Ep. 55 – Superbugs & Smart Treatments Podcast

All right, welcome back to The Equine Vet Connect Podcast.

 

Here at Countryside Equine Hospital.

 

Dr. Caitlyn’s back with us today.

 

Great topic.

 

Yeah.

 

I think it’s coming up more and more.

 

Definitely something we discuss a lot.

 

Something we are concerned about every day.

 

And really true, I think this is something that every one of our listeners needs to be concerned about.

 

Yes.

 

More than just from your animal, but just life in general.

 

It affects us too.

 

Yes.

 

So we’re going to talk about antibiotic resistance today.

 

Yes, we are.

 

It’s kind of a cool topic.

 

Yeah.

 

So one of the things I found interesting is, do you know the history behind the first antibiotic?

 

Yes.

 

Yeah.

 

Penicillin.

 

Penicillin.

 

Now that you asked me, I’m going to forget all of it, but I am familiar.

 

Yes.

 

It was actually a German invention.

 

And they smuggled the spores that grew penicillin out of Germany.

 

The scientists that figured this out actually had those spores covering his jacket, his like suit jacket.

 

Oh.

 

And they flew him out.

 

He already escaped the country with only the clothes on his back.

 

The penicillin spores were actually in his jacket.

 

See, I didn’t know all of this.

 

This is why you needed to tell the story because you know a lot more than I do.

 

Yes.

 

And so they got him out of Germany, then smuggled him out of Europe to the US.

 

And he brought these spores that he’d been researching to the US.

 

And this was the birth of penicillin.

 

Pretty cool history.

 

Yeah, it is.

 

It’s recent.

 

Yeah.

 

Antibiotics are not, in the grand scheme of things, as far as like, you know, Eastern medicine and everything, like they’re very new.

 

Very.

 

Yeah.

 

And the downside is, bacteria have been around forever.

 

Oh, yeah.

 

And these guys have been living and thriving, doing well forever.

 

Yeah, literally since the dawn of time.

 

Yes.

 

Yeah.

 

When you look for, like, when people look for, or scientists look for signs of life on other planets, they’re looking for bacteria and those teeny tiny little organisms that are simple, but they, you know, they evolve and they change to adapt to their environment and survive.

 

And they’ve survived for millions of years doing this.

 

They adapt incredibly rapidly, incredibly well.

 

But you’re dealing with something that’s got a generation life cycle of like 24 hours.

 

Right.

 

These things, they learn.

 

Yes.

 

These little bitty guys, they learn.

 

Because I mean, you think about it you can find bacteria in Antarctica where it’s like zero.

 

In the ice caps, yeah.

 

You can find them in the little hot pots, hot in Yellowstone.

 

That’s part of the way that they date when they do like the ice sampling, the core sampling, is they look at the bacteria that’s in there and they, that’s how they help date things and like they’re just, they’re just, they’re living everywhere.

 

Yes, they’re everywhere.

 

They learn how to adapt, which is cool.

 

But downside, since we invented antibiotics, as soon as we came up with a way to fight them, they started fighting back.

 

Correct.

 

And so, antibiotic resistance is real.

 

It is.

 

It is.

 

Absolutely.

 

I remember I got excited when we decided we were going to talk about this, because I am a nerd, but also I remember, this has stayed with me since undergrad.

 

I was in my microbiology class and one of the first days in lecture, they posted this video or they started playing this video and it’s a giant agar gel plate essentially, which is how we plate bacteria and things.

 

And they did on each end, there was no antibiotic, and then each there was like each section, they would increase the concentration of the antibiotic tenfold.

 

And so they did like a time lapse of it.

 

And so they plated this bacteria on each end.

 

And you can physically watch the bacteria, they grow, grow, grow till they get to the next segment.

 

And then they pause.

 

And then you can see a couple offshoots that start to grow because they’ve made changes and they’ve adapted.

 

And then they reproduce and it spreads, spreads, spreads till they get to the next one.

 

And then they pause.

 

And the same thing.

 

And it is so interesting because you can physically see it.

 

Because like you said, these things are reproducing, you know, every 24 hours.

 

And so they, you could physically see them adapt and overcome each concentration of antibiotics.

 

And then they went through and they mapped and basically figured out, you know, how many different strains there now were.

 

And all these things, like, we’ll have to link it.

 

It’s really interesting.

 

That’s really cool.

 

Yeah.

 

And it’s stayed with me ever since.

 

Like it’s embedded in my brain and I will not forget it because it’s real.

 

Like you can see it in real time happening.

 

And that’s just with one antibiotic at different concentrations.

 

That’s not even introducing other antibiotics that they can then adapt to.

 

So it’s cool.

 

It’s really interesting.

 

It’s really cool.

 

I’m like you, I’m a nerd.

 

So the whole microbiology thing was pretty fascinating to me.

 

It is.

 

And that’s, you know, a lot of what we’re dealing with, I’d probably say 50% of the cases that we’re dealing with in VetMed are going to involve some type of an antibiotic.

 

This is a commonly used thing.

 

And our generation, antibiotics have always been around.

 

We’ve always been developing new ones.

 

We’re always like, oh, don’t worry about it.

 

We got another antibiotic.

 

But if you look, the number of antibiotics that are coming on the market now versus what, you know, we started out with penicillin.

 

That one’s rocking on for a long time.

 

And then we started developing the macrolides.

 

We started developing the aminoglycosides, the cephalosporins.

 

I mean, we were just cranking new antibiotics.

