August 16, 2024 • 25 mins
Unlock the mysteries of Hansen's disease with us as we welcome acclaimed dermatopathologist, Dr. Mara Dacso. Through her journey from medical school in Galveston to her significant work in Baton Rouge, Dr. Dacso shares her extensive knowledge on leprosy, often termed the "great mimicker". Learn how the varied clinical presentations—from minor skin patches to severe systemic reactions—pose challenges for diagnosis and why it's crucial to consider leprosy in differential diagnoses. We'll also touch on unique transmission vectors, including armadillos and soil, and the prognosis for those who receive timely treatment.
Ever wondered why dermatologists and not infectious disease docs are often the first to diagnose leprosy in the U.S.? Dr. Dacso breaks down this phenomenon, revealing the diagnostic process and the importance of recognizing symptoms such as anesthetic lesions and enlarged nerves. Navigate through the complexities of treatment protocols recommended by the WHO, including the use of multi-drug therapy and the role of the National Hansen's Disease Program in combating drug resistance. Join us for an eye-opening conversation that underscores the critical importance of timely diagnosis and treatment in the fight against Hansen's disease.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 2 (00:09):
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 1 (00:17):
Coming to you from the University of Texas Medical
Branch and the GalvestonNational Laboratory.
Speaker 2 (00:21):
This is Infectious Science, where enthusiasm for
science is contagious.
Welcome back to the InfectiousScience Podcast.
This is Dr Matthew Dasho, herewith Camille Ledoux, and a real
special guest who is joining usfrom Dallas, texas, a not only a
friend of the podcast, but Iwould even say family of the
(00:45):
podcast, because this is noneother than Dr Mara Dasho, my
sister, who is a practicingdermatopathologist and also
someone who happens to have agreat deal of expertise in
Hansen's disease, which, as weknow and we'll discuss in more
detail, is caused byMycobacterium leprosy.
(01:05):
So, mara, welcome to thepodcast.
Speaker 3 (01:09):
Hi Dr Dasho.
From Dr Dasho.
Speaker 2 (01:12):
Maybe, to start, you can tell us a little bit about
your background, how you gotinto working with Hansen's
disease and what got youinterested in leprosy to begin
with.
Speaker 3 (01:23):
Yes, absolutely.
My interest in Hansen's diseasereally started before I started
residency.
So I was a medical student inGalveston and I decided to do an
international health andtropical medicine master's in
Spain and it just so happenedthat I also had an interest in
(01:45):
public health, infectiousdisease.
And then I discovered aninterest in leprosy, because we
actually did have adermatologist expert in leprosy
who saw patients in her clinicthat I ended up working with
one-on-one.
That was really helpful on theclinical side and I was able to
do some research.
But then in Galveston actually Idid an elective and I ended up
(02:08):
going to Baton Rouge, which isthe center of Hansen's disease,
the National Hansen's diseaseprogram in Baton Rouge.
I ended up meeting the directorthere doing some research and I
really just sort of fell intothis interest, this niche, and
so that sort of led to moreresearch, which then led in my
clinical years when I was doingmy residency, ultimately in
(02:29):
dermatology, discovered more ofan interest, ended up doing more
research, and then he, thedirector, ended up actually
retiring early and he said oh,so you're now going to be
following in my footsteps.
By the way, I've been doingthis for 25 years Now it's your
turn.
So now I'm reading pathologyfor the National Hansen's
disease program from Dallas andI go there periodically and help
(02:52):
run their laboratory.
So that's kind of my side gig,but it's been really great.
I've loved working with them.
Speaker 4 (02:57):
It is something that's rare, but it's not as
rare as you think when we firstwere recording, we were talking
about how this is such a slowgrowing pathogen that clinical
presentations can really varypretty widely.
When you do see this in clinic,do you find that it's getting
caught early?
What clinical presentations doyou see?
Or is it people that are on alater?
Speaker 3 (03:18):
stage.
Unfortunately it's across theboard.
So we call leprosy the greatmimicker because it really can
look like anything.
If it's not on the brain youare probably going to miss it.
It can range clinically fromjust a hypopigmented or light or
white colored patch that may bea little anesthetic, all the
way over to nodules and plaquesand more severe presentations.
(03:42):
So unless you're thinking aboutit, you may miss it.
And I think that's one of thethings that happens is that
people go undiagnosed for a longperiod of time and they may not
think of it because it's notusually itchy, it's not usually
painful, and then they just havethis rash that persists.
So unless you see adermatologist or you see someone
that thinks to biopsy this orthinks about leprosy, you may
(04:04):
miss it.
The other thing that happens isthat people can present with
something called an immunologicreaction.
So, depending on the type ofleprosy you have, your body may
mount an immune response to theantigen, so to the bacilli, and
then it can present withneuropathy.
It can present with systemicsymptoms like fever and just
(04:28):
really, really sick people.
Their skin is really angry,they may have nodules and they
may even have vasculitis andarthralgias.
So you have to think about it.
You also have to think to askthe questions about their
exposures.
Speaker 4 (04:40):
In any past history we were talking about how people
often think of armadillos whenthey think of leprosy.
Do you find that in Texasthat's a pretty common
denominator for past exposures,or does it really vary where
people have?
Speaker 3 (04:54):
been exposed.
Well, we know that armadillosget highly infected with M
leprae, and so we think that,because you can trace the region
of the country, that you mightsee more of the nine-banded
armadillo.
You can sometimes see morePantz's disease.
The issue is that sometimes itdoesn't always equate.
And so then what?
(05:14):
Is it still the armadillo, oris there something else going on
?
So there are more and morepapers coming out on some of the
other mechanisms oftransmission that might be
occurring.
