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Hello and welcome to
Chattering with iCatCare.

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I'm Yaiza Gomez Mejias, iCatCare
Veterinary Community Coordinator

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and host of this month's podcast.

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Our clinical spotlight today is
focused on pathogenic organisms in

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the gastrointestinal tract of cats.

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I will be interviewing Katie McCallum
and Giulia Cattaneo, authors of

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this month's Spotlight article
titled 'Feline enteropathogens and

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molecular diagnostics: benefits,
limitations and clinical applications'.

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As all articles in the Journal of Feline
Medicine and Surgery, it is open access,

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and can be found on the journal website.

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But before delving into the world of
gastrointestinal guests, Anna Maria Tiozzo

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Ambrosi will talk about her JFMS Open
Report Case, which has been awarded this

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year as the best JFMS practitioner paper.

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So Anna Maria is the first author of the
JFMS Open Report Practitioner Best Paper

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Award, Hypokalaemic myopathy associated
with iatrogenic hypercorticism in a cat,

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and given the reduced alternatives to
steroids in cats compared to dogs and

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their apparent resistance to them, your
report really helps us understand that

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this may not always be the case and that
we can certainly see adverse effects as

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a result of the long-term administration.

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So would you like to start by
explaining, well, where are the

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clinical signs that prompted the
cat's journey to the veterinary clinic

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in this case, which I believe were
not too typical for hypercorticism.

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No.

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In fact, the main clinical
signs were lethargy, hindlimb

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weakness with plantigrade stance
and above all, ventroflexion of

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the neck for one days duration.

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There  wasn't  alopecia, for
example, that typically we can

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see in use of steroid in cat.

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You didn't see any curly ears, you
didn't see any other clinical sign

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consistent with  hypercorticism?

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Yes.

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And what, what was the cat's clinical
history before the onset of these signs?

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He was 12 years old, but he was fine.

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He was fed with an hydrolysed
diet and he had been treated with

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methylprednisolone acetate at dose
of 20 mg for cat intramuscularly

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twice a year for six years
for a seasonal pruritus.

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So

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it was a, the,

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the cat had some, some sort
of a skin hypersensitivity?

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Yes.

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And what

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were the key findings from the initial
blood work and how did you interpret them?

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Considering the blood, the clinical signs,
I decided to perform blood exams  and I

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saw marked increase of muscle enzymes.

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And overall from hemogas, I
saw a severe hypokalaemia.

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In fact, the liver of potassium
was 2.2 millimoles per litre.

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And so this

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finding suggested a hypokalaemic myopathy.

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And

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I read you, you also used
something we don't often hear of.

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You did the urine fractional
excretion of potassium.

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Yes.

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fraction of potassium was 19.04%
and, uh, this result suggested a

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renal elimination of a potassium and
not the gastrointestinal problems.

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So it was an external lab test, right?

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Yes.

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So, so if I understood you
well, it excluded renal disease

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as a cause of the hypokalemia.

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Yes.

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Because the urine specificity
gravity was  normal.

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How did you carry out the diagnostic
workup and, and what else did you find?

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The first thing I
thought that  Orazio will

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have an hyperaldosteronism
because he was an old cat and

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because there was a hypokalemia.

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But then I decided to perform
an abdominal ultrasound.

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I put the Orazio on the left side and the
right side, and I put him on the back.

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And after 30 minutes, 45 minutes of
abdominal ultrasound, I finally found

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the adrenal glands and they were
small considering the dorsoventral

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axis diameter of the caudal pole,
0.16 cm and 0.17 cm, and so a  few

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things didn't make sense to me.

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The first question is why
did Orazio have hypokalemia?

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And then why were adrenal glands so small?

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And so then I remembered what
the owner told me during the

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visit, the use of steroid for
six years, even if twice a year.

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So I decided to perform an ACTH
stimulation test and the result

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show an adrenal suppression.

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Well, well done for, for persisting at the
ultrasound and, and finding the adrenal

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glands, which we know it's not easy.

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You were really thorough and, and you
highlighted before how important it

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is to take a good clinical history
because without knowing that the

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cat had had steroids in the past it
would have been more challenging.

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As you described in your report,
you had a few  differentials in the

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first place, and how did you narrow
down your list of differentials?

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Yes, I consider the
different diagnosis the cause

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of hyperkalemia.

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For example, hyperthyroidism.

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But in our case, the total TT4 was normal.

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Then diabetes mellitus.

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But in this case, there wasn't glycosuria.

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And the following day, during the
hospitalisation, the glycemia was normal.

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Another differential diagnosis was
hyperaldosteronism, but in this case, the

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adrenal gland were normal and there was
a low level serum of hormone aldosterone.

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Then, for example, chronic kidney disease.

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In fact, we know that the cat with
chronic kidney disease could have

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hypokalemia in 30% because, or for a low
intake of potassium with the diet, or

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for polyuria and

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polydipsia, or for vomiting or diarrhoea.

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But in this case, the urine
specific gravity was normal

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after potassium level was normal and above
all, the urea and creatinine was normal.

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And the last differential diagnosis

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was a renal tubular acidosis.

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But,both bicarbonate and
the blood PH was normal.

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Well done.

