Good evening, everybody, and welcome to tonight's webinar. My name is Bruce Stevenson, and I had the honour and privilege of chairing tonight's webinar. As it's a member's webinar, I don't think I need to do too much housekeeping.
Remember to use the Q&A box to drop any questions, and we will get to as many of those as we can at the end. If we don't, we'll pass them on to Maggie and ask her pretty pleased to help us and answer as many as what we can. So it is my privilege tonight to introduce Doctor Margie Shirk.
Margie graduated from Ontario Veterinary College in 1982. In 1986, she opened cats only veterinary clinic in Vancouver in Canada. This is the third feline clinic in North America.
She became a board certified feline specialist, the first year the specialty became available and has maintained her certification ever since. Since 2008, she has been a consultant and an educator speaker, speaking internationally and teaching online. Margie has co-edited the Journal of Feline Medicine and Surgery for 23 years.
She has served extensively in the American Association of Fetline Practitioners, as well as other veterinary organisations. Margie, welcome to the webinar, vet, and it's over to you. Thank you, Bruce.
It's a pleasure to be here. I'm looking forward to, talking about a variety of gastroenteric syndromes in cats. And of course, there are many, many, as a consequence, while I have selected a few here, I won't even make it through all of these, so I apologise for that ahead of time.
I probably, I really wanted to teach placing in an esophagostomy tube because that's something that every one of us can do and should, should be prepared to do, on a, on any day, a given day. But I will see where I, what I get to. So, without further ado, let me start with what we commonly call inflammatory bowel disease, but that is actually a misnomer.
We should be talking about chronic enteropathies, and I'll talk about the progression or supposed progression from IBD to lymphoma, as well as diagnosing small cell lymphoma. So IBD is actually a histopathologic diagnosis. We can't really make the diagnosis any other way.
We can't make it by, through ultrasound or through, the clinical signs or the clinical findings. Chronic enteropathy, on the other hand, is a broader term. It describes the a syndrome of diarrhoea, vomiting, and weight loss of more than 3 weeks' duration.
So, generally, what we're talking about is chronic enter. And it may be during those three weeks, it may be intermittent or continuous. Some cats with chronic enteropathy have inflammatory bowel disease or lymphocytic plasmacytic enteropathy, which again, is a better term, because inflammatory bowel disease tells you nothing.
It just tells you there's inflammation in the bowel. It doesn't tell you anything whatsoever about, the aetiology or, therefore, how to treat it. Lymphocytic plasmacytic enteritis, or entopathy.
Is a, a descript describes the types of cells that are, are aggregating, and other cats will have lymphoma or less common causes. So chronic enteropathy or IBD can be food responsive, occasionally antibiotic responsive, but that's generally not where we want to go with it. Steroid responsive or idiopathic and non-responsive.
So it is more accurate to refer to chronic enteropathy pending a diagnosis. And what we see with the architectural changes of of of associated with chronicity, be it chronic enteropathy or true lymphocytic plasmacytic enteritis, the the lymphocytic plasmacytic form of IBD of inflammatory disease. Is that we see crypto edoema and blunted villa.
So in the image on the left-hand side, you can see the edoema in the crypto area and the, blunted villi. It's not strictly the increase in, in numbers of cells. So that's why you need, a, a biopsy.
So, the history and differentials, it's chronic, it's, you know, non-responsive generally. You've tried diet, you have, tried to deworm, you've tried, some, some diets. Weight loss can be dramatic depending on where the, the, changes are present.
If they're in the, if they're, significant in, distribution, lots of it in the small. Bowel stool character varies widely. It may be large or small, bowel diarrhoea or possibly no diarrhoea.
They may have a voracious appetite, again, if it's localised, in the small bowel. And sometimes they don't use the litter box, so someone may be coming to you because their cat is defecating outside of the box. Otherwise, there's an unremarkable history.
And differentials, we've got a long list of differentials that could present with the same or similar signs. Some of them are regional such as histoplasmosis, geographically regional. Some of them are, anatomically regional such as adenocarcinoma, and, or maybe in the liver, it could be in the pancreas.
Lots of different things that. Cause this. And as I learned from Doctor Alice Wolf, many, many years ago, who's one of the four fathers or mothers of, feline medicine, is that FIP, FELV, and FIV should be on the differential list, pretty much every differential list in a, in cats because they can present in many different ways.
So, what we want to start with is a therapeutic trial of evaluating for any allergens possible. So because that could be dietary hypersensitivities, we're gonna use a limited antigen or indeed a, true, hypoallergenic diet, and deworm them, because parasites are protein in the gut, as is hair, treat for hair balls. We want to get rid of any protein allergens.
Well, all allergens are protein as far as I am aware, and, get rid of those. Prebiotic has been suggested, but we really don't have any scientifically studied evidence for that. Then we're gonna do an abdominal ultrasound.
Consider doing the cabolamine folate, FPLI or FTLI, looking for pancreatitis or exocrine pancreatic insufficiency, respectively. And then the next step would certainly be biopsy, where we want to be getting good quality biopsies and good numbers of biopsies, surgical vers or endoscopic, and I'll touch on that later. Now, one of the main documents that I want to refer to here, and this is in the reference list, there's also the QR code here, is the ACBIM consensus statement guidelines on diagnosing and distinguishing low-grade neoplastic from inflammatory lymphocytic chronic enteropathies in cats, and that was published in 2023.
