October 1, 2024 • 27 mins
Dr George Moncrieff and Dr Roger Henderson share their wisdom on viral infections. In the first of three episodes on this topic, they’ll cover cytopathogenic rashes, where the virus is present in the skin lesion.
Along with sharing their top six viral facts, they’ll talk you through:
- Viral warts
- Herpes simplex infections
- Chickenpox
- Shingles
- Orf
- Molluscum contagiosum
For each of these conditions, they’ll discuss what the virus is up to, share their experiences on the available treatments and complications that you should be aware of in primary care.
Thank you to our kind sponsor AproDerm, who provide a comprehensive range of quality emollients designed for the management of dry skin conditions, including eczema, psoriasis and ichthyosis.
To simplify the process of finding the most suitable emollient for each patient, they have developed a remarkable solution: the AproDerm Emollient Starter Pack. This pack conveniently combines all four of their emollients in a single prescription, enabling patients to identify their ideal emollient more efficiently, aiding both compliance and adherence.
Find out more: https://aproderm.com/aproderm-emollient-starter-pack/
LI: https://www.linkedin.com/company/fontus-health-ltd/
Got some feedback for us? Please rate and review Rash Decisions to help us keep creating educational podcasts for you.
Is there a dermatology topic you’d like us to explore? Email us at info@aproderm.com, and we’ll do our best to cover it.
The views expressed in this podcast are of Dr George Moncrieff and Dr Roger Henderson. Fontus Health has not influenced, participated, or been involved in the programme, materials, or delivery of educational content.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:08):
Hey George, do you want to hear a joke?
No thanks.
Oh good, I was really lookingforward to watching a documentary
about origami last night, but whenit came to it, I wasn't able to.
It was pay-per-view.
Oh, for goodness sake.
Now, today, George and I willbe talking about the problem
of viral skin infections, whichyou can imagine is a huge topic.
I like to think of viralrashes in two broad groups,
(00:31):
cytopathogenic and paraviral.
And in this episode, we'll explore thecytopathogenic rashes where the virus is
present in the skin lesions themselves.
So, from pesky viral warts tothe infamous chickenpox and
molluscum, we'll be covering it all.
So stay tuned and play the music.
(00:59):
So, welcome once again to thisRash 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 was the Chair
of the Dermatology Council for England.
(01:21):
This is the first of three episodesabout viral skin infections.
Next time, we'll be talking aboutparaviral rashes, such as measles.
Obviously, that's a real worryat the moment because of the fall
in the MMR vaccination uptake.
We'll also look at things likeFifth disease and pityriasis rosea.
And you definitely don't want to missthe last episode, where we'll be joined
(01:42):
by a very special guest, where she'llbe telling us all about the rarer viral
illnesses, such as Kawasaki disease,smallpox, and obviously Covid-19.
So, do make sure to follow RashDecisions so you don't miss any of those.
Now in our bacterial skin podcast, whichwe hope you listened to, George and I
put our heads together and came up withour 'top six facts', which was such
(02:05):
good fun to do, and which went down sowell with all of you, we thought we had
to share another one with you today.
So, I'm going to kick [off] with one ofmy favourites, so up first, we previously
told you that the cells in our bodieswere outnumbered by bacteria 10 to 1.
Well, there are ten times as many virusesin our bodies as there are bacteria.
(02:27):
So, this goes off the scale.
I really like that one.
It's amazing, isn't it?
And we don't really know whatthe role of these viruses might
be, what role they're playing.
That's absolutely right, George, andthat brings [me] on to fact three,
which is that the future of controllingserious bacterial infections is
actually probably with viruses.
(02:49):
Now, phages are viruses thatonly attack and kill bacteria.
Their role at present is still verymuch in the research phase, and one
of the problems is that each phagehas to be developed as a bespoke agent
for a particular bacteria, so they'renot available instantly, in other
words, off the shelf, for treatinglife-threatening bacterial infections.
(03:12):
So as an area of research,I find this really exciting.
It's reassuring to know that there's stuffgoing on there, isn't there, that means
we might have something when finally, thetime of antibiotics has come to an end.
Viruses are spread by direct contact,often through droplet spread.
The enteroviruses, things like coxsackieand polio and even the echoviruses, as
(03:36):
well as, of course, things like norovirus,are spread by the faeco-oral route.
Again, physical contact there.
When someone with a viraemia, orindeed someone who has virus in their
tonsils or upper airways, coughsor sneezes, droplets containing
viruses are distributed into the air.
Now you might be surprised to learnthat these can travel at a speed of 100
(03:58):
miles an hour, so they can hit a wall afew metres away from you if you sneeze
without covering your nose and mouth.
And if there's no draft, i.e.
there's no wind or anything, theseviral particles can remain suspended
in the air for a very long time.
Absolutely, indeed they can, and wethink they're able to hang in the air for
minutes, or even in some cases, hours.
(04:21):
We also mustn't forgetthe impact of touch.
So, if you touch your face or yournostrils and you've got a viraemia,
then you touch a hard surface.
Again, that can hang around for avery long time on those hard surfaces.
Rashes caused by a virus,they're called exanthems.
But viruses aren't the only causes ofexanthemata, and this rash can easily
(04:43):
be confused with things like drugreactions, secondary syphilis, graft
versus host reactions, and many more.
And many viral infections can alsoinclude a rash on the mucosal surfaces,
and obviously we're thinking ofthe mouth as a good example there,
and these are called enanthemata.
So 'X' on the outsideand 'N' on the inside.
(05:04):
Great way of remembering it, yeah.
Now, number six, viruses obviouslydon't respond to standard antibiotics,
or other antimicrobials, but wedo have some antivirals for some
viruses, notably of course theherpes viruses and the pox viruses.
Yes, and I think we're goingto touch on some of those.
That's a good list, George.
(05:25):
So, let's start at some of thecytopathogenic rashes first, and I'm
going to start with an old favouritehere, which we all know, viral warts.
Yeah, they're a nightmare, aren't they?
They're caused by a variety of humanpapillomaviruses, and they're easily
spread by direct contact with a case orvia a fomite, as we've been discussing.
