Saving brains: malaria in pregnancy leads to cognitive deficits in offspring

October 4, 2015November 17, 2015 ~ Betty ~ 1 Comment

OLYMPUS DIGITAL CAMERA — The malaria clinic at Nalufenya Children’s Hospital in Jinja, Uganda (Credit: Chloe McDonald)

In the global effort to eradicate malaria, the focus has often been on the number of lives saved—through insecticide-treated bed nets, artemisinin-based therapies, vector control and other strategies. Equally important in this fight is the concept of saving brains, particularly in young children.

Malaria is caused by an infection with the parasite Plasmodium falciparum and can manifest as either an uncomplicated or severe disease. The most severe neurological complication is cerebral malaria, a disease that disproportionally affects young children because they have not yet developed immunity against Plasmodium parasites. More than 785,000 children under the age of nine living in sub-Saharan Africa are affected by cerebral malaria each year. The idea of saving brains becomes especially relevant in this population because cerebral malaria can have long-lasting effects on the cognitive function of these children. An early study found that children who developed cerebral malaria were roughly three and a half times more likely to have a cognitive deficit than children who did not have malaria. Importantly, researchers observed this difference two years after the initial episode of cerebral malaria and long after the disease itself had been treated.

If exposure to malaria at a young age could have long-lasting effects on the cognitive abilities of children, what happened when that exposure happened much earlier? Like during pregnancy? In a new study published in PLoS Pathogens, a team of researchers led by Dr. Chloë McDonald and Dr. Kevin Kain showed that malaria in pregnancy leads to cognitive impairments in the offspring that persist into adulthood. Continue reading →

Phages fight back: how anti-CRISPRs interfere with the bacterial immune system

September 23, 2015November 16, 2015 ~ Betty ~ 4 Comments

A transmission electron micrograph of phage JBD93, which contains an anti-CRISPR gene. (Credit: Joe Bondy-Denomy)

So nat’ralists observe, a flea
Hath smaller fleas that on him prey;
And these have smaller fleas to bite ‘em.
And so proceeds Ad infinitum.

Jonathan Swift, 1733

When the Anglo-Irish satirist wrote these words nearly two centuries ago, he could not have known just how far down the tree of life his observations would hold true. These predator-prey relationships exist beyond the plains of Africa or the jungles of Borneo. They extend to the realm of microscopic organisms and to the world of bacteria and the teeny tiny, itsy bitsy viruses that prey on them. These viruses are called bacteriophages, or phages for short.

Like human and other animal viruses, phages rely completely on their host for reproduction. They enter a bacterial cell and hijack the cellular machinery to make new phages until the cell is literally bursting with viral cargo. A torrent of phages is unleashed that go on to infect more bacteria and continue the cycle.

But bacteria are not helpless victims in this story. They have a large arsenal of anti-phage weapons to keep phages out and prevent them from taking over. Perhaps the coolest of these weapons is the CRISPR-Cas system. First discovered in 2007, the CRISPR-Cas system functions as the bacteria’s immune system. It is both a memory keeper and a hitman. Every time a bacteria survives a phage infection (which doesn’t happen often), the CRISPR-Cas complex takes a small piece of phage DNA and adds it to the bacteria’s own DNA, gradually building a database of unique DNA fingerprints from every phage that has ever tried to kill it. In other words, bacteria with CRISPR-Cas systems are able to “learn” from their previous phage encounters and acquire immunological memory based on those experiences—a trait that was previously thought to be unique to animals.

“It’s the first example of a single cell, simple [bacteria] having an adaptive immune system,” says Dr. Joseph Bondy-Denomy, a faculty fellow at the University of California, San Francisco. “The adaptability of CRISPR is very, very rapid. I think that’s why it’s so exciting.” Continue reading →

Less toxic staph cause more severe disease

September 12, 2015September 12, 2015 ~ Betty ~ Leave a comment

A scanning electron micrograph of methicillin-resistant Staphylococcus aureus and dead human immune cells. (Credit: National Institute of Allergy and Infectious Diseases. CC BY 2.0)

We hear a lot about toxins in the news these days. Specifically, the hidden toxins lurking in the food we eat, the household products we use, the air we breathe and why we need to go on a juice cleanse to detox our bodies, lose weight and feel great!

But right now, let’s ignore those exaggerations and pseudoscience (because that’s a lengthy post in and of itself) and talk about real toxins. Real bacterial toxins. These toxins are proteins made and secreted by bacteria that help them establish an infection and cause disease. Staphylococcus aureus, commonly known as staph, is one species of bacteria that deploys a large and diverse arsenal of toxins. Most people carry staph bacteria asymptomatically on their skin and in their noses. In certain individuals, such as those with a weakened immune system, the bacteria can cause a wide spectrum of diseases from minor skin and soft tissue infections to life-threatening pneumonia and bloodstream infections. A key component of the bacteria’s survival strategy are the toxins that damage tissues and attack immune cells to interfere with the host’s defense system. Toxins are also responsible for disease symptoms such as the skin lesions commonly seen in patients with a staph infection.

Given the important role that toxins play in establishing and maintaining an infection, it would be logical to assume that the more toxins a bacteria produces, the more severe the infection. Until recently, that was the prevailing belief in the research community. Continue reading →