MRSA Pneumonia Explained Clearly by | Part 1

By Adem Lewis / in , , , , , , , , , , , , , , , , , /

Wow welcome to another MedCram lecture
we’re going to talk about Mrs a infections here’s what we’re going to
cover in the next four videos a brief review of the differences between MSS a
mrs a health care required mrs a and community-acquired mr NSA will talk
about the risk factors for mrs a variance factors that typically make
community-acquired mrs a worse than hospital acquired pneumonia and will
illustrate chest x-ray and CT findings for mrs a pneumonia we’ll talk about the
clinical decision and diagnosis of mrs a will compare vancomycin and linezolid
for primary treatment options we’ll also talk about tell events and pros and cons
and how it compares with vancomycin and wide variety of agents may not be ready
for primary consideration for mrs a pneumonia we’ll also talk about specific
treatment considerations for community-acquired mrs a and finally
we’ll tie it all together and review before we talk about mrs a let’s talk a
little bit more general about infections from Staphylococcus aureus staff and
Latin means grape-like and then caucus means like a grouping so this would be
like a grape like grouping this is what it looked like under the microscope and
then aureus if you’ll notice the periodic table au is the symbol for gold
and they notice that these colonies were were gold and looking and so that’s
where we came up with Staphylococcus aureus it’s basically a very
opportunistic bacteria it likes to invade likes to go in and it can cause
some very bad infections specifically in the skin but also in the lungs and
there’s two major types or branches of Staphylococcus aureus two major types of
infections and it has to do with the antibiotics that we use for a
Staphylococcus aureus in both situations of course it’s a Staphylococcus aureus
it will have a sa but the antibiotic specifically that we use as a litmus
test to find out whether or not this staph aureus of is one type or another
it’s something called methicillin otherwise can be used as oxacillin
methicillin is the one that we use so the ones that are sensitive to
methicillin are called methicillin sensitive Staphylococcus aureus and the
ones that are resistant are called methicillin-resistant Staphylococcus
aureus so we have MSS a specifically and Mrs a obviously Mrs a is not sensitive
to methicillin and as a result of that there’s a whole class of antibiotics
which can’t be used against it it’s resistant to it it does nothing for it
and the patient gets worse and this can be seen in a number of different
situations so methicillin sensitive basically you can use a wide variety of
different antibiotics mr sa is also likewise divided into two groups which
you may not be aware of there are actually two types of mrs a one of them
is known as the healthcare acquired M R s a and the other one is known as the
community-acquired M R s a and as it turns out the community acquired mr sa
is very very variant we’ll talk about that a little bit in just a bit the
hospital acquired or healthcare acquired mr sa is the ones that we typically see
in the hospital but there’s been more of a blurring and we’ll talk a little bit
more about that so just be aware that there’s a healthcare associated mr sa
and there is a community acquired mr sa both of these are resistant to
methicillin of course and then there’s methicillin sensitive we’re going to
talk a little bit about the epidemiology we’ll talk about the clinical features
specifically as it relates to pneumonia and I’ll talk about the treatment and
the treatment options that we have today for this ok so we’re going to talk about
Mrs a just in general Mrs a has been described all the way
back to the 1960s and what they noticed is that this strain of staphylococcus
aureus was resistant to methicillin that’s how it got its term mr sa this
incidence since the 1960s has definitely increased without a question and in fact
to the point now if you would take a look at all the
different types of strains for instance in an intensive care unit about 60
percent of the staff of coccus aureus is M RSA and this is this is growing and
that accounts for about 90,000 infections per year so that’s pretty
significant now how does this work there’s something called penicillin
binding proteins so penicillin binding proteins specifically the penicillin
binding protein 2a is coded by the gene you may see this the MEC a gene and this
MEC a gene which can be you know shared around to different types of staph
aureus they can all get this penicillin binding protein which basically in
activates methicillin so that methicillin doesn’t work so it all boils
down to this penicillin binding protein to a coda for by the MEC a gene and this
is a mobile genetic elements for two bacteria that don’t normally have this
ability to be resistant to methicillin so you can get new generations it can be
transferred and so this is a real problem because if we have a lot of this
going around we get more and more antibiotic resistance so that’s M RSA
let’s talk a little bit about the different types of M R say that we
alluded to earlier okay so there’s the healthcare acquired mr si let’s talk
about that one first the thing that you’ve got to know about these two
different types is that they were identified based on the risk factors and
in the environment in which they were found and so they’re named for their
history and so you can see that the healthcare acquired mr si was a
particular strain of mr sa that was seen in hospitalizations and so typically we
would see these in people who have been in the hospital for greater than 48
hours or within 12 months of being in the hospital if they came in from the
outside so in other words these were people that were discharged to a
healthcare facility or they came back into the hospital but have been just
recently hospitalized or in a nursing of some sort or they were in the
hospital and this happened two or three four or five days after they were
hospitalized now this has been increasing in prevalence since oh the
1980s 1990s once it got to around the 2000s 2010 the prevalence started to
even out maybe even go down a little bit and we’ll talk about why and I can
allude to that the community-acquired amorous a started to increase in terms
of that if you word however to compare Mrs a to M s sa okay especially this
healthcare acquired mr saye the healthcare acquired mr sa had patients
that had increased length of stays in the hospital increased mortality that’s
comparing it to the MS SA and this makes sense right because if you have someone
with MS si you’re going to generally speaking select the right antibiotic up
