Companion Quarterly vol27 no3 Sept 2016 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 27, No. 3 | September 2016

VOLUME 27 NO 3 SEPTEMBER 2016

Angiostrongylosis in dogs and cats

Haemotropic Mycoplasma infections

Proactive management of canine atopy

A case of feline orofacial pain syndrome

Bravecto for earmites: a case study

Volume 27 | No. 3 | September 2016 ISSN No. 1173-6941 EXECUTIVE COMMITTEE 2016 cas@vets.org.nz

CONTENTS

President

Brendon Bullen

Companion Quarterly

Operations Manager Rochelle Ferguson

Treasurer

Aimee Brooker

Committee Members Helen Beattie Warren Stroud John Munday Catherine Watson Toni Anns Natalie Lloyd

EDITORAL COMMITTEE Sarah Fowler (Editor) Genevieve Rogerson Angus Fechney Christine Moloney (Advertising) Janice Thompson Simon Clark

Address for submitting copy/ correspondence

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

Advertising Manager

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

NZVA website www.nzva.org.nz

2 Editorial 4 Highlights from CAS Executive Meeting

6 CAV Noticeboard 8 CAS Service Awards 2016 10 Mailbox 12 What is your diagnosis? Philip S. Hyndman

14 Angiostrongylosis

Boyd R Jones, W.E. Pomroy,

20 Haemotropic Mycoplasma

(Haemoplasma) infections in New Zealand cats Janice Thompson

24 Recent advances in the

diagnosis and staging of chronic kidney disease in dogs and cats Graham Swinney

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

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

28 The proactive management of 30 Can the English Bulldog be

Newsletter design and setting

32 Feline orofacial pain syndrome

Penny May T 021-255-1140 E penfriend1163@gmail.com

fixed?

Nikki Frost

36 Efficacy of Bravecto against earmites in 16 hound puppies Hannah Bain, Hugh Hasselman

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.

canine atopic disease Duncan Graham

Cover photograph pixabay.com

40 Specialist profile - Brent Higgins

42 2016 NZVA Conference 46 NZVJ Companion Animal

Digest: Volume 64, 4, 2016

48 Massey News 49 What is your diagnosis: The answer

Vets in Stress Programme

Animal Council Update

24 Hour Freephone Confidential Counselling Service

52 New Zealand Companion 53 History of the New Zealand 54

Companion Animal Register Pieter Verhoek Guidelines for Authors

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 Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

EDITORIAL

Registration and regulation of Allied Veterinary Professionals The New Zealand Veterinary Nurses Association is currently working towards registration and regulation of Allied Veterinary Professionals (AVP). The definition of an Allied Veterinary Professional includes everyone working “in a clinical capacity to provide animal healthcare under the direction of a veterinarian” and includes veterinary nurses, veterinary technologists, rural animal technicians, large animal veterinary technicians and veterinary nursing assistants. This has come about through an understanding that regulation is an important part of maintaining quality, safety, and wellbeing of the veterinary profession as a whole. The aim is to encourage professionalism, and promote AVPs’ importance as a vital part of providing quality veterinary care. CAV is fully supportive of this initiative and believe this will be a huge positive step forward for the veterinary industry. Regulation will provide consistency of education so that there is clear distinction between the different qualifications available, and make it easier to determine exactly what training has been provided. This will make AVPs accountable for their own professional practice and conduct, and will require maintenance of competency including CPD. This will also align New Zealand with international standards of practice. These changes should make it easier for us to provide truly ‘team-based healthcare’ for our patients and clients,

and I’m sure this will translate into better healthcare outcomes. The NZVNA has appointed a special committee, the Allied Veterinary Professional Regulatory Council (AVPRC) with the task of initiating the move toward professional regulation. This will function currently as a working group of NZVNA, but the long-term vision is for this to become an independent body with functions similar to the VCNZ. Ideally this will sit in a combined umbrella with VCNZ to aid communication and collaboration throughout the entire veterinary industry. A voluntary register has been established which is available for all Allied Veterinary Professionals to join, currently this has 250 members and is growing rapidly. This will be a long-term plan, as ultimately regulation will require NZ legislative changes. The NZVNA is very encouraging of feedback and would like to hear views from the veterinary profession. The best contact address for more information or feedback is regulation@nzvna.org.nz. l Brendon Bullen,

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

WORKING TO PROMOTE AND SUPPORT COMPANION ANIMAL PRACTICE IN NEW ZEALAND

Highlights from the CAS Executive Committee meeting 19 May 2016, Wellington

Homeopathic vaccinations

New graduate support

NZ Kennel Club

Dangerous dogs

Members have raised concerns about puppies being presented having being treated with homeopathic vaccinations, and paperwork that claims these provide protection against viral diseases. We have alerted the ACVM group to these claims and based on this there compliance team is investigating.

We committed to supporting the NZKC new canine health and welfare officer with technical advice and articles for their Dogworld magazine.

Antimicrobial resistance issues

Currently CAS recommends the FECAVA guidelines for NZ vets to follow for selecting and using antimicrobials. To future proof the industry on this front we need to promote understanding about how resistance develops and measures that can be taken to reduce resistance development. This education needs to be extended to the public as their expectation around treatment needs to be adjusted to allow best practice by the veterinarian. We saw an opportunity for health and veterinary services to work together on this topic.

The NZVA mentoring scheme has also being revamped this year with a pilot scheme underway that has seen considerably more support and training being provided to mentors. The effectiveness of this training will be assessed following the course and rolled out more widely if appropriate.

A taskforce has been formed to update the NZVA Dangerous Dog Position Statement. This complex issue requires a comprehensive detailed response from multiple groups, with vets in a pivotal position to effect a societal wide change in what it means to be a responsible dog owner.

Supporting veterinary students

The committee plans to further support our up and coming companion animal veterinarians by meeting with them annually on campus. This August we have arranged for Kelly Buckle to present on exotic diseases in companion animals, and win hearts with the ever popular pizza lunch. l

Whatâ&#x20AC;&#x2122;s in a name?

Would a rose smell so sweet by any other name? Well we certainly hope so! At the last AGM a resolution was passed to ask the NZVA board's permission to grant a change of name, this has been given and we are now all members of the Companion Animal Veterinarians Branch of the NZVA. The Companion Animal Vets branch will continue to promote and support companion animal practice in New Zealand, and we look forward to less convoluted explanations to others when we are introducing ourselves!

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

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. Applications are usually considered at the end of March and September each year. We have $10,000 per annum to grant and are very keen to have this resource utilised to support and promote companion animal veterinarians. 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.

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

CAV/CAHF Project Grant 2016 The Companion Animal Health Foundation is a charitable trust that acts as the research funding arm for CAV. Funding applications from CAV members are invited in March and September for research projects that will enhance companion animal health and welfare.

WINNER

Article of the Issue

Bernie Vaatstra

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

“Congenital cerebellar malformation resembling Dandy-Walker syndrome in a Jack Russell Terrier x Fox Terrier puppy” June 2016 | Volume 27 (2) | Pages 26–29

EYEVET Services Limited

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

NEWS IN BRIEF

CAS Service Awards 2016

We are very pleased to announce that the CAS Service Awards for 2016 have been awarded to Dr. Pru Galloway and Dr. Kate Hill. These awards were presented at the CAS dinner during the 2016 NZVA Conference in Hamilton in June.

Kate Hill

Photo courtesy of Kate Hill

Kate graduated from the University of Queensland in 1996. After a year in small animal practice she returned to the University of Queensland as a junior resident in small animal medicine. In 1999, Kate undertook a residency in small animal medicine at Purdue University, Indiana. She is a diplomat of the American College of Veterinary Internal Medicine (ACVIM), and is also a registered veterinary specialist with the Australasian Veterinary Boards Council. After a year as clinical faculty at Purdue University, Kate moved to the University of Tennessee for 2 years as an assistant professor in small animal medicine. Kate joined Massey University in July 2005 as a Senior Lecturer in Small Animal Medicine and is a Director of the centre for service and working dog health. Kate joined the CAS technical advisory group in 2006, becoming a member of the CAS executive in 2007. She served for seven years, resigning in 2014 when she moved to Brussels. During this time she has been heavily involved with continuing education for CAS. Kate has shared her knowledge with us through articles for the CAS newsletter, by speaking to us at various regional branches, as well as at our annual conference in 2008. She has used these opportunities to update us on endocrinology in companion animals, antimicrobial use and working dog health 8

issues. Recently we made use of research she undertook on canine tail injuries to support our submission to government to ban tail docking. Kate was responsible for developing the medicine module of the CAS veterinary refresher scheme and this has been of great value to veterinarians re-entering companion animal practice after a break, as well as to the profession in general in terms of retaining skilled practitioners. Kate was also on the scientific committee that supported the Auckland WSAVA congress in 2013. This committee of three knowledgeable and well connected veterinarians underpinned the scientific programme using their professional networks and connections. This effort was integral to the success of the congress, and made a large contribution to advancing our collective knowledge. l

Pru Galloway

Photo courtesy of Pru Galloway

Pru graduated from Massey University with distinction in 1987. After three years in private practice she completed a residency in feline medicine at Bristol University and in 1997 she became a Fellow of the Australian and New Zealand College of Veterinary Scientists. For New Zealand, this meant we had our very first, and only, registered specialist in feline medicine. Pru then established a referral service â&#x20AC;&#x153;Catmedâ&#x20AC;? in Wellington and has been active in managing the difficult end

of feline medicine cases for both local veterinarians and through telephone consultations, many others throughout NZ. In 1999, Pru facilitated the establishment of the CAS branch when it was Wellingtonâ&#x20AC;&#x2122;s turn to host the committee. This committee, chaired by Helen Beban then developed into a national committee model that we follow today. Pru has made an enormous contribution to educating NZ veterinarians on feline medicine topics. This contribution to our education has included Vetscript articles, lectures at Massey, regional branch seminars, and regular contributions to the CAS Newsletter. The NZVNA has also benefited from her expertise as a regular speaker at their conferences. Special mention should be made of the work Pru did in 1999 to support the CAS stream of the annual conference, when the headline speaker withdraw at short notice. Pru presented four seminars, developed at short notice to ensure that the show could still go on. Pru Galloway is also active in feline matters internationally. She is on the veterinary advisor panel for International Cat Care, and has served on the chapter examination committee of the feline branch of the ANZCVS, as well as the editorial board of the Journal of Feline Medicine and Surgery. Pru played an integral role in the success of the WSAVA 2013 Congress held in Auckland, both by presenting and as a member of the scientific committee that put together the speakers programme. The quality of the speakers presenting at WSAVA was instrumental in the success of the congress and was largely down to the professional networks that Pru Galloway, Kate Hill and Richard Jerram have developed. This award while recognising the professional support that Pru has given CAS and its members over the years, would not be complete without also mentioning how nice she is! Pru not only advances the field of feline veterinary knowledge by distilling vast amounts of knowledge into convenient take home packages for busy veterinarians, but also retains a high level of compassion for her clients, their cats and is a caring colleague. l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

MAILBOX

Dear Editor ..... I CONGRATULATE WOOLLETT, Forsyth and Beugnet for their timely well constructed article "Survey of fleas, ticks and gastrointestinal helminths in cats and dogs in New Zealand" (CAS Newsletter 27(1), 32–38, 2016). Their review of published research into the prevalence of gastrointestinal helminths in dogs yielded sparse studies of selected populations of dogs. I would like mention another study in working dogs by Dr T. Busch in the 1980s and more general data from two Auckland practices from the early ’70s to mid ’80s. The Busch study was of about 120 working dogs in South Auckland and I think this was published in the forerunner to the CAS Newsletter (T. Busch, pers. comm.). The second lot of data was of approximately 12,000 faecal examinations performed in-house between 1972–1985 from dogs presented to the Dominion Road Veterinary Hospital in central Auckland and dogs presented between 1972–1983 to the Forrest Hill Veterinary Clinic on Auckland's North Shore. The report of the Busch study cannot be located at this point but Dr Busch recalls that the surprising feature was the low incidence of Toxocara canis; only one 4-month-old dog. Our estimate of the well/unwell dog in the 12,000 dog-sample data was approximately 50:50 with gastrointestinal signs accounting for the majority of "unwell" dogs. The methodology was generally the same as Woollet et al. in both the Busch study and our large data set. Differences we recall included the use of a saturated nitrate salt solution before changing to saturated sugar. We combined faeces from three consecutive defaecations of these dogs because we were advised that Trichuris vulpis was an unreliable egg producer. Our data summary (it was never designed as a study) suggested that T. canis was a very rare finding in adult dogs: less than 0.5%. The findings of the Busch, Woollett and O'Connell studies together with our historic data support O'Connell's suggestion that the there is probably an effective immune response to this parasite in healthy adult dogs. A notable exception from our data was a Greyhound with postpartum metritis. This dog had diarrhoea with hookworm, roundworm and whipworm eggs. Unfortunately we did

not record enough information to make any conclusions about seriously ill animals being more subject to T. canis infestation. Hookworm eggs were present in about 2% of faecal samples in our data and 12 % of samples had Trichuris eggs. Our view after 4–5 years of collecting this data was that a faecal sample from apparently well dogs should be examined for parasite eggs on an annual basis. This practise determined whether anthelmintics were required and if they were, established the timing of repeat treatments given the varying pre-patent periods of the various helminth species. Cats seem always to come second (if only in the literature). It is disappointing then that Woollet et al. fail to mention the gastric helminth Ollulanus tricuspis in cats. The current incidence is unknown in New Zealand but it does occur and affected cats frequently have large numbers of worms. We suggest that cats that vomit frequently should have vomitus examined directly for worms. Vomiting can be induced in cats with an empty stomach. This will give a sample that is more amenable to examination. Ollulanus infection is likely to be unrecognised if not investigated in cats. – Allan and Cheryll Bell

References

Collins GH, Charleston WAG. Ollulanus tricuspis and Capillaria putorri in New Zealand cats. New Zealand Veterinary Journal, 20, 82, 1972 Guy PA. Ollulanus tricuspis in domestic catsprevalence and methods of post mortem diagnosis. New Zealand Veterinary Journal, 32, 81–2,1984 Bell AG. Ollulanus tricuspis in a cat colony. New Zealand Veterinary Journal, 32, 85–7, 1984 l

.............................................................................................. I REALLY ENJOYED reading the Companion Quarterly June Issue’s article entitled “Tooth resorption in a cat”. It was informative and the key learning was to extract cat’s teeth properly. What concerned me with the article though were sentences like “No intraoral radiographs were taken at the first dental procedure” which was repeated later in the article. While these statements are factually correct, I worry when I see sentences like this. Although intra-oral radiography is best practice this is often not possible for a range of factors. These

include the veterinary practice does not have dental radiography equipment, the practice is not willing to invest in this equipment or the client is not able to pay for this diagnostic procedure. If I put my paranoia hat on the tut-tut tone of these sentences borders on possible denigration of a veterinary colleague in my opinion. This is interesting in light of the latest newsletter from the Veterinary Council of New Zealand. This does nothing for the first opinion-referral veterinary surgeon relationships. I am also concerned that in these increasing litigious times an “ambulance chasing” lawyer will find these statements and accuse a veterinary surgeon of malpractice and incompetence. Perhaps the author of the article just needed to word the best practice use of intra-oral radiography in a different way. Over the years there have been many dental procedures with tooth extractions done by experienced practitioners, without dental radiographs, with no problems encountered. Complications happen and revision procedures need to be carried out. I would hate to see the day where first opinion veterinary surgeons will not do simple tooth extractions in practice because they do not have all the “right” equipment. I cannot see many veterinary surgeons following paragraph 3c of Veterinary Services from the VCNZ’s Code of Professional Conduct i.e. The practice resources must be sufficiently managed in order to meet the minimum standards expected. Resources include but are not limited to: staff, equipment, facility and inventory, with their employer. Doing a tooth extraction well versus referring to a dental specialist has cost implications for many owners and possible animal welfare issues if the owner cannot afford to go down this road.

