Challenges of Antibiotic Resistance

Challenges of Antibiotic Resistance

– Tonight’s program is sponsored by the College
Scholar’s Program. This program provides a stipend to JCCC faculty,
both full and part-time, for the development of two research presentations, one of which,
of course, is taking place tonight. And either a guest lecturer in the classroom,
or a faculty seminar on the topic of the presenter’s choice. College Scholars was started by Dr. Jim Leiker
to provide a platform for JCCC faculty to present their research projects. Those of us who are involved in this program
feel it’s important for a number of reasons. First, community college professors, of course,
the emphasis is on teaching. So this gives community college faculty a
chance to explore their own research interests. Second, I think that pursuing your own research
interests makes faculty, of here we have two extraordinarily wonderful examples, better
teachers because they can bring new insights, and new enthusiasm, to the classroom. And I think there’s a lot of students who
are these-students of these professors who would say that’s exactly what happens in the
classroom, in their classroom. And then, finally, it’s a way for the community
to understand the resource that they have at JCCC, and the resource that they have in
the faculty. So community members have come to every one
of these presentations, and there’s always a lively back and forth, and exchange of questions
and answers at the end, after the presentation is over. So it’s a chance for the members of the community,
and faculty, to meet and get to know a little more about each other. So now, on to tonight’s speakers. Heather Seitz received a PhD in Microbiology
and Immunology from the University of North Carolina, Chapel Hill, in 2006, and joined
the faculty at JCCC in 2007. Melanie Harvey received a PhD in Inorganic
Chemistry from Vanderbilt University in 2000, and joined the JCCC faculty in 2008. Both Dr. Harvey and Dr. Seitz have published
extensively in scholarly journals, and have presented, also extensively, at academic conferences. They are also sought after speakers for both
their teaching and research expertise. As professors at Johnson County Community
College, they have collaborated to turn their classrooms into living laboratories, and encourage
their students to become part of the solution to the problem of antibiotics resistance. Dr. Seitz’s students run experiments on local
soil samples to isolate bacteria, while Dr. Harvey’s students characterize the antibiotic
compounds. Dr. Seitz and Dr. Harvey are two of about
200 educators around the world who are engaged in this type of experimentation in their classrooms. They are part of the Small World Initiative,
a program started at Yale University, that has the dual purpose of encouraging students
to pursue careers in science and to crowdsource the search for new antibiotics. Their innovative teaching, and their commitment
to JCCC, has won Dr. Harvey and Dr. Seitz numerous awards, among them the Distinguished
Service Award, and the Burlington Northern Santa Fe Railway Award, both of which are
presented to faculty who demonstrate excellence in teaching and service. I am very pleased to have both of them here
tonight. Ladies and gentlemen, Dr. Melanie Harvey,
and Dr. Heather Seitz. (applause)
– Good evening, and thank you, Sarah, that was a very warm introduction. So tonight’s talk is going to be about the
challenge that we’re facing with antibiotic resistance. We’re going to be talking a little bit about
the statistics on antibiotic resistance in the United States today, the history of antibiotics,
how they work, and how is it that bacteria can become resistant? Some important classes of antibiotics, and
we’ll talk about the antibiotics of last resort, as well as discuss a little bit of the chemical
structure of those important classes. We’ll be talking about what’s being done to
develop new antibiotics, both here at JCC, as well as nationwide, and international efforts. And, lastly, we’ll talk a little bit about
our research into finding new antibiotics. That will be primarily the focus of our second
talk on Wednesday, April 19th at noon, in this exact auditorium. So if you’d like to come back to hear more
about our specific research results, feel free. We would love to have you. So we take antibiotics for granted. Today, my son is sick, and probably has strep
throat. I know that tomorrow I will probably take
him to the doctor and he will be prescribed an antibiotic, and he will get better. I have faith in that, right? I know that that’s the reality that I live
in right now. But that reality is precarious, right? I want to introduce you to a little girl. She is two years old. She is from Connecticut. And in September of 2016, she went on vacation
with her family in the Caribbean. And it was a wonderful two week vacation filled
with lots of food from the local markets, including goats and chicken meat. And they had a wonderful vacation. But about two days before they returned to
the United States, this little girl fell ill with some diarrhea. Immediately upon return to the United States,
they took her to the pediatrician, right? And the pediatrician was involved in a new
effort called the Pathogen Detection Network. So they took a sample from this little girl’s
stool, from her diarrhea, and sent it to the Pathogen Detection Network. Immediately began treating her with an antibiotic. Because she had been visiting the Caribbean,
and there’s a lot more diversity in the types of pathogens that you might see in the water,
and the food samples there, they treated her with a slightly unusual antibiotic for that
case, Paromomycin, which is primarily prescribed for amoebic dysentery, or a parasite like
dysentery, that we typically don’t see in the United States. That turned out to be one of the best things
that they did for this little girl. She recovered just fine. And she was released from the hospital, and
made a full recovery. But that entry into the Pathogen Detection
Network showed us how close a call she came, right? So they analyzed the sample by DNA analysis
and found an important antibiotic resistance gene called MCR-1. And it, it turns out that the bacteria she
was infected with, E-coli, had this resistance gene. This is an antibiotic of last resort. So had they used the traditional antibiotics
to treat her, they would have found that no antibiotics that they had tried would be effective. That is not an isolated case, unfortunately. Each year in the United States more than 2
million people will get sick, every year here, from an antibiotic resistant infection. That is more than the entire state of Nebraska,
which is where I’m from, right? That’s why I care about those people. And of those 2 million people, 23,000 of them
will die every year in the United States. That is half the student population at Johnson
County Community College, and the entire population of K State University. That’s a lot of deaths from antibiotic resistant
infections. So what happened before antibiotics? – Okay, so before antibiotics, your chances
of dying from a bacterial infection were very high. In fact, in 1910, 46% of the deaths in the
United States were from infectious disease. By the year 2010, that number had dropped
to just 3%. The difference is both vaccinations and antibiotics. Now people were using antibiotics before they
realized they were using antibiotics. We do know that some ancient cultures used
moldy bread in infected wounds, or in wounds to prevent infection. So they didn’t even realize what they were
doing, but they were, in fact, using an antibiotic. We’ve also found evidence in mummies. They found evidence of tetracycline, and they
have deduced that it was in their process of brewing beer that they were actually also
making, growing a bacteria that produced tetracycline. So in their regular diet they were taking
antibiotics. And they’ve also seen that Egyptians that
were in this group had lower incidents of bacterial infections. Okay, so the miracle drug that I want to just
tell you about the story of a little bit, is the first time that antibiotics were available
worldwide. And that is Penicillin. This is Alexander Fleming, and he is credited
as the first person to publish the discovery of Penicillin. And he was studying bacteria. He went on holiday for two weeks. And he came back, and here is a photograph
