Ending the arms race with infectious diseases | Janelle Ayres | TEDxSanDiego

Ending the arms race with infectious diseases | Janelle Ayres | TEDxSanDiego


Translator: Ilya Bychkov
Reviewer: Denise RQ “It is now time to close the book
on infectious diseases and declare the war
against pestilence won.” It is something we all want. We all want to live in a world
free of infectious diseases. Think about when you watch movies
like, “Contagion” or “Outbreak.” or when you watch the news coverage on the Ebola virus
or more recently, the Zika virus. How did seeing those things make you feel? They freaked you out, right? Infectious diseases
evoke legitimate feelings of fear in every single one of us, because none of us is free from the threat
of contracting an infection. The quote that I began with is from
the US Surgeon General from the 1960s. He made this statement in response
to the success of the early antibiotics. It is a statement that accurately reflects
the overall sentiment of the time: which is that because we had such great success
with the early generation of antibiotics, infectious diseases were soon
going to become a worry of the past. I want to tell you about one
person’s war against an infection that took place just last year. That is my dad’s. In January of 2015,
my dad became very sick. It took the doctors
a few weeks to figure it out, but they realized that he had gallstones, and he would have to have
his gallbladder removed. That diagnosis was actually
a relief to all of us, because gallstones are very common
in the United States, and gallbladder removal surgery is one of the most commonly performed
surgeries in the country. So this is basically standard
operating procedure for his doctors. We couldn’t imagine that anything
serious could possibly go wrong. Actually, nothing serious did go
wrong with his surgery. It went quite well.
He was discharged from the hospital, but 12 hours after his discharge,
my mum sent me a text. It said, “He can’t walk.
I have to call an ambulance. I don’t know what’s wrong.” My family is up in the Bay Area; I was down here in San Diego
when this happened. So my sister was communicating to me
from the ICU my dad’s symptoms. I’m the only biologist in my family, so you can imagine how confused they were. How could 12 hours ago
my dad be perfectly healthy, and discharged from the hospital, and now he is laying paralyzed
in a bed in the intensive care unit? But after I heard his symptoms,
I knew exactly what had happened. My dad had sepsis. If you don’t know what sepsis is this is a life-threatening condition that occurs when your body’s response
to an infection is so powerful that it begins damaging
its own tissues and organs. It’s pretty much a death sentence because it has mortality rates
greater than 80%. I dropped everything. I had to rush home. I had to get to the hospital
to be with him and to talk with his doctors. It felt like I couldn’t get there
fast enough. First, my flight was delayed. Then I had to battle Bay Area traffic
for over two hours. I was certain that he was going to be gone
by the time I got to the hospital. But he wasn’t. When I walked into his room in the ICU, my dad waived to me and gave me
one of his classic thumbs up that I had seen 1,000 times growing up. The doctors confirmed
that he did have sepsis. What happened is that his gallstones
went undetected for so long, that his gallbladder became infected. From there, the bacteria
spread into his bloodstream, and then infected his vertebrae,
and that caused his paralysis. It was his body’s response
to the bacteria being in the blood that caused him to have sepsis. The treatment strategy
proposed by his doctors was really the only option
they had available for them: to administer broad spectrum antibiotics and to hope for the best. I sat there for a week with my dad, and I can remember obsessively
watching his vitals monitors, hoping the next blood pressure read
was going to be higher, or the next ventilator read
was going to be lower. I was looking for any indication that the infection was actually
responding to the antibiotics. But the numbers never got better, because he had
an antibiotic-resistant infection, making the only strategy that was
available to him completely useless. After nine days, my dad lost
his war against an infection and he passed away. It is because of the global spread
of the antibiotic resistance, and our current strategies
for treating infectious diseases that my dad died. We are further away than ever from closing
the book on infectious diseases. But why? If we really had such great success
with the early generation antibiotics, how is it possible
that we screw things up so badly that we now are in far worse condition
than we were 50 years ago? And the main issue is our perspective on
how we should be dealing with problems. When we are faced with the challenge, we think that in order to solve
that challenge, we have to annihilate
the source of the problem. If you have a mouse in your house,
you set traps to try to kill that mouse. If you have a weed in your yard, you spray toxic chemicals
all over your yard to try to kill that weed and prevent
new ones from coming in. Infectious diseases are
no exception to this mentality. All of our current strategies
to fight infectious diseases are based on the question: how do we fight infections? As a result, we declared a war
against infectious diseases. We put all our efforts
into developing weapons in the form of antibiotics and antivirals
in order to win this war. But bacteria and viruses
are incredibly slippery targets. They can evolve so quickly resistance
to our weapons, making them obsolete. So what do we do? Our solution has been
to just make more new weapons, make more antibiotics,
make more antivirals. It’s not surprising that the microbes have
evolved resistance to our new weapons. So our perspective is fueling
an ever escalating arms race between us and the infectious diseases. The scary fact is it’s
an arms race we can never win. The second issue, in addition
to driving drug resistance, is that there is a fundamental issue
with this perspective, if we actually want to develop therapies that will enable a patient
to survive an infectious disease. To help you understand
what I mean by this, I want to continue with the war analogy. In an actual war, there is
combat between soldiers. But that combat
does not occur in isolation. Something that can happen is what’s called
“the collateral damage of war,” which is the unintentional
or incidental damage that can occur to civilians,
property, economy, and the society. The same principle
can be applied to an infection that’s occurring in a patient’s body. So if we have a septic patient, there is going to be bacteria,
virus, or even fungus that has entered their bloodstream. Their immune system
is going to recognize that foreign invader and it’s going to mount a killing response
to try to fight that infection. But that fight
is not occurring in isolation. What happens is, basically, every other physiological system
in the patient’s body becomes damaged: the liver, the kidneys,
the intestine, lungs, the cardiovascular system,
all get damaged. You can give
a septic patient antimicrobials, and they might be effective
at killing the infection, but you are left with a patient that has suffered extreme
collateral damage to his body. For my dad, even if his infection
was sensitive to the antibiotics, the likelihood of him
to surviving was very low because he suffered so much physiological
damage from the infection. What he needed were therapies
that would fix that physiological damage. He wasn’t given any drugs that do that
because those drugs don’t exist; because we haven’t been approaching
infectious diseases from the right perspective. So if we’ve been asking
the wrong question, what is the question
that we should be asking? Instead of asking,
“How do we fight infections?”, we should be asking
“How do we survive infections?” I know that a single word change
from “fight” to “survive” seems simple, but by making the single change, we’ve completely changed
the meaning of the question. If we can understand
the answer to this question, we will completely change the way
we treat infectious diseases. We will be able to develop
drugs, therapies, strategies that will enable the patient
to survive an infection without driving drug resistance
in the microbial populations. Because these drugs will be
fixing the collateral damage that’s happened in the patient’s body rather than targeting the microbe
that’s causing the infection. I became very interested in this question,
“How do we survive infections?” when I was getting my PhD
at Stanford about ten years ago. We all know that our bodies
have an immune system, and this immune system is important for recognizing microbes
that are invading our body, and it is important for mounting
a killing response against these microbes to fight the infection. We found in addition to our immune system, our bodies encode
a distinct defense system that we call the tolerance defense system. This tolerance defense system
is absolutely necessary for our ability to survive infections. It protects us from mortality by preventing and fixing
the collateral damage that happens to our bodies
during infectious diseases. This is really exciting
because it means that if we can find out how this tolerance defense system
is working in our bodies, we can change the way
we treat infectious diseases, we will be able to develop therapies that overcome the limitations
of current strategies that are available, we can develop strategies
that promote survival without driving drug resistance. So then how do we go about doing this? This is actually a main goal
of my team at the Salk Institute. We’re committing to understanding
this tolerance defense system so that we can make this a reality. We take a variety of approaches
to address this goal, but one of our main approaches
that we’re really excited about, and that we have already
been successful with is we’re leveraging our interactions
with beneficial microbes. Right now all of you have
about three pounds of bacteria that are living on you body surfaces
exposed to the environment. If we sprinkle in some viruses
and some fungus, now you have your microbiome. Your microbiome is
absolutely essential for your health. We have an evolutionary theory,
that has lead us to predict that the microbiome has evolved mechanisms
to turn on our tolerance defense system. It can effectively manipulate
this defense system to promote our health. We are using the microbiome to teach us
how to turn tolerance defenses on, to teach us what they are,
how to manipulate them to promote health. We are using these microbes
as platforms for drug design so that we can move this into the clinic. For example,
we’ve recently identified an E. coli that lives in the intestines
of healthy individuals. This E. coli has taught us
that we can cure infectious diseases by mediating communication between the immune system,
our fat tissue, and our skeletal muscle, by preventing collateral damage
in the form of skeletal muscle wasting. In pre-clinical trials, just by orally administering
this E. coli to the model patients, we can cure sepsis, bacterial pneumonia,
typhoid fever, and infectious diarrhea without the need for a single antibiotic. I think that’s amazing. I think it’s exciting (Applause) I think it opens up a promising future for our ability to treat
and cure infectious diseases. My lab will continue to do this. We are committed to it,
but we can’t do it alone. We are all vulnerable to the threat
of contracting an infectious disease. We are all terrified of that threat. But if you leave here
with one thing today, I want you to leave here
believing that there is hope to get us out of the mess
that we got ourselves into. The first step to this
is really changing our perspective going from “How do we fight infections?”
to “How do we survive infections?” All of you: doctors, scientists,
health care officials, drug companies need to make
that perspective shift. We have the technology
and knowledge to do it. We have to make that shift,
because it’s only then when we’ll truly be able to close
the door on infectious diseases and end the war against pestilence. Thank you. (Applause)

