Cockroaches, Alligators & Other Weird Sources of New Drugs

Cockroaches, Alligators & Other Weird Sources of New Drugs


Antibiotics are one of humankind’s most amazing
discoveries. Ever since that fateful day in 1928 when Scottish physician Alexander Fleming
noticed a funny mold growing in one of his petri dishes, antibiotics have been kicking
bacterial butt. That famous mold, of course, was producing
penicillin, the founding antibiotic superstar, which has since extended the average human
life by at least a decade. It fundamentally changed the face of medicine. Antibiotics,
or antimicrobials, are basically selective poisons designed to either kill or slow the
growth of bacteria to the point where your body’s own immune system can clean up. These
drugs target a specific part of bacteria or some important stage in their development
without damaging the body’s host cells. And they’re really great their job. Until they
aren’t. Lately, antibiotic technology has been having
a hard time keeping pace with bacterial evolution. We’ve talked here on SciShow about how lots
of your die-hard, go-to favorite antibiotics are starting to lose their mojo in the face
of sneaky and rapidly evolving bacteria. The US Centers for Disease Control and Prevention
estimates that at least 2,000,000 Americans became infected with drug-resistant bacteria
in 2012, and 23,000 of them died as a result. These superbugs are deadly serious and could
quickly unleash a global health crisis if we don’t find a way to keep them in check.
The problem is we’ve already hit up many of the most obvious sources of antibiotics, like
fungi, which includes penicillin, and synthetic molecules.
Fortunately, we humans have big, delicious brains, and some of the best of them are hard
at work trying to invent all-new ways to kill dangerous bacteria or find other organisms
on the planet that are better at it than we are so we can steal their secrets. And while
they’re finding some promising leads, I gotta say, they’re looking in some pretty weird
places. [Intro] You know how everyone jokes that after some
big global disaster, only cockroaches will survive? Well, we recently found what may
partially explain their famous, and infuriating, tenacity. Research from the University of
Nottingham suggests that certain insects, like roaches and locusts, have brain tissues
that are infused with super-powered antibiotic juju. The researchers found nine different
antibiotic molecules tucked into the roaches’ nervous systems that may be protecting them
from otherwise lethal bacteria. They’re all a type of molecule known as peptides, short
chains of amino acids that make up proteins, kinda like proto-proteins. And these peptides
are specific to the bugs’ brains. They seem to be chemicals that roaches” brain cells
use to communicate with each other, y’know, whenever a cockroach is sitting around thinking
about stuff, which I guess can happen, and although we’re not sure how these peptides
actually work, laboratory tests have shown that they’re incredibly effective at eliminating
some of our least favorite bacteria, like the most dangerous strains of e.coli, which
cause gastrointestinal infections. And even MRSA, a super-resistant type of staphylococcus
bacterium that can cause unstoppable deadly infections in humans, particularly in hospitals.
In lab trials, these roach brain molecules killed over 90% of MRSA bacteria, without
harming any host cells. So I can guess what you’re thinking: shut
up and take my money! Well, hold on a sec, because we’re a bit away from having cockroach
brains on the pharmacy shelves. There’s still loads of technical hurdles to overcome, tests
to conduct, basic things we need to figure out, like how exactly these molecules work.
But roaches aren’t the only hardy animals out there. Alligators are some of the Earth’s
most rugged beasts. They essentially live in cesspool swamps teeming with bacteria and
fungus and other microbes, and more than that, they’re known brawlers. Put just a few territorial
800 pound toothy reptiles together in a dirty swamp, and you will no doubt come out with
some serious bite marks and bloody wounds, even missing limbs. But amazingly, what you
probably won’t find are any infections. This got some bayou scientists to thinkin’!
Dr. Mark Merchant, a biochemist at McNeese State University in Louisiana, helped conduct
a decade long study that investigated what makes alligators so unusually resistant to
bacterial and fungal infection. Turns out, it’s in their blood. An alligator’s
immune system is largely innate, meaning it can fight off harmful micro-organisms without
having any prior exposure to them. They just pop right out of their eggs ready to do battle.
We humans also have some innate immunity, provided by things like our skin and white
blood cells, but a big part of our immunities are adaptive, meaning we often develop a resistance
to specific diseases only after being exposed to them. Which of course is not ideal all
the time, but alligators get to skip this step. Researchers examining blood samples from American
alligators isolated their infection fighting white blood cells and then extracted the active
proteins working in those cells. And these two included a special class of peptides which
seemed to have a knack for weakening the membranes of bacteria, causing them to die. When pitted
against a wide range of bacteria including drug-resistant MRSA, these tough little peptides
proved to be effective killers. They also wiped out 6 of 8 strains of candida albicans,
a type of yeast infection that’s particularly troublesome for AIDS and transplant patients
with weakened immune systems. Such compounds may also be found in similar animals, like
crocodiles, Komodo dragons, and the skins of some frogs and toads. So far, lab trials
have shown that gator blood can kill at least 23 different strains of bacteria including
salmonella, e.coli, staph, and strep infections AND even a strain of HIV. For now, scientists
are working to find the exact chemical structures at work in four of these promising chemicals
and pinpoint which types are best at killing which microbes. One problem so far: high concentrations
of gator blood serum have already been found to be so powerful that they are toxic to human
cells. So other biologists are taking a different approach in the search for the next generation
of antibiotics. Rather than looking at other animals, they’re
exploring strange, new places, like cave soils and deep-sea sediments. Researchers have recently
discovered evidence of promising new fungi strains living way down in hundred million
year old nutrient-starved sediments in the Pacific Ocean. Everyone thought this was a
near-dead zone for life, too harsh and remote an environment for something like fungi to
survive in. Just a decade ago, the only living things known to inhabit such deep sediment
layers were single-celled bacteria and archaea, organisms known to flourish in extreme environments.
But while examining dredged up sediments from as deep as 127 meters into the sea floor,
scientists found fungi of at least eight different types, four of which they successfully cultured
in the lab. Some of the fungi even belonged to the genus Penicillium, which we have to
thank for the development of penicillin. Now, we’re not exactly sure how old these fungi
are, but they are definitely quite old and maybe, more importantly, they appear to have
been living in isolation for eons. If that’s the case, they may have evolved specific and
unusual defenses against bacteria, which, just like their penicillin kin in that famous
petri dish, could end up being a new and powerful source of antibiotics.
And there’s one more strategy that scientists are using, one that works in espionage as
well as in medicine. And that is seeing what the enemy is up to.
While exploring life in strange new places around the world, some biologists are looking
for bacteria that have never been exposed to our drugs, but still appear to be naturally
resistant to them. Wherever we find the most naturally resistant
bacteria, we might also find natural antibiotics that we never knew about.
And here, one of the most promising leads is again in one of the hardest-to-reach places:
New Mexico’s Lechuguilla cave, a place that was isolated from all human contact until
it was discovered in the 1980’s. One of the many fascinating things that scientists
have discovered here is that the cave bacteria seem to be resistant to everything.
Even though they’ve never been exposed to us or our drugs, all of the bacteria have
proven to be resistant to at least one major antibiotic, and many tend to fend off more
than a dozen of the most powerful antimicrobials we have. This suggests to scientists that
the bacteria have evolved to be this way because they live in an environment that’s rich in
naturally occurring antibiotics, ones that the germs we live with up here on the surface
have never encountered. Now we just have to find out what exactly
those compounds are. So look, I’m not going to lie to you: we have
a lot of work to do. While we might discover a new super-drug lurking
in a cave or under the sea or in a cockroach’s head, there’s a big difference between finding
a substance that cleans house in a petri dish and actually putting a new antibiotic in the
vein of a human patient. So the bummer is, as promising as some of
these bold new discoveries may be, none of them has yet yielded an actual marketable
drug. Still, there’s a long list of successful antibiotics
that we’ve managed to derive from strange sources, starting with Dr. Fleming’s rogue
fungus. So if we keep exploring strange new places
and studying how other animals deal with the problems we’re facing, we just might find
the next penicillin before the superbugs get the best of us. Thanks for watching this SciShow Infusion,
especially to our Subbable subscribers. To learn how you can support us in exploring
the world, just go to Subbable.com. And as always, if you want to keep getting smarter
with us, you can go to YouTube.com/SciShow and subscribe.

