Of the feline vaccine preventable diseases, FeLV is arguably the deadliest, with reported mortality rates of up to 90% within 3 years of infection.1-3 The ability of FeLV to cause immune suppression, bone marrow disorders, and lymphoma/leukaemia makes it an important cause of morbidity and mortality in domestic cats. Recognising this, the World Small Animal Veterinary Association (WSAVA) has recently reclassified FeLV as a core vaccine in areas where it is endemic.4
What’s the risk?
Exposure risk may be higher than you think!
Recent research demonstrates that although the prevalence of deadly progressive FeLV infections in Australia is 0.5%, almost 1 in 7 Australian cats with outdoor access have been exposed to the virus (regressive or abortive infections) and therefore been at risk of its severe consequences.5
Progressively infected cats represent just the ‘tip of the iceberg’ of pet cats in Australia that have been exposed to FeLV.
– unexposed (84%)
FeLV infection status of healthy, client-owned cats with outdoor access predominantly from Eastern Australia. Not to scale. Approximately 2.5% of cats were unclassifiable as FeLV-unexposed or abortive due to insufficient samples being available for further antibody testing.5
Simple protocol for optimal compliance
FeLV is now classified as a core vaccine by the WSAVA Vaccination Guidelines Group and the American Association of Feline Practitioners (AAFP) for young cats and adult cats with outdoor access and can easily be incorporated into a feline vaccination protocol.4,6
Fel-O-Vax® 5 provides a highly effective and convenient option to protect cats against this potentially fatal disease.
Young cats are most at risk of FeLV and at the kitten stage, future lifestyle is often unknown. Vaccination from 8 weeks of age allows for optimal protection in these early months. Furthermore, most Australian adult cats will have outdoor access and be at continued risk, making it simple to continue this protection into their adult years. At the first annual vaccination, if the cat is deemed strictly indoors, an F3 vaccine can be given as recommended.
Kitten/adult
Suggested
4. Squires, R. A. et al. (2024)
Westman, M. et al. (2019) The Diagnosis of Feline Leukaemia Virus
6. Stone, A. E., et al. (2020)
C&T
Issue 320 | September 2025
Control & Therapy Series
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...not what he/she should have done, BUT WHAT HE/SHE DID, right or wrong, the full details, revealing the actual “blood and dung and guts” of real practice as it happened, when tired, at night, in the rain in the paddock, poor lighting, no other vet to help.
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Over the years, we have been privileged to see past CVE Directors Dr Doug Bryden AM and Dr Bill Howey OAM recognised in the Queen’s/King’s Birthday Honours. This year we are so proud to congratulate the C&T Veterinary Editor, Dr Richard Malik, for being awarded Member of the Order of Australia (AM) for significant service to veterinary science, particularly in the field of medicine and infectious diseases.
Last issue we acknowledged the 60th Anniversary year of The CVE with an historical timeline celebrating some important milestones. I apologise for some mistakes in the representations of these awards for Drs Bryden and Howey which have been corrected: cve.edu.au/our-story
I am excited that another great C&T issue is now in your hands. These days, if you want the latest veterinary knowledge, you can have it in seconds. It’s a golden age for access but also an age of overwhelm. Endless scrolling and fact collecting can miss something important: the lived texture of veterinary life. This is where a well-told case captures more than the diagnosis—it brings to life the uncertainty and the decision points that shape outcomes. It is a snapshot of real practice with all its messiness. These stories slow us down and invite us to walk alongside a colleague, to learn not just what they did but also why they did it.
We aim to make the latest and emerging veterinary content not only accessible but also meaningful and relevant. For over 55 years, The C&T has been sharing interesting cases contributed from the veterinary community—stories that showcase the incredible diversity that presents to veterinary practice. This issue features stories from colleagues on snake bites, microscopic investigations in a case where a rabbit left 1/3 of its body weight behind in the practice and more!
I invite you to engage with these cases and indulge in the experience of others. Let them spark curiosity, challenge assumptions and remind you that veterinary medicine is as much about the story as the science.
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Complications Following Brown Snake Envenomation
Only a Vet’s Dog Could Have this Many
Nicole Whitehouse BVSc/BVBio (Hons)
Wagga Wagga Veterinary Hospital
e. waggavet@waggavet.com.au
e. nikki.whitehouse@waggavet.com.au
t. 02 6926 0900
C&T No. 6084
Nikki is based in Wagga Wagga, where she works as a mixed practice veterinarian.
She has a special interest in Emergency and Internal Medicine, and gets to practice these areas a bit too often on her own pets.
Initial Presentation
Sasha is a 42 kg 10-year-old-female neutered Great Dane cross from Wagga Wagga, NSW. Around 1pm in November, she was found collapsed in the yard, after being seen to be normal 20 minutes prior. She was transferred to hospital, where she was assessed within 15 minutes of being found.
Sasha was markedly obtunded on presentation, blue mucous membranes, CRT 2s and HR 160BPM. She produced massive amounts of bloody diarrhoea. A Vet-BLUE and AFAST revealed a gall bladder halo sign, and no free abdominal or thoracic fluid. She was initially treated with a 20mL/kg bolus of intravenous Lactated Ringers Solution and oxygen by mask. At this stage, our most likely differential diagnoses for her were snake envenomation and anaphylaxis. She was administered Tiger-Brown 8100IU Antivenom (Padula Serums Pty Ltd) in case of envenomation, diluted 1:1 with saline and administered over 10 minutes.
Initial Diagnostics
Sasha had a coagulation panel performed, which showed normal PT and elevated APTT (>200, 75-105). A comprehensive panel revealed mild haemoconcentration (HCT 0.65, 0.37-0.62) and a mild increase in ALT (194, 10-125).
At this stage, a dead brown snake was found in the yard near where she had collapsed, and she was treated with an additional 2050IU Multi-Brown snake Antivenom (Summerland Serums Pty Ltd). Following treatment with the second vial, her colour was pink, CRT 1s, HR 120 and her mentation was improved. She was kept on intravenous fluid therapy and was clinically well.
Second presentation
Twenty-four hours after initial presentation, Sasha vomited and seemed flat. Reassessment revealed an unexpected irregularly irregular tachyarrhythmia. This was monitored by ECG and progressed into ventricular tachycardia overnight (HR consistently >180, pulse deficits present). She was treated with both boluses of lidocaine and a lidocaine CRI (2mg/kg boluses repeated up to 5 times as needed; up to 80mcg/kg/min). She had a short-lived response to intravenous boluses and intermittently developed a polymorphic ventricular tachycardia. Repeat biochemistry revealed a mild hypoproteinemia (50, 52-82), consistent with a mild hypoalbuminaemia (19, 22-39), which was attributed to her diarrhoea. Her ALT had increased to 400 (10-125) and her electrolyte panel was unremarkable.
Sasha was started on sotalol (80mg PO BID). Her arrhythmia improved over the next 24 hours and she was discharged home on sotalol and ondansetron (8mg PO BID), both of which were tapered after one week. She had some bruising and several areas of ulceration of her skin where ECG clips had been applied. These were clipped and cleaned and were presumed to be due to poor perfusion.
Third presentation
Two weeks after her initial snake envenomation, Sasha represented for thickened, oozing and blackened skin along her right ear and side, and ulcerations to both front feet. She was anaesthetised for full assessment, potential debridement and biopsy.
Upon clipping, it became apparent that wounds were distributed across her right side. Differentials included hypoperfusion to these sites at time of collapse and/ or thermal injury. As she had never laid on this side in hospital, nor did she have a heat mat placed at any time, we suspect these were burns from lying on hot concrete at the time of her initial collapse or sun exposure (Note: She was found near but not on a concrete surface). Hypoperfusion alone was considered less likely given ulcerative lesions on the right side of both forefeet.
Based on this, we elected to remove the burn eschar and send a sample for culture and susceptibility testing. All diseased tissue was removed, and the wound was closed with extensive reliance on undermining of subcutaneous
1
2
3 4 5 6
Figure 1. Sasha presented with extensive thickening, and scabbing of the skin
Figure 2. The distribution of lesions became clearer with clipping
Figure 3. Intraoperative photo postdebridement of eschar
Figure 4. Post-operative day 1
Figure 5. Post-operative day 1
Figure 6. Sasha 8-weeks post initial snake envenomation
tissue and several layers of absorbable PDO2/0 in simple interrupted and continuous patterns. Skin closure where possible with minimal tension was performed with 3/0 polypropylene in a cruciate pattern. Areas that could not be closed were managed with external tie down bandages. These were initially placed with Solugel™ and manuka honey in combination on the open wounds, with bandages being changed frequently (initially q6-8h) as soon as strike through occurred.
Ongoing management
Culture and susceptibility testing revealed multi-resistant Enterobacter cloacae and Enterococcus sp. She was started on a combination of trimethoprim sulphadiazine and amoxicillin-clavulanate post operatively for 2 weeks.
Eight weeks later, with several bandage changes and a collection of T-shirts in her wardrobe, Sasha is almost completely healed.
Discussion
This case report provides an opportunity to explore sequelae that are not often seen following Brown Snake Envenomation. Her initial response to antivenom and supportive care, aligns well with what we would expect where a potential envenomation is treated promptly, with almost 90% of dogs that are diagnosed with Brown Snake Envenomation surviving to discharge.¹
Sasha’s second presentation highlighted the potential for severe cardiac arrhythmias following Brown Snake
envenomation. Cardiac arrhythmias following Brown Snake envenomation in dogs have not been frequently reported in the veterinary or human literature.² However, it is known that Brown Snake Envenomation can cause severe cardiovascular effects. Brown snake venom contains prothrombin activators that have been postulated to result in thrombosis and pulmonary outflow obstruction, leading to haemodynamic collapse and hypotension. ³ This is supported by the presence of gall bladder oedema (characterised by the ‘halo sign’), which is a sign of venous congestion, and poor return of blood to the heart. Therefore, we suspect that the venom indirectly resulted in myocardial injury, and subsequent reperfusion injury that caused the ventricular arrhythmias several days after the initial insult.
Furthermore, burns are known to cause a systemic inflammatory response that can contribute to myocardial ischaemia and subsequent arrhythmias. When skin is severely burned, it can take 7-10 days for the eschar to develop, fitting this history. By classifying this as a thermal burn, this would be classed as a third-degree burn covering 35% of total body surface area (TBSA), which we would expect to have significant metabolic complications.⁴
Perhaps one of the most concerning aspects of Sasha’s recovery was the development of multi-resistant infections following her thermal injuries. The wound culture revealed Enterobacter cloacae and Enterococcus species, both of which are known to be opportunistic pathogens. These organisms are often resistant to multiple antibiotics, presenting a challenge in veterinary medicine, especially in critically ill patients who are already immunocompromised due to systemic shock and the effects of venom. The presence of resistant infections underscores the importance of stringent infection control protocols in the hospital setting and the utilisation of culture and sensitivity testing.
Additionally, Sasha’s skin ulcerations, most likely related to poor perfusion, thermal injury and likely worsened by prolonged contact with ECG clips, further emphasise the importance of monitoring skin integrity in critically ill patients. These ulcerations were properly managed, cleaned, and treated with antibiotic therapy, but they serve as a reminder of the potential for hospitalacquired injuries in critically ill patients, especially when prolonged monitoring or equipment is used.
Sasha’s case is an example of the variety of challenges that can be seen and managed, including shock, arrhythmias, thermal injuries, and resistant infections. Despite the complexity of her case medically, she responded well to treatment and her case is a fantastic example where persistence and nursing care can result in fantastic outcomes for our patients.
Figure 7. Sasha 14-weeks post initial snakeenvenomation
Figure 8. Fully healed at 16-weeks
References
1. Allen GE, Brown SGA, Buckley NA, O’Leary MA, Page CB, et al. (2012) Clinical Effects and Antivenom Dosing in Brown Snake (Pseudonaja spp.) Envenoming — Australian Snakebite Project (ASP-14). PLOS ONE 7(12): e53188. https://doi.org/10.1371/ journal.pone.0053188
2. Day, SK., Nash, KJ., Midwinter, MJ. and Goodwin, WA., A retrospective analysis of clinical features, management and outcomes in dogs and cats with Eastern Brown Snake envenomation (2016–2022). Aust Vet J. 2025; 103: 77–87. https://doi.org/10.1111/avj.13399
3. Heller, J., Mellor, D., Hodgson, J., Reid, S., Hodgson, D. and Bosward, K. (2007), Elapid snake envenomation in dogs in New South Wales: a review. Aust Vet J. 85: 469-479. https://doi. org/10.1111/j.1751-0813.2007.00194.x
4. Garzotto, CK. 2015. “Thermal Burn Injury.” In Small Animal Critical Care Medicine , by Deborah C. Silverstein and Kate Hopper. Missouri: Elsevier Saunders.
Comment Courtesy of
Rob Webster BVSc FANZCVS
Animal Emergency Australia
104 Eastlake St, Carrara QLD 4211
e. rwebster@aes.email
What a lucky girl!
Well done to the clinical team, and the author for sharing a great story of case management with a fortunate and well-deserved outcome!
Some comments which I hope are useful to the readers of The C&T
– Treat the horse, not the zebra!
Snake envenomation is a complex and multi-systemic insult requiring early intervention often before diagnosis is confirmed. In areas with a high prevalence of snake bite, envenomation should be at the top of the DDX list during high season so that treatment is not delayed.
It is interesting that in this case the patient had clinical signs and pathology consistent with anaphylaxis, but snake bite was confirmed when the dead snake was located AFTER treatment. The decision making was appropriate and can be supported by considering the relative prevalence of the two conditions in Wagga Wagga in summer and how this affects the rate of ‘false positive’ and ‘false negative’ test interpretation.
The test results could be supportive of either condition, but because snake bite is of high prevalence, false negatives are the more frequent error. Anaphylaxis is far less common, so the false positives are the most frequent error. In other words, treat the most likely disease, especially if it is rapidly fatal like snake envenomation.
– Antivenom
Sasha received just over 6000 units of brown snake antivenom during the first hour of treatment which is an appropriate dose. Padula and Leister showed that 4000 units of antivenom neutralised all serum venom in 4 dogs with brown snake envenomation where quantitative venom levels were measured before and after antivenom administration. Day and Nash from the University of Queensland published a retrospective analysis of 240 dogs and 98 cats with brown snake envenomation in which antivenom administration was strongly correlated with improved survival, but there was no association between improved survival and greater than 4000 units of antivenom.
Both those studies were conducted using patients from South-East Queensland, so care must be taken extrapolating their results in other regions where there are likely to be differences in the yield of venom, and potentially the venom components. A reasonable principle in managing this envenomation is to administer antivenom ‘in excess’ to the likely serum venom concentration.
– Thermal burn
What a doozy!
I have unfortunately been associated with multiple patients over the years who have suffered significant burns like this one. My patients developed their burns in hospital rather than from recumbency prior to arrival, and I have learned the difficult lesson that heat pads and hot water bottles are unsafe for patients, because prolonged skin contact and/ or poor circulation reduces dissipation of heat and will unpredictably result in extensive, full thickness burns which can also lead to significant systemic problems (I suspect the ventricular tachycardia and the hypoalbumenaemia may be attributable). The team here managed the burn well. There is always room for debate on eschar removal, and whether to close or maintain as an open wound, but recovery and cosmetic result here both seem excellent.
– Multi-drug Resistant Infection
Was diagnosed because you looked for it. Well done. There is a high prevalence within hospitals, and also the community and we will only know the prevalence through better sampling and testing.
Final Thoughts
What a great job. I am glad Sasha went home healthy despite these complications and the lethal envenomation she presented for.
It could have been worse, imagine if Sasha was a nurse’s dog???
Have you ever examined how your practice handles its sterile goods?
Are you aware of the financial, environmental, or labour impacts of these processes?
