Companion Quarterly Vol 29 No1 March 2018

COMPANION QUARTERLY – Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA

Companion Quarterly

OFFICIAL NEWSLETTER OF THE COMPANION ANIMAL VETERINARIANS BRANCH OF THE NZVA Volume 29, No. 1 | March 2018

VOLUME 29 NO 1 March 2018

How to get the most from your skin biopsies

Diagnosis of hypoadrenocorticism in dogs

Calling time on Scottish folds

Practical dental homecare info

Snippets from WSAVA 2017

Volume 29 | No. 1 | March 2018 ISSN No. 2463-753X EXECUTIVE COMMITTEE 2018 cav@vets.org.nz

CONTENTS

President

John Munday

Companion Quarterly

Operations Manager Rochelle Ferguson

Treasurer

Aimee Brooker

Committee Members Simon Clark Nina Field Toni Anns Natalie Lloyd Paula Short

EDITORAL COMMITTEE Sarah Fowler (Editor) Bart Karalus Crystal Loh Ian Millward Juliet Matthews Simon Clark Shanaka Sarathchandra

Address for submitting copy/ correspondence

Sarah Fowler 66 Callum Brae Drive, Rototuna, Hamilton 3210 T (H) 07 845 7455 | M 027 358 4674 E sarah.fowler@gmail.com

Advertising Manager

Christine Moloney 25 Manchester St, Feilding T 06 323 6161 | F 06 323 6179 E christine.moloney@totallyvets.co.nz

NZVA website www.nzva.org.nz CAV website www.cas.nzva.org.nz

2 Editorial 4 CAV activities and meeting highlights

8 CAV Noticeboard 10 What is your diagnosis?

Gabriel Hagard

12 Information on the proposed

release of rabbit calicivirus (RHDV1) K5 in New Zealand CAV Executive Committee

16 Calling time on Scottish folds Sarah Fowler, Rochelle Ferguson, John Munday

22 Diagnostic techniques: how to

get the most from a skin biopsy Duncan Graham

26 Diagnosis of

hypoadrenocorticism in dogs Boyd R Jones, Anne Kim, Lucy Lane

Copyright

The whole of the content of the Companion Quarterly is copyright, The Companion Animal Veterinarians Branch of the NZVA (CAV) and The New Zealand Veterinary Association (NZVA) Inc.

32 Practical dental homecare information Janine van Dam

Cover photograph

Magdeline Soo's dearest buddy Einstein basks in the evening sunlight and considers his good fortune.

36 Conference report: 42 Congress Charlotte Mathews,

Newsletter design and setting Penny May T 021-255-1140 E penfriend1163@gmail.com

Disclaimer The Companion Quarterly is a non peer reviewed publication. It is published by the Companion Animal Veterinarians Branch of the NZVA (CAV), a branch of the New Zealand Veterinary Association Incorporated (NZVA). The views expressed in the articles and letters do not necessarily represent those of the editorial committee of the Companion Quarterly, the CAV executive, the NZVA, and neither CAV nor the editor endorses any products or services advertised. CAV is not the source of the information reproduced in this publication and has not independently verified the truth of the information. It does not accept legal responsibility for the truth or accuracy of the information contained herein. Neither CAV nor the editor accepts any liability whatsoever for the contents of this publication or for any consequences that may result from the use of any information contained herein or advice given herein. The provision is intended to exclude CAV, NZVA, the editor and the staff from all liability whatsoever, including liability for negligence in the publication or reproduction of the materials set out herein.

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nd

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WSAVA

38 A week with ... Feline medicine specialist, Pru Galloway Susan Murray

42 NZVJ Abstract 44 What is your diagnosis? The answers

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47 New Zealand Companion 48

Animal Health Foundation update CPD Record

Vets in Stress Programme 24 Hour Freephone Confidential Counselling Service

0508 664 981 Helps you solve personal and work problems, including: Relationship problems Drug and alcohol issues Work issues Change Stress Grief

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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EDITORIAL

Welfare and puppy adoption I hope everybody had an enjoyable holiday period and are feeling refreshed and looking forward to an exciting year keeping companion animals healthy. Lots of things have happened in the CAV sphere in the 3 months since the last Companion Quarterly. However, in this editorial I will focus on only two of the recent events; the Trade Me ban on selling brachycephalic dogs and the recent Listener articles on dogs in New Zealand.

As a child I remember visiting Japan and being taken to a pond that contained goldfish with deformed fins and eyes that bulged out from the sides of their heads.

The fish could hardly swim and many had cloudy eyes. Understandably I assumed these fish were all suffering from some nasty disease. Imagine my surprise then when our guide proudly told us that these were extremely valuable, exceptionally high quality, fancy goldfish that had been bred over many generations specifically to have deformed fins and bulgy eyes.

Interesting, I thought, but what’s in it for the fish?

I remembered those fish from my formative years when Trade Me announced their ban on selling English and French bulldogs and Pugs. While the Trade Me ban will not stop these dogs from being sold by other methods, it has raised awareness for welfare concerns in brachycephalic breeds. This is extremely important because, like the guide in Japan who would never have considered his goldfish may have been suffering, many people in the public were completely unaware that having a pushed-in face could negatively impact welfare. While CAV doesn’t think that banning breeds is the best way to solve welfare issues, we welcome the publicity it has generated.

The ban has been extremely effective in making people wonder whether it really is such a good idea to breed a dog that bears such little resemblance to its naturallyevolving ancestors. After I had read the news story on ‘Stuff’, I read the user comments. While it is accepted that these comments do not necessary reflect those of the general population, I was pleasantly surprised that the majority of people who left a comment supported Trade Me’s ban and suggested that it should have gone further.

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As veterinarians we are in the unique situation of having a foot in both camps regarding issues relating to companion animal breeding. We have clients who are breeders, but we also feel a responsibility to improve the welfare of companion animals. As a child I had a neighbour who bred English bulldogs. This neighbour really loved her dogs and considered herself the most responsible breeder in New Zealand. Despite the fact that her dogs snuffled, had trouble walking, suffered from skin diseases, and were all born by elective caesarean, she was convinced her bulldogs were all happy balls of good health. One difficulty we will face as vets will be to convince such people that the dogs they breed are welfare-compromised and must be bred in ways that improve health. Furthermore, these dogs can be made healthier without destroying a breeder’s life work or even produce a dog that is no longer recognisable as that breed. Many breeders will challenge the possibility their dogs are not healthy with examples of 15-yearold brachycephalic dogs that died after being hit by a car when chasing a rabbit.

However, it is important to remember that studies of pugs and French bulldogs revealed that at least 50% of the dogs had altered breathing that interfered with their ability to exercise normally due to cosmetic traits that have been deliberately selected for. That significant numbers of dogs suffer for their looks is unacceptable. While it will take a long time and a large shift in public attitudes to convince everybody that many brachycephalic dogs are currently welfarecompromised, hopefully the Trade Me ban has started a conversation that will result in more pressure for breeders to produce healthy happy dogs rather than produce dogs with the most exaggerated physical features possible.

As a committee, CAV discussed the Trade Me ban at length. While we support the goal of the ban, the current ban has the disadvantage of not including other welfare-compromised breeds of dogs and cats. Worse, some might think that because Trade me hasn’t banned, for example Boston terriers, Shar peis or Scottish fold cats, these breeds don’t have compromised welfare. While recognizing the flaws in Trade Me’s ban, CAV hopes this will be a good starting point for many

additional conversations regarding how puppies are bought and sold in New Zealand.

Just before the news of the Trade me ban came out, CAV contributed to an excellent series of articles in the Listener (13 January 2018 edition for any who missed it). These articles covered problems in the greyhound industry, the rise of unregulated ‘puppy farms’ in New Zealand, and the best way to source a new puppy.

In the article we explained the importance of seeing the parents of any puppy prior to purchase. This enables prospective owners to ensure that the puppy’s parents are well looked after and healthy and ensures that by purchasing the puppy you are not supporting a ‘puppy farm’. Of course, it always has to be remembered that lots of dogs are euthanatised in New Zealand every day and, as my muttley (beautifully long nosed!) dogs will attest, adoption from a shelter is another excellent option. CAV have developed a resource regarding ethically sourcing a dog and this is available to the public on the NZVA website. A Dog Breeding Toolkit for Veterinarians is also available on the CAV webpage, under the resources section [Eds note: an abbreviated version of this is printed on page 20 of the December 2017 issue of Companion Quarterly].

The latest developments, along with the proposed welfare regulations due to take effect in October this year, signals improving animal welfare standards in New Zealand. People in New Zealand do seem to be more aware of welfare issues in our companion animals. Hopefully this will translate into a greater willingness to adopt animals from shelters or, if they have to buy a specific breed, they buy from a breeder who prioritises health and temperament over cosmetic traits. CAV applauds the decision by Trade Me as well as the decision by Animates to work with the SPCA to rehome unwanted cats and dogs and not sell puppies that could have been supplied from ‘puppy farms’.

The increasing awareness of the importance of welfare issues in our pets is excellent news both for companion animals in New Zealand and for companion animal veterinarians.

John S. Munday CAV President l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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WORKING TO PROMOTE AND SUPPORT COMPANION ANIMAL PRACTICE IN NEW ZEALAND

CAV activities and meeting highlights

Proposed release of RHDV1 K5 in 2018 CAV made a submission to ACVM on the proposed release of this virus, requesting that the following concerns are considered in the risk assessment.

• The risk to animal welfare posed by release of RHDV1 K5 due to its potential to cause unnecessary pain and distress to owned rabbits and unreasonable pain and distress to wild rabbits.

• The ability of RHDV1 K5 to actually be an effective tool in achieving the aim of long term control of the wild rabbit population.

If the virus is approved for release, CAV have also requested that the release date allows sufficient time and is widely publicised so that all rabbit owners are made aware of the risks and have time to get their rabbits vaccinated and implement biosecurity measures to mitigate the risks to their pets. The full submission is available on the CAV website.

For more information, see page 12.

Federation of Asian Small Animal Veterinarians Associations

CAV have been a member of this association since its formation in 2007, along with Australia, Malaysia, Korea, Japan, China, India, Hong Kong, Singapore, Philippines, Sri Lanka, Taiwan and Thailand. Pieter Verhoek (previous CAV President) served a term as FASAVA President in 2014.

The primary focus of FASAVA is providing education. They achieve this by holding an annual conferences (the last one held with ASAV on the Gold Coast in 2017), with every third year combining with WSAVA when it is in the Asia region (this will be in Singapore this year).

FASAVA also subsidise education in developing countries such as Cambodia and Laos. CAV believe that we have a 4

responsibility as a privileged member of the global veterinary community to support those veterinarians in countries that have still to develop robust veterinary standards and animal welfare systems. To this end, CAV have joined other several other well established FASAVA members and signed an MOU to each contribute USD $1000 annually for three years to a common fund to assist the provision of veterinary CPD to countries like Cambodia and Laos.

Regular updates on this initiative will be provided to members through articles in the Companion Quarterly.

Research into methicillin resistant Staphylococcus psuedintermedius (MRSP)

Funding for a project led by Massey University’s David Wilkinson to assess MRSP carriage by New Zealand dogs was approved by the Companion Animal Health Foundation in the final funding round for 2017. It is important to the ongoing health of our canine population that we have a good understanding about resistance patterns in New Zealand, and this project is expected to improve our understanding of the current situation and potential risks.

Cat Management Strategy Group

This group plans to continue, post the release of the Cat Strategy Management Plan, with representatives from NZVA, RNZSPCA and the Morgan Foundation.

They will meet twice yearly and set up a website with contact details.

Veterinary medicines section of the VCNZ Code of Professional Conduct

CAV, along with many veterinarians, made a submission to the Veterinary Council of New Zealand on the proposed changes to the veterinary medicines section. CAV were in support of improved stock control requirements, and stricter controls around prescribing

antibiotics of critical importance. It is vital that the profession demonstrates good stewardship of medicines to retain prescribing privileges. The proposals to require hard copy recording for controlled drugs and the extensive requirements for counselling owners on adverse events prior to dispensing medications were not supported.

Round up of Responsible Breeding initiatives in 2017

Following the release of the National Animal Welfare Advisory Committee (NAWAC) opinion on selective breeding in March 2017, CAV contributed to an article published on the Stuff website that was widely publicised, about the welfare issues facing brachycephalic dogs. CAV have also written and contributed to two other articles in Vetscript on the topic of responsible breeding, and developed an ethical guide to sourcing a dog for the NZVA website.

Working with Dogs NZ, CAV supported their seminar held for veterinarians and breeders in October, on responsible breeding practices and have plans to jointly run more of these in other parts of the country in 2018. Cat Fancy have also expressed interest in being involved with these, and we are looking at how we can also include cat breeders as they also face similar problems with brachycephalic issues.

A dog breeders toolkit for veterinarians has been developed (available on the CAV website under practice resources) to assist veterinarians provide advice on breeding healthy dogs.

CAV participated in a Listener article on puppy farming and irresponsible breeding to highlight welfare concerns occurring where there is no regulation for those commercially breeding cats and dogs.

With NAWAC supporting CAV’s position for a ban on the breeding of Scottish folds, we are working on raising

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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awareness of the problems associated with this breed (see the article in this issue) in the profession, with the breed registries and the public.

also the psychological wellbeing of the cats and dogs in their care.

A position statement on responsible breeding is currently being developed for 2018 release, to support lobbying for cat and dog breeding regulations such as those already in place in many other countries.

CAV share the concerns raised in the latest WSAVA global dental guidelines about the welfare issues seen with an increase in non-veterinarians offering anaesthesia-free dentals. We do not believe that groomers possess the required skills to competently provide dental care, with examples of severe periodontal disease being overlooked during so called “dentals” performed by groomers. CAV contributed to an article in the February Vetscript highlighting these concerns.

