C&T Series Issue 313

C&T

Centre for Veterinary Education

Control & Therapy Series Issue 313 | D e cember 2023

29 Major Winner—Veterinary Management of Free-Ranging Native Birds Dr Timothy Portas

Hairball Conundrums

7

Feline Hyperaesthesia

13

A Bit of a Problem in Equine Welfare

23

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C&T Issue 313 | December 2023

Control & Therapy Series

PUBLISHER Centre for Veterinary Education Veterinary Science Conference Centre Regimental Drive The University of Sydney NSW 2006 + 61 2 9351 7979 cve.publications@sydney.edu.au cve.edu.au Print Post Approval No. 10005007 DIRECTOR Dr Simone Maher EDITOR Lis Churchward elisabeth.churchward@sydney.edu.au EDITORIAL ASSISTANT Dr Jo Krockenberger joanne.krockenberger@sydney.edu.au VETERINARY EDITOR Dr Richard Malik DESIGNER Samin Mirgheshmi ADVERTISING Lis Churchward elisabeth.churchward@sydney.edu.au To integrate your brand with C&T in print and digital and to discuss new business opportunities, please contact: MARKETING AND SALES MANAGER Ines Borovic ines.borovic@sydney.edu.au

DISCLAIMER All content made available in the Control & Therapy (including articles and videos) may be used by readers (You or Your) for educational purposes only.

Knowledge and best practice in this field are constantly changing. As new research and experience broadens our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. You are advised to check the most current information provided (1) on procedures featured or (2) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications.

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Engage With Your Profession.............................................................2 From the Director................................................................................2 Congratulations to Bill Howey..........................................................22 Congratulations to the Distance Education class of 2023! ������ 46

Small Animal Hereditary Haemophilia A in a Young Dog Maddie Roberts...................................................................................4 Hairball Conundrums

Winner

Rachel Korman & Alison Jukes ������������ 7

Companion Animal Zoonoses Guidelines - Boehringer Ingelheim................................................................................................ 7 Research Roundup............................................................................. 10 Feline Hyperaesthesia Syndrome Clare Rusbridge.................. 11 Feline Hyperaesthesia: Wally’s Story Sue England................... 13 Cautionary Tails

Simone Maher................................................... 14

Low Dose Radiation as a Possible Treatment for Cystitis ��������� 18 Tincture of Time: Some Brief Tick Paralysis Facts Rick Atwell.......................................................................................... 27 Perineal Hernia Repair......................................................................28 Dog Diet Study.....................................................................................28

L arge Animal A Large Scale Poisoning Event in Cattle Caused by Cape Tulip Daniel Reiner, Julie Wayne & Jeremy Rogers .......................... 16 Cancer Eye of Cattle Mac Kneipp............................................... 19

Winner Best Visuals

A Bit of a Problem in Equine Welfare: What is the Role of Veterinarians? Andrea Harvey.....................................................23

Perspective Veterinary Management of Free-Ranging Native Birds Timothy Portas..................................................................................29

What's Your Diagnosis?

What’s Your Diagnosis?

Natalie Courtman & Beth McDonald..............................................3 After-Hours Dystocia Case in a Multiparous Beef Cow Robert Mills........................................................................................ 44

Major Winner

From the Director

The unique C&T Series was established in 1969 by our first Director Dr Tom Hungerford OBE BVSc FACVSc HAD who wanted a forum for uncensored and unedited material, to get the clinicians writing:

"

not the academic correctitudes, not the theoretical niceties, not the super correct platitudes that have passed the panel of review… not what he/she should have done, BUT WHAT HE/SHE DID, right or wrong, the full detail, revealing the actual ‘blood and dung and guts’ of real practice as it happened, when tired, at night, in the rain in the paddock, poor lighting, no other vet to help.

The C&T forum gives a ‘voice’ to the profession and everyone interested in animal welfare. You don’t have to be a CVE Member to contribute an article—please send your submissions to Dr Jo Krockenberger. joanne.krockenberger@sydney.edu.au

Join In! The C&T is not a peer-reviewed journal.

We are keen on publishing short, pithy, practical articles (a simple paragraph is fine) that our readers can immediately relate to and utilise. Our editors will assist with English and grammar as required.

"

I enjoy reading the C&T more than any other veterinary publication.

-Terry King, Veterinary Specialist Services, QLD

Thank You to All Contributors The C&T Series thrives due to your generosity.

Winners Major Winner Prize: A CVE$400 voucher Veterinary Management of Free-Ranging Native Birds Timothy Portas............................................................................29 Winners Prize: A CVE$100 voucher Hereditary Haemophilia A in a Young Dog Maddie Roberts............................................................................4

Suddenly it’s December again and as usual, our final edition of the C&T for the year is a bumper one indeed.

The submission awarded our major winner prize is by Timothy Portas, with a practical run down on veterinary management of free-ranging native birds. A hallmark of this time of year for many is juvenile birds being brought into clinics; management of nestlings and fledglings is covered by Timothy, along with many of the common ailments of birds. Make sure you share this article with your colleagues and keep it within easy reach.

Andrea Harvey provides some thought-provoking commentary on the use of bits in horses, challenging us to question whether ubiquitous use has blinded us to the negative impact they may have. A must read for any horseriding vets!

Daniel Reiner, Julie Wayne and Jeremy Rogers report on a cattle poisoning event caused by cape tulip which makes for a fascinating read. Mac Kniepp’s article on cancer eye in cattle was awarded best visuals – take a look and you’ll see why.

There is plenty of other great reading too.

A heartfelt thank you to all of our contributors throughout the year – it is your generosity in taking the time to compile and share your thoughts, experiences and case studies that makes this publication possible. And of course, thank you to all of our readers and sponsors.

Hoping you all have a fulfilling end to 2023, and there seems no more appropriate wish for the new year than peace – in homes, hearts and communities.

Happy reading,

A Large Scale Poisoning Event in Cattle Caused by Cape Tulip Daniel Reiner, Julie Wayne & Jeremy Rogers ..................... 16 Simone

Best Visuals

Prize: A CVE$100 voucher

Cancer Eye of Cattle Mac Kneipp........................................ 19

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Control & Therapy Series – Issue 313 December 2023

Authors’ views are not necessarily those of the CVE

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Engage With Your Profession

Dr Natalie Courtman Associate Professor of Veterinary Clinical Pathology VPDS laboratory Sydney School of Veterinary Science e. natalie.courtman@sydney.edu.au t. +61 2 9351 3099

The skin and subcutaneous tissues were erythematous and extensively thickened over the ventral abdomen bilaterally, extending down both hindlimbs to the stifle region and cranially to caudal thorax. The thickening consisted of coalescing nodules with areas of ulceration and draining sinus tracts, as shown in the image of the ventral skin below (Figure 1).

Fine needle aspirates (FNA) were obtained from two subcutaneous nodules and impression smears from the ulcerated surfaces and stained with rapid Romanowsky stain (Rapid Diff, Australian Biostain). Images of the cytology smears are shown below in Figures 2 and 3.

Dr Beth McDonald Specialist in Veterinary Dermatology University Veterinary Teaching Hospital Sydney, VPDS e. beth.mcdonald@sydney.edu.au C&T No. 5993 A 5-year-old, 6.39kg neutered female domestic longhaired cat was referred to the dermatology service of the University Veterinary Teaching Hospital Sydney with a 2-year history of inflamed ventral abdominal skin and underlying nodular subcutaneous tissues with draining sinuses. The cat had shown a partial response to doxycycline 50mg SID and had also been treated with 0.7mLs of 80mg/mL cefovecin injections subcutaneously (Cerenia, Zoetis). It was then treated for a month with a combination of 5mg daily 5mg prednisolone and 7mg/ kg cyclosporin. The lesions worsened and this treatment was stopped 3-4 weeks prior to presentation. The cat had been licking at the affected areas.

Figure 2. FNA from subcutaneous nodule (500x magnification)

Figure 3. FNA from subcutaneous nodule (500x magnification)

QUESTIONS − What is your diagnosis based on the cytology? − What are the main differentials for the gross skin lesions?

Email your answer to cve.marketing@sydney.edu.au. The best answer will be published in the March 2024 C&T and the winner will be entitled to a CVE$100 voucher towards continuing education of their choice. 

Figure 1. Image of ventral abdominal skin lesions

Centre for Veterinary Education

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Control & Therapy Series – Issue 313 December 2023

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What’s Your Diagnosis?

Winner

Hereditary Haemophilia A in a Young Dog Dr Maddie Roberts BVSc (Hons 1) FANZCVS Registered Specialist in Small Animal Medicine e. maddie.roberts@sydney.edu.au C&T No. 5994 A 13-week-old male entire Staffordshire Bull Terrier presented to a referring veterinarian for acute onset of lethargy. The patient was acquired from a breeder in QLD at 8-weeks-of-age. Vaccination and worming preventatives were appropriate for age. The patient had been fed a commercial puppy diet and had no known history of scavenging.

The other dog in the household, a 5-year-old maleneutered Staffordshire Bull Terrier, was reported to be clinically well.

Physical examination was unremarkable, and the patient was discharged with no specific treatment and view for outpatient monitoring at home.

The patient represented to the referring veterinarian the following morning for subtle bruising on the ventral abdomen. The patient had been bright and alert in comparison to admission the day prior. There had been no known exposure to rodenticides.

On physical examination the puppy was bright and alert with a heart rate of 160 beats per minute (bpm), respiratory rate of 36 breaths per minute and a rectal temperature of 38.5°C. The patient was noted to have a swelling on the medial left thigh, with normal muscle tone. A bruise overlying this swelling extending to the inguinal region was noted.

A complete blood count, serum biochemistry and inhouse coagulation times were performed. A normocytic hypochromic moderately regenerative anaemia was apparent, with a PCV of 0.3 L/L (reference interval {RI} 0.37 – 0.56 L/L), absolute reticulocyte count of 151x10⁹/L and a hypoproteinaemia (52g/L, RI 55–79 g/L).

Biochemistry revealed moderate hyperphosphataemia (2.77mmol/L, RI 0.8 – 1.8mmol/L). IDEXX In House citprothrombin time (PT) was normal (16.0 seconds, RI 11.0 – 17.0) and activated partial thromboplastin time (APTT) was prolonged (186 seconds, RI 72 – 102.0). The patient received two 5mL/kg Hartmann’s boluses and was discharged with view for referral to the internal medicine

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team at the University Veterinary Teaching Hospital, Sydney (UVTHS) the following day.

The patient presented to the emergency service at UVTHS the same evening for lethargy and abdominal pain. On physical examination the patient was quiet but alert. The vital parameters were similar to those obtained at the referring clinic (HR 160bpm, RR 32 breaths per minute, rectal temperature 38.4°C). The patient was observed to have ongoing ecchymoses involving the left inguinal region and medial aspect of left thigh, with a new finding of tense, painful abdomen. PCV / TP was stable compared to previous haematology (PCV 0.3 L/L; TPP 0.58g/L). A point-of-care ultrasound (POCUS) of the abdomen revealed anechoic fluid within the retroperitoneal space. Abdominal radiographs (figures 1 and 2) identified enlargement of the retroperitoneal space with fluid streaking and ventral displacement of the descending colon. Fluid collection for analysis was not performed due to concern of a coagulopathy. The patient was treated with methadone analgesia (Ilium methadone 10mg/mL; 0.3mg/kg) and IV fluid therapy (Hartmann’s at maintenance rates (Body weight 0.75 x 70 / 24) mL/hr).

The following morning the patient was referred to the internal medicine team. The patient was noted to be bright and alert. Vital signs including heart rate, respiratory rate and temperature were within normal limits, with the heart rate consistently measuring at 112-120 bpm. Mucous membranes were pink and moist with no petechiae noted. The patient was normotensive, with a Doppler measurement of 115 mmHg systolic (size 2 cuff, forelimb). The retroperitoneal enlargement had substantially reduced and no signs of abdominal or retroperitoneal pain were apparent. There was no sign of joint effusion nor evidence of melena or haematochezia on rectal examination.

Upon review of the patient history and diagnostic results, differentials considered for a prolonged APTT with normal PT and platelet count included defects of the intrinsic coagulation pathway, haemophilia A (factor VIII {FVIII} deficiency), haemophilia B (factor IX deficiency {FIX}), deficiencies in factor XI, XII, contact factor deficiencies, disseminated intravascular coagulation (DIC) or presence of anti-phospholipid antibodies.

Von Willebrand’s Disease or thrombocytopathies were considered less likely based on the magnitude of APTT prolongation. Due to the normal hepatic biochemistry, synthetic liver dysfunction was considered unlikely. An artifact of collection was considered unlikely based on the degree of prolongation and evidence of ecchymoses in the patient.

A complete blood count was repeated and revealed a normocytic normochromic moderately regenerative

Control & Therapy Series – Issue 313 December 2023

Authors’ views are not necessarily those of the CVE

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Entitled to a CVE$100 voucher

An abdominal ultrasound was performed to evaluate the abdominal swelling and discomfort. This indicated the presence of a small volume of anechoic fluid within the retroperitoneal space and engorgement of the cisterna chyli (Figure 3). No sonographic changes to the liver, gastrointestinal tract or urogenital system were observed. Due to the concern of an underlying coagulopathy and perceived reduction in retroperitoneal fluid accumulation, ultrasound guided centesis of the retroperitoneal space was not performed.

As a defect of secondary haemostasis was suspected, treatment with fresh-frozen plasma was recommended for provision of clotting factors in an attempt to attenuate further bleeding. Fresh frozen plasma was declined by the owner for reasons that were not readily apparent. Vitamin K was considered; however, given the normal PT and no clinical history of liver disease (picky appetite, nausea, vomiting, ptyalism, seizures) or biochemical changes to suggest hepatic dysfunction) nor rodenticide exposure, it was not administered. The patient was supported with Hartmann’s intravenous fluid therapy at maintenance rates. Analgesia was discontinued due to repeatably low pain scores.

The following morning the patient was quiet and hemodynamically unstable (HR 160 bpm, thready femoral pulses, pale mucous membranes, BP of 95mmHg). New changes to physical examination included discomfort on extension of the neck. While the patient was able to ambulate, he was noticeably weaker than previously.

Repeat PCV / TP was stable from the day prior, and a POCUS of the thorax indicated the presence of a moderate volume of pericardial effusion without sonographic signs of cardiac tamponade. C-reactive protein (CRP) was 88mg/L (VCHECK Fluorescent immunoassay; RR <20mg/L).

External coagulation times confirmed a normal PT (7.4 seconds, RR 5.4 – 10.7) and prolonged APTT (27.4 seconds, RR 10.7 – 18.4 seconds) and mild hyperfibrinogenemia (4.7g/L RR 1.8 – 2.7 g/L).

Based on the strong suspicion of an inherited coagulopathy, marked clinical deterioration overnight and blood products being declined, the patient was humanely euthanised. A post-mortem evaluation was not performed at the owner’s request. Following euthanasia, subtle joint effusion was noted on examination.

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The FVIII assay subsequently returned at an undetectable level (<0.1IU/ml RR >4.0). A canine von Willebrand Factor (wVF) assay was within reference range (83CU/dL, RR 50 – 180CU/dL).

Discussion The decision to discuss this case in the C&T forum was to raise awareness of inherited coagulopathies in young dogs. Based on the clinical history, disease progression and diagnostic test results, Haemophilia A (FVIII deficiency) was considered most likely for this patient.

