September 3, 2025 • 49 mins
War is a vector of disease. The battlefield isn't just a place where bullets fly—it's where pathogens thrive and evolve. Throughout human history, war and disease have been inseparable companions, creating perfect storms of contagion that affect soldiers and civilians alike.
Our journey begins in the Boer War concentration camps where measles swept through malnourished populations. We explore how the densely packed, unsanitary conditions created an environment where this highly contagious virus could spread with unprecedented severity, even among adults who typically have greater resistance.
The trenches of World War I became breeding grounds for tuberculosis—a disease that claimed millions of lives with no effective treatment available beyond isolation, nutrition, and exposure to fresh air and sunlight. It would be decades after the war ended before the first effective medications were developed in the 1940s.
War doesn't just spread existing diseases—it creates conditions for new ones to emerge. During World War II, when farming ceased in the occupied Crimean Peninsula, overgrown grasslands became habitats for wildlife and the ticks they carried. When Russian soldiers reclaimed the area in 1944, they encountered what would later be identified as Crimean-Congo hemorrhagic fever. Similarly, the Korean War saw the emergence of Hantavirus among US soldiers.
Perhaps most alarming is our exploration of the current Russia-Ukraine conflict, where overstretched medical systems have accelerated antimicrobial resistance to frightening levels. Klebsiella pneumoniae from Ukrainian wounds exhibits carbapenem resistance rates ten times higher than those observed anywhere else in Europe. These resistant strains are already crossing borders, detected in six European countries and as far away as Japan.
The displacement of populations, collapse of healthcare infrastructure, and ecological disruptions caused by conflict create ripple effects that extend far beyond the battlefield. As one expert reminds us, perhaps "more effective than any vaccine, is peace."
Subscribe, share, and join us next time as we continue exploring the intricate connections between human activity and disease emergence. The more we understand these relationships, the better prepared we'll be to face future health challenges.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 2 (00:07):
This is a podcast about One Health the idea that
the health of humans, animals,plants and the environment that
we all share are intrinsicallylinked.
Speaker 3 (00:15):
Coming to you from the University of Texas Medical
Branch and the GalvestonNational Laboratory.
Speaker 2 (00:19):
This is Infectious Science.
Where enthusiasm for science?
Speaker 4 (00:23):
is contagious infectious science, where
enthusiasm for science iscontagious.
Hello everyone, and welcomeback to Infectious Science.
Today we are talking about warand pathogens.
There are very few examples ofprolonged peace in history, and
the human penchant for war hasin history, and continues today,
to significantly exacerbate thespread of infectious diseases.
(00:44):
We've previously talked abouthow globalization exposes us to
diseases that previously wereonly endemic in a specific
region or locale.
Just like globalization, waralso increases contagion,
because wherever groups ofpeople move, so too does disease
.
Whether masses of people aremeeting on a battlefield or
forcibly displaced by conflict,disease, the constant companion
(01:06):
of humanity, tends to follow.
In addition to this, war alsoincreases disease by disrupting
public health infrastructure andmaking resources scarce, which
can result in malnutrition orthe use of unclean water, all of
which increase ourvulnerability to pathogens.
We have selected some historicand modern examples of how war
has shaped the spread and naturepathogens.
So let's dive in.
(01:26):
Alex, you had the first war inour chronological history.
Do you want to start?
Speaker 1 (01:31):
My name is Alexander Alvarado, for today's episode of
the Infectious Science Podcast,talking about war and disease.
I'm going to be talking aboutthe Boer War and about measles
outbreaks in British-runconcentration camps during the
later phase of the war, and soI'm going to give some
background as far as some of theunderlying tensions that led to
(01:51):
the war, talk a bit more aboutthe Boer War itself and then
talk more about measles virusand how the war ultimately
changed the spread of measlesitself and the course of disease
that measles is able to cause.
So the United Kingdom formallyannexed the Cape Colony, which
is an area that encompasses muchof the western coast of South
Africa, following the signing ofthe Convention of London in
1814 with the Netherlands, inthe aftermath of one of the last
(02:16):
of the Napoleonic Wars, the Warof the Sixth Coalition, and so
the British ended up inpossession of a territory which
had a population of Dutch andHuguenot settlers that came over
as a result of Dutch activitiesin the colony over the past two
centuries and the indigenouspeoples that had long been on
(02:38):
the land, and there weresignificant political
(03:01):
disagreements between theBritish were curtailing the
practice of slavery and theunwillingness of the British
administration to go and expandthe colony to enable these
semi-nomadic boar cattle herdersto expand their range.
And ultimately this led forsome of these settlers, some of
these boars, to opt, over thecourse of largely the 1830s
(03:22):
through the 1850s, to settle inthe interior of South Africa in
order to live beyond the courseof largely the 1830s through the
1850s, to settle in theinterior of South Africa in
order to live beyond thejurisdiction of the British, to
live outside of the boundariesof the Cape Colony.
In time, these settlementscoalesced into some of these
Dutch settler republics, theseBoer republics, including states
like the Orange Free State andthe South African Republic.
(03:45):
And these states, they were hitby an influx of foreigners as a
result of the discovery of goldin 1884, the Whitwater Strand
Gold Rush, and largely Britishnationals ended up emerging into
the South African Republiclooking for gold.
And there were fears,ultimately, among a number of
these Boer residents in theRepublic that the amount of
(04:07):
British residents, which in timecame to outnumber the Boers,
that these British nationalswould amass enough political
clout to push for the absorbanceof the independent state into
the British Empire.
And there were continueddisputes regarding what the
rights of these foreignresidents should be and upon the
duration required for them toattain citizenship, etc.
(04:28):
In order for the Boers to findsome ways to dilute the
political power of these Britishnationals and these foreigners
who had come seeking for gold,pushing back on that.
And so the British attempted tonegotiate with the South
African Republic regarding thenature of the rights of these
foreigners who had come seekingfor gold.
But the collapse ofnegotiations between the British
(04:50):
and the Boer states ultimatelyled to the Orange Free State and
the South African Republic toboth declare war against the
United Kingdom.
Initial Boer victories in 1899,a mobilization by the British,
one of the largest at the time,enabled ultimately the capture
(05:14):
of both states in 1900 and oflarge swaths of territory.
And so, with the collapse ofthe central states that
initially started to wage thewar, with continued, though,
civilian support and the natureof the decentralized structure
of command for the Boer armiesand local knowledge of the land,
the climate was ripe for Boerguerrilla warfare to continue
(05:37):
the struggle for longer againstthe British.
And the British ultimatelydecided, in order to go about
suppressing the spate ofguerrilla warfare and to enable
the end of this war, tried toessentially detach the Boer
military forces that werecontinuing to battle against
them, from the civilianpopulation and from the
(05:59):
resources that they relied uponfrom the civilian population,
like food, and so they destroyedBoer farmsteads and settlements
, they burned crops and theydisplaced the population, both
Boers and the indigenous peoplesof that land.
They displaced them into thesespecially constructed
concentration camps, and so thusthis enabled the Boer
(06:20):
guerrillas to be deprived ofcivilian cover that they could
otherwise blend into, as well asof civilian support and the
material resources that theycould use in order to further
continue their campaign againstthe British.
And these camps were ratherdensely populated and were known
for having poor sanitation andhad limited food rations, both
(06:42):
as a result of the limitationsof the time as well as British
policy that exacerbated thesituation.
So relations of knownguerrillas received smaller
rations than others, and theindigenous African detainees
lacked a guaranteed food ration,unlike some of the Boers, and
were thus forced to work forfood, unlike Boer detainees, and
(07:03):
received nutritionallyimbalanced rations when they did
receive rations, as a result ofpseudoscientific misconceptions
of dieting at the time, and asa result, this was a population
that, between the stresses ofwar, which is known to
negatively affect the immunesystem, and the widespread
nature of malnutrition in adensely populated area.
(07:25):
This gives you animmunocompromised population in
an area where infectiousdiseases can easily spread, and
in many ways this was almost theperfect storm for a measles
outbreak.
And so measles virus itself is aparamyxovirus that has a
non-segmented RNA viral genomewhich is capable of causing the
disease of measles in humans,and so viral infection is
(07:49):
largely caused through aerosoltransmission, be it through
direct contact or in contactwith infected surfaces.
And so measles virus itself, ittends to infect these airway
epithelial cells and specializedlung immune cells, the latter
of which may include, say, thesealveolar macrophages, and
alveolar macrophages, bybecoming infected, may end up
(08:12):
trafficking measles virus tolocal lymph tissue, enabling
subsequent infection of morespecialized immune cells, some
naive B cells as well as memoryT and B cells.
And this is mediated through themeasles virus interaction with
the SLAM receptor, otherwiseknown as CD150, which is this
surface receptor that'sconserved among some of these
(08:33):
cell types.
And as a result of theinfection of some of these
specialized immune cells, andparticularly these memory B and
T cells, and the necessary celldeaths caused by the immune
system, this response to go andkill the measles virus cells
that were targeted to otherorganisms and, essentially,
their replacement by thesepopulations of BNT cells that
(09:08):
are specific to measles virusspecifically, it enables an
increasing amount ofsusceptibility to other
pathogens and thisimmunosuppression can last for
some time, even after the fullresolution of the course of
disease of measles itself.
It can prove to be quiteproblematic, but in terms of
measles disease itself.
So basically, after a 7 to 14incubation period you start to
(09:29):
experience some of the signs ofa nonspecific febrile illness.
So a fever, cough, rhinitis.
These are some of the thingsthat may start to emerge, and,
in conjunction with some ofthese prodromal symptoms,
conjunctivitis, coplic spot anda maculopapular rash are rather
characteristic of measles virus.
Infection and the spread of thevirus to further within the
(09:52):
lungs and into the brain maylead to pneumonia and
encephalitis respectively, andso pneumonia can be caused by
other pathogens as a result ofmeasles-induced
immunosuppression, or directlyby measles, due to the sort of
damage that measles can cause tothe lung itself.
And pneumonia is often theprimary cause of measles death,
(10:14):
be it indirectly or directly asa result of measles virus
infection.
And it's worth noting thatmeasles virus is highly
contagious.
It has an R0 value of about 12to 18, which really points to
the contagiousness of measlesvirus itself, as a number of
otherwise naive, uninfected,susceptible individuals can
(10:37):
ultimately become infected byjust one case.
And so, in a densely populatedarea, in the absence of modern
day vaccines for measles virusand in a population that was
highly immunosuppressed, theseBritish-built concentration
camps for the Boers and for theindigenous people of the Boer
(10:58):
republics really enabled a rapidspread of measles virus, and it
enabled further these highdegrees of mortality to it,
higher even in adult cases thannormal, because the measles
virus largely tends to be adisease of the youth right.
Once infected with it you mayhave lifelong immunity, but it
(11:18):
is particularly hard on youngerpeople.
These outbreaks were somewhatunique, though, with relatively
higher case fatality rates inadults, which was a new
development that in many wayscould probably be attributed to
the stressors of the camp andthe nature of the concentration
camps in general in terms of thedense degree of the population
and the malnutrition that theywere experiencing.