(05:46):
They're therefore most common onthe hands and around the face.
Verrucas are human papillomavirusinfections on the feet, and they're
usually picked up by walking barefootin a public area, such as a swimming
pool, or around a swimming pool.
They're most common in children andyoung adults, probably because in
adults we've become immune to mostof the important ones, but they
(06:09):
can persist for many, many years.
The viruses effectively hide withinthe cell nucleus, protecting them
from our immune system, and so theytake over the cell's organelles and
are hidden from antiviral treatments.
That accounts for the poor responsethey have to tropical treatments.
Such as liquid nitrogen and all the paintsand things that we apply like salicylic
(06:31):
acids, which are trying to split thecells up a bit and expose the virus.
Yeah, they can be a real nuisance andtake an awful long time to get better.
There's another viral skin problem,though that can be certainly more
than a nuisance, which I alwayslook out for because I really don't
like it, and that's herpes simplex.
We really mustn't forget aboutthat one initially, must we?
(06:54):
It can be nasty, can't it?
Yeah.
The initial infection with aherpes simplex virus is often
asymptomatic actually, but it canbe very nasty with a very severe
herpetic, usually gingivostomatitis,so bleeding, swollen, nasty gums.
The virus then travels usually backto the geniculate nucleus, and it
(07:15):
doesn't get any further than that.
But following this initial infection,the virus typically remains dormant in
that geniculate ganglion, and in mostindividuals causes no further issues.
However, some unfortunate peoplehave recurrent cold sores, where
painful vesicles appear whenevertheir skin temperature is raised.
(07:37):
So that can be from a fever, hencecold sores, but also premenstrually, or
even following a sauna or sunbathing.
They also tend to come out during episodesof reduced immunity, including simple
things like stress, but also pregnancy.
And in this situation, the active lesionsare shedding virus, and the patient is
(08:00):
contagious through skin-to-skin contact.
Yeah.
Individuals with atopic eczemaare especially vulnerable
to herpes simplex virus.
If you didn't hear us talk in ourpodcast about atopic eczema, then do
have a listen because it's a good one.
That's really interesting, why is that?
Why are people with atopic eczema morevulnerable, would you say, George?
(08:23):
Well, one of the big reasons is that deepin the epidermis, in the stratum spinosum,
we produce over 3,000 antimicrobialagents, called antimicrobial peptides.
These are our body's naturalantibiotics, things like the
defensins and cathelicidin which isconverted to its active agent, LL-37.
(08:48):
These antimicrobial peptides arecritical at combating HSV infection.
But, the inflammatory interleukinsthat are produced in atopic
dermatitis, things like IL-4 andIL-13 decrease the production
of these antimicrobial peptides.
So that explains why patients with ADare particularly vulnerable to getting
(09:11):
eczema herpeticum, which is a potentiallylife-threatening and serious infection.
In eczema herpeticum, monomorphic, i.e.
they're all the same shape, quitesmall, usually two to four millimetres,
inflammatory eroded areas develop.
It's usually, but not invariably,on the face, probably because
(09:35):
the skin there is quite thin andvulnerable to eczema generally.
Patients with this complicationof atopic dermatitis can become
critically ill, quite rapidly.
So, if you see somebody with it, I woulddefinitely recommend treating them, but
I'd also recommend if you're not sendingthem into hospital, that you contact
them in a few hours because they can gofrom being well to being ill quite fast.
(09:59):
I think it needs urgenttreatment with aciclovir.
And if there's any even remoteconcern that your patient is ill,
they should be admitted immediatelyfor intravenous aciclovir.
Interestingly, I was talking with DrMorgan, who's going to be joining us
in our third podcast on this topic,and she says that there's a novel
anti-herpes drug called, wait for it,amenamevir, which is not yet available
(10:23):
in the UK, but is currently being usedin Japan, and will be an option for that.
Another interesting thing to say isthat our biologics that knockout IL-4
and 13 for atopic eczema, things likedupilumab, I'd be very interested to
see whether patients on those don't everget eczema herpeticum, because they're
(10:43):
no longer having the IL-4 and 13 levelsthat knockout the antimicrobial peptides.
I haven't seen that in any literature yet,but it's something I'm looking out for.
Oh, that will be interesting.
Now, as you know, there's this bigdrive for minor self-limiting illnesses
to go to community pharmacists ratherthan into primary care practices.
(11:05):
And one of the viral illnessesthat I think community pharmacists
may be seeing a lot more of as aconsequence is chickenpox, because
obviously it's much more common.
Most people are less likely to havesignificant health issues, but not all.
Right, well that's right, yes, we'll betalking about poxviruses with Dr Morgan
in our third podcast on this topic.
(11:26):
But sadly, this infection, chickenpox,remains common, and I think you'll
agree with me, it's one of thecurrencies we see in general practice.
Absolutely.
And I think that's sad, becausechickenpox is confined to humans.
We have an excellent, albeitquite expensive, vaccine.
So, it is potentially completelypreventable, it can be a very serious
(11:51):
infection, and it just doesn't need tobe a rite of passage through childhood.
No, chickenpox parties shouldbe a thing of the past.
Absolutely.
So, let's talk about, how contagiousit is, because there can be a little
bit of misinformation or some mythsand inaccuracies about how chickenpox
(12:12):
is spread and the timescale involved.
Right, well, the incubation period,which is the time from exposure
to the onset of the rash, isactually quite long with chickenpox.
It's between two and three weeks.
Prior to the onset of any skinchanges, the patient develops
a coryzal illness with fever.
At that stage, if you look in theirmouth, you might see an enanthem with
(12:34):
small painful ulcers on a red base.
Patients are contagious from the startof that coryzal illness until the last
crop of spots have formed dry crusts.
That's usually around about seven toten days after the onset of the rash.
So, they're contagious foraround about a fortnight.
(12:55):
The lesions themselvesactually harbour the virus.
But when you've got chickenpox,it's mostly spread through
droplets, from coughing.
You've got a viraemia and when youcough you spread the virus into
the air and then people inhale it.
That's the main means of contact.
The virus is a cytopathogenic virus,so you have the virus in the lesions.
