Episode Transcript
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(00:08):
Hey George, I'm really excited.
Oh no, I know I'm goingto regret this, but why?
Well, basically, I'vegot an audience of two.
So we're essentially ina comedy club here now.
Oh no, no, please.
So when I moved up to Scotland,I went into a bakery in Glasgow,
and I said to the baker, "Is thata custard tart or a meringue?"
He said, "No, you're right.
(00:29):
It's a custard tart."
Anyway, tough audience.
You just don't improve, Roger.
We covered cytopathogenic and paraviralrashes in our previous two episodes,
And for this next episode, we're goingto be exploring the more rare and
odd viral skin infections, includingKawasaki disease [and] Covid-19.
(00:54):
And as an extra treat, we're joined byour very special guest, Dr Marina Morgan,
Consultant Clinical Microbiologistat Royal Devon and Exeter Hospital.
So sit back, turn the volume up and getready for another insightful episode.
Play the music.
(01:21):
Hello and welcome once again tothis Rash Decisions podcast, where
we look at skin-related issues,conditions and treatments in an
interesting and informed way.
I'm Dr Roger Henderson.
I'm a GP with a long-standinginterest in this area of health.
And I'm Dr George Moncrieff.
I was also a GP, although I've now retiredfrom my practice, and I'm a former Chair
(01:42):
of the Dermatology Council for England.
So today we're going to be talkingabout a collection of odd rashes
that are likely to be linked to avirus, but which are very tricky to
pin down as to their exact cause.
And I'm delighted to introduce thefabulous Dr Marina Morgan, who you
may remember was also with us for ourpodcast on bacterial skin infections.
(02:04):
And as I mentioned earlier, Marina isa Consultant Clinical Microbiologist at
[the] Royal Devon and Exeter Hospital.
So welcome to the podcast, Marina.
It's really good to have you back withus today, and we must have done something
right for you to agree to come back.
Thank you.
It's a great privilegeand an honour to be here.
Thank you very much.
And welcome from me, Marina, as well.
(02:25):
It's lovely to have you.
Thank you so much.
Really is great to have you here with us.
Absolutely.
Now we've got a fair bit to covertoday, Marina, so we're going to look
at a hotchpotch of odd rashes that I'mconvinced must have a viral aetiology,
possibly as paraviral immune reactions,but no single viral agent has been
(02:46):
attributed to any individual condition.
So I'm going to take a deep breathand I'm going to start with Pityriasis
lichenoides et varioliformis acuta.
Fortunately for me, PLEVA, for short.
Now, if I'm brutally honest, George,I haven't seen this too many times,
or I haven't seen it for a yearor two now, unless I have, and
(03:09):
I've actually misdiagnosed it.
I'm surprised.
I certainly saw this regularly.
And certainly as a GP I had colleaguesreferring their patients with difficult
rashes my way, but I'd say I probably sawhalf a dozen cases a year or so of PLEVA.
It's especially in the late spring andthe early autumn and typically what
(03:29):
we see is a young adult with a mildlyitchy rash on their limbs and trunk.
And it's pityriasiform, as I'vesaid before, comes from the Greek
word meaning 'like a husk of bran'.
So it has a rather husk like,very fine surface scale.
The individual lesions are typicallyovoid, slightly erythematous, and have
(03:54):
that collarette of pityriasiform scale.
And it's called pityriasislichenoides because it often has a
slight look of lichen planus to it.
Now, you'll remember that lichen planus iswhat's known as an interface dermatitis.
It occurs at the junction betweenthe epidermis and the dermis.
(04:15):
And so, unlike eczema and psoriasis,which are up in the epidermis, where the
light just reflects quite superficially,here the light has to travel down
through the epidermis and into theupper dermis before it reflects back.
Now, the more the light goes down, themore red light is filtered out, just
leaving the blue end of the spectrum.
(04:36):
That's why lichen planus has a rathermore violaceous colour to it, as do
the other interface dermatitises.
PLEVA can also have a rather moreviolaceous colour, so hence lichenoides.
And this eruption can last from severalweeks or months, but I've actually seen
it lasting years, and when that happens wecall it pityriasis lichenoides chronica.
(05:03):
Actually interesting, there's an evenmore severe end of the spectrum where
the lesions become ulceronecrotic andthat's known as Mucha-Habermann's disease.