So there's a possibility thatthere's a soil-borne incidence
going on here.
So maybe it's something that'sin the soil, maybe it's passed
by another microbe that we don'tknow about that's able to
(05:36):
transmit the mycobacteria.
So we really don't have aclear-cut answer.
But we know that the armadillocarries it, and if you do have
exposure to armadillos, there'sa possibility.
But we just don't have thatclear, clear, clear-cut answer
why people are getting it butdon't necessarily have exposure
to armadillos.
Speaker 4 (05:56):
What's the prognosis for patients?
So say, they've come in,someone was thinking about it
and actually kind of wentthrough a path to actually get a
diagnosis.
Then sort of what does it looklike?
Speaker 3 (06:06):
Well, of course, the most important thing is to
diagnose it and then what I tryto do, at least from the
pathology end, is help toidentify what type of leprosy it
is, because it exists along aspectrum and it can exist
depending on your immunologicresponse and how you mount that
response.
Again, it could be you respondreally really briskly to the
(06:29):
mycobacterium and you just havea few lesions, and then some
people don't mount a responseand they have tons of lesions
and they're covered and have ahigh burden, high load of
mycobacteria.
So I think that's somethingthat you have to always think of
again in the back of your mind,but just understanding that it
exists along this spectrum.
(06:50):
And when you diagnose them,then you also have to decide how
you're going to treat them,because the tuberculoid or the
type of leprosy where you're onthe spectrum, where you're
really mounting that goodresponse, we would treat that in
a different way than someonewho is not mounting a very good
response and they have tons ofbacilli and they're highly
infected and they may need moretreatment for longer periods of
(07:12):
time.
Gotcha.
Speaker 4 (07:13):
Okay, that makes sense.
And then I'm really curious.
So I come from a bacteriologybackground and I've always heard
that epilepary is notculturable.
And so how then do youdifferentiate between, like the
different types like you weretalking about earlier?
Speaker 3 (07:28):
So you're right.
So you can't culture it inmedia and it only grows really
at that perfect temperature.
I don't want to misspeak, but Iwant to say it's 32 degrees
Celsius.
I have to look again.
I'm sorry about that, butbasically it's difficult to
culture in media and you can'tculture it.
So we rely on histology.
Basically they're seeing themycobacteria in H&E stain
(07:52):
sections I'm sorry on fightstain sections, and then we also
use PCR.
So we, especially at theNational Hansen's disease
program, do PCR on all of theblocks that we receive and we do
PCR for M leprae but also for Mlepromatosis, which is another
mycobacteria that causes leprosyand it manifests in a very
(08:15):
clinically indistinguishable way.
But it is distinguished justbased on a couple of little
biogenetic differences.
So we do differentiate the twoand again, pcr is the way to go.
If you don't see it in stainedsections then it doesn't mean
that you don't have it, becauseit may be so rare that in the
(08:37):
sections you may not even see itbecause you're cutting through
the block and maybe the bacillusis not there.
It may just take one to causethat type of reaction.
So it can be challenging.
But PCR you're looking at ahundred of those sections, so
your chance of finding it isbetter.
Speaker 4 (08:55):
And I was also curious how large of the portion
of our population that'sactually immune to Hansen's
disease, and it's quite high,and really it takes repeat
exposures over many, many monthswith someone who's untreated to
even potentially end upcontracting M leprosy.
What have you found?
Do you think that if there's agenetic predisposition to it in
(09:15):
certain families or in groups,or is it that someone has been
around someone for anexceptionally long period of
time?
Speaker 3 (09:24):
Yeah, that's a really good question because actually
only 5% of the population couldpotentially get leprosy, so 95%
of us will not get it.
Our bodies are going to takecare of the infection.
So then you have to extrapolatethose 5% of the population.
What makes them similar andwhat makes them different?
And even though we don't have,again, a clear-cut answer, we do
(09:46):
see it more prevalent incertain groups and certain
ethnic groups and certainpopulations that live in certain
places, for example, micronesia.
Leprosy is actually veryprevalent and a lot of people
are exposed in that area.
And why?
Well, it may just begenetically that they're
predisposed, it may beenvironmental.
(10:07):
There's a lot of potentialsthere.
So I think that when you lookat why someone's getting it and
why someone's not, again, thechances are very, very good that
you're not going to get it.
But if there's a strong familyhistory, if there's someone in
your family that has beeninfected and you've been around
them for long periods of time,you could get it Absolutely.
(10:28):
But again it could also be thatyou're in the same family.
Your dad may have lepromatousleprosy, which is again we're on
that end of the spectrum whereyou get heavily infected and you
may not.
So I think the jury's still outthere, but it's very
interesting question and why wesee it in certain groups.
Speaker 2 (10:44):
Now, Mara, I think you have the unique
characteristic is that you haveseen folks who are suffering
from this condition and we don'tsee it that often, so don't
always have a good idea of theclinical presentation and also
the epidemiological background.
There's certain populationsthat we know may be affected
(11:05):
more disproportionately folkscoming from endemic areas.
There's the migration of folksfrom those endemic areas.
So can you say a little bitmore about what you've seen
clinically and what the spectrumof disease looks like and what
populations that you see aremost affected by Hansen's
disease?
Speaker 3 (11:24):
I deal mostly with the diagnosis of leprosy, but I
still have encountered patientswho have been dealing with
leprosy and they're certainlyvery diverse.
I've been involved in thosecases, even though they may not
be my patients, and it goes frompeople who are actually just
born and raised in Florida, incentral Florida or in Louisiana
(11:46):
or in Texas, and they may nothave a family history, but all
of a sudden they develop a rashthat hasn't been diagnosed and
someone does a biopsy and itshows that it's positive.
