Jenny Fisher – A Celebration of Faculty Research ~IUN~

Jenny Fisher – A Celebration of Faculty Research ~IUN~


Alright so I think most of us would agree
that the development of antibiotics was one of
the biggest medical breakthroughs, maybe even in history. Beginning with World War
Two when penicillin was introduced and saved countless lives of soldiers on the
battlefield and then had widespread use globally. This was really hailed for good
reason as a miracle drug. From everything, from infections like sepsis that would
have been a death sentence to maybe common STD’s like gonorrhea, these could
all be fixed with penicillin. But even in these halcyon days of this new kind of
miracle cure there was still something lingering that we still had this specter
sort of resistance already appearing. Before penicillin ever went to market
there were already staph aureus species that were resistant to this. So how could
that happen? Well long before humans were even a twinkle in the eye of the
universe bacteria and the soils had been carrying on this biological arms race
for millions of years producing the antagonistic molecules that we know as
antibiotics to kind of gain a foothold over other organisms in the soil to
out-compete them for resources and these other bacteria then evolved resistance
to that slowly a little at a time maybe lots of them died off a few survived and
passed those genes on and bacteria responded by creating new antibiotics
and other bacteria responded to that by creating new resistance and so this was
all fine and good until we appeared on the scene and started selecting for
resistance by the overuse and abuse to some degree of antibiotics, but where we
really made this jump was when these genes were sort of weaponized
or mobilize from the bacterial chromosomes on to something called
plasmids. So up here you’ll see a plasmid and a plasmid is an extra chromosomal
piece of DNA that can move around and some of them give resistance to one drug
or maybe two drugs or this one gives resistance to five different classes of
antibiotics all at once. So rather than millennia of evolution, we
suddenly jump from you know a worm to a mammal in terms of the abilities and the
and the huge jump that these plasmids can make in the evolution of organisms. All right so then we have this pressure to keep these plasmids and this is where
we get something I like to call the super bug. Now the name sounds really
cute, but don’t be fooled. These things are deadly. Super bugs are what we call
bacteria that have become resistant to almost every single class, if not every
class of the main frontline antibiotics and shown here is a representation of
super gonorrhea that is making its way around the globe and that’s what they
call it so the CDC refers to as super gonorrhea and what was formerly this
riddle like kind of really a minor embarrassment of an STD that you could
from the first slide you could see you could cure with a shot of penicillin in
four hours is now these strains are treatable only with the last line one
class of last resort antibiotics so this is this is scary but it’s a lot more
scary if it’s something that causes a much more severe disease than
gonorrhea. So something like sepsis or blood stream infections
essentially. If a patient comes into the hospital dying of sepsis, they don’t have
time to go through treatment after treatment and have antibiotics fail. If
health practitioners don’t know about emerging and resistance or super bugs
that are on the rise they can’t prepare for them and they can’t respond
appropriately to the needs of their patients. So hopefully here’s where we
come in. In some of my previous, and this is gonna sound really glamorous,
working with sewage, comparing this to the human gut microbiome we found that
sewage does a really good job of reflecting what the human gut microbiome
looks like, so the idea that I had was that we can use sewage as a way to do a
cheap epidemiological study by taking a single sample of pooled human gut
microbiome from an entire community at once. We can look at the antibiotic
resistance that they’re carrying and then we can figure out for a given
community what the risks are of potentially different antibiotics and
the important part here is that we want to look at commensal bacteria as well as
pathogens because pathogens are not our only concern here. Okay so think back to
that plasmid I showed you with those five different types of resistance that
they could get. It’s not just bad bacteria that carry these plasmids. Good
bacteria can pick them up just as easily. We have a lot more good bacteria than we
have bad and those are not necessarily enemies. Sometimes they share these
plasmids with one another. So the problem is that we can have our good bacteria
carrying this resistance and potentially sharing it with pathogens, but our bodies
and the clinics are not the only place that bacteria reside of course. So
anywhere we have overlaps between humans and our bacteria you know the
environment, soil, water, farm animals, urban infrastructure, these are all
potential reservoirs of resistance and so this is where my lab and I sample. We
sample sand from the beaches, we sample impacted recreational waters, we sample
sewage and septic tanks and things like that and we use a bunch of traditional
microbiological techniques. We grow bacteria on plates just like you would
expect exposing them to different antibiotics seeing which ones survive. We
also take a DNA based approach. So we look for the presence of these plasmids. We look for specific genes that can confer different types of antibiotic
resistance and then we look for the presence of those genes on the plasmids
to show that they can be potentially spread around and shared
and so it should come as no surprise to people that we have found some of them. We’ve found a lot of resistance which is not surprising and this matches pretty
well with what we’re seeing in hospitals. We can compare it to their antibiogram
that they’ve developed but we don’t want to just reflect what we’re seeing. We
want to be predictive. We want to create an early warning system for emerging
resistance that is not showing up yet in hospitals. So one of these things that
we’re concerned about is colistin. Colistin was a drug that kind of fell
out of favor in the 80s because it’s very highly toxic to people but it got
picked up for use in animal agriculture particularly as a growth enhancer for
swine farms in China, so they feed it to the pigs that makes them get fat faster. But in 2015 they found resistance, colistin resistance, on a plasmid in
these pigs, then a few months later they find it in commercial meat. A few months
later they find it in a patient in New York, so this spreads globally and
very quickly. So we have also found colistin resistance. We have found it in
sewage, we have found it in the environment, we have found it in
commensal bacteria are good bacteria, and we’ve found in pathogens. So it’s here. So
I’m predicting that, and this is so gloom and doom, sorry, but then
it’s only a matter of time before we have an untreatable coalesced and
resistant super bug case here in Northwest Indiana, but my hope is that we
can continue to monitor this and that maybe we can find the next super bug
before it finds us. Thank you. (Applause)

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