Don’t get me wrong I am all for dental radiography, doing the job properly and being paid appropriately for our time, skill, knowledge and financial investment. This however is not the real world for the majority of first opinion veterinary surgeons. Most veterinary practitioners are doing an excellent job in our current working environment. Regards, Robert Bird BVSc, Massey 1990 (Dist), MANZCVS, MVM (CA) l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

What is your diagnosis? THE QUESTIONS… PHILIP S. HYNDMAN

BVSc, Zoetis Companion Animal Rotating Intern. Massey University Veterinary Teaching Hospital. An 8-year-old female spayed Minature Schnauzer presented with a large mass on the ventral aspect of her neck that had first been noticed by the owners 3 weeks prior to presentation as a small mass. The owners reported no hypersalivation, inappetence, vomiting, change in behaviour or other signs of discomfort. The owners were also concerned about increased respiratory noise while she was sleeping over the previous few nights. The patient was otherwise fit and healthy with no other significant health concerns or relevant historical findings. On clinical examination an approximately 5 x 3 x 1.5 cm (parallel to the sagital plane) mildly lobulated subdermal mass was identified in the ventral cervical region lying predominantly right of midline. It had a homogenous, firm, soft-tissue consistency and was freely mobile within the subcutaneous tissue. The mass appeared well demarcated from the surrounding tissue superficially although differentiating the mass from the trachea, oesophagus, and cervical musculature was difficult. During palpation no hypersalivation, excessive swallowing, pain or discomfort was noted. Following a full physical examination, all vital parameters were within reference limits with no appreciable lymphadenopathy or other abnormalities. Water, syringed into the mouth, was swallowed normally. No coughing or other abnormalities were noted at this time. She was sedated with 0.3 mg/kg butorphanol I/V and orthogonal radiographic views obtained (Figure 1). 1 What are your radiographic findings? 2 What are your differential diagnoses? A fine needle aspirate was then performed with a 22 gauge 1-inch needle. Two

Figure 1. Ventrodorsal oblique (a) and left lateral (b) radiographic views of the cervial spine. In the ventrodorsal oblique view the ventral neck and cranial cervical spine is lateralized to the right. Image provided by Dr.

Richard Munn, Levin & Horowhenua Veterinary Centre Ltd.

Figure 2. Photomicrographs of cytological preparation from fine needle aspirate of the cervical mass. Magnification 500x.

samples were obtained, from proximal and distal within the mass. No negative pressure was applied and the needle was redirected and advanced three times with each aspirate. A firm soft-tissue density with an occasional “gritty” texture consistent with mineralization was noticed while the needle was being redirected within the mass. The samples obtained were grossly sanguineous in appearance with the FNA sites bleeding mildly following the procedure. The following

images were obtained from in-house cytology (Figure 2). 3 What are your differential diagnoses for the mass following in-house cytology given the clinical presentation? 4 How would you proceed with further diagnostics and intervention? l Answers revealed on page 49

Contact: Philhyndman88@gmail.com 12

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

FEATURE ARTICLE

Angiostrongylosis BOYD R JONES, ONZM, BVSc, FACVSc, DECVIM-Ca and W.E. POMROY, BVSc, Dip Vet Clin Stud, PhD Diseases that do not occur in New Zealand may be of little interest to us. However, with global warming the potential change in distribution of some of these diseases may put cats and dogs in this country at risk. In addition many of you will do your OE in other countries and some diseases are being diagnosed with increasing frequency in those countries. This is true for Angiostrongylus vasorum (in UK, Europe, Canada, North America) and Angiostrongylus cantonensis (Australia, Asia, Pacific region). Disease due to each parasite is becoming more prevalent and extending its natural range into new geographic areas (Morgan et al. 2005). Slugs and snails are the intermediate hosts for both parasites. There are parallels between the epidemiology of A. vasorum and A. cantonensis in UK and Australia. In New Zealand we should be aware of both diseases. It may only be a matter of time before they are on our list of differential diagnoses.

Angiostrongylus vasorum

A. vasorum is a nematode with an indirect life cycle. Primary hosts are wild and domestic dogs in which the parasite lives in the right heart and pulmonary arteries. They are slender worms up to 2.5 cm long and they can live for longer than 2 years in a dog. The females lay eggs which travel to the pulmonary capillaries where they hatch releasing L1. The L1 larvae are coughed up, swallowed and excreted in faeces. Intermediate hosts include aquatic and terrestrial slugs and snails. Paratenic hosts include frogs which have eaten infected slugs and snails. The prepatent period is approximately

Photo courtesy of Bayer Animal Health

28–108 days. Dogs become infected by eating an intermediate or paratenic host which contains the L3 larvae. The free-living phase of the life cycle is similar to the cat lungworm Aelurostrongylus abstrusus which is in the same taxonomic grouping, the Metastrongyloidea. A. vasorum was first reported in France and has since been recognised in many countries including England, Wales, Ireland, Germany, Denmark, Canada and South America. Recently, there have been sporadic reports from countries previously considered free from infection. The factors resulting in the change to reported distribution of A. vasorum include:

• Increased awareness of the disease by veterinarians • Milder climate changing the distribution and abundance of mollusc hosts • Increased prevalence of foxes which act as disease reservoirs • The role of wildlife

Clinical signs

Cough, dyspnoea and tachypnoea are the most common cardiorespiratory signs. Coughing occurs due to the physical presence of the parasite and the associated inflammatory response. Concurrent bacterial infection occurs in some dogs. Clinical signs of a coagulopathy are variable and include petechiae, ecchymoses and

Contact: IVABS, Massey University, Palmerston North

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

scleral haemorrhage (Figure 1). The cause of bleeding is not well understood. Dogs commonly have mild increases in prothrombin and partial thromboplastin times with mild thrombocytopaenia. Bleeding can occur in animals with normal coagulation profiles.

A. vasorum is thought to lead to a compensated state of disseminated intravascular coagulation (DIC) (Adamantos et al. 2015). Immune-mediated thrombocytopaenia, reduced concentration of factors V and VIII and acquired von Willebrand’s factor deficiency have been reported. Central nervous system signs are also reported and are associated with haemorrhage or less commonly larval migration. Severe pulmonary hypertension can lead to signs of cor pulmonale.

Clinical pathology

Eosinophilia is present in 35–50% of cases and hyperglobulinaemia in 75%. Hypocalcaemia occurs occasionally. If haemorrhage is present (epistaxis, airway haemorrhage, haematuria, haemarthrosis) there may be anaemia and coagulation parameters may be abnormal: thrombocytopenia, prolonged PT/PTT, prolonged buccal mucosal bleeding time.

Thoracic radiography

Radiological signs are variable with signs of bronchial thickening and a multifocal or peripheral alveolar pattern (Boag et al. 2004) (Figure 2).

Definitive tests

Baermann flotation of faeces has low sensitivity as larvae are shed intermittently. Repeat sampling or testing of 3-day pooled samples increases accuracy. Direct faecal smears are easy and quick to perform but have low sensitivity (approximately 60%). PCR analysis also has low sensitivity. ELISA testing of blood for antigens produced by adult worms has excellent sensitivity and specificity.

Treatment

Figure 1. Episcleral haemorrhage in a dog with Angiostrongylus infection (Courtesy Dr Barbara Gallagher, University College Dublin).

In the UK imidacloprid/moxidectin and milbemycin are licensed to treat angiostrongylosis. Fenbendazole (20–50 mg/ kg p.o. q24 h for 5–21 days) is effective but is not licensed for treatment. One study compared imidacloprid/moxidectin spot-on solution and fenbendazole in the treatment of naturally affected dogs with A. vasorum and showed efficacies of 85% and 91% respectively. These drugs are efficacious under field conditions but not 100% (Willesen et al. 2007). Regular anthelmintic treatment is likely to reduce but not eliminate the risk of disease (Morgan and Shaw 2010). Steroids may be indicated if clinical signs worsen when the adult worms are killed.

Prevention

In endemic areas prophylactic treatment with an effective drug is sensible and if used in the prepatent period clears infection or reduces parasite numbers (e.g. milbemycin or imidacloprid/ moxidectin).

Figure 2. Lateral radiograph of a dog with respiratory signs due to Angiostrongylus infection (Courtesy Hester McAllister, Diagnostic Imaging, University College Dublin).

To reduce the risk of exposure, limit dogs’ access to slugs and snails and stop the dog eating them. Remove faeces regularly and remove dog toys etc from the lawn/ground at night.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Neural angiostrongylosis

Angiostrongylus cantonensis, commonly known as the rat lungworm, is present in Australia and the Asia-Pacific region. It is endemic to the coastal areas of Queensland and New South Wales. Importantly, there is a changing geographical distribution with increasing prevalence in south eastern Australia in dogs and in humans (Lunn et al. 2012; Mahdis et al. 2015). A. cantonensis is endemic to Queensland but from 1989 the geographic distribution in humans and dogs has extended south into New South Wales and metropolitan Sydney. It is an emerging infectious disease affecting dogs on the eastern seaboard of Australia. The disease is also seen increasingly as a neurological disease in horses, possums, birds (tawny frogmouths) and simians in captivity. Some references indicate a possibility for cats to be infected but to date there are no reports of this occurring. The peak incidence of infection seems to be in May (autumn). The adult lungworms reside in the pulmonary vessels of rats, the definitive host. The L1 larvae migrate to the airways from the lung capillaries, pass up the trachea, are swallowed and passed in rat faeces. Intermediate hosts (slugs and snails) ingest the larvae which develop to the L3 stage. A variety of animals such as frogs can act as paratenic hosts. Rats and other mammals including dogs and humans ingest molluscs/ paratenic hosts containing these larvae. The L3 larvae penetrate the gut and migrate to the brain and/or spinal cord where they develop to sub-adults before they then migrate to the pulmonary arteries via the venous system. The infection in animals other than rats does not reach patency but some development in the CNS may occur.

Clinical signs

Neural angiostrongylosis was first described in Australia by Mason (1976, quoted by Lunn et al. 2012) in south eastern Queensland. Affected dogs are mostly young and show nervous signs which range from mild ataxia and paresis to severe ascending paralysis, hyperaesthesia, incontinence, convulsions, coma and death. Larvae damage the CNS but it is probably the host’s reaction to the dying larvae or to their shed cuticle that contributes most to the onset of clinical signs.

Diagnosis

Diagnosis is based on the clinical signs (they can look similar to Neospora in young dogs!!) and rarely is there a history of the dog being seen to eat slugs. Eosinophilic pleocytosis in CSF is characteristic and suggestive of A. cantonensis. The presence of anti A. cantonensis IgG in CSF demonstrated by ELISA testing is supportive and currently this is the most specific test available. PCR testing and other diagnostic tests for Angiostrongylus spp. show promise (Lunn et al. 2012) and may become alternative laboratory diagnostic methods in the future.

The role of anthelmintics in treating affected dogs is controversial as a rapid “kill” of larvae may result in a sudden release of parasite antigen, worsening the clinical signs as there is a significant immunological component to the CNS inflammation. There may be anthelmintic strategies to prevent infection and the long acting moxidectin preparations used to prevent heartworm may have a role.

Risk of introduction to New Zealand

At present, for imported dogs, there are no specific tests/ treatments required for A. vasorum other than those that relate to a general treatment for nematodes prior to arrival (see box for current MPI policy re angiostrongylosis). Could dogs undergoing this treatment protocol still enter NZ infected? Maybe; whilst the risk is currently low, climatic changes with the increased incidence of A. vasorum in dogs in other countries and the incomplete efficacy of registered anthelmintics could allow introduction to NZ. A. cantonensis is more likely to be introduced accidentally with an infected intermediate host/ paratenic host as rodents (other than laboratory animals) cannot be imported.

References

Adamantos S, Waters S, Boag A. Coagulation status of dogs with naturally occurring Angiostrongylus vasorum infection. Journal of Small Animal Practice 56, 485–90, 2015 Aghazadeh M, Jones MK, Aland KV, Reid SA, Traub RJ, McCarthy JS, Lee R. Emergence of neural angiostrongylosis in eastern Australia. Vector-borne and Zoonotic Diseases 15, 184–90, 2015 Boag AK, Lamb CR, Chapman PS, Boswood A. Radiographic features of 16 dogs affected with Angistrongylus vasorum. Veterinary Record 158, 426–30, 2004 Gallagher B, Brennan SF, Zarelli M, Mooney CT. Geographical, clinical, clinicopathological and radiographic features of canine angiostrongylosis in Irish dogs: a retrospective study. Irish Veterinary Journal 65, doi 10.1186/2046-0481-65-5, 2012 Lunn J, Lee R, Smaller J, MacKay BM, King T, Hunt GB, Martin P, Krockenberger MB, Spielman D, Malik R. Twenty two cases of neural angiostrongylosis in eastern Australia (2002–2005) and a review of the literature. Parasites and Vectors 5, 70–88, 2012 Morgan ER, Shaw SE, Brennan SF, De Waal TD, Jones BR, Mulcahy G. Angiostrongylus vasorum: a real heartbreaker. Trends in Parasitology 21, 49–51, 2005 Morgan ER and Shaw SE. Angiostrongylus vasorum infection in dogs: continuing spread and developments in diagnosis and treatment. Journal of Small Animal Practice 51, 616–21, 2010 Walker AG, Spielman D, Malik R. Canine neural angiostrongylosis: a case control study in Sydney dogs. Australian Veterinary Journal 93, 195–99, 2015 Willesen JL, Kristensen AT, Jensen AL, Heine J, Koch J. Efficacy and safety of imidicloprid/moxidectin spot-on solution and fenbendazole in treatment of dogs with naturally occurring Angiostrongylus vasorum (Baillett 1886) Veterinary Parasitology 147, 258–64, 2007 l

Treatment

There is usually a good response to glucocorticoids which reduce inflammation associated with dead or moulting A. cantonensis larvae but the response may vary and may be absent. Steroids should be continued for at least 6–8 weeks. Permanent neurological deficits may occur in recovered dogs.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

INDUSTRY NEWS

Shedding light on the complexities of anaesthesia Appropriate premedication, smooth induction, stable maintenance, rapid recovery, and accurate analgesia are the goals of an integrated anaesthetic plan. Throw in patient variation, increasing procedural complexities, increasing owner expectations and knowledge, and it becomes no easy task.

the non-pregnant patient? Easy to read, practice relevant information covering the entire anaesthetic process, with a quick reference guide for when you need a quick-time refresher, is presented in concise Library pieces. With regular new additions, the Library is a valuable clinic resource that keeps growing.