But it also could be people whohave immigrated from other
countries and do not haveresources, and maybe they were
(12:08):
diagnosed or maybe they wereeven partially treated in their
home country, but then come tous and present either with a
reaction, so they may present toan ER and no one knows their
history.
And then all of a sudden youhave someone coming in that has
diffuse rash, joint pains, verysick, and no one really knows
(12:28):
what to do.
They treat it as something else.
So I think that these people,the people who are coming from
other countries especially, whodon't have resources, who don't
have access to healthcare and toinsurance, will come in,
present to the ER and then theymay get lost.
And unless you have that, onemember of the healthcare team
that thinks to call someone,whether from the Hansen's
(12:51):
program or a local Hansen'sclinic, to say, hey, this might
be leprosy, what do we do?
These people may slip throughthe cracks.
So I think it's reallyimportant that we're thinking
about this disease, becausethere are people that are coming
in who may or may not have beentreated and they're potentially
at a disadvantage because we'renot thinking about it as
(13:12):
clinicians either.
Speaker 4 (13:14):
I have two follow-up questions to that.
That's very, very interesting.
One is why do you think thatthe majority of cases in the
United States are diagnosed indermatology clinics versus
something like an infectiousdisease clinic?
Part of my PhD program is doingclinical encounters and so we
go to infectious disease clinicsand we shadow and they're
trying to think of like anythingand everything, but certainly
(13:37):
when I was getting into theliterature on this, it really
seems like it's diagnosedoftentimes by dermatologists.
So why do you think that is?
And then also, how susceptibleis the organism to antibiotics?
Speaker 3 (13:48):
So I think that most people are presenting to derm
because there tends to be a rashinvolved.
Typically there's a rash, notalways.
Actually, some forms of leprosyare pure neural, where you
don't have a rash at all.
And that's even morechallenging because then they go
to neurology and get this workup until someone potentially
does a nerve biopsy.
But most of the people whopresent to DERM have a rash and
(14:14):
DERM does what DERM does best,which is biopsy.
And then dermatopathologists ifyou're sending to a
dermatopathologist who istrained to look at these
biopsies and then come up withthe diagnosis or at least a
differential diagnosis stain thetissue to look for organisms.
If they don't see organisms,then they may send it.
(14:36):
There's a high possibility thatthis is leprosy, whether there's
anesthesia.
So if the lesions areanesthetic, that's also very
important to think of.
So it's not just rash.
Are the lesions anesthetic?
Are nerves enlarged?
And you can even test for that.
You can see.
Sometimes when the nerves areenlarged or the ulnar nerve is
enlarged you can say hey, oh, mygoodness, maybe that nerve is
(14:56):
inflamed.
But in derm clinics we aretrained to biopsy and as long as
the dermatologist is doing acorrect biopsy, which we always
recommend a punch biopsy to getall the way down to fat so you
can see the nerves.
Then a lot of times at leastthe pathologist should have a
suspicion that this could be andthen know from there okay,
(15:18):
stain it up, okay, maybe itneeds to get PCR.
So that's kind of the chain ofevents.
But a lot of these people do goto germ.
And then what was the secondpart of your question.
Speaker 4 (15:28):
I'm curious about how susceptible it is to
antibiotics, particularlybecause when I think of
mycobacterium I of course thinkof tuberculosis, and that is
exceptionally long course ofantibiotics.
But for something like Lepre,is it a short course?
Is it exceptionally long courseof antibiotics?
But for something like leprosy,is it a short course?
Is it a long course?
And then, based on that, howsusceptible is it Like?
Is there resistance to certainclasses?
Speaker 3 (15:49):
So that's a great question.
So the WHO will treat leprosywith something called multi-drug
therapy.
So Dapsone, rifampin andClefazanine are the three drugs
that are used, varyingfrequencies and durations.
Typically, though, if you'refollowing WHO protocol, the
(16:09):
possebacillary or thetuberculoid form of leprosy is
treated for a little bit lesstime six months to a year and
then if it's multibacillary orlepromatous, where it's again
that spectrum where there's highburden of bacilli and lots of
lesions, then you're going totreat for longer and you're
treated with three drugs.
Now most clinicians are actuallytreating with a little bit of a
(16:31):
different regimen and it'scalled ROM, but rifampin,
ofloxacin, minocycline ormoxifloxacin, and doing it for a
little bit of shorter timeperiods because a lot of these
medicines are not well toleratedA lot of laboratory issues and
anemia etc.
But the medicines are longerperiod of time, number one to
(16:51):
treat fully.
But in terms of resistance,that does occur.
It does occur not often, butthat's also something that we
can test for genetically.
So if you send your specimen tothe National Hansen's Disease
Program, you actually can havethe tissue tested for resistance
, and so we look at certaingenes and look to see if those
(17:11):
genes are expressed in differentways to determine if there's
resistance.
Speaker 4 (17:16):
Okay, that's very cool.
And then so, when someone hascompleted the course, how are
they cleared?
Is it that they've completedthe six months to a year of
antibiotics?
Do they have to have a clearbiopsy?
Kind of no continuing symptoms?
Speaker 3 (17:31):
That's a really good question too.
So if you complete the fulltreatment, so if you complete
your multidrug therapy regimen,we do consider those patients
treated.
Now, the issue with leprosy isthat the bacillus can remain in
the tissue and typically doesfor many years after treatment,
because even though the DNA maybe present, the organism itself
(17:52):
is dead.
It just takes years and yearsfor that organism to be broken
down and removed from thetissues so it still can mount a
reaction, it still can presentlesions and still cause issues
with morbidity.