 

If you look, that’s slowing down because we’re getting less and less ways to develop these antibiotics.

 

I mean, we’re still looking for, we’re always looking for new ones.

 

But scientists are having to work harder and harder to come up with new ways to kill these guys.

 

Yeah, there’s only so many ways that you can slow them down or kill them without harming the host.

 

Right.

 

So you have to, you know, there’s a lot of science that goes into understanding, you know, the bacteria and the cell cycle and all of those things.

 

But yeah, it’s slowing way down.

 

So our options are limited.

 

And in human medicine, you know, you have even more options.

 

But in veterinary medicine, our options are limited even more because we don’t have access to or shouldn’t have access to all of those that we use for human medicine.

 

So one of the things we have to really worry about in horses, if you want to talk about a class of medications that can have a profound effect.

 

Oh, yeah, it’s the antibiotic in horses because you have to be very careful when choosing antibiotics because some of these antibiotics can induce and that they can have an antibiotic induced colitis, which is this very severe diarrhea.

 

We used to call it colitis X, and we found out, no, that was the antibiotic we gave them.

 

Yeah.

 

And basically, it can kill off all the bugs in the GI track that keep this GI track functioning.

 

And so we have to be very careful, especially in equine med, on our antibiotic choices.

 

Right.

 

Because some of these, great, we killed the infection.

 

But we also.

 

But we just killed the host.

 

Yes.

 

Because like we talked about, bacteria living everywhere, I mean, they are commensals.

 

Like they are in your skin, they are in your gut, they are everywhere.

 

There’s areas in the body that are sterile that don’t have bacteria.

 

But a lot of the, a lot of big sections of the body do have bacteria, and they have a function there.

 

They help us, you know, we have a symbiotic relationship with these guys.

 

And so if we kill them off, that’s not good.

 

There’s been a lot of research in the human realm now about, you know, your gut microbiome and all the things, and how it really affects, you know, a lot of things in your physiology.

 

And it’s true, but the same is said for horses.

 

And if we kill them off, because we are not judicious with our antibiotic choices, we’re going to have a bad day.

 

Yes.

 

Yeah.

 

And out of that, we’ve developed newer techniques, which we’ll get into to help overcome the resistance.

 

And talk about a little bit, you know, proper selection.

 

You know, there’s a lot of things that go into how can we get as close as possible.

 

Because if an infection is resistant to an antimicrobial, and that’s the one we use, we will continue to make a resistant population, can actually make the population even more resistant.

 

Because they see it, it doesn’t kill them.

 

They’re like, oh, we just got stronger.

 

Right.

 

Yeah.

 

And the only ones that it doesn’t kill, those that figured out how to survive.

 

So we kill off the ones we can, and then we’re left with these super bugs that we can’t kill.

 

Correct.

 

So this is a very important thing to make sure we hit on the correct antibiotic.

 

Yeah.

 

So we’ve gotten excited.

 

But so antibiotic resistance is, or antimicrobial resistance is the ability for bacteria to fight off or resist being killed or slowed down by our antibiotic of choice.

 

There’s lots of different ways that bacteria, basically once one bacteria in a population develops this ability or develops these genes, there’s lots of different ways that then it can spread to other bacteria.

 

One of those is vertical transmission.

 

So when it sexually reproduces and transfers genes, just like your mom transferred genes to you.

 

But the other one that bacteria do is called horizontal gene transfer, and it’s very interesting.

 

There’s one way that one bacteria will form what’s called a pilus.

 

A pilus?

 

I don’t ever say that right.

 

Pilis.

 

Yeah.

 

It’s basically like a little hair-like projection that it shoots out, and it pokes them into another bacteria, and then they shoot genetic material called a plasmid across this little highway, and then it gets into the other bacteria, and it integrates itself into the DNA, and then that new cell or that new bacteria now has the genes as well.

 

It can do that.

 

There’s these really cool things.

 

I’m like seeing all this microbiology stuff in my brain, and it’s like a little movie.

 

It’s just so cool.

 

There’s this thing called a bacteriophage, which is a virus that can infect one bacteria and basically suck up its genetic material.

 

And if it has resistance to genes, then it goes and it infects another bacteria, and it injects it.

 

Like, that’s the whole thing.

 

It’s like a sci-fi movie.

 

It’s crazy.

 

The other one is if a bacteria dies or like explodes or something, and there’s just genetic material floating around, other bacteria can just like pick it up and just integrate it in.

 

Yeah.

 

Yeah.

 

It’s like a battlefield pick up.

 

Yeah.

 

You lost your weapon.

 

Oh, I’ll take your weapon.

 

Right.

 

You get a better weapon than I do.

 

I’ll go fight.

 

Yeah.

 

And so then they incorporate all of this genetic material with, and it may have resistance genes.

 

It may not.

 

It’s luck of the draw.

 

But they’re changing and adapting so quickly.

 

That’s how this happens as quickly as it does.

 

Well, this isn’t happening over years.

 

This is happening in days.

 

Oh yeah.

 

This is like as this infection is going, all these things can be happening.

 

Yeah.

 

And every like nidus of infection is different.

 

So every like bacteria also do this thing called a biofilm, which is where they basically coat themselves in this slime and they make an environment that is suitable for them.

 

But even within that little biofilm, there’s different areas, like one might have a lower area of oxygen, one might have a higher area of oxygen, one might have, you know, different, it’s just little different mini environments within that environment.