Your clinic likely sterilizes surgical instruments and implants using one or more of the following methods:
Single-use blue wraps around some form of basket
Single-use paper or sealable plastic pouches
Reusable cloth drapes
Reusable rigid sterilization containers
Single-use wraps (or blueys) are inexpensive and widely available. However, they are designed for one-time use and then discarded, contributing significantly to a practice’s waste stream, which ultimately ends up in landfills. Australians produce approximately 21.6 billion tonnes of landfill each year, with hospital single-use goods being a notable contributor.¹ Additionally, blueys cannot act as rigid barriers, and sharp instruments can perforate them, compromising kit sterility. If accidental perforation occurs, it’s unlikely you would even be aware of it. Wrapping a kit also takes time, which is something most nurses have in short supply.
Single-use paper or sealable plastic pouches are also inexpensive and commonly available. They allow small quantities of instruments to be contained and sterilized but also end up as landfill. Being non-rigid, they are also susceptible to accidental perforation.²
Reusable cloth drapes are relatively expensive and have been used for many decades. Although they are disposed of infrequently, they need to be washed and dried after each use. Consider the water, detergent, electricity, and nursing time required for each use.³
Reusable rigid sterilization containers are typically made of aluminium. While they require a larger upfront cost, their lifespan is incomparable, as rigid containers can last for more than a decade. If you calculate the processing cost per kit, a practice can see savings as soon as the second year of ownership, simply by comparing it to the cost of consumables that would have been used instead.⁴
References:
3. Exploring the Safety and Environmental Impact of Sterilization Techniques.
4. Sustainability | Reducing the Environmental Impact of Sterilization Packaging for Surgical Instruments in the Operating Room: A Comparative Life Cycle Assessment of Disposable versus Reusable Systems (mdpi.com)
QUESTION
Seen an intriguing case recently?
Send us a high resolution image/s to pose the Q. and an article on how you treated it to appear in the following issue.
anSwer
What’s YOUR Diagnosis?
C&T No. 6070, Issue 319 Jun 2025
Multifocal Lesions in a Cat
Mark Krockenberger
Professor of Veterinary Pathology
Registered Specialist Veterinary Pathologist
Sydney School of Veterinary Science
Sydney Infectious Diseases
Read the history and see all the images here cve.edu.au/CandT-6070
1. What is your diagnosis?
Multifocal cryptococcosis involving skin and oral cavity.
ANSWER
Read How Would You Treat This Case? on page 12 and send in your answer.
The best and most complete will be published in December and wins the CVE$300 Voucher.
The images of the fine needle aspirate cytology stained with DiffQuik reveal large numbers of variably sized circular yeast cells with a thick cell wall and a narrow negatively stained extracellular capsule. Narrow-necked budding of the yeasts, while not particularly prominent, is evident in both images. It appears that these yeasts are in an extracellular and intracellular location. While there is no scale provided, it appears that some of these are perhaps surprisingly small (I would estimate they may be ranging in size from 2-10 microns in diameter).
The other major possibilities are histoplasmosis and sporotrichosis. The small forms of the fungus present are consistent with these other fungi, however the large forms are not so consistent. The presence of capsule and evidence of narrow-necked budding is also more consistent with cryptococcosis rather than histoplasmosis or sporotrichosis.
In different parts of the world these other differentials may require more consideration, however both these diseases are rare in Australia compared to cryptococcosis.
2. Explain the likely pathogenesis of the disease process.
Cryptococcosis is a relatively common fungal disease globally in cats. The disease is almost invariably caused by members of the Cryptococcus neoformans species complex or Cryptococcus gattii species complex, but rarely other species from the genus Cryptococcus may cause disease in animals and people. It is worth noting that the two species complexes are made up of multiple species (C. neoformans species complex is comprised of C. neoformans, C. deneoformans and a C. neoformans/C. deneoformans hybrid; while the C. gattii complex is comprised of C. gattii, C. deuterogatii, C. bacillispora, C. tetragattii, C. decagatti ) that are identified by genomic differences, however diagnostic labs are generally reporting these fungi as the two species complexes and any distinct difference in pathogenesis between species within the species complex remains unclear.
These fungi are environmental fungi and are found in many different environments. Classically, members of the C. neoformans species complex are associated with bird excreta and various trees in the environment, and the C. gattii species complex are associated with different trees and C. gattii is particularly associated with eucalypts in Australia.
Generally, pathogenesis involves inhalation or direct inoculation of the organism. It is possible in this case that the primary lesion is in the rostral nasal cavity or in the rostral oral cavity. Of course, it is not impossible for the primary lesion to be in other parts of the respiratory tract or even elsewhere in the alimentary tract (very unusual for a cat). In this particular case, it appears that there has been dissemination of the organism to the skin multifocally, although I am not quite sure from the images of the exact distribution of the cutaneous lesions. Dissemination is also supported by the tongue lesions (multifocal differing size lesions in oral cavity).
The relatively small capsule makes me consider that the strain infecting this cat is more likely to be in the C. neoformans species complex. Members of the C. gattii species complex generally have more prominent large capsules.
The size of the fungus, intracellular and extracellular distribution, cutaneous dissemination, makes me wonder about whether it may be a strain of C. deneoformans (used to be described as C. neoformans serotype D). C. deneoformans is found more commonly in Europe but can also be found globally, including in Australia.
The speciation of the fungus requires fungal culture to be performed. Antifungal susceptibilities are generally quite predictable but can also be performed by specialist laboratories.
A suitable diagnostic tool to consider in these cases is cryptococcal antigen serology. There are point of care kits that can be used, although my experience is that the IMMY Cryptococcal Lateral Flow Assay (immunochromatography assay) is reliable and an excellent screening test. We usually confirm positive results from this test in the laboratory by a latex agglutination test (LCAT). You could look at this research paper (Krockenberger, MB, C Marschner, P Martin, G Reppas, C Halliday, LJ Schmertmann, AM Harvey, R Malik (2020). Comparing immunochromatography with latex agglutination
testing for the diagnosis of cryptococcosis in cats, dogs and koalas. Medical Mycology 58:39-46 https://doi.org/10.1093/mmy/myz010). Occasionally false results occur in any diagnostic test (Teh A, E Pritchard, SL Donahoe, R Malik, M Krockenberger (2024). A case of disseminated cryptococcosis with abdominal involvement due to Cryptococcus neoformans species complex in a Ragdoll cat and false-negative cryptococcal antigen lateral flow tests due to the postzone phenomenon. Australian Veterinary Journal 102:316-312 https://doi.org/10.1111/ avj.13329 )
In this particular case, while we expect the cryptococcal antigen serology to be positive, because of the relatively narrow capsule size it may have a relatively low serum antigen titre. The advantage of the LCAT titre is that it’s decline or otherwise over the treatment period can be used as a measure of therapeutic progress. Therapy is long term (months to years) and requires dedicated owners. Therapeutic drug level monitoring may be considered in cases where normal drug dosages do not seem to be having the expected results, and in this setting, it can be worth determining susceptibility data during the course of therapy as sometimes the isolated organism develops mutational resistance if a single azole used for therapy.
3. What is the significance of the disparate location of the lesions?
I suspect that the period of 3-months of cortisone therapy has assisted the fungus to disseminate by dampening down the immune response to the organism, although we do see dissemination with widespread skin lesions sometimes without immunosuppressive therapy.
My presumption is that the 3-months of cortisone therapy have assisted this fungus to invade the host and also to disseminate (likely haematogenously), although a role of the cryptococcal species in this dissemination is also possible.
Figure 2. Fine needle aspirate of nodule
What’s YOUR Diagnosis?
C&T No. 6071, Issue 319 Jun 2025
Sick Puppy
Maddy Reichstein
Southern Tablelands Veterinary Hospital
105 Robinson St
Goulburn
e. southerntablelandsvets@gmail.com
C&T No. 6086
Billie was a 6-week-old female entire chocolate Labrador puppy and on initial presentation, she was brought in with a singular 1-2mm scabbed lesion on the left dorsal eyelid, suspected to possibly be from a fight with a litter mate.
The puppy was otherwise well at home and only the singular scab was noted. The puppy then represented 6 days later with bilateral mucopurulent discharge, marked chemosis, periocular ulceration/crusting and multiple pustules on the inner pinna and muzzle. The mandibular lymph nodes were also enlarged. The puppy was quiet but still eating, drinking, toileting well.
Read the history and see all the images here cve.edu.au/CandT-6071
Juvenile Cellulitis
Billie was started on 1mg/kg prednisolone SID PO for 4 weeks with weekly rechecks to alter dosing with her weight. She initially was also started on oral amoxyclav 12.5mg/kg BID PO and Tricin eye ointment BID for 7 days. After 4 weeks, the prednisolone was reduced to EOD for 2 weeks then every third day for a week before being discontinued. Each visit showed progressive improvement and Billie was otherwise well at all stages of treatment. No signs of relapse have been seen since finishing her medication.
Discussion
Juvenile cellulitis, also called puppy strangles, is a rare immune-mediated skin disease typically affecting dogs aged 3 weeks to 6 months. It presents acutely with facial swelling (muzzle, eyelids), followed by papules, pustules, and nodules on the face, ears, and submandibular region. These lesions may drain, crust and marked submandibular lymphadenopathy— sometimes with abscessation—is characteristic. Pruritus is usually absent, though pain and systemic signs (fever, lethargy, anorexia) are common. In severe
Figure 1. A & B; Billie at presentation. Note the periocular lesions and lesions in the external ear canal.
Figure 2. Billie at most recent check up
cases, joint pain or sterile arthritis can occur. Though primarily seen in young puppies, rare cases in juvenileadult dogs (up to 4 years) are reported.
Breed predisposition is suspected, with Golden Retrievers, Gordon Setters, Dachshunds, and pointers over-represented. Familial clustering supports a genetic component.
Pathogenesis is immune-mediated and idiopathic. Histopathology reveals sterile pyogranulomatous inflammation involving macrophages and neutrophils, suggesting a Type IV hypersensitivity or innate immune dysregulation. The disease may begin as primary lymphadenitis with secondary skin involvement. No infectious agent has been confirmed. Anecdotal links to vaccination exist but remain unproven.
Molecular insights are emerging. Cytokines like IL-1, IL-6, TNF-α are likely involved. Corticosteroid response indicates immune dysregulation. Experimental use of JAK inhibitors (e.g., oclacitinib) shows promise in refractory cases. No specific autoantigen or gene mutation has been identified, but studies are underway in high-risk breeds.
Diagnosis is clinical, based on signalment and lesion pattern. Differential diagnoses include bacterial cellulitis, demodicosis, dermatophytosis, distemper, adverse drug reactions, and immune-mediated dermatoses. Cytology typically reveals sterile pyogranulomatous inflammation. Misdiagnosis can delay care.
Treatment centers on high-dose corticosteroids (1–2 mg/kg/day of prednisone), often producing rapid improvement. Therapy is tapered gradually over 4–8 weeks. Relapse risk increases with premature tapering. Adjunct antibiotics may be used for secondary infections. Topical antiseptics (e.g., chlorhexidine) and analgesia support recovery.
Steroid-sparing agents like cyclosporine (Atopica) are effective in severe or refractory cases. JAK inhibitors are under investigation. Doxycycline may offer adjunctive benefit but is less preferred in puppies due to dental risks.
Prognosis is excellent with early treatment. Most dogs recover completely with minimal scarring. Recurrence is rare in puppies but more frequent in adult-onset cases. Long-term immune dysfunction is not typically seen. Follow-up during and after treatment ensures relapse is detected early.
Juvenile cellulitis is a self-limiting but dramatic inflammatory disease of young dogs. Prompt immunosuppressive therapy leads to full recovery in most cases. Emerging research into immunopathogenesis and cytokine modulation may lead to more targeted therapies in the future.
References
1. Bajwa J. Juvenile cellulitis (juvenile sterile granulomatous dermatitis and lymphadenitis) in a 9-week-old puppy treated with prednisolone-cyclosporine combination therapy. Can Vet J. 2022;63(3):313-316
2. Inga A, Griffeth GC, Drobatz KJ, Goldschmidt KH, Mauldin EA. Sterile granulomatous dermatitis and lymphadenitis (juvenile cellulitis) in adult dogs: a retrospective analysis of 90 cases (2004–2018). Vet Dermatol. 2020;31(3):219-e47
3. Thomas R. Dermatology emergencies: Juvenile cellulitis. Proceedings of CVC Veterinary Conference, 2015
4. Kansas State Univ. Diagnostic Lab (Brown A, Ganta C). Juvenile Cellulitis in a Four-Month-Old Chinese Crested Puppy – Case Study. Diagnostic Insights Newsletter. Jan 2020
5. Miller WH, Griffin CE, Campbell KL. Muller & Kirk’s Small Animal Dermatology, 7th ed. Elsevier; 2013:695-699
6. White SD, Rosychuk RA, et al . Juvenile cellulitis in dogs: 15 cases (1979–1988). J Am Vet Med Assoc . 1989;195(11):1609-1611
7. Park C, et al. Combination of cyclosporine A and prednisolone for juvenile cellulitis concurrent with hind limb paresis in 3 puppies. Can Vet J. 2010;51(11):1265-1268.
8. Oclacitinib mechanism of action – Food and Drug Administration Freedom of Information Summary, Apoquel® (oclacitinib), 2013. (Demonstrates JAK1 inhibition of cytokines relevant to canine inflammation.) Read here cve.edu.au/320-best-answer
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How Would YOU Treat This Case?
Jorid Nordaker BVSc
Master of Teaching (Secondary Science) Clinical Veterinary Registrar
University Veterinary Teaching Hospital Sydney
Caitlin Lowe Final year vet student, SSVS, The University of Sydney e. jorid.nordaker@sydney.edu.au
C&T No. 6087
A 4-year-old MN DSH cat was presented for chronic ulcerative dermatitis and an ulcer on the hard palate.
He was FIV FeLV negative and had a moderate non regenerative anaemia, mild hypoalbuminemia, ALB;GLOB Ratio 0.6, moderate eosinophilia and mild to moderate hyperbilirubinaemia.
An impression smear of the skin lesions revealed many eosinophils.
– How would you treat this case?
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Photos courtesy of Jorid Nordaker
Figure 1 A & B. Skin lesions
Figure 2. Impression smear cytology
replieS & CommentS
John Sandford, Vet
Clifton Hill Vet Clinic, Melbourne
e. jandk@jsandford.com.au
C&T No. 6088
Reply No. 1
Multi-Billion-Dollar Pet Food Fraud Review
Read cve.edu.au/cnt-6082
I would like to comment on Dr Pete Coleshaw’s review of Dr Tom Lonsdale’s book.
I have not read the book but know well Tom Lonsdale’s views on the pet food industry. I wonder if at least part of the book is confusing the feeding of dry food causing some weird deficiencies / conditions with what I think is the main problem—that of causing major dental problems because of the lack of chewing per se. NO dog or cat EVER CHEWS dry food. People hear a crack or crunch and ASSUME its chewing. True chewing consists of abrading ALL surfaces of ALL teeth along with massaging ALL gum-tooth crevices which is where I believe 99% of all dental problems arise A video of a dog eating dry food with its molars might be too difficult to arrange so I ask has ANYONE EVER seen a dog CHEWING dry food with its incisors? I’d give a big prize to anyone who could video such an event. Both dogs and cats would normally consume any dry food with their molars and only if too big would they ever use their incisors ( and I don’t know of any dry food that big ).Even so, they would only crush it a fraction before taking it to their molars for a further slight crushing and then swallowing but NEVER CHEWING it as in a relatively large piece of meat or bone. Felines and canines in the wild obviously would never get dry food and that should give us the basic reasoning to explain the problems of feeding dry food (from at least the dental hygiene aspect).