he took of what he found. And this is a plate where he was growing,
these little white dots represent, these actually are staff. So he was growing staff, but then there was
this contaminant, and it turns out that contaminant was Penicillium notatum. And what was interesting about this that stood
out to him was the fact that in this whole region here you see that the staff, it looks
like the staff was there, but it died, okay? So then he started studying this Penicillium
notatum to see what is it making, what is it producing, that is killing the staff? And he ended up, at first he called it the
mold broth. But then he shortened it to just call it Penicillin. So he would extract the Penicillin. He did have a little trouble isolating the
Penicillin specifically, the chemical, because it was very unstable, the way he was trying
to isolate it. So he would just use this mold broth. So then some folks at Oxford worked on this. Norman Heatley, first, was able to successfully
extract the Penicillin drug molecule. And Edward Abraham used a new technique at
the time, column chromatography, to help remove impurities and clean, you know, purify it. And then Howard Florey, in 1940, he started
testing it on mice that had bacterial infections to see, you know, if it would cure their bacterial
infections. This process required, at this time, a lot
of this mold broth. And so, they had, they hired a bunch of ladies,
they called them Penicillin girls, and they paid them hourly to maintain these cultures,
and to grow lots and lots of mold. And, in fact, they needed, at that time, to
do the testing that he was doing, they needed 500 liters a week. And the reason I spelled mould like this is
really because these folks are all British, and so I just went with their spelling, right? Okay, so then Florey used it on the first
patient, and I believe I read that it was his wife who knew of somebody, and they just
decided to try it out on this guy. So there’s this policeman, and he is 43 years
old, and he was pruning his roses, and he accidentally scratched the side of his mouth. But then he developed a horrible infection. In fact, it was so bad that it had taken over,
you know, his, he had abscesses on his face, and they had to remove one of his eyes. And it was infecting his lungs. And so he was going to die. And they thought, well, this is the kind of
candidate that we want to try this on, is somebody who if, you know, he was going to
die if we don’t do something. So this is where they started. They injected him with Penicillin, and he
made a remarkable recovery. He was eating, feeling better. But then they ran out. Because, remember, they had, you know, all
these 500 liters a week, which just to test some mice. So they needed a lot more for a human. And, unfortunately, ran out of it, and he
died five days later. So at that point they said, “Okay, we’re only
going to use this, for our first clinical trials, we’re only going to use this on children
at this point, and only when they’re, like, as a last resort, like, to try to save them. And that way we won’t need as much on a child
as we would a grown man.” So this is the first, here’s an example of
the first girl, I believe, she was the first one, right? Yeah. And this is taken, this was in 1942, and here
is, you can just tell from this picture that she is in a really bad state with an infection,
a bacterial infection. Picture three is after four days of Penicillin. Picture four is after nine days, and then
five and six shows after she’s made a full recovery. So this was kind of, like, amazing, because
if you imagine how many people were dying. And just imagine, you know, cutting yourself
pruning roses, and that’s a death sentence. That seems bizarre to us today. But this is really the reality of what people
were living in when they didn’t have antibiotics available. Okay, so they needed a lot more, and it was
the middle of World War II. And, you know, Britain was in no shape to
be mass producing something like this. All of their chemical plants were focused
on the war efforts, and they did not have, it was not a good time for them to be mass
producing Penicillin, and to sort this out. So they looked to the United States for help. And this guy is Andrew Moyer, he’s the director
of the USCA’s northern research laboratory in Peoria, Illinois. And he was doing agriculture research. And one of the things he was doing was, he
had a lot of byproducts from the wet mill processing of corn, and he’s always trying
to find a use for that. So that was just a thing that they seemed
to try it on everything. But he worked out that if he added this corn
steep liquor to the fermentation medium that he was growing this mold in, and he substituted
lactose, which is the sugar in milk, for sucrose, which is table sugar. He substituted those in the culture medium
that he’s growing it in, and he actually increased the yield 10-fold. So suddenly now they can grow it, 10 times
as much Penicillin in the same volume. And so then the, this became like an important
part of the war effort, really. If you imagine all the soldiers that are being
injured, and a lot of their injuries are susceptible to infection, this was very important that
they really mass produce this and make it available. So they, basically, the War Production Board
was formed, and they talked to all the chemical companies in the U.S., and they chose 21 companies
to participate in this effort. And they would grow these molds in big fermentation
vats, where it was aerated, and they really maximized how much they could get. This was a big production. And Pfizer was the first commercial plant
that was opened. And I just wanted to show you this because,
I think what’s interesting, and it started making me think about the World War II generation,
even, and that sense of, at that time, of not so much individualism, as much as like
doing things for the good of everybody. They really had very much of that sense of
sacrificing for the many. But they did this whole campaign, because
they needed people to get on board. It took a collaborative effort of more than
one country, and it took scientists that were working in government, in academia, in hospitals,
in, you know, in all different, in chemical plants, in all, in industry. It took all of them working together to bring
about this mass production of Penicillin and make it available to the world. So I think that that– And so they launched
this whole campaign of just letting people know, like, this is important to everybody,
and we should care about this. – All right, so we’ve learned that Penicillin
was originally found, made by a fungus, right? So we know that fungus can make antibiotics. But bacteria can also make antibiotics. And you think, that’s interesting, because
these drugs are designed to kill bacteria, and to kill fungi. But bacteria do this, they make these antibiotics
as natural byproducts in their environment. So we all know animals of every species, and
bacteria, and fungi included, they all want to stake out their own little claim, right? Their own little picket fences, as you were. So they all want to compete for the space
and nutrients in their local environment. And an environment like the soil has millions
of bacteria per gram. So they all want that little piece of that. So these bacteria and fungi make these compounds,
these antibiotics, to help secure their little space, to make sure everybody else stays out
of their little zone. And I’ll show you a picture of what that looks
like on an agar plate later in our talk. So think of it like little picket fences that
these bacteria are producing. Now it’s really important that the compounds
that a bacteria makes don’t kill that particular bacteria. So I want to take you all back to biology
class for a minute, and talk about the difference between a bacterial cell and a human cell. So bacteria, over here on the left, are much
smaller than their human cell counterparts, and they are much simpler in design. They have very few components to the cell. And there is a wide variety and diversity
in how these bacteria are created. So we have bacteria with a certain type of
yellow coating, or cell wall, called gram-negative bacteria. And we have other bacteria that have a very
