Companion Quarterly Vol 29 No2 June 2018 by Companion Quarterly

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. 2 | June 2018

VOLUME 29 NO 2 June 2018

Feline immunodeficiency virus in New Zealand

FALPS: a fatal inherited disease of British shorthair cats

Leptospirosis in dogs: an emerging problem?

Feline idiopathic hypercalcemia

Report: Highlights from Veterinary Ophthalmology course

Volume 29 | No. 2 | June 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 Alison Pickering Becky Murphy Paula Short

EDITORAL COMMITTEE Sarah Fowler (Editor) Bart Karalus 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

2 Editorial 4 CAV activities and meeting highlights

6 CAV Noticeboard 8 What is your diagnosis? Matthew Kopke

10 News in Brief: prize winners

for CAV Continuing Education Grants for 2018

12 Mandatory tests for the Dogs

NZ Accredited Breeders Scheme

20 Feline autoimmune

lymphoproliferative syndrome (FALPS): a fatal inherited disease of British shorthair cats Danielle Aberdein

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

24 Feline immunodeficiency virus

in New Zealand: should we test? should we vaccinate? and does it even cause disease? John S Munday, Nick J Cave

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.

Cover photograph

Buck, a huntaway/heading dog cross who works on a dairy farm in Richmond Downs. Photo courtesy of Crystal Loh.

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

28 Feline idiopathic hypercalcemia Susan Murray

34 Leptospirosis in dogs: an emerging problem? Janice Thompson

Conference Report: highlights from the course in Veterinary Ophthalmology II at the European School for Advanced Veterinary Studies: Part I Jos van Hees

What is your diagnosis? The answers

New Zealand Companion Animal Health Foundation update

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.

47 Massey News 48 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 2 | June 2018

EDITORIAL

Critical thinking is critical As an academic who spends a significant proportion of their time doing research I had a nasty experience a couple of months ago. As I was out walking my dogs, I was listening to a ‘Planet Money’ podcast. The story started with a peer-reviewed paper that had recently been published in a high-impact well-respected journal that proved that extrasensory perception (ESP) was real. On reading this paper, a different researcher was forced to conclude that one of two possibilities were true. Either ESP was indeed real or that the research that proved ESP was real was somehow flawed. This led the second researcher to re-run, using identical methods, 100 experiments that had been previously published in high-tier peer-reviewed journals. Amazingly, of the 100 previously-published studies only 39 could be repeated with the results obtained in 61 studies different to those previously published. While a number of explanations for this low rate or repeatability were proposed, the most likely seemed to be publication bias. This bias develops because only studies that show a significant effect will be published. For example, I compare treatment A with treatment B and the p-value that I chose for the level of significance in my study is 0.05. As a p-value of 0.05 means that there is a 1 in 20 chance that the effect seen is purely down to random chance, if 20 different researchers do the same experiment, one will see a significant effect just due to luck. The 19 studies that did not show a significant effect won’t get published because they don’t show anything new. However, the one study that did show a significant effect will get published and this is now taken as conclusive evidence that treatment A is better than treatment B.

The experiments described in the podcast were all carried out on human subjects and my initial reaction was that veterinary studies were sure to be much better. However, the more I thought about it, the less sure I was. Compared to studies on human patients, veterinary studies tend to be much smaller and sample sizes of less than 20 are not unusual. Additionally, studies investigating new treatments or procedures in humans have to be blinded and placebo controlled. In contrast, few veterinary studies are adequately blinded or include appropriate controls. In my experience blinding of an experiment is absolutely essential because it is impossible for any researcher to avoid observational bias. This bias does not develop consciously, but even if I am not ‘hoping’ for any experimental outcome, I have found that I unconsciously interpret changes within samples differently when I know which group a sample comes from compared to when I am blinded. Likewise, appropriate controls are essential and too often in veterinary medicine we are forced to try and compare a new treatment or procedure to highly inaccurate ‘historical data’. Such limitations can be unavoidable, but do raise the question of whether or not the level of repeatability for studies in veterinary medicine would be better than the level of repeatability found in the studies done in humans. Why do I mention these rather depressing facts in an editorial in CQ that prides itself on containing relevant research results? I mention this because as a profession we always have to remain somewhat skeptical. This skepticism definitely includes things that our clients may bring to our attention from

the internet. However, as even studies published in peer-reviewed journals may later be proven incorrect, we have to retain our critical thinking ability and not simply believe everything we read in textbooks or in journals. The veterinary profession is progressing rapidly and it is worth remembering that many accepted ‘facts’ 20 years ago have now been shown to be incorrect. Likewise, I think it is very important that our profession is careful about new treatments and therapies. While there are undoubtedly many outstanding new treatments available, it is important that we recognize that for many there is little or no convincing evidence for their use. I would hate to see the veterinary profession lose credibility by failing to acknowledge the lack of evidence-based support for new products and procedures that we may be recommending to clients. During my teaching at Massey, there is always the moment when a 5th year student realizes that not all lecturers agree with each other. I always think that this is a very positive thing as it demonstrates to the students that there still remains a level of uncertainty in veterinary medicine. I always encourage the students to do some reading and make up their own minds. Considering the results of the repeatability experiment, I think remaining open to new information and critically evaluating the current information is more important than ever. One thing that history has taught us is that some of the things that we are certain about today will be proven to be wrong tomorrow. John S. Munday CAV President l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

WORKING TO PROMOTE AND SUPPORT COMPANION ANIMAL PRACTICE IN NEW ZEALAND

CAV activities and meeting highlights

Dog control enforcement

Following the Christchurch City Council’s short-lived decision to require dogs classified as menacing to wear muzzles when in both private and public places, CAV published an article in The Spinoff criticising the current breed specific focus of our dog control laws. This was picked up by other media outlets and resulted in further media attention for our position on dangerous dog control in both radio and print media outlets. Through this channel, we highlighted the major flaw in the Dog Control Act, where dogs are identified as being risky based solely on their breed. We also made suggestions around bringing in a tiered classification system based on actions and considering the context of the attack. Members can read more about the NZVA position on dangerous dog control under the policies/companion animal health and welfare tab on the NZVA website. This policy is also due for review in 2018, so any comments from members would be welcomed.

Communications to support the release of RHDV1 K5 in 2018

Following approval from MPI for the registration and release of RHDV1 K5 in New Zealand, CAV supported NZVA’s communications to the general public and veterinarians on how to best protect nontarget rabbits.

Greyhound Racing New Zealand (GRNZ) welfare committee work

CAV have provided a NZVA advisor to the GRNZ welfare committee since 2016. This committee recently reviewed the GRNZ welfare standards for their registered dogs. While there is still much work to be done regarding the welfare of racing greyhounds, it was pleasing to see the GRNZ board adopt all the recommendations made by the GRNZ welfare committee, particularly around breeding management. This will mean stricter restrictions on the ages that female dogs can be bred and the number of litters they have, bringing them into line with the CAV responsible breeding guidelines. 4

NZVA Policies updates

The responsible dog and cat ownership policies, and the euthanasia policy updates are in the final stages of approval and should be available to members and the public from the NZVA website in June. Feedback was sought in May on a reviewed position on electronic behaviour modifying collars, and a CAV position on selective breeding. Work is underway on a comprehensive de-sexing policy to replace the current pre-pubertal policy and an update on our dangerous dog position statement. For policies that contain information helpful to the general public, a project is planned to present these in a user-friendly format and create a public section on a new CAV website to showcase them.

World Small Animal Veterinary and Federation of Small Animal Veterinary Associations

Meetings for both these organisations will be held during the annual WSAVA congress in Singapore this September. Natalie Lloyd and Peter Verhoek are both attending this meeting allowing Natalie to also represent CAV at WSAVA while Pieter Verhoek will represent CAV at FASAVA.

2018 Wellbeing project

Work has begun on CAV’s wellbeing initiatives for 2018. CAV members will be asked to participate in the workplace mental health barometer survey undertaken by researchers at Massey University. The aim of this survey is to better understand the mental health of the New Zealand workforce. Members are encouraged to participate in this confidential academically designed survey. All results are sent directly to the researchers at Massey, who operate under a strict code of ethics. If 50 (or more) CAV members participate, we will have the opportunity to have the CAV membership data group reported separately from the national group. This will allow us to benchmark ourselves to other occupations across New Zealand, giving us a better understanding of how the mental health of veterinarians

compares with the mental health of other professions. As scientists, we will all understand the power of acquiring New Zealand-based and veterinaryspecific metrics that can be used to develop future initiatives to best support veterinary wellbeing.

RxVet/CAV A week with…

This scholarship attracted seven worthy applicants and a random draw was required to determine the two successful recipients. Dermatology appeared to be a hot topic, with Raewyn Creevy and Juliet Matthews both being awarded scholarships to spend a week seeing referral dermatology practice at The Skin Vet in Auckland with Debbie Simpson.

Hill’s Pet Nutrition/CAV Educating the Educators Scholarship

This initiative, sponsored by Hill’s Pet Nutrition, Massey School of Veterinary Sciences and NZVA VetLearn, is pleased to support our New Zealand specialists travelling overseas for their continuing professional development. The really great part of this is that they then bring back this knowledge to share with CAV members through articles in the Companion Quarterly and the wider veterinary profession through regional branch presentations. In the March round we are proud to support Assoc. Prof. Andrew Worth, Dr. Damian Chase, Dr. Debbie Simpson, Dr. Richard Jerram and Dr. Trudi McAlees. We can look forward to many great articles and regional branch talks from them covering emergency medicine, dermatology, and surgical topics. Again, we are thankful to our three sponsors, Hill’s Pet Nutrition, VetLearn and Massey School of Veterinary Science who work with CAV to make this all happen.

Executive committee member updates Aimee Brooker, who has served as Treasurer since 2014, will hand over this role at the AGM in June to Simon Clark, who joined CAV in 2017. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

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

Boyd Jones Anne Kim Lucy Lane

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

“Diagnosis of hypoadrenocorticism in dogs" March 2018 | Volume 29 (1) | Pages 26–30

EYEVET Services Limited

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

What is your diagnosis? THE QUESTIONS… MATTHEW KOPKE, Small Animal Internal Medicine Resident, School of Veterinary Science, Massey University A 6-year-6-month-old, female spayed Staffordshire Bull Terrier presented with recurrent seizure activity, several times per day over the preceding two-week period, and more recent development of lethargy, altered mentation and hyporexia. The owners reported that the dog was not on medication, had not been fed any unusual foods and had no known access to toxins. However, they did report that they were currently renovating their house. A venous blood sample was obtained for serum biochemistry (including liver function tests, blood glucose and inhouse ammonia testing) and a complete blood count (CBC). The CBC revealed normal red blood cell, white blood cell and platelet counts, however, basophilic stippling of approximately 50% of the red blood cells along with a marked increase in the number of nucleated red blood cells (specifically metarubricytes), was appreciated (Figure 1). No significant findings were described on serum biochemistry. A urine sample was obtained via cystocentesis, and urinalysis revealed moderate glucosuria and urine specific gravity of 1.028.

Figure 1. This is not a photomicrograph of blood from the dog in this case but illustrates clinicopathological changes typically seen in similar cases including hypochromic RBC (which are also called target cells, arrowhead), RBC containing iron inclusions or siderocytes (arrows), nucleated RBC (nRBC), and basophilic stippling of mature RBC (B) and nRBC (Wright’s stain, 1000x magnification). eClinPath.com (accessed 6 May 2018).

Questions:

1. What is this dog’s problem list? 2. What are your differential diagnoses for these problems? 3. How would you arrive at a definitive diagnosis?

Answers on page 44

Contact: M.Kopke@massey.ac.nz

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

NEWS IN BRIEF

Prize winners for CAV Continuing Education Grants for 2018 Every year CAV has a draw to select two practitioners, one new member and one continuing member to receive a prize of $500 towards companion animal continuing education from VetLearn. The winners for 2018 were Joanna Bruin (new member) and Shanaka Sarathchandra (continuing member).

Joanna is a companion animal veterinarian at Dargaville Veterinary Centre in Northland. She is planning on putting the prize money towards the 'Radiology refresher for the companion animal practitioner workshop' to be held in Auckland in November. Jo will have no problem ticking off the CVE component of her CPD requirements after attending the 'Cytology workshop' and the NZVA Megaconference earlier in the year.

Shanaka is clinical lead veterinarian for Pet Doctor’s Hamilton clinics. He would like to say a big “Thank you!” to CAV for the totally unexpected prize. He plans to put it towards the 'Companion animal reproduction workshop' in August since it is held locally and it covers a subject that he would like to become more knowledgeable in. l

Joanna vaccinating an abandoned pup before sending her off to a great new home. Photo courtesy of Joanna Bruin.

Photo courtesy of Shanaka Sarathchandra.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

CAV UPDATE

Mandatory tests for the Dogs NZ Accredited Breeders Scheme Dogs NZ have a list of recommended health tests for each breed they register available on their website (https://www.dogsnz.org.nz/pdfs/breedhealth-tests.pdf). The tests include DNA sampling, cardiac and eye certification, along with orthopaedic assessments through radiographs and examinations. To support this list, CAV have compiled a list of the mandatory tests required for the Dogs NZ Accredited Breeders Scheme with information on when to perform the test, who performs it, when it needs to be repeated and how it should be reported. It is important that, as veterinarians, we encourage open reporting of health results to Dogs NZ. To build a true representation of the health of a breed, all test results should be submitted, not just those that are “acceptable”. It is only by testing and accurate recording of the results that the resultant data will have the power to transform the health and welfare of the pedigree breeds by reliably informing breeding decisions. The days of breeders being stigmatised for poor test results are long gone. Those breeders that have the foresight to undertake the responsibility and costs associated with testing then using those results to improve the health and welfare of their puppies must be celebrated and supported.