front even if you’re giving them like Rocephin or ampicillin or something like
that there’s a good chance especially if you’re using one of these
second-generation penicillins like methicillin etc that you’re going
to hit the MS sa with Mrs a unless you’re using Vanko in these situations
or other antibiotics that we’ll talk about later you’re not going to get and
therefore mortality is going to go up especially if it’s a very severe
infection okay let’s talk about CA Mrs a and I think we’re going to get into this
a little bit later but the two big areas and this is the biggest one that this
was seen was in the skin and the soft tissue this was pretty big about in the
early 2000s mid 2000s what was happening was is that they were starting to see in
high schools and colleges that gym equipment football equipment were
getting colonized with this type of CA Mrs a and these students were coming
down with horrible mrs a infections that were a lot more difficult to treat than
the type of infections that they were seeing in the hospital this was also
seen in intravenous drug users so in the 1980s we’re also getting these
types of infections and why was it that the community-acquired in other words
the strain of mr sa that was seen in the community why was it acting so different
well it’s because of this thing called the the pant on Valentine factor and
this is a very lends factor I don’t want to get too much into it but there was
also causing leukocidin toxins and there’s different antibiotics that could
make the toxins worse and there’s other antibiotics that could make it better
there’s still some argumentation about which type of antibiotic is better for
this the bottom line that you need to know is that the type of strain of mr sa
that was seen in the community and is actually increasing and in fact
overtaking this strain that was seen in the hospital is very very variant and
very aggressive difficult to treat and has a increased mortality the other
thing that you can see especially if this causes a pneumonia is you get a
severe necrotizing pneumonia that sometimes the only way you can make them
better is to surgically remove that portion of the lung so the thing is is
that because these strains were first identified this one here in the
community and this one here in the hospital we kind of looked at this
differently you know if the mr sa is coming from the hospital is generally
going to be a hospital-acquired mr sa and of course if it’s coming from the
community we got to be concerned that it’s a much more aggressive and very
lended community acquired mr sa the fact of the matter is now is we’re starting
to see a blurring of these two types so in other words we could actually see
this strain occurring in the hospital setting and we could see this strain
occurring in the community setting and so it’s very important to look at the
types of strains and see how the behavior of this of this bacteria is
let’s talk about risk factors what are the risk factors that you’ve got to look
for in page specifically to be worried about mr
essay in general so let’s talk about these risk factors and they kind of go
for both of course the most obvious is going to be you know previous antibiotic
use because we know that this causes resistance specifically cephalosporins
which is kind of scary because we use that all the time and community acquired
pneumonia but the one that is associated the most is fluoroquinolones like
levaquin let’s just say in general it’s fluoroquinolones and that one is
big-time associated and we use that all the time in community acquired pneumonia
the other one is HIV and this specifically goes for the community
acquired em RSA believe it or not things that wouldn’t surprise you
hemodialysis catheters these are catheters that are left in place they
get em RSA all the time long-term acute care facilities or sub
acute care facilities obviously this is going to be big time if there’s
colonization or there’s contact in other words very poor hand-washing then that
goes along with the environment again risk factors antibiotics HIV
hemodialysis casts so catheters these Quinton catheters long-term acute care
facilities colonization contact environment so I think you’ve know and
understand a little bit about what Mrs a is where it comes from it’s basically
staph aureus it’s basically a resistant strain you know what the protein is it’s
a penicillin binding protein it comes from the MEK a gene there are different
variants factors which makes community-acquired mrs a much worse than
the run-of-the-mill hospital-acquired pneumonia in fact let’s look at a
survival curve and I’ll distinguish that that’ll make it very clear between these
two okay so let’s draw a graph here let’s look at survival
so on this we’re looking at survival and here we’re looking at days post
admission and let’s say in the blue we’re going to look at those that are
the pant on Valentine leuco side and toxin negative so that would be like
your basically your hospital-acquired m RSA and then we can also look at the
yellow which is the pant on valentine leukocidin toxin positive
community-acquired mrs a so in terms of that the survival was pretty poor
basically going down here and lever leveling out at about 30% whereas the
survival for the hospital-acquired one and again this is kind of blurring was a
little bit more like this in terms of the survival as you can see here in this
situation you can see clearly that the survival is much worse in the community
acquired one because of that that toxin so next let’s talk a little bit of some
of the manifestations of mrs a pneumonia and staff pneumonia particularly and and
what we could see you

8 thoughts on “MRSA Pneumonia Explained Clearly by | Part 1

  1. See videos 2 through 4 of the MRSA Pneumonia series at
    Includes quizzes after each video

  2. thanks for the video- I'm not in med school, I'm an engineer/programmer, but i survived MRSA (cavitary) pneumonia (as well as going fully septic with it + the legions on the skin, almost lost my arm & foot), was treated w/vanco… just trying to understand what happened to me on a deeper level since my doctors don't explain it at a detail level that I want.

  3. Can this be acquired by dental surgery (removal of wisdom teeth)? My sister in law, currently staying in my home (but has been in hospital for about 2 days now due to blood poisoning & just diagnosed with an internal version of MRSA [?] & some sort of severe issue with her heart as well, requiring heart surgery). She had her wisdom teeth removed a few weeks ago. She'd been getting sicker & sicker, but finally taken to hospital against her will.

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