However, staff training helps. Jurox, manufacturer of premium anaesthetic induction agent Alfaxan®, knows that anaesthesia is about more than just making an animal go to sleep, and is committed to providing in-clinic training and support customised to the particular needs of the practice.

Jurox’ commitment to supporting the best practice anaesthesia in New Zealand clinics reflects a growing range of veterinary anaesthesia and analgesia products. In recent times, Jurox has launched Medetate (medetomidine), Butordyne (butorphanol), Antipam (atipamazole), and most recently Bupredyne (buprenorphine). Bupredyne is the first multi-dose vial of buprenorphine in New Zealand and is the result of research dedicated to the veterinary industry.

Anaesthesia varies according to the patient, procedure, drugs, and people involved, and no two anaesthetics are identical. Understanding the nuances of how all the elements work together to create a good outcome or present a challenge is vital to managing a successful anaesthetic, and developing a knowledgeable and resourceful peri-operative team. Developed by Jurox’ veterinary team, including members of the Anaesthesia and Analgesia Chapter of the Australian and New Zealand College of Veterinary Scientists, the in-clinic training presentation covers everything from risk assessment and minimisation, understanding premedicants and induction agents, to specific scenarios such as old, young and C-section patients.

Source: Jurox Pty Ltd

Suited to both vets and nurses, and delivered by well-trained Jurox Territory Managers, the presentation is tailored to answering the questions and concerns of the practice, and helping to improve the everyday practice of anaesthesia. Complementing the presentation’s content is the other element of clinic support, the Alfaxan Anaesthesia Library. Split into two parts, the Library is a physical clinic resource containing information on getting the most out of Alfaxan, useful for new users and those more experience, as well as specific anaesthetic scenarios that may differ from a routine anaesthetic due to patient population or disease state. For example, what should you do for a geriatric patient? How does the pregnant patient presenting for caesarean-section differ from

If you would like to find out more, book a training session at your practice, or start your own Anaesthesia Library, please get in touch with Jurox on 0800 587 696. l

Source: Pixabay.com

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

FEATURE ARTICLE

Haemotropic Mycoplasma (Haemoplasma) infections in New Zealand cats JANICE THOMPSON BVSc,

PhD, Gribbles Veterinary, Palmerston North.

Abbreviations

Mycoplasma haemofelis: Mhf “Candidatus” Mycoplasma haemominutum: CMhm “Candidatus” Mycoplasma turicensis: CMt

Introduction

Feline haemoplasmas are organisms that were formerly known as Haemobartonella felis and that were initially considered to be rickettsias (Grindem et al. 1990; Foley and Peterson 2001) but have now been reclassified as Mycoplasmas based upon the development of PCR tests and examination of 16S ribosomal RNA gene sequences (Messick, 2004). They are small gram negative rods that cannot be cultured (Foley and Peterson 2001). The designation of “Candidatus” has been given to some species that have been incompletely characterised. Haemoplasmas are small epierythrocytic organisms that lack a cell wall. They contain circular double stranded DNA and little other internal structure. Mycoplasma spp other than haemoplasmas cause many forms of disease other than anaemia (Messick 2004). In a recent detailed review two forms of Mycoplasma were described and denoted as the large or Ohio form which causes feline infectious anaemia and the small or California form which appears to have low virulence (Messick 2004). The large form is now known as Mycoplasma haemofelis (Mhf ), the small form known as “Candidatus” Mycoplasma haemominutum (CMhm). More recently Contact: janice.thompson@gribbles. co.nz, Ph 06 356-7100

another species called “Candidatus” Mycoplasma turicensis (CMt) has also been described in cats, initially in Switzerland but has now been shown to be present in other countries (Novacco et al. 2011; Sykes 2010). It is a diagnosis made by only by PCR and has not been seen by light microscopy (Novacco et al. 2011; Sykes 2010). “Candidatus” Mycoplasma haematoparvum, a canine haemoplasma, was also identified by PCR in two cats in the USA but reportedly there has been no further detection of this species in cats (Sykes 2010). Haemoplasmas sit in a small indentation on the surface of the RBC with a clear zone separating the organism from the RBC. They are connected to the RBC by fine fibrils. It is noted that Mhf may rapidly disappear from RBCs and reappear at a later time, both in splenectomised and nonsplenectomised animals. This is thought to result from phenotype switching and disappearance of the fibrils. The phenotype switching is thought to cause development of a carrier state and to contribute to its ability to survive in vivo, perhaps by developing a carrier state, disguising cytoadherence antigens and/or establishing infection in another cell type. Reappearance of the cytoadherent ability and allows for transfer of the organism between hosts by vectors possibly including fleas (Messick 2004). However the actual mode of transmission remains unknown and infection is prevalent in regions where fleas are uncommon (Sykes 2010). There is an increased prevalence of Mhf and CMhm in older male non-pedigree cats suggesting that transmission may also result from fighting. DNA from both CMt and CMhm but not Mhf was found to be present in the saliva of infected cats (Barker and Tasker 2013). Vertical transmission from queens to kittens during pregnancy, at birth or via lactation has been suggested but not proven (Barker and Tasker 2013).

Characteristics of the different species of feline haemoplasmas

Mhf often causes severe regenerative anaemia in affected cats (Barker and Tasker 2013; Messick 2004; Sykes 2010). Anaemia usually develops as a result of direct damage to the RBC and/or immune mediated haemolytic anaemia in the form of extravascular haemolysis, although some infected cats may have intravascular haemolysis. Infected cats have a positive coombs test. Increased osmotic fragility and decreased RBC lifespan have been noted (Sykes 2010). While Mhf is considered highly pathogenic, CMhm is considered to be of low pathogenicity (Foley and Peterson 2001; Sykes 2010). Clinical signs were shown to be minor and while a mild decrease in RBC parameters was observed, the decrease may cause the RBC parameters to decrease from high normal to low normal, or from low normal to marginally below the reference interval. These cats may become carriers with reappearance of the organism following immunosuppression from various causes. Most CMhm infections are described as chronic and asymptomatic. Co-infection with FeLV has been shown to cause more significant anaemia (Sykes 2010). CMt was first identified in Switzerland and has since been found in a number of other countries (Sykes 2010). Infection is thought to cause either mild anaemia (Novacco et al. 2011; Sykes 2010) or occasionally severe anaemia (Sykes 2010) although the severe anaemia was seen in a cat immunosuppressed by glucocorticoids. Numbers of organisms are usually very low. It has not been identified by light microscopy and PCR is needed to determine if there is coinfection with the other species (Basker and Tasker 2013).

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

In addition to the different species of feline haemoplasmas, different strains within each species are also believed to exist (Barker and Tasker 2013)

Haemoplasmas in New Zealand

Mhf, CMhm and CMt have all been identified in New Zealand by PCR (Barker and Tasker 2013; Jenkins et al. 2013). Surveys carried out using PCR have identified all three of these species in cats in New Zealand. In one survey of cats tested by PCR 31% of cats were found to be infected. Of these CMhm was present in 25% of infected cats. Mhf was present in 7.5% of infected cats and CMt present in 4.5% of infected cats. Co-infection with multiple species was also identified (Jenkins et al. 2013). Multiple co-infections have also been diagnosed by PCR via Gribbles Veterinary in Palmerston North. These co-infections include combined infections with either two or all three Mycoplasma species present in the same cat (Unpublished data: Gribbles laboratory).

Diagnosis

Both Mhf and CMhm organisms can be observed on RBCs in blood smears during routine haematological evaluation. They are present as small structures on the surface of RBCs and although they are noted to be different in size, accurate identification can only be made by PCR. Organisms of both are visible by light microscopy. CMhm is approximately 0.3 μm in diameter and about half the size of Mhf, which is approximately 0.6 μm in diameter (Foley and Pederson 2001). CMt has not been seen by light microscopy (Barker and Tasker 2013). Sometimes the organisms may be very obvious but overall the sensitivity and specificity of diagnosis by light microscopy is not good and depends on the experience of the haematologist, the age of the blood sample and stage of disease. In addition artefact such as stain sediment and other RBC structures such as Howell Jolly bodies may be confused with organisms (Barker and Tasker 2013). Mycoplasma organisms may be obvious but differentiation between the different species is not feasible by light microscopy. If the blood sample is old, organisms may drop off the RBCs and be present in the background and therefore may be very difficult to

differentiate from stain sediment and other artefact. Numbers of organisms may decrease quickly to due loss of ability to adhere to RBCs (Messick 2004) so while anaemia may be present the causative organism may not be obvious. Suspicion of Mhf infection may be raised by the presence of severe regenerative anaemia and autoagglutination of the RBCs with an absence of other causes of severe anaemia. Organisms may or may not be seen (Sykes 2010). The number of infected RBCs may decline from 90% to less than 1% in under 3 hours. Sequestration of the organism in splenic and pulmonary macrophages is a possible explanation. It has been suggested that recovered cats may remain carriers for years with re-activation of disease due to stress, steroids, severe disease (Sykes 2010). If there is severe regenerative anaemia and organisms are seen on RBCs then Mhf is the very likely cause. If the anaemia is mild the possible differential diagnoses include per-acute Mhf infection and/or co-infection with one of the other species. A further blood sample should show development of a more severe anaemia if Mhf is present. If the anaemia remains mild but organisms are present on the RBCs then it is very possible that one of the lowly virulent species is present. Accurate differentiation of infective organisms requires PCR since there may be single or multiple Mycoplasma species present. Further diagnostics are also needed to identify any underlying disease that may be causing immunosuppression if one or both of the lowly virulent species are present. Underlying disease includes concurrent infection with retroviruses and also administration of corticosteroids for any reason (Barker and Tasker 2013; Sykes 2010. It has been noted that cats co-infected with FeLV and CMhm reportedly may be more likely to develop myeloproliferative disease than cats infected with FeLV alone (Sykes 2010). The presence of a persistent severe non-regenerative anaemia along with visualisation of organisms on RBCs also requires examination for concurrent disease causing immunosuppression because non-complicated infection with Mhf is usually regenerative. For example if chronic renal failure is present along with anaemia then the anaemia may be a result of the renal failure and PCR is needed to identify any Mycoplasmas

seen on the RBCs. If the organisms are CMhm then this may be a result of concurrent disease rather than the cause of disease.

Treatment

The recommended treatment for Mhf is doxycycline at 10 mg/kg/day PO for a minimum of 2 weeks and blood transfusions may be required. Alternatively enrofloxacin at a dose rate of 5 mg/kg/day PO may be used (Sykes 2010). Pradafloxacin at dose rates of 5 mg/kg daily orally or 10 mg/kg daily are also suggested (Barker and Tasker 2013). It is noted that the use of glucocorticoids to suppress immune mediated haemolytic anaemia is controversial given the glucocorticoids may reactivate a latent infection however they may be required where antibiotics alone are not successful or where diagnosis is uncertain (Sykes 2010). Also note that infections with CMhm in New Zealand cats are reasonably common (Barker and Tasker 2013; Jenkins et al. 2013) and asymptomatic, so perhaps cats that may be used as potential blood donors should be tested by PCR to prevent inadvertent infection of cats receiving blood transfusions (Basker and Tasker 2013).

References

Barker E, Tasker S. Haemoplasmas: Lessons learnt from cats. New Zealand Veterinary Journal 61, 184–92, 2013 Foley JE, Pederson NC. “Candidatus Mycoplasma haemominutim” a lowvirulence epierythrocytic parasite of cats. International Journal of Systematic and Evolutionary Biology 51, 815–7, 2001 Grindem CB, Corbett WT, Tomkins MT. Risk factors for Haemobartonella felis infection in cats. Journal of American Veterinary Association 196, 96–9, 1990 Jenkins KS, Dittmer KE, Marshall JC, Tasker S. Prevalence and risk factor analysis of feline haemoplasma infection in New Zealand domestic cats using real time PCR. Journal of Feline Medicine and Surgery 15, 1063–9, 2013 Messick JB. Hemotrophic mycoplasmas (hemoplasmas): a review and new insights into pathogenic potential. Veterinary Clinical Pathology 33, 2–13, 2004 Novacco M, Boretti FS, Wolf-Jackel GA, Riond B, Meli ML, Willi B, Lutz H, Hofmann-Lehmann R. Chronic “Candidatus Mycoplasma turicensis” infection. Veterinary Research 42, 59–66, 2011 Sykes JE. Feline hemotropic mycoplasmas. Journal of Veterinary Emergency and Critical Care 20, 62–9, 2010 l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

FEATURE ARTICLE

Recent advances in the diagnosis and staging of chronic kidney disease in dogs and cats Graham Swinney is Medical Affairs Veterinarian/ Internal Medicine Consultant for IDEXX Laboratories

GRAHAM SWINNEY, BVSc (Hons), DVCS, FANZCVS (Canine Medicine) Chronic kidney disease (CKD) is a common disease in both dogs and cats. The incidence of CKD increases with advancing age, and some studies report an incidence of up to 30% in cats over 15 years of age (Lulich et al. 1992). The prevalence reported in dogs varies between studies, and has been reported as low as 0.37% in UK practices (O’Neill et al. 2013), 5.8% in four US teaching hospitals (Bartlett et al. 2010) and 10% in geriatric dogs (Brown 2013). Early diagnosis and management potentially may influence the rate of progression and quality of life. The clinical presentation of patients with CKD may vary. In dogs there is commonly polydipsia and polyuria, but this may not be noted until later stages of the disease in cats. In more advanced stages of the disease there may be non-specific clinical signs such as weight loss, poor body condition, inappetance, lethargy, dehydration and in some cases vomiting in the face of a uraemic gastropathy and ulceration. In the early stages of disease the physical examination may be unremarkable, but palpable changes in the kidneys may be noted in cats – in some cases there may be small, irregular and firm kidneys, but sometimes one or both kidneys may be enlarged (as may happen with infiltration, ureteral obstruction, polycystic kidneys). As the disease advances changes noted may include poor body condition, a poor haircoat, dehydration, palpation abnormalities Contact: NZVP: 0800 838 522