(11:39):
And so, over the course of the1900 to 1902 period in which
these camps were still operable,there were about 47,000
civilians, be they Boer settlersor the indigenous peoples, that
died in these British camps.
Roughly about 30% of thesedeaths are estimated to have
been as a result of measles.
(12:00):
In some of these camps, over50% of children's deaths were
due to measles and over 10% ofadult deaths were due to that
same disease.
And I think that really speaksto the nature of how these
specially constructedenvironments, these temporary
environments, and the nature ofwar can significantly affect the
spread of infectious disease,and it's something to be
(12:23):
cognizant of in modern conflicts.
Even to this day, there arecertainly still issues with that
, with a number of wars that arefought and with the breakdown
of sanitation systems and of theemergence of, in some cases,
hastily constructed, denselypacked refugee camps and further
this outbreak, I think, is abit of a cautionary tale.
(12:43):
This points to the destructivecapacity of measles virus when
it's not being mitigated bythings like widespread vaccine
uptake and antivirals and theresources that we have today,
and I think it certainly pointsto how, when we have infectious
diseases that can't becontrolled by some of these
therapeutics, or if there's somereluctance to go about using
some of these therapeutics, theconsequences can be rather
(13:06):
disastrous for the population.
Thankfully, there have been nolingering effects to this day of
the measles epidemic in theBritish concentration camps, but
the camps themselves and thedegree of death that ultimately
pervaded in them is still inmany ways a cause of concern for
what happened over the courseof that war, and certainly a
(13:27):
story is worth attention, and soI figured that I talk about it
a bit more today in this segment.
Back over to you.
Speaker 5 (13:34):
Awesome.
Thanks, alex.
It's always so good to learnand understand things that you
really knew nothing aboutbeforehand.
I really like using theserecordings and these sessions
that we have to learn for myselfand study things I was
previously interested in butmaybe didn't know too much about
specifically, and the war andthe disease process that I
(13:55):
wanted to focus on for ourrecording session today was
actually the relationshipbetween tuberculosis and World
War I, tuberculosis and WorldWar I.
So, as we here know,tuberculosis is caused by
mycobacterium tuberculosis.
It has two phases really, orthree, I guess, if you want to
consider latent phase as a phase.
But primary tuberculosis is notso infectious for most people
(14:19):
and most people's immune systemsdo fight off the infection at
this stage.
However, from primarytuberculosis can become latent.
So it's basically yourinfection is held at bay, but
it's still present in the bodyby your immune system.
However, certain triggers thatdepress the immune system can
cause that infection to becomereactivated, and that's called
(14:42):
secondary tuberculosis.
Just want to make sure all thatsounds right, matt, sound good
on your end.
Speaker 2 (14:47):
Sounds very good on my end.
Yeah, doing great.
Speaker 5 (14:49):
Awesome, okay, so actually in World War I, before
the war, tuberculosis itself wasa pretty rampant disease
process and of course, with warbringing so many people into
close quarters and of coursewith war bringing so many people
into close quarters, it reallycaused a massive spike in
tuberculosis cases.
Specifically in World War Ithey didn't really use
(15:15):
particularly great screeningmethods for tuberculosis.
So, if I'm correct, matt, nowof course we do our physical
exam, we do certain tests totest whether or not a person has
tuberculosis they're actuallyspecific for testing for
tuberculosis and of course alsodoing chest x-rays seemed as
pretty routine for screening forthe infection.
But back then we didn't havex-rays used in the screening
(15:39):
process for tuberculosis and wereally just used physical exam
and history to screen.
For that Is it pretty difficultto actually diagnose primary
tuberculosis just off a physicalexam.
Speaker 2 (15:52):
Yeah, I mean it really depends on the context.
I've seen a lot of peoplearound the world with
tuberculosis infection and itdoes have a very typical
presentation A lot of peoplepresent with chronic.
It's a chronic infectiousdisease, right Like something
that's indolent, very slowmoving, slow growing.
Fever, chills, night sweats,weight loss are often very
(16:14):
common and it was a reason thatback in those days they called
it consumption, because peoplelooked as though they were being
consumed by the pathogen.
So clinicians of those dayswere pretty adept at diagnosing
tuberculosis even without allthe fancy diagnostic tools.
Now they may have over-calledsome things tuberculosis because
we didn't have the moleculartests and, dennis, I won't push
(16:36):
you on when Robert Kochelaborated the first real
diagnostics for tuberculosis anddescribed the bacterium, but
these were things that werebeing deployed at the time.
But probably physical diagnosisand history, you know,
obviously, palpating lymph nodes, assessing for the clinical
signs and symptoms, listening tothe lungs, these were probably
(16:58):
as good as we got.
But you know, because it tendsto travel in populations, you
would certainly see it inclusters, in people who are in
close quarters.
So I think you rightlymentioned war does tend to
produce disruptions in a lot ofthe public health control
measures that we typically relyon for peace and stability
during peace and stability times.
So you know it's not surprisingspikes in infectious pathogens
(17:22):
during those times of upheaval.
Speaker 5 (17:24):
Yeah, absolutely Completely agree.
And speaking of how you seethese increases and these spikes
in the community in World War Iand, as I'm sure, in all the
other wars we're going to talkabout today, it's important to
note that these diseases didn'tjust infect and affect soldiers.
Right, there were so manycivilians that were at the other
(17:46):
end of this infection and alsodied.
And specifically in World War I, there's not a great count for
how many people died fromtuberculosis just in those years
of the actual war, butestimates are in the millions,
and so that just shows howhorrible this disease was at
that time.
And specifically so becauseback then, in World War I's
(18:07):
years, we didn't actually have acure or treatment for
tuberculosis.
So back then the treatmentreally was just isolation,
nutrition and sunlight, fromwhat I could read.
So fresh air, sunshine that wasthe best that we could do and
pretty aggressive disease.
So without an actual treatment,without an actual cure, it's
(18:33):
clear to see why it took so manylives back then.
From what I can see and fromthe research that I did, the
first treatments that weredeveloped were actually in 1943.
It was streptomycin was thefirst treatment used for TB.
I don't specifically believethat's used nowadays, matt,
correct me if I'm wrong, but Idon't think so.
They use it in resistance.
Speaker 2 (18:52):
So in people who have treatment failure it's a second
line treatment.
There you go.
Or it can be used in people whohave complicated TB, things
like cerebral TB or likemeningitis, tb, meningitis,
things like that.
Sometimes in treatment failuresthey'll use streptomycin.
(19:13):
So it's not ideal.
There's other alternatives andit depends on the country too.
In countries where there is,for example, high prevalence of
multidrug resistant tuberculosis, you tend to use more things
like quinolones, which is whyyou don't see them prescribed as
widely for general respiratoryinfections in some other
countries.
It's because you want toreserve those kinds of things
(19:34):
for TB treatment, because theycan be quite effective in the
second line treatment.
But I think Camille is going tobe getting into more
antimicrobial stuff later on.
But you're right onStreptomycin certainly is not
first line.
Speaker 5 (19:44):
It has a lot of toxicities you're right on,
streptomycin certainly is notfirst line.
It has a lot of toxicities.
Interesting, yeah, and I thinkmedication that we do so use as
first line.
I know TB, we typically willthrow a few medications at it as
a first line treatment.
But isoniazid specifically atleast from the textbooks, from
what I know is considered one ofthe first line treatments and
that was specifically broughtout and used in 1952 from what I
(20:07):
could see.
So it really shows a solid 20,30 years after World War I
finished we didn't reallydevelop, I guess, common
treatments for TB until then.
So it just really shows howaggressive this disease process
was, how hard it is to treat,and highlights just the effect
that it had overall onpopulations throughout World War
(20:28):
I, which was the first worldwar, right, and so there were so
many countries that cametogether, so many countries
involved.
Really just you're able tounderstand, when you think about
it from that aspect, howtuberculosis had such a rampant
effect and a really detrimentaleffect on the population.
Speaker 2 (20:45):
Yeah, no, that's right on.
We treat people now with fourdrugs.
There's the drugs that stop thebacteria from replicating those
are bacteriostatic and thenthere's bactericidal, the ones
that kill it, and so you need acouple of different ways to get
at this because it's just likein so much of medicine we need
drugs to attack things that arefast growing, so we're good at
that.
We're less good at attackingthings that are slow growing, so
(21:07):
this one needs a lot of help tobe able to treat it.
And you're right, times of war,times of disruption, and in a
time where these drugs, thesecountermeasures, are not readily
available and you're displacingpopulations and it wasn't so
much, as I understand it, of amilitary issue, as much as it
was for the populations in thecountries that were experiencing
the war and hosting theseconflicts, that were most
(21:30):
affected by these contagionsduring World War I.
And it wasn't just TB.
We had a lot of sexuallytransmitted infections, typhoid,
malaria, so a lot of otherpathogens went rampant during
the times of these wars.
Speaker 5 (21:45):
Yeah, I completely agree.
I actually settled on TV andWorld War I specifically because
I just finished reading ahistorical fiction book that was
set in the time of both WorldWar I and World War II, but it
specifically talked about theestablishment of a preventorium
I think is how you pronounce itwhere they would isolate
patients with tuberculosis, andit was cool to pull that into
this.
Speaker 6 (22:05):
What's the name of the book with?
Speaker 5 (22:06):
tuberculosis and it was cool to pull that into this
what's the name of the book.
Speaker 2 (22:12):
I have the book right here.
Give me one second.
Well, while she's getting thebook, I'll just say that Sir
William Osler, who lived from1849 to 1919, the father of
modern medicines.
He wrote the first real seminalmedical textbook of medical
management called the Principlesand Practice of Medicine, and
tuberculosis slash consumptionfeatures heavily in his textbook
.
He has a whole chapterdedicated to it and, like you
(22:33):
said, Christina, there wereprecious few things you could do
.
Osler was a fan of prescribingopium in these circumstances
because it was good for cough,it was good for pain and
obviously there were othercountermeasures that they would
try.
But when you read these oldtextbooks you realize they were
working mostly with publichealth control measures.
(22:53):
They can go to altitude, gooutside in the sunlight.
Tuberculosis bacilli do notlike UV light, they do not like
circulating air and so when yougo to a ward, especially in
Southern Africa or other placeswhere TB is highly prevalent,
when there's a TB ward, it'lloften be very well lit, the
windows will be open and thefans will be blasting, in
(23:14):
addition to all of the maskingand other countermeasures that
we have, because people knowthat it's those environmental
things that are also going tohelp contain the contagion.
Speaker 5 (23:23):
Wow, that's really interesting.
I didn't know that.
And then, Dennis, for yourquestion.
The book is called the Women ofChateau Lafayette, so pretty
good book.
Speaker 2 (23:33):
I can only hear Hamilton saying Lafayette.
Speaker 5 (23:37):
No, yeah, they actually talk about Hamilton in
the book too.
So if you can't get enough ofHamilton, read the book.
