Our lab recently published an article in PeerJ describing the succession of the bacterial microbiome in the ileum of commercial turkeys, and the relationship between this bacterial succession and a condition known as Light Turkey Syndrome or LTS. I thought it might be useful to describe the history surrounding this condition in a little more detail.
LTS has been talked about by commercial turkey growers in Minnesota for nearly 10 years. When I first started talking to industry people about LTS, several notable observations surfaced. First, this condition is different than classical disease conditions with known pathology in commercial turkeys. LTS does not involve any known pathology in the digestive or respiratory systems. This is different from a condition known as Poult Enteritis and Mortality Syndrome (PEMS), where there is notable watery droppings in poults, dehydration, stunting, spiked mortality, and acute enteritis. LTS is a benign condition, with only two primary observations that are considered abnormal: 1) high variations in weights between poults within a flock, and 2) lower-than-average flock market weights on the order of 1-3 pounds per bird.
So, LTS is a problem that is much different than classical diseases seen in the turkey industry over the past fifty years. Dr. Sally Noll’s lab first looked at flocks experiencing LTS to see if there were any notable differences between lighter and heavier birds within the same commercial flock. They first looked for some common gut pathogens, including Salmonella, Campylobacter, E. coli, astroviruses, rotaviruses, and reoviruses. They found no differences between lighter and heavier birds in the presence of these potential pathogens, and they found no differences overall between lighter and heavier flocks for the presence of these potential pathogens. They also did histological analyses of gut and immune tissue and measured xylose absorption on these birds, and found no major differences between light and heavy birds/flocks. To some extent, this ruled out active disease, gut development, and immune status as causes of LTS.
What about external factors? Here are some anecdotal observations. Poults hatched from the same source in Minnesota go to farms within Minnesota and elsewhere in the world. The industry has tracked the market weights of these flocks over a number of years, on farms that have very similar management systems and similar nutritional plans. Based upon an expected market weight established using flocks outside of Minnesota, the vast majority of flocks within Minnesota rarely achieve these weights.
LTS can be reproduced via inoculation studies. Inoculation of research flocks with fecal homogenates from LTS flocks depresses growth. This suggests something about the gut microbiome that induces LTS. There are a lot of additional refined animal experiments that are needed to fully understand the nature of the gut microbiome-LTS relationship. Is there an unknown bacteria or virus in LTS flocks that asymptomatically depresses growth and performance? Or more likely, is it shifts in the entire gut microbiome that impacts growth and development? Now that we know the succession of bacteria in the turkey ileum and how it is impacted or slowed in LTS flocks, can we modulate it? And is this approach enough to solve the LTS problem?