complicated, thick cell wall that are called gram-positive bacteria. So there’s lots of different kinds of bacteria
that have different components that are shown here in this cartoon diagram. And that’s important because as bacteria create
an antibiotic, that antibiotic is oftentimes for a different kind of bacteria than they
are. So gram-negative bacteria might make an antibiotic
that harms gram-positive bacteria, for example. Now these cells are very different than human
cells. So if we are going to take an antibiotic,
the goal of that drug is to kill the bacteria without harming our own cells. So these drugs also have to be designed to
not harm any of the complicated workings of our own cells. So hopefully you can see from this cartoon
that there’s a lot of stuff going on inside that cell, right? There’s a lot of organelles, and complicated
machinery that all works together inside of our own cells, and the drugs that we take
can’t harm any of that. So it becomes very difficult to pinpoint those
exact differences that bacteria have that human cells do not have. So how do these antibiotics actually work? So antibiotic drugs target many different
places in the bacterial cell that are different and unique from those human cells. So we know that there are antibiotics that
target the DNA structures, so this is the instructions to make all the proteins of the
cell. So your DNA encodes all the things that you
need, and the enzymes that copy the DNA and RNA in the bacterial cell are slightly different
than the ones in human cells. So we have a whole class of drug that targets
those enzymes. We have antibiotics that target the cell wall. We’ll talk more about Penicillin, you’ve already
heard a little bit about Penicillin. But we’ll talk more about how it works. And those are drugs that target that yellow
coating around the bacteria that is definitely different than what we have in our human cells. We have drugs that target the cell membrane,
and drugs that target the ribosomes. So these are the little machines inside of
your cell that take your DNA and turn it into proteins, right? And there’s slight differences in how these
ribosomes are made to how human ribosomes are made. So there’s whole classes of drugs, and you
can see the list of the different antibiotics here, that target those ribosomes And lastly,
it’s important to note, that there’s a class of drugs that work to inhibit the metabolism
of a bacteria. So bacteria can live in places that we can’t
live, right? They can live in toxic waste, they can live
in the soil, they can live without oxygen. They can do amazing things that we cannot
do. And most of that is because of enzymes that
are involved in their metabolism and growth. So we can use antibiotics to target those
differences without harming our own cells. So how is it that these antibiotics, that
these bacteria, become resistant to antibiotics? So every time we try to pull out a weapon,
they pull out a bigger, sort of, defense. So bacteria are smart, and they’re very adaptable. Their DNA can change rapidly, much more rapidly
than human DNA changes over time. And those changes in the DNA can lead to some
important resistance factors. So you can have a change in the bacteria’s
DNA that does not allow the drug to get into that cell. So a change in the DNA changes what the cell
wall looks like, and the drug can no longer get in. You can have a change in the DNA of the bacteria,
and now an enzyme that may have been involved in metabolism can now break apart the drug,
the antibiotic drug. So it can just chop it in half. You can have a change in the DNA that alters
the place where the antibiotic binds. So antibiotics are these little red balls,
right? So the antibiotic is supposed to bind to this
component, a change in the DNA can change that protein to a different shape. And the antibiotic can no longer bind. And the last mechanism that I want to talk
about, and one that you’ll see, sort of, us talk about throughout the talk, is you can
change a pump. So this is a channel through the membrane,
and bacteria have lots of these for transporting things across the membrane, and you can have
a change in the DNA that alters this pump, and so, instead of pumping out the metabolism
product that it was supposed to pump out, it now pumps out the antibiotic, right? Think about when you try to feed a baby peas
for the first time, they just spit it right back at you, right? That’s my, that’s what I see in my head, right? So that efflux pump, it just pumps it right
back out. And that’s a really effective way for these
bacteria to become resistant. So how do these changes in the DNA happen? So changes in the DNA happen, they can happen
randomly. Every time the bacteria divides, it copies
all of its bases, its millions of bases of DNA. And sometimes the enzymes that do that make
a mistake. So you can have a random mutation. Those random mutations are more likely to
occur if the environment that the cell is in is stressed, meaning it’s not quite the
right temperature, or not quite the right oxygen level, or it contains antibiotics. So if you have a sub-optimal level of antibiotic
drugs, so a low-level of antibiotic drugs, it’s not quite killing the bacteria, but it’s
causing a lot of stress on that bacteria. That bacteria is having a hard time doing
its job of metabolizing and growing, you are more likely to have these mistakes, or mutations,
occur. So here we see a change in the DNA that’s
caused randomly. And it’s created an efflux pump here in this
little red arrow. In a population of cells where there is one
mutant bacteria, this mutation can slowly change over time, right? And I want to show you an example of, sort
of in real time, how these random mutations can occur. Now before we look at this video, I want you
to know this is a high stress environment, so one of those environments where you see
lots more mutations then you might otherwise see. Okay, so again, that’s unlike what you would
see in the human body. We don’t have, thankfully, increasing amounts
of antibiotics over time. But with that selective pressure, with that
increased amount of antibiotics, you can accumulate those mutations at a pretty rapid pace. Now that is not the most dangerous type of
mutation, or antibiotic resistance, that we’re worried about. Bacteria can share their DNA. I love this cartoon. It was on a shortcut through the hospital
kitchens that Albert was first approached by a member of the antibiotic resistance. So we see two bacteria here, and this particular
bacteria’s looking a little shady, and he’s sharing his DNA with another bacteria. And this is a mechanism that bacteria can
do. They can use their, their DNA can be on mobile
elements called plasmids. And these are specially designed pieces of
DNA, they are designed for sharing. So bacteria, in their natural environment,
they do clonal proliferation, meaning they clone and copy themselves identically. It’s not a very good idea for robust diversity,
so humans, we don’t clone each other, right? Because we like the diversity that we see
around us, and that makes us a healthier population. So bacteria have these mobile elements to
help them survive in complex environments where there might be additional stress. And so bacteria of the same species, right? These guys look sort of the same, can share
this bacteria on plasmids, but interestingly and scarily, right, there are, bacteria of
different types can share their DNA. So in our opening case with the two-year-old
from Connecticut, she actually was infected with a strain of E-coli that had at one point
gotten some DNA from a shigella bacteria. So different kinds of bacteria can share their
DNA and cause resistance, and not just different bacteria, but viruses can infect bacteria
and share DNA, and increase the spread of these mobile elements. Now let’s think about that for a second as
we look back at our example of the population. So if a bacteria is introduced that has this
mobile element, so notice the red mutation here is on a separate piece of DNA, one that’s
easily shared between different bacteria, we can much more quickly see the spread of
these antibiotic resistance genes. So that gene that that little girl had from
Connecticut, was actually on one of these mobile elements, which makes it an incredibly
scary type of infection. Now I want to talk for a second about the