Policy updates

The NZVA Responsible Cat and Dog Ownership policies have been reviewed and updated. There is an increased emphasis on the need for owners to provide, not only for the physical, but

Dentistry

Committee member updates

Pauline Calvert has resigned after serving a three year term on the committee. Pauline has been a highly valued member of the committee, and a valued source of information drawn from her experience in companion animal practice and her extensive pharmacological knowledge (she is an examiner and past president of the pharmacology chapter of the ANZCVS).

We thank her very much for the contribution she has made to CAV (this was her second stint on the committee) and congratulate her on being appointed President of AGCARM (the first woman to hold this position!). l

Would you like to see your pet on the cover of Companion Quarterly?

We now have a new cover photo for each issue of Companion Quarterly. This means we are always on the lookout for suitable photos. Photos selected for the cover must be landscape orientation (or able to be cropped to this), crisp and well focused, and of high resolution (at least 300 DPI). They must also be well composed and interesting.

Please send any suitable images to the Editor (sarah.fowler@ gmail.com). If however you have a favourite snap of your fur-family that’s not quite up to cover standards, please send that in too: photos that are not selected for the cover may be printed on the back inside cover.

WINNER

Article of the Year

Jeffrey Clyne

“Opioids and gastro-oesophageal reflux, regurgitation and vomiting in the perianaesthetic period.”

June 2017 | Volume 28 (2) | Page 24–29

EYEVET Services Limited

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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The CAV Noticeboard Hill’s Pet Nutrition/CAV Educating the Educators Scholarship This scholarship provides assistance for veterinary educators to attend advanced level continuing education events outside New Zealand, in exchange for articles, reports and presentations on their area of interest.

Through this partnership, we recognise the importance in supporting our leading veterinarians’ participation in international conferences to ensure they remain up to date, and disseminate this knowledge to the wider CAV membership.

This scholarship is open to both CAV members and non-members. Successful applicants are

usually specialists in their field but we also support those who have developed advanced skills in a specialist area.

If you would like to partner with us to improve the knowledge of NZ veterinarians, then see our website, or contact cav@vets.org.nz for application forms and a list of the terms and conditions.

We are very grateful to Hill’s Pet Nutrition as the principle sponsor along with support we receive from the Institute of Veterinary, Animal and Biomedical Sciences and VetLearn.

CAV/CAHF Project Grant 2018 The Companion Animal Health Foundation is a charitable trust that acts as the research funding arm for CAV. Funding applications are invited in March and September for research projects that will enhance companion animal health and welfare.

See the CAHF website (www.healthypets.org.nz) to find out how we are supporting projects on elbow dysplasia, bone marrow sampling techniques and FIV

WINNER

Article of the Issue

Duncan Graham

prevalence. Any queries on how to make an application or donate contact Rochelle Ferguson (CAV Operations Manager) on cav@vets.org.nz

G SCH RAN OL TS & AR SH Ava IPS ilab CAV le to me mb ers

“Book Review: Diagnostic Techniques in Veterinary Dermatology: a review of two recently published textbooks" December 2017 | Volume 28 (4) | Pages 44–48

EYEVET Services Limited

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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What is your diagnosis?

THE QUESTIONS… GABRIEL HAGARD, BVSc

Case history

A 6-year-old spayed female Labrador Retriever weighing 23 kg, was presented for apparent excessive thirst starting after a recent stay at a boarding kennel. Water consumption was not measured and the increase in thirst was a subjective observation. No polyuria nor pollakiuria were reported by the owner. However, the dog lived semi-rurally, spending most of the time outdoors and was not closely monitored.

Vaccinations were up to date, including for leptospirosis. Her appetite was reported to be normal and the diet consisted of Royal Canin Labrador Retriever kibble. There was no known access to anticoagulant toxins. Previous clincal history included laparotomy and jejunal enterotomy to remove a foreign body (sock) obstruction a year prior to the current problem.

Clinical findings

Clinical examination was unremarkable. The dog’s demeanour was bright and alert and she was afebrile. The patient was lean, with a body condition score of 4/9. There was no evidence of dehydration. Mucous membranes appeared normal, with no icterus. Heart rate was normal. The urinary bladder was moderately full and non-painful. No abnormalities, such as distention or masses were noted on abdominal palpation.

There was no abdominal pain or hepatomegaly. Kidneys were palpable and of a normal size and contour. Chest auscultation was unremarkable.

In order to investigate the cause of the potential polydipsia, cystocentesis was performed to obtain a urine sample. A dipstick showed glucose 4+, and no detectable ketones, blood or protein. The urine specific gravity, measured with a refractometer, was 1.025. A venous blood sample was obtained and submitted to NZVP, Hamilton for complete blood count (CBC) and a serum chemistry panel including fructosamine concentration. The CBC was within normal limits. Serum biochemistry (Table 1) revealed mild elevations of alkaline phosphatase (ALT) and aspartate aminotransferase (AST). Alkaline phosphatase (ALP), urea, creatinine, calcium and fructosamine were within reference ranges. Blood glucose was not measured. Total protein and phosphate were marginally reduced and bicarbonate was mildly elevated. (See Table 1)

Contact: Newstead Veterinary Services, 161 Morrinsville Rd, Hamilton, gabriel@hagard.net

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Table 1. Serum biochemistry results for a 6-year-old female spayed Labrador Retriever presenting with a history of apparent polydipsia.

Testa Fructosamine Creatine kinase AST ALT ALP Bilirubin Total protein Albumin Globulin Albumin:globulin ratio Urea Creatinine Amylase Lipase Cholesterol Calcium Phosphate Sodium Potassium Na:K ratio Chloride Bicarbonate Anion gap

Results 272 414 108 121 77 1.3 50 29 21 1.4

Unit μmol/L U/L U/L U/L U/L μmol/L g/L g/L g/L -

Reference range 225–365 0–609 0–79 0–75 0–185 0.0–6.0 52–75 26–44 19–36 0.9–2.1

4.2 72 697 30 6.2 2.32 0.95 149 4.7 32 112 25.3 16

mmol/L μmol/L U/L U/L mmol/L mmol/L mmol/L mmol/L mmol/L mmol/L mmol/L mmol/L

2.6–10.2 45–135 30–1020 13–200 3.0–8.0 2.20–3.00 1.00–3.00 139–153 3.5–5.6 27–40 105–128 18.0-24.0 17–27

a Analytes greater than the reference range are indicated in red while those lower than the reference range are indicated in blue.

To confirm that the finding of glycosuria was persistent, urinalysis was repeated 3 days later and a reading of 4+ for glucose was again obtained on a dipstick. At this stage blood glucose was also measured and found to be normal (5.0 mmol/L; reference range; 3.5–5.5 mmol/L).

The Questions

1. What are this dog’s major problems?

2. What are your differential diagnoses for these problems?

3. What tests would you do to confirm your diagnosis?

Answers on page 44

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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CAV UPDATE

Information on the proposed release of rabbit calicivirus (RHDV1) K5 in New Zealand CAV Executive Committee

Background

The New Zealand Rabbit Coordination Group are seeking approval from Ministry for Primary Industries (MPI)/ ACVM to introduce a Korean variant of the rabbit calicivirus already present in New Zealand. The applicants hope that the Korean variant (RHDV1 K5 or K5) will overcome the natural resistance that the NZ wild rabbit population has developed to the existing virus (RHDV1 v351). In naĂŻve rabbits, there is no difference in morbidity and mortality between RHDV1 v351 and K5.

Canterbury regional council has applied to MPI for approval to introduce and use RHDV1-K5 for pest rabbit management.

MPI plan to carry out a risk assessment of the strain, including an assessment of its benefits and any risk it poses to pet and farmed rabbits. The consideration will take into account animal welfare, biosecurity and public health. This includes the risk to pet and farmed rabbits and the availability of protection by a vaccine. MPI advise that RHDV1 K5 will only be approved if it meets the requirements under both the ACVM and Biosecurity Acts.

MPI has sought feedback to ensure that all potential areas of concern are identified, and how any risks could be managed, before any decisions are made. CAV have made a submission on behalf of the NZVA. The submission emphasised the importance of having both an effective vaccine available that owners can rely on to protect their pet Contact: cav@vets.org.nz

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Source: Sarah Fowler

rabbits, and an education campaign so that owners understand how best to protect their pet rabbits.

If approved, the group plan to release the virus in March/April 2018 in New Zealand. It will be released nationally including Canterbury, Otago, Marlborough, Southland and Bay of Plenty regions. The virus is then expected to spread nationwide.

Cylap vaccine

The vaccination that is registered for use against RHDV1 v351 in New Zealand rabbits (Cylap; Zoetis), does not claim to have efficacy against K5. The NSW Department of Primary Industries implemented a pilot study through the Invasive Animals CRC to determine the suitability of Cylap to protect domestic and production rabbits from RHDV1 K5.

The experiment compared the mortality of a small number of vaccinated and unvaccinated rabbits that were infected with a high dose of RHDV1 K5 thirty days post vaccination. All of the rabbits that were vaccinated with Cylap survived the infection and none of the unvaccinated rabbits survived.

K5 was released in Australia in autumn 2016. Since the introduction of the new strain into Australia, Zoetis have had no reports of lack of efficacy for Cylap related to RHDV1-K5 infection. Australian scientists have reported that RHDV1-K5 virus is present in the wild rabbit samples but had not been present in any vaccinated domestic/pet rabbits.

Based on the Cylap pilot trial and the Australian data, the indications are that Cylap will provide protection against K5, despite not having a registered claim.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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Source: https://pixabay.com

How to protect NZ domestic rabbits Vaccination

Rabbits at risk of exposure to K5 should be vaccinated with Cylap and kept upto-date.

The label recommendation is for Cylap to be administered at 10–12 weeks, followed by an annual booster.

The Melbourne Rabbit Clinic (Australia’s first dedicated rabbit and guinea pig clinic) recommends the following protocol for Cylap administration to protect against K5 – adding one extra booster 4 weeks after the initial vaccination: Vaccinate at 10–12 weeks of age, give a booster at 14–16 weeks, then ongoing 12-monthly boosters.

The Australian Veterinary Association have recommended a much more aggressive protocol, however you must bear in mind that they are also responding to the risks from RHDV2, a strain of calicivirus not present in

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New Zealand. Their recommendation for beginning vaccination at 4 weeks and giving boosters 6-monthly are in response to RHDV2 risks, not K5.

• Regularly decontaminate equipment

In all instances vaccination should be administered to healthy animals, and a risk/benefit discussion with each owner is strongly recommended.

Adverse events include skin reactions, inappetence and malaise. Off-label use of the vaccination should only be done with consent from the owner.

•

Biosecurity measures

• Control insects (especially flies and fleas) as much as possible both indoors and outdoors. Flies are the main vector through which the virus is spread • Remove uneaten food on a daily basis • Keep your pet rabbit indoors where possible • Rabbit-proof your backyard to prevent access by wild rabbits

• • •

and materials including cages, hutches, bowls etc, with either 10% bleach or 10% sodium hydroxide Limit contact between and handling of unfamiliar pet rabbits Wash hands, shoes and clothing after handling other than your own rabbits Avoid cutting grass and feeding it to rabbits if there is the risk of contamination from wild rabbits.

Infected rabbits should be isolated and disposed of in a manner that will minimise environmental contamination.

Information for owners

This webpage has been set up to inform rabbit owners and may be helpful for client to reference: www.landcareresearch.co.nz/science/ plants-animals-fungi/animals/vertebratepests/biological-control-of-rabbits/petrabbit l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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CAV UPDATE

Calling time on Scottish folds SARAH FOWLER , Editor Companion Quarterly, ROCHELLE FERGUSON and JOHN MUNDAY, CAV Executive

Introduction

The National Animal Welfare Advisory Committee (NAWAC) released their “Opinion on Animal Welfare Issues Associated with Selective Breeding” earlier this year, agreeing with the concerns raised by CAV on the health of Scottish fold cats.

NAWAC stated in their report that the “Scottish Fold breed should be banned on welfare grounds.”

History of the breed

The breed was developed in Scotland in the early 1960s from a white barn cat ‘Susie’ that developed a mutant gene causing folded ears (Figure 1a). A breeding programme was started and the breed was registered with the Governing Council of the Cat Fancy (GCCF) in Great Britain in 1966. Along with the characteristic ear folds, the cats also typically have short legs and short thick tails (Figure 1b). All Scottish fold cats can trace their pedigree back to Susie.

a

In 1971, the breed was banned by the GCCF after it was discovered the same genetic defect that causes the folded ears also resulted in severe arthritis. The Federation Internationale Feline (FiFe) will also not recognise the breed.

Despite the significant welfare cost associated with crippling arthritis, the breed gained favour and continued in the United States. The breed remains popular there and around the world, particularly in Japan.

Pathophysiology

The autosomal dominant mutant gene causes osteochondrodysplasia (FOCD). This is a developmental abnormality that produces cartilage that is not strong enough to support the ear in an upright position, causing the ear to fold. The cartilage defect also affects cartilage on articular surfaces, so that a highly progressive degenerative joint disease develops.

The altered gene has been identified as TRPV4 (Gandolfi, et al. 2016), which encodes a calcium-permeable ion channel, although how the mutation in TRPV4 affects the development of cartilage is currently unknown. Histologically, death of chondrocytes within articular cartilage and defective maturation of chondrocytes in the growth plate are seen.

Contact: CAV@vets.org.nz

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b Figure 1. Photographs of Scottish fold cats showing (a) the folded ears and b) the short legs and short thick tail typical of the breed.

Photo credit: Pixabay.com and R. Malik.