Cockroaches, Alligators & Other Weird Sources of New Drugs


Antibiotics are one of humankind’s most amazing
discoveries. Ever since that fateful day in 1928 when Scottish physician Alexander Fleming
noticed a funny mold growing in one of his petri dishes, antibiotics have been kicking
bacterial butt. That famous mold, of course, was producing
penicillin, the founding antibiotic superstar, which has since extended the average human
life by at least a decade. It fundamentally changed the face of medicine. Antibiotics,
or antimicrobials, are basically selective poisons designed to either kill or slow the
growth of bacteria to the point where your body’s own immune system can clean up. These
drugs target a specific part of bacteria or some important stage in their development
without damaging the body’s host cells. And they’re really great their job. Until they
aren’t. Lately, antibiotic technology has been having
a hard time keeping pace with bacterial evolution. We’ve talked here on SciShow about how lots
of your die-hard, go-to favorite antibiotics are starting to lose their mojo in the face
of sneaky and rapidly evolving bacteria. The US Centers for Disease Control and Prevention
estimates that at least 2,000,000 Americans became infected with drug-resistant bacteria
in 2012, and 23,000 of them died as a result. These superbugs are deadly serious and could
quickly unleash a global health crisis if we don’t find a way to keep them in check.
The problem is we’ve already hit up many of the most obvious sources of antibiotics, like
fungi, which includes penicillin, and synthetic molecules.
Fortunately, we humans have big, delicious brains, and some of the best of them are hard
at work trying to invent all-new ways to kill dangerous bacteria or find other organisms
on the planet that are better at it than we are so we can steal their secrets. And while
they’re finding some promising leads, I gotta say, they’re looking in some pretty weird
places. [Intro] You know how everyone jokes that after some
big global disaster, only cockroaches will survive? Well, we recently found what may
partially explain their famous, and infuriating, tenacity. Research from the University of
Nottingham suggests that certain insects, like roaches and locusts, have brain tissues
that are infused with super-powered antibiotic juju. The researchers found nine different
antibiotic molecules tucked into the roaches’ nervous systems that may be protecting them
from otherwise lethal bacteria. They’re all a type of molecule known as peptides, short
chains of amino acids that make up proteins, kinda like proto-proteins. And these peptides
are specific to the bugs’ brains. They seem to be chemicals that roaches” brain cells
use to communicate with each other, y’know, whenever a cockroach is sitting around thinking
about stuff, which I guess can happen, and although we’re not sure how these peptides
actually work, laboratory tests have shown that they’re incredibly effective at eliminating
some of our least favorite bacteria, like the most dangerous strains of e.coli, which
cause gastrointestinal infections. And even MRSA, a super-resistant type of staphylococcus
bacterium that can cause unstoppable deadly infections in humans, particularly in hospitals.
In lab trials, these roach brain molecules killed over 90% of MRSA bacteria, without
harming any host cells. So I can guess what you’re thinking: shut
up and take my money! Well, hold on a sec, because we’re a bit away from having cockroach
brains on the pharmacy shelves. There’s still loads of technical hurdles to overcome, tests
to conduct, basic things we need to figure out, like how exactly these molecules work.
But roaches aren’t the only hardy animals out there. Alligators are some of the Earth’s
most rugged beasts. They essentially live in cesspool swamps teeming with bacteria and
fungus and other microbes, and more than that, they’re known brawlers. Put just a few territorial
800 pound toothy reptiles together in a dirty swamp, and you will no doubt come out with
some serious bite marks and bloody wounds, even missing limbs. But amazingly, what you
probably won’t find are any infections. This got some bayou scientists to thinkin’!
Dr. Mark Merchant, a biochemist at McNeese State University in Louisiana, helped conduct
a decade long study that investigated what makes alligators so unusually resistant to
bacterial and fungal infection. Turns out, it’s in their blood. An alligator’s
immune system is largely innate, meaning it can fight off harmful micro-organisms without
having any prior exposure to them. They just pop right out of their eggs ready to do battle.
We humans also have some innate immunity, provided by things like our skin and white
blood cells, but a big part of our immunities are adaptive, meaning we often develop a resistance
to specific diseases only after being exposed to them. Which of course is not ideal all
the time, but alligators get to skip this step. Researchers examining blood samples from American
alligators isolated their infection fighting white blood cells and then extracted the active
proteins working in those cells. And these two included a special class of peptides which
seemed to have a knack for weakening the membranes of bacteria, causing them to die. When pitted
against a wide range of bacteria including drug-resistant MRSA, these tough little peptides
proved to be effective killers. They also wiped out 6 of 8 strains of candida albicans,
a type of yeast infection that’s particularly troublesome for AIDS and transplant patients
with weakened immune systems. Such compounds may also be found in similar animals, like
crocodiles, Komodo dragons, and the skins of some frogs and toads. So far, lab trials
have shown that gator blood can kill at least 23 different strains of bacteria including
salmonella, e.coli, staph, and strep infections AND even a strain of HIV. For now, scientists
are working to find the exact chemical structures at work in four of these promising chemicals
and pinpoint which types are best at killing which microbes. One problem so far: high concentrations
of gator blood serum have already been found to be so powerful that they are toxic to human
cells. So other biologists are taking a different approach in the search for the next generation
of antibiotics. Rather than looking at other animals, they’re
exploring strange, new places, like cave soils and deep-sea sediments. Researchers have recently
discovered evidence of promising new fungi strains living way down in hundred million
year old nutrient-starved sediments in the Pacific Ocean. Everyone thought this was a
near-dead zone for life, too harsh and remote an environment for something like fungi to
survive in. Just a decade ago, the only living things known to inhabit such deep sediment
layers were single-celled bacteria and archaea, organisms known to flourish in extreme environments.
But while examining dredged up sediments from as deep as 127 meters into the sea floor,
scientists found fungi of at least eight different types, four of which they successfully cultured
in the lab. Some of the fungi even belonged to the genus Penicillium, which we have to
thank for the development of penicillin. Now, we’re not exactly sure how old these fungi
are, but they are definitely quite old and maybe, more importantly, they appear to have
been living in isolation for eons. If that’s the case, they may have evolved specific and
unusual defenses against bacteria, which, just like their penicillin kin in that famous
petri dish, could end up being a new and powerful source of antibiotics.
And there’s one more strategy that scientists are using, one that works in espionage as
well as in medicine. And that is seeing what the enemy is up to.
While exploring life in strange new places around the world, some biologists are looking
for bacteria that have never been exposed to our drugs, but still appear to be naturally
resistant to them. Wherever we find the most naturally resistant
bacteria, we might also find natural antibiotics that we never knew about.
And here, one of the most promising leads is again in one of the hardest-to-reach places:
New Mexico’s Lechuguilla cave, a place that was isolated from all human contact until
it was discovered in the 1980’s. One of the many fascinating things that scientists
have discovered here is that the cave bacteria seem to be resistant to everything.
Even though they’ve never been exposed to us or our drugs, all of the bacteria have
proven to be resistant to at least one major antibiotic, and many tend to fend off more
than a dozen of the most powerful antimicrobials we have. This suggests to scientists that
the bacteria have evolved to be this way because they live in an environment that’s rich in
naturally occurring antibiotics, ones that the germs we live with up here on the surface
have never encountered. Now we just have to find out what exactly
those compounds are. So look, I’m not going to lie to you: we have
a lot of work to do. While we might discover a new super-drug lurking
in a cave or under the sea or in a cockroach’s head, there’s a big difference between finding
a substance that cleans house in a petri dish and actually putting a new antibiotic in the
vein of a human patient. So the bummer is, as promising as some of
these bold new discoveries may be, none of them has yet yielded an actual marketable
drug. Still, there’s a long list of successful antibiotics
that we’ve managed to derive from strange sources, starting with Dr. Fleming’s rogue
fungus. So if we keep exploring strange new places
and studying how other animals deal with the problems we’re facing, we just might find
the next penicillin before the superbugs get the best of us. Thanks for watching this SciShow Infusion,
especially to our Subbable subscribers. To learn how you can support us in exploring
the world, just go to Subbable.com. And as always, if you want to keep getting smarter
with us, you can go to YouTube.com/SciShow and subscribe.

Cockroaches, Alligators & Other Weird Sources of New Drugs


Antibiotics are one of humankind’s most amazing
discoveries. Ever since that fateful day in 1928 when Scottish physician Alexander Fleming
noticed a funny mold growing in one of his petri dishes, antibiotics have been kicking
bacterial butt. That famous mold, of course, was producing
penicillin, the founding antibiotic superstar, which has since extended the average human
life by at least a decade. It fundamentally changed the face of medicine. Antibiotics,
or antimicrobials, are basically selective poisons designed to either kill or slow the
growth of bacteria to the point where your body’s own immune system can clean up. These
drugs target a specific part of bacteria or some important stage in their development
without damaging the body’s host cells. And they’re really great their job. Until they
aren’t. Lately, antibiotic technology has been having
a hard time keeping pace with bacterial evolution. We’ve talked here on SciShow about how lots
of your die-hard, go-to favorite antibiotics are starting to lose their mojo in the face
of sneaky and rapidly evolving bacteria. The US Centers for Disease Control and Prevention
estimates that at least 2,000,000 Americans became infected with drug-resistant bacteria
in 2012, and 23,000 of them died as a result. These superbugs are deadly serious and could
quickly unleash a global health crisis if we don’t find a way to keep them in check.
The problem is we’ve already hit up many of the most obvious sources of antibiotics, like
fungi, which includes penicillin, and synthetic molecules.
Fortunately, we humans have big, delicious brains, and some of the best of them are hard
at work trying to invent all-new ways to kill dangerous bacteria or find other organisms
on the planet that are better at it than we are so we can steal their secrets. And while
they’re finding some promising leads, I gotta say, they’re looking in some pretty weird
places. [Intro] You know how everyone jokes that after some
big global disaster, only cockroaches will survive? Well, we recently found what may
partially explain their famous, and infuriating, tenacity. Research from the University of
Nottingham suggests that certain insects, like roaches and locusts, have brain tissues
that are infused with super-powered antibiotic juju. The researchers found nine different
antibiotic molecules tucked into the roaches’ nervous systems that may be protecting them
from otherwise lethal bacteria. They’re all a type of molecule known as peptides, short
chains of amino acids that make up proteins, kinda like proto-proteins. And these peptides
are specific to the bugs’ brains. They seem to be chemicals that roaches” brain cells
use to communicate with each other, y’know, whenever a cockroach is sitting around thinking
about stuff, which I guess can happen, and although we’re not sure how these peptides
actually work, laboratory tests have shown that they’re incredibly effective at eliminating
some of our least favorite bacteria, like the most dangerous strains of e.coli, which
cause gastrointestinal infections. And even MRSA, a super-resistant type of staphylococcus
bacterium that can cause unstoppable deadly infections in humans, particularly in hospitals.
In lab trials, these roach brain molecules killed over 90% of MRSA bacteria, without
harming any host cells. So I can guess what you’re thinking: shut
up and take my money! Well, hold on a sec, because we’re a bit away from having cockroach
brains on the pharmacy shelves. There’s still loads of technical hurdles to overcome, tests
to conduct, basic things we need to figure out, like how exactly these molecules work.
But roaches aren’t the only hardy animals out there. Alligators are some of the Earth’s
most rugged beasts. They essentially live in cesspool swamps teeming with bacteria and
fungus and other microbes, and more than that, they’re known brawlers. Put just a few territorial
800 pound toothy reptiles together in a dirty swamp, and you will no doubt come out with
some serious bite marks and bloody wounds, even missing limbs. But amazingly, what you
probably won’t find are any infections. This got some bayou scientists to thinkin’!
Dr. Mark Merchant, a biochemist at McNeese State University in Louisiana, helped conduct
a decade long study that investigated what makes alligators so unusually resistant to
bacterial and fungal infection. Turns out, it’s in their blood. An alligator’s
immune system is largely innate, meaning it can fight off harmful micro-organisms without
having any prior exposure to them. They just pop right out of their eggs ready to do battle.
We humans also have some innate immunity, provided by things like our skin and white
blood cells, but a big part of our immunities are adaptive, meaning we often develop a resistance
to specific diseases only after being exposed to them. Which of course is not ideal all
the time, but alligators get to skip this step. Researchers examining blood samples from American
alligators isolated their infection fighting white blood cells and then extracted the active
proteins working in those cells. And these two included a special class of peptides which
seemed to have a knack for weakening the membranes of bacteria, causing them to die. When pitted
against a wide range of bacteria including drug-resistant MRSA, these tough little peptides
proved to be effective killers. They also wiped out 6 of 8 strains of candida albicans,
a type of yeast infection that’s particularly troublesome for AIDS and transplant patients
with weakened immune systems. Such compounds may also be found in similar animals, like
crocodiles, Komodo dragons, and the skins of some frogs and toads. So far, lab trials
have shown that gator blood can kill at least 23 different strains of bacteria including
salmonella, e.coli, staph, and strep infections AND even a strain of HIV. For now, scientists
are working to find the exact chemical structures at work in four of these promising chemicals
and pinpoint which types are best at killing which microbes. One problem so far: high concentrations
of gator blood serum have already been found to be so powerful that they are toxic to human
cells. So other biologists are taking a different approach in the search for the next generation
of antibiotics. Rather than looking at other animals, they’re
exploring strange, new places, like cave soils and deep-sea sediments. Researchers have recently
discovered evidence of promising new fungi strains living way down in hundred million
year old nutrient-starved sediments in the Pacific Ocean. Everyone thought this was a
near-dead zone for life, too harsh and remote an environment for something like fungi to
survive in. Just a decade ago, the only living things known to inhabit such deep sediment
layers were single-celled bacteria and archaea, organisms known to flourish in extreme environments.
But while examining dredged up sediments from as deep as 127 meters into the sea floor,
scientists found fungi of at least eight different types, four of which they successfully cultured
in the lab. Some of the fungi even belonged to the genus Penicillium, which we have to
thank for the development of penicillin. Now, we’re not exactly sure how old these fungi
are, but they are definitely quite old and maybe, more importantly, they appear to have
been living in isolation for eons. If that’s the case, they may have evolved specific and
unusual defenses against bacteria, which, just like their penicillin kin in that famous
petri dish, could end up being a new and powerful source of antibiotics.
And there’s one more strategy that scientists are using, one that works in espionage as
well as in medicine. And that is seeing what the enemy is up to.
While exploring life in strange new places around the world, some biologists are looking
for bacteria that have never been exposed to our drugs, but still appear to be naturally
resistant to them. Wherever we find the most naturally resistant
bacteria, we might also find natural antibiotics that we never knew about.
And here, one of the most promising leads is again in one of the hardest-to-reach places:
New Mexico’s Lechuguilla cave, a place that was isolated from all human contact until
it was discovered in the 1980’s. One of the many fascinating things that scientists
have discovered here is that the cave bacteria seem to be resistant to everything.
Even though they’ve never been exposed to us or our drugs, all of the bacteria have
proven to be resistant to at least one major antibiotic, and many tend to fend off more
than a dozen of the most powerful antimicrobials we have. This suggests to scientists that
the bacteria have evolved to be this way because they live in an environment that’s rich in
naturally occurring antibiotics, ones that the germs we live with up here on the surface
have never encountered. Now we just have to find out what exactly
those compounds are. So look, I’m not going to lie to you: we have
a lot of work to do. While we might discover a new super-drug lurking
in a cave or under the sea or in a cockroach’s head, there’s a big difference between finding
a substance that cleans house in a petri dish and actually putting a new antibiotic in the
vein of a human patient. So the bummer is, as promising as some of
these bold new discoveries may be, none of them has yet yielded an actual marketable
drug. Still, there’s a long list of successful antibiotics
that we’ve managed to derive from strange sources, starting with Dr. Fleming’s rogue
fungus. So if we keep exploring strange new places
and studying how other animals deal with the problems we’re facing, we just might find
the next penicillin before the superbugs get the best of us. Thanks for watching this SciShow Infusion,
especially to our Subbable subscribers. To learn how you can support us in exploring
the world, just go to Subbable.com. And as always, if you want to keep getting smarter
with us, you can go to YouTube.com/SciShow and subscribe.

