September 3, 2024 • 34 mins
In this episode, your hosts Dr George Moncrieff and Dr Roger Henderson are joined by Consultant Clinical Microbiologist Dr Marina Morgan to discuss some of the potentially very serious bacterial skin infections...
Delving straight in with necrotising fasciitis, the trio cover how patients come to get this bacterial infection and, as it's so easy to miss this diagnosis, the signs and symptoms you should be looking out for in primary care.
They then move onto discussing the secrets to diagnosing Panton-Valentine Leukocidin (PVL). Spread by close skin contact, they will be imparting key tips that you can share with your patients to reduce the risk of them passing on this devastating staphylococcus aureus infection.
Ending with Lyme disease, which is now endemic in many parts of the UK, they discuss the likelihood of catching this tick-bourne infection, along with how you should treat someone who presents to you with the associated erythema migrans rash.
But, if that isn’t enough, this episode also explores antibiotic resistance, and why primary care physicians should be reserving antibiotics for the more serious infections.
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.
Episode Resources:
- The Lee Spark NF Foundation Education Video: https://nfsuk.org.uk/education/severe-group-a-streptococcal-infections-leading-to-necrotising-fasciitis/
- The Lee Spark NF Foundation: https://nfsuk.org.uk/
- Morgan, M. (2005) 'Hospital management of animal and human bites', The Journal of Hospital Infection, 61(1), pp. 1-10.
- Morgan, M. et al. (2024) 'Group A beta-haemolytic streptococcal infection in children', BMJ, 385 (8426), doi: https://doi.org/10.1136/bmj-2023-077561
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:08):
Hello, and welcome once again tothis Rash Decisions podcast, where
we look at skin-related issues,treatments, and conditions 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
(00:28):
of the Dermatology Council for England.
In the last two podcasts on bacterial skininfections, George and I spoke about the
common bacterial ones, such as impetigoand bacterial folliculitis, as well as
the more serious ones like cellulitis,scarlet fever, and secondary syphilis.
We described both their clinicalrepresentations and their treatments.
(00:51):
But today we're going to be talking aboutsome potentially very serious bacterial
skin infections, in the third of threepodcasts we've been doing about them.
If you heard our first two, we do hopeyou enjoyed them and remember, we talked
about a special guest for this podcast.
Well, I'm delighted tosay she's with us today.
And it's the fabulous Dr Marina Morgan.
(01:11):
Now, Marina is a Consultant ClinicalMicrobiologist, at the Royal Devon and
Exeter Hospital and out of her multipleinterests, these include necrotising
infections, especially fasciitis andPVL-associated disease, which I'm
certain we're going to be talking about.
And she developed the Exeter protocolfor treating necrotising fasciitis,
(01:32):
which dramatically reduced mortalityfrom this condition in her area.
Marina, welcome to the podcast.
It's so good to have you with us today.
And I suppose the first thing tosay is, did I miss anything out?
Thank you very much.
No, I don't think you did actually.
I'm just a bug lady.
So I deal with bugs.
[Laughing]
(02:01):
Welcome Marina and Roger mentionedin his introduction, necrotising
fasciitis, and I'd like to gostraight into that if I may, please.
Because, there's only a relatively smallnumber of cases in the UK and I believe
that's around about 650, per year.
But it's a truly catastrophic infection.
And I think it's one that we,particularly in primary care, must
(02:22):
remain vigilant to at all times.
If we can recognise it earlyand manage it aggressively,
it can make a big difference.
I've only seen it once andyou don't forget it, do you?
She was a young woman who'd knockedher leg at the gym developing
a large bruise on her shin.
She, as I'm sure everybody would, shetook some ibuprofen for a couple of days,
(02:45):
but then came to see me when the painhad become excruciating, unbearable.
In fact, it was almost impossible tohave a proper communication with her
because of the intensity of the pain.
And I think it was that, that caused meto realise what we're likely to be dealing
with here, and therefore admit urgently.
So, what are your thoughts there, Marina?
(03:08):
Well, firstly, I think that's anabsolutely excellent diagnosis
because it's so easy to miss it.
Necrotising fasciitis in its generalterm, just means you've got necrotic
fascia, and any bug can do it.
The first type, the most commontype to diagnose is really
easy, you can't really miss it.
It takes a while to develop, thepatients don't get very sick, but
you can see something early on.
(03:29):
And these are the kind of patientswho have lots of comorbidities.
The bugs responsible are mixed organisms,a very different pathology, mouldering,
and not that difficult to diagnose,because it's a more chronic presentation.
The one that you spotted had to be agroup A strep necrotising fasciitis.
So, am I right in thinking that inyounger people it's more likely to
(03:49):
be a group A strep and just a singlebug, whereas perhaps in a nursing
home or an older person, peoplewith comorbidities, it might be a
mixed group of organisms causing it?
To an extent, yes.
Unfortunately, the bugsdon't read the textbooks, and
they don't follow the rules.
[Laugh] No.
So you can't, you can't 100%sort of legislate for that.
Can I go back just to the verybeginning, and I apologise for this.
(04:11):
I have to do a little bit of very basicbacteriology, but it might help set
the scene for what I'm going to say.
I tell the medical students thatif you imagine you're wearing a
blue dress, I'm exuding positivity.
I'm a very positiveperson most of the time.
And so on the outside of me, I've gotthis blue dress and the bugs on the
outside of me, on my skin are blues.
They're cold, so they'reblue, but actually they stain
(04:31):
blue with the gram stain.
It's just a way of remembering it.
So your skin infections generallytend to be Gram-positive.
So staphylococci and streptococci.
Whereas if you've got, gut typeinfections, or urine infections mainly,
which is obviously near the gut, they tendto be from organisms that are inside of
you, and, they have to be usually, and theway of remembering it is that inside you
(04:52):
it's warm, and so the bacteria are pink.
So pink bacteria are Gram-negativein the terminology, and
Gram-positive is the skin bacteria.
So, when you come to necrotisingfasciitis, any bacterium and some
fungi can cause it, really rarely.
But really what we're talking about, theones that GPs [are] absolutely, devastated
by if they miss it and it's so easy todo, are the Gram-positive, the group A
(05:14):
strep, sometimes with the staph aureus.
And the problem with themis that it can be any age.
But typically, you get somebody who'snormally pretty fit and healthy.
And a lot of people, if they thinkabout NEC fasc, expect it to be some
sort of traumatic injury, to havesome sort of penetrating trauma.
But the majority that I see, and I'veseen over 150 now, group A strep NEC
(05:36):
fasc's, they've actually come in with abit of a flu-like illness, and they've
had some sort of severe pain somewhere.
Absolutely typically, it would be a youngchap playing rugby, pulling a muscle.
And what you need, it's rather likehaving the holes in the cheese lining up.
A set of very unfortunatecircumstances that come together
and give you this particular idealenvironment for the bugs to grow.
(06:01):
So you happen to have a group A strepin your throat, something happens to
make the group A strep go into yourbloodstream, you have a bacteraemia,
which you normally get rid of quiteeasily because the neutrophils come out,
they gobble up the bugs, and they dieof indigestion, and that gives you pus.
So, your little bit of bacteraemiais normally got rid of.
If you're diabetic, your neutrophilsdon't chase the bacteria so fast,
(06:23):
they can't kill them so quickly.
If the bacteria gets into the deeptissues, because they circulate
all the way through the body, theycan be a little bit more difficult
to get at by the neutrophils.
And if you've got a traumatised area,if you've pulled a muscle genuinely,
you've exposed vimentin, which is amuscle protein that acts like Velcro
and sucks in the group A strep.
(06:45):
So what's that called again, Marina?
Vimentin.
V I M E N T I N.
Vimentin.
Right, it's a new one for me.
So you have this sort of perfect scenariowhere you've got an exposed surface, you
happen to have a, a group A strep that'sevaded the defence mechanisms, tootling
through near the fascia, near the muscle,it gets grabbed in and it's deep down.
(07:07):
And if your neutrophils can't get at itvery quickly, it starts multiplying and
every 20 minutes, these bugs divide.
Add to which, if you've had a trauma,your first response normally is to go
and get some Brufen or some sort ofnon-steroidal, and some painkillers.
And the problem with thatis that it's threefold.
It keeps your temperature down, soyou don't realise how unwell you are.
(07:27):
It makes the pain less, so youpresent later to any medical help.
But the majority of the problems arethat the way that non-steroidal's work,
they actually dismantle the inflammatorymechanism, the cyclooxygenase pathway.