 

But that biofilm is different than the biofilm on the horse across the stall.

 

Like so every infection is different and they all can have different changes in different genetic material.

 

And it’s just, it’s a whole thing.

 

It is really cool.

 

Yeah.

 

And it is, I think the, when you’re talking about the plasma transfer, that’s my favorite.

 

It’s like looking over, seeing your buddy like, oh, you’re going to need what I got.

 

Here you go.

 

I’m going to shoot you.

 

Have this plasmon.

 

Here you go, have a plasmon.

 

Yeah, it’s crazy.

 

Yeah.

 

And there, I was reading about it and they’re finding a lot of other ways that there’s transmissible genetic elements basically, which is what they’re called, that they can transfer them lots of other ways too.

 

And it’s just like, they are just living in their own little universe doing their thing.

 

Well, and forever we thought the way this worked was we just have the bacteria that survive.

 

Well, then they reproduce.

 

But then we found out like, no, no, no, they’re teaming up.

 

It’s like all bacteria are friends.

 

So here, have some of my stuff.

 

Yeah.

 

And that’s been the cool thing when they start typing out these genomes and actually looking at the DNA sequences and watching these things get passed.

 

I mean, if you’re a nerd, this is, this is like right up there.

 

It’s legit.

 

Like it is, when I say it’s like a sci-fi movie, I’m not kidding.

 

Like it’s, if you look up some of the like animations that they’ve done on this stuff, it looks, it’s bizarre, but it happens.

 

And it’s so real.

 

And it’s been happening for millions of years.

 

Yes.

 

It’s so cool.

 

Yeah.

 

So our little, you know, we come up with these anti-microbials and they’re like, oh man, we’ve been fighting this forever.

 

Like, come on, let’s do this.

 

Yeah.

 

I mean, they go after it.

 

So, you know, I think the biggest thing we’re looking at this is, when we’re attacking an infection, we have to always keep in the back of our mind anti-microbial resistance.

 

And this is why when people call in, they’re like, oh, I just need an antibiotic.

 

I just need this.

 

I just need it.

 

It’s just an antibiotic.

 

Do you?

 

It’s not just an antibiotic.

 

Correct.

 

There’s times and a place to use them.

 

And then there’s a lot of things that go into which antibiotic we’re going to pick.

 

Yeah.

 

Knowing what types and knowing what type of bacterial infection you’re dealing with.

 

We do a lot of cytologies here.

 

We’re actually looking at them.

 

Are we dealing with cocci?

 

Are we dealing with rods?

 

And then the greatest separator of bacteria is Gram-negative and Gram-positive.

 

If you go all the way back to that first biology class you took in grade school, you’re looking through the microscope.

 

Are they blue or are they red?

 

Well, Dan doesn’t know.

 

I don’t know.

 

Every time I do a Gram scan, somebody tells me, is this blue or red?

 

How did you get through HISTO?

 

You get really good at cell architecture.

 

I guess.

 

You get really good.

 

So when I took HISTO, that was my freshman year of vet school.

 

I never thought about that with you being colorblind.

 

I was terrified they’d find out.

 

You didn’t know?

 

No, I knew I was.

 

Yeah, but they didn’t know?

 

Well, no, because I thought if they found out, they would kick me out of vet school.

 

No, they would help you.

 

Well, I didn’t want them to know that.

 

Oh my gosh.

 

My other thought was, if I’m going to go do this, color is important.

 

You’re going to have to figure it out.

 

I got to figure it out.

 

Yeah.

 

So I mean, I can memorize.

 

Like, you tell me what color a tube is, I can tell you the anticoagulant in the Senate.

 

I mean, yeah.

 

I memorized them all.

 

I got to Histo.

 

I figured out, like, I can’t tell.

 

Like, when they start talking about the purple versus this, I couldn’t tell that, but I can be like, oh, I can see that structure.

 

That looks like an eosinophil.

 

I can’t tell that it’s bright pink, but it looks like an eosinophil.

 

That’s an eosinophil.

 

It’s all lobulated.

 

I can tell you.

 

Oh, man.

 

I can look at the nucleus and give you an idea what kind of cell it is.

 

That would be awful.

 

See, but you missed out because Histo, some of the most beautiful slides.

 

You know, maybe I did, maybe I didn’t.

 

Oh, man.

 

I had a great time.

 

Okay.

 

Anyway, but yeah, that’s how I got through.

 

Gram positive versus gram negative.

 

We digress.

 

Gram positive versus gram negative.

 

So that’s our first differentiation.

 

And that’s one of the things that we get younger vets in.

 

I can’t believe I’m starting to be the old guy now.

 

I always tell them like, if you got an infection, because it’s three to five days to get the culture back.

 

Yeah.

 

If you just look at the cytology, and you figure out cocci versus rods, then you run a gram stain.

 

Gram negative versus gram positive.

 

You can narrow your choice down a lot.

 

Yeah.

 

Because then you don’t have to go grab the biggest, baddest guy in the fight.

 

Right.

 

You got a bunch of gram negative rods, grab an amino glycoside.

 

Yeah.

 

Maybe you don’t need to go with one, like a, like a, a baytril.

 

Maybe you can do just a genomycin.

 

So when we talk about antibiotics, we make different choices because antibiotics come in several different classes.

 

Like we’ve talked about, you know, your amino glycosides, floroquinolones, macrolides, the cephalosporins, all of those things.

 

The next thing is, is it bactericidal or bacteriostatic?

 

So does it kill the bacteria or does it slow it down?