#TomorrowsDiscoveries: Preventing Bacterial Infections – Lloyd Miller, M.D., Ph.D.

#TomorrowsDiscoveries: Preventing Bacterial Infections – Lloyd Miller, M.D., Ph.D.


>>Lloyd: Many bacteria
are becoming increasingly resistant to antibiotics,
which complicates treatment and creates a serious
threat to public health. Methicillin-resistant Staph
aureus, commonly known as MRSA, causes nearly 90% of
bacterial skin infections, such as abscesses and cellulitis. These infections result in
over 10 million outpatient and emergency room visits and
500,000 hospital admissions per year in the United States. My name is Lloyd Miller, and
to provide an alternative to antibiotics, my research group studies the specific immune
responses that help clear MRSA skin infections. We are basically looking for
ways to engage the body’s own defenses to fight off
these dangerous infections. We hope that our
discoveries will translate to vaccines and
immunotherapies to combat MRSA and other antibiotic-resistant pathogens. (light music)

Infection, Contamination, and Nosocomial Control must see Video

Infection, Contamination, and Nosocomial Control must see Video


There are over two million hospital acquired
infections each year and 80,000 deaths per year are attributed to infections developed
in hospitals. The blood pressure cuff is the only medical
device not routinely cleaned or disaffected between patients
All research studies conclude that reused blood pressure cuffs are contaminated and
are a source for cross contamination even reused disposable cuffs
Approximately 440,000 patients that enter the hospital and will contract the hospital
acquired infection at a cost estimated to be $10,000,000,000 per year. If only 1% of
these infections caused by contaminated blood pressure cuffs that cost would be $100,000,000
per year Cuff-Guard is the only disposable cover for
blood pressure cuffs Place the contaminated cuff inside the Cuff-Guard
Pull the two sided tape Seal like an envelope in seconds
Now you have an uncontaminated cuff to place on your patient to prevent the spread of disease Make sure that you are protected

10 Most Infectious Diseases

10 Most Infectious Diseases


[Background Music Starts] From slowly evolving illnesses, to those imminently
fatal death sentences, we count down the 10 most infectious diseases. NUMBER 10: Rabies
Rabies is fatal if not treated immediately. You contact Rabies typically after being bitten
by an animal (or feasibly another human) that has rabies. The thing is, you should seek
treatment any time you are bitten, because the chance of surviving Rabies if treatment
begins after symptoms pop up is about 8%. Those aren’t very good odds. Ever heard
of ‘foaming at the mouth’? That’s Rabies. The disease kills about 55,000 people every
year, and people who contract the disease must live with vicious side effects like acute
pain, violent movements, and mania. NUMBER 09: Smallpox
There’s a reason why we worked so hard to rid the world of Smallpox. Once you have Smallpox,
your body, including your mouth and throat, will become littered with pussing, fluid filled
bumps. The disease has killed 300 million since 1800 alone, but it has been around since
about 10,000 BC. Just pray that you don’t get hemorrhagic Smallpox, which causes bleeding
to occur under your skin, which sours your body, earning it the nickname, ‘black pox’. NUMBER 08: Tuberculosis
Be careful when you see someone sneeze, because that’s how Tuberculosis spreads. It’s
no laughing matter, either, as over one third of the population is infected with Tuberculosis.
However, this is likely just a latent form and the symptoms will never arrive. If they
do, however, which is about a one in ten probability, you’re in for a rough ride. Coming in at
a 50% mortality rate and killing 1.5 million people a year, Tuberculosis’s main target
is usually the lungs, but will move around attacking other organs, including a male’s
testicles. If you have a weak heart, mute this for a second—Tuberculosis can, at times,
erode the pulmonary artery, causing your lungs to fill with blood. NUMBER 07: Influenza
Influenza, more commonly referred to as the flu, is seen as less of a threat today simply
because we have the means to treat it. But, that wasn’t always the case. In today’s
day and age, people will only get the flu a couple times and get over it pretty quickly
with some over the counter drugs or an annual flu shot. However, in 1918, things were a
little different. The Spanish Flu killed 100 million people—including many young and
healthy people. The reason for this was because the flu could turn an immune system against
the patient’s body, meaning the healthier you were, the more deadly the virus became.
These days, strains of the flu are appearing to grow stronger, so let’s hope we don’t
see anything like the Spanish Flu any time soon. NUMBER 06: Anthrax
Yes—Anthrax makes this list. Why? It’s a bacterial infection that’s super lethal.
Before Anthrax became a household name after the attack on September 11th, 2001, it was
still just as lethal, and wreaked havoc all over the world. Anthrax is insanely fatal.
Even one of the ingredients is aptly named, ‘Lethal Toxin’. Anthrax is most dangerous
through inhalation, ingestion, or through broken skin. Diarrhea is usually the first
symptom, with death following within a few days to two weeks. Anthrax is one of history’s
worst villains. An island in Scotland was marked uninhabitable for 50 years after Anthrax
contaminated the area. Burning is one of the only ways to kill Anthrax—all around, it’s
a vicious beast. NUMBER 05: Cholera
Cholera is a terrifying infectious disease that has struck fear in the heart of man all
throughout history. Cholera spreads through contaminated food and water—allowing the
disease to spread like fire. It has killed millions, and to this day, kills 120,000 people
or more each year. Cholera can cause patients to produce 5 gallons of diarrhea a day. Today,
if you can find treatment, you only have about a one percent chance of dying. However, there
are strains that can kill within 2 hours. NUMBER 04: Bubonic Plague
If there is one disease that can top Cholera, it’s the Bubonic Plague. Here’s why. Bubonic
Plague has one death toll at 100 million that swept Europe in the Middle Ages, and then
another death toll from the Roman Empire that knocked out 50 million people. The Roman Empire
at its peak topped out at an estimated 90 million people—accounting for 20% of the
world population at the time. That means the Bubonic Plague decimated a huge portion of
the globe in one swoop. Sadly, such a massive disease is transmitted by simple rat fleas—which
also die. Sad, we know. The Japanese also used the Bubonic Plague as a weapon against
the Chinese in World War II. If you think that’s horrific, imagine the fourteenth
century—where diseased bodies were flung over the walls of cities under attack NUMBER 03: AIDS
As of today, more than 30 million people have died of AIDS, with another 40 million listed
as infected. There’s still no cure in sight, and current methods of treatment can be very
expensive. What makes AIDS so terrifying is that it makes the human body far more susceptible
to Tuberculosis, hepatitis, and several forms of cancer. We’ll do our part and spend the
next few moments saying something very important. Safe sex will save your life. You do not want
AIDS. Using protection against STD’s and HIV is the smartest thing you can possibly
do. Be safe. Always. NUMBER 02: Ebola
Ebola is incredibly lethal if not treated immediately. Some outbreaks have seen upwards
of 90% and higher mortality rates. Native to central Africa, cases in the 1970’s started
cropping up due to what was found out to be indigenous wildlife. But, that’s about as
specific as it gets. No one truly knows where Ebola came from. Humanity believes that some
animal species carries it, but we have no idea what species that is. If you contract
Ebola, pain can start anywhere in the body—resulting in multiple organ failure and certain death
within most untreated cases. Those who do get treated, however, can make a full recovery.
No one has used Ebola as a biological weapon yet, though that is a major fear that permeates
all throughout the world. NUMBER 01: MRSA
We’re not sure why this is, or how it came to be, but the disease makes modern medicines
unusable. MRSA contains what’s known as a ‘Superbug’ which causes boils and lacerations
of the skin—and can kill within 24 hours. All strains of MRSA that exist are resistant
to our modern day antibiotics. Why? These strains, unlike other, more treatable diseases,
are far more pathogenic—and brutal. MRSA can cause a flesh eating condition, systemic
infections, a flesh eating infection that targets lung tissue, bone infections, bloodstream
infections, and an infection that targets the heart. The scariest part is these diseases
show that they’re getting stronger. Perhaps the use of antibiotics by mankind will come
at a terrifying price.