You mentioned exotoxins inthe previous podcast, George.
Exotoxins are produced, they'reproteins made inside the
(07:48):
bacterium and exported out.
The way to remember it,exotoxins, exported out.
And there is a whole myriad of exotoxins.
Some that make you go brightred, like scarlet fever, and
some that will digest tissues.
And this is why group A strep iscalled the flesh-eating virus.
It's not a virus, but, you know, that'sthe way that the newspapers report it.
(08:08):
So your exotoxins are produced and group Astrep produce a lot of leukocidal toxins.
They kill white cells.
So if you imagine somebody sitting therewith a machine gun, firing out bullets at
the advancing army of neutrophils, they'reexploding them before they get near them.
So, the neutrophils that domake it through the onslaught of
these toxins, get to the fascia.
(08:29):
They eat the bugs there, but thenthey can't kill them because the
non-steroidal completely stops theneutrophils killing any ingested bacteria.
It stops production ofintracellular enzymes and peroxides.
So, streps can survive the wholemechanism of being able to kill
the ingested bacteria by producingsuperoxides and hydrogen peroxide
(08:50):
being completely abrogated.
So, you've got a perfectsetting to develop a NEC fasc.
You've got somebody who for somereason may be immunocompetent,
may be immunosuppressed, um,diabetics are more likely to get
all sorts of necrotising fasciitis.
You have bacteria in the deep tissues.
You have, particularly with the groupA strep, it has this myriad capacity
(09:11):
for different exotoxin production.
And if it's producing the rightexotoxins, then you get your
different scenarios of presentation.
So, the GP will see the patients atthe very beginning or at the very end.
And at the very beginning, they feel abit unwell, the bacteraemia is giving them
shivers and shakes, and they feel they'vegot sort of influenza-type problems, and
(09:31):
it's a viral infection, it looks like.
Later on, they get the pain, agonisingpain somewhere, which might be
totally out of the blue, or it mightbe associated with a previous injury
that has exposed the muscle, etc.
etc., and the bugs get downinto it near the fascia.
Then a bit later along in thespectrum, they'll actually present
with something more focal, and asthe infection comes to the surface,
(09:54):
you start getting skin changes.
Now the problem with group Astrep is that when it's in the
superficial layer, it's over the fat.
Whereas the deep fasciallayer is over the muscle.
So if bugs are down in the deep fascia,they're way down deep in the iceberg.
Really difficult forneutrophils to get at.
And you can't see anything atthe skin level for a long time
until the infection ascends.
(10:15):
If it's a superficial fasciallayer, then it can be mistaken
for a simple cellulitis, asort of more deep cellulitis.
And sometimes you'll find the calciumdrops and things like that, but that's
very much a secondary care evaluation.
So your infection is in oneof these fascial layers.
It starts, the bugs aremultiplying every 20 minutes.
Streptococci produce lots of exotoxins.
(10:37):
When they reach a concentration inthe tissues where they've used up all
the available nutrition, and they'reentering what we call stationary phase.
When they do that penicillins don'twork because they are beta-lactam
antibiotics that only work onstopping cell wall assembly.
So if they're not making cellwalls, penicillins won't work.
So penicillins work when you'vegot a lowish number of bugs.
(10:58):
But they're completely inactive andthey also don't penetrate very well
because you've got thrombosis goingon and you've got tissue swelling.
You've got compartment syndromehappening if it's a leg or arm.
So all these things are happeningall together and towards the end
of the spectrum you've got the deepinfection, loads of exotoxins being
produced, lots of different types.
Some will give the patient vomitingand diarrhoea so it's misdiagnosed
(11:19):
as gastroenteritis, some justmention incidentally they've got
the pain, there's not much to see soyou don't think it's that serious.
But if a patient comes to seeyou with cellulitis, and they're
heading into opiates, they havenot got a simple cellulitis.
So, going back to your patient, George,it was fantastic that you spotted it,
and so many people wouldn't spot it,because it's only just becoming compulsory
(11:41):
now to include necrotising fasciitisin the medical student curriculum.
Hitherto, it hasn't been.
And it's because of, you know, a lot of,intense lobbying by various groups...
Yep.
There's been very, very little taughtand people don't understand it.
The two patients I can recallwhere I have been unable to
communicate with the patient becausethey are in such severe pain.
(12:02):
One had an ectopic and theother had necrotising fasciitis.
So, clearly the intensity of pain in thissituation is about as bad as it can be.
But that pain, is that dueto damage to the nerves?
Yes, what happens as the bugs spreadacross the fascia you get thrombosis
to the nerves and you get agonisingpain in the centre as the inflammation
(12:23):
and infection ascends to the skin.
If you imagine the top of an iceberg,the iceberg emerging out of the ocean.
The very centre, epicentre of the skinsurface will be very, very painful
and then gradually becomes numb as thenerves die, and then it spreads out.
So the very edge of thespreading lesion will be very
painful and the centre will die.
Right.
But it all depends where yousee the patient at that point.
(12:44):
So if you see somebody late, painwill no longer be a major feature?
The deep pain...
Or may not be.
It may not be, but that's very, very late.
By that time, it's easy because you'vegot obvious full thickness necrosis.
You've got black lesions and blisterswith serosanguineous fluid in them.
Ghastly, I can imagine.
Yeah.
At that point, it basically needsa lot of surgery, doesn't it?
(13:05):
I mean, you need a surgeon who's goingto be a bit cut and thrust really,
going to take out far more thanmight at first seem to be necessary.
You need pretty bold surgery, don't you?
Absolutely, what you don't want to dois to pussyfoot around this and have
some junior surgeon looking at itand saying it doesn't look too bad,
it's you know, not that serious, youknow [the] patient's pain is better.
(13:27):
We've got them on opiates.
They're comfortable.
You're tempted to think that maybeyou've got time to do a biopsy.
But time to debridement is of the essence.
We shouldn't be doing a frozen section.
It's a total waste of timethinking of doing that.
Maybe we've got time to do someMRIs, but basically, if you
think you've got a NEC fasc, e.g.
if the pain score is 8, 9, 10 out of10, and the CRP is really high, you've
(13:51):
got to get in there and debride.
And before the surgery, you'vegot to load them up with really
big domestos antibiotics.
Antibiotics to cover all the bugs.
Majority ones are the group A strep,so you need something that will switch
off those exotoxins, and those are twoantibiotics, linezolid and clindamycin,
because penicillins don't work, remember,when the bugs get into stationary phase.
So what was the firstone, clindamycin and?
(14:13):
Linezolid.
Yes.
Linezolid is available in generalpractice, but it's rarely needed.
In empirical treatment of necrotisingfasciitis, we use it to cover all
Gram-positives, including MRSA, and itswitches off the production of the toxins.
We add piperacillin-tazobactam ormeropenem for the Gram-negatives, until
we're absolutely sure what the bugs are,by looking at them under the microscope.
(14:36):
As a complete aside from that, doyou have concerns about our use
in primary care of clindamycinso freely for things like acne?
Are we going to increase therisk of that antibiotic becoming
less useful for this sort of rarebut incredibly severe infection?
It's a very good point, actually.
It's spread around.
(14:56):
Clindamycin is a very popularantibiotic to use topically for acne.
It is.
I hasten to add I haven't useda topical antibiotic for acne
for over 20 years, but, uh...
It's a very good antibiotic,and as I say, it switches off
toxins, so it's very popular.
There's also a clindamycin vaginalcream, which is extremely good for
women with vulvovaginitis due togroup A strep, or trying to decolonize
(15:17):
from MRSA, if they're carrying itintravaginally, which sometimes happens.
But, in answer to your question,yes, you don't want to use anything
too liberally, because things willbecome resistant quite quickly.
The clindamycin resistance ratefor a group A strep, a couple of
years ago, was anything between11 and 16%, and that's old data.
That's already quitefrightening, isn't it?
Yeah.
Yeah, and doxycycline's even worse.
So whatever you use,you will get resistance.
(15:39):
Again, that's an antibiotic that wethrow around in, in dermatology, a lot,
for its anti-inflammatory side effects.
That's fascinating, reallyinteresting, I've learnt a lot already.
The other thing we mentioned brieflyin our introduction was PVL, or
Panton-Valentine Leukocidin staphylococcalinfection, described by Sir Philip
(16:02):
Noel Panton and Francis Valentine,almost a hundred years ago in 1932.
Now I have to say that if any ofour listeners have a deep knowledge
of this, we'll happily award themthe Rash Decisions prize goldfish.