Cardiac certificate Age: Repeat: Performed by: What is involved:

Reporting:

Any age Annually while in breeding programme. Examination must have been performed within 12 months of mating. Veterinarian Identify the dog presented for testing by microchip. Testing involves heart auscultation by a veterinarian and completion of a Dogs NZ Application for Congenital Cardiac Database form. Include the microchip number of the dog examined. The method is detailed on the form. If findings are normal, the certificate is valid for 12 months. If a murmur or abnormal rhythm is noted, referral to a cardiologist or veterinarian with a special interest in cardiology is recommended. Complete the Application for Congenital Cardiac Database form (available from the CAV website)

Dermoid sinus checks in puppies Age: Repeat: Performed by:

What is involved:

Reporting:

DNA testing Age: Repeat: Performed by: What is involved:

Reporting: 12

From 6 weeks of age No need to repeat once tested. Most breeders do this themselves on neonatal puppies, then repeat weekly until they go to their new home. Veterinarians may be asked to certify a dermoid sinus isn’t present at the first vaccination visit. Identify the dog presented for testing by microchip. A dermoid sinus can be felt in young puppies. It is characterized by the presence of a tuft of hair protruding from each sinus and is sometimes complicated by infection. The skin from the back of the head to the tail is examined visually and by palpation. The most common places for this defect to occur are on the midline at the back of the neck and on the midline of the rump – so in front of and behind the ridge. If there is any doubt as to whether a sinus is present or not shaving the hair in the suspected area can reveal the external opening in the skin. The Rhodesian Ridgeback Association has more information on this condition on their website: http://www.nzridgebackassn. co.nz/dermoid-sinus/ Report the result of the physical examination in a letter, including the dog’s microchip number and pedigree name (if known)

Can be performed at any age No need to repeat once tested. Veterinarian or approved microchip implanter Identify the dog presented for testing by microchip. Check the Dogs NZ breed health test list on their website to find which DNA tests are recommended for the breed of dog you are testing. Testing kits are provided by the DNA testing companies. The test kits will provide a return package for the sample that usually includes any biosecurity labelling requirements if sending outside of New Zealand. The microchip must be verified and recorded at the time of sampling. Include the pedigree name on the submission form if it is available. Accepted Dogs NZ providers for this test include: Orivet, Animal Network and Equine Parentage Animal Genetics (based at Massey University). Provide a copy of test results to the breeder.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Elbow dysplasia Age:

12 months of age and over. The NZVA scheme has an option to score at 1 year of age, those with a 0 score are eligible for rescoring after 2 years of age.

Repeat:

No need to repeat once tested.

Performed by:

Veterinarian

What is involved:

Identify the dog presented for testing by microchip. A radiograph of a flexed mediolateral view of each elbow (one view per radiograph). General anaesthesia, while not mandatory, is recommended. The microchip number and if known, pedigree name should be included on the form and radiographs The radiograph is submitted to a recognised scheme for scoring. Dogs NZ recognised schemes include the NZVA elbow dysplasia scheme, the Australian Canine Hip and Elbow Dysplasia Scheme (CHEDS), the Orthopaedic Foundation for Animals (OFA) and the British Veterinary Association elbow dysplasia scheme.

Reporting:

Complete Application for Hip/Elbow Dysplasia Database (available on the CAV website) and provide a copy of the original Elbow Scoring Report.

Exocrine pancreatic insufficiency Age:

Awaiting confirmation from Dogs NZ

Repeat:

Likely 12-monthly, but awaiting confirmation from Dogs NZ

Performed by:

Veterinarian

What is involved:

Identify the dog presented for testing by microchip. Submit a blood sample for a TLI assay.

Reporting:

Eye certificate

Provide a copy of the test results to breeder.

Age:

Any age

Repeat:

Annually while in breeding programme. Examination must have been performed within 12 months of mating

Performed by:

Dogs NZ-approved eye vet

What is involved:

Refer the breeder to an approved Dogs NZ eye vet for this assessment. See the Dogs NZ website (http://ab.dogsnz.org.nz/Health/Health%20Test%20Info) for a list of currently approved veterinarians and their contact details.

Gonioscopy Age:

Performed from 12 months of age.

Repeat:

This is a specific test for glaucoma, and once performed does not need to be repeated.

Performed by:

Dog NZ-approved eye vet

What is involved:

Refer breeder for this assessment. See the Dogs NZ website (http://ab.dogsnz.org.nz/Health/Health%20Test%20Info) for a list of currently approved veterinarians and their contact details.

Hemivertebrae Age:

From 12 months of age. No need to repeat test.

Repeat:

No need to repeat once tested.

Performed by:

Veterinarian takes radiographs and submits for scoring

What is involved:

Identify the dog presented for testing by microchip. A lateral and VD view of the spine from C1 to L7 is required. The microchip number and, if known, pedigree name should be included on the form and radiographs. There are no schemes for scoring hemivertebrae in NZ. It is suggested that veterinarians submit their radiographs to Dr Mariano Makara in Australia. See her website (http://www.vetscoring.com/) for forms and instructions for uploading x-ray files. This site gives useful information on the condition for breeders: http://www.veterinarypartner.com/Content. plx?P=A&A=2554&S=1&SourceID=42

Reporting: 14

Finalised report provided to breeder.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Hip dysplasia â&#x20AC;&#x201C; PennHIP method Age:

From 16 weeks of age. No repeat testing needed.

Repeat:

No need to repeat once tested.

Performed by:

PennHIP accredited veterinarian

What is involved:

Identify the dog presented for testing by microchip. PennHIP assessment consists of three separate radiographs taken under general anaesthetic or heavy sedation: the distraction view, the compression view and the hip-extended view. The distraction view and compression view are used to obtain accurate and precise measurements of joint laxity and congruity. The hip-extended view is used to obtain supplementary information regarding the existence of osteoarthritis (OA) of the hip joint. (The hip-extended view is the conventional radiographic view used to evaluate the integrity of the canine hip joint.) The PennHIP technique is more accurate than other schemes, and it has been shown to be a better predictor for the onset of OA. For more information refer to Antech Medical (http://info.antechimagingservices.com/pennhip/navigation/general/what-isPennHIP.html) who administer the scheme. They have Information on becoming accredited to take and submit PennHIP radiographs. There is no charge to complete the training to become accredited. These Youtube video by Andrew Worth: (https://www.youtube.com/watch?v=8akAM3BF-xc&feature=youtu.be) explain why NZVA have moved to PennHIP for veterinarians.

Reporting:

Complete the Application for Hip/Elbow Dysplasia Database (available on the CAV website) and include a copy of the original PennHIP report.

Hip dysplasia â&#x20AC;&#x201C; Willis method Age:

Minimum age for testing depends on the scheme. The Australia National Kennel Club will accept a submission from 12 months of age, however the Orthopaedic Foundation for Animals has a minimum age at testing of 2 years.

Repeat:

No need to repeat once tested.

Performed by:

Veterinarian

What is involved:

Verify the presented dogs identity by microchip. A radiograph of a VD view of the hips, including femurs and patella. The use of general anaesthesia or heavy sedation is highly recommended. See this site from Veterinary Imaging Associates for advice on positioning for hip scoring (http://www.onlinevets.com/Hip_Elbow_Dysplasia_Evaluation_Tips_Submission.pdf). The microchip number and if known, pedigree name should be included on the form and X-rays. Australian National Kennel Club administer the Canine Hip and Elbow Dysplasia Scheme (CHEDS) that scores hips based on the Willis/BVA method. The form to make submissions can be downloaded from this website: http://ankc.org.au/media/6592/ankccanine-hip-v7.pdf. Send them to one of the veterinarians listed here: http://ankc.org.au/media/6593/ankc-ltd-cheds-radiologist-panelv6.pdf. Other Dogs NZ recognised schemes include the Orthopaedic Foundation for Animals (OFA) and the British Veterinary Association (BVA)

Reporting:

Complete Application for Hip/Elbow Dysplasia Database (available on the CAV website) and include original CHED report.

Legg-Calve-Perthes disease Age:

From 12 months of age.

Repeat:

No need to repeat once tested.

Performed by:

Veterinarian

What is involved:

Check with Dogs NZ

Reporting:

Complete the Application for Legg-Calve-Perthes Database form (available on the CAV website).

Nephritis Age:

As old as possible prior to first mating.

Repeat:

Annually while in breeding programme. Examination must have been performed within 12 months of mating.

Performed by:

Veterinarian

What is involved:

Verify the presented dogs identity by microchip. Collect urine sample and send to laboratory for a urine protein creatinine ratio. Breeding stock should have a protein:creatinine ratio no greater than 0.3.

Reporting:

Veterinarian completes the Application for Kidney Database form (available on the CAV website). Note the form has not been updated from the previous 0.5 cutoff limit.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Patella luxation Age: Repeat: Performed by: What is involved:

Minimum of 1 year of age. Annually while in breeding programme. Examination must have been performed within 12 months of mating. Veterinarian Verify the presented dog's identity by microchip. Palpate the patellae. Record and grade the laxity and position of the patellae.

Reporting:

The following are grades of patella luxation: • Grade 1 – The patella can be luxated manually at full extension of the stifle joint, but returns to the trochlear groove when released. • Grade 2 – There is frequent patellar luxation, but the patella naturally returns to the trochlea. • Grade 3 – The patella remains in a luxated position, though it can be manually returned to the trochlea. • Grade 4 – The patella is permanently luxated, and cannot be returned to the trochlea. Instructions for the examination are available from the Dogs NZ form. Veterinarian completes Application for Patellar Luxation Database form (available on the CAV website).

Polycystic kidney disease Age: Repeat: Performed by: What is involved:

Test as late as possible prior to breeding. Annually while in breeding programme. Examination must have been performed within 12 months of mating. Veterinarian skilled in ultrasonography with access to an ultrasound that produces diagnostic quality images. Verify the presented dogs identity by microchip. Ultrasound examination of the kidneys. Affected animals show at least three renal cysts, with cysts present in both kidneys. Other family members with cysts confirm that they are inherited and not an insignificant finding or due to another disease.

Reporting:

If fewer than three cysts are detected, or if cysts are only seen in one kidney a retest in 6–12 months is recommended to ensure the dog is not in the early stages of the disease. The dog should not enter the breeding programme until after the test has been repeated. Report from veterinarian performing the test, including the microchip number.

Portosystemic shunt (PSS) Age: Repeat:

Prior to first mating. No need to repeat if test results are normal.

Performed by: What is involved:

If abnormal results, further investigation is required. If PSS can be ruled out by the further testing, there is no need to repeat. Veterinarian Verify the presented dog’s identity by microchip, include this on the submission form. Perform a fasting and 2-hour post prandial serum bile acid test.

Reporting:

This test is not specific for PSS, so if suspicious results are received, particularly in animals with no clinical signs of PSS, further investigation is warranted. Consider repeating the test in 4–8 weeks, and/or referral to a specialist for an abdominal ultrasound. Copy of the blood test results provided to breeder

Thyroid testing Age: Repeat: Performed by: What is involved:

Test as late as possible prior to breeding. Annually while in breeding programme. Examination must have been performed within 12 months of mating. Veterinarian Verify the presented dog’s identity by microchip, and include this on the submission form. Collect a serum blood sample. 2 mL of serum is needed for testing. If specimen is to be stored for more than 12 hours prior to shipping, frozen storage of separated serum is recommended. Submit to Gribbles Laboratory for the NZKC ABS Thyroid Panel (Free T4, TSH and TgAA).

Reporting:

Interpret results using the guidelines provided on the form Complete Application for Thyroid Database form (available on the CAV website) and provide breeder with a copy of the test results.

Transitional vertebrae Age: Repeat: Performed by: What is involved:

From 12 months of age. No need to repeat once tested. Veterinarian Verify the presented dog’s identity by microchip. Perform VD and lateral views of the caudal lumber and sacral vertebra. The microchip number and if known, pedigree name should be included on the radiographs.

Reporting:

Examine the radiograph for transitional vertebrae. If any concerns refer to a radiologist for interpretation. Copy of an radiograph report provided to breeder.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

CLINICAL UPDATE

Feline autoimmune lymphoproliferative syndrome (FALPS): a fatal inherited disease of British shorthair cats DANIELLE ABERDEIN LLB(Hons), BVSc,

MVS, PhD

What is FALPS?

FALPS is an autosomal recessive inherited disease of British shorthair (BSH) cats presenting as marked generalised lymphadenopathy in young kittens. The disease was first seen in BSH kittens in Australia from the mid-1990s and in NZ from 2008. FALPS progresses quickly, currently has no known treatment, and affected kittens usually die or require euthanasia shortly after diagnosis. While FALPS clinically mimics lymphoma, additional testing confirms FALPS as a nonneoplastic T-cell proliferation.

