00:01
Now, this slide is a little bit difficult to read but we’ll
go through each one individually.
00:05
We’re now talking about classic diseases associated with
each organism.
00:10
Clostridium botulinum, the classic disease has associated
with it anything
what you could think of which is flaccid which is loss of
muscle contraction,
so, generalized weakness, typically, a descending flaccid
paralysis.
00:26
Meaning, starting here up the head and then, going down
toward the toes
which is different from some other classic neurologic
diseases such as Guillain-Barré syndrome
which is an ascending weakness but botulinum causes
descending weakness, blurred vision,
ultimately paralyzing the respiratory muscles, the
diaphragm, the intercostal muscles,
and so, the patients die from a respiratory arrest unless
they are ventilated and managed.
00:56
As we mentioned just a little bit ago, infant botulism
causes a floppy baby syndrome
and this typically will be seen by a baby several months of
life
who has been -- or has been exposed through spores to honey
or some other infected material
who then becomes less and less vigorous.
01:15
They may lie in the crib, be very floppy hence the name and
more importantly,
they will be unable to eat all that vigorously.
01:24
These are babies who may come in to the hospital with the
notice
that he just doesn’t seem to be eating properly, he just
lies there all the time
and I thought babies were supposed to be much more active.
01:36
So, it’s a difference from normal which brings the baby in
to see medical care.
01:40
And then, there can be wound associated botulism which is
very similar
to what we’ve just described for the classic form
except that it’s introduced via a wound but into the
bloodstream.
01:51
This is different from a treatment use of botulinum toxin or
Botox
into a specific area to relax a specific muscle typically to
do with some sort of plastic surgery or a facial surgery.
02:04
Now, C. difficile, this causes pseudo-membranous colitis,
why pseudo-membranous?
Because the toxins in combination poison the gut membranes,
the gut layers causing disruption of those layers and
sometimes the purulent,
instead the disease related to that is so prominent that
under visualization from an endoscope
when one does endoscopy, it looks as if there’s a whole
additional layer of gut there.
02:34
In fact, that’s all cellular debris and purulent pus.
02:39
Patients with pseudo-membranous colitis have a very foul
smelling what’s called the c. diff stool.
02:46
Nurses especially and other healthcare providers will be
able to tell you from a distance
when a patient has c. diff stool cuz it is a very prominent,
very odoriferous diarrhea.
02:58
Patients with Clostridium perfringens.
03:01
If they’re lucky, they’ll only have the enterotoxin
production from the organism
and they’ll have a food poisoning which can again be a
cholera-like watery diarrhea with a lot of abdominal cramps.
03:15
However, clostridium perfringens is far more classically
associated
with gas gangrene, necrotizing enterocolitis, cell death.
03:24
So, patients with Clostridium perfringens may have a
disruption of normal stool or intestinal barriers,
or they may have stool contamination of a wound.
03:34
Ultimately, thy develop fevers, hemorrhagic bullae, tissue
necrosis,
and a very significant fowl smelling brownish discharge.
03:45
Similarly, in Necrotizing enterocolitis which as the name
says is necrotizing or death of the cells lining the gut.
03:54
These patients can have abdominal pain followed by vomiting
and bloody diarrhea.
03:59
Typically, Necrotizing enterocolitis is seen in very young
infants
who have some sort of disruption of the normal gut barriers
but it can be introduced in immunocompromised patients or
patients
with underlying gut disorders who are older.
04:15
And then, cellulitis and fasciitis can be compromised by
many organisms
which if it includes Clostridium perfringens may develop the
gas gangrene appearance that we just described.
04:28
And then, finally, Clostridium tetani/tetanus.
04:31
Generalized tetanus typically is a gradual or a subacute
onset over about one week
and patients may present initially with sweating and
irritability
but then, they’ll develop various elements of muscle
contracture, trismus
as we’ll see in a picture at the end of this talk is sort of
a sardonic grin.
04:51
In fact it looks just like this. If you can on your own
right now
and I promise I won’t look clench every single muscle which
you have, feel how that feels,
see what it does to your face and you’ll get a sense for why
we would call tetanus locked jaw.
05:08
In fact, it just seems like you’re clenching down on your
teeth to the point of where they might break.
05:14
Patients then develop this opisthotonus, sardonic grin
and if the muscle clenching continues in complete contrast
to botulism where everything is relaxed,
here, everything is contracted but yet the still point is
respiratory failure ensues.