It was a good one, but that'sall I have for TB World War I.
I think, dennis, you have thenext war and pathogen that we're
going to talk about today, soyou want to take over.
Speaker 6 (23:54):
Yeah, absolutely.
I want to talk about a diseasethat was discovered during World
War II and it's also a goodexample of how war can shape or
can create ecologicaldisturbances and modifies the
landscape and that leads to anoutbreak of diseases that rely
(24:16):
on the ecological complexitythat's then disturbed through
war and I'm going to talk aboutmy favorite pathogen.
I've been very humble.
I've never really talked aboutCrimean Congo hemorrhagic fever
here on this podcast, my mainfocus.
But Crimean Congo hemorrhagicfever was discovered in 1944 in
the Crimean Peninsula and whathad happened is the Crimean
(24:40):
Peninsula.
I think everybody at this pointin time has an idea where that
is located in time has an ideawhere that is located.
With the Crimean War and withthe Ukrainian War, the Crimean
Peninsula was occupied by Germansoldiers for many years and in
1944, the Russian soldiers werepushing the German soldiers out
(25:00):
of the Crimean and also out ofparts of the East and pushing
them back towards Central Europe, and during the occupation the
farming in this area had stopped.
You can imagine, during anoccupation, everything stops
right.
The farmers don't take care oftheir fields, so grass overgrows
, pests maybe, come in.
A lot of wild animals likerabbits, hares, mice, you name
(25:24):
it.
They come in, they can hide inthe grass and they often bring
other vectors with them, and sothey brought in quite a number
of ticks.
And so what happened in 1944 is, when the Crimean Peninsula was
reoccupied by the Russians,roughly 200 Russian soldiers
fell ill with a hemorrhagicfever, and it was very severe,
(25:46):
and the spotlight really quicklyfell on the ticks, because the
tick density was so high in thatarea.
The grass that had overgrown,the rabbits that had come in,
that brought the ticks, and soon.
So there were ticks crawlingall over the place and they
caused a very severe disease,hemorrhagic fever, with high
fatality rates.
And what the Russians did isthey dispatched a team that had
(26:09):
already discovered a new diseasein 1937 in the far east of
Russia, and Mikhail Chumakov,like a famous virologist, was
sent and was to investigate thecase, identify the pathogen.
This took a long time, it tookdecades until they finally
figured out that it's a buniavirus, and they had a lot of
(26:32):
suspicion what it could be, andit took them a long time to
figure it out.
And in the meantime, in the1960s, another virus had been
discovered in the Congo, inCentral Africa, and that's why
they then found out that thoseare the same diseases and that's
why it has this funky name,crimean-congo hemorrhagic fever,
(26:52):
because they thought it was twodifferent diseases.
But in the 1960s they actuallyrealized it's the same disease
and neither the Russians nor thepeople in Africa wanted to
budge and that's why they cameup with that name.
Speaker 5 (27:04):
That's interesting.
I didn't realize that that'swhere the namesake comes from,
that's really cool, Camille.
Speaker 6 (27:10):
what are your thoughts?
Speaker 4 (27:11):
I was just curious.
Why do you think it took themso long to figure out what virus
it was?
Was it just the moleculartechniques were not there?
Was it something else?
Speaker 6 (27:20):
Yeah, now, looking back, you can only speculate.
Back then they did a lot of thethings.
They would grind up the ticks,they would take blood from the
patients and they would injectit into any animal that they can
get their hands on, from catsto you name it.
They also injected it intoprisoners, prisoners of war, and
, yeah, that was a commonoccurrence back then, and they
(27:41):
were able to isolate Rickettsia.
But this turned out to be acontamination later on, and the
reason why it took them so longis that what we hear in the West
I don't know if that's corrector not is people in Africa, for
example, had worked with mice asan isolation technique suckling
mice and the Russians had notdone that.
But once the Russians used thistechnology and used animals as
(28:04):
an isolation mechanism,specifically suckling mice, they
were able to isolate the virus.
Like you said, camille, it wasa different type of technology
that was used to detect thedisease.
So I want to also add on aquick story about another bunya
virus, another war.
This is specifically the KoreanWar, which was from 1951 to
(28:26):
1954, I think, and again somesort of ecological disturbance
led to the discovery of thevirus.
The virus, just likeKorean-Ming-Kongo it took
decades to isolate the viruslater on and the agent was
identified as Hantan virus.
It's a river that runs throughKorea and so in 1951, 54, around
(28:51):
that time during the Korean Warthey had roughly 3,500 UN
soldiers.
So United Nations soldiers wereaffected by this really severe
disease, with case fatalityrates up to 10%.
And then once they gottreatment and they had better
care, the case fatality ratewent down to 5%.
But the disease back then waspresented with high fever,
(29:14):
headache, bleeding, kidneyfailure, leading to severe
illness and death in otherwisehealthy young soldiers.
And once they had an idea whatthe exposure mechanism is, which
is rodents rodents carry thedisease they were able to
contain the transmission andreduce the transmission.
But again it took them quite awhile.
(29:36):
It took probably like fourdecades really to identify and
to characterize the causativeagent of Korean hemorrhagic
fever.
And that's another classic storyin virology and it's a classic
example in military medicine.
And you can imagine having adisease going on during the war.
(29:56):
We talked about this with TB.
It strains medical resources,it makes the forces that are
fighting less efficient andeverybody's concerned,
especially if they don't knowhow the disease is transmitted.
If you're interested in this,look up Korean War and Hantan
virus.
It's like one of the hallmarksin bunyal virus virology and I
(30:17):
think then we're going on to thecurrent war, camille.
Speaker 4 (30:21):
One of the current wars?
Speaker 2 (30:22):
yeah, Dennis, I love the way that you described
especially the One Healthelements of how these pathogens
emerged in times of war, and youdescribed the environmental
disruption leading to animalencroachment, vector growth and
propagation and then sort of theperfect storm, if you will, of
factors coming together to allowthese diseases to emerge or to
(30:44):
reemerge.
And so I was thinking about whenyou were talking about Congo
especially.
I thought about there was thistime in the mid 1800s.
We use this a lot in our publichealth teaching where we talk
about the African sleepingsickness outbreaks that took
place during sort of colonialtimes in Central and East Africa
and a lot of war, a lot ofconflict, a lot of disruption
(31:08):
and the increase in abundance oftsetse flies were largely
related to changes to theenvironment from the movement,
the mass movement of populationsaway from areas that they had
taken care of.
And as we think about war as acontext for disease emergence
and for pathogens, it really isthinking about not just the boom
(31:29):
boom that happens but thesocial, economic, cultural and
environmental disruption thattakes place during times of war
that many point to as sort ofinflection points of when many
diseases have emerged orre-emerged.
So if you pay attention toinfectious diseases.
Then you also want to payattention to war and conflict,
(31:50):
because these two are intimatelytied.
Speaker 6 (31:53):
Yeah, that's very true.
One thing that always comes tomind when I read about these
stories and when I learn aboutthese stories is this was also a
very different time.
Right Nowadays, when a newdisease emerges, probably within
days or weeks, we know what itis.
Right, we hear these stories oh, there's something suspicious
going on in this country, xyz.
And then a week later we hearit's Marble Virus or it's in
(32:17):
Seoul, right and back.
Then it took them decades andthey had these symptomology.
They called it Koreanhemorrhagic fever or they called
it Crimean fever or Crimeanhemorrhagic fever, and for
decades nobody knew what it was.
Can you imagine this?
Can you imagine living in atime where people fall sick and
die and nobody has an answerwhat it was?
(32:39):
Nobody can even tell you.
It was crazy times.
I think we're very lucky tohave the diagnostic capabilities
that we have nowadays.
Speaker 5 (32:47):
Yeah, I completely agree, dennis, and I think it's
important to also put that intocontext when we're talking about
just in general not even justin wartime, but in general, like
whenever there is a new diseasethat presents itself right the
reason that we're able to detectthings earlier and develop
treatments and stuff like thatearlier is because the
(33:09):
technology has advanced in a waythat is so beneficial to us as
a population.
It's not necessarily somethingis being done unethically or
something's being done that'smaybe not up to standard.
Our technology has advancedincredibly, and while, yes, it's
still not perfect, that's thedirection we want to be moving
(33:29):
right, because that's how we cansave so many more lives, and so
I think it really is amazing tosee that transition from 40, 50
, 60 years ago to now, howrapidly we're able to respond as
a society to these newencroaching pathogens.
Speaker 4 (33:44):
I absolutely agree with that as well, and I think
that before we had the kind ofglobalized connectivity of
researchers sharing informationback and forth, which is so
valuable and really helps usmaintain surveillance and keep
everyone safe, before we wereable to identify these diseases
there was so much fear, and Ithink that's where we saw a lot
of things cropping up around.
You know, disease was linked tomorality, right, so like people
(34:07):
had this idea that they couldkeep themselves safe in a way if
they were just like good enoughor something like that, or that
being sick said something abouta person or whatever, and I
think we've talked about that onprevious episodes.
I think I got into this field,into infectious diseases, with
kind of that hope that we couldstart to move away from that and
more towards just caring aboutpeople because they're people
and treating them because wehave whatever's available,
(34:28):
whether that's a vaccine or goodantivirals or good antibiotics.
Speaker 5 (34:32):
It takes me back to the miasmas that we've
previously talked about, camille.
I think there was like a linein the book, or some paragraph
or something like that, thattalked about how it was.
You know, associated with thesmell of a person is how
susceptible they are to diseaseand stuff like that.
So the nobility were able tosurround themselves with nice
smelling gardens and goodperfumes, and that would keep
(34:55):
the diseases away.
Versus the other status levelsweren't able to do that because
they didn't have the, I guess,resources to do so, nor the
space, as we know, and so theywere presumed to be a dirtier or
more sickly population becauseof so.
Speaker 4 (35:12):
Yeah, and I think if there is a miasma, war is the
miasma right.
If there is something that'slike just going through and
spreading disease, it's warright.
So, like war is the equivalentof kind of our modern miasma of
this can spread very quickly andspill over right.
Wars spill over borders andthey spill over groups of people
and drive all of these changes.
And a lot of times it can verymuch be something that if it's
(35:34):
not happening to you, it's nothappening in your backyard, it's
invisible, right, and thisinvisible spread of pathogens
until it does show up on yourdoorstep.
And that's actually how I cameto this episode was thinking
about one of the current wars,which is the Russian-Ukrainian
War, and so, for context, thatbegan on February 24th 2022.
I can actually remember where Iwas when this war began.
(35:54):
It's ongoing, as of thisrecording, and, like many
conflicts throughout history,this war has really shaped
pathogens.
So what I first saw about thisit came out in November 2024.
It was an article published byScience and basically the
article was saying that theprophylactic use of
broad-spectrum antibiotics inUkrainian triage centers was
really promoting drug-resistantbacteria.
(36:16):
It's really interesting.