I can always tell if a dog or cat gets dry food only – ALL premolars and molars are quite clean on the very tips but the side and gum arears have varying amounts of tartar and receding gums (depending on age ) – see photo 1 from the review as an example. The tiny clean tooth tips is the give-away that the dry food is ONLY contacting these points. Once that apparent contradiction is pointed out to the owner, (preferably by using photos as well as the split second observation on their own pet on the exam table ) most people understand. However, talking about raw bones etc to compensate for the total lack of cleaning is often too big an ask for the average died-in-the-wool convenient dry pet food feeding owner I have other points such as boredom control and lack of house demolition to try and push the bone feeding
principle. As a dog owner, I have no real problem feeding dry food BUT my dog gets a raw bone every day of its life to make up for the otherwise total lack of tooth cleaning, and at 5 years of age its teeth are like photo 2 from the review as once again an example—Also, my 15-year-old cat got daily dry food and a bone every day of it’s life and had every single original tooth when euthanased ( lung cancer ). I never touched it’s teeth (see photo 3) (Photo 4 had slight tartar in the last 6 weeks of life ). I realize N=1 dog and 1 cat, but surely this is a starting point of any dry food-bone chewing discussion.
Reply No. 2
Dry Food For Cats—An Historical Accident?
Read cve.edu.au/cnt-6075
I am very surprised that in the above article, when mention of obesity comes up, no mention what-so-ever is made of the feeding frequency / quantity of food (dry or wet) consumed. While I certainly go along with the concepts mentioned—that of higher water intake in natural diets, different carbohydrates / protein levels in commercial diets etc, I am very surprised that no mention was made of the part that overfeeding of dry food plays in obesity rather than just attributing it to dry food per se
One of my standard questions for at least 55 of my last 59 years in practice is: How often do you feed your cat?
About 90% of people who feed their cat approximately ad lib will say twice daily, and when pressed, add that they top it up on and off! I will admit that I do not know why ALL ad lib dry food fed cats do not end up obese (but 99% do end up as fussy eaters). Surely, to keep the article concise / accurate, the feeding frequency / quantity should have been eliminated. Ad lib or permanent excess intake by cats would be very rare in nature.
– Can a cat get obese on ‘insufficient’ dry food? Or to put it another way,
– If one fed a cat ALWAYS accurately according to its weight, would it suffer any known consequences other than the question of the cat might whinge for more? Also,
– Could a cat on a natural type diet but excessive in quantity (say as in a zoo), become obese? I rather think so. So, quantity, would again be relevant.
Comment
Randolph Baral
Paddington Cat Hospital
210 Oxford Street
Paddington NSW 2021
t. 0293806111
e. paddington@catvet.com.au
Thank you to Dr John Sandford for his comments in relation to my article: Dry Food For Cats—An Historical Accident?
He notes, ‘I am very surprised that no mention was made of the part that overfeeding of dry food plays in obesity rather than just attributing it to dry food per se
In my article, I start the section about obesity with a direct comparison of caloric density:
"If you compare any brand of dry food to its equivalent form of wet food, for the same volume (say, 100g), the dry form has approximately 5 times as many calories’ and go on to say ‘we could infer that cats evolved to meet their caloric requirements from a diet much less calorie dense than dry food.
The inference is that due to its high caloric density, dry food easily enables overfeeding beyond caloric requirements.
Feeding frequency is often misunderstood. The very act of eating results in thermogenesis, i.e. there is energy expenditure due to eating itself. My expectation from this is that feeding more frequently will result in greater energy expenditure as long as feeding more regularly does not result in higher caloric intake. My approach to clients has therefore been to recommend multiple daily feeds of small quantities.
In answer to Dr Sandford’s specific questions
1. Can a cat get obese on ‘insufficient’ dry food? Any cat (or other species) eating insufficient calories of any style of food will lose weight. It is difficult to feed insufficient calories of dry food because it so energy dense. Most cats’ maintenance requirements of maintenance dry food are approximately 2/5ths of a cup per 24 hours.
2. If one fed a cat ALWAYS accurately according to its weight, would it suffer any known consequences other than the question of the cat might whinge for more? If a cat is fed maintenance caloric requirements that meets all nutritional requirements, there should be no physiological consequences. Note, that I don’t believe that a solely dry food diet is able to meet all nutritional requirements for cats (as detailed in the article). Additionally, cats have limited means to communicate with us; ‘whingeing’ has a negative connotation that neglects that the communication is because of hunger.
3. Could a cat on a natural type diet but excessive in quantity (say as in a zoo), become obese? I rather think so. So, quantity, would again be relevant. Any diet that exceeds caloric requirements will result in weight gain. Diets based on the nutrient profile that cats evolved to eat are less calorie dense so, in many cases, satiety helps prevent eating excess to caloric requirements of such a diet. It is important to consider diet ‘quantity’ in terms of energy.
Giant Mass in a Senior Rabbit
Tanni Sima BVB/DVM
Karim Chammas BVSc. MANZCVS (Feline)
Beecroft Vet
19A Wongala Crescent, Beecroft NSW 2119
t. 02 8914 0828
e. info@beecroftvet.com.au
C&T No. 6089
Signalment, History & Clinical Presentation
A 14-year-old male neutered lop ear rabbit was presented with a giant mass on his right lateral thigh. The mass started appearing two to three years ago as a single small nodule and, according to the owners, it did not bother him. The previous clinician took a FNA cytology and it was diagnosed as a lipoma. The owner was advised to monitor the mass. However, the mass had enlarged over the past two years to the point it was severely impacting the quality of his life. Lumpectomy was discussed in the consult and euthanasia was offered based on the age of the rabbit, the size of the mass, and quality of life. The risk of anaesthesia was discussed and owners elected surgery.
Physical Exam
On physical exam, a 20 - 25 cm diameter soft mobile subcutaneous pendulant mass was attached to the right lateral thigh (Figure 1). There was no pain on palpation and manipulation. The patient’s mobility was severely compromised, but he was able to sit and right himself. The rabbit also had a mild right-sided head tilt and marked pineal-pedal reflex of the right ear. No circling, falling or other neurological signs were observed. Cytology was taken, and a moderate number of yeasts were found in both ear canals. Otoscope exam showed a moderate amount of cerumen in the right external ear canal. The rest of the physical exam was within normal limits.
Head tilt is a common condition for lop ear rabbits. Ear infections and Encephalitozoon cuniculi were suspected, the diagnosis and treatment of which are beyond the scope of this article.
Anaesthesia & Analgesia
An intravenous catheter was placed in the right lateral ear vein. The rabbit received 0.05 mL (0.3 mg/ kg) butorphanol and 0.05 mL (3 mg/kg) ketamine intravenously as premedication and induction. The dose is calculated based on the estimate weight post lumpectomy. He was maintained on isoflurane and oxygen by mask. A bolus of 0.05 mL butorphanol was given intravenously during the surgery. The anaesthesia was stable. Postoperatively, he received 0.5 mg/kg meloxicam and 1 mg/kg metoclopramide subcutaneously and take-home meloxicam by mouth. He was syringe-fed critical care and had active warming during the postanaesthesia period.
Surgery
A skin incision was made over the lateral surface of the mass and blunt dissection was performed to peel away the connective tissue (Figure 2). A large blood vessel was ligated at the base of the mass and the wound was sutured up with 3/0 PDS.
Gross pathology
The mass weighed 750 grams. For comparison, the rabbit weighed 2.5 kg before the lumpectomy (30% of the body
Figure 1. The mass after shaving.
Figure 2. Incision over the mass
weight). Histopathology was recommended to confirm the original diagnosis of lipoma, but the owners declined due to cost constraints. Post-surgery, the mass was transected, and the mass consisted of abundant amounts of fibrofatty oily soft tissue resembling adipose tissue (Figure 3 ).
Cytology
Five FNA and cytology samples were taken, out of the clinician’s interest. The cell population consisted of large numbers of vacuolated and well-differentiated adipocytes. As such, the original diagnosis of a lipoma remained the most likely diagnosis based on the gross appearance of the mass and the results of the in-house cytology.
Post Surgery
The rabbit recovered well post-surgery and started eating the second day. Two weeks post-surgery the sutures were intact and the owner reported the rabbit’s mobility and quality of life had markedly improved.
Discussion
Lipoma is a benign, non-viral related tumour of mesenchymal origin. In rabbits, surgery is considered if the mass is impeding the mobility, affecting grooming, or causing irritation. The prognosis is usually good postsurgical removal. The limitation of this case is that the mass was not submitted for histopathology confirmation.
Diagnosis of the lipoma was therefore based on physical exam, gross appearance and cytology. Another possible differential diagnosis is liposarcoma, although this was considered less likely based on the gross appearance and cytology findings. The main factor to consider in this case, and rabbit surgery in general, is the risk of general anaesthesia. In rabbits, the peri-anaesthetic mortality rate is five times higher than that of cats and dogs due to their higher metabolic rates, oxygen consumption, and smaller lung capacity. Especially in this case, the patient is senior and has other pre-existing conditions. This case result shows that large mass removal in senior rabbits can still be performed when the options are between euthanasia and surgery. However, the risk of rabbit anaesthesia should be discussed with the owner before surgery.
Figure 3. Resected mass
Figure 4. 2 weeks post-surgery
Figure 5. 4 weeks post-surgery
Amphotericin B Availability for Veterinary Use in Australia
Richard Malik1 & Mark Krockenberger2
1 Centre for Veterinary Education
² Sydney School of Veterinary Science
The University of Sydney
C&T No. 6090
There are two formulations of amphotericin B currently available for veterinary use in Australia.
1. Liposomal Amphotericin B – AmBisome
This is the liposomal formulation used almost exclusively in human medicine today. It is less nephrotoxic than the original. Must be given intravenously. Expensive—around $280 per 50 mg vial.
Once reconstituted, it must be used within 24 hours. No storage permitted. Effective but cost-prohibitive for most veterinary cases.
2. Amphotericin B Deoxycholate—Fungizone & Generic Equivalents
This is the original formulation, solubilised with bile salts (giving it a yellow colour). Once widely used in human medicine, it has been replaced by liposomal forms. Now used almost exclusively in veterinary medicine. Human-grade products are still available— mostly manufactured in India. Medsurge previously stocked it reliably, but availability declined after COVID. Currently available through HL Pharma at about $140 per 50 mg vial.
New Product – Amphotin B
BOVA Compounding has now stepped in with Amphotin B—a human grade amphotericin B deoxycholate injection made in India. Each vial contains 50 mg. Price: as of July 2025 $65 per vial. Needs to be reconstituted with sterile water for injection.
This makes treatment of serious fungal infections in animals far more accessible. It can be given IV, subcutaneously and intraperitoneally. Importantly, the vial can be frozen and thawed many times—provided excellent sterility is maintained—and this make it far more cost effective for use in cats and small dogs.
How to Order
–
Order online via: bovavet.com.au
Select the product as shown in the online catalogue.
– Alternatively, submit a written prescription using your clinic’s standard template.
Note: A hard copy of the prescription, signed in ink, must be posted to BOVA within 24 hours of submission.
Immunotherapy & Palliative Management for Metastatic Adenocarcinoma
Moira van Dorsselaer BVSc
The Cat Clinic Hobart
150 New Town Rd
New Town TAS 7008
e. moira@catvethobart.com.au
t. +613 6227 8000
C&T No. 6091
Presentation & Initial Assessment
Little, a nearly 16-year-old cat weighing 5.86 kg (BCS 5/9), presented to our clinic for a second opinion after a recurrence of adenocarcinoma, likely of salivary origin, with metastasis to regional lymph nodes. The mass had returned within 4 months of the initial surgical excision and was now firm, irregular, large, and deemed inoperable.
Prior to Little’s presentation, we had been in discussions with Dr Chris Weir regarding our first immunotherapy case—a 21-year-old cat diagnosed with a squamous cell carcinoma of the upper lip. Given Little’s condition, I discussed the potential for immunotherapy with his owners, who were eager to explore any possible treatment options.
Treatment Initiation
Following consultation with Dr Chris Weir and Dr Richard Malik, Little was started on a regimen of:
– Palladia (toceranib phosphate) 2.5 mg/kg
– Maropitant 4 mg once a day
– Mirtazapine 1.8 mg/dose once a day
Administered once daily, 3 times per week.
We arranged for the original biopsy sample to be sent to Dr Weir for immunotherapy formulation. In parallel, we discussed the potential use of Stelfonta (tigilanol tiglate) but concluded that the size of the masses and the risk of significant post-treatment wounds outweighed the benefits. Instead, Dr Weir provided nanoparticles to be
combined with injectable carboplatin (50:50 ratio) for intralesional injections.
Initial Procedure & Intralesional Injections
Little was sedated with:
– Dexmedetomidine – 6 µg/kg
– Methadone 0.3 mg/kg.
He was induced with alfaxalone and maintained on isoflurane anaesthesia. Thoracic radiographs were taken, revealing no pulmonary metastasis. However, severe osteoarthritis in both elbows was noted, and meloxicam was initiated for pain management.
The carboplatin-nanoparticle mixture was injected into the masses using a Luer-lock syringe. The masses were firm, making injection challenging, particularly into an intraoral lesion, where the liquid just leaked out. A fentanyl patch (25 µg/hr) was applied to his tail, and he was discharged. Unlike previous cases where I had used Stelfonta, Little exhibited no significant post-treatment pain.
Immunotherapy Initiation & Progress
Three days post-injection, Little received his first IM immunotherapy injection (0.4 mLs in the right hind limb). He showed no adverse reactions. Weekly IM immunotherapy injections continued for 4 weeks, alongside his palladia/maropitant/mirtazapine regimen.
By the second injection the masses appeared to have changed in texture and possibly reduced in size. He had also gained 170 g.
At his fifth injection (4 weeks after the last weekly dose):
– His weight had dropped 100 g.
– He had developed hypertension (BP 180 mmHg), likely as a response to the Palladia; so was started on amlodipine (0.625 mg/day).
– Overgrooming with hair loss on the left flank and inguinal regions was noted.
– The masses were similar in size but appeared more discrete and non-painful.
Continued Management & Emerging Challenges
Over the following months, Little continued monthly immunotherapy injections. His overgrooming worsened, his owners thought possibly due to stress from medication administration. Despite weight fluctuations, his quality of life remained very good, although the oral lesion continued to enlarge.
By his seventh immunotherapy injection, his weight and blood pressure were stable, but the overgrooming had significantly worsened, despite Bravecto spot-on treatment the month prior. The masses remained unchanged.
Two weeks later, Little presented lethargic and anorexic, which was highly unusual for him. His weight was stable and he still had generalized flank and ventral hair loss which was moist; however, it was acutely painful along his lumbar spine and hind end, which was suspected to be trauma-related. Treatment was initiated:
– Methadone (0.3 mg/kg IM)
– Fentanyl patch (25 µg/hr)
– Solensia (frunevetmab) injection SCI
– Antibiotics for suspected secondary skin infection
Palladia/maropitant/mirtazapine was paused until appetite improved and a discussion about his quality of life was had, should he not improve to his old self. Two days later, a wound consistent with a cat bite was discovered, explaining the acute pain. With treatment, Little returned to his normal self quickly.
Further Adjustments & Transition to Intralesional Palladia
At his next visit, Little had regained weight and was stable. However, his oral lesion continued to enlarge, though it did not yet affect appetite or behaviour. Overgrooming improved, with noticeable hair regrowth. We were unsure if this was due to the antibiotics or analgesia from the Solensia and fentanyl patch.
Due to insufficient sample availability, we were unable to continue immunotherapy beyond 8 injections. His owners declined further biopsy for additional samples. After consultation with Dr Weir, we trialed intralesional Palladia NP (toceranib phosphate, 0.5mg/mLs, mixed 50:50 with nanoparticles (provided by Dr Weir), injected into right submandibular masses under anesthesia. Given my experience the last time, I decided against attempting to inject intralesionally into the oral lesion.