Source: pixabay/com

as described, and possibly pale mucous membranes, oral ulceration and uraemic breath. If there is systemic hypertension there may be consequences such as tortuous retinal vessels, retinal haemorrhages and possibly retinal detachment. The diagnosis of CKD involves a combination of blood and urine testing. Typically there is a loss of concentrating ability when approximately 66% of nephron function is lost, and azotaemia typically develops when there is approximately 75% loss of nephron function. In more advanced CKD the combination of inadequate urine concentrating ability (<1.030 in dogs and <1.035 in cats) and azotaemia supports the diagnosis, but there may be more challenges for diagnosis earlier in the disease process. Serum creatinine and

urea are the most routine biochemical tests to aid in diagnosis. Blood urea can be affected by non-renal factors however, such as dehydration, hepatic function, gastrointestinal haemorrhage and the protein content of the diet. Creatinine, a breakdown product of muscle, is a better indication of renal function than urea, but can be impacted by loss of muscle mass. The sensitivity of creatinine can be increased by monitoring the creatinine level over time – a significant upward trend in creatinine, even if still within the reference interval may aid in the earlier diagnosis of CKD. Other serum biochemical changes may include hyperphosphataemia, changes in serum calcium, metabolic acidosis, and in some cases hypokalaemia. Haematology may reveal a non-regenerative anaemia. The

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

urinalysis should be complete to look for proteinuria, casts, or any signs of an infection. A urinary protein to creatinine ratio should be considered if the urine sediment is inactive to objectively assess the degree of proteinuria. If significant proteinuria is present there may be hypoalbuminaemia or hypercholesterolaemia noted on the serum biochemical profile.

SDMA – A new kidney biomarker

Symmetric dimethylarginine (SDMA) is a new renal function test offered by IDEXX Laboratories. SDMA (a methylated form of the amino acid arginine), along with other methylated arginines, are produced in every nucleated cell. The methylation of arginine residues plays a role in RNA processing, protein shuttling and signal transduction. SDMA is released into circulation during protein degradation, almost exclusively by the kidneys (Kielstein et al. 2006). There are three important attributes of SDMA: 1 It is a biomarker for kidney function 2 It increases earlier than creatinine 3 It is specific for kidney function Assessment of the Glomerular Filtration Rate (GFR) using a clearance test is the gold standard for assessing kidney function, but it is complicated and expensive to undertake, so is rarely performed in clinical practice. A metaanalysis of 18 studies of human patients showed SDMA correlated highly with GFR (r=-0.85) (Kielstein et al. 2015). A recent study of 24 female dogs that were carriers of an X-linked hereditary nephropathy also showed a strong correlation between SDMA and GFR (R2 =0.85), and an even tighter correlation in affected male dogs (R2 =0.95) (Nabity et al. 2015). A close correlation of SDMA and GFR has also been demonstrated in cats (R2 =0.82) (Braff et al. 2014). As discussed earlier serum creatinine typically may not increase beyond the reference interval until 75% of kidney function is lost, making it a late stage marker of kidney disease. A study published in 2014 of 21 cats with CKD showed that SDMA increased on average 17 months earlier than creatinine, and on average when there was a 40% reduction in the GFR (Hall et al. 2014a). In this study with a GFR value of 30% below the median set as indicating reduced renal function, SDMA had a sensitivity of 100%, and a specificity of 91%, and 26

the two ‘false positive’ cases identified had a GFR 25% below the median value. The sensitivity of serum creatinine in the study was between 17% and 50% depending on the cut-off value used. A similar study undertaken in dogs showed SDMA increased on average 9.5 months earlier than serum creatinine (Yerramilli et al. 2014). SDMA is specific to kidney function, as is creatinine in most cases. Serum creatinine concentrations however can be affected by lean body mass, which may be significant in older animals, or those losing body condition as a result of illness. There has been a study published that showed that in aging cats lean body mass and creatinine decreased, despite the fact the GFR was falling. The SDMA increased as GRF fell, and showed no correlation to lean body mass (Hall et al. 2014b). A similar study in dogs showed no correlation between SDMA and lean body mass (Hall et al. 2015). The International Renal Interest Society (IRIS) has provided guidelines on the staging and management of renal disease for a number of years now. The staging has been based on a fasting serum creatinine, with sub-staging based on arterial blood pressure and proteinuria. IRIS have recently modified their staging guidelines based on the availability of testing for SDMA concentrations (Anonymous et al. 2016). One implication of the utility of SDMA is earlier diagnosis of kidney disease. If the SDMA concentration is elevated in the face of a normal serum creatinine, early kidney disease is likely. This should prompt an investigation for an underlying cause, which potentially could direct specific therapy. Management strategies can be commenced, and the knowledge of the presence of early renal disease may influence drug choices and anaesthetic management. Finally, an appropriate monitoring strategy can be determined based upon the individual needs of each patient.

References

Anonymous. IRIS CKD Guidelines Updates 2014–2015. http://www.iris-kidney. com/pdf/staging-of-ckd.pdf (Acessed 11 July 2016). International Renal Interest Society, 2016 Bartlett PC, Van Buren JW, Neterer M, Zhou C. Disease surveillance and the referral bias in the veterinary medical database. Preventative Veterinary Medicine 94, 264–71, 2010

Braff J, Obare E, Yerramilli M, Elliott J, Yerramilli M. Relationship between serum symmetric dimthylarginine concentration and glomerular filtration rate in cats. Journal of Veterinary Internal Medicine 27, 1699–701, 2014 Brown SA. The Merck Veterinary Manual: Renal dysfunction in small animals. http:// www.merckvetmanual.com/mvm/ urinary_system/noninfectious_diseases_ of_the_urinary_system_in_small_ animals/renal_dysfunction_in_small_ animals.html. (Accessed February 8, 2016). Merck and Co. Inc, Kenilworth, NJ, USA, 2013 Hall JA, Yerramilli M, Obare E, Yerramilli M, Jewell DE. Comparison of serum concentrations of symmetric dimethylargine and creatinine as kidney function biomarkers in cats with chronic kidney disease. Journal of Veterinary Internal Medicine 28, 1676–83, 2014a Hall JA, Yerramilli M, Obare E, Yerramilli M, Yu S, Jewell DE. Comparison of serum concentrations of symmetric dimethylarginine and creatinine as kidney function biomarkers in healthy geriatric cats fed reduced protein foods enriched with fish oil, L-carnitine, and medium chain triglycerides. The Veterinary Journal 202, 588–96, 2014b Hall JA, Yerramilli M, Obare E, Yerramilli M, Melendez LD, Jewell DE. Relationship between lean body mass and serum renal biomarkers in healthy dogs. Journal of Veterinary Internal Medicine 29, 808–14, 2015 Kielstein JT, Salpeter SR, Bode-Boeger SM, Cooke JP, Fliser D. Symmetric dimethylargine (SDMA) as an endogenous marker of renal function – a meta-analysis. Nephrololgy Dialysis Transplantation 21, 2446–51, 2006 Lulich JP, Osborne CA, O’Brien TD, Polzin DJ. Feline renal failure: questions, answers, questions. Compendium: Continuing Education for the Practicing Veterinarian 14 127–53, 1992 Nabity MB, Lees GE, Boggess MM, Yerramilli M, Obare E, Yerramilli M, Rakitinin A, Aguiar J, Relford R. Symmetric dimethylarginine assay validation, stability and evaluation as a marker for the early detection of kidney disease in dogs. Journal of Veterinary Internal Medicine 29, 1036–44, 2015 O’Neill DG, Elliott J, Church DB, McGreevy PD, Thomson PC, Brodbelt DC. Chronic kidney disease in dogs in UK veterinary practices: prevalence, risk factors and survival. Journal of Veterinary Internal Medicine 27, 814–21, 2013 Yerramilli M, Yerramilli M, Obare E, Jewell DE, Hall JA. Symmetric diethylarginine (SDMA) increases earlier than serum creatinine in dogs with chronic kidney disease (CKD), [ACVIM Abstract NU-42]. Journal of Veterinary Internal Medicine 28, 1084–5, 2014 l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

FEATURE ARTICLE

The proactive management of canine atopic disease DUNCAN GRAHAM BVSc, BSc (hons), Animal Dermatology NZ, Nelson Canine atopic disease (CAD), like its human counterpart, is a chronic disease that waxes and wanes; it responds to treatment and then at some point, especially without treatment, relapses. It has both acute and chronic flares. These flares are annoying to both owners and veterinarians attempting to manage the disease, and more importantly, uncomfortable for the canine patient. If these flares are not controlled, they lead to chronic changes. The knowledge that human atopy is a chronic condition where relapses are common, combined with new research showing that clinically normal skin in atopic patients is not normal, and does not have normal barrier function, has led to the concept in human medicine of proactive treatment as opposed to reactive treatment. Instead of the clinician reacting to an acute flare, acting as the ambulance at the bottom of the cliff, she tries to proactively establish a barrier to prevent the patient going over the cliff. In the management of the human atopic patient, this has been specifically applied to the use of topical treatments to prevent or delay flares or relapses. Similarly in canine atopics, histological studies of non-lesional, clinically normal, skin has demonstrated that there is sub-clinical inflammation. Trans-epidermal water loss studies of normal skin of canine atopics have also shown that the barrier function of noninflamed non-lesional skin is impaired. Canine dermatologists have taken this knowledge and are promoting proactive treatment versus reactive treatment. A recent article published in Veterinary Dermatology (Lourenco et al. 2016) Contact: duncan@animaldermatology.co.nz

Source: https://pixabay.com

described a double-blinded placebocontrolled study of 41 client owned dogs with spontaneous canine atopic disease. The researchers looked at the likelihood of relapse in the 21 dogs treated proactively, on 2 consecutive days with hdrocortisone aceponate (HCA) versus 20 dogs that were treated in a similar fashion with placebo. The study had two phases: initially all dogs were treated with two pumps once daily of HCA until remission of symptoms was achieved. Remission was defined as when the dog dropped below a predefined score of 60 on the lesional scoring system called the CADESI (canine atopic disease extent and severity index). This scoring system does not directly measure pruritus. However the investigators felt it gave a good index of remission. Once remission was achieved, immediately phase two was started. This meant that, as previously mentioned, each animal was treated either with HCA or placebo on two consecutive days per week. Each animal was examined every two weeks for the first 45 days, then monthly, or sooner in the case of relapse. A full examination and CADESI scoring was done at every visit.

They found that placebo-treated dogs were 3.5 times more at risk of an acute flare than HCA-treated dogs. The median time to relapse was 115 days in HCA-treated dogs and 33 days in placebo-treated dogs. Fifty days after phase two started more than 85% of placebo-treated dogs had relapsed compared to two of the HCA-treated dogs. Relapse rates of HCA-treated dogs were 60% at 100 days and 80% at 180 days. There were no adverse effects in any of the HCA-treated dogs. Skin atrophy had been seen previously in one study but was not reported in this one. This is important: we are using topical treatment as opposed to systemic treatment to avoid side effects. This is obviously a great improvement. However, the relapse rate in the HCAtreated dogs, even though it is much better than non-treated dogs (placebo dogs), does indicate the importance of managing client expectations. They must realize at the outset that it is likely their dog will flare; perhaps not for six months but sooner or later, even with proactive topical treatment, he will relapse and need to be seen so that the clinician can make the appropriate

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

modifications to the treatment regime. They will then need to flip over into a management strategy for acute flares. This is true even in the most well managed cases; it is not the fault of the owner or the clinician. It is the nature of the disease. Instead of being dismayed at a relapse after several months, we should be pleased the flare-free gap has been as long as it has. I think managing expectations, giving clients a realistic idea of what is possible and what is not possible, is a very important, if somewhat overlooked, aspect of the management of CAD. It should be pointed out that the dogs in this study were allowed concurrent allergen-specific immunotherapy (ASIT) and therapeutic shampooing. There is no free lunch; CAD takes a large amount of owner input to manage well. Part of this involves explaining to the owner what proactive treatment is trying to do – extend the interval between relapses. Without that kind of explanation, they may not see the sense of treating normal skin in what appears to be a relatively itch-free dog. This concept of proactive management of atopy in both human and animals is being promoted as a new way of managing the disease. To a certain extent it is true: we know from the histopathological studies that non-lesional skin is not normal. We know from the trans-epidermal water loss studies that

even non-inflamed, non-reactive skin is a poor barrier, allowing antigens to penetrate, and micro-organisms to overgrow. However, clinicians have known for many years that to manage atopic patients, it is often necessary to keep them on longterm, systemic, antipruritic, anti-inflammatory medications, often corticosteroids. The new twist, in both human and canine atopic management, is using topical medications to do this. Previously this was done with systemic medications. In both human and canine medicine, the recent introduction of topical corticosteroids that have little if any systemic effect makes this an even more compelling scenario.

Reference

Lourenço AM, Schmidt V, São Braz B, Nóbrega D, Nunes T, Duarte-Correia JH, Matias D, Maruhashi E, Reme CA, Nuttall T. Efficacy of proactive long-term maintenance therapy of canine atopic dermatitis with 0.0584% hydrocortisone aceponate spray: a double-blind placebo controlled pilot study. Veterinary Dermatology 27, 88–92, 2016

The author has received continuing education support and payment for lectures from Royal Canin and Virbac NZ. This report was not requested by either company. l

RESEARCH NEWS

Can the English Bulldog be fixed? breeding and compared their genotype to that of 37 English Bulldogs presented to the UCDavis Veterinary Clinic for health problems.

The origins of this polarizing breed lie approximately 400 years ago when a small number of probably mastiff-like dogs were bred to produce a strong and ferocious fighting dog for use in bull-baiting. Over time breeders manipulated the dog’s appearance from this aggressive fighter to the chubby, squat, stertorous household pet of today. In the process of selection the Bulldog’s gene pool underwent several reductions in size. The English Bulldog of today has a median life-span of only a little over 8 years and is prone to a wide range of breed-related health issues. There are high rates of congenital conformational birth defects in pups – splay legs, cleft palate, flat chests, and brachycephalic obstructive airway syndrome is a leading cause of health problems and death in the breed. They are also prone to chondrodysplasia, leading to elbow and hip dysplasia and spinal problems, and a range of skin, dental, cardiac, and ocular conditions.