They quoted a lot of differentpeople in this article and one
of them was Jason Bennett, whowas the director of the Walter
Reed Army Institute of Research,saying multi-drug-resistant
organisms, and he stated thatit's eye-opening just how
incredibly resistant some of thebacteria coming out of Ukraine
are.
I haven't seen anything like it, and what I think is
interesting about this is thatseeing multi-drug resistance
(36:39):
rise, or any drug resistancerise, isn't likely new, but we
have the technology now to seeit happening in real time, and
there's certainly been a lot offunds poured into Ukraine, and
so we are seeing this happen in.
I want to talk about isKlebsiella pneumoniae.
This is a bacteria it's known tocause one in five deaths that
(37:07):
are attributed to antimicrobialresistance globally and has been
reported to be hyper virulentand pan drug resistant when
cultured from Ukrainiancasualties, and that's from a
December 2024 article in theJournal of Infection.
What allows Klebsiella often tobe so notoriously resistant to
antibiotics is that it can formbiofilms, so that's the bacteria
is there, and then there's thislike mucousy membrane and it
can be very difficult forantibiotics to penetrate and
(37:28):
actually stop the bacteria fromeither multiplying or kill the
bacteria off.
And what's really wild aboutthis is that 80% of Ukrainian
Klebsiella genome sequence carrya gene that is known as NDM1.
It makes them resistant to awhole class of antibiotics, and
that class is carbapenems.
This rate of resistance tocarbapenems in Klebsiella is 10
(37:53):
times higher than anywhere elsein Europe.
Even just since 2022, you haveseen that dramatic of a shift
that we now see resistance inKlebsiella that is 10 times
higher than the rest of Europeto a whole class of antibiotics,
which really can limit yourtreatment options for people, as
you were talking about earlierwith tuberculosis, the concern
(38:15):
isn't only for soldiers, right,so it's not just for Ukrainian
soldiers and people, socivilians will be affected.
But the reality is that, on aglobal scale, human health is
very intertwined and theseresistant microbes really do
have the potential to spreadbeyond Ukraine.
Speaker 5 (38:31):
Yeah, Camille, and something that's particularly
scary from what you mentioned.
Correct me if I'm wrong on that, but if I'm correct,
carbapenems are also consideredthe last line of defense and are
used for a lot of multi-drugresistant infections.
And so to have an entire familyof Clamsiella that is
completely resistant to theentire class of carbapenems,
(38:53):
that's pretty intense.
Speaker 2 (38:54):
Yeah, carbapenem resistance is a pretty scary
evolution of antimicrobialresistance.
Speaker 6 (39:00):
Camille, I have a question for you.
It's probably a very naivequestion, but how does the
antibiotic resistance occur?
What is producing this?
I know Klebsiella is somethingthat you also find in a
nosocomial setting, in ahospital setting quite often,
and is it soldiers being injured, then going to hospital being
treated with antibiotics, notgiven the full course?
(39:21):
So because of some, can youexplain that a little bit more
to me?
Speaker 4 (39:31):
Yeah, so the CDC is basically stating that the war
has stressed Ukrainian healthsystems, so that's part of it,
and that really creates anenvironment where antimicrobial
resistant bacteria can thriveand really quickly spread, not
only within the country butacross borders.
But also, what you're seeing isyou're basically seeing these
mass casualty events, right?
So not only are hospitalspotentially being shelled,
they're also seeing a hugeinflux in people that are
wounded, whether those aresoldiers or civilians, and
(39:53):
there's a shortage of staffing,which is also a problem, right?
So if you have one nurse who'ssupposed to be managing all
these people, can he or shereally physically like, take all
the infection preventionmatters?
You know, washing your hands,changing your gloves?
Your resources are limited, soyou're potentially spreading
something that one person hasbrought in.
But you also are seeing that intriage centers, oftentimes we
(40:14):
use these what's known as broadspectrum antibiotic treatments
just to see if they can catchsomething to improve someone's
health outcomes, and it's reallyunderstandable why we do that,
right?
Even in the United States,likely, if you came into some
emergency rooms and you werewounded badly enough, they might
still do that to be like hey,you are probably going to get an
infection from whatever this is, we're just going to give you
(40:35):
broad spectrum antibiotics.
When you start to do that on apopulation level, I think that's
when you start to see whatwe're seeing right now.
That's occurring in Ukraine,and what's wild about this is
that Ukrainian refugees that arefleeing the war, or injured
soldiers that are beingevacuated to receive medical
care, are actually bringing thisresistant bacteria with them.
So it's been found in sixEuropean countries as well as as
(40:57):
far away as Japan.
So this is definitely moving.
And again, this is going backto that idea of you know, war is
miasma, right, people might notbe tuning into the fact that
there's this war going on.
People get empathy, fatigue,they see it happen and then they
stop eventually.
But the effects of it are veryreal and are definitely going to
impact our intertwined health.
And I think about antimicrobialresistance a lot, and that's
(41:20):
because globally, it's reallyknown to cause more deaths than
other health threats likemalaria or HIV, and the WHO has
even declared antimicrobialresistance as one of the top 10
public health threats tohumanity.
So this is not like a jokingmatter in any sense, and
conflict zones are really thesecradles of antimicrobial
resistance and that might be.
(41:41):
Again, the health systems arestressed, you're running out of
staff, you're also just doingbroad spectrum treatments, but
also just the nature of thewounds that we see currently in
wars.
Right, if you are being hit bya bullet or by shrapnel, it
enters the body and can embedpathogens really deeply in the
tissues, which is an ideal placefor them to thrive.
And the triage centers thenreceiving these people who are
(42:05):
potentially severely wounded aredoing kind of whatever they can
.
They're throwing whatever theycan to see if something sticks
and just to potentially improvepatient outcomes.
And so we're seeing not just thecarbapenem resistance, but
there was investigation intosome soldiers who have passed,
and one of them, who hadsuccumbed to sepsis, was found
to have extensivelydrug-resistant bacterial strains
.
Those are known as XDR.
And another investigation of adifferent soldier found nine
(42:28):
extensively drug-resistantbacterial strains.
That's not something that wenormally see, right, and this is
something that we really needto be thinking about and
thinking about how do we preventthese from happening?
Yes, preventing conflict isgreat if you can, but that's
often such a difficult thing toeven draw something like a war
to a close right and finding away to still manage people's
(42:49):
health and to protect everyonethere, as well as your entire
global community.
Your war is not just going to bein one place, right, the
effects of it are going tospread out Instead of being
thrown into a pond.
You see all these ripples, andthere's a quote that I just
wanted to share just to end withthat it's from Dr Scott Pallett
, who's a physicianmicrobiologist at the Royal
Center for Defense Medicine, andhe said that the level of drug
(43:10):
resistance we are seeing inUkraine heralds the peril of the
post-antibiotic era, and that'ssomething we've talked about
previously before that we really, in many cases, have relied onp
throat to make sure they don'tjust have the flu or COVID or
something, before we just givethem antibiotics, and this is
(43:46):
something that it's ourresponsibility.
Once we have technology whichis something we've talked about
in this episode Once you havethe technology, you can identify
something.
It's our responsibility to useit so we can be good stewards of
the therapeutics that we dohave.
Speaker 2 (44:00):
Yeah, I like that.
Camille, I think your pointreally drives home something
that I think we all know aboutwar and conflict and its
relationship with infectiousdiseases, which is that you may
see on the television thatthere's a war happening in some
other part of the world andthink it doesn't really affect
me, but the truth is that theemergence of infectious
(44:21):
pathogens affects all of us.
Right?
Because if vaccination ratesfall in a particular area that's
experiencing conflict, ifanimal migration or vector
emergence takes place in a placewhere the bullets are flying
and people are having to leavetheir homes, feral animals are
roaming, there's no publichealth infrastructure to help
(44:42):
vaccinate or call stray animals.
When you think of all thesystems, protections that keep
us safe from pathogens emergence, then you think of how
disruptive war is to thosestructures.
You can see that really weshould all be worried anytime we
see a conflict around the world, not to say that we're in any
(45:03):
position to stop it.
It's not a video game.
These are complex geopoliticalsituations, but I do think that
if we are trying to advisepeople who are either in our
clinics or our public healthauthorities, or even people in
our community who may notunderstand these areas of
interconnectedness.
(45:24):
I think, thinking of theseexamples that you guys have all
described TB, antimicrobialresistance, crimean Congo is a
viral emergence.
History is riddled withexamples of wartime and conflict
being an inflection point forthe emergence of a new pathogen
or the re-emergence of an oldone.
And so I think, just as we seean unprecedented amount of
(45:48):
conflict in the world, payingattention to those things, it's
not just how it affects thosepopulations, it's also how it
might eventually spill over andaffect us.
Speaker 6 (45:56):
So how it might eventually spill over and affect
us Absolutely and I think, toour listeners, we've only picked
a few examples.
I think this was just reallyjust the tip of the iceberg.
I think we could have gone onand on, going back centuries and
different wars, and we reallyjust gave you a little overview
of some things that we areinterested in.
(46:18):
One thing as we were talkingabout this, I realized we didn't
really talk about humandisplacement.
Right, I talked about animalmovements and so on, but the
displacement that war causescauses ripple effects, camille
said, like all over the world,and I think this should be a
five episode season.
Almost right, I think this wasjust really the surface, for
(46:40):
sure.
Speaker 2 (46:40):
Yeah, and if you look at, sometimes people will ask
why is there so much militaryfunding for infectious disease
research?
And when you think about it,what do we want?
We want to keep our soldierssafe.
We want to keep our militarysafe.
We also know they're going toplaces where they're going into
places where they can be exposedto these pathogens.
(47:01):
So some of the greatestinnovations in vaccinology, in
diagnostics, have taken placethrough entities like the Naval
Medical Research Units, whichwere founded really as a
mechanism to promote researcharound the world as part of
defense, because it's not justhow many guns you can make, it's
also can you keep your militaryworkforce safe and can you
(47:24):
address the health needs of thepopulations that are being
affected.
It is all interrelated and Idon't see global health security
going away anytime soon.
So I think this is a reallygood topic, guys, very timely
topic, and I can guarantee youfive years, 10 years, when we're
all you guys are almost as grayas I am, and when you get there
, I think we'll still be havingthese discussions about war and
(47:49):
conflict and its effect oninfectious diseases, because
it's a tale as old as time.
Speaker 6 (47:53):
All right, any last words?
I think that's again anothercool episode.
Thanks, camille, for pickingthe topic and to our listeners,
I hope you enjoyed this as muchas we enjoyed it.
Speaker 2 (48:08):
Any last take-home messages, what do you think?
Can we say give peace a chance.
Can we say something?
I agree Too trite.
Speaker 4 (48:12):
I like that Give peace a chance.
Speaker 2 (48:16):
Maybe more effective than any vaccine is peace.
That's more.
Maybe more effective than anyvaccine is peace guys.
Peace, peace and stability.
So it's a good.
Those are good, good things forus to take away, but it's
always good to see you guys.
Thanks for letting me invadethe podcast again.