But can you remind us a bit more about[what] PVL infection is and what we
need to know about it in primary care?
(16:24):
Right, from the point of viewof the primary care physician,
PVL, Panton-Valentine Leukocidin,is just another exotoxin.
So that means it's produced insidethe bug, it spreads out, and it
actually kills the white cells.
It is a leukocidal toxin.
So in response to that, your body overmakes neutrophils to compensate for
(16:44):
their destruction, and so patientspresent with even a minor trauma
with recurrent boils and abscesses.
It used to be that recurrent boilsand abscesses was the domain of
diabetics, but nowadays, to behonest, I don't see diabetics with it.
I see loads of PVL staph aureusinfections, and it can be in anybody, but
particularly young people, people who arefit, people who are in contact sports.
(17:06):
It's a skin-spread bacterium,so you need close contact with
somebody else who's got it.
Um, so contact sports, sharing wetsuits,toothbrushes, sleeping with somebody.
Sharing towels, hanging towels close uptogether in the bathroom, using a gym and
throwing your towel into an ice bucket,jumping in an ice bath with loads of
other athletes, who've probably got it.
(17:27):
There was a lovely outbreak some yearsago, at a prestigious international
meeting where wrestlers were afflictedwith boils, particularly on their bottoms.
I was told on good authority that as wellas the skin to skin contact that's so
inevitable in wrestling, for some reason,sharing of jockstraps had occurred.
Just beggars belief, really,but that's well recognised.
(17:47):
People do very strange things.
I've seen somebody who's had notrouble with their skin whatsoever
until seven months ago and sincethen they've just gone from one
nasty, deep abscess to another.
Abscesses on their ankles, abscesseson their bottom, abscesses everywhere.
Just nasty, deep infections.
Just suddenly going from nothing,from nought to ninety, or a hundred
(18:07):
miles an hour, with infection.
Until I came across PVL infections,I thought invasive group A strep was
the worst infection I'd ever seen.
But fulminant PVL staph aureuspneumonia is far, far worse.
Most labs can't test their isolatesof staph aureus for PVL production.
So like us, if we suspect PVL on aclinical basis, we have to send our
(18:31):
isolate to the reference lab for testing.
Although less than 2% of the staph aureuscausing bacteraemias in the UK were found
to produce PVL, this is actually prettyold data, from over 15 years ago, and we
have no idea of the percentage of UK staphaureus isolates that produce PVL now.
For example, in Exeter only a fewyears ago, we found 15% of the
(18:56):
patients with infected wounds attendingour emergency department had staph
aureus that was producing PVL.
PVL staph aureus is transmitted by closecontact with an infected person's skin.
So, it spreads in families andbetween sleeping partners especially.
Also, at risk, are patients withskin trauma, so those who inject
(19:20):
drugs, and closed communities,such as boarding schools, prisons,
and military establishments.
So, the key to diagnosis clinically,is simply asking the right questions.
Is there someone close to youwith recurrent skin infections?
Do you play contact sports?
Do you use a gym where peoplehave boils and abscesses?
(19:44):
You get the clues to the presence ofPVL infection from the background.
It's like being a good GP, youjust ask the right questions.
So once you think they might have it, thenif you look at the old guidelines, I was
part of the guideline committee that didit, but unfortunately, they're completely
out of date and they don't work.
We didn't know that at the time.
It's taken some years to findout, but they recommended MRSA
(20:05):
type decolonization, and remember,it doesn't have to be an MRSA.
It can be a fluclox sensitive MSSA.
It can be any staph that can produce PVL.
But historically, it was theMRSAs from America, the USA...
Yeah, America's had a big problemwith MRSA, hasn't it, and PVL.
Absolutely.
Whereas, in the UK, it'salmost invariably MSSA.
(20:25):
Yep.
And that probably accounts for whywe're a little bit more relaxed about
it in the UK than they are in America.
I think the problem is that thestrains have changed a lot, and
so what you've got, you've got avery promiscuous gene that will hop
between different types of staph.
So the American strain, the PVL gene, hashopped between lots of other different
(20:47):
kinds of staph now, and there's lotsthat are producing it, and I think
they're producing it in different amounts.Different skins are different as well.
So, um, the actual environment ofcertain skins is not conducive to it.
So you have a very, very complexsituation of who's actually got
PVL carriage, but once they've gotit, the old guidelines would say
that you treat them like an MRSA.
(21:08):
You decolonize them withan antiseptic lotion.
Chlorhexidine we used to use.
You can decolonize nasally withantiseptics like mupirocin, Naseptin®,
Octenisan®, that sort of thing.
And whereas five days seem to work fora lot of the old MRSAs, nowadays, if
you've got the PVL gene inside a staph,it seems to make it far more stickable
(21:28):
and far more spreadable, and it'sreally, really difficult to shift it.
Hence, I tend to use 10 daysdecolonization, not the five that's
recommended in current guidelines.
We've had a lot of cases where it'sgone around families and if you
just treat one, nothing happens.
You need to treat thewhole family at least once.
I then treat again anybodythat's actually got lesions.
(21:49):
Now the easiest way to do it is, I findlocally, is to give three months of
treatment, ten days once a month forthree months of a decolonization regimen.
Give antibiotics that aresuitable for that bug.
If it's an MRSA, doxycycline isusually pretty good because most
of them are still sensitive.
Fluclox isn't quite so good.
It doesn't get quite such goodlevels on the skin, but it
(22:10):
gets into the abscesses okay.
If they're big abscesses, theyneed incising and draining.
Lesions should be covered.
Patients shouldn't be jumping intoswimming pools and sharing towels
and spreading it here and there.
They need to be treated properly and theyneed to be aware of the infection risks.
But the most significant problem,happily very rare, is PVL pneumonia.
(22:31):
Yeah, yeah.
So, if you just acquire your staphaureus from contact with somebody who's
got PVL on their skin, it'll get intoyour skin and particularly up your nose.
Your oropharynx becomes colonized.
Then if you have an intercurrentviral infection, or suppose you're
a heavy smoker, you can actuallydamage your mucociliary escalator
(22:52):
so the bugs don't get swept out.
In other words, you can get aninhalational secondary chest infection.
The problem is that PVL staphpneumonia is a necrotising pneumonia.
The necrotising exotoxins attackblood vessels, causing haemorrhage
and infarction, and this resultsin a characteristic haemoptysis
and death of the lung tissues.
(23:13):
PVL staph aureus pneumonia is a trulydreadful disease, and once established,
it's very, very difficult to treat.
So the diagnosis has to be early,rather like invasive group A strep.
The mortality of PVL staphpneumonia can be as high as 65%,
though we've got it down to about15% in Exeter with great effort.
(23:34):
Hence, the main reason in my mind fordecolonizing patients that are carrying
PVL staph on their skin is to lessenthe spread of PVL staph to others
who've not encountered it before.
The carriers eventually developantibodies and are then far less
likely to get invasive infection, butpeople they're spreading it to have
no protective antibodies and they willbe most at risk of invasive infection.
(23:57):
The contacts yes.
...they will then get serious pneumonia.
And it's a really nastyhaemorrhagic pneumonitis, isn't it?
Or pneumonia, it really is, as you say,very high mortality and very aggressive.
Absolutely ghastly.
But that's fascinating, their contactswho first encounter it, then get
it as an inhalation complication.
Yes, you can get a haematogenous spreadto the lungs from a skin lesion, e.g.
(24:20):
a blister or an abscess, and thatcan cause a haematogenous pneumonia.
Gosh, fascinating, gosh,I'm learning so much.
Moving on, something we are seeingincreasingly commonly is Lyme disease.
And I believe this is now endemicin the UK, coming right across
the country, including Scotland.
I've had a couple of casesrecently from Scotland.
(24:40):
Indeed, I actually had a casefor a young woman who had not
travelled out of Bicester.
And she hadn't travelledout of Bicester for months.
And she had Lyme disease.
In fact, she fortunatelypresented with a classic rash.
But I gather the, the tick thattransmits this infection, it's
called Ixodes ricinus, is the tickin the UK, but this is moving further
(25:02):
north with global warming, whichis a frightening thought, isn't it?
Another disease that's going toget more common as the world warms
up and that mite can survive.
Let's have just a few wordsand thoughts about Lyme disease
in our last five minutes.
Okay, it is pretty well endemic.
Partly because the sheep aren'tbeing dipped, they can live on sheep,
deer, all sorts of large animals.