Defective endochrondral ossification leads to shortening and distortion of the metatarsal and metacarpal bones. It is also accompanied by progressive periarticular new bone formation and accelerated degenerative joint disease.

In homozygous cats, the condition leads to limb deformity and degenerative joint disease, often evident on radiographs from 7 weeks of age. The subsequent disability and chronic pain markedly impacts quality of life and frequently leads to euthanasia at an early age.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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While it was originally thought that arthritis and degenerative joint disease was restricted to homozygous animals, more recent studies have found that all Scottish folds, including heterozygotes, have some degree of FOCD as determined by radiographically visible bone changes (Malik et al. 1999; Chang et al. 2007; Takanosu et al. 2008). Logically, this is not surprising.

If the defective cartilage is unable to support the weight of the pinna, it appears unlikely to be strong enough to have normal function when lining a joint.

Heterozygotes do, however, exhibit variable clinical signs. Malik et al. (1999) describe the case histories of ten heterozygote cats showing that while some were severely affected as to require euthanasia before 2 years of age, others were apparently clinically asymptomatic at 4, 5, and 11-years-old.

Diagnosis

A diagnosis of FOCD is suspected based on breed, pedigree and the following, clinical signs:

• lameness • reluctance to jump • stiff, stilted gait • short, misshapen distal limbs • swelling of plantar tarsometatarsal regions • short, thick inflexible tail.

FOCD is confirmed by characteristic radiological findings (Figure 2) which include irregular shape and size of tarsal, carpal, metatarsal and metacarpal bones, phalanges and caudal vertebrae, narrowed joint spaces and progressive new bone formation around joints of distal limbs.

Treatment

FOCD is an incurable progressive disease. Therapy is supportive, consistent with other degenerative joint disease protocols.

The mainstay of management is non-steroidal antiinflammatories, supported by weight management, and environmental modification (soft bed, ramps). Other therapies such as, pentosan polysulphate, omega-3 supplements, other neutraceuticals and physiotherapy have been suggested, but are currently unproven.

In the past a variety of approaches have been used for severely affected individuals, including ostectomy of tarsal exostoses, pantarsal arthrodesis and radiation therapy, with limited success. Autologous stem cell therapy has been suggested as a treatment but it is currently unknown if this is beneficial.

Euthanasia is often required at an early age.

Heterozygote controversy

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Figure 2. Lateral radiographic view of the hindlimbs and tail of a Scottish fold cat showing severe FOCD. Note the irregular shape and size of tarsal, metatarsal bones and phalanges, narrowed joint spaces, and progressive new bone formation around the joints of the distal limbs and tail, including marked tarsal exostoses. Photo credit: R. Malik.

NZCF have considered de-registering the breed outright, but have instead opted for a testing and management proposal.

They have drafted a policy, that is yet to be implemented that recommends:

• Annual examinations including x-rays and examination for •

In discussing this breed with New Zealand Cat Fancy, it is well accepted by breeders that they should avoid breeding homozygous Scottish folds. Breeders do, however, debate the degree to which heterozygous cats are affected by FOCD, whether all heterozygotes are affected, and if by breeding less affected cats together the problems may reduce over time.

•

However, even in the most responsible breeding programs, it is unavoidable that progeny with FOCD will be produced and will suffer from crippling arthritis. CAV do not accept that this “collateral damage” is a reasonable approach to manage cat welfare.

•

•

any evidence of lameness, stiffness or pain and with those affected not used for breeding and desexed.

DNA tests to ensure no fold-to-fold matings are inadvertently taking place because of the variable expression of the actual ear folding. Cats with two copies of the mutation to be desexed.

All breeding cats microchipped for tracking of testing.

Identity certified by the veterinarian doing testing (including DNA tests).

Pet owners purchasing kittens must agree to allow NZCF or other researchers to contact them periodically with regards the health of their cat.

Review of this policy in association with the data provided from breeders in 5 years’ time.

It is likely that once implemented, these requirements will be a mandatory requirement to register a kitten. It is concerning

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however that this work has yet to have any date set for implementation.

The reluctance by NZCF to de-register the breed is, in part, due to the ability of breeders to continue breeding Scottish folds outside the confines of NZCF. There is an alternative cat pedigree register in New Zealand, Catz Inc which will register the Scottish fold (along with the newly introduced Munchkin cat breed, which NZCF refuses to recognise due to welfare concerns). NZCF believe that until there is a government-backed mechanism to ban a breed, the best welfare protection they can afford Scottish fold cats is to have them bred in accordance with NZCF rules (once they are implemented).

CAV breeding recommendations

CAV believes that breeding cats for a certain look when aware of the substantial risks that many cats will develop a painful, untreatable disease, is unethical and to the detriment of animal welfare.

Since FOCD is a highly penetrant genetic disease frequently leading to chronic

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pain and reduced quality of life, for ethical and welfare reasons, all cats carrying this mutation should not be bred.

This welfare issue is quite different to those seen in brachycephalics which have received a lot of attention recently.

Because this problem is associated with a single gene that can be simply eliminated within one generation, CAV recommends that MPI implement an animal welfare regulation to ban the breeding of Scottish folds in New Zealand. A similar ban already exists in the state of Victoria in Australia.

CAV calls for all Scottish fold breeders to move instead to the Scottish shorthair. This breed has the same breed characteristics as the Scottish fold but without the crippling genetic mutation and folded ears.

“There exists sufficient information to know that breeding these cats is cruel… vets and cat breeders who condone this practice have no scientific basis with which to defend this practice.

They are not breeding cats – they are perpetuating a disease state” (Malik 2016).

References

Chang J, Jung J, Oh S, Lee S, Kim G, Kim H, Kweon O, Yoon J, Choi M. Osteochondrodysplasia in three Scottish fold cats. Journal of Veterinary Science 8, 307–9, 2007 Gandolfi B, Alamri S, Darby WG, Adhikari B, Lattimer JC, Malik R, Wade CM, Lyons LA, Cheng J, Bateman JF, McIntyre P. A dominant TRPV4 variant underlies osteochondrodysplasia in Scottish fold cats. Osteoarthritis and Cartilage 24, 1441–50, 2016 Malik R. Cute and condemned to suffering: it’s time to ban the breeding of mutant cats. https://theconversation.com/ cute-and-condemned-to-suffering-itstime-to-ban-the-breeding-of-mutantcats-65874 (accessed 19 December 2017).

The Conversation, Parkville, Victoria, Australia, 2016 Malik R, Allan GS, Howlett CR, Thompson DE, James G, McWhirter E C, Kendall K. Osteochondrodysplasia in Scottish fold cats. Australian Veterinary Journal 77, 85–92, 1999 Takanosu M, Takanosu T, Suzuki H, Suzuki K. Incomplete dominant osteochondrodysplasia in heterozygous Scottish fold cats. Journal of Small Animal Practice, 49, 197–9, 2008 l

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CLINICAL UPDATE

Diagnostic techniques: how to get the most from a skin biopsy DUNCAN GRAHAM BVSc, BSc (Hons), Animal Dermatology NZ Of all the dermatological diagnostic tests, cytology gives the most information, the quickest and the most cheaply, for a wide range of dermatological problems. Unfortunately, there are a number of dermatological diseases that cytology does not deal with adequately. A multiple-site skin biopsy, either with a biopsy punch or a wedge biopsy, is often the next step.

However, a multi-site biopsy is expensive, somewhat invasive (at the very least it needs sedation) and time consuming to perform. It can however give a great deal of information; it is a very powerful diagnostic tool.

Despite these positives, not uncommonly, owners and veterinarians are disappointed with the results: either the biopsy is considered to be nondiagnostic or it doesn’t add very much to what is already known. There are a number of reasons for this outcome, many of which can be avoided.

Keith Linder’s presentation at the 2017 North American Veterinary Dermatology Forum (NAVDF), entititled “Taking skin biopsies – a pathologist’s perspective” deals with the problem of how to get more from your biopsies. It is the best and the most succinct discussion I have seen, and is, overall, a brilliant discussion of how to get the most from your skin biopsy. In a recent review of Diagnostic techniques in Veterinary Dermatology

by Ariane Neuber and Tim Nuttal (Companion Quarterly 28 (4), 2017), I grizzled about the lack of guidance on taking a biopsy. Keith Linder has supplied it.

Contact: duncan@animaldermatology.co.nz

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He lists ten basic principles of skin biopsy.

misdiagnosis of pyoderma rather than hypersensitivity.

1. Biopsy early in disease investigation 2. Biopsy before treatment or 3 weeks after treatment withdrawal, if stable 3. Treat bacterial skin infections, if any, prior to biopsy 4. Do not scrub or prep the skin prior to biopsy 5. Use appropriate pain management, local anaesthesia etc.

6. Collect six punch biopsies (8 mm in diameter) for histology or wedge biopsies 7. Biopsy primary lesions that are active, newer and nearly fully developed; avoid secondary lesions and inactive lesions 8. Provide history, lesion description, pruritus status, treatment response and differentials (italics and bold are mine) 9. Provide digital pictures 10. Work with a dermatopathologist

In one primary (possibly) disease, mucocutaneous pyoderma (MCP), with a differential of discoid lupus erythematosus (DLE), it is recommended to pre-treat with antibiotics. The lesions will clear if it is MCP but, although they may slightly improve, they will not resolve if it is DLE.

Most of these principles are well known and not at all controversial, just good common sense. I want to draw your attention to the seeming contradiction between point 2 and point 3. Point 2 is really referring to treatments that actually change the histological findings, for example, corticosteroids. In most cases, point 3 is specifically referring to microbial overgrowth, and should probably be extended to pre-treating Malassezia overgrowth as well. The problem with microbial overgrowth is that it obscures some of the features of the underlying disease, or in the case of pemphigus foliaceus and superficial pyoderma there may be shared features, i.e. acantholtytic keratinocytes. In a hypersensitivity case, the features of pyoderma may obscure those of the initiating cause (allergy) leading to a

As Keith Linder points out, the most important ways to avoid a disappointing biopsy result are to 1. select the right patient 2. select the right lesion types and 3. know where to biopsy specific lesions. These three points are the most important aspects of taking a biopsy and getting results that satisfy you and your client.

The only principle i find controversial is the need to take six 8 mm punches.

From the point of view of the pathologist, the more the better. From the point of view of the animal and the clinician, there are some serious downsides to taking that many large samples: time, and the potential for chewing out sutures, leaving large gaping holes, are both substantially increased. In many cases, I would question whether you need to take so many samples. Most of the time, four punch biopsies of 6 mm-diameter will give you enough information. However, I would bow to Keith on this.

Point 1: Not every skin problem, not every skin disease, should be biopsied.

Diagnostics should not be seen as a way of milking the cash cow. As Linder points out, biopsies do not differentiate between the different causes of most pruritic diseases, especially when allergies or ectoparasites are important differentials. Most endocrine alopecias are not differentiated by biopsy. I think the underlying premise of point one is:

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always have a list of differentials that you are trying to prove or disprove when you biopsy. If you can’t come up with differentials, then you should refer the case. A biopsy is not a hail mary pass, it is a way of proving or disproving differential diagnoses.

Point 2: Secondary lesions rarely give good information on biopsy. Linder says to only biopsy active primary lesions (papules, nodules, plaques, masses, pustules, vesicles and bullae). In my experience, this is often not possible but is desirable. The other complication is that some lesions can be either primary, secondary or both. Examples of these lesions are scaling, crusts, alopecia, atrophy and depigmentation.

However you can avoid biopsying obviously non-informative secondary lesions like lichenification, hyperpigmentation, and excoriations. Ulcers should be avoided if possible, especially ones due to self trauma (see below).

In some ways, general practitioners have an advantage in differentiating primary from secondary lesions given their closer relationship with the animal. Linder recommends “Observation of the temporal development of lesions, clinical context, skin lesion combinations and clinical evidence of self-trauma” to help distinguish between primary and secondary lesions. It is much easier in general practice to hospitalise an animal and watch the progression of lesions. I spend considerable time with owners trying to tease out what the lesion looked like at its earliest stage. Usually by the time I see an animal, all primary lesions have substantially changed into their secondary forms.

Now we come to point 3, which is the most exciting part of Linder’s presentation. This is what I complained about: that the recent book Diagnostic Techniques in Veterinary Dermatology did not have a guide, even a table or diagram that described where you should biopsy certain types of lesions. Before this article, the only text that gave this sort of information was Skin Diseases of the Dog and the Cat by Thelma Gross et al. It is an excellent text but not readily available. The old advice to biopsy the margin of the lesion is tossed aside, and each type of lesion is biopsied in the area that is going to give the most information about the pathogenesis of the lesion. As Linder points out, this varies from lesion to lesion. Alopoecic lesions give the most information in the centre of the lesion as do ischemic dermatopathies and lesions involving the panniculus.

Linder recommends biopsying the more fully developed areas of primary skin lesions. Unfortunately the area of fullest development may be at the margin, or in the centre, or an intermediate area. You may need to take the whole lesion.

The other important point he makes is that the active area may not be at the complete recognisable margin. He uses the examples of erythema and hyperpigmentation: they may be the most peripheral change, but they don’t usually give very much information because they are not specific changes. He suggests that the biopsy would be more informative if it was taken just inside this rim of change, where there is epidermal atrophy, erosions and “smoothing”. Smoothing refers to the loss of skin architectural details. The classic example of this is

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the loss of the cobblestone appearance of the nasal planum in DLE. He recommends biopsying active lesions within individual lesions, with signs of activity being adjacent erythema and recent expansion. Healed areas, either central or peripheral, should be avoided, as should scars.

Table 1 can be used as a quick guide of where to biopsy.