diversity that we see in bacteria. So we’ve talked a little bit about how bacteria
can come in different shapes and sizes, but in our gastrointestinal tract, imagine that
we have a collection of bacteria. Most of that bacteria is good bacteria, it
does good things for us. It helps break down our nutrients, it helps
us digest our food, it helps us stay healthy because there’s not space in nutrients for
the dangerous pathogens to set up shop. There’s a lot of research now talking about
the human microbiome, right? So you can send off and find out what your
microbiome profile is. So we know that this is a very complex and
diverse environment. If we have this mutant bacteria, and we destroy
all of the competition in that environment, the only thing left is this resistant bacteria. So how would we go about doing that? Well when I take my son to the doctor tomorrow,
he’s most likely going to be prescribed a broad-spectrum antibiotic. And what does that word mean? Well, broad-spectrum means an antibiotic that
is effective against many different types of bacteria. In many cases, it kills off a lot of the normal
bacteria that you have in your gastrointestinal tract. Remember, these drugs don’t know which one
is the pathogen, and which one are the good bacteria. So in the case of a broad-spectrum antibiotic,
if we have this one mutant bacteria, we’ve killed off all of the competition. We now have more space and nutrients, right? What we see is a selection for that resistant
bacteria. So every time we use antibiotics, we select
for those that are resistant. In the case of a broad-spectrum antibiotic,
that is all that’s left. So what happens if we take a narrow-spectrum
antibiotic? And these are drugs that are harder to prescribe,
because you have to be more confident about what kind of infection your patient might
be experiencing. So a narrow-spectrum antibiotic is only going
to work against one type. And so if we do that in a situation, we kill
off only one kind of the bacteria, and we’re left with those good guys that can then proliferate
and create that coating to help us protect against the pathogen and the potentially resistant
bacteria. So they can help us compete for space in nutrients. And we see much less spread of that mutation,
that resistant bacteria. So how do these antibiotic resistant bacteria
spread in a population? And this graphic is from the CDC. And it starts here with George, right? He got some antibiotics that applied some
stress in his gastrointestinal tract, and he developed a resistant bacteria in his gut. So he may have gone, and been a part of a
healthcare facility, like a hospital, or a nursing home, where the people in those, the
encounters in that environment, are highly susceptible to these types of infections. So that is one way, we call that sort of hospital-acquired
resistance. Or, George could have gotten better, and gone
home, and he could still have passed it around with his friends and family. How you share a microbiome with the people
that you are closest with, right? So you have similar bacteria. And so George could have shared those resistant
bacteria with the people that he cares about. Now that is one side of the story. When people have those resistant bacteria,
they can spread them in the population. That’s the side that we typically think of. But we also have to pay attention to this
other side. So, in agriculture, there is wide-spread antibiotic
use. And so those antibiotics inside the animal
gut also can develop resistance. And if we don’t handle, or cook, those meats
properly, from those animals, we can also be exposed to those resistant bacteria. And the fertilizer or other water that’s been
contaminated with those animal feces can also spread those drug resistant bacteria through
our vegetables, right? So these resistant bacteria can spread in
the population in many different ways. Now what can be done about this? Well this is the CDC report from 2014, talking
specifically to prescribers, so doctors that prescribe antibiotics. And they say, order recommended cultures before
antibiotics are given. So let’s think of the last time a kid that
you know, or you, suffered from bronchitis, or an ear infection. Did you walk out of the doctor’s office with
an antibiotic script? Did you wait 48 hours before getting that
antibiotics? No, right? Now, if that’s the first recommendation every
time we prescribe an antibiotic, why isn’t it being followed, right? Well we don’t tend to go to the doctor when
we’re kind of sick, maybe getting sick, right? We go to the doctor as a last resort. We are very sick. Our child is very sick. We can’t miss any more work, or school, or
whatever commitments we have, we need to get better now. So patients have a responsibility in this. We don’t want to wait 48 hours. Can you imagine if a kid has a terrible fever
for two days, you take him to the doctor, and the doctor says, “Yeah, just sit on that
for two days, and I’ll call you back.” Right? As parents and even people that have been
sick, that’s not acceptable. The other side of this is the money, right? So it costs a lot of money to run the tests
to prescribe those special narrow-spectrum antibiotics. The insurance companies don’t want to pay
for that, you don’t want to pay for that. And it takes a lot of time and resources. So it’s very difficult to follow this first
recommendation from four physicians. They should also make sure that the dose is
appropriate, and to make sure to check back in 48 hours later and adjust the prescription,
right? Which also doesn’t always happen at the rate
that we like to see. Now we can’t always control what we walk out
of the doctor’s office with. But some behaviors that you can contribute
to, that can help reduce the spread of antibiotic resistance. Don’t seek antibiotics for those viral infections. Remember, every time we use an antibiotic,
we select for resistance. We increase the number of antibiotic resistant
bacteria in the environment. Don’t take antibiotics that are just lying
around, right? So if somebody didn’t finish their antibiotics,
we’ll get to that one in a second, but those antibiotics are either expired, you might
be allergic to them, they are prescribed at a dose that is not you. So if you take little kids, that is not the
same size as me, right? Or they are old and expired, so there’s lots
of reasons why you shouldn’t take antibiotics that have in the cabinet. Don’t stop taking your antibiotics until they
are gone. So remember that the stress that we put these
bacteria under when we take antibiotics can increase the rate of their mutations. So if you take antibiotics just long enough
to feel better, but you haven’t killed all those bacteria, they will remember, right? They are more likely to have those mutations. So you want to make sure that all of the bacteria
that you’ve been sick with are dead, right? They are gone. So take that entire prescription. And should you have any issues with antibiotic
resistance, you always want to make sure to talk to your doctor promptly if you don’t
feel better after taking your full course of antibiotics. So those are some things that are within your
realm of control, right? That you could do to help spread, help prevent
the spread of antibiotic resistance. – Okay, so there was a, I’m not a microbiologist,
I’m a chemist, and there were a lot of terms, when I started working with Heather, that
I had to learn. And one of the big differences is when you
hear her talk about gram-negative and gram-positive, I was like, “What does that even mean?” And I liked this visual here, because it really
shows us that this is gram-positive, and this is gram-negative. And, basically, lots of antibiotics will treat
against gram-positive bacterial infections, lots of antibiotics will kill those. The gram-negative bacteria are the ones that
have all the tricks. They have all of the resistance kind of arsenal
that they can pull. And so those are much more difficult to treat. And so, really, when we talk about needing
new antibiotics, we’re really focusing on ones that can fight back against gram-negative
bacteria. So if we wanted to classify antibiotics, there’s
a good number of different types that we could put up. I could put lots of chemical structures up
here. But they, basically, I wanted to focus on