So again, defining that GI signs have been lasting for 3 weeks or longer, after ruling out infectious, metabolic and extraintestinal causes such as hyperthyroidism. Or, liver disease, then you're thinking food responsive enteropathy, inflammatory or steroid-responsive enteropathy, most commonly is, is, lymphocytic plasmacytic and small cell or low grade intestinal T cell lymphoma, which I probably will refer to as small cell lymphoma rather than LGITL. So it, these both are common in older cats, and certainly the prevalence of diagnosing elementary lymphoma has increased.
Oops. So differentiating the differentiating these two conditions, the, the strictly inflammatory versus the neoplastic, there is an overlap of clinical signs and as well as laboratory data, imaging, and histopathologic findings. Small cell lymphomas are characterised by monoclonal or.
Oligoclonal rearrangements of the lymphocyte receptors, but clonality is not equivalent to malignancy. That's important to recognise. Not all reactive lesions, so the, the inflammatory ones are polyclonal.
So histopathology remains key. So, when is it one versus the other? In this study back now, 12 years ago, Doctor Gary Norsworthy looked at chronic small bowel disease in, in 100 client-owned domestic cats.
And he found that the most common diagnoses were chronic enteritis and intestinal lymphoma. And in these cats with, with small bowel disease signs and ultrasonographically thickened small bowel, they were all biopsied. 49 of them had enteritis, so lymphocytic plasma lymphocytes and plasma cells, more so than eosinophils, and 46 had small cell lymphoma.
So that's really remarkable that there were so many with lymphoma. It was almost a 50/50 split. He did not, unfortunately, comment on how many of them, had both.
So pathogenesis, maybe it's regressive feline leukaemia virus and small cell lymphoma, depending on the subtype of feline leukaemia in a positive CAT, but there are no studies of regressive FELV and LPE. Certainly, mucosa invading bacteria are more common in cats with large smell lymphoma than in small cell lymphoma. And intravascular bacteria are only found in those individuals with large cell lymphoma.
So, probably not, an, an infectious in that. What about dysbiosis? Dysbiosis promotes inflammation and malignant transformation in people and in non-feline animal models, but there's again, no difference in the bacterial populations between cats with LPE and small bow a small cell lymphoma.
What about chronic inflammation? Well, chronic inflammation in people and in cats, and certainly when we're thinking about, melanomas, when we're thinking about breast cancer in, in people, chronic inflammation can promote oncogenesis, and there is frequent coexistence of these two chronic chronic inflammatory and and small cell lymphoma presentations in cats. Is it a continuum?
The, certainly the duration of clinical signs in cats with neoplasia is longer than in those with, inflammation, which makes sense if the first one, if one comes before the other. There is a study that shows that environmental tobacco smoke exposure increases the risk of, increases the risk of lymphoma on any body part, not just in the bowel, in cats, significantly. Disruptions in crosstalk, the communication between the immune system, the intestinal environment, and the microbiome in a genetically predisposed individual is probably the, the, underpinning pathogenesis, which then gets exacerbated by one of these other things I just mentioned.
So from the these guidelines, anything with the blue is now a callout box from these guidelines where they make statements, they give the evidence level and then the panel of six members votes on if they strongly agree, agree, or whichever as so the consensus guidelines. So there are currently no known pathognomonic signalment or clinical findings that can reliably distinguish between lymphoplasmacytic enteritis and small cell lymphoma in cats because both conditions overlap with a wide range of presentations, including no clinical signs at all. The age of the individuals, the, cats with small cell lymphoma are older, but there is overlap.
Breeds that are predisposed, domestic short hairs, while they are the largest breed period, and, and Siamese, as well as some of the other oriental cats would fall in there as well. And then sex neutered male. So, in, I differing from, from dogs, weight loss is, is the, most common sign in feline chronic enteropathy.
80 to 90% of cats lose weight, 70 to 80% have vomiting, 60 to 70% have anorexia, and, 50 to 65% of diarrhoea. Many that have sarcopenia and low body condition score, and muscle loss predominates. So we see these very thin cats.
So they may also, there may be, you may palpate segmental or diffusely thickened intestinal loops. There may be abdominal discomfort or pain, often in the cranial abdomen, which makes you think about the pancreas. Possibly, there is concurrent pancreatitis, with or without cholangitis, or there are no clinical findings, making it especially difficult.
So again, it is a chronic insult, and we don't know whether severe lymphoplasma cytic enteritis is precancerous or not. We don't know. And if it is, the mechanism is unknown.
But speculating when, when we do have a transition from chronic inflammation to neoplasia, it, it may look similar to this. Where is it tends to be located? Anywhere, anywhere.
The, the neoplasia tends to be in the jujunum more than the ileum, more than the duodenum, and those certainly more commonly than the stomach or the colon. If there is neoplasia in the stomach, it's most likely a large cell lymphoma, so bad disease. If it's in the colon, it's more likely to be inflammation, so good disease.