It's really good to seeeverybody and I learned
something new from all of youevery time it's never an
invasion.
Speaker 5 (48:36):
This is your home.
Speaker 4 (48:37):
You always have a space on the podcast couch.
Speaker 6 (48:40):
All right, Thanks everybody.
Speaker 5 (48:43):
Thanks so much again, guys, for listening.
Speaker 3 (48:47):
Thanks for listening to the Infectious Science
Podcast.
Be sure to hit subscribe andvisit infectiousscienceorg to
join the conversation, accessthe show notes and to sign up
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Speaker 2 (48:58):
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Speaker 3 (49:07):
Also, don't hesitate to ask questions and tell us
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To get in touch, drop a line inthe comments section or send us
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Speaker 2 (49:16):
So we'll see you next time for a new episode, and in
the meantime, stay happy stayhealthy, stay interested.
This is a podcast about One Health the idea that
the health of humans, animals,plants and the environment that
we all share are intrinsicallylinked.
Speaker 3 (00:15):
Coming to you from the University of Texas Medical
Branch and the GalvestonNational Laboratory.
Speaker 2 (00:19):
This is Infectious Science.
Where enthusiasm for science?
Speaker 4 (00:23):
is contagious infectious science, where
enthusiasm for science iscontagious.
Hello everyone, and welcomeback to Infectious Science.
Today we are talking about warand pathogens.
There are very few examples ofprolonged peace in history, and
the human penchant for war hasin history, and continues today,
to significantly exacerbate thespread of infectious diseases.
(00:44):
We've previously talked abouthow globalization exposes us to
diseases that previously wereonly endemic in a specific
region or locale.
Just like globalization, waralso increases contagion,
because wherever groups ofpeople move, so too does disease
.
Whether masses of people aremeeting on a battlefield or
forcibly displaced by conflict,disease, the constant companion
(01:06):
of humanity, tends to follow.
In addition to this, war alsoincreases disease by disrupting
public health infrastructure andmaking resources scarce, which
can result in malnutrition orthe use of unclean water, all of
which increase ourvulnerability to pathogens.
We have selected some historicand modern examples of how war
has shaped the spread and naturepathogens.
So let's dive in.
(01:26):
Alex, you had the first war inour chronological history.
Do you want to start?
Speaker 1 (01:31):
My name is Alexander Alvarado, for today's episode of
the Infectious Science Podcast,talking about war and disease.
I'm going to be talking aboutthe Boer War and about measles
outbreaks in British-runconcentration camps during the
later phase of the war, and soI'm going to give some
background as far as some of theunderlying tensions that led to
(01:51):
the war, talk a bit more aboutthe Boer War itself and then
talk more about measles virusand how the war ultimately
changed the spread of measlesitself and the course of disease
that measles is able to cause.
So the United Kingdom formallyannexed the Cape Colony, which
is an area that encompasses muchof the western coast of South
Africa, following the signing ofthe Convention of London in
1814 with the Netherlands, inthe aftermath of one of the last
(02:16):
of the Napoleonic Wars, the Warof the Sixth Coalition, and so
the British ended up inpossession of a territory which
had a population of Dutch andHuguenot settlers that came over
as a result of Dutch activitiesin the colony over the past two
centuries and the indigenouspeoples that had long been on
(02:38):
the land, and there weresignificant political
(03:01):
disagreements between theBritish were curtailing the
practice of slavery and theunwillingness of the British
administration to go and expandthe colony to enable these
semi-nomadic boar cattle herdersto expand their range.
And ultimately this led forsome of these settlers, some of
these boars, to opt, over thecourse of largely the 1830s
(03:22):
through the 1850s, to settle inthe interior of South Africa in
order to live beyond the courseof largely the 1830s through the
1850s, to settle in theinterior of South Africa in
order to live beyond thejurisdiction of the British, to
live outside of the boundariesof the Cape Colony.
In time, these settlementscoalesced into some of these
Dutch settler republics, theseBoer republics, including states
like the Orange Free State andthe South African Republic.
(03:45):
And these states, they were hitby an influx of foreigners as a
result of the discovery of goldin 1884, the Whitwater Strand
Gold Rush, and largely Britishnationals ended up emerging into
the South African Republiclooking for gold.
And there were fears,ultimately, among a number of
these Boer residents in theRepublic that the amount of
(04:07):
British residents, which in timecame to outnumber the Boers,
that these British nationalswould amass enough political
clout to push for the absorbanceof the independent state into
the British Empire.
And there were continueddisputes regarding what the
rights of these foreignresidents should be and upon the
duration required for them toattain citizenship, etc.
(04:28):
In order for the Boers to findsome ways to dilute the
political power of these Britishnationals and these foreigners
who had come seeking for gold,pushing back on that.
And so the British attempted tonegotiate with the South
African Republic regarding thenature of the rights of these
foreigners who had come seekingfor gold.
But the collapse ofnegotiations between the British
(04:50):
and the Boer states ultimatelyled to the Orange Free State and
the South African Republic toboth declare war against the
United Kingdom.
Initial Boer victories in 1899,a mobilization by the British,
one of the largest at the time,enabled ultimately the capture
(05:14):
of both states in 1900 and oflarge swaths of territory.
And so, with the collapse ofthe central states that
initially started to wage thewar, with continued, though,
civilian support and the natureof the decentralized structure
of command for the Boer armiesand local knowledge of the land,
the climate was ripe for Boerguerrilla warfare to continue
(05:37):
the struggle for longer againstthe British.
And the British ultimatelydecided, in order to go about
suppressing the spate ofguerrilla warfare and to enable
the end of this war, tried toessentially detach the Boer
military forces that werecontinuing to battle against
them, from the civilianpopulation and from the
(05:59):
resources that they relied uponfrom the civilian population,
like food, and so they destroyedBoer farmsteads and settlements
, they burned crops and theydisplaced the population, both
Boers and the indigenous peoplesof that land.
They displaced them into thesespecially constructed
concentration camps, and so thusthis enabled the Boer
(06:20):
guerrillas to be deprived ofcivilian cover that they could
otherwise blend into, as well asof civilian support and the
material resources that theycould use in order to further
continue their campaign againstthe British.
And these camps were ratherdensely populated and were known
for having poor sanitation andhad limited food rations, both
(06:42):
as a result of the limitationsof the time as well as British
policy that exacerbated thesituation.
So relations of knownguerrillas received smaller
rations than others, and theindigenous African detainees
lacked a guaranteed food ration,unlike some of the Boers, and
were thus forced to work forfood, unlike Boer detainees, and
(07:03):
received nutritionallyimbalanced rations when they did
receive rations, as a result ofpseudoscientific misconceptions
of dieting at the time, and asa result, this was a population
that, between the stresses ofwar, which is known to
negatively affect the immunesystem, and the widespread
nature of malnutrition in adensely populated area.
(07:25):
This gives you animmunocompromised population in
an area where infectiousdiseases can easily spread, and
in many ways this was almost theperfect storm for a measles
outbreak.
And so measles virus itself is aparamyxovirus that has a
non-segmented RNA viral genomewhich is capable of causing the
disease of measles in humans,and so viral infection is
(07:49):
largely caused through aerosoltransmission, be it through
direct contact or in contactwith infected surfaces.
And so measles virus itself, ittends to infect these airway
epithelial cells and specializedlung immune cells, the latter
of which may include, say, thesealveolar macrophages, and
alveolar macrophages, bybecoming infected, may end up
(08:12):
trafficking measles virus tolocal lymph tissue, enabling
subsequent infection of morespecialized immune cells, some
naive B cells as well as memoryT and B cells.
And this is mediated through themeasles virus interaction with
the SLAM receptor, otherwiseknown as CD150, which is this
surface receptor that'sconserved among some of these
(08:33):
cell types.
And as a result of theinfection of some of these
specialized immune cells, andparticularly these memory B and
T cells, and the necessary celldeaths caused by the immune
system, this response to go andkill the measles virus cells
that were targeted to otherorganisms and, essentially,
their replacement by thesepopulations of BNT cells that
(09:08):
are specific to measles virusspecifically, it enables an
increasing amount ofsusceptibility to other
pathogens and thisimmunosuppression can last for
some time, even after the fullresolution of the course of
disease of measles itself.
It can prove to be quiteproblematic, but in terms of
measles disease itself.
So basically, after a 7 to 14incubation period you start to
(09:29):
experience some of the signs ofa nonspecific febrile illness.
So a fever, cough, rhinitis.
These are some of the thingsthat may start to emerge, and,
in conjunction with some ofthese prodromal symptoms,
conjunctivitis, coplic spot anda maculopapular rash are rather
characteristic of measles virus.
Infection and the spread of thevirus to further within the
(09:52):
lungs and into the brain maylead to pneumonia and
encephalitis respectively, andso pneumonia can be caused by
other pathogens as a result ofmeasles-induced
immunosuppression, or directlyby measles, due to the sort of
damage that measles can cause tothe lung itself.
And pneumonia is often theprimary cause of measles death,
(10:14):
be it indirectly or directly asa result of measles virus
infection.
And it's worth noting thatmeasles virus is highly
contagious.
It has an R0 value of about 12to 18, which really points to
the contagiousness of measlesvirus itself, as a number of
otherwise naive, uninfected,susceptible individuals can
(10:37):
ultimately become infected byjust one case.
And so, in a densely populatedarea, in the absence of modern
day vaccines for measles virusand in a population that was
highly immunosuppressed, theseBritish-built concentration
camps for the Boers and for theindigenous people of the Boer
(10:58):
republics really enabled a rapidspread of measles virus, and it
enabled further these highdegrees of mortality to it,
higher even in adult cases thannormal, because the measles
virus largely tends to be adisease of the youth right.
Once infected with it you mayhave lifelong immunity, but it
(11:18):
is particularly hard on youngerpeople.
These outbreaks were somewhatunique, though, with relatively
higher case fatality rates inadults, which was a new
development that in many wayscould probably be attributed to
the stressors of the camp andthe nature of the concentration
camps in general in terms of thedense degree of the population
and the malnutrition that theywere experiencing.
(11:39):
And so, over the course of the1900 to 1902 period in which
these camps were still operable,there were about 47,000
civilians, be they Boer settlersor the indigenous peoples, that
died in these British camps.
Roughly about 30% of thesedeaths are estimated to have
been as a result of measles.
(12:00):
In some of these camps, over50% of children's deaths were
due to measles and over 10% ofadult deaths were due to that
same disease.
And I think that really speaksto the nature of how these
specially constructedenvironments, these temporary
environments, and the nature ofwar can significantly affect the
spread of infectious disease,and it's something to be
(12:23):
cognizant of in modern conflicts.
Even to this day, there arecertainly still issues with that
, with a number of wars that arefought and with the breakdown
of sanitation systems and of theemergence of, in some cases,
hastily constructed, denselypacked refugee camps and further
this outbreak, I think, is abit of a cautionary tale.