Clinical signs

Kittens affected by FALPS are normal at birth but typically develop signs of FALPS around 6–10 weeks of age, including:

• A rapidly progressive and often dramatic generalised non-

painful lymphadenopathy, with all peripheral lymph nodes usually affected and easily palpable (Figure 1). Abdominal distension due to a combination of marked visceral lymphadenopathy, splenomegaly and hepatomegaly. Variable anaemia. Non-specific signs of failure to thrive, poor growth (compared with unaffected littermates), lethargy and reduced appetite. In many cases, these are the only clinical signs observed by affected kittens’ owners or breeders; in some cases, owners or breeders of affected kittens do not recognise any clinical signs at all. Clinical cases of FALPS are therefore possibly under-diagnosed. To date, all reported cases of FALPS have been fatal or required euthanasia on humane grounds by 5 months of age.

• • •

Differential diagnoses

The main differential diagnoses for FALPS are multicentric lymphoma and lymph node hyperplasia (“reactive lymphadenopathy”) due to various causes of antigenic stimulation. Multicentric lymphoma in cats can cause similar clinical signs and clinical pathology to those seen in kittens with FALPS. As Contact: D.Aberdein@massey.ac.nz

Figure 1. Photograph of a 12-week old FALPS-affected BSH kitten with markedly enlarged cervical and mandibular lymph nodes.

in lymphoma, the cytology and histology of enlarged lymph nodes in FALPS-affected kittens usually reveals a monomorphic population of lymphocytes effacing normal nodal architecture, although in some cases variable numbers of plasma cells are also present. If immunohistochemistry (IHC) is also performed, the majority of lymphocytes present within the enlarged nodes of FALPS-affected kittens typically show a CD3+ immunophenotype (consistent with T-cells). The results of nodal cytology, histology and immunohistochemistry in kittens with FALPS are therefore usually suggestive of T-cell lymphoma, and many early cases of FALPS were initially misdiagnosed as lymphoma. However, specialised testing (typically PARR or “clonality” testing, not currently available in NZ) will usually confirm a non-neoplastic T-cell proliferation within multiple lymph nodes and other lymphoid tissues of FALPS-affected kittens. Even if PARR testing is not available, lymphoma should be considered a very unusual diagnosis in any kitten under 6 months of age (FALPS-affected kittens are usually less than 5 months and often much younger), particularly in

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

cases where multiple related or sibling kittens are similarly affected, and further investigation of other causes of lymphadenopathy – including FALPS – should be undertaken. Lymph node hyperplasia secondary to a wide range of antigenic stimulation (e.g. hypersensitivity, FeLV or FIV infection) is another cause of nodal enlargement in cats and kittens, and may cause enlargement of multiple peripheral nodes similar to FALPS. Ruling out these other potential causes of lymphadenopathy is recommended (e.g. with FeLV and FIV testing, thorough clinical exam, and lymph node cytology). In contrast to FALPS, nodal hyperplasia does not typically cause such marked enlargement of all peripheral lymph nodes, splenomegaly or hepatomegaly. Cytology of hyperplastic nodes also usually shows a more mixed cell population than that seen in FALPS cases (with many small lymphocytes and plasma cells, and often neutrophils, eosinophils and macrophages seen, depending on the underlying cause). FALPS should therefore be considered as a potential differential diagnosis in any BSH or BSH-cross kitten (including mixed-breed kittens where the pedigree is unknown) under 5 months of age with enlargement of multiple peripheral lymph nodes.

Genetic basis for FALPS

FALPS is due to a monogenic autosomal recessive mutation in the Fas ligand gene. The mutation responsible for the disease causes a premature stop codon in the gene, leading to a truncated Fas ligand protein which is unlikely to trigger effective lymphocyte apoptosis. Kittens homozygous for the mutation go on to develop FALPS, while heterozygotes are clinically unaffected but carry the mutation and may pass it to their offspring.

What can be done?

Since the genetic mutation underlying FALPS was confirmed in 2016, genetic testing is now available to identify FALPS carrier cats using buccal (cheek) swabs, which are easily collected and submitted by owners or breeders. Blood (EDTA or lithium heparinised) can also be tested, but buccal swabs are generally preferred. Testing is currently available through Massey University in New Zealand as well as through UK-based labs as set out below.

Massey University

Attention: Dr Dani Aberdein School of Veterinary Science – Massey University Tennant Drive Palmerston North 4474 Sample requirements: Buccal swabs email: D.Aberdein@massey.ac.nz Please email before sending samples or for information on collection and sending. If swabs are sent from outside NZ, import documentation must also be attached to the swab package – please email for details. Turnaround: 2-4 weeks Price: $50 + GST

Langford Vets

Diagnostic Laboratories Langford Vets Churchill Building Langford BS40 5DU United Kingdom email: labs@langfordvets.co.uk Sample requirements: Buccal swabs Turnaround: unknown Price: £35.40 (including VAT)

Breeding recommendations

As FALPS appears consistently lethal at a young age and carriers do not show clinical signs, genetic testing prior to mating is recommended for all BSH and BSH-cross cats (which includes the Scottish Fold, Selkirk Rex and Manx breeds). Ideally, cats identified as carriers

should be desexed and not used for breeding. However, where desexing a carrier cat is not immediately practical (e.g. in a cattery with a small number of breeding cats), carriers may still be mated, but should be mated only to confirmed non-carriers (i.e. confirmed by genetic testing). Such matings will not produce FALPS-affected kittens, but may produce further carrier kittens; accordingly, all offspring of these matings should also be tested. These recommendations are also endorsed by the BSH Breed Section of the NZ Cat Fancy. If widely adopted, they should reduce the occurrence of and ultimately eradicate FALPS from the NZ BSH breeding population within a relatively short period of time.

Prevalence of the affected allele and the New Zealand situation

A recent (2017) study published in the NZVJ suggests carriers of the mutant FALPS allele are relatively common in the BSH breeding population in NZ, with 22% of clinically healthy BSH cats across three NZ breeding catteries identified as carriers (heterozygotes) on genetic testing. Two of the three catteries tested had not previously observed cases of FALPS in their breeding cats. However, since that study, many NZ-based BSH breeders have begun to test their breeding cats and have reportedly adopted the breeding recommendations above, which should result in a reduction in the occurrence of FALPS and carrier cats in NZ. The prevalence of the mutant allele in Australian BSHs is currently unknown. However, given the reports of FALPS in Australian BSH kittens since the 1990s, the occurrence of the mutant Fas ligand allele is likely to be similar to that found in NZ. Studies of the frequency of the allele and carrier state in Australian BSH cats are currently in progress. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

CLINICAL UPDATE

Feline immunodeficiency virus in New Zealand: should we test? should we vaccinate? and does it even cause disease? JOHN S MUNDAY, BVSc, PhD, DipACVP, and NICK J CAVE, BVSc, MVSc, PhD,

DipACVN

Feline immunodeficiency virus (FIV) is a retrovirus that was first isolated in 1987 from a group of cats that were suffering from high rates of chronic diseases. Due, at least in part, to its close relationship with human immunodeficiency virus, this new feline virus received intensive research interest. Experimental infection by FIV caused marked lymphocyte depletion and significant immunosuppression and FIV was associated with a multitude of clinical presentations including fever, lethargy, anorexia, emaciation, vomiting, cystitis, diarrhoea, haemopoietic disorders, dermatitis, otitis, lymphadenopathy, stomatitis, neurological disease, ocular disease, abscesses, renal insufficiency/ failure, hepatic disease, and upper respiratory tract infection. Due to the immunosuppression observed in experimentally infected cats, the disease syndrome associated with FIV was designated ‘feline acquired immunodeficiency syndrome (feline AIDS)’ and a vaccine was developed and promoted. While experimental infection is well recognised to cause severe clinical disease, the extent to which natural infection by FIV causes disease is less clear. While a number of diseases were initially associated with infection by FIV, more recent research has frequently reported either weak or no associations between natural FIV infection and Contact: School of Veterinary Science, Massey University. Tel 06 350 4525

disease in cats. The current evidence that natural FIV infection causes disease in cats is now reviewed. Of the clinical diseases that FIV has been associated with, there is possibly the greatest evidence supporting a role of this virus in chronic gingivostomatitis (FCGS) and it has been suggested that as many as a half of cats naturally infected with FIV may develop this disease (Hartmann 2012). However, while associations between FIV and FCGS have been reported in some studies (Ravi et al. 2010; Kornya et al. 2014; Burling et al. 2017), associations have not been consistently detected and no association between FIV and FCGS were reported in studies from the United States, Australia and Germany (Belgard et al. 2010). The lack of a consistent association between FIV and FCGS suggests that, FIV may be one of a number of factors that result in disease. The probability that FCGS is highly multifactorial is supported by the recent evidence that infection by calicivirus and Pasteurella multocida are also associated with FCGS in cats. Although rates of infection of FIV in New Zealand cats are approximately twice as high as rates in cats in the United States of America (USA), there is no evidence of any difference in rates of FCGS between New Zealand and the USA. In a review published in 2012, FIV was reported to be associated with a 5-fold increased risk of B-cell lymphoma in cats. However, as FIV could not be detected in the cancers, the role of FIV in neoplasia development was uncertain (Hartmann 2012). FIV infection has also been associated with cutaneous squamous cell carcinomas (SCC) of cats, although as cats allowed outdoors are at increased risk of both FIV infection and UV-induced SCC, this association was probably

coincidental (Hutson et al. 1991). FIV infection was not associated with any significant increase in neoplasia in studies of cats from Canada and Australia (Ravi et al. 2010; Liem et al. 2013). FIV has also been associated with the development of neurological disease that typically manifests as behavioral changes rather than motor defects (Hartmann 2012). Changes in the behavior of cats may or may not be associated with histological evidence of inflammation. This syndrome is reported to be dependent on the FIV strain and no increased neurological disease was observed in FIV-infected cats in Canada or Australia (Ravi et al. 2010; Liem et al. 2013). While natural infection by FIV can cause a reduction in blood lymphocyte number, whether this causes clinically relevant immunosuppression is less certain (Hartmann 2012). Human immunodeficiency virus was discovered due to a sudden increase in disease caused by infectious agents that had previously thought to be nonpathogenic. In contrast, studies of cats in Australia and Canada found no increased rate of infectious disease in FIV-positive cats (Ravi et al. 2010; Liem et al. 2013). A key observation in human AIDS patients is that the marked immunosuppression reduces efficacy of therapies making secondary infections difficult to treat. Currently there is little evidence that natural infection by FIV changes the response of diseases to appropriate therapy. Due to the differences between human AIDS and the clinical syndromes seen in FIV-infected cats, the appropriateness of the term ‘feline AIDS’ is now controversial (Hartmann 2012). Studies in North America have revealed that cats that are clinically unhealthy are

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

more likely to be FIV-positive (Burling et al. 2017). This finding suggests that FIV does cause disease in cats. In contrast, a study of cats in Australia did not detect any increased rate of FIV infection in unhealthy cats compared to healthy ones (Norris et al. 2007). While the cause of these different results is uncertain, it may be due to differences in the pathogenicity of the strains of FIV in Australia and North America. Interestingly although strains of FIV in North America may be more pathogenic, studies in USA and Canada have not found significant differences in the lifespan of cats infected by FIV compared to non-infected cats (Ravi et al. 2010; Hartmann 2012). As stated by Liem et al. (2013), “assigning clinical relevance to FIV infection in individual cats represents a considerable clinical challenge”. This difficulty is clinically important for two reasons. Firstly, should we test for FIV? Secondly, should we vaccinate against FIV? A diagnostic test should only be done if the result will change some aspect of the treatment for that patient. In the case of testing for FIV, as 5–10% of New Zealand cats are infected by FIV, between 1 in 10 and 1 in 20 of all submitted feline blood samples with be FIV positive. However, detecting FIV infection in a sick cat does not in any way prove that the cat is sick because of FIV. In addition, as there is no evidence that concurrent FIV infection changes the treatment or prognosis of any secondary infection, the detection of FIV cannot be used as a justification to alter normal treatment protocols. As making treatment decisions on the basis

of detecting a common, potentially lowly-pathogenic virus is simply not supported by current scientific evidence it is difficult to imagine a justification for testing a sick cat for FIV in New Zealand. Vaccinating cats against FIV is controversial in two ways. Firstly, if natural infection by FIV doesn’t cause significant disease and does not appear to shorten the lifespan of infected cats, does the benefit of protecting against the virus outweigh any potential risks associated with vaccination? Secondly, a study in Australia revealed that vaccination using the Fel-O-Vax FIV vaccination did not significantly protect against subsequent FIV infection (Westman et al. 2016). As reported in a recently-completely PhD thesis undertaken at Massey University, this vaccine similarly failed to protect against subsequent FIV infection in New Zealand cats. The poor protection against FIV infection in New Zealand may be most likely to be due to the different strains of FIV virus that are common in this country. While each veterinarian and client have their own level of risk they find acceptable, the apparent poor efficacy of the vaccine in New Zealand and the uncertainty regarding the clinical significance of FIV infection are considerations that should be discussed with clients.