 

Is it time dependent or concentration dependent?

 

How does it work?

 

Does it work on the ribosome?

 

Does it work on, you know, there’s lots of different ways that antibiotics actually work on those bacteria.

 

But then what class of bacteria does it actually, like what’s the spectrum is what we call it.

 

So is it broad spectrum?

 

Is it more of a narrow spectrum?

 

Does it work on aerobes or versus anaerobes?

 

Does it work on gram positives, gram negatives?

 

Like all of these things go into it.

 

And so if we know what bacteria we’re dealing with or what population of bacteria we’re dealing with, then we can look at all of our choices and make a better choice, make a more narrow targeted choice.

 

And then the other one you deal with too is where’s the infection at?

 

Certain antibiotics penetrate other places better than others.

 

You could have the right antibiotic, but if it doesn’t like to go that structure, then like we know like cephalosporins love the lungs.

 

They love to go to the lungs.

 

So that’s a great one to use.

 

We know like chloramphenicol, for whatever reason, it loves to go into bones.

 

So that gives us an idea like based on our infection, these are actually all the things that are going through your vet’s mind when we go to treat infection.

 

That whole list that Caitlyn just ran down, we’re gonna go through every one of those.

 

Now, I mean, we may just be standing there staring at it for a minute, and you’re like, they’re just looking at it.

 

They’re just buffering.

 

No, we’re going through this mental checklist in our head, do, do, do, do, do, do, do, what’s my initial choice?

 

Right.

 

And then we factor antimicrobial resistance into it, and we say, okay, is this the right choice?

 

Is it going to contribute to your resistance because it may not work?

 

Or do we want to pick a lower tier because we might not need to go for the big guns?

 

We might be able to knock this out with some soap and water and decontamination, and then come in with a lower tier antibiotic and proper wound care and all of these things if it’s a wound.

 

There’s a lot of other things that we can do other than just antibiotics to manage these things as well.

 

Because that’s one of the things like dealing with horses, you have to be very careful and we try to minimize our use because of the fear of a colitis and then also we’re limited in what we have.

 

So these are very important steps we have to take.

 

Yeah.

 

When people call in and they’re like, oh, well, I just put it on some SMZs.

 

I’m like, oh.

 

And then the other thing is, so the things that go into antibiotic resistance is overuse and misuse of antibiotics.

 

Yes.

 

So underdosing antibiotics, so not giving them the proper dose for the size of the animal or for the proper course of treatment, so how long you’re treating them.

 

Those can both contribute to antibiotic resistance as well, because you are, if you’re underdosing, you’re essentially, you know, you’re exposing that population of bacteria to a lesser degree than they’re supposed to see.

 

And so it’s not going to kill off everything.

 

And then, like you said, you’re going to breed more resistant bacteria.

 

That’s why your doctor and your veterinarian both, when we tell you, like, we need you to finish the course.

 

We mean it.

 

Yes.

 

You’re going to look, the horse may look better in 48 hours.

 

That’s not when we stop.

 

If we said seven days, go the seven days.

 

Treat past resolution of clinical signs.

 

Yes.

 

Yes.

 

Do not ease up.

 

Do not quit.

 

Correct.

 

You have to keep going.

 

Yeah.

 

This is one of the biggest things for stopping, or trying to minimize the chance of resistant infections.

 

Yeah.

 

Which is why I really don’t like just handing out antibiotics everywhere, because, again, right dosage, right length of time, right antibiotic.

 

You want to have bute and banamine on hand, or different topicals on hand for things to happen?

 

Sure.

 

But we don’t just willy-nilly give out antibiotics anymore because we can’t.

 

I mean, several years ago, like the Veterinary Feed Directive came out for food animals and changed how we prescribe antibiotics to food producing species because of this.

 

Well, you’ve got to remember, this isn’t just about animal safety, but this is about yours as well.

 

These bacteria aren’t limited to just people or just animals.

 

Bacteria can leave animals and go to people, so we don’t need to be-

 

And vice versa.

 

Right.

 

Yeah.

 

We don’t need to be creating superbugs in animals.

 

That can then infect people.

 

Because you talk about, like, so hospital-acquired infections, like MRSA in people, so multi-drug-resistant Staphylococcus aureus is what MRSA stands for.

 

That is a superbug.

 

And when people get it, it’s scary, because we don’t have, we can’t treat it anymore.

 

Because this bug has seen, or this bacteria has seen, so many antibiotics in a hospital setting and so many disinfectants that it has become multi-drug-resistant and it’s, I mean, it is a serious thing.

 

CDC spends a lot of time trying to figure out what to do about these multi-drug-resistant strains.

 

And it’s not just MRSA anymore.

 

Yeah.

 

It’s E coli.

 

Yeah.

 

The Salmonella’s, they’re getting good at this.

 

And that’s the other reason, you know, I hate going to a human hospital.

 

I just do, but, ugh.

 

We always say, you know, a hospital is no place for a healthy horse.

 

No.

 

Because it’s not.

 

You know, we keep everything clean, and we do all these things, but, you know, the longer a horse stays here that doesn’t need to be here, or humans stay in a hospital that don’t really need to be in a hospital, their chance of picking up a hospital-acquired infection goes up.

 

And so we don’t want to do that.

 

The World Health Organization said that antimicrobial resistance is in the top 10, like top 10 global problems facing public health now.

 

It’s, it’s, it’s real.

 

Yes.

 

Yeah.