So neuropathy, nerve damage,lesions, it certainly can be
longstanding.
And that's really the big thingwith Hansen's disease is that
(18:13):
the sequelae, which are usuallyneurologic, which are usually
the neuropathy and the loss ofsensation, is really what causes
the most disability over time.
And that's the biggest problem.
It's diagnosing it, yes,treating it, yes, but then what
happens to these people?
A lot of them end up at a greatdisadvantage because they're
not getting their rehabilitationthat they need, and that's
(18:35):
another thing that the programdoes is occupational therapy,
physical therapy, wound care tohelp these people who are
dealing with the sequelae Gotcha.
Speaker 4 (18:43):
Yeah, no, that's definitely something I think
that can often slip through thecracks Like oh, like we're
treating this, but notnecessarily all the downstream
effects of it, and that'sdefinitely really important to
ensure that people have qualityof life, and so people six
months to a year on antibiotics,that's a very long time.
Do you find that there's a lotof compliance with the regimen,
because that's an exceptionallylong time to take antibiotics?
(19:05):
Do you think that that is abarrier to care, that a lot of
people will take it and thendrop off, or?
Speaker 3 (19:11):
I don't know if there's statistics or not yeah,
I don't know about percentages,but absolutely, and a lot of
people do directly observedtherapy.
So DOT and they'll have thepatients come in for their
monthly visits and have themtake the medicine in front of
them, especially if they're kids, for example, if you're
treating a kid.
But I think it really is on theclinician to be doing this
(19:33):
follow-up for their patients andmaking sure that they're taking
their medicines and seeing themregularly.
And that can certainly be achallenge for people who don't
have access.
I mean, these people have to goto a free clinic and the
Hanson's clinics around thecountry I think there are eight
of them Uh, me on that but thoseclinics are government funded.
(19:54):
They are free of charge, themedicines are free of charge.
So if you get these peoplehooked in to the right places
and to the clinics that exist,they are going to get the care
they need and they'll get thelab monitoring.
But it takes several steps,especially in our system, to get
them there and they may not.
So I think we're absolutelyunderdiagnosing.
In the United States wetypically diagnose about maybe
(20:18):
200 cases a year, but I thinkthat number is definitely
underestimated because we'remissing patients that just can't
get in or they're misdiagnosed.
Speaker 4 (20:27):
We had previously talked about that, where in
infectious disease, anything itcan get very like us versus them
.
Even if you look at the webpage, I think for the CDC it's like
oh, most M leprosy infectionsare acquired outside the United
States, but that's notnecessarily true and I think
what you were saying just kindof brings me into that important
point.
But it's stigmatizing tosuggest that it's coming from
(20:49):
outside borders, when bordersare things that we've made up
and it's definitely here.
Speaker 3 (20:53):
Totally Absolutely.
It is here, and a lot of thecases are coming in from people
who are from the United Statesthat we see not all of them, but
a good number of them and so wecan't continue to think that
this is just something that iscoming from people from other
countries and they're the oneswho are getting exposed and
(21:13):
bringing it into our country.
That's not the case at all,especially leprosy.
We just still have so much tolearn and we certainly can't
stigmatize those individuals.
It still is a very stigmatizingdisease, right, and so I think
that dates back years and yearsand years and biblical times,
and so I think that there's alot to that, and culturally too.
(21:34):
So people coming from othercountries that you can't even
say leprosy.
That's why we call it Hansen'sdisease, because of the stigma
that is associated with thatword.
Speaker 4 (21:43):
That's definitely a major thing that we really
discussed that this is stillsuch a stigmatized disease and
that can be a barrier to carebut can also lead to negative
health outcomes for peoplebeyond the physical right, from
a mental health perspective,especially because, if you think
about it, when people sayleprosy, the idea of that is
that that was the original moralunclean disease and we've seen
(22:04):
that later in other diseases aswell.
So I think in the 80s HIV wasalso viewed that way until there
was a lot of activism andpushback.
And so is there activism aroundHansen's disease to change the
perspective of it.
Or do you think that there'snot enough cases where that's
being done or there's notfunding for it?
Speaker 3 (22:22):
I think that certainly we need to bring more
voice to this disease.
The issue, of course, is thatit's exceedingly rare, and so
when you have a rare disease,it's not funded well and it's
not given a lot of attention,and so you end up with some
resources, not a lot, and so,unless you really can know where
(22:44):
to look and know where theseprograms are and where these
resources are, it's verynebulous.
And then, on top of that, thisis a government program that
really funds the research andfunds the clinical work.
So I think that it'schallenging to get the public
eye involved in this disease.
Most people don't even think itexists anymore, and so it's
(23:06):
challenging.
It really really is.
It's hard to know what the nextsteps are, because it's so rare
, but yet it's really important.
And it's still relevant, butyet it's rare.
So I think we have a lot ofwork yet to come and hopefully
it will continue along theselines, but we'll also have more
clinicians interested who willsupport us Absolutely.
(23:36):
I think that everyone would wantthis disease to be eradicated.
In fact, the WHO has put forththese goals for eradication that
keep going on and on.
We want to eradicate in 2000and then 2010 and then 2020.
I think that the lesson here isthat it's still with us and
although we want it to beeradicated, this is a much more
complex issue than justmedicines.
This is really kind ofidentifying those at risk and
(24:00):
then treating them, but thenalso following them and making
sure that we are addressing allof the encompassing issues that
come from this disease, and it'scertainly very, very much
socioeconomic.
We're dealing with thesepsychological impacts, I think,
down the road that also canaffect someone's life profoundly
(24:22):
.
So I think we as cliniciansreally do need to keep this in
the forefront of our minds andalso just educate yourself on
just basic presentations ofleprosy.