But usually it's a fairly mild illnessand people have tried various things like
antibiotics for it, but I don't know.
Do you see this, Marina, or does it notreally come your way into secondary care?
(05:25):
Well, I've never actually seenit, not that I know to, actually.
[Inaudible]
Right, that says it all, doesn't it?
Right, yes, okay.
So we keep it in generalpractice on the whole, or
perhaps into dermatology circles.
And the antibiotics are notbeing used to kill the bacteria.
They're being used, I think, todampen down the inflammatory reaction.
So I think we're basically seeing itprobably in primary care, um, although
(05:45):
my primary care colleagues do seem tobe a bit unfamiliar with it, but it's
definitely out there and there's a wholelot of different pityriasiform rashes.
If I just digress, sorry, pityriasisversicolor, which is caused by a yeast,
the pityrosporum We've talked aboutpityriasis rosea, which is almost
certainly a resurgence of the humanherpes viruses 6 and 7, I think it is.
(06:07):
There's pityriasis alba, which isessentially nothing more than a patch
of very, very mild eczema, usually onthe face, and becomes more apparent
at the end of the summer when thatskin isn't developing a nice tan.
But people often try a prolongedcourse of a tetracycline or a macrolide
antibiotic for PLEVA, sometimes theycan help a bit, probably more due to
(06:27):
their anti-inflammatory side effectsthan any true antibacterial role.
But it's definitely not somethingthat causes me any great worry.
It's obviously unpleasant for patients andit's a bit itchy and it doesn't look very
nice, but it's not dangerous in any way.
There's another one I probably oughtto talk about that people often haven't
seen or don't think they've seen, andthat's something called lichen striatus.
(06:48):
I saw a case of that actuallyjust a few weeks ago.
It's an odd entity that typically presentsin a child aged between about five and 15.
Interestingly, it's morecommon in girls than boys, but
that's not absolutely definite.
And this rash follows Blaschko'slines, usually down the limb or down
the back or the back of the buttock,and it's virtually without symptoms.
(07:10):
It can be a bit uncomfortable, inwhich case a simple emollient, for
example something like AproDerm®Colloidal Oat [Cream], will be
very useful at relieving that.
And there appears to be some seasonalvariation, so that raises the thought
that it might be due to a virus.
Perhaps influenza has been suggested,even HVZ, herpes varicella-zoster.
(07:31):
Is that something thatcomes your way, Marina?
Not again that I've seen, butI'll keep an eye on it because it
sounds pretty interesting actually.
I think we'll hit bingo soon.
I agree it's not that common, um,and it's called lichen striatus
because it's got certain similarities,I suppose, to lichen planus.
You have tiny little sort of whitebumpy, pinky bumps, often in a
(07:55):
line, and a perfectly well child.
Another odd entity, a really odd entitythat we occasionally see is, and this
is a unilateral rash in a young child.
It typically occurs around thearmpit and then down onto the chest.
And it's got this long name.
It's a unilateral laterothoracicexanthem of childhood.
(08:16):
And it typically occurs on thesort of close to the shoulder area.
So we sometimes call it APEC, standingfor asymmetric because it's just
on one side, periflexural, becauseit's close to the flexure of the
axilla, exanthem of childhood.
And it's uncommon, self-limiting,unilateral exanthem.
Typically seen in little childrenaged about two or three years old.
(08:39):
Again, slightly morecommon in girls than boys.
It can easily be confused becauseit's got a bit of scale to it.
So it can be confused being asymmetrical.
It makes us immediately think,"Could this be a fungal infection?"
But it's almost certainlya response to a virus.
It lasts for several weeks or months,and then it goes, and it's presumed
[just] to be due to some kind of seasonalvariation and clustering of cases,
(09:02):
must account for it having some kind ofviral cause, but that remains elusive.
Other candidates that are being consideredinclude the parainfluenza viruses,
adenoviruses, again, human herpesviruses 6 and 7, and even EB viruses.
That's really fascinating stuff,George, and some of those are new to me.
One condition, though, thatmay be more familiar, to people
(09:24):
listening is Kawasaki disease.
I've seen this once in my career.