 

And it’s interesting because if you go look, they’ve done some work in like third world countries.

 

Their risk of hospital-acquired infection is actually much lower than here in the first world.

 

Because the first world, we’ve been cranking out these antibiotics and had access to them willy-nilly, been able to do whatever we wanted to do.

 

We’ve been growing this population of superbugs.

 

Other places that have not been as aggressive with antimicrobial use, whether it be from an access standpoint, their risk is much lower because they have not bred these superbugs.

 

And first world, we’ve done a great job breeding superbugs.

 

That’s what we’ve done best.

 

Yeah, and things that we can do as far as, like I said earlier about not just reaching for antibiotics, but cleanliness is huge.

 

Like, you decontaminate before you use your antibiotics.

 

Like, you get rid of as much bacteria as you possibly can before you reach for that next step.

 

There’s lots of, like, dilution is the solution to pollution, as we always say.

 

Just getting as much out as you possibly can so that you have a smaller population that you then have to work on is helpful too.

 

But yeah, it’s really serious.

 

I mean, they’ve said in the next couple of decades, we’re going to be very limited on what antibiotics we actually have available to us that still work.

 

And that’s scary.

 

Well, and that’s where that kind of leads into our next topic is, how do you make these decisions?

 

The gold standard is now, and I think will continue to be the culture and sensitivity.

 

We grow these bacteria, we type them.

 

We actually do antibiotic trials to see what they’re sensitive to and what they’re not.

 

And we get that report back and we know what we’re dealing with.

 

And it’s been kind of interesting because now, with PCR, we’re doing this faster.

 

Because they’re able to go in and genetically type these plasmids we talked about.

 

And they’re like, we see this gene is going to be resistant to these antimicrobials.

 

I actually was looking into, when I was digging into this years ago, we’re looking at bringing culture and sensitivity that’s in house.

 

There’s actually a QTPCR machine that can crank out a lot of this data in as little as six hours.

 

Yeah.

 

Six hours, we can identify what bacteria it is.

 

Yeah.

 

And then also identify likelihood of resistance to certain antibiotics.

 

The gold standard will always be the little disk or the little dilution wells to know like, all right.

 

This is where we’re at.

 

Yeah.

 

This one killed it.

 

Nope.

 

This one’s growing a lot.

 

Great.

 

We got genomycin in this well.

 

Yeah.

 

It killed the infection.

 

We got the ceftiofur in this one.

 

It was happy as a clam and grew well.

 

Don’t use that one.

 

Don’t use that one.

 

So that will always be the gold standard.

 

And we may, this is why we always make the caveat, if we do culture something, we may still start them on antibiotic that day, day one.

 

But we’ll say, when we get this culture and sensitivity back, we might have to change course.

 

And that’s okay.

 

We’re still going to make an educated decision on our first choice antibiotic.

 

But based on the culture, we might have to go to something else.

 

But we’re going to do that.

 

We’re not going to change three times because you’re just guessing at that point.

 

Well, I like to say that the first one’s called, we take a SWAG at it.

 

You know what swag stands for?

 

That’s a scientific wild ass guess.

 

So we’re going to take a swag at this thing.

 

We’re going to use all the knowledge we’ve got.

 

We’re going to make the best decision we can.

 

And that first antibiotic we go to, it is a guess.

 

Oh man.

 

But it’s like, we like to narrow it down.

 

It’s a scientific guess.

 

It’s a scientific one.

 

But then we’re going to…

 

We need to make that a bumper sticker.

 

You know, swag.

 

Take swag at it.

 

So, but we’re going to get that culture.

 

We’re going to send it out to the lab.

 

We’re going to get it to grow.

 

They’re going to report back to us.

 

You know, and that’s like one of the things we’re always looking at.

 

What’s the fastest way we can get that back?

 

We pick a lot of our lab choices on how fast we can get that result back.

 

I’m like running back into the clinic with my swab, like send it!

 

Can we get this out UPS now?

 

Can they come right here, right this second, please?

 

Yes, let’s get this lab today.

 

Yeah, I’m like checking in the office every day.

 

I’m like, has it come in yet?

 

Has it come in yet?

 

Because that’s, when you have that, we get a report back and it’s going to tell us what they’re resistant to, what they’re sensitive to.

 

But then we’re going to start, that’s when the next step comes in.

 

It’s like, okay, where is this infection?

 

What’s the best delivery route for this medication?

 

Which one of these?

 

I’ve got four drugs that it’s sensitive to.

 

Why don’t you just don’t pick one based on?

 

Oh yeah, I didn’t even talk about that, like route of administration and will they take it?

 

And can we get it and how expensive is it?

 

Oh yeah, all that.

 

We look through and then that’s when the next round of decisions.

 

Sometimes it comes in, you got a whole bunch of R’s, which stands for resistance.

 

And you’re like, oh crap.

 

And you got one S and you’re like, this is where we’re at.

 

Yeah.

 

We got one S, one sensitive.

 

Yeah.

 

So.

 

That’s a multi-drug-resistant bacteria, so.

 

So getting that culture and sensitivity.

 

Again, it goes back, you’ve heard this on this podcast a hundred times.

 

And like, if you can, if you learn anything from this podcast, one, the most expensive medication is one that doesn’t work.

 

Correct.

 

Two, get an accurate diagnosis.

 

Correct.

 

Like narrow your target down to where you can hit what you’re aiming at.

 

And that’s what that culture helps us do.

 

Yeah.

