Stuart Reid's epidemiological study of one strain of salmonella showed both animals and humans tended to pass the disease across specie, but not very often.
Reid is a veterinarian and quantitative epidemiological researcher from the Royal Veterinary College in London. He explores relationships between human and animal health issues, including antibiotic resistance and antibiotic-resistant bacteria.
A few years ago Reid and co-researchers began studying a troublesome strain of salmonella called Salmonella Typhimurium DT104. They examined long-term surveillance data on antimicrobial resistance, specifically in Scotland, for Salmonella Typhimurium DT104 isolates from "concurrently sampled and sympatric human and animal populations." This strain is a virulent and drug-resistant pathogen.
Among the 5,200 total isolates, they found 65 resistance phenotypes, 13 of those unique to animals, 30 of them unique to humans and 22 common to both. Of those 22 common isolates, 11 were identified first in the human isolates, whereas only five were identified first in the animal isolates. This is an indication of direction of travel. Hence, the 11 found first in humans implies they moved from humans to animals. The five identified first in animals and later in humans would imply movement from animals to humans.
Reid said 22 shared profiles is a statistically lower number than they would expect if the bacteria were flowing freely between the two populations.
He and the other researchers concluded that animals and humans generally have different strains of the bug and that animals are unlikely the source of if for humans in a paper published in 2011.
In fact, Reid said, the most likely explanation for the animal-human sharing is a third, fourth and maybe even a fifth source of DT104.
Reid said he was attacked for publishing the data. One of the criticisms was that he and his research partners only used phenotypic data, meaning the bugs they were examining and quantifying were only tested for their actual traits, such as resistance and human or animal host.
To follow up, Reid said the team has begun collecting genetic data on the same project they previously tested phenotypically. The data is not fully analyzed yet but he said this week it is looking like it will produce much the same results as the first study.
Ultimately, Reid said, this study just adds to the understanding researchers have that the entire ecosystem and all its parts are interrelated and share bacteria and antibiotic resistance. Only that understanding together with the work of cooperation can achieve the goal of managing antimicrobial products wisely.
"We need to stop playing the blame game because it won't move us forward," Reid said.