References

Belgard S, Truyen U, Thibault JC, Sauter-Louis C, Hartmann K. Relevance of feline calicivirus, feline immunodeficiency virus, feline leukemia virus, feline herpesvirus and Bartonella henselae in cats with chronic gingivostomatitis. Berl Munch Tierarztl

Wochenschr 123, 369–76, 2010 Burling AN, Levy JK, Scott HM, Crandall MM, Tucker SJ, Wood EG, Foster JD. Seroprevalences of feline leukemia virus and feline immunodeficiency virus infection in cats in the United States and Canada and risk factors for seropositivity. Journal of the American Veterinary Medical Association 251, 187–94, 2017 Hartmann K. Clinical aspects of feline retroviruses: a review. Viruses 4, 2684–710, 2012 Hutson CA, Rideout BA, Pedersen NC. Neoplasia associated with feline immunodeficiency virus infection in cats of southern California. Journal of the American Veterinary Medical Association 199, 1357–62, 1991 Kornya MR, Little SE, Scherk MA, Sears WC, Bienzle D. Association between oral health status and retrovirus test results in cats. Journal of the American Veterinary Medical Association 245, 916–22, 2014 Liem BP, Dhand NK, Pepper AE, Barrs VR, Beatty JA. Clinical findings and survival in cats naturally infected with feline immunodeficiency virus. Journal of Veterinary Internal Medicine 27, 798–805, 2013 Norris JM, Bell ET, Hales L, Toribio JA, White JD, Wigney DI, Baral RM, Malik R. Prevalence of feline immunodeficiency virus infection in domesticated and feral cats in eastern Australia. Journal of Feline Medicine and Surgery 9, 300–8, 2007 Ravi M, Wobeser GA, Taylor SM, Jackson ML. Naturally acquired feline immunodeficiency virus (FIV) infection in cats from western Canada: prevalence, disease associations, and survival analysis. The Canadian Veterinary Journal 51, 271–6, 2010 Westman ME, Malik R, Hall E, Harris M, Norris JM. The protective rate of the feline immunodeficiency virus vaccine: an Australian field study. Vaccine 34, 4752–8, 2016 l

Source: pixabay/com

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

FEATURE ARTICLE

Feline idiopathic hypercalcemia

This article was written as part of the requirements for receiving the RxVet/CAV A Week With….Scholarship

SUSAN MURRAY, BVSc, Companion Animal

Veterinarian

Introduction

Hypercalcemia is defined as elevated calcium levels in the blood, and develops when entry of calcium into the extracellular fluid overwhelms the mechanisms that maintain a normocalcemic state. Significant hypercalcemia has negative effects on a variety of organ systems, most notably the renal, gastrointestinal and neuromuscular systems. These effects can cause symptoms including but not limited, to weakness, muscle twitching, seizures, exercise intolerance, muscle wasting, lethargy, vomiting, diarrhoea, constipation, inappetance, polyuria/ polydipsia, haematuria and stranguria. There are many causes of hypercalcemia in cats (see Table 1). The most common diagnoses in cats with persistent elevations in ionised calcium (iCa) are idiopathic and malignancy, followed by chronic kidney disease (CKD). The syndrome of idiopathic hypercalcemia (IHC) in cats has emerged over the last two decades and appears to be increasing in frequency. The cause of IHC remains elusive. Table 1: HARDIONS-G acronym for differential diagnoses for hypercalcemia in cats. (De Brito Galvao et al. 2014) H: Hyperparathyroidism, houseplants, hyperthyroidism A: Addison’s disease, aluminium toxicity, vitamin A toxicity R: Renal disease D: Vitamin D toxicosis, drugs (psoriasis cream, vitamin D-based creams, cholecalciferol rodenticide) dehydration, DMSO I: Idiopathic, infectious, inflammatory O: Osteolytic, osteomyelitis, bone infarct, diagnoses N: Neoplasia, nutritional G: Granulomatous disease

If a persistent increase in total calcium (tCa) is detected in a cat, iCa concentrations should be measured as this is the biologically active form of calcium. This can be performed on an in-house analyser, such as an i-STAT or VetStat, or blood can be sent to a commercial veterinary pathology laboratory. Samples sent to the latter must immediately be put into a redtop serum tube anaerobically, then spun down, and sent chilled but not frozen. Prediction of iCa from the tCa measurement is not accurate, especially when there is concurrent chronic kidney disease. Contact: Matamata Veterinary Services, 26 Tainui Street, Matamata

History and physical exam may raise suspicion of a particular cause for the hypercalcaemia but confirmation requires further testing. The magnitude of elevation of tCa concentration in serum cannot be used to make a diagnosis of the underlying cause. Patients with malignancy-associated hypercalcemia are usually systemically unwell, since it takes a reasonably large tumour burden to produce enough parathyroid hormonerelated peptide (PTHrP) to cause hypercalcemia. The less sick the cat presents, the more likely it is to be IHC. In cases of vitamin D toxicosis, measurement of concentrations of 25 (OH) vitamin D3 and 1,25 (OH)2 vitamin D3 in serum is recommended to secure a diagnosis. Imaging can help detect neoplasia/granuloma as an underlying cause of hypercalcaemia but ideally concentrations of parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) in serum should be measured as well. Currently these two tests are not available in New Zealand, and are very costly as the serum samples must be frozen and shipped on dry ice to the USA. A diagnosis of idiopathic hypercalcaemia can be made when all other causes of hypercalcaemia are excluded. Often cats with IHC are asymptomatic or have mild signs at diagnosis. They can range in age from <1–20 years and there is no obvious sex predilection. In one study of 427 cats, the mean age for presentation was 9.8 years, long-haired cats were over represented, both genders were equally represented, almost half the cats had no clinical signs, and 18% had mild weight loss (Schenk 2004). Some cats with IHC develop CKD due to persistent hypercalcemia, and cats with CKD may develop IHC over time. Treatment of hypercalcemia usually targets the dysregulated mechanism that is responsible for the elevated concentration of calcium in serum (e.g. surgery for primary hyperparathyroidism), however in IHC, as the mechanism is unknown, treatment is symptomatic. When monitoring therapy for IHC, it is important to measure iCa. Excess calcium is toxic to cells, particularly the central nervous system, gastrointestinal tract, heart and kidneys, and mineralisation of soft tissues is a common complication. The need for treatment in cases of IHC increases as the concentrations of iCa increase or clinical signs become obvious. Ongoing hypercalcemia can be lethal in those that develop CKD or urolithiasis and aggressive treatment in these cases is necessary. Treatment of IHC depends on the severity of the hypercalcaemia (in terms of iCa concentration), the degree of clinical signs, biochemical alterations and urinary parameters including the presence of uroliths (see Table 2). Treatment options include fluid therapy, diet, and medication with bisphosphonates and glucocorticosteriods. Uncommonly, severe hypercalcemia necessitates emergency supportive care

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

including fluid therapy, along with treatment to support renal and/or cardiac function. Table 2: Treatment plan for cats with idiopathic hypercalcemia with no/mild clinical signs. Modified from De Brito Galvao et al. 2014. Ionised Ca concentration

Clinical signs

Treatment recommendation

<0.25mmol/L above the upper reference range

No evidence of calcium toxicitya

monitor iCa concentration every 1–3 months

<0.25mmol/L above the upper reference range

Evidence of calcium toxicitya

Nutritional management

>0.25mmol/L above the upper reference range

Nutrition, fluids and medical management

a Evidence of calcium toxicity includes increased BUN, creatinine and/or phosphorus, decreased USG or urinary stones, or gastrointestinal signs such as constipation, weight loss, vomiting.

Diet is one of the most important tools for managing IHC. Normocalcemia may be restored after a change to an appropriate diet, and is a good option if the patient is clinically stable and iCa elevation is mild. Diets designed to reduce formation of calcium oxalate stones (e.g. Royal Canin Urinary S/O, Hills c/d Multicare) are restricted in calcium, promote less urinary acidification, and some are restricted in oxalic acid. High-fibre diets (e.g. Royal Canin Satiety, Hills r/d and w/d) have been reported to restore normocalcaemia in some cats (McClain et al. 1995) but other studies showed no beneficial effect (Midkiff et al. 2000) of increasing dietary fibre. Diets for treatment of renal disease have low calcium and phosphorus concentrations but the low phosphorus can enhance renal calcitrol synthesis and exacerbate hypercalcaemia and so are not recommended. If the elevation in iCa concentration is moderate to severe, or if a diet change is not successful after a trial of 6–8 weeks, then treatment with a bisphosphonate can be considered. These drugs reduce the activity and number of osteoclasts breaking down bone. Adequate hydration is important for cats being treated with bisphosphonates because these drugs may be nephrotoxic especially at higher doses, and bone necrosis has also been reported. Erosive oesophagitis is known to occur in humans taking bisphosphonates (Mohn et al. 2009), however the risk of development of oesophagitis in cats appears to be low. To be safe, butter may be applied to the cat’s lips to increase licking and salivation and then follow the dose with 5–6 mls of water. The starting dose for bisphosphonates is 10 mg/cat weekly, given orally. To maximise intestinal absorption, bisphosphonates should be given after a 12-hour over-night fast followed by a further 2 hours of fasting. iCa concentrations should be rechecked after 3–4 weeks of treatment and the dose rate increased if necessary by 10 mg increments every 3–4 weeks. If 30 mg/cat per week is insufficient to reduce iCa concentration to within the reference range, then prior to adding other medications, it is recommended to recheck the diagnosis of IHC by repeating testing of serum concentrations of PTH, PTHrP, and 25-hydroxyvitamin D, chest radiographs and abdominal ultrasound (with aspirates of liver and spleen to rule out mast cell disease and lymphoma).

Treatment with glucocorticosteriods may be considered when bisphosphonate therapy has not restored normocalcaemia. They are thought to decrease serum calcium concentrations by decreasing intestinal and renal tubular calcium absorption and mobilisation of calcium from the skeleton. Prednisolone may be given orally at a dose of 5 mg/cat/day for a month before reevaluation and this dose increased after evaluation by 5 mg increments monthly as needed. Some cats need as much as 15–20 mg to restore normocalcaemia, however 50% of cats will become normocalcaemic with 5–10mg prednisone daily. Other treatment regimes include promoting calciuresis with fluid therapy and diuretics. Potential future treatment options include calcimimetics such as cinacalcet, however the author is unaware of any published studies using these in the management of hypercalcaemia in cats.

Case study

A 2-year-old female spayed Persian cat was first presented to Catmed referral service in June 2017 for investigation of hypercalcemia. She was an indoor cat living with one other healthy cat. She was a fussy eater and was fed Royal Canin Persian dry food with other wet food. She had initially presented to the referring veterinarian with chronic weight loss and intermittent vomiting (clear fluid or bile on average weekly). A serum biochemistry panel taken by the referring veterinarian had shown a persistent increase in tCa and increased iCa concentrations.

Initial clinical evaluation

On physical examination, she was noted to have marked brachycephalism, bilateral mild chemosis and mucoid discharge at her medial canthus, with a normal retinal exam. Her heart rate was 140 beats/minute, respiratory rate was 102 breaths/ minute, blood pressure was 120 mmHg and temperature 38.7°C. The blood pressure and heart rate were noted to be low considering she was a nervous cat. She weighed 3.15 kg and had a body condition score of 4/9. A neurological exam was normal. Her submandibular lymph nodes or salivary glands were mildly increased in size, but otherwise there was no palpable lymphadenomegaly. Abdominal palpation was unremarkable.

Further diagnostic testing

The cat was admitted for blood tests and imaging. A venous blood sample was obtained by jugular venepuncture for serum biochemistry (Table 3) and a urine sample by cystocentesis for urinalysis (Table 4). Due to her relatively low blood pressure and slow heart rate, a cardiac ultrasound and electrocardiogram was undertaken. However, the findings of these tests were unremarkable. An I/V catheter was placed, fluid therapy was initiated with 0.9% saline at 12 mL/hour to provide cardiovascular support and the cat was anaesthetised. A 3-view radiographic study of the thorax and abdomen ("catogram") showed no evidence of pulmonary masses or bone lysis. Similarly abdominal and ventral cervical ultrasound were unremarkable (i.e. no evidence of masses or parathyroid enlargement). Fine needle aspirates were taken from the submandibular lymph nodes/salivary gland, liver and spleen to rule out mast cell tumour or lymphoma. All were unremarkable.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Table 3. Serum biochemistry results for samples taken on day 1 from a 2-year-old Persian cat under investigation for hypercalcemia. Analytea

Resultb

Reference range

Packed cell volume

26–45%

Total protein

54–82 g/L

160

150–165 mmol/L

3.8

3.5–5.8 mmol/L

125

112–129 mmol/L

Albumin

22–44 g/L

Alkaline phosphatase

10–90 U/L

Alanine aminotransferase

20–100 U/L

Amylase

473

300–1100 U/L

Bilirubin

2–10 μmol/L

Urea

8.3

3.6–10.7 mmol/L

Ca (total)

3.35

2–2.95 mmol/L

Phosphate

1.21

1.10–2.74 mmol/L

Creatinine

27–186 μmol/L

Glucose

5.2

3.9–8.3 mmol/L

Globulin

15–57 g/L

7.353

7.2–7.4

Total CO2 c

Na c

151

150–165 mmol/L

3.6

3.5–5.8 mmol/L

Ionised calcium c

1.72

1.2–1.32 mmol/L

Creatine kinase d

203

0-344 IU/L 37C

Phosphate d

1.33

1.30–2.80mmol/L

Ca (total)

3.07

25 Vitamin D c

Requested

16–25 mmol/L

1.81–2.70mmol/L Pending

a Analytes were measured on an in-house VetScan blood analyser except where indicated by footnotes. b Results shown in red text are greater than the reference range for that parameter c These parameters were measured on in-house i-STAT blood analyser d These results were provided by New Zealand Veterinary Pathology.