(13:16):
And what happens is you get crops ofsmall red bumps, which are quite itchy.
They rapidly develop intoclear-filled vesicles, which then
mature into pus-filled pustules.
And those then breakdown and form dry crusts.
And crops of spots continue to appearfor the first few days of the illness.
(13:37):
So, you see lesions at different stagesof development, gradually evolving,
and so it's when the last crop ofspots have finally got to the dry crust
phase that you're no longer contagious.
Yep.
A very rare complication, one that Ithink we need to think about though, of
chickenpox, is Reye’s encephalopathy.
This is virtually only seen whena child is also given aspirin.
(14:02):
So, I generally go out of my wayto advise parents to avoid this.
That's a great takeaway point, George.
And I suppose one of the messagesof the wayside pulpit with this
podcast, I'd be saying, avoidaspirin in cases of chickenpox.
I mean, we should be avoiding itanyway, in children, but anyone
with chickenpox, avoid aspirin.
And I think there's another one here,which we sometimes forget, and I'm
(14:24):
going to chip in with my smokingcessation hat on, and remind, all the
healthcare professionals listening.
If you see an adult with chickenpox,ask them if they smoke, and this always
tends to raise an eyebrow in them,but there's a good reason for that.
Yeah.
You're so right.
Although it's uncommon in adults,we do see it from time to time.
(14:44):
And here, as you say, the mostimportant thing to establish
is whether the patient smokes.
Because smoking exposes them to a highrisk of developing chickenpox pneumonitis.
Which, I've never seen that in an adultwith chickenpox who doesn't smoke.
Chickenpox pneumonitisclassically presents about one
to six days after the rash.
(15:04):
And it can be lethal.
It can.
So, after recovery, we will know thatthe patients have had this, because
if you do a chest x-ray, you see thatmiliary shadowing on their chest x-ray.
But it's a reallyfrightening complication.
So, if I had an adult developchickenpox, and they were a smoker,
I would be keeping a very close eyeon them or getting them admitted.
(15:26):
Similarly, chickenpox in someonewho's immune suppressed, or indeed
in anyone over 21, particularlyif they've got a widespread
exanthem, can become very serious.
And by immune suppressed, I meanthings like even a short course of
oral steroids, for example, for asevere asthma attack, can render
that patient dangerously vulnerableto chickenpox for up to three months
(15:49):
after the steroids have been stopped.
I think this is such an important message.
Yeah.
If I see a child, a young child, and Ineed to put them on steroids, perhaps
for an acute asthma attack, one of thefirst questions I'll ask the parents
is, "Has your child had chickenpox?"
And I think that if they haven't,they need to be advised to seek help
(16:12):
urgently, if they come into contactwith chickenpox or if they themselves
develop any early signs of it becausein that situation zoster immunoglobulin
or aciclovir could be life-saving.
Children have died, developingchickenpox, even a few months
after finishing a short course ofsteroids, for example, for asthma.
(16:33):
Yes.
Similarly, chickenpox inpregnancy can be a disaster.
So, I always check to see whethera woman of childbearing age
has had chickenpox as a child.
And if she can't remember ordoesn't know, I would suggest that
she thinks about vaccination, asvaccination before conception can
prevent chickenpox in pregnancy.
(16:53):
Obviously, you don't alwaysget the chance to do that.
If a mother does come into contactwith chickenpox, which, let's
face it, is hardly unlikely.
She might have other childrenwho come home and get chickenpox.
Stored blood, taken at the time ofbooking, can be retrieved and tested.
So, when we take our booking bloods,that blood is saved, and they can go back
(17:14):
and they can test it for chickenpox IgG.
If that is absent then that helpsus to inform any decision regarding
whether after exposure, theyshould be given ZIG or aciclovir.
Noting, of course, that's anunlicensed use in pregnancy, but
probably a wise decision and onethat needs to be thought about.
(17:36):
Yeah, that's a fantastic takeawaythere, George, and sometimes
we do forget about that.
Now before I'm going to move on to ournext condition, I just wanted to take
the time to say a few words about ourkind sponsor, AproDerm®, and their range
of emollients that include creams, gel,ointment, all formulated to soothe,
moisturise, and protect our skin affectedby a whole range of dry skin conditions.
(17:59):
And if you've listened to our podcastbefore, you'll know that myself and
George are huge fans of AproDerm®.
Now, why?
Well, their complete rangeis suitable from birth.
They're free from common irritantsand sensitisers, which is vitally
important, obviously, as well asbeing vegan-friendly and cruelty-free.
So, they really do tick all theboxes, and I would suggest that we
(18:21):
make it our go to emollient range.
I'm going to come on to shinglesnext, and if there's one condition
that has more old wives taleslinked to it, I have yet to meet it.
I mean, going back to medieval times,when it was known as the 'belt of roses
from Hell', I've lost count of the timesI've heard myths such as, if shingles
goes all the way round the body andmeets in the middle, then it's fatal.
(18:45):
And I'm sure you've heard a fewcrackers as well, too, George.
I have, but I haven't heard that one.
And if that were the case, itwould be crossing two dermatomes.
And if I saw shingles crossingdermatomes, I'd be very concerned
about the patient's immune status.
Yes.
Shingles in someone who is immuneincompetent for whatever reasons can
be a very nasty condition indeed.
(19:07):
Yeah.
Shingles, as we all know, is due toreactivation of the patient's own
chickenpox virus that's been lyingdormant in their dorsal root ganglia since
they had chickenpox usually as a child.
And the onset of this painfulrash is heralded by pain
in that affected dermatome.
Now, contrary to many textbooks,shingles is not uncommon in
(19:30):
children and young adults.
During lockdown, my four year oldgranddaughter had abdominal shingles
while she was staying with us.
Wow.
In children, it's typicallya very mild illness.
The rash is barely painful, and it doesn'tnormally need any treatment at all.
In fact, I don't generally rush totreatment in someone under 50 with
(19:54):
shingles, but certainly in anyone over50 and the older they are, the more
eager I am to get going with treatment.
Agreed.
Of course, the sooner that isstarted, the better, ideally
before any rash has developed.