Holy Hallucinations 22: Termites and Tosspots

Holy Hallucinations 22: Termites and Tosspots


This is a response to BereanBeacon’s video,
“Termites Place Hex on Evolution.” But before I begin, I’d like to correct
a couple of gross oversights from Holy Hallucinations 21 where I neglected to mention a pair of
great Youtubers who produce material in the areas of philosophy and theology. So if you
haven’t yet been exposed to the fascinating and educational videos of philosophy professor
SisyphusRedeemed, or the eloquent and beautiful deconversion and theological productions of
Evid3nc3, then you really should head over to their channels and click the yellow button.
So now, back to the subject of this episode and that’s the user BereanBeacon and one
particular example of the seemingly endless feast televisual craptitude that you can find
on his channel. I’ll be referring to you as BB for the purposes
of this response, so I hope you don’t take offense, but if you do feel so inclined then
I’d hold off until you see the rest of the video because I can assure that my little
nickname for you is going to be the least of your worries.
Like many of your videos, this one features an episode of the anti-science radio show
“Creation Moments” featuring a feeble-minded, geriatric creationist named Ian Taylor. It
seems Mister Taylor’s sole qualifications for disparaging evolutionary biology are an
undergraduate degree in metallurgy and the willingness and ability to lie like the pope
at an HIV prevention workshop. But lest I be accused of indulging in baseless
ad hominem attacks, let’s take a look at what the old fossil had to say about the evolution
of termites, and then ‘ll explain exactly why he’s either talking straight out of
his arse or has his head stuck up it. “The nest was discovered in in fossilized
wood from Big Bend National Park in Texas. Other scientists examined the grains under
a microscope and found that they were hexagonal in shape. That distictive shape told them
that the grains were termite droppings, and these droppings were identical to those made
by modern termites. With this discovery, they holes in the fossilized wood suddenly made
sense.” It’s hardly surprising of course to hear
a creationist talking crap, because it sometimes seems that that’s all they’re capable
of doing when placed in front of a microphone. The discovery that your rationally challenged
colleague’s referring to was published by David Rohr and colleagues in the peer-reviewed
journal Geology in January, 1987. The fact that this particular episode of “Creation
Moments” was broadcast in March of 2011 is a testament to the breathtakingly fast
pace at the cutting edge of modern Creation Research.
Now on the whole, Taylor makes a reasonable summary of this part of the paper apart from
his description of the fossilized frass as being “identical” to that of modern termites.
The authors of the actual paper do make an argument that the droppings are termitic in
origin because among extant insects only termites and roaches produce hexagonal droppings. They
argue against the possibility that the frass was produced by roaches, firstly because the
pellets were too small; secondly, because modern wood boring roaches prefer to live
in rotting wood and the petrified specimen in question appeared to be sound; and finally
because of the similarity of the distribution of the fossilized frass within the wood and
that of modern origin. At no point, however, do the authors state
that the frass is identical to extant termite fecal pellets, which begs the question as
to why this shriveled old fart said they did. I suspect that what he was doing was opening
the gate to prepare the way for him to drive through his muck-spreader and really start
spraying his shite. But before we see him completely lying his
nuts of for Jesus, let’s watch him as he starts up his tractor.
“The wood had been tunneled out in the same way that modern termites tunnel wood. the
nest was in the centre of the wood, just like modern termite build their nests. These ancient
termites had placed their droppings around the edge of the nest. Modern termites do the
same thing to plug any air leaks and to prevent draughts. In short, every evidence says that
termites from the time of the dinosaurs were built just like modern termites and that they
behaved in the same was as modern termites.” Once again, our budding manure magnate deliberately
overstates the case. Nothing in the paper in any way says, implicitly or explicitly,
that the insects in questions were, ”built just like modern termites.” In fact in their
conclusions the authors clearly state, and I quote, “Because the material reported
here is in the form of trace fossils, and no termites were preserved with the frass,
it is impossible to definitely prove that termites were responsible.
Now, the authors do indeed argue that termites were responsible for both the nest and frass,
and that this fossil is the oldest known example of both. And they also contend that this specimen
represents one of the earliest pieces of evidence of social behavior in insects. However arguing
and contending are very much different to stating as fact, and while these authors do
point to similarities between various aspects of these remains and their extant counterparts,
they never claim that they’re identical because they don’t have the evidence to
justify doing so. In fact, it’s very interesting to just compare
the language used by this creationist cretin and the scientists whose words he’s mining
like a dung beetle that’s just discovered an elephant’s outhouse. While Rohr and colleagues,
like all good scientists, use more circumspect and intellectually honest language when putting
forward their interpretations of the evidence, Taylor resorts to the dogmatic absolutism
of the religious zealot who, certain of the infallible truth of his scripture, can’t
even conceive of the possibility of being wrong.
So at no stage did the paper say anything about the morphology of these animals themselves,
but it appears that this wrinkled old prune doesn’t feel in any way restrained by such
trivialities as common decency or the facts. It seems that Mister Taylor is either demonstrating
the true value of his metallurgy degree in the area of evolutionary paleobiology, or
merely being a compulsive liar. Of course he is a creationist apologist, so perhaps
I shouldn’t be surprised. So with all that said. I’d love to ask this
stupid old bastard exactly which of the more than 2000 species of extant termites he thinks
these invisible fossils are “just like?” That comment alone speaks volumes about the
childish and simplistic mind that we’re dealing with here.
And now we get back to the question of why Farmer Taylor is so insistent on misrepresenting
this physical evidence. So now that he’s fired up his John Deere, let’s take at look
at what he’s been planning to do with it. “That there is no evidence of termite evolution
in this nest agrees perfectly with the Bible’s claim that all things reproduce after their
kind.” And there we have it. With this devious sleight
of hand the creatard claims that these ancient termites that weren’t actually in the fossil,
that produced similar fecal pellets and that behaved in a similar manner, are in fact the
same as the termites that are alive today, and so evolution must not occur. One can only
wonder whether he read the same paper I did. Or whether he read it at all.
And so a 65-million year-old fossil that was found in a late Cretaceous formation and in
itself conclusively negates biblical creation and a young earth is, with a generous dollop
of dishonestly, a liberal sprinkling of sophistry and a side dish of reprehensible lies is served
up as proof positive for the Abrahamic creation myth. And here I’ve been for the past year
arguing that there’s no such thing as magic. Of course, there’s nothing new here, just
a rehashing the same dismal failed arguments we’ve heard time and time again with organisms
such as crinoids, various mollusks, shrimp and plants and, of course, coelacanths, otherwise
colloquially known as living fossils. All your deceptive little muck-raker’s done
is substitute the word “termite” as an excuse to spew out the same old pathetically
unconvincing bullshit. This argument of course completely ignores
the well-documented concept of evolutionary stasis. It’s been clearly understood for
decades that evolutionary lineages can and do remain relatively stable morphologically
over periods of millions of years in the absence of dramatic changes in selective pressures.
This stasis is maintained, at least in part, by the statistical stabilization of gene pools
in large populations by allele dilution and gene flow, although the exact contributions
of these and other factors are the subject of active debate and research by today’s
evolutionary biologists. Thus, given a sufficiently large breeding population and a sufficiently
stable environment evolutionary theory easily accounts for phenotypic persistence, be it
in snails, or shrimp or fish or termites. However, over longer periods of time even
this persistence of phenotypes begins to apply only to gross morphology. Zoologists and paleontologists
with the appropriate training and experience are able to easily distinguish similar species
within the fossil record and to differentiate extant species from their extinct relatives,
even creating mathematical algorithms to quantify these differences.
Of course none of this matters to the fatuous creatards who try to propound this stunted
and sickly runt of an argument in its many forms. The fact that this concept has been
explained countless times does nothing to prevent them from gleefully interpreting stasis
as an absence of any evolutionary process at all, presumably by conceitedly using a
maxim along the lines of “it looks the same to my ignorant and untrained eye, so it is
the same.” By way of an example, let me quote from a
random paper I selected on trilobite morphology that demonstrates the detail and precision
used by a trained professional: “Granulation is coarsest on the posterior half of the axial
rings, on the glabella and cheeks, and on the pleural ribs of thorax and pygidium (pahy-jid-ee-uhm);
furrows are finely granulated to smooth.” In contrast the creationists who make these
arguments about living fossils essentially simply assert the lack of any evolutionary
change with no evidence or argument and no reference to any specific specimens or morphological
features. Essentially they best they can do is: “sure looks the same, don’t it? Hyuk,
hyuk.” That might impress you, BB, but it elicits an entirely different response from
anyone who can tell the difference between a laboratory and a lobotomy.
Now, before I wrap up this section, let’s get back to the subject of termites so I can
show you what a little real research can do. Based on morphological analyses of extant
species and on the fossil record it’s been long accepted that termites and cockroaches
are descended from a common roach-like ancestor. Unsurprisingly more recent DNA analysis has
confirmed this to be the case, providing three independent verifications of the evolutionary
relationships of these insects. Additionally, Mastotermes darwiniensis, the
most roach-like of the termites is the only one that carries an endosymbiotic bacterium
that’s common to all cockroaches. Researchers predicted that these Blattabacteria should
have co-evolved their hosts and recently conducted a molecular analysis of a number of roaches
and termite and their respective microbial symbionts. The resulting phylogenies of both
insects and bacteria were almost identical, and provided a breathtaking validation of
evolutionary theory, for only evolution both predicted and provides an explanation for
the convergence of these cladograms. This is just one example of the countless
equally impressive pieces of evidence that all converge inexorably to the same conclusion:
that evolution is a fact that is beautifully explained by the theory of the same name regardless
of what cretins like Ian Taylor have to say about it. And if he doesn’t like it – then
he can stick it up his compost heap. So now that I’ve dealt with that, it’s
time to turn my attention back to you BB. I have to say that I initially found the second
half of your video a little surreal as it was, to put it mildly, a bit of a non-sequitur.
I’m not sure whether this was an editing error on your part or merely a sign of a short
attention span, but you changed the subject faster than William Lane Craig after an honest
question. So, let’s do the same and take a look at
what you had to say about that stale and rancid puddle of Creationist vomit known as the Life
Science Prize. “They could easily shut down us creationists
by simply taking doctor Mastropaulo’s challenge and defeat him. If they have any evidence
they could bring us to an embarrassing halt as creationists. They could silence out voice.
They could make us look like morons.” Of course it wouldn’t take a scientist accepting
this challenge to make creationists look like morons because they’ve been doing a bang-up
job of that themselves for over a century. And if you don’t believe me then just take
a look at some of the many fine examples of stupendous fuckwittery from your fellow mentally
castrated intellectual eunuchs right here on Youtube.
So now let’s get back to the challenge. Firstly, let me point out that your faith
in your apparent hero, Joseph Mastropaolo, is as misplaced as your faith in your pitifully
childish and patently fallacious fairy tales. You see, it seems that the good doctor is
a kinesiologist with a PhD in the field, although, according to his entry in creationwiki, not
a particularly good one since his record of 6 peer-reviewed publications in an academic
career of over 26 years is about as impressive as a pair of hamster testicles dangling off
of a bull elephant. So while this may qualify him to comment on
the correct posture for a creationist to adopt while talking endless wank to avoid a case
of terminal brain-strain, it hardly fosters confidence in his ability to debate the veracity
of evolutionary theory with even a moderately qualified biologist. I strongly suspect that
if such a debate ever took place he’d be picking the shrapnel out of his arse for a
year afterwards. Secondly, it took just five minutes for me
to find two published accounts of exactly how Mastropaulo and his slimy henchmen reacted
when Biology Professors Michael Zimmerman and non-other than Richard Dawkins probed
them by pretending to be interested in a debate. It was more than amusing to read how their
enthusiasm dried up faster than a suspicious stain on a priest’s trousers after choir
practice when anyone even vaguely resembling an unbiased and/or qualified adjudicator was
suggested. The desperation in their frenzied attempts to extricate themselves from the
possibility of being called on their bullshit was nothing short of palpable despite the
liberal seasoning of false bravado. From just these two accounts it should, be
more than blindingly obvious to anyone whose brain isn’t seeping out of their anal sphincter
that Mastropaulo has no intention in participating in a debate. This particularly odious and
dishonest little reptile uses the façade of a genuine challenge to publicize his intellectually
indefensible position, and this is no more evident than the fact that anyone who declines
to participate in his charade is automatically adjudged to have lost the debate by default.
As a result he’s collected more so-called victories than an evangelical preacher has
venereal diseases and proudly displays his dishonesty on his web page, presumably either
because he’s too stupid to realize exactly how big a douchebag this makes look like or
because he thinks it’s OK to be a lying tosspot as long as you’re doing it for Jesus.
So, aside from this being a tactic that I might expect from a fifth grader that takes
the “short bus” to school, it’s one of the most underhanded and reprehensible
kinds of behavior imaginable. If this is the kind of lying pustule you need to fall back
on to cling to your primitive superstitions, BB, then perhaps you need to ask yourself
whether they’re really worth clinging to. Because from where I’m standing it appears
that you’re tossing very things your religion is supposed to stand for into the same cesspit
that Joseph Mastropaulo’s wallowing in. “They don’t do it because the rules for
Life Science Prize restrict them to real science. Not propaganda. Not the power of the pulpit.
They also have many pulpits in their favor. Not the power of that headlines. They’re restricted
to science and that’s why they won’t contend for the Life Science Prize.”
So presumably it was this fear of debating “real” science that compelled Michael
Zimmerman to suggest that the judge be at least a member of the National Academy of
Science? Presumably this is also why he suggested a definition of evolution (that is, “change
in allele frequency over time”) that has been in virtually, and I quote, “every biology
textbook for the past half century.” Scared of science, BB? Really?
If your Doctor Douchbag was so keen to debate science, then can you explain why he wouldn’t
accept these quite reasonable terms? Why he insisted that this scientific debate could
only be adjudicated by a superior court judge? Better still, can you explain why he wouldn’t
even accept Zimmerman’s suggestion of using an ordained priest, Dr Francisco Ayala as
a judge? Could it be that it was because Ayala is a past president of the American Association
for the Advancement of Science and a member of the National Academy of Science? Could
it be that Mastropaulo didn’t explain why Ayala was unacceptable because he was too
busy browning his kecks at the prospect of being shown up for what he really is?
So you see, BB, if by “science” you mean what every sane and rational human being on
the planet understands by that word, then it’s pretty clear that the only one avoiding
a debate on it is your Doctor Dickhead. If, on the other hand, by “science” you mean
that hazy, ill-defined concept that seems to roughly approximate to “anything that
conflicts with my delusional belief system”, (you know,the same usage that I’ve heard
coming from such monumental Youtube fucktards such as Nephilimfree and Eye2EyeIIIV?), then
you might have a point. Because at the end of the day, working scientists
have much better and much more productive things to be doing with their time than pandering
to the hallucinations of a bunch of feeble-minded, deceitful simpletons.
So quite frankly, BB, you and Joseph Mastropaulo can take your pathetic and transparently dishonest
little challenge and stick it back up where it belongs to keep it safe and warm. Because
all you’re doing by parading it around so proudly in public is demonstrating quite clearly
how your Beacon is running on only a 5-watt bulb.