His ongoing, now severe, skin inflammation between his hind legs prompted a prednisolone (5 mg SID) trial.
Outcome & Final Months
Eight days post-intralesional Palladia, the neck masses ulcerated and bled, but also flattened and softened, with no associated pain. Little remained bright and active.
By December 2024, Little’s weight had dropped to 5.25 kg. He had a moist excoriation over the right jugular region where he had the intralesional palladia/
nanoparticles (see images) and the oral mass had continued to increase in size. Despite ongoing weight loss and his skin issues, his quality of life remained good—he had even caught and eaten a rabbit.
Medications at this stage included:
i. Palladia (15 mg, once daily, 3 times per week)
ii. Amlodipine (0.625 mg SID)
iii. Prednisolone (5 mg SID)
iv. Pregabalin (12.5 mg BID)
v. Mirtazapine (1.8 mg PRN)
By January 2025, Little gained 140 g, and his condition remained stable, except for the oral mass, which was now constantly bleeding. After discussions with his owners, we acknowledged that euthanasia would likely be necessary in the near future.
Reflection & Future Considerations
This case highlights the potential of immunotherapy for inoperable neoplasia, particularly in regions like Tasmania, where radiation therapy is unavailable.
Despite his diagnosis, Little has lived an additional 12 months with good quality of life, a significant improvement given the initial prognosis his family was given. It remains uncertain whether continued immunotherapy would have further prolonged survival had more sample been available.
Little was our third case utilising immunotherapy with Dr Chris Weir, and we are excited to explore its potential in future cases.
Figure 1. Prior to nanotherapy
Figure 2. Lesion at the time of the initial injection
Figure 3. 1 week post nanoparticle injection
Figure 4. Moist excoriation over the right jugular region where he had the intralesional palladia/nanoparticles
Figure 5. By January 2025, Little gained 140 g, and his condition remained stable, except for the oral mass which had continued to grow 1 2 3 4 5
Cancer Vaccine— Another Option for Animals
Lynne Bodell
Bodell Lynne Veterinary Clinic
56 Chaston St
Wagga Wagga NSW 2650
t. +61269255570
e. info@lynnebodellvetclinic.com.au
C&T No. 6092
Isabella is a 13-year-old F(N) 4.9 kg Papillon who, apart from arthritis, is in excellent health.
In the first week of September 2024, her owner noticed a small skin lump just below the right carpal joint which she initially thought was related to the arthritis, but which then grew rapidly.
On 16 September, the dog presented for assessment—the lump was approximately the size of a squash ball, cystic and hyperaemic, wrapped around the carpus—about 2/3rds of the leg.
FNA result
The cellularity of the sample was too low to reach a diagnosis in this case (consistent with provided history of
difficult sample exfoliation). Occasional mesenchymal/ spindle cells were present, and these showed some features of atypia which could reflect a neoplastic (e.g. soft tissue sarcoma) or reactive (e.g. fibroplasia) process though there was no clear evidence of inflammation.
Due to the high risk of the lump ulcerating and the rapid rate of growth, after discussion with the owner, we opted to remove lump and send for histopathology. The owner totally rejected amputation, chemotherapy and referral.
The lump was removed on 19 September—the tumour margins appeared well defined (typical of soft tissue sarcoma); however, its deeper extent was closely adhered to nerves, tendons and blood vessels and we were unable to remove all tumour from these areas. We also opted to be conservative with skin margins under the circumstances, so we were able to get primary skin closure.
Histopathology Result
Soft tissue sarcoma, grade 3, high mitotic index of 24, therefore a high risk of recurrence and possible metastases.
Cancer Vaccine
I had read about an autologous nanoparticle cancer vaccination (CANCV) which had been developed by Dr Chris Weir. After discussions with the owner and Dr Weir, we were keen to try this option. The vaccine was made from the paraffin block of the tumour. On 3rd October, Isabella started on the cancer vaccinations, which were
Figure 1. Isabella
Figure 2. Low and high-power histopathology images of Isabella’s lump
given IM. The frequency in this case was weekly for weeks 1 – 4, then fortnightly for the next injection, and then monthly.
There have been no adverse reactions to the vaccine to date and the dog (who is not the bravest soul) tolerates the injections well.
The wound on the leg healed very well; we had stopped bandaging by 8 October and apart from some scar tissue, there has been no sign of recurrence as of time of writing (mid-January 25) and the area is now fully haired.
Considering the rapid initial growth of this tumour, the fact that it was not completely removed and the grading of this tumour, I would have expected recurrence by now if we had not started the vaccinations.
The owner is aware that at best we described this as palliative, although to date the cancer vaccine has exceeded our expectations. We are looking to now reduce frequency of the vaccine to every 3 months (unless recurrence and then would increase again).
The CANCV in this case has been a very cost-effective option (a fraction of the price of chemo) with no side effects to date. It can be used concurrently with other medications (e.g. pred, chemo, etc) if required, on a variety of different tumours and gives us another option.
Acknowledgement
I need to thank Dr Chris Weir (Dog Oncology Group) for all his time and advice with this case—you have made one dog and owner very happy.
Postscript: At the beginning of February we opted to reduce Isabella’s vaccination frequency to monthly. In hindsight this was a mistake because in early March the tumour started to regrow quite rapidly. We reverted back to weekly vaccinations which slowed the growth but eventually the owner opted for euthanasia in late April. Dr Weir advised that it was likely that the tumour had mutated slightly and hence not as susceptible to the vaccine. We live and learn, so if I had a similar aggressive tumour I would not try and reduce the frequency. Either way Isabella probably had 6 months more QOL than she would have had without the vaccines.
Read C&T No. 6027 CANCV-4—Canine Autologous Nanoparticle Cancer Vaccine (V4): Immunotherapy For Dogs by Dr Chris Weir cve.edu.au/CandT-6027
Feline Aortic Thromboembolism
Diana Azevedo
BSc ISFM CertFN & DipFN RVN icatcare, UK
C&T No. 6093
Aortic thromboembolism (ATE) is an acute syndrome, commonly secondary to cardiac disease and frequently seen in feline patients due to a combination of characteristic factors. Patients presenting with this disease frequently have a poor to guarded prognosis at presentation and, although the clinical signs might depend on the location of the obstruction, these cats are commonly extremely painful, paraparetic/ paraplegic, tachycardic and tachypnoeic. Care and monitoring for these patients can be challenging due to the high risk of cardiovascular decompensation and their poor prognosis.
Aetiology and pathophysiology
An ATE is a relatively common medical emergency in cats presenting to practice, with potentially devastating consequences. This disease process is the result of a blood clot (thrombus) formation that dislodges or fragments and travels (as an embolism) through the aorta.1–3
ATE is seen in cats with severe heart disease, especially hypertrophic cardiomyopathy (HCM), but can develop in cats with dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM) and unclassified cardiomyopathy (UCM).1,2 ATE has also been reported in patients with arrhythmia, such as atrial fibrillation or as part of arrhythmogenic right ventricular cardiomyopathy, and in cats without underlying heart disease, including cats with pulmonary neoplasia (clot and/or tumour embolisation), other conditions associated with hypercoagulability (eg, protein-losing disorders) and thyroid disease.1,2
Two retrospective studies showed cardiac disease to be the most common cause of ATE in cats (90%¹ and 69%⁴) and for this reason, this article focuses on ATE of cardiac origin.
Thrombus formation and embolisation
The three main risk factors for thrombus formation are described by Virchow’s triad3,5–7 (Figure 1): – blood stasis; – hypercoagulable state; and – endothelial damage.
Virchow’s Triad
Endothelial damage Hyper coagulable state
Cats with severe heart disease have a higher risk of clot formation in comparison with dogs.6,8 Regardless of the diagnosis, the cardiac disease process involves chamber enlargement, especially the left atrium, and secondary decreased blood flow velocity in the left atrium and left auricular appendage.⁶
Under physiological conditions, the preserved endothelium and normal laminar blood flow prevent platelet aggregation and normal blood flow removes activated coagulation factors (fibrinogen, Factor VIII antithrombin, etc).⁵ However when this endothelium is damaged secondarily to heart disease, these processes are compromised, and the thrombotic process is triggered, promoting platelet aggregation and subsequent activation of the intrinsic clotting cascade.5,6 In addition, different studies have shown that cats with heart disease present with higher levels of coagulation factors and lower levels of coagulation inhibitors in comparison with healthy cats.5,8,9
The most frequent embolisation site is the terminal aorta (aortic trifurcation), where it is known as a saddle thrombus, which causes complete or partial obstruction of blood to the hindlimbs leading to paresis/paralysis. Other embolization sites include the brachial artery, and visceral blood vessels, including mesentery, kidneys, brain and lungs.³
Imhoff showed that bilateral aortic ligation alone is not enough to mimic a thromboembolic event because the collateral circulation is not affected.10 The ATE
Figure 1. Virchow’s triad describes the three categories that contribute to thrombosis
Increased left atrial size
Stretched atrial cardiomyocytes
causes mechanical occlusion of the aorta but also releases vasoactive substances, such as serotonin and prostaglandins which lead to vasoconstriction affecting the collateral circulation as well.
Incidence
There are some breeds that are predisposed to HCM, such as Ragdoll, Maine Coon, Sphynx, Birman and Scottish Fold, but mixed-breed cats are more often reported to have HCM/ ATE. In addition, in some studies, the male cat is more likely to be diagnosed with ATE, and this may be linked to the fact that HCM has a higher prevalence in males than in females.11–13
Presentation and physical examination
Cats develop ATE suddenly and, due to their lifestyles and the fact that they are masters at hiding symptoms, this acute presentation can be the first sign of heart disease. Owners report sudden vocalisation/distress, open-mouth breathing and paresis/paralysis as the most common presenting signs.3,6,12 The sudden onset is not only distressing to the cat but also to the owner.
In some cases, the outdoor cat re-appears ‘off its back legs’ after some days missing from the home. Other clinical signs will depend on the embolisation site. Table 1 describes the clinical signs resulting from the different embolisation sites.
Embolisation site
Clinical signs
Brachial artery Neurological deficits in the forelimbs
Table 1. Clinical signs of aortic thromboembolism by embolisation site
As mentioned before, the most frequent embolisation site is the aortic trifurcation, and the diagnosis can be reached with a physical examination based on the five cardinal signs – the five Ps (Figure 2)
– Pain: Acute and severe, especially in the first 6–24 h due to poor perfusion and ischaemic myopathy. After 24 h, the cat might not react to pain stimulation secondary to loss of sensory and motor function.1,2,3,12,13
– Paralysis or paresis: Depending on the degree of tissue affected and whether there is partial or complete obstruction.
– Pulselessness: Not always easy to assess, especially in obese, distressed and/or painful cats. In these cases, using the Doppler to search for a pulse may be helpful.
– Poikilothermy: Low rectal temperature is often seen. Lower temperatures are recorded in affected limbs rather than in unaffected limbs.1,6,13
– Pallor: Pads and nail beds of affected limbs are frequently pale or cyanotic due to poor perfusion.
It was initially thought that cardiovascular decompensation was the main cause of ATE but Flanders suggested that ATE might be the cause of cardiovascular decompensation.14
Consequences and complications of ATE
The severity of complications will depend on the duration of the obstruction, how complete it is and how much the collaterals are affected, but it is all secondary to ischaemic necrosis.⁴
Reperfusion syndrome
The hypoperfusion of tissue distal to the obstruction will lead to activation of the ischaemic cascade where cells switch from aerobic to anaerobic processes of energy production.
This process is inefficient and harmful in the long term, leading to increased lactate levels (hyperlactataemia) and metabolic acidosis, leakage of potassium out of the cells and the death of the cells.
When the obstruction is resolved and the blood circulation is restored, the cells of the immune system, including neutrophils and macrophages, will flood the ischaemic area and activate the inflammatory cascade, increasing the production of cytokines, which can have negative effects on every body system.15
Partial motor recovery
Amputation of the hind limb or digits might be advised when the tissue necrosis is too severe or when
Figure 2. The five Ps of aortic thromboembolism
self- trauma is present due to neuropathic pain. Affected cats can develop pitting oedema and local hair loss (Figure 3)
Further diagnostics and potential findings
Arrhythmia
Hyperkalaemia may induce arrhythmias, including wide complex tachycardia (Figure 4) due to changes in the resting membrane potential.16 Atrial fibrillation is also associated with atrial damage secondary to severe cardiac disease. Cats with congestive heart failure (CHF) can present with other conduction disturbances such as right bundle branch block or fascicular block.11 These disturbances can be misinterpreted as having ventricular origin because of the abnormal width and appearance of the QRS, although these disturbances have a P wave associated with the QRS as they originate in the sinus node unlike the ventricular rhythms (atrioventricular dissociation) (Figure 5) 17
Heart murmur
A heart murmur alone is not indicative of heart disease in cats. Cats can present with:
– heart disease without a heart murmur; – heart disease with a murmur; and – heart murmur without heart disease – physiological or benign murmur; for example, dynamic ventricular outflow tract obstruction, midventricular obstruction, aortic flow on the audible range.
The fourth heart sound (S4), or atrial gallop, is associated with atrial contraction and end-diastolic ventricular filling in a less compliant ventricle with concentric hypertrophy of the wall consistent with HCM.
Tachypnoea and dyspnoea
These clinical signs might be secondary to the presence of pulmonary oedema/pleural effusion but also to stress and/or pain.
Abnormal breathing sounds
Crackles and other abnormal breathing sounds are associated with pulmonary oedema.
Further investigations
These should be performed once the patient has a stable respiratory rate and should be stopped if causing distress.
Blood testing
Emergency or minimal database might be required which could include renal parameters, electrolytes, blood gases and lactate. Frequently, these patients present with hyperkalaemia, azotaemia, hyperphosphataemia, increased lactate and creatine kinase and hyperglycaemia induced by stress.
Figure 4: Hyperkalaemia may induce arrhythmias including wide complex tachycardia. Image courtesy of Davies Veterinary Specialists
Gallop sound
Figure 3. After surviving severe and prolonged reperfusion syndrome, Buddy developed pitting oedema (a) leading to localised hair loss (b) and consequent digital amputation (c). Images courtesy of Andrea Cox
Echocardiography
Cats with HCM will typically present with left atrial and left auricular enlargement, left ventricular concentric hypertrophy and diastolic dysfunction. The presence of spontaneous echocardiographic contrast (SEC), which has a swirling smoke-like appearance on echocardiography, represents aggregation of erythrocytes in the enlarged left atria, and is indicative of stasis (reduced blood flow).9,11 In some cases, a thrombus might be seen in the left auricle or left atrium (Figure 6) The presence of increased B-lines (narrow-based ‘comet tails’ can be supportive of pulmonary oedema but is not specific to the aetiology.
Radiography
This is the most appropriate imaging modality to diagnose/confirm CHF. The presence of oedema and/or pleural effusion, in addition to cardiomegaly, will confirm the diagnosis (Figure 7)
Nursing considerations on the acute presentation
Analgesia
Regular pain scoring must be performed using comprehensive and adequate scales such as the Glasgow Feline Composite Measure Pain Scale or Feline Grimace
Scale. Full mu- opioids (methadone and fentanyl) should be used in the first 24–72 h. Following the RCVS Code of Conduct for Veterinary Nurses, buprenorphine might be adequate if the pain score reflects the choice.3,6
Oxygen supplementation
Stressed patients with HCM have an increased oxygen demand, which is more significant if there is evidence of congestive heart failure (pulmonary oedema/pleural effusion). When supplementing oxygen in an incubator or oxygen tent, it is essential to maintain a controlled temperature because active warming will cause vasodilation and blood redirection, which can worsen the reperfusion syndrome in these patients.⁶ To avoid hyperthermia, ice packs should be placed inside the tent/incubator and/or on top of it.