Several in-house tests are available to evaluate coagulation in both general and referral practice, with the most utilised including a manual platelet count, inhouse complete blood count analysis (platelet number) and coagulation times (APTT, PT and ACT). Other inhouse diagnostic that are not as readily available include PIVKA assays and thromboelastography.

The APTT assay is an indicator of coagulation factors of intrinsic and common pathways, including factors VIII, IX, X and XII. While the activated clotting time (ACT assay) measures the same pathways, the APTT is more sensitive to clotting factor deficiencies. For an individual factor to cause a prolongation in APTT, the factor level needs to be less than 30% of normal (Stockham & Scott 2008). This assay is not without limitations, as several processes can contribute to prolongation including artifact of collection (activation of clotting factors in vitro), inadequate blood volume per citrate tube, increasing the amount of citrate:plasma, marked erythrocytosis or previous heparin therapy. Patients with low circulating fibrinogen (aids in formation of fibrin, required in secondary haemostasis) can also have a prolonged APTT. Due to these limitations, collecting an appropriate volume of blood per citrate tube and validating any in-house result with an external panel that includes fibrinogen is recommended.

Factor VIII circulates with vWF as a non-convalent complex, with vWF serving as a stabilising and protective molecule. Von Willenbrand disease, a disorder of primary haemostasis, is the most common hereditary bleeding disorder in dogs and exists as three types (and subtypes within). Clinical signs of vWB disease can include mild to severe mucosal haemorrhage, cutaneous bruising and prolonged haemorrhage from trauma. Staffordshire Bull Terriers are not a breed with a reported predilection for any type of vWB disease. Although uncommon, prolongations of APTT have been reported with this disease (Stockham and Scott 2008). A simple buccal mucosal bleeding time (BMBT) could have been used to rule out this differential while vWF levels were pending.

A prolonged BMBT time (greater than 4 seconds) would have supported this diagnosis;, however, other diseases

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anaemia with a PCV of 0.29 L/L and absolute reticulocyte count of 189 x 10⁹/L. The platelet count was within normal range (315 x 10⁹ /L; RR 150 – 539). A mild inflammatory leukogram with left shift was evident (band neutrophils 0.4 x 10⁹/L RR <0.1; neutrophil count 10.4 x 10⁹/L RR 3.1 – 9.0). An external coagulation panel, factor VIII assay and vWF assay were requested through Vetnostics Diagnostic Services.

Haemophilia A is an inherited X-linked disorder whereby affected dogs (most often male due to mode of inheritance) present with spontaneous bleeding in the subcutaneous tissue or joints (Nichols et al 2010). Canine breeds with known genetic mutations include the Boxer and German Shepherd and, at present, genetic testing is available via OriVet (Melbourne). De novo mutations can occur sporadically in individuals (Barr and Michael 2012).

Following the euthanasia of this patient the bitch was tested for both known variants and was verbally reported to have a negative result. This would suggest potentially a new genetic mutation in this patient.

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such as thrombocytopathies or vasculitis can also lead to this result.

Figure 1. Right lateral abdominal radiograph indicative of enlargement of retroperitoneal space with fluid streaking (green arrows) and ventral displacement of colon (red arrow)

There are several aspects of case management that are worthy of discussion. At several timepoints, fresh frozen plasma was recommended in attempt to attenuate further haemorrhage. Fresh-frozen plasma is a stored canine blood product obtained from centrifugation of whole blood (the other component, packed red blood cells, is removed, and stored separately). Fresh-frozen plasma contains all coagulation factors (except for platelets) in addition to fibrinogen, albumin, protein C, protein S, antithrombin and tissue factor pathway inhibitor. The provision of coagulation factors in dogs with haemophilia results in haemostasis and cessation of bleeding. In scenarios where fresh frozen plasma is not available, whole blood can also be used; the limitation of this product is a greater fluid volume that may lead to fluid overload. Cryoprecipitate, a portion of plasma containing fibrinogen, vWF and FVIII can also be used in these cases however use is limited by lack of availability (Barr and McMichael 2012).

In the absence of fresh frozen plasma or a blood transfusion, some may ask why there was not consideration for the administration of vitamin K when liver disease or deficiency were placed on the differential list. This was largely due to the exceptionally low index of suspicion based on highly controlled home environment, the other dog being clinically well, and no evidence of synthetic liver failure (of which a loss of greater than 70% of function is required to be lost to see abnormal results) nor sonographic abnormalities of the liver.

If this patient had been nursed through this event, further diagnostics that would have been performed including external coagulation times and a factor VIII assay 4 - 6 weeks after discharge. The intent of this window would be to maximise opportunity for any ‘normalisation’ of factor levels. Management recommendations would include avoidance of trauma (which is challenging in a multi-dog household) and should any signs of spontaneous haemorrhage occur to seek veterinary care and consider the use of fresh frozen plasma to minimise ongoing haemorrhage.

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Figure 2. Ventrodorsal abdominal radiograph indicative of displacement of descending colon to the left (red arrow)

Figure 3. Transabdominal ultrasound of the right kidney identifying a small volume of anechoic fluid abutting the kidney (blue arrow)

Control & Therapy Series – Issue 313 December 2023

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Attempts have been made to reach the breeder of this patient to recommend an external coagulation panel be performed in all offspring and to retire the bitch from the breeding pool. If any other pups had prolongations in aPTT, external Factor VIII levels would be recommended.

Tracing of this patient’s pedigree and whole genome sequencing of any confirmed offspring with the disease could also aid in identifying a new aberrant mutation contributing to this disease.

Have you had a Staffordshire Bull Terrier with unexplained bleeding and a prolonged APTT? Please contact Dr Maddie Roberts at Sydney University (Maddie. roberts@sydney.edu.au).

References Nichols TC et al 2010 Prevention of spontaneous bleeding in dogs with hemophilia A and hemophilia B, Hemophilia 16(supp 3): 19-23 Stockham SL & Scott MA 2008 Fundamentals of Veterinary Clinical Pathology, 2nd edition Barr JW & McMichael M 2012 Inherited disorders of hemostasis in dogs and cats, Topics in Companion Animal Medicine 27(2)53-58. 

Hairball Conundrums Rachel Korman & Alison Jukes Cat Specialist Services 1-15 Lexington, Underwood, QLD t. +61 7 3841 7011 e. drkorman@catspecialists.com.au C&T No. 5995 Hairballs are a common problem in long-haired cats and owners often think it’s normal. Is there more to it?

Unfortunately, there’s little published evidence assessing the frequency of hairballs in cats. One owner survey found 10% of apparently ‘normal’, domestic shorthaired cats vomit hairballs compared to 20% of domestic longhaired cats (Cannon, JFMS 2013). In studies of feral cats, urban free-living cats and zoo cats, hair ball prevalence was low although some urban free-living cats had hair in their stomachs on necropsy.

Grooming is a normal feline behaviour and the feline tongue is adapted with keratinous barbs, which encourage ingestion of fur when grooming. On average, a domestic shorthair cat loses 28 g of hair per kg bodyweight annually, with 75% of this hair being ingested and found in stools (Hendriks et al. 1998). Most cats pass this fur undigested in stools but sometimes hair can accumulate forming trichobezoars. Increased frequency of hair ball production may suggest the cat is ingesting an excessive amount of hair or has an underlying gastrointestinal disorder preventing normal hair elimination.

So what should you do if an owner mentions their cat vomits (or coughs!) hairballs frequently in their annual health check or brings them to the clinic for the problem?

A great new resource published by Boehringer Ingelheim.

Frequent hair ball production should raise suspicion for excessive hair ingestion due to pruritis (e.g. flea infestation, atopy, hypersensitivity), overgrooming due to pain or a behavioural disorder. Working through these differential diagnoses is sensible e.g. flea combing and discussing ectoparasitic prophylaxis with the owner, followed by considering a diet trial for underlying hypersensitivities.

If a clear region of overgrooming exists (e.g. over the flank), then investigating for pain (e.g. ureteral stone obstruction or spinal disease) could be considered.

The author has seen a cat with left sided ureteral stones whose only symptom was a sudden onset of hair barbering over the left flank. This behaviour resolved with analgesia and subsequent passage of the ureterolith.

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In human medicine, prophylactic administration of plasma or recombinant factor VIII is encouraged to mitigate severe bleeding events. Screening for bloodborne infectious disease is required for plasma derived products with well documented outbreaks of HIV and hepatitis C in recipients during the 1970s and 80s.

Novel therapies that have been investigated include gene therapy (currently in early trials) and the use of monoclonal antibodies.

Figure 2. Hairball – vomited up

Figure 3. An ultrasound image of the stomach of the same patient above. The blue arrow demonstrates the hyperechoic and shadowing hair filling the stomach. The double headed arrow demonstrates the stomach wall.

Hair balls can also result secondary to altered gastrointestinal motility from chronic GI diseases such as inflammatory bowel disease or dietary intolerance or hypersensitivities. Ileus secondary to increased sympathetic stimulation from chronic pain, stress or dehydration can occur. When diagnosed and appropriately treated, it is not unusual for hairball production to decrease.

It is important to question owners about diet and stool consistency. Physical examination should include assessment of body weight, body and muscle condition scoring and trends reviewed to see if the patient is losing weight or condition. This should prompt further investigations for GI disease if present.

Normal gastrointestinal tract motility depends on finely co-ordinated, contractile smooth muscle activity that forces contents distally (or proximally during vomiting).

Contractions occur under the influence of excitatory neurotransmitters (e.g. acetylcholine). A combination of contraction and relaxation mixes, grinds and ultimately results in propulsion of ingesta. There are Page 8

Figure 4. This image shows the giant hair ball following gastrotomy for removal. This hairball weighed approximately 320 g. According to the world’s best source of information (the internet) the biggest hairball recorded was 12.5 cm wide and weighed 350g.

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Figure 1. This right lateral radiograph demonstrates an enormous hair ball in the stomach of a Maine Coon with an anxiety disorder resulting in overgrooming of both his own coat and his litter mates’ coat. The stomach is entirely filled with hair.

The staples in the craniodorsal abdomen are from a previous adrenalectomy.

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3 recurring phases of interdigestive activity—namely motor quiescence, irregular contractions and giant contractions. Cats prone to hair balls may have a lack of housekeeper contractions in the stomach resulting in poor gastric peristalsis.

Diet composition affects gastrointestinal motility. High or low fibre content did not appear to affect gastric emptying time; however a larger meal size did, and triangular kibble took longer to clear from the stomach than round kibble despite no correlation with kibble surface area and gastric emptying time. (Armbrust et al Vet Radio Ultrasound 2003, Goggin et al. Am J Vet Res 1998) If hair balls reach a size to cause a partial or complete obstruction, these typically lodge in the pylorus or the ileo-caeco-colic junction. Cats subsequently present with inappetence, vomiting and abdominal pain.

Oesophageal hair balls (which probably form in the stomach and get caught when being vomited) may cause oesophagitis and strictures but appear less commonly (Squires, JSAP 1989).

Figure 5. Better out than in. Not from a sheep, but from a 4 kg British Shorthair. I’m still itchy 4 years later.

Hair balls can be identified on diagnostic imaging, particularly when they reach a substantial size. If they are causing a partial obstruction, they are more difficult to identify.

Options to reduce hairball formation − Diet change y Cats with IBD or dietary intolerance may respond to an elimination diet. y

y

Anti-hair ball diets have insoluble fibre added and larger kibble size to encourage gastric emptying.

Cellulose addition specifically raises faecal hair excretion (Beynen, All about Feed 2015). It likely does this through preventing accumulation of hairs in the stomach and increasing transfer of loose hairs into the duodenum and accelerating gastric transit time.

There is no evidence that compares the use of dry diets versus wet diets for altering hairball production.

− Grooming y Daily grooming (although it is important to remove as much hair as possible rather than just loosen it) or even better, a ‘lion clip’ − Encouraging increased gastric emptying y Feed smaller meals frequently to help speed up gastric emptying. − Lubricants y These may help prevent the hairs from coalescing into a big ball. Liquid paraffin (in the form of Catalax gel, Laxatone gel or similar) is generally well tolerated, but syringing must be avoided to prevent aspiraCentre for Veterinary Education

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Figure 6. The patient in question prior to his surgery for hair ball removal. Biopsies were obtained from the stomach, duodenum, jejunum and ileum to assess for underlying GI disease; however, these were unremarkable. The patient is highly anxious and it is likely this has contributed to his overgrooming behaviour. He has responded well to anxiolytic medication and regularly clipping, both of himself and his litter mate.

tion pneumonia. Again, evidence is limited. Richard Malik likes hemp oil (e.g. Hempooch) as an easy and safe way to get lubricant into the stomach; it also provides a nice mix of fatty acids and gives the coat improved gloss. − Medical management y Prokinetic agents (e.g., metoclopramide, cisapride or prucalopride) are rarely required for most cats; however, those with marked dysmotility (e.g., cats with idiopathic megacolon) will benefit from administration and these drugs could be trialled in cats where the frequency of hair balls has not responded to the above management options. 

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Due to its comprehensive content, this course is spread over 2 years to allow the busy practitioner to fully engage with the content whilst maintaining life balance.

cve.edu.au/de-feline-medicine The International Society of Feline Medicine is the veterinary division of the pioneering cat welfare charity International Cat Care. Trusted by vets and nurses, it provides a worldwide resource on feline health and wellbeing, via the Journal of Feline Medicine of Surgery, by fostering an international community of veterinary professionals with a shared vision of feline welfare, and supporting professional development with practical CPD. Additionally, International Cat Care’s website provides a valuable resource of accurate information delivering what both vets and cats would want owners to know.

Research Roundup Welcome to Research Roundup where we bring you summaries of the latest feline research. Included are articles on the practical use of POCUS in cats with ureteral obstruction, the significance of thrombocytosis and barriers to the measurement of blood pressure.

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The ISFM & AAFP are partners with the CVE in delivering the Feline Medicine Distance Education course.

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Feline Hyperaesthesia Syndrome C&T No. 5996

Clare Rusbridge BVMS PhD DECVN FRCVS Clare is Professor in Veterinary Neurology at the University of Surrey and Senior Neurologist at Wear Referrals. She was awarded a Bachelor of Veterinary Medicine and Surgery from Glasgow University in 1991 and became a Diplomate of the European College of Veterinary Neurology after a residency in Veterinary Neurology and Neurosurgery at the Royal Veterinary College. She became an RCVS Specialist in Veterinary Neurology in 1997 and was awarded a PhD from Utrecht University in 2007. She has spent over 25 years researching Chiari malformation, syringomyelia and maladaptive pain. As a result of this work, she received the JA Wight Memorial award in 2011, was made Fellow of the Royal College of Veterinary Surgeons (meritorious contribution to knowledge) in 2016, received an RCVS Impact award in 2022 and was awarded the Pet Plan Charitable Trust Scientific Award for 2023.

Feline hyperaesthesia syndrome (FHS) is a poorly understood maladaptive pain condition that is a diagnosis of exclusion. Treatment with neuropharmacological agents is indicated in a minority of cases, and only after addressing environmental needs according to the ‘five pillars’ framework and taking a systematic approach to rule out dermatological causes and other causes of spinal or tail pain.