So, if a patient presents with painin a dermatome area, and one of the
common sites is in the ophthalmicregion, headache on that side coming on
(20:16):
suddenly, definitely not crossing themidline, a strictly unilateral pain.
Then I have a low threshold forthinking about shingles in that
situation and trying to get in withsomething very safe like aciclovir
even before the rash has appeared.
Once the patient's had the rash formore than 48 to 72 hours, two or three
days, there really is little benefitfrom these antiviral treatments.
(20:40):
Another interesting point, whichagain is contrary to the textbooks,
as GPs, we regularly see someone,perhaps a grandparent, who's come
into contact with chickenpox.
For example, perhaps a grandchildthey've been asked to look after,
because of the child being ill.
And then the grandparentgoes down with shingles.
And I think what's happening here is thattheir immune system, which normally keeps
(21:03):
the virus at bay, focuses on the exposureto this virus and reduces its surveillance
on the dormant virus, allowing that toescape from the dorsal root ganglia.
Yeah.
Now, ophthalmic shingles is particularlyimportant, because it accounts for between
10 and 25% of all cases of shingles.
And of course, this involves thefirst branch of the trigeminal nerve.
(21:26):
But just beyond the ganglia, behind theeye the nasociliary branch comes off.
It comes off from the main trunk to supplysensation to the side of the nose, both
inside and out, also the cornea, andalso the upper lid conjunctiva, and a few
other areas on the face, but not below thenose, as well as having ciliary branches,
(21:48):
which then penetrate the eyeball.
So, that little bit of neuroanatomyis important, because if you have got
ophthalmic shingles, and you've got anysymptoms or signs, on the side of the
nose, either on the inside or outside,extension of the rash into that area, i.e.
Hutchinson's sign, there is arisk of eyeball involvement, and
(22:08):
therefore orbital ophthalmic shingles,with a serious risk to eyesight.
If you see signs of shingles in thisarea, in someone with ophthalmic
shingles, I'd recommend, if they've gota positive Hutchinson's sign, you should
involve an ophthalmologist urgently.
I agree.
Pick up the phone.
That's one of the situations.
Pick up the phone.
Yeah, absolutely.
That day.
(22:28):
Now, when I was a GP for one of thebiggest agricultural universities in
the country, I often saw young adultswho were terrified they'd picked up
some terrible illness on a Saturdaynight, and they were really relieved
when I told them they had a reallysimple to treat problem, including
no treatment at all, and that wasn'tgoing to cause them any embarrassment.
And of course, I'm talking here about orf.
(22:50):
I wasn't quite sure whereyou're going with that, Roger.
But yes, orf is well recognised bythe farming community, isn't it?
And this infection, which isvirtually always painful, is caused
by a very large parapoxvirus.
It generally produces a solitary,large, often haemorrhagic blister at
the site of infection, and it typicallycomes from an infected sheep or goat.
(23:13):
Occasionally it comes fromfencing, where the sheep may rub
their lesion encrusted mouths.
And it usually lasts for, waitfor it, six to seven weeks,
and it is often complicated bysecondary bacterial infections.
I've seen lymphangitis, introduced by orf.
Treatment is, well, we haven'treally got anything terribly useful.
(23:34):
It's usually self-limiting and usuallynothing other than keeping the lesions
covered and analgesia is recommended.
Obviously, any secondary bacterialinfection should be treated.
DermNet NZ mention imiquimod topically,I haven't had any experience with that.
But I have to say, the next time I seethis, I'll probably try Clinisept+,
which has over 90% hypochlorous in it.
(23:57):
I believe secondary care do havetreatment options for disseminated
orf, things like cidofovir.
But I've never seen that and would,of course, in that situation,
discuss it with a microbiologist.
Yeah, of course.
You mentioned Clinisept+, andI certainly am now recommending
it in those situations.
But there's another condition Ithink we could use Clinisept+ for,
(24:18):
which is molluscum contagiosum.
And if I had a pound, for everyworried parent wanting to know how
to get rid of little Janet or John'smolluscum, I'd be recording this podcast
sipping a cocktail in the Bahamas.
But if we're being brutally honest,there's really no clear treatment
that works really well, is there?
No, I haven't had much experience yetof using Clinisept+ for this, but I
(24:39):
certainly would next time I see it.
Molluscum is a common infection.
It's easily recognised by our colleagues.
It almost invariably affects children, andit behaves rather like a wart, persisting
and increasing in numbers over many years.
And of course, like warts,if you scratch them, you just
autoinoculate and you can spread them.
The individual lesions are firm,pearly white to cream coloured
(25:01):
papules, measuring usually betweentwo to six millimetres, with an
umbilicated central depressed area.
And this is considerably more commonin children with atopic eczema, where
it seems to develop in patches ofuncontrolled eczema, and often then
spreads, forming numerous lesions.
You can get giant molluscum wherethey're over a centimetre or two,
(25:24):
and there I'd be worried aboutimmune suppression, notably HIV.
So, if you see a giant molluscum,you need to be worried there
But coming back to your question, I agree.
Treatments are generally prettydisappointing and it's often wise to
encourage them just to leave thingsalone, though that can take years.
We used to talk about dipping an orangestick in phenol and attacking one of
(25:47):
them, and that could sometimes triggerthe immune system to clear the lot.
But nowadays we've got 5% potassiumhydroxide solution, that's
MolluDab®, and that's appliedtopically, that can sometimes help.
I would certainly, as I've said,consider Clinisept+ next time I see this.
What I would do is I would get someClinisept+, or the patient can buy
Clinisooth+ over the counter, and Ijust soak a dressing in the solution
(26:11):
and hold that in contact for about 20minutes, twice a day for a few weeks.
Cantharidin 0.7%, which is alsoknown as Spanish fly, and comes from
the blister beetle, topically, issaid to work very well, and half of
treated cases clear within 12 weeks.
But it's not licensed in theUK, and of course, is limited by
(26:34):
side effects such as priapism.
You know, it used to be used asan aphrodisiac in Roman times.
So, it's not licensed yet in theUK, but I think watch this space.
Yeah, absolutely.
