Less toxic staph cause more severe disease

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)
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

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Bacteria from tobacco plant roots provide protection against sudden-wilt disease

A tobacco field in Tennessee (Credit: ajgarrison3. CC BY 2.0)
A tobacco field in Tennessee (Credit: ajgarrison3 via Flickr. CC BY 2.0)

As humans, we rely on the community of microbes in our gut to help us thrive. These microorganisms, collectively known as the gut microbiome, serve many purposes. Chief among them are helping us breakdown food into nutrients that our bodies can absorb and use and preventing harmful pathogens from taking hold.

So what is a poor plant to do without a gut? Use its root microbiome of course! The root microbiome is the collection of bacteria and fungi that live in the soil in and around the plant’s roots. The root microbiome is remarkably diverse and fluid in its composition. One gram of soil from the roots can contain up to one billion bacteria from as many as 10,000 different species. To compare, one millilitre of intestinal fluid from a human contains similar numbers of microbial cells but they represent only 500 to 1000 different species.1

The relationship between a plant and its microbial co-dwellers is generally one of give and take—the plant secretes carbon-rich sugars through its roots to feed the microbes and the microbes help the plants take up more nutrients from the soil and prime its immune system. Beyond this, we know surprisingly little about just what and how exactly all those microbial partnerships are contributing to plant health.

Dr. Ian Baldwin leads a group of researchers in the department of molecular ecology at the Max Planck Institute for Chemical Ecology in Germany. His team uses the wild tobacco plant Nicotiana attenuata to study the complex interactions between plants and microbes. In a paper published last week in the Proceedings of the National Academy of Sciences, the researchers describe how the root microbiome rescued plants from sudden-wilt disease. Continue reading

The curious case of Neisseria and the seven-carbon sugar

A scanning electron micrograph showing Neisseria gonorrheae bacteria (blue) infecting a type of human immune cell called a neutrophil (gold). (Image: Ryan Gaudet)
A scanning electron micrograph showing Neisseria gonorrhoeae bacteria (blue) infecting a type of human immune cell called a neutrophil (gold). (Image: Ryan Gaudet)

Walking into the little lunchroom in the back of the lab, I am greeted by a row of empty wine bottles. Celebratory drinks in the lab usually mean a manuscript’s been accepted for publication and when there’s that many empty bottles, you know it must be a pretty good journal. As I attempt to work out a wine to impact factor conversion in my head, the lab door opens and Ryan Gaudet (pronounced good-ie) walks in. Gaudet, a PhD student in the lab of Dr. Scott Gray-Owen at the University of Toronto, is the lead author of a paper recently published in the journal Science about a new signalling molecule produced by the bacteria Neisseria gonorrhoeae. It was for this paper that he and his labmates were celebrating.

To fully appreciate and understand this paper, we need to go back more than a decade to the early 2000s, when Adrienne Chen, an undergraduate student working in the Gray-Owen lab, noticed something peculiar: when cells infected with HIV were exposed to N. gonorrhoeae, HIV genes suddenly turned on and normally silent genes became expressed. This was a compelling finding because co-infection of HIV with the sexually transmitted infection gonorrhoea (caused by N. gonorrhoeae) is known to increase HIV shedding and enhance male-to-female transmission. A few years later, the mysteries of the gonorrhoea-HIV relationship drew Dr. Rebecca Malott, a postdoctoral fellow, to the Gray-Owen lab where she began a project aimed at trying to figure out how Neisseria bacteria turned on HIV gene expression.

That’s when the detective work began. Continue reading