Clinical signs The classic clinical signs of feline hyperaesthesia syndrome (FHS) are lumbar hyperaesthesia, rippling skin, vocalisation and episodes of attacking or overgrooming the tail causing soft tissue damage or mutilation (Figure 1).¹ It is reputedly more common in Siamese, Burmese, Himalayan and Abyssinian cats and typically signs appear between 1 and 4 years. Commonly described signs include:

be difficult to distract during an episode. The personality of the cats is often described as highly aroused (anxious, aggressive, restless, constantly wandering and pacing) and the behaviour may be provoked by petting/stroking and may be more likely when anxious or stressed.

Pathogenesis The pathognomonic signs of FHS is contraction of the panniculus carnosus (cutaneous trunci) muscle which is intimately attached to the skin and fascia, hence the other monikers of FHS being ‘rolling skin syndrome’ or ‘twitchy cat disease’. The main function of panniculus carnosus is to shake off unwarranted foreign bodies or stimuli.² The most common cause of rippling skin is skin irritation which induces this reflex.

However, rippling and twitching of the skin are also observed when a cat is highly aroused and frustrated, that is, emotionally rather than physically irritated.³ A negative emotional state can also explain the other behaviours seen with FHS. For example, brief, intense grooming behaviour directed to the shoulder or base of the tail is a typical displacement activity seen when a cat is frustrated (Figure 2).³ Frustrated cats also rapidly switch between behaviours and thrash their tails. Anxious or very aroused cats may have mydriasis, piloerection or be hypervigilant.³ The suggestion that FHS is a seizure disorder, is spurious and likely based on a positive response by some cats to anti-epileptic drugs with anxiolytic or analgesic activity.

Likewise, an aversion to being touched on the back and improvement on medication used to treat neuropathic pain, does not confirm spinal pain. FHS is often used as an umbrella term for cats exhibiting signs of excessively twitchy skin-to-tail mutilation and this is likely

− dilated pupils; − appearing annoyed with, twitching or biting at the tail; − rippling skin on the back just above the tail; − sensitivity to touch around the tail and spine; and − personality change.

There may be self-mutilation characterised by biting, licking, chewing and plucking of the hair, and the cat may Centre for Veterinary Education

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Figure 1. Overgrooming of the tail is a classic sign of feline hyperaesthesia syndrome

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The author’s first-line therapy is gabapentinoids and second-line therapy is topiramate. The prognosis is fair if the above systematic approach is taken.

References 1. Amengual Batle P, Rusbridge C, Nuttall T, et al. Feline hyperaesthesia syndrome with self-trauma to the tail: retrospective study of seven cases and proposal for an integrated multidisciplinary diagnostic approach. J Feline Med Surg 2019; 21: 178–185.

Figure 2. Intense grooming behaviour is a typical displacement activity in a frustrated cat

2. Naldaiz-Gastesi N, Bahri OA, López de Munain A, et al. The panniculus carnosus muscle: an evolutionary enigma at the intersection of distinct research fields. J Anat 2018; 233: 275–288.

inappropriate. However, it is possible that some cats may be experiencing abnormal sensations and these cases may have some sort of neuropathic pain or itch disorder.

3. Ellis SLH. Recognising and assessing feline emotions during the consultation: History, body language and behaviour. J Feline Med Surg 2018; 20: 445–456.

Diagnosis

4. Ellis SLH, Rodan I, Carney HC, et al. AAFP and ISFM feline environmental needs guidelines. J Feline Med Surg 2013; 15: 219–230.

Diagnostic work-up of affected cats includes ruling out all other possible explanations (in particular, skin disease), assessing environmental triggers and investigating for spinal pain. Cats with caudal spinal pain typically have behavioural signs of restricted movement, for example, reduced jumping or tail movements (Figure 3). When assessing the environmental triggers, it is important to ascertain the contextual information, such as:

5. Favrot C, Steffan J, Seewald W, et al. Establishment of diagnostic criteria for feline non-flea-induced hypersensitivity dermatitis. Vet Dermatol 2012; 23. DOI: 10.1111/j.1365- 3164.2011.01006.x.

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− where the behaviour occurs; − who was there (owner and other animals) and how they reacted; and − what was happening immediately before.

It is especially important to ascertain how the owners react to the behaviour, past and present, as for many owners, the sight of their cat behaving in an ‘odd’ manner can be very distressing and repeated attempts to interrupt the behaviour can inadvertently lead to increasing levels of arousal and a subsequent worsening of the behavioural signs.

Figure 3. Cats with caudal spinal pain may find it difficult to jump

Treatment and prognosis As for feline orofacial pain syndrome (FOPS), addressing environmental needs according to the ‘five pillars’ framework is essential, not optional.⁴ Pruritic skin disease should be ruled out with: − skin scrapes and cytology (Figure 4); − control of ectoparasites; − fungal culture; − responses to a 6–8-week restriction diet; and − response to immune-modulating therapy (e.g. allergen-specific immunotherapy, glucocorticoids or ciclosporin).⁵

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Figure 4. Puritic skin disease should be ruled out with skin scrapes and cytology

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A diagnosis of a maladaptive pain syndrome can only be made after environmental needs and dermatological causes have been ruled out. In this instance, medication for neuropathic pain can be tried.

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Feline Hyperaesthesia: Wally’s Story Sue England e. justmates@optusnet.com.au C&T No. 5997

Sue (pictured here with Tyson) is a feline enthusiast who is passionate about rescue animals, wildlife and nature.

It also looked as if he was being attacked by fleas; surely not as he was only treated a week or two previously. I did treat

him again to be sure.

I tried to comfort him and calm him, but even while holding him, the twitching did not seem to settle. The only comfort he found was hiding away in his cubby bed. I had come to believe that he may be suffering with feline hyperaesthesia so I began reaching out to Richard Malik for his thoughts.

Wally is a 10-year-old male, neutered Domestic Shorthaired cat who came to me around 7-months-ofage of age as a stray. He seemed to be a very normal cat that just meowed a lot.

He had always been a happy cat and got along with other cats easily, living mostly outdoors in a secure backyard.

A few years after Wally had been with me, he encountered a stray cat that entered the backyard. The cats ended up in quick fight, but Wally seemed ok and went about his day.

The following day I gave Wally his breakfast and realised he was playing in an erratic way, running up and down his scratching post, darting across the enclosure.

Wally video 2

I opened his enclosure and let him into the backyard so he could run around but instead he raced straight under the house, meowing deeply. This behaviour was very out of character for him.

Wally has days he seems normal then there are days he has very obvious attacks.

Some triggers are stress, windy days and if he eats too much and makes himself feel sick. Other times I can’t figure out why he is having an attack.

While having his good days, you can still see the occasional tail flick and minor twitching, so he never seems to be 100% symptom free.

Wally video 1 I encouraged him back into his enclosure, watched him closely and realised what first looked like him playing and having fun was in-fact something more.

I noticed him rolling his skin, flicking his ears and tail, twitching, getting up and dashing across the enclosure, meowing loudly for no reason.

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Wally video 3

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− I have tried CBD with no luck. − I have also tried Gabapentin at 50mg twice a day. This does help a little but not enough; the more he had the more sedate he becomes. − I have been reluctant to try other medications so far for fear of causing too much sedation as I still want him to be a cat without being too sedated.

Being confined to his pet bed brings him comfort

Wally video 4

View here the 5 videos of Wally as well as C&T No. 5638 'Cat wheels to exercise cats' also contributed by Sue England.

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Video 5. Wally on a typical day (4 years post hyperaesthesia diagnosis) 

To err is to be human,” wrote Alexander Pope. “Success is not final, failure is not fatal: It is the courage to continue that counts,” Churchill proclaimed. An African proverb announces that “Only those who do nothing never make mistakes".

—Brookings

Cautionary Tails Simone Maher Director, Centre for Veterinary Education e. simone.maher@sydney.edu.au C&T No. 5998

I recall doing the admission consult—everything seemed fine, the owners reported the cat was BAR and living his best life indoors and out. I do remember clocking the heart sounds were displaced to the right—but the morning was busy, the clients kept chatting (even through my “just one moment” shushing signal which rarely failed). So I didn’t think too much of it.

Quite some time ago, I was working in a clinic which performed high-volume desexings. Often these animals had not been seen by a vet prior to their admission for spey/neuter under a voucher scheme.

But then… after the cat was induced, just as prepping started, he went into marked respiratory distress. A quick X-ray showed a diaphragmatic hernia—likely traumatic, some time ago, and (because cats are amazing) he had recovered to be apparently clinical normal.

I have a distinct memory of a delightful blue male cat, which had wandered into the lives of a family as a young adult. They had had the cat many months and under the subsidised scheme were now in a position to get it vaccinated, microchipped and desexed.

Fortunately, this story had a happy ending. We were in a position to perform corrective surgery and had access to discretional funding that covered the lion’s share of the bill. He recovered well and went on to live an even better life. But I will never forget the feeling of absolute dread

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So it was this case that I recalled some time later when again I saw a cat for health check prior to admission for desexing and noticed the heart sounds were very muffled. Again, the cat was clinically normal. I almost dismissed it—then checked myself and recommended a quick lateral radiograph. This kitty had a (likely congenital) pericardioperitoneal hernia. The outcome this time was a little different—the owners chose not to pursue any further diagnostics or treatment and decided to just take puss home to live out his life. But I am so bloody glad I didn’t just go ahead and knock that cat out (I have catastrophised that scenario many times!!).

The moral to my cautionary tale? Learn from my mistake!

Trust your gut and have confidence in your competence at physical examinations. If heart sounds in a cat seem a bit off—pause for a second and reevaluate. You might just avoid a disaster.

What’s old is new again!

Claire Wade suggested this new column and contributed the first article published in Issue 255 June 2009.

Prompting this comment from Dr Pat Cole, retired vet. ‘...Claire is to be admired for her refreshingly honest approach and attitude to the C&T Series. In large animal practice I am sure we would all remember our first bovine caesarian and how difficult it was and yet how much easier it became as the years rolled by.’

Use the QR code above to read Claire Wade’s Letter to the Editor followed by her C&T article and Pat Coles’ subsequent Letter to the Editor.

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...‘what he/she did, right or wrong, the full detail, revealing the actual “blood and dung and guts” or real practice as it happened....’

Tom Hungerford

The words of Tom Hungerford on the back cover inspired me to contact you and share my idea. The mistakes we remember in practice are the ones that we wish we could go back and do-over, even if they weren’t catastrophic.

I wish I had access to C&T before I made some mistakes, and I wondered if a regular article or column could be included to allow practitioners to share some of the doozies to help others avoid them? Obviously these would need to be anecdotal to avoid legal issues, and not specify names or practices, but they should be based on true cases.

Every time I stuffed up I felt I was the only practitioner who had ever made that mistake and that every other vet knew more about pharmacokinetics, anaesthetics, or sonography. Knowing that I was not completely alone in making errors would have helped in coping and thereby learning more from mistakes. Reading of other’s errors may also have helped me from avoiding the same mistake.

I understand how difficult it would be for practitioners to publish their mistakes, however if it were done confidentially, I feel sure a lot of valuable information may be shared.

Let’s make this a regular column!

The first contributor (published anonymously if preferred) to this re-instated column wins the voucher towards continuing education; cve.edu.au

With our compliments

cve.edu.au

+61 2 9351 7979

CVE$200

Send to cve.marketing@sydney.edu.au

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when he crashed on the prep table and the image of that quick lateral radiograph is burnt into my mind.

Entitled to a CVE$100 voucher

A Large Scale Poisoning Event in Cattle Caused by Cape Tulip Dr Daniel Reiner BSc DVM Willunga Veterinary Services, Mount Compass, SA e. dreiner476@gmail.com

Dr Julie Wayne BVSc(hons MVSC MANZCVS (Pathobiology) DACVP (Anatomic Pathology) Gribbles VETLAB

Jeremy Rogers PIRSA, SA C&T No. 5999 Introduction

Necropsy findings Necropsy was performed on two dead cows. Findings included myoglobinuria, excessive rumen fluid, severe small intestine and abomasum mottling with dark blood, haemorrhagic kidney and lungs, pericardial effusion and hepatomegaly.

Further autopsies were performed on Monday 26 June and the suspected diagnosis at this point was cape tulip (Moraea sp) poisoning .

Although rumen contents were closely examined, no plant material that resembled cape tulip was seen. There were large stands of cape tulip in the bush block area, on swampy land, and there was evidence of grazing by cattle. It was noted that cattle had also been chewing on the bark of trees in the same location. Most dead cattle appeared to have died without struggling, many had aborted, and most were found dead amongst the trees/ shrubs, rather than in the cape-tulip-infested area.

It was estimated that more than 100 cows died in this event.

Both one-leafed cape tulip (Moraea flaccida) and two-leaf cape tulip (Moraea miniate) are serious pasture weeds in WA, SA and VIC. All parts of cape tulip contain toxic levels of cardiac glycosides of the bufadienolide type, with cattle being the most affected species.¹ Additionally, the plant is difficult to manage as it reproduces through both corms and seeds. Corms are the underground storage organ that provides resistance to unfavourable weather conditions and makes identification of the plant difficult.²

Subsequent action

A producer in the Fleurieu peninsula of SA lost over 100 of 200 cattle that had been grazing in a neighbour’s ‘bush block’ during stormy weather in June. The cattle, due to calve in a few weeks and in good body condition, were poisoned by cape tulip.

Cape tulip poisoning was confirmed from characteristic post-mortem changes that typically affect heart muscle and abomasum. Serum pepsinogen (an indicator of abomasum damage) was very high. Salmonella spp. were not detected in tests and an Anthrax ICT conducted on one cow was negative.

History A group of approximately 200 springer cows six weeks off calving and of mixed ages were moved into a neighbour’s paddock, as severe weather was expected. This block had bush and shelter but poor grass availability and a large amount of mature bracken fern. The block had been grazed each year, but in summer to manage fire risk. On Saturday 24 June, four days after moving cattle to this block, the owner found approximately 30 dead cattle and on Sunday 25 June approximately another 30 dead. The dead cattle appeared to have epistaxis. Prior to death, affected cows walked slowly before collapsing and dying and looked very uncomfortable and in pain.

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Bracken fern poisoning was suspected initially. The remaining cattle were immediately moved out of the bush block on to adjacent paddocks. Deaths continued after the remaining cattle were relocated to adjacent paddocks. Some became recumbent and were treated for metabolic conditions, but most did not respond to treatment.

Laboratory findings

Histopathology revealed moderate multifocal to coalescing acute myocardial degeneration, segmental acute small intestinal mucosal haemorrhage and moderate multifocal lymphocytic abomasitis which is attributed to probable previous parasitism and likely to be unrelated to cape tulip. The main finding was within the myocardium. In these sections, lesions were widespread but subtle. Multifocal myocardial degeneration is described in cases of cape tulip poisoning and may cause death by affecting conductivity throughout the heart. Cardiac lesions such as these can also cause death by cardiac arrhythmia. This finding is non-specific but well recognised in cases of poisoning by plants containing cardiac glycosides, including cape tulip.

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Winner

were between 300-400mm high, with no flowers, so they could have been immature plants.

References 1. One-leaf Cape tulip: declared pest WA Agriculture and food, 2020 2. Cape tulip—how and when to control. Landscape South Australia and PIRSA 3. Poisonous plants of Australia Selwyn Everest Rev edition 1981

Discussion

4. Cape Tulip—what you should know. WA Dept Ag factsheet

This tragic event occurred as an inadvertent consequence of hungry cattle exposed to a very toxic plant previously unknown to the owner. It is not unusual for producers to be unaware of the dangers of cape tulip as livestock raised in areas that have it rarely ingest it.

