Monthly Archives: December 2013

The story behind “Light Turkey Syndrome” in Minnesota

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?


What is a Superbug??


You hear it every day in the popular press. It instills fear upon its very mention in a news release. But what exactly is a “Superbug?”

Let’s start with a search for “Superbug” on the internet. I did a google search and came up with a few definitions:

Maryn McKenna is a science writer and author of the popular book “Superbug.” She has written some fantastic blogs under the Wired Science blog Superbug. Her book focused on methicillin-resistant Staphylococcus aureus (MRSA), and her blogs have had a major emphasis on multidrug resistant (MDR) bacteria and the implications of antibiotic use on the rise of MDR bacteria. So, it would seem from Maryn’s standpoint that MDR bacteria with pathogenic potential represent a Superbug. That seems pretty logical to me.

Wikipedia states that “pathogens resistant to multiple antibiotics are considered multidrug resistant (MDR) or, more colloquially, superbugs.” States the same that McKenna implies.

Merriam-Webster dictionary defines Superbug as “a pathogenic microorganism and especially a bacterium that has developed resistance to the medications normally used against it.”

It looks like most sources agree on the definition of a Superbug. A pretty simple and straightforward one at that.

Now we get into shades of grey. What if we have trouble defining MDR and/or defining pathogen? For example, what if we find an MDR E. coli isolate on retail chicken such as that reported in the recent Consumer Reports investigation? The authors of this article spend a great deal of time discussing the implications of pathogen contamination of retail meat. But, if you look at the data, the prevalence of true pathogens of concern (such as Salmonella) is actually quite low, while E. coli isolation is more frequent. Still, they lump these together as “presence of bacteria on retail meat”. To make it clear, the classical diarrheagenic E. coli such as O157:H7 are not found on chicken. The biggest risk of E. coli in chicken is that some of these E. coli may have the potential to cause extraintestinal infections in humans, such as urinary tract infections (although this is still a controversial topic). However, the majority of E. coli from poultry do not seem to possess this potential. Survey studies such as the one conducted by Consumer Reports do not distinguish between whether or not an E. coli isolated from a chicken breast actually represents a possible human pathogen.

Let’s also look at the same report and their discussion of MDR. Their data (presented here) illustrates that MDR in pathogens of concern is again very low. Yet, they chose to lump all bacteria together in statements such as “Our test results found that 49.7 percent of our samples contained at least one multidrug-resistant bacterium.” This is again a shady area of the use of the word Superbug, since by definition it is a pathogen that has acquired MDR. Lumping all of these bacteria together as potential Superbugs is not appropriate. If the data were parsed to categorize Superbugs by pathogen type and MDR phenotype, then the data would be much less convincing. While it is convenient and sensational to lump them all together, it is an inappropriate use of the data.

Fortunately, the CDC is taking a lead on a better definition of Superbug. An article in CNN describes CDC’s proposal to categorize Superbugs by threat level. The levels are “urgent,” “serious,” and “concerning.” Those falling in the urgent category include MDR Clostridium difficile (C dif infections), carbapenem resistant Enterobacteriaceae (Klebsiella, E. coli, and Salmonella resistant to carbapenems), and Neisseria gonorrhoeae (causative agent of gonorrhoeae).

So, it seems that we are on the path to appropriately defining a Superbug, taking into account not only that a pathogen is MDR but also the ability of said pathogen to cause disease and hamper antibiotic treatment. A final issue is what policies should be taken to reduce the spread of these Superbugs. Here is probably the most important point – not all Superbugs become so in the same way. Some, such as CRE, pick up plasmids that make them MDR. Others acquire mutations that make them MDR over time. And they all spread differently, some through horizontal gene transfer, some through clonal dissemination, some using both. It is frustrating to see the media and activist groups misuse definitions to promote an agenda. Take, for example, the National Resources Defense Council, which starts this recent article with the following statement: “Feeding low levels of antibiotics to cows, pigs and chickens that aren’t even sick breeds “super bugs” — dangerous germs that are able to fight off antibiotics that spread to our communities and families.”

Now, I don’t disagree that we should judiciously use antibiotics in all settings, including animals. But as I have stated before, blanket statements such as the above one by NRDC are inappropriate. First, it implies that Superbugs as a whole are all impacted by use of subtherapeutic antibiotics in animal agriculture. Not true. Also, none of these reports ever reference articles demonstrating that subtherapeutic use of antibiotics in animals drives the emergence of Superbugs. I challenge you to do literature searches for articles demonstrating in a controlled experiment that this is the case. Believe me, I have tried, and there is nothing out there that convincingly demonstrates that this happens. This is why USDA/FDA have been lobbying for educated removal of certain drugs from animal production versus the mass removal of all antibiotics under a given claim. I think we really need to better consider the underlying science of policy making in this country, and support more science to make better decisions.

All this said, Superbugs are real. The name provokes a lot of unimaginable thoughts to people reading an article. We as humans are very good at sensationalizing and placing blame, less effective at promoting the right forms of change. Using a more concise definition of Superbug, let’s also promote the necessary science to address issues and solutions, rather than using public fear to promote changes in the absence of science.