I remember fortunately diagnosing itcorrectly with a child who wasn't too
unwell when I saw them, um, thoughtthey had Kawasaki disease and admitted
them and was extremely sick by thetime that they got to hospital.
(09:45):
Although their life was saved,unfortunately, they lost most of
their fingers and some toes duringtheir time in intensive care.
And that's exactly the problemwith Kawasaki as to what it can do.
Yeah, I think I've probably seenabout four cases and your case
sounds awful, Roger, and youcertainly don't forget them, do you?
No, that's one that stuck with me.
(10:06):
Yeah.
Fortunately, it's a very raredisease and I'm sure Marina
will have some thoughts on this.
But I'm sure it's due to some kindof toxic shock reaction to maybe a
bacterial superantigen or perhapssome kind of immune complex problem.
Various agents have beenconsidered, I know, like human
herpes virus 8 and even rickettsia.
But have you got any thoughts on, onthe aetiology, what's going on here?
(10:29):
That's absolutelyfascinating, but so tragic.
Roger's child would have had a veryrare complication of Kawasaki disease,
Kawasaki disease shock syndrome.
Kawasaki seems to be a combinationof genetic susceptibility and Asian
children, typically Japanese arevery susceptible, combined with an
overreaction to a superantigen, whichis usually bacterial, but can be viral.
(10:51):
So your theory about herpes and flu,it might also be true, but because
it's a superantigen reaction, itlooks a bit like toxic shock and it's
still very, very murky as to whatactually is the cause of Kawasaki.
Goodness, yeah, it'sfrightening, isn't it?
And it usually presents, Ibelieve, in boys more than girls,
and quite young, aged 2 to 5.
(11:15):
How I think of it is they have aspectacularly high fever, often
well over 40, with bilateralred, sore, non-discharging eyes.
Then they get these very swollen, crackedlips, and a strawberry-looking tongue.
The other feature that would certainlyhighlight and make me think about
it is they get massive, and I meanmassive, cervical lymphadenopathy,
(11:37):
very large glands in the neck,over one and a half centimetres.
They really are big.
Then they go on to get a widespread,rather non-specific, maculopapular
rash, again with some rednesson the palms and the soles.
Any infant with an unexplained andparticularly high fever, or a prolonged
fever, would make me think about this.
(11:58):
And the biological response,such as that rash, for example,
should raise the suspicion ofKawasaki disease, shouldn't it?
Absolutely, George.
Particularly if the fever's going onfour or five days, as you say, it's
the length of time of the rash as well.
Big lymph nodes, over one and a halfcentimetres, so really big lymph nodes.
Swollen hands and feet, and atemperature of more than 38.
(12:20):
More than four or five days with arash and fissured mucous membranes is
the absolutely classical presentation.
Now, the real problem is that actuallywe've realised that there are two other
conditions that can mimic this veryclosely, particularly the new one,
MIS-C and streptococcal toxic shock.
So MIS-C, which is M IS - C, stands for Multisystem
(12:41):
Inflammatory Syndrome in Children.
We've had one or two cases down here inExeter, and MIS-C produces a Kawasaki-like
manifestation, erythematous or urticarialrash, with a mucositis that also has
a conjunctivitis, and a periorbital,and palmar and plantar oedema.
So, all three of these syndromes,Kawasaki's, MIS-C, and toxic shock,
(13:04):
they have the same ultimate cause, theresults of a dysregulated immune response.
Kawasaki's and MIS-C are particularlysimilar, they present with a rash,
which can be hands and feet, cervicallymphadenitis, and the persisting fever,
high temperature for three or five days.
The children really look ill, and theyneed to be referred as quickly as you can.
(13:26):
Because they need cardiac testingand the blood testing to establish
diagnosis and start the treatment.
Happily, now we're going a littlebit further out of the acute Covid
events, MIS-C is becoming much rarer.
And we've got morechildren being vaccinated.
But the clues to the diagnosis wouldinclude a recent Covid infection.
That's within the last two to six weeks.
(13:48):
And if they present with gastroenteritis.
Both diarrhoea and vomiting andabdominal pain that can be bad enough
they're admitted to hospital [with]an acute abdomen and then they'll
often develop shock and myocarditis.