Insect anesthesia helps to expose bug guts while still alive

Insect anesthesia helps to expose bug guts while still alive


In the past, getting an inside look at living
bugs was difficult. during CT scans, the critters would crawl
and squirm — causing image smearing and artifacts. Like many animals, insects become sedentary
when exposed to high CO2 environments, so researchers at the University of Western Ontario
had an idea. Scientists subjected Colorado Potato Beetles
to a constant flow of CO2. Within seconds, the insects were not moving,
but still alive. With the beetles immobilized, researchers
were able to get some of the clearest images of bug guts to date. With the exception of a few older males, the
subjects were easily woken up, and the exposure to radiation and CO2 didn’t seem to harm the insects. The researchers say that with this quick and
safe method of knocking out bugs, clearer looks at insect insides are in the near future, while still on the inside of the bug

The End of Antibiotics and the Future of Fighting Infections

The End of Antibiotics and the Future of Fighting Infections


Thank you all for coming. Tonight we’re going to talk about a very serious
subject. Um, the situation that we face with antibiotic
resistant bacteria. Antibiotics were once the silver bullet that
seemed to be able to cure just about everything. Now we look at 23,000 antibiotic resistant
bacterial infections every year. So let me introduce you to our panelists. Our first participant is the Director of the
Wisconsin Institute for Discovery at the University of Wisconsin-Madison. She was a science advisor to President Barack
Obama. Please welcome Jo Handelsman. Our next participant is a professor at Rockefeller
University where he is head of the Laboratory of Bacterial Pathogenesis and Immunology. Please welcome Vincent Fischetti. Our next participant is an associate professor
of Immunobiology and Microbial Pathogenesis at The Salk Institute. Please welcome Janelle Ayres. Our next participant is the Evnin Associate
Professor at Rockefeller University. Please welcome Sean Brady. and finally the Singer Professor of Medicine
in Microbiology, and the Director of the Human Microbiome Program at NYU School of Medicine. Please welcome Martin Blaser. Uh so, I thought that maybe a way to start
would be to show a video. This was an experiment that was done at Harvard
where basically scientists created at sort of gigantic petri dish, sort of kind of the
size of an air hockey table basically, and they seeded it with bacteria on either side
and then basically laced it with antibiotics. Starting at the edge with pretty mild levels
and then as you go further in, it gets more and more deadly until the central band has
a thousand times the lethal dose for Ecoli. It’s really kind of mind blowing. We’re going to see the bacteria, so just sort
of hanging out there and now they’re multiplying. This is sort of time lapse, so when they hit
that point, what they’re encountering that as antibiotics and then how are they getting
past it? I mean you can see them. It takes a little bit of time and what they’re
waiting for is growth of one or a very small number of cells in the population that are
already resistant. And so although there were many, many billions
of cells crossing the plate, probably one in a million would have resistance to the
antibiotic, so once those started dividing and- So they’re dividing and one in a million just
happens to gain this power to get past it? Well, they always had the power. It was preexisting in the population, but
then when the whole population is, the rest of the population is stopped by the antibiotic
because they’re inhibited by it. Then those few that are resistant start proliferating
and then they take over and that’s exactly what it looks like in similar terms when it’s
in the body, you know, you take an antibiotic and most of the bacteria will die, but there
will be preexisting mutants in the population that are resistant. That’s great. Well not great, but it’s amazing. It is definitely not great. Yeah, no it didn’t. I know, I know. Don’t get me wrong. We think of antibiotics as, as the sort of
heroic triumph of science. I mean, how did, how did we get to enjoy the
benefits of antibiotics? I mean, how did that begin? Well, it started with a chance discovery from
a by Sir Alexander Fleming. In the UK, who found a fungus on his plate
that was clearly inhibiting growth of staphylococcus on, on the Petri dish, and he recognized what
it was that this was a compound that was diffusing into the Auger and determined that it was
what we now know of as penicillin, but it was many years before it can be used in any
kind of broad scale way because he discovered that in 1929 and by the start of World War
II, we still, we’re not using antibiotics and they weren’t in general use. Why not? I mean you, you discover a drug, you know,
put it into practice. I mean, what was the holdup? They couldn’t make enough of it. That fungus produced some but not enough to
go into large scale production. And so during the war a scientist named Ken
Raper was worked for the USDA in Peoria and he decided as a war effort to put out the
call for penicillin producing strains of penicillium mold. So he told everybody in Peoria to collect
as many fruits and vegetables with that green blue fuzzy thing that you see on your bread
and fruit to bring those to his lab. And people did and he had this large collection
and it turned out it was his own technician who has gone down in history, as Moldy Mary
now. Her name was actually Mary Hunt and she brought
in the winning cantaloupe and it had a strain of penicillium mold that produces more penicillin
than any other natural strain to this day. And so they started, they moved it right into
commercial production and started pumping out large amounts of penicillin and they have
enough to be able to ship it the penicillin to the troops in Europe. And so World War Two was the first war in
which more people died directly of bullets and bombs than the infections that accompanied
them. Wow. So, and then once, once the war is over, then
antibiotic start to become more of just a general medicine for the public in general,
right? Yeah. And at the same time there was interest in
soil bacteria that produced antibiotics. And, and then after the war there was just
this explosion of knowledge of people, culturing organisms from the soil, screening them for
antibiotics and then moving into production. And so we had dozens of antibiotics coming
onto the market in the next decades. Sean, I mean, how would you sort of describe
like the sort of, the overall benefit of these discoveries of penicillin and some of these
other early antibiotics? I mean, what I mean overall, like in terms
of lives saved or someone, what are we looking at in terms of the scale of this? I think one of the figures that penicillin
alone has saved 100 million lives. And that’s penicillin alone. Yeah. So if you think about that single picture
that Joe talked to you, you see it in almost any microbiology textbook. That image has probably saved more lives than
anything in the history of science. So you want one kind of thing in your office,
you should hang that picture as a scientist because it’s made a larger impact on human
health than anything but, but that, that whole discovery, even today we’re still using those
antibiotics. So. So that’s the initial discovery, then you
think about almost everything that came out of what we call the golden age of antibiotics,
the forties, fifties, and sixties. So people were finding things not just on
cantaloupe but in other- They are culturing soil bacteria largely and
finding antibiotics. Almost every class of antibiotics that we
use today was discovered in that that time period. We have relied on antibiotic defense really
of those molecules and continually using versions of those molecules up until today. And that’s why we’re in the position we are
today. We, we’ve largely ceased discovering antibiotics
after the golden age, the late sixties, early seventies. Because we thought we were done. We thought we had solutions to these problems. That’s how good those initial discoveries
were. How, how much of an impact they made on human
health. What’s your sense of like when it started
to become clear that things weren’t going so well? Like when? When do you think that the sort of scientific
medical community said, I think we have a problem? Well that happened pretty quickly. I mean we were seeing resistant organisms
to penicillin early on. It was, it started Like a matter of a few years after? Probably a year or two After the introduction of penicillin. Exactly we already started to see early stages
of resistance, but you know, was it an organism here, an organism there, but, but it was occurring
at that time and it’s been occurring at an accelerated rate since then. Right. So Marty, what do you think is, what would
you say would be like one of the main factors that explain sort of how we got to this point
in terms of resistance? Like what are we doing that is causing all
of these bacteria now to be just so dangerous? So, uh, the short answer is that Darwin was
right and that is that there is survival of the fittest. It’s selection. We are using antibiotics in such magnitude
because of the miraculous nature of antibiotics, both the public and the profession says, well,
why don’t we just treat this person with antibiotics even if their symptoms are minimal. So there’s enormous pressure, selective pressure
of antibiotic use and it’s just, it’s just a mathematical certainty that there’ll be
resistance, but it’s not linear. It’s, it’s geometric because of the properties
of bacteria growing. Yes, but you have to remember that bacteria
come, most of them come from the soil and antibiotics are in the soil, so they’ve learned
for millions of years how to deal with antibiotics. So the systems are there for as long as you. If you expose them to antibiotics, those systems
become heightened, then become resistant. So they, they’ve seen these drugs or similar
drugs or antibiotics type molecules for hundreds and hundreds of thousands, millions of years. Marty, you, you’ve also been talking a lot
and writing a lot about the fact that our antibiotics are not precision weapons that
you know, you use them against Ecoli, MRSA, and so on, but that’s not the only thing that’s
going to affect. Yeah, so so antibiotics came of age when we
were, when we were really trying to eliminate these bad pathogens, but no one really considered
what was the effect of the antibiotics or the normal bacteria living in the body, the
normal bacteria that we call the microbiome, but now it’s clear that that when you take
an antibiotic for a skin infection or lung or urinary tract infection, that antibiotic
is getting everywhere in the body and it is selecting for resistant organisms in that
body. That’s suppressing some organisms and other
organisms are coming up and maybe some organisms are becoming extinct as well. So these are organisms that we might actually
depend on. It might be actually beneficial for us. And so in fact we know that one of the main
defenses against infection are our residual. Our normal organisms there, there, there,
the coast guard, they are protecting against invaders. They don’t want to share their turf and 50
years ago it was shown that if you pretreat mice or other laboratory animals with antibiotics
and then give them a pathogen like Salmonella, the, the level of Salmonella that it takes
to kill the mouse goes down by four logs, you know, by 10,000 falls. So Sean, I mean someone might say like, well
we have all these gigantic pharmaceutical companies. There’s lots of money that they can throw
at the problem. You know, there was penicillin and then there
were other things I can think of mycin and you know, you know, science marches on. So we’ve got like more in the pipeline, right? That’s the unfortunate thing. We have almost nothing in the pipeline. Almost nothing. You can, you can ascribe that to a number
of different reasons. We don’t get in a crisis because of one thing,
but we get in it because many things came together that we probably didn’t foresee. One of them being that our first round of
antibiotics worked so well right? That golden age of antibiotics when we were
describing them, people thought we were done and so so over the next ensuing 30 years antibody
