An Infectious Disease Researcher in our Midst: A Q&A with Bruce Kimball

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Chemical ecologist and Monell Member Bruce Kimball, PhD recently transitioned permanently to Monell from the U.S. Department of Agriculture (USDA) after being co-located at Monell for over 12 years. We asked him – via email (social distancing!) – how his work may possibly inform the COVID-19 pandemic. One of his most recently published papers with USDA colleagues, in PLOS Neglected Tropical Diseases, describes a new method for monitoring raccoon and striped skunk vaccination programs using volatile chemical signals of immunization detected in the animals’ scat. This non-invasive monitoring of wildlife populations using fecal volatiles has enabled, for the first time, a link between volatile compounds and adaptive immunity. This strategy could become an important resource for monitoring viral infections in wildlife species, perhaps in a manner that could prevent future pandemics.

Q. First, how did a chemical ecologist get involved in chemosensory research and now basic immunology?

A. This arises from my own interests in chemical ecology and animal behavior along with the 40-year history of USDA research at Monell. Initially, my research focused on diet selection and how animals interpret chemical cues in their foraging environment. However, shortly after arriving at Monell in 2007, I started collaborating with Gary Beauchamp and Kunio Yamazaki on individual odor and how body odors are altered by health perturbations.

Bruce Kimball, PhD

Q. Tell us more about your research on viral infection and odors within animals of the same species and how that might relate to COVID -19.

A. After a few years of research, it become abundantly obvious that every health perturbation altered body odors. From this, I became interested in the mechanisms behind these alterations. A significant part of my research is related to cellular immunity and how cells recognize pathogens. This type of immune response is called innate immunity and is comprised of different components including physical barriers like our skin and mucous in our respiratory tracts and a suite of specialized cells that function as initial sentinels that recognize foreign pathogens. Cellular recognition of viruses, as well as gram-positive and gram-negative bacteria, appear to each give rise to different molecular signals in the infected host. However, within these broad categories, the cellular processes I am studying don’t appear to differentiate between different types of viruses for example. Indeed, we would expect an influenza virus to generate the same odor response as a coronavirus. 

I have also worked in a related area called adaptive immunity – for example, my recently published work with raccoons and skunks. In this type of immune response, specific antibodies are produced by the hosts’ immune system after being exposed to a pathogen such as the COVID-19 virus. Whether or not specific changes occur in body odors is the million dollar question. In practice, at this point in my research, I don’t have data to point to that says we could tell the difference between a flu virus and COVID-19 using volatiles, though I am hopeful it may be possible.

Q. Does your research speak to the spread of disease? What have you published on avian flu?

A. An important feature of many zoonotic diseases is their origins in wildlife. One way to prevent pandemics from ever starting would be to identify these viruses before they can mutate and infect humans. Influenza is one such disease. My published work in this area – and what we now know – is that when ducks are infected with an avian influenza, it results in a change in fecal volatiles. In addition to instrumental analyses of feces, we trained mice, ferrets, and dogs to differentiate feces from ducks before (healthy) and after experimental infection with a low pathogenic avian influenza. This suggests another tool for monitoring avian influenza in wild birds. Ever since the 2009 H1N1 influenza, such surveillance in wild birds has been extensive – which reflects a known pathway for new human influenzas. 

What we are seeing with COVID-19 is pretty much the same pandemic scenario. Typically, a virus moves from wildlife to domestic animals (often to pigs), it mutates, and is then transmitted to humans. As has been surmised by researchers since the COVID-19 spillover occurred, this is probably how COVID-19 started: a coronavirus circulating in bats passed through another animal and mutated, making it virulent and transmissible in humans. My research does suggest that surveillance of viruses in wildlife and domestic animals could possibly be achieved via monitoring fecal volatiles.

Q. Tell me about your research on discriminating bacterial from viral infection to also discriminate COVID-19 from other viral infections.

A. I think it is important to note that most of our data suggests that individual viruses cannot be discriminated from each other through their changes to body odors. However, it appears that body odor can tell us whether a sick animal has a viral or bacterial infection. Our current model indicates that the cellular response to viruses is different from the cellular response to gram-negative bacteria, which is different than gram-positive bacteria. When we immunized mice with two very different vaccines and looked for volatile differences related to what should have been two different adaptive responses, trained mice did not recognize them to be different. Arising from this finding, we have focused on cellular immunity and pathways activated by cellular recognition of pathogens.  

Q. How might this work relate the current pandemic?

A. It is important to realize that I am not a physician, bacteriologist, virologist, or epidemiologist! In disease surveillance, our research suggests that viruses may be detected in animals before humans ever become infected. In human disease detection, this research could be of tremendous value in diagnosing bacterial infection, thus ruling out viral infection, to facilitate proper prescription of antibiotics. Many bacterial infections, such as sinusitis and gastroenteritis, would all benefit from a rapid test for bacterial vs viral cause – typically diagnosed now by clinical symptoms, or waiting it out, as it were, and if one gets better in a prescribed time, it was viral.

Q. What does your wide-ranging research portend for public health and infectious disease studies in the near and not-so-near future?

A. My ideas are based on the eventuality of another pandemic down the road. We know the etiology of these viral pandemics, and they all involve mutation as the virus moves from wildlife to humans. Pigs seem to play a major role in allowing wildlife-borne viruses to become virulent in humans. Importantly, we really should not be concerned about just one type of virus (SARS and COVID-19 are coronaviruses, but swine flu is an influenza virus). If our data is correct that every virus will produce the same volatile signal, we could theoretically construct a detection system that identifies any viral infection in pigs – which could prevent the pathogen from ever being transmitted to humans and creating the next pandemic.