Source: pixabay.com

A recent article by Pedersen et al. (2016) in Canine Genetics and Epidemiology reports the results of the first study to use genome-wide DNA analysis to investigate genetic diversity of English Bulldogs rather than pedigree data. The authors looked at a variety of genetic markers across the genome of 102 registered English Bulldogs used for

They found that English Bulldogs, whether healthy breeding stock or sick animals potentially the product of puppy mills, had very low genetic diversity. This is due to their small founder populations and the artificial genetic bottlenecks imposed during the transition from aggressive fighter to cuddly pet. The authors conclude that while some phenotypic and genetic diversity remains in the breed it is questionable whether this is enough to provide the raw material to make the health improvement the breed desperately needs.

References

Pedersen NC, Pooch AS, Liu H. A genetic assessment of the English bulldog. Canine Genetics and Epidemiology 3, 6 DOI: 10.1186/ s40575-016-0036-y, 2016 l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

CASE REPORT

Feline orofacial pain syndrome NIKKI FROST, BVSc, Franklin Vets, Pukekohe

Case history

Puzzle (Figure 1), a 14-year-old female spayed Burmese cat presented with a 3-month history of tooth chattering after eating. Clinical exam revealed thick tartar on her maxilliary premolar teeth and a fractured right mandibular canine tooth. At 4.65 kg she had a body condition score of 5/9. The rest of her physical exam and preanaesthetic blood tests were unremarkable. Puzzle was anaesthetized and the fractured tooth extracted using a surgical approach and a mucoginigval flap that was sutured back in place. Upon waking from anaesthesia, Puzzle was seen pawing at her mouth, however this was assumed to be due to the sutures causing irritation. She was discharged with postoperative analgesia consisting of meloxicam (Metacam oral suspension for cats, Boehringer Ingelheim, New Zealand) at a dose of 0.04 mg/kg orally once daily. Puzzle represented 7 days later for her post-operative check and the owner reported that the pawing was continuing. This was assumed to be due to irritation from the sutures so these were removed. However Puzzle represented another 7 days later and the owner reported that the pawing had intensified and she had started traumatising her right lip with her claws. Clawing was seen to occur after eating or grooming. Since the meloxicam was not effective, Puzzle was prescribed buprenorphine (Temgesic, Reckitt Benckiser, U.K.) to be given into the buccal pouch at a dose of 0.013 mg/kg twice daily. This was also unsuccessful in controlling the clawing and over the next 3 days the intensity with which she clawed at her mouth increased. Based on the intensity of the attempted self-mutilation with no real response to analgesics, one of the differential diagnoses considered was Feline Orofacial Pain Syndrome (FOPS). Consequently treatment with phenobarbitone (PSM Healthcare, Auckland, New Zealand) at 2 mg/kg twice daily was initiated. This dose resulted in heavy sedation but only partially reduced the self-trauma after 3 weeks. At this point treatment was switched to 100 mg gabapentin (22 mg/kg) PO, 12-hourly (Nupentin, Mylan, Auckland, New Zealand). This is a very a high dose (normal dose for a cat is 3–10 mg/kg) but was given because the owner found it too hard to divide the capsules and refused to pay for compounding. This dose was effective at reducing self-trauma but the effect waned after

Figure 1. Puzzle. Photo courtesy of Nikki Frost

about 10 hours, so the dose was increased to three times daily. She was maintained on this dose of gabapentin for 2 months, after which it was then decreased to 100 mg twice daily with no reduction in efficacy and so was then was reduced to 100 mg once a day. After several months of good control of the self-trauma, Puzzles’ owner decided to stop the medication completely. Within 48 hours she resumed pawing at her mouth. Treatment with gabapentin was resumed, initially 100 mg twice a day and when that only partially reduced the signs, the dose was increased again to three times a day but this dose again was only partially effective. The decision was made to add amitriptyline (ArrowAmitriptyline, Actavis, Auckland, New Zealand) to her treatment regime, at a dose of 1 mg/kg 12-hourly. Within 12 hours of the first dose, Puzzle stopped clawing at her mouth. However her owner found optimal reduction of signs occurred when the two medications were given 2 hours apart (gabapentin at 7 am and 7 pm and amitriptyline and 9 am and 9 pm) to lengthen the duration of action. Due to the stress and restriction of having to medicate her cat four times a day, Puzzles’ owner elected euthanasia, nine months after the initial dental procedure.

Contact: nfrost@fvs.co.nz

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Discussion – feline orofacial pain syndrome

FOPS is a condition characterized by acute and severe oral and facial pain (Rusbridge et al. 2010) resulting in episodes of exaggerated licking and chewing movements and pawing at the mouth. Typically these episodes occur in most patients after discomfort is triggered by movement of the mouth as occurs with eating, drinking or grooming (Gandolfi et al. 2013). More severe cases result in self-mutilation of the tongue, lips and buccal mucosa. Usually the mutilation is unilateral or, at least, more severe on one side (Rusbridge et al. 2010).

Pathophysiology

FOPS shares similarities with trigeminal neuralgia in humans. In this condition a combination of peripheral disturbance or damage such as dental disease, and cerebral brainstem disinhibition of the trigeminal apparatus results in a paroxysmal neural discharge and reverberation of pain impulses when an oral pain trigger is elicited (Heath and Rusbridge, 2010). In FOPS, it has been suggested that not only is there nerve dysfunction causing neuropathic pain but also dysfunction of the processing of sensory information from the trigeminal nerve within the brain. Trigger factors for peripheral sensitization include tooth eruption, dental disease, dental treatment and other oral lesions such as mouth ulceration (Rusbridge et al. 2010, Southerden 2013).

anaesthesia. The inciting cause for the development of FOPS may be related initially to oral lesions and/or extraction of affected teeth. However if clinical signs abate after addressing these oral lesions or erupting teeth then a diagnosis of FOPS is much less likely. The characteristic symptoms of exaggerated mouth movements and (often unilateral) pawing at the mouth, possibly leading to self inflicted injuries (Figure 2) usually occurring after eating or grooming increase the index of suspicion for this diagnosis. Elimination of all other causes of orofacial pain such as trauma to the teeth or the supporting oral skeletal or soft tissues structures, tooth resorption, temporomandibular joint disease, myositis, otitis media and CNS lesions must be made (Southerden 2013).

External factors such as stress also appear to play a part in the development of this condition (Heath and Rusbridge, 2010). Situations which may cause anxiety such as living in a multicat household, introduction in a new kitten, moving house, a cattery stay or change in the family situation have been linked to the onset of FOPS episodes in some cats (Rusbridge et al. 2010).

Signalment

A recent retrospective study by Rusbridge et al. (2010) showed the mean age at onset of clinical signs was 7.1 years. However there appeared to be two peaks; one at 6 months (coinciding with eruption of permanent dentition) and another at 10–12 years. Recurrence of signs of self-trauma occurred in 70% cases at a mean interval of 2 years. No significant sex predisposition was observed. The study showed that 92% of cases were Burmese or Burmese-cross cats however FOPS has also been reported in domestic shorthair, Siamese, British shorthair, Tonkinese, and Somali cats. A genomic study of affected cats suggested an association of FOPS with a region of chromosome C1 within the low-density lipoprotein receptor related protein 1 gene. The protein this gene encodes is expressed in the central nervous system and has been implicated in other pain-related syndromes such as migraines in humans (Gandolfi et al. 2013).

Diagnosis

Diagnosis of FOPS is made on the basis of appropriate signalment, elimination of other explanations, and identification of contributory causes. Full-mouth radiographs should always be recommended for cases where the intensity of clinical signs is not matched by the clinical findings, along with a comprehensive oral health assessment under general

Figure 2. An example of the type of self-inflicted oral trauma that may be seen with FOPS. Photo courtesy of Nikki Frost

Treatment

Treatment of FOPS should include elimination of possible trigger factors such as dental disease. In the study by Rusbridge et al. (2010), of 53 cats with FOPS who had dental lesions, the signs of FOPS improved in 35 of them following the treatment of those lesions. In some cats, the signs of FOPS started following a dental procedure (Rusbridge et al. 2010) as dental treatment itself may also cause peripheral nerve sensitisation (Southerden 2013). Standard analgesic drugs such and non steroidal antiinflammatories and opioids may help in mild cases of FOPS. However anti-convulsant drugs, such as phenobarbitone, diazepam and gabapentin appear to give the most effective relief in terms of elevation of clinical signs. This is likely due to their effect on the GABA receptors in the dorsal horn and trigeminal ganglion which control the propagation of pain signals (Rusbridge et al. 2010). Possible options for managing FOPS are listed in Table 1.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Table 1: Drug options for treatment of FOPS (Plumb 2005, Rusbridge et al. 2010)

Drug Phenobarbitone Diazepam

Recommended dose 2–3 mg/kg BID 0.2–1 mg/kg BID

Carbamazepine

25 mg BID

Gabapentin Amitriptyline Amantadine

10–20 mg/kg BID–TID 0.5–1 mg/kg BID 3 mg/kg SID

In the retrospective study by Rusbridge et al. (2010), no single drug appeared to be the perfect treatment, however phenobarbitone and diazepam appeared most effective with 88% and 86% cases responding effectively, 6% and 7% having a partial response and 6% and 7% not responding respectively. This shows that, as in the case described here, trial and error may be required to find a drug that will work for a particular patient. Removing sources of stress and the use of Feliway (Ceva Animal Health, France) may also help reduce

Comments First choice of treatment Risk of idiosyncratic liver failure so not recommended Monitor haematology (may cause aplastic anaemia) and liver enzymes (concern for hepatotoxicity) Only moderately effective Only effective in a small number of cats

signs (Rusbridge et al. 2010). Use of an Elizabethan collar or bandaging the paws may be required if self-mutilation is severe (Heath and Rusbridge 2010). Prognosis for resolution is fair. In the retrospective study by Rusbridge et al. (2010), 12/113 cats were euthanased due to ongoing or recurrent signs associated with FOPS, while 33/113 required permanent medication to control clinical signs and 53/113 were managed through episodes and then were able to be weaned off medication. For teething kittens, medication can usually be

withdrawn when the canines were fully erupted, however 10/18 of the kittens in the study had recurrent episodes with four of those ten requiring permanent medication. Seventy-five of the 113 cats in the study had recurrent on ongoing episodes.

References

Gandolfi B, Rusbridge C, Malik R, Lyons LA. Your Getting on my Nerves! The Feline Orofacial Pain Syndrome. Proceedings of the Tufts’ Canine and Feline Breeding and Genetics Conference, 2013 Heath S, Rusbridge C. Feline Orofacial Pain Syndrome. Proceedings of the 3rd AVA/NZVA Pan Pacific Veterinary Conference, Dental Stream, June, 2010. Plumb DC. Plumbs Veterinary Handbook (5th Edn). Blackwell Publishing, Ames USA, 2005 Rusbridge C, Heath S, Gunn-Moore DA, Knowler SP, Johnston N, McFadyen AK. Feline orofacial pain syndrome (FOPS): a retrospective study of 113 cases. Journal of Feline Medicine and Surgery 12, 498-508, 2010 Southerden P. Feline Orofacial Pain Syndrome. Proceedings of the 2013 BSAVA Congress, 2013. l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

CASE REPORT

Efficacy of Bravecto against ear-mites in 16 hound puppies Hannah Bain is a Technical Advisor (Companion Animal and Equine) for MSD Animal Health

HANNAH BAIN, BVSc (Dist.), MSD Animal Health and HUGH HASSELMAN, BVSc, VetSouth Gore

Introduction

Otodectes cynotis is a common mite of dogs and particularly cats (Forsyth 2013), found worldwide. Puppies and kittens appear to be more susceptible. Mites live on the surface of the ear canal, and feed on epidermal debris and tissue fluid. The resultant dry, dark debris is said to look like coffee grounds. Clinical signs may include pruritis and head-shaking, but infestations can be subclinical. In heavy infestations mites may leave the ear canal, causing infestations of the head, neck, and tail head. O. cynotis mites are readily transferred between hosts during close contact, and infestations are prevalent in animal shelters and breeding establishments (Arther et al. 2015). Clinical signs will usually prompt otoscopic examination, and diagnosis is made by observation of mites in swabs of the ear canal. The life-cycle is around 21 days, and treatment should be effective (or continued) beyond this timeframe so that larvae hatching from incubating eggs can be killed (Curtis 2004). When treating O. cynotis infestations, all in-contact dogs and cats should be included in the treatment programme. In addition, the environment, bedding and grooming equipment should be thoroughly cleaned as mites are capable of surviving for several weeks to months away from the host (Curtis 2004). As well

as miticidal agents, cleaning of the ear canal to remove exudate is an important part of treatment. Additionally, treatment for secondary bacterial/fungal infection and inflammation may be required. Otic preparations can be useful for topical treatment of ear mites, and some products are registered for this indication in New Zealand.

hunting hounds. They were found to be in generally good health, however the examining veterinarian noted headshaking and otic exudate in several pups. A swab of the exudate was taken with a cotton bud from several pups and a smear examined microscopically. Numerous mites (Figure 2) were seen which were identified as O. cynotis.

Systemic products are useful due to their longer efficacy. Those registered for use against O. cynotis in New Zealand include (not necessarily limited to) those containing imidacloprid/ moxidectin (Advocate®); and selamectin (Revolution®). Studies with these two products report efficacy one month after either a single application (Six et al. 2000; Shanks et al. 2009) or two applications one month apart (Six et al. 2000; Davis et al. 2007; Shanks et al. 2009; Arther et al. 2015). Bravecto chewable tablets contain fluralaner, an isoxazoline that has proven efficacy against fleas, the endemic New Zealand tick (Haemaphysalis longicornis) and Demodex species mites (generalised demodicosis) for 12 weeks. Efficacy against a range of other tick species exotic to New Zealand has also been demonstrated. This case summary outlines a New Zealand treatment trial of Bravecto chewable tablets against earmite (O. cynotis) infestation in dogs.

Figure 1. Several of the hound puppies

Case description

Sixteen, 12-week-old Harrier hound puppies (Figure 1) were presented for physical examination and vaccination. The pups were housed together in good facilities and intended for use as

Figure 2. Example of an ear-mite from one of the hound pups

Contact: hannah.bain@merck.com

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

On the basis of widespread ear-mite infestation in a controlled population of pups, the opportunity for a treatment trial with Bravecto (MSD Animal Health, Upper Hutt, New Zealand) was considered. One unpublished field-study1 demonstrated excellent efficacy of fluralaner against O. cynotis in dogs (n=16). Bravecto is registered for the control of fleas, ticks and Demodex spp. mites in dogs from 8 weeks of age and at least 2 kg bodyweight. Therefore Bravecto was considered a safe and valid choice for a treatment trial.