the three major places where we get them, and design them. And the first is, you know, we have natural
antibiotics, and these would-be ones that are made by a fungus, or a bacteria, and we
just extract it and use it as is, right? Purify it, and then that’s our drug. Like Penicillin, like original Penicillin. Okay, so that would be completely natural. Most of our antibiotics are what we call semi-synthetic,
in that we’ve taken them from nature. We’ve taken them from the bacteria, produced
them, and then we alter them in some way. In a chemical lab, they’ve worked out some
kind of way to make a derivative of it, and change up the structure. And a lot of that is to decrease side effects,
or to combat these resistant things, these tricks that the bacteria are doing. I want to show you-Oh, yeah, and then the
last one is completely synthetic, and that would be an antibiotic that we have just made
from, we don’t need a bacteria or something living to make our starting material for us. We’re just going to assemble them in a lab,
okay? So I want to point out a couple things, and
then I’m going to tell you a little bit, I’m going to explain a little bit about Penicillin,
and how it works, and how a bacteria can be resistant to Penicillin, just as an example. I think it’s a really interesting one. Okay, so first I want to show you just a little,
for those of you that maybe haven’t had chemistry, or haven’t had much of it, but I just want
to point out the important thing to us here is, you see this little square ring? See the square? This is a beta-lactam ring, okay? And you see it in Penicillin as well. This is called a beta-lactam. And all these little places here, these are
carbons, they’re just not shown. Chemists understand that those are all carbons. Okay, so this is a beta-lactam ring, and I’m
going to talk a little bit about that. It’s an important part of Penicillin. And this is a, this is cephalosporin, this
is a class of antibiotics. And we are on the fifth generation of them
as far as, like, changing them up to combat antibiotic resistance. They have altered them, chemists have altered
them, at this alpha-1, alpha-2, A-2, A-1, A-3, different places for different reasons,
okay? And so they’re on, lots of generations have
come, and they keep developing new ones. So let me get back to Penicillin. This beta-lactam ring, and then, of course,
cephalosporin works very similar. What happens is, Penicillin enters a bacteria
cell, and there’s this thing called the Penicillin binding protein, PBP is what we’ll call it
for short. The Penicillin binding protein, and it has
one job. And obviously, they named it because of what
Penicillin does to it. But it has one job, and its job is to make
the cell wall of the bacteria stronger. So what it does is, it actually makes cross-links,
it builds these cross-links in the cell wall, and it makes it stronger. So that’s its one job, all right? So Penicillin enters the cell, and it binds
to this PBP. And then the PBP can’t do its job, okay? So it binds to it, and then after it binds,
this beta-lactam ring opens, and it binds, and then it binds permanently to that PBP,
and then it can’t do its job. And then what happens is, the cell wall doesn’t
have all of those cross-links it needs, it’s weak. It has weaknesses that make it, you know,
break down, and the bacteria cell dies, okay? So, in response to that, bacteria have evolved
to be able to, through mutations of their DNA, they now can make, when they’re resistant
to Penicillin, they make something called beta-lactamase. And beta-lactamase is an enzyme that when
Penicillin enters the cell, then beta-lactamase goes and binds to the Penicillin, opens that
beta-lactam ring, it opens that ring, and then Penicillin can’t do what it was going
to do. It cannot, it doesn’t, it’s not able to then
bind to the PBP, and so then the PBP just, you know, keeps doing its job, and the bacteria
cell is fine. And I might just point out that one of the
reasons that PBP binds Penicillin is because it looks to it like what it’s supposed to
be binding. It looks, the similar, very similar structure
to what it’s supposed to be doing. So it thinks it’s doing its job, and it’s
binding to something else that makes it permanently unable to do its job. Okay, so, the cell then has this beta-lactamase
that it makes. And so then what chemists have done is develop,
they change up like this R group here, or whatever’s over here, and they change that
to make it where that beta-lactamase can’t bind to the Penicillin, and so then the Penicillin
can still do its job. So it’s like we keep coming back with the
bigger gun, you know? It’s like nature makes a way around what we
designed. And then chemists have to design something
else that can overcome that thing that they have, that nature has come up with. So it’s that kind of thing going. All right, so completely synthetic. I did want to put this one on here. I think it’s interesting. The fluoroquinolones, they are, they are useful. Doctors prescribe them, and I know that my
mother-in-law’s had some of these before, but she was pretty ill. They have now, the FDA, this is completely
synthetic, but the FDA issued a strong warning last year and just said, “If you have another
option, don’t prescribe these, because the side effects of them turn out, have turned
out to be pretty severe if you do have side effects from it. And it’s not worth the risk if there’s another
option.” So they, we’re talking nerve damage, muscle
damage, tendons, and it’s sometimes permanent and debilitating. So they have a new warning on this. And, you know, side effects are often a small
population, but if that’s you, they always want to weigh the risks of what could possibly
happen with the benefit. And so now, this particular class, many of
them, they are only prescribing if they don’t have another good alternative. Okay, this slide just shows a few that Heather’s
going to talk about. But these are some of our drugs of last resort. These are kind of big guns that we pull out. And I show you this to show you the complexity
of these molecules, too. I think even if you haven’t had a lot of chemistry,
or seen, been used to looking organic structures, you can appreciate the complexity of these
molecules. And I will say this, it sounds simple to change
up something, like, we’ll just change this little group over here. But it’s incredibly complicated, because they
have to, natural products chemists have to come up with reactions that will change one
part of a molecule, but not mess with the rest of it. And often that includes some elaborate steps
around it, or protecting this stuff over here with a reaction, and then doing this other
reaction, and then coming back and taking these producting groups off. And it’s very, it’s very complicated, and
it takes many years to work out some of these. And sometimes there’s just road blocks to
these syntheses. And I’m going to talk a little bit more about
this in a little bit, but I think it’s your turn now. We’re tag teaming. – Okay, so these are antibiotics of last resort. And so when we look at the statistics in the
United States of all the different kinds of antibiotic resistance, we see all of the different
kinds of strains. The strains that are resistant to these antibiotics
are the ones that we’re most worried about. So what are those bacteria, and what are those
kind of infections? So carbapenem resistant enterobacteriaceae,
CRE, are a growing concern because, again, they’re resistant to one of those antibiotics
of last resort. So if they don’t pull those antibiotics out,
we hope that they have lowered amounts of resistance. But we’re seeing resistance to even those,
those last resort antibiotics. Especially the bacteria that have NDM-1, or
KPC-2, because those are on those mobile elements, those plasmids. So when you see this particular type of strain
in the news, or you read in the journals, I know you all are reading the journals, if
you see these particular types of genes popping up, you’ll know those are more dangerous,
because that gene can be shared with many different kinds of bacteria, and passed through
populations much faster. I’ve mentioned this before, but our two-year-old
from Connecticut had this MCR-1 gene, which is a colistin-resistant gene. Colistin, again, is one of those big, complicated