discovery programs, both in academic and industrial settings largely shut down and so there are
almost no pharmaceutical industries that are putting at least the effort they used to put
in to finding antibiotics. The second thing is then if we’d been using
antibiotics, the same ones for 30 years, that means they don’t cost us anything anymore. They’re all generics. You can get an antibiotic for somewhere between
free and twenty cents a day in many parts of the world, so now you have an infrastructure
that doesn’t exist and you have a financial structure that doesn’t support the development
of antibiotics. So we are at a certain point trying to figure
out how to restart that pharmaceutical industry and how to make it worthwhile to restart it. Have to be some major things changed. It’s in direct competition with chronic disease
which is much more lucrative for the companies because it drug you take for the rest of your
life is obviously going to make them more money than a drug you take for five days and
then stop, and so even even now with the crisis that we all know we’re in, very few companies
want to move back into that area. And what they’re doing is taking a drug that
worked, became, an organism, becomes resistant, and they just make a modification on that
drug. It’s cheaper for them to do that than to start
from the beginning and now the virus can become resistant much more rapidly. So they work for maybe a year or two and then
they can’t use them anymore. Marty. And then there’s yet another problem and that
is that bacteria don’t respect borders and so what that means is that if, if a resistant
organism arises in another country like India or China, it doesn’t take too long for it
to come over here and because antibiotics are so inexpensive and because people think
that they’re so miraculous. In many of these countries, people are able
to get antibiotics over the counter, no prescription necessary. Parents are giving their kids 10 courses of
antibiotics a year in, in some recent studies funded by the Gates Foundation, tremendous
antibiotic pressure, very low cost, but somebody’s making money on those antibiotics. Resistant organisms are arising and then there
are the crossing all over the world, So this, so this sort of cheap marketplace
of antibiotics over the counter and so on is even helping to drive on- The whole antibiotic market is broken. Antibiotics are in one sense too cheap and
and, and are therefore overused and abused. And on the other hand there’s no incentive
to create new antibiotics that we want to keep and put in reserve for important infections,
which won’t affect tens of millions of people so that there isn’t that market. So the market, the economic model for antibiotics
is just broken. Just, just to put a number on that, right? Yeah. So the most recent, they’re going to differ
a little bit, but let’s say the six months, recent antibiotics that came to market made
about $10,000,000 each last year. 10, 10 million each. Right? Okay, that seems like a lot of money, but
just let’s say you’ve done all the clinical trials you need and now you need to synthesize
a production scale an antibiotic. It’s $150,000,000 investment, right? And the reason these things make a little
money is, is you don’t want to use them. You don’t want to use in this frontline defense,
right? You want to put them in reserve until you
absolutely need them. And so where’s the incentive? If, if forget the hundreds of millions you
put into development, just to make the thing costs you 10 times which you can sell it for,
sell it for a year. We really have to rethink how we, how we market
these things, how we as a community decide we’re going to put antibiotics in reserve
and put an upfront and of realization that these things are there. We need to pay for them as a community because
we’re going to need them some day. Alright, so let’s, let’s brighten things up
a bit by like actually, you know, you folks are actually working on things. So maybe we’ll start. We’ll start with antibiotics themselves, with
new antibiotics. So with Jo and Sean’s work. So, so, so you’ve been going back to the soil,
the soil that brought us all these original drugs. You think you think there are more there for
us to find? I do. I’m so, for a long time I went to other methods
for antibiotic discovery and you’ll hear about some of those that Sean’s developed soon,
but the reason I did that was that there were some references from the nineties that said
that the soil was mined. It was fully tapped and I’ve gone back to
the data and I can’t find the data and so now I question whether that’s really true
because in the ensuing decades my lab just spontaneously discovered antibiotics, novel
antibiotics from soil that hadn’t been discovered and we weren’t even looking in some cases. And so I. It just occurred to me one day, wait a minute,
it’s not mined if we’re finding them and so that’s the approach we’re taking is going
back and asking what is the frequency of new compounds? There was one paper that said the rediscovery
rate would be 99 percent, so if you found 100 compounds, 99 of them would be already
known. Well that’s actually not so bad if it’s true
because we can look at a lot more than 100 compounds with today’s methods, but. But I’m not even sure that that’s true because
it wasn’t really based on at least published data. Maybe somebody in a pharmaceutical company
has the data, but we haven’t seen it. So are there particular places that you like
to go look for new antibiotics? In a particular soil that is you like or is
it just in your backyard? Well, we’re looking at across the world, so
we have a worldwide network of undergraduate students. Undergraduates who are a fantastic and very
creative workforce. So we developed a course that is known as
the Small World Initiative and it’s taught in 15 countries and all over the United States
and about 10,000 students a year take the course and they dig up soil from whatever
environment is interesting to them and they come up with more interesting reasons than
I ever would for why an environment is interesting. And and so they have this great variety of
soils. They’re isolating very interesting antibiotic
producing organisms and now we have to go into the next stage which is figuring out
what antibiotics are produced. So we think that if we have 10,000 students,
each one gets at least 10 antibiotic producing organisms per year. That’s a lot of candidates. And so if we can crank through enough of them,
even if that one percent rediscovery or 99 percent rediscovery rate is correct, we still
have a lot of new compounds to look at. So Sean, what kind of approach are you taking
to searching for these, these new antibiotics? So about 20 years ago now, I guess, Jo and
a few other people were thinking along these ideas, thinking about is there a reservoir
in soil still of, of natural products and, and the thing that that percolated to the
top of the thinking of these people was that there’s data from even longer ago, maybe 120
years ago that it appears we don’t culture most of the bacteria out of the environment,
that actually the bugs we’ve been playing with represent a small fraction of the bacteria
in the environment. So let me ask you, so if you like take a sample
of a little sample of soil, first of all, like how many microbes are in there and how
much DNA are you talking about that you’re looking at from all of them? So it depends on whose numbers, let’s say
is there’s thousands, maybe 10,000 different microbes of which we culture about one percent. Just one percent,. Just one percent. And again, people have done better nowadays,
but they don’t solve the other problem, which is even if we can culture bacteria, we don’t
turn on their genes. Right? So even if you can bring bacteria in the lab,
they don’t know how to turn on the genes, they’re gonna make antibiotics for us. And so, so what we want to do is just look
at their DNA and you can get huge amounts of DNA at least in the context of molecular
biology out of a single gram of soil. And so it’s the coming together of this idea
that we can culture bacteria. We can sequence their genomes and we can. We can mess with genes, right genes in ways
that we can turn them on that really allows you to untapped this reservoir that’s been
tapped or untapped. So. So Vincent, I wanted to, to kind of shift
gears here and look at a way of dealing with bacteria that’s totally doesn’t involve antibiotics
at all. Um, there’s, and this is, this is kind of
a long running idea of basically sending the enemies of bacteria against them. I mean, can you explain the idea of this kind
of approach? What was sometimes called Phage therapy? Well phage therapy actually started before
antibiotic therapy. So, um, it was discovered by D’Herelle about
100 years ago. He discovered a, he had a vessel in the, it
was cloudy with bacteria and suddenly it disappeared, just disappeared in his eyes. And he said some things in there that killed
the bacteria, figured out that it was, it was a virus, a virus that only infected bacteria,
bacteria phage, it’s called. And that started a revolution at the time
to use phage to control infection. It was well before antibiotics. So these, so these viruses, they’re back,
they’re known as bacteria phage. So what are we looking at? So the blue thing is bacteria. The blue thing is the bacteria and the ring
around that is the cell wall of bacteria. When it attaches, it injects its DNA into
the cell and once that DNA gets into the cell, it takes over the self for the production,
a new virus particles and once those virus particles are produced, the phage have a problem. They have to get out of that organism and
they solve the problem by producing an enzyme called the lysine that drills a hole in the
cell wall. And since the pressure inside the bacteria
is greater than the external environment, the organism explodes and releases the bacteria
phage that had been produced in the environment. And that’s phage therapy using those phage
to kill the organism directly. What we’ve done is now taking that enzyme,
the specific enzyme that drills a hole in the cell wall, we can produce it recombinantly,
and when you add that enzyme externally, it does precisely what it did from the inside,
drills a hole in the wall membrane externalizes and kills the organism, so we’ve developed
the enzyme that the phage now uses to release its progeny phage. You could use phage themselves and that’s
called phage therapy as a means to control bacteria, but you can use the enzyme to to
accomplish the same thing. And there are particular species of phages
that can go after particular species of bacteria? The very specific, that’s the problem with
phage therapy is that they’re highly specific for the organism that you’re going after. So in order to kill, for instance of Staph
Aureus, you’ll need to produce a cocktail of maybe five or six or 10 or 15 phage to
get around the chance of organisms becoming resistant because the bacteria become resistant
very rapidly to phage. So they getting resistant to the phages as
well. Antibiotics, they’re just evolving, But that’s. That’s the normal system. The phage are trying to get into the organism,
the bacteria trying to keep them out. So that balance has been going on for a billion
years. Nobody wants to win that war, phage that want
to win because if they win, all is gone. If the bacteria when. Well they can’t get enough DNA into them to
to, to, to modulate their, their, their DNA themselves. Right. Because bacteria are taking in. They are taking in DNA and so they need that. That acquisition of phage DNA that doesn’t
kill them, that allows them to pick up genes if they, allows them to survive much more
rapidly. So then there’s this molecule that phage make,
this enzyme called lysine, and so you want to just try just using lysine rather than
the whole virus. We’ve been using lysine for almost 20 years
now. We have lysine and the beauty of lysine is
that they are very specific for the organism. We don’t see resistance, we’d never seen resistance. We’ve been doing this for 20 years that they
cannot become resistant to lysines because they’d have to remodel their cell walls, so
it would take them a very long time to become resistance. Probably hundreds of years before they become
resistant to actual lysines. So those are anthrax organisms and we’ve added