Think about it.
Think about it if you see arash or someone has a numb
lesion.
If you keep it in the back ofyour mind, then you're not going
to miss it.
All right, thank you, it is mypleasure.
This was really fun.
I hope we can do it againsometime in the future, but I
(24:43):
would love for anyone else tocontact me if they're interested
or they have questions.
I hope that conversations willcontinue.
Speaker 1 (24:54):
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Speaker 1 (25:11):
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Speaker 2 (25:18):
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This is a podcast about One Health the idea that
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we all share are intrinsicallylinked.
Speaker 1 (00:17):
Coming to you from the University of Texas Medical
Branch and the GalvestonNational Laboratory.
Speaker 2 (00:21):
This is Infectious Science, where enthusiasm for
science is contagious.
Welcome back to the InfectiousScience Podcast.
This is Dr Matthew Dasho, herewith Camille Ledoux, and a real
special guest who is joining usfrom Dallas, texas, a not only a
friend of the podcast, but Iwould even say family of the
(00:45):
podcast, because this is noneother than Dr Mara Dasho, my
sister, who is a practicingdermatopathologist and also
someone who happens to have agreat deal of expertise in
Hansen's disease, which, as weknow and we'll discuss in more
detail, is caused byMycobacterium leprosy.
(01:05):
So, mara, welcome to thepodcast.
Speaker 3 (01:09):
Hi Dr Dasho.
From Dr Dasho.
Speaker 2 (01:12):
Maybe, to start, you can tell us a little bit about
your background, how you gotinto working with Hansen's
disease and what got youinterested in leprosy to begin
with.
Speaker 3 (01:23):
Yes, absolutely.
My interest in Hansen's diseasereally started before I started
residency.
So I was a medical student inGalveston and I decided to do an
international health andtropical medicine master's in
Spain and it just so happenedthat I also had an interest in
(01:45):
public health, infectiousdisease.
And then I discovered aninterest in leprosy, because we
actually did have adermatologist expert in leprosy
who saw patients in her clinicthat I ended up working with
one-on-one.
That was really helpful on theclinical side and I was able to
do some research.
But then in Galveston actually Idid an elective and I ended up
(02:08):
going to Baton Rouge, which isthe center of Hansen's disease,
the National Hansen's diseaseprogram in Baton Rouge.
I ended up meeting the directorthere doing some research and I
really just sort of fell intothis interest, this niche, and
so that sort of led to moreresearch, which then led in my
clinical years when I was doingmy residency, ultimately in
(02:29):
dermatology, discovered more ofan interest, ended up doing more
research, and then he, thedirector, ended up actually
retiring early and he said oh,so you're now going to be
following in my footsteps.
By the way, I've been doingthis for 25 years Now it's your
turn.
So now I'm reading pathologyfor the National Hansen's
disease program from Dallas andI go there periodically and help
(02:52):
run their laboratory.
So that's kind of my side gig,but it's been really great.
I've loved working with them.
Speaker 4 (02:57):
It is something that's rare, but it's not as
rare as you think when we firstwere recording, we were talking
about how this is such a slowgrowing pathogen that clinical
presentations can really varypretty widely.
When you do see this in clinic,do you find that it's getting
caught early?
What clinical presentations doyou see?
Or is it people that are on alater?
Speaker 3 (03:18):
stage.
Unfortunately it's across theboard.
So we call leprosy the greatmimicker because it really can
look like anything.
If it's not on the brain youare probably going to miss it.
It can range clinically fromjust a hypopigmented or light or
white colored patch that may bea little anesthetic, all the
way over to nodules and plaquesand more severe presentations.
(03:42):
So unless you're thinking aboutit, you may miss it.
And I think that's one of thethings that happens is that
people go undiagnosed for a longperiod of time and they may not
think of it because it's notusually itchy, it's not usually
painful, and then they just havethis rash that persists.
So unless you see adermatologist or you see someone
that thinks to biopsy this orthinks about leprosy, you may
(04:04):
miss it.
The other thing that happens isthat people can present with
something called an immunologicreaction.
So, depending on the type ofleprosy you have, your body may
mount an immune response to theantigen, so to the bacilli, and
then it can present withneuropathy.
It can present with systemicsymptoms like fever and just
(04:28):
really, really sick people.
Their skin is really angry,they may have nodules and they
may even have vasculitis andarthralgias.
So you have to think about it.
You also have to think to askthe questions about their
exposures.
Speaker 4 (04:40):
In any past history we were talking about how people
often think of armadillos whenthey think of leprosy.
Do you find that in Texasthat's a pretty common
denominator for past exposures,or does it really vary where
people have?
Speaker 3 (04:54):
been exposed.
Well, we know that armadillosget highly infected with M
leprae, and so we think that,because you can trace the region
of the country, that you mightsee more of the nine-banded
armadillo.
You can sometimes see morePantz's disease.
The issue is that sometimes itdoesn't always equate.
And so then what?
(05:14):
Is it still the armadillo, oris there something else going on
?
So there are more and morepapers coming out on some of the
other mechanisms oftransmission that might be
occurring.
So there's a possibility thatthere's a soil-borne incidence
going on here.
So maybe it's something that'sin the soil, maybe it's passed
by another microbe that we don'tknow about that's able to
(05:36):
transmit the mycobacteria.
So we really don't have aclear-cut answer.
But we know that the armadillocarries it, and if you do have
exposure to armadillos, there'sa possibility.
But we just don't have thatclear, clear, clear-cut answer
why people are getting it butdon't necessarily have exposure
to armadillos.
Speaker 4 (05:56):
What's the prognosis for patients?
