Hello and welcome to Chattering with iCatCare.
I'm Yaiza Gomez Mejias, iCatCare Veterinary Community Coordinator
and host of this month's podcast.
Our clinical spotlight today is focused on pathogenic organisms in
the gastrointestinal tract of cats.
I will be interviewing Katie McCallum and Giulia Cattaneo, authors of
this month's Spotlight article titled 'Feline enteropathogens and
molecular diagnostics: benefits, limitations and clinical applications'.
As all articles in the Journal of Feline Medicine and Surgery, it is open access,
and can be found on the journal website.
But before delving into the world of gastrointestinal guests, Anna Maria Tiozzo
Ambrosi will talk about her JFMS Open Report Case, which has been awarded this
year as the best JFMS practitioner paper.
So Anna Maria is the first author of the JFMS Open Report Practitioner Best Paper
Award, Hypokalaemic myopathy associated with iatrogenic hypercorticism in a cat,
and given the reduced alternatives to steroids in cats compared to dogs and
their apparent resistance to them, your report really helps us understand that
this may not always be the case and that we can certainly see adverse effects as
a result of the long-term administration.
So would you like to start by explaining, well, where are the
clinical signs that prompted the cat's journey to the veterinary clinic
in this case, which I believe were not too typical for hypercorticism.
No.
In fact, the main clinical signs were lethargy, hindlimb
weakness with plantigrade stance and above all, ventroflexion of
the neck for one days duration.
There wasn't alopecia, for example, that typically we can
see in use of steroid in cat.
You didn't see any curly ears, you didn't see any other clinical sign
consistent with hypercorticism?
Yes.
And what, what was the cat's clinical history before the onset of these signs?
He was 12 years old, but he was fine.
He was fed with an hydrolysed diet and he had been treated with
methylprednisolone acetate at dose of 20 mg for cat intramuscularly
twice a year for six years for a seasonal pruritus.
So
it was a, the,
the cat had some, some sort of a skin hypersensitivity?
Yes.
And what
were the key findings from the initial blood work and how did you interpret them?
Considering the blood, the clinical signs, I decided to perform blood exams and I
saw marked increase of muscle enzymes.
And overall from hemogas, I saw a severe hypokalaemia.
In fact, the liver of potassium was 2.2 millimoles per litre.
And so this
finding suggested a hypokalaemic myopathy.
And
I read you, you also used something we don't often hear of.
You did the urine fractional excretion of potassium.
Yes.
fraction of potassium was 19.04% and, uh, this result suggested a
renal elimination of a potassium and not the gastrointestinal problems.
So it was an external lab test, right?
Yes.
So, so if I understood you well, it excluded renal disease
as a cause of the hypokalemia.
Yes.
Because the urine specificity gravity was normal.
How did you carry out the diagnostic workup and, and what else did you find?
The first thing I thought that Orazio will
have an hyperaldosteronism because he was an old cat and
because there was a hypokalemia.
But then I decided to perform an abdominal ultrasound.
I put the Orazio on the left side and the right side, and I put him on the back.
And after 30 minutes, 45 minutes of abdominal ultrasound, I finally found
the adrenal glands and they were small considering the dorsoventral
axis diameter of the caudal pole, 0.16 cm and 0.17 cm, and so a few
things didn't make sense to me.
The first question is why did Orazio have hypokalemia?
And then why were adrenal glands so small?
And so then I remembered what the owner told me during the
visit, the use of steroid for six years, even if twice a year.
So I decided to perform an ACTH stimulation test and the result
show an adrenal suppression.
Well, well done for, for persisting at the ultrasound and, and finding the adrenal
glands, which we know it's not easy.
You were really thorough and, and you highlighted before how important it
is to take a good clinical history because without knowing that the
cat had had steroids in the past it would have been more challenging.
As you described in your report, you had a few differentials in the
first place, and how did you narrow down your list of differentials?
Yes, I consider the different diagnosis the cause
of hyperkalemia.
For example, hyperthyroidism.
But in our case, the total TT4 was normal.
Then diabetes mellitus.
But in this case, there wasn't glycosuria.
And the following day, during the hospitalisation, the glycemia was normal.
Another differential diagnosis was hyperaldosteronism, but in this case, the
adrenal gland were normal and there was a low level serum of hormone aldosterone.
Then, for example, chronic kidney disease.
In fact, we know that the cat with chronic kidney disease could have
hypokalemia in 30% because, or for a low intake of potassium with the diet, or
for polyuria and
polydipsia, or for vomiting or diarrhoea.
But in this case, the urine specific gravity was normal
after potassium level was normal and above all, the urea and creatinine was normal.
And the last differential diagnosis
was a renal tubular acidosis.
But,both bicarbonate and the blood PH was normal.
Well done.