Intravenous (IV) catheter placement
IV catheter placement and blood drawing (when appropriate) might take multiple attempts to avoid cardiovascular decompensation.
Monitor for reperfusion syndrome
– Severe hyperkalaemia due to tissue damage can lead to serious complications. Insulin is usually used to promote cellular uptake of potassium to reduce the levels within the circulating blood. When administering insulin, glucose levels need to be closely monitored and frequently supplemented.5,15
– If the hyperkalaemia is causing ECG abnormalities, calcium gluconate might be added to stabilise the
Figure 6. Thrombus in left atrium (red circle). Yellow arrows show enlarged left atrium, blue dashed arrow shows atrial fibrillation. Image courtesy of Davies Veterinary Specialists
Figure 7. Cardiomegaly with oedema and or pleural effusion on radiography confirms a diagnosis of congestive heart failure. Image courtsey of Dr Lara Barron
Figure 5. ECG showing right bundle branch block. Image courtesy of Davies Veterinary Specialists
cardiac cell membrane. Calcium gluconate will not affect potassium levels.5,15
– Sodium bicarbonate might be added to reduce metabolic acidosis, as a buffer, but only when severe as this drug is associated with adverse reactions.5,15
Treat CHF
– Loop diuretics (eg, furosemide or torsemide): diuretics are the foundation of CHF treatment and control. In case of poor compliance, it is important to advise the owner that if this drug is discontinued, the animal might deteriorate quickly.
– Aldosterone antagonists (eg, spironolactone): high concentrations of aldosterone have negative effects such as sodium retention and increased risks of arrhythmia.18
– Thrombolytic drugs: such as tissue plasminogen activator (TPA). Administration of TPA within 6 h of the thromboembolitic event has shown some improvement in restoration of the arterial lumen and functional recovery, but further research is needed to demonstrate evidence for their benefit.3,6,19
Cat friendly care
The use of feline-friendly interaction/ handling techniques is key for these patients, as stress will increase myocardium oxygen demand which will put strain on the heart, causing further decompensation.20
Points to consider:
– When possible, topical local anaesthetic cream should be used to facilitate blood sampling or IV catheter placement.
– Patients should be placed in a calm and quiet environment but continue to be closely monitored.
– ‘Less is more’ approach.
– A hiding place can be offered. This must facilitate continued close monitoring without the need to disturb the patient and can be as simple as a cover over part of the cage door.
– Use of different techniques to give tablets, including:
y gentle restraint;
y gelatine capsule for multiple tablets;
y pill popper;
y use of a towel to gently and lightly wrap the cat; and
y use of soft yoghurt-like texture products (eg, Webbox lick-e-lix) if the cat is food-motivated.
Some tablets such as clopidogrel can be bitter, and for this reason, hiding this medication in the food might result in food aversion.
Nursing considerations after initial stabilisation
Monitor resting respiratory rate (RRR)
Patients with active CHF will have a consistently increased resting respiratory rate due to pleural effusion and/or pulmonary oedema. If the RRR is consistently above 30 breaths per minute (bpm), or there is evidence of increased respiratory effort, the clinician must be informed as the dose of diuretics might have to be adjusted.3,15
Monitor for anorexia
Patients in practice might be anorexic just for the simple fact they are in a different environment with stressors such as strange smells and noises. Adding this to azotaemia, stress related to paresis/paralysis, discomfort and a significant number of new medications, and these patients might not ingest the recommended daily calorie intake. If they do not ingest a minimum of 50% of the daily resting energy requirement, the placement of a nasogastric feeding tube might be advised to avoid hepatic lipidosis.20,21
Monitor pain
ATE is a painful process and not only during the acute presentation. Depending on the duration of obstruction, the cat might still be very painful after the body dissolves the clot and blood flow resumes.
As mentioned above, when the obstruction is present for longer periods, the patient might not feel pain due to nerve damage.1–3,12,13
Monitor ECG for arrhythmias
Wide complex tachycardia can be haemodynamically significant and is life-threatening because it can progress to ventricular fibrillation, which is an arrest rhythm. Lidocaine is typically used as a first-line treatment for ventricular tachyarrhythmias, but it is rarely indicated in cats due to their increased sensitivity to this drug and potential side effects such as altered mentation and vomiting. In addition, this sodium channel blocker is
contraindicated in patients with derangements as it can promote worsening of arrhythmias.17 The correction of potassium values might reverse the abnormal rhythm.
Cats with severe heart disease can also present with atrial fibrillation, which is often a high-rate arrhythmia.
Persistently increased heart rate can induce/ worsen chamber enlargement (tachycardia-induced cardiomyopathy). This arrhythmia is usually treated with calcium channel blockers or beta blockers, although the latter should be avoided in cases of CHF.22
Blood sampling
Frequent blood sampling is needed to evaluate reperfusion syndrome and renal function.
Physiotherapy
This should be avoided in the first 72 h, as this might worsen the reperfusion syndrome. After this period, physiotherapy, including hindlimb massage for 30 mins three times daily for a week, might improve collateral circulation and prevent muscle contraction.3,6,12
Monitoring for re-embolisation
Vocalisation, distress, increased levels of pain, tachypnoea, dyspnoea, and increased potassium levels should be monitored.
Ongoing nursing considerations
Patients with CHF might need regular blood sampling because diuretics can cause prerenal azotaemia and hypokalaemia. It is imperative to decrease the stress of these patients when coming back to practice for reassessment because the additional stress increases the myocardial oxygen demand, which might destabilise the control of CHF.
Owners should be provided with information on how to make the visit to the veterinary clinic less stressful, such as:
– How to introduce the carrier.
– Use of pheromones.
– Discuss with the veterinary surgeon the use of gabapentin, as this drug has minimal cardiovascular effects and reduces the cat’s anxiety.20
International Cat Care’s guide, ‘Visiting your vet ’, has all the information to help owners with this process.
Advise cat owners to use the following techniques to increase food and water intake to prevent cardiac cachexia and dehydration.20
– Use ceramic bowls instead of plastic or metal.
– Place multiple water bowls around the house. Put a glass with water in the cat’s favourite place (eg, the window).
– Add tuna water (not brine) to give some flavour.
– Add ice cubes to the cat’s water bowl.
– Offer different textures and flavours of food (not at the same time).
– Warm up the food.
– Keep food and water bowls separated.
International Cat Care’s guides, ‘Increasing water intake’ and ‘Inappetence’, have information to help owners encourage their cats to drink/eat. All International Cat Care’s cat carer guides are available at: https://icatcare. org/advice-cat- carer-guides
Demonstrate to the owner how to perform passive range of motion exercises, as this should be continued at home if well tolerated.
Prognosis
The median survival time for patients with CHF, secondary to primary HCM, is between 596 and 732 days, but this decreases significantly with an ATE event (184 days).11
In a study of 250 cats by Borgeat et al, 61.2% of the cats were euthanased at presentation and 11.6% were euthanased or died within the first 24 h after starting treatment.13 Early detection of complications such as acute kidney injury and reperfusion syndrome, and prompt intervention might be linked with better outcome.23
The owner should be given all the information to be able to make an informed decision. The prognosis of ATE is guarded to poor at presentation, but there are some negative prognostic indicators:⁶
– Rectal temperature less than 37.2°C.
– Presence of gallop sound.
– Presence of CHF.
– Reduced heart rate.
– Both hindlimbs affected (70–75%).23
– Previous ATE events.
On a more positive note, Guillaumin suggests that recent research in thrombolytic drugs and the advanced information on long-term treatment options could improve the prognosis for cats suffering from a thromboembolic event.23
Conclusions
Cats with advanced heart disease present a particular set of characteristics that predispose them for thrombus formation, which can travel away from the heart and cause serious and potentially fatal complications. A high number of cats presenting to practice with ATE are euthanased due to the severity of this acute process, or later when their primary disease process progresses. There are limited treatment options for these cases and not all patients respond to the available treatment.
Additionally, the high risk of cardiovascular decompensation increases the challenge for veterinary nurses to handle, care and monitor these patients. Regardless of the owner’s decision, veterinary nurses are in the best position to advocate for these patients to ensure the best care, and nursing ATE patients can be as equally rewarding as it can be heartbreaking.
References
1. Smith SA, Tobias AH, Jacob KA, et al. Arterial thromboembolism in cats: acute crisis in 127 cases (1992–2001) and long-term management with low-dose aspirin in 24 cases. J Vet Intern Med 2003; 17: 73–83.
2. Atkins CE, Gallo AM, Kurzman ID, et al. Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985–1989). J Am Vet Med Assoc 1992; 20: 613–618.
3. Fuentes VL. Arterial thromboembolism: risks, realities and a rational first-line approach. J Vet Intern Med 2012; 14: 459–470.
4. Laste NJ and Harpster NK. A retrospective study of 100 cases of feline distal aortic thromboembolism: 1977–1993. J Am Anim Hosp Assoc 1995; 31: 492–500.
5. Stokol T, Brooks M, Rush JE, et al. Hypercoagulability in cats with cardiomyopathy. J Vet Intern Med 2008; 22: 546–552.
6. Aherne M. Feline arterial thromboembolism. Today’s Veterinary Practice 2021: 38–48.
7. Schoeman JP. Feline distal aortic thromboembolism: a review of 44 cases (1990–1998). J Feline Med Surg 1999; 1: 221–231.
8. Hathcock JJ. Flow effects on coagulation and thrombosis. Arterioscler Thromb Vasc Biol 2006; 26: 1729–1737.
9. Schober KE and Maerz I. Assessment of left atrial appendage flow velocity and its relation to spontaneous echocardiographic contrast in 89 cats with myocardial disease. J Vet Intern Med 2006; 20: 120–130.
10. Imhoff RK, Production of aortic occlusion resembling scute aortic embolism syndrome in cats. Nature 1961; 192: 979–980.
11. Ferasin L. Feline myocardial disease 2: diagnosis, prognosis and clinical management. J Feline Med Surg 2009: 11, 183–194.
12. Hassan MH, Abu-Seida AM, Torad FA, et al. Feline aortic thromboembolism: presentation, diagnosis, and treatment outcomes of 15 cats. Open Vet J 2020; 10: 340–346.
13. Borgeat K, Wright J, Garrod O, et al. Arterial thromboembolism in 250 cats in general practice: 2004–2012. J Vet Intern Med 2014; 28: 102–108.
14. Flanders J. Feline aortic thromboembolism. Compendium of Continuing Education for the Practicicing Veterinarian 1986; 8: 478–484.
15. Moise NS. Thromboembolism in the cat. Proceedings of the World Small Animal Veterinary Association World Congress, 2005.
16. Norman BC, Côté E and Barrett KA. Wide- complex tachycardia associated with severe hyperkalemia in three cats. J Feline Med Surg 2006; 8: 372–378.
17. Fox P R. Feline cardiomyopathy. Procedings of the World Small Animal Veterinary Association World Congress, 2003.
18. Ames MK and Atkins CE. Beyond furosemide: the role of diuretics in congestive heart failure part 2 – spironolactone. https://todaysveterinarypractice.com/cardioloy/ the-role-ofdiuretics-in-congestive-heart- failure-part-2-spironolactone/ (2016, accessed 20 May 2024).
19. Cambournac M, Damoiseaux C, Guillaumin J, et al. Multicentric aortic thromboembolism retrospective study in 158 cats: the MATERS study [abstract]. J Vet Emerg Crit Care (San Antonio) 2022; 32: S2–S37.
20. Rodan I, Dowgray N, Carney HC, et al. 2022 AAFP/ISFM cat friendly veterinary interaction guidelines: approach and handling techniques. J Feline Med Surg 2022; 24: 1093–1132.
21. Taylor S, Chan DL, Villaverde C, et al. 2022 ISFM consensus guidelines on management of the inappetent hospitalised cat. J Feline Med Surg 2022; 24: 614–640.
22. Kittleson MD and Côté E. The feline cardiomyopathies: 2. Hypertrophic cardiomyopathy. J Feline Med Surg 2021; 23: 1028–1051.
23. Guillaumin J. Feline aortic thromboembolism: recent advances and future prospects. J Feline Med Surg 2024; 26. DOI: 10.1177/1098612X241257878
The International Cat Care Veterinary Society (formerly ISFM) is the veterinary membership division of pioneering cat welfare charity International Cat Care (iCatCare), bringing together a global community of veterinary professionals dedicated to improving the lives of cats worldwide. Trusted by vets and nurses, it provides professional development and CPD through access to expert knowledge resources, including the Journal of Feline Medicine and Surgery (JFMS). The iCatCare website is also a trusted resource of information and guidance for veterinary professionals, cat owners and caregivers
iCat Care Research Roundup
Welcome to Research Roundup where we bring you summaries of the latest feline research. In this issue we have some varied subjects from insect diets to feline infectious peritonitis, and we encourage you to have a look at this month’s Clinical Spotlight review article that discusses physical therapy.
Read here: cve.edu.au/rr-september-25
The Rise of Equine Assisted Reproduction Techniques in Australia
Gus Ruiz DVM MS MANZCVS (Reproduction) Dipl. ACT
Senior clinician - Specialist in Veterinary Reproduction (Theriogenology)
Sydney School of Veterinary Science and Camden Equine Centre
e. gus.ruiz@sydney.edu.au
C&T No. 6094
Assisted reproductive technologies (ART) in horses have undergone significant advancement over the past two decades, with ovum pick-up (OPU), intracytoplasmic sperm injection (ICSI), and more recently, in vitro fertilisation (IVF) emerging as key tools for enhancing fertility management and genetic progress in elite equine breeding programs. Despite their widespread adoption in Europe and North America, the use of OPU–ICSI remains notably limited in Australia, even as interest among breeders and veterinarians continues to grow. However, uptake is expected to increase soon associated with increasing availability of training for veterinarians and commercial laboratories with the experience to achieve reliable and repeatable success rates. This article provides an overview of the current status of these biotechnologies in Australia, examines the challenges limiting their broader implementation, and explores future directions for their integration into clinical and breeding practice.
Impact of Advanced Reproductive Technologies in Equine Breeding Programs
Oocyte Pick-Up (OPU) and Intracytoplasmic Sperm Injection (ICSI) represent advanced assisted reproductive technologies in horses that effectively bypass several natural reproductive processes (ovulation, fertilisation within the reproductive tract and early embryonic development in utero). Instead, oocytes are harvested directly from the ovaries via transvaginal aspiration (OPU), matured in vitro, and fertilised by the direct injection of a single sperm cell (ICSI) into the oocyte (See Video & Figure). Together, they offer an alternative to conventional artificial insemination (AI) and embryo
transfer (ET) programs by increasing reproductive efficiency in breeding programs by:
– Enabling breeding from genetically valuable subfertile mares (associated with uterine pathology, hormonal imbalances, ovulation issues, recurrent embryo loss)
– Enabling breeding from subfertile stallions. It also allows a more efficient use of stallions with limited availability of semen (i.e. deceased stallions) by using a single semen straw for 8-10 ICSI sessions, compared to traditional AI where multiple straws are used for a single breeding.
– Adding flexibility and conveniency, as eliminates the traditional dependence on the breeding season, allowing oocytes to be collected and embryos to be produced throughout the year providing unprecedented flexibility for managing high performance mares and stallions’ timelines
– Supporting international genetic exchange by cryopreserving and shipping embryos worldwide
– Increasing embryo production efficiency compared to traditional breeding techniques such as ET. The average embryo production per OPU-ICSI session is between 1.5 to 2 embryos worldwide, compared to an average embryo recovery of 0.7 (or 70%) per flushing.
– Assisting in research and genetic conservation of endangered equine breeds or rare genetics lines.