Treatment protocol

On the day of treatment with Bravecto (Day 0), the pups were 13 weeks old, and weighed 8–13 kg. The pups had previously been treated orally at the appropriate dose for their weight for internal parasites with Drontal Allwormer (Bayer Animal Health, Auckland, New Zealand), at 4, 6, 8, 10 and 12 weeks of age, and vaccinated (Vanguard Plus 5, Zoetis, Auckland, NZ) at 12 weeks of age. On Day 0 the pups were treated orally with Bravecto chewable tablets appropriate to their individual weight, to achieve the clinical dose of 25–56 mg/kg. On Days 0, 7, 14 and 35 the pups’ ear canals were examined visually using an otoscope. The number of mites in each ear was estimated and the scores for both ears averaged together to generate the mite score where 0 = 0 mites, 1 = 1–4 mites, 2 = 5–10 mites and 3 = >10 mites. Similarly, the amount of debris/cerumen observed in the ear canal was scored according to the following categories, 0 = none, 1 = slight, 2 = moderate and 3 = severe. On Day 14, pups with moderate or severe ear-canal debris scores were treated with Epi-Otic (Virbac, Hamilton, New Zealand) ear cleaner. Between Days 14 and 35, eight pups were rehomed and left the premises, therefore could not be included in the Day 35 examination.

Results

The results are shown in Tables 1. On Days 14 and 35, no mites were found in any of the pup’s ears. By Day 35, the debris scores had reduced in most pups. No adverse events were reported.

Discussion

In this group of pups, mite counts were reduced to zero in all pups within 14 days after treatment with Bravecto. As there was no control group, it cannot be confirmed that results were due to treatment, however this result is consistent with a previous field-study1 where a control group confirmed the reduction in mites was associated with treatment. As several of the pups were not available for the Day 35 count, and some pups had been treated with Epi-Otic ear cleaner on Day 14, the Day 35 results must be interpreted with caution.

Table 1. Results of treatment trial with Bravecto for pups with otitis externa due to Otodectes cynotis ear mites. The proportion of pups assigned to each score category for number of mites and amount of otic debris is shown

n Mite scorea 0 1 2 3 Otic debrisb 0 1 2 3

0 16

Days after Treatment 7 14 16 16

35 8

0 5 (31%) 3 (19%) 8 (50%)

9 (56%) 7 (44%) 0 0

16 (100%) 0 0 0

8 (100%) 0 0 0

0 11 (69%) 5 (31%) 0

1 (6%) 13 (81%) 2 (13%) 0

4 (25%) 9 (56%) 3 (19%) 0

1 (13%) 7 (87%) 0 0

a Mite score = average of number of mites in left and right ear estimated by visual examination of ear canals and categorised as 0 = 0 mites, 1 = 1–4 mites, 2 = 5–10 mites and 3 = >10 mites. b Ear canal debris score = average amount in left and right ears estimated by visual examination of ear canals and categorised as 0 = none, 1 = slight, 2 = moderate and 3 = severe.

References

Arther RG, Davis WL, Jacobsen JA, Lewis VA, Settje TL. Clinical evaluation of the safety and efficacy of 10% imidacloprid + 2.5% moxidectin topical solution for the treatment of ear mite (Otodectes cynotis) infestations in dogs. Veterinary Parasitology 2015, 210, 64, 2015 Curtis CF. Current trends in the treatment of Sarcoptes, Cheyletiella and Otodectes mite infestations in dogs and cats. Veterinary Dermatology 15, 108–114, 2004 Davis WL, Arther RG, Settje TS. Clinical evaluation of the efficacy and safety of topically applied imidacloprid plus moxidectin against ear mites (Otodectes cynotis) in client-owned cats. Parasitology Research 101, 19, 2007 Forsythe PF. Feline otitis. Proceedings of British Small Animal Veterinary Congress 2013 Shanks DJ, McTier TL, Rowan TG, Watson P, Thomas CA, Bowman DD, Hair JA, Pengo G, Genchi C, Smothers CD, Smith DG. The efficacy of selamectin in the treatment of naturally acquired aural infestations of Otodectes cynotis on dogs and cats. Veterinary Parasitology 91, 283, 2009 Six RH, Clemence RG, Thomas CA, Behan S, Boy MG, Watson P, Benchaoui HA, Clements PJ, Rowan TG, Jernigan AD. Efficacy and safety of selamectin against Sarcoptes scabiei on dogs and Otodectes cynotis on dogs and cats presented as veterinary patients. Veterinary Parasitology 91, 291, 2000 l

The long duration of efficacy of Bravecto against other ectoparasite species may also be favourable in treating ear-mites. These results indicate that Bravecto may be effective against Otodectes cynotis in dogs, however further investigation is needed to fully assess the therapeutic efficacy against this species. MSD Animal Health, data on file.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

CAV SPECIALIST PROFILE

Brent Higgins

BVSc, CertSAS, DiplECVS The Specialist Profile is a regular feature that aims to provide an insight into the path New Zealand veterinarians have taken to achieve specialisation.

THIS ISSUE TONI ANNS TALKS TO BRENT HIGGINS WHO IS A REGISTERED SPECIALIST IN SMALL ANIMAL SURGERY BASED AT VETSPECS IN CHRISTCHURCH. HE ALSO SPENDS TIME DEVELOPING ORTHOPAEDIC PRODUCTS AT OSSABILITY, THE COMPANY WHICH HE COFOUNDED.

What is your specialty, and how many years have you been practicing as a registered specialist?

I sat and passed my European College of Veterinary Surgeons exam 5 years ago and became a specialist soon after.

Where did you obtain your veterinary degree, and did you move directly into a residency from there? My undergraduate degree was at Massey. I then worked as a cattle vet in Australia for 2 years before heading to the UK and

Brent Higgins with the TTA Wedge System Osteotomy Guide developed by OssAbility the company he co-founded. Photo credit: OssAbility

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

practicing in small animal clinics. I started specialist training at Liverpool in 2006.

What drove you to specialise, and why did you choose surgery? I was dissatisfied with the quality of my clinical skills and yearned to just perform complex surgery. Why? Orthopaedic surgery is richly and immediately satisfying. You’ve either nailed the surgery and the patient will do well or there is an error and you have more to learn. You’ve got to deliver perfection and I like that challenge.

Explain the process you took to become a registered specialist?

I started working for free one day a week at a local specialist clinic in the UK. They eventually gave me a job as a surgical intern – working crazy hours. But I loved it and got to scrub in on cases and understand the process of surgery. I realised surgery was less about the blade and more about thinking and problem solving. Performing surgery is actually such a small part of the whole process of successful treatment – the true brilliance of surgery is in the decision-making outside of theatre. That internship helped me get a 3-year residency at the University of Liverpool. This was three years of pretty intense training with leading British surgeons. It was an amazing experience: fun but hard work. There were a lot of other residents at Liverpool so it was like being part of a family – we socialised together a lot. At the end I had spent 10 years away from NZ and I wanted to come home. I was fortunate to complete my training for one more year with Dr. Helen Milner in Christchurch at Vetspecs.

What do you like most about your job? Now I have my dream job… but its taken me till I'm age 39 to get there. On Mondays and Tuesdays I work as a specialist surgeon at VetSpecs seeing orthopaedic cases. For the rest of the week I work at OssAbility (the company I co-founded) developing orthopaedic products.

After my specialist exams were done I yearned for a creative outlet. I tried dancing and making music videos and searching for what I perceived was missing. That creative pull didn't let me settle.

specialist and that time was filled only with training and not much else. I was happy to give it my all and I think that’s the key. Specialist training takes a lot of time but it is also a lot of fun. Working with truly talented people is magical.

When I decided to become a parttime surgeon and focus on product development that was a confusing time as it was so soon after completing specialist training. But now it all makes sense and looking back I can connect the dots. Through founding OssAbility I get to create things that benefit other’s lives – surgeons as well as patients. It is an incredible feeling to have an idea and be able to bring it into existence. The opportunity to create mixes so well with the clinical work at VetSpecs.

What do you think is the future of surgery?

What is the worst part of your job?

It’s hard when a surgery is imperfect and you get a complication – I’m very hard on myself and that has an impact which I’m trying to be better at managing. I think all of us feel like that. This is the reason I believe technology will increasingly become important to us as clinicians: education and experience can only go so far and it’s hard to transfer these things to others. In contrast we can use technology to help us make better pre and intraoperative decisions and deliver better results for our patients. Technology just makes us better vets.

What advice would you give to someone thinking of specialising? Go for it! The heart always wins so you must follow your dreams. But be prepared for the training to take over your life for a few years. You will need to dive in deep! I recommend first spending time at a specialist clinic and seeing how the game works – it’s different to general practice.

What do you think about vets specialising later in their careers, after a significant period of time in general practice? I had been a GP for 6 years before starting specialist training. It then took me another few years to become a

Technology is changing all industries at an exponential pace. Think driverless cars, automated food production, communication. Surgery is one industry already being changed through technology and that change is occurring rapidly. Without this change surgery is just too subjective, too reliant on the expertise and emotions of humans. We created the OssAbility TTA Wedge System to remove that subjectivity. Surgeons no longer need to go through that painful learning curve. They can focus on the patient and use the technology we developed to be confident in the great results they are going to get. It means surgeons can sleep at night after they’ve done a surgery because the system makes surgery easier. That’s the future of surgery – technology helping us deliver great outcomes.

How did OssAbility begin?

OssAbility started with just me and an engineer when we worked together on his research of 3D printed titanium implants. The TTA Wedge System is just the beginning of a life-time developing products to help surgeons. We’ve now got a small team of engineers and share an office with a company producing implants for humans. It’s a pretty exciting environment to be working in.

What’s next for you?

Orthopaedics can be so much simpler. We can deliver excellence every time we perform surgery if we have the right tools. That’s what I’m trying to create at OssAbility and apply at Vetspecs. I want to develop the tools so that every vet can perform great surgery. Thankfully, NZ surgeons love being part of this mission and contributing to this dream. It’s probably the most exciting and creative time of my life, and it’s just the beginning. l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Worlds in Fusion 2016 NZVA Conference, 21â&#x20AC;&#x201C;24 June 2016, Claudelands, Hamilton

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Worlds in Fusion 2016 NZVA Conference, 21â&#x20AC;&#x201C;24 June 2016, Claudelands, Hamilton

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Worlds in Fusion 2016 NZVA Conference, 21â&#x20AC;&#x201C;24 June 2016, Claudelands, Hamilton

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

New Zealand Veterinary Journal Companion Animal Digest Volume 64, 4, 2016

Here we present brief summaries of the articles from the most recent issue(s) of the New Zealand Veterinary Journal that are likely to be of interest to companion animal veterinarians. Remember, even if you are not a subscriber to the print version of NZVJ, all NZVA members have free online full-text access to the NZVJ at http://www.sciquest.org.nz/nzvj

SARAH FOWLER BSc, MSc,

PhD, BVSc Editor, Companion Quarterly and Scientific Editor, NZVJ

How to ensure your nurses enjoy their job and keep turning up!

Relationships between workplace wellbeing, job demands and resources in a sample of veterinary nurses in New Zealand D Gardner and S Kimber Pages 224â&#x20AC;&#x201C;229

Why they did it

The work of veterinary nurses and technicians may be emotionally demanding, unpredictable, variably mundane and complex, with long hours. These job demands may lead to feelings of burn-out, cynicism and intentions to leave the job. Given the potential impact on individuals, veterinary businesses, clients and patients, there has been surprisingly little research into how these workplace demands affect vet nurses psychological wellbeing.

What they did

Veterinary nurses were asked to take part in an online survey in which nine variables (such as Job demands, Job resources, work engagement and emotional exhaustion) were assessed using questions or statements and the nurses asked to report how much they agreed with the statement. Statistical methods were then used to assess relationships among the variables studied.

What they found

Increasing job demands were related to emotional exhaustion, which led, unsurprisingly to increased cynicism and intentions to leave. However, demanding work need not be exhausting: when nurses were provided with sufficient resources in the form of equipment, skills, co-workers, time etc., this reduced emotional exhaustion and also benefited nurseâ&#x20AC;&#x2122;s family life. Feeling engaged with their work reduced both exhaustion and intentions to leave. Positive team relationships also helped nurses deal with a highly demanding job environment.

Take-home message

This study provides some important preliminary information to help create healthier workplaces for veterinary nurses. Sufficient job resources must be available to help nurses deal with their demanding work. Without these resources, nurses are vulnerable to emotional exhaustion and may resolve to leave the job.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Chronic relapsing pyoderma in a New Zealand dog caused by multi-drug resistant MRSP First report of a mecA-positive multidrug-resistant Staphylococcus pseudintermedius isolated from a dog in New Zealand AG Bell, GW Coombs, B Cater, C Douglass Pages 253-256

Why they did it

Globally MRSP infection is a major clinical problem of dogs, their owners and for the veterinarians who treat them. While MRSP is no more virulent than methicillin-susceptible S. pseudintermedius, successful treatment of canine pyoderma caused by MRSP can be very difficult and is a risk for infectionvulnerable dogs. This is the first report of a canine infection caused by MRSP in New Zealand.

What they did

This article reports a single case of a Sealyham terrier from Hamilton, which was referred to a specialist dermatologist for management of persistent skin disease involving numerous episodes of pododermatits, otitis and pyoderma, probably with underlying atopy, over a period of 6 years.

What they found

Upon presentation to the dermatologist the dog was diagnosed with mucocutaneous pyoderma (nasal, lip margins and peri-anal), superficial spreading pyoderma and focal deep pyoderma. The infecting organism was identified as Staphlococcus pseudintermedius which was resistant to numerous antimicrobials including oxacillin (a surrogate for methicillin) and carried the mecA gene which confers resistance to B-lactam antimicrobials.

The dog was treated with rifampicin (100 mg/day orally) for 2 weeks and topical cream containing mupirocin was applied to the nose, lips and anus 2–3 times daily. Due to the risk of hepatotoxicity, cefpodoxime was substituted for the rifampicin, followed by enrofloxacin when the lesions worsened. Before cure could be achieved the dog was euthanased due to collapse, pyrexia and signs of renal disease.