 

And we’re not using, we’re not supposed to use antibiotics as a preventative either.

 

No.

 

You, unless there’s active infection there, you’re not supposed to reach for antibiotics.

 

You’re not supposed to, you’re not going to look at something and be like, oh, that looks like it could be kind of scary.

 

Like if it’s not scary, don’t touch it.

 

No, minimize your use.

 

Yeah.

 

And that culture and sensitivity is what really helps.

 

And it’s kind of interesting when we talk about, when you’re looking at a lot of these cultures, is a lot of the older antibiotics that have fallen out of favor, that we quit using, and it’s been 10 or 15 years since they were mainstream.

 

What we’re starting to see now is those older antibiotics that they’re resistant to, because we’ve thrown so many new things at them, they’ve lost their resistance to some of these older antibiotics.

 

They’re starting to work again.

 

Yes.

 

Some of those first-generation cephalosporins that we had resistance to, now they’re actually working again.

 

Some of the tetracyclines, I mean, tetracycline, everything was resistant to tetracycline.

 

Well, now it’s actually coming back and working quite well.

 

So it’s interesting, again, how fast they develop.

 

But that’s why that culture and sensitivity is so important, because one that you may not typically reach for, that may be the one that fixes our problem.

 

Mm-hmm.

 

Even within the same class, like I’ve had one that it was resistant to enterofloxacin but susceptible to marbofloxacin.

 

So it’s in the same class.

 

But I was like, okay, well, obviously, I have to go for the marbo, which is not one that we typically use.

 

But I’m like, okay, well, it works.

 

And some of the things we do is different techniques of administration allow us to overcome some of this resistance as well.

 

One of them can be just topical use.

 

We have this problem right here.

 

We may use a topical antibiotic.

 

We may mix that antibiotic with something else like a tricide, because you can do what’s called a biofilm assay now.

 

If you’re doing these biofilms, you can do this biofilm assay.

 

What that is, is we can combine that antibiotic with something like a peroxide.

 

We can combine it with a tricide.

 

And that allows us to overcome some of those resistance mechanisms.

 

Break that biofilm down.

 

Right.

 

Yeah.

 

And so, if you’re dealing with some of these multi-drug resistance, a lot of times I’ll have them do that biofilm assay, because that will, that gives me a clue like, okay, yeah, we’ve got a bunch of resistance, but turns out if I’ll mix this with peroxide and use it topically, I’ll get rid of the infection.

 

Very common in the reproduction world.

 

We’re treating uterine infections.

 

So, there’s different things we can do to actually modify these antibiotics so they would do work better.

 

Yeah.

 

Yeah.

 

But the only way we’re gonna know that, culture and sensitivity, biofilm assays, get it to the nerds, let them help us.

 

Yeah.

 

Because there’s, it’s not just the genes, and there’s lots of other mechanisms, physical mechanisms that bacteria use to fight off the antibiotics as well.

 

So, they’re, like we said, they’re made to survive.

 

Like they are, they’re resilient little things.

 

One of my favorite techniques, I love a regional limb profusion.

 

Oh, yeah.

 

Yeah.

 

This is a really cool technique, where we, being a foot guy, use this a lot.

 

Yeah.

 

But we end up putting a tourniquet, and we inject the antibiotic into the area we need it, into one of the vessels.

 

But we have a tourniquet, depending on where it’s at, we may just have, we’ll put a tourniquet above it.

 

Sometimes if the wound’s higher up in the leg, we’ve got it above and below.

 

And we put that systemic dose of, well, sometimes lower, some of them are full systemic doses, some of them are a much lower dose.

 

But we put it in there, let this tourniquet stay on for about 20, 30 minutes, and it gives a very high tissue concentration, exactly where we need it.

 

And that will allow us to overcome some of these resistances as well, by really pushing our concentration up.

 

Without the systemic side effects.

 

So there’s, you know, in some classes of antibiotics, they can be really hard on the kidneys.

 

They can be really hard on, you know, as they go through and they get processed by the body, they can wreak some havoc, not just colitis, but, you know, like I said, problems with the kidney, problems with the liver, things like that.

 

So if we can avoid those side effects in these stronger hitting antibiotics and just put them right where we need them, that’s super helpful.

 

Especially in some of these, they’re cost prohibitive.

 

But when you’re using a tenth of the dose, and you’re focused on that one area.

 

And I think one way to think about it is we’re evaluating the ability of a bacteria to kill its MIC, minimum inhibitory concentration.

 

These numbers don’t actually mean anything, it’s just an example.

 

But if you have like, let’s say you’re talking about amikacin, and the report comes back and it’s got like a ten times MIC, we’ll kill this.

 

We know when we actually give these drugs systemically, we can actually look up what will our tissue concentration be.

 

And it says amikacin will work at a ten times MIC.

 

Well, we know if we give it systemically, we may only get five times MIC.

 

Safely.

 

Safely.

 

Yeah.

 

But if we do it as a regional limb, Oh, we can get ten all day long.

 

We get a hundred times MIC.

 

And so all of a sudden, this one with intermediate sensitivity becomes useful if the right technique is picked.

 

Correct.

 

Yeah.

 

And it’s, I mean, you can, like Dan was saying, there’s topical.

 

You can do oral administration, which then we have to look at absorption and bioavailability and all of those things.

 

You can do injectable, whether it’s intravenous or intramuscular, depending on the formulation.

 

Like, you know, we look at all of these things and we’re adjusting, like we were just talking about metronidazole, rectally the other day.