lysine to them and you could see what happens to them. This is real time. They just explode and disappear. So you can take 10 billion organisms in a
test tube and add up five few micrograms of lysine, within a couple of minutes, they’re
gone, so it works quite well. We have enzymes and they’re quite specific,
so you don’t run into the problem, the antibiotic problem where you kill everything. Your normal floor and the and the organism
you’re trying to kill that. Quite the, the, the, the staff enzyme will
kill staff. Anthrax enzyme kills anthrax. So you, you’re, you’re targeted killing. You’re not affecting your normal flora. So why isn’t everybody using lysine? I mean, what’s the, what are the challenges
that you still face? Well, we’re in clinical trials right now phase
two. Phase one showed that it was quite safe. We’re in phase two in the hospital. So about 117 patients which would sure be
done by the end of this year, treating MRSA infections, endocarditis, MRSA, septicemia
and Endocarditis. Heart infections? Heart valve infections and septicemia, bacteremia
and we’ll know by the end of the year. So Janelle, I mean you had touched on this
earlier about, you know, maybe paying more attention to our own sort of host health in
terms of dealing with these infections and you know, you’re, you’ve been doing a lot
of research into, into tolerance. Maybe you could sort of describe sort of the
overall idea that you’re pursuing and then how do you know how that might translate into
an actual treatment for a patient? Yeah. So I think that the, uh, what is evident to
me with our perspective, uh, in developing antibiotics and antibiotic history and the
approaches that have been described by my fellow panelists is that they’re all based
on the question of how do we kill microbes and developing ways to kill microbes. And we are approaching this from a different
perspective. We actually want to understand what it takes
to enable a patient to return back to a healthy state and to survive infectious diseases. And um, there’s, we, I talked about sepsis
and how in sepsis and this is the case with other infectious diseases as well, there’re
significant physiological damage that occurs and that leads to physiological dysfunction. And in order for a patient to return to a
healthy state and to survive an infection, they have to be able to. You have to be able to alleviate that damage
that’s occurred, um, and, and restore the patient back to normal physiological function. And our assumption is that if we just kill
the pathogen, we should be able to do that, but that’s not necessarily the case. You can have patients where antibiotics are
effective in them, but the physiological damage that they’ve endured kills the patient anyways. And so there’s, we are taking a variety of
approaches to understand, um, if our body encodes ways to protect us from infectious
diseases by promoting health and alleviating physiological damage. And about 10 years ago now, we discovered
that in addition to our immune system, which protects us from infections by killing pathogens,
we’ve discovered that we encode a distinct defense strategy that we call the cooperative
defense system. And this is a defense system that, um, is
essential for us to survive infections. And it protects us by executing what we call
tolerance mechanisms or disease tolerance mechanisms. And these are mechanisms that our bodies encode
that alleviate physiological damage during microbial interactions. And so these are mechanisms that promote our
health without killing the pathogen, so you can induce these, um, tolerance responses
in, um, a host and they will be perfectly healthy and survive the infection despite
having the pathogen present in their body. Um, and we like this approach because this
provides a new avenue for treating infectious diseases that will enable us to promote survival
of the patient, but they also, um, in theory should be what we call anti-evolution proof,
meaning that pathogens should not evolve resistance to such strategies because we’re targeting
the, the patient and the physiology that’s affected by the, um, the infectious disease
without having a negative impact on microbial fitness. It almost sounds like the microbiome is so,
so complex with hundreds or thousands of species that, how would you ever disentangle it well
enough to be able to make it into medicine? You have to have a hypothesis. You have to conduct clinical trials. Clinical trials have advanced cancer therapy. They’ve converted HIV infection from a lethal
disease to a completely treatable disease with longterm step-by-step clinical trials. That that’s what the field needs. Of course, that’s what we need in to to restore,
to have working antibiotics, to develop new antibiotics as well. Yep. Sean. We do similar things with the human microbiome
to do the soil because we look at the molecules that these bugs make and we’ve in fact found
antibiotics that are effective against MRSA. So these are. These are antibiotics made in our bacteria
living inside of us. Coded by the bacteria living inside of us. And we’re sort of antibiotics factories. Yeah, we, yeah. We may not need to undergraduates anymore. We may just have to mine our own microbiome. Or the undergraduates’. To add to the complexity, we also have bacterial
phage in our gut and they are modulating. So we have phages that are attacking our bacteria
inside of us all the time. We eat, drink phage all the time. Ten trillion phage pass through our gut into
our tissues everyday, everyday. So they’re everywhere. There’s 10th of the 31 phage on earth, so
they’re everywhere. We eat, drink phage all the time, so they’re
in our gut, they’re modulating the organism up and down, so you have a bloom of phage
and they are killing these particular organism. You have a reduction in up in that organism. We don’t know what physiological effects it
has on our bodies, but it has to have an effect and, and understanding the modulation of phage
and our gut flora is a, is another area that people are starting to look at. And then Janelle, like your own body is then
responding to all these different things going on inside of you. I mean. Absolutely, it’s a bi-directional relationship. So, um, we’re, we’re recognizing the microorganisms
that are in our intestine, but also some microbes induce host responses or immune responses
to that are not effective against themselves, but will be effective against other microbes
within the community. So, um, through this, bi-directional communication,
it goes back to ecology 101. They’re, they’re using the host to also shape
that ecosystem. So I’m gonna open it up to questions in a
little bit. But before I do that, I just wanted to get
a sense from all of you about sort of the human side of all of this. I mean, we, we talked about how the industry
incentives are all quite perverse and you know, it takes time and effort to find these
antibiotics or to develop these other alternatives. So are there, do you see changes in a good
direction in terms of, of, you know, creating a sort of these scientific or social customs
or, or, or procedures to help get us towards this better situation where you might use
the, these things? Or are we just going to, you know, like not
be able to define these replacements because there isn’t enough support for it. And Marty, what do you think? The bottom line is that we need to be better
stewards of antibiotics. We could create 10 new antibiotics or 10 new
lysines, but unless we use them better, uh, the, uh, the resistance will get to us. The bacteria are, are selected for resistance. So we’re, we have to reduce the variation
in antibiotic use. They’re using antibiotics a lot less in Sweden
than they are here. People are just as healthy as we are here. There’s a lot of regional variation in antibiotic
use. There’s variation from doctor to doctor, the
the practice, the public have to be better stewards. Understand that antibiotic use has cost. We’re using it as if it had no cost. So you think that we could even now, I mean
not even talking about these amazing possibilities that we’ve just discussed, you think that
we could reduce the amount of antibiotics that patients are taking and still be protecting. That will help us decrease the pressure. You know, one of the questions is why did
C diff move out of the hospital into the community? Why did MRSA move from the hospital into the
general community? But we might be able to get it back in. Right. So Janelle you were just nodding before. I mean, do you think. I think there’s some great data from antibiotic
clinical trials from 1920s and 1930s where with certain trials, the, the group that received
the placebo, 80 percent of them did just fine. We can clear infections on our own. We can survive infections on our own, um,
and I think a lot of times by the time a patient shows up to the clinic to get the antibiotics,
they, there are studies to suggest that they’ve already cleared the infection and now they’re
just getting antibiotics because they have some residual symptoms from the infection. So I completely agree with Marty that if we
can just temper our use of current, um, antibiotics that will help significantly. And what about you Sean? You were just talking about like, um, how
much money an antibiotic might make and how much money is required to do it. So like how do you, how do you even, how do
you get those thing numbers to balance out? I think the good thing is we’ve seen this
tremendous effort in the past decade to try and solve the discovery problem. We still need more money there, but we clearly
see there’s global impetus to say we need more antibiotics. Maybe there’re, I think there’re 50 recognized
major efforts in the past decade to, to support antibiotic discovery internationally. So I see that going in the right direction. I really do. I don’t know that it’s going to happen fast
enough, we’ll ever get enough money, but that’s in the right direction, but it’s the post
antibiotic issue. Not only our use, but how do we market it? How do we, how do we let those things survive? I still think we have a lot of hard thinking
to think about how we’re, how we’re going to do that and I don’t think we have, we have
a solution. We have great examples we can go to. There are lots of things that countries do
to put things in reserve. You can say our army is in reserve until we
need it. Right? We pay a lot of money for that. Why not think of same models for antibiotics
that we have them developed. They’re in reserve. We pay for them prior to their use, but before
we need them. I mean there’s a lot of thought that has to
go into that, but to me that’s where the gap is at the moment, but we need more money for,
for, for development of antibiotics. We see money flooding in. We still need more, but there’s really still
this question of how do we use them afterwards and how do we finance that worries me. What might help is the fact that we’ve been
using for years and decades or a broad spectrum antibiotics and they’re killing everything
and the reasons for that is when you’re sick, you go to the hospital and the clinician needs
to know what he’s going to treat you with. If he doesn’t know the bug that’s causing
the infection he has to give you something that’s broad spectrum. If we had diagnostics at the bedside, so if
someone comes into the hospital and we know exactly what organism’s causing the infection
you can treat with an antibiotic that is specific for that organism. Would have very little effect on your normal
flora, but we’re not at that point. We’re close. Our hospitals now can identify the organism
fairly quickly. Fairly quickly meaning what kind of time scale? Hours, so we’re at hours from days to hours. And if that. If you can do that, then you have antibiotics
that are more channeled to the organism that you’re killing, which would cause less side
effects. And I think that that might be a way to survive
this type of issue that we’re having right now. And then what about sort of uh, these, um,
less, we’ll call them less conventional things like phage therapy or using lysines or so. And do you like in terms of getting a regulatory
approval for these things, do you do, do you think that that is able to move forward quickly
enough or. Or are we, do we need a better way to sort
of like take in new ideas and try to get them approved to be used? Well, the lysine therapy has been quite successful
