Jun 22, 2021
In this episode, we host Dr. Philip Hardwidge, associate director of the Center on Emerging and Zoonotic Infectious Diseases in the Department of Diagnostic Medicine and Pathobiology at Kansas State University. Dr. Hardwidge’s research focuses on understanding, treating and preventing diarrheal disease caused by bacterial pathogens. These pathogens represent important threats to food safety, biosecurity and animal health. His research team is tackling the fundamentals of biochemical interactions, leading to a better understanding of mitigation methods.
The Many Paths of Pathogens with Dr. Philip Hardwidge, associate director of the Center on Emerging and Zoonotic Infectious Diseases
We have to be as scientists extremely open and and generally
willing to share data be transparent about our
raw data and like other aspects in life know when to ask for help.
Something to chew on is a podcast devoted to the exploration and discussion of global food systems produced by the Office of Research Development at Kansas State University. I'm Maureen Olewnik. Coordinator of Global Food Systems.
I'm Scott Tanona. I'm a philosopher of Science.
We welcome back co-host Dr. Jim Stack Professor of Plant Pathology.
Diarrheal disease caused by bacterial pathogens is a challenge in both humans and animals in many instances the introduction of pathogens in animal systems causes illness and in some cases is carried through meat processing affecting contamination of food meant for human consumption. Studies of food safety at K-State includes fundamental through applied research. The importance of research in the area of pathogenic bacteria has been addressed in several of our podcasts to date. Most focusing on the applied research in testing, monitoring, and mitigating potential contamination of food products. However, the basic molecular biology of host pathogen interaction is not well understood. In today's podcast, we will talk with Dr. Philip Hardwidge, Associate Director of the Center on Emerging and Zoonotic Infectious Diseases here at K-State. His study of host pathogen interaction has led to a better understanding of the mechanisms by which pathogens enter and colonize in a host system. With studies leading to an understanding of how this impacts autoimmune disorders, cancer, and more.
I would like to welcome Dr. Philip Hardwidge to the podcast. Dr. Hardwidge is the Associate Director of NIH and Cobra Center on Emerging and Zoonotic Infectious Diseases. I am hopeful that he will explain to us exactly what all that means. Before we get started in talking about your current activities, Dr. Hardwidge could we maybe get a little bit of understanding of who you are, what your background is, and what brought you to K-State. What brought you to the area of study that you're in, today.
Thanks for having me on this podcast series. I'm from the midwest, Michigan and Illinois. My father was a Pfizer scientist and we happened to be living in Central Illinois when I was a high school student, so he gave me some interest in Microbiology and Chemistry, so I ended up doing a Microbiology degree at the University of Illinois, and wanted to develop a research program kind of at the interface between Biochemistry and Microbiology, so I knew from a fairly early age where my career would hopefully head. I did a PHD at the Mayo Clinic Graduate School
in Rochester, Minnesota. So, Mayo is a very famous hospital. They also have a very robust graduate training program. And after that, I did a postdoc at the University of British Columbia in Vancouver Canada. Primarily because one of the leading E Coli Microbiologists was running his laboratory in Vancouver and when I finished my education I took an Assistant Professor Position in South Dakota State University back in 2005. There were some unique opportunities to help develop their graduate program, and I had the opportunity to work with germ-free piglets which are a very nice model for some types of E Coli diseases.
I was then recruited to the University of Kansas Medical Center and then subsequently recruited to Kansas State University where I've been since 2012.
Great, thank you for the overview there. In the introduction, I referenced the Center on Emerging and Zoonotic Infectious Diseases. Can you tell us a little bit about what that is at K-State and what your goals are there?
Sure, so we call this CEZID, Center on Emerging and Zoonotic
Infectious Diseases. This is an NIH Center that's administered by
Dr. Juergen Richt and myself. So, [Dr.] Juergen is a Virologist. I
am a Bacteriologist and we're both interested in looking at
virulence factors. So, namely what features of pathogens. What
components of bacteria and viruses cause diseases in humans and
animals. We're also looking at host pathogen interactions. And to
do this we use basic science. So fundamental aspects of how
bacteria and viruses work. How they cause disease, and we also take
translational approaches that can be InVitro in test tube[s], lab
experiments, or in large animal models of disease. So overall,
we're attempting to advance our understanding of new or emerging
infectious diseases, or zoonotic diseases, those pathogens that can
cross the interface between animals and human beings. So Covid-19
is a great example of both cases. It has recently emerged, and it
is Zoonotic. It's believed to have originated from bats, so you
know within this center. [Dr.] Juergen and I administer the
day-to-day operations, but we’re heavily interested in mentoring
junior scientists. So, there are four primary projects each
Principal Investigator works on a different pathogen that examines
one emerging or zoonotic infectious disease and then there are five
pilot projects. So smaller projects we funded with some seed money,
and then there are two research cores, uh, to help develop the
research infrastructure here at K-State.