CDC media briefing on healthcare-associated infections, March 26, 2014

CDC media briefing on healthcare-associated infections, March 26, 2014


>>>GOOD MORNING.
I’M BARBARA REYNOLDS. WE’LL BEGIN IN JUST ONE MINUTE.
FOLLOWING A BRIEF VIDEO.>>>On any given day, about 1 in 25 hospital patients
have an infection caused by their medical care. Almost half of these
patients are 65 or older. There are 5 places where
patients are most likely to get infections: in the
bloodstream, the urinary tract, the gut, and the two most
common places are the site of surgery and the lungs. The germs most likely to cause
healthcare associated infections include: C. difficile, or
deadly diarrhea, Staph, including the drug-resistant
type known as MRSA, a family of germs known
as Enterobacteriaceae, that include CRE the “nightmare
bacteria,” Enterococcus, which can be resistant to
an important antibiotic, vancomycin, and Pseudomonas,
which can cause infections of the lungs and bloodstream. One in every 9 patients who gets
an infection will die during their hospitalization. Over the last several years,
great progress has been made in preventing some infections. For example, bloodstream
infections in patients with central lines
have been nearly cut in half in the last 5 years. But more work needs to be done. CDC’s goal is to eliminate
all healthcare-associated infections. We work 24/7 to save
lives and protect people.>>>AGAIN, WELCOME TO CDC’S MEDIA BRIEFING ON HEALTH
CARE-ASSOCIATED INFECTIONS. I’D LIKE TO WELCOME NOT ONLY
THOSE, OUR GUESTS IN THE ROOM IN MEDIA, BUT ALSO THOSE OF US
JOINING US WEBCAST AND SATELLITE TODAY.
I’D LIKE TO INTRODUCE OUR TWO SPEAKERS.
FIRST SPEAKING WILL BE DR. MICHAEL BELL, AN EXPECT IN
INFECTION PREVENTION AND PATIENT SAFETY.
DR. BELL TRAVELED THE WORLD PROVIDING INFECTION PREVENTION
CONSULTATION FOR OUTBREAKS OF COMMON GERMS AND EXOTIC VIRUSES
LIKE EBOLA. DR. BELL IS CURRENTLY THE DEPUTY
DIRECTOR OF THE CDC’S DIVISION OF HEALTH CARE QUALITY
PROMOTION. THE DIVISION IS RESPONSIBLE FOR
PATIENT SAFETY ISSUES IN MEDICAL FACILITIES.
WITH DR. BELL’S LEADERSHIP, THE DIVISION CREATES INFECTION
PREVENTION GUIDELINES, RESEARCHES NEW PREVENTION
STRATEGIES, INVESTIGATES OUTBREAKS IN HEALTH CARE
FACILITIES AND PROVIDES WORLD CLASS LABORATORY EXPERTISE FOR
MICROBES THAT CAUSE HEALTH CARE RELATED INFECTIONS, INCLUDING
ANTIBIOTIC RESISTANT THREATS. JOINING US ALSO TODAY IS
VICTORIA NAHOOM OF ATLANTA, EXECUTIVE DIRECTOR OF THE SAFE
CARE CAMPAIGN. SHE HAS A COMPELLING STORY TO
TELL. AND WE ARE SO PLEASED THAT
VICTORIA IS ABLE TO JOIN US TODAY TO REPRESENT PATIENTS
NATIONALLY WHO HAVE BEEN IMPACTED BY HEALTH CARE
ASSOCIATED INFECTIONS. AFTER THEIR BRIEF REMARKS WE’LL
OPEN IT UP FOR QUESTIONS. DR. BELL?
>>>GOOD AFTERNOON. SOONER OR LATER EVERYONE IS
LIKELY TO BECOME A PATIENT SOMEWHERE.
WE GO TO THE HOSPITAL HOPING TO GET BETTER, AND IN MANY CASES WE
DO. BUT NOT ALWAYS.
AS A DOCTOR I WANT ALL OF MY PATIENTS TO BECOME WELL AND STAY
HEALTHY. BUT SOME THINGS STAND IN THE
WAY, INCLUDING HEALTH CARE ASSOCIATED INFECTIONS.
CDC IS KNOWN FOR HANDLING OUTBREAKS, BUT IT’S MORE
IMPORTANT TO BE SCANNING THE HORIZON FOR THE NEXT IMPORTANT
THREAT THAT NEEDS TO BE TACKLED. WE UNDERTOOK A MAJOR STUDY TO
FIND OUT WHAT KINDS OF INFECTIONS ARE AFTFECTING
PATIENTS IN HOSPITALS. THE REPORT SHOWS THAT AS A
NATION WE ARE MOVING IN THE RIGHT DIRECTION.
BUT THERE’S A GREAT DEAL OF WORK STILL TO BE DONE.
DESPITE THE PROGRESS WE’VE SEEN, THREE QUARTERS OF A MILLION
PATIENTS EVERY YEAR END UP WITH HEALTH CARE ASSOCIATED
INFECTIONS. WE FOUND THAT ON ANY GIVEN DAY,
AS YOU SAW IN THE GRAPHIC, ONE OUT OF 25 HOSPITALIZED PATIENTS
HAS AN INFECTION. AND OF THOSE PEOPLE, 1 OUT OF 9
GO ON TO DIE THIS IS NOT A MINOR ISSUE.
THE COMPARISONS YOU’RE LIKELY TO WANT TO MAKE ARE WITH THE 2007
REPORT THAT WAS BASED ON HISTORICAL INFORMATION GOING
BACK INTO THE LATE ’90s. I WANT TO CAUTION YOU THAT THIS
IS NOT NECESSARILY APPLES TO APPLES.
IT’S MORE LIKE APPLES TO PEARS. YOU CAN SEE THERE’S A TREND FOR
THINGS BEING BETTER, BUT THE MINOR DETAILS PROBABLY ARE NOT
COMPARABLE. THE REPORT WE’RE RELEASING TODAY
IS IMPORTANT BECAUSE IT WAS DESIGNED TO GATHER INFECTION.
I THINK THE QUALITY OF THOSE DATA ARE BETTER THAN THOSE WE
HAD TO WORK WITH BEFORE. THE REPORT SOUNDS THE ALARM
ABOUT THE THREATS WE NEED TO BE ADDRESSING.
IT TELLS US, AS YOU SAW LUNG INFECTION, GUT INFECTION,
INFECTIONS RELATED TO SURGERY AND URINARY CATHETERS ARE AT TOP
OF THE LIST OF THINGS CAUSING PROBLEMS FOR HOSPITAL PATIENTS.
IT SHINES THE LIGHT ON SEVERAL IMPORTANT PATHOGENS, THE GERMS
RESPONSIBLE FOR MANY OF THESE INFECTIONS.
AT THE TOP OF THE LIST IS CDIF IT CAUSES ANTIBIOTIC RESISTANT
DIARRHEA. TODAY THE TYPE OF BACTERIA
SPREAD IN THIS COUNTRY HAS SUCH A STRONG TOXIN, THIS IS A VERY
SEVERE INFECTION REQUIRING COLON REMOVAL IN SOME CASES.
STAPH INFECTIONS ARE A PROBLEM, INCLUDING MRSA.
AND FINALLY WE’RE SEEING A LOT OF INFECTIONS RELATED TO THE
ACA. THIS IS A FAMILY OF BACTERIA HAS
INCLUDES E. COLI, MANY COMMON ORGANISMS THAT LIVE IN THE GUT
AND NEED TO BE THERE FOR US TO BE HEALTHY.
THE CHALLENGE THAT WE SEE IS THAT SOME OF THOSE BACTERIA, THE
NIGHTMARE BACTERIA ARE NOW COMPLETELY UNTREATABLE.
THAT MEANS THAT AS A DOCTOR, I HAVE NOTHING LEFT I CAN OFFER A
PATIENT WHO HAS AN INFECTION LIKE THIS IN THE HOSPITAL.
THE MICROBES WE’RE TALKING ABOUT NOW ARE ALSO IN LAST YEAR’S
ANTIBIOTIC RESISTANCE THREAT REPORT.
THAT IS THE REPORT WE RELEASED LOOKING AT HOW MUCH OF A PROBLEM
ANTIBIOTIC RESISTANCE IS. THEY’RE ALSO AT THE CENTER OF
THE PRESIDENT’S FY-15 BUDGET INITIATIVE, WHERE HE’S TRYING TO
DRIVE PROGRESS BY CUTTING SOME OF THESE INFECTIONS BY 50% OR
MORE IN FIVE YEARS. THIS IS A MAJOR AND IMPORTANT
INVESTMENT IN MAKING SURE HOSPITAL CARE REMAINS SAFE.
IT’S NOT ALL BAD NEWS. SOME SUCCESSES WE’RE SEEING ARE
IN PROTECTING THE MOST FRAGILE PATIENTS, THE PATIENTS IN
INTENSIVE CARE UNITS. WE’VE SEEN GOOD PROGRESS
PREVENTING BLOOD STREAM INFECTIONS RELATED TO CENTRAL
LINES. CENTRAL LINES ARE THE PLASTIC
CATHETERS THAT GO OFF OF THE SKIN IN THE NECK AND INTO THE
MAJOR VESSELS OF THE HARD. WE NEED THEM TO PROVIDE GOOD
MEDICAL CARE TO PROVIDE MEDICATION, THEY’RE ALSO A
FREEWAY FOR BACTERIA TO GET INTO THE BLOOD STREAM.
SO, MAKING SURE WE HANDLE THOSE CATHETERS PERFECTLY EVERY TIME
IS A MAJOR PUSH THAT WE’VE MADE. WE HAVE SEEN THAT THE NUMBER OF
THESE INFECTIONS HAVE GONE DOWN BY ALMOST HALF SINCE 2008.
THIS IS GREAT PROGRESS. THERE’S MORE WORK TO BE DONE.
S THERE’S ALSO PROGRESS IN THE
INFECTIONS IN SURGERY. THERE’S BEEN ABOUT A 20%
REDUCTION IN INFECTIONS AFTER SURGERY SINCE 2008.
IS 20% ENOUGH? I DON’T THINK SO BUT THE
PROGRESS IS MOVING IN THE RIGHT DIRECTION.
IN CONTRAST, URINARY TRACT INFECTIONS RELATED TO CATHETERS
IN THE BLADDER ARE MORE STUBBORN.
WE ARE NOT SEEING THE SAME RAPID PROGRESS.
IN A WAY, MAYBE THAT’S NOT A BIG DEAL, BUT THEY’RE NOT AS SEVERE
AN INFECTION. PEOPLE DON’T TEND TO DIE
IMMEDIATELY FROM A BLADDER INFECTION LIKE THEY DO FROM A
BLOOD STREAM INFECTION. BLADDER STREAM INFECTIONS ARE A
BROAD DRIVER OF BROAD SPECTRUM ANTIBIOTIC USE.
WHEN BROAD SPECTRUM ANTIBIOTICS ARE GIVEN, IT WIPES OUT THE
BACTERIA IN THE GUT AND OPENS UP THE PROBLEM FOR CDIF.
SO YOU THINK YOU’RE HAVING A TRIVIAL INFECTION WITH THE
BLADDER, THEN YOU’RE FIGHTING FOR YOUR LIFE.
WE ARE SEEING A STALLING OUT OF PROGRESS IS SOMETHING THAT WE’RE
WORKING ON SPECIFICALLY. THE CHALLENGE WITH ANTIBIOTIC
RESISTANCE CAN’T BE OVERSTATED. WE FOUND THAT OVER HALF OF