Table 1 Lesion type Erosions, ulcers

Draining tract, fissure

Patches, macules

Haemorrhage Leukotrichia Crusts

Scale Papules Nodules, plaques, masses Vesicles, bullae, pustules Epidermal collarettes Lichenification Atrophy (full thickness) Epidermal atrophy

Alopecia

Mucinosis Pannicular, S/C lesions

Lesion site to biopsy Avoid biopsy if possible Deep wedge perpendicular to ulcer margin Avoid shallow punch from centre Avoid punch biopsy Large wedge biopsy with draining tract in middle of biopsy Collect multiple wedges Sample for culture Biopsy active margin, especially areas with erythema with depigmented macules Biopsy grey rather than white areas; they are more actively depigmenting Avoid smoothing out the epidermal surface architecture.

Biopsy centre, dorsally.

Biopsy centre of lesions, taking multiple samples with an 8 mm punch Keep crusts intact on the surface of the biopsy. Submit any crusts that fall off.

Pretreat with antibiotics to clear up infection..

Biopsy central area of scale (5–6 punches) Papules centred in punch. 5–6 x 6–8 mm punch biopsies 1–2 wedges of margins where 70–80% of wedge has lesional tissue Keep fragile lesions intact. Wedge for large lesions.

Avoid Avoid If full thickness atrophy (epidermis + dermis) biopsy centrally Multiple biopsies from actively expanding margins, include a small section of normal skin Centre of lesion, 6 x 8 mm punch biopsies.

If expanding, biopsy active area inside the margin.

Submit a normal sample labelled as such.

Biopsy centre with multiple punches Biopsy centre lesion, wedge biopsy. Avoid marginal tissue as this is non-diagnostic.

I would like to thank Keith Linder for a fantastic article.

Texts

Linder, KE. Taking skin biopsies – a pathologist’s perspective.

Proceedings of the 30th North American Veterinary Dermatology Forum. Pp 77–80, 2017 Gross, EL, PJ Ihrke, EJ Walder, VK Affolter. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. Blackwell Science Ltd, Oxford, UK. 2005 l

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FEATURE ARTICLE

Diagnosis of hypoadrenocorticism in dogs BOYD R JONES BVSc,

FACVSc, DECVIM-Ca, ANNE KIM and LUCY LANE, final year veterinary students, Murdoch University, WA, Australia

Introduction

Hypoadrenocorticism (Addison’s disease) has been referred to as “the Great Pretender” due to its ability to mimic other common diseases in the dog and thereby present a diagnostic challenge for clinicians (Klein and Peterson 2010a). The October 2017 Veterinary Update from the Veterinary Council of New Zealand provided a summary of concerns from their Complaints Assessment Committee (Butler, 2017) regarding investigations (or rather a lack of) of a dog which had previously been diagnosed with hyperadrenocorticism and was being treated with the steroidogenesis inhibitor trilostane (sold as Vetoryl). The dog became ill but hypoadrenocorticism was neither diagnosed nor treated appropriately by the attending veterinarians. Clearly, Addison’s disease is a potential outcome in any dog treated with trilostane and its diagnosis should have been pursued or treatment implemented urgently. This brief article reviews some aspects of hypoadrenocorticism and its diagnosis.

Pathogenesis

Addison’s disease is due to insufficient production of glucocorticoids and mineralocorticoids. It commonly affects young-to-middle aged female dogs, and is more common among Standard Poodles, West Highland White terriers, Wheaten terriers, Rottweilers and Great Danes. Hypoadrenocorticism may have a primary cause i.e. immunemediated destruction of the adrenal glands, or rarely, may occur secondary to a lack of ACTH secreted from the Contact: B Jones, 28 Princes St, Kauri Point, RD 3, Katikati, 3170 26

pituitary gland (Klein and Peterson 2010a; Bøysen and McMurray 2017) Dogs with hyperadrenocorticism in which steroidogenesis is being suppressed by treatment with trilostane or mitotane (also known as o’p-DDD and sold as Lysodren) or which have had an adrenal gland surgically removed, are also at risk for developing hypoadrenocorticism.

The adrenal cortex is made up of three layers; the outer zona glomerulosa which produces mineralocorticoids including aldosterone, and the middle zona fasiculata and inner zona reticularis both of which produce glucocorticoids and androgens. Decreased production of glucocorticoids impairs energy metabolism, vascular tone and integrity and inhibits the stress response while reduced aldosterone secretion impairs regulation of water and electrolyte balance by the kidneys leading to marked electrolyte abnormalities particularly hyponatraemia, hypochloridaemia and hyperkalaemia, and metabolic acidosis.

History and clinical presentation

Addison’s disease is characterised by vague and non-specific clinical signs that can be attributed to multiple body systems and to other diseases (Klein and Peterson 2010a). Clinical signs may “wax and wane” with periods of apparent good health while other dogs show progressive deterioration. The number of clinical signs, their severity and the rapidity of progression vary from dog to dog. Clinical signs may be similar in a dog that is mildly affected to one that is profoundly ill. Klein and Peterson (2010a) record the most common clinical signs reported by owners include: poor appetite (85–90%), weakness (51–75%), weight loss (40–50%), diarrhoea (35%), polyuria/polydipsia (17–25%), tremors/ shaking (17–27%), collapse (10%), and painful abdomen (8%). Haematemesis, haematochezia, melaena, ataxia and seizures were also reported.

The most common findings identified on physical examination by a veterinarian again depended on severity and ranged from mild dehydration to collapse and shock with weak pulses, poor capillary refill and hypothermia.

The most common findings were; lethargy (87%), thin body condition (82%), weakness (68%), shock and collapse (27%), bradycardia (24%), weak pulses (25%), haematochezia/ melaena (17%) and abdominal pain (7%) (Klein and Peterson 2010a). It is clear there is a “theme” in the findings observed by owners of the affected dogs and primary care veterinarians, but none are pathognomonic for hypoadrenocoorticism. There must be an index of suspicion of hypoadrenocorticism if a dog shows the above signs. If you don’t “think it” you won’t diagnose hypoadrenocorticism and request suitable diagnostic tests.

Clinical and laboratory findings

Serum biochemistry and complete blood count (CBC) changes are non-specific for the diagnosis of hypoadrenocorticism, however they may aid in arousing suspicion of the disease. Common serum biochemistry findings include hyponatraemia and hyperkalaemia, azotaemia, hypercalcaemia, hypoglycaemia, hypoproteinaemia, hypocholestrolaemia, and elevated liver enzymes (ALT or AST) (Gold et al. 2016, Wakayama et al. 2017).

A Na:K of ≤1:24 is a strong indication for hypoadrenocorticism. CBC changes may include non-regenerative anaemia, eosinophilia and lymphocytosis. The lack of a stress leukogram despite an obviously sick dog is a typical finding.

Atypical hypoadrenocorticism

A small proportion (5–10%) of animals with primary hypoadrenocorticism have normal electrolyte values (Van Lanen and Sande 2014). It was previously thought that these patients were only deficient in glucocorticoids and had normal concentrations of

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mineralocorticoid production and that this was due to damage to the adrenal cortex which was isolated to the glucocorticoid secreting layers. This was termed “atypical” hypoadrenocorticism.

However, recent studies (Baumstark et al. 2014) have revealed that dogs with atypical hypoadrenocorticism do have reduced mineralocorticoid production. Measurements of serum hormone concentrations showed that, after stimulation with ACTH some animals with normal electrolyte concentrations, had decreased cortisol and aldosterone responses indicating they were deficient in both glucocorticoids and mineralocorticoids.

These findings raise the question of how animals with reduced mineralocorticoid production are able to maintain normal electrolyte concentrations. It may be that if sodium intake is sufficient to maintain extracellular fluid volume and the flow rate in the renal distal tubule, then the potassium concentration may be maintained. Studies have also shown that dogs with atypical hypoadrenocorticism may also go on to develop electrolyte abnormalities. Thus the “atypical case” maybe be a stage in the continuum of adrenal destruction and such cases should be carefully monitored, especially with regard to electrolyte concentrations.

Along with vague or specific laboratory findings, a range of nonspecific clinical signs such as lethargy, anorexia, vomiting and diarrhoea, contribute to confusion regarding diagnosis early in the course of the disease (Klein and Peterson 2010 b; Gold et al. 2016; Wakayama et al. 2017).

Patients with hypoadrenocorticism can deteriorate quickly and progression of the condition can be life threatening, therefore it is critical to obtain accurate diagnosis at an early stage as possible.

Diagnostic tests for hypoadrenocorticism

Basal serum cortisol concentration

Measurement of basal serum or plasma cortisol concentration is considered a reliable screening test for patients with clinical signs and serum biochemistry results consistent with a diagnosis of hypoadrenocorticism (Bovens et al.

2014; Gold et al. 2016). Dogs with basal cortisol concentrations of >55 nmol/L can reliably be excluded as having hypoadrenocorticism. The cut-off value of >55 nmol/L has excellent sensitivity (99.4%), with negative 28

predictive value of 99.8% (Gold et al.

2016). However, specificity of this cut-off is low (67%), so cortisol concentrations less than 55 nmol/L should not be interpreted as confirming a diagnosis of hypoadrenocorticism. A recent study (Gold et al. 2016) showed that a cut-off of <5.5 nmol/L for basal cortisol concentration had specificity of 99.1% and sensitivity of 81.6% for predicting dog with hypoadrenocorticism with excellent positive predictive values.

Furthermore, there was no difference in basal cortisol concentrations observed in dogs with hypoadrenocorticism which had normal or abnormal electrolyte concentrations. While this suggests a cut-off of <5.5 nmol/L could be used to confirm a diagnosis of hypoadrenocorticism, the authors of this study were careful to state that additional investigation is required to substantiate this finding. Lennon et al. (2007) measured basal cortisol concentrations in 123 dogs with suspected hypoadrenocorticism and concluded that a cortisol concentration <27.59 nmol/L had 100% sensitivity and 98.2% specificity in detecting dogs with hypoadrenocorticism, but emphasised the requirement for an ACTH stimulation test if adrenal function was to be assessed. Measurement of basal serum cortisol is a practical alternative to the ACTH stimulation test (see below), as it is less expensive, requires a single blood sample and does not require expensive ACTH and the cortisol assay is widely available. However, it has limitations as to what can be concluded if basal cortisol concentrations fall between 5.5 and 55 nmol/L, Definitive diagnosis by undertaking an ACTH stimulation test is still required for most clinical cases. Nevertheless, measurement of a low basal cortisol concentration in a dog with supportive clinical signs and laboratory findings make a diagnosis of hyoadrenocorticism very likely. If you are in doubt treat the dog with fluids and dexamethasone (see below) and do an ACTH stimulation test later, after the crisis if you think it necessary to do so.

ACTH stimulation test

A definitive diagnosis of hypoadrenocorticism requires measurement of the adrenal reserve with an ACTH stimulation test. The cortisol concentrations in serum is measured before and after the administration of ACTH. In normal dogs, the adrenal glands respond to the ACTH stimulus

with increased production of cortisol. If the patient has hypoadrenocorticism, there will be reduced response to the ACTH by the adrenal glands, and usually a low cortisol concentration in serum is measured both before and after ACTH administration. A value <55 nmol/L after ACTH administration confirms a diagnosis of hypoadrenocorticism, whereas a concentration >138 nmol/L excludes it (Cohen and Feldman 2012).

Different diagnostic laboratories may have different cut-off values for the ACTH stimulation test used support or exclude a diagnosis of hypoadrenocorticism depending on the technique they use to measure cortisol. Check with your laboratory for full details.

Synthetic ACTH, available in NZ as Synacthen (in 250 µg vials), is used for the test. Previously it was recommended to use 250 µg/dog for ACTH stimulation testing in dogs. However 5 µg/kg has also been shown to be effective (Lathan et al. 2008). The lower dose reduces cost without inaccuracy. Unused ACTH from the vial maybe frozen in aliquots for use with another case. A protocol for ACTH testing is shown in Box 1. Blood must be collected for cortisol measurement before any treatments are administered, and remember that prednisone, prednisolone or hydrocortisone may cross react with some cortisol assays producing falsely elevated values.

Box 1. ACTH stimulation test protocol Collect blood sample for measurement of basal cortisol concentration in plasma or serum Administer synthetic ACTH (Synacthen) I/V or I/M at 250 μg/dog or 5 µg/kg 60 minutes later, collect a second blood sample for measurement of cortisol Store both samples at 4°C, submit together to diagnostic laboratory Interpretation: For most dogs with primary hypoadrenocorticism both the preand post- ACTH cortisol concentrations are <20 nmol/L (check your laboratory reference values

Treatment of hypoadrenocorticism

An acute Addisonian crisis in a dog represents a true medical emergency, due to severe hypovolemia, dehydration, hypotension, electrolyte derangements, and acid-base abnormalities.

Appropriate treatment should be instituted rapidly at the same time that the definitive diagnostic workup

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is begun. The goals of therapy include correcting hypovolemia, hypotension, electrolyte imbalances (particularly hyperkalemia and hypoglycaemia), and acid-base abnormalities, and providing corticosteroid supplementation. Sodium chloride (0.9%) should be administered at I/V 60–90 mL/kg/hour (shock rates) for the first 1–2 hours and the flow rate adjusted as vital signs improve. This will replace the sodium deficit and reduce hyperkalaemia by dilution, restore renal perfusion and improve metabolic acidosis. Due to these effects, additional specific therapy to address high potassium concentration may not be needed. However if lifethreatening bradyarrhythmia is present or if fluid treatment has not improved potassium concentrations within 30–60 minutes, insulin with dextrose, sodium bicarbonate or calcium gluconate may be considered (Klein and Peterson 2010b). If the dog is hypoglycaemic, an I/V bolus of 50% dextrose (0.5–1.0 mL/kg) should be administered.