In this case, hungry cattle in late-stage pregnancy were moved into a sheltered area that contained some large stands of cape tulip, and limited available good quality pasture.

Rapidly removing the cattle from exposure to this plant undoubtably saved many lives in this case. As little as 1 kg of cape tulip can kill adult cattle and the time until death is dose dependant. Some poisoned cattle will survive but develop diarrhoea—presumably because of gut irritation.

The toxin, a cardiac glycoside (bufadienolide) acts on heart muscle and produces nausea, blurred vision, dizziness and diarrhoea.³ The post-mortem changes described in this case; haemorrhage in heart muscle, gut irritation, particularly fourth stomach and large bowel, were typical of cape tulip poisoning.

Figure 2. Severe inflammation of the abomasum in a freshly dead cow

Affected cattle have a very inflamed abomasum and die rapidly often without struggling. Due to the amount of inflammation present, toxicity is likely to be very painful.

Unfortunately, there is no treatment, and eradicating the plant can be difficult. Table 1 (below) describes the lifecycle and strategy for control of the plant. In this infestation, no flowers were visible, but the plants tend not to flower until 2-3 years old.⁴ The plants observed

Figure 3. A freshly dead cow who aborted

Cape Tulip Calendar Summer Jan

Feb

Autumn Mar

Apr

May

Leaves emerge after Autumn rains

Winter Jun

Jul

Aug

Spring Sep

Flowering stems emerge

Oct

Nov

Dec

Flowering

CONTROL- hand remove CONTROL- metsulfuron methyl CONTROL- Glyphosate + metsulfuron-methyl CONTROLGlufosinateammonium Plant dormant

Seed set

Figure 1. Cape Tulip Calendar Centre for Veterinary Education

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Other possible causes included nutritional deficiencies (potentially copper, but unlikely with this history) and other toxins including 1080 or plants containing fluoroacetate. Changes in liver and kidney were nonspecific but suggestive of sublethal toxic cellular injury.

In the kidney, there was likely myoglobinuric nephrosis.

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Figure 4. Thickening and haemorrhage in large bowel

Figure 5. A dense sward of Cape Tulip and grass

Low Dose Radiation as a Possible Treatment for Cystitis

Study’s Cystitis Remedy so Effective that NC State Ready to Offer Treatment to Cats Data is pending on the study’s final cat, treated with low-dose radiotherapy last month, but the researchers say every other cat has shown improvement, with most never having another episode of cystitis.

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Cancer Eye of Cattle

that OSCC more commonly occurs on the lateral limbus (corneoscleral junction) and conjunctiva, and more often on the most exposed corneal epithelium along the line where the eyelids meet,¹ but OSCC also occurs on the lower eyelid, medial canthus and third eyelid.

Mac Kneipp BVSc MVS MANZCVS PhD Border Veterinary Surgery 26 Herbert Street

OSCC Can Be Categorised Into Stages.

Goondiwindi QLD 4390 t. 0746713688 C&T No. 6000 The two main groups of ocular diseases of cattle are inflammatory lesions, labelled as ‘pinkeye’ and neoplasms, labelled as ‘cancer eye.’ It is not always easy to differentiate between them and more than one disease process can occur in the same eye (see tables).

Pinkeye and cancer eye are umbrella terms, that is, they are the clinical presentation of a variety of different diseases.

Cancer eye in cattle is most often ocular squamous cell carcinoma (OSCC), a chronically progressive and invasive cancer of epithelial origin.¹ OSCC is the most common malignant tumour of cattle, affecting up to 20% of cattle in some herds², and accounting for 33% of total condemnations of mature cattle in NSW abattoirs from 2010 to 2014.³ Despite being well recognised by cattle vets worldwide, much of our knowledge about OSCC is presumed, not proven. It is not even known for certain what causes OSCC. The aetiology appears multifactorial. UV damage and unpigmented epithelial tissue are thought to be major component causes but it has not been possible to experimentally reproduce OSCC. In addition to being white-faced (bally) and exposed to strong sunlight, other risk factors may include genetics, increasing age (average age 8-years-old and rare in less than 3-years-old), gender (female), high plane of nutrition, living at high altitude, and viruses; including papillomaviruses and herpesviruses.⁴ The individual cow’s immune response may prove to be the most important risk factor.

OSCC has been reported in different breeds but is most common in Hereford, Hereford cross, and Friesians and has been shown to be heritable. Anecdotally, our clinic attends less cancer eye of cattle now compared to 25 years ago. This has coincided with a shift away from farming Herefords and towards black Angus and Wagyu.

Similarly, predilection sites for OSCC lesions may be, at least partially, dictated by amount of pigment and level of exposure. Pigment (melanin) is photoprotective.

OSCC occurs more in unpigmented tissues. Anatomical features such as the eyelids and third eyelid (nictitating membrane) may protect against exposure. It is stated

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On the eyeball and third eyelid there are 3 or 4 OSCC stages—plaque, papilloma, carcinoma in situ, and squamous cell carcinoma. Whilst staging may help decision making, all stages may not be seen and the change to aggressiveness and malignancy is on a continuum. Stage 3, carcinoma in situ, is usually when it is becoming malignant. Stage 4 carcinoma may invade tissues of the eye, entire orbit, and regional lymph nodes.

For eyeball OSCCs up to stage 2 or even 3, a superficial keratectomy or ‘scraping’ (local anaesthetic and scalpel scraping of OSCC tissue) may be curative in up to about 50% of cases, beyond that surgical enucleation is usually indicated. OSCC of the third eyelid can appear serious as it may prolapse the membrane and bleed, and it is stated that these cancers can be highly aggressive,⁴ but in my experience, they are the easiest and most rewarding OSCC to treat. They can often be extirpated (complete surgical removal) with good margins simply by removing the entire third eyelid. Just a bit of local and snip off the third eyelid. Most do not recur.

OSCCs of the true eyelids are more problematic. On the eyelids there are 3 stages—keratoma, carcinoma in situ, and SCC. Stages 2 and 3 of true eyelid OSCC are rarely cured by surgery alone as you cannot get decent margins unless you remove the entire, often healthy, eye along with all the tissues in the globe. (Thus, making the surgery an ‘exenteration’ rather than ‘enucleation’).

This operation feels more like butchery than surgery to me and is redundant if it is only done so the cow can subsequently be sent to slaughter. I think it would be more humane to allow vets to write a ‘fit-for-slaughter’ certificate rather than gouging their eyes out, waiting for them to recover, and then sending them to slaughter.

Alternative or adjunctive treatments to surgery for all forms of OSCC include cryotherapy (double freeze-thaw to -25° C), chemotherapy, and immunotherapy such as intralesional BCG (Bacillus Calmette–Guérin vaccine), or IL-2. When OSCC is proven to be an immune-mediated disease, specific immunomodulating treatments and gene targeting will further improve disease outcomes.

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Winner - Best Visuals Entitled to a CVE$100 voucher

Plaque

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Papilloma

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Carcinoma in situ

Squamous cell carcinoma

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Table 1. OSCC of eyeball and third eyelid can be divided into 3 or 4 stages

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Table 2. Non-neoplastic lesions with similar clinical presentation to OSCC

Inflammatory lesions are commonly labelled as ‘pinkeye’…

…or ‘just pinkeye’

Blepharitis (dermatophilus)

Warts (papillomavirus)

Corneal dermoid

Trauma

Trauma

Trauma

Eyelid laceration

Periorbital fat

Cornea 'devolved' back to skin

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Keratoma

Carcinoma in situ

Squamous cell carcinoma

Table 4. Mixed inflammatory and neoplastic lesions

Table 5. Treatments of OSCC

‘Ex situ’ third eyelid with SCC

Carcinoma in situ 2W post op

Ablation before suturing

References 1. Tsujita, H. and C.E. Plummer, Bovine ocular squamous cell carcinoma. Veterinary Clinics: Food Animal Practice, 2010. 26(3): p. 511-529.

2. Spradbrow, P.B., J.L. Samuel, and W.R. Kelly, Ocular lesions in slaughtered cattle in Queensland. Australian Veterinary Journal, 1985. 62(6): p. 203-205.

3. Bailey, G., Primefact 1422: Cancer eye in cattle, in Primefact, N. DPI, Editor. 2015, NSW Government: Online.

4. Rankin, A.J. and G.A. Sutton, Livestock Ophthalmology, in Slatter’s Fundamentals of Veterinary Ophthalmology, D.J. Maggs, P.E. Miller, and R. Ofri, Editors. 2018, Elsevier: St. Louis, Missouri. p. 471-495. 

CONGRATULATIONS! Dr Bill Howey BVMS GradDipEd MACVSc MRCVS OAM FANZCVS Bill was recently presented the AVA Fellowship Award for his significant contribution to the field of veterinary science.

Bill needs no introduction to CVE members having been a veterinary consultant to the CVE (then the PGF) for many years before serving as the Director from 2000-2002. Bill produced over 80 ‘TimeOut' seminars throughout Australia attended by over 1,000 vets and delivered some major CVE/PGF courses, specifically equine.

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Figure 1. Presentation of AVA Fellowship Award made by AVA President Dr Bronwyn Orr

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Table 3. OSCC of eyelids can be divided into 3 stages

The article is timely, as the FEI Equine Ethics & Wellbeing Commission has recently been completed. The social license of equestrian sport is increasingly under scrutiny, and Dr Cook highlights that the use of bits is one of the things that needs to change if equestrian sport is to maintain its social license to operate. In fact, as he points out, there is substantial enough evidence now that the use of bits directly contravenes with FEI’s own ‘Code of

Andrea Harvey BVSc PhD DSAM(Fel) DipECVIM-CA MANZCVS (Animal Welfare) MRCVS

Sustaining the social licence of equestrian sport (Cook 2023)

C&T No. 6001

Abstract: The horse is a nose-breathing animal that, at liberty, runs with a closed mouth and sealed lips. The bit is an Iron Age tool that breaks the lip seal, suffocates, and hurts a horse. In horseracing, the bit is a probable cause of premature fatigue, falls, catastrophic accidents, and sudden death.

Pain alone is evidence enough and reason for change. Equestrian sport administrators are urged to conduct bit-free trials and adjust their rules to comply with the physiology of the horse, i.e., to permit bit-free competition. A step that would get the process under way would be for administrators to discover for themselves the benefits of riding bit-free.

Dr Robert Cook, Professor Emeritus in Equine Surgery at Tufts University, Massachusetts, has intimate knowledge and experience of the equine head, neck and respiratory tract after a long and distinguished veterinary career as an equine ENT surgeon and researcher. His impressive list of peer-reviewed publications covers many upper and lower airway topics such as exercise induced pulmonary haemorrhage, recurrent laryngeal neuropathy, guttural pouch mycosis, progressive ethmoid haematoma, epiglottal entrapment, dorsal displacement of the soft palate, chronic bronchitis, epistaxis, headshaking, and a range of aspects of ENT radiology and endoscopy.

Through this work he became increasingly aware of the multitude of health and welfare issues caused by the use of metal bits and has been publishing on this for the last 24 years. This substantial body of research, however, has been largely overlooked by mainstream equestrian industries, and indeed by the veterinary profession. Now at 92 years of age, Dr Cook is still writing articles on this topic, and advocating for change in the equine industry.

Box 1. Sustaining the social licence of equestrian sport (Cook 2023)

What are the welfare issues?

The metal bit was introduced to equestrianism in the iron age (1200-1100BC); yet, in the 21st century equipped as we are with vastly superior knowledge and years of scientific evidence of the array of welfare issues caused by bit pain and interference with the upper airway, metal bits are still widely used in the equine industry. In Dr Robert Cooks most recent article in Horses and People, he says it’s time to draw the iron age to a close (see box 1).

Dr Cook’s article lays out the fascinating chronology of the use of bits from the iron age until today, the changes in animal welfare legislation and the formation of various equine welfare-orientated organisations, the scientific scrutiny of bit use and associated publications, and significant events in advocacy for the use of bit-free bridles.

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Dr Cook summarises the welfare issues (and the scientific evidence behind them) associated with the use of metal bits. This includes bit-induced oral pain and the array of secondary behavioural and training problems that result, facial neuralgia, dental and interdental space pathology, breathlessness and hypoxia secondary to upper airway obstruction with secondary disorders such as exerciseinduced pulmonary haemorrhage, and possibly increased risk of falls, and injuries. Bit-induced pain and airway interference is indisputable, with compelling scientific evidence (Cook 1988, 1999, 2003, 2011, 2019a,b,c, 2020, 2021a,b, Cook and Strasser 2003, Mellor and Beausoleil 2017, Cook and Mills 2009, Cook and Kibler 2018, Mellor 2019a, 2019b, 2020a, Tuomola 2022).

The facial signs of pain in the horse have been well documented over the last decade (Della Costa et al. 2014, Gleerup et al. 2015) and on close scrutiny, many features of the ‘facial grimace’ can be readily identified in horses being ridden with a bit.

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A Bit of a Problem in Equine Welfare: What is the Role of Veterinarians?

of the behavioural signs of bit-induced pain in the horse are so common that they are regarded as being normal for the horse and are overlooked. This common fallacy has been well named ‘bit-blindness’ (Mellor 2020a, b).

Dr Cook goes on to admit that he had been a ‘blindto-the-bit’ veterinarian and rider for 45 years before recognising the bit as a foreign body in a horse’s mouth (Cook 1999, 2000). Similarly, I myself, despite the wealth of information already available by this time, was also a ‘bit-blind’ veterinarian and rider for 13 years before I became aware of bit related issues (Figure 1).

He further describes how bit usage quickly teaches a young horse an abundance of unwanted, bit-avoidance behaviours, for example gaping mouth, headshaking, tongue-retraction, tongue-over-bit, and choking-up (Cook 2012b, Mellor 2020a).

The majority of veterinarians graduating today are also just as ‘bit blind’ as Dr Cook was when he graduated as a veterinarian nearly 7 decades ago, despite the enormous advances in animal welfare science and equine medicine, and the greater understanding of, and recognition of, pain, alongside the growing body of evidence specifically around bit-induced welfare problems. Why is this? Why is something so important that impacts so many horses on a daily basis totally overlooked in veterinary education and by so many equine veterinarians?

What additional benefits arise from riding ‘bit-free’?

A dramatic reduction in these conflict behaviours has been documented when horses are ridden bit-free (Cook and Kibler 2018). This finding has been replicated in a recent study where bit-free horses had fewer ridden hyperreactive behaviours (bucking, spooking, rearing and bolting) and better relative welfare scores for management, and during riding and handling compared to the horses ridden with a bit (Luke et al. 2023). As such, bit-free riding is likely to result in fewer rider injuries from falls resulting from these hyperreactive behaviours. Riding bit-free has also been associated with riders taking greater pleasure in riding and a feeling a better sense of harmony with their horse (Cook and Kibler 2022). As Dr Cook says ‘once riders give bit-free a trial they will often vow to never again put a bit in a horse’s mouth. The strongest resistance to the idea of riding bit-free comes from those who have never given it a trial.’ This certainly fits with my personal experiences when I was introduced to bit-free riding by trainer Carlos Tabernaberri. I have never ridden with a bit since and certainly feel that my horses are much more relaxed during riding and that I have an enhanced relationship with them as a result.

Why is the veterinary profession not more aware of these issues?