Well, I think we've really had a nicewalk through some of the most common
viral infections that we tend to see inour practices, the common currencies,
(26:55):
and we really do hope you've enjoyed it.
Roger and I really hope that you'lljoin us again in two weeks time,
when we'll be talking about paraviralskin rashes, such as measles and
rubella, currently a really hot topic.
We'd also like to thank our sponsor,AproDerm®, for all their help in putting
these Rash Decisions podcasts together.
We couldn't have done it without them.
(27:16):
Absolutely.
And if you do like what you hear,and we really hope you do, do take a
moment to rate and review us whereveryou get your podcasts, because it
really does help us put togetherthe content that you want to hear.
But until the next time,it's goodbye from George.
Goodbye.
And as always, it's goodbye from me.
Goodbye.
Hey George, do you want to hear a joke?
No thanks.
Oh good, I was really lookingforward to watching a documentary
about origami last night, but whenit came to it, I wasn't able to.
It was pay-per-view.
Oh, for goodness sake.
Now, today, George and I willbe talking about the problem
of viral skin infections, whichyou can imagine is a huge topic.
I like to think of viralrashes in two broad groups,
(00:31):
cytopathogenic and paraviral.
And in this episode, we'll explore thecytopathogenic rashes where the virus is
present in the skin lesions themselves.
So, from pesky viral warts tothe infamous chickenpox and
molluscum, we'll be covering it all.
So stay tuned and play the music.
(00:59):
So, welcome once again to thisRash 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 was the Chair
of the Dermatology Council for England.
(01:21):
This is the first of three episodesabout viral skin infections.
Next time, we'll be talking aboutparaviral rashes, such as measles.
Obviously, that's a real worryat the moment because of the fall
in the MMR vaccination uptake.
We'll also look at things likeFifth disease and pityriasis rosea.
And you definitely don't want to missthe last episode, where we'll be joined
(01:42):
by a very special guest, where she'llbe telling us all about the rarer viral
illnesses, such as Kawasaki disease,smallpox, and obviously Covid-19.
So, do make sure to follow RashDecisions so you don't miss any of those.
Now in our bacterial skin podcast, whichwe hope you listened to, George and I
put our heads together and came up withour 'top six facts', which was such
(02:05):
good fun to do, and which went down sowell with all of you, we thought we had
to share another one with you today.
So, I'm going to kick [off] with one ofmy favourites, so up first, we previously
told you that the cells in our bodieswere outnumbered by bacteria 10 to 1.
Well, there are ten times as many virusesin our bodies as there are bacteria.
(02:27):
So, this goes off the scale.
I really like that one.
It's amazing, isn't it?
And we don't really know whatthe role of these viruses might
be, what role they're playing.
That's absolutely right, George, andthat brings [me] on to fact three,
which is that the future of controllingserious bacterial infections is
actually probably with viruses.
(02:49):
Now, phages are viruses thatonly attack and kill bacteria.
Their role at present is still verymuch in the research phase, and one
of the problems is that each phagehas to be developed as a bespoke agent
for a particular bacteria, so they'renot available instantly, in other
words, off the shelf, for treatinglife-threatening bacterial infections.
(03:12):
So as an area of research,I find this really exciting.
It's reassuring to know that there's stuffgoing on there, isn't there, that means
we might have something when finally, thetime of antibiotics has come to an end.
Viruses are spread by direct contact,often through droplet spread.
The enteroviruses, things like coxsackieand polio and even the echoviruses, as
(03:36):
well as, of course, things like norovirus,are spread by the faeco-oral route.
Again, physical contact there.
When someone with a viraemia, orindeed someone who has virus in their
tonsils or upper airways, coughsor sneezes, droplets containing
viruses are distributed into the air.
Now you might be surprised to learnthat these can travel at a speed of 100
(03:58):
miles an hour, so they can hit a wall afew metres away from you if you sneeze
without covering your nose and mouth.
And if there's no draft, i.e.
there's no wind or anything, theseviral particles can remain suspended
in the air for a very long time.
Absolutely, indeed they can, and wethink they're able to hang in the air for
minutes, or even in some cases, hours.
(04:21):
We also mustn't forgetthe impact of touch.
So, if you touch your face or yournostrils and you've got a viraemia,
then you touch a hard surface.
Again, that can hang around for avery long time on those hard surfaces.
Rashes caused by a virus,they're called exanthems.
But viruses aren't the only causes ofexanthemata, and this rash can easily
(04:43):
be confused with things like drugreactions, secondary syphilis, graft
versus host reactions, and many more.
And many viral infections can alsoinclude a rash on the mucosal surfaces,
and obviously we're thinking ofthe mouth as a good example there,
and these are called enanthemata.
So 'X' on the outsideand 'N' on the inside.
(05:04):
Great way of remembering it, yeah.
Now, number six, viruses obviouslydon't respond to standard antibiotics,
or other antimicrobials, but wedo have some antivirals for some
viruses, notably of course theherpes viruses and the pox viruses.
Yes, and I think we're goingto touch on some of those.
That's a good list, George.
(05:25):
So, let's start at some of thecytopathogenic rashes first, and I'm
going to start with an old favouritehere, which we all know, viral warts.
Yeah, they're a nightmare, aren't they?
They're caused by a variety of humanpapillomaviruses, and they're easily
spread by direct contact with a case orvia a fomite, as we've been discussing.
(05:46):
They're therefore most common onthe hands and around the face.
Verrucas are human papillomavirusinfections on the feet, and they're
usually picked up by walking barefootin a public area, such as a swimming
pool, or around a swimming pool.
They're most common in children andyoung adults, probably because in
adults we've become immune to mostof the important ones, but they
(06:09):
can persist for many, many years.
The viruses effectively hide withinthe cell nucleus, protecting them
from our immune system, and so theytake over the cell's organelles and
are hidden from antiviral treatments.
That accounts for the poor responsethey have to tropical treatments.
Such as liquid nitrogen and all the paintsand things that we apply like salicylic
(06:31):
acids, which are trying to split thecells up a bit and expose the virus.
Yeah, they can be a real nuisance andtake an awful long time to get better.