Table 4. Urinalysis results for urine sample from Persian cat with hypercalcemia Analyte

Result

Urine specific gravity pH

1.045 7

Protein

Blood

Red blood cells

1–5

White blood cells

None

Crystals

None

Epithelial cells

Bacteria

None

Urine protein:creatinine ratioa

0.25

Non-proteinuric ≤0.2; borderline ≥0.2 – <0.4; proteinuric ≥0.4

Serum biochemistry results showed that both iCa and tCa concentrations were higher than the reference range confirming that the cat was hypercalcaemic. The most common cause of hypercalcaemia in cats is idiopathic. However, to reach this diagnosis, all other causes for hypercalcaemia must be excluded. Imaging, including radiography and ultrasonographic examination of the neck and abdomen, and fine needle aspirates of lymph nodes liver 32

and spleen, did not show any evidence of neoplasia. Serum biochemistry and urine testing indicated normal renal function. There was no know access to vitamin D toxin, and measurement of serum vitamin D concentration was pending and expected to take up to 2 weeks for a result. Testing for PTH and PTHrP was discussed with the owner. However as this costs in excess of $1000 the owner declined to pay for this testing.

Management

To supporting recovery from general anaesthesia and to promote calciuresis, I/V saline (0.9%) was continued at 12 mL/hour until the cat was discharged that afternoon. Saline was selected as the I/V fluid as it does not contain calcium. Instructions were given to begin feeding a controlled-calcium diet (Hill’s Prescription Diet Feline c/d Multicare; Hill’s Pet Nutrition). The cat was returned to the referring clinic daily for the next 4 days to allow administration of 100 mL 0.9% NaCl S/C to promote calciuriesis. Six days after the initial visit, the cat was re-admitted to Catmed. Her cardinal signs were normal, weight was stable and physical examination was unremarkable. She was given her daily SC bolus of 0.9% saline and blood and urine samples were taken so that measurement of iCa and urinalysis could be repeated. The iCa concentration remained elevated at 1.75 (reference range 1.2–1.32) mmol/L. Urinalysis showed a urine specific gravity of 1.044, and trace protein. Given the signalment and diagnostic results, IHC was considered the most likely cause of this cat’s hypercalcaemia. As the iCa concentration was markedly high and hadn’t decreased with diet and fluid therapy, it was elected to start treatment, with alendronate (Fosamax; Merck Sharp & Dohme) a bisphosphonate, at 10 mg/cat orally once weekly. Subcutaneous fluid therapy was reduced to alternate day treatment for three further treatments given at the referring veterinary clinic. The purpose of this treatment was to promote calciuresis but also to ensure hydration, as alendronate can be nephrotoxic. The controlled-calcium diet was continued.

Follow-up care

One month after discharge the cat was eating well and vomiting less frequently. Physical examination was unremarkable and her weight had increased by 300 grams to 3.46 kg. Urinalysis showed that UPCR was within normal range indicating that the mild proteinuria had resolved. The results of the vitamin D testing were received which were within normal limits at 75 nmol/L (reference rang 57.2–207 nmol/L) ruling out vitamin D toxicosis. The cat’s iCa concentration was markedly reduced though still mildly elevated at 1.35 (reference range: 1.2–1.32) mmol/L. The excellent response to Fosamax and the weight gain further supported a diagnosis of idiopathic hypercalcaemia. The owner was advised to monitor the vomiting and continue feeding c/d Multicare biscuits and treating with 10 mg Fosamax weekly. At a recheck 7 weeks later, the cat was bright and responsive, her physical exam was unremarkable, and she had gained a further 100 g of weight. Her iCa concentration was somewhat increased on the last measurement at 1.41 mmol/L so her dose of Fosamax was increased to 20 mg weekly. After another 5 weeks, the owner reported that she was only vomiting occasionally and the vomit was consistent with furballs. Physical examination was again unremarkable. However, she had lost 100 g of weight and her iCa concentration was still elevated at 1.4 mmol/L so her dose of Fosamax was again increased to 30 mg PO weekly (this is the maximum dose). The owner was advised that the cat should

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

be assessed again in another month and if the iCa concentration did not reduce then repeating the diagnostic testing and starting treatment prednisolone could be considered.

Discussion

The typical presentation of hypercalcaemia in cats is a long-haired cat with a non-specific illness, mild weight loss and vomiting, as was seen with the cat described here. As the iCa concentration was more than 0.25 mmol/L above the top of the reference range, it was recommended to start Fosamax early in the course of management rather than waiting to see if diet alone would decrease calcium concentrations. In this case not all differential diagnoses for the underlying cause of the hypercalcaemia had been ruled out, as the PTH and PTHrP testing had not been undertaken due to costs. However the cat’s signalment and lack of evidence for diseases causing hypercalcaemia on imaging and routine blood testing made a working diagnosis of idiopathic hypercalcaemia reasonable.

In summary, hypercalcaemia in cats can present in many different ways and may be an incidental finding well worth investigating. The work up and management can be very rewarding and increase quality and quantity of life.

Acknowledgements

Thanks especially to Pru Galloway for allowing me to spend the week with her, and Pet Vet Lower Hutt for allowing the scholarship to be undertaken in their practice. Thanks also to RxVet for support of the RxVet/CAV A Week With….scholarship.

Selected references and recommended reading

De Brito Galvao JF, Chew DJ, Schenck PA. Feline idiopathic hypercalcemia. In: Bonagura JD, Twedt DE (Eds.). Kirks Current Veterinary Therapy XV. Pp. 242–8. Elsevier Saunders, St Louis, MO, USA, 2014 Feldman EC. Disorders of the parathyroid glands. In: Ettinger SJ, Feldman EC (Eds). Textbook of Veterinary Internal Medicine (7th Edtn). Pp. 1722–51, Saunders Elsevier, St Louis, MO, USA, 2010

Finch NC. Hypercalcaemia in cats: the complexities of calcium regulation and associated clinical challenges. Journal of Feline Medicine and Surgery 18, 387–99, 2016 McClain HM, Barsanti JA, Bartges JW. Hypercalcemia and calcium oxalate urolithiasis in cats: a report of five cases. Journal of the American Animal Hospital Association 35, 297–301, 1995 Midkiff AM, Chew DJ, Randolph JF, Center SA, DiBartola SP. Idiopathic hypercalcemia in cats. Journal of Veterinary Internal Medicine, 14, 619–26, 2000 Mohn KL, Jacks TM, Schleim KD, Harvey CE, Miller B, Halley B, Feeney WP, Hill SL, Hickey G. Alendronate binds to tooth root surfaces and inhibits progression of feline tooth resorption: a pilot proof-of-concept study. Journal of Veterinary Dentistry 26, 74–81, 2009 Savary KC, Price GS, Vaden SL. Hypercalcaemia in cats: a retrospective study of 71 cases (1991–1997). Journal of Veterinary Internal Medicine 14, 184–9, 2000 Schenck PA. Calcium metabolic hormones in feline idiopathic hypercalcemia. Journal of Veterinary Internal Medicine 18, 442, 2004 Schneck PA, Chew DJ. Idiopathic hypercalcemia in cats. Waltham Focus 15, 20–4, 2005 l

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 2 | June 2018

FEATURE ARTICLE

Leptospirosis in dogs: an emerging problem? JANICE THOMPSON, BVSc

(Dist), PhD, Clinical Pathologist

Leptospira and their hosts in New Zealand

Leptospires include a very large number of organisms. Traditionally the genus Leptospira was divided into L. interrogans that included over 200 pathogenic serovars, and L. biflexa that included 60 saprophytic nonpathogenic environmental organisms. Using this division, the serovars were defined by agglutination after crossabsorption with homologous antigen. Additional serovars have also been isolated but have yet to be named (Levett 2001). There is now another more complicated system for classifying leptospires in which the species are divided into genomospecies based on DNA hybridisation. There is also further system that combines the different serotypes with the genomospecies classification. In addition, there are also multiple strains of some serovars (Levett 2001). Much more recently sequencing of the 16S rRNA gene has given yet another more complicated method of

identifying Leptospira species. In this system Leptospires may be categorised as pathogenic, intermediate, nonpathogenic and “other” (Morey et al. 2006). Historically the Copenhageni serovar has usually been considered the most important serovar that causes leptospirosis in New Zealand dogs, following contact with infected rats. The early reviews of canine leptospiral infections dealt almost exclusively with Copenhageni (Ellison and Hilbink 1990). This resulted from epidemiological work done in the 1970’s and1980’s where surveys were carried out on possible vectors (Hathaway 1981; Marshall and Manktelow 2002). Infected animals may be either maintenance hosts or accidental hosts for the infective serovar. This original epidemiological work identified the ship rat (Rattus rattus), mice (Mus musculus) and hedgehogs (Erinaceus europaeus) as maintenance hosts for Ballum and Norway rats (R. norvegicus) as maintenance hosts for Copenhageni and Ballum depending the geographical location of the rats. In the Waikato and Auckland regions, Norway rats

were identified as being infected with Copenhageni and in the southern parts of the North Island Norway rats were identified as infected with Ballum. Cattle are maintenance hosts for Hardjo and pigs are maintenance hosts for Pomona and Tarassovi (Hathaway 1981). So dogs in the northern regions of the North Island that came into contact with rats may have become infected with Copenhageni and it was rarely diagnosed elsewhere (Ellison and Hillbink, 1990). In addition to the more commonly discussed serovars, there is an additional serovar, Balcanica, in which the maintenance host is the possum (Trichosurus vulpecula) and more than 80% of adult possums were reportedly infected (Hathaway, 1981). Theoretically animals coming into contact with possums in some bush habitats, for example huts in the bush, may therefore also become infected with Balcanica. However routine testing for Balcanica is not carried out in diagnostic laboratories. Balcanica has reportedly been isolated from humans, cattle and pigs in Eastern Europe although there is a suggestion that it may cross react with Hardjo (Hathaway, 1981). Experimental

Take-home message 1. In New Zealand, dogs are susceptible to leptospiral serovars Copenhageni, Pomona, and Hardjo and Tarassovi. 2. Dogs are infected as a result of contact with livestock and/or rodents. 3. Infection may be more common in wet warm conditions. 4. The current canine vaccine is designed for protection against Copenhageni and there is no information regarding crossprotection against the other serovars. 5. Serological testing against all serovars is required to make a definite diagnosis because non-specific titres due to crossreaction with non-infective serovars are common. Unless all serovars are tested, the actual infective serovar may be missed. 6. Dogs that are azotaemic and/or have hepatobiliary disease may be infected with leptospirosis, particularly if they are residing in farming environments. 7. If a low serological titre is obtained initially then a second sample 7–10 days later is needed to make a diagnosis.

Contact: Gribbles Veterinary, Palmerston North, Phone: 063567000; Email: janice.thompson@gribbles.co.nz

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

et al. (2013) surveyed a wide range of dogs and tested for serovars Pomona, Hardjo, Copenhageni and Ballum, but not Tarassovi. O’Keefe et al. (2002) tested for Hardjo, Pomona, Copenhageni, Grippotyphosa but not Canicola and Tarassovi. These surveys included serology on apparently normal dogs (O’Keefe 2002) and blood sourced from dogs at the Massey University Teaching Hospital plus submissions to New Zealand Veterinary Pathology (Harland et al. 2013). Serology to Canicola and Grippotyphosa was negative in all dogs. O’Keefe et al. did not test for Ballum and Harland et al. found a small number of dogs with titres to Ballum, and that the titres to Ballum were much lower than titres for other serovars. In these surveys, positive titres to Hardjo, Pomona and Copenhageni were found, with titres to Hardjo being more prevalent among those breeds used as working dogs compared to other dog breeds. Cases of leptospirosis caused by Pomona have also been described in dogs in New Zealand (Thompson 2012; Thompson and Taylor 2015). There is also a report of combined Tarassovi and Pomona infection in a pack of hounds in South Auckland (Mackintosh et al. 1980).