(12:43):
This points to the destructivecapacity of measles virus when
it's not being mitigated bythings like widespread vaccine
uptake and antivirals and theresources that we have today,
and I think it certainly pointsto how, when we have infectious
diseases that can't becontrolled by some of these
therapeutics, or if there's somereluctance to go about using
some of these therapeutics, theconsequences can be rather
(13:06):
disastrous for the population.
Thankfully, there have been nolingering effects to this day of
the measles epidemic in theBritish concentration camps, but
the camps themselves and thedegree of death that ultimately
pervaded in them is still inmany ways a cause of concern for
what happened over the courseof that war, and certainly a
(13:27):
story is worth attention, and soI figured that I talk about it
a bit more today in this segment.
Back over to you.
Speaker 5 (13:34):
Awesome.
Thanks, alex.
It's always so good to learnand understand things that you
really knew nothing aboutbeforehand.
I really like using theserecordings and these sessions
that we have to learn for myselfand study things I was
previously interested in butmaybe didn't know too much about
specifically, and the war andthe disease process that I
(13:55):
wanted to focus on for ourrecording session today was
actually the relationshipbetween tuberculosis and World
War I, tuberculosis and WorldWar I.
So, as we here know,tuberculosis is caused by
mycobacterium tuberculosis.
It has two phases really, orthree, I guess, if you want to
consider latent phase as a phase.
But primary tuberculosis is notso infectious for most people
(14:19):
and most people's immune systemsdo fight off the infection at
this stage.
However, from primarytuberculosis can become latent.
So it's basically yourinfection is held at bay, but
it's still present in the bodyby your immune system.
However, certain triggers thatdepress the immune system can
cause that infection to becomereactivated, and that's called
(14:42):
secondary tuberculosis.
Just want to make sure all thatsounds right, matt, sound good
on your end.
Speaker 2 (14:47):
Sounds very good on my end.
Yeah, doing great.
Speaker 5 (14:49):
Awesome, okay, so actually in World War I, before
the war, tuberculosis itself wasa pretty rampant disease
process and of course, with warbringing so many people into
close quarters and of coursewith war bringing so many people
into close quarters, it reallycaused a massive spike in
tuberculosis cases.
Specifically in World War Ithey didn't really use
(15:15):
particularly great screeningmethods for tuberculosis.
So, if I'm correct, matt, nowof course we do our physical
exam, we do certain tests totest whether or not a person has
tuberculosis they're actuallyspecific for testing for
tuberculosis and of course alsodoing chest x-rays seemed as
pretty routine for screening forthe infection.
But back then we didn't havex-rays used in the screening
(15:39):
process for tuberculosis and wereally just used physical exam
and history to screen.
For that Is it pretty difficultto actually diagnose primary
tuberculosis just off a physicalexam.
Speaker 2 (15:52):
Yeah, I mean it really depends on the context.
I've seen a lot of peoplearound the world with
tuberculosis infection and itdoes have a very typical
presentation A lot of peoplepresent with chronic.
It's a chronic infectiousdisease, right Like something
that's indolent, very slowmoving, slow growing.
Fever, chills, night sweats,weight loss are often very
(16:14):
common and it was a reason thatback in those days they called
it consumption, because peoplelooked as though they were being
consumed by the pathogen.
So clinicians of those dayswere pretty adept at diagnosing
tuberculosis even without allthe fancy diagnostic tools.
Now they may have over-calledsome things tuberculosis because
we didn't have the moleculartests and, dennis, I won't push
(16:36):
you on when Robert Kochelaborated the first real
diagnostics for tuberculosis anddescribed the bacterium, but
these were things that werebeing deployed at the time.
But probably physical diagnosisand history, you know,
obviously, palpating lymph nodes, assessing for the clinical
signs and symptoms, listening tothe lungs, these were probably
(16:58):
as good as we got.
But you know, because it tendsto travel in populations, you
would certainly see it inclusters, in people who are in
close quarters.
So I think you rightlymentioned war does tend to
produce disruptions in a lot ofthe public health control
measures that we typically relyon for peace and stability
during peace and stability times.
So you know it's not surprisingspikes in infectious pathogens
(17:22):
during those times of upheaval.
Speaker 5 (17:24):
Yeah, absolutely Completely agree.
And speaking of how you seethese increases and these spikes
in the community in World War Iand, as I'm sure, in all the
other wars we're going to talkabout today, it's important to
note that these diseases didn'tjust infect and affect soldiers.
Right, there were so manycivilians that were at the other
(17:46):
end of this infection and alsodied.
And specifically in World War I, there's not a great count for
how many people died fromtuberculosis just in those years
of the actual war, butestimates are in the millions,
and so that just shows howhorrible this disease was at
that time.
And specifically so becauseback then, in World War I's
(18:07):
years, we didn't actually have acure or treatment for
tuberculosis.
So back then the treatmentreally was just isolation,
nutrition and sunlight, fromwhat I could read.
So fresh air, sunshine that wasthe best that we could do and
pretty aggressive disease.
So without an actual treatment,without an actual cure, it's
(18:33):
clear to see why it took so manylives back then.
From what I can see and fromthe research that I did, the
first treatments that weredeveloped were actually in 1943.
It was streptomycin was thefirst treatment used for TB.
I don't specifically believethat's used nowadays, matt,
correct me if I'm wrong, but Idon't think so.
They use it in resistance.
Speaker 2 (18:52):
So in people who have treatment failure it's a second
line treatment.
There you go.
Or it can be used in people whohave complicated TB, things
like cerebral TB or likemeningitis, tb, meningitis,
things like that.
Sometimes in treatment failuresthey'll use streptomycin.
(19:13):
So it's not ideal.
There's other alternatives andit depends on the country too.
In countries where there is,for example, high prevalence of
multidrug resistant tuberculosis, you tend to use more things
like quinolones, which is whyyou don't see them prescribed as
widely for general respiratoryinfections in some other
countries.
It's because you want toreserve those kinds of things
(19:34):
for TB treatment, because theycan be quite effective in the
second line treatment.
But I think Camille is going tobe getting into more
antimicrobial stuff later on.
But you're right onStreptomycin certainly is not
first line.
Speaker 5 (19:44):
It has a lot of toxicities you're right on,
streptomycin certainly is notfirst line.
It has a lot of toxicities.
Interesting, yeah, and I thinkmedication that we do so use as
first line.
I know TB, we typically willthrow a few medications at it as
a first line treatment.
But isoniazid specifically atleast from the textbooks, from
what I know is considered one ofthe first line treatments and
that was specifically broughtout and used in 1952 from what I
(20:07):
could see.
So it really shows a solid 20,30 years after World War I
finished we didn't reallydevelop, I guess, common
treatments for TB until then.
So it just really shows howaggressive this disease process
was, how hard it is to treat,and highlights just the effect
that it had overall onpopulations throughout World War
(20:28):
I, which was the first worldwar, right, and so there were so
many countries that cametogether, so many countries
involved.
Really just you're able tounderstand, when you think about
it from that aspect, howtuberculosis had such a rampant
effect and a really detrimentaleffect on the population.
Speaker 2 (20:45):
Yeah, no, that's right on.
We treat people now with fourdrugs.
There's the drugs that stop thebacteria from replicating those
are bacteriostatic and thenthere's bactericidal, the ones
that kill it, and so you need acouple of different ways to get
at this because it's just likein so much of medicine we need
drugs to attack things that arefast growing, so we're good at
that.
We're less good at attackingthings that are slow growing, so
(21:07):
this one needs a lot of help tobe able to treat it.
And you're right, times of war,times of disruption, and in a
time where these drugs, thesecountermeasures, are not readily
available and you're displacingpopulations and it wasn't so
much, as I understand it, of amilitary issue, as much as it
was for the populations in thecountries that were experiencing
the war and hosting theseconflicts, that were most
(21:30):
affected by these contagionsduring World War I.
And it wasn't just TB.
We had a lot of sexuallytransmitted infections, typhoid,
malaria, so a lot of otherpathogens went rampant during
the times of these wars.
Speaker 5 (21:45):
Yeah, I completely agree.
I actually settled on TV andWorld War I specifically because
I just finished reading ahistorical fiction book that was
set in the time of both WorldWar I and World War II, but it
specifically talked about theestablishment of a preventorium
I think is how you pronounce itwhere they would isolate
patients with tuberculosis, andit was cool to pull that into
this.
Speaker 6 (22:05):
What's the name of the book with?
Speaker 5 (22:06):
tuberculosis and it was cool to pull that into this
what's the name of the book.
Speaker 2 (22:12):
I have the book right here.
Give me one second.
Well, while she's getting thebook, I'll just say that Sir
William Osler, who lived from1849 to 1919, the father of
modern medicines.
He wrote the first real seminalmedical textbook of medical
management called the Principlesand Practice of Medicine, and
tuberculosis slash consumptionfeatures heavily in his textbook
.
He has a whole chapterdedicated to it and, like you
(22:33):
said, Christina, there wereprecious few things you could do
.
Osler was a fan of prescribingopium in these circumstances
because it was good for cough,it was good for pain and
obviously there were othercountermeasures that they would
try.
But when you read these oldtextbooks you realize they were
working mostly with publichealth control measures.
(22:53):
They can go to altitude, gooutside in the sunlight.
Tuberculosis bacilli do notlike UV light, they do not like
circulating air and so when yougo to a ward, especially in
Southern Africa or other placeswhere TB is highly prevalent,
when there's a TB ward, it'lloften be very well lit, the
windows will be open and thefans will be blasting, in
(23:14):
addition to all of the maskingand other countermeasures that
we have, because people knowthat it's those environmental
things that are also going tohelp contain the contagion.
Speaker 5 (23:23):
Wow, that's really interesting.
I didn't know that.
And then, Dennis, for yourquestion.
The book is called the Women ofChateau Lafayette, so pretty
good book.
Speaker 2 (23:33):
I can only hear Hamilton saying Lafayette.
Speaker 5 (23:37):
No, yeah, they actually talk about Hamilton in
the book too.
So if you can't get enough ofHamilton, read the book.
It was a good one, but that'sall I have for TB World War I.
I think, dennis, you have thenext war and pathogen that we're
going to talk about today, soyou want to take over.
Speaker 6 (23:54):
Yeah, absolutely.
I want to talk about a diseasethat was discovered during World
War II and it's also a goodexample of how war can shape or
can create ecologicaldisturbances and modifies the
landscape and that leads to anoutbreak of diseases that rely
(24:16):
on the ecological complexitythat's then disturbed through
war and I'm going to talk aboutmy favorite pathogen.
I've been very humble.
I've never really talked aboutCrimean Congo hemorrhagic fever
here on this podcast, my mainfocus.
But Crimean Congo hemorrhagicfever was discovered in 1944 in
the Crimean Peninsula and whathad happened is the Crimean
(24:40):
Peninsula.
I think everybody at this pointin time has an idea where that
is located in time has an ideawhere that is located.
