Lets take a look at Eosinophilic lung disease
now. And before we move on though, the segway
here, is the fact that it’s, well, for the
most part, once again, hypersensitivity in
exposure. However, with
hypersensitivity pneumonitis, you did not
necessarily see eosinophils. Is that understood?
If that is not clear and you don’t have
a firm grasp of that, go back and take a look
at that table, so that you’re… that and
the criteria. That would be the two most important.
Now, under Eosinophilic lung disease, this
means that the patient was exposed to, we’ll
take a look at the number of issues in which
now the patient has developed what? Eosinophilia.
Clear? Defining characteristics needed to
diagnose Eosinophilic lung disease (ELD) include,
number 1, peripheral blood with eosinophilia.
So, you have an increase in WBC, and specifically
it will be increase in eosinophils. With
abnormalities of pulmonary imagining. Who
are you going to… what part of lung are
you going to affect more so? Good. The interstitium.
The lung tissue eosinophilia demonstrated
in transbronchial or open lung biopsies.
Eosinophil is the name of the
game here, and increased eosinophils
in bronchioalveolar lavage. Stop here. Would
you tell me. Lets say that your patient
was growing birds or raising birds and your
patient maybe was working in a type of a silo,
whatever it may be. That’s hypersensitivity
pneumonitis. They’re not feeling too well.
On bronchoalveolar lavage, what you’re going to
find there? Good. A low CD4 to CD8 count.
That was criteria number two. Here, with the
etiologies and differentials that I’ll give
you for Eosinophilic lung disease. Here, the
bronchioalveolar lavage will show you, eosinophils.
All three bullet points: blood, biopsy, lavage
What are my differentials? Lets begin.
Drug-induced, toxin-induced. NSAIDs. You’ve
heard of patients who is “allergic to drugs”
such as NSAIDs. The usual suspects here for
antibiotics, especially sulfonamides, penicillins,
phenytoin, maybe even L-tryptophan. Good.
These will be one’s in which, upon exposure,
the patient has now developed Eosinophilic
lung disease. Next.
So those were drugs. What if your patient...
let’s walk through the various types of,
what’s known as Loeffler’s syndrome. So
these will be helminths. For example, Ascaris
lumbricoides. Crazy worm. Where is
it? In my intestine. How big is it? I
don’t know, it’s huge. What does it do?
It’s like an alien in your intestine and
it burrows through the intestine. Gets
into where? The blood. And it goes where?
Transpulmonary. Would you tell me as
to, well, what you require to properly kill
your helminth? Oh yeah, you need eosinophils
Dr. Raj. There you go.
So, here we have Eosinophilic lung disease
which is caused by what? Helminthic infections.
Understand something. If it doesn’t invade…
what do you mean doesn’t invade? Where did
you find this Ascaris initially?
In the intestine. If it doesn’t invade,
you are not going to find eosinophilia. Is
that understood? An important clinical distinction.
If this thing actually invades through the
intestine. Here it comes, you see it? Here
I come, I’m coming into the blood and I’m
going to the lung, then you’ll have
eosinophilia. That must be understood in many
of these helminths. Lets continue.
Hookworm. We have Ancyclostoma duodenale.
We have Strongyloides stercoralis. What does
this one do? This thing is so strong that
it will actually penetrate through your foot
when you step on it. So therefore this might
be a patient who has HIV, and immunocompromised.
Imagine this thing burrowing through your
foot, the sole of it, my goodness, your sole.
Not this one, but the sole, underneath your
foot is so thick and this strong worm can
get through? Yeah, it can. Gets into blood,
transpulmonary. What’s this called?
Loeffler syndrome. Let me give you
a little bit more information that you will find
to be interesting. Lets continue.
Tropical. Well here, you end up having
what? Wuchereria bancrofti. What does this
organism do? It literally blocks off, whom?
It blocks off the lymph nodes, doesn’t it?
So, if you block off your lymph, then what
then happens? You have lymphedema. Sometimes
this lymphedema is so bad that it’s amazing
actually that, you can find patients in
developing countries in which, I’m gonna
be a little exaggerated here, but they’re
literally, they are putting their scrotum
in a wheelbarrow and bringing it in into the
clinic. That is rather large. Welcome to elephantiasis
is what I’m getting at. Could I be any more
dramatic? So, welcome to Loeffler. Look for
Another one simple, Brugia malayi.
Another one will be, this is a good one.
A direct lung parenchymal invasion and this
is called paragonimiasis. This is directly
lung parenchymal invasion whereas the other
ones result in eosinophilia via transpulmonary.
Is that clear?
Then we have the ones that love to go through
haematogenous. So heavy haematogenous seeding
helminth include your Trichonella, the disseminated
strongyloid, the visceral larva migrans, cutaneous
and schistosomiasis. So these are important
ones from microbiology that you’ve covered.
I would know some of these and as to how they’re
involved with different manifestations in
your patient and, ultimately, in the lung,
may result in what kind of disease? Eosinophilic
lung disease. Often times, you call this Loeffler.