Sounds like it's a great center, and could you say something about why zoonotic diseases deserve such a focus, or what's important about them?
Okay yeah, so obviously we've learned a lot more, or the public has learned a lot more, with the Covid- 19 pandemic. But you know zoonotic disease diseases, or zoonoses, are diseases caused by viruses or bacteria that can spread between humans and animals, or animals and humans. So, in many parts of the world there's very close association between animals and humans. So, farming systems can be quite different compared with what we're familiar with in the United States. So, there's very close contact between humans and animals and some good examples would include Influenza. So, we have the flu circulating in chickens and in pigs. These viruses can mutate and suddenly become able to infect human cells and cause disease. Antibiotic resistance is an issue. So, we've tended to treat food animal diseases. So bacterial infections of pigs and cows with very large quantities of antibiotics to control their infections and to promote weight gain. Well, this can evolve antimicrobial resistance in these organisms and some of these pathogens can also infect human beings. So, antimicrobial use in agriculture can have a direct impact on our ability to treat human infections. And then there are vector-borne diseases. So, bacteria and viruses that can be spread or transmitted by mosquitoes, ticks, and fleas. For example, so that the insect, the mosquito or flea, can provide a conduit between an animal and a human being. So, as the mode of transmission. So, many of these diseases are extremely serious. They're relatively new. They're emerging, and the the life cycle, this animal to human interface, explains why they're why they are called a zoonotic diseases.
Great, thanks! And could you describe two, sort of, some of the different projects you, said there's a course of on going ones, and then some pilot ones. So, I don't know which, pick a couple just to give us a sense of some of the work that's going on in a little more detail. love to hear some more.
Okay, so yeah, within our CEZID program, we have four very exciting primary research projects. One of them directed by Dr. Tom Platt, in the Division of Biology, looks at a pathogen known as shigella flexneri. Shigella has a lot of similarities to the hemorrhagic E Coli, the hamburger E Coli, E Coli o157 h7. He's very interested in the environmental behavior of Shigella. So what must Shigella do to survive in aquatic environments versus survive when Shigella has colonized a human host. And many of those molecular mechanisms are very different. The pathogen has to do, you know, many different things make many different proteins depending whether it's living in the environment, or within a human. [Dr.] Stephanie Shames studies Legionella. So, many of you may have heard
the term Legionnaires Disease from this outbreak in the air conditioning vent in a convention in Philadelphia many decades ago. So, Legionella is the pathogen that causes this human disease. And [Dr.] Stephanie studies some of the specific proteins that legionella uses to subvert host defense mechanisms. Bacteria and viruses have evolved
very elaborate mechanisms to short-circuit or subvert our natural host defense. My own laboratory studies those mechanisms as well. So, that's [Dr.] Stephanie's focus. We also have a Flavivirus project, Japanese Encephalitis Virus, Yellow Fever Virus these are Flaviviruses. [Dr.] Scott Huang is trying to design live attenuated vaccines to control flaviviruses. And finally, [Dr.] Nick Wallace is studying Papillomavirus. Papilloma Viruses are believed to cause non-melanoma skin cancer, but the mechanism is not understood. So, [Dr.] Nick's studies are designed to start to understand at a molecular level what's going on between Papillomavirus and skin cancer.
If I could ask a question, you indicate that you're looking at certain proteins to maybe influence the outcome in a human infection, or an animal infection for that matter. We have a lot of vaccines for viral diseases, but relatively few for bacterial diseases. What's the strategy for, you know, using these proteins to prevent disease?