Glucocorticoid supplementation is essential during the crisis and should be administered in conjunction with fluid therapy; hydrocortisone sodium succinate, 10 mg/kg I/V every 3–6 hours or prednisolone sodium succinate, 5 mg/ kg every 3–6 hours or dexamethasone sodium phosphate (a single dose of 0.5–1 mg/kg). I/V fluids are required for at least 48 hours and should be tapered slowly and medications adjusted as the dog’s condition improves.

electrolyte concentrations. Dogs that have ‘atypical’ hypoadrenocorticism will require lifelong glucocorticoid treatment and may, at a later date require mineralocorticoid supplementation.

Once stabilised dogs may be discharged on maintenance therapy. Dogs that have ‘typical’ hypoadrenocorticism with electrolyte abnormalities at the time of diagnosis, will require ongoing mineralocorticoid and variable glucocorticoid supplementation. Dogs receiving fludrocortisone get some glucocorticoid effect and may only need glucocorticoid administration at times of identified stress e.g. boarding in kennels. Dogs receiving injectable desoxycorticosterone pivalate which has no glucocorticoid activity may require glucocorticoid supplementation (Bøysen and McMurray 2016). The determination of suitable dose rates depends on the response of the individual patient to treatments and careful monitoring of

Summary

Long-term management with fludrocortisone (1.5 µg/kg/day as a starting dose) is the treatment of choice for dogs with sodium and potassium dysregulation with this dose being adjusted up or down until sodium and potassium concentrations are within the reference intervals. An alternative treatment option is desoxycorticosterone pivalate administered intramuscularly, monthly (see above). Readers are referred to suitable references (Lathan and Tyler 2005; Klein and Peterson 2010b; Bøysen and McMurray 2016) or suitable textbooks for more detailed information on the long-term management of hypoadrenocorticism.

If a dog with hyperadrenocorticism, under treatment with trilostane or mitotane develops hypoadrenocorticism, stop administering the drug and, after stabilising the hypoadrenocorticism, only reintroduce trilostane or mitotane when there is a significant response to an ACTH stimulation test indicating a return of excess cortisol secretion i.e. hyperadrenocorticoidism. This event is more likely to occur in dogs treated with trilostane than mitotane where ongoing treatment for hypoadrenocorticism may be required due to permanent destruction of the adrenal cortices.

In conclusion, naturally occurring hypoadrenocorticism is a disease of low prevalence but in dogs under treatment for hyperadrenocorticism with trilostane or mitotane, hypoadrenocorticism is highly likely if they become ill. In practices where diagnostic investigation is limited due to cost and/ or unavailability of ACTH stimulation testing, the measurement of basal serum cortisol can be used to reach a tentative diagnosis in patients with suspect clinical signs consistent with hypoadrenocorticism. If the dog has critical clinical signs then treatment must begin immediately without waiting for confirmation of a low basal cortisol or “flat line” ACTH stimulation test result.

References

Butler S. Zebra hoof beats: the risk of pattern matching. https://testbed01.wonderlab. co.nz/2017/10/20/zebra-hoof-beats-therisk-of-pattern-matching/ (accessed 12 November 2017). Veterinary Council of New Zealand, Wellington, NZ Baumstark M, Sieber-Ruckstuhl N, Müller C, Wenger M, Boretti F, Reusch C. Evaluation of aldosterone concentrations in dogs with hypoadrenocorticism. Journal of Veterinary Internal Medicine 28, 154–9, 2014 Bovens C, Tennant K, Reeve J, Murphy K. Basal serum cortisol concentration as a screening test for hypoadrenocorticism in dogs. Journal of Veterinary Internal Medicine 28, 1541–5, 2014 Bøysen S, McMurray J. Hypoadrenocorticism. Veterinary Ireland Journal 6, 89¬–92,2016 Cohen T, Feldman E. Comparison of IV and IM formulations of synthetic ACTH for ACTH stimulation tests in healthy dogs. Journal of Veterinary Internal Medicine 26, 412–4, 2012 Gold A, Langlois D, Refsal K. Evaluation of basal serum or plasma cortisol concentrations for the diagnosis of hypoadrenocorticism in dogs. Journal of Veterinary Internal Medicine 30, 1798–805, 2016 Klein SC, Peterson ME. Hypoadrenocorticism: part I. Canadian Veterinary Journal 51, 63–9, 2010a Klein SC, Peterson ME. Hypoadrenocorticism: part II. Canadian Veterinary Journal 51, 179–84, 2010b Lathan P, Tyler J. Canine hypoadrenocorticism: diagnosis and treatment. Vetfolio-Compendium 27, 121–32, 2005 Lathan P, Moore G, Zambon S, ScottMoncrieff J. Use of a low-dose ACTH stimulation test for diagnosis of hypoadrenocorticism in dogs. Journal of Veterinary Internal Medicine 22, 1070–3, 2008 Lennon EM, Boyle TE, Hutchins RG, Friedenthal A, Correa MT, Bissett SA, Moses LS, Papich MG, Birkenheuer AJ. Use of basal serum or plasma cortisol concentration to rule out a diagnosis of hypoadrenocorticism: 123 cases.

Journal of the American Veterinary Medical Association, 231, 413–6, 2007 Wakayama J.A, Furrow E, Merkel LK, Armstrong PJ. A retrospective study of dogs with atypical hypoadrenocorticism: a diagnostic cut-off or continuum?

Journal of Small Animal Practice 58, 365–71, 2017 Van Lanen K, Sande A. Canine hypoadrenocorticism: pathogenesis, diagnosis and treatment. Topics in Companion Animal Medicine 29, 88–95, 2014 l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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FEATURE ARTICLE

Practical dental homecare information This article was written as part of the requirements for receiving the Hillâ&#x20AC;&#x2122;s Pet Nutrition/CAV Educating the Educators Scholarship

JANINE VAN DAM, BVSc MANZCVS (Dentistry

and Oral Surgery)

Introduction

Over 85% of dogs and over 50% of cats older than 4 years of age have periodontal disease. There is also a trend in pet ownership toward smaller dogs. As smaller dogs are more likely to have periodontal disease due to both overcrowding and genetics (as well as many other factors) it is important that, from the first vaccination, we inform owners about the need for prophylactic dental homecare. To be able to form an individual plan that works for each owner, veterinarians need to make sure they up to date with which products are currently available, which are not recommended and if there is evidence to prove a product will be effective.

A number of companies that produce products to be used in dental homecare make unsubstantiated claims. In order to help veterinarians make informed decisions about which dental products to recommend, the Veterinary Oral Health Council was formed in 1997. Based in the United States, and endorsed by many veterinary organisations worldwide, the council gives a seal of approval to products which have proven in controlled studies to retard the growth of plaque and/or tartar. The councilâ&#x20AC;&#x2122;s website is www.vohc.org.

From the moment an animal wakes up after having its teeth descaled and polished the plaque biofilm, made up of organic and inorganic material derived from saliva, gingival crevicular fluid and bacterial products, is already forming on the teeth. The aim of homecare is daily plaque removal. Calculus (tartar) is formed from the precipitation of minerals from the saliva within the plaque biofilm. It is primarily made up of calcium phosphate. Once calculus has formed it cannot controlled with homecare alone.

Each animal and client is different so veterinarians need to be practical and realistic when setting up a regime for a client to follow. Homecare can control gingivitis but not periodontitis.

Once periodontitis sets in, a professional clean and descale at a veterinary clinic will be needed.

Mechanical removal of plaque and tartar

Tooth brushing is still the gold standard for home dental care, however owner compliance is only around 5% for a dog and less than this for a cat. To be effective teeth need to be brushed at least every other day, however, due to the issues with owner compliance, advising owners to brush daily is recommended. The aim is to disrupt the plaque biofilm. Brushing teeth also promotes gum health, stimulates saliva flow which in itself has a cleaning action in the mouth, and promotes gingival health.

Contact: janine@petdentistry.co.nz

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Photo courtesy of pixabay.com

It is recommended to start when the pet is young, with deciduous teeth, and just get them used to having the brush in the mouth and always give a treat afterward so it is a positive experience.

Toothpastes are available which are generally abrasive and also can contain enzymes which kill plaque bacteria. They are not essential, but often used since they are flavoured so the taste is pleasant to the animal, making the brushing procedure a more positive experience. It is most important to brush the buccal (outside) teeth as the tongue usually does a good job at stopping plaque build-up on the lingual surface. Tooth brushes specifically for animals with two sets of bristles for lingual and buccal surfaces are available, however it is not essential to use such a brush. A soft bristled toddlerâ&#x20AC;&#x2122;s tooth brush is also effective, and if it will increase owner compliance due to the cheaper cost, then it should be considered as an option. The recommended method for brushing teeth is the modified Bass technique. For the maxillary teeth, the bristles are angled 45 degrees upwards and the tooth brush is moved in a circles at the gingival-tooth margin. For the mandibular teeth the bristles are angled 45 degrees downwards.

It is a good idea to show clients how to do this, and to provide them with a tooth brush to get the routine started. With such low levels of owner compliance, routine dental check-ups are recommended. If it is obvious compliance is low then an alternative treatment method should be discussed.

Dental diets

Dental diets are complete and balanced diets for the animal and can be fed long term. Diets differ in the way in which they work.

Some dental diets contain kibble which breaks in such a way that the fibrous nature of the kibble helps to remove the tartar and plaque on the crown. Other dental diets contain polyphosphates

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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which chelate the minerals in the saliva that cause tartar to form. These diets make the teeth look clean because they remove the tartar but they do less to stop plaque accumulation (and plaque bacteria are what actually causes periodontal disease).

Be sure to check what type of dental diet you have in your clinic.

Some diets have VOHC approval for plaque and tartar (such as Hill’s products), others only for tartar (Eukanuba) and some have had no studies completed.

Dental treats

These generally work with texture causing the tartar to be mechanically removed as the animal chews. They are not a complete and balanced diet. There are treats available with the VOHC seal of approval. Greenies, for example, have the seal for both plaque and tartar in dogs.

Purina Proplan Dental Crunch and Greenies have the VOHC seal for tartar in cats. They should not be given to animals under 6 months of age. There are too many dental treats on the market to mention them all individually, so I will go concentrate on the products that are frequently used by clients.

Rawhide chews and pig’s ears assist in stimulating saliva flow and exercising the teeth and gums. There is some evidence to show they do reduce plaque and tartar build up, however the client should be warned of problems that can occur due to choking and obstruction of the GI tract.

There can also be problems with bacterial contamination.

There is no evidence to show that feeding bones and natural diets helps with oral health. Studies looking at feral versus domesticated dogs and cats have shown that although the feral animals have lower calculus scores, the amount of periodontal disease is the same. When feeding bones there is an increased risk of fractured teeth, gastric upsets, constipation and salmonellosis. As such, feeding these diets and treats is not recommended.

The American Veterinary Dental College does not recommend feeding cows hooves, dried natural bones or hard nylon products as dental chews as they are too hard and do not mimic the effect of an animal tearing meat off a carcass. They also recommend pets are supervised when given a chew toy due to the risk of GIT obstruction.

New dental treats on the market by Oravet contain a substance called delmopinol in the centre of the chew which is actually a barrier sealant. This

34

means it covers the crowns of the teeth in a layer that stops plaque being able to adhere to the teeth. Currently Oravet dental hygiene chews only have the VOHC seal for tartar.

Dental sealants

These products are relatively new to the market in New Zealand. They cover the teeth with a substance to stop plaque and tartar adhering to the teeth. Oravet (active ingredient delmopinol), has the barrier sealant in the centre of the chew.

It works best if given daily. It is liked by some owners as they don’t have to get their hands near the pet’s mouth. There have been reports that it may turn the pet’s faeces a greenish colour. Another product recently available in New Zealand is Sanos. This is a self-hardening liquid bandage device that aids in gingival and oral health. It is applied by the veterinarian after a descale and polish when the dog or cat is under a general anaesthesia. It is recommended to use a non-fluoride toothpaste prior to applying Sanos as the fluoride affects the binding agents. The mouth should be rinsed and the teeth dried with a swab then air dried. The liquid is then applied to the teeth both bucally and lingually, then lightly air dried again.

It is effective for 6 months. The teeth should not be brushed for 7 days after application to allow the product to harden.

If the animal has CUPS (chronic ulcerative paradental stomatitis) then for the initial week Maxiguard oral cleansing gel can be applied to retard plaque. Sanos has the VOHC seal plaque and tartar in dogs (2011).

Sanos has been around in the USA for a long time. It is particularly useful as a prophylactic product on animals such as small dogs, which we know are likely to have periodontal problems in the future. Some clinics are offering it as a prophylactic treatment and applying the product when the pet is desexed then at regular intervals after that.

Plaque/tartar-inhibiting chemicals

Chlorhexidine gluconate is in oral rinses and is known to reduce gingivitis, however it has some limitations. Long term use can cause discolouration of teeth, reduce sense of taste and increase the rate of calculus formation. It also needs sufficient contact time in the mouth to be effective.

Zinc ascorbate is mainly used in cats as a plaque retardant and is currently available in New Zealand as Maxiguard oral cleansing gel. It is licenced for use

in dogs and cats and a small amount is applied daily to the gum above the upper molars. It is also available as dental wipes.

Although it has been widely used in the USA for around 30 years it does not have VOHC approval, however a protocol for a study has recently been approved, so an outcome should be known soon. This product needs to be kept refrigerated or in a cool dark place. The zinc also binds to volatile sulphur compounds which helps to reduce oral malodour.

Polyphosphates are used as an additve in dental diets as mentioned previously, and prevent formation of calculus but have no little effect on plaque formation.

