasn't been a human-to-human case of transmission in America since 1924, an average of seven new cases are reported every year in the U.S. From 2010 to 2015, there were 3248 cases, including 584 deaths, reported worldwide, according to the World Health Organization.

Yersinia pestis, the flea-borne bacteria that's most often responsible for plague, infects rodents; humans are “incidental hosts,” who can acquire the infection if bitten by an infected flea or rodent. Compared to the 14th century, when the Black Death spread wildly, or the late 19th century, when 10 million people died of the disease after it traveled from Hong Kong to port cities worldwide, most people today live in more sanitary conditions and have less frequent contact with the rodents most likely to carry the infected fleas. Today, 95 percent of plague cases originate in parts of sub-Saharan Africa and Madagascar.

The most common of the three strains of plague is the notorious bubonic plague, which causes painful swollen lymph nodes (also called buboes) and was responsible for Europe's Black Death—so named because internal hemorrhages caused by the infection make the skin appear black. But the pitbull that infected four Colorado residents carried the rarer respiratory strain of pneumonic plague, which is contagious when the infected person coughs up infected particulates. There is also septicemic plague, the most lethal form, which infects the blood, and most often occurs when plague virus has gone undetected and is allowed to spread.

In the U.S., you're generally only at risk of contracting plague in late spring to early fall if you've been in a rural or semi-rural area of the West, especially New Mexico, Arizona, or Colorado, and have had contact with fleas or rodents including ground squirrels, chipmunks, prairie dogs, or rats. And even then, the risk is low.

Only the pneumatic version of plague is contagious from human to human (though untreated bubonic plague can become pneumonic), but you have to be coughed upon, or receive fluid from an infected person upon an open wound or directly into your mouth or nose.

Plague symptoms mimic any flu—fever, chills, headache, difficulty breathing or coughing—but people have been known to cough up blood with the pneumonic variety. If you've been in a rural area, or camping, and come down with these symptoms two to three days later, it's best to go to a hospital.

Now for some good news: While untreated plague is quite deadly, people with plague who are treated with antibiotics within 24 hours of infection have strong recovery rates.

So while it's good to be aware and take precautions, the chances of another plague pandemic remain slim.

This story was originally published in 2015 and has been updated. 

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