Of course it makes complete sense that the bit would cause pain, airway obstruction and related issues, when we take a minute to think logically about it. However, bit use has become so accepted that it is easy to be blind to these issues, until they are pointed out.

Dr Cook describes how for thousands of years, use of metal bits has been ‘standard practice’. As a result, many

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Figure 1. Riding my horse, Connie, cross-country in 2010, having been a bit-blind veterinarian for 10 years.

What are the wider consequences of ‘bit blindness’?

The consequences of bit blindness in veterinarians also has worrying wider implications on our ability to recognise some forms of pain in horses, in addition to missing potential underlying causes of behavioural problems, airway problems, poor performance and sudden death.

Whilst the profession has developed exceptional advances in recognising some forms of pain, such as foot and limb pain, recognition of oral pain has appeared to lag behind. Indeed, advances in equine dentistry and addressing dental causes of oral pain, have

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Dr Cook has also presented evidence of bit pain being a potential cause of sudden deaths by triggering the trigemino-cardiac reflex (Chowdhury and Schaller 2015, Cook 2022). Bit interference with the upper airway may also cause several common respiratory disorders that are currently classified to be of unknown aetiologies.

This includes dorsal displacement of the soft palate, epiglottal entrapment, dynamic collapse of the larynx and trachea, scabbard trachea deformity, exercise induced hypoxaemia and subsequent recurrent laryngeal neuropathy, and negative pressure pulmonary oedema.

Contents

occurred much more recently than advances in equine orthopaedics, and recognition of dental pain is still very much an emerging area.

Some of the wider issues associated with lack of recognition of bit-induced pain, airway obstruction and poor performance are readily identifiable in the literature. For example, just this year a paper on medical causes of racehorse poor performance unassociated with lameness (Lo Feudo et al. 2023) identified equine asthma, exercise-induced pulmonary haemorrhage, dynamic upper airway obstructions, cardiac arrythmias, and exertional myopathies to be common causes of poor performance, with no mention at all about the potential role of bits in the aetiology of these conditions.

Furthermore, as is usually the case, evaluating response to removal of the bit was not part of the poor performance diagnostic protocol. Another study evaluated whether subtle lameness in racehorses was associated with changes in facial expressions (Anderson et al. 2023), concluding that there were inconsistent associations between lameness status and facial grimace scores. However, all horses were evaluated with bits in their mouths, and therefore likely had altered facial expressions due to bit pain, which was not considered or discussed in this study.

What should we do as veterinary professionals?

In a recent review of mouth pain in horses, Professor Emeritus in Animal Welfare Science, David Mellor concluded:

"

So, how might we proceed? We cannot simply ignore the bit problem, which has now been identified so clearly. Inaction when a problem is not apparent is understandable. Inaction once a significant problem has been recognized is unacceptable. Recognition of such a problem brings with it an ethical responsibility to act (Mellor 2020a) .

As a profession, we clearly have a moral obligation to not only recognise this issue and pay attention to the overwhelming evidence for the realm of health and welfare problems caused by the use of bits, but also to act in a way to achieve positive change.

This issue is not only relevant to equine veterinarians, but also to: any veterinarians that ride horses or have children that ride horses; those that spectate in any equestrian sports; and any involved in welfare advocacy.

In his review on bit pain, David Mellor lays out some recommendations for a way forward (Mellor 2020a) and; in my own opinion, as a profession we have an obligation to promptly implement the following:

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Figure 2. Riding my horse, Nyx, in 2023, in a ‘sidepull’ bitless bridle. After being a bit-blind veterinarian for 13 years, I became aware of the issues associated with metal bits and changed to bit-free riding.

− Familiarise ourselves with the literature in this area − All veterinarian horse riders should try bit-free riding to experience the benefits firsthand and lead by example by choosing to ride in a pain-free, bit-free bridle (Figures 2 and 3) − Address this topic in veterinary undergraduate teaching and equine veterinarian CPD − Participate in the education of clients and other equine professionals − Consideration in diagnostic ‘work-ups’ by removing the bit in all investigations of airway problems, poor performance, lameness and behavioural/training issues − Advocating for allowance of ‘bit-free’ riding in competitions and riding clubs − Alteration of standard autopsy protocols (Cook 2022) to gain a better understanding of causes of sudden death, particularly applicable to racehorses − Updating of position statements by professional bodies and organisations to reflect current knowledge

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Cook, W.R. (2019a): Horsemanship’s elephant-in- the-room; the bit as a cause of unsolved problems affecting both horse and rider. https://en.weltexpress. info/2019/02/15/horsemanships-elephant-in-the-room-the-bit-as-a-causeof-unsolved-problems-affecting-both-horse-and-rider/ Cook, W, R (2019b): Man bites Horse. Man bites horse – weltexpress.info Cook, W, R (2019c): “Clearing the Air on the Bit-free Debate,” NovemberDecember Issue, Horses and People Magazine Cook, W.R. (2020): Man to Horse: an urgent message – bits cause pain (The Horse’s Hoof, Fall issue, 2020) Cook, W.R. (2021a): Pain-free Horsemanship https://en.weltexpress.info/2021/09/29/pain-free-horsemannship/ Cook, W.R. (2021b): Towards a Pain-Free Future for Horses (Unpublished manuscript 21 5 Towards a Pain-Free Future for Horses 032022) Cook, W.R. (2022): Sudden death in the racehorse https:// worldbitlessassociation.org/resources/sudden-death-in-the-racehorse/ Cook, W.R. and Kibler, M (2022): The effect of bit-induced pain in the horse on the feelings of riders about riding. https://worldbitlessassociation.org/ resources/the-effect-of-bit-induced-pain-in-the-horse-on-the-feelings-ofriders-about-riding-2022/ Dalla Costa, E.; Minero, M.; Lebelt, D.; Stucke, D.; Canali, E.; Leach, M.C. (2014).

Figure 3. The ‘Robert Cook cross-under’ bitless bridle, Development of the Horse Grimace Scale (HGS) as a Pain Assessment Tool in modelled by my horse Nyx.Pain-free, bit-free bridles Horses Undergoing Routine Castration. PLoS ONE 9, e92281. should be used in combination with good training techniques and only light pressure from the rider’s hands. Gleerup, K.B.; Forkman, B.; Lindegaard, C.; Andersen, P.H. (2015). An equine pain face. Vet. Anaesth. Analg, 42, 103–114.

References

Anderson, K.A.; Morrice-West, A.V.; Wong, A.S.M.; Walmsley, E.A.; Fisher, A.D.; Whitton, R.C.; Hitchens, P.L. Poor Association between Facial Expression and Mild Lameness in Thoroughbred Trot-Up Examinations. Animals 2023, 13, 1727. https://doi.org/10.3390/ani13111727

Luke, K.L, McAdie, T, Bradley, Smith, P, Amanda K, Warren-Smith (2023): Bit use and its relevance for rider safety, rider satisfaction and horse welfare in equestrian sport. Applied Animal Behaviour Science 259, 105539 https://doi. org/10.1016/j.applanim.2023.105855

Chowdhury T and Schaller B.J. (2015): Trigeminocardiac Reflex. Elsevier, Amsterdam, London, Tokyo

Lo Feudo, CM, Stucchi, L, Conturba, B, Stancari, G, Zucca, E, Ferrucci, F. Medical causes of poor performance and their associations with fitness in Standardbred racehorses. J Vet Intern Med. 2023; 1- 14. doi:10.1111/jvim.16734

Cook, W.R. Williams, R.M.; Kirker-Head, C.A.; Verbridge, D.J (1988): Upper airway obstruction (partial asphyxia) as the possible cause of exercise induced pulmonary hemorrhage in the horse: a hypothesis. J. eq. vet. sci. 8,11-26.

Mellor, D.J. and Beausoleil, N.J. (2017): Equine welfare during exercise: An evaluation of breathing, breathlessness and bridles. Animals. 7, 41 doi:10.3390/ ani7060041

Cook, W.R. (1999): Pathophysiology of bit control in the horse. J Equine Vet Sci. 19: 196-204

Mellor, D.J. (2019a) Equine welfare during exercise 1. Do we have a bit of a problem? https://www.slideshare.net/SAHorse/equine-welfare-duringexercise-do-we-have-a-bit-of-a-problem

Cook, W.R. (2000): A solution for respiratory and other problems caused by the bit, Pferdeheilkunde 16, 333-351 Cook, W.R. (2003): Bit-induced Pain; a cause of fear, flight, fight, and facial neuralgia in the horse. Pferdeheilkunde, 19,18.

Cook, W.R. and Strasser, H. (2003): Metal in the Mouth: The Abusive Effects of Bitted Bridles. Sabine Kells, Qualicum Beach, BC, Canada Cook, W.R. and Mills, D.S. (2009): Preliminary study of jointed snaffle vs. crossunder bitless bridles: Quantified comparison of behaviour in four horses.

Equine Vet. J.41, 827-830 Cook, W.R (2011): Damage by the bit to the equine interdental space and second lower premolar. Equine Vet Educ. 23, 355-360

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Mellor, D.J (2019b) Equine welfare during exercise 2. Do we have a bit of a problem? https://www.youtube.com/watch?v=rY4yEC7lhco Mellor, D.J. (2020a) Mouth Pain in Horses: Physiological Foundations, Behavioural Indices, Welfare Implications, and a Suggested Solution. Animals, 10(4):572. doi: 10.3390/ani10040572.

Mellor, D.J (2020b). Bit Blindness. VetScript 33(9), 32-34; VetScript is the Monthly Magazine of the New Zealand Veterinary Association.

Tuomola, K (2022): Doctoral dissertation, Helsinki University.Vandermark, S and Wilkins, C (2019): Trying to see the whole picture. Horses and People Magazine, August 16, 2019

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Cook W.R. and Kibler, M. (2018): Behavioural assessment of pain in 66 horses, with and without a bit. Equine Vet Educ. 31, 551-560 https://doi.org/10.1111/ eve.12916

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Tincture of Time

Some Brief Tick Paralysis Facts Professor Emeritus Rick Atwell C&T No. 6002 1.

Different tick antiserum (TAS) brands had different electrophoretic patterns (Atwell, (2008) UQ, S of VS, Diag. Lab., Archived data)

2. In an ‘In Practice’ dog study (42 sites), there were different TAS use patterns but no difference in mortality data re the brand of TAS used. (Atwell et al 2008. n=506 data archived Merial /BI)

different mechanisms, even allowing for local versus general paralysis, in both people and animals, channels for Na+, Ca ++ and K+ are involved, proportional to varying toxin characteristics Holland and Atwell (2009) CVE, C&T (296) 5771:36

3. TAS (even pre-dosed) will not block all the effects of tick toxins, especially cardovascular (Campbell, PhD, U of Q)

10. It is feasible that some ticks in different areas could have different combinations of toxins, in varying proportions. (AVJ letter Holland and Atwell). If true, this could explain varying clinical signs (areas, between seasons etc.), why some very small ticks can be highly toxic, why some very engorged ticks produce no signs (in nonimmune hosts), and why some TAS-producing dogs can develop TP with placement of ticks.

4. There are multiple toxins (n=19) (Tick Vaccine Lab, U of Q) secreted by I holocyclus; a minority of which may not secrete anything that induces clinical disease. (Cooper, PhD, Uni of Syd).

5. Tick toxins vary geographically e.g., 100km apart, SE Qld/ NE NSW (Song et al (2011) Int. J. Parasitology 41:871). based on variation of mRNA, and possible protein variations.

6. Clinical signs (and overall case toxicity) vary geographically e.g., coastal versus inland, using visual analogue scoring systems (VAS). (Atwell et al (2008), n=506, data archived Merial/BI) 7.

Double (2mL/kg)volume (n=53) TAS dosing (blinded, random, controlled, client dog study) had no effect on survival (West Chermside Vet Hosp; Atwell et al, (2006) data archived) Halved cat (TAS) doses had no effect on disease survival (n=10) (non-random, uncontrolled, pilot data only). Both studies may suggest a trend, but lack enough case numbers to prove significance, and generate interpretive power.

8. Astute owners most probably notice signs of weakness in their dogs before we detect illness— individualized, early, subtle, repeatable signs exist (AVJ Letter, Atwell et al) which owners may simply report as ‘dog seems off’ or is ‘quiet.’

Early disease was associated with dogs being less active, barking less, no jumping etc. ‘Figure of 8’ walking best revealed early signs of weakness e.g., left back leg when dog is turning rightwards.

9.

Why people usually get local paralysis (e.g., facial nerve paralysis) and dogs, general systemic disease, is still not known. Less commonly the reverse signs occur (i.e., child systemic; dogs with local) Human and animal tick toxicity seems to be affected by

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11. Clinical outcome is dependent on many factors, but older dogs (7 years plus) are progressively more susceptible (Atwell et al, (2008) n=506 data archived Merial/BI).

Breeds weight and gender status have no effect on mortality, but brachycephalic TP mortality prevalence has not been reported in a large, controlled study.

12. It is unknown why this tick (and similar Indian and European ticks) usually only have one tick per host—80%. (10% had 2 ticks and 10%>2). (Atwell et al (2008) n=506 data archived Merial/BI).

13. A self-experienced descriptive case of generalised TP (in an older male person) revealed many factors that our patients cannot relay (eg. double vision) and suggested his signs were of a descending nature.

14. Botulism is very similar to TP re the pathophysiology, the ‘trickle toxin’ nature of the toxicity, the delayed later use of antisera (i.e., when clinical signs are well apparent) and the necessity of critical care to dramatically improve survival (Rao et al (2021) m.m. weekly review 70:1).

15. The host/ tick interface is a major factor—are there local allergy or inflammatory responses to ‘disable’ attachment/ feeding sites? What is the immune status of the host? What is the best TAS dose and timing? What is the TAS tissue penetration rate, toxin supply rate, toxin transit time and

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16. There is adequate evidence, to suggest less TAS (per case) could be used (Westwood et al (2013) AVJ) 91:49) and that immediate use of TAS is essential to maximise its effect.

A small window may exist post admission when the maximum TAS effect occurs. (Atwell et al (2008)), n=506, data archived Merial/BI.

Amendment to C&T No. 5984

Perineal Hernia Repair Issue 312, September 2023 C&T No. 6003 With thanks to CVE member Dr John Sandford for drawing this to our attention and Dr Glenn Shea, Senior Lecturer in Veterinary Anatomy at the Sydney School of Veterinary Science, for providing the below anatomical description, clarifying the terminology used in the article.

aponeurosis lies level with the caudal part of the sternum, so that over the abdominal wall, the muscle is present rather than its aponeurosis. What Walmsley & Wallace have described as the “external leaf of the rectus abdominis aponeurosis” is the external lamina of the rectus sheath, formed by the aponeurosis of the external abdominal oblique, with contributions from the underlying aponeurosis of the internal abdominal oblique at the level described and illustrated. Together with the internal lamina of the rectus sheath (formed from the aponeurosis of the transverse abdominis at this level), deep to the rectus abdominis, these aponeuroses of the lateral abdominal wall muscles surround the rectus abdominis on their way to creating the linea alba, but do not attach to the rectus abdominis en route.’

This clarification is important because use of the rectus abdominis aponeurosis instead of the external lamina (as intended by the authors), would be impractical and not achieve the purpose of the surgery. This highlights the importance of using correct veterinary anatomical nomenclature in clinical science.

Note: The C&T Series editors welcome feedback, clarification, and discussion on all of our articles. Thanks to our readers for engaging in discussion.