Delmopinol hydrochloride is the new chemical agent found in Oravet chews. It forms a preventative barrier to stop plaque and calculus build up over time. It has VOHC acceptance for tartar control (2016).

Papain, pomegranate, yucca and cinnamon are just some of the naturally occurring antioxidants and microbial agents that are found in the formulation of Healthy Mouth products. These are available in gel, water additive and dental spray formulations which are sold only through vets. It is currently not available in New Zealand. It does have the VOHC seal for plaque control.

Water additives are easy for clients to give, so compliance is high. Aquadent is available in NZ. This product contain xylitol which at high levels can effect blood glucose levels and also can be toxic to the liver. It also contains chlorhexidine in small amounts. Studies done have shown that it helps retard plaque and tartar but it does not have the VOHC seal of approval.

Clients should be warned of the potential toxicity if large amounts are ingested.

In conclusion, there are many different products available to help prevent gingivitis in animals. The gold standard is still tooth brushing, however owner compliance is a significant limitation. It is exceedingly important when a pet goes home after having a dental procedure that the owner is made aware of the need for ongoing homecare to retard the build-up of plaque and the related problems of gingivitis and periodontitis.

This article is based on the seminar given

by Dr Caiafa at the FASAVA conference, August 2017. The proceedings of the seminar have been uploaded, with permission, to the NZVA website at http:// www.nzva.org.nz/dentalhomecare should you wish to read them. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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CONFERENCE REPORT

42nd WSAVA Congress Copenhagen, Denmark, September 2017

CHARLOTTE MATHEWS,

BVSc.

When a Princess opens a congress, you know it’s going to be a good week!

Princess Marie of Denmark welcomed all the attendees to WSAVA Congress 2017 in Copenhagen, Denmark. A royal welcome is a fairly high standard to keep throughout a week, but Copenhagen did not disappoint!

Being my first time in Europe, I was fairly in awe of all the history and buildings as it was. However Copenhagen was beautiful in it’s own right. The first impression you get when arriving is that it’s clean, green and safe (especially having just spent time in London) with awe inspiring buildings and architecture.

Oh, and bikes, bikes everywhere and not a helmet in sight! Copenhagen is the capital of Denmark and is an 850-year-old harbour town. Hans Christian Anderson is its most famous resident; a fact they are very proud of as demonstrated by a statue of the little mermaid being the top tourist attraction.

As mentioned, bikes are a huge part of the city, with bike paths beside most roads. These are not marked very clearly for Kiwi tourists like me, leading to a very close call nearly getting run down… luckily I don’t understand Danish expletives! Something that astounded me was just how close you could get to the royals and palaces in Copenhagen.

Amalienborg Palace is where the Queen, Prince Frederik and Princess Mary live (Figure 1a). There are four palaces, one on each corner of a square, a square that anyone can walk through. You

can literally walk up to the Queen’s window, minding the one guard outside. Another highlight was the canal tour. This begins at beautiful Nyhavn (Figure 1b), where most of the iconic pictures of Copenhagen are taken, and takes you along a network of canals through the city, passed a lot of famous buildings and gives you a nice taste of the city. And yes, the danish pastries are worth the flight (Figure 1c)!

The WSAVA Congress was held at the Bella Center which is a sight to behold, with two large black and white towers zig-zagging their way 23 stories up forming the adjoining hotel, a feat of innovative Scandinavian architecture. The first day was the WSAVA Assembly Meeting, with representatives from member nations and groups within WSAVA. It was an interesting day seeing the inner workings of WSAVA. During the morning we were put into regions, with Asia/Oceania being the smallest but definitely not the quietest. The brainstorming session was about the idea of being a “Global Community” of veterinarians; how this looks, and how we can better assist each other in ultimately improving animal and human health and welfare. It was eye opening to hear about different countries struggles and limitations when practicing medicine. Such as when the Sri Lankan representative asked me if I used gaseous anaesthesia during surgery, turns out it is too expensive in Sri Lanka.

a

b

c

Figure 1. (a) One of the four palaces that make up the royal residence of Amalienborg. (b) A view along the 17th-century waterfront at Nyhaven. (c) Danish pastries!

Contact: charlotte.matthews2@gmail.com

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

The afternoon was the WSAVA business meeting. Associate and full memberships were granted to a number of organisations around the world. There was a vote for allowing Cuba to remain on an associate membership after 16 years, which was extremely contentious. The application was ultimately granted.

The next 4 days were filled with loads of interesting lectures, with nine lecture streams running each day. Healthy breeding was front and centre throughout, with a worldwide demand for action on hereditary diseases especially brachycephalic airway disease. This culminated in a well-attended Brachycephalic Dog Panel Discussion. WSAVA was also excited to release their Global Dental Guidelines during the Congress.

Here are some of my take home points from lectures:

• De-escalate the type of antibiotic being used (e.g. broad or

• • •

• • •

•

• •

multi to narrow or single) if a culture and sensitivity indicates that it will be effective. And always consider topical therapy in pyoderma.

An epidermal collarette is specific for a superficial staphloccal infection, with bacteria prominent at the leading edge of the scale.

It is useful to establish a normal resting respiratory rate for an individual over 10 occasions at home when monitoring for signs of heart failure (pre clinical disease).

In IMHA, combining prednisone with another immunosuppressant helps decrease unwanted steroid side effects for the owner. Splenectomy as an adjunct to immunosuppression also looks promising in refractory IMHA cases.

Use hidden sutures for closing gingiva after tooth extraction in cases of gingivostomatitis to reduce irritation.

Try to preserve maxillary canine teeth in cats as extraction changes the conformation between the canine teeth.

When closing an enterotomy/anastomosis, be mindful of how much pressure you put on the suture line during the leak test, is it physiological? Adding unnecessary additional sutures can make the area ischaemic.

The most important thing to treat in otitis externa is the inflammation. Also, don’t forget about biofilms and searching for the nidus of re-infection if they are present (around pinna, on beds etc.).

Biomarkers for heart disease (pro-BNP and cTnI) are helpful for motivating further testing but are not diagnostic.

A grain free diet is not a carbohydrate free diet. The newer gluten free alternatives are not as well researched as of yet, as they haven’t been used as much.

Figure 2. Creating original “Danish” house music at the Danish Party Night.

I also had the pleasure of attending the Danish Party Night (Figure 2); a great night where Scandinavian food, design and music were showcased. The highlight of the evening was when we were all given 1 of 4 street instruments, buckets, sticks or shakers, to “play”. A cacophony of sound broke out as we were all led in creating our very own (surprisingly in time) Danish house music. Those Danes really know how to get a party started!

It was great to see 11 other Kiwis had made the trip to Copenhagen as well. It was especially heartening hearing from other delegates I met, that “Auckland WSAVA was THE BEST Conference!” upon learning I was from New Zealand. CAV, you certainly left an impression on the world!

Thank You to CAV for the opportunity to attend WSAVA 2017.

It was a fantastic experience with lots of learning and a great reason to visit a beautiful city. Bring on Singapore 2018! l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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A WEEK WITH ...

… Feline medicine specialist, Pru Galloway This article was written as part of the requirements for receiving the RxVet/CAV A Week With… Grant

SUSAN MURRAY, BVSc, Small Animal

Veterinarian,

I must admit I was full of trepidation (working mother guilt) as to whether I could leave my family and job for a week, when I was considering applying for the “A week with” grant. When I finally decided to apply it was the night before submissions were due, and it was late. I put together what I thought was an average application and was therefore very surprised to find myself one of the lucky recipients. Leaving Dad in charge I headed for the capital.

I was very privileged to spend my week with Pru Galloway, who manages Cat Med, a feline medicine specialist service. Pru was extremely welcoming and worked wonders at rekindling my ethusiasm for both cats and doing a great medicine workup.

Pru generally sees 2–4 (or more) referral cases a day, and does phone veterinary consults, as required, where time allows.

Being a referral practice, the clients are amazingly committed and it was so refreshing to be working with people who wanted the absolute best for their pets, committed to a full and thorough work up, and who did their utmost to follow the advice given.

Pru is very thorough and systematic with her clinical practice, starting with a detailed and thorough history taking process.

Many of the patients already had long histories, so prior to the consult we read the histories noting relevant details and ideas, and gaining an understanding of the case. A detailed history was then gathered from the owner during which Pru was very good at extracting relevant information, and I gained a better appreciation of how to ask questions in an open ended manner. There were a number of very detailed clinical note templates that I have come home with in an attempt to revitalise the detail of my histories.

I thought I did a relatively thorough clinical examination but Pru definitely taught me some extra tricks of the trade. She made taking blood pressure in a cat looking amazingly easy, and I will definitely be attempting many more blood pressure readings in consults in the future. For several cases, we also did retinal exams to assess the significance of high BP measurements

The author with her AWW mentor, Pru Galloway (R). Photo courtesy

of the author.

in the consult and I was amazed that I could actually see and appreciate retinal changes. I also learned that proteinuria (measured by a urine protein:creatinine ratio) can be a hint for persistent hypertension at home.

I was lucky enough that throughout the week I was exposed to many different cases, and some days we even managed themes. Some of the information that I collected in note form included:

Contact: Matamata Veterinary Services, 26 Tainui Street, Matamata

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Inappropriate urination issues

An adult male neutered Siamese cat was presented for inappropriate urination issues. With a thorough medical work up we were able to confirm this was in fact a behavioural issue, and with a detailed environmental assessment were able to identify several changes that may help manage his problem. I would recommend reading the AAFP guidelines (http://journals.sagepub.com/ doi/pdf/10.1177/1098612X14539092 for diagnosing and solving house soiling behaviour (guidelines/questionnaire for clients/take home notes). This case gave me renewed enthusiasm and ideas for trying to assist cats that end up in these situations, but a committed owner and time are required, not a rushed 15 minute consult.

Toxoplasmosis

• Can cause many disease processes including but not limited to uveitis, fever, malaise, myositis, weight loss, anorexia, seizures/neuro signs, icterus,

•

• •

•

diarrhoea, pancreatitis (more often than we know), intersitial/alveolar lung pattern (bad prognosis for toxoplasma pneumonitis), pleural effusion, myocarditis. Toxoplasma cysts can encyst in many locations.

During primary infection (typically in the cat’s first year of life when it hunts or is fed raw meat) cats often develop self-limiting small bowel diarrhoea.

Gold standard diagnosis is finding tachyzoites in affected tissue. PCR can confirm their identification.

As there can be interassay variance with Toxoplasma titres, when measuring rising titres approximately 3 weeks apart, ask the lab to hold the first sample until the second sample is taken so they are run together on the same day.

Treat with clindamycin 12.5 mg/kg, every 12 hours, PO for a minimum of 4 weeks or 2 weeks after resolution of clinical signs. This often causes small bowel diarrhoea at this dose.

Give with food to minimise nausea/ vomiting. If needed give Cerenia at 2 mg/kg, once daily, PO an hour before clindamycin. Clindamycin sends the toxoplasmosis into remission but it can recur it the animal becomes immunosuppressed. Pru isn't a fan of trimethoprim sulpha as it is bitter and so cats tend to be difficult to medicate.

Upper respiratory tract (URT) work-up for persistent sneezing/nasal discharge • Calicivirus doesn't wax and wane • Herpesvirus may become latent and

recur with stress. Can cause turbinate necrosis, then with secondary bacterial infection can lead to rhinosinusitis, and turbinate osteomyeltitis, which requires long courses of antimicrobials i.e. 4–6 weeks.

• If you can treat this osteomyelitis/ rhinosinusitis with long course of antimicrobials then next time it flares, consider famciclovir (40 mg/ kg every 8–12 hours, PO, for 2 weeks)

Allan Bell Dermvet-online Consultancy service by a Registered Specialist in Veterinary Dermatology (for veterinarians in the South Island and from Wellington as far north as Lake Taupo) For cases where referral is difficult but help is required.

Contact dermvet.bell@xtra.co.nz for cost estimates and protocol

Allan Bell BVSc MACVSc (canine med) FACVSc (dermatology)

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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•

•

•

•

to stop the next acute flare of the herpes i.e. give as soon as the early signs are seen. This is available from pharmacies, over the counter as ‘Famciclovir Once (a box of 3 x 500 mg tablets; Apohealth). Reduce dose with renal disease. Pru checks a liver panel 7 days after starting, as there have been reports of hepatopathy in humans taking famciclovir. If used long term, consider performing occasional CBCs and measuring serum creatinine concentrationsto monitor for neutropenia and renal disease (recommeneded by Plumb’s Veterinary Drug Handbook, 2015).

Herpes is intermittently shed so PCR tests must be performed when clinical signs are present, whereas calicivirus is continuously shed so tests should positive if this virus is present. PCR can detect respiratory vaccinal viruses so be mindful of this if the cat has been vaccinated recently.

Zithromax (azithromycin): is antimicrobial and reduces biofilm. Use when other antibiotics haven't worked (e.g. doxycycline). Use Zithromax 40mg/ml powder for oral suspension.

This contains 600 mg of azithromycin and you add 9 mLs of water to produce 15 mLs of solution. Dose 1 mL PO, once daily for 5–7 days then twice weekly (long half life).

Nasal culture can be useful. While any bacteria grown are usually a secondary infection, this provides information on antimicrobial sensitivities and identifies Pseudomonas which informs your antibiotic selection/management.

Traumatic nasal flush: consider this if stertor is present and you are concerned there is a nasal/ nasopharyngeal mass. Intubate, pack back of the throat with a swab, block other nostril and flush 10 mL warm saline quickly into sealed nostril. Then pull out swab to see if any chunks of tissue have been caught on it.

Mycoplasma

• Can be an URT commensal, but usually significant if found in the lower respiratory tract.

• Can do a PCR test for Mycoplasma on fluid obtained by bronchoalveolar

40

lavage (BAL). Pru sends samples to Colorado State University, cost to the veterinarian via NZVP is >$NZ200.

• Doesn't respond to amoxicillinclavulanic acid but is usually sensitive to doxycycline.

Coughing cats and chest radiographs

• Intubate with a sterile ET tube, • Pass a sterile 6–8 Fr feeding tube • •

• Bronchial pattern on radiographs:

•

•

• •

need BAL to distinguish diagnoses.

Eosinophilic BAL fluid suggests parasites or allergy/asthma, neutrophilic fluid suggests inhaled irritants causing chronic bronchitis (not allergic) or infection (e.g. Mycoplasma, Bordetella). Differentiating these is important as the diagnosis dictates the treatment needed.

Asthma: commonly causes collapse of right middle lung lube with mucus due to short vertical bronchus. May see anterior shift of diaphragm on VD view due to reduced lung volume with collapse (vs. consolidation where lung volume remains unchanged).

Interstitial pattern: Pru describes this as like looking through net curtains. The underlying structures such as aorta and caudal vena cava can be seen but not as clearly as usual.

Alveolar pattern: dense “trees in fog”, unable to see through to the aorta and CVC at all.

Check the caudal extremity of lung lobes on the lateral view.

If they extend past T13 with a flattened diaphragm, this suggests hyperinflation with air trapping, due to bronchoconstriction

Bronchoalveolar lavage (now not such a scary procedure) • Choose your patient carefully; they

must be stable breathing room air.

• Premedicate with butorphanol or acepromazine/buprenorphine, preoxygenate for 10 minutes, and give 10 breathes of inhaled Ventolin (salbutamol).

• Use a pulse oximeter to monitor haemoglobin saturation.

• Induce with ketamine/diazepam I/V as the ketamine is a mild bronchodilator.

• •

(softer) or urinary catheter down the ET tube until gentle resistance is met.

Pass 2–3 x 5 mL aliquots of warmed saline into tube and quickly suction back out.

It’s helpful if the anaesthesia is light enough to allow the cat to gently cough when the warmed saline is instilled.

Give atropine slowly, I/V on completion to help dry up secretions.

Have Ventolin injection on hand (emergency bronchodilator).

Hypercalcaemia

• Clinical signs: anorexia, weight loss, •

• • •

intermittent vomiting, vague clinical signs.

Affected cats have high concentrations of total calcium in serum or some just have high concentrations of ionised calcium. Ionised calcium must analysed as it is the biologically active form of calcium.

Excess calcium precipitates in the kidneys and muscles (metastatic calcification).

In cats, the most common cause is idiopathic followed by malignancy and chronic kidney disease In dogs, malignancy is most likely but other causes include vitamin D toxicosis due to ingestion of pest bait or psoriasis cream (dogs lick their owners).

I would like to thank Pru for allowing me to spend the week with her, and also the other veterinarians and nurses I met in the practice. As well as the clinical knowledge I gained, I also learned many valuable gems of information in relation to systems and how better to use Vision software.

Thanks to RxVet and CAV for this opportunity, I think it is a great initiative and was well worth the nerves it took to make my way south to the big smoke.

Dad and the kids survived just fine. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

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NZVJ ABSTRACT

Recovery of brodifacoum in vomitus following induction of emesis in dogs that had ingested rodenticide bait KH PARTON, EK WILLSON, MG COLLETT and LH BOOTH New Zealand Veterinary Journal, 66(1), pp. 41â&#x20AC;&#x201C;43, 2018

AIM: To assess the benefit of inducing emesis in dogs that have ingested rodenticide bait containing brodifacoum (BDF), by determining the amount of BDF in bait recovered from the vomitus relative to the estimated amount consumed.

METHODS: Between 2014 and 2015 samples of vomitus from seven dogs that ingested rodenticide baits containing BDF were submitted by veterinarians in New Zealand. All seven dogs had been given apomorphine by the veterinarian and vomited within 1 hour of ingesting the bait. Some or all of the bait particles were retrieved from each sample and were analysed for concentrations of BDF using HPLC. Based on estimations of the mass of bait consumed, the concentration of BDF stated on the product label, and the estimated mass of bait in the vomitus of each dog, the amount of BDF in the vomited bait was calculated as a percentage of the amount ingested.

RESULTS: For five dogs an estimation of the mass of bait ingested was provided by the submitting veterinarian. For these dogs the estimated percentage of BDF in the bait retrieved from the vomitus was between 10â&#x20AC;&#x201C;77%. All dogs were well after discharge but only one dog returned for further testing. This dog had a normal prothrombin time 3 days after ingestion.

CONCLUSIONS AND CLINICAL RELEVANCE: The induction of emesis within 1 hour of ingestion can be a useful tool in reducing the exposure of dogs to a toxic dose of BDF. The BDF was not fully absorbed within 1 hour of ingestion suggesting that the early induction of emesis can remove bait containing BDF before it can be fully absorbed. https://doi.org/10.1080/00480169.2017.1379915 l

In the same issue of the New Zealand Veterinary Journal, also see the following peer-reviewed correspondence: Discovery of the feline fur-mite Lynxacarus radovskyi in a cat resident in New Zealand. J Nichols and ACG Heath. NZVJ 66 (1), 50-55, 2018 https://doi.org/10.1080/00480169.2017.1391140

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What is your diagnosis?

THE ANSWERS… 1. What are this dog’s major problems?

• PU/PD (with perhaps less than ideally concentrated urine) • Glycosuria (with euglycemia) • Mild elevation of ALT/AST 2. What are your differential diagnoses for these problems?

PU/PD • Renal insufficiency (eg chronic renal failure, acute kidney injury, leptospirosis) • Diabetes mellitus • Diabetes insipidus (central or congenital nephrogenic) • Hypercalcemia • Hypokalemia • Drug-induced • Hepatic insufficiency Glycosuria • Diabetes mellitus • Renal tubular disease (idiopathic) • Fanconi syndrome • Primary renal glucosuria Elevation of liver enzymes (ALT and AST) • Hepatocyte damage due to: o Primary liver disease (e.g. hepatitis, drugs/toxins, trauma, neoplasia) o Secondary to extra-hepatic diseases (e.g pancreatitis, gastrointestinal disease, diabetes mellitus, hyperadrenocorticism, congestive heart failure) • AST may also be increased by muscle damage and haemolysis Glycosuria in the presence of euglycemia is suggestive of Fanconi syndrome where a renal tubular defect impairs resorption of glucose, electrolytes, amino acids and low molecular weight proteins, which are lost in the urine. Diabetes mellitus is ruled out by normoglycemia and a normal fructosamine concentration. The serum biochemistry results were not consistent with CRF, hypercalcemia or hypokalemia and there were no clinical signs or history suggestive of drug/toxin exposure, trauma, or GIT/pancreatic disease.

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Fanconi syndrome may be congenital or acquired. The acquired form may be caused by exposure to a variety of renal toxins (heavy metals, antibiotics, other medications) or secondary to a number of primary diseases including copper storage hepatopathy which generally causes elevated activities of liver enzymes as seen here.

Leptospirosis was considered unlikely due to the absence of any typical clinical signs such as fever, anorexia, dehydration, petechiae/ecchymoses, vomiting, diarrhoea, respiratory signs, painful kidneys, icterus or neurological signs. Lower urinary tract disease was considered less likely owing to the absence of any observed pollakiuria, as well as the absence of haematuria and proteinuria on urinalysis.

3. What tests would you do to confirm your diagnosis?

Glucosuria in the presence of normoglycemia raises the clinical index of suspicion of Fanconi syndrome. To support this diagnosis, the degree of aminoaciduria can be determined. This can be performed by assessing amino acid concentrations in paired serum and urine samples or by determining the ratios of amino acids to creatinine in the urine.

To investigate liver disease, a variety of tests may be carried out. Standard “sick animal” serum biochemistry panels measure the concentrations of molecules (or activities of enzymes) that typically change in response to hepatobiliary disease.

• Detection of increased liver enzyme activities in serum due to either increased leakage (ALT, AST) from damaged cells or upregulation in response to hepatocyte damage (ALP, GGT).

• Altered concentration of markers of liver function: o Bilirubin: typically elevated in serum when normal enterohepatic circulation of bile is disrupted i.e. cholestasis. o Cholesterol: may decrease in liver failure (or increase with cholestasis).

o Urea: may decrease due to reduced conversion of ammonia to urea. o Plasma proteins: the concentration of many proteins including albumin are reduced due to impaired hepatic synthesis.

• Measurement of pre- and post-prandial serum bile acids: hepatic dysfunction (reduced function, PSS, biliary obstruction) allows bile acids to spill over into serum. This is a sensitive test for hepatic dysfunction and is useful before jaundice can be detected, but it is not part of a standard sick animal panel and must be requested separately.

As none of these blood tests are specific for particular types of hepatic disease, liver biopsy to obtain a sample of tissue for liver histopathology may be required to obtain a diagnosis.

As many clotting factors and other molecules involved in haemostasis are synthesised in the liver, animals with evidence of hepatic failure should have clotting times tested (APTT, PT or PTT) before any procedure likely to result in haemorrhage is carried out. In animals with a bleeding disorder, cytology of liver cells obtained via ultrasound-guided fineneedle aspirate may still provide useful information (though the agreement with results determined by biopsy is only about 30%).

Diagnosis and management

Laboratory urinalysis revealed that the ratios of glycine (23.8; reference range 0–10.6) and cystine (1.8; reference range 0–0.7) in the urine were elevated relative to creatinine. The excessive loss of these amino acids in the urine supports a diagnosis of Fanconi syndrome. The ratios of the other amino acids to creatinine were within normal limits.

On the same day, a prothrombin time was measured and found to be slightly elevated (12.2 seconds; reference range 7.0–11.0 seconds). On discussion with a veterinary pathologist the slight increase in PT was decided to be of no concern as there was no evidence of hepatic failure (i.e. glucose, cholesterol, urea and albumin

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

concentrations were within normal limits), there was no evidence of haemorrhage into body cavities or mucous membranes, and there was no history of possible access to anticoagulant toxins.

Fanconi syndrome may be caused by a limited range of aetiologies: either inherited (in Basenjis) or acquired.

Acquired causes include primary diseases such as leptospirosis, primary hypoparathyroidism, copper storage hepatopathy, and exposure to renal toxins such as gentamicin and heavy metals.

It has also been associated with the feeding of jerky treats. This dog had no evidence of leptospirosis, being afebrile, with no vomiting or diarrhoea, no icterus, stiffness or abdominal pain, and no ocular or neurological signs. There was no known history of exposure to renal toxins such as gentamicin, heavy metals or ingestion of jerky treats. There were no biochemical changes to suggest primary hypoparathyroidism, specifically no hypocalcaemia or hyperphosphataemia.

The diagnosis of Fanconi syndrome together with biochemical evidence of mild liver damage and a known breed predisposition to copper hepatopathy, prompted a decision to obtain liver biopsies. Extra-hepatic causes of mild elevations of liver enzymes were considered unlikely because of an absence of typical clinical findings for these conditions. These included pancreatitis, hyperadrenocorticism, congestive heart failure, and gastrointestinal disease. The decision was made to obtain surgical biopsies of the liver rather than the less invasive ultrasound-guided needle-core biopsies due to the ability to directly visualise any gross pathology of the liver, a lower risk of inadvertent vessel laceration, and, in particular, the possibility of superior diagnostic sample quality. One report has demonstrated that core-needle biopsies missed histological changes found in surgical samples in 52% of cases (Willard, 2010).

The patient was anaesthetised and a midline coeliotomy performed. The liver was found to be a normal size and shape with a slight yellow-orange tint. A biopsy was taken using the “guillotine” method and half this sample was preserved in formalin for histology while the other was kept fresh for quantitative copper analysis.

Both samples were submitted to SVS Laboratories (Hamilton).

Histopathology revealed mild to moderate swelling of hepatocytes with multifocal hydropic degeneration and moderate to dense diffuse intra-hepatocellular goldenbrown pigment. Hepatocellular and lobular architecture were retained. There

was no evidence of significant fibrosis, active necrosis or inflammation. Staining with rhodanine showed intracytoplasmic aggregates of copper within hepatocytes of the centrilobular to mid-zonal areas of the liver. The concentration of copper in the liver was elevated (2400 µmol/kg; reference range 500–1600 µmol/kg).

Based on the accumulation of copper within the liver, a diagnosis of copper storage hepatopathy was made. The centrilobular distribution of copper granules was suggestive of a primary copper storage disease. In the absence of a history of toxin/ drug exposure or clinical signs suggestive of other conditions, it was presumed that the Fanconi syndrome was secondary to excessive copper accumulating in the kidney.

Treatment for Fanconi syndrome consists of removing/treating the underlying cause if present and treating any electolyte abnormalities. As the measured electrolytes were normal (other than a marginally low phosphate) and the degree of renal damage appeared mild, the dog was treated with a prescription diet for liver disease which contains low copper levels (Canine L/D dry and canned food; Hill’s Pet Nutrition) and oral medications to support liver function. These medications consisted of 11 mg/kg ursodeoxycholic acid (Ursosan; BNM Group), 17 mg/kg s-adenosyl-L-methionine (Samylin;VetPlus) and 2.3 mg/kg silybin (Samylin;VetPlus) daily for 60 days.

The dog was re-examined 3 weeks after starting treatment. The owner reported that polydipsia subjectively appeared to have resolved. It was not possible to confirm resolution of any polyuria as the dog was largely unobserved whilst urinating. Urine was tested with a dipstick which showed no evidence of glycosuria.

A blood sample submitted for serum biochemistry to monitor kidney and liver function. This showed improvement in liver enzyme activities. AST was within the reference range and ALT activity had reduced (98 U/L; reference range 0–75 U/L).

The concentration of urea in serum was now slightly below the reference range (2.3 mmol/L; reference range 2.6–10.2 mmol/L).

Seven weeks after starting treatment the dog was examined again. Polydipsia was still absent and all liver enzyme activities were within normal limits. The medications were discontinued 1 week later. However, the dog will need to be fed the copper-restricted prescription diet indefinitely

Discussion

Fanconi syndrome is an uncommon syndrome characterised by a proximal renal tubular defect that leads to

inadequate resorption of many urine constituents, including glucose, bicarbonate, amino acids and other electrolytes (Yearley et al. 2004; Giger et al.

2015). Abnormal glucose reabsorption by the proximal renal tubule leads to glycosuria and osmotic diuresis (Yearley et al. 2004; Kerl et al. 2010). Glycosuria, with euglycemia or hypoglycemia, is the classic finding of Fanconi syndrome (Giger et al. 2015; Kerl et al. 2010). Due to the osmotic diuresis polyuria and polydipsia are the most common signs associated with Fanconi syndrome (Yearley et al.

2004). Other signs may include vomiting, diarrhoea, weakness, lethargy, weight loss, poor hair coat, dehydration, and other signs of uraemia (Kerl et al. 2010). If left untreated, Fanconi syndrome can lead to renal tubular acidosis, renal papillary necrosis, chronic renal failure and death (Yearley et al. 2004).

Fanconi syndrome can be inherited or acquired. Most cases of inherited Fanconi syndrome are found in Basenjis (Yearley et al. 2004; Giger et al.

2015). Acquired Fanconi syndrome has been associated with leptospirosis, gentamicin administration, primary hypoparathyroidism, copper storage hepatopathy and various toxicoses including consumption of jerky treats (Hooper and Roberts, 2003; Abraham et al.

2006; Kerl et al. 2010; Carmichael et al. 2014; Major et al. 2014; Igase et al. 2015).

Copper storage hepatopathy occurs when excessive amounts of copper accumulate in the liver. High hepatic copper concentrations can occur from ingestion of excessively high amounts of copper in the diet, an inherited gene mutation of hepatocellular copper transport proteins, or liver damage that leads to an inability to maintain a neutral copper balance (e.g. cholestasis) (Center 2010). While many breeds have an increased incidence of excess copper storage, a genetic cause for the condition has been identified in Bedlington Terriers and Labrador Retrievers (Center, 2010). Fieten et al. 2016). In one study of Labrador Retrievers with chronic hepatitis, positive staining for copper was found in 15/17 liver biopsies (Shih et al.

2007). Copper hepatopathy has also been reported in dogs that were exposed to excessive levels of dietary copper (van den Ingh et al. 2007).

Excess copper is cytotoxic to hepatocytes.

Free copper ions can catalyse the formation of hydroxyl radicals which can have damaging effects on lipids, nucleic acids, and proteins (Giger et al. 2015) leading to impaired protein synthesis, nuclear injury and oxidative membrane damage (Center, 2010). Mitochondrial and cell membrane injury lead to cell necrosis

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and apoptosis of hepatocytes (Center, 2010) and ultimately liver cirrhosis can result (Twedt, 2009).

Serum biohemistry changes in dogs with copper storage hepatopathy reflect hepatocellular damage and cholestatic disease. Elevations in ALT, AST, GGT, and ALP are common. Histopathology with copper-specific stains is required to make a definitive diagnosis of copper hepatopathy.

The distribution of copper granules within the liver can help determine if copper accumulation is a primary or secondary problem. With primary disease, copper accumulates in zone 3 (centrilobular) hepatocytes and is also found in regenerative nodules and other hepatocytes. With secondary disease, copper accumulation is found only in areas adjacent to cellular injury (Hoffman, 2007).

Other histopathologic abnormalities can include cirrhosis, necrosis, and chronic inflammatory changes (Twedt, 2009).

In severe copper hepatopathy, where the liver copper concentration exceeds 9500 µmol/kg, treatment with copper chelation is recommended using either D-penicillamine or trientine. Zinc supplementation can then be used as a maintenance therapy. Zinc decreases intestinal absorption of copper, but may not be tolerated in many dogs due to gastrointestinal side-effects. Dietary restriction of copper intake is an important part of therapy and can most easily be achieved with a hepatic prescription diet (Center, 2010). Supportive therapy for copper hepatopathy with ursodeoxycholic acid, vitamin E, s-adenosylmethionine and silybin may be helpful (Center, 2010, Twedt, 2009).

Fanconi syndrome is treated by identifying and treating the underlying cause wherever possible. Supportive treatment of Fanconi syndrome can be provided by supplementation of vitamins, minerals, amino acids and bicarbonate. Correction of the metabolic acidosis caused by bicarbonate loss in particular, can dramatically slow disease progression and minimise renal damage (Yearley et al. 2004; Kerl et al. 2010 ; Fieten et al. 2016).

Resolution of Fanconi syndrome and successful management of copper storage hepatopathy in this dog was presumed based on normalisation of clinical signs, serial serum biochemistry

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testing, and urinalyses. This case is similar to a previously published case report of three dogs with transient acquired Fanconi syndrome associated with copper storage hepatopathy (Appleman et al.

2008). The dogs in this previous report were a Clumber Spaniel, a West Highland White Terrier and a Cardigan Welsh Corgi.

Differences between this case and those described by Appleman et al. (2008) include that the hepatopathy in the three other dogs was more severe than that seen in the Labrador Retriever described here, and those dogs were treated with copper chelation therapy rather than a copper-restricted diet alone. In all cases the outcome was excellent.

Learning points

• Fanconi syndrome is an uncommon differential for polyuria/polydipsia.

• Fanconi syndrome and concurrent liver enzyme elevations should raise the suspicion for copper storage hepatopathy.

• Liver biopsy should be considered early in the course of investigation of liver disease, especially if a breed-related hepatopathy is suspected.

• Successful treatment of copper storage hepatopathy should result in the resolution of Fanconi syndrome.

Acknowledgements

Thank you to Sandra Forsyth at SVS Laboratories, Hamilton for advice on interpretation of coagulation results and to Mark Bestbier, also at SVS, for interpretation of liver biopsies.

References

Abraham LA, Tyrrell D, Charles JA. Transient renal tubulopathy in a racing Greyhound. Australian Veterinary Journal 84, 398–401, 2006 Appleman EH, Ci anciolo R, Mosenco AS, Bounds ME, Al‐Ghazlat S. Transient acquired Fanconi syndrome associated with copper storage hepatopathy in 3 dogs. Journal of Veterinary Internal Medicine 22, 1038–42, 2008 Carmichael N, Lee J, Giger U. Fanconi syndrome in dogs in the UK. Veterinary Record 174, 357–8, 2014 Center SA. Emerging syndrome of copper-related hepatotoxicity. Wild West Veterinary Conference 2010.

Fieten H, Gill Y, Martin AJ, Concilli M, Dirksen K, van Steenbeek FG, Spee B,

van den Ingh TS, Martens EC, Festa P et al. The Menkes and Wilson disease genes counteract in copper toxicosis in Labrador retrievers: a new canine model for copper-metabolism disorders. Disease Models and Mechanisms 9, 25–38, 2016 Giger U, Brons A, Mizukami K, Slutsky J, Raj K, Fitzgerald CA, Strickland S, Sewell AC, Henthorn PS. Update on Fanconi syndrome and cystinuria. World Small Animal Veterinary Association World Congress Proceedings 2015.

Hoffman G. Chronic hepatitis and copper metabolism in Labrador Retrievers.

ECVIM- A Congress 2007.

Hoffmann G, van den Ingh TSGAM, Bode P, Rothuizen J. Copper-associated chronic hepatitis in Labrador Retrievers.

Journal of Veterinary Internal Medicine 2006 20, 856–61, 2006 Hooper AN, Roberts BK. Fanconi Syndrome in Basenji Dogs. World Small Animal Veterinary Association World Congress Proceedings 2003 Igase M, Baba K, Miyama TS, Noguchi S, Mizuno T, Okuda M. Acquired Fanconi syndrome in a dog exposed to jerky treats in Japan. Journal of Veterinary Medical Science 77, 1507–10, 2015 Kerl M E, Ettinger S J, Feldman E. Renal Tubular Diseases. In: Textbook of Veterinary Internal Medicine (7th Edtn).

Ettinger SJ, Feldman EC (Eds). Pp. 2062–8. Saunders Elsevier, St. Louis, MO, USA, 2010.

Major A, Schweighauser A, Hinden S E, Francey T. Transient Fanconi syndrome with severe polyuria and polydipsia in a 4-year old Shih Tzu fed chicken jerky treats. Schweizer Archiv Fur Tierheilkunde 156, 593–8, 2014 Shih JL, Keating JH, Freeman LM, Webster CR. Chronic hepatitis in Labrador Retrievers: clinical presentation and prognostic factors. Journal of Veterinary Internal Medicine 21, 33–39, 2007 Twedt DC. Chronic hepatitis and copper hepatopathies in the dog. Western Veterinary Conference 2009. van den Ingh TS, Punte PM, Hoogendijk EN, Rothuizen J. Possible nutritionally induced copper-associated chronic hepatitis in 2 dogs. Veterinary Record 161, 728, 2007 Willard MD. Inflammatory canine hepatic disease. In: Textbook of Veterinary Internal Medicine (7th Edtn). Ettinger SJ and Feldman EC (Eds). Pp. 1637–42.

Saunders Elsevier, St. Louis, MO, USA, 2010 Yearley JH, Hancock DD, Mealey KL. Survival time, lifespan, and quality of life in dogs with idiopathic Fanconi syndrome. Journal of the American Veterinary Medical Association 225, 377–83, 2004 l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

Companion Animal Health Foundation update Promoting animal health and welfare to benefit companion animals in New Zealand

CATH WATSON, CAHF

Chair, www.cahf.org.nz

Project updates

CAHF is excited to report we have been able to fund a highly relevant project proposed by Dr. David Wilkinson into MRSP carriage on dogs in New Zealand.

The project has several objectives, not the least of which is to calculate the prevalence of MRSP in healthy dogs in NZ, along with the identification of the resistant strains, to help us better understand the risk to our patients and clinics. The success of this project will hopefully also lead to the establishment of a reference bank of isolates for future research, as well as database for identification specific to New Zealand.

Keep an eye out for your clinic’s invitation to take part in this project.

CAHF funds are available to anyone with a project which meets the trust

criteria for funding, which can include educational and welfare projects as well as research – as long as it will benefit companion animals in New Zealand. If you’d like to check whether your project meets the Trust criteria, visit www.cahf. org.nz or contact cav@vets.org.nz Unfortunately we weren’t able to fund every project we would have liked to, from this last round purely because of limited funds. We urgently need to secure the future of CAHF. This is our industry and it is our patients and pets that ultimately will benefit, so…..

Can you raise $500?

We are asking for the support of all practices in New Zealand and individual veterinarians to raise at least $500 each annually, a sum which would secure the future of the Foundation and ensure it works as planned to help our pets enjoy better and healthier lives. Every dollar

will be used to help combat health and welfare problems encountered by companion animals in New Zealand.

By joining our $500 Project, we are asking practices to pledge to raise $500 by whatever means they can; external fundraising events, organizing your own internal fundraiser for your practice, or simply by making an individual donation.

Please visit our updated website http:// www.cahf.org.nz/help/donate for details.

We now also have a Give-A-Little page: https://givealittle.co.nz/org/healthypets.

Supporting the Foundation will clearly demonstrate to your staff, your clients and your suppliers that you invest in the health of pet companion animals and that you support the veterinary profession through the Foundation.

If you wish to register your practice as an annual $500 practice supporter for the CAHF use the online registration form on the website www.cahf.org.nz l

Photo courtesy of pixabay.com

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CPD RECORD

Read articles from Companion Quarterly 29(1) March 2018

Date of Activity: …………………………

Activity description Read articles in the March 2018 issue of Companion Quarterly (tick those that apply) o o

What is Your Diagnosis (Gabriel Hagard) Information on the proposed release of rabbit calicivirus (RHDV1) K5 in New Zealand (CAV Exec. Committee) o Calling time on Scottish folds (Sarah Fowler, Rochelle Ferguson, John Munday) o Diagnostic techniques: how to get the most from a skin biopsy (Duncan Graham) o Diagnosis of hypoadrenocorticism in dogs (Boyd Jones, Anne Kim, Lucy Lane) o Practical dental homecare information (Janine van Dam) o Report: WSAVA Congress (Charlotte Mathews) o A week with….Feline medicine specialist, Pru Galloway (Susan Murray) o ………………………………………………………………………………………………………… o ………………………………………………………………………………………………………… o …………………………………………………………………………………………………………

Activity type: Category: Self-directed activity Self-Directed Activity Type: Updating knowledge or preparatory reading/research Hours claimed: VCNZ Points (0.5 per hour reading): Reflective record: Actual learning outcomes and the impact on your practice What did you teach or learn from this activity? ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................

How do you think this will impact on your practice? ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................

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Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 1 | March 2018

COMPANION QUARTERLY â&#x20AC;&#x201C; Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA

Companion Quarterly

OFFICIAL NEWSLETTER OF THE COMPANION ANIMAL VETERINARIANS BRANCH OF THE NZVA Volume 29, No. 1 | March 2018

VOLUME 29 NO 1 March 2018

How to get the most from your skin biopsies

Diagnosis of hypoadrenocorticism in dogs

Calling time on Scottish folds

Practical dental homecare info

Snippets from WSAVA 2017