Welcome to Chattering With iCatCare, the official monthly podcast of International Cat Care, hosted by Yaiza Gomez-Mejias (Veterinary Community Co-ordinator). Each month, we chatter about cats and cat-friendly practices with industry experts and contributors to The Journal of Feline Medicine and Surgery. Each episode contains highlights from our longer discussions and interviews, which are accessible to iCatCare members at portal.icatcare.org. If you would like access to our full episodes, would like to become an iCatCare Veterinary Society Member, or find out more about our Cat-Friendly schemes, visit icatcare.org.
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
full version of the podcast and all
the other member benefits including
congress recordings, monthly webinars
and clinical clubs, the discussion forum
and much more at portal.icatcare.org.
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