Figure 1. Transmission electron micrographs of leptospires within renal tissue. (A) A leptospire (L) within the proximal convoluted tubule of a calf, 14 days after infection with Pomona (x22,500). The microvilli appear normal. (B) A leptospire in oedema fluid (Oe) migrating between renal tubular epithelial cells in the kidney (x25,000). From Thompson 1984.

work in sheep and cattle suggested that Balcanica is unlikely to be spread via these species although sporadic infection may occur (Mackintosh et al. 1981). Dogs are considered accidental hosts for the pathogenic serovars of leptospire present in New Zealand and infection depends on contact with a maintenance host excreting leptospires usually via the urine. In maintenance hosts,

leptospiruria tends to persist for long periods or even a lifetime. It is thought that localisation of leptospires in the proximal convoluted tubules of the kidneys of maintenance hosts (Figure 1) gives some protection from humoral immunity, thus prolonging survival of the bacteria (Marshall and Manktelow 2002; Hathaway 1981). More recent serological surveys tested dogs throughout New Zealand. Harland

In recent months, leptospirosis in livestock in New Zealand has been the subject of several articles that discussed the serovars identified, the increasing incidence of the Tarassovi serovar in cattle (Heuer et al. 2017) and an increasing incidence of leptospirosis within meat workers. There is a very general informal discussion of Pomona and Hardjo but not of Tarassovi (Littlewood 2017; Philps 2017). In the past, Tarassovi has been associated with pigs rather than cattle, and pigs have been regarded as the maintenance host (Hathaway 1981). Recently there has also been anecdotal discussion by various epidemiologists about increased numbers of human leptospirosis cases over the wet winter months. Dogs on farms work in the same environmental conditions as their human owners and are likely to have greater exposure, via conjunctiva, mucus membranes and skin abrasions (Sykes et al. 2011) with urine and puddles of contaminated water without the benefit of protective gear. Thus conditions causing increased incidence of human leptospirosis are also likely to cause leptospirosis in dogs.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Diagnosis of leptospirosis

Consensus statements on leptospirosis have been formulated for North America and Europe (Sykes et al. 2011; Schuller et al. 2015). While overseas data may be useful, it should also be noted that these countries have a different range of leptospiral serovars present compared to New Zealand. Serovars reported in Germany include Icterohaemorrhagiae, Canicola, Gryppotyphosa, Bratislava and Saxkoebing (Geisen et al. 2007). In North America serovars reported include Grippotyphosa, Icterohaemorrhagiae, Pomona, Autumnalis and Bratislava; with only one reported instance of dog with titre to Hardjo (Birnbaum et al. 1998; Tangeman and Littman 2013). Clinical syndromes reported overseas include renal and hepatic disease, DIC, pulmonary syndromes, bleeding tendencies, uveitis and occasionally pancreatitis and abortions (Sykes et al. 2011). It cannot be assumed that the epidemiology and clinical syndromes seen in New Zealand are the same as those seen overseas due to differences in serovars, maintenance hosts and environmental conditions. Environmental conditions include factors affecting the density of the maintenance hosts, which determine the amount environmental contamination, plus the likelihood of infection cycling within the maintenance host population. Environmental conditions also include factors such as the amount of moisture/ humidity and the temperature as these affect the survival of the organisms in the environment and hence the likelihood of an accidental host becoming infected. Thus when considering the epidemiology of leptospirosis, all factors such as whether the infected animal is an accidental host or a maintenance host, and its ecology, plus the environment must be understood in order to understand the spread of a specific serovar. It is important to note that because different leptospiral serovars have antigens in common, positive serology may be obtained to both the infective serovar and also to other non-infective serovars. Titres obtained from a single antibody/serology test may not be to the infective serovar. In early stages of infection, the non-specific titres caused by cross-reactivity may be higher than that of the infective serovar and it is only on repeat testing that the infective 38

serovar is identified by a significantly higher titre (Miller et al. 2011; Thompson and Taylor 2015). Furthermore, unless titres to a range of leptospiral serovars are measured, the infective serovar may be completely missed. Cross-reactions to non-vaccinal serovars may also occur and higher titres may be seen if the dog has ongoing exposure to field strains of Leptospira following vaccination (Sykes et al. 2011). Leptospiral vaccines available in New Zealand cover a limited range of serovars. The Copenhageni serovar has traditionally been regarded the most important cause of leptospirosis in dogs in New Zealand (Ellison and Hillbink, 1990) and the vaccines registered for use in dogs in New Zealand contain the serovar Icterohaemorrhagiae for protection against Copenhageni. There is no information on cross-protection for dogs against leptospiral serovars other than Icterohaemorrhagiae and Copenhageni (vaccine product information for Nobivac Lepto 1, MSD Animal Health; Leptoguard, Zoetis NZ). Tarassovi is not included in the 3-way leptospirosis vaccine for cattle in NZ (vaccine product information; Virbac NZ) so vaccinated cattle may theoretically become infected and excrete Tarassovi. Dogs are susceptible to leptospirosis and where azotaemia and/or hepatobiliary disease are seen, particularly in dogs in contact with farmed livestock and rodents, leptospirosis should be considered as a likely differential diagnosis. Dogs from rural environments exposed to livestock may be infected with either Pomona, Hardjo or Tarassovi. Outbreaks in dogs overseas have been associated with warm temperatures, slow moving and stagnant water and following periods of higher rainfall (Sykes et al. 2011). Anecdotally the winter of 2017 in New Zealand was warmer and wetter than usual, and it was interesting to note that when the weather became much drier, and associated with droughtlike conditions, the numbers of dogs with suspected leptospirosis decreased markedly. When considering a potential case of leptospirosis, in order to make an accurate diagnosis, all potential infective serovars must be considered. Livestock in New Zealand may be infected with Pomona, Hardjo and now Tarassovi, and in dogs exposed to livestock, these serovars should be considered in addition to Copenhageni. If practitioners

try to select one serovar to test and do not test the others, then it is possible any titre obtained may be a nonspecific titre due to cross-reaction with a non-infective serovar and the infective serovar may be completely missed. The importance of considering all serovars has been well demonstrated in a clinical case in which an infected dog was monitored. Initially this dog was PCR-positive and then, once antibody developed, became PCR-negative. The first serological responses consisted of relatively low titres to Hardjo and Copenhageni and Pomona. However with further monitoring, over 10 days, serological responses to Hardjo and Copenhageni remained relatively very low while the Pomona titre eventually became extremely high (Thompson and Taylor 2015). Non-specific cross-reactions to nonvaccinal serovars may also occur. Here, where antibody was measured in vaccinated dogs, non-specific antibody titres were seen to serovars not present within the vaccine, similar to those seen in the infected dog described above (Thompson and Taylor 2015). Higher titres to the vaccinal serovars may be seen if there is ongoing exposure to field strains following vaccination (Sykes et al. 2011). Tarassovi was added to the canine leptospirosis panel because of the possible exposure of dogs to infected cattle and the likelihood of measurement of non-infective titres to any serovar. Where low titres are measured it is necessary to repeat the serology in 10–14 days in order to make a definite diagnosis. It is also important to understand the timelines around infection and the development of antibody. Infection is followed by an incubation period then development of clinical signs. The animal will be leptospiraemic and leptospiruric until antibody develops (Levett 2001). In accidental hosts, once antibody develops leptospires are cleared first from the blood and then later from the kidney. Hence early in infection, animals with leptospiral infection are serologically negative but positive to PCR-based tests that detect leptospiral DNA. Exact times for the development of antibody are variable and depend on infective dose, and individual animal susceptibility. Both serology and PCR testing may be needed to make a diagnosis (Thompson and Taylor 2015). Identification of the

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

actual serovar requires serology. The PCR test used by Gribbles Veterinary identifies “pathogenic” leptospires (i.e. the serovars of leptospires that are known to cause disease rather than those that do not cause disease) but does not identify the specific serovar. There are species-specific identification techniques using the 16S rRNA gene sequencing that can identify specific Leptospira species (Morey et al. 2006) which can be accessed if considered necessary. Culture of leptospires is not routinely used for diagnosis of clinical cases, as this requires special media, and leptospires are difficult and slow to grow (Sykes et al. 2011). Please see VetScript, pages 44–46, April 2018, for a discussion of canine leptospirosis cases received at Gribbles Veterinary Palmerston North during August and September 2017, including the serovars found to be causing infection.

References

Ellison RS, Hilbink F. Leptospiral infections in New Zealand dogs. Surveillance 17 (2), 15–6, 1990 Geison V, Stengel C, Brem S, Muller W, Greene C, Hartman K. Canine leptospirosis infections – clinical signs and outcome with different suspected Leptospira serogroups (42 cases). Journal of Small Animal Practice 48, 324–8, 2007

Harland AL, Cave NJ, Jones BR, Benshop J, Donald JJ, Midwinter AC, Squires RA, Collins-Emerson JM. A serological survey of leptospiral antibodies in dogs in New Zealand. New Zealand Veterinary Journal 61, 98–106, 2013 Hathaway SC. Leptospirosis in New Zealand: An ecological view. New Zealand Veterinary Journal 29, 109–12, 1981 Heuer C, Yupiana Y, Collins-Emerson J, Benshop J, Weston J, Wilkinson D, Vallee, E, Wilson P, Marchant R. Leptospira shedding in dairy herd: new findings. VetScript 30 (5), 44–6, 2017 Levett P. Leptospirosis. Clinical Microbiology Reviews 14, 296–326, 2001 Littlewood K. IVABS Research update. Leptospirosis in New Zealand: an international perspective. VetScript 30 (9), 12, 2017 Mackintosh CG, Blackmore DK, Marshall RB. Isolation of Leptospira interrogans serovars tarassovi and pomona from dogs. New Zealand Veterinary Journal 28, 100, 1980 Mackintosh CG, Marshall RB, Thompson JC. Experimental infection of sheep and cattle with Leptospira interrogans serovar balcanica. New Zealand Veterinary Journal 29, 15–19, 1981 Marshall RB, Manktelow BW. Fifty years of leptospirosis research in New Zealand: a perspective. New Zealand Veterinary Journal 50, 61–3, 2002 Miller MD, Annis KM, Lappin MR, Lunn KF. Variability in results of the microscopic agglutination test in dogs with clinical leptospirosis and dogs vaccinated against leptospirosis. Journal of Veterinary Internal Medicine 25, 426–32, 2011

Morey RE, Galloway RL, Bragg SL, Steigerwalt AG, Mayer LW, Levett PN. Species-specific identification of Leptospiraceae by 16S rRNA gene sequencing. Journal of Clinical Microbiology 44, 3510–6, 2006 O’Keefe JS, Jenner JA, Sandifer NC, Antony A, Williamson NB. A serosurvey for antibodies to Leptospira in dogs in the lower North island of New Zealand. New Zealand Veterinary Journal 50, 23–5, 2002 Philp M. Leptospirosis: time for a rethink. (A shadow on the slaughter board). VetScript 30 (6), 28–32, 2017 Schuller S, Francey T, Hartmann K, Hugonnard M, Kohn B, Nally JE, Sykes J. European consensus statement on leptospirosis in cats and dogs. Journal of Small Animal Practice 56, 159–79, 2015 Sykes JE, Hartmann K, Lunn KF, Moore GE, Stoddard RA, Goldstein RE. ACVIM Consensus statement on leptospirosis: diagnosis, epidemiology, treatment and prevention. Journal of Veterinary Internal Medicine 25, 1–13, 2011 Tangeman LE, Littman MP. Clinicopathologic and atypical features of naturally occurring leptospirosis in dogs: 51 cases (2000–2010). Journal of the American Veterinary Medical Association 243, 1316–22, 2013 Thompson J. Leptospirosis: Pathogenesis and RBC destruction. PhD thesis, Massey University, Palmerston North, 1983 Thompson J. Leptospirosis in dogs in New Zealand. VetScript 25 (6), 8–11, 2012 Thompson J, Taylor D. Diagnosis of leptospirosis in dogs. VetScript 28 (3), 18–20, 2015 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.

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

CONFERENCE REPORT

Highlights from the course in Veterinary Ophthalmology II at the European School for Advanced Veterinary Studies (ESAVS): Part I Toulouse, France, 26–30 June 2017 This article was written as part of the requirements for receiving the Hill’s Pet Nutrition/CAV Educating the Educators Grant

JOS VAN HEES, BVSc

(Hons), MANZCVS, Special interest veterinary practitioner in ophthalmology. I was fortunate to be awarded a Hill’s Pet Nutrition/CAV Educating the Educators Scholarship to assist in attending the ESAVS Ophthalmology II course in Toulouse, France. This week-long course, held at the National Veterinary School of Toulouse (Figure 1), focused on ophthalmology surgery with over 50% of the time spent in wet labs practising eyelid, corneal and lens surgery and the remainder of the time spent in lectures. The attendees were mainly from Europe and I was the only attendee from ‘downunder’. Fortunately, the lectures were in English – albeit with a few French words thrown in. The following is notes on a selection of topics relevant to small animal veterinarians that were covered in the course lectures. Part II, to be published in the September issue of Companion quarterly will cover skin diseases of the eyelids, ocular pathology and neoplasia of the orbit, adnexa and eyelids.

Contact: Queenstown Eye Vet Ltd, PO Box 2900, Wakatipu, 9349, NZ 027-417-2932

Diseases of the globe

From a lecture by Alain Regnier (National Vet School Toulouse, France)

Occular anatomy

The globe is composed of three layers:

outward rotation of the eye. Abducens Nerve (VI) innervates the lateral rectus muscle and retractor oculi muscle. Injury leads to medial strabismus.

•

Strabismus • Fibrous tunic: the sclera and cornea • When the extraocular muscles do • Uvea: anterior (iris and cilary body) and not work correctly, the axes of the posterior (choroid) Nervous layer: retina and optic nerve

two eyes are misaligned this is called strabismus.

•

The diameter of the globe of dogs and cats is approximately 20–25mm. The extraocular muscles which move the globe and hold it in place include:

• 4 rectus muscles: dorsal, ventral, lateral

and medial – move the eye in their respective directions. dorsal oblique muscle: internally rotates the eye ventral oblique muscle: external rotation of the eye retractor oculi muscles: retract the globe to protect the eye The eye muscles are innervated by the:

• • •

• Oculomotor Nerve (III) innervates

the dorsal, ventral and medial rectus muscles and the ventral oblique muscle. Injury results in lateral strabismus. Trochlear Nerve (IV) innervates the dorsal oblique muscle. Injury leads to

•

Congenital strabismus

• Inherited in Siamese cats: the eyes

converge, and they may have a fine pendular nystagmus. In Siamese and other albinotic animals most of the optic nerve fibres cross over in the optic chiasm, while in normal animals only 60% of fibres cross over. The strabismus is an adaption to abnormal retinal projections to the brain and these cats do not show visual impairment. Congenital hypoplasia of the extraocular muscles has been reported in Miniature Poodles resulting in deviation of the eyes.