 

You can give metronidazole orally, but, and it’s better absorbed that way, but horses will not eat when you put them on metronidazole.

 

I mean, your appetite just drops completely off, and you have to eat to heal.

 

So we’ll give metronidazole per rectum, but we have to, we know that it’s not absorbed as well, so we have to increase our dose to overcome that and get back to our concentration.

 

So all of these things are going on in our little brains as we’re trying to figure out and make a plan.

 

So it’s not, you know, we’re not just reaching blindly into the back of the truck and pulling out the first thing we’re thinking of.

 

There’s a lot of thinking that goes into it.

 

And what’s also interesting is the regionality of antibiotics.

 

Yeah.

 

Just even like, because I talked about this with you guys when I first started, I was here for my working interview and I was like, what’s your recipe for cellulitis here?

 

Like what works here?

 

Because what works here and what works an hour and a half, two hours up the road in Aiken, totally different.

 

Oh yeah, like I went from Kentucky.

 

There was antibiotics like you did not give in Kentucky.

 

Yeah.

 

Because you were going to get a colitis.

 

That’s just what it is.

 

And I get here and people are like, oh, we just give this.

 

I’m like, no.

 

Oh, I can’t.

 

But it works here.

 

And like I talked to friends of mine in California, they’ve got an entirely different microbiome out there.

 

Different things work, different things don’t.

 

Yeah.

 

So, regionality plays a big role.

 

So we’re making that swag.

 

We’re looking at past experiences with this type of a situation.

 

And this allows us for a better choice.

 

Yeah.

 

But I would definitely say one of the big take aways from today is going to be like, if your vet recommends a culture and sensitivity, it is 100 percent worth the money to do it and allow them to do it.

 

Because that’s going to give you the most information and allow you to make the best educated decision that you can and you’re going to be able to clear that infection faster, better, get faster healing, and you’re also going to have less resistance, hopefully.

 

You’re going to do it cheaper, too, because the cost of a culture and sensitivity is the same cost of switching an antibiotic.

 

So really, it’s a cost-neutral deal.

 

So if you’re looking at it from a money perspective, it’s cost-neutral.

 

And if we can get that choice wiser, like you said, you’re three to four antibiotics deep.

 

Like, we’re just throwing crap at the wall, hoping it sticks.

 

And you’ve also set yourself up in future infections to have a harder time, because now the body and all your gut, like all the bacteria on the skin, all the bacteria in the gut, they have all seen these antibiotics now.

 

So they have also acquired resistance genes and things.

 

And so, you know, you’re just, it’s a, every horse is like its own soup of bacteria.

 

And every time you put an antibiotic in there, the whole soup is getting it.

 

And so it’s, it’s not just the infection that you’re treating now, but it’s any infection you might treat in the future.

 

Right.

 

So.

 

No, it’s, it’s critically important.

 

Culture and sensitivity, 100%, if there was anything I want people to get today is.

 

Please do it.

 

Please.

 

Yeah.

 

Like I think it’s one of the most important things.

 

And it’s, it’s, most of the time it’s easy.

 

Like if you’re dealing with a wound, we come in, I’m going to swab it first thing, I’m going to set that to the side, and then I’m going to tackle the wound.

 

Right.

 

If we’re dealing with lungs, we’re going to do a transtrachial wash, we’re going to get a little sample, we’re going to plate it, we’re going to send it off for culture, we’re going to look at it under the microscope, see what we’ve got.

 

Like, it’s not getting that sample most of the time, it’s not that difficult.

 

No.

 

So.

 

No, we do that a lot.

 

And I tell people, I look at some of these respiratory effects, it’s like, I’m going to go do a cytology in a gram stain, and then you may have to come by and pick up an antibiotic later.

 

I’m not going to leave one now because I don’t know what I’m dealing with.

 

Right.

 

Let me go home.

 

It’s going to take, like, by the time I get back, you’re delaying treatment by a couple hours.

 

Get back to the clinic, run this culture, or run the cytology and the gram stain.

 

And it’s like, okay, I got gram-positive cocci in here.

 

Let me grab a bottle of exceed.

 

Oh crap, I got gram-negative rods.

 

I need to grab genomycin.

 

So I can get that first swag pretty close in just a few hours.

 

Now I’m waiting on the culture to come back.

 

And it’s always like that game, like, did I pick right?

 

Did I pick right?

 

Did I pick right?

 

And then you get your, you get your susceptibility back and you’re like, woo-hoo.

 

Yes.

 

I did it.

 

Yeah.

 

Throw yourself a little party.

 

So yeah, doing, doing her party.

 

Exactly.

 

And like doing things the right way just doesn’t take that much longer.

 

It’s not that much more expensive.

 

And in the long run, you’re going to win a lot more.

 

You’re going to win a lot more.

 

Yeah.

 

And so again, back to my horse is sick.

 

Let me just throw it on SMZs.

 

Please don’t.

 

Don’t.

 

We’re not, we’re not saying that just to be, you know, crotchety veterinarians that don’t want, that want to make money off of you.

 

We’re saying it because it’s critically important, not only for your horse, but also for public health and people.

 

Like, antibiotic resistance is, it’s real, and it’s getting scarier and scarier every year.

 

Like, it’s, and in small animal medicine, too.

 

I mean, it’s just, it’s very real, and it’s not going to go away.

 

We talk about this a lot in derm cases.

 

The hardest thing I run into is when I go look at the derm case, and I’m dealing with the nasty, everybody calls it rain rot, but dermatophytosis.

 

I got this nasty bacterial skin infection, a pyoderma.

 

And I said, all right, let’s go through the history.

 

What all have we done?

 

Well, we had some SMZ, so we did that.

 

That didn’t work.

 

We had some leftover of this, so we threw this at it.

 

I’m like, one, there should be nothing left over.

 

But we digress.

 

Yeah.

 

And so by the time we get there, this has been going on for three weeks.

 

We were on random antibotic number three, and we’re losing this game, and you get this culture, and it comes about with some nasty multi-drug-resistant staph.

 

And you’re like, huh, now I gotta combat this, when the right choice would have avoided where we’re at now.

 

Because that’s usually the call, right?

 

It wasn’t that bad, so I treated with this, and then it just kept getting worse, so I treated with this, and it got worse, so I treated with this.

 

And then by the time we get there, we’re like, it’s bad.

 

Whereas the first phone call, we could have knock this out, and we had never gotten to this.

 

And not to mention all the topicals and things that people will put on there that don’t help, and it’s just like, just call us.

 

We can knock this out better, more efficient.

 

Like, ugh.

 

Yeah, we just want to help.

 

Let us help, please.

 

So, yeah, there’s a lot more that goes into antibiotics than just throwing some pills at it.

 

Yeah, and I think I would get so many calls when you could still buy penicillin at like a feed store.

 

Oh, I would get so many calls.

 

It’s like, well, I gave it one shot of penicillin at this dose, and I was like, ugh.

 

10 cc’s of penicillin.

 

That was always the thing.

 

One time, one time.

 

I was like, that is so grossly under-dosed.

 

I can’t even, like, it makes me twitch.

 

Like, I just, I’m like, you just, I mean, you might as well just pour it on him, because it, I mean, just, just throw it away.

 

I’d say the penicillin and the SMZ were the two that, those get me the most.

 

It’s like, just because you have them, don’t mean you can just throw it at them and hope.

 

Don’t do it.

 

Hope ain’t a plan.

 

No, hope is not a plan.

 

Right antibiotic.

 

Correct.

 

Because we’ve got some that we know, like, the lungs, man, that is typically a cephalosporin all day long.

 

They love to go there.

 

Skin, cephalosporin’s not going to get the job done.

 

Just not going to happen.

 

So, there may be times where we reach for the SMZ, but we’ve got a really good case for why we did that.

 

Yeah.

 

It’s not…

 

One antibiotic doesn’t just…

 

It’s not a blanket.

 

It doesn’t do everything that all of its family members do.

 

So, you know, kind of end everything this way.

 

What are your key takeaways?

 

If people learn anything from this podcast, what do you hope they get out of it?

 

I would say just because you have it in your at-home pharmacy doesn’t mean you need to use it.

 

Culture and sensitivity, all the time, every time.

 

And please follow our directions to the letter.

 

Finish the antibiotics, do it at the right timing.

 

Like, when you tell me you have antibiotics left over from the last time, my eye’s gonna start twitching.

 

I’m gonna get mad because you shouldn’t, because that means you didn’t follow directions, and I really need you to follow directions in this instance.

 

I think the only thing I would add would be, if your horse won’t take the antibiotic in the form we prescribed, let us know.

 

Like, if you’re like, he won’t eat anything in his feed, and if you try to syringe it to him orally, he will kill us all.

 

Okay.

 

Cool.

 

We can work with that.

 

We’ll make another plan.

 

Yep.

 

Or if two days in, he no longer will take the antibiotic, let us know.

 

Yeah, don’t wait for three more days just because it’s a Sunday.

 

Call us and tell us, because if you’ve just done those first two days, and then you quit for three days, that’s going to potentially make our antibiotic, when we start it back up again, not work as well.

 

So we need to know as soon as it happens.

 

Let us know.

 

Well, Dr. Cait, thanks for being here today, and all the people here at Countryside Equine.

 

We’re still pretty fired up, loving to do this podcast.

 

April, thanks for filming this.

 

Kasey, thanks for editing all this.

 

We’ve got a great team up here.

 

Everything from the podcast team to the techs and staff that work here, I love our team.

 

It’s a good place to be.

 

Yes, ma’am.

 

So thank you.

 

And most of all things for our listeners out there, y’all keep this going and we really enjoy it.

 

And we’re going to keep cranking out those episodes.

 

We’re going to keep putting more and more out.

 

So again, if y’all got questions, comments, send them in, be happy to get to them.

 

We’re still working on some of these little short videos.

 

So when people do have questions, we’re going to be attaching those.

 

We’ve got little short videos to answer your questions on, you know, when you listen to the podcast, you’re like, oh, I wonder about this.

 

We’re going to try to get those answered.

 

Bear with us, you know, we still got real jobs, still got to pay the bills around here.

 

So keep the lights on.

 

And then one day maybe we’ll be professional podcasters.

 

I don’t know if I’m cut out for it.

 

I love being a vet.

 

I ain’t going to lie to you.

 

I gotta go get my hands dirty.

 

I can’t sit here for too long to get antsy.

 

I was thinking about the other day, I’ve been a vet now for 16 years, and I’m just as excited today to go to work as it was the first day.

 

You beat the statistic, Dan.

 

Good job.

 

Love it.

 

Love it.

 

Love it.

 

Love it.

 

So again, thanks everybody for listening.

 

We’ll see y’all next week.

 

Take care.