There's another viral skin problem,though that can be certainly more
than a nuisance, which I alwayslook out for because I really don't
like it, and that's herpes simplex.
We really mustn't forget aboutthat one initially, must we?
(06:54):
It can be nasty, can't it?
Yeah.
The initial infection with aherpes simplex virus is often
asymptomatic actually, but it canbe very nasty with a very severe
herpetic, usually gingivostomatitis,so bleeding, swollen, nasty gums.
The virus then travels usually backto the geniculate nucleus, and it
(07:15):
doesn't get any further than that.
But following this initial infection,the virus typically remains dormant in
that geniculate ganglion, and in mostindividuals causes no further issues.
However, some unfortunate peoplehave recurrent cold sores, where
painful vesicles appear whenevertheir skin temperature is raised.
(07:37):
So that can be from a fever, hencecold sores, but also premenstrually, or
even following a sauna or sunbathing.
They also tend to come out during episodesof reduced immunity, including simple
things like stress, but also pregnancy.
And in this situation, the active lesionsare shedding virus, and the patient is
(08:00):
contagious through skin-to-skin contact.
Yeah.
Individuals with atopic eczemaare especially vulnerable
to herpes simplex virus.
If you didn't hear us talk in ourpodcast about atopic eczema, then do
have a listen because it's a good one.
That's really interesting, why is that?
Why are people with atopic eczema morevulnerable, would you say, George?
(08:23):
Well, one of the big reasons is that deepin the epidermis, in the stratum spinosum,
we produce over 3,000 antimicrobialagents, called antimicrobial peptides.
These are our body's naturalantibiotics, things like the
defensins and cathelicidin which isconverted to its active agent, LL-37.
(08:48):
These antimicrobial peptides arecritical at combating HSV infection.
But, the inflammatory interleukinsthat are produced in atopic
dermatitis, things like IL-4 andIL-13 decrease the production
of these antimicrobial peptides.
So that explains why patients with ADare particularly vulnerable to getting
(09:11):
eczema herpeticum, which is a potentiallylife-threatening and serious infection.
In eczema herpeticum, monomorphic, i.e.
they're all the same shape, quitesmall, usually two to four millimetres,
inflammatory eroded areas develop.
It's usually, but not invariably,on the face, probably because
(09:35):
the skin there is quite thin andvulnerable to eczema generally.
Patients with this complicationof atopic dermatitis can become
critically ill, quite rapidly.
So, if you see somebody with it, I woulddefinitely recommend treating them, but
I'd also recommend if you're not sendingthem into hospital, that you contact
them in a few hours because they can gofrom being well to being ill quite fast.
(09:59):
I think it needs urgenttreatment with aciclovir.
And if there's any even remoteconcern that your patient is ill,
they should be admitted immediatelyfor intravenous aciclovir.
Interestingly, I was talking with DrMorgan, who's going to be joining us
in our third podcast on this topic,and she says that there's a novel
anti-herpes drug called, wait for it,amenamevir, which is not yet available
(10:23):
in the UK, but is currently being usedin Japan, and will be an option for that.
Another interesting thing to say isthat our biologics that knockout IL-4
and 13 for atopic eczema, things likedupilumab, I'd be very interested to
see whether patients on those don't everget eczema herpeticum, because they're
(10:43):
no longer having the IL-4 and 13 levelsthat knockout the antimicrobial peptides.
I haven't seen that in any literature yet,but it's something I'm looking out for.
Oh, that will be interesting.
Now, as you know, there's this bigdrive for minor self-limiting illnesses
to go to community pharmacists ratherthan into primary care practices.
(11:05):
And one of the viral illnessesthat I think community pharmacists
may be seeing a lot more of as aconsequence is chickenpox, because
obviously it's much more common.
Most people are less likely to havesignificant health issues, but not all.
Right, well that's right, yes, we'll betalking about poxviruses with Dr Morgan
in our third podcast on this topic.
(11:26):
But sadly, this infection, chickenpox,remains common, and I think you'll
agree with me, it's one of thecurrencies we see in general practice.
Absolutely.
And I think that's sad, becausechickenpox is confined to humans.
We have an excellent, albeitquite expensive, vaccine.
So, it is potentially completelypreventable, it can be a very serious
(11:51):
infection, and it just doesn't need tobe a rite of passage through childhood.
No, chickenpox parties shouldbe a thing of the past.
Absolutely.
So, let's talk about, how contagiousit is, because there can be a little
bit of misinformation or some mythsand inaccuracies about how chickenpox
(12:12):
is spread and the timescale involved.
Right, well, the incubation period,which is the time from exposure
to the onset of the rash, isactually quite long with chickenpox.
It's between two and three weeks.
Prior to the onset of any skinchanges, the patient develops
a coryzal illness with fever.
At that stage, if you look in theirmouth, you might see an enanthem with
(12:34):
small painful ulcers on a red base.
Patients are contagious from the startof that coryzal illness until the last
crop of spots have formed dry crusts.
That's usually around about seven toten days after the onset of the rash.
So, they're contagious foraround about a fortnight.
(12:55):
The lesions themselvesactually harbour the virus.
But when you've got chickenpox,it's mostly spread through
droplets, from coughing.
You've got a viraemia and when youcough you spread the virus into
the air and then people inhale it.
That's the main means of contact.
The virus is a cytopathogenic virus,so you have the virus in the lesions.
(13:16):
And what happens is you get crops ofsmall red bumps, which are quite itchy.
They rapidly develop intoclear-filled vesicles, which then
mature into pus-filled pustules.
And those then breakdown and form dry crusts.
And crops of spots continue to appearfor the first few days of the illness.
(13:37):
So, you see lesions at different stagesof development, gradually evolving,
and so it's when the last crop ofspots have finally got to the dry crust
phase that you're no longer contagious.
Yep.
A very rare complication, one that Ithink we need to think about though, of
chickenpox, is Reye’s encephalopathy.
This is virtually only seen whena child is also given aspirin.
(14:02):
So, I generally go out of my wayto advise parents to avoid this.
That's a great takeaway point, George.