antibiotics we saw on the previous slide as an antibiotic of last resort. And then, we know that there are certain classes
of bacteria that we’re always a little bit worried about. So mycobacterium tuberculosis causes the disease
TB, or tuberculosis. It infects one-third of the world’s population. Mycobacterium, itself, is an unusual bacteria
in that it has an extra layer, or coating, on its cell wall that makes it incredibly
difficult to treat. Antibiotics don’t penetrate that bacteria
very well, period, and so the drugs that we can use to get into this particular bacteria
have to be taken for six to nine months in some cases. That’s a long time to be on antibiotics. So when we see bacteria like mycobacterium
that is resistant to multiple drugs, there’s an incredibly growing concern. Vancomycin-resistant enterococci, and MRSA,
some of you guys have heard of MRSA, methicillin-resistant Staphylococcus aureus, used to be called methicillin-resistant,
now we tend to call it multi-resistant, because these types of bacteria are often resistant
to more than one class of antibiotic. And then, lastly, the escape group. So this is a group of bacteria, mostly gram-negative,
although we have a staph in here, an enterococcus, that we’re concerned with overall. So these are the ones that are the most concerning
strains of bacteria that we want to develop new antibiotics for. And I’ll show you in a minute my students,
they work on these bacteria, safe relatives of them, we don’t use the dangerous pathogens
in the lab, but we use, we call them escape relatives. And we use this class of, these classes of
bacteria to screen and find those new antibiotics. So, I showed you before, the concern that
we have with agricultural use. So of all the antibiotics that are used, only
30% are used by humans. 70% are consumed by animals in our food chain,
right? In our global food web. Now, you think, well, wow, that’s a lot of
sick animals. Actually, if you look only at the dark blue
parts of the pig here, and the chicken, that is the percentage of the antibiotics that
are used to actually treat a sick animal. Most of the antibiotics are used in agriculture
to increase growth promotion, to make the animals bigger faster. Or, prophylactically, as prevention. So we just heard, in my previous slide, that
humans should not take antibiotics if they are not sick with a bacteria that the antibiotic
treats. Yet we use 70% of our antibiotics in agriculture
improperly, right? So not to treat an active illness in the animal. Now, maybe those are different antibiotics,
right? So it turns out, that’s not true, either. So many of the antibiotics that we use in
agriculture are also used in humans. So a recent study last year from China showed
that over 20% of the chickens produced are resistant to colistin, that antibiotic of
last resort that we were just talking about. So colistin is used in agriculture production,
and yet it’s our secret weapon that we keep locked away in a cabinet. So this is a growing problem that we see. Now, antibiotic resistance isn’t new, it’s
making the news now because it’s getting a little bit scarier, but from the time of discovery
of Penicillin here in blue, in 1928, with Alexander Fleming, we’ve known about resistance. Even Alexander Fleming, in his own notebook,
said, “Watch out, use these drugs carefully, because they will become resistant, bacteria
will become resistant.” And so that was first identified in 1940. And we can see that the different classes
of antibiotics, tetracycline was pretty quickly found to be resistant. And this last group, the fluoroquinolones,
they were actually documented resistant cases before it was really widespread, so the same
year, right? So it’s not a new problem, and it’s not a
problem that we predict is going to go away. The problem here is that in the past 30 years,
there has not been a new class of antibiotics discovered, right? Now what does that mean for us, right? So we know that we came close with our two-year-old
from Connecticut. But this is a report from January of 2017,
so just a few months ago, a Nevada woman, she was 70, had traveled to India to be with
family, and had come back. She had had some hip and leg fractures, and
got an infection that was what we call pan-resistant, resistant to every known antibiotic used in
humans. And she passed away from that super bug resistant
bacteria. Okay. What can be done? – Yeah. – I’m definitely a lot more gloom, and you’re
more- – Yeah. Okay, so the Pew Charitable Trust actually
published an article, it’s pretty interesting, about sort of a scientific road map for antibiotic
discovery, that if you’re interested in reading their report, you should look it up. It’s very easy to find. But, basically, the ways that, the pathways
forward to get new antibiotics, first off, basic research. Understanding what are the bacteria doing
that’s making them resistant? We need more basic research funding, because
it’s that, it’s organic chemists, you know, having better research as far as, like, what
kind of reactions are available to them that they know they can try to make new drugs. So basic research always needs to be funded. And that’s one of the things that people have
a hard time funding because they want it to relate to some, like how am I going to get
my money back out of this. They want it to be some kind of an investment,
and it’s an investment in our future, really. Any time that they invest in basic research,
because we’re going to need it down the road. Building chemical libraries tailored for antibiotic
discovery. One of the big things is sharing information,
sharing options, building some kind of like systematic, you know, storehouse for information
that can be shared is going to be really important. Natural products. Now, we need to get creative, and I’m going
to talk about this in just a second. But we need to start getting creative to find
more new natural products. As nature evolves, as bacteria are evolving,
and they are getting a better arsenal, we should be able to tap into that and find better
antibiotics that they are making. We need to share better, knowledge, materials,
and expertise, as particularly related to antibiotics. And this is much of what they talked about
is what we need to happen. We need more partnerships between public and
private. When I talked about during World War II where
everybody kind of got together and decided to tackle this problem together, right now
pharmaceutical companies are not interested so much in antibiotics because there’s not
a lot of money to be made in it. Unfortunately, if you use an antibiotic very
much, it becomes not effective, right? Because resistance will be built up against
it. So we’re not, we’re talking about needing
to spend time and energy developing something that may not pay off, because to actually
have a great antibiotic, it means that you hold it under lock and key and only use it
when you have to. There’s not money in that. So much of the work on this is being done
by national labs, government funded research, in academia, and those places. And so, but we do need partnerships where
everybody’s working together. Crowdsourcing is a great thing, and we’re
going to talk a little bit more about the Small World Initiative, just briefly. We promise not to keep you here all night. We’re getting close. But crowdsourcing and academia is a really
good way of putting a lot of people on this, on this project, and screening lots of samples. Okay, so how many natural antibiotics do you
think are found in soil? And this is your question, Joe, what do you
think? – That’s a loaded question. – Just give us a guess. – Five. – Five. Okay, well let me tell you that every antibiotic
that we have talked about today, you can find that in soil. All of the bacteria, all of, every fungi that
we have talked about, we can find those in soil. And so, actually, the dirt is a great place
to look for new antibiotics. In fact, all of these drugs of last resort
are found from bacteria, they’re made, initially, by bacteria that you can find in soil in certain
parts of the world. Somewhere in the world you can find it in
the dirt. Okay, so I’m going to tell you about the two,
sort of the cutting edge, like, here’s the game changer kind of research things that
have come out in the last few years. These are very complicated projects to pull