Okay so, if I understand your question right. There are therapeutic strategies so we have ways to treat diseases that have already occurred, or we have preventative measures such as vaccines. Bacterial, many bacteria, are challenging to tackle with vaccines. There can be great variation in the surface of bacteria. The outer membrane proteins, for example, are often targeted by vaccines. This is essentially the outside of a bacterium. These can be very highly variable between strains among different strains. So, it's hard for a cocktail of vaccine proteins to really be effective in preventing disease. There's an emerging strategy known as anti-virulence compounds where we attempt to not kill the bacteria using antibiotics, but we attempt to subvert the bacterium's ability to cause disease. That's also something my laboratory is developing.
How does that work?
Okay, so the the classic antimicrobial penicillin, for example, you know, inhibits cell wall integrity in the bacterium, so the bacterium lyses and dies. There are many antibiotics used that block the ability of a bacterium to make new protein, bacterial cell then dies. Resistance is a major problem here. So, the more often you challenge a group of bacteria with these antimicrobials. The more frequently you select for mutants mutations in the bacterial genome that will allow it to resist those antibiotics. So, one emerging concept is to not try to kill the bacterium, but try to simply block its ability to colonize a human host, or secrete a toxin that would be deleterious to a human or an animal. And that's thought it would be much less prone to the evolution of resistance mechanisms. We're not trying to destroy or kill the bacterium. We're simply targeting a very small component of its biology, namely its ability to cause disease. Some of these targets are a little less obvious to identify. So the cell wall is a very obvious and effective target for antimicrobials. Some of the mechanisms that bacteria use to block the immune system. These are being targeted for these anti-virulence therapies, but they've only been identified and studied relatively recently.
Yeah, thank you. So yeah, so that's cool. So the idea is not just that we haven't targeted this stuff, yet. So it's new, but that even ongoing application of these to it's basically blocking a side effect of what the bacterium's up to. Right? And lets it still propagate and continue on, because you're not sort of killing off only a subset of them. You're not forcing evolution, right? So, that the virulence isn't part of isn't something that it would sort of act against.
Exactly, that's the concept. So, a good example is perhaps the hemorrhagic E Coli this is a devastating disease. If humans acquire this organism, but it's typically an accidental infection, so through undercooked ground beef, contaminated produce, humans occasionally get E Coli infections. Extremely serious, potentially fatal disease but this organism lives very naturally in the intestines of cattle. So, it's a commensal organism. It does no harm to the cattle. So, it's not really something that one would would do a blanket antimicrobial attack on. There there may be a mechanism by which we can have a more selective targeting of their virulence functions. So prevent disease but not select for uh resistant strains of this organism.
Yeah, that's that's really neat, and and you said you're looking at some of those these interactions too in your own lab. Could you say what you're working on in this area?
Yeah so, I became interested in this area through some serendipitous scientific conferences, a few years ago. My lab had always been interested in the biochemistry of bacterial proteins that are able to block the immune system of the human host. So, some bacteria such as E Coli and Salmonella have a secretion system. So, they have a nano scale needle and syringe like machine that allows them to inject proteins into the intestinal cells. They are colonizing so this nano machine allows the bacterium to manipulate the human cells, and try to prevent the cells from establishing a dialogue with the immune system. So the biochemistry of these proteins, how they've evolved to bind signaling hubs in this innate immune system, what enzymatic activities they have to inhibit host proteins. Very fascinating to me, but it became clear through some collaborative discussions, that some of these proteins might be good targets for anti-virulence therapies. And they also might be good model proteins that could be used to study the immune system more generally. In other words, bacteria and viruses have evolved to inhibit the immune system. Can we use some of their examples to build other drugs that would function as anti-inflammatories. That's kind of the direction my lab has gone in the last five or six years.
So, you're turning this then to not just how can we prevent more more disease, right sort of, how can we learn from from what these bugs are doing to actually address other concerns like right?
Exactly, so, if we take, and that's you know that's the value of of basic science and basic molecular microbiological studies, if we really take a close look at what nature has already done. What evolutionary pressures have selected for, we can learn a lot about how organisms interact with each other. And specifically with regard to the immune system and inflammation, we can see very clear examples from bacteria and viruses. They have very very effective anti-inflammatory strategies. So E Coli and Salmonella for example, are great masters of inhibiting inflammatory responses. Well, if one looks at other diseases, other human diseases, such as Psoriasis, which is skin inflammation, cancer, diabetes, inflammatory bowel disease. These all have some common features in that some of the inflammatory signals proteins known as Cytokines are overproduced in too high abundance. So, can we take some of the bacterial strategies that block the production of these proinflammatory proteins, take the bacterial proteins, modify them detoxify them make them friendly for use, and turn them into lead compounds for new new drugs. So that's an emerging area of many laboratories. It's a concept known as drugs from bugs. The bugs are the bacteria and viruses perhaps. They can suggest to us novel therapeutic strategies to controlling inflammation.