‘There Are No Benign Procedures At All’
While OPU is generally considered a safe and well-tolerated procedure, it is not without risks. Complications can range from minor and self-limiting to severe and potentially life-threatening. Minor complications are reported to be of up to 1% and they may include rectal irritation, transient fever and mild colic. These typically occur during or shortly after the procedure and are often resolved with minimal intervention. Major complications, although rare at approximately 0.1%, can be serious and include ovarian or peritoneal inflammation and/or infection (peritonitis), hemorrhage, rectal tears and perforation and death due to severe complications.
The success and safety of OPU depends on rigorous patient selection, technical proficiency, and adherence to animal welfare standards. Candidate mares should be evaluated not only for genetic merit but also for behavioural suitability and overall reproductive and general health to mitigate procedural risks. The technique requires precision and consistency, achievable through structured training under experienced veterinary supervision. Central to ethical practice is the prioritisation of animal welfare, which includes the use of
appropriate sedation and analgesic protocols to minimise discomfort, and the careful scheduling of procedures.
At the University of Sydney’s Equine Centre Camden, advanced reproductive technologies are led by reproduction specialists Dr Gus Ruiz and Dr Rory Nevard. Their expertise supports both clinical services and formal training in ovum pick-up (OPU), contributing to the development of veterinary professionals in this specialised field. As part of the University of Sydney, the Equine Centre Camden integrates high-quality clinical care with veterinary education, ensuring excellence in both outcomes and learning.
Current Status & Challenges of OPU–ICSI in Australia
Despite growing interest among breeders and veterinarians, the application of OPU-ICSI remains significantly underutilised in Australia compared to its widespread adoption in Europe and North America. Several key factors contribute to this limited uptake:
– A primary barrier is the shortage of veterinarians with advanced training in OPU—a technically demanding procedure that requires both theoretical knowledge and substantial hands-on experience under expert supervision. Inadequate technique not only compromises oocyte recovery rates but also poses risks to mare health, underscoring the need for structured training programs and consistent practice, which are currently scarce in Australia. –
Another major constraint is the limited availability of laboratories equipped to support equine in vitro embryo production. Successful embryo development to the blastocyst stage requires specialised infrastructure, tightly controlled culture conditions, and skilled embryologists experienced in handling equine gametes. At present, only a small number of Australian laboratories demonstrate reliable and repeatable success. While interest in offering OPU services locally is increasing, many veterinarians lack access to laboratories capable of supporting the full OPU–ICSI workflow.
timeline. The process starts with the aspiration of immature oocytes via OPU at a referral clinic, followed by selection, package and transportation of immature oocytes to the laboratory, where maturation for 28-32hrs will occur followed by intracytoplasmic sperm injection (ICSI). The injected oocytes are then cultured in vitro for 7 to 9 days until blastocyst stage is reached. Developed embryos are either transferred fresh into synchronised recipient mares or cryopreserved via vitrification. The entire in vitro embryo production process from OPU to blastocyst formation takes approximately 9 to 11 days.
At the University of Sydney’s Equine Centre in Camden, our objective is to establish an advanced reproduction service that supports both academic research and industry application. A central focus of this initiative is the training of veterinary practitioners in OPU technique, with the objective of improving procedural efficiency and clinical outcomes. By optimising OPU protocols, the goal is to achieve the desired annual embryo yield from as few as two to three sessions per mare. This approach has the potential to reduce procedural frequency, thereby minimising stress, lowering associated costs, and enhancing overall animal welfare. Such outcomes align with the University of Sydney’s broader mission of integrating high-quality clinical care with veterinary education and innovation focusing on animal welfare.
Summary & Future Directions on the Implementation of OPU–ICSI in Australia
The integration of OPU-ICSI represents a significant advancement in equine assisted reproduction, maximising reproductive efficiency by increasing genetic value of individuals with desired genetics, allowing marketing of genetics around the world and adding flexibility and conveniency to equine breeding programs. The success of this technique depends on careful mare selection, technical proficiency, and a commitment to minimising procedural impact. When performed by trained veterinarians with precision and appropriate clinical oversight, OPU–ICSI can yield high-quality embryos with fewer sessions, reducing stress and improving welfare outcomes. Moving forward, the broader clinical adoption of OPU–ICSI in Australia will depend on expanding laboratory infrastructure and implementing targeted training programs for both veterinarians and embryologists.
Video 1. Intracytoplasmic Sperm Injection (ICSI) showing a matured equine oocyte at the metaphase II (MII) stage while is aligned and then injected with a single selected sperm (visible within the injection needle). Video courtesy of Dr Andres Gambini, University of Queensland.
cve.edu.au/320-video
The Advantages of Self-paced Learning
Asynchronous learning allows you to learn in your own time and at your own pace without being tied to someone else’s schedule. It’s stress-free because there is no deadline and you study when you choose. Importantly—you choose the order of topics. Continuing Education becomes more meaningful when it is selfdriven because you have a clear purpose for what you want to get out of your learning. You’re in control: Choose to take as little or as long as you like to fully engage with the learning process to truly grasp the concepts.
12 TimeOnline OnDemand Courses for Vets
CVE Members enjoy a 50% discount on these courses.
Price: $150 for CVE Members
Duration: Self-paced CPD points: 5
Care of Rabbits & Rodents TimeOnline OnDemand
Speaker: Olivia Clarke
BSc BVMS MANZCVS (Unusual Pets, Avian)
cve.edu.au/emergency-care-rabbits-and-rodents
Using AI for Your Clinical Notes Will Save You Time & Save Your Sanity
It’s several hours past closing time. It’s dark outside, and the nurses have all gone home, but you are still frantically typing away. As usual, you tried to keep up with the notes during the day, but things got busy, and now you’re missing dinner with your family because you have so much paperwork to catch up on. You’re hungry, you’re tired, and to be honest you can’t remember exactly what Fluffy’s body temperature was this morning, and you are wondering if it is okay to just write 38.4°C.
A new era in veterinary practice
Until a few months ago, we all accepted this as the norm—just one of the downsides to being a veterinarian. Then, seemingly overnight, a new era arrived.
Our clinic started using a generative artificial intelligence (AI) program to help with our medical records and it has been revolutionary. Suddenly, notes are quickly and easily completed as we go. Appointments are more efficient and we are running behind schedule less often. We can better connect with our patients and clients without worrying about typing notes during our consultations. We have more time to focus on clinical care. The accuracy of our records has probably improved too, with less details being skipped or muddled. Plus, best of all, we are all finishing work on time—at least most days. The dream!
How it works
Generative AI scribing tools are software programs that can transcribe the conversation between the
clinician and the client during a consultation, and then use AI to summarise the visit and create a medical record. They are becoming increasingly common in the human medical field, and now many veterinary hospitals have started using these tools as well.
Note: This is not a sponsored post—it’s just a great program!
There are several different programs available, and we trialled a few, but we currently use Heidi Health. This is designed for use in human medical practices but is very flexible and adapts well to veterinary practice. It is a separate program to our clinical records software (we use Petbooqz) but can be integrated if desired.
I’m going to be honest, I don’t fully understand how these AI programs work. I’m not a computer programmer, and I’m guessing you are not either. Don’t let this put you off—do you truly understand how your phone works, or the internet? Generative AI is just the latest advancement in technology and, just like previous advances, it can seem daunting at first. However, there is no doubt that it can be a very useful tool when you know how to make it work for you.
We sign in to Heidi Health through a web browser, and have installed microphones to the computers so that it can easily pick up on the conversation in the room. You can also use the program through a phone app if preferred.
As the client enters the consult room, I click ‘start transcribing’ on the program. I then completely ignore the computer for the rest of the consultation, unless I need to check details on the previous records. I chat to the client, gathering history as usual, with no need to type at the same time. The client might waffle on about their holiday plans, but I don’t let that bother me, as I know the program will filter that out.
I examine the patient and make sure to vocalise findings out loud–‘His heart rate is 160 today, no murmur, his lung sounds are normal… His teeth do have some mild tartar but no gingivitis…’.
The client feels like I am just naturally talking to them, and they seem to appreciate that I take the time to explain what we are doing on the exam. (How many clients don’t even realise you are doing an examination when you are looking at or touching their pet?).
I verbally summarise our assessment and treatment plan with the client and finish up the appointment. The client
leaves with a smile, feeling like I am the most thorough and communicative vet in the world. I then click ‘stop transcribing’ and then the real magic happens. After stopping recording the magic happens.
It has been listening to the conversation, cut out all of the extraneous details and small talk, and distilled it down to the relevant facts mentioned. It re-orders the information into a logical, clear framework, based on our preferred template. The result is a clear, concise visit summary in whatever style or structure we wish. I quickly read the summary, tweak a few details here or there, and then copy it into the medical record. The visit has now taken me about one minute to write up, rather than the usual 5-10 minutes.
Astonishingly accurate
I am a stickler for thorough and accurate medical records, and yet I feel like it often does a better job than I would, particularly for complex cases with multiple comorbidities. The notes are astonishingly accurate, though not 100%; as with any computer program, it’s not perfect.
In particular, our program does sometimes get the names of drugs confused or misspelled. However, it does learn over time, so the more you use it, the better it gets. There can be details that are missed, but that is usually because I forget to mention something out loud. Not surprisingly, human error is much more common than computer error.
Of course, we do have to be sure not to rely on the program completely. The veterinarian must still read and edit the report given to ensure it fully reflects the case.
What else can AI do?
We’re just getting started and are frequently coming up with new ways to use the software. With our current program, it is quick and easy for us to create new templates for common scenarios and use them to format clinical records as needed. Even without the client in the room, I will often transcribe myself summarising a case verbally to make records for surgeries, dental procedures, ultrasound reports, or other procedures. I can even ask it to convert my notes into a discharge summary to email to the client.
While at our clinic we are mostly using AI for note-taking, there are numerous other potential applications for using AI tools that will probably become a common part of clinical practice soon enough. AI can be helpful for creating client handouts, reviewing the latest literature on particular conditions, considering differentials, and interpreting results. You can even try free online AI tools such as ChatGPT or Perplexity for these types of functions, though programs specifically designed for
clinical uses would presumably be more accurate. The Vet Vault Podcast has a great episode (#141) on the use of AI in practice and how to build your own AI clinical tools, ensuring the program only draws from information sources that you know and trust.
Of course, information provided by generative AI should never be fully relied upon—just like Google, or even our old textbooks! It can make mistakes or fill in gaps in knowledge with inaccurate information. We still need to use our own clinical judgement and double check sources. At the end of the day, we are the ones responsible for clinical decision making.
What do the clients think?
Most clients seem happy for us to use the program and seem to appreciate the extra focus we can give them and their pet during the visit. Transcription software is now fairly common among human general practitioners and so most people are familiar with the idea. To ensure the clients feel comfortable with being recorded, we have information about it on our website, in email reminders, and have signs and pamphlets in the reception and consulting rooms. Clients always have the ability to opt out. I can think of only one client who stated that she did not consent to being recorded, and so we simply reverted to the traditional notetaking approach.
Final thoughts
While it can be daunting to see such a dramatic change in technology, nobody wants to get left behind. Consider AI programs as just another tool that you can use to make your clinical work easier, more efficient, and more accurate. It’s time to embrace the new era, focus on your patient care, and go home before your dinner gets cold.
Further Reading/listening
Follow the link for further reading about AI in veterinary medicine and a summary of some of the most popular AI scribe programs in Australia at time of publication. cve.edu.au/ai-320
ChatGPT in veterinary medicine: a practical guidance of generative artificial intelligence in clinics, education, and research https://www.frontiersin.org/journals/veterinary-science/ articles/10.3389/fvets.2024.1395934/full
Animal Disease Insights—New Dashboard Providing Access to 20 Years of Global Disease Intelligence
Navneet Dhand
Director, Asia Pacific Consortium of Veterinary Epidemiology (APCOVE)
e. navneet.dhand@sydney.edu.au
C&T No. 6096
Animal Disease Insights is a new, free web-based dashboard launched by One Health Epi Consulting to provide veterinary practitioners, epidemiologists, policymakers, and other stakeholders with comprehensive access to 20 years of global animal disease data. The platform consolidates official outbreak data into interactive visualisations, enabling rapid assessmentofemergingdiseasethreatsworldwide.
The dashboard features three main sections designed to meet diverse user needs:
– World Tab: Offers a global overview of 130 animal diseases, showing distribution patterns, top affected countries by outbreaks, cases, or deaths, and breakdowns by host species and pathogen types.
– Country Tab: Provides detailed, 20-year historical outbreak data for individual countries. For example, government veterinarians can examine foot-andmouth disease outbreaks on interactive maps and access event-specific details.
– News Tab: Aggregates media reports and tracks weekly and monthly coverage trends, helping users detect emerging issues such as avian influenza, African swine fever or rabies incursions.
Practitioners can utilise Animal Disease Insights for various applications, including pre-purchase or import risk assessments, updating clinic biosecurity protocols with current disease spread information, educating clients through visual media trends, and
preparing evidence-based presentations with longterm disease trend data.
The platform complements existing resources like the World Organisation for Animal Health’s (WOAH) World Animal Health Information System (WAHIS) by integrating news coverage and offering a userfriendly interface tailored for quick, evidence-based decision-making.
One Health Epi Consulting is committed to supporting the veterinary and public health community by providing high-quality disease intelligence at no cost.
Future enhancements aim to incorporate social media data to capture real-time public and media sentiment, further enriching the platform’s capacity to monitor and predict disease trends dynamically. This will enhance its utility for veterinary professionals, policymakers, and researchers in managing animal health risks effectively.
Overall, Animal Disease Insights represents a significant advancement in global animal health surveillance. By providing accessible, comprehensive, and timely disease data, the platform supports improved disease surveillance, biosecurity planning, and informed policy development worldwide.
Figure 1. Image courtesy of Mark Stevenson
Pathophysiology of Feline Chronic
Gingivostomatitis & Juvenile Gingivitis:
Insights Into Novel Medical Management
Richard Malik & Andrea Harvey
Centre for Veterinary Education and Sydney School of Veterinary Science, The University of Sydney
Perspective No. 166
Editor’s Note
The first section has a lot of history and theory. If you are impatient by nature, or a surgeon, save time by reading the last section ‘A New Way Forward’ on page 41.
If you are interested in immunopathogenesis and how disease causation evolves with increasing knowledge, then start at the beginning.
Introduction
Feline chronic gingivostomatitis (FCGS) is a severe, chronic inflammatory disease of the oral cavity in domestic cats (Felis catus) Clinically, affected cats present with oral pain, drooling, halitosis, difficulty eating (dysphagia or inappetence), weight loss, and poor grooming due to discomfort. Importantly, FCGS is distinct from simple gingivitis or periodontal disease: by definition, the inflammation in FCGS extends beyond the gingival margin to involve the oral mucosa and caudal stomatitis. Furthermore, the extent of inflammation is greatly disproportionate to the amount of tartar and plaque present. Current evidence suggests that FCGS results from an inappropriate or exaggerated immune response to chronic antigenic stimulation in the mouth. Proposed antigenic triggers include plaque bacteria (oral microbiome), viruses, and even dietary components or allergens.
Feline calicivirus (FCV) has long been implicated as a major factor, and other infectious agents (feline herpesvirus, feline immunodeficiency virus, feline leukemia virus, etc.) and stressors have also been associated with FCGS (discussed further below).
This article will examine in detail the roles of the oral microbiome, dietary factors, viral infections, and immune dysregulation in the pathophysiology of gingivostomatitis in cats (including the juvenile gingivitis variant).
The Feline Oral Microbiome in Gingivostomatitis
The oral cavity of cats harbors a rich and diverse microbiome, composed of numerous bacterial species (and to a lesser extent fungi and other microbes) that normally exist in a balanced ecosystem. When this balance is disrupted – for example, by inadequate oral hygiene, underlying disease, or immune disturbances –dysbiosis can occur, allowing pathogenic or opportunistic bacteria to overgrow. Cats with FCGS often show evidence of periodontal disease (tartar/calculus accumulation, gingivitis, alveolar bone loss) indicating chronic plaque buildup. A key feature of FCGS is that the amount of inflammation is greatly disproportionate to the amount of tartar present.