off, but they’re really cool, okay? So this first one is more of a microbiology,
and then the second one will be a chemist approach. This one was published in Nature in 2015. And any time you have a paper in Nature or
Science, those are the two, it’s a game changer. To get published in those, they’re game changers. Well this one was really cool. Okay, my favorite fun fact that I have learned
in this whole thing working with Heather, is that 99% of bacteria found in soil can’t
be grown in the traditional way in the lab. In other words, we’ve been going, and we’ve
been getting soil samples, and we’re looking for bacteria and growing them up in the lab,
and we’re just scratching the surface, because 99% of the bacteria that are in our samples
that we collect in our yard, those of you that are in her class, 99% of those bacteria,
we aren’t even seeing them, okay? So that’s what’s crazy. So we have all of that to tap into, potentially. Well, this group, they found teixobactin,
and it is a new class of bacteria. And it was, basically what they did was, they
took a soil sample, they diluted it down until they got single cells. They put them in a semipermeable membrane,
which for those of you that have had chemistry, you’ll know what that means. But, it’s basically a membrane that allows
stuff to go in and out, but not the cell. That bacteria has to, is stuck in there, almost
like a little jail, a little cage. So it’s like a little cage, and then they
buried them in the ground. So they’re in the dirt, in their little cage. So they’ve got the benefit of, everything
that’s in the soil can go in and out of this cage, but the bacteria is stuck in there. So then they grew them that way. And, in that, they were able to isolate this
new bacteria, and so far, all of the bacteria they’ve tested it against, nothing is resistant. So that is a very encouraging, that’s a very
encouraging finding. And that’s why they’re in nature, because
this is super cool. Okay, so, but this research, I was talking
to Heather about it, and she was like, this is really hard. Like, what they had to do, and the amount
of work they had to do to get single cells, and bury them, and do this work, this is very
hardcore research that who knows how many, and how long, and wow. This is some tough work. But they got, it paid off big. Okay, and then the next one is the chemistry
one. This one was also published in Nature. This was last year. And this is a group from Harvard. These are the macrolides, this is a class
of compounds. And, basically, this is erythromycin, which
is in that class of compounds, they all have this big ring here. And they, usually, using this as a starting
point, this whole class of compounds would be made by taking this as a starting point,
and then changing it to make it a better drug, or make it a different drug, or combat some
kind of resistance that has developed. Okay, but what this group did was, they started
with little building blocks, smaller molecules, and then they could make all kinds of versions
of those, and they figured out a process for putting those pieces together to build these. So instead of making a semi-synthetic one,
they built a completely synthetic one from smaller building blocks. It’s a very complicated process, but the fact
that they were able to build it, instead of relying on nature to make their starting material,
allowed them to make over 300 new candidates. Where normally someone would spend years to
try to make one new candidate, they were able to make, find a process for making 300 new
candidates that now they can screen them, and test them, and see how, you know, see
how they work out. So this is a pretty exciting way that chemists
were able to sort of, this natural product development is, this type of organic chemistry
is, these people are long-suffering. And they’re very hard core, it takes a long
time. But they were able to really come up with
a ton of compounds. So that’s also a very exciting thing. Okay, we’re just going to tell you about our
work real quick, just a brief intro. And most of, we’ll go into detail on Wednesday
next week, if you come to that presentation. But go ahead. – Yeah. So in 2012, Jo Handelsman at Yale, in the
Center for Scientific Teaching, developed a program called the Small World Initiative. And her goal was to bring authentic research
into the classroom, as well as solve a global crisis of antibiotic resistance. So just a small task she was trying to accomplish. She went on to then be President Obama’s advisor
for antimicrobial research, one of his advisors. And what they did was, after they got the
program up and running at Yale, they then expanded and trained faculty all over the
country, and all over the world, to do this program. So you can see here a map showing all the
different faculty groups all over the country. And here is our blue dot right here. This is, I started working on this, and I
did the training, and became a Small World Initiative faculty member in fall of 2014. I was then joined a few semesters later by
Jamie Cunningham, also in the Microbiology Department. And then about the same time, or about thereabouts,
we started our collaboration with Dr. Harvey. So we’ve been doing this for now seven semesters
in the classroom. And let me just give you a really quick overview
of what that looks like. So my students, this should be familiar, right? So students get to pick and decide what soil
sample they want to bring in. We’ve also had environmental samples from
ponds, from sand, from bee pollen, and lots of different kinds of soil samples. And they take that soil sample, and they grow
it on agar plates. So here, each of these little circles is a
pile of bacteria, we call a colony. And you can see, even on this plate, that
these bacteria have made those picket fences, right? They’ve secreted that antibiotic, and created
a little zone around themself. So here is a colony of bacteria, and you see
this little ring around it. Here’s one here, and here, and here, and here. So we call these candidates, right? So the students collect these bacteria onto
a collection plate, or a patch plate. And students typically get between five and
15 different bacteria that they will find in their soil sample, or their environmental
sample. We then match them up with those escape relatives. So we match them up with those bacteria that
we really need to find an antibiotic to. So in this bottom panel here, you can see
a student’s bacteria, and it’s secreting an antibiotic that, in this case, is killing
staph, staphylococcus. So that’s one of those escape pathogens that
we’re all worried about. Now the rest of the semester we do all the
same things that you would typically see in a microbiology lab. We do gram staining, where they characterize
their candidates through staining. Biochemical and metabolic testing. And we send the samples off for DNA sequencing. So they get to identify their bacteria using
a genetic approach. At that point, we have a pretty good collection
of viable candidates that I then hand off to Melanie’s class. – So one thing that makes ours unique here,
is that, as far as we know, we’re the only ones, only partnership between microbiology
and chemistry. And you actually approached me really early
on, and I started working with honor students, but it was hard to accomplish a whole lot. It’s just been much more productive to have
a whole class of students participating. So we’re a little unique in that. And part of that, comes with that, is we’re
making it up as we go, because we did not have a lot of colleagues to ask, “Hey, what
are you doing?” To go, you know, “What’s your next step?” So we’re kind of, we started it off just sort
of making up as we go, and then we did find one group at Yale that had partnered with
a chemist for a while, and what they were doing was pretty much what we had decided
to do, so that was like, “All right!” We felt really good about ourselves, because
we had- – We were in the same field! – Separately come to the same conclusions
that that’s how we should approach this. So right now, my Chem-140 lab, and I have
one student here tonight that’s in that class, what we’re doing is, we basically take plates
of the bacteria that we’re interested in looking at, and we’re extracting. We’re using a certain protocol to extract