So say, they've come in,someone was thinking about it
and actually kind of wentthrough a path to actually get a
diagnosis.
Then sort of what does it looklike?
Speaker 3 (06:06):
Well, of course, the most important thing is to
diagnose it and then what I tryto do, at least from the
pathology end, is help toidentify what type of leprosy it
is, because it exists along aspectrum and it can exist
depending on your immunologicresponse and how you mount that
response.
Again, it could be you respondreally really briskly to the
(06:29):
mycobacterium and you just havea few lesions, and then some
people don't mount a responseand they have tons of lesions
and they're covered and have ahigh burden, high load of
mycobacteria.
So I think that's somethingthat you have to always think of
again in the back of your mind,but just understanding that it
exists along this spectrum.
(06:50):
And when you diagnose them,then you also have to decide how
you're going to treat them,because the tuberculoid or the
type of leprosy where you're onthe spectrum, where you're
really mounting that goodresponse, we would treat that in
a different way than someonewho is not mounting a very good
response and they have tons ofbacilli and they're highly
infected and they may need moretreatment for longer periods of
(07:12):
time.
Gotcha.
Speaker 4 (07:13):
Okay, that makes sense.
And then I'm really curious.
So I come from a bacteriologybackground and I've always heard
that epilepary is notculturable.
And so how then do youdifferentiate between, like the
different types like you weretalking about earlier?
Speaker 3 (07:28):
So you're right.
So you can't culture it inmedia and it only grows really
at that perfect temperature.
I don't want to misspeak, but Iwant to say it's 32 degrees
Celsius.
I have to look again.
I'm sorry about that, butbasically it's difficult to
culture in media and you can'tculture it.
So we rely on histology.
Basically they're seeing themycobacteria in H&E stain
(07:52):
sections I'm sorry on fightstain sections, and then we also
use PCR.
So we, especially at theNational Hansen's disease
program, do PCR on all of theblocks that we receive and we do
PCR for M leprae but also for Mlepromatosis, which is another
mycobacteria that causes leprosyand it manifests in a very
(08:15):
clinically indistinguishable way.
But it is distinguished justbased on a couple of little
biogenetic differences.
So we do differentiate the twoand again, pcr is the way to go.
If you don't see it in stainedsections then it doesn't mean
that you don't have it, becauseit may be so rare that in the
(08:37):
sections you may not even see itbecause you're cutting through
the block and maybe the bacillusis not there.
It may just take one to causethat type of reaction.
So it can be challenging.
But PCR you're looking at ahundred of those sections, so
your chance of finding it isbetter.
Speaker 4 (08:55):
And I was also curious how large of the portion
of our population that'sactually immune to Hansen's
disease, and it's quite high,and really it takes repeat
exposures over many, many monthswith someone who's untreated to
even potentially end upcontracting M leprosy.
What have you found?
Do you think that if there's agenetic predisposition to it in
(09:15):
certain families or in groups,or is it that someone has been
around someone for anexceptionally long period of
time?
Speaker 3 (09:24):
Yeah, that's a really good question because actually
only 5% of the population couldpotentially get leprosy, so 95%
of us will not get it.
Our bodies are going to takecare of the infection.
So then you have to extrapolatethose 5% of the population.
What makes them similar andwhat makes them different?
And even though we don't have,again, a clear-cut answer, we do
(09:46):
see it more prevalent incertain groups and certain
ethnic groups and certainpopulations that live in certain
places, for example, micronesia.
Leprosy is actually veryprevalent and a lot of people
are exposed in that area.
And why?
Well, it may just begenetically that they're
predisposed, it may beenvironmental.
(10:07):
There's a lot of potentialsthere.
So I think that when you lookat why someone's getting it and
why someone's not, again, thechances are very, very good that
you're not going to get it.
But if there's a strong familyhistory, if there's someone in
your family that has beeninfected and you've been around
them for long periods of time,you could get it Absolutely.
(10:28):
But again it could also be thatyou're in the same family.
Your dad may have lepromatousleprosy, which is again we're on
that end of the spectrum whereyou get heavily infected and you
may not.
So I think the jury's still outthere, but it's very
interesting question and why wesee it in certain groups.
Speaker 2 (10:44):
Now, Mara, I think you have the unique
characteristic is that you haveseen folks who are suffering
from this condition and we don'tsee it that often, so don't
always have a good idea of theclinical presentation and also
the epidemiological background.
There's certain populationsthat we know may be affected
(11:05):
more disproportionately folkscoming from endemic areas.
There's the migration of folksfrom those endemic areas.
So can you say a little bitmore about what you've seen
clinically and what the spectrumof disease looks like and what
populations that you see aremost affected by Hansen's
disease?
Speaker 3 (11:24):
I deal mostly with the diagnosis of leprosy, but I
still have encountered patientswho have been dealing with
leprosy and they're certainlyvery diverse.
I've been involved in thosecases, even though they may not
be my patients, and it goes frompeople who are actually just
born and raised in Florida, incentral Florida or in Louisiana
(11:46):
or in Texas, and they may nothave a family history, but all
of a sudden they develop a rashthat hasn't been diagnosed and
someone does a biopsy and itshows that it's positive.
But it also could be people whohave immigrated from other
countries and do not haveresources, and maybe they were
(12:08):
diagnosed or maybe they wereeven partially treated in their
home country, but then come tous and present either with a
reaction, so they may present toan ER and no one knows their
history.
And then all of a sudden youhave someone coming in that has
diffuse rash, joint pains, verysick, and no one really knows
(12:28):
what to do.
They treat it as something else.
So I think that these people,the people who are coming from
other countries especially, whodon't have resources, who don't
have access to healthcare and toinsurance, will come in,
present to the ER and then theymay get lost.
