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microbiology

Some ‘Hospital-Acquired’ Infections Traced to Patient’s Own Microbiome

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Bacteria in both blood and gut

Caption: New computational tool determines whether a gut microbe is the source of a hospital-acquired bloodstream infection
Credit: Fiona Tamburini, Stanford University, Palo Alto, CA

While being cared for in the hospital, a disturbingly large number of people develop potentially life-threatening bloodstream infections. It’s been thought that most of the blame lies with microbes lurking on medical equipment, health-care professionals, or other patients and visitors. And certainly that is often true. But now an NIH-funded team has discovered that a significant fraction of these “hospital-acquired” infections may actually stem from a quite different source: the patient’s own body.

In a study of 30 bone-marrow transplant patients suffering from bloodstream infections, researchers used a newly developed computational tool called StrainSifter to match microbial DNA from close to one-third of the infections to bugs already living in the patients’ large intestines [1]. In contrast, the researchers found little DNA evidence to support the notion that such microbes were being passed around among patients.


A Bacterium Reaches Out and Grabs Some New DNA

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Credit: Dalia Lab, Indiana University, Bloomington

If you like comic book heroes, you’ll love this action-packed video of a microbe with a superpower reminiscent of a miniature Spiderman. Here, for the first time ever, scientists have captured in real-time—and in very cool detail—the important mechanism of horizontal gene transfer in bacteria.

Specifically, you see Vibrio cholerae, the water-dwelling bacterium that causes cholera, stretching out a hair-like appendage called a pilus (green) to snag a free snippet of DNA (red). After grabbing the DNA, V. cholerae swiftly retracts the pilus, threading the DNA fragment through a pore on the cell surface for stitching into its genome.


Has an Alternative to Table Sugar Contributed to the C. Diff. Epidemic?

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Ice cream sundae

Thinkstock/piyaphat50

Most of us know how hard it is to resist the creamy sweetness of ice cream. But it might surprise you to learn that, over the past 15 years or so, some makers of ice cream and many other processed foods—from pasta to ground beef products—have changed their recipes to swap out some of the table sugar (sucrose) with a sweetening/texturizing ingredient called trehalose that depresses the freezing point of food. Both sucrose and trehalose are “disaccharides.” Though they have different chemical linkages, both get broken down into glucose in the body. Now, comes word that this switch may be an important piece of a major medical puzzle: why Clostridium difficile (C. diff) has emerged as a leading cause of hospital-acquired infections.

A new study in the journal Nature indicates that trehalose-laden food may have helped fuel the recent epidemic spread of C. diff., which is a microbe that can cause life-threatening gastrointestinal distress, especially in older patients getting antibiotics and antacid medicines [1, 2]. In laboratory experiments, an NIH-funded team found that the two strains of C. diff. most likely to make people sick possess an unusual ability to thrive on trehalose, even at very low levels. And that’s not all: a diet containing trehalose significantly increased the severity of symptoms in a mouse model of C. diff. infection.


Creative Minds: Giving Bacteria Needles to Fight Intestinal Disease

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Cammie Lesser

Cammie Lesser

For Salmonella and many other disease-causing bacteria that find their way into our bodies, infection begins with a poke. That’s because these bad bugs are equipped with a needle-like protein filament that punctures the outer membrane of human cells and then, like a syringe, injects dozens of toxic proteins that help them replicate.

Cammie Lesser at Massachusetts General Hospital and Harvard Medical School, Cambridge, and her colleagues are now on a mission to bioengineer strains of bacteria that don’t cause disease to make these same syringes, called type III secretion systems. The goal is to use such “good” bacteria to deliver therapeutic molecules, rather than toxins, to human cells. Their first target is the gastrointestinal tract, where they hope to knock out hard-to-beat bacterial infections or to relieve the chronic inflammation that comes with inflammatory bowel disease (IBD).


Expanding Our View of the Human Microbiome

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Girl and her micrbiomeMany people still regard bacteria and other microbes just as disease-causing germs. But it’s a lot more complicated than that. In fact, it’s become increasingly clear that the healthy human body is teeming with microorganisms, many of which play essential roles in our metabolism, our immune response, and even our mental health. We are not just an organism, we are a “superorganism” made up of human cells and microbial cells—and the microbes outnumber us! Fueling this new understanding is NIH’s Human Microbiome Project (HMP), a quest begun a decade ago to explore the microbial makeup of healthy Americans.

About 5 years ago, HMP researchers released their first round of data that provided a look at the microbes present in the mouth, gut, nose, and several other parts of the body [1]. Now, their second wave of data, just published in the journal Nature, has tripled this treasure trove of information, promising to further expand our understanding of the human microbiome and its role in health and disease [2]. For example, the new DNA data offer clues as to the functional roles those microbes play and how those can vary over time in different parts of the human body and from one person to the next.


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