Now, this slide is a little bit difficult to read but we’ll go through each one individually.
We’re now talking about classic diseases associated with each organism.
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.
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.
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.
They may lie in the crib, be very floppy hence the name and more importantly,
they will be unable to eat all that vigorously.
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.
So, it’s a difference from normal which brings the baby in to see medical care.
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.
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.
Now, Clostridioides 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.
In fact, that’s all cellular debris and purulent pus.
Patients with pseudo-membranous colitis have a very foul smelling what’s called the c. diff stool.
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.
Patients with Clostridium perfringens.
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.
However, clostridium perfringens is far more classically associated
with gas gangrene, necrotizing enterocolitis, cell death.
So, patients with Clostridium perfringens may have a disruption of normal stool or intestinal barriers,
or they may have stool contamination of a wound.
Ultimately, thy develop fevers, hemorrhagic bullae, tissue necrosis,
and a very significant fowl smelling brownish discharge.
Similarly, in Necrotizing enterocolitis which as the name says is necrotizing or death of the cells lining the gut.
These patients can have abdominal pain followed by vomiting and bloody diarrhea.
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.
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.
And then, finally, Clostridium tetani/tetanus.
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.
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.
In fact, it just seems like you’re clenching down on your teeth to the point of where they might break.
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.
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.
There can be localized tetanus.
If there’s been local introduction of the tetanus toxin,
then, right near the wound, one can have twitching and spasms.
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.
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.
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.
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.
But many times when patients present with respiratory failure, it’s too late.
That binding at the nervous system motor junction has already occurred
and it is a very difficult binding to compete with, with the antitoxin.
Clostridioides difficile, 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.
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.
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.
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.
And Clostridium tetani, obviously, the best treatment is prevention,
so, having up to date vaccination with the tetanus toxoid vaccine is highly supportive.
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.
Here then with this last slide of the talk are two pictures which were equally interesting.
I suggest you maybe put them aside if you’re about to have dinner.
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.
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.
On the right slide of the slide is the patient with lockjaw as I had mentioned before and you can see that sardonic grin.
Every muscle is contracted in this patient’s face and even if you look at the neck,
you can see prominent neck musculature.
This is a patient who would be in danger of losing his respiratory drive as well.
So, one species, four different subspecies, a whole wide range of disease.
Of all of those, the one you are very likely and most likely to see will be disease related to c. diff.
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.