Read the article here:

‘Aponeuroses are fibrous sheets that serve as origins/ insertions of muscles, and the rectus abdominis has its caudal attachment to the prepubic tendon, and its cranial attachment via an aponeurosis that continues over the ventral thoracic wall to blend with the cranial part of the sternum and first costal cartilage.

The junction between rectus abdominis muscle and

Dog Diet Study Do you have a foodie dog? Ever wondered how the diet you feed them could give them a long and healthy life?

Help us find out by registering your dog to participate in our study!

We want to know how preparation of dog food may optimise quality of life in dogs. Specifically, we want to determine whether diet is only influenced by nutrients present, or whether processing level also matters. To do this, we’re comparing the effect of a standard highquality kibble food versus a minimally processed whole food on the health of pet dogs. Participating owners will feed their dog a series of two different diets for two weeks each (following a transition period), monitor their feeding behaviour and collect some small stool samples. Owners would also bring their dog to the UVTHS on three occasions for clinic visits. These involve minor Page 28

blood sampling of the dogs so that we may measure their glycaemic response, metabolites, immune function and hormone levels, while stool samples will be used for gut microbiome analysis. Together, this invaluable data will help us determine how different processing levels of food affect dog physiology.

Dogs over 10 kg in weight, between 2-10 years old and generally healthy are eligible for the study.

By participating, you’ll receive free, vet-approved dog food and a free health check of your dog, and you’ll be contributing towards important research in dog health. The study is being conducted by the University Veterinary Teaching Hospital and Charles Perkins Centre, in collaboration with an industry partner (Lyka).

To learn more, email us at: usyd-dog-diet.study@sydney.edu.au

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toxin binding rate to ‘tissue targets’, (Chend K et al Sci. Rep. 2016;6:29446) and finally, host susceptibility, and expression of ongoing disease, to us, as clinicians—there is still much to know!

Major Winner

− masked lapwing (Vanellus miles)

Perspective No. 160

Veterinary Management of FreeRanging Native Birds Timothy Portas BVSc MVSc MANZCV DACZM RSPCA Queensland Wildlife Hospital e. tportas@rspcaqld.org.au

Coraciiformes − laughing kookaburra (Dacelo novaeguineae)

Passeriformes − noisy minor (Manorina melanocephala) − Australasian figbird (Sphecotheres vieilloti) − black-faced cuckoo-shrike (Coracina novaehollandiae) − Australian magpie (Gymnorhina tibicen) − butcher birds (Cracticus spp.) − pied currawong (Coracina novaehollandiae) − crows (Corvus spp.) * Not all species occur in all states

Introduction Avian species are the predominant taxonomic group presenting for veterinary evaluation in Australia, often constituting equal to or greater than 65% of wildlife hospital admissions. Australia is home to some 830 species of wild birds.

Species commonly presenting for veterinary evaluation*: Psittaciformes − rainbow lorikeet (Trichoglossus haematodus) − scaly-breasted lorikeet (Trichoglossus chlorolepidotus) − sulphur crested cockatoo (Cacatua galerita) − galah (Eolophus roseicapilla) − corellas (Cacatua spp.) − Australian king parrot (Alisterus scapularis) − rosellas (Platycercus spp.)

Anseriformes − Pacific black duck (Anas superciliosa) − Australian wood duck (Chenonetta jubata) − Black Swan (Cygnus atratus)

Megapodes − Australian brush-turkey (Alectura lathami)

Columbiformes − crested pigeon (Ocyphaps lophotes)

Caprimulgiformes − tawny frogmouth (Podargus strigoides)

Gruiformes − purple swamp hen (Porphyrio porphyrio) − dusky moorhen (Gallinula tenebrosa)

Pelicaniformes − Australian white ibis (Threskiornis moluccus)

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Charidriiformes

The prize is a CVE$400 voucher

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For definitive identification of bird species presented for veterinary evaluation the following resources are recommended: − Pizzey G, Knight F, Pizzey S. (2012) The Field Guide to the Birds of Australia, 9th Edition. Harper Collins, Sydney. − Day N, Simpson K. (2019) Field Guide to the Birds of Australia. Viking Press, New York. − https://www.birdsinbackyards.net/finder − Morcombe’s Birds of Australia app available for Apple and Android Despite the large number of species that occur in Australia, most birds presenting for veterinary evaluation are likely to be of a limited number of species that have adapted well to urban and peri-urban environments.

Aside from the common native species listed above, several exotic species have well established feral populations in Australia and may also be commonly presented. These include the rock pigeon (Columba livia), the spotted turtle dove (Streptopelia chinensis), the common myna (Acridotheres tristis), the European blackbird (Turdus merula) and the common starling (Sturnus vulgaris). In most states these birds are considered pests and it may be illegal to treat and rehabilitate these species; euthanasia at the point of admission is recommended.

This module provides information on husbandry, nutrition, restraint and handling and diseases or conditions that are likely to be seen by veterinarians working in the field of wildlife rehabilitation. For a more complete account of diseases and medical conditions seen in free-ranging birds see: Thomas NJ, Hunter DB, Atkinson CT. (2007) Infectious Diseases of Wild Birds. Wiley-Blackwell, Ames.

Atkinson CT, Thomas NJ, Hunter DB. (2008) Parasitic Diseases of Wild Birds. Wiley-Blackwell, Ames.

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Disclaimer: many of the drug doses cited in this module constitute off-label use and have not undergone pharmacokinetic or pharmacodynamic studies in the species described. Physiological differences mean that the absorption, distribution, and metabolism of these drugs may vary significantly compared with domestic birds and between species. Clinicians should use these drugs with caution.

Husbandry All wild birds should be housed separately from domestic dogs and cats in a quiet environment, preferably with subdued lighting. Birds that present ‘fluffed up’ or showing other signs of general debility will benefit from being placed in a temperature and humidity-controlled environment such as a Vetario Intensive Care Unit (https://atxvet.com.au/product/ vetario-intensive-care-t50m/) or Rcom Bird ICU Brooder (https://eshop.bellsouth.com.au/Rcom-Incubators) until triage and initial evaluation have occurred. These units are also suitable for housing nestlings and recently fledged juveniles while awaiting transfer to a licensed rehabilitator or wildlife hospital.

For short to medium term medical treatment, medium to larger sized birds of many species can be housed in standard domestic animal hospital cages. Cages should be equipped with perches made from natural materials and some natural foliage for security. Smaller species will require cages with suitably sized wire or mesh and an appropriate design to prevent escape. Flighty or nervous species such as quails, kingfishers and brush-turkeys will injure themselves in hard walled enclosures and are best housed in soft mesh crates. Raptors and waterfowl require specialised housing and should be transferred to a specialist facility as soon as possible.

Nutrition in captivity Injured or sick birds may be dehydrated and hypoglycaemic on presentation and will benefit from the administration of an oral electrolyte or glucose solution such as Vetafarm Poly Aid Plus (https://vetafarm.com.au/ product/poly-aid-plus/) or Wombaroo/Paswell First Aid for Birds (https://www.wombaroo.com.au/product/firstaid-for-birds/) as part of the initial stabilisation process.

The diet and/or nutritional requirements of many native bird species are incompletely understood. However, for the purposes of feeding birds requiring short term veterinary care they can be divided into broad groups on the basis of diet: see Table 1 below. While many species rely primarily on a principal dietary component, they will frequently consume a wide array of other food items. The diet is also likely to vary depending upon stage of life and season.

Commercial or home-made artificial diets are offered to wild birds in captivity as sourcing and replicating the diversity of foods consumed in the wild is not possible.

Natural food items are incorporated where possible to promote natural foraging behaviour and provide enrichment.

A complete discussion of captive diets for birds is beyond the scope of this document and readers are referred to the following resources: − Koutsos E (2016). Foundations in Avian Nutrition.

In: Current Therapy in Avian Medicine and Surgery (Ed Speer BL). Elsevier, San Diego. Pp 142-149. − Orosz SE (2014). Clinical Avian Nutrition. Veterinary Clinics: Exotic Animal Practice 17, 397-413. − wombaroo.com.au/wp-content/uploads/2020/12/ Wombaroo-Bird-Booklet.pdf − wombaroo.com.au/product-category/bird-foods/ − vetafarm.com.au/product-category/birds/ − vetnutritionsolutions.com.au/exotics

NUTRITIONAL CATEGORY

PRINCIPAL DIETARY COMPONENT

SPECIES EXAMPLE

Herbivore

Grasses, sedges, leaves, bulbs, aquatic vegetation

Geese, ducks, swans, swamp hens

Nectarivore

Nectar, pollen

Lorikeets, honeyeaters

Granivore

Seeds, grains

Finches, parrots, doves and pigeons

Frugivore

Fruits

Pigeons, fig-birds and orioles, koels and channel-bill cuckoos

Carnivore

Vertebrate prey

Raptors, kookaburras, magpies, butcher birds

Insectivore

Invertebrate prey

Masked lapwing, tawny frogmouths, swallows and swifts, magpie larks

Piscivore

Fish

Pelicans, cormorants, some raptors, herons

Table 1. Broad nutritional categories of Australian native birds commonly presenting for veterinary evaluation.

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Ladds P. (2009) Pathology of Australian Native Wildlife.

CSIRO Publishing, Melbourne.

The ability to confidently handle and manually restrain birds will reduce the risk of injury to the handler and reduce the risk of injury and stress to the bird. Manual restraint should only be used for very brief physical examinations, the administration of medications or to assist feeding. Anaesthesia is recommended for longer procedures. Injuries may occur as the result of bites or from claws and talons. Some species such as butcherbirds have hooked beaks and can deliver painful bites, while friar birds have needle sharp claws that can be used to good effect. Gannets and cormorants have serrated edges to their beak and can deliver painful bites. Raptors have extremely powerful talons and can cause significant damage if not restrained correctly. Eye protection should be worn when handling birds such as darters, cormorants, gannets and herons.

Many smaller species can be restrained without the use of protective equipment while larger species can be effectively restrained with the use of light weight towels. Gloves should generally be avoided. In addition to immobilising beaks or claws, the wings of the bird should generally be restrained against the body to prevent the bird injuring itself or escaping. For larger species such as pelicans and black swans, two people are often required to safely and effectively restrain the bird.

Most species can be safely anaesthetised using isoflurane in oxygen delivered via mask for both induction and maintenance. Fasting for 3-4 hours is recommended for nectarivores such as lorikeets as there is a high risk of regurgitation and aspiration due to the liquid nature of the crop contents. Wild birds that present sick or injured often have not eaten for some time prior to presentation; fasting is generally not required. However, checking to see that the crop is empty prior to anaesthesia is prudent. For short procedures intubation is generally not required. In waterfowl such as ducks, placement of a face mask over the beak causes stimulation of trigeminal nerve receptors inducing a stress response resulting in apnoea and bradycardia. Intravenous alfaxalone or propofol, given to effect, results in a smoother, shorter induction and avoids activation of the stress response in these species. Pre-oxygenation prior to induction is recommended for birds exhibiting obvious signs of injury or illness. On recovery from anaesthesia birds should be lightly restrained until sufficiently coordinated and allowed to recover in a quiet, darkened and thermally appropriate environment.

A detailed account of avian anaesthesia is beyond the scope of this document and readers are referred to the following resources: − Gunkel C, Lafortune M. (2005) Current techniques in avian anaesthesia. Seminars in Avian and Exotic Pet Centre for Veterinary Education

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Medicine 14, 263-276. DOI: 10.1053/j.saep.2005.09.006 − Speer BL. (2018) Basic anaesthesia. In: BSAVA Manual of Avian Practice (Eds Chitty J, Monks D). British Small Animal Veterinary Association, Gloucester. Pp 232-241. − lafeber.com/vet/avian-anesthesia-webinar − vin.com/apputil/content/defaultadv1. aspx?pId=11349&catId=34746&id=5328309

Common diseases of free-ranging native birds Parasitic diseases Throat worm Aetiology Cheilospirura gymnorhinis is found in the oral cavity and pharynx of fledgling magpies, with the same or similar parasite found in currawongs, butcher birds, and possibly magpie larks and black-faced cuckoo shrikes (Ladds 2009, Hall and Rose 2021).

Clinical signs Nodular lesions with a nematode protruding from the centre are present on the oral mucosa surrounding the tongue and glottis. Infestations with this parasite are typically mild and self-limiting although heavy burdens can block the glottis, impeding prehension and ingestion of food resulting in debilitation. (Figure 1) Diagnosis A presumptive diagnosis can be made on the basis of the characteristic clinical signs. A similar parasite Syngamus trachea, the gape worm, is occasionally found in the pharynx and throat of free-ranging native birds.

Treatment Moxidectin applied topically (although efficacy is unknown) and manual removal of the parasites are the mainstay of treatment.

Neuroangiostrongyliasis Aetiology Neuroangiostrongyliasis is caused by the aberrant migration of the larvae of the rat lung worm, Angiostrongylus cantonensis, in the brains of affected birds causing a granulomatous encephalitis and meningitis (Ma et al. 2013). Birds acquire the parasite after ingesting snails and slugs, the intermediate hosts of the parasite. Affected birds include tawny frogmouths, gang gang and yellow-tailed black cockatoos (Monks et al. 2005). In one study angiostrongyliasis was responsible for clinical disease in 80% of tawny frogmouths exhibiting neurological signs (Gelis et al. 2011). A seasonal pattern of infection in late summer and autumn has been observed in tawny frog mouths in the Sydney region.

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Restraint and anaesthesia

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Figure 2. Loss of the righting reflex in a tawny frogmouth with neuroangiostrongyliasis.

Clinical signs Clinical signs include depression, weight loss, and an inability to fly, perch (due to pelvic limb paresis) or right themselves. (Figure 2) Diagnosis No antemortem diagnostic tests are available and the condition must be differentiated from trauma and organochlorine toxicity. Definitive diagnosis is by morphological examination of the worms recovered post mortem and supportive histological findings.

Treatment Anthelmintics are generally considered to be contraindicated as death of the parasite results in a severe inflammatory response and worsening of clinical signs. Variable results have been reported following the use of dexamethasone in birds (Gelis et al. 2011).

Successful treatment with steroidal and nonsteroidal anti-inflammatory therapy and fenbendazole has been reported in flying foxes (Reddacliff et al. 1999). Freeranging tawny frog-mouths are frequently in an advanced state of disease at presentation and euthanasia may be the most appropriate option.

Figure 1. Severe throat worm infection in a sub-adult Australian magpie.

Knemidocoptes spp.

Aetiology Disease associated with Knemidocoptes intermedius is seen in wild pied currawongs, magpies, forest ravens and superb lyre birds (Jaensch et al. 2003, Holz et al. 2005).

Knemidocoptes pilae causes disease in psittacines.

Transmission between birds is likely via direct contact or contaminated nesting or roosting sites.

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Figure 3. Hyperkeratosis associated with Knemidocoptes intermedius infestation in a pied currawong

Figure 4. Severe knemidocoptic mange, caused by Knemidocoptes pilae, in a sulphur crested cockatoo with concurrent circovirus infection.

Clinical signs

Clinical signs

Marked hyperkeratosis is the primary clinical sign. The lower limbs of currawongs, magpies and ravens are affected. In severe cases there are markedly raised and thickened crusts; lesions may cause deformities and the loss of digits (Figure 3). Affected birds are often severely debilitated at presentation. In psittacines the skin of the head, vent and feathered areas of the pelvic limbs are also affected (Portas et al. 2017). (Figure 4)

Infection in most birds is subclinical. Moderate to severe skeletal myositis occurs in pied currawongs and, to a lesser extent, magpies (Lederer et al. 2002). Affected birds exhibit weight loss and an inability or reluctance to fly or are found immobile or ataxic on the ground.