MIS-C children are also usually alot older, they're seven to nine
compared to Kawasaki, which isusually two to five years of age
And I believe they don't have thesame sex difference that Kawasaki
(14:12):
do either Kawasaki's more boys.
Whereas this is equal boys and girls.
Is that right?
Yeah, pretty well.
Yeah, and it's also more common inchildren of colour, isn't it, as well?
Yes, MIS-C, is far commonerin the African, African
Caribbean and Hispanic patients.
That's very, very useful.
Thanks.
So, when thinking about toxic shock,which is more my home ground really,
(14:36):
again, it's a common cause of a widespreadrash in very sick, febrile children.
It's very acute.
They've not been suffering for fouror five days, with a spreading rash.
They're not too bad, theyget a bit grizzly and they
get really sick very quickly.
And they're very hypotensive andneed a lot of intravenous fluids
when you get them into hospital.
And by definition, all the staphylococcaltoxic shock patients have to have a rash.
(15:00):
It's part of the definition.
But only 50% of streptococcal toxicpatients will actually have a rash.
So, just to recap, because it's prettycomplicated, but I think essentially,
a sick child with a rash, on the palmsand soles too, with lymphadenopathy
and mucositis, you've got to askthe parents whether they've had
Covid in the last four or six weeks.
(15:21):
Or whether they had more recentcontact with a streptococcal
type illness, impetigo,tonsillitis, something like that.
And if they've been unwell withCovid recently, and they now have an
inflammatory syndrome with swollen handsand feet, and particularly if they've
got abdominal symptoms, then thatwould really point to it being MIS-C.
Whereas a child with a temperature ofmore than four days, massive cervical
(15:42):
lymphadenopathy, you know, greater thanone and a half centimetres, bilateral
conjunctivitis without any pus, thatis unwell with a rash also on the
palms and soles, and particularlywith the lip fissuring, that's
going to point you towards Kawasaki.
Whereas a more acutely ill child withshock, rash, gastroenteritis appearing,
and a conjunctival suffusion, so pinkeyes, with a history of streptococcal
(16:06):
contact, is much more likely tohave streptococcal toxic shock.
Either way, these children need tobe in hospital as soon as possible.
Mercifully, none of theseconditions is that common.
But I'm sure it's our role ingeneral practice to be vigilant
and to jump when necessary.
And I think this brings me back toa point that I say to everybody I
(16:26):
talk to who works in primary care.
And that is that every patient,and I mean [with] every patient
make a conscious decision.
Are they unwell?
In which case I'm not too concerned.
They can head off home.
Or are they ill?
And if they're ill, you need to jump andyou don't see an ill patient that often,
(16:52):
maybe just three or four times a year.
But when you see somebody who'sill, and a child in particular,
the signs can be really subtle.
Um, it can be really subtle, both inlittle children and in older people.
And when you see someonewho's ill, you need to jump.
So for example, the child who's climbingup my curtains and jumping around the
(17:16):
place and playing around and being anuisance and won't let me examine them.
I don't really need to examine them.
They've given me all the informationI need, but the child who lies there
limp and pathetic and pale and floppy.
NICE have produced a very usefultable of things like heart rates and
respiratory rates and tone and so on.
(17:36):
I just stand back and make avery, very conscious decision.
Have I got somebody infront of me who's ill?
And when they are, I would considergetting a 999 ambulance to get them
to a place where they can be manageddefinitively and urgently, not go
with their parents in the car lateron this afternoon or whatever.
They need to get there fast.
(17:57):
And we need a very low index of suspicionfor conditions like Kawasaki and these
other conditions, because it does demandthis urgent admission for things like
aspirin, and immunoglobulin, assumingthey survive the acute illness, but
to prevent the late complications ofthings like coronary artery aneurysms,
which occur in up to a quarter of cases.
And I believe there's also a linkwith ischaemic heart disease.
(18:20):
But I think to wait for that feature thateveryone seems to remember, which is that
the skin on the palms and the soles canpeel, is the way to diagnose Kawasaki.
It's absolutely not.
That's a very, very late sign.
Furthermore, it's by no means specific.
You see it, for example,with scarlet fever.
Lots of things can cause peelingof the palms and the soles.
So just because someone's skin ontheir palms is peeling, it just
(18:43):
means they've had a major illness.
And you should not be relying on that.
