Oct. 15 (UPI) -- Bloodstream infections acquired during a hospital stay have been traced to patients' own bodies -- rather than nurses and doctors -- according to a new study.
Stanford scientists found the infections specifically originate from patients' large intestines. The researchers believe their findings, published Monday in the Nature Medicine, can lead to addressing the risk factors responsible for these infections.
"Until now, we couldn't pinpoint those sources with high confidence," Dr. Ami Bhatt, an assistant professor of hematology and of genetics at Stanford, said in a press release. "That's a problem because when a patient has a bloodstream infection, it's not enough simply to administer broad-spectrum antibiotics. You need to treat the source, or the infection will come back."
Roughly 40 percent of immunocompromised patients, which includes about 23,000 recipients of bone marrow transplants each year, develop bloodstream infections during their two- to six-week hospital stays, the researchers noted. And they are at risk for repeated rounds of infection.
The researchers used new bioinformatics software to rapidly and accurately identify where these infections originated.
They analyzed blood and stool samples collected from 30 patients who had incurred bloodstream infections upon undergoing bone marrow transplant procedures between early 2015 and 2017 at Stanford Hospital.
Because it would be nearly impossible to size up every patch of tissue on or in the body for suspect microbes, the researchers chose to focus on the gut with its 1,000 to 2,000 microbial species.
"Often, these bugs aren't intrinsically pathogenic," Bhatt said. "They're perfectly well-behaved in the gut. It's only when they show up in the wrong place -- due, for example, to leaking through a disrupted intestinal barrier into the bloodstream -- that they cause trouble."
The researchers had to analyze an immense amount of data by analyzing their entire genomic sequences to ferret out tiny differences. The researchers said this can involve the difference between drug susceptibility and drug resistance, as well as a relatively benign infections and a virulent ones.
From each patient's stool sample, they extracted the combined DNA of microbial inhabitants by using whole-genome sequencing methods.
"Just finding E. coli in a patient's blood and again in that patient's stool doesn't mean they're the same strain," Bhatt said.
The researchers then analyzed the genomes of all the individual microbial strains in each patient's stool.
The researchers compared pinning down individual strains to the reassembly of many hundreds of different photographs that have been chopped into small pieces, mixed together and deposited in a single bag. And the bag contains fragments of several copies of each photo.
To compare these gut-resident microbial-genome "photos" with the microbial strains of the bloodstream pathogens, the researchers designed a computational tool, called StrainSifter, that contained detectable levels of exactly the same bacterial strain that had caused those patients' bloodstream infections.
"Because the gut normally harbors more than 1,000 different bacterial strains, it's looked upon as a likely culprit of bloodstream infections, especially when the identified pathogen is one known to thrive inside the gut," Bhatt said. "But while this culpability has been assumed -- and it's an entirely reasonable assumption -- it's never been proven. Our study demonstrates that it's true."
Generally, any given patient's bloodstream pathogen didn't match microbial strains found in other patients' blood or stool samples.
"I don't think we're passing around active infections among one another as often as has been assumed," Bhatt said. "Our results suggest that people are the most likely source of their own infections. Maybe we need to get rid of this idea of 'catching' others' infections, and give more thought to the health of our own resident microbial ecosystems."