Multiple pale foci of necrosis and inflammation may be evident in the pectoral muscles. (Figure 5) Neurological signs predominated in nankeen kestrels (Raidal and Jaensch 2000). Anaemia, failure to thrive and mortality may also occur in young birds of other species. Anaemia and hepatomegaly appear to be common in juvenile fig birds and orioles. (Figure 6)

Diagnosis Diagnosis is by demonstration of the mite through microscopic examination of skin scrapings, although lesions in affected birds are characteristic.

Diagnosis

Treatment Treatment with macrocyclic lactones is effective in mild cases while euthanasia is recommended in severe cases.

Leucocytozoonosis Aetiology A common infection, usually asymptomatic, and often found concurrently with other haematozoans, in wild Australian birds. The organism is transmitted between birds by blackflies (Simuliidae) in which the parasite undergoes sexual reproduction. Morbidity and mortality have been reported in pied currawongs, Australian magpies, grey butcherbirds, nankeen kestrels, noisy minors, Australasian fig birds, olive-backed orioles and tawny frogmouths (Adlard et al. 2004, Pierce et al. 2004, Jiang et al. 2019).

Antemortem diagnosis is by demonstration of gametocytes in peripheral blood smears and cytological examination of feather pulp smears in juvenile birds.

(Figure 7) The use of PCR for diagnosis has been reported but is not commercially available. Histopathology can be used to demonstrate the presence of schizonts and associated inflammation.

Treatment Effective treatment regimens have not been established although there is anecdotal evidence to suggest pyrimethamine may be effective in juvenile fig birds.

Euthanasia is indicated in severe cases.

Trichomoniasis Aetiology A protozoan disease of the upper gastrointestinal tract caused by the flagellate Trichomonas gallinae.

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Clinical signs Clinical signs include emaciation, inappetence, diarrhoea, weakness, depression, and the presence of faecal material around the vent.

Diagnosis Diagnosis is my demonstration of the organism on wet preparations of faecal samples or intestinal contents (post mortem). Spironucleus spp. can be differentiated from other enteric protozoa by the presence of two anterior nuclei and eight flagella.

Treatment An effective treatment regimen for this disease has not been established and mortality is high.

Figure 5. Multifocal areas of necrosis and inflammation in a pied currawong associated with Leucocytozoon spp.

Trichomonas gallinae is an introduced parasite of the feral rock pigeon, although indigenous species have recently been described from native pigeons (Forrester and Foster 2008). The organism has a direct life cycle but can survive for several hours in contaminated water. Affected species include pigeons, doves and raptors.

Clinical signs Affected birds may exhibit anorexia, dysphagia and weight loss.

Characteristic cream to caseous yellow plaques may be evident in the oropharynx. (Figure 8) Diagnosis Demonstration of the organism (motile, flagellated protozoa) by microscopic examination of wet preparations taken directly from the lesion or a crop wash.

Treatment Metronidazole (50 mg/kg PO sid for 7 days) or carnidazole (20-30 mg/kg PO once) are generally effective treatments.

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Bacterial diseases Necrotic enteritis Aetiology Clostridium perfringens is the primary pathogen implicated in necrotic enteritis, although other bacteria such as Escherichia coli have also been isolated from affected birds. The disease has been reported in free-living rainbow and scaly-breasted lorikeets and king parrots in Australia (McOrist and Reece 1992). Carbohydrate overload has been implicated as a predisposing factor and cases are seen predominantly in late winter and early autumn. All sex and age classes are affected.

Clinical signs Affected birds may die per-acutely or exhibit diarrhoea, inappetence, an inability to fly or stand, depression and may regurgitate clear fluid.

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disease in free-ranging king parrots, galahs and sulphur-crested cockatoos (Philbey et al. 2002). The natural host for the organism is unknown but transmission is via the faeco-oral route.

In king parrots the disease is seen most commonly in juveniles, occurs predominantly during the winter months and is associated with high levels of mortality.

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Figure 6. Hepatomegaly in a juvenile Australasian fig bird associated with Leucocytozoon spp.

Figure 7. Leucocytozoon spp. gametocytes in a peripheral blood smear of an Australasian fig bird.

Diagnosis

Clinical signs

Diagnosis is based on clinical signs, isolation of Clostridium perfringens and suggestive histopathological lesions. PCR has been used to determine the specific toxin (alpha, beta etc.) present.

Many birds may be asymptomatic carriers. In clinically ill birds, signs associated with the respiratory and gastrointestinal tracts predominate and may include diarrhoea, nasal and ocular discharge, dyspnoea, weight loss, green/yellow urates and depression.

Treatment An effective treatment regimen for this disease has not been established.

Chlamydiosis Aetiology Chlamydiosis is caused by bacteria in the genus Chlamydophila. Chlamydophila psittaci has been widely reported from a wide range of bird species within Australia and globally. However, C. gallinacea and other Chlamydiales have been reported from crimson rosellas and galahs in Australia (Stokes et al. 2021). A recent study in south-east Queensland demonstrated a prevalence of 28.54% in free-ranging birds and demonstrated novel chlamydial species (avian C. abortus, C ibidis and C pneumoniae) in a range of novel avian hosts (Kasimov et al. 2022). In free-ranging Australian birds chlamydiosis is seen primarily in pigeons, doves and parrots; the disease is considered endemic in these populations.

Chlamydiosis has also been reported from free-ranging superb lyrebirds and short-tailed shearwaters (Ladds 2009). Transmission is via the faeco-oral route or respiratory tract secretions.

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Diagnosis A modified ELISA for detection of antibodies to Chlamydia psittaci in whole blood or serum is available as a patient side test kit (ImmunoComb Avian Chlamydophila psittaci Antibody Test Kit; Biogal Galed Laboratories) and can be used for ante mortem detection of the disease. An indirect fluorescent antibody test is also available for ante mortem diagnosis of the disease. PCR can be performed on fresh liver and spleen (post mortem) or swabs from the cloaca, upper respiratory tract or conjunctiva (ante mortem). Culture can be performed on fresh spleen or liver, cloacal or conjunctival swabs although this requires specialised transport media and specialised culture techniques.

Treatment Doxycycline hydrochloride (60 mg/kg IM q 7 days) is generally an effective treatment. A minimum treatment period of 45 days has been recommended although a shorter treatment period of 21 days was effective in one study (Guzman et al. 2010). Chlortetracycline hydrochloride may also be administered in water although therapeutic doses may not be achieved.

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Figure 8. Oropharyngeal plaque associated with trichomoniasis in a Peregrine falcon.

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Figure 9. Loss of outer primary feathers in a juvenile rainbow lorikeet due to psittacine beak and feather disease.

Viral diseases Psittacine beak and feather disease Aetiology A common disease of fledgling rainbow and scaly breasted lorikeets. The causative agent, beak and feather disease virus, a Circovirus, is relatively widespread in free-ranging psittacine populations in Australia (Raidal 2012). Young birds are typically affected but disease may be seen in birds of any age. Acute and chronic forms of the disease occur.

Clinical signs The typical clinical presentation in lorikeets includes the loss of outer primary flight and tail feathers (Figure 9). Remaining feathers may be dystrophic (shortened, retained feather sheaths, annular constriction of and

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haemorrhage within the calamus) and are easily lost (Figure 10). In cockatoos the pulviplumes are often first affected; the powder-down patch becomes bare and as a result the plumage is dull and the beak is glossy.

The beak of affected birds may become elongated before eventually fracturing or sloughing off. Secondary diseases, a result of immune suppression, may be present.

Diagnosis Diagnosis is via a combination of polymerase chain reaction (whole blood or feather material), haemagglutination (feather material) assay and haemagglutination inhibition (serum, plasma or whole blood) assay. However, the clinical presentation is characteristic and a presumptive diagnosis can be made on the basis of clinical signs.

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There is no treatment, birds are persistently infected and euthanasia of affected birds is recommended.

Pox virus Aetiology Avian pox is caused by viruses in the genus Avipoxvirus with transmission predominantly via biting insects; transmission may also be via direct physical contact and fomites. The majority of avipoxviruses infecting wild birds remain uncharacterised; however, a novel pox virus has recently been characterised from magpie larks (Sarker et al. 2021). Pox virus infection has been reported from a wide variety of free-ranging native Australian birds (Annuar et al. 1983).

Clinical signs

Figure 10. Annular constriction of and haemorrhage within the calamus of a feather from a rainbow lorikeet with psittacine beak and feather disease.

Three distinct syndromes are recognised in wild birds worldwide but nodular lesions on unfeathered skin appears to be the most common lesions observed in the butcherbird-magpie clade in the greater Brisbane region, although cases involving extensive necrosis of the beak are seen infrequently. (Figure 11) Diagnosis Lesions are characteristic and a diagnosis is supported by characteristic histological changes. Definitive diagnosis requires electron microscopy or virus isolation although this is rarely warranted (or available) in the clinical setting.

Treatment The disease is generally self-limiting and treatment is not indicated unless pox lesions affect the eyes or the bird’s ability to prehend food. Birds presenting for veterinary evaluation frequently have extensive lesions. Euthanasia is indicated where extensive lesions are present such as those disrupting the architecture of the beak or affecting the eyelids to such an extent that vision is limited.

Toxicoses Botulism Aetiology

Figure 11. Severe pox virus associated lesions affecting the beak and periocular skin of an Australian magpie.

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Botulism is caused by toxins produced by multiple serotypes of the bacterium Clostridium botulinum. The disease is seen most frequently in water dwelling species such as ducks, swans, ibis and pelicans; although all birds are likely susceptible (WHA, 2019). The disease has a seasonal prevalence with outbreaks occurring most commonly in summer and autumn in Australia.

Proliferation of Clostridium botulinum is dependent upon environmental conditions including low oxygen

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Treatment

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Figure 12. A Pacific black duck with botulism.

environments, sufficiently high ambient temperature and a high protein substrate (Rocke and Bollinger, 2007).

Outbreaks can occur repeatedly at specific locations.

Clinical signs The disease is characterised by progressive weakness, paresis and flaccid paralysis. Affected birds struggle to fly and as the disease progresses birds lose the ability to fly and eventually walk. The muscles of the neck maybe affected and the nictitating membrane may protrude in some cases. Death occurs when the muscles responsible for respiration become paralysed. (Figure 12) Diagnosis A presumptive diagnosis can be made on the basis of suggestive clinical signs, lack of lesions at necropsy and appropriate environmental conditions. Obtaining a definitive diagnosis can be challenging: a capture enzyme-linked immunoassay (cELISA) and PCR can be used to detect botulinum toxin, although these tests are not routinely available in all states and territories.

Treatment There is no specific treatment for the disease and treatment is limited to the provision of supportive care.

Supportive care includes oral or parenteral fluid therapy, administration of charcoal slurries, assist feeding and lubricating eye drops. Birds may require several weeks of supportive care before being sufficiently recovered for release.

Clinical signs Tawny frogmouths with organochlorine toxicity are found weak, unable to fly and exhibit a range of neurological symptoms including opisthotonos, dilated pupils, leg extension and head tilt (Charles 1995). Exposure to high doses of organophosphates in birds can result in death without premonitory signs. Clinical signs of organophosphate and carbamate exposure include acute neurological symptoms, hyper-salivation, emesis, respiratory distress, diarrhoea, paralysis of the feet. In addition to these clinical signs a myriad of sub-lethal effects that have the potential to reduce reproduction and survival have been demonstrated following exposure to organophosphates and carbamates.

Diagnosis

Pesticide toxicities Aetiology Pesticide toxicity events appear to be reasonably common in free-ranging birds with organophosphate Centre for Veterinary Education

and, to a lesser extent, organochlorine toxicities most frequently reported (Hall and Rose 2021). In many events the specific toxin involved remains unknown. Most poisonings are associated with agricultural chemicals that have been deliberately or accidentally misused or disposed of. Organophosphate associated with toxicity include e fenthion, fenamiphos, parathion, diazinon, malathion, famphur, phorate, terbufos and chlorpyrifos.

Carbamates include carbofuran, aldicarb and carbaryl.

Organochlorines associated with toxicities include methoxychlor, aldrin, dieldrin, chlordane, toxaphene, lindane, DDT, DDE and heptacholor epoxide and endrin.

Exposure most commonly occurs due to ingestion of contaminated food but can occur through dermal and inhalation routes of exposure.

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Encephalomyelitis of lorikeets (clenched-claw syndrome)

Treatment

Aetiology

The use of atropine blocks receptors targeted by these drugs while pralidoxime chloride (2-PAM) is a cholinesterase reactivator. Emetics, cathartics and adsorbents limit further absorption from the gastrointestinal tract. Supportive treatment includes fluid therapy and nutritional support.

A neurological syndrome of uncertain aetiology occurring in rainbow lorikeets in coastal New South Wales and, to a lesser extent in south-east Queensland and Victoria.

Birds may be affected at any time of the year and subadult and adult birds are affected. A viral aetiology has long been proposed but the causative agent not identified (McOrist and Perry 1986). More recently an Avulavirus has been proposed as a potential cause of this syndrome (Chang et al. 2020).

Diseases of unknown aetiology Lorikeet paralysis syndrome Aetiology A disease syndrome of unknown aetiology that seasonally (October – June) affects rainbow, and to a lesser extent, scaly-breasted lorikeets in south-eastern Queensland (Lacasse et al. 2021). Extensive investigations into the cause of the syndrome have not revealed an underlying aetiology although no evidence of infectious disease and most common toxins and pesticides have been excluded.

This disease syndrome is distinct from encephalomyelitis of lorikeets (clenched-claw syndrome), a nonsuppurative encephalitis of possible viral origin, heavy metal toxicoses and various other neurological syndromes of undetermined aetiology in lorikeets. This disease is postulated to be caused by a neuromuscular toxin; most likely plant associated.

Clinical signs

Clinical signs Affected birds initially present sitting on their hocks with clenched claws but are otherwise bright and alert.

Progressive paralysis may occur.

Diagnosis A presumptive diagnosis can be made on the basis of clinical signs. There are no gross lesions but a nonsuppurative encephalomyelitis is evident on histology.

Treatment An effective treatment regimen for this disease has not been established.

Black and white bird disease Aetiology

A presumptive diagnosis can be made based on clinical signs. Supportive clinical pathology findings include a leucocytosis, elevations in creatine kinase, AST and uric acid.

A syndrome of acute mass mortality of undetermined aetiology seen predominantly in magpies, pied currawongs, pee wees and Australian ravens from the east coast of New South Wales (Hall and Rose 2021). The disease has been suspected in a smaller number of other species at other locations in Queensland and Victoria.

There are recent anecdotal reports of the disease in Western Australia. All age and sex classes are affected, although more males than females have been affected in some outbreaks (Jarratt and Rose 2016). A viral aetiology is suspected but remains unproven (Wildlife Health Australia 2017).

Treatment

Clinical signs

Prognosis is dependent upon the severity of clinical signs at presentation. Birds with less severe clinical signs (able to walk and swallow) have a good chance of recovery over a period of 2-8 weeks with supportive care including parenteral fluid administration, lubricating eye drops and assist feeding. Birds that are unable to stand and have lost both their blink and swallow reflexes and those whose clinical signs progress rapidly generally have a poor prognosis even with intensive nursing care and euthanasia is warranted.