(25:24):
We get in the way, we take the place ofthe larger animals, and we walk through
the grass and they leap onto our legs.
Yes you can get it in Bicester.
I removed a tick from my husband as he waswalking up the stairs and I spotted it.
He was wearing shorts and I thought"My goodness, he's got a tick."
He said, "Oh god, get it off me."
I said, "Not until I've had a photograph."
And it's really quite difficult to spot.
They're quite small.
And so that's why a lot of peopledon't realise they've actually
(25:45):
got them because they don't...
As they feed, they get bigger, don't they?
As they feed on blood, they get bigger.
They do.
And then they're more obvious.
But that's why it's vital to checkthe kids when you've been out walking
and make sure they haven't got any...
Yeah I've certainly removed them fromthe back of my children's neck, my
grandchildren's necks after they'vebeen walking in Isabella Plantation
in Richmond Park, for example.
So at bath time you see thetick there and you get it off.
(26:07):
Goodness.
Certainly in London, in inner cities,you certainly get them, because [there
are] lots of wild animals around.
And I know there's been a Lymearthritis in a dog in Wimbledon.
So, you know, yes, it's everywhere.
You can't say you're not going to get it.
It's not just the deer, is it?
It's voles, it's cattle, it's horses,a whole load of different animals
can have the ticks living on themand breeding on them, but they
don't live and breed on us, do they?
(26:30):
No, but what they do do, if youinterrupt their feeding, they will
regurgitate blood back into it.
And if they happen to be an infectedtick, then you get the infection.
Not all ticks carry Borrelia.
About one in seven, isn't it, in the UK?
Very good question.
I couldn't give the exact[answer], because the problem
is, it depends where you sample.
Because there are areas whereyou don't have infected ticks.
But that's probably about right.
Yeah, but I think it'sabout one in seven, yeah.
The way to remove it, with a tickremoval and ideally anticlockwise.
(26:54):
For goodness sake, don'tuse lighted cigarettes.
That isn't a good way to do it.
And take the ticks off.
And basically, we don't recommendtreating empirically, tick bites,
because most of them aren't bitten byinfected ticks, and if you get them
off early, there's a lot less chanceof the infection being transmitted.
I read somewhere that if you getthe tick off in the first 24 hours,
(27:14):
the likelihood of going on to getLyme disease, even if the tick was
infected, is very small indeed.
So I think the trick isto get them off quickly.
I agree, if you get an O'Tom tickremover, ideal, but I wouldn't wait for
Amazon to deliver it in two days time.
I'd get it off first, and thenhave an O'Tom tick remover for
(27:35):
next time, would be my advice.
Absolutely.
I think only about a third of patientswith Lyme disease actually manifest the
rash, the erythema chronicum migransrash, this rapidly spreading, almost
target like rash with a red edgeand then paler centre and then the
tick bite not always in the middle.
(27:56):
And of course you can get multipleerythema chronicum migrans with some of
the, particularly some of the Europeanvariants of Lyme disease, can't you?
The evolution of the rash is interestingand if somebody pitches up with what looks
like erythema migrans and they haven'tgot a history of a tick bite, that doesn't
mean to say they haven't got it because...
No.
If they've had one tick bite five yearsago, they've obviously [been] in that area
(28:19):
where ticks would be, so they've missedthe tick bite that's actually set it.
Just because they don't remembera tick bite doesn't mean
to say they haven't got it.
So follow the NICE guidelinesand clinically you treat them.
If they've got erythema migrans,you, you treat them on spec and
you follow the NICE guidelines.
We have rather strange length of courses.
I think it's something like,azithromycin for 17 days or
something strange, or doxycyclineor amoxicillin for three weeks.
(28:42):
It's a spirochaete, isn't it?
So it would respond very well to apenicillin, I would have thought.
Interestingly, no.
The problem is with children undereight or nine, it's difficult
to justify using doxycycline.
Doxycycline is the best treatment.
No, I agree with children, yeah.
And so we tend to useamoxicillin for children.
Azithromycin, although it works asimilar sort of way, it's not a cell
wall acting antibiotic, it's sortof okay from that point of view,
(29:04):
because it's the most peculiar bug.
Generally speaking, if you canpossibly get a patient onto
doxy, I would treat with doxy.
Right.
Yeah.
Yeah.
And what are your thoughtsabout things like chronic Lyme?
People who are complaining thatthey have chronic Lyme disease?
It's an absolute nightmare for themand for the medical establishment
because there's so many thingsthat give you a chronic fatigue,
(29:25):
chronic illness, feeling awful.
I'm not one of the microbiologiststhat says chronic Lyme disease can't
exist because you can never saynever in microbiology or medicine.
And so there must be some people that dosuffer with a genuine chronic infection.
Must be.
But discerning those from the peoplewho are just suffering the chronic
inflammatory response to having hadthe infection, which is what most
(29:46):
microbiologists feel is probablywhat's happening, and that's why
doxycycline works so well and theyfeel better on it because it's
an anti-inflammatory antibiotic.
So, it's really difficult to kind ofget your head around Lyme disease and
we're learning all the time and allwe can do is just keep working at it.
Marina, I'm really sorry.
We've run out of time.
I've been distracting you too much.
(30:07):
I was hoping we would get on to talkingabout meningococcal septicaemia and
Waterhouse–Friderichsen syndrome and,uh, all sorts of other things from
toxic shock through to even anthrax.
Which I think is something that as GPs,no bad thing that we just vaguely aware
that anthrax is something, if you've gota really nasty black lesion that's sort
(30:29):
of suddenly appeared and looks horrible,um, just to have that at the back of your
mind for that odd case, we may well comeacross it in the next 50 years, but this
has been absolutely fascinating already.
Finally, I think one thing I justwant to quickly say is that one
thing I say to all my students andmy registrars is, "With every single
(30:51):
patient encounter, every single one,sit back and make a conscious decision.
Are they unwell?
In which case, I'm not concerned.
Or are they ill?"
And signs of illness can be very,very subtle and easily missed,
particularly in little children,particularly in older people.
(31:12):
And I think this dovetailsso nicely with Martha's Law.
It's a situation where I say,listen to what the family is saying.
They know, they will spot the subtleclues that we might otherwise miss.
But I think the things like,you know, the child is running
around the consulting room.
I don't need to examine [them].
If they're climbing up the curtain andunder my desk, they can get on with
it, and I'm not going to examine them.
(31:33):
It's the child who sits there limpand has a delayed capillary refill
time, maybe a low oxygen sat. Theircolour's poor, they're listless, you
pick up their arm and they drop it.
So I think with all these illnesses,whether it's meningococcal meningitis,
or whether, which we haven't covered,or whatever, I think that it's so
important to make that conscious decision.
(31:54):
"Am I faced with somebody here who's abit ill, doesn't matter, or are they ill?"
Can I just come in there and saythat, absolutely the most important
thing of all is the parents.
Parents look after the children.
If they say their child's not well, andif they've seen healthcare professionals
in the last 24 hours or 36 hours already,then that's the worry for group A strep
(32:15):
because it's such an insidious pathogen.
And an interesting thing about group Astrep, it makes people outside themselves.
So even when they've got toxic shock,even when they've got NEC fasc, they
go to that sort of detached phaseand they're sort of not with it.
It's most peculiar.
And that's another sign, forcertainly the adults and the children
as well that works very well.
Well, goodness me, Marina, I've lost trackof how much I've learnt from you today.
(32:38):
And I'm sure our listenerswould have gained so much
too from all your expertise.
Thank you so much for givingus all your valuable time.
But before we do let you go, isthere anywhere our listeners can
go to get more information on someof the things we've talked about?
Absolutely.
I can heartily recommend theLee Spark Foundation website.
There's an educational video onstreptococcal infections that
(33:00):
we made basically, most of usdid it at the RD&E in Exeter.
It's very useful as a, learningexercise for, paramedics, clinical
staff, non-clinical staff, and even,members of the public, on the sort
of complications and what to lookfor with streptococcal infections.
And I'm very happy for the healthcarepeople who might be listening to this.
I'm very happy to be emailed.
(33:20):
I've got loads of papers and information[that] I'm very happy to provide.
Well, Marina, thank you so much foryour time and your expertise, and we'd
love to take a note of that resource sothat we can add it to the information
we have attached to this podcast.
Absolutely wonderful stuff.
George and I do hope you foundthis podcast as interesting
and as helpful as we have.
(33:41):
And that you've enjoyed the previoustwo on bacterial skin infections.