Nature did it first.
Nature did it first. So, let's learn from nature. There are many ways to, you know, look for potential new therapeutics. There's random libraries of small molecules, there are you know very robust computational strategies, so letting machine learning, computer strategies to predict chemical interactions, or take a look at what bacteria and viruses have already done.
The work is fascinating and clearly taking a lead, from as you said, what nature has already done is obviously a very effective approach. I'm wondering, with the new N-bath Center going in, kind of in your backyard, what kind of interaction do you see going on between the work you're doing and that center? Is it going to be, kind of running parallel to one another? Do you have direct input in what's happening up there, or direct activities going on in the future?
So, there are obvious parallels between the, you know, the National Bio and Agro Defense Facility, NBAF. It is literally right next door to our CEZID program, and to our laboratories. So, we're very interested in looking for partnerships certainly there will be a lot of training opportunities. So much of the workforce at NBAF is likely to come out of K-State. So, one of our missions is to train this new workforce, both with the book knowledge and the hands-on laboratory skills that will make them good contributors to NBAF. There's a lot of parallels in the mission, you know, so to protect the food supply, to protect agriculture, to protect the population against zoonotic diseases. So, there's good interface between CEZID and NBAF. So, definitely we're interested in establishing collaborations. Dr. Juergen Richt, my collaborator, he's already established several collaborations. We work with the Plum Island facility, already. This is the laboratory that's essentially moving from the Long Island area to become NBAF. So many of the projects are already in place, and certainly we'll see a lot of growth in the coming years about how to safeguard food animal health public health and really preserve our agricultural economy from various threats.
Earlier, you mentioned the E Coli outbreaks that have occurred as a consequence of produce and because of those outbreaks over the past, probably five to ten years, been a lot of research looking at E Coli and Salmonella in particular, and whether plants actually play a role in their life history. And clearly they they do. That it's not really just an incidental occurrence of those organisms perhaps being sprayed on these these plants with irrigation water or something like. That in fact there's compelling data that they truly infect the plants and that they've actually documented an upregulation in expression of effector genes, and things like that. So, there seems to be some strong relationship between E Coli Salmonella and the plants. And I'm just wondering if you're aware of any evidence of that plant component actually helping to drive the evolution of those species or the emergence perhaps of new pathotypes. Because we we know that the plant pathogenic bacteria as well as as some of these share secretion systems and that some of our closely some of the plant pathogens that are closely related to the enterics, you know, have multiple secretion systems. And I'm just wondering if there's any evidence that you're aware of that there's a drive in the evolutionary process for some of the zoonotics? Some of these human pathogens like E Coli or Salmonella.
Yeah, that's a fascinating question. So thanks for bringing that up. It's very clear that a lot of what bacteria do when they interact with human or animal cells also occurs when bacteria need to interact with plant surfaces. So for example, the elaboration of surface appendages for adherence. The pili, the the swimming apparatus called the flagellum, these are all up regulated by by contact with plant surface. Gaining entrance at wound sites or cracks between root hairs there's a lot of physiological similarity between the human intestine and some aspects of plant cell boundaries where these mechanisms are conserved. Whether plant interaction drives the evolution of bacterial pathotypes, or not, is unfortunately rather poorly understood. And I think a lot of that is a function of scientists taking a human-centric view to a lot of what these pathogens do. So, we tend to take the view, and I'm also to blame, bacteria exists to cause disease in people to cause diarrhea, in terms of these intestinal pathogens to cause respiratory illness, of course that's not the case. So, most infections are accidental. The only goal, if a bacterium were to have a goal, is to replicate so to find food source and to replicate. So, our view is often a little bit warped, and we don't give appropriate coverage to what might be going on in the environment. So when new virulence factors emerge. Are sporadic accidental human infections really driving that evolution? Most likely not. More likely the interaction in the between the bacterium and its environment, whether that's in water or with produce, on spinach or lettuce, this is more likely the the driving factor to evolving new bacterial path types. But it's poorly understood. Some of the model systems are are less well developed. Plants also have immune systems, so I've mentioned a few times about an ability of these bacteria to inhibit human immune systems. Well, plants also have immune responses to infection. They essentially try to wall off the infected cells to limit the spread of the infecting pathogen. But again, these bacteria have ways to evade that plant immune system. Secretion Systems are well conserved in how they block human versus plant functions. So, I think this area should be studied much more extensively. I think if more funding were available to really look at the what forces drive the evolution of these bacteria we would learn much more. To some extent, that's a product of our funding system. In that it tends to be slanted towards immediate tangible therapeutic benefits to humans or food animals, and at times basic science inquiry can be ignored or at least underfunded. So, I would target as you suggest this area as a potential rich area of investigation.