And unless you have that, onemember of the healthcare team
that thinks to call someone,whether from the Hansen's
(12:51):
program or a local Hansen'sclinic, to say, hey, this might
be leprosy, what do we do?
These people may slip throughthe cracks.
So I think it's reallyimportant that we're thinking
about this disease, becausethere are people that are coming
in who may or may not have beentreated and they're potentially
at a disadvantage because we'renot thinking about it as
(13:12):
clinicians either.
Speaker 4 (13:14):
I have two follow-up questions to that.
That's very, very interesting.
One is why do you think thatthe majority of cases in the
United States are diagnosed indermatology clinics versus
something like an infectiousdisease clinic?
Part of my PhD program is doingclinical encounters and so we
go to infectious disease clinicsand we shadow and they're
trying to think of like anythingand everything, but certainly
(13:37):
when I was getting into theliterature on this, it really
seems like it's diagnosedoftentimes by dermatologists.
So why do you think that is?
And then also, how susceptibleis the organism to antibiotics?
Speaker 3 (13:48):
So I think that most people are presenting to derm
because there tends to be a rashinvolved.
Typically there's a rash, notalways.
Actually, some forms of leprosyare pure neural, where you
don't have a rash at all.
And that's even morechallenging because then they go
to neurology and get this workup until someone potentially
does a nerve biopsy.
But most of the people whopresent to DERM have a rash and
(14:14):
DERM does what DERM does best,which is biopsy.
And then dermatopathologists ifyou're sending to a
dermatopathologist who istrained to look at these
biopsies and then come up withthe diagnosis or at least a
differential diagnosis stain thetissue to look for organisms.
If they don't see organisms,then they may send it.
(14:36):
There's a high possibility thatthis is leprosy, whether there's
anesthesia.
So if the lesions areanesthetic, that's also very
important to think of.
So it's not just rash.
Are the lesions anesthetic?
Are nerves enlarged?
And you can even test for that.
You can see.
Sometimes when the nerves areenlarged or the ulnar nerve is
enlarged you can say hey, oh, mygoodness, maybe that nerve is
(14:56):
inflamed.
But in derm clinics we aretrained to biopsy and as long as
the dermatologist is doing acorrect biopsy, which we always
recommend a punch biopsy to getall the way down to fat so you
can see the nerves.
Then a lot of times at leastthe pathologist should have a
suspicion that this could be andthen know from there okay,
(15:18):
stain it up, okay, maybe itneeds to get PCR.
So that's kind of the chain ofevents.
But a lot of these people do goto germ.
And then what was the secondpart of your question.
Speaker 4 (15:28):
I'm curious about how susceptible it is to
antibiotics, particularlybecause when I think of
mycobacterium I of course thinkof tuberculosis, and that is
exceptionally long course ofantibiotics.
But for something like Lepre,is it a short course?
Is it exceptionally long courseof antibiotics?
But for something like leprosy,is it a short course?
Is it a long course?
And then, based on that, howsusceptible is it Like?
Is there resistance to certainclasses?
Speaker 3 (15:49):
So that's a great question.
So the WHO will treat leprosywith something called multi-drug
therapy.
So Dapsone, rifampin andClefazanine are the three drugs
that are used, varyingfrequencies and durations.
Typically, though, if you'refollowing WHO protocol, the
(16:09):
possebacillary or thetuberculoid form of leprosy is
treated for a little bit lesstime six months to a year and
then if it's multibacillary orlepromatous, where it's again
that spectrum where there's highburden of bacilli and lots of
lesions, then you're going totreat for longer and you're
treated with three drugs.
Now most clinicians are actuallytreating with a little bit of a
(16:31):
different regimen and it'scalled ROM, but rifampin,
ofloxacin, minocycline ormoxifloxacin, and doing it for a
little bit of shorter timeperiods because a lot of these
medicines are not well toleratedA lot of laboratory issues and
anemia etc.
But the medicines are longerperiod of time, number one to
(16:51):
treat fully.
But in terms of resistance,that does occur.
It does occur not often, butthat's also something that we
can test for genetically.
So if you send your specimen tothe National Hansen's Disease
Program, you actually can havethe tissue tested for resistance
, and so we look at certaingenes and look to see if those
(17:11):
genes are expressed in differentways to determine if there's
resistance.
Speaker 4 (17:16):
Okay, that's very cool.
And then so, when someone hascompleted the course, how are
they cleared?
Is it that they've completedthe six months to a year of
antibiotics?
Do they have to have a clearbiopsy?
Kind of no continuing symptoms?
Speaker 3 (17:31):
That's a really good question too.
So if you complete the fulltreatment, so if you complete
your multidrug therapy regimen,we do consider those patients
treated.
Now, the issue with leprosy isthat the bacillus can remain in
the tissue and typically doesfor many years after treatment,
because even though the DNA maybe present, the organism itself
(17:52):
is dead.
It just takes years and yearsfor that organism to be broken
down and removed from thetissues so it still can mount a
reaction, it still can presentlesions and still cause issues
with morbidity.
So neuropathy, nerve damage,lesions, it certainly can be
longstanding.
And that's really the big thingwith Hansen's disease is that
(18:13):
the sequelae, which are usuallyneurologic, which are usually
the neuropathy and the loss ofsensation, is really what causes
the most disability over time.
And that's the biggest problem.
It's diagnosing it, yes,treating it, yes, but then what
happens to these people?
A lot of them end up at a greatdisadvantage because they're
not getting their rehabilitationthat they need, and that's
(18:35):
another thing that the programdoes is occupational therapy,
physical therapy, wound care tohelp these people who are
dealing with the sequelae Gotcha.