in moving through the system. Phage therapy has an issue, because phage
therapy is, is a concoction of many phage to control a particular infection. And since you could make a cocktail, I can
make a different cocktail that causes the same infection. There is no IP so there’s no incentive. The develop phage therapy if it does work
to some degree, but there’s no incentive there. But if you have a defined molecule then that,
I think that the pathway to get it out out the door is quite good. Alright. So Jo, I’m just curious, are you, when you
look ahead 50 years, do you see the sort of the dark picture they recast earlier or do
you, are you optimistic? I mean what’s. I’m always the optimist, but I also have to
be tempered by the fact that we developed a plan for antibiotic development and stewardship
when I was in the White House and there were some really simple things in there that could
have been done like stewardship of antibiotics in hospitals. So CDC has an eight point plan of what hospitals
are supposed to do. We found that only 50 percent of hospitals
in the United States followed that very, very simple plan, like having a strategy for an
antibiotic use in the hospital, training personnel in antibiotics. It. It was really kind of depressing and appalling
and we identified all the things mentioned here and then many others that we need to
steward the antibiotics, use them less, have better diagnostics so that we know when to
use them and we don’t even use the tools today that we have like diagnostics. I’ve, I’ve done this survey completely unscientific. I shouldn’t even talk about it, but it’s my
little way of keeping tabs on the docks. I asked in my lab, when people go for a sore
throat, go to the doctor, what do they do? And 10 years ago there was never a test. They just gave them the antibiotics in every
case. And then slowly we started seeing the strep
test, strep throat test being used. But even today, fewer than half are getting
a test before they get antibiotics. That just seems irresponsible to me. Any guesses why? I mean Marty, what do you? I mean you’re the doctor? I mean why, what? I mean what, it doesn’t make sense. It’s the problem of transparency, the medical
profession and the public overestimate the benefit of antibiotic and they underestimate
the cost, the effects of antibiotics. And so, uh, we, we have, we have to fix that
and I, I really agree about narrow spectrum antibiotics, you know, and, and as I said,
antibiotics are falsely inexpensive, why, why give someone a $500 or $5,000 antibiotic
when you can treat them with a $5 antibiotic. So the market’s broken, but we need to use
tax money just like we need to use tax money to buy interstate highways, uh, that, that’s
a public. Antibiotics are public good. We have to invest in, in, in antibiotics that
will protect our future, uh, as, as a public good. Okay, um, we have microphones. A question right in the back there. Thank you first off for the presentation,
that was really useful. Um, I just have two quick questions. So first I’m being. So how advanced and what are the, what is
the percentage accuracy on these diagnostic tools? Can they either be improved or is it just
because these current antibiotics are cheaper, they’re just not getting that much visibility. And my second question is, are there currently
government programs that are in place or in the pipeline? And the reason I ask this is because there’re
orphan diseases out there that don’t have a large market either, but yet there are a
lot of government programs that incentivize the innovations for this space. So I’m wondering if that’s something that’s
happening in the pipeline right now that will encourage innovation in the space. Great. So let’s, uh, let’s, uh, let’s take these
one at a time. So Vince maybe you could start us off in terms
of the diagnostics. Is it just a case that we already have really
good diagnosis but then they’re just not being used enough? Or are there a possibility to develop new
kinds of technology to really get these things identified fast? Well, right now they’re doing it by DNA analysis. So how does that work? You just get a number of organisms, a few
organisms from swab and they can take it and put it, extract the DNA, put it through a
machine and identify certain genes certain pathogens have. And they can do that within hours. Sometimes they’d have to grow the organism
very for only a few generations to get more organisms so they can extract more DNA. But it’s quite quite accurate. It just takes a little more time. It’s not at the bedside. It’s a few hours, but it’s better than what
we used to have which was overnight. We’d have to culture it, let the grow, organisms
grow overnight and then even another test usually two days before you get the identification. When you say at the bedside, are you saying,
I mean like a doctor comes, a nurse comes and takes your temperature at the bedside,
takes your blood pressure at the bedside or you’re saying- Well like a rapid strep test is in a sense
at the bedside. You can swab the throat and put it into a
solution that digests the organism and they have an antibody that identifies a molecule
on that organism. You can do that within 20 minutes. You get the results of that experiment. That’s at the bedside. We’re not there yet, but we’re close. And are hospitals like. It sounds from your, from your survey, I would
guess that maybe hospitals are a little slow to really snap up the best of these diagnostics. They are used. Some are and some aren’t. Just like the simple practices to reduce antibiotic
resistance, which don’t cost any money and in most cases some adopt them and some don’t. And Marty, I mean most antibiotics used in the United
States and most countries are used in outpatients. They’re not used, so the focus, 90 percent
of the antibiotics are used in outpatient, and most of the antibiotics are used for upper
respiratory infections, which we know that a big fraction are viral and are not bacterial
at all, so viral infections don’t respond to antibiotics. So we need a rapid diagnostic that will tell
whether that outpatient walking in has a viral infection or bacterial infection. In the doctor’s office as well. If we had that tool, we could eliminate a
lot of unnecessary antibiotic testing. One of the problems is that the antibiotic
costs $5. The test might cost $500. So our health system isn’t, It’s not working. Okay. So after we get fix antibiotic problem, we’ll
fix the healthcare system, right? Or first, what if, at the same time. Anyway, the second question was about what? What are, what are there? Are there any special government programs
that are actually like trying to, to push research about resistance forward with what’s
happening? So as, as you mentioned, I’m on this commission
that Jo was involved in setting up called PACCARB, which is President Obama set it up
by executive order and, and our mandate is to combat antibiotic resistant bacteria and
we have five different areas, surveillance, stewardship, new diagnostics, therapeutics
and international efforts working with other countries. So as, as part of these and, and the executive
order, uh, money’s have gone into something called BARDA, which is to develop new antibiotics,
to put money in, to make it more economically viable, to develop antibodies, to look at
antibiotics like orphan diseases as well. They’re, they’re special stipulations that
make it more attractive for companies to make products for orphan diseases. Great. Any more questions? Is prevention still a big thing in terms of
the washing of the hands thing, is that still the best thing we can do? I have one little version of that. I try not to touch anything when I go to the
men’s room. Does that work? So soap and water works. There’s no question, but on the other hand,
there are all these antibacterial products, uh, that are killing the good bacteria. Good bacteria help protect us against the
bad bacteria against the invader. So are they doing more good or good? Doing more harm. And I don’t know either. These things have hardly been tested and the
people who make them aren’t particularly interested in testing. So we should, we should just talk a little
bit about. I mean, we’ve lot, I’ve been talking a lot
about the gut, but the skin is covered in bacteria, right? And it’s a completely different flora than
we have in our gut or our mouth or our ears. In fact, the two hands differ a left and right. So. And are they, are they, are they doing, are
they doing good things for me right now? Yeah. They’re protecting your skin just like they
protect any surface they’re on, they’re good guys. You have to get used to this respect for the
microbes thing. Okay, okay, now I can handle this. And so, so if you use these sort of hand sanitizers
with the antibacterials- There are times to use them in the hospital,
it’s very important to use them because you have a lot of bad bacteria transmitting in
hospitals. So washing the hands and a variety of different
ways is important. And during flu season it’s very important
because flu is transferred by people’s hands. But if you take all of that collectively,
maybe that’s three percent of the time. The other 97 percent of the time, the benefit
is just leaving our microbes alone. I think the biggest thing any of us can do
is treat our flu symptoms very respectfully. Stay home, not, so you don’t transmit it,
wash your hands with soap. Purell won’t help with flu, but uh, that much
but certain, oh, well yeah, get get you saying get the shot. Get a vaccine. That’s right, and because I think more antibiotics
are given for flu like symptoms that turn out to be viral, but we don’t have the test
to prove that than probably any other disease, so I think if we kept the flu under control
and that can be controlled just by behaviors and washing hands and breathing in people’s
faces. When? Usually November or December till our early
March events. Vince? You have to realize that 90 percent of infections
come in through the mucous membranes. They’re not coming in on your hands. They are coming in through mucus membranes. Your eyes, your your genital track. So when you touch something that’s contaminated,
you’re not getting infected through your skin. It’s when you touch your nose, or you touch
your mouth that the organism then gets it. That’s how it gets in. You have to have a wound. Your skin is a barrier. The only other way is a wound. You’re bringing the organism from where the
other, whatever you picked up and you touch your nose and how many times you touch your
nose and your mouth. About 12 times an hour for the average person. Wow. In the back there. I think multiple of you stadia, but you were
basically because you were using bacteria. No, because you were developing and what do
you got? Penicillin and all which came from soil bacteria
and therefore the soil bacteria had natural built in resistance to the compound you were
using. A question, is it possible to synthetically
generate proteins or protein analogs which would bind to sites or would interfere in
other ways with mechanisms for which things have not developed resistance to because they
weren’t. They aren’t actually naturally occurring equivalent
to penicillin. Yeah. That’s actually an interesting point is that
I think they’ve done studies right where like they would look at old soil and actually actually
find that there were some resistance, resistant microbes like before the invention of antibiotics. That’s right. They’re all over it. My, my group has studied a site in Alaska
that’s essentially as pristine as you can find a site on earth and it has very little
exposure to antibiotics and we find a large array of antibiotic resistance genes. We also have found that when, purely synthetic
antibiotics had been introduced on the market, resistance has even faster in some cases than
to the naturally occurring ones. Penicillin’s been on the market for what,
60 or more 70 years and it’s still useful. Some of the this synthetic antibiotics can’t
even be used anymore because there’s so much resistance, so we’re dealing with evolution. I think that’s the answer to the question
of why there’s no universal cure or prevention because we’re dealing with evolving organisms. So I guess the lesson is that bacteria are
pretty awesome. They really are. All right. Well let’s give a hand for our panelists. Thank you for coming.