And I suppose one of the messagesof the wayside pulpit with this
podcast, I'd be saying, avoidaspirin in cases of chickenpox.
I mean, we should be avoiding itanyway, in children, but anyone
with chickenpox, avoid aspirin.
And I think there's another one here,which we sometimes forget, and I'm
(14:24):
going to chip in with my smokingcessation hat on, and remind, all the
healthcare professionals listening.
If you see an adult with chickenpox,ask them if they smoke, and this always
tends to raise an eyebrow in them,but there's a good reason for that.
Yeah.
You're so right.
Although it's uncommon in adults,we do see it from time to time.
(14:44):
And here, as you say, the mostimportant thing to establish
is whether the patient smokes.
Because smoking exposes them to a highrisk of developing chickenpox pneumonitis.
Which, I've never seen that in an adultwith chickenpox who doesn't smoke.
Chickenpox pneumonitisclassically presents about one
to six days after the rash.
(15:04):
And it can be lethal.
It can.
So, after recovery, we will know thatthe patients have had this, because
if you do a chest x-ray, you see thatmiliary shadowing on their chest x-ray.
But it's a reallyfrightening complication.
So, if I had an adult developchickenpox, and they were a smoker,
I would be keeping a very close eyeon them or getting them admitted.
(15:26):
Similarly, chickenpox in someonewho's immune suppressed, or indeed
in anyone over 21, particularlyif they've got a widespread
exanthem, can become very serious.
And by immune suppressed, I meanthings like even a short course of
oral steroids, for example, for asevere asthma attack, can render
that patient dangerously vulnerableto chickenpox for up to three months
(15:49):
after the steroids have been stopped.
I think this is such an important message.
Yeah.
If I see a child, a young child, and Ineed to put them on steroids, perhaps
for an acute asthma attack, one of thefirst questions I'll ask the parents
is, "Has your child had chickenpox?"
And I think that if they haven't,they need to be advised to seek help
(16:12):
urgently, if they come into contactwith chickenpox or if they themselves
develop any early signs of it becausein that situation zoster immunoglobulin
or aciclovir could be life-saving.
Children have died, developingchickenpox, even a few months
after finishing a short course ofsteroids, for example, for asthma.
(16:33):
Yes.
Similarly, chickenpox inpregnancy can be a disaster.
So, I always check to see whethera woman of childbearing age
has had chickenpox as a child.
And if she can't remember ordoesn't know, I would suggest that
she thinks about vaccination, asvaccination before conception can
prevent chickenpox in pregnancy.
(16:53):
Obviously, you don't alwaysget the chance to do that.
If a mother does come into contactwith chickenpox, which, let's
face it, is hardly unlikely.
She might have other childrenwho come home and get chickenpox.
Stored blood, taken at the time ofbooking, can be retrieved and tested.
So, when we take our booking bloods,that blood is saved, and they can go back
(17:14):
and they can test it for chickenpox IgG.
If that is absent then that helpsus to inform any decision regarding
whether after exposure, theyshould be given ZIG or aciclovir.
Noting, of course, that's anunlicensed use in pregnancy, but
probably a wise decision and onethat needs to be thought about.
(17:36):
Yeah, that's a fantastic takeawaythere, George, and sometimes
we do forget about that.
Now before I'm going to move on to ournext condition, I just wanted to take
the time to say a few words about ourkind sponsor, AproDerm®, and their range
of emollients that include creams, gel,ointment, all formulated to soothe,
moisturise, and protect our skin affectedby a whole range of dry skin conditions.
(17:59):
And if you've listened to our podcastbefore, you'll know that myself and
George are huge fans of AproDerm®.
Now, why?
Well, their complete rangeis suitable from birth.
They're free from common irritantsand sensitisers, which is vitally
important, obviously, as well asbeing vegan-friendly and cruelty-free.
So, they really do tick all theboxes, and I would suggest that we
(18:21):
make it our go to emollient range.
I'm going to come on to shinglesnext, and if there's one condition
that has more old wives taleslinked to it, I have yet to meet it.
I mean, going back to medieval times,when it was known as the 'belt of roses
from Hell', I've lost count of the timesI've heard myths such as, if shingles
goes all the way round the body andmeets in the middle, then it's fatal.
(18:45):
And I'm sure you've heard a fewcrackers as well, too, George.
I have, but I haven't heard that one.
And if that were the case, itwould be crossing two dermatomes.
And if I saw shingles crossingdermatomes, I'd be very concerned
about the patient's immune status.
Yes.
Shingles in someone who is immuneincompetent for whatever reasons can
be a very nasty condition indeed.
(19:07):
Yeah.
Shingles, as we all know, is due toreactivation of the patient's own
chickenpox virus that's been lyingdormant in their dorsal root ganglia since
they had chickenpox usually as a child.
And the onset of this painfulrash is heralded by pain
in that affected dermatome.
Now, contrary to many textbooks,shingles is not uncommon in
(19:30):
children and young adults.
During lockdown, my four year oldgranddaughter had abdominal shingles
while she was staying with us.
Wow.
In children, it's typicallya very mild illness.
The rash is barely painful, and it doesn'tnormally need any treatment at all.
In fact, I don't generally rush totreatment in someone under 50 with
(19:54):
shingles, but certainly in anyone over50 and the older they are, the more
eager I am to get going with treatment.
Agreed.
Of course, the sooner that isstarted, the better, ideally
before any rash has developed.
So, if a patient presents with painin a dermatome area, and one of the
common sites is in the ophthalmicregion, headache on that side coming on
(20:16):
suddenly, definitely not crossing themidline, a strictly unilateral pain.
Then I have a low threshold forthinking about shingles in that
situation and trying to get in withsomething very safe like aciclovir
even before the rash has appeared.
Once the patient's had the rash formore than 48 to 72 hours, two or three
days, there really is little benefitfrom these antiviral treatments.
(20:40):
Another interesting point, whichagain is contrary to the textbooks,
as GPs, we regularly see someone,perhaps a grandparent, who's come
into contact with chickenpox.
For example, perhaps a grandchildthey've been asked to look after,
because of the child being ill.
And then the grandparentgoes down with shingles.