Speaker 4 (18:43):
Yeah, no, that's definitely something I think
that can often slip through thecracks Like oh, like we're
treating this, but notnecessarily all the downstream
effects of it, and that'sdefinitely really important to
ensure that people have qualityof life, and so people six
months to a year on antibiotics,that's a very long time.
Do you find that there's a lotof compliance with the regimen,
because that's an exceptionallylong time to take antibiotics?
(19:05):
Do you think that that is abarrier to care, that a lot of
people will take it and thendrop off, or?
Speaker 3 (19:11):
I don't know if there's statistics or not yeah,
I don't know about percentages,but absolutely, and a lot of
people do directly observedtherapy.
So DOT and they'll have thepatients come in for their
monthly visits and have themtake the medicine in front of
them, especially if they're kids, for example, if you're
treating a kid.
But I think it really is on theclinician to be doing this
(19:33):
follow-up for their patients andmaking sure that they're taking
their medicines and seeing themregularly.
And that can certainly be achallenge for people who don't
have access.
I mean, these people have to goto a free clinic and the
Hanson's clinics around thecountry I think there are eight
of them Uh, me on that but thoseclinics are government funded.
(19:54):
They are free of charge, themedicines are free of charge.
So if you get these peoplehooked in to the right places
and to the clinics that exist,they are going to get the care
they need and they'll get thelab monitoring.
But it takes several steps,especially in our system, to get
them there and they may not.
So I think we're absolutelyunderdiagnosing.
In the United States wetypically diagnose about maybe
(20:18):
200 cases a year, but I thinkthat number is definitely
underestimated because we'remissing patients that just can't
get in or they're misdiagnosed.
Speaker 4 (20:27):
We had previously talked about that, where in
infectious disease, anything itcan get very like us versus them
.
Even if you look at the webpage, I think for the CDC it's like
oh, most M leprosy infectionsare acquired outside the United
States, but that's notnecessarily true and I think
what you were saying just kindof brings me into that important
point.
But it's stigmatizing tosuggest that it's coming from
(20:49):
outside borders, when bordersare things that we've made up
and it's definitely here.
Speaker 3 (20:53):
Totally Absolutely.
It is here, and a lot of thecases are coming in from people
who are from the United Statesthat we see not all of them, but
a good number of them and so wecan't continue to think that
this is just something that iscoming from people from other
countries and they're the oneswho are getting exposed and
(21:13):
bringing it into our country.
That's not the case at all,especially leprosy.
We just still have so much tolearn and we certainly can't
stigmatize those individuals.
It still is a very stigmatizingdisease, right, and so I think
that dates back years and yearsand years and biblical times,
and so I think that there's alot to that, and culturally too.
(21:34):
So people coming from othercountries that you can't even
say leprosy.
That's why we call it Hansen'sdisease, because of the stigma
that is associated with thatword.
Speaker 4 (21:43):
That's definitely a major thing that we really
discussed that this is stillsuch a stigmatized disease and
that can be a barrier to carebut can also lead to negative
health outcomes for peoplebeyond the physical right, from
a mental health perspective,especially because, if you think
about it, when people sayleprosy, the idea of that is
that that was the original moralunclean disease and we've seen
(22:04):
that later in other diseases aswell.
So I think in the 80s HIV wasalso viewed that way until there
was a lot of activism andpushback.
And so is there activism aroundHansen's disease to change the
perspective of it.
Or do you think that there'snot enough cases where that's
being done or there's notfunding for it?
Speaker 3 (22:22):
I think that certainly we need to bring more
voice to this disease.
The issue, of course, is thatit's exceedingly rare, and so
when you have a rare disease,it's not funded well and it's
not given a lot of attention,and so you end up with some
resources, not a lot, and so,unless you really can know where
(22:44):
to look and know where theseprograms are and where these
resources are, it's verynebulous.
And then, on top of that, thisis a government program that
really funds the research andfunds the clinical work.
So I think that it'schallenging to get the public
eye involved in this disease.
Most people don't even think itexists anymore, and so it's
(23:06):
challenging.
It really really is.
It's hard to know what the nextsteps are, because it's so rare
, but yet it's really important.
And it's still relevant, butyet it's rare.
So I think we have a lot ofwork yet to come and hopefully
it will continue along theselines, but we'll also have more
clinicians interested who willsupport us Absolutely.
(23:36):
I think that everyone would wantthis disease to be eradicated.
In fact, the WHO has put forththese goals for eradication that
keep going on and on.
We want to eradicate in 2000and then 2010 and then 2020.
I think that the lesson here isthat it's still with us and
although we want it to beeradicated, this is a much more
complex issue than justmedicines.
This is really kind ofidentifying those at risk and
(24:00):
then treating them, but thenalso following them and making
sure that we are addressing allof the encompassing issues that
come from this disease, and it'scertainly very, very much
socioeconomic.
We're dealing with thesepsychological impacts, I think,
down the road that also canaffect someone's life profoundly
(24:22):
.
So I think we as cliniciansreally do need to keep this in
the forefront of our minds andalso just educate yourself on
just basic presentations ofleprosy.
Think about it.
Think about it if you see arash or someone has a numb
lesion.
If you keep it in the back ofyour mind, then you're not going
to miss it.
All right, thank you, it is mypleasure.
This was really fun.
I hope we can do it againsometime in the future, but I
(24:43):
would love for anyone else tocontact me if they're interested
or they have questions.
I hope that conversations willcontinue.
Speaker 1 (24:54):
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 (25:00):
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 1 (25:11):
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 (25:18):
So we'll see you next time for a new episode, and in
the meantime, stay happy stayhealthy, stay interested you.
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