Recent studies using genomic sequencing have confirmed that cats with FCGS have an altered oral microbiome compared to healthy cats. Genera such as Porphyromonas, Treponema, and Fusobacterium (obligate anaerobic bacteria often associated with periodontal disease) were found to be significantly more
Figure 1. FCGS in a cat; extensive disease of the caudal pharynx persisted despite full mouth extraction
abundant in the mouths of FCGS-affected cats than in healthy controls. Porphyromonas gulae, a species related to the Porphyromonas bacteria that cause periodontal disease in dogs and humans, has been isolated from cats with stomatitis.
One notable finding was that Bergeyella zoohelcum (a Gram-negative bacterium) was abundant in healthy cats and proposed as a biomarker of a normal feline oral microbiome. Overall, microbiome data implies that FCGS involves a state of oral dysbiosis. The inflammation and tissue damage in FCGS could create an environment favouring anaerobes, while the overgrown microbes provide continual antigenic stimulation that drives further inflammation.
Dietary Factors & Oral Health
Dietary and nutritional factors can influence the oral environment and potentially play a role in gingivostomatitis, although direct causal links are not yet well defined. In one epidemiological survey, it was noted that food residues in the mouth predispose cats to microbial proliferation and dental plaque build-up, which in turn triggers gingival inflammation. Some veterinarians advocate that incorporating dry food or dental diets may help mechanically reduce plaque, though this alone is insufficient to prevent FCGS in susceptible cats, while other colleagues think that a high carbohydrate diet actually favours multiplication of undesirable bacteria. Beyond plaque, there is speculation that food allergens or additives could play a role in oral inflammation for some cats. Nutritional status in general can modulate immune function. Poor nutrition could further impair oral mucosal healing and immune response, creating a vicious cycle. In summary, while diet is not considered a primary cause of FCGS, it influences oral hygiene and possibly immune responses. More research is needed to determine if any specific diet can meaningfully prevent or mitigate feline gingivostomatitis.
Viral Agents & Feline Gingivostomatitis
Feline calicivirus (FCV) is the viral agent most strongly linked to FCGS. In chronic gingivostomatitis, FCV has been detected at high frequency in affected cats, suggesting a persistent infection or carrier state might trigger ongoing inflammation. This implies that FCV presence correlates with the occurrence and severity of stomatitis.
Interestingly, experimentally induced lesions did not invariably progress to chronic disease, indicating that while FCV can trigger stomatitis, additional factors (or host idiosyncrasies, likely genetically programmed e.g., less than optimal immune response) are required for the chronic, immune-mediated condition to develop.
Despite decades of association, it remains debated whether FCV is a primary cause of FCGS or a co-factor. In a recent cohort of 61 stomatitis cats, the percentage of cases positive for calicivirus antigen was high, suggesting active viral presence. The working hypothesis is that chronic FCV infection in the oral tissues provides constant antigenic stimulation and mucosal damage, which triggers the cat’s immune system to mount an excessive, inappropriate inflammatory response. In a situation reminiscent of FIP, the immune response causes florid inflammation, but perhaps because of missing key component of cell mediated immunity, the virus persists in the tissues despite ongoing inflammation. Notably, no particular ‘virulent’ biotype of FCV specific to stomatitis has been confirmed—rather, chronic FCV carriers often harbor antigenically variable virus strains (due to mutation under immune pressure), which may help the virus persist by evading the host’s immune response.
Other viruses have also been implicated in FCGS, especially those that affect the immune system. Feline herpesvirus (FHV-1) primarily causes respiratory and ocular disease, but it can rarely cause oral ulcerative lesions as well. Given that routine feline vaccines protect against both FCV and FHV, it is notable that inadequate vaccination was identified as a risk factor for FCGS in at least one study. In the authors’ experience, many cats with FCGS originated from shelters or rescue organisations where early vaccination was incomplete, consistent with early exposure to calicivirus being critical to the later development of this syndrome.
Chronic retroviral infections can predispose cats to severe stomatitis as well. Some authorities suggest cats with FCGS should be tested for FIV/FeLV, as positivity is not uncommon. In general, FIV-infected cats are known to often suffer severe gingivitis/stomatitis as part of their chronic infections. Importantly, cats co-infected with FCV and feline foamy virus (a retrovirus, sometimes found in multi-cat environments) or co-infected with FeLV tend to have poorer response to stomatitis treatment.
Overall, viral agents—especially FCV—are considered major contributors to FCGS pathogenesis. However, not every FCV carrier develops stomatitis, and some stomatitis cats do not have detectable FCV on PCR testing (pointing to other causes, poor sampling, or potential problems with selection of PCR primers). The interplay between viral infection and host immune response is critical, as described next.
Immune Dysregulation & Inflammation
A hallmark of feline gingivostomatitis is an immunopathologic reaction in the oral tissues. Both CD4+ helper T-cells and CD8+ cytotoxic T-cells are
present, with studies noting an overrepresentation of activated CD8+ T cells in blood and tissue of FCGS cats. This suggests that the disease is driven by antigenspecific immune responses (T and B cell responses to oral antigens) that become pathogenic. Chronic inflammation is thought to be a result of the immune system attacking oral tissues or persistently activated by antigens in dental plaque and/or viruses.
Pro-inflammatory cytokines are abundantly expressed in FCGS lesions. IL-6 and IL-8 are key cytokines in driving neutrophil infiltration and acute phase inflammation, and their strong activation in FCGS mucosa confirms a highly inflammatory microenvironment. In one study, pathways related to innate immunity (neutrophilic inflammation) were also enriched, highlighting that both the innate and adaptive arms of the immune system are engaged in FCGS.
Why do certain cats develop this maladaptive immune response? It may be that some individuals are genetically predisposed to an overzealous immune reaction. The presence of periodontal disease or retained roots can provide a nidus for chronic inflammation, which is why extracting teeth often helps (removing the major sources of plaque-antigen stimulation), indicating that in those cats, the immune system remains triggered by remaining antigens or perhaps has become self-perpetuating. The overproduction of immune mediators (like cytokines, prostaglandins, matrix metalloproteinases) leads to destruction of gingival connective tissue and bone (periodontal ligament and alveolar bone are often lost in chronic cases). The result is a painful, ulcerative oral environment where normal mucosal barriers are broken down, and secondary bacterial infections can further complicate healing.
Importantly, FCGS is not simply periodontitis it is an immune-mediated mucositis that goes beyond what typical tartar-induced gingivitis would cause.
Immune dysregulation is underscored by the fact that immunosuppressive medications often provide relief (albeit temporary) and by the success of immunemodulating therapies (like cyclosporine or stem cells, as discussed later).
Juvenile gingivitis (sometimes called juvenile hyperplastic gingivitis) is an oral inflammatory condition occurring in young cats, typically under 1 year-of-age, around the time the permanent teeth erupt. Clinically, these young cats exhibit marked gingival redness, swelling, and sometimes a proliferative or hyperplastic gum line soon after the adult teeth come in (Figure 2). There may also be a rapidly progressive component where periodontal attachment loss occurs early (juvenile periodontitis) in severe cases.
The pathophysiology of juvenile gingivitis is not fully understood, but it is thought conventionally to be an exaggerated inflammatory reaction to the normal bacterial colonisation that accompanies tooth eruption. There is speculation that this could be partly immunemediated or even involve viral triggers, and the authors think calicivirus infection (as a chronic viral carrier) is actually the key underlying disease process. Many authors believe juvenile gingivitis is multi-factorial, with plaque bacteria being the primary driver but immune system quirks making the response unusually severe. Notably, despite the intense inflammation, juvenile gingivitis often is self-limiting.
Traditionally, management of juvenile gingivitis has focused on aggressive plaque control and supportive care during the period of susceptibility. In cases with gingival overgrowth, surgical gingivectomy can remove excess tissue and reduce pseudopockets. If the condition fails to respond to these measures and progresses, some cats may require extractions of the affected teeth to control pain and disease progression. In contrast, the authors believe this dogma is incorrect, and the principal treatment should be directed at the underlying calicivirus infection, with no requirement for gingivectomy and the like.
The relationship between juvenile gingivitis and adult FCGS is not definitively established—not all juvenile cases go on to develop chronic stomatitis. Both conditions share the feature of immune hyper-responsiveness to oral antigens, though juvenile gingivitis is often transient whereas FCGS is chronic and persistent.
Figure 2. A young cat with ‘juvenile gingivitis’ due to calicivirus. Gum tissue was RT-qPCR positive for calicivirus, as one might expect.
Therapeutic Responses to Pharmacologic Interventions
Management of FCGS is challenging and, according to the literature, often requires a combination of dental, surgical and medical approaches. About 50–60% of cats achieve clinical remission of stomatitis after extensive extractions, and another ~20–30% improve substantially, although they are not completely cured. These refractory cases (and partial responders) require ongoing medical therapy to control inflammation and pain.
Traditionally, the mainstay of medical therapy has been immunosuppressive and anti-inflammatory drugs to ‘tamp down’ the overactive immune response. However, chronic steroid use gives rise to significant side effects (diabetes, immunosuppression, muscle wasting, etc.) and invariably loses effectiveness over time.
Interferon Therapy & Immune Modulation
Recombinant feline interferon-omega (rFeIFN- ω) has emerged as a therapeutic option for FCGS, particularly in cases associated with calicivirus. Feline IFN- ω is a Type I interferon (like IFN- α ) that has been licensed in some countries for treatment of feline viral diseases. In FCGS, interferon can be applied either by injection or oro-mucosally (sprayed in the mouth). Experimental studies suggest rFeIFN- ω is roughly as effective as corticosteroids in managing stomatitis lesions, with the advantage of an antiviral mechanism that could eventually reduce calicivirus load. Indeed, the antiviral effects of omega-interferon might have been underestimated in determining the reason it is effective in these cases, if given for a sufficiently long duration of therapy.
Apart from interferon, the immunosuppressant cyclosporine has shown efficacy in chronic stomatitis. Since FCGS is T-cell mediated, cyclosporine can help ‘calm the immune attack’ in the mouth. Cyclosporine is often used in stomatitis cats that are refractory to steroids or when steroids are contraindicated. The success rate varies, but some cats maintain long-term remission on cyclosporine. A common concern is whether cats treated with cyclosporine are at risk of developing toxoplasmosis, and commonly clindamycin is given at the same time to try to prevent this happening, and also for its effect on anaerobic bacteria in the lesions.
Importantly, antibiotics are frequently administered to FCGS cats, but usually as adjunct therapy rather than a definitive solution. However, long-term antibiotic therapy risks fostering resistant bacteria and usually does not cure FCGS since the primary issue is immune dysfunction.
Given the strong association between feline calicivirus and chronic stomatitis, it makes sense that antiviral therapy directed at FCV might ameliorate the disease. Recent advances—some spurred by SARS-CoV-2 (COVID-19) research and feline infectious peritonitis (FIP) treatments—have identified antivirals that are effective against RNA viruses in cats.
One of the newest candidates is molnupiravir, a broadspectrum antiviral that acts as a nucleoside analogue to induce lethal mutagenesis in RNA viruses. Molnupiravir is actually a prodrug given to improve bioavailability over its primary metabolite, the nucleoside EIDD-1931, which is converted to the active antiviral nucleotide triphosphate, which is the active antiviral.
In a pilot trial (2025), eight FCV-positive cats with chronic gingivostomatitis that had failed full-mouth extractions were enrolled to receive molnupiravir or placebo. By the end of the trial, 4/5 treated cats showed improved oral lesion scores and 2/5 had a marked decrease in calicivirus shedding, whereas none of the 3 untreated control cats showed improvement. This work was presented at the ACVIM forum in June. These results are very promising: they suggest that suppressing FCV replication with an antiviral can lead to clinical remission of stomatitis in at least a subset of cases. Further research with larger samples and longer follow-up is needed, but this proof-of-concept indicates antivirals deserve a place in the FCGS treatment arsenal when viral infection is confirmed.
Besides molnupiravir, other antivirals and antiviral strategies have been explored. Broad-spectrum antivirals like GS-441524 (a nucleoside analogue used to treat FIP) theoretically could also have activity against FCV, but this remains speculative. If a stomatitis cat is positive for FIV or FeLV, managing those conditions (e.g., antiretroviral drugs like AZT for FIV, or interferon for FeLV) might indirectly help the oral disease by improving overall immune function, though evidence is anecdotal.
In summary, antiviral therapy targeting FCV is an exciting new avenue for FCGS management. As these treatments are refined, they hold promise for cats that suffer chronic oral inflammation associated with persistent viral infection. Our unpublished work in Sydney over the last three years has confirmed that molnupiravir is a highly effective treatment for cats with FCGS, although we use it in concert with doxycycline to manage the bacterial dysbiosis and low dose meloxicam to reduce the overactive inflammatory component within the lesions.
Emerging Therapies: Mesenchymal Stem Cells
One of the most promising emerging therapies for refractory FCGS is the use of mesenchymal stem cell (MSC) therapy. MSC can secrete cytokines and factors that dampen overactive immune cells, promote tissue healing, and even effect antiviral supportive actions by improving the host’s immune response. Initial pilot studies about a decade ago showed dramatic improvements in cats with stomatitis that received intravenous stem cell therapy, especially those that had not responded to other treatments.
In a 2023 long-term study by Soltero-Rivera et al., cats were observed for 2–9 years post-treatment. Importantly, many of these cats had been candidates for euthanasia due to unrelenting pain prior to MSC therapy, and after treatment they experienced a restored quality of life. Approximately one-third of cats treated did not improve significantly (true non-responders), indicating MSCs are not a panacea for all cases. Adverse effects of MSC infusion were relatively minor: about 34% of cats had transient reactions like fever or vomiting around the time of infusion, but these were self-resolving transfusion-like reactions, and no long-term negative effects were noted. Autologous cells may have slightly faster efficacy in some reports, but allogeneic cells are more practical to use in clinical settings (they can be banked and readily administered without the need for harvesting from the current patient).
Mechanistically, MSC therapy in FCGS is thought to work by modulating the immune response. Essentially, they help turn off the chronic inflammatory response by restoring immune balance. A fascinating development is that a specific allogeneic MSC product (using uterinederived MSCs from spay-neuter clinic donors) has been in advanced clinical trials and was recently on track for conditional FDA approval as a treatment for feline stomatitis. Veterinary stem cell companies and academic centers (e.g., UC Davis, which has spearheaded much of the FCGS MSC research) are optimistic that this therapy will become a standard of care for refractory cases.
Beyond stem cells, other emerging or adjunct therapies include laser ablation of inflamed tissue, plasmarich protein injections to promote healing, and novel immunotherapies (such as IL-2 or IL-10 modulation).
In conclusion, stem cell therapy represents a significant breakthrough for a subset of stomatitis cats that do not respond to conventional treatments. As with any innovative therapy, cost and access are considerations,
but the potential to cure or induce long-term remission in a disease that was previously often an end-of-line scenario (euthanasia due to intractable pain) is a remarkable advancement in feline medicine.
Conclusions
Feline gingivostomatitis is a complex syndrome with multifactorial pathophysiology. The feline oral microbiome in FCGS shifts toward a dysbiotic state rich in anaerobes, which likely fuels inflammation further. Among infectious agents, feline calicivirus stands out as a key player associated with FCGS development, although other viruses like FHV-1 and FIV can influence disease severity and progression.