If you haven't caught up withthose yet, do have a listen.
And if you like what you hear, then dorate and review us wherever you get your
podcasts as it really does help us tokeep producing quality content for you.
Or even better, get in touchwith questions or suggestions
for future podcasts as we doreally love to hear from you.
(34:03):
In the meantime, Roger and I do hopeyou'll join us again in a couple of
weeks time when we'll be discussinganother key area of dermatology
that we need to be aware of.
We'd also like to thank our sponsor,AproDerm®, for all their help in putting
these Rash Decisions podcasts together.
We couldn't do it without them.
So until the next time,it's goodbye from Marina.
(34:24):
Goodbye.
Thank you.
It's goodbye from George.
Goodbye.
And as always, it's goodbyefrom me and we'll see you then.
Goodbye.
Hello, and welcome once again tothis Rash Decisions podcast, where
we look at skin-related issues,treatments, and conditions 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
(00:28):
of the Dermatology Council for England.
In the last two podcasts on bacterial skininfections, George and I spoke about the
common bacterial ones, such as impetigoand bacterial folliculitis, as well as
the more serious ones like cellulitis,scarlet fever, and secondary syphilis.
We described both their clinicalrepresentations and their treatments.
(00:51):
But today we're going to be talking aboutsome potentially very serious bacterial
skin infections, in the third of threepodcasts we've been doing about them.
If you heard our first two, we do hopeyou enjoyed them and remember, we talked
about a special guest for this podcast.
Well, I'm delighted tosay she's with us today.
And it's the fabulous Dr Marina Morgan.
(01:11):
Now, Marina is a Consultant ClinicalMicrobiologist, at the Royal Devon and
Exeter Hospital and out of her multipleinterests, these include necrotising
infections, especially fasciitis andPVL-associated disease, which I'm
certain we're going to be talking about.
And she developed the Exeter protocolfor treating necrotising fasciitis,
(01:32):
which dramatically reduced mortalityfrom this condition in her area.
Marina, welcome to the podcast.
It's so good to have you with us today.
And I suppose the first thing tosay is, did I miss anything out?
Thank you very much.
No, I don't think you did actually.
I'm just a bug lady.
So I deal with bugs.
[Laughing]
(02:01):
Welcome Marina and Roger mentionedin his introduction, necrotising
fasciitis, and I'd like to gostraight into that if I may, please.
Because, there's only a relatively smallnumber of cases in the UK and I believe
that's around about 650, per year.
But it's a truly catastrophic infection.
And I think it's one that we,particularly in primary care, must
(02:22):
remain vigilant to at all times.
If we can recognise it earlyand manage it aggressively,
it can make a big difference.
I've only seen it once andyou don't forget it, do you?
She was a young woman who'd knockedher leg at the gym developing
a large bruise on her shin.
She, as I'm sure everybody would, shetook some ibuprofen for a couple of days,
(02:45):
but then came to see me when the painhad become excruciating, unbearable.
In fact, it was almost impossible tohave a proper communication with her
because of the intensity of the pain.
And I think it was that, that caused meto realise what we're likely to be dealing
with here, and therefore admit urgently.
So, what are your thoughts there, Marina?
(03:08):
Well, firstly, I think that's anabsolutely excellent diagnosis
because it's so easy to miss it.
Necrotising fasciitis in its generalterm, just means you've got necrotic
fascia, and any bug can do it.
The first type, the most commontype to diagnose is really
easy, you can't really miss it.
It takes a while to develop, thepatients don't get very sick, but
you can see something early on.
(03:29):
And these are the kind of patientswho have lots of comorbidities.
The bugs responsible are mixed organisms,a very different pathology, mouldering,
and not that difficult to diagnose,because it's a more chronic presentation.
The one that you spotted had to be agroup A strep necrotising fasciitis.
So, am I right in thinking that inyounger people it's more likely to
(03:49):
be a group A strep and just a singlebug, whereas perhaps in a nursing
home or an older person, peoplewith comorbidities, it might be a
mixed group of organisms causing it?
To an extent, yes.
Unfortunately, the bugsdon't read the textbooks, and
they don't follow the rules.
[Laugh] No.
So you can't, you can't 100%sort of legislate for that.
Can I go back just to the verybeginning, and I apologise for this.
(04:11):
I have to do a little bit of very basicbacteriology, but it might help set
the scene for what I'm going to say.
I tell the medical students thatif you imagine you're wearing a
blue dress, I'm exuding positivity.
I'm a very positiveperson most of the time.
And so on the outside of me, I've gotthis blue dress and the bugs on the
outside of me, on my skin are blues.
They're cold, so they'reblue, but actually they stain
(04:31):
blue with the gram stain.
It's just a way of remembering it.
So your skin infections generallytend to be Gram-positive.
So staphylococci and streptococci.
Whereas if you've got, gut typeinfections, or urine infections mainly,
which is obviously near the gut, they tendto be from organisms that are inside of
you, and, they have to be usually, and theway of remembering it is that inside you
(04:52):
it's warm, and so the bacteria are pink.
So pink bacteria are Gram-negativein the terminology, and
Gram-positive is the skin bacteria.
So, when you come to necrotisingfasciitis, any bacterium and some
fungi can cause it, really rarely.
But really what we're talking about, theones that GPs [are] absolutely, devastated
by if they miss it and it's so easy todo, are the Gram-positive, the group A
(05:14):
strep, sometimes with the staph aureus.
And the problem with themis that it can be any age.
But typically, you get somebody who'snormally pretty fit and healthy.
And a lot of people, if they thinkabout NEC fasc, expect it to be some
sort of traumatic injury, to havesome sort of penetrating trauma.
But the majority that I see, and I'veseen over 150 now, group A strep NEC
(05:36):
fasc's, they've actually come in with abit of a flu-like illness, and they've
had some sort of severe pain somewhere.
Absolutely typically, it would be a youngchap playing rugby, pulling a muscle.
And what you need, it's rather likehaving the holes in the cheese lining up.
A set of very unfortunatecircumstances that come together
and give you this particular idealenvironment for the bugs to grow.
(06:01):
So you happen to have a group A strepin your throat, something happens to
make the group A strep go into yourbloodstream, you have a bacteraemia,
which you normally get rid of quiteeasily because the neutrophils come out,
they gobble up the bugs, and they dieof indigestion, and that gives you pus.
So, your little bit of bacteraemiais normally got rid of.
If you're diabetic, your neutrophilsdon't chase the bacteria so fast,
(06:23):
they can't kill them so quickly.
If the bacteria gets into the deeptissues, because they circulate
all the way through the body, theycan be a little bit more difficult
to get at by the neutrophils.
And if you've got a traumatised area,if you've pulled a muscle genuinely,
you've exposed vimentin, which is amuscle protein that acts like Velcro
and sucks in the group A strep.
(06:45):
So what's that called again, Marina?
Vimentin.
V I M E N T I N.
Vimentin.
Right, it's a new one for me.
So you have this sort of perfect scenariowhere you've got an exposed surface, you
happen to have a, a group A strep that'sevaded the defence mechanisms, tootling
through near the fascia, near the muscle,it gets grabbed in and it's deep down.
(07:07):
And if your neutrophils can't get at itvery quickly, it starts multiplying and
every 20 minutes, these bugs divide.
Add to which, if you've had a trauma,your first response normally is to go
and get some Brufen or some sort ofnon-steroidal, and some painkillers.
And the problem with thatis that it's threefold.
It keeps your temperature down, soyou don't realise how unwell you are.
(07:27):
It makes the pain less, so youpresent later to any medical help.
But the majority of the problems arethat the way that non-steroidal's work,
they actually dismantle the inflammatorymechanism, the cyclooxygenase pathway.
You mentioned exotoxins inthe previous podcast, George.
Exotoxins are produced, they'reproteins made inside the
(07:48):
bacterium and exported out.
The way to remember it,exotoxins, exported out.
And there is a whole myriad of exotoxins.
Some that make you go brightred, like scarlet fever, and
some that will digest tissues.
And this is why group A strep iscalled the flesh-eating virus.
It's not a virus, but, you know, that'sthe way that the newspapers report it.
(08:08):
So your exotoxins are produced and group Astrep produce a lot of leukocidal toxins.
They kill white cells.
So if you imagine somebody sitting therewith a machine gun, firing out bullets at
the advancing army of neutrophils, they'reexploding them before they get near them.
So, the neutrophils that domake it through the onslaught of
these toxins, get to the fascia.