Take-home message

Veterinarians should be aware that multi-drug resistant MRSP is present in New Zealand Around 50% of healthy dogs are colonised with S. psuedintermedius and it is a common cause of skin and ear infections. Treatment of such infections caused by MRSP is difficult due to the limited number of effective and available antimicrobials. The authors stressed the need for veterinarians to carefully assess the response of canine pyoderma to antimicrobial treatment and perform culture and sensitivity (including to oxacillin) if infections do not respond to treatment.

Corrigendum The New Zealand Veterinary Journal Companion Animal Digest in the Companion Quarterly 27(2) 2016 contained a summary on page 34 of the article by Ryan Cattin titled “Distribution of blood types in a sample of 245 New Zealand non-purebred cats” which contained an error. The summary stated that: Type A cats given type B blood may experience anaphylaxis haemolysis and death with the lifespan of transfused cells are significantly reduced in type B cats given type A blood. The correct sentence should read: Type B cats given type A blood may experience anaphylaxis haemolysis and death with the lifespan of transfused cells are significantly reduced in type A cats given type B blood. l

Article Awards

Thinking about writing up an article for Companion Quarterly? Remember practitioners or veterinary students whose articles are accepted for publication are eligible for the following awards and prizes: • Articles accepted for publication (practitioners): $150 • Article accepted for publication (students): $50 (note: in error this was given as $100 in the June 2016 issue of Companion Quarterly) • Best article of the issue prize: $100 • Best article of the year prize: $400 (sponsored by Eyevet Services) • Best student article of the year prize: $400 (sponsored by VetEnt) Note: Articles submitted by companies or as part of the requirements for receiving a CAS grant are not eligible for prizes.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Massey News People

It is with sadness that we announce that Richard Kuipers von Lande is leaving the VTH at the end of August after 10 years as a key member of the small animal surgical team. Richard is heading to the UK with his family to be closer to relatives and will be venturing into private referral practice. Whilst on faculty, Richard completed residency training and became a fellow of the Australian and New Zealand College of Veterinary Scientists. During his tenure, Richard has contributed immensely to both the teaching programme and the referral service. He will be sorely missed and will be remembered for his dedication to teaching through his tutorials and practical sessions and his MacGyver abilities to fabricate myriad teaching aids and surgical constructs. We wish you well Richardo and hope to see you back some time in the future. It is with great pleasure that we can announce that Sarah Hill – our internal medicine registrar – has successfully passed the primary examinations of the American College of Veterinary Surgeons. This qualifies her to sit the final part of the examination to become a Diplomat of the College. Sarah will be heading to new pastures soon but is currently on the medicine service in a clinical capacity. Last month we said goodbye to our 2015 crop of rotating interns and we have welcomed the new intake into the Small Animal Hospital: Ester Quilez, Kevin Kang, Karolina Roszak, Matthew Yeung, Rayan Rouch and Sophie Lovell.

Patrons Day advance notice

This years Companion Animal Patrons Day will be on the 2nd of December. This is our annual CPD day, free to any Patron of the VTH. If you are outside or referral area and still want to come there is a reasonable priced attendance fee to cover catering and support the VTH. Patrons Day has been annually sponsored by Zoetis NZ.

VTH research projects

A reminder that we are actively recruiting cases for several clinical research trials. All research at the VTH is conducted with informed client consent and is optional. Where applicable the project has been approved by the Massey University Animal Welfare Committee. We are looking for cases of: • Suspected Cushing’s disease – blood sampling and analysis • Appendicular osteosarcoma – novel limb sparing using 3D titanium printing • Lumbosacral stenosis – novel stabilisation using 3D titanium printing • Angular limb deformity – computer assisted surgery using 3D-printed guides • Talo-crural instability in working dogs – new method of stabilisation of repair • Condylar fractures of the humerus in working dogs – CT study of contralateral limb. To find out more contact the MUVTH on 063505329 and ask for the Small Animal Clinical Trials Technician. l

The intern programme allows recent graduates to extend their learning in a teaching hospital environment and is part of the pathway to specialization for many. The interns work in the 24-hour MU Pet Emergency Centre as well as rotating through the medicine and surgery referral service, anaesthesia and radiology.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

What is your diagnosis? THE ANSWERS… 1 What are your radiographic findings? There is a ventral mass effect with dorsal displacement of the caudal two-thirds of the cervical trachea. This mass has a homogenous softtissue opacity in the ventral cervical region with no obvious cystic or other structures noted. The mass is more difficult to visualize and appreciate on the lateral projection. No orthopedic abnormalities are noted within the cervical vertebrae. It is difficult to appreciate the involvement of local structures in relation to this mass from these images. 2 What are your differential diagnoses? • Neoplastic mass: thyroid adenoma/ carcinoma, secondary metastasis to the thyroid gland, carotid body tumor, leiomyosarcoma • Oesophageal foreign body • Cellulitis/granuloma/infectious mass, i.e. para-oesophageal abscess, foreign body with resultant inflammatory/infectious tissue • Salivary gland inflammation or neoplasia • Lymphadenopathy (submandibular, medial retropharyngeal, cervical) – unlikely due to size of the mass 3 What are your differential diagnoses for the mass following in-house cytology given the clinical presentation? The slides show significant blood contamination with large numbers of normal erythrocytes and a normal population of inflammatory cells. This suggests the mass is not inflammatory in origin. In multiple views of the slide a moderate number of clumped, relatively uniform cells with mostly central nuclei and indistinct cytoplamic borders can be seen. Free nuclei can also be seen. These features are typical for thyroid epithelial cells. Thyroid epithelial cells occaisionally contain dark blue

granules, however this was not observed in these slides. The epithelial cells exhibit mild pleomorphisim and anisokaryosis indicating the mass is neoplastic. Given the history, physical examination and cytological findings the most likely differential diagnosis is a neoplastic mass of thyroid origin. However, other neoplasias cannot not be rulled out including plasma cell tumor, mast cell tumor, lymphosarcoma, melanoma and histiocytoma. Cytology is a useful diagnostic tool to confirm or increase a clinicians suspicion of thyroid neoplasia, however, this is not a reliable means to distinguish benign from malignant neoplasms as masses which appear cytologically benign may be highly malignant (Tobias and Johnston 2012). A definitive diagnosis and more accurate distinction of malignancy is based on capsular and/or vascular invasion assessed via histology (Feldman et al. 2015). 4 How would you proceed with further diagnostics and intervention? Additional survey and diagnostic imaging was performed to investigate the mass’ location relative to closely associated sensitive structures, assess local invasion of tissues, allow surgical excision planning and scan for distant metastasis. Blood testing was performed prior to anaesthesia including serum biochemistry and electrolyte analysis, a complete blood count and serum thyroxine analysis. Most canine thyroid tumors are endocrinologically nonfunctional with approximately 10% of affected canine patients reported to be hyperthyroid and approximately 55–60% euthyroid (Alleman and Choi 2010; Tobias and Johnston 2012). Serum thyroxine levels in this patient were low (10 nmol/L; reference range 20–66 nmol/L). Clinical

hypothyroidism only results after 80% destruction of both thyroid glands. Since thyroid neoplasia is typically unilateral and euthyroid sick syndrome may supress thyroxine levels, care must be taken in interpreting this measurement (Feldman et al. (2015). No other irregularities consistent with hypothyroidism were observed in this patient’s history, clinical examination or blood testing. Computed tomographic (CT) imaging (Figure 3) was performed on the cervical neck, thorax, and abdomen. This included images (Figure 3b) taken after I/V administration of iohexol (Omnipaque), an iodinated contrast agent. This technique improved the identification of the extent and borders of the vascular cervical mass. No evidence of local tissue invasion or distant metastasis was identified with advanced imaging.

Treatment:

With the presenting clinical history, physical and diagnostic findings, and a tentative diagnosis of thyroid neoplasia, surgical en bloc excision was pursued providing both definitive diagnosis following histology, and treatment for this patient. A midline ventral cervical incision exposed a large mass bulging laterally between the sternocephalicus and sternohyoideus muscles. The caudal laryngeal nerve was identified adhered to the medial aspect of the mass which required careful blunt dissection to elevate it from the surface of the mass. The mass appeared grossly non-invasive with a good areolar fascia surrounding, assisting marginal en bloc resection. The lateral retropharyngeal lymph node was also removed. The excised mass was submitted for histology and diagnosed as a compact thyroid adenocarcinoma. The tumour was surrounded by a capsule; there was no vascular invasion outside the capsule.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Figure 3. (a) CT image at the level of the 3rd cervical vertebra. (b) CT view at the same level 45 seconds after IV adminstration of iodinated contrast medium.

Follow-up thyroid function testing and imaging was recommended to monitor for possible metastasis and remaining thyroid tissue function. The patient was discharged following routine post-operative recovery. The owners reported that she was doing well on a follow-up phone consultation 3 weeks following surgery.

Discussion: thyroid neoplasia

Thyroid tumors are relatively common in canine patients accounting for 1.2–3.8% of all canine tumors and 10–15% of all canine head and neck tumors (Withrow and Vail 2007; Campos et al. 2014). While thyroid adenomas account for 30–50% of thyroid masses identified at necropsy, they are usually small, non-invasive incidental lesions that are clinically silent (Withrow and Vail 2007). Malignant thyroid tumors, however, are usually large and easily palpable and so comprise approximately 90% of all clinically detected thyroid tumors. The majority (up to 75%) of malignant thyroid tumours occur unilaterally (Liptak 2007; Tobias and Johnston 2012; Feldman et al. 2015). Thyroid tumors can also arise from ectopic thyroidal tissue, present within the tongue, ventral neck (usually lateral to the trachea), cranial mediastinum or heart base (Alleman and Choi 2010; Tobias and Johnston 2012). Thyroid carcinomas in canine patients

are typically large, highly vascular and poorly encapsulated masses that readily invade or surround local tissues including the trachea, oesophagus, cervical musculature and neurovascular structures (Tobias and Johnston 2012; Feldman et al. 2015). Distant metastasis is common, most frequently to the pulmonary parenchyma and regional lymph nodes with the majority of lymphatic drainage in a cranial direction (Alleman and Choi 2010; Feldman et al. 2015). Two known risk factors for the development of thyroid neoplasia include thyroiditis resulting in hypothyroidism, and exposure to ionizing radiation, with iodine deficiency/ excess, and a chronic excess of thyroidstimulating hormone secretion also suggested (Feldman et al. 2015).

Presenting clinical signs/signalment

Typically patients with thyroid carcinomas are middle-aged to older (median age at diagnosis 9–11 years) presenting with a palpable mass in the ventral cervical region as the main complaint from the client (Withrow and Vail 2007). Other commonly reported signs resulting from a mass effect and/ or local invasion include; coughing, tachypnea, dyspnea, dysphagia, dysphonia, stridor or stertor, dysphagia, weight loss, vomiting, regurgitation, retching, anorexia, horners syndrome

due to invasion of the vagosympathetic trunk, and facial oedema (Withrow and Vail 2007; Feldman et al. 2015). When thyroid tumors are functional (i.e. produce thryroid hormone), additional clinical symptoms of hyperthyroidism may be detected. No sex predilection has been reported in the literature with breeds believed to be at increased risk including Boxers, Beagles, Golden Retrievers and Siberian Huskies (Feldman et al. 2015). Most thyroid masses are firm, irregular in shape, nonpainful and relatively unmovable appearing embedded into surrounding tissue. As the thyroid gland is not normally palpable in the dog and most thyroid masses are carcinomas, any mass identified in this region warrants further investigation. The mobility of a palpable mass is a poor indicator of whether a tumour is histologically invasive (Deitz et al. 2014).

Diagnostic imaging

Useful diagnostic imaging modalities include; ultrasound, CT, magnetic resonance imaging (MRI) and scintigraphy. Diagnostic imaging provides valuable information to increase suspicion of a thyroid tumor, guide FNA sampling, investigate the location of closely associated sensitive structures, assess local invasion of tissues, investigate for distant metastasis and enable tailored treatment.

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Survey imaging as a minimum should always be pursued prior to intervention as approximately 30–40% of dogs with thyroid carcinomas have been found to have metastatic disease at initial presentation with 60–80% developing metastasis during the course of the disease (Withrow and Vail 2007; Tobias and Johnston 2012; Feldman et al. 2015). Imaging should be focused on the most common sites for metastasis, including the pulmonary parenchyma and regional lymph nodes, with a secondary focus for possible metastasis to the abdominal viscera and skeleton (Tobias and Johnston 2012). A prospective study of 13 dogs comparing ultrasound, CT, and MRI for diagnosing histologically or cytologically confirmed thyroid carcinomas, identified sensitivities of 79%, 85%, and 93%, and specificities of 33%, 100%, and 67% respectfully (Taeymans et al. 2013). Findings identified MRI imaging to be the preferred modality for preoperative diagnosis and staging as it most closely matched histology for local tissue invasion.

Local anatomy

The paired thyroid glands lie lateral to the cranial cervical trachea with the caudal laryngeal nerve running dorsomedially in close proximity to each gland. Lymphatic draininge from the thyroid gland is predominantly cranial to the deep cervical lymph node, which can be absent in a good proportion of dogs. Subsequently, the retropharyngeal lymph node is a common site for drainage and subsequent identification of metastasis. The four small parathyroid glands lie intimately associationed with the thyroid glands. The two internal parathyroid glands are embedded within the caudal poles of the respective thyroid glands while the external parathyroid glands are typically found close to the cranial dorsolateral margin of each of the thyroid glands although their location may vary.

Surgical and/or oncological management

Withrow and Vail (2007) estimate that only 25–50% of thyroid carcinomas are amenable to surgical treatment at the time of initial diagnosis. Freely movable, non-invasive masses, identified with advanced imaging, should be managed surgically via marginal resection at a plane adjacent to the tumor capsule (Withrow and Vail 2007). Given the location of closely associated sensitive structures, it is encouraging to note that marginal resection of such masses does not appear to increase the risk of recurrence (Feldman et al. 2015). This less aggressive approach should result in less postoperative complications which in addition to routine surgical complications of infection, dehiscence, delayed healing and seroma formation can include; clinical hypocalcemia, laryngeal paralysis, and extensive hemorrhage. (Feldman et al. 2015). External beam radiation, radioactive iodine and chemotherapy have also been described in the literature as limited primary and adjunctive therapies for canine thyroid tumours where surgical intervention is not applicable. The general prognosis for malignant thyroid tumors is regarded as guarded to poor. Prognostic factors for thyroid carcinomas include the degree of mobility, histomorphologic criteria of malignancy, and tumor stage (Feldman et al. 2015). Large tumor volumes (>20 cm3), bilateral disease and cervical vascular invasion are poor prognostic indicators correlated with high metastatic rates (Campos et al. 2014). Without treatment, the median survival time for malignant thyroid carcinomas is approximately 3 months. With appropriate treatment and management, however, median survival times are increased up to 36 months with surgery alone (mobile carcinomas) and 45 months with surgery and adjunctive external beam radiation therapy (Liptak 2007). Local recurrence

rates have been reported at 30% following thyroidectomy (Liptak 2007). Recommended follow-up monitoring includes frequent physical examination, diagnostic imaging for local and distant metastasis, and blood testing for calcium levels and thyroid function.