The incredible (endangered) biodiversity of the Amazon rainforest | Jorge Rodrigues | TEDxUTA

The incredible (endangered) biodiversity of the Amazon rainforest | Jorge Rodrigues | TEDxUTA


Translator: Deborah Oliveira
Reviewer: Denise RQ Host: Our next speaker is
a Brazilian native and microbiologist with deep interests in biodiversity
and ecosystem functionality of the Amazon rainforest. In order to shed light on these and other
microbial ecosystems in question, he uses high-throughput
genomic technologies to study microorganism environments as diverse as tropical forests
and termite hindguts. Today, he serves as an Assistant Professor
within the Department of Biology at UTA. Please welcome Jorge Rodrigues. (Applause) Jorge Rodriguez: For the next ten minutes, I’m going to try to convince you
that Dr. Seuss has been lying to you. (Laughter) I hope that if I convince you of that,
you will go back home, buy more Dr. Seuss books,
and read to your kids, with your siblings, friends,
grandkids, and so on. Why do I say that? Because it is my own experience
when I started working in the Amazon. I was really interested
in learning more about the Amazon. If I am going there, I want to find out
what is already there. And if I am going to be there, I want to find out
if something is going to eat me, who is going to eat me there, right? So what I did was to collect a whole bunch
of information about the Amazon. I collected books, readings, videos. And I started reading all of this. But the book that really caught
my attention was this book. Why is that? Well, because it is all about
the rainforest. So I said, “This is
the must-read book for me.” If I am going there, I should read
more and more about this book. So I start reading this book
and what happened was that the book starts talking
about the rainforest and the patterns, the dry seasons
and the rainy seasons of the forest. I thought, “Oh, that is very interesting!
Let me continue reading this.” The next topic was about the locations. It told me where rainforests are located. But I am a scientist, and as a scientist
I don’t just trust data. I really want to find out
what is going on with the data. So what I did was to connect with people who could tell me more about the Amazon,
or about the rainforest. I found one expert, and the expert was seven years old. I asked him, “Where are
the locations of the rainforest?” He told me, “Rainforests are located
in Central and South America, they are also located in Africa in countries like Congo, Zaire,
Gabon, Madagascar, and back again we have rainforest in countries like the Philippines,
Thailand, Malaysia, New Guinea.” I compared the information
the expert gave me with the information
that I got from the book, and they both matched. So I am going to read
more and more about this book. The next topic in the book
was about the biodiversity. It talks about the biodiversity
of plants and of animals. I said, “I am going
to get there to the Amazon, and it is going to be like a zoo to me, because I am going to see all kinds
of animals, all kinds of plants.” It turns out that when I got there
that is what I saw. A pretty dark place,
and this is the middle of the day. I thought, “Wait a minute, all those books promised me
that I would see something else!” Actually, the books told me that 25% of all terrestrial species
are present in the Amazon. 25%. The books told me
that in a 100 by 100 square meters, I would find more plants
than in the entire European continent. Imagine the entire Europe. In a 100 by 100,
you can see more plants there. In a single tree, I can see
80 different species of ants. And if you multiple this number of insects
by the number of plants, you would find a staggering number of 42,000 different insects
in a hectare of the Amazon. If this is not enough for you, the majority of them
have not been described. We don’t know what they are doing there. And something that is
a bit more related to us: in a single sampling expedition,
we can find 72 different species of bats. If you are in the US,
we have 42 species of bats. In a single expedition, we could almost double
the number of bat species in the Amazon. I did not see any animals there. I was still wondering, “What is happening?
Why don’t I see all those animals?” And I would be OK with that,
not seeing any animals there, but the problem is
that the landscape is changing. The Amazon is changing quite fast. This is a satellite picture
of part of the Amazon forest. Every little orange dot you see is a fire. A fire that started to change the land. How do we do that? You remove all the hardwood and sell it. Then you slash everything to the ground. Next, you let it dry. When the dry season comes,
you set everything on fire. And that fire will burn for days and days,
sometimes for weeks and weeks. Once everything is turned to ashes,
you sow with grass and move cattle in. There are lots and lots of cattle there. So this idea of changing the land
from forest to pasture is really changing the biodiversity
in the Amazon forest. Why is that? Because this is the most important factor affecting biodiversity losses
in the Amazon. It is more important
than the CO2 increase, more important than climate change. It is the most important
man-made alteration going on in tropical systems these days. Just to give you an example, this is the area where we do
our sampling in the Amazon. In 1975, it was a sea of green. If we looked from the airplane,
we’d only see trees all over the place. In 14 years, that is what we saw. Lots and lots of changes. This is called a fishbone
structure of development. You have a road, and in both sides of it,
you have clearing of the land transforming the forest into pasture. The road continues, and you see more; more and more changes. If the landscape is changing,
then all inhabitants are changing as well. You know that plants
and animals will change. You have a forest with hundreds of plants, and then you have
one single plant now: a grass species. You have all kinds of animals,
all animals I didn’t see before, and now you have
one single species of animal: a cow. But there are lots of microbes there
I don’t see, and I know they’re there. Those are tiny little microbes. I have one gram of soil here on my hand., a little gram of soil. In this gram of soil,
I have 100 million microbes. There are 10,000 species of microbes
in this little gram of soil. They are all changing, so I am here today to tell you
they are changing as well; not only plants and animals change
but microbes change as well. The research that we do in the Amazon
tells us that the microbial communities in the Amazon soil
are increasing in similarity. What does that mean? It means that the microbes are becoming
more and more the same. They are becoming more and more
equal to each other. Genetically, they are becoming
more and more similar to each other. Why is that important? I have two reasons for you. The first reason is related
to the environment. Environments, ecosystems
provide us some services, and microbes as well. We don’t know that on a daily basis, but you have more microbial cells
than human cells. In the Amazon, those microbes are responsible
for recycling all nutrients. All dead carcasses of animals
are recycled by microbes. All leaves that fall from the trees
are recycled by microbes. So microbes are responsible
for all the biogeochemical cycles. If you are changing those microbes, then those biogeochemical cycles
will be altered as well. Now imagine the Amazon, that place that is the largest forest
terrestrial ecosystem in the world. If this ecosystem is changing,
then the Earth is changing. That is the first reason. The second reason is because microbes
are reservoirs of new antibiotics. They are reservoirs
of new biotechnological products. They are reservoirs
of cancer-fighting drugs. In fact, there are at least
120 prescribed drugs these days that came from the forest. If we are losing all those microbes,
we are losing the opportunity of finding new drugs, new antibiotics,
new biotechnological products. This is a picture that I took
during my last trip in the Amazon. When we are removing wood from the forest, we are not removing only wood,
we are removing something with it. I just told you that,
the microbes are disappearing. If the microbes are disappearing,
we are removing something else: their genes, those antibiotics
that we are supposed to find. You and me, we are all
driving that truck together. You like it or not, you are responsible
for driving that truck. As a responsible driver, or as a driver,
the question for you to ask is: “Should I step on the gas pedal
and go for it as fast as I can, or should I slow down a little bit and find the safest route
for me to keep going?” Thank you very much. (Applause)

What Is Loneliness Doing to Your Brain?

What Is Loneliness Doing to Your Brain?


Today we’re talking about loneliness;
not to be confused with introversion, or social anxiety, while those subjects are worthy topics. Loneliness actually has been defined in many ways: “a state of solitude or being alone,”
“inability to find meaning in one’s life….” Okay, this is already a downer, so look at
a picture of a panda. Aw, it’s cute! Now I want a panda. I’m gonna overnight one to my crib. I’m gonna do that. Of course, we’re not the only generation
to experience loneliness, even though listening to The Weeknd
really does make it feel like that. Health insurance provider Cigna recently published a study citing that 18-22 year olds have the highest “loneliness score,”
followed by millennials, then Generation X… so yeah,
young people, we just killin’ it right now. Generation Z cited that they feel people are
around them but they aren’t really with them, feel shy, and they feel like people
don’t know them very well. The old man in me really wants to say, “these
kids right now are out here spending too much time on the Twitters and the Fortnites!”,
but that’s not exactly what Cigna found. Cigna cited lack of an IRL social life
as part of the problem, saying that “levels of in-person interactions, physical and mental wellness,
and life balance” are better predictors of loneliness
than social media alone. So, if your IG game is on point but you like to hang
out with your friends, you should be good… but if social media IS hanging out with your
friends, go outside! Humans are social mammals and need social interaction to survive; that’s
part of why solitary confinement in prisons is so torturous. Why do that to ourselves
on the outside? “Y’all best go out to the quarry for some stickball and a swim!” You know, I’m not doing this voice again. One study breaks down three types of loneliness. Situational loneliness is when unpleasant events
or circumstances cause us to retract from society. Developmental loneliness can hinder
our capacity to balance individualism and intimacy. (Psychological disorders like depression or schizophrenia could cause developmental loneliness). And finally, internal loneliness, when a self-perception of worthlessness intensifies
the feeling of being alone. This got dark again, bring in another panda pic. Lifestyle influences our neurophysiology, so lonely people perceive the world very differently. For instance, people suffering from loneliness tend to see benign events as more threatening,
living in self-defense mode… even in their sleep. Some research suggests that lonelier
people have more restless sleep patterns, which could impact cognitive development. Research suggests that there are
neural correlates for loneliness. A 2009 study revealed that lonelier people
showed less activation in brain centers associated with reward when viewing pictures of people in pleasant situations, and less activation in parts of the brain linked to empathy when viewing images of people
in unpleasant situations. Other researchers also discovered that neurons in the dorsal raphe nuclei are sensitive to social isolation. Those neurons in question, taken together
with the ones from the ventral striatum, deal with the reward neurotransmitter dopamine. So, it’s possible that low social interactions=less dopamine=less feeling good. Of course,
the latter study was run with mice, so more research is always needed. On top of that, a meta-analysis from 1980 to 2015
found that loneliness and its accompanying
depression was as bad as smoking 15 cigarettes a day, and is a risk factor for mortality.
This is so dark; bring in the pandas! Please, don’t leave, don’t leave! I’m
not gonna leave you on a downer. Loneliness is a social epidemic, yes,
but there are remedies. Don’t replace friendships and happiness with likes and text messages.
Go out and meet people! Humans need social interaction in real life –
it’s developmentally necessary. Easier said than done, but remember, you’re
not alone in feeling alone. And if you’ll excuse me, I have a panda
waiting for me at home. I did order one, and I can’t wait to play with it. Yo, thanks so much for watching. If you’re
like, “ooh, I need a little bit more loneliness content!” watch this video about what solitary
confinement does to your brain. And if you’re like, “that’s a little bit too dark for me,”
watch this video about pandas watching… watching porn? Watch this video about pandas
watching porn. Thanks for watching my video, and also, subscribe to Seeker for more videos! Pandas watching porn?
I’m definitely gonna hafta watch that. I gotta find out what’s going
on with pandas.

