Stories about: infectious disease

Food for thought: How your microbiome celebrates Thanksgiving

Image of microbiome superimposed over a Thanksgiving turkeySeth Rakoff-Nahoum, MD, PhD, a Boston Children’s Hospital physician-scientist who does infectious disease research and is taking an evolutionary approach to understanding the human microbiome and its effect on health, offers us some insight into what’s happening to the bugs in our gut as a result of the Thanksgiving meal. 

Q: Does the traditional American Thanksgiving meal affect the human microbiome?

A: Anything you put in your body has the potential to affect your microbiome, and Thanksgiving dinner is no different.

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Another microbiome perspective: The host holds the leash

Abstract depiction of the microbiome

Most scientists and clinicians accept that the human microbiome impacts a person’s nutrition, immune system function, physical health and perhaps even mental illness, but exactly how or why is not well understood. Now, taking an evolutionary approach, a Boston Children’s Hospital infectious disease researcher suggests the host may play a more active role in controlling the microbiome than previously appreciated.

“I think we need to re-evaluate the way in which we think about the microbiome,” says Seth Rakoff-Nahoum, MD, PhD, a physician-scientist at Boston Children’s in the Divisions of Infectious Diseases and Gastroenterology, whose perspective was published today in Nature.

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Of bugs, genes, development and intestinal biology

genes intestinal developmentThe collection of bacteria and other microorganisms living in our intestines—our microbiota—is now understood to play an important role in our physiology. Recent research indicates that it helps regulate our metabolism, immune system and other biological processes, and that imbalances in the microbiota are associated with everything from inflammatory bowel disease to diabetes.

Seth Rakoff-Nahoum, MD, PhD, wants to take this understanding to a new level. An infectious disease clinical fellow at Boston Children’s Hospital, he has systematically probed how genetics interact with environment—including the microbiota—to shape intestinal biology during different stages of development.

His investigations provide interesting clues to disorders that have their origins early in life, ranging from necrotizing enterocolitis in newborns to Hirschsprung’s disease (marked by poor intestinal motility) to food allergies.

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Infecting bacteria show surprising genetic diversity; we may need to adapt too

New research may change the way we culture and treat infections. (Burkholderia cepacia complex, CDC/Wikimedia Commons)
New research may change the way we culture and treat infections. (Burkholderia cepacia complex, CDC/Wikimedia Commons)

Ed. note: A longer version of this story appeared on Harvard Medical School’s website.

A boy with cystic fibrosis develops a potentially deadly Burkholderia dolosa infection in his lungs. Various genetic mutations allow some bacterial strains to survive assaults from his immune system and antibiotics, while others perish. Eventually, the strongest mutant dominates the B. dolosa colony.

Right? Maybe not, say the authors of a new study. Examining sputum samples from infected patients, they found that dozens of different kinds of B. dolosa may coexist in that boy’s lungs—each adapting and surviving in different ways. The findings, published last month in Nature Genetics, warn of possible shortfalls in the way infections are currently cultured and treated.

“We found that when a pathogen like B. dolosa infects us, it diversifies. Many cells discover ways to survive, and these successful mutants coexist,” says senior author Roy Kishony, PhD, professor of systems biology at Harvard Medical School.

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Bacteria use pain as a weapon

It’s bad enough that invasive infections are painful. New work suggests that pain is only a means to an end for virulent bacteria: It’s how they suppress our immune system.

Staph found near fibers from pain neurons
Invasive methicillin-resistant Staphylococcus aureus (labeled by green fluorescent protein) are found close to pain nerve fibers (labeled by red fluorescent protein) in dermal skin tissue following infection

Previously, the pain from invasive infections like meningitis, necrotizing fasciitis, urinary tract infections, dental caries and intestinal infections was thought to be due to the body’s immune response, causing the infected tissue to become inflamed and swollen.

Not so, says Boston Children’s Hospital neuro-immunologist Isaac Chiu, PhD. Studying invasive skin infections caused by methicillin-resistant Staphylococcus aureus (MRSA) in live mice, his team’s research demonstrates that the pain is induced by the bacteria themselves, and kicks in well before tissue swelling peaks.

Adding outrage to insult, once the pain-sensing neurons are activated, they suppress the immune system, potentially allowing the bacteria to proliferate, finds the study, published last week in Nature.