(08:29):
They eat the bugs there, but thenthey can't kill them because the
non-steroidal completely stops theneutrophils killing any ingested bacteria.
It stops production ofintracellular enzymes and peroxides.
So, streps can survive the wholemechanism of being able to kill
the ingested bacteria by producingsuperoxides and hydrogen peroxide
(08:50):
being completely abrogated.
So, you've got a perfectsetting to develop a NEC fasc.
You've got somebody who for somereason may be immunocompetent,
may be immunosuppressed, um,diabetics are more likely to get
all sorts of necrotising fasciitis.
You have bacteria in the deep tissues.
You have, particularly with the groupA strep, it has this myriad capacity
(09:11):
for different exotoxin production.
And if it's producing the rightexotoxins, then you get your
different scenarios of presentation.
So, the GP will see the patients atthe very beginning or at the very end.
And at the very beginning, they feel abit unwell, the bacteraemia is giving them
shivers and shakes, and they feel they'vegot sort of influenza-type problems, and
(09:31):
it's a viral infection, it looks like.
Later on, they get the pain, agonisingpain somewhere, which might be
totally out of the blue, or it mightbe associated with a previous injury
that has exposed the muscle, etc.
etc., and the bugs get downinto it near the fascia.
Then a bit later along in thespectrum, they'll actually present
with something more focal, and asthe infection comes to the surface,
(09:54):
you start getting skin changes.
Now the problem with group Astrep is that when it's in the
superficial layer, it's over the fat.
Whereas the deep fasciallayer is over the muscle.
So if bugs are down in the deep fascia,they're way down deep in the iceberg.
Really difficult forneutrophils to get at.
And you can't see anything atthe skin level for a long time
until the infection ascends.
(10:15):
If it's a superficial fasciallayer, then it can be mistaken
for a simple cellulitis, asort of more deep cellulitis.
And sometimes you'll find the calciumdrops and things like that, but that's
very much a secondary care evaluation.
So your infection is in oneof these fascial layers.
It starts, the bugs aremultiplying every 20 minutes.
Streptococci produce lots of exotoxins.
(10:37):
When they reach a concentration inthe tissues where they've used up all
the available nutrition, and they'reentering what we call stationary phase.
When they do that penicillins don'twork because they are beta-lactam
antibiotics that only work onstopping cell wall assembly.
So if they're not making cellwalls, penicillins won't work.
So penicillins work when you'vegot a lowish number of bugs.
(10:58):
But they're completely inactive andthey also don't penetrate very well
because you've got thrombosis goingon and you've got tissue swelling.
You've got compartment syndromehappening if it's a leg or arm.
So all these things are happeningall together and towards the end
of the spectrum you've got the deepinfection, loads of exotoxins being
produced, lots of different types.
Some will give the patient vomitingand diarrhoea so it's misdiagnosed
(11:19):
as gastroenteritis, some justmention incidentally they've got
the pain, there's not much to see soyou don't think it's that serious.
But if a patient comes to seeyou with cellulitis, and they're
heading into opiates, they havenot got a simple cellulitis.
So, going back to your patient, George,it was fantastic that you spotted it,
and so many people wouldn't spot it,because it's only just becoming compulsory
(11:41):
now to include necrotising fasciitisin the medical student curriculum.
Hitherto, it hasn't been.
And it's because of, you know, a lot of,intense lobbying by various groups...
Yep.
There's been very, very little taughtand people don't understand it.
The two patients I can recallwhere I have been unable to
communicate with the patient becausethey are in such severe pain.
(12:02):
One had an ectopic and theother had necrotising fasciitis.
So, clearly the intensity of pain in thissituation is about as bad as it can be.
But that pain, is that dueto damage to the nerves?
Yes, what happens as the bugs spreadacross the fascia you get thrombosis
to the nerves and you get agonisingpain in the centre as the inflammation
(12:23):
and infection ascends to the skin.
If you imagine the top of an iceberg,the iceberg emerging out of the ocean.
The very centre, epicentre of the skinsurface will be very, very painful
and then gradually becomes numb as thenerves die, and then it spreads out.
So the very edge of thespreading lesion will be very
painful and the centre will die.
Right.
But it all depends where yousee the patient at that point.
(12:44):
So if you see somebody late, painwill no longer be a major feature?
The deep pain...
Or may not be.
It may not be, but that's very, very late.
By that time, it's easy because you'vegot obvious full thickness necrosis.
You've got black lesions and blisterswith serosanguineous fluid in them.
Ghastly, I can imagine.
Yeah.
At that point, it basically needsa lot of surgery, doesn't it?
(13:05):
I mean, you need a surgeon who's goingto be a bit cut and thrust really,
going to take out far more thanmight at first seem to be necessary.
You need pretty bold surgery, don't you?
Absolutely, what you don't want to dois to pussyfoot around this and have
some junior surgeon looking at itand saying it doesn't look too bad,
it's you know, not that serious, youknow [the] patient's pain is better.
(13:27):
We've got them on opiates.
They're comfortable.
You're tempted to think that maybeyou've got time to do a biopsy.
But time to debridement is of the essence.
We shouldn't be doing a frozen section.
It's a total waste of timethinking of doing that.
Maybe we've got time to do someMRIs, but basically, if you
think you've got a NEC fasc, e.g.
if the pain score is 8, 9, 10 out of10, and the CRP is really high, you've
(13:51):
got to get in there and debride.
And before the surgery, you'vegot to load them up with really
big domestos antibiotics.
Antibiotics to cover all the bugs.
Majority ones are the group A strep,so you need something that will switch
off those exotoxins, and those are twoantibiotics, linezolid and clindamycin,
because penicillins don't work, remember,when the bugs get into stationary phase.
So what was the firstone, clindamycin and?
(14:13):
Linezolid.
Yes.
Linezolid is available in generalpractice, but it's rarely needed.
In empirical treatment of necrotisingfasciitis, we use it to cover all
Gram-positives, including MRSA, and itswitches off the production of the toxins.
We add piperacillin-tazobactam ormeropenem for the Gram-negatives, until
we're absolutely sure what the bugs are,by looking at them under the microscope.
(14:36):
As a complete aside from that, doyou have concerns about our use
in primary care of clindamycinso freely for things like acne?
Are we going to increase therisk of that antibiotic becoming
less useful for this sort of rarebut incredibly severe infection?
It's a very good point, actually.
It's spread around.
(14:56):
Clindamycin is a very popularantibiotic to use topically for acne.
It is.
I hasten to add I haven't useda topical antibiotic for acne
for over 20 years, but, uh...
It's a very good antibiotic,and as I say, it switches off
toxins, so it's very popular.
There's also a clindamycin vaginalcream, which is extremely good for
women with vulvovaginitis due togroup A strep, or trying to decolonize
(15:17):
from MRSA, if they're carrying itintravaginally, which sometimes happens.
But, in answer to your question,yes, you don't want to use anything
too liberally, because things willbecome resistant quite quickly.
The clindamycin resistance ratefor a group A strep, a couple of
years ago, was anything between11 and 16%, and that's old data.
That's already quitefrightening, isn't it?
Yeah.
Yeah, and doxycycline's even worse.
So whatever you use,you will get resistance.
(15:39):
Again, that's an antibiotic that wethrow around in, in dermatology, a lot,
for its anti-inflammatory side effects.
That's fascinating, reallyinteresting, I've learnt a lot already.
The other thing we mentioned brieflyin our introduction was PVL, or
Panton-Valentine Leukocidin staphylococcalinfection, described by Sir Philip
(16:02):
Noel Panton and Francis Valentine,almost a hundred years ago in 1932.
Now I have to say that if any ofour listeners have a deep knowledge
of this, we'll happily award themthe Rash Decisions prize goldfish.
But can you remind us a bit more about[what] PVL infection is and what we
need to know about it in primary care?
(16:24):
Right, from the point of viewof the primary care physician,
PVL, Panton-Valentine Leukocidin,is just another exotoxin.
So that means it's produced insidethe bug, it spreads out, and it
actually kills the white cells.
It is a leukocidal toxin.
So in response to that, your body overmakes neutrophils to compensate for
(16:44):
their destruction, and so patientspresent with even a minor trauma
with recurrent boils and abscesses.
It used to be that recurrent boilsand abscesses was the domain of
diabetics, but nowadays, to behonest, I don't see diabetics with it.
I see loads of PVL staph aureusinfections, and it can be in anybody, but
particularly young people, people who arefit, people who are in contact sports.
(17:06):
It's a skin-spread bacterium,so you need close contact with
somebody else who's got it.
Um, so contact sports, sharing wetsuits,toothbrushes, sleeping with somebody.
Sharing towels, hanging towels close uptogether in the bathroom, using a gym and
throwing your towel into an ice bucket,jumping in an ice bath with loads of
other athletes, who've probably got it.
(17:27):
There was a lovely outbreak some yearsago, at a prestigious international
meeting where wrestlers were afflictedwith boils, particularly on their bottoms.
I was told on good authority that as wellas the skin to skin contact that's so
inevitable in wrestling, for some reason,sharing of jockstraps had occurred.
Just beggars belief, really,but that's well recognised.
(17:47):
People do very strange things.
I've seen somebody who's had notrouble with their skin whatsoever
until seven months ago and sincethen they've just gone from one
nasty, deep abscess to another.
Abscesses on their ankles, abscesseson their bottom, abscesses everywhere.
Just nasty, deep infections.
Just suddenly going from nothing,from nought to ninety, or a hundred
(18:07):
miles an hour, with infection.
Until I came across PVL infections,I thought invasive group A strep was
the worst infection I'd ever seen.
But fulminant PVL staph aureuspneumonia is far, far worse.
Most labs can't test their isolatesof staph aureus for PVL production.
So like us, if we suspect PVL on aclinical basis, we have to send our
(18:31):
isolate to the reference lab for testing.
Although less than 2% of the staph aureuscausing bacteraemias in the UK were found
to produce PVL, this is actually prettyold data, from over 15 years ago, and we
have no idea of the percentage of UK staphaureus isolates that produce PVL now.
For example, in Exeter only a fewyears ago, we found 15% of the
(18:56):
patients with infected wounds attendingour emergency department had staph
aureus that was producing PVL.
PVL staph aureus is transmitted by closecontact with an infected person's skin.
So, it spreads in families andbetween sleeping partners especially.
Also, at risk, are patients withskin trauma, so those who inject
(19:20):
drugs, and closed communities,such as boarding schools, prisons,
and military establishments.
So, the key to diagnosis clinically,is simply asking the right questions.
Is there someone close to youwith recurrent skin infections?
Do you play contact sports?
Do you use a gym where peoplehave boils and abscesses?
(19:44):
You get the clues to the presence ofPVL infection from the background.
It's like being a good GP, youjust ask the right questions.
So once you think they might have it, thenif you look at the old guidelines, I was
part of the guideline committee that didit, but unfortunately, they're completely
out of date and they don't work.
We didn't know that at the time.
It's taken some years to findout, but they recommended MRSA
(20:05):
type decolonization, and remember,it doesn't have to be an MRSA.
It can be a fluclox sensitive MSSA.
It can be any staph that can produce PVL.
But historically, it was theMRSAs from America, the USA...
Yeah, America's had a big problemwith MRSA, hasn't it, and PVL.
Absolutely.
Whereas, in the UK, it'salmost invariably MSSA.
(20:25):
Yep.
And that probably accounts for whywe're a little bit more relaxed about
it in the UK than they are in America.
I think the problem is that thestrains have changed a lot, and
so what you've got, you've got avery promiscuous gene that will hop
between different types of staph.
So the American strain, the PVL gene, hashopped between lots of other different
(20:47):
kinds of staph now, and there's lotsthat are producing it, and I think
they're producing it in different amounts.Different skins are different as well.
So, um, the actual environment ofcertain skins is not conducive to it.
So you have a very, very complexsituation of who's actually got
PVL carriage, but once they've gotit, the old guidelines would say
that you treat them like an MRSA.
(21:08):
You decolonize them withan antiseptic lotion.
Chlorhexidine we used to use.
You can decolonize nasally withantiseptics like mupirocin, Naseptin®,
Octenisan®, that sort of thing.
And whereas five days seem to work fora lot of the old MRSAs, nowadays, if
you've got the PVL gene inside a staph,it seems to make it far more stickable
(21:28):
and far more spreadable, and it'sreally, really difficult to shift it.
Hence, I tend to use 10 daysdecolonization, not the five that's
recommended in current guidelines.
We've had a lot of cases where it'sgone around families and if you
just treat one, nothing happens.
You need to treat thewhole family at least once.
I then treat again anybodythat's actually got lesions.
(21:49):
Now the easiest way to do it is, I findlocally, is to give three months of
treatment, ten days once a month forthree months of a decolonization regimen.
Give antibiotics that aresuitable for that bug.
If it's an MRSA, doxycycline isusually pretty good because most
of them are still sensitive.
Fluclox isn't quite so good.
It doesn't get quite such goodlevels on the skin, but it
(22:10):
gets into the abscesses okay.
If they're big abscesses, theyneed incising and draining.
Lesions should be covered.
Patients shouldn't be jumping intoswimming pools and sharing towels
and spreading it here and there.
They need to be treated properly and theyneed to be aware of the infection risks.
But the most significant problem,happily very rare, is PVL pneumonia.
(22:31):
Yeah, yeah.
So, if you just acquire your staphaureus from contact with somebody who's
got PVL on their skin, it'll get intoyour skin and particularly up your nose.
Your oropharynx becomes colonized.
Then if you have an intercurrentviral infection, or suppose you're
a heavy smoker, you can actuallydamage your mucociliary escalator
(22:52):
so the bugs don't get swept out.
In other words, you can get aninhalational secondary chest infection.
The problem is that PVL staphpneumonia is a necrotising pneumonia.
The necrotising exotoxins attackblood vessels, causing haemorrhage
and infarction, and this resultsin a characteristic haemoptysis
and death of the lung tissues.
(23:13):
PVL staph aureus pneumonia is a trulydreadful disease, and once established,
it's very, very difficult to treat.
So the diagnosis has to be early,rather like invasive group A strep.
The mortality of PVL staphpneumonia can be as high as 65%,
though we've got it down to about15% in Exeter with great effort.
(23:34):
Hence, the main reason in my mind fordecolonizing patients that are carrying
PVL staph on their skin is to lessenthe spread of PVL staph to others
who've not encountered it before.
The carriers eventually developantibodies and are then far less
likely to get invasive infection, butpeople they're spreading it to have
no protective antibodies and they willbe most at risk of invasive infection.
(23:57):
The contacts yes.
...they will then get serious pneumonia.
And it's a really nastyhaemorrhagic pneumonitis, isn't it?
Or pneumonia, it really is, as you say,very high mortality and very aggressive.
Absolutely ghastly.
But that's fascinating, their contactswho first encounter it, then get
it as an inhalation complication.
Yes, you can get a haematogenous spreadto the lungs from a skin lesion, e.g.
(24:20):
a blister or an abscess, and thatcan cause a haematogenous pneumonia.
Gosh, fascinating, gosh,I'm learning so much.
Moving on, something we are seeingincreasingly commonly is Lyme disease.
And I believe this is now endemicin the UK, coming right across
the country, including Scotland.
I've had a couple of casesrecently from Scotland.
(24:40):
Indeed, I actually had a casefor a young woman who had not
travelled out of Bicester.
And she hadn't travelledout of Bicester for months.
And she had Lyme disease.
In fact, she fortunatelypresented with a classic rash.
But I gather the, the tick thattransmits this infection, it's
called Ixodes ricinus, is the tickin the UK, but this is moving further
(25:02):
north with global warming, whichis a frightening thought, isn't it?
Another disease that's going toget more common as the world warms
up and that mite can survive.
Let's have just a few wordsand thoughts about Lyme disease
in our last five minutes.
Okay, it is pretty well endemic.
Partly because the sheep aren'tbeing dipped, they can live on sheep,
deer, all sorts of large animals.
(25:24):
We get in the way, we take the place ofthe larger animals, and we walk through
the grass and they leap onto our legs.
Yes you can get it in Bicester.
I removed a tick from my husband as he waswalking up the stairs and I spotted it.
He was wearing shorts and I thought"My goodness, he's got a tick."
He said, "Oh god, get it off me."
I said, "Not until I've had a photograph."
And it's really quite difficult to spot.
They're quite small.
And so that's why a lot of peopledon't realise they've actually
(25:45):
got them because they don't...
As they feed, they get bigger, don't they?
As they feed on blood, they get bigger.
They do.
And then they're more obvious.
But that's why it's vital to checkthe kids when you've been out walking
and make sure they haven't got any...
Yeah I've certainly removed them fromthe back of my children's neck, my
grandchildren's necks after they'vebeen walking in Isabella Plantation
in Richmond Park, for example.
So at bath time you see thetick there and you get it off.
(26:07):
Goodness.
Certainly in London, in inner cities,you certainly get them, because [there
are] lots of wild animals around.
And I know there's been a Lymearthritis in a dog in Wimbledon.
So, you know, yes, it's everywhere.
You can't say you're not going to get it.
It's not just the deer, is it?
It's voles, it's cattle, it's horses,a whole load of different animals
can have the ticks living on themand breeding on them, but they
don't live and breed on us, do they?
(26:30):
No, but what they do do, if youinterrupt their feeding, they will
regurgitate blood back into it.
And if they happen to be an infectedtick, then you get the infection.
Not all ticks carry Borrelia.
About one in seven, isn't it, in the UK?
Very good question.
I couldn't give the exact[answer], because the problem
is, it depends where you sample.
Because there are areas whereyou don't have infected ticks.
But that's probably about right.
Yeah, but I think it'sabout one in seven, yeah.
The way to remove it, with a tickremoval and ideally anticlockwise.
(26:54):
For goodness sake, don'tuse lighted cigarettes.
That isn't a good way to do it.
And take the ticks off.
And basically, we don't recommendtreating empirically, tick bites,
because most of them aren't bitten byinfected ticks, and if you get them
off early, there's a lot less chanceof the infection being transmitted.
I read somewhere that if you getthe tick off in the first 24 hours,
(27:14):
the likelihood of going on to getLyme disease, even if the tick was
infected, is very small indeed.
So I think the trick isto get them off quickly.
I agree, if you get an O'Tom tickremover, ideal, but I wouldn't wait for
Amazon to deliver it in two days time.
I'd get it off first, and thenhave an O'Tom tick remover for
(27:35):
next time, would be my advice.
Absolutely.
I think only about a third of patientswith Lyme disease actually manifest the
rash, the erythema chronicum migransrash, this rapidly spreading, almost
target like rash with a red edgeand then paler centre and then the
tick bite not always in the middle.
(27:56):
And of course you can get multipleerythema chronicum migrans with some of
the, particularly some of the Europeanvariants of Lyme disease, can't you?
The evolution of the rash is interestingand if somebody pitches up with what looks
like erythema migrans and they haven'tgot a history of a tick bite, that doesn't
mean to say they haven't got it because...
No.
If they've had one tick bite five yearsago, they've obviously [been] in that area
(28:19):
where ticks would be, so they've missedthe tick bite that's actually set it.
Just because they don't remembera tick bite doesn't mean
to say they haven't got it.
So follow the NICE guidelinesand clinically you treat them.
If they've got erythema migrans,you, you treat them on spec and
you follow the NICE guidelines.
We have rather strange length of courses.
I think it's something like,azithromycin for 17 days or
something strange, or doxycyclineor amoxicillin for three weeks.
(28:42):
It's a spirochaete, isn't it?
So it would respond very well to apenicillin, I would have thought.
Interestingly, no.
The problem is with children undereight or nine, it's difficult
to justify using doxycycline.
Doxycycline is the best treatment.
No, I agree with children, yeah.
And so we tend to useamoxicillin for children.
Azithromycin, although it works asimilar sort of way, it's not a cell
wall acting antibiotic, it's sortof okay from that point of view,
(29:04):
because it's the most peculiar bug.
Generally speaking, if you canpossibly get a patient onto
doxy, I would treat with doxy.
Right.
Yeah.
Yeah.
And what are your thoughtsabout things like chronic Lyme?
People who are complaining thatthey have chronic Lyme disease?
It's an absolute nightmare for themand for the medical establishment
because there's so many thingsthat give you a chronic fatigue,
(29:25):
chronic illness, feeling awful.
I'm not one of the microbiologiststhat says chronic Lyme disease can't
exist because you can never saynever in microbiology or medicine.
And so there must be some people that dosuffer with a genuine chronic infection.
Must be.
But discerning those from the peoplewho are just suffering the chronic
inflammatory response to having hadthe infection, which is what most
(29:46):
microbiologists feel is probablywhat's happening, and that's why
doxycycline works so well and theyfeel better on it because it's
an anti-inflammatory antibiotic.
So, it's really difficult to kind ofget your head around Lyme disease and
we're learning all the time and allwe can do is just keep working at it.
Marina, I'm really sorry.
We've run out of time.
I've been distracting you too much.
(30:07):
I was hoping we would get on to talkingabout meningococcal septicaemia and
Waterhouse–Friderichsen syndrome and,uh, all sorts of other things from
toxic shock through to even anthrax.
Which I think is something that as GPs,no bad thing that we just vaguely aware
that anthrax is something, if you've gota really nasty black lesion that's sort
(30:29):
of suddenly appeared and looks horrible,um, just to have that at the back of your
mind for that odd case, we may well comeacross it in the next 50 years, but this
has been absolutely fascinating already.
Finally, I think one thing I justwant to quickly say is that one
thing I say to all my students andmy registrars is, "With every single
(30:51):
patient encounter, every single one,sit back and make a conscious decision.
Are they unwell?
In which case, I'm not concerned.
Or are they ill?"
And signs of illness can be very,very subtle and easily missed,
particularly in little children,particularly in older people.
(31:12):
And I think this dovetailsso nicely with Martha's Law.
It's a situation where I say,listen to what the family is saying.
They know, they will spot the subtleclues that we might otherwise miss.
But I think the things like,you know, the child is running
around the consulting room.
I don't need to examine [them].
If they're climbing up the curtain andunder my desk, they can get on with
it, and I'm not going to examine them.
(31:33):
It's the child who sits there limpand has a delayed capillary refill
time, maybe a low oxygen sat. Theircolour's poor, they're listless, you
pick up their arm and they drop it.
So I think with all these illnesses,whether it's meningococcal meningitis,
or whether, which we haven't covered,or whatever, I think that it's so
important to make that conscious decision.
(31:54):
"Am I faced with somebody here who's abit ill, doesn't matter, or are they ill?"
Can I just come in there and saythat, absolutely the most important
thing of all is the parents.
Parents look after the children.
If they say their child's not well, andif they've seen healthcare professionals
in the last 24 hours or 36 hours already,then that's the worry for group A strep
(32:15):
because it's such an insidious pathogen.
And an interesting thing about group Astrep, it makes people outside themselves.
So even when they've got toxic shock,even when they've got NEC fasc, they
go to that sort of detached phaseand they're sort of not with it.
It's most peculiar.
And that's another sign, forcertainly the adults and the children
as well that works very well.
Well, goodness me, Marina, I've lost trackof how much I've learnt from you today.
(32:38):
And I'm sure our listenerswould have gained so much
too from all your expertise.
Thank you so much for givingus all your valuable time.
But before we do let you go, isthere anywhere our listeners can
go to get more information on someof the things we've talked about?
Absolutely.
I can heartily recommend theLee Spark Foundation website.
There's an educational video onstreptococcal infections that
(33:00):
we made basically, most of usdid it at the RD&E in Exeter.
It's very useful as a, learningexercise for, paramedics, clinical
staff, non-clinical staff, and even,members of the public, on the sort
of complications and what to lookfor with streptococcal infections.
And I'm very happy for the healthcarepeople who might be listening to this.
I'm very happy to be emailed.
(33:20):
I've got loads of papers and information[that] I'm very happy to provide.
Well, Marina, thank you so much foryour time and your expertise, and we'd
love to take a note of that resource sothat we can add it to the information
we have attached to this podcast.
Absolutely wonderful stuff.
George and I do hope you foundthis podcast as interesting
and as helpful as we have.
(33:41):
And that you've enjoyed the previoustwo on bacterial skin infections.
If you haven't caught up withthose yet, do have a listen.
And if you like what you hear, then dorate and review us wherever you get your
podcasts as it really does help us tokeep producing quality content for you.
Or even better, get in touchwith questions or suggestions
for future podcasts as we doreally love to hear from you.
(34:03):
In the meantime, Roger and I do hopeyou'll join us again in a couple of
weeks time when we'll be discussinganother key area of dermatology
that we need to be aware of.
We'd also like to thank our sponsor,AproDerm®, for all their help in putting
these Rash Decisions podcasts together.
We couldn't do it without them.
So until the next time,it's goodbye from Marina.
(34:24):
Goodbye.
Thank you.
It's goodbye from George.
Goodbye.
And as always, it's goodbyefrom me and we'll see you then.
Goodbye.
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