•

Acquired strabismus results from:

• Lesions of cranial nerves III, IV, and VI. • Globe proptosis results in damage to the medial rectus and other extraocular muscles. Immune mediated inflammation of the extraocular muscles seen in Shar

•

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

• Can be associated with blindness as the patient is unable to

hold a steady gaze Most commonly associated with vestibular disease May be seen in cross-eyed Siamese cats (convergent strabismus)

• •

Changes in globe size Congenital

• Anophthalmos: congenital absence of the eye • Microphthalmos: congenital small eye. This is common

in dogs, but rare in cats. May be inherited in Dobermans, Miniature Schnauzers, Australian Shepherds and Collies and can be associated with other congenital disorders such as cataracts, persistent pupillary membranes, anterior segment disorders, iris colobomas and retinal dysplasia. If mild, then function of the eye may be normal. Small globe size can lead to entropion.

Acquired

• Phthisis bulbi: decrease in globe size usually due to severe

intraocular inflammation secondary to endophthalmitis, trauma or chronic glaucoma leading to reduced aqueous production. Enucleate if painful or causing purulent conjunctivitis. Buphthalmos: enlargement of globe due to prolonged increase in intraocular pressure (glaucoma) or more rarely due to an intraocular tumour. The enlarged globe leads to tear film problems, exposure keratitis and trauma to the eye. If the eye is non-functional and painful enucleation is necessary. An alternative is evisceration and insertion of an intrascleral prosthesis. Endophthalmitis: is inflammation of the entire uveal tract and Panophthalmitis is inflammation of all the tissues of the globe. Causes include infection due to trauma, postsurgery and endogenous (mycoses). Signs include pain, decreased vision, red eye, chemosis, cloudy cornea (oedema), hypopyon (purulent material in the anterior chamber), vitreal inflammation and retinal detachment. The posterior segment is often not visible. Treatment involves systemic broad-spectrum antibiotics and subconjunctival injections of gentamycin or tobramycin. Prognosis is poor.

• c

•

Proptosis of the globe Figure 1. (a) The course was held at the National Veterinary School in Toulouse. The course masters (veterinary ophthalmologists) Professor Peter Bedford, Dr Alain Regnier (seen here (b) with the author, centre), and Dr Jean-Yves Douet were excellent tutors. We had access to one operating microscope per two participants (c) and practicing corneal and lens surgery on pig’s eyes greatly improved my microsurgical skills and confidence in surgical technique.

Pei, Irish Wolfhounds, Akitas and Golden Retrievers leads to progressive strabismus. Bilateral divergent strabismus can be associated with congenital hydrocephalus.

•

Nystagmus

• Involuntary, periodic and rhythmic oscillation of the eyes • Movement can be pendular, jerky, rotatory or fluttering

• Proptosis is forward displacement of the globe with

entrapment of the eyelids behind the equator. Traumatic ocular proptosis is an ocular emergency usually caused by motor vehicle accidents or bite wounds to the head. It is most common in brachycephalic breeds of dogs that have shallow orbits and require less trauma to luxate the eye. Less common in dolichocephalic dogs and rare in cats, which usually have suffered significant ocular trauma and it is often not possible to save the globe. Complications include avulsed extraocular muscles, torn optic nerve, hyphaema and retrobulbar haemorrhage, globe rupture (indicated by a soft globe) and dried cornea. In milder cases, the above complications may not occur.

• • • • •

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Prognosis:

• Contrary to earlier opinions that

dilated pupils were associated with a poor prognosis, the current thought is that pupil size is not a good indicator of vision prognosis. Diffuse hyphaema is a negative predictor for saving vision, as are retinal detachment, optic disc swelling, and retinal or vitreal haemorrhages if these can be viewed. If multiple extra-ocular muscles are avulsed, the globe is ruptured, or the optic nerve is transected then replacement of the globe is not recommended.

•

Surgical treatment of globe proptosis:

• This is a true ocular emergency after

stabilizing the trauma patient. Protect the globe with antibiotic ointment. After general anaesthesia and surgical preparation of the peri-orbital area with a 1:10 solution of povidone Iodine, the globe is cleansed with sterile saline. A lateral canthotomy may be required to facilitate repositioning of the globe. The eyelid margins are pulled in front of the globe equator. The lids may be everted and pulled up with Allis tissue forceps or 3–4 simple interrupted sutures of 4.0 nylon can be placed in the eyelids which are then pulled anteriorly to bring up the eyelids while gentle pressure is placed on the globe using a scalpel handle. Two to three temporary tarsorraphy sutures are placed for 2–3 weeks. Perioperative and postoperative treatment includes topical 1% atropine eye drops, topical antibiotic, and systemic antibiotics and corticosteroids for 7–10 days.

• •

•

Complications of globe proptosis:

enucleation may be a better option to avoid the ongoing medical costs associated with complications. Enucleation is the preferred treatment if multiple extraocular muscles are avulsed, the optic nerve is transected, or the cornea or sclera is ruptured.

Surgery of the globe

From a lecture by Alain Regnier (National Vet School Toulouse, France)

Enucleation

• Removal of the globe, nictitating

membrane and eyelid margin. Indications include: u extensive laceration of the globe u chronic glaucoma with buphthalmos u phthisis bulbi with secondary problems u proptosis of the globe, u panophthalmitis u ocular tumours u relief of intractable ocular pain.

•

Transconjunctival approach:

• Advantage is minimal haemorrhage

and better exposure to the optic nerve, but greater risk of leaving behind abnormal tissue. This is the best method unless you suspect an ocular tumour extending through the sclera, or if there is panophthalmitis extending into extraocular orbital tissue. A lateral canthotomy improves exposure. An incision is made in the bulbar conjunctiva 4–5 mm behind the limbus and is extended 360°. The conjunctiva is separated from the episclera and blunt dissection is continued caudally close to the sclera. The extraocular muscle insertions are identified and cut. Dissection is continued until the optic nerve is identified. The optic nerve is cut with curved scissors and the nictitating gland and membrane are removed. Surgicel haemostatic sponge may be placed in the orbit to control haemorrhage.

•

• • •

• Important! Avoid excessive traction on

the optic nerve as it may cause damage to the optic chiasm, especially in the cat. This can lead to vision loss in the fellow eye. The lid margins are removed with scissors. The bulbar conjunctiva and episclera are sutured with a simple continuous 4/0 absorbable suture, followed by simple interrupted sutures in the skin. Mild ipsilateral epistaxis may appear after surgery due to lacrimal drainage of orbital blood and the owner should be warned that their pet could sneeze blood.

• • •

Intraocular prosthesis insertion:

• A silicone orbital prosthesis can be

placed in the orbit prior to closure to prevent unsightly indentation of the skin over the orbit. This is contraindicated if the reason for enucleation was orbital neoplasia or panophthalmitis. Cats show a high extrusion rate of prostheses.

• •

Transpalpebral approach:

• Allows better vision of the orbit,

reducing the risk of leaving abnormal tissue behind the globe. Causes more haemorrhage from the eyelids and potentially places more traction on the optic nerve so is not recommended in cats.

•

Exenteration:

• Removal of the globe with all the soft tissues of the orbit.

• Used for orbital tumours with orbital extension, or panophthalmitis with orbital contamination.

Complications of enucleation and exenteration:

•

• Post-operative swelling. • In cats: traction leading to damage to

•

• Lateral strabismus due to rupture of

medial rectus muscle – sometimes resolves. Corneal ulceration and kerratoconjunctivitis sicca (dry eye) Lagophthalmos, keratitis, and phthisis bulbi Vision loss: only 20–30% regain vision – more likely with brachycephalic dogs. In cats the facial bones are often fractured, and the fellow eye may be blind from traction of the optic chiasma.

• •

• If costs are a concern for the owner,

•

the optic chiasm resulting in blindness in the other eye. Draining fistulas from incomplete removal of the caruncle, the third eyelid gland and conjunctival goblet cells. Orbital emphysema in brachycephalic dogs. This is caused by air moving up the nasolacrimal duct.

•

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Evisceration and intrascleral prosthesis (ISP) implantation:

• IOL placement can also reduce

post-operative posterior capsule opacification by retarding the migration of corneal endothelium.

• This involves removal of the intraocular contents leaving the corneoscleral fibrous tunic of the globe and filling this with a silicone implant. An ISP results in a more cosmetic appearance than enucleation – the dog has an eye that moves. The cornea may remain clear or appear black from pigmentation or grey due to fibrosis. Indications include blind painful eyes suffering from end-stage glaucoma, non-infectious panuveitis or severe non-perforating trauma. Contraindications include severe corneal disease, intraocular tumours and infectious endophthalmitis.

•

• •

Mesh implant:

• An alternative to an ISP is using 2.0–4.0

non-absorbable suture material and a horizontal and vertical continuous suture pattern to create a mesh by anchoring sutures across the orbit from the periosteum. This reduces the postoperative indentation of the skin.

Surgery of the lens

From a lecture by Alain Regnier (National Vet School Toulouse, France)

The lens is a soft, transparent, biconvex structure located between the vitreous and iris, and its function is to focus light onto the retina. Without a lens, a dog will be hypermetropic which means farsighted so its close vision will be blurry.

Cataract extraction

Cataracts are a leading cause of vision impairment in dogs. Clinical trials indicate medical therapy for cataracts is fruitless.

• If vision is to be restored, a cataractous

lens must be removed. In young animals, cataracts may spontaneously resorb. Microsurgery and phaecoemulsification has given cataract extraction a good success rate. Aphakic (without a lens) dogs can function quite well without intraocular lens (IOL) placement. IOL placement will improve visual acuity.

• • •

Patient selection:

• Dogs can adjust to incomplete lens

opacity or monocular blindness, so surgery is not indicated in dogs with unilateral cataract or immature cataracts. Cataract extraction is indicated when the dog is bumping into objects and not able to maintain a normal lifestyle, i.e. with bilateral cataracts approaching maturity. It is essential to select patients without pre-existing eye diseases that could compromise the outcome, e.g. keratitis, KCS, uveitis, glaucoma and retinal disease such as progressive retinal atrophy (PRA). A dog with PRA will develop cataracts but will have visual impairment and retinal changes prior to cataract development so will be nonvisual regardless of the presence of cataracts. Dogs with uveitis that is causing cataracts or lens-induced uveitis (LIU) because of hyper-mature cataracts will likely have a poor post-operative result. Pupillary light responses (PLR) are unreliable as a sole method for assessing visual potential because PLR can persist with advanced retinal degeneration and conversely PLR may be absent with iris atrophy with intact vision, as in aged poodles. Electroretinography is the most reliable method for assessing retinal function. Ultrasonography is useful to detect retinal detachment and vitreal opacities. Diabetes and other concurrent disease should be managed prior to surgery. Fractious, aggressive or highly excitable pets are not good candidates for surgery as they will require regular pre and post-op medication and may risk injury to the eye when handled.

•

• • • •

Surgical procedure for cataract extraction:

• Surgical details will not be discussed here. Combinations of topical and systemic corticosteroids and non-

steroidal anti-inflammatory drugs (NSAID) are required pre, peri and post operatively. The eye must also be monitored carefully for glaucoma. Removal of the lens by an extracapsular technique using phaecoemulsification with the use of viscoelastics during surgery gives the best results.

•

Success rates and complications:

• Success means vision is present,

the degree of which is assessed by menace response, maze negotiation and tracking behaviour. Recent data suggests that with phaecoemulsification, short-term success is between 90–95% and it drops to 85% several years after surgery. Intra-operative complications: haemorrhage, vitreous prolapse, tear of the posterior lens capsule, lens material dropping into the vitreous, and lens subluxation. Short-term post-operative complications: intraocular pressure spikes, acute uveitis, retinal detachment, bacterial endophthalmitis and corneal oedema. Long-term complications: chronic uveitis, glaucoma (3–17%), posterior synechiae, retinal detachment (5% of dogs – minimized by controlling post-op inflammation), and posterior capsule opacification (22% of dogs within 2 years of surgery) which usually does not significantly obstruct vision. Not all complications will compromise vision and some may be managed effectively medically.