HOSPITALIZED PATIENTS END UP GETTING AN ANTIBIOTIC AT SOME
POINT. THIS IS A HUGE AMOUNT OF
ANTIBIOTIC PRESSURE. WE’RE FOCUSING ON IMPROVING THE
PRESCRIBING OF ANTIBIOTICS SPECIFICALLY BECAUSE THESE
NIGHTMARE BACTERIA AND DEADLY DIARRHEA ARE SUCH A THREAT TO
PATIENT HEALTH. WE WANT TO SEE EVERY HOSPITAL IN
THE COUNTRY HAVING A STRONG ANTIBIOTIC STEWARDSHIP PROGRAM
SO THEY CAN MAKE SURE ALL PRESCRIPTIONS ARE AS SOUND AND
APPROPRIATE AS POSSIBLE. SO HOW ELSE DO WE USE THE
INFORMATION THAT WE’RE REPORTING?
THE DATA WE PROVIDE AT CDC DRIVES ACTION.
AT THE STATE AND FEDERAL LEVELS WE USE THIS DATA TO FIND THE
FACILITIES THAT ARE STRUGGLING WITH ONE OR MORE TYPES OF
INFECTION. THEN WE TRY TO TARGET RESOURCES
TOWARDS THOSE AREAS. USING THIS TARGETED APPROACH, WE
HAVE SEEN SEVERAL SUCCESSES AT THE STATE LEVEL.
FOR EXAMPLE, IN FLORIDA, THERE’S A 35% REDUCTION OF THOSE
CATHETER-ASSOCIATED URINARY TRACT INFECTIONS.
THIS IS GREAT. IN GEORGIA, WE HAVE CUT BLOOD
STREAM INFECTIONS IN BABIES IN ICUs BY ALMOST A HALF THIS
TARGETED APPROACH IS A WAY TO USE LIMITED RESOURCES BECAUSE NO
ONE IS FLUSH WITH MONEY RIGHT NOW.
AS EFFECTIVELY AS POSSIBLE, TARGETING THE BIGGEST PART OF
THE PROBLEM. LASTLY, I’D LIKE TO SAY A WORD
ABOUT WHAT CAN YOU DO AS A PATIENT.
I’M ALWAYS ASKED WHAT IS IT THAT I CAN DO TO PROTECT MYSELF IN
THE HOSPITAL OR A LOVED ONE? THE SHORT ANSWER IS ASK
QUESTIONS. IT’S HARD, BUT YOU HAVE TO ASK
QUESTIONS. THE QUESTIONS TO ASK ARE THINGS
LIKE HAVE YOU WASHED YOUR HANDS? IT SOUNDS BASIC, BUT IT’S
IMPORTANT. AND YOU CAN ASK IT IN A NICE
WAY. YOU CAN SAY I’M SURE YOU JUST
WASHED YOUR HANDS T WOULD MEAN A LOT TO ME AND MY MOTHER IF YOU
WOULD WASH THEM AGAIN. WE’RE VERY WORRIED ABOUT
INFECTIONS IN THE HOSPITAL. YOU CAN ASK QUESTIONS ABOUT THE
CATHETERS YOU HAVE. IF YOU HAVE A CATHETER IN PLACE,
ASK EVERY DAY CAN THE CATHETER COME OUT TODAY?
IN FACT, BEFORE YOU HAVE A CATHETER PUT IN, WHEN YOU’RE
TALKING TO YOUR SURGEON, ASK HER HOW LONG WILL I HAVE TO HAVE A
CATHETER AFTER MY PROCEDURE? IF SHE SAYS TWO DAYS, STARTING
DAY TWO, START ASKING CAN THE CATHETER COME OUT TODAY?
THEY SAID IT WOULD COME OUT TODAY.
FINALLY ASK ABOUT TESTING. ARE YOU DOING TESTS TO MAKE SURE
I’M ON THE RIGHT ANTIBIOTIC? IF SO, YOU KNOW, TELL ME ABOUT
IT. THESE QUESTIONS ARE VERY HARD TO
ASK IF YOU’RE A PATIENT RECEIVING CARE.
YOU HAVE PLENTY TO THINK ABOUT. I THINK IT’S A GOOD IDEA TO
BRING A FRIEND OR FAMILY MEMBER WHOSE MAIN JOB IT IS TO BE THE
PERSISTENT ASKER OF THOSE QUESTIONS.
BECAUSE AT THE END OF THE DAY, THE DOCTORS, THE NURSES, THE
ENTIRE MEDICAL TEAM WANTS YOU TO GET BETTER.
EVEN THOUGH IT MIGHT BE ANNOYING FOR A MINUTE, IT’S A HELPFUL
REMINDER TO HAVE HAND WASHING, CATHETER REMOVAL AND APPROPRIATE
ANTIBIOTIC USE AT THE TOP OF THEIR MINDS.
THERE’S A HUGE AMOUNT OF INFORMATION IN THESE REPORTS
WE’RE RELEASING TODAY. I DON’T WANT TO LOSE SIGHT OF
THE FACT THAT EVERY NUMBER YOU SEE IN THE REPORT IS A PERSON.
THESE ARE PATIENTS WHO WENT TO THE HOSPITAL TO RECEIVE CARE,
AND IN SOME CASES THEY GOT INFECTIONS THAT KEPT THEM IN THE
HOSPITAL LONGER, IN A FEW CASES THEY DIED.
THIS IS SOMETHING THAT DRIVES THE EFFORTS AT CDC TO ELIMINATE
HEALTH CARE-ASSOCIATED INFECTIONS.
I WISH I COULD BE INTRODUCING OUR NEXT SPEAKER UNDER DIFFERENT
CIRCUMSTANCES, BUT I’M HONORED TO SHARE THE PODIUM TODAY WITH
MRS. VICTORIA NAHUM FROM THE SAFE CARE CAMPAIGN.
SHE AND HER HUSBAND ARMANDO ARE STRONG ADVOCATES FOR PATIENT
SAFET SAFETY.
>>THANK YOU, DR. BELL. GOOD AFTERNOON.
IN AN 11-MONTH PERIOD BETWEEN NOVEMBER OF 2006 AND OCTOBER OF
2007, THREE DIFFERENT MEMBERS OF MY FAMILY REPRESENTING THREE
DIFFERENT GENERATIONS OF MY FAMILY WERE INFECTED BY HEALTH
CARE ASSOCIATED INFECTIONS IN THREE DIFFERENT HOSPITALS IN
THREE DIFFERENT STATES. SO AT THE END OF THAT TIME WE
LOST OUR SON JOSHUA TO A DRUG RESISTANT GRAM NEGATIVE
INFECTION THAT SURROUNDED HIS BRAIN AND IT WAS SO VIRULENT IT
PUSHED PART OF HIS BRAIN INTO HIS SPINAL COLUMN.
IN DOING SO IT EFFECTIVELY RENDERED HIM A PERMANENT
VENTILATOR DEPENDENT QUADRIPLEGIC.
SO TWO WEEKS LATER, JOSHUA DIED FROM HIS INFECTION.
HE WAS ONLY 27. SO, IN OUR GRIEF IN TRYING TO
UNDERSTAND, YOU KNOW, HOW AND WHY THESE INFECTIONS WERE SO
FREQUENTLY APPEARING ALL OVER THE COUNTRY, MY HUSBAND ARMANDO
AND I REACHED OUT TO THE CDC FOR ANSWERS IN ATLANTA.
THEY WERE CLOSE BY. I WANT TO TELL YOU GRACIOUSLY
THEY MET WITH US. IN THE EIGHT YEARS SINCE OUR
ORIGINAL MEETING, THEY HAVE BECOME GREAT PARTNERS AND
MENTORS AND ENCOURAGERS IN OUR WORK TO PREVENT OTHER FAMILIES
FROM EXPERIENCING SIMILAR FATES. OUR ORGANIZATION, SAFE CARE
CAMPAIGN, WORKS WITH HOSPITALS AND HEALTH CARE SYSTEMS TO HELP
THEM DO JUST THAT. THE NEW INFECTION NUMBERS, THE
DATA TODAY REPRESENTS A FORWARD STRIDE IN OUR SHARED WORK.
COMPONENTS INCLUDING GUIDELINES TURNED INTO CHECKLISTS AND DATA
TRANSPARENCY AS WELL AS PAY FOR PERFORMANCE INITIATIVES HAVE
HELPED PREVENT INFECTION, UNNECESSARY HARM AND MANY TRAGIC
DEATHS. WHILE INWARDLY I BREATHE A SMALL
SIGH OF RELIEF THAT ANNUAL INFECTIONS AND MORTALITIES ARE
DIMINISHING, I REMAIN EXTREMELY CAUTIOUS REGARDING THE GROWING
THREAT OF ANTIBIOTIC RESISTANCE AND THE DIRE IMPACT OF ITS
POTENTIAL DANGER TO AMERICAN HEALTH CARE.
TODAY I WANT PEOPLE, HEALTH CARE WORKERS AND PATIENTS ALIKE TO
UNDERSTAND THEY HAVE THE POWER. YOU GUYS HAVE THE POWER TO
PREVENT HEALTH CARE ASSOCIATED INFECTIONS.
PROFESSIONAL CAREGIVERS CAN MAKE THE DEFINITIVE DIFFERENCE BY
PRACTICING COMPULSIVE HAND HYGIENE AND ALWAYS FOLLOWING
OTHER BEST PRACTICES AT THE BETSIDE.
PATIENTS, PATIENTS CAN PREVENT THEIR OWN INFECTIONS AND
POTENTIAL INFECTIONS IN LOVED ONES BY DOING EASY THINGS LIKE
DR. BELL SUGGESTED WHEN HE WAS UP HERE A FEW MINUTES AGO.
THINGS LIKE ASKING QUESTIONS, INSISTING ON PROPER HAND HYGIENE
EVERY TIME BY ANYONE WHO TOUCHES THEM, EVEN FAMILY MEMBERS.
ESPECIALLY THEIR DOCTOR. AND EDUCATING THEMSELVES ON HOW
TO SAFELY RECEIVE MEDICAL CARE — THIS IS REALLY
IMPORTANT. YOU DON’T JUST SLAP DOWN AND SAY
TAKE CARE OF ME. YOU HAVE TO NAVIGATE WHAT WILL
HAPPEN TO YOU. IN DOING SO, THAT CAN SAVE YOUR
LIFE. THANKFULLY WE ARE REALIZING ONCE
AND FOR ALL WE’RE ALL IN THIS TOGETHER YET OUR SINGULAR AND
VERY PERSONAL ROLES AND HOW WE DELIVER AS WELL AS RECEIVE CARE
LEAVES US ACCOUNTABLE FOR OUR OWN ACTIONS.
THANK YOU SO MUCH. WELL, I HOPE YOU APPRECIATE
AS MUCH AS I DO THE COLONURAGE CONVICTION THAT IT TAKES TO
SHARE THAT STORY. IT’S WHY CDC HAS MADE THIS SUCH
A HIGH PRIORITY. DIANE, ON THE PHONE, IF YOU
COULD GIVE INSTRUCTIONS TO CALLERS, I WILL TAKE QUESTIONS
NOW FROM THE ROOM. THANK YOU.
TO ASK A QUESTION, PLEASE PRESS STAR 1.
YOU WILL BE PROMPTED TO RECORD YOUR NAME.
TO WITHDRAW YOUR REQUEST, PLEASE PRESS STAR 2.
ONE MOMENT, PLEASE, WHILE WE WAIT FOR THE FIRST QUESTION.
>>ERIN FROM NBC. THE STATISTIC OF 1 IN 9 PATIENTS
WHO DIE, I’M ASSUMING THAT’S AS A RESULT OF THE HOSPITAL
ACQUIRED INFECTION, IT WASN’T ANOTHER COMORBIDITY THAT
OCCURRED? THAT’S A PERFECT QUESTION.
NO. OF ALL THE PATIENTS WHO HAD
INFECTIONS 1 OUT OF 9 OF THEM WENT ON TO DIE DURING THEIR
HOSPITAL STAY. THERE’S A POSSIBILITY THAT
SOMETHING ELSE WAS CONTRIBUTING TO THAT DEATH, BUT IT’S
DIFFICULT TO TEASE THAT OUT. SO WE’VE SIMPLIFIED THE NUMBERS
1 IN 9. THE DATA THAT YOU’RE
PRESENTING, DID ANY STATES STAND OUT AS PERFORMING WELL WITH
REDUCING INFECTIONS? ANY STATES THAT PERFORMED WORSE?
DO YOU HAVE THAT COMPARISON? I WISH THERE WERE.
IF THERE WAS A PERFECT STATE, WE COULD COPY EVERYTHING THEY’RE
DOING AND SPREAD IT ACROSS THE OTHER 49.