I was just going to say your center must be a rich experience for the students. I'm just wondering, how do you maximize that? I mean with the aggregation of expertise you have there and the diversity of projects that could be a pretty rich environment for certainly a graduate experience. I was just wondering how you might comment on it?
Yeah, thank you. We're very excited we're in the second year of this program and one of the main goals is to bring along the next generation of of scientists. So, not only are we mentoring the the junior faculty, you've heard some of their research projects already. Another component of that is mentoring their own students, and postdocs students, can be undergraduates, masters students, PHD students, and the mentoring can be direct or indirect. So, certainly we've seen pretty significant growth in student numbers. Each lab seems to be getting more and more students. We've started several journal clubs. We've discussion programs. We bring in distinguished scientists to speak with students and faculty. So, we try to bring in leaders of the of the various fields have scientific discussions with students. Really set the foundations for their growth, as we've discussed, we do need an immediate workforce as NBAF comes online. But, we also need the the next generation of basic scientists to populate our university laboratories. So, we're also seeing a rapid increase in research infrastructure. So, several new pieces of technology are now new to K-State. So we have single cell capability. So, we can isolate single cells from various tissues work with them in isolation do single cell sequencing, single cell gene expression, analysis. We have new live cell microscopes again. This was not available here until recently. So, I'm very excited that we have a really first-rate group of faculty. We have many people interested in highly capable of student mentoring. And we're really developing first-rate technology, so students can get hands-on experience with techniques that will make them very marketable to academic or industry careers.
In many respects progress is a function of the relationship between science and technology, and probably for the last 500 years it's been kind of a push-pull relationship where one feeds the innovation of the other, or feeds off of the innovation of the other, and it is more of philosophical question. Do you think at this point though we science has become more dependent upon technology to the point where it influences the questions that we ask?
I think there can be a tendency for that. So it's very easy to get excited about a new machine, and then frame scientific questions around what that machine is capable of doing. So for example, if you get a new live cell microscope the tendency can be, let's do all experiments focused on live cell microscopy. But, I'm not too concerned. I think you know good science is done through the classic scientific method, and tried and true technologies are often still the best approach to solving problems. So for example, my postdoc yesterday showed me a very nice set of data that have solved a year-long problem for us. He was using genetic techniques in Salmonella established in the 1960s. But he was he was aware of the older literature, he could recognize the value of that more dated technology, and he knew it was appropriate for the question he was asking. So, it is a challenge, technology makes it some things easier. But, they can kind of cloud our understanding of some of the basic concepts. So, I think there's room for both, but I guess I'll point out that there's been a lot of very important scientific discoveries that are essentially accidental. They're serendipitous, so really it's our job to do well-controlled experiments, have testable hypotheses, have good robust record-keeping practices, and then keep our eyes open, because if we see something unexpected or unusual we want to be able to follow that up, and be confident it's not just a laboratory mistake. So, all the fundamental training students learn in Chemistry 101, in undergraduate, keep a good notebook, rigor, and reproducibility, I think you know these fundamental issues are always going to trump any technological advance, in terms of how we move this field forward.
You've been talking about basic science a lot and about the accidental things that pop up right from just doing some work. And then, you know, as you said in your own work, you know moving to how this might, some discoveries, might actually apply to treating autoimmune disorders and things like that. Right? So, how do you think about either, you know, an individual scientist or the scientific community doing this balance of the, you know, let's work on some really basic questions that we, and we just want the answers to, and we don't really know what the application will be. To then, noting where there might be, you know, some something really useful applied and sort of starting to follow down that path. To then, sort of hey we have a very specific question. Like, you know, Covid, and we have to address.So how do you balance that as either an individual, or as a research group, or as a wider community? What thoughts [do] you have on that?