Connecting with Tiny Insect Brains through Virtual Reality | Dr. Shannon Olsson | TEDxChennai

Connecting with Tiny Insect Brains through Virtual Reality | Dr. Shannon Olsson | TEDxChennai


Translator: Suyeon Ji
Reviewer: Peter van de Ven I’d like to start by having
everyone close their eyes and think about all the decisions
that you’ve made so far today. Now, I suppose the first decision
you must have made is to get out of bed, and I’m hoping that the last decision
you’ve made is to start listening to me. Please open your eyes. We’re constantly making decisions, even the path that you took to get
to where you are at this very moment was an entire series of decisions: if you should move,
when you should move, even how you should move. Now, what if you’re a fly? Insects also have to make decisions about if, when,
and how they should do things. Should they fly or should they walk? Should they eat, should they wait? And where should they go
to find their food? And just like us, insects have to take
information from the world around them as well as internal information –
hunger, thirst, hot, and cold – and then decide. Why should we even care
about the decisions of a tiny fly? It seems so inconsequential to our lives. In fact, insects are some of the very
first animals to emerge on this planet. They are nearly half a billion years old. If you add up all the species of insects
that exist on this planet today, it is nearly equal to all other
forms of life put together, all species of bacteria, fungi –
even you and me. While we often think of insects as pests
that bring disease or destroy our crops, they also serve incredibly important
ecosystem services, such as pollination and reducing waste,
like these termite mounds do. They have survived mass extinctions,
and we cannot survive without them. And I believe that understanding
the decisions that these tiny animals make is not only essential
for the future of this planet but can also teach us about ourselves
and our own decision making. And that is important
for treating neurological disorders, improving education,
predicting financial trends, even generating artificial intelligence. But the fact of the matter is we don’t even know
how the tiny brain of an insect, with only 100,000 neurons, makes decisions. So how can we possibly
comprehend the human mind, when we have 80 billion neurons. To start, maybe we should think
about the decisions themselves. We humans understand
each other’s decisions by making a connection with each other
through an emotion called empathy. Now, this photograph was taken
after I’d had a very horrible day at work. And I’m sure you’ve all
had days liked these, and I’m sure you all know what you
feel like at the end of those days. And my then five-year-old daughter,
Grace, noticed how I was feeling, and she came up to me, and she gave me
what I most needed at that very moment, which was a warm embrace. See, Grace was practicing empathy. It’s perhaps the most profound
of human emotions, and it’s often confused with sympathy. But sympathy is when you
feel bad for someone, or you’re thinking about another person,
but empathy is very different. It’s feeling along
with another individual. It’s connecting with them
on such a deep level that you share their experiences
as if they were your own. Now how can you possibly empathize
with a fly, to understand their decisions. You can’t talk to them, and they’re too small and too quick
for you to follow them around and observe their decisions
as they make them. You simply can’t put yourself
into their world. Perhaps, instead,
you can put them into our world, into a world that we create just for them, so we can give them choices and observe the decisions
that they make in real time, exactly as they make those decisions. But now, if you’re going
to build a world for a fly, you’d better have an architect. Pavan, could you please say hello? Pavan Cowshick: Hello. Shannon Olsson: This is Pavan Cowshick. (Applause) He’s a graduate student in the lab, and when Pavan joined the lab
three years ago, I asked him to do nearly the impossible – I asked him to build a universe
for an insect. And that’s exactly what Pavan has done. So here’s the world
that we’ve created for a fly. It’s an artificial world,
so it’s a virtual reality arena. And the most important part of this arena
is, of course, the fly itself, which you see here right in the middle. And it can fly, and it can move its legs, but it’s held in place
so it doesn’t fly out of the world. We have a camera that can film
the fly’s behaviors as it moves, and we have a panoramic display. Many insects have very large eyes so they can literally see
in the back of their heads. So our display also has to wrap
around the insect in 360 degrees. The last two components are actually
what sets our arena apart from virtual reality that you might have
for humans or for other animals. And that’s that we give our fly
both a wind direction and also an odor. In the real world, when insects
are flying to objects at a distance, it often can’t see them. So it uses its sense of smell
to locate plants or fruits or flowers or whatever are the objects
of its affection. This is not unlike
if you’ve ever lost your cell phone, and you call it up, and you follow the ring tone
until you can locate where that phone is. Insects do a similar thing, but instead
of using sound, they use smell. And the wind direction
is actually what tells them where the smell is coming from
and where they can locate the object. So this is, right here – I will show you – part of the arena. And you can see how tiny it actually is. And that’s because it’s actually
made for a fly and not for us. And I’m going to show you also a fly. So, this fly is balancing
on a ball right now. Now you can see that it’s flying. If you zoom in on it – there you go. This fly is actually flying in this world,
but in this world – there you go again. In this world, it’s actually
looking at me right now. And it’s not getting any wind and odor other than what it’s getting
from the air around it. In the real world, when this insect
is flying around and making its decisions, it will move within the world
when it makes its choices. But I’m holding it in place,
which means instead of the world moving while the insect flies, we have to move the world
around the insect. This is how we do it. This is the cockpit
of a virtual reality arena. So this is what the visual part
of our arena looks like. You see two trees on it,
and it looks a bit distorted because, as I said,
in reality it’s wrapped in 360 degrees, so this is what it looks like
when it’s unwrapped. And you can see the fly
down there at the bottom. This is a still frame,
so it’s not yet moving. When a fly wants to move left or right,
it changes how it beats its wings. If it wants to move left,
it beats its wings very hard on its right. If it wants to move right,
it beats its wings hard on its left, and that’s how it turns. So in our world, we pay attention
to those wing beats, and we turn the world
in response to those wings, so the fly is actually driving the world. Now, in the video, you’ll see,
when we start on the right, you’ll see the trajectory
that the fly would be making if it were actually flying in this world. So you can see this fly
is making a choice to go to this tree. This is an apple fly,
and these are apple trees, so it really likes them. If you observe
the trajectory on the right, you’ll see that it’s gone to the tree, and it’s actually flying
in and around the branches of the tree and circling them. And now we’ll give it
the same choice again, and it will actually fly
to the trees with apples. And if you watch very closely, you’ll notice that as it gets very
close to these objects, very close to the leaves of the apples, it actually will throw its legs out. And in the real world,
it does this for two reasons: either it’s about to crash into something,
or it wants to land on it. And this is how we truly know
that this fly is making decisions because it actually is detecting these
virtual objects as if they were real. So we’re using the power
of this technology as a way to present
these animals with choices and observe through their eyes, through their antenna,
and through their behavior how they make decisions, and how these tiny brains can make
such complex choices in the world. And we feel that this
is extremely important, not only for understanding
decision making in general but for a much bigger reason. So often, in today’s digital
and urban world, we forget our connection with nature. We forget how important the plants
and animals around us are for the food we eat, the water we drink,
and the very land that we live on. So I hope that when you leave today,
go home, go outside in your garden or even inside your house
and try to find an insect – an ant, a grasshopper, maybe even a fly – and try to watch it for a little bit, and think about all the decisions that it must have made to get to the exact
place that you are right then. And also realize
that many of those decisions are not all that different than the kind
of decisions that you might make. Because we’re all connected
on this planet. And in the end, our two worlds are exactly the same. Thank you. (Applause)

Magnetic Termites: Leading You Out of the Australian Outback

Magnetic Termites: Leading You Out of the Australian Outback


Hi Guys. I am Trisha with Insectopia here to talk to
you about magnetic termites. These termites build tall mounds that some
people say bear a resemblance to headstones. They build them in plains and they all face
the same direction. Mostly North-South, which is where they get
the name magnetic. But why in the world would they build a mound
that is 9-12 feet high with a North/South axis of 7 feet, and an East/West axis of only
3 feet? The leading hypothesis for their North/South
orientation is, temperature control. In the early morning the termites spend their
time on the east wall to warm up. By noon, when the day is hottest and the sun
is directly overhead in the Australian Outback, the termite mound is thin so the mound does
not have a large amount of surface area that the sun can heat. As the day is ending, the mound can pick up
enough heat to make it through the night. How does this help you? Well, now with the knowledge that the termite
mounds are built North to South. The next time that you are lost and wandering
around the Australian Outback and you run into one of these mounds, you will have a
50/50 shot at picking North instead of walking around completely lost. Before we dive into this mound, I want to
clear up a common misconception. Termites are eusocial cockroaches. Let’s try to clear this up a little, termites
are a kind of cockroach and are closer related to grasshoppers, praying mantids, and walking
sticks than they are to ants. This has to do with termites having an incomplete
metamorphosis and ants having a complete metamorphosis. Now, let’s look inside of this mound. In each mound there are varying ages of individuals
from eggs to adults and the individuals are specialized for different jobs. These special groups of individuals are called
castes. The 5 castes are: queen, king, soldier, worker,
and reproductive. The life cycle of a termite mound goes something
like this: The queen lays every egg in the colony and
is the mother to every individual in the colony other than the king. The eggs are cared for by the workers. In fact, the workers do all of the hard work
in the colony. They clean and repair the nest, gather food
and water, care for the young, construct the tunnels and galleries, and control the numbers
of soldiers and reproductives by killing and eating them based on chemical cues. The workers are very busy. Every single worker in the termite mound is
a nymph and most of them will stay nymphs for their entire life. These insects never molt into adulthood! It is as if most termites live in Peter Pan’s
Neverland. The lucky few individuals that come into adulthood
turn into either soldiers or reproductives. The soldiers have large mandibles and it is
their job to protect the colony. The reproductives gain wings and will wait
around in the colony until the external conditions are right so that they can go on a mating
flight. On a mating flight, a reproductive female
and a reproductive male will mate and become a king and queen. They will land on the ground and shed their
wings. The queen will find an ideal location to start
a colony. At that point, it is the king’s job to tend
for the colony and the eggs until there are workers to do these jobs. The king will stay by the side of the queen
in her chamber for the rest of his life. The queen will become as large as a human
index finger and lay an egg every 3 seconds. She actually becomes so large that she is
no longer able to move or leave the chamber that she is in. The workers will carry the eggs to another
chamber and care for them. This is how the cycle starts anew. These are real life pictures of the magnetic
termite’s mounds. This is what a termite looks like in real
life. On the left you can see an egg on the right
you can see a worker. On the left you can see a soldier and on the
right you can see a reproductive. On this final slide you can see a queen. Thank you for listening! If you have any questions about magnetic termites
or a thought on which caste you would be if you were a termite, let us know in the comment
section below! Make sure to like, comment, and subscribe
for more videos like this one. I will be posting videos frequently. Come and check out our next epic insect tale.

From the Headlines: Bed Bugs with Louis Sorkin

From the Headlines: Bed Bugs with Louis Sorkin


When I feed them, sometimes it’s once a month,
or sometimes longer, usually, there’s a little bump that starts, it swells within an hour
it’s totally gone and then maybe six hours or more is when the little red marks show
up. I got more interested in bed bugs back in the late eighties when someone actually
brought one in to look at. Now again, there are more people in the world who are interested
in this insect and trying to learn more about it, too. How to get rid of it and how to manage
it and just to learn more about its biology. I’m looking at the behavior because trying
to find a chink it its armor is actually trying to find out something that can be manipulated
in its behavior to assist you in either monitoring or removing the insect from the environment.
Media coverage online or on television, explains about searching the bed, searching the mattress,
searching behind the walls, look in the walls, look behind pictures, picture frames, and
the problem is that most of the media then doesn’t show you what bed bugs really look
like, so you really don’t have any idea of what you’re looking for. They only show adult
bed bugs and that one-sixth of the population is a quarter-inch long or less than a quarter-inch
long, but reddish-brown, and that’s an adult bed bug. But the youngest bed bugs are about
a millimeter when they’re born and they’re pale white, and they blend in with the background.
Well, a small infestation could actually be just one female who has mated and then she’s,
you know, in your home, on a package you brought in, or clothing, or something, and that’s
all it needs, ’cause then she produces a few hundred eggs in her lifetime, but she’ll probably,
in the first month, lay five to ten eggs, and then she’ll have to mate again in order
to have sperm to produce more eggs, then she’ll have to feed to make more eggs and also nourish
the sperm she would have inside her. You wait too long to get rid of an infestation, your
population of bed bugs really increase and you have them in so many more places of your
home than you have started months before. There is no magic bullet to get rid of bed
bug infestations. If there were one product that worked that way, then we wouldn’t have
a problem anymore.