With the Crimean War and withthe Ukrainian War, the Crimean
Peninsula was occupied by Germansoldiers for many years and in
1944, the Russian soldiers werepushing the German soldiers out
(25:00):
of the Crimean and also out ofparts of the East and pushing
them back towards Central Europe, and during the occupation the
farming in this area had stopped.
You can imagine, during anoccupation, everything stops
right.
The farmers don't take care oftheir fields, so grass overgrows
, pests maybe, come in.
A lot of wild animals likerabbits, hares, mice, you name
(25:24):
it.
They come in, they can hide inthe grass and they often bring
other vectors with them, and sothey brought in quite a number
of ticks.
And so what happened in 1944 is, when the Crimean Peninsula was
reoccupied by the Russians,roughly 200 Russian soldiers
fell ill with a hemorrhagicfever, and it was very severe,
(25:46):
and the spotlight really quicklyfell on the ticks, because the
tick density was so high in thatarea.
The grass that had overgrown,the rabbits that had come in,
that brought the ticks, and soon.
So there were ticks crawlingall over the place and they
caused a very severe disease,hemorrhagic fever, with high
fatality rates.
And what the Russians did isthey dispatched a team that had
(26:09):
already discovered a new diseasein 1937 in the far east of
Russia, and Mikhail Chumakov,like a famous virologist, was
sent and was to investigate thecase, identify the pathogen.
This took a long time, it tookdecades until they finally
figured out that it's a buniavirus, and they had a lot of
(26:32):
suspicion what it could be, andit took them a long time to
figure it out.
And in the meantime, in the1960s, another virus had been
discovered in the Congo, inCentral Africa, and that's why
they then found out that thoseare the same diseases and that's
why it has this funky name,crimean-congo hemorrhagic fever,
(26:52):
because they thought it was twodifferent diseases.
But in the 1960s they actuallyrealized it's the same disease
and neither the Russians nor thepeople in Africa wanted to
budge and that's why they cameup with that name.
Speaker 5 (27:04):
That's interesting.
I didn't realize that that'swhere the namesake comes from,
that's really cool, Camille.
Speaker 6 (27:10):
what are your thoughts?
Speaker 4 (27:11):
I was just curious.
Why do you think it took themso long to figure out what virus
it was?
Was it just the moleculartechniques were not there?
Was it something else?
Speaker 6 (27:20):
Yeah, now, looking back, you can only speculate.
Back then they did a lot of thethings.
They would grind up the ticks,they would take blood from the
patients and they would injectit into any animal that they can
get their hands on, from catsto you name it.
They also injected it intoprisoners, prisoners of war, and
, yeah, that was a commonoccurrence back then, and they
(27:41):
were able to isolate Rickettsia.
But this turned out to be acontamination later on, and the
reason why it took them so longis that what we hear in the West
I don't know if that's corrector not is people in Africa, for
example, had worked with mice asan isolation technique suckling
mice and the Russians had notdone that.
But once the Russians used thistechnology and used animals as
(28:04):
an isolation mechanism,specifically suckling mice, they
were able to isolate the virus.
Like you said, camille, it wasa different type of technology
that was used to detect thedisease.
So I want to also add on aquick story about another bunya
virus, another war.
This is specifically the KoreanWar, which was from 1951 to
(28:26):
1954, I think, and again somesort of ecological disturbance
led to the discovery of thevirus.
The virus, just likeKorean-Ming-Kongo it took
decades to isolate the viruslater on and the agent was
identified as Hantan virus.
It's a river that runs throughKorea and so in 1951, 54, around
(28:51):
that time during the Korean Warthey had roughly 3,500 UN
soldiers.
So United Nations soldiers wereaffected by this really severe
disease, with case fatalityrates up to 10%.
And then once they gottreatment and they had better
care, the case fatality ratewent down to 5%.
But the disease back then waspresented with high fever,
(29:14):
headache, bleeding, kidneyfailure, leading to severe
illness and death in otherwisehealthy young soldiers.
And once they had an idea whatthe exposure mechanism is, which
is rodents rodents carry thedisease they were able to
contain the transmission andreduce the transmission.
But again it took them quite awhile.
(29:36):
It took probably like fourdecades really to identify and
to characterize the causativeagent of Korean hemorrhagic
fever.
And that's another classic storyin virology and it's a classic
example in military medicine.
And you can imagine having adisease going on during the war.
(29:56):
We talked about this with TB.
It strains medical resources,it makes the forces that are
fighting less efficient andeverybody's concerned,
especially if they don't knowhow the disease is transmitted.
If you're interested in this,look up Korean War and Hantan
virus.
It's like one of the hallmarksin bunyal virus virology and I
(30:17):
think then we're going on to thecurrent war, camille.
Speaker 4 (30:21):
One of the current wars?
Speaker 2 (30:22):
yeah, Dennis, I love the way that you described
especially the One Healthelements of how these pathogens
emerged in times of war, and youdescribed the environmental
disruption leading to animalencroachment, vector growth and
propagation and then sort of theperfect storm, if you will, of
factors coming together to allowthese diseases to emerge or to
(30:44):
reemerge.
And so I was thinking about whenyou were talking about Congo
especially.
I thought about there was thistime in the mid 1800s.
We use this a lot in our publichealth teaching where we talk
about the African sleepingsickness outbreaks that took
place during sort of colonialtimes in Central and East Africa
and a lot of war, a lot ofconflict, a lot of disruption
(31:08):
and the increase in abundance oftsetse flies were largely
related to changes to theenvironment from the movement,
the mass movement of populationsaway from areas that they had
taken care of.
And as we think about war as acontext for disease emergence
and for pathogens, it really isthinking about not just the boom
(31:29):
boom that happens but thesocial, economic, cultural and
environmental disruption thattakes place during times of war
that many point to as sort ofinflection points of when many
diseases have emerged orre-emerged.
So if you pay attention toinfectious diseases.
Then you also want to payattention to war and conflict,
(31:50):
because these two are intimatelytied.
Speaker 6 (31:53):
Yeah, that's very true.
One thing that always comes tomind when I read about these
stories and when I learn aboutthese stories is this was also a
very different time.
Right Nowadays, when a newdisease emerges, probably within
days or weeks, we know what itis.
Right, we hear these stories oh, there's something suspicious
going on in this country, xyz.
And then a week later we hearit's Marble Virus or it's in
(32:17):
Seoul, right and back.
Then it took them decades andthey had these symptomology.
They called it Koreanhemorrhagic fever or they called
it Crimean fever or Crimeanhemorrhagic fever, and for
decades nobody knew what it was.
Can you imagine this?
Can you imagine living in atime where people fall sick and
die and nobody has an answerwhat it was?
(32:39):
Nobody can even tell you.
It was crazy times.
I think we're very lucky tohave the diagnostic capabilities
that we have nowadays.
Speaker 5 (32:47):
Yeah, I completely agree, dennis, and I think it's
important to also put that intocontext when we're talking about
just in general not even justin wartime, but in general, like
whenever there is a new diseasethat presents itself right the
reason that we're able to detectthings earlier and develop
treatments and stuff like thatearlier is because the
(33:09):
technology has advanced in a waythat is so beneficial to us as
a population.
It's not necessarily somethingis being done unethically or
something's being done that'smaybe not up to standard.
Our technology has advancedincredibly, and while, yes, it's
still not perfect, that's thedirection we want to be moving
(33:29):
right, because that's how we cansave so many more lives, and so
I think it really is amazing tosee that transition from 40, 50
, 60 years ago to now, howrapidly we're able to respond as
a society to these newencroaching pathogens.
Speaker 4 (33:44):
I absolutely agree with that as well, and I think
that before we had the kind ofglobalized connectivity of
researchers sharing informationback and forth, which is so
valuable and really helps usmaintain surveillance and keep
everyone safe, before we wereable to identify these diseases
there was so much fear, and Ithink that's where we saw a lot
of things cropping up around.
You know, disease was linked tomorality, right, so like people
(34:07):
had this idea that they couldkeep themselves safe in a way if
they were just like good enoughor something like that, or that
being sick said something abouta person or whatever, and I
think we've talked about that onprevious episodes.
I think I got into this field,into infectious diseases, with
kind of that hope that we couldstart to move away from that and
more towards just caring aboutpeople because they're people
and treating them because wehave whatever's available,
(34:28):
whether that's a vaccine or goodantivirals or good antibiotics.
Speaker 5 (34:32):
It takes me back to the miasmas that we've
previously talked about, camille.
I think there was like a linein the book, or some paragraph
or something like that, thattalked about how it was.
You know, associated with thesmell of a person is how
susceptible they are to diseaseand stuff like that.
So the nobility were able tosurround themselves with nice
smelling gardens and goodperfumes, and that would keep
(34:55):
the diseases away.
Versus the other status levelsweren't able to do that because
they didn't have the, I guess,resources to do so, nor the
space, as we know, and so theywere presumed to be a dirtier or
more sickly population becauseof so.
Speaker 4 (35:12):
Yeah, and I think if there is a miasma, war is the
miasma right.
If there is something that'slike just going through and
spreading disease, it's warright.
So, like war is the equivalentof kind of our modern miasma of
this can spread very quickly andspill over right.
Wars spill over borders andthey spill over groups of people
and drive all of these changes.
And a lot of times it can verymuch be something that if it's
(35:34):
not happening to you, it's nothappening in your backyard, it's
invisible, right, and thisinvisible spread of pathogens
until it does show up on yourdoorstep.
And that's actually how I cameto this episode was thinking
about one of the current wars,which is the Russian-Ukrainian
War, and so, for context, thatbegan on February 24th 2022.
I can actually remember where Iwas when this war began.
(35:54):
It's ongoing, as of thisrecording, and, like many
conflicts throughout history,this war has really shaped
pathogens.
So what I first saw about thisit came out in November 2024.
It was an article published byScience and basically the
article was saying that theprophylactic use of
broad-spectrum antibiotics inUkrainian triage centers was
really promoting drug-resistantbacteria.
(36:16):
It's really interesting.
They quoted a lot of differentpeople in this article and one
of them was Jason Bennett, whowas the director of the Walter
Reed Army Institute of Research,saying multi-drug-resistant
organisms, and he stated thatit's eye-opening just how
incredibly resistant some of thebacteria coming out of Ukraine
are.
I haven't seen anything like it, and what I think is
interesting about this is thatseeing multi-drug resistance
(36:39):
rise, or any drug resistancerise, isn't likely new, but we
have the technology now to seeit happening in real time, and
there's certainly been a lot offunds poured into Ukraine, and
so we are seeing this happen in.
I want to talk about isKlebsiella pneumoniae.
This is a bacteria it's known tocause one in five deaths that
(37:07):
are attributed to antimicrobialresistance globally and has been
reported to be hyper virulentand pan drug resistant when
cultured from Ukrainiancasualties, and that's from a
December 2024 article in theJournal of Infection.
What allows Klebsiella often tobe so notoriously resistant to
antibiotics is that it can formbiofilms, so that's the bacteria
is there, and then there's thislike mucousy membrane and it
can be very difficult forantibiotics to penetrate and
(37:28):
actually stop the bacteria fromeither multiplying or kill the
bacteria off.