Thanks, that's one of the toughest aspects, at least personally for me as a professor. How focused and narrow do we get in terms of the minutia of a protein. So, do we need to understand every atom of every protein? Versus when are we ready to apply this to a disease? Translate this into a real therapeutic. I think we have to be as scientists extremely open, and generally willing to to share data, be transparent about our raw data, and like other aspects in life, know when to ask for help. So, most of my translational endeavors in terms of anti-virulence compounds bacterial proteins used to inhibit the immune system have really resulted because I shared data very early on with with someone at a meeting, or a conference, or invited lecturer, and they had a slightly different way of of looking at the data. So, I viewed it in one direction. That I understand how this protein works, and an outsider to my specific field was able to ask a broader question. So, oh if you know that this protein blocks the immune system, have you ever thought about trying this? Or, I know a friend at my institution who could take your protein and try it in their mouse model of inflammation, for example. So it is a challenge. We're constricted by funding opportunities, so it's more comfortable to kind of stay siloed, and work on what we’re recognized as experts to do. But, I think it's far more important to take these leaps of faith, and try to work with translational scientists who might really see the application of your basic discovery, and be able to help you apply it to a broader application. And of course, there's a lot of complexities with university licensing and patenting data ownership, but we have all the university resources to help us with that.
You've been talking a lot about individual organisms that you work with. Have you done any work with the way those organisms interact with one another different types? And what I'm kind of getting at is the microbiome activities that are being tested and looked at in various areas across campus. Does your work specifically get into that area?
Yeah, thank you. We have worked a little bit with the microbiome, and that's something I haven't mentioned yet in this discussion. So, you mentioned the naturally occurring commensal, or beneficial organisms that that colonize all of our mucosal surfaces. So, the microbiota or microbiome, another aspect of the success of a bacterium or virus, if we think about a human infection it's not just the immune system of the host that challenges the pathogen. It's also the bacteria that line the respiratory tract, the intestinal tract, the genital tract, the skin. So, that's another barrier, and it's actually one of our defense mechanisms, essentially. So, how do bacterial pathogens interact with the microbiome? We've done a few studies in that area. So, we've mostly used mouse models to study where we can do fecal transplantation, to study what makes certain strains of mice more resistant, or more susceptible to bacterial infection. And a lot of that susceptibility is driven, not by the strain of mouse per se, but rather which intestinal microbes are harbored within that mouse. So, the microbiome really does play an important role in dictating disease susceptibility. So again, it's interesting to do a survey, to understand what bacteria are present in the gut, what are the correlates of resistance, and susceptibility. But, it's even more interesting, to then use that information to start to tailor different treatments, so the pre and probiotic industry is extremely robust in this area. There's opportunities for collaboration to make animals more resistant to infections, or are more robust at gaining weight over their development time. And there's also fundamental aspects of how the microbiome dictates immune responses so we may again learn a lot from how the microbiome can dampen the immune system in terms of generating new anti-inflammatory compounds. If you take an animal and you rid it of the microbiome, or you develop a germ-free animal in the laboratory, for example, you tend to see very potent anomalously high inflammatory responses. Suggesting, that one job of the microbiome is to dampen the immune system and really make it selective towards pathogens, rather than, towards random insults or challenges. So, this is a huge area to study. We've collaborated with several groups here on various organisms to do surveys of the microbiome, and we're hoping to apply some of this knowledge to potentially discover new therapeutic strategy.
Very much so, absolutely. Do you have any questions for us, [Dr.] Phillip?
I think we've covered kind of the highlights, and I think I've given you a good flavor of how I approach science, and what my main interests are.
Thank you very much. I enjoyed the discussion. Yeah, really enjoyed the discussion.
Thank you, Thank you all.
Thank you, [Dr.] Maureen
Yeah, thanks much! bye-bye bye-bye!
If you have any questions or comments you would like to share check out our website athttps://www.k-state.edu/research/global-food/ and drop us an email.
Our music was adapted from Dr. Wayne Goins’s album Chronicles of Carmela. Special thanks to him for providing that to us. Something to Chew On is produced by the Office of Research Development at Kansas State University.
Keywords: Center on Emerging and Zoonotic Infectious Diseases, Disease, Global Food Systems, Kansas State University, Pathobiology, Research