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And yes, I suppose that the high blood
pressure made things a little bit

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confusing and it, it was good to see
that the white coat effect can drive

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the blood pressure really, really high.

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Yeah.

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Now I will interview  Katie McCallum
and Giulia Cattaneo about Feline

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enteropathogens and molecular diagnostics.

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We know microorganisms are
part of the gastrointestinal

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tract and make things work.

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When do they cause enteric disease?

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So part of the paper has
been quite challenging.

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What we wanted to do is, there is a lot
of literature out there and a lot of

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prevalence data out there, which will
look at cats with diarrhoea and cats

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that don't have diarrhoea, and they'll
try and ascertain whether there's a

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higher prevalence in the cats  with
diarrhoea, and that's all very well.

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But then you have five or six of these
studies with different populations

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of cats, different detection methods,
making the whole thing quite difficult.

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So what we aim to do is to, to get
prevalence data and combine it all.

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And what that ended up showing us was
that the prevalence in diarrheic cats

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was very similar to non diarrheic cats.

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But obviously with the caveat that
by combining all these studies,

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there's lots of different factors
that we haven't taken into account.

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The problem with  enteropathogens
is so many of them are subclinically

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shared, so the clinical relevance of
them is not known for all of them.

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What we do know is there are some risk
factors reported in multiple studies.

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The big one is your shelter, multi
cat household situation where you get

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outbreaks of diarrhoea, and that's
probably because you've got stressed cats.

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There's high disease burden and exposure
to disease, high housing  densities,

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lots of movement of cats in and out as
well and concurrent diseases as well.

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So I think when you have lots and lots
of cats in the same place, particularly

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with diseases, let's mention coronavirus.

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The prevalence of fecal shedding of
enteric coronavirus hugely increases in

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a shelter cat setting in most situations.

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The other thing that that's been looked
at is seasonality, and we actually only

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found one study looking like in any
great detail about seasonality, and we

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didn't find it particularly clinically
useful in that they looked at, are

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there peaks of bacterial protozoal viral
infections, depending on the season,

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and I don't think that makes a big
difference to how I would approach a case.

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Other risk factors are diets, and
I'm going to bring up raw feeding.

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I'm gonna do it very carefully.

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Raw feeding is something that,
that is quite up and coming.

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There's a lot of owners
raw feeding their cats now.

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We know there has been a link to certain
enteric diseases, including salmonella,

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and there's also more recent papers
showing that cats fed raw diets have

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been shown to get tuberculosis in the UK.

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It is a contentious subject
because the problem is you

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can't actually prove causality.

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Just because they're having a raw
diet doesn't mean that the salmonella

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has necessarily come from that.

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It might just be increasing these cats
exposure to these diseases rather than

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actually being the true cause of that.

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I'm going to leave it at that, but
raw diets do need to be looked at.

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And the final risk factor is just age.

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If I have a young cat presenting
with diarrhoea, I'm much more likely

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to do infectious disease testing
than an older cat because their

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immune system isn't well developed.

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They have a more stresses,
vaccinations, neutering.

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They're more likely to pick up infections.

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And from my my side of things,
breed or genetics is important.

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For example, tritrichomonas, this
is the pathogen which we see more

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commonly in our pedigree breeds.

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So Bengals, Persians,
Siamese,  Abyssinians.

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So something to to think about why
this disease affects pedigrees.

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It's still a little bit hazy, but
certainly can help hone in our

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diagnostic methods and choose the
best testing for these individuals.

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With regards to health status, again,
going back to immunosuppression,

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increasing the risk or the propensity to
develop clinical signs in cats previously

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asymptomatic for carriers of pathogens.

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Interesting to look at
interactions between pathogens,

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co-infection, or co carriers.

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For example, cryptosporidium and
tritrichomonas can have accentuating

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effects on each other in terms of disease.

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But looking at gastrointestinal disease,
GI health, we need to think about

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clostridial bacteria, the forms that might
lie dormant, spore form, the vegetative

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form, which is actively growing.

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Different microclimates in the GI tract
might allow these  clostridial bacteria

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to convert to that vegetative form,
and essentially then cause  disease.

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Increased concentration of primary
bowel acid can help shift from the

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spore form to the actively growing form.

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Favourable intestinal conditions
might shift towards a disease.

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Antibiotics are another big factor at
they lead to dysbiosis and therefore

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shifts in competition by, you know,
originally commensal bacteria are

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wiped out, and then potentially
allowing propagation of bacteria

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that are pathogenic or opportunistic.

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And then chronic inflammatory
enteropathy, we have disruption

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of the normal GI barrier.

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Potential for development of disease
by pathogens that would otherwise

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be kept at bay with normal barrier.

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And we know that we have
chronic enteropathy.

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Potentially there is a genetic basis, for
example, in dogs TLR receptor mutations.

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Thank you for listening.

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If you are an iCatCare Veterinary Society
member don’t forget you can access the

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full version of the podcast and all
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and much more at portal.icatcare.org.

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If you are looking for more free CPD from
International Cat Care, on the 30th of

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September, Dr. Becky Mullis will host
an open access webinar titled 'Caring

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for the ageing cat, managing common
conditions and maintaining their weight'.

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We’ll be back again next month with more
from the world of feline medicine and JFMS