And what's really wild aboutthis is that 80% of Ukrainian
Klebsiella genome sequence carrya gene that is known as NDM1.
It makes them resistant to awhole class of antibiotics, and
that class is carbapenems.
This rate of resistance tocarbapenems in Klebsiella is 10
(37:53):
times higher than anywhere elsein Europe.
Even just since 2022, you haveseen that dramatic of a shift
that we now see resistance inKlebsiella that is 10 times
higher than the rest of Europeto a whole class of antibiotics,
which really can limit yourtreatment options for people, as
you were talking about earlierwith tuberculosis, the concern
(38:15):
isn't only for soldiers, right,so it's not just for Ukrainian
soldiers and people, socivilians will be affected.
But the reality is that, on aglobal scale, human health is
very intertwined and theseresistant microbes really do
have the potential to spreadbeyond Ukraine.
Speaker 5 (38:31):
Yeah, Camille, and something that's particularly
scary from what you mentioned.
Correct me if I'm wrong on that, but if I'm correct,
carbapenems are also consideredthe last line of defense and are
used for a lot of multi-drugresistant infections.
And so to have an entire familyof Clamsiella that is
completely resistant to theentire class of carbapenems,
(38:53):
that's pretty intense.
Speaker 2 (38:54):
Yeah, carbapenem resistance is a pretty scary
evolution of antimicrobialresistance.
Speaker 6 (39:00):
Camille, I have a question for you.
It's probably a very naivequestion, but how does the
antibiotic resistance occur?
What is producing this?
I know Klebsiella is somethingthat you also find in a
nosocomial setting, in ahospital setting quite often,
and is it soldiers being injured, then going to hospital being
treated with antibiotics, notgiven the full course?
(39:21):
So because of some, can youexplain that a little bit more
to me?
Speaker 4 (39:31):
Yeah, so the CDC is basically stating that the war
has stressed Ukrainian healthsystems, so that's part of it,
and that really creates anenvironment where antimicrobial
resistant bacteria can thriveand really quickly spread, not
only within the country butacross borders.
But also, what you're seeing isyou're basically seeing these
mass casualty events, right?
So not only are hospitalspotentially being shelled,
they're also seeing a hugeinflux in people that are
wounded, whether those aresoldiers or civilians, and
(39:53):
there's a shortage of staffing,which is also a problem, right?
So if you have one nurse who'ssupposed to be managing all
these people, can he or shereally physically like, take all
the infection preventionmatters?
You know, washing your hands,changing your gloves?
Your resources are limited, soyou're potentially spreading
something that one person hasbrought in.
But you also are seeing that intriage centers, oftentimes we
(40:14):
use these what's known as broadspectrum antibiotic treatments
just to see if they can catchsomething to improve someone's
health outcomes, and it's reallyunderstandable why we do that,
right?
Even in the United States,likely, if you came into some
emergency rooms and you werewounded badly enough, they might
still do that to be like hey,you are probably going to get an
infection from whatever this is, we're just going to give you
(40:35):
broad spectrum antibiotics.
When you start to do that on apopulation level, I think that's
when you start to see whatwe're seeing right now.
That's occurring in Ukraine,and what's wild about this is
that Ukrainian refugees that arefleeing the war, or injured
soldiers that are beingevacuated to receive medical
care, are actually bringing thisresistant bacteria with them.
So it's been found in sixEuropean countries as well as as
(40:57):
far away as Japan.
So this is definitely moving.
And again, this is going backto that idea of you know, war is
miasma, right, people might notbe tuning into the fact that
there's this war going on.
People get empathy, fatigue,they see it happen and then they
stop eventually.
But the effects of it are veryreal and are definitely going to
impact our intertwined health.
And I think about antimicrobialresistance a lot, and that's
(41:20):
because globally, it's reallyknown to cause more deaths than
other health threats likemalaria or HIV, and the WHO has
even declared antimicrobialresistance as one of the top 10
public health threats tohumanity.
So this is not like a jokingmatter in any sense, and
conflict zones are really thesecradles of antimicrobial
resistance and that might be.
(41:41):
Again, the health systems arestressed, you're running out of
staff, you're also just doingbroad spectrum treatments, but
also just the nature of thewounds that we see currently in
wars.
Right, if you are being hit bya bullet or by shrapnel, it
enters the body and can embedpathogens really deeply in the
tissues, which is an ideal placefor them to thrive.
And the triage centers thenreceiving these people who are
(42:05):
potentially severely wounded aredoing kind of whatever they can
.
They're throwing whatever theycan to see if something sticks
and just to potentially improvepatient outcomes.
And so we're seeing not just thecarbapenem resistance, but
there was investigation intosome soldiers who have passed,
and one of them, who hadsuccumbed to sepsis, was found
to have extensivelydrug-resistant bacterial strains
.
Those are known as XDR.
And another investigation of adifferent soldier found nine
(42:28):
extensively drug-resistantbacterial strains.
That's not something that wenormally see, right, and this is
something that we really needto be thinking about and
thinking about how do we preventthese from happening?
Yes, preventing conflict isgreat if you can, but that's
often such a difficult thing toeven draw something like a war
to a close right and finding away to still manage people's
(42:49):
health and to protect everyonethere, as well as your entire
global community.
Your war is not just going to bein one place, right, the
effects of it are going tospread out Instead of being
thrown into a pond.
You see all these ripples, andthere's a quote that I just
wanted to share just to end withthat it's from Dr Scott Pallett
, who's a physicianmicrobiologist at the Royal
Center for Defense Medicine, andhe said that the level of drug
(43:10):
resistance we are seeing inUkraine heralds the peril of the
post-antibiotic era, and that'ssomething we've talked about
previously before that we really, in many cases, have relied onp
throat to make sure they don'tjust have the flu or COVID or
something, before we just givethem antibiotics, and this is
(43:46):
something that it's ourresponsibility.
Once we have technology whichis something we've talked about
in this episode Once you havethe technology, you can identify
something.
It's our responsibility to useit so we can be good stewards of
the therapeutics that we dohave.
Speaker 2 (44:00):
Yeah, I like that.
Camille, I think your pointreally drives home something
that I think we all know aboutwar and conflict and its
relationship with infectiousdiseases, which is that you may
see on the television thatthere's a war happening in some
other part of the world andthink it doesn't really affect
me, but the truth is that theemergence of infectious
(44:21):
pathogens affects all of us.
Right?
Because if vaccination ratesfall in a particular area that's
experiencing conflict, ifanimal migration or vector
emergence takes place in a placewhere the bullets are flying
and people are having to leavetheir homes, feral animals are
roaming, there's no publichealth infrastructure to help
(44:42):
vaccinate or call stray animals.
When you think of all thesystems, protections that keep
us safe from pathogens emergence, then you think of how
disruptive war is to thosestructures.
You can see that really weshould all be worried anytime we
see a conflict around the world, not to say that we're in any
(45:03):
position to stop it.
It's not a video game.
These are complex geopoliticalsituations, but I do think that
if we are trying to advisepeople who are either in our
clinics or our public healthauthorities, or even people in
our community who may notunderstand these areas of
interconnectedness.
(45:24):
I think, thinking of theseexamples that you guys have all
described TB, antimicrobialresistance, crimean Congo is a
viral emergence.
History is riddled withexamples of wartime and conflict
being an inflection point forthe emergence of a new pathogen
or the re-emergence of an oldone.
And so I think, just as we seean unprecedented amount of
(45:48):
conflict in the world, payingattention to those things, it's
not just how it affects thosepopulations, it's also how it
might eventually spill over andaffect us.
Speaker 6 (45:56):
So how it might eventually spill over and affect
us Absolutely and I think, toour listeners, we've only picked
a few examples.
I think this was just reallyjust the tip of the iceberg.
I think we could have gone onand on, going back centuries and
different wars, and we reallyjust gave you a little overview
of some things that we areinterested in.
(46:18):
One thing as we were talkingabout this, I realized we didn't
really talk about humandisplacement.
Right, I talked about animalmovements and so on, but the
displacement that war causescauses ripple effects, camille
said, like all over the world,and I think this should be a
five episode season.
Almost right, I think this wasjust really the surface, for
(46:40):
sure.
Speaker 2 (46:40):
Yeah, and if you look at, sometimes people will ask
why is there so much militaryfunding for infectious disease
research?
And when you think about it,what do we want?
We want to keep our soldierssafe.
We want to keep our militarysafe.
We also know they're going toplaces where they're going into
places where they can be exposedto these pathogens.
(47:01):
So some of the greatestinnovations in vaccinology, in
diagnostics, have taken placethrough entities like the Naval
Medical Research Units, whichwere founded really as a
mechanism to promote researcharound the world as part of
defense, because it's not justhow many guns you can make, it's
also can you keep your militaryworkforce safe and can you
(47:24):
address the health needs of thepopulations that are being
affected.
It is all interrelated and Idon't see global health security
going away anytime soon.
So I think this is a reallygood topic, guys, very timely
topic, and I can guarantee youfive years, 10 years, when we're
all you guys are almost as grayas I am, and when you get there
, I think we'll still be havingthese discussions about war and
(47:49):
conflict and its effect oninfectious diseases, because
it's a tale as old as time.
Speaker 6 (47:53):
All right, any last words?
I think that's again anothercool episode.
Thanks, camille, for pickingthe topic and to our listeners,
I hope you enjoyed this as muchas we enjoyed it.
Speaker 2 (48:08):
Any last take-home messages, what do you think?
Can we say give peace a chance.
Can we say something?
I agree Too trite.
Speaker 4 (48:12):
I like that Give peace a chance.
Speaker 2 (48:16):
Maybe more effective than any vaccine is peace.
That's more.
Maybe more effective than anyvaccine is peace guys.
Peace, peace and stability.
So it's a good.
Those are good, good things forus to take away, but it's
always good to see you guys.
Thanks for letting me invadethe podcast again.
It's really good to seeeverybody and I learned
something new from all of youevery time it's never an
invasion.
Speaker 5 (48:36):
This is your home.
Speaker 4 (48:37):
You always have a space on the podcast couch.
Speaker 6 (48:40):
All right, Thanks everybody.
Speaker 5 (48:43):
Thanks so much again, guys, for listening.
Speaker 3 (48:47):
Thanks for listening to the Infectious Science
Podcast.
Be sure to hit subscribe andvisit infectiousscienceorg to
join the conversation, accessthe show notes and to sign up
for our newsletter and receiveour free materials.
Speaker 2 (48:58):
If you enjoyed this new episode of Infectious
Science, please leave us areview on Apple Podcasts and
Spotify, and go ahead and sharethis episode with some of your
friends.
Speaker 3 (49:07):
Also, don't hesitate to ask questions and tell us
what topics you'd like us tocover for future episodes.
To get in touch, drop a line inthe comments section or send us
a message on social media.
Speaker 2 (49:16):
So we'll see you next time for a new episode, and in
the meantime, stay happy stayhealthy, stay interested.
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