from that, and try to isolate whatever it is they’re making that’s killing other bacteria. We want to try to isolate that antibiotic. And so then we try to separate it using a
technique that we would do in this lab anyway, which is TLC. It’s a classic organic chemistry thing, chromatography. It’s where you separate parts of a mixture. And then we put those in plates. We send them back to Heather. She’s not done, she has, I keep her busy. So we send them back to her, and she pours
agar on them with bacteria embedded in it, and, basically, we see, did we isolate something
that’s inhibiting growth of bacteria? And then we’ve gone on to do things like try
separating them more, and isolating those components. This is the part we’re kind of working out
the details of right now. But we have had some interesting results,
some promising ones, as far as, like, we’ll isolate something that does inhibit growth. So we feel like we’re on the right track. And we’re sort of able to do this with a whole
class of students. It’s a good way to sort of screen all the
candidates, and then we can spend more focused time on the ones that look more promising
with the different procedures that we’re using right now. But we’re also always kind of improving our
procedures and approach, and trying something new. We’ve tried a number of things in just the
few semesters that I’ve been doing it with this class. We keep making it better, and it’s going better
every time. The best part is that all of our students
get to participate in authentic research. So we’re really interested in the outcome,
but we’re also interested in the process, and the opportunity that our students have. And it’s a pretty unique one, and a lot of
people don’t get that kind of experience, especially not in your first year of a science
class. So that’s a pretty cool thing. Okay, so we’ve done poster sessions every
semester with our students where they present their research. And, you know, they can put this on their
resume, present it at an actual thing, because it’s totally legit. People go around and grill them and everything. No, not really, just kidding. No, actually, people are very interested in
what you’re doing, so they’ll come around and they’ll ask you what you did. I’m going to-
– Don’t scare them. – Scare them, okay, okay, sorry. Anyways. – It’s like in two weeks. – It’s very exciting, it’s very fun to show
off what you’ve done, okay? And so, so everyone, it’s a very, science
is always a community thing. And so it’s a very cool thing to be a part
of something like this. So we’ve done poster sessions every time,
and we have had, so far, over 400 student researchers that have participated here at
Johnson County Community College. We have sequenced 189 different bacteria. We have presented 191 posters and done chemical
analysis on 46 different samples so far. So it’s been a really cool thing, and it’s
something where we’ve been able to incorporate, you know, include a lot of people, and they
get to be a part of it. So it’s been a great opportunity. Okay, and I think we’re done, so if you have
questions for us. I know we kept you a long time, but there’s
two of us, so we talk a lot. But if you have questions, we’d love to hear
them right now. So. Yes, Joe. – The proliferation of the antibiotics (inaudible)
what effect does that have? It’s pretty balanced. Is there any research going here in the food
corridor on that? – There’s not. There’s a lot of work way higher than my pay
grade in the government trying to understand the impact of that and how do you control
that. So, again, it’s a bottom dollar issue, right? So they want to make the biggest chicken the
fastest, and the cheapest, because we all want our chicken nuggets to be $1.00, right? And so it becomes a problem with trying to
impose regulation, or impose sanctions, or even taxes on those antibiotics, and it’s
not just the United States, it’s a global problem. So 20% of chicken in China is resistant to
colistin. Has bacteria that are resistant to colistin. – Yeah, and, you know, we don’t have a culture
that likes regulation on things, especially if it’s going to cost. And so that is the problem. It’s like, who’s going to tell me I can’t
do this? And like you said, you know, when it’s an
international issue, those are even harder to get everybody on board. We’re so global that we are, and we’re so
interconnected, that what other countries do, and the things that they cause to happen,
we’re all affected by it, everyone’s affected, including, we affect other people, they affect
us. Matthew? – Getting back to what (inaudible) was saying
and what Joe brought up as well. Are there any international organizations
working to remediate livestock antibiotic usage or the over-usage on the chicken farms
especially? – There is a number of non-profit groups that
are trying to impact change and bring awareness. And the World Health Organization has it on
their radar. But, unfortunately, it’s very difficult to
get many countries to sign on to regulations like that. – Yeah? – With the bodies fighting off any kind of
infection, it creates antibodies, do those antibodies help at all to combat the infection? And like what happens (inaudible) cells in
antibiotics used in, like, the infection? – Absolutely, yeah. So the time before antibiotics, right, we
had to rely on our natural defenses. And so antibodies are proteins that our body
makes as a natural defense to the pathogens that we’re infected with. So they certainly do work in any infection
process, hopefully, if you’re healthy. But antibiotics are just a way to avoid that
infection. Antibodies take about two weeks to develop
fully, the highest number we get, and so we don’t want to be sick that long. So we use these drugs to help reduce the length
of the infection, and get healthier faster. – It seems a lot of the research is done in
wet labs. Is there any computer simulation that can
be done that could possibly go a lot faster? – Yeah, so this, was it this fall? – Yeah. – Oh, it seems so long ago. – No, wait, what semester is this? This is spring. It was in service this semester. – It was in service. – It was January. – So in January, I brought in-
– Sorry. – A lot has happened this semester. In January, I brought in some training from
a group called Genome Solver, and one of the things that they do is trying to bring authentic
research into dry labs, or lecture settings. And they use a bioinformatics approach. So they taught us some tools to search databases
of peptides, and to look at modeling, and trying to predict genetic elements that might
be important. And doing that dry lab part of it. Doing a computer bioinformatics approach. But so far, we just had the training in January,
apparently, and we haven’t had a full implementation of that yet. Barry. – 30 years ago, what was the trigger to stop
the development, historically. What factors were causing it? – Yeah, the pharmaceutical companies, they,
there’s a great documentary called “Hunting the Nightmare Bacteria.” And it’s on PBS. And they interviewed the different pharmaceutical
companies to find out exactly why did they drop out of that market. And they’ll tell you it’s a portfolio decision,
right? So there are drugs like cholesterol lowering
medications, and ADHD medications, and anti-depressants that people take every day for the rest of
their life. Those are way more valuable to that for-profit
pharmaceutical company than these antibiotics. And even vaccines, which is another way that
we can combat infectious disease, everybody, hopefully, right, gets vaccinated. And so that’s a lot more profit for that pharmaceutical
company then a drug that, again, you don’t really want to use for a long period of time. – It’s almost like a cultural shift in our
culture towards money driving everything instead of, you know, I mean… Science has always been, you know, sometimes
you’re just curious, and you just want to make things better, and you’re not thinking
about, you know, making a buck. So… Other questions? Well thank you guys so much. – So much. – You’ve been a wonderful audience, we appreciate
it. (applause)

One Reply to “Challenges of Antibiotic Resistance”

  1. Its was really productive ….great work… I am an under graduate medical microbiology student , working on some plant extract against MRSA (MDR)..

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