You will never make a diagnosisof Kawasaki in time to make a
difference for your patient.
You'll miss that window of opportunityto intervene when you could have
prevented some of those really importantside effects and complications.
Absolutely, I couldn't agree more.
There's that old adage, justlisten to your gut feeling,
(19:05):
listen to that sixth sense.
I think that's saved me a lot oftimes, more times than I care to think.
So just listen to that sixthsense and don't ignore it.
Um, you touched on Covid-19 there Marina,and we now know we should be thinking
of Covid both acute and long-term ashaving the potential to impact every
(19:26):
single area of the body from the topof the head to the bottom of the feet.
So since Covid washed up on ourshores, what have you been seeing
in your workload linked to it?
Just about every kind of rashI could imagine actually.
It's most bizarre.
When I was training many years ago, I wastold that syphilis was the great mimicker.
(19:47):
Um, but now Covid seems to be to blamefor most of the odd rashes I see.
[I] couldn't agree more Marina.
It's quite extraordinary isn't it,the spectrum of rashes that we see
with Covid-19 from simple chilblainsor something called perniosis,
which is most commonly seen in youngpeople, where it's almost certainly
(20:08):
due to a high level of interferon.
So you could, in fact, if you wantedto call it an interferonopathy,
which is caused by their innateimmune system producing interferon.
So it's a very vigorous and effectiveinnate immune response to the more
maculopapular, um, papular vesicularrashes, which can then become
haemorrhagic or even urticarial.
(20:30):
The livedo, which we see in very, veryill patients, can be a sort of pointer
towards the fact that the patient hasn'treally got much chance of making it.
It's a very bad prognosticfeature if you see a livedo rash.
So it's an extraordinaryspectrum, isn't it?
And if I'm honest, it was when I sortof looked at this during Covid and
was reflecting on the spectrum ofrashes that I was thinking, they're
(20:53):
all having the same virus, but whyare their illnesses all so different?
And why is their experience so different?
And perhaps, what does the skin rash tellus about the outcome and their prognosis?
Could the skin be a, window into that?
Now, I'm probably barking up thewrong tree here, but it made me think
(21:15):
that, well, in a young person, with avigorous, innate immune response, and
a high interferon level, immediatelyfollowing infection, they will knock
down their viral load, which isgood for their long-term prognosis.
But they then get theinterferonopathy, they get the
Covid toes, they get the chilblains.
(21:35):
But in an older person, whose innateresponse might be a little bit more
sluggish, that allows a much, muchgreater viral load to hit the patient.
And that's then subsequentlyfollowed by a massive adaptive immune
response and the cytokine storm.
And it's then the cytokine storm thatcauses all the endothelial damage, and
(21:57):
hence the macular vesicular rashes and thelivedo rashes, which can become necrotic
and all the other more severe rashesassociated with more severe disease.
And then that endothelial damage goeson to affect the kidneys, the heart, the
lungs, the brain, the gut, and so on.
So the rash to some extent cangive you a window into what their
(22:18):
immune system is doing and thereforewhat their prognosis might be.
And it was what made me start thinkingabout why we have paraviral rashes, i.e.
due to the immune response,and cytopathogenic viruses.
Anyway, that's where mythoughts have been developing.
Does it make any sense to you at all,Marina, or am I completely bonkers?
(22:40):
Nope.
I think there's an awful lot of truthin what you say, actually, George.
The trouble is, we're stillin that awful position of not
knowing, really, what's going on.
We're just at the frontier of beingable to put it all together, I think.
I think of it this way, it's the Venndiagrams just don't overlap well enough
for us to figure it out properly.
Interesting.
(23:01):
Very interesting.
As always, George and I do hope youfound this podcast as interesting
[and] as helpful, as we have.
And that you've enjoyed the previoustwo we've done on viral skin problems.
But if you haven't caught upwith those yet, do have a listen.
if you like what you hear,then do rate and review us
wherever you get your podcasts.
It really does help us keepproducing quality content for you.
(23:24):
Or you can get in touch with questionsor suggestions for future podcasts,
as we really do love to hear from you.
But, until then, it's goodbye fromour very special guest, Marina.
Goodbye.
It's goodbye from George.
Goodbye.
And as always, it's goodbye from me.
Goodbye.