•

Surgery for a luxated lens

• The lens may luxate anteriorly through the pupil or posteriorly dropping back into the vitreous. Luxated lenses are removed by the intracapsular technique – i.e. removal of the lens nucleus, cortex and intact lens capsule through a large corneal incision. A cryoprobe is used to pull the lens out. Any vitreous that moves forward into the anterior chamber is excised to prevent obstruction of the filtration angle and subsequent glaucoma. Posterior lens luxation may also be managed medically. l

•

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

What is your diagnosis? THE ANSWERS… 1. Problem list: a) Recurrent seizure activity with associated altered mentation b) Metarubricytosis with basophilic stippling of erythrocytes c) Glucosuria with normal serum glucose levels 2. Differential diagnoses a) Differentials for seizure activity can broadly be categorized into intracranial and extracranial causes. 1. Extracranial causes include metabolic (liver disease, renal disease, hypoglycemia, hypocalcemia, sodium imbalance, thiamine deficiency) and toxic (drugs, heavy metals, pesticides, ethylene glycol, caffeine/ methylxanthines, mycotoxins). 2. Intracranial causes include the broad categories of degenerative, neoplastic, infectious, inflammatory, traumatic, vascular, and of course idiopathic causes. b) Differentials for metarubricytosis include lead toxicity, heat stroke (dog), bone marrow injury (cats), dyserythropoeisis, and abnormal splenic function. c) Differentials for glucosuria (with normoglycemia): are primary renal glycosuria and proximal tubular nephropathy/Fanconi-like syndrome (due to acute pyelonephritis, pancreatitis, consumption of pet jerky treats, drug therapy (gentamicin, tetracycline), congenital defect (particularly Basenjis), leptospirosis, neoplasia, primary hypoparathyroidism, toxins (copper, heavy metals, including lead). 3. How would you arrive at a definitive diagnosis? Lead toxicity appears on the list of differential diagnosis for all three of the dog’s major problems. To rule this in/out requires measurement of the concentration of lead in serum. 44

Diagnosis:

The concentration of lead measured in this case was >0.6 mg/L (reference range <0.2 mg/L) the highest detection limit for the test, confirming the diagnosis of chronic lead toxicity. Presumably the source of the lead was accidental ingestion of dust/flakes of old leadcontaining paint released into the dog’s environment during the renovation of the owner’s house. Diagnosis of lead toxicosis may be difficult, especially in the absence of known exposure, and because of the insidious nature of clinical signs and progression of the disease. Potential sources of lead include old paints, lubricants, solder, batteries, toys, and ornaments, amongst others. Clinical signs are often variable, however, typically involve a combination of neurological and gastrointestinal signs such as lethargy, inappetence, vomiting, diarrhea and constipation being most commonly reported, with behavioral changes, regurgitation, and seizure activity less frequently documented. Despite such variability, certain classical clinical findings may be identified with diagnostic testing, including metarubricytosis, basophilic stippling of erythrocytes and presence of radioopaque material in the gastrointestinal tract, that may help increase the index of suspicion. More recently, additional clinical manifestations of lead toxicity have been identified, including proximal tubular nephropathy leading to Fanconilike syndrome (King 2016), and detection of glucosuria and proteinuria on urinalysis.

Management:

The dog was treated with a chelation agent, D-penicillamine at 40 mg/kg (recommended dose range; 33–55 mg/kg, dependent on tablet size available), administered orally, three times daily, approximately 30 minutes prior to feeding. A minimum of 2 weeks

treatment is advised, with some literature suggesting the need for up to 4 weeks of therapy. Unfortunately, in this case, despite advice to the contrary, the dog continued to be exposed to lead, neurological signs progressed despite treatment, and the owners elected euthanasia.

Discussion:

One of the major effects of lead toxicity is the inhibition of enzymes containing free sulfhydryl groups. This is of particular importance with regards to haem synthesis, which ultimately results in a decrease in the circulating red blood cell population, leading to increased production and release of immature and stippled red blood cells, as was described here (metarubricytosis, basophilic stippling). Formation of reactive oxygen species also plays a role, leading to red blood cell membrane damage and fragility. In terms of the neurological signs associated with lead toxicity, several mechanisms have been proposed, including interference with neurotransmitter release, substitution of calcium for lead, and formation of reactive oxygen species. Lead has also been found to accumulate within the cells of the proximal renal tubules. Within these cells, lead interferes with mitochondrial function and disrupts energy-dependent processes such as the active reabsorption of glucose, bicarbonate, amino acids, proteins and electrolytes. The result in this case was the loss of glucose in the urine, which in the presence of serum glucose levels within normal limits, is consistent with Fanconi-like syndrome. In the past, cases of lead toxicity accounted for as much as 42.5% of the total number of poisoning cases presented to a university veterinary hospital (Prescott 1983). This same study reported 58.6% of accidental poisonings in dogs being the result of lead intoxication (Prescott 1983). More

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

recently however, the incidence of lead toxicity is assumed to be uncommon, with only sporadic reports in the literature. This is most likely due to fewer potential sources of lead, with lead-free petrol and paints replacing those used in the past. Treatment of lead poisoning is centered around preventing ongoing exposure to the source of lead and appropriate chelation therapy. Chelation agents that do not bind lead within the gastrointestinal tract (GIT) are preferred (i.e. those that solely bind lead within the blood, promoting excretion via the urine), since binding within the GIT may enhance absorption and worsen clinical signs. Ideally, dimercaptosuccinic acid (succimer) should be used, however, this unfortunately cannot be sourced through human pharmacies in New Zealand. In an acute setting, with known exposure, or as was described in this case, repeat exposure, calcium ethylenediaminetetraacetic acid (CaEDTA) is also a good option. However, this needs to be administered

subcutaneously, four times daily, for 5 days, at a dosage of 25 mg/kg (diluted in dextrose 5% to a concentration of 10 mg/ml). The need for hospitalization and the associated costs precluded the use of CaEDTA in the case described here. D-penicillamine, which is primarily used to treat copper hepatopathy, has been shown to have some benefit in cases of lead poisoning. The main drawback with this agent is that it does bind residual lead in the GIT and so may enhance further lead uptake. Potential side-effects that have been reported with use of D-penicillamine are mostly gastrointestinal in nature, including nausea and vomiting, and these may require cessation of therapy (if severe), or a reduction of the dose and close, continued monitoring. Prior to a reduction in the lead content of paints in the 1970s, lead toxicity was associated with significant morbidity and mortality in both humans and animals. More recent literature however, suggests a good prognosis with early diagnosis and appropriate chelation therapy such as CaEDTA.

References:

King JB. Proximal tubular nephropathy in two dogs diagnosed with lead toxicity. Australian Veterinary Journal 94, 280–4, 2016 Mastrorilli C, Welles EG, Hux B, Christopherson PW. Botryoid nuclei in the peripheral blood of a dog with heatstroke. Veterinary Clinical Pathology 42, 145–9, 2013 Morgan RV, Moore FM, Pearce LK, Rossi T. Clinical and laboratory findings in small companion animals with lead poisoning: 347 cases (1977–1986). Journal of the American Veterinary Medical Association 199, 93–7, 1991 Plumb DC. Plumb’s Veterinary Drug Handbook Eighth Edition, PharmaVet Inc, Stockholm, WI, USA, 2015 Prescott CW. Clinical findings in dogs and cats with lead poisoning. Australian Veterinary Journal 60, 270–1, 1983 Yabuki A, Iwanaga T, Giger U, Sawa M, Kohyama M, Yamato O. Acquired Fanconi syndrome in two dogs following long-term consumption of pet jerky treats in Japan: case report. Journal of Veterinary Medical Science 79, 818–21, 2017 l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 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

The March funding round has been and gone, and CAHF are pleased to report we are funding two further projects. The first, by Andrew Worth, will explore whether the angle of screw placement for calcaneo-tibial screws used in Achilles tendon injuries, influences the success or failure of stabilisation. The second, by John Munday, will looks at whether we can improve the treatment of feline oral squamous cell carcinomas by using immunohistochemistry to detect p16 and p53 proteins. Andrew has also had two previously completed projects funded by CAHF recently published in the May 2018 issue of NZVJ, so keep an eye out for these:

• Leitch BL and Worth AJ. Mechanical testing of a steel-

reinforced epoxy resin bar and clamp for external skeletal fixation of long-bone fractures in cats. NZVJ 66 (3), 144–53, 2018 [https://doi.org/10.1080/00480169.2018.1443406] Soo M, Lopez-Villalobos N and Worth AJ. Heritabilities and genetic trends for elbow score as recorded by the New Zealand Veterinary Association Elbow Dysplasia Scheme (1992–2013) in four breeds of dog. NZVJ 66 (3), 151–61 [https:// doi.org/10.1080/00480169.2018.1440652] [Ed’s note: both are downloadable for free by CAV members from sciquest.org.nz] 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

•

Can you raise $500?

A huge thank you to the practices who have expressed an interest in this project, and especially to Tauranga Vet Services who have been busy handing out CAHF brochures to clients and already made a successful donation through our Give-ALittle page. Several other practices have signed up and are taking on the challenge – have you? 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.

Photo credit-Juliet Matthews.

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. Donations can also be made through our Give-ALittle 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 CAHF would also like to thank the on-going generous support we have from CAV, Vet Centre Marlborough, Waikiwi Vet Services, and Boyd Jones, as well as thank the Small Animal Medicine chapter of ANZCVS for their recent generous donation. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

Massey News New Head of School (of) Veterinary Science

The Veterinary program at Massey University has a new name and a new Head of School. The College of Science has been restructured and the former institutes, of which IVABS, the Institute of Veterinary, Animal and Biomedical Sciences was one, have been reorganised. IVABS has been split into a School of Agricultural Sciences and a School of Veterinary Sciences. And as the result of the changes and a global search, a new Head of the Vet School has been appointed. Professor Jon Huxley becomes the 11th school head in the 56-year history of the Vet School. Prior to commencing at Massey, Professor Huxley was at the University of Nottingham, joining in 2006 as one of the School of Veterinary Medicine and Science’s founding academic staff. He has held the position of Professor of cattle health and production since 2011 and was the head of the Division of Veterinary Surgery from 2011 to 2014. His academic career has focused on dairy cow health and endemic diseases of dairy cattle, particularly lameness and the impact of the housed environment on animal health and welfare. However, he has also had extensive experience developing and delivering veterinary education.

People

Associate Professor Andrew Worth has returned to the Veterinary Teaching Hospital after a nine-month leave of absence during which he spent time at the Royal Veterinary College in Potters Bar as a soft tissue surgeon. Kat Crosse and Wendy Baltzer were running the small animal surgical service with intermittent locum coverage for that time and are to be commended for maintaining a full referral service in difficult circumstances. There is a global shortage of surgeons and radiologists willing to work in university practice and there is a full time surgical position currently being advertised to take the team back to four. In March Kat Crosse and Wendy Baltzer attended the Veterinary Orthopaedic Society meeting in Snowmass, Colorado. This conference offers cutting-edge research abstracts and state-of-the-art lectures, and is the pinnacle of the ortho conference circuit – as well as being an amazing opportunity to ski/snowboard. Kat will soon be heading to the UK for a couple of months to begin a collaborative research project in brachycephalic airway syndrome. She is part of an initiative that involves Dogs NZ, aimed at reducing the incidence of brachycephalic airway syndrome.

Oncologist Valerie Poirier has recently spent time in Guelph, Canada at the Animal Cancer Centre, at work on her PhD, and will spend further time there in 2018. Andrew Worth recently attended the PennVet Working Dog Conference in Philadelphia, USA. This biannual event is targeted at the working dog industry and brings together trainers, breeders, government organisations and veterinarians. The University of Pennsylvania Working Dog Centre was founded by Cindy Otto after the events of 9/11. She has created a unique dog training and research centre that seeks to improve training outcomes for working dogs. Much of the work focuses on scenting and fitness. The MU WDC is planning to bring Cindy Otto to New Zealand as part of our Working Dog Research Colloquium. She will be speaking on canine olfaction in September at Palmerston North. Richard Burchell is leaving Massey for Tropical North Queensland, and a new post as an Internist at James Cook University’s Veterinary Teaching Hospital in Townsville. Associate Professor Craig Ruaux has joined the Small Animal Medicine service in his stead. Craig is a Queensland BVSc graduate and also has a PhD from the University of Queensland. He held a research position at Texas A&M University and is a Diplomat of the American College of Small Animal Medicine. He most recently held an Associate Professorship at Oregon State University. It’s the time of year when our interns complete their year rotating through the VTH. Our interns provide 24/7 care through the MU Pet Emergency Centre and there is a fair chance that if you have referred an afterhours case, it was one of these hard working folk who looked after it. We wish Suzanne Busser, Mackenna Dent, Harvey Saunders, Shawn Chandrakumar, Linda Kungiesingh and Soscha Ten Cate all the best for their futures and thank them for their efforts. Soscha has been accepted into an emergency and critical care residency at The Ohio State University. Shawn will be starting an internal medicine internship at the Veterinary Specialty Hospital of San Diego in California. Harvey Saunders will be starting his surgical internship at Animal Referral Hospital in Brisbane. Suzanne Busser will be staying at the MUVTH for a 6-months oncology stint, while Linda Kungiesingh will be going home to the Caribbean for a well-deserved break prior to starting her new adventures and Mackenna Dent is still working out her internal medicine future. l

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 2018

CPD RECORD

Read articles from Companion Quarterly 29(2) June 2018

Date of Activity: ………………………… Activity description Read articles in the June 2018 issue of Companion Quarterly (tick those that apply) o o o

What is Your Diagnosis (Mathew Kopke) Mandatory tests for the Dogs NZ Accredited Breeders Scheme (CAV) Feline immunodeficiency virus in New Zealand: Should we test? Should we vaccinate? And does it even cause disease? (John Munday and Nick Cave) o Feline autoimmune lymphoproliferative syndrome (FALPS): A fatal inherited disease of British shorthair cats (Danielle Aberdein) o Leptospirosis in dogs: An emerging problem? (Janice Thompson) o Feline idiopathic hypercalcemia (Susan Murray) o Report: Highlights from the Course in Veterinary Ophthalmology II: Part I (Jos van Hees) o ………………………………………………………………………………………………………… 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? ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ ............................................................................................................................................................................................................................................................................................................ 48

Companion Quarterly: Official Newsletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 29 No 2 | June 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. 2 | June 2018

VOLUME 29 NO 2 June 2018

Feline immunodeficiency virus in New Zealand

FALPS: a fatal inherited disease of British shorthair cats

Leptospirosis in dogs: an emerging problem?

Feline idiopathic hypercalcemia

Report: Highlights from Veterinary Ophthalmology course