IF THERE WAS ONE THAT WAS PARTICULARLY TERRIBLE, WE COULD
PUT ALL OF OUR RESOURCES THERE. AS IT TURNS OUT, STATE BY STATE,
SOME PLACES ARE HAVING SUCCESS WITH SOME INFECTIONS, NOT
OTHERS. IT’S A VERY MIXED PICTURE.
OTHER QUESTIONS IN THE ROOM? DIANE, DO WE HAVE A QUESTION ON
THE PHONE, PLEASE? YES, WE DO.
WE HAVE A QUESTION FROM MIKE STOBE, ASSOCIATED PRESS.
YOUR LINE IS OPEN. Caller: THANK YOU FOR TAKING
MY QUESTION. YOUR ANNOUNCEMENT TODAY COULD BE
TAKEN BY SOME AS GOOD NEWS. DAN, WE JUST LOST MIKE ON THE
OVERHEAD. PERHAPS WE LOST DIANE AS WELL.
>>ONE MOMENT. WE’LL GET HIM RIGHT BACK ON THE
LINE AGAIN. OKAY.
>>BEAR WITH ME. YOUR LINE IS OPEN, MIKE.
>>Caller: CAN Y’ALL HEAR ME? YES.
>>Caller: THANK YOU FOR TAKING THE QUESTION.
THIS — WHAT YOU PRESENTED TODAY COULD BE SEEN BY SOME AS GOOD
NEWS. THESE ARE NUMBERS THAT SUGGEST
ESTIMATES THAT SUGGESTED THAT THERE WERE NEARLY 2 1/2 TIMES AS
MANY HOSPITAL INFECTIONS IN A YEAR AS THE NUMBERS YOU
PRESENTED FROM THE 2011 SURVEY. I GUESS I WAS WONDERING IF YOU
COULD TALK A BIT MORE ABOUT THE CONTEXT OF THIS DATA?
WHERE ARE WE IN THE EVOLUTION OF DATA COLLECTION?
YOU SAID A LITTLE BIT ABOUT THAT.
YOU TALKED ABOUT THE APPLES AND PEARS, BUT ARE THESE REALLY THE
MOST SOLID NUMBERS WE’VE HAD? AND IF THERE HAVE BEEN
IMPROVEMENTS IN FIGHTING HOSPITAL INFECTIONS, COULD YOU
SAY A LITTLE MORE ABOUT WHAT GENERALLY TYPE OF MEASURES HAVE
ACCOUNTED, FOR EXAMPLE, THE IMPROVEMENT IN BLOOD STREAM
INFECTIONS THAT YOU MENTIONED? IF YOU COULD ADDRESS THAT.
THANKS. SURE.
SO, FIRST AND FOREMOST, THIS IS PROBABLY THE BEST QUALITY OF
DATA WE’VE HAD IN A VERY LONG TIME TO LOOK AT THE BURDEN AND
TYPE OF INFECTIONS WE’RE SEEING IN HEALTH CARE.
THE PREVIOUS ESTIMATES, I THINK, ARE USEFUL IN A VERY BIG
PICTURED, NONGRANULAR KIND OF WAY TO SAY THAT IT USED TO BE
BIGGER, NOW IT SEEMS TO BE SMALLER, BUT THEY DEFINITELY ARE
NOT THE SAME METHODOLOGY. I WOULDN’T COMPARE THEM
DIRECTLY. BUT THERE SEEMS TO BE A TREND.
THE REASON FOR DOING THIS BECAME CLEAR WHEN WE DID THE ORIGINAL
PUBLICATION IN 2007, WHERE WE HAD TO USE ALL SORTS OF
DIFFERENT PUBLICATIONS AND DATA SOURCES TO COBBLE TOGETHER A
PICTURE. THAT LED TO THE PROCESS THAT
ALLOWED US TO DO THE SURVEY WE WERE PUBLISHING TODAY.
IT TOOK A PILOT IN 2009, FOLLOWED BY EXPANSION IN THE
NEXT YEAR. THAT PROCESS WAS A DIRECT
RESPONSE TO THE DIFFICULTY OF GETTING A BURDEN ESTIMATE FROM
THE PREVIOUS PUBLICATION. HAVING SAID THAT, THIS IS MORE
THAN JUST THAT BURDEN ESTIMATE. THE PLACES WHERE WE HAVE SEEN
SUCCESS ARE THINGS — INFECTIONS LIKE CENTRAL LINE ASSOCIATED
BLOOD STREAM INFECTIONS, VENTILATOR ASSOCIATED
PNEUMONIAS, THINGS THAT HAPPEN IN INTENSIVE CARE UNITS.
ORIGINALLY THIS WAS THE PLACE WHERE THE SICKEST PATIENTS WERE,
THESE ARE THE INFECTIONS THAT HAD THE GREATEST THREAT TO
PATIENT WELLBEING. THOSE THINGS WE FOCUSED ON UP
FRONT. THEY ARE THE THINGS WE FOLLOW
MONTH BY MONTH, YEAR BY YEAR. WE TRACK THESE THINGS, THAT’S
PART OF WHAT POPULATES THE PROGRESS REPORT THAT WAS ALSO
RELEASED. AT THE SAME TIME WEING ABOUT WH
MEASURING IN THAT SYSTEM. THIS SURVEY ALLOWS US TO LOOK AT
EVERY INFECTION HAPPENING ON THAT DAY AND FIGURING OUT WHAT
ELSE IS OUT THERE. SOME OF THAT ELSE IS IS THE
PNEUMONIAS. OF THE PNEUMONIAS THAT MADE UP
25% OF INFECTIONS, MORE THAN HALF HAD NOTHING TO DO WITH THE
INTENSIVE CARE UNIT. MORE THAN HALF WERE ON THE WARD
WHAT ARE THOSE? WE’RE TEASING THAT APART SO WE
CAN UNDERSTAND THE NEXT LEVEL OF PREVENTION IS.
IN THE INTENSIVE CARE UNIT WE KNOW IF YOU RAISE THE HEAD OF
THE BED, DO METICULOUS ORAL CARE SO THERE’S LESS BACTERIA
DEVELOPING THERE, AND REDUCE SEDATION, THESE THINGS ARE
ASSOCIATED WITH PREVENTING THOSE PNEUMONIAS WHAT IS THE
EQUIVALENT BUNDLE OF PRACTICES FOR A PATIENT NOT ON A
VENTILATOR? IS IT PERHAPS RELATED TO
SEDATION? COULD IT BE THESE PEOPLE ARE
USING TRANQUILIZERS? BECAUSE HOSPITALS ARE, LET’S
FACE IT, NOISY PLACES. MAYBE THE DOWN SIDE TO GETTING
GOOD SLEEP IS THAT YOU’RE MORE LI
LIKELY TO INHALE SALIVA OR STOMACH CONTENTS.
IF WE FIND A LOT OF THESE INFECTIONS ARE CAUSED BY PNE
USHU PNEUMOCOCCUS, WE CAN PREVENT
THAT. WE CAN LOOK AT PLACES WE’RE NOT
ROUTINELY MEASURING AND SAY WHICH OF THESE THINGS NEEDS THAT
LEVEL OF ATTENTION DIRECTED TOWARDS IT NEXT.
ANOTHER BIG CHUNK OF THIS WAS THE DEADLY DIARRHEA,
CLOSTRIDIUM DIFFICILE. THAT THENEED FOR ANTIBIOTIC
STEWARDSH STEWARDSHIPS IN EVERY HOSPITAL.
THAT’S HOW WE’RE USING THIS PARTICULAR STUDY TO FIND OUT
WHERE ELSE WE NEED TO LOOK AND GET A BETTER ESTIMATE OF HOW BIG
THE PROBLEM IS WE HAVE A COUPLE IN THE ROOM.
PLEASE. WHOEVER WAS FIRST.
DON’T FIGHT. I’M DIANA DAVIS FROM WSB IN
ATLANTA. WHAT YOU JUST ELUDED TO, IT
MENTIONS SOME THINGS YOU’RE LOOKING AT.
ARE YOU ALSO LOOKING AT IF STAFFING SHORTAGES, PROBLEMS,
OVERLOADED STAFF, IF THAT MAY BE CONTRIBUTING TO SOME OF THIS?
>>THE STAFFING QUESTION IS A HUGE CHALLENGE.
I WISH THERE WERE GOOD DATA THAT PROVED A CERTAIN AMOUNT OF
STAFFING LED TO A BETTER OUTCOME.
WE DON’T HAVE DATA TO SAY THAT. I KNOW MANY FACILITIES ARE
STRUGGLING WITH THE STAFFING QUESTION.
WE SEE THIS NOT ONLY IN HOSPITALS, BUT IF YOU COMPARE
HEALTH CARE TEN YEARS AGO TO WHEN THE 2007 NUMBERS WERE
RELEASED, THINGS ARE DIFFERENT. A LOT OF CARE THAT USED TO ONLY
TAKE PLACE IN INTENSIVE CARE UNITS IS NOW BEING PROVIDED
ONWARDS. THE STAFFING IS NOT SAME.
THE LEVEL OF TRAINING MAY NOT BE THE SAME.
SIMILARLY, THE THINGS THAT HAPPENED ONWARDS ARE NOW
HAPPENING IN NURSING CARE HOMES. IT’S WHERE ARE WE PROVIDING THIS
CARE? PART OF THE WORK THE CDC IS
ENGAGED IN NOW IS MAKING IT POSSIBLE FOR US TO REACH INTO
NURSING HOMES, AMBULATORY SURGERY FACILITIES TO GIVE THE
SAME SORTS OF DATA THAT INFORM OUR QUALITY IMPROVEMENT QUESTION
LIKE WE DO IN HOSPITALS. AS SOON AS WE HAVE INFORMATION
THAT SAYS STAFFING SHOULD BE EXACTLY THIS, I WILL BE HAPPY TO
TRUMPET THAT. ONE FOLLOW UP.
PATIENTS BEING AGGRESSIVE OR FAMILY MEMBERS IF THE PATIENTS
ARE NOT ABLE TO SPEAK FOR THEMSELVES, HOW DO YOU GET
PEOPLE OVER THE INTIMIDATION OF BEING IN A HOSPITAL, SAYING —
CHALLENGING A DOCTOR. WHAT’S YOUR MESSAGE TO PEOPLE
WATCHING THIS RIGHT NOW ABOUT THEIR — GEE, I DON’T WANT TO BE
RUDE. GEE, THAT’S IMPOLITE.
>>IT’S HARD. WHEN MY OWN MOTHER WAS IN THE
INTENSIVE CARE UNIT, I FOUND IT HARD TO PIPE UP.
IF I FIND IT HARD, I CAN’T IMAGINE WHAT IT’S LIKE FOR
EVERYBODY ELSE. WHEN A FRIEND OF MINE WAS
RECENTLY IN THE INTENSIVE CARE UNIT, TWO OF US, ANOTHER FRIEND
AND MYSELF, WE TOOK TURNS BEING THE BAD COP.
WE SUPPORTED EACH OTHER. IT’S EASIER TO DO WHEN YOU
DECIDE UP FRONT I’M GOING TO BE THE BAD COP TODAY.
IT’S HARD TO DO. BUT IT’S VERY IMPORTANT THAT
PEOPLE TRY. DO WE HAVE A CALL FROM THE —
YES, PLEASE. [ INAUDIBLE ].
>>I JUST HAD A QUESTION, WHEN WE’RE USING THE STATE FIGURES.
SO, FOR EXAMPLE, IN GEORGIA, THE CLASS B NUMBER IS DOWN 33%.
THAT’S COMPARED TO THE NATIONAL BENCHMARK.
IS IT FAIR TO SAY WE HAD A DROP IN GEORGIA OF 33%?
OR IS THAT COMPARED TO THE NATIONAL BENCHMARK?
I’M WONDERING WHETHER THAT’S ACCURATE GIVEN THAT DEPENDING ON
WHERE GEORGIA STARTED. RIGHT.
DEPENDING ON WHERE YOU STARTED IS THE KEY TO THE QUESTION.
THE BASELINES FOR MANY OF THESE NUMBERS IS 2006 TO 2008.
WE HAVE BEEN REPORTING PROGRESS YEAR BY YEAR.
SO, CONTINUING TO SHOW THAT SAME ARROW IS NOT AS HELPFUL AT THIS
POINT SINCE IT’S 2014. THAT’S WHY WE COMPARED IT TO THE
NATIONAL PROGRESS LEVEL. SO, WHEN YOU SAY THAT, YOU KNOW,
THERE’S A 30% IMPROVEMENT IN GEORGIA COMPARED TO THE
NATIONAL. IT’S ONLY COMPARED TO THE
NATIONAL. IS IT ACCURATE TO SAY THAT’S
A LOWER NUMBER THAN WE’VE SEEN NATIONALLY?