And I think what's happening here is thattheir immune system, which normally keeps
(21:03):
the virus at bay, focuses on the exposureto this virus and reduces its surveillance
on the dormant virus, allowing that toescape from the dorsal root ganglia.
Yeah.
Now, ophthalmic shingles is particularlyimportant, because it accounts for between
10 and 25% of all cases of shingles.
And of course, this involves thefirst branch of the trigeminal nerve.
(21:26):
But just beyond the ganglia, behind theeye the nasociliary branch comes off.
It comes off from the main trunk to supplysensation to the side of the nose, both
inside and out, also the cornea, andalso the upper lid conjunctiva, and a few
other areas on the face, but not below thenose, as well as having ciliary branches,
(21:48):
which then penetrate the eyeball.
So, that little bit of neuroanatomyis important, because if you have got
ophthalmic shingles, and you've got anysymptoms or signs, on the side of the
nose, either on the inside or outside,extension of the rash into that area, i.e.
Hutchinson's sign, there is arisk of eyeball involvement, and
(22:08):
therefore orbital ophthalmic shingles,with a serious risk to eyesight.
If you see signs of shingles in thisarea, in someone with ophthalmic
shingles, I'd recommend, if they've gota positive Hutchinson's sign, you should
involve an ophthalmologist urgently.
I agree.
Pick up the phone.
That's one of the situations.
Pick up the phone.
Yeah, absolutely.
That day.
(22:28):
Now, when I was a GP for one of thebiggest agricultural universities in
the country, I often saw young adultswho were terrified they'd picked up
some terrible illness on a Saturdaynight, and they were really relieved
when I told them they had a reallysimple to treat problem, including
no treatment at all, and that wasn'tgoing to cause them any embarrassment.
And of course, I'm talking here about orf.
(22:50):
I wasn't quite sure whereyou're going with that, Roger.
But yes, orf is well recognised bythe farming community, isn't it?
And this infection, which isvirtually always painful, is caused
by a very large parapoxvirus.
It generally produces a solitary,large, often haemorrhagic blister at
the site of infection, and it typicallycomes from an infected sheep or goat.
(23:13):
Occasionally it comes fromfencing, where the sheep may rub
their lesion encrusted mouths.
And it usually lasts for, waitfor it, six to seven weeks,
and it is often complicated bysecondary bacterial infections.
I've seen lymphangitis, introduced by orf.
Treatment is, well, we haven'treally got anything terribly useful.
(23:34):
It's usually self-limiting and usuallynothing other than keeping the lesions
covered and analgesia is recommended.
Obviously, any secondary bacterialinfection should be treated.
DermNet NZ mention imiquimod topically,I haven't had any experience with that.
But I have to say, the next time I seethis, I'll probably try Clinisept+,
which has over 90% hypochlorous in it.
(23:57):
I believe secondary care do havetreatment options for disseminated
orf, things like cidofovir.
But I've never seen that and would,of course, in that situation,
discuss it with a microbiologist.
Yeah, of course.
You mentioned Clinisept+, andI certainly am now recommending
it in those situations.
But there's another condition Ithink we could use Clinisept+ for,
(24:18):
which is molluscum contagiosum.
And if I had a pound, for everyworried parent wanting to know how
to get rid of little Janet or John'smolluscum, I'd be recording this podcast
sipping a cocktail in the Bahamas.
But if we're being brutally honest,there's really no clear treatment
that works really well, is there?
No, I haven't had much experience yetof using Clinisept+ for this, but I
(24:39):
certainly would next time I see it.
Molluscum is a common infection.
It's easily recognised by our colleagues.
It almost invariably affects children, andit behaves rather like a wart, persisting
and increasing in numbers over many years.
And of course, like warts,if you scratch them, you just
autoinoculate and you can spread them.
The individual lesions are firm,pearly white to cream coloured
(25:01):
papules, measuring usually betweentwo to six millimetres, with an
umbilicated central depressed area.
And this is considerably more commonin children with atopic eczema, where
it seems to develop in patches ofuncontrolled eczema, and often then
spreads, forming numerous lesions.
You can get giant molluscum wherethey're over a centimetre or two,
(25:24):
and there I'd be worried aboutimmune suppression, notably HIV.
So, if you see a giant molluscum,you need to be worried there
But coming back to your question, I agree.
Treatments are generally prettydisappointing and it's often wise to
encourage them just to leave thingsalone, though that can take years.
We used to talk about dipping an orangestick in phenol and attacking one of
(25:47):
them, and that could sometimes triggerthe immune system to clear the lot.
But nowadays we've got 5% potassiumhydroxide solution, that's
MolluDab®, and that's appliedtopically, that can sometimes help.
I would certainly, as I've said,consider Clinisept+ next time I see this.
What I would do is I would get someClinisept+, or the patient can buy
Clinisooth+ over the counter, and Ijust soak a dressing in the solution
(26:11):
and hold that in contact for about 20minutes, twice a day for a few weeks.
Cantharidin 0.7%, which is alsoknown as Spanish fly, and comes from
the blister beetle, topically, issaid to work very well, and half of
treated cases clear within 12 weeks.
But it's not licensed in theUK, and of course, is limited by
(26:34):
side effects such as priapism.
You know, it used to be used asan aphrodisiac in Roman times.
So, it's not licensed yet in theUK, but I think watch this space.
Yeah, absolutely.
Well, I think we've really had a nicewalk through some of the most common
viral infections that we tend to see inour practices, the common currencies,
(26:55):
and we really do hope you've enjoyed it.
Roger and I really hope that you'lljoin us again in two weeks time,
when we'll be talking about paraviralskin rashes, such as measles and
rubella, currently a really hot topic.
We'd also like to thank our sponsor,AproDerm®, for all their help in putting
these Rash Decisions podcasts together.
We couldn't have done it without them.
(27:16):
Absolutely.
And if you do like what you hear,and we really hope you do, do take a
moment to rate and review us whereveryou get your podcasts, because it
really does help us put togetherthe content that you want to hear.
But until the next time,it's goodbye from George.
Goodbye.
And as always, it's goodbye from me.
Goodbye.
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