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A Lego-like approach to vaccine design

A syringe made of Legos.
A robust, reproducible vaccine with low risk of side effects is hard to come by. A new design strategy could balance the benefits and risks of different vaccine approaches while making them as easy to build as Legos. (seanmichaelragan/Flickr)

A good vaccine should confer robust, long-lasting immunity against a given pathogen without causing side effects. Striking this balance has fueled a long-standing debate over whole-cell and acellular vaccines.

Whole-cell vaccines rely on killed or weakened pathogens. Acellular or subunit vaccines contain only defined sets of antigens known to stimulate an effective immune response against the pathogen in question.

Both approaches have their strengths and weaknesses. Whole-cell vaccines carry a bacterium’s full complement of antigens and can activate many arms of the immune system at once. And they are inexpensive to manufacture. But these vaccines can be hard to reproduce and run the risk of causing frequent or serious side effects.

Acellular vaccines are very reproducible and run a much lower risk of side effects. But the immune responses they trigger aren’t as robust or durable, as evidenced by the recent failures of the acellular pertussis vaccines.

What if you could bring together the effectiveness of a whole-cell vaccine and the safety and reproducibility of an acellular one? That’s what Boston Children’s Hospital’s Fan Zhang, PhD, Yingjie Lu, PhD, and Richard Malley, MD, want to do with the Multiple Antigen Presenting System, or MAPS.

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A vaccine that works in newborns?

If we could immunize infants at birth, far more could be protected from infections.(DFID-UK Dept for International Development)

Right now, immunizations against most infections begin at 2 months of age. But that leaves newborns at risk for infections like rotavirus, whooping cough and pneumococcus during a highly vulnerable time.

In resource-poor countries, this is a serious problem: Many children see a health care provider only at birth, so may miss their chance to be protected. Worldwide, each year, more than 2 million infants under 6 months old die from infections, especially pneumonia. If we could immunize infants at birth, it would be a huge win for global health.

Unfortunately, though, newborns don’t respond to most vaccines. Their immune systems are too immature—which is why few vaccines for newborns exist.

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Modeling sepsis in newborns: toward better detection and treatment

Sepsis, a serious, hard-to-diagnose threat in the NICU, can interfere with a baby's development even when cleared with antibiotics. (Image: Army Medicine/Flickr)

Sepsis, or bacterial infection of the bloodstream, is a grave threat to premature infants in the neonatal intensive care unit (NICU) who have catheters and intravenous lines. Even when antibiotics clear the infection itself, the inflammation that it causes can do just as much damage. Not only can sepsis and the resulting inflammation interfere with fragile preemies’ ability to gain weight, but a growing literature suggests that they can impair brain development.

Preventive measures can now avoid many cases of sepsis, but those that slip through can be hard to detect in newborns.

“Newborns can’t speak, and they have unique immune systems, so they tend not to have fevers or show clinical signs,” explains Ofer Levy, MD, PhD, of the Division of Infectious Diseases at Boston Children’s Hospital. “There may be irregular breathing or increased heart rate, or the baby may be acting a little ‘off,’ but these signs are pretty nonspecific. There’s a tremendous need for better diagnostics in this field.”

Levy and colleagues recently described a mouse model that, for the first time, captures the effects of sepsis on the newborn immune system. They and others have begun using it to identify diagnostic markers and better treatments.

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Innovation Day at Children’s Hospital Boston: A preview

Valentine's Day is Innovation Day (image: Richard Giles/Flickr)

In a series of 17 short TED-style talks next Tuesday, February 14, clinicians and scientists from Children’s will present new products, processes and technologies to make health care safer, better and less expensive. The event, from 1-5 p.m. Eastern, is sponsored by the Innovation Acceleration Program. It’s now running a wait list, but you can also watch the live stream or track the proceedings on Twitter (#iDay) or via @science4care. Here’s a small sampling of next week’s presenters; for details, read the press release or view the full agenda.

Diagnosing lazy eye when it’s most treatable: in preschoolers

If lazy eye, or amblyopia, is caught early – ideally, before age 5 – it’s easily treated by patching the “good” eye, forcing the child to use and strengthen the weaker eye. But if it goes unnoticed, the weak, unused eye can slowly go blind,

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