Affected birds are bright and alert but exhibit progressive neurological signs including an inability to fly then stand, an inability to right themselves and respiratory distress. A haemorrhagic enteritis may be present in some birds. Reflexes are preserved and there is rapid progression to death within 12-24 hours.

Affected birds develop a syndrome of ascending flaccid paralysis and progressively lose the ability to fly, develop a hopping and, eventually, ataxic gait, exhibit characteristic voice changes, lose the ability to blink and eventually swallow.

Diagnosis

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Diagnosis A presumptive diagnosis can be made on the basis of clinical signs and characteristic histological

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and storage methods may vary between diagnostic laboratories.

Treatment Supportive care including parenteral and oral fluids and assist feeding has been reported to be effective in a small number of affected birds (Jarratt and Rose 2016).

Wasting syndrome in sub-adult galahs and corellas Aetiology A syndrome of uncertain aetiology seen in sub-adult galahs (Doneley 2012) and little corellas characterised by emaciation, weakness and diarrhoea. The disease appears to be multifactorial. All birds presented to the RSPCA Queensland Wildlife Hospital tested for beak and feather disease virus were positive despite the lack of typical clinical signs. Birds were variably infected with Macrorhabdus ornithogaster, Spironucleus species and/or enterovirus. A syndrome of circovirus mediated immune suppression associated with opportunistic secondary infections is proposed.

Clinical signs Affected birds exhibit marked emaciation and often have diarrhoea staining of the feathers surrounding the vent. Birds are weak and sometimes mistaken for pets by members of the public due to their quiet (weakened) nature.

Diagnosis The clinical presentation is highly suggestive and can be further supported by demonstrating characteristic Spironucleus-like organisms in fresh faecal samples, Macrorhabdus organisms on gram stains or wet preparations of faecal samples, supportive histopathology and polymerase chain reaction (whole blood or feather material), haemagglutination (feather material) assay and haemagglutination inhibition (serum, plasma or whole blood) assay for beak and feather disease virus.

Fishing hook ingestion and hook and line entanglement are common presentations in and water fowl such as swans and ducks and in piscivorous species such as a pelicans, gulls, cormorants and darters. String, plastic and human hair can become entwined on the feet of a range of avian species but is seen most commonly in pee wees, magpies, crows and currawongs.

Clinical signs Birds that have collided with vehicles will often have evidence of impact trauma including beak injuries, pectoral muscle bruising, fractures of the appendicular skeleton (often open), and respiratory distress associated with pulmonary contusions. Birds that have collided with glass will often have evidence of impact trauma affecting the beak (contusions or fractures) and/or pectoral muscles (bruising). Affected birds are often unable to fly due to concussion and/or fractures, especially of the coracoid, clavicle, keel and less commonly the humerus or radius and ulna. Birds that have been entangled in barbed wire or fruit netting frequently present still entangled within sections of wire or netting.

Birds that have ingested fish hooks may have sections of line trailing from the oral cavity. The skin of the pelvic limbs and patagium are common sites in which hooks become lodged and fishing line entanglement of the wings and pelvic limbs is common. Birds with entanglement of the feet may have deep lacerations and swelling of the digits. In severe cases there is exposure of tendons and bone and sometimes necrosis of digits.

Diagnosis

Treatment An effective treatment regimen for this disease has not been established.

Diagnosis is based on history, clinical examination and radiographic findings.

Treatment

Miscellaneous conditions Trauma Aetiology Trauma associated with vehicular or glass collision is common in avian species in urban and peri-urban environments. Species commonly presenting as a result Centre for Veterinary Education

of vehicular trauma include lorikeets, cockatoos, galahs, corellas, kookaburras, raptors, tawny frogmouths, noisy miners and magpies. Species commonly presenting as a result of glass collision include lorikeets, pigeons and doves, kingfishers and honeyeaters. Barbed wire and fruit-netting entanglement, usually involving the patagium, is also commonly seen in birds from periurban and rural environments. Patagial injuries are frequently severe due to prolonged struggling or the rescuer’s attempts to remove the bird from the barbed wire.

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Where birds have been concussed following collisions and have not sustained fractures, prognosis is usually good with supportive care (analgesia and fluid administration, and the provision of warmth and cage rest). Standard avian orthopaedic procedures can be undertaken to repair fractured long bones. Open fractures, fractures that involve or are close to joints

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changes (multisystemic perivascular inflammation, hepatic necrosis, non-suppurative inflammation and myodegeneration of cardiac and skeletal muscle, and non-suppurative encephalitis).

The prognosis for hook removal depends upon the location within the gastrointestinal tract and ease of surgical access if required. The prognosis for recovery following foreign body entanglement of the lower limbs depends on the length of time and extent of the entanglement.

Nutritional secondary hyperparathyroidism Aetiology The aetiology of this condition is incompletely understood but may be associated with anthropogenic provision of foods with an inverse calcium to phosphorous ratio such as mincemeat and seeds.

Additional potential causes include reduced biodiversity of prey species, inappropriate calcium to phosphorous ratios in invertebrate prey and xenobiotic exposure (Tangredi 2007).

Clinical signs Affected fledglings have excessively pliable beaks, folding fractures of long bones, keel deformities, poor plumage and tend to hock sit rather than stand.

Diagnosis A presumptive diagnosis can be made on the basis of clinical and radiographic findings. Osteopenia is the principle histological finding.

Treatment Mild cases can be treated with calcium supplementation (Vetafarm Calcivet, https://vetafarm.com.au/product/ calcivet-50ml/), dietary correction and supportive care.

Birds with skeletal changes are unlikely to survive in the wild and euthanasia is recommended.

Management of nestlings and fledglings Juvenile birds can be broadly divided into those that are precocial and those that are altricial. Altricial species are born in an underdeveloped state and require extensive parental care to survive. Precocial species are born at an advanced stage of development and require no, in the case of brush turkeys, or limited parental care, in the case of some waterfowl and shorebirds, for survival.

Precocial species leave the nest straight or shortly after hatching.

Juvenile altricial birds can also be classified according to their stage of development: − hatchling – usually 0-3 days post hatching, unable to thermoregulate, unfeathered

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− nestling – usually 3-13 days old, beginning to thermoregulate, feathers developing − fledgling – usually 13 days old or older, feathers developed and learning to fly Hatchling or nestling birds that have fallen from the nest need to be returned for ongoing parent rearing or transferred to an experienced wildlife rehabilitator for hand-rearing. Fledgling birds are learning to fly and are frequently found out of the nest. The parents are often nearby and will continue to feed and care for these birds. In many instances these birds could be reunited with their parents. However, well-meaning but poorly informed members of the public often take these birds and present them to private veterinary clinics or wildlife hospitals. Members of the public presenting healthy fledgling birds should be encouraged to return these fledglings to the location where they were found and referred to the following guides for reuniting fledgling birds: rspcaqld.org.au/blog/fact-check/baby-birdseason#:~:text=To%20try%20to%20reunite%20 the,and%20baby%20birds%20from%20predators wildcare.org.au/species-information/ birds/#:~:text=Please%20the%20baby%20bird%20 into,your%20local%20wildlife%20rescue%20 group.&text=Download%20our%20Baby%20Bird%20 Poster,create%20a%20make%2Dshift%20nest yumpu.com/en/document/read/11609598/how-do-imanage-baby-birds-currumbin-wildlife-sanctuary Chicks of altricial species usually have a well-developed begging response and will gape readily when hungry or offered food. Identifying the species is important in order to provide appropriate food to the chick whilst in care. A detailed account of hand-rearing juvenile birds is beyond the scope of this document and readers are referred to Duerr and Gage (2020) for more detailed information.

Veterinary assessment of nestlings and fledglings All nestling and fledgling birds should be carefully examined for signs of potential trauma sustained from falls or attempted predation. Long bone fractures and air sac rupture are common findings. The general demeanour and hydration status of the bird should be assessed. Dehydration is a common finding and should be corrected prior to offering solid food. Oral electrolyte solutions such as Vetafarm Spark Electrolyte Bird Supplement, Wombaroo/Paswell First Aid for Birds or Vetafarm Spark Electrolyte Bird Supplement can be administered by syringe or crop needle in cases of mild to moderate dehydration where the bird is otherwise bright and alert. Subcutaneous fluids can

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and comminuted fractures are likely to have a poor prognosis.

(Podargus strigoides) in Western Australia. Parasitology Research. 118. DOI: 10.1007/s00436-019-06317-7.

Many nestlings and some fledglings are hypothermic on presentation and should be gradually warmed by placing in a warmed, humidity-controlled environment such as a Vetario Intensive Care unit, Rcom Bird ICU Brooder or a Brinsea Products Brooder/Intensive Care Unit.

Lacasse C, Rose K, Allen M, Ward MP, Pulscher LA, Giles A, Hall J, Phalen DN. (2021) Investigation into clinicopathological and pathological findings, prognosis, and aetiology of lorikeet paralysis syndrome in rainbow lorikeets (Trichoglossus haematodus). Australian Veterinary Journal. 10, 432-44.

Kasimov V, Dong Y, Shao R, Brunton A, Anstey SI, Hall C, Chalmers G, Conroy G, Booth R, Timms P, Jelocnik M. (2022) Emerging and well‐characterized chlamydial infections detected in a wide range of wild Australian birds.

Transboundary and Emerging Diseases. https://doi.org/10.1111/tbed.14457

Medical problems in hand-reared wild birds frequently relate to deficiencies in captive husbandry (incorrect diet, incorrect feeding frequency, poor hygiene, temperature fluctuations etc.) and a complete review of husbandry practices is warranted when assessing sick nestling or fledglings in care.

References Adlard R, Peirce M, Lederer R. (2004) Blood parasites of birds from south-east Queensland. Emu. 104, 191-196. DOI: 10.1071/MU01017.

Annuar BO, Mackenzie JS, Lalor PA. (1983) Isolation and characterization of avipoxviruses from wild birds in Western Australia. Archives of Virology 76, 217229.

Chang W, Eden J, Hall J, Shi M, Rose K, Holmes EC. (2020) Meta-transcriptomic analysis of virus diversity in urban wild birds with paretic disease. Journal of Virology. doi.org/10.1101/2020.03.07.982207 Charles J. Organochlorine toxicity in tawny frogmouths. Proceedings of the Australian Committee of the Association of Avian Veterinarians, Dubbo. 1995:13541.

Doneley B. (2012) Weight Loss Syndrome in Juvenile Free‐living Galahs (Eolophus roseicapillus). Proceedings of the Association of Avian Veterinarians Australian Committee, Annual Conference 2012, pp 9-11.

Duerr RS, Gage LJ. (2020) Hand-Rearing Birds, 2nd Edition. Wiley Blackwell, Hoboken.

Forrester DJ, Foster GW. (2008) Trichomonosis. In: Parasitic Diseases of Wild Birds (Atkinson CT, Thomas NJ, Hunter DB eds). Wiley-Blackwell, Iowa. Pp 120153.

Guzman DS, Diaz-Figueroa O, Tully T, Ciembor P, Morgan T, Walden M, Poston RP, Flammer K, Mitchell MA, Ritchie B. (2010) Evaluating 21-day doxycycline and azithromycin treatments for experimental Chlamydophila psittaci infection in cockatiels (Nymphicus hollandicus). Journal of Avian Medicine and Surgery.

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Hall J, Rose K. (2021) Common Diseases of Urban Wildlife: Birds. Taronga Conservation Society Australia, Sydney.

Holz PH, Beveridge I, Ross A. (2005) Knemidocoptes intermedius in wild superb lyrebirds (Menura novaeholandiae). Australian Veterinary Journal 83, 374-375.

Jaensch SM, Raidal SR, Hobbs RP. (2003) Knemidocoptes intermedius in a wild currawong (Strepera graculina). Australian Veterinary Journal 81, 411.

Jarratt C, Rose K. (2016) Mass mortality event in Australian magpies and Australian ravens in NSW in 2015. Proceedings of the Association of Avian Veterinarians Australian Committee, Annual Conference 2016, pp 23-27.

Est. 1965

Ma G, Dennis M, Rose K, Spratt D, Spielman D. (2013) Tawny frogmouths and brushtail possums as sentinels for Angiostrongylus cantonensis, the rat lungworm. Veterinary Parasitology 192, 158-165.

McOrist S, Reece RL. (1992) Clostridial enteritis in free-living lorikeets (Trichoglossus spp.), Avian Pathology, 21:3, 503-507, DOI: 10.1080/03079459208418868.

Monks DJ, Carlisle MS, Carrigan M, Rose K, Spratt D, Gallagher A, Prociv P. (2005) Angiostrongylus cantonensis as a cause of cerebrospinal disease in a yellowtailed black cockatoo (Calyptorhynchus funereus) and two tawny frogmouths (Podargus strigoides). Journal of Avian Medicine and Surgery 19, 289-293.

Peirce MA, Lederer R, Adlard RD, O’Donoghue PJ. (2004) Pathology associated with endogenous development of haematozoa in birds from southeast Queensland. Avian Pathology, 33, 445-450, DOI: 10.1080/03079450410001724076 Philbey AW, Andrew PL, Gestier AW, Reece RL, Arzey KE. (2002) Spironucleosis in Australian king parrots (Alisterus scapularis). Australian Veterinary Journal. 80, 154-60. doi: 10.1111/j.1751-0813.2002.tb11381.x. PMID: 12019702.

Portas T, Jackson B, Shamsi S, Raidal SR. (2017) Beak and feather disease virus carriage by Knemidocoptes pilae in a sulphur-crested cockatoo (Cacatua galerita). Australian Veterinary Journal 95, 486-489.

Raidal SR. (2012) Avian circovirus and polyomavirus disease. In: Fowler’s Zoo and Wild Animal Medicine Current Therapy Volume 7 (Eds Miller RE, Fowler ME).

Elsevier Saunders, Missouri. Pp 297-303.

Raidal SR, Jaensch SM. (2000) Central nervous disease and blindness in Nankeen kestrels (Falco cenchroides) due to a novel Leucocytozoon-like infection. Avian Pathology 29, 51-56. doi: 10.1080/03079450094289.

Rocke TE, Bollinger TK. (2007) In Infectious Diseases of Wild Birds. Thomas NJ, Hunter DB, Atkinson CT (eds) Wiley-Blackwell, Iowa. Pp 377-416.

Sarker S, Athukorala A, Raidal SR. (2021) Molecular characterisation of a novel pathogenic avipoxvirus from an Australian passerine bird, mudlark (Grallina cyanoleuca). Virology 554, 66-74, https://doi.org/10.1016/j.virol.2020.12.011.

Stokes HS, Martens JM, Jelocnik M, Walder K, Segal Y, Berg ML, Bennett ATD. (2021) Chlamydial diversity and predictors of infection in a wild Australian parrot, the Crimson Rosella (Platycercus elegans). Transboundary and Emerging Diseases 68, 487–498.

Tangredi BP. (2007) Environmental factors associated with nutritional secondary hyperparathyroidism in wild birds. Avian and Poultry Biology Reviews 18, 47-56.

Wildlife Health Australia. (2017) WHA fact sheet: Neurological disease in “black and white” birds in Australia. Wildlife Health Australia.

Wildlife Health Australia. (2019) WHA fact sheet: Botulism in Australian wild birds.

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Jiang Y, Brice B, Nguyