Now that we've wrapped up this
case of codylomata acuminata,
we do need to further discuss the various
manifestations of herpes simplex virus
which has so many different
manifestations on the skin.
We alluded to genital herpes in this case, but HSV causes
a lot more trouble than just the occasional herpes.
Let's take a look at HSV1 first and
then we'll take a look at HSV2.
So as you can see right off the bat,
the prevalence of HSV1 is 66% worldwide,
so it's a wildly endemic viral infection.
And as I mentioned, there are multiple skin and systemic
manifestations and we'll go through some of them today.
It's transmitted via mucosal secretions and
oftentimes, if you have an active herpetic lesion,
as you might imagine,
it's much more likely to be transmitted
cause the virus is living in that
lesion and is being secreted.
We'll talk more about the difference between a primary
HSV infection versus secondary reactivation infection.
So here we can talk about the difference between
the primary and secondary infection with HSV1.
Primary infection is the initial infection.
After inoculation, there's about a 2 to 12-day period
of incubation before you can develop gingivostomatitis.
A milder version is shown here but essentially, gingival stomatitis
can just involve a few ulcers on the back of the hard palate
or it can present much more floridly with
significant mucosal inflammation, edema, ulceration
and hemorrhagic crusts on the
lips and on the buccal mucosa.
This presentation is oftentimes
accompanied by lymphadenopathy,
fever, malaise, headaches and severe
pharyngitis with odynophagia,
which as you might imagine,
might impair a patient's ability to swallow,
particularly since this can occur in children.
In contrast, a seconday HSV1 presentation or
reactivation occurs in about 20 to 40% of people
who have previously been infected and it
could be months or years before somebody has a
secondary reactivation of HSV1.
These lesions are triggered by
different types of exposures.
It could be excess sunlight, it could
be a fever due to some other infection
or just psychological stress, trauma to the
area like if you bite your cheek or your tongue
and in folks who are immunocompromised, they're
much more likely to have these reactivations
especially as you get older or if you have any other types of
infections going on that could compromise your immune system.
The most classic lesion is shown here with this
herpes labialis lesion at the vermilion border.
Remember the vermilion border is the junction between
normal skin and the beginnings of the mucosa of the lip.
Interestingly enough, these lesions are often preceeded
by pain, paresthesias, maybe even just some itchiness
that the patient will experience a few
days before the appearance of the vesicles
so they have a little bit of a
warning that these are coming.
Rarely, patients will have some
systemic symptoms but typically
it's not nearly as acute a presentation
as someone having a primary lesion.
Okay, so here's a list of all of the HSV1 manifestations
even though this list is not even fully comprehensive.
We've already talked about herpetic gingivostomatitis.
We've talked about herpes labialis and cold sores.
The next stop we'll talk about
herpetic whitlow, this is a old term
but it basically refers to an HSV1 infection
of a finger or around the fingernail.
As you might imagine, these are relatively common
in kids who are constantly getting cuts in the skin
and essentially HSV1 just penetrates the
dermis and causes a local infection.
Next stop is genital herpes which
we've talked about previously.
Just a reminder that while HSV2 is the
most likely cause of genital herpes,
HSV1 can also cause those lesions.
Now, we already discussed erythema multiforme
earlier on this section but I'll just remind you,
that you wouldn't find HSV1 itself in any
of the lesions of erythema multiforme.
Remember, it represents an immune-mediated
hypersensitivity reaction to the virus,
rather than a manifestation of
the virus itself in the skin.
In contrast, those first five lesions on the left side of our
screen would actually yield HSV1 if you were to biospy them.
Next stop, herpetic keratitis.
This is actually an ophthamologic emergency
involving HSV1 infection of the cornea itself
and you could see this with flourescene
on the slit lamp exam as well.
Next stop are a variety of
neurologic manifestations of HSV.
This can include herpes encephalitis,
aseptic meningitis and Bell's palsy.
That's the one that's shown here
with 7th cranial nerve palsy.
Having spoken about HSV1, let's shift
the gears and start talking about HSV2.
The prevalence of HSV2 in
high-income countries is about 16%
and this also have a primary infection presentation
and a secondary reactivation presentation.
First up, primary infection after inoculation,
patients will experience bilateral genital ulcers
with lymphadenopathy, fevers,
myalgias and potentially,
if the lesions exist around the urethral
os, you may have some dysuria as well.
In contrast, after that spontaneously resolves, a number of
patients will present with reactivation or secondary infection.
This is characterized by small erosions,
maybe some vesicles on an erythematous base
and they're unlikely to have systemic
symptoms at the time of presentation.
Diagnosis is fairly straightforward,
there's a number of different ways to do it
but the most sensitive and specific
approach is gonna be with PCR testing.
Direct flourescent antibody testing is also useful though
it doesn't quite have the same sensitivity and specificity
and a viral culture can be done but the sensitivity is not
very high and of course it can take some time to obtain.
Serology, I should just point out, is effectively useless
because the prevalence of HSV1 and HSV2 is so high,
it's not gonna tell you if there's seropositivity
explains their current presentation.
Simply unroof a vesicle, swab the
lesion and send it off to the lab.
To treat these lesions acutely as long as you catch
it early, you can use valcyclovir or acyclovir
but if it's been several days into the lesion,
it's probably just gonna resolve on its own.
Subsequently, if a person has recurrences,
multiple recurrences overtime,
patients oftentimes take prophylactic valcyclovir
or acyclovir to prevent future infections.
Alright, so we've covered HPV, HSV,
measles, molluscum contagiosum,
what a lecture.
We'd be remiss however, if we
didn't discover quickly this rash.
You've gotta be able
to recognize this one.
Painful, unilateral, vesicular rash, common
in the elderly and immunocompromised.
You guessed it, it's
shingles caused by VZV.
This is a painful, dermatomal vesicular rash, common
in the elderly and immunocompromised as I said.
While it's caused by reactivation
of latent varicella zoster virus,
it can be complicated by some
pretty severe infections.
Involvement of the V5 ophthalmic branch, which can
cause potentially vision-threatening inflammation,
but more commonly, about 10-15% of patients who
get shingles will develop postherpetic neuralgia.
This is a painful neuropathy that persists for more than 90 days
after the dermatologic inflammation has long since resolved.
This condition can be debilitating for patients and requires the use
of a variety of the gabapentinoid kind of medications to cool it down.
Otherwise, when it's initially presenting, as long as you
catch it early, you can treat sometimes with steroids.
You can use antivirals but once it's passed the initial
vesicular stage and it's starting to crust over,
those medications are less likely to be effective.
And of course, we now have vaccines to try and prevent
this infection or reactivation with things like zostavax.
which patients are recommended to get once
they have gotten above a certain age.