Now, there is an important point that I need
to bring to your attention. If you have such
strict, intense eosinophilic reaction taking
place in the lung known as Loeffler, is it
possible that you might then also affect your
adjacent structure? What is then adjacent
to the left lung? Right here, by the apex,
fifth intercostal space. The heart.
And so therefore, what if you had Eosinophilic
heart disease? You know what that’s called?
You do. That’s called Endomyocardial fibrosis.
Right? In the US, extremely uncommon, but
if you take some of these tropical countries,
interesting, huh? Tropical countries, which
is kind of like what we see here with these
helminths. Then could you have eosinophilic
damage to the heart? Yes, you could. What’s
that called again? That’s called Endomyocardial
fibrosis. Now, be careful, because at some
point, you need to distinguish that from what’s
called your Endocardial fibroelastosis and
that’s found with your young infants. Lets
Now, here we have what’s known as your acute
eosinophililc type of pneumonia. And the acute
eosinophilic type of pneumonia, as you can
expect it to be is rather rapid. Patients
have been fire-fighters during 9/11, HIV-patients
and smokers. So during this time, lets
say that… crazy, a building just collapsed
during 9/11, you’re a fire-fighter in the
middle of that, trying to save. What are you
going to breathe in? All kinds of things.
And so during this time when you’re breathing
in who-knows-what, you might then have a acute
eosinophilic type of reaction. Is that understood?
Rapid development of acute respiratory failure.
HIV-patient, immunocompromised, smokers, perhaps.
They will have acute febrile illness for less
than a week’s duration. And once again
here, it will be non-productive cough because
it’s the interstitium that is being involved.
Acute eosinophilia. Acute type of conditions.
Emergency type of fire-fighters
or emergency type of calls that are taking
The chronic, as the name applies. 50-60% of
your patients will then exhibit some type
of atopic reaction. What does this mean? This
would mean this individual was exposed to
some type of allergen. What does atopic mean?
Remember atopic asthma, in obstructive? Isn’t
that the majority of your asthma patients?
Of course, it is. With atopia or, excuse me,
atopy, then that patient may also have atopic
type of eczema. Asthma, eczema. Long period
of time, been exposed to allergen, now developing
what? Eosinophilic. Now, be very careful because
if this patient was, once again, working as
a farmer, that’s a hypersensitivity pneumonitis.
You see that? That is not Eosinophilic lung
disease. You must keep that separate.
Next, with chronic type of eosinophilic, predominantly
occurs in women, non-smokers and some of them
been exposed to post-radiation breast cancer
therapy. Huge. Radiation therapy for breast.
Chronic eosinophilic lung disease.
Next. Well, under this, now we have a condition
in which we have huge granulomas. So this
then brings us to Eosinophilic granulomatosis
with polyangiitis. In other words, this is
Churg-strauss. Now with Churg-strauss, a
couple of things that I wish to bring to your
attention. First and foremost, it is P-ANCA
+. What does P-ANCA stand for? What’s
that P stand for? It means perinuclear and
it stains for MPO which is myeloperoxidase.
Is that clear? So, another name for P-ANCA,
as you know, is MPO, myeloperoxidase. Whenever
you think about ANCA +, you should be thinking
about your blood vessels that are affected
and also other organs. No exception. Vasculary
disorder characterised by, sinusitis,
asthma, peripheral blood eosinophilia.
Do you see which one of these condition, oh,
excuse me, which one of these presentations
is not found in Granulomatosis with polyangiitis,
formally known as Wegener? Obviously, the
eosinophilia, right? Lets continue.
Here’s the sole form of vasculitis that
is associated with eosinophilia and lung involvement.
The sole type of lung disease. The integumentary,
cardiovascular system, GI, renal, neurologic
systems may also be involved. Remember, these
ANCA + can affect many organs.
Even in Wegener, now currently known as Granulomatosis
with polyangiitis, which is a C-ANCA +, another
name for C-ANCA, proteinase 3. Do you understand
with every little thing that we do? It’s about
me making sure that I tie it in to other differentials
and other things that you see around in medicine,
but you have to have a proper way of organising
things. Let me be your anchor so that I can
get you where you need to be. Lets continue.
Now, you have Allergic bronchopulmonary aspergillosis
(ABPA). What is this patient exposed to? Good.
Aspergillus, fumagatus perhaps. What does it
do? It then elicits a immunologic eosinophilic
type of reaction. Now this is usually in
a backdrop of a patient who already kinda
has an atopic type of condition. So this
might be asthma, or patient that might have
cystic fibrosis. That’s an important one
where it colonises the airway, you’re not
able to properly get rid of your organism.
It’s stuck. Obstructive, asthma, cystic
fibrosis. I don’t have my mucociliary
clearance. The histologic findings of, pay
attention, bronchocentric granulomatosis is
important. Bronchiolitis and eosinophilic
pneumonia and mucoid impaction can lead to
bronchiectasis. What does that mean to you?
Infection, foul-smelling sputum, fibrosis
and respiratory compromise. Be careful. Go
through that order, bronchocentric type of
granulomatosis, you end up destroying your
bronchioles, yet once again. Bronchiolitis
eosinophilic pneumonia. This is allergic bronchopulmonary