Does lab work help, such as, you know, doing a CBC serum biochemistry panel, a urinalysis, and faecal analysis, as well as a total T4 and retroviruses, because we need to rule out other differentials. Unfortunately, no, it's not, it's gonna help us rule out other differentials, but it doesn't differentiate between inflammatory disease and neoplasia. What about imaging?
Radiographs, there's no benefit over ultrasound, other than, you know, availability, possibly and cost, and then maybe ease of interpretation depending on what the, what you as a practitioner are used to interpreting. But abdominal ultrasound to assess other organs and identify abnormal segments is useful, but not to differentiate between lymphoplasma cytic enteritis and small cell lymphoma, unfortunately. So small cell lymphoma can be, we used to think of it as, as being, well, certainly segmental, but also having, more, more imaginations of thickenings of the jujual wall.
But this, here you can see someone with chronic enteropathy has a thickened wall where this arrow is pointing, compared to normal, but this could equally well, unfortunately, be, a small cell lymphoma. Well, an ultrasound, you're, you're likely to see diffuse thickening in in any layers of the bowel wall, in the small bowel. These are very common.
And the ultrasonographic abnormalities in the mucosa were highly predictive of mucosal histopathologic lesions, but they don't correlate, but the thickened mucosa, submucosa, I beg your pardon, or muscularis did not correlate with histopathologic lesions, different from what I was taught or what used to be believed. Ultrasonographic and pathologic changes occur even in clinically healthy cats. So the musculars to submucosa ratio of being greater than one was indicative of an abnormal bowel segment, but there is no difference found between inflammatory or, or neoplasia tissues.
So this gets to be really frustrating. One study showed differences in the junal nodes, in that the, in neoplastic, patients with neoplasia have rounder, thicker, more hypoechoic nodes than with . with, inflammation, but that's gonna vary from the change of the time that you see them and the, the hydration status of the cat, etc.
And there's also a greater chance of mild effusion, abdominal effusion with neoplasia than LPE. Overall, larger lymph nodes, both groups of cats will have larger lymph nodes than healthy cats, so it doesn't differentiate. OK.
So what does this give us then? I mean, we're right now, we're working on index of suspicion and having ruled out other things. So, with the, the gold standard is a collection of intestinal tissue biopsies.
And there's no clearly demonstrated superiority in quality for biopsy specimens obtained by laparotomy, which should be full thickness versus endoscopic. Because poor technique can affect quality and ample diagnostic evaluation for both methods. And it has been shown that all inflammatory and neoplastic lesions are present in the laminopropria.
Therefore, if mucosal samples, as endo endoscopic samples of sufficient quality are procured, a diagnosis is possible without obtaining full thickness biopsy specimens. Because of limited access, however, to the jujunum by endoscopy, jujunal lesions, which is, oh, by the way, where the majority of the small cell lymphomas were, cannot be reliably sampled. So, I did want to mention with endoscopy, the way one can maximise the diagnostic utility.
Certainly, using a flexible endoscope is valuable, but it has to be performed carefully, so that the results are meaningful. We need to get ideally 12, good, 12 good quality diag specimens for them to be diagnostic. And what you can do with, with this, should you have endoscopy is perform upper GI endoscopy.
Then, it's, and then while your patient is anaesthetized, you surg you surgically prep their abdomen and, and perform intraoperative evaluation. Of the jujunum and ileum using the endoscope. So making evaluating the outside just as you would with any exploratory celiotomy or laparotomy, exploring the, the abdomen, looking at, you can biopsy the lymph nodes, you can biopsy based on your ultrasound if it seems warranted.
The pancreas or the liver, or whatever else seems to be abnormal or you're suspicious of. And then you make an incision in the, in, in the distal, duodenum, put a purse string suture around that and make a, pass your endoscope through that, opening, pull the bowel up over the, over the endoscope. And anywhere that things look abnormal on the inside of the bowel, you Ask someone to place a stay suture.
And you can then, after you withdraw the endoscope and pull that purse string suture closed, you can then, or suture it closed in another way. You can then do full thickness biopsies from each of those, each of the, at each of those, at each of those, stay suture marks. One could also do laparoscopy.
That's also possible to do. And there's been certainly good, essentially, that's doing, full thickness. There's no difference in surgical duration, etc.
So, how do we differentiate between lymphocytic plasmaytic enteropathy and intestinal lymphoma? Do we, how, how do we do this? Well, there's still controversy as to whether full thickness biopsies are preferable.
In fact, because they, because mostly in the dunum and ileum, which you can't reach using endoscopy. That would favour doing full thickness, but both conditions currently in some counts, so you may be fine doing, just the one good quality endoscopic biopsies are less risky for the patient, but they must have, be of good quality. So, to this, the evidence level, was a 2 out of 3 and 4 out of 6 members strongly agreed.
So we can really say endoscopic biopsies, but if you really want to get the dejunum, you're gonna have to do a little bit more acrobatics, and otherwise full thickness biopsy the usual route. So we have to do, you know, histopath isn't, isn't, isn't going to tell us, too much, but it will tell us if it's a chronic, condition because of the morphologic changes. It is the, gold standard for diagnosing chronic enteropathy.
The alignment of samples is, for processing is critical, and attaching them to attaching the samples to cucumber slices or synthetic sponges can be very helpful for the processing. Still, pathologists may disagree. They don't all agree on what is normal.
Many of them just report, you know, large numbers or great, great increase in numbers of lymphocytes and plasma cells suggestive of lymphocytic plasmacytic anthopathy, despite the fact that they're not reporting about the chronicity of the lesions. So, while there was a, a, a wonderful paper in 2008, standard form for assessment of duodenal, as well as other tissues, mucosa, and, very few people, a pathologists, unfortunately, use it. And still, there are many exceptions.
So we still have to proceed with special stains, immunohistochemistry, immuno phenotyping, and, or clonality tests. So, clonality can be an important part of the diagnostic evaluation. However, it must be interpreted in conjunction with clinical, histopathologic, and immunohistochemical results, and cannot be used as a sole means to reclassify cases.
Because, as I said before, you can have polyclonal, not all LPEs are polyclonal, and not all small cell lymphomas are monoclonal. So, if we're looking at immunohistochemistry, we can be doing PCR, PCR for antigen receptor rearrangement or PAR. I always have to write it out because I don't remember what, what it stands for.
And it, it generally, is a reflection of whether it's neoplastic or reactive inflammatory. But again, not conclusive here. So, single spike, is, is generally associated with neoplasia, multiple spikes are associated with reactive or inflammatory changes.
You use blood, stained non-fixed and non-cover slipped slides are OK. Formal and fixed samples are also OK. 91% of confirmed feline lymphoma is detected with par, but a negative result does not rule out lymphoma.
So what about flow cytometry? Again, immunohistochemistry here, immuno phenotyping. It stains live cells with fluorescently labelled antibodies that bind to proteins on cell surface.
And different proteins, are expressed by different cell lines, as you can see in the images on the right. And if there's a homogeneous cell line, it, it's more consistent. With neoplasia versus a heterogeneous, cell, cell lineage, which is more consistent with the reactive process.
So which test should you choose at this website that you can see on the bottom, and I believe it's also on the, sheet with the, references. But if, if it's not, maybe just take a quick screenshot, a screen. Shot here, CSU, CVMBs.
Colostate.edu, etc. Which test should I choose?
They've got a very good table. I've broken it up here so that the cat stuff is all together. But here you can see which types of cells, which types of samples you need, and, which indication you have and what test is, is best.
So we're still out there. These tests compliment each other and aren't definitive on their own, as I've already said. But does it even matter?
From a clinical, from a clinician's perspective, from the cat's perspective, from the client's perspective, who cares? Well, in this is a a probably and possibly an academic point of view. And in this article, differentiating inflammatory bowel disease from alimentary lymphoma and cats doesn't matter?
Will a comprehensive diagnostic evaluation of cats with chronic enteropathy change prognosis or treatment? Probably not. I mean, large cell lymphoma, most definitely, but small cell lymphoma, they're probably going to live for 4 years or, or, or longer on with treatment.
Prognosis and treatments strategy may change, on the, based on the underlying diagnosis with further research. That's this author's cry. It may not be appropriate for every individual, but it should be available and without scientific curiosity and research, advancing the field, the the profession won't advance.
So, you, you know, in this, in this case, I would consider that we need to rule out other conditions. We need to rule out, large cell lymphoma, and mostly we can do that. Certainly, we can do that with histopathology, and, and oftentimes we can do that with ultrasound, but we want to, if we want to get more information, we may need to go further.
Which brings me to treatment options. First steps after diagnostic workup and ruling out other causes, including don't forget parasites. We're gonna do a dietary trial.
This is before we do all of this, this, this lengthy, workup. Up to 3 weeks of an exclusive diet, no treats, no milk from the cereal bowl, no human foods, nothing whatsoever, no insects, no mice, that you can use. A gastrointestinal type diet or a limited antigen novel protein diet, or ideally, I think, starting right away with a hydrolyzed protein diet, or possibly with a home-cooked recipe that has been balanced by, a, veterinary nutritionist, someone who is, is a, a diplomat in veterinary nutrition.
You can also ask for help with balanceit.com. Then, if we, the first trial doesn't work, it may need 2 or 3 or 4 different diets sequentially, which most people aren't, aren't, up for doing.
I get it from a nutritionist's perspective or an allergist perspective that this is, is logical, but we're, we are talking about human behaviour. And then if all dietary trials fail, offer biopsies. I'm far more likely after the first trial to offer biopsies.
If, however, biopsies aren't available, then we can start a steroid or antibiotic trial. Now, I am very concerned about responsible antibiotic stewardship. So I'm not likely going to jump on that.
So I'm, I'm far more likely to jump on a. Steroid trial because it's highly, it's unlikely that it's infectious, cause, and, therefore, steroids should not be making it, it worse. So corticosteroids and wait on the antibiotic trial until other treatments have failed.
So we're gonna do diet with for, for lymphocytic plasma cytic enteropathy, diet plus pre prednisolone, starting at 2 milligrammes per kilogramme per day, either once, a day or divided, half 1 milligramme, per kilogramme, given twice a day. Taper by 25% every 3 weeks, 3 to 4 weeks to the. Lowest effective dose.
Bedesonide is an alternative for diabetic cats. However, it's, I don't know what, success you have had. I have not used a lot of it, because in the few cats that I have used it in, it has not worked very well.
If there is maabsorption present, then we should probably start with dexamethasone subcutaneously. If there is, if the, chronic enteropathy is refractory, then we want to add chlorabusil. And chlorambucil, we can do it either, in a metronomic way or in a pulse way.
I prefer the metronomic way where they, where a cat gets 2 milligrammes, every 2 days if they're a large cat or every 3 days if they're a smaller cat. Very scientific, but low doses of chemotherapy drugs are given continuously over a long period of time, which modulates the tumour microenvironment due to the cytotoxic, antiangiogenic and immune modulatory effects. Alternately, one can give 20 milligrammes per metre squared, orally every 2 weeks or 15 milligrammes per.
Squared for 4 days every 3 weeks. I just like, I think it's simpler for clients to go, you know, and, and, and if you go, Monday, Wednesday, Friday, Monday, Wednesday, Friday for a larger cat or or Monday, Wednes Monday, Thursday, Monday, Thursday for a smaller cat, I think it's easier for clients to do. So, what about if you've got small cell lymphoma?
There were 3 groups in, in a study back in 2009. 1st group got oral prednisolone and high dose pulse, chlorambuils. So, as, then the second, group got modified Madison, Wisconsin, multi-agent, and the third group got a combination of both protocols.
There was good to excellent response in three quarters of, of this small group of cats, 17 cats. earlier, 10 years earlier, Fondacaro et all had found that the disease-free interval was a good 5.8 to 49 months, with using the chlorambuil 2 milligrammes, as I, I've said, every 2 or 3 days.
And then, just after this paper had been published, Stein published that the overall response rate was in fact 96% with a media. In clinic, clinical remission of 786 days. And in that paper, she, rescued these cats.
100% of them were rescued using chlo cyclophosphamide and, glucocorticoid together. So, in general, because it's so easy and it can be done at home, I do, oral prednisolone with the, metronomic, chlorambucil. What's the prognosis?
Well, with, lymphocytic plasmacytic enteropathy diet plus prednisolone plus or minus chlorambucil, gosh, they can go years and years and years, can't they? Whereas with small cell lymphoma, with prednisolone and chlorambusil, maybe changing diet, it's, it's a, they still go for, you know, I've, I've shown they can go for 4 years, they can, that's, it's a good disease. It's a good disease to have.
OK. So changing thoughts there, we'll talk about adjusting the microbiome, because I did mention that microbiome may be affected. We're all well familiar with pictures of this sort.
This is for for humans, and looking at all the various Different things that can cause upsets in the microbiota, inflammatory cytokines, metabolites, etc. Etc. So it's a, a real question of of balance.
So this biosis or imbalance of bacteria is also caused by bacterial or viral infection or parasites, not just by inflammation as we've been, or neoplasia, as we've been talking about here. Diet or diet change, these rapid changes, drug therapy might change. Or altered gut secretions due to concurrent disease.
And this can result in maldigestion and maabsorption, a dietary intolerance or hypersensitivity, which is gonna look like, which is a form of LPE and inflammation. So are there changes in the gastrointestinal microbiome with chronic enteropathy? Well, in a very recent paper, 2024, it, it was shown that in fact, there are, whereas previously it was believed not, that it was primarily in a decrease in diversity from the healthy cat with balanced metaboli.
And balance a widely diverse gut microbiota to in inflammatory disease versus small cell lymphoma, where you can see there's quite a difference in the proportion of different types of bacteria, as well as altered metabolites. So what about the faecal microbiome? Looking at the faecal microbiome in cats with inflammatory disease or alimentary small cell lymphoma.
There was a lower micro lower faecal microbial microbial diversity, . The dysbiosis patterns were similar to those in people with inflammatory bowel disease or irritable bowel disease rather. And as you can see, there's a decreased number of obligate anaerobes and increased numbers of facultative anaerobes.
One, this is a, a very old paper that I did want to point out, cause I probably, you, you don't get to see the Canadian Veterinary Journal. And, and this was a very good, study that Doctor Scott Weiss, who is a god in all things, infectious, if you don't already subscribe to worms and the Worms and Germs blog, I would recommend that you do, worms and germs blog.com.
And, he, he looked at studying, he want to evaluate labels, and labels and how accurately they reflected the bacterial contents of commercial probiotics. This was back in 2011. So undoubtedly different things that were available, and these were for marketed for use in animals.
What he did was he purchased 25 probiotics. He scrutinised the labels, and then they actually enumerated the bacterial contents. 21, only 21 of the products listed specific microorganisms.
Well, right there, I suspect that your 11 of your eyebrows has gone up a little bit. Then, in 15 of the 25, so 60% of the products, they, listed expected bacterial numbers. So, again, not so great, but better than nothing.
One or more of the organisms were misspelt on the labels of 7 out of the, 22 of the products that bothered to list specific organisms. Viable growth ranged from 0 to 2 times 10 to 9 colony forming units per gramme. Only 4 out of 15, 27% of the products that had specific claims of viable organisms met or exceeded their label claim.
So hopefully both your eyebrows are reaching for your hairline now, and only two of these also had an acceptable label which properly described the contents. So big deficiencies in veterinary probiotic quality remain. Veterinarians and owners should scrutinise commercial probiotics and demand evidence of quality control and efficacy.
So, very sketchy indeed. So currently, this is a, a, a paper from 2020, says currently selection of bacterial strains for most commercial probiotic products is mostly based on their ability to survive the passage through the stomach and small intestine, their ability to adhere to mucus, and in vitro, so so plate, immunomodulation, not looking at actually, what the, what the bacteria, it, it is good at doing. So what we want to look for is that they consistently meet the label claim that there are independently published clinical data for the species, and these two, the Fortafloide Fortiflora SA and Proviable DC which hope.
You have these. I do have published clinical data, and there is published and, and, soon to be published data on the Visiome vets. So these ones are, at least do, have what in them what they say, and they can get through the gut without being without deteriorating and can grow and are stable.
So how past, present, and future of gastrointestinal microbiota research in cats. This is a paper that you might want to check out, efficacy of probiotic, prebiotics, symbiotic, and postbiotic supplementation on gastrointestinal Health in Cats, a systemic, systematic review and meta-analysis from 2024 in JSAP unfortunately concludes that current data highlight the need for further research, especially. Focused, on at-risk groups and sick cats before advocating the use of biotic supplementation.
So while it is something we can do, and it may be something that doesn't cause harm, I'm always cautious using that, that phrase because it may in fact cause harm in that if the person, if the client. Is using up their relationship with their cat to administer something to that cat that, that their time and their financial resources, that we don't know works, that's doing harm. I think we're better off to use, to, to use those resources, it for things that we do know work.
All right. So where am I at? 40 minutes.
Hmm. OK, let's see what I can do here. Talking about unexpected weight loss and maintenance of body condition, and feeding the vomiting cat and feeding tubes, I unfortunately, won't be able to teach.
So weight loss may indicate subclinical disease and should be investigated. Evaluating percentage weight change is very easy and very helpful. Because we, by maintaining weight and lean body mass, we can delay morbidity and mortality.
On unhealthy musculoskeletal changes, differentials are certainly age associated sarcopenia, but also inadequate dietary protein. Sometimes we're feeding a diet that doesn't have enough protein in it for them to, store muscle, in which case, in order to, in order to, function, they have to metabolise their own, muscle, which is not good for their kid. Kidneys either.
And it could also be that they're not eating enough protein, not eating enough, because it's, it's painful for them to get there. They may, as most older cats have a decreased ability to digest and absorb protein. That is an, an age related change.
And they may have an increased need if they have a disease such as, kidney disease, such as heart disease, such as neoplasia because of disease associated chachexia. The plus they may have increased loss if they have, not very common, but if they have, glomerul nephritis or, or something like that. Now, remember, we have body condition scoring, and we have muscle condition scoring.
And body condition scoring looks at the adequacy of calories. This cat is getting, an, the ideal amount of calories. This cat is getting too few calories.
This cat is getting too many calories. However, it doesn't tell us where those calories are coming from. Are they fat source calories, carbohydrate source calories, or protein calories?
Muscle mass tells us about protein calories. So with the muscle condition scoring, what we have now is normal muscle mass, and we're, when we stroke the head, when we just, excuse me one sec. Oh God this.
When we stroke the cat's head down their spine, and we also look at their, you know, feel their, their hip bone, their their scapula, and see if they've got muscle wasting in the thigh. So, normal muscle mass feels like when you, stroke your palm with your palm up across your, your, Whatever this part of your, your hand is called. And when you mild loss on the top right, is when you turn your hand over and you feel across your knuckles.
You can see, now we can start to feel the, the scapula, the, the spinal, the vertebral, bumps, etc. Then bottom left is moderate. Muscle mass, which is when I turn my hand sideways, but only partially, drop my fingers and what it feels like across my knuckles.
And severe muscle loss is when I make a fist and I feel across the knuckles like that. So, normal, mild, moderate, severe. All right.
So now you know how to do that. You can also have high body condition score with low muscle mass, such as in this obese cat who's got a high body condition, but she has no muscles, she's got sarcopenic obesity. All right.
So we've already talked about the different things that can cause muscle wasting associated with, feeding. Remember, any time you send a diet home, whether it's a maintenance diet, whether it's a kitten diet, whether it's a diet for kidneys, for, hydrolyzed protein, whatever it might be, you are performing a dietary trial of N equals 1. And you need to see, just as you do, if you're doing treatment for, I don't know, cholangitis, and you get them back to recheck the liver enzymes, you need to get them back and see how is their coat, how is their weight?
How is their, are their body and muscle condition scores. So doing those, performing those, on, on every single cat. It still is, is, it's not really controversial, but maybe, I don't know, the protein requirements increase in older cats because they've got decreased appetite.
So we need to make more biologically available and more protein, for them. They have a decreased ability to digest nutrients. They may have catabolic disease, some have sarcopenia.
So we need to be very cautious with protein, restriction. That's a whole another conversation, isn't it? Feeding tips, we wanna make sure that there's space between water and food.
They don't have to have their plate of food and their mug of tea. Right beside each other the way we do. They don't want the litter tray anywhere near the food.
We don't want to be in the in the loo with with the, the toilet, and being on the ground with with a blanket and the food and our water right there, we would find that quite disgusting as well. The bowls should be wide, especially in the clinic, so their whiskers aren't being impaired by interfered with, so that they can't sense, if someone is coming air movement. It should be quiet.
Cats like to hunt alone and eat alone private, . Warming may be helpful. And so we don't want to change diets in the clinic where they already are frightened.
We want to change them at home. And they need to be easy to access. This little kitty is having a hard time with the stairs, so we would want to make sure that there's food on every level for her.
Now, sarcopenia and cachexia, I've mentioned those two. How are they different? Well, both have decreased lean body mass and both predict disability, but sarcopenia is a nutrition-related disorder of ageing.
That may or may not have concurrent illness. It's characterised by a gradual generalised loss of strength and muscle, resulting in dis in disability, predisposing to disease, decreasing quality of life and death. It'd be nice if it decreased death, but it, that's sort of terrible grammar.
is it, whereas caexia is characteristic of certain diseases including hyperthyroidism, neoplasia, congestive heart failure. So, weight loss is an early sign of chronic kidney disease. We know this.
Getting a baby scale, this is, I have one right on the, on my window ledge, that I, I weigh my cats on regularly. And with chronic kidney disease, we know that weight loss begins 3 years before we can even make the diagnosis with SDMA, with creatinine, with urine-specific gravity, with FGF 23. Actually, I don't know about that one.
That hasn't been looked at. Cancer, renal disease, hyperthyroidism, a different paper. Look at weight loss began 2.5 years before death.
Other diseases, weight loss began 3 and 3/4 years before death. So, we want to be weighing cats early on so that we can, because if we can change nu through through nutrition, get them to stop losing weight, we can, decrease morbidity and mortality. In fact, with large cell lymphoma, cats who lost more than 5% of weight during treatment had much sort of survival time than those who maintained their weight, the same disease.
With other cancers, cats with slightly increased or ideal body condition scores survived up to 6 times longer than if they were underweight. With heart failure, the best outcome is if, if an individual human or cat is normal or slightly increased, so a 6 out of 9, which I sort of figure I am, so I, rather than constantly berating myself for that, I think, well, if I get heart failure or cancer, I'm gonna have a better. Outcome, before treatment rather than being underweight or obese.
And this is called the obesity paradox. Being slightly overweight or ideal weight improves outcomes for cats with heart disease and with cancer. So our goal is, it must be to maintain weight as cats age.
So, I'm gonna skip the eating behaviour components here. I did want to mention here, OK. Why is she or he not eating enough?
We want to be thinking illness, but not just illness, palatability, nausea, vomiting, pain, anxiety, difficulty accessing food, either psychologically because they've got to go past something or someone that scares them, or because there are stairs or, they have to jump over something. Pain could be in the mouth, could be in the, the, osteoarthritis. Lots of different reasons.
Could it also be boredom with food. And what should I do if he or she is vomiting? Well, nutritional support is essential.
Cats, because they are designed to eat 8 to 10 small meals a day. Meals of about 35 calories, 8 to 10 times a day, which is the equivalent of a mouse, and 35 calories is, it actually works out to be, about 10 to 15 pieces of dry food, and then wet food depends on the wet food. So we want to control vomiting.
We need to avoid fasting. Cats don't fast. In fact, as, as I hope you're aware, the AFP, now called the feline VMA anaesthesia guidelines, as well as the Aha anaesthesia guidelines, American Animal Hospital Association, recommend fasting cats no longer than 3 to 4 hours before anaesthetizing them.
12 hours is not appropriate for cats or most dogs either. So we want to control vomiting, avoid fasting, and we need to provide adequate, balanced, nutrition, both good quality and quantity. They are all good carnivores, and they survive with, on a balanced protein-based diet.
They need to be getting up approximately, this is just a rule of thumb, nothing, nothing accurate. I generally, cause if you're not doing anything, this is a lot better than, than, . Not using a formula.
50 kilocalories per kilogramme, ideal weight per day, not obese weight, not skinny weight. 50k cals per kid, ideal weight per day, that contains 5 to 5.4 grammes of protein per kilogramme ideal weight per day.
Cats are protein pigs. You consider that we need 1 to 2 grammes of protein per pound. Per day.
So 1 to 2, so about, you know, 2, to maybe 4 per kilo. And cats need, 5 to 5.4 grammes of protein per kilo.
And then appetite stimulants, of course, but if somebody's vomiting, we need to, we need to deal with the vomiting first. And we need to optimise hydration because hydration makes you, dehydration makes you nauseous. Dehydration gives you a headache.
Dehydration makes you feel, inappetent. How we can use H2 antagonists or proton pump inhibitors, or go straight to an antiemetic, which is what I think most of us would prefer to do. And here are, drugs and doses.
How is dehydration like a hangover? Well, dehydration plus acidosis, plus oxidative stress and inflammation is a hangover. And many older cats, this is one of mine, who is no longer, unfortunately, dehyd.
Hydration causes intent or hangovers inappetence or anorexia, nausea, vomiting, lethargy, pain. I mean, you look at Nimitz, and he clearly has a headache, withdrawn or grumpy, constipated, and what is it that clients call us about? Their cat's inappetent, nauseous, and we're reaching for appetite stimulants and antiemetics, and, and, let's make sure we always remember to give fluids as well.
So, and it's not just important in the hospital. It's also very important that at home, we raise bowls if needed, we get them away from water, we make it it easy to access. We can use tempting foods.
Tomato paste is something that many cats like, licky licks or. True or, cat it or whichever brand of, of, these tube pastes are very useful. But remember, they're only about, at least with, true.
I don't know what Licky Licks, it's 9 calories, 7 to 9 calories per tube. And remember, cats need, 50k cows per kilogramme ideal weight. Catnip may be helpful to stimulate dried fish, dried, chicken, may be helpful as well.
We certainly have drugs we can use as well, and Capriorin has been cleared in, in the United States for, chronic kidney disease. But how much is enough? We need to calculate.
Senior cats may actually need 70 kilocalories because they don't absorb as well. 70k cals per kilogramme ideal weight per day. We need to calculate and communicate how much that they, they, they, they need, and then they need to monitor.
Just the last couple of slides here, cause I'm well aware of what time we're at, Bruce. A patient from the, from the, AAFP, IS pardon me, this is from the ISFM. Sam Taylor led this, these consensus guidelines.
An assessment tool for identifying the need for nutritional support. You can see this is a decreased food intake for 3 to less than 3. 3 to 5 days, greater than 5 days, less than 80%, which isn't, you know, most people can't tell the difference between 100% and 80% resting energy requirement, but you can see it gradually increases to the risk level, presence of weight loss, vomiting or diarrhoea, if it's severe.
A low body condition score, not even severe low, muscle condition score, moderate to severe loss, mild. Loss hypoalbuminemia. Expected course of illness, the duration there less than 2 days, all the way up to greater than 3 days, which most things are.
And a patient with 2 or more high risk factors present should receive nutritional support immediately once stabilised. Patients with fewer than 2 risk factors should be closely monitored and reassessed daily. And of course, the methods of feeding, we have oral assisted.
I don't call it force feeding, that's really bad languaging versus tubes. We have nasal esophageal tubes and esophageal tubes. Each one has advantages and disadvantages, what they may need an anaesthetic.
Some of them don't, when you can start using them, how long you can use them, what types of foods you can use, and how well the patient accepts them. I don't think they accept any or any tubes, na, esophageal tubes very well at all, but we want to start early. Now, the last thing I want to say here, and I'm talking about feeding tubes that would is gonna have to be another, webinar which hopefully I'll be invited to do.
But oral assisted, this is a very bad way to, to perform this, this, treatment. The first thing is, what I would ask you is, what is the oral capacity of a cat? Not even a kitten, but of a cat, an adult cat.
Well, the answer to that. If you hopefully come up with a number in your head, is about 0.5 mL.
So if you're using a 12 mL syringe, such as this individual in this picture is using, there's no way that you can administer half a mL at a time. So it's no wonder that the cat will shake their head and try to get away and won't be able to swallow. So when about the largest syringes you can use would be 3 CC syringes.
But the, the problem with that too is if you, like I, reuse these syringes, they often get really sticky. So, you're probably better off to use 1 mL syringes. And so, instead of using 3 12 cc syringes for 36 mLs of food, you're gonna need to use 12, 3 C syringes or 36 1 cc syringes or whatever.
So, again, no time to, to go into these things, right now, and I most certainly apologise for that. Let me just, skip quickly to, there, the, I do want to mention that there's some fabulous, resources that the ISFM has put together with, about, inhabitants, as well as, feeding tubes, and you can, certainly, get to those with optimising we, we want to be proactive. Alleviate pain, calculate the nutritional needs and make sure that they get them.
Try different bowls and different diet types, appetite stimulants, antiemetics, get feeding tubes in early and correct underlying, problems. And I, again, I apologise that I am unable to talk about gallbladders or, or more than that. Margie, thank you so much for your, info tonight and sharing your knowledge with us.
I know that I speak for myself, and I'm sure I speak for everybody else when, we, I say, it was fantastic, and we would love to have you back. We'll have to get, Beck and them on to organise another webinar for, OTubes and, and the likes. Because, those are essential when you have, a, a sick kitty.
They really are. It's, it's, in my opinion anyway, they're about as important as fluids. Yes.
Yeah, hydration, nutrition, analgesia, and meeting behavioural needs in order to reduce stress. Those are the four keys to well-being. Yeah, absolutely.
And, and keys to, to quality of life as well. Yes, indeed. Yeah, fantastic.
Well, I, we haven't had any questions coming through at all. I think everybody that's listening like me is sat transfixed. They haven't even thought about questions because they've been riveted by what you've been sharing with us.
So thank you so much for your time tonight. We really appreciate it and we look forward to having you back.