Juvenile gingivitis in cats shares some parallels by featuring an outsized inflammatory reaction in the young animal’s mouth, but it often eventually resolves with maturity and aggressive dental care. Therapeutically, the approaches to FCGS are evolving from purely symptomatic treatment (antibiotics, steroids, extractions) toward targeted interventions: immunomodulators like interferon-omega to curb viral replication and immune activation, direct antivirals like molnupiravir/EIDD1931 to eliminate the key triggering viral antigens, and regenerative medicine such as mesenchymal stem cells to restore immune equilibrium. Nonetheless, some cases remain frustratingly refractory, highlighting the need for continued research.
With a better understanding of the pathophysiology, veterinarians can develop earlier diagnostic markers and more effective, specific treatments—turning this once life-long debilitating disease into a manageable or even preventable condition for our feline companions.
Editor’s Note
Start overleaf if you just want the basic facts and not the background and history.
A New Way Forward
To reiterate, FCGS is a debilitating inflammatory disease affecting the oral mucosa of cats presenting as ulcerative and/or proliferative inflammatory process extending from the gingiva to the caudal pharynx. The foundational understanding of gingivostomatitis in cats was established by Pedersen (1991) and further expanded by Ross Harley’s PhD research at Bristol Veterinary School (see reference 7 in the bibliography), with both investigators emphasising the critical role of calicivirus.
Over the past three decades, however, complex and often contradictory findings have emerged, complicating and in some respects hindering the clinical approach to managing FCGS.
After initial primary infection with calicivirus, affected cats mount a robust antibody-mediated (AMI) and cell-mediated immune response (CMI) to clear FCV from oral tissues. FCGS occurs when these processes are unbalanced, so the virus and the inflammatory response to its presence persist. Dietary factors may also play a role, especially when ultra-processed carbohydraterich kibble is a major part of the affected cat’s diet. Additionally, bacterial biofilms displaying striking dysbiosis have been identified in affected tissues, reinforcing the notion that both viral and bacterial factors trigger an inappropriate immune response which favours disease progression.
CONCLUSION
FCGS is a multifactorial disease influenced by viral infection, immune dysfunction, and environmental factors. A multidisciplinary approach incorporating antivirals, immunomodulation, and adjunctive therapies has the potential to significantly improve clinical outcomes and quality of life for feline patients.
Old Treatment Modalities
Surgical Management
The historical dogma is that full-mouth or partialmouth dental extractions remain the gold standard treatment, providing long-term resolution or substantial improvement in maybe 60% of cases. Lower success
rates are commonly seen by practitioners who are not experts in performing this radical surgical procedure. Although there is a wealth of evidence supporting this approach, intuitively this would appear to be an unattractive option for most cats and most owners.
Full mouth extraction is an aggressive, painful surgical intervention involving prolonged or multiple general anaesthetics, and can be associated with moderate morbidity, high cost and delayed convalescence. Although most cases are improved, a substantial proportion of cases still have residual disease even after healing has occurred. Presumably, extraction removes chronic antigenic stimulation by elimination of virus-infected tissues, facilitating viral clearance and immune resolution. Some cats, however, continue to exhibit caudal pharyngeal inflammation post-extraction, necessitating additional medical intervention.
Corticosteroids such as prednisolone provide temporary relief but are not viable for long-term management due to adverse effects. If they are used, when the doses are later terminated the condition recurs, sometimes worse than it was initially. This is because corticosteroids favour viral persistence and multiplication!
Cyclosporine has shown excellent efficacy in controlling refractory cases by inhibiting T-cell activation and reducing proinflammatory cytokine expression. It is also used in a conceptually similar condition in dogs, i.e. Canine Chronic Ulcerative Stomatitis (CCUS) or Canine Ulcerative Paradental Stomatitis (CUPS; but which older Australian vets would refer to as ‘trench mouth’), in concert with metronidazole.
Mesenchymal stem cell (MSC) therapy has emerged as a promising option, with studies showing normalisation of CD4/CD8 ratios and resolution of clinical signs in some refractory cases but only following full mouth extraction.
Antiviral Therapy – Way of The Future?
Recent advancements in feline antiviral therapies have produced a paradigm shift in the treatment of FCVassociated FCGS. Molnupiravir (prodrug) and its active metabolite, EIDD-1931, have demonstrated efficacy in eliminating FCV from the oral mucosa, paralleling their success in treating feline infectious peritonitis (FIP). Mefloquine and nitazoxanide have also shown antiviral activity against FCV, warranting further investigation as therapy. Prolonged treatment courses are necessary to fully clear FCV from gingival and pharyngeal tissues, like protocols used in FIP therapy.
Additional therapeutic interventions, such as highenergy laser therapy, have shown potential in eradicating viral reservoirs within gingival tissue.
Our Current Recommended Therapeutic Regimen
The tide turned during the resurgence of feline antiviral therapies, which gave veterinarians worldwide a greater confidence in using antiviral drugs. This movement began with the use of famciclovir for herpetic infections caused by FHV-1 and gained momentum with GS-441524 and GC376 for feline infectious peritonitis (FIP).
We believe the most promising agent for treating calicivirus is EIDD-1931 and its prodrug molnupiravir.
Research by Jacqui Norris’s group indicated that mefloquine also exhibits effective activity against calicivirus, while other teams, including one from the University of NSW and a feline physician (Dr Emily Pritchard), advocate for nitazoxanide.
Our preferred treatment for calicivirus is molnupiravir and its metabolite, EIDD-1931, due to their established efficacy against FIP. All three medications we utilise (EIDD-1931, doxycycline, half-dose meloxicam) can be safely administered to kittens with acute calicivirus, adult cats with acute virulent disease, and those with calicivirus-associated gingivostomatitis.
A combination protocol incorporating low-dose oral meloxicam (to reduce the inflammation), doxycycline (to mitigate bacterial dysbiosis), and molnupiravir or EIDD-1931 (for antiviral action) has yielded excellent results in the hands of the authors. This regimen often leads to marked clinical improvement within 2–3 months, allowing for medication tapering and potential discontinuation.
Mirtazapine (2 mg once a day; oral or transdermal) is frequently included to stimulate appetite in affected cats.
Much like treating FIP, prolonged treatment courses are necessary to eliminate calicivirus from the gingival and caudal pharyngeal tissues. With input from BOVA Compounding, we have developed a stable drug combination that includes low-dose oral meloxicam to reduce the inflammatory response and thereby make the cats more comfortable, doxycycline to combat bacterial
dysbiosis and for its immunomodulatory effects, and EIDD-1931 for its long-term antiviral action.
We administer these treatments, either directly onto the lesions, or mixed with two equal meals of canned cat food or fresh meat, using a specially designed paste which is palatable and ‘adhesive’. The rationale is as follows: we wish to have the drug work initially in the oral cavity and gums at very high concentrations and subsequently be absorbed and target the same tissues by achieving effective blood levels. We chose EIDD1931 so that the active antiviral would work LOCALLY from the get-go, in comparison to molnupiravir which needs to be activated in the liver to become an effective antiviral agent. Additionally, we often include 2 mg of mirtazapine daily (given separately orally or transdermally) to encourage a strong appetite.
Patients typically show immediate initial improvement, likely due to doxycycline and meloxicam. Over 1-3 months, the benefits become sustained, resulting in substantial recovery, allowing for discontinuation of all the medications.
We have used this approach in cats with residual disease after whole mouth extractions and also in cats with calicivirus-associated gingivitis where full-mouth extractions have not been performed, including cases of juvenile gingivitis. Ideally, these cats should receive thorough dental care and the extraction of any teeth that
Figure 3. A cat with FCGS before (A) and after (B) therapy with molnupiravir/meloxicam and doxycycline. The cat has continued to do well following discontinuation of all drugs. The dates are provided on the photographs.
are loose or exhibit lytic changes (in alveolar bone or teeth) on dental radiographs. It can also be used in cats and kittens with acute calicivirus disease, including cats with prominent lingual ulcers.
It is essential to note that this approach is still a work in progress. Some cats may require higher doses of EIDD1931, and we may explore the sequential or combination use of mefloquine or nitazoxanide in the future. Continued research and clinical experience will help refine these treatment strategies to enhance outcomes for affected cats. Thorough and comprehensive case notes (that include details of diagnosis, treatment schedule, response to treatment [including photos] and details of suspected adverse events) will allow retrospective assessment and analysis.
Practice Tip
It is worth keeping a tub of this combination paste in the pharmacy* in case you are presented with an acute case of calicivirus disease, whether it be a nasty virulent calicivirus strain, or just a normal calicivirus involved in a kitten with cat flu. This product will provide symptomatic relief and be an effective antiviral, with the proviso that you maintain hydration by force-feeding, syringing A/d or cream treats, or IV fluid therapy to protect the kidneys during administration of low oral meloxicam. The disease course will be markedly foreshortened. If you are not sure if herpetic disease (FHV-1) is present also, add in Famvir at 40 mg/kg BID to TID.
*Vets are legally allowed to order medicines from pharmacies either by prescription (i.e. for an individual animal) or via written order. The written order does not need to comply with the same requirements that a prescription does i.e. no need for animal owner details or a need to be for a specific animal. Vets can order via written order the quantity they need 'for emergency use'. It is the responsibility of the prescribing veterinarian to determine if a medicine is likely to be needed immediately and when it isn’t in the animal’s best interests to wait the time it takes (often several days) to order and receive a compounded medicine. So, the medicine ordered via written orders, can sit on a vet’s shelf until dispensed by the vet. The vet can then dispense and label the amount they give to the owner from the shelf stock. A vet shouldn’t dispense an amount of a compounded medicine that will expire before the label says. Some of Bova’s products have long shelf lives, others not so long, so it really depends on the formula and the stability data.
Figure 4. A cat with FCGS and a non-healing lingual ulcer before (A & B) and after (C) therapy with molnupiravir/meloxicam and doxycycline. The cat has continued to do well following discontinuation of all drugs. The dates are provided on the photographs.
Figure 5. A cat with calicivirus-associated juvenile gingivitis before and after therapy with molnupiravir/ meloxicam/ doxycycline. The cat has continued to do well following discontinuation of all drugs.
Figure 6. Label for palatable paste containing EIDD1931, doxycycline monohydrate and meloxicam in the optimal ratios for treatment of calicivirus associated stomatitis
Figure 7. A different cat with FCGS/juvenile gingivostomatitis before (above) and after (below) molnupiravir/meloxicam/doxycycline therapy. Image courtesy of Chantal Celindano.
Therapeutic regimen using the BOVA combination paste product
Dose rate – number of clicks (1 click = 0.25mL) per 3 kg of cat, twice a day, with food
i. A 3 kg cat should get 1 click twice a day
ii. A 4.5 kg cat should get 2 clicks in the AM, and one click in the PM
iii. A 6 kg cat should get 2 clicks BID
Each click (=0.25mL) contains EIDD-1931 51mg/0.25mL, Doxycycline 15mg/0.25mL, Meloxicam 0.0375mg/0.25mL.
Presented as 35mL pack size in the Topi-click device with a syringe.
Contextualised Care/Spectrum of Care
This novel management approach focusing on antiviral treatment rather than surgical removal of teeth is currently controversial amongst some veterinary dentists given the current limited evidence base. However, the importance of contextualised care/spectrum of care has become well recognised, acknowledging that there are different ways to approach treatments, depending on specific circumstances of the individual animal and their caregivers, and the context in which care is delivered. This approach emphasises tailoring care to individual circumstances which includes holistic patient specific needs, client preferences, and financial limitations, encouraging a flexible and patient-centred approach.
The authors therefore consider that it is critical that less invasive and less expensive treatment options are able to be offered, in the interests of best patient welfare and affordability to clients, particularly given that these cases tend to be more prevalent in low socioeconomic communities.
Ethical Considerations in Treatment Selection
One of the most debated aspects of FCGS management is the ethical consideration of full-mouth extractions. Ethical decision making with any treatment should include
i. Treatment efficacy
ii. Patient welfare impacts (discussed below)
iii. Other adverse impacts of treatment
iv. Client preferences
v. Cost
Most clients would have a strong preference for medical management if it were efficacious. Whilst it is early days in clinical trials, results to date from different researchers across the world are extremely promising. Welfare impacts on patients are substantially reduced if surgical intervention is not required or can be minimised. Some cases may still require dental extractions where there is dental pathology, and full dental evaluation is always recommended, but there may be benefit in reducing inflammation with medical management prior to dental extractions in these cases— a contextualized individual patient approach is advised Medical management is substantially less expensive which can be a key component in determining whether these cases are successfully managed or not—many owners of these patients simply cannot afford extensive dental extractions. The only concern raised with antiviral therapy by some clinicians is the contribution to resistance of these antivirals. Whilst this is a valid concern, in the authors’ opinions this is not an ethical justification to withhold an efficacious antiviral treatment for a viral disease.
Welfare Considerations in Treatment Selection
Applying the Five Domains Model for assessing patient welfare enables a scientific, holistic and objective approach to assessing welfare impacts of management interventions. This involves assessing impacts in the four physical/functional Domains of Nutrition, the Physical Environment, Health, and Behavioural interactions (with other animals, people and the environment) and through evidence from physiology, behavioural science and neuroscience, inferring impacts on the animal’s mental experiences.
Surgical intervention has greater negative impacts on patient welfare through the frequency of reduced voluntary nutrition in the peri-operative period, risk of dehydration associated with reduced food intake and general anaesthesia, requirement for hospital admission and the associated anxiety/fear, the requirement for prolonged or multiple general anaesthesia and the associated risks, pain associated with surgery, impacts on behaviour in both the peri-operative period and potential longer term behavioural impacts from full mouth extractions. Conversely, medical management has very few welfare impacts restricted mainly to the impacts of administering medications since the recommended treatment regimens have limited side effects.
In summary, some researchers, including the authors of this article, argue that antiviral therapies offer a less invasive alternative to extensive dental extractions, potentially reducing the need for radical surgical interventions. This may circumvent an extremely expensive procedure associated with substantial morbidity for the feline patient.
Is treatment a choice between medical or surgical approaches or should both be used?
To be clear, the authors are not necessarily suggesting a choice between medical and surgical treatment but rather are recommending a contextualised and individual patient-centred approach to management decision making, which includes the option of antiviral treatment. Dental evaluation is recommended, and some extractions may still be required. However, it is likely that many patients will benefit substantially from antiviral therapy, and whether any required tooth extractions are performed before or after such therapy should be considered on a case-by-case basis.
In summary, gingivostomatitis in cats remains a complex and challenging condition influenced by a viral component, immune response discrepancies, and environmental factors. By leveraging advancements in antiviral treatments and adapting therapeutic protocols to address the specific needs of each individual cat, we have the potential to improve the quality of life for many feline patients suffering from this condition.
Chronological Bibliography
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19. Verstraete FJM, Lommer MJ. Oral and maxillofacial surgery in dogs and cats. 2nd ed. St. Louis: Elsevier, 2019.
20. Hennet P, Steffen F, Graf F, et al . Comparative efficacy of recombinant feline interferon omega versus glucocorticoids in refractory calicivirus-positive cats with caudal stomatitis. J Vet Intern Med 2020;34(3):1266–1273.
21. Vapniarsky N, Arzi B, DuRaine G, et al . Histological, immunological, and genetic analysis of feline chronic gingivostomatitis. Front Vet Sci 2020;7:310.
22. Arzi B, Clark K, Sundstrom D, et al . Therapeutic efficacy of mesenchymal stem cell transplantation in feline chronic gingivostomatitis: a randomized controlled trial. Stem Cell Transl Med 2020;9(6):636–649.
23. Fried WA, Lockett S, Hummel J, et al. Use of unbiased metagenomic and transcriptomic analyses to investigate the association between feline calicivirus and chronic gingivostomatitis in cats. Am J Vet Res 2021;82(5):381–394.
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This is an independent article, it was not commissioned and there are no conflicts of interest to declare.
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