I’M ASSUMING THAT MEANS GEORGIA’S KIND OF LAGGING BEHIND
THE NATION IN PROGRESS. SO, I WILL LET OUR
SPECIALISTS IN THAT ARENA ADDRESS THIS NEXT.
AGAIN, I THINK THE REASON FOR PRODUCING THIS REPORT AT ALL IS
TO PUSH, JUST AS I’M BEING PUSHY WHEN IT COMES TO ASKING
QUESTIONS AT THE BEDSIDE, WE’RE BEING PUSHY WHEN IT COMES TO
STATE COLLEAGUES, HEALTH CARE COLLEAGUES SAYING, LOOK, THERE’S
MORE TO BE DONE. PAUL, JONATHAN, DO YOU WANT TO
SAY A WORD? JUST TO JUMP IN.
MIKE IS CORRECT. WE’RE COMPARING BACK TO THE
NATIONAL BASELINE. WE DO DO COMPARISON IN THE
PROGRESS REPORT THAT COMPARES THE STATE PROGRESS TO THE REST
OF THE NATION WITHOUT THE STATE EXCLUDED.
THERE’S A CONCLUSION. WHETHER THE STATE’S PROGRESS IS
SIGNIFICANTLY DIFFERENT FROM THE REST OF THE NATION, AGAIN, LIKE
MIKE ALSO ELUDED TO, THAT DIFFERS BETWEEN THE DIFFERENT
INFECTION TYPES. WE’RE NOT LOOKING AT A COMPOSITE
MEASURE AS A WHOLE. I’LL FOLLOW UP ALSO BY SAYING
THAT THESE THINGS TEND TO TAPER OFF.
AND WE DON’T WANT TO PENALIZE PLACES THAT ARE DOING A GREAT
JOB BECAUSE THEY’RE DOWN SO LOW THERE’S NOT A LOT OF PROGRESS
LEFT TO MAKE. YOU’LL SEE US CONTINUING TO WORK
WITH THE ISSUE OF BASELINES IN DIFFERENT WAYS OF PRESENTING THE
DATA SO WE CAN GIVE A CLEAR PICTURE OF HOW WE’RE PROGRESSING, WHERE WE NEED WORK, BUT ALSO WITHOUT TAKING AWAY THE SUCCESS OF A PLACE THAT’S GOTTEN SO LOW THAT THERE’S NO PLACE ELSE TO GO. DO WE HAVE A CALL FROM THE
PHONE, PLEASE? WE DO HAVE A QUESTION FROM
DANIEL WHITE, YOUR LINE IS OPEN. Caller: THANK YOU GUYS FOR
TAKING MY CALL. THE CDC PROJECTS THAT WITH THE
$30 MILLION IN FUNDING REQUESTED BY THE PRESIDENT’S FISCAL YEAR
’15 BUDGET THAT IT’S ANTIBIOTIC RESISTANCE INITIATIVE COULD
ACHIEVE A REDUCTION IN HEALTH CARE INFECTION.
YOU GUYS PROJECT THIS WOULD SAVE A NUMBER OF LIVES, PREVENT
HOSPITALIZATIONS AND CUT MORE THAN 2 MILLION IN COSTS.
HOW WOULD THE A.R. INITIATIVE ACCOMPLISH THIS?
>>THE A.R. INITIATIVE IS IN THE FY-15 PRESIDENT’S BUDGET.
IT IS TO IMPROVE OUR ABILITY TO TRACK THE INFECTIONS.
IMPROVE THE ABILITY TO GET THE DATA TO TELL US WHERE THE HOT
SPOTS ARE. IMPROVE THE NATION’S CAPACITY TO
DO THE LABORATORY TESTING THAT’S NEEDED TO FIGURE OUT WHICH OF
THESE GERMS IS CAUSING THE PROBLEM. ALSO BOOSTER OUR ABILITY TO PUT, AS THEY SAY, BOOTS ON THE GROUND
IN PLACES THAT ARE HAVING A PROBLEM AND ACTUALLY DELIVER
ASSISTANCE TO IMPROVE PRACTICES. IS THERE ANOTHER QUESTION ON THE
PHONE? WE DO HAVE A QUESTION FROM
MARY ANN ROSER, YOUR LINE IS OPEN.
>>Caller: THANKS. I’M WONDERING IF WE HAVE DATA ON
INDIVIDUAL FACILITIES AND STATE RANKINGS.
I HAD A SECOND PART TO THAT. WE DO PROVIDE HOSPITAL LEVEL
DATA FROM THE CENTERS FOR MEDICARE MEDICAID SERVICES
HOSPITAL COMPARE WEBSITE. OUR NATIONAL HEALTH CARE SAFETY
CDC DATA GETS HANDED OFF TO CMF, THEY CAN PUBLIC THOSE
INFECTION RATES BY HOSPITAL WITH THE ADDRESS FOR EVERY HOSPITAL
THEY SUPPORT WITH CMF MONEY. Caller: SO WE HAVE THOSE FOR
THIS YEAR? YES.
>>Caller: AND STATE RANKINGS FOR THE REPORT TODAY, DO YOU
HAVE THAT? WHEN YOU SAY STATE
RANKINGS — Caller: I’M IN TEXAS.
ARE WE NEAR THE BOTTOM OR — NO.
WE DON’T HAVE THAT. THE PROBLEM HERE IS YOU MIGHT BE
AT THE BOTTOM FOR ONE INFECTION TYPE, BUT YOU MIGHT BE LEADING
THE PACK FOR ANOTHER. SO IT DOESN’T REALLY HELP
ANYBODY TO SAY ONE STATE IS GOOD OR BAD.
>>Caller: DO YOU HAVE ADVICE FOR THE PUBLIC ABOUT USING
ANTI-BACTERIAL SOAP? I UNDERSTAND.
THERE’S A HUGE AMOUNT OF COMMERCIAL PRODUCT OUT THERE.
REALLY PLAIN SOAP AND WATER WORKS REALLY WELL FOR ALMOST
EVERYTHING. USING IT CONSTANTLY IS A GOOD
THING. ALCOHOL HAND RUBS ARE A GREAT
THING. WHEN I’M TRANSITING IN AIRPORT,
I’M CONSTANTLY USING THEM. FOR SOME THINGS,
ANTI-MICROBIAL SOAP SOLUTIONS ARE IMPORTANT.
IF YOU’RE ABOUT TO HAVE SURGERY, YOUR DOCTOR MAY SAY TAKE A
SHOWER WITH THIS SOAP TWICE IN THE NEXT COUPLE OF DAYS SO YOUR
INFECTION RISK IS LOWER. THERE’S A ROLE FOR ALL OF THESE
THINGS. FOR ROUTINE DAY IN AND DAY OUT
USE, AT MY HOUSE I USE A NICE SOAP THAT SMELLS LIKE FLOWERS.
THAT’S FINE. YOU DON’T NEED ANYTHING SPECIAL.
WE HAVE TIME FOR TWO MORE QUESTIONS.
>>Caller: THANK YOU. [ INAUDIBLE ].
>>WE DON’T COME OUT AND SAY DON’T USE ANTI-BACTERIAL SOAP.
WE ARE SPECIFIC ABOUT WHERE WE SAY IT SHOULD BE USED.
WHAT WE WANT PEOPLE TO DO, THOUGH, IS FOCUS ON KEEPING
THEIR HANDS CLEAN AT ALL TIMES. ESPECIALLY IN HEALTH CARE
SETTINGS. ANOTHER QUESTION ON THE PHONE?
>>DAN CHILD’S, ABC NEWS, YOUR LINE IS OPEN.
>>Caller: THANK YOU VERY MUCH FOR TAKING MY QUESTION.
WITH REGARD TO THE PROBLEM OF ANTIBIOTIC RESISTANCE THAT YOU
WERE TALKING ABOUT, WHERE ARE WE IN TERMS OF NEW APPROACHES TO
THESE UNTREATABLE INFECTIONS THAT YOU MENTIONED AND WILL WE
GET A SECOND CHANCE TO GET IT RIGHT WITH ANTIBIOTICS?
IF SO, WHEN? GREAT QUESTION.
SO, AS A NATION IN ADDITION TO PREVENTING ANTIBIOTIC RESISTANCE
IN ORGANISMS BY BETTER ANTIBIOTIC USE, AND IN ADDITION
TO NOT LETTING THE ORGANISMS SPREAD FROM PATIENT TO PATIENT
WITH GOOD HAND HYGIENE G INFECTION CONTROL, WE’RE ALSO
SUPPORTING THE GENERATION OF NEW ANTIBIOTICS.
THE CHALLENGE THAT WE HAVE IS THAT IT TAKES A LONG TIME TO GO
FROM SOME RARE CHEMICAL IN A JUNGLE TO SOMETHING THAT WE KNOW
IS SAFE AND EFFECTIVE FOR HUMAN BEINGS.
DURING THAT SPAN OF TIME, WHAT WE HAVE RIGHT NOW IS PRETTY MUCH
IT. SO A LOT OF THE VERY INTENSE
WORK WE’RE DOING WITH REGARD TO ANTIBIOTIC STEWARDSHIP AND
PREVENTION OF RESISTANCE IS AB THESE HANDFUL
OF ANTIBIOTICS THAT STILL WORK FOR US EFFECTIVE AND AVAILABLE
FOR THE NEXT, WHO CAN SAY, SEVEN, EIGHT YEARS MAYBE BEFORE
WE HAVE A NEW TRULY USEFUL ANTIBIOTIC THAT HAS COME THROUGH
THE PIPELINE. THERE’S THAT PIECE OF IT.
YOU ALSO TALKED ABOUT OTHER APPROACHES.
THERE IS AN INTERESTING AREA OF WORK, NOT COMPLETELY MATURE YET.
OF OTHER WAYS TO TAKE CARE OF INFECTIONS.
SOME OF YOU MAY HAVE HEARD ABOUT MEDICAL HONEY.
THERE ARE WAYS TO TREAT WOUNDS THAT SEEM TO BE SUCCESSFUL, IF
THERE’S OVERWHELMINGLY SUPPORTIVE DATA, WE MAY BE
RECOMMENDING TO DO THAT ROUTINELY.
WE’RE NOT QUITE THERE YET. I THINK THE DESPERATION WITH
WHICH SOME OF THESE INFECTIONS ARE BEING APPROACHED IS LEADING
TO INTERESTING NEW APPROACHES. LASTLY, THE QUESTION OF WILL WE
GET A SECOND CHANCE IS AN IMPORTANT ONE.
THERE ARE TWO PIECES TO THIS. ONE IS, ONCE WE DO HAVE NEW
ANTIBIOTICS, IF WE TREAT THEM THE WAY WE’VE BEEN TREATING THEM
UP UNTIL NOW, WE’LL LOSE THOSE QUICKLY AS WELL.
I GUARANTEE IT. IT’S LIKE ORDERING A NEW CREDIT
CARD WHEN YOU’RE BANKRUPT. IT DOESN’T WORK.
THE FLIP SIDE IS WHEN YOU DON’T USE AN ANTIBIOTIC FOR A LONG
TIME, BACTERIA STOP FIGHTING IT. SO ONE OF THE MEDICATIONS THAT
WE USE FOR THE NIGHTMARE BACTERIA IS A THING CALLED
COLLISTIN. IT’S A TERRIBLE DRUG TO USE,
BECAUSE THE SIDE EFFECTS ARE HORRIBLE.
SO IT STILL WORKS. IN DESPERATION, WE’RE USING
THAT. THERE’S A POSSIBILITY THAT WITH
VERY GOOD ANTIBIOTIC STEWARDSHIP, USING LESS BROAD
SPECTRUM ANTIBIOTICS AND USING THEM AS WIDELY AS POSSIBLE, WE
MAY BE ABLE TO MOVE THE NEEDLE BACK A LITTLE BIT FOR SOME OF
THESE BACTERIA. Caller: THANK YOU.
>>THANK YOU. THIS CONCLUDES TODAY’S MEDIA
BRIEFING ON HEALTH CARE-ASSOCIATED INFECTIONS.
THANK YOU, DR. BELL. THANK YOU, VICTORIA.
FOR MEDIA ATTENDING TODAY’S BRIEFING IN PERSON, WE ARE
JOINED BY THE MEMBERS OF THE GEORGIA STATE HEALTH DEPARTMENT, THE QUALITY IMPROVEMENT ASSOCIATION, AND THEY’RE
AVAILABLE FOR INTERVIEW ALSO. FOR THOSE NOT IN THE ROOM, MEDIA
WHO HAVE FOLLOW-UP QUESTIONS OR REQUESTS FOR INTERVIEW, PLEASE
CALL CDC’S MEDIA LINE AT 404-639-3286 OR E-MAIL
[email protected] THANK YOU.

Fighting Infection with Phages

Fighting Infection with Phages


Modern medicine faces a serious problem. Thanks in part to overuse and misuse of antibiotics,
many bacteria are gaining resistance to our most common cures. Researchers are probing possible alternatives
to antibiotics, including phages. Dr. Shayla Hesse: “So, bacteriophages, or we like to call them
phages for short, are naturally-occurring viruses that infect and kill bacteria. Their basic structure consists of a head,
a sheath, and tail fibers. The tail fibers are what mediate attachment
to the bacterial cell. The DNA stored in the head will then travel
down the sheath, and be injected inside the cell. Once inside the cell, the phage will hijack
the cellular machinery to make many copies of itself. Lastly, the newly-assembled phages burst forth
from the bacterium, which resets their phage life cycle and kills the bacterium in the process. Someday, healthcare providers may be able
to treat MRSA and other stubborn bacterial infections using a mixture of phages, or a
“phage cocktail.” Dr. Randall Kincaid: “The process would be first to identify what the pathogen is that’s causing the infection, so the bacterium is isolated, and characterized,
and then there’s a need to select a phage in a process known as screening of phage,
that are either present in a repository or in a so-called phage library, that allows
for many of the phages to be evaluated for effectiveness against that isolated bacterium.” Phages were first discovered over a hundred
years ago, by a French Canadian named Felix d’Herelle. They initially gained popularity in eastern Europe. However, Western countries largely abandoned
phages in favor of antibiotics, which were better-understood, and easier to produce in
large quantities. Now, with bacteria like these gaining resistance
to antibiotics, phage research is gaining momentum in the United States once again. NIAID recently partnered with other government
agencies to host a phage workshop, where researchers from NIH, FDA, the commercial sector, and
academia gathered to discuss recent progress. NIAID also conducts and supports research
on phages. “The research that I’m working on now is
aimed at answering the question of what makes a good phage for phage therapy. There’s a diversity of phages out there,
and how do we choose, or engineer, the best phages for use for therapeutic purposes.” Through research on phages, and other efforts,
NIAID is committed to outpacing antimicrobial resistance.

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.