References

Alleman AR, Choi US. Endocrine System. In: Alleman AR, Andreasen CB, Avery AC, Avery PC (eds). Canine and Feline Cytology. Second Edtn. Pp 383–94. Elsevier Saunders, St Louis, MO, USA 2010 Campos M, Ducatelle R, Rutteman G, Kooistra HS, Duchateau L, de Rooster H, Peremans K, Daminet S. Clinical, pathologic, and immunohistochemical prognostic factors in dogs with thyroid carcinoma. Journal of Veterinary Internal Medicine 28, 1805–13, 2014 Deitz K, Gilmour L, Wilke V, Riedesel E. Computed tomographic appearance of canine thyroid tumours. Journal of Small Animal Practice 55, 323–9, 2014 Feldman EC, Nelson RW, Reusch C, Scott-Moncrieff CJ. Canine and Feline Endocrinology. Fourth edition Pp 204–11. Elsevier Saunders, St Louis, MO, USA 2015 Liptak JM. Canine thyroid carcinoma. Clinical Techniques in Small Animal Practice 22, 75–81, 2007 Taeymans O, Penninck DG, Peters RM. Comparison between clinical, ultrasound, CT, MRI, and pathology findings in dogs presented for suspected thyroid carcinoma. Veterinary Radiology and Ultrasound 54, 61–70, 2013 Tobias KM, Johnston SA. Thyroid and Parathyroid Glands. In: Seguin B, Brownlee L (eds). Veterinary Surgery: Small Animal 1st Edtn. Pp 709–23. Elsevier Saunders, St Louis, MO, USA, 2012 Withrow SJ, Vail DM. Withrow and MacEwen's Small Animal Clinical Oncology. Pp 592–6, Elsevier Saunders, St Louis, MO, USA, 2007 l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Companion Animal Health Foundation Update Firstly a huge thank you to all those who supported CAHF at the NZVA Conference! I hope you had a great time with your fellow colleagues, and came away with refreshed knowledge along with new tips and tricks. CAHF looks forward to continuing to support research that advances our knowledge in companion animal veterinary medicine, which the generously donated funds will go towards. CATH WATSON, Chair

internal fundraiser for your practice, or simply by making an individual donation.

Companion Animal Health Foundation

On that note, I’d like to gently remind you all that CAHF is a charity established by CAV to directly benefit companion animals in New Zealand, not only by supporting research relevant to New Zealand, but we’d also like to support projects which promote public knowledge in New Zealand on companion animal issues, along with welfare work and projects relating to the well-being of all companion animals. The next funding round closes for applications on 30th September 2016. The trustees are keen to support veterinarians and nurses in clinical practice who have projects relevant to the CAHF aims, so applications from those in clinical practice will be given favourable consideration in this next funding round. To enable this funding to continue, CAHF needs further support financially, so we have come up with a challenge for you all…we’re challenging every practice in NZ raise $500!

Could your practice raise $500 or more? We need your support

The Companion Animal Health Foundation (CAHF) was founded in 1996 with the goal of improving the health and wellbeing of our companion animals. The CAHF is a registered independent charity (CC32372) operated in association with the New Zealand Veterinary Association. The CAHF has supported investigations into important health problems of pets in New Zealand over the last 10 years but support has been limited because the foundation is reliant on charitable donations from the veterinary profession and from the public.

Source: https://pixabay.com

Pets are subjected to many diseases, injuries and abuse. However, while there are several charities devoted to the prevention of cruelty to pets, few are concerned with the improvement of companion animal health through improved medical care, surgery, and an understanding of sociological issues related to pets in New Zealand. The CAHF supports and assists veterinarians and veterinary nurses to undertake investigations into the problems associated with companion animals; medicine, surgery, and investigations on the relationships between animals, pet owners and the veterinary profession. The goal of the CAHF is to help veterinarians to help pets enjoy longer and healthier lives.

Support the future of pet health by donation to the CAHF

We are asking for the support of all practices in New Zealand and individual veterinarians to raise at least $500 each, a sum which would secure the future of the CAHF and ensure it works as planned to help our pets enjoy better and healthier lives. Every dollar will be used to help combat health and welfare problems encountered by companion animals in New Zealand. By joining our $500 Project, we are asking practices to pledge to raise $500 by whatever means they can; external fundraising events, organizing your own

It is important that we raise the profile of the CAHF amongst the general public. There is a CAHF brochure for you display in your practice and we hope that individual pet owners will also see the vital importance of New Zealand-based investigations into pet diseases and will also be willing to donate to the CAHF. Remember that fundraising activities that encourage owners to take part, help us, and also advance your practice profile.

What’s in it for you?

If you join our $500 Project we will provide you with a certificate that will identify you or your practice as a committed CAHF supporter. Donations of $2000-plus and $5000 or more will be designated as Silver and Gold supporters respectively, and certification will reflect that status. Remember all donations over $5 are tax deductible. We have a dedicated area on our website (www.healthypets.org.nz) where your practice, as a supporter will be also identified. The website also has information about the CAHF, its Trustees, activities and current projects. There will be a site for notices and photos of practice and other fundraiser events in support of CAHF. Supporting the CAHF 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 CAHF.

So what’s next?

We will be in contact with you soon. However, if you wish to register your practice as an annual $500 practice supporter for CAHF, use the online registration form on the website www. healthypets.org.nz l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

History of the New Zealand Companion Animal Register PIETER VERHOEK, CAV/

NZVA representative to NZCAR, NZCAT

What is the NZCAR? NZCAR is the acronym for the New Zealand Companion Animal Register; i.e. the database that contains the details of microchipped companion animals and their owners and whose primary function is the repatriation of lost pets in New Zealand. The website is www. animalregister.co.nz Why was the NZCAR established? This story starts in the late 1990s when the Labour Government of the day wanted to introduce a means to tackle the dangerous dogs issue that was rearing its ugly head. In the late 1990s a young girl was severely bitten by a large mastiff-type dog and this attracted a lot of media attention. In response to this, the government of the dayâ&#x20AC;&#x2122;s reaction was to establish the National Dog Database (NDD). The Local Government working group built a model which connected dog to owner with a microchip for management purposes only and with the passage of time have come to realise the limitations. The NDD was never created with repatriation of lost pets in mind and was never intended to involve cats or any other species. All of this occurred despite intense lobbying from NZVA. In the mid 2000s the New Zealand Companion Animal Council (NZCAC), under the chairmanship of ex-NZVA President Dr Ross Blanks, began a discussion to solve this problem; i.e. to establish a separate microchip database for ALL companion animals of any species, with the sole purpose of repatriation, i.e. the ability to return lost animals back to their owners.

A working group, which included stakeholders from; NZVA, CAS (now CAV), RNZSPCA, New Zealand Kennel Club (NZKC), New Zealand Cat Fancy (NZCF) and the NZCAC itself, began work in earnest. Over a short period of time a business plan was drawn up and expressions of interest in establishing and managing the database were asked for which resulted in Animal Register Ltd being awarded the contract. Each of these stakeholders loaned NZCAC $8000 to establish the NZCAR, as the NZCAC at the time did not have sufficient funds to construct the database and infrastructure. This seed funding has since been re-paid. Of note is, the NZCAC owns the software of the microchip database. The web-based database began accepting registrations in September 2007. In the first month of operation 115 animals were registered, while nowadays the average monthly registrations are between 6000â&#x20AC;&#x201C;8000.

Some facts about NZCAR:

- There are now about over 800 organisations registered with either implanter or enquiry status to the NZCAR - 56.9% of registrations are cats - 42.2% of registrations are dogs - the remaining are rabbits, goats, horses, birds, turtles, rats, fish and some others!! - as at July 2016 over 470,000 animals are registered - profits from the NZCAR are used to help fund the NZCAC as well as other companion animal charities and projects within New Zealand. Over $2.8 million has been raised since 2007. - owners can access their own information 24/7 to report a pet missing, update address and phone

details or to change the contact details. They can also use the 0800 support line which operates 8.30am to midnight, and has an emergency contact and message service outside these hours. A key feature of the NZCAR is that all changes on the system are logged and no change of contact details is permitted without the consent of the listed primary contact. This is essential and very important, because sadly disputes over ownership occur quite often. Another important fact is that NZCAR is not a legal ownership database. When the NZCAR was founded the NZCAC also created the New Zealand Companion Animal Trust to manage the profits, but this is a topic for another article. There are numerous success stories since the establishment of the NZCAR. One story in particular worth relating is following the Christchurch earthquake in February 2011 the NZCAR was actively involved in supporting the Canterbury SPCA to get all lost pets home. Of those found cats and dogs that were microchipped, over 80% of owners were notified within 2 hours. However found pets that were not microchipped often took days to get back home. This stretched resources and tracking owners was extremely time consuming for the rescue organisations involved. Subsequent to the earthquake NZCAC, NZCAT, NZCAR and Animal Register Ltd also donated over 12,500 microchips and free registrations for the pets of Christchurch. This project had a combined value in excess of $160,000. Without widespread public support of the NZCAR this level of donation for pets and pet owners in Christchurch would not have been possible. l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

Instructions for Authors submitting articles to the Companion Quarterly SARAH FOWLER (Editor), for

the Companion Quarterly Editorial Committee

The Companion Quarterly is published quarterly in the first week of March, June, September and December of each year. The printing costs are covered by the advertisements. There is therefore a limit of about 55–60 pages to the size of each issue. There is a balance between political issues, articles for continuing education and other news. Authors are expected to submit their articles and conference in a final form suitable for publication. If practitioners wish assistance with writing, please contact the editor. Also look at previous issues to see the layout.

Articles

The article should have a title. Following the title the names of the authors, their degrees, titles, contact details should be present. Submit articles preferably by email, or disk if this is not possible. Submit articles in adequate time for reading and alterations before publication. Contributions must be original. Articles or extracts from articles may be completely copied only if there is permission from the original authors and source of publication. It is the responsibility of the author(s) rather than the editorial committee to obtain this permission. The author(s) should disclose if they have published the same article or a very similar article elsewhere. Articles that are clearly editorials/advertising will be labelled as such at the discretion of the editorial committee. These include articles/editorials that are repeated from other publications such as VetScript and that contain obvious product placement comments.

Proof reading

The authors should proof read their article looking for mistakes, spelling errors, omitted details. While the editorial committee reads through the articles, the articles should be presented error-free.

Articles and conference reports from recipients of grants and scholarships It is the responsibility of recipients of any grants and scholarships to supply any conference reports and articles written as part of the requirements in the final form suitable for publication.

References

A list of references should be supplied if appropriate. Follow the guidelines for the New Zealand Veterinary Journal for method of reporting of references. The number of references should be kept to a reasonable number relative to the length of article. Keep numbers of references to a minimum when discussing a single point, i.e. do not be repetitive with numerous references when a few will do. The editorial committee will omit references if the list is judged to be excessively long.

Figures

Good quality illustrations that clearly illustrate the necessary points should be submitted with the article. Submit any photos or graphics in their original forms (i.e. JPG, PDF, TIF files) as they lose their clarity when extracting them from Word or Publisher documents. If positions of figures are not obvious from the text, send a hard copy or some other form of instruction as to where they should be placed. Figures should be clearly numbered labelled as to top and bottom where necessary. Features on the figures should be clearly labelled by the author(s). The figure captions should be concise and accurate, and supplied with the text on a separate page at the end of the article. Diagrams/figures can be copied from textbooks only if there is permission from the original author and the source is clearly acknowledged. It is the responsibility of the author(s) to obtain this permission before submitting the article to the Quarterly editorial committee.

Timing of article submission and publication

Articles will be published as soon as possible after submission. The newsletter goes out in the first week of March, June, September and December. Articles therefore need to be submitted at least one month before (i.e. by the end of January, April, July and October) but preferably earlier to allow one month for the collation, printing, binding and posting of the Quarterly. Depending on when the articles are received, the size of that particular issue and the need for refereeing, at the editor’s discretion articles may be held over for a later issue.

Refereeing

Articles may be sent to appropriate people in that field of expertise for refereeing/proof reading if the editorial committee deems this

is necessary. This is to ensure accuracy within the text to protect readers, the authors CAV and the clients and the patients of veterinary practitioners.

SciQuest and the NZVA website

Selected scientific articles will be placed on the SciQuest website for access by NZVA. There will be a delay of a year to ensure that practitioners still see a benefit in becoming CAV members. The entire newsletter is now being placed on the CAV website but the most recent issues (i.e. those within a year of publication) are available only to CAV members.

Article of the issue and student article

Prizes are sponsored for the best case report and general article in each quarterly issue. The best overall article in each category for the year is then decided in May and the overall prize awarded at the Annual dinner in June. The members of the editorial committee will judge the articles on their clarity, conciseness, and usefulness to practitioners. Articles that are submitted to the Quarterly as part of an obligation due to the author(s) receiving Educating the Educator or Study/ Research Grants from CAV are not eligible for the article of the issue prizes. Articles submitted by the editor and the members of the editorial committee are also not eligible for the prizes. There is a separate undergraduate student article competition.

Planning a case report? Some hints as to how do so!

When writing an article take time to look at how articles in other journals are arranged. While articles for the Quarterly are not as detailed as the NZVJ the information needs to be arranged in a logical manner to make it easy for the reader to follow. Therefore follow some logical headings as detailed below. Not all of these headings will need to be used in all articles and some may be combined depending on the type of case and amount and type of information available. • Introduction • History • Clinical signs • Materials and methods • Results (of investigations e.g. laboratory results, radiography). • Discussion • Conclusion • Acknowledgments • References. l

Companion Quarterly: Official Newletter of the Companion Animal Veterinarians Branch of the NZVA | Volume 27 No 3 | September 2016

NZVA COMPANION ANIMAL SOCIETY NEWSLETTER

New Zealand Veterinary Association

Companion Animal Society Volume 27 No 1 March 2016

In This Issue ...

• Management of diabetes mellitus in cats • Diskospondylitis – a casebased review • Parasites in NZ cats and dogs - a survey • Conference report: American Veterinary Dental Forum 2015 • Specialist Profile: Robyn Gear • NZVJ Companion Animal Digest • What is your diagnosis?

VOLUME 27 NO 1 MARCH 2016