05:31
The diaphragm fails to work, the intercostal muscles are
completely contracted,
patients are unable to breathe and they develop what may be
called wooden chest similar
to like if your chest were made of wood, you’d have no
ability to contract and breathe.
05:45
There can be localized tetanus.
05:48
If there’s been local introduction of the tetanus toxin,
then, right near the wound, one can have twitching and
spasms.
05:56
This is perhaps an early warning indicator that the patient
needs further treatment to prevent generalization of the
tetanus
and in fact, without a whole lot of luck or without
intervention,
that patient is destined to develop generalized tetanus.
06:12
So, what do we do about all of these?
Can we do anything about all of these infections?
Again, let’s start with Clostridium botulinum. How do we
prevent it?
Well, the best thing is to prevent introduction of the spore
containing organism into foods in the first place
or if it may be present to properly treat the foods through
heating
and then, proper canning so that the spores don’t have a
chance to be developed and produced from the organism.
06:40
Then, if the patient develops botulism, then, there is an
antitoxin
to introduce an immunologically based therapy to bind out
the toxin itself
so that it has an inability to bind to its nervous system
targets.
06:57
If however the patient has already presented with
respiratory failure,
they require intubation, ventilator support, and then,
attempted
to treat the underlying source with penicillin, getting rid
of any -
a repository of the contaminated food if that’s what it is.
07:15
But many times when patients present with respiratory
failure, it’s too late.
07:21
That binding at the nervous system motor junction has
already occurred
and it is a very difficult binding to compete with, with the
antitoxin.
07:30
If the patient has developed c. difficile due to presence of
an antibiotic
which has been knocking out the normal flora, well, then,
stop that antibiotic
and hopefully, allow the normal flora to reintroduce.
07:43
Sometimes, however, that is not enough and so, we will
actually target the Clostridioides difficile itself
with an oral antibiotic or an antibiotic which is not well
absorbed,
Metronidazole, Flagyl, is one such antibiotic. However, it
is well absorbed through the gut
but in the process of being absorbed, it can actually start
to treat the underlying Clostridioides difficile infection.
08:08
Vancomycin and importantly, not intravenous Vancomycin but
oral Vancomycin
which is poorly absorbed at all meaning that it is very
present and able to treat the Clostridioides difficile
within the lumen, the interior of the gut.
08:24
And then, Bacitracin is a third antibiotic which many have
tried
but typical recommended treatment regimens start with the
course of Metronidazole
and then, if failure occurs, go straight to oral Vancomycin.
Clostridium perfringens,
wound care, wound care, wound care because once the organism
is present in a contaminated or infected wound,
the only way to get it out truly is to take it out, to
breathe the site accompanied
by a high dose penicillin to try to treat any systemic
presence of the organism.
08:57
And Clostridium tetani, obviously, the best treatment is
prevention,
so, having up to date vaccination with the tetanus toxoid
vaccine is highly supportive.
09:07
There also is passive immunization with tetanus
immunoglobulin or a passive immunomodulatory regimen
and then, along with that wound, debridement if a wound is
present,
supportive care if the patient has lost respiratory drive,
then, treatment with underlying penicillin.
09:25
Here then with this last slide of the talk are two pictures
which were equally interesting.
09:32
I suggest you maybe put them aside if you’re about to have
dinner.
09:35
On the left side is a picture of a foot with gas gangrene
from clostridium perfringens and as you can see,
there are bullae present, there’s tense edema of the foot
with some erythema
from all the edema factor which is present.
09:49
You can see copious purulence discharge from the site itself
and I guarantee you that that foot would smell quite
horribly from even quite a distance.
09:59
On the right slide of the slide is the patient with lockjaw
as I had mentioned before and you can see that sardonic
grin.
10:06
Every muscle is contracted in this patient’s face and even
if you look at the neck,
you can see prominent neck musculature.
10:14
This is a patient who would be in danger of losing his
respiratory drive as well.
10:19
So, one species, four different subspecies, a whole wide
range of disease.
10:25
Of all of those, the one you are very likely and most likely
to see will be disease related to c. diff.
10:31
I won’t show you a picture of that because once you’ve
smelled c. diff stool,
a picture is not even close to the smell which is worth
10,000 words but different diseases,
different toxins, different pathogenesis, but all quite
significant and all quite important to know.