And yes, I suppose that the high blood pressure made things a little bit
confusing and it, it was good to see that the white coat effect can drive
the blood pressure really, really high.
Yeah.
Now I will interview Katie McCallum and Giulia Cattaneo about Feline
enteropathogens and molecular diagnostics.
We know microorganisms are part of the gastrointestinal
tract and make things work.
When do they cause enteric disease?
So part of the paper has been quite challenging.
What we wanted to do is, there is a lot of literature out there and a lot of
prevalence data out there, which will look at cats with diarrhoea and cats
that don't have diarrhoea, and they'll try and ascertain whether there's a
higher prevalence in the cats with diarrhoea, and that's all very well.
But then you have five or six of these studies with different populations
of cats, different detection methods, making the whole thing quite difficult.
So what we aim to do is to, to get prevalence data and combine it all.
And what that ended up showing us was that the prevalence in diarrheic cats
was very similar to non diarrheic cats.
But obviously with the caveat that by combining all these studies,
there's lots of different factors that we haven't taken into account.
The problem with enteropathogens is so many of them are subclinically
shared, so the clinical relevance of them is not known for all of them.
What we do know is there are some risk factors reported in multiple studies.
The big one is your shelter, multi cat household situation where you get
outbreaks of diarrhoea, and that's probably because you've got stressed cats.
There's high disease burden and exposure to disease, high housing densities,
lots of movement of cats in and out as well and concurrent diseases as well.
So I think when you have lots and lots of cats in the same place, particularly
with diseases, let's mention coronavirus.
The prevalence of fecal shedding of enteric coronavirus hugely increases in
a shelter cat setting in most situations.
The other thing that that's been looked at is seasonality, and we actually only
found one study looking like in any great detail about seasonality, and we
didn't find it particularly clinically useful in that they looked at, are
there peaks of bacterial protozoal viral infections, depending on the season,
and I don't think that makes a big difference to how I would approach a case.
Other risk factors are diets, and I'm going to bring up raw feeding.
I'm gonna do it very carefully.
Raw feeding is something that, that is quite up and coming.
There's a lot of owners raw feeding their cats now.
We know there has been a link to certain enteric diseases, including salmonella,
and there's also more recent papers showing that cats fed raw diets have
been shown to get tuberculosis in the UK.
It is a contentious subject because the problem is you
can't actually prove causality.
Just because they're having a raw diet doesn't mean that the salmonella
has necessarily come from that.
It might just be increasing these cats exposure to these diseases rather than
actually being the true cause of that.
I'm going to leave it at that, but raw diets do need to be looked at.
And the final risk factor is just age.
If I have a young cat presenting with diarrhoea, I'm much more likely
to do infectious disease testing than an older cat because their
immune system isn't well developed.
They have a more stresses, vaccinations, neutering.
They're more likely to pick up infections.
And from my my side of things, breed or genetics is important.
For example, tritrichomonas, this is the pathogen which we see more
commonly in our pedigree breeds.
So Bengals, Persians, Siamese, Abyssinians.
So something to to think about why this disease affects pedigrees.
It's still a little bit hazy, but certainly can help hone in our
diagnostic methods and choose the best testing for these individuals.
With regards to health status, again, going back to immunosuppression,
increasing the risk or the propensity to develop clinical signs in cats previously
asymptomatic for carriers of pathogens.
Interesting to look at interactions between pathogens,
co-infection, or co carriers.
For example, cryptosporidium and tritrichomonas can have accentuating
effects on each other in terms of disease.
But looking at gastrointestinal disease, GI health, we need to think about
clostridial bacteria, the forms that might lie dormant, spore form, the vegetative
form, which is actively growing.
Different microclimates in the GI tract might allow these clostridial bacteria
to convert to that vegetative form, and essentially then cause disease.
Increased concentration of primary bowel acid can help shift from the
spore form to the actively growing form.
Favourable intestinal conditions might shift towards a disease.
Antibiotics are another big factor at they lead to dysbiosis and therefore
shifts in competition by, you know, originally commensal bacteria are
wiped out, and then potentially allowing propagation of bacteria
that are pathogenic or opportunistic.
And then chronic inflammatory enteropathy, we have disruption
of the normal GI barrier.
Potential for development of disease by pathogens that would otherwise
be kept at bay with normal barrier.
And we know that we have chronic enteropathy.
Potentially there is a genetic basis, for example, in dogs TLR receptor mutations.
Thank you for listening.
If you are an iCatCare Veterinary Society member don’t forget you can access the
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If you are looking for more free CPD from International Cat Care, on the 30th of
September, Dr. Becky Mullis will host an open access webinar titled 'Caring
for the ageing cat, managing common conditions and maintaining their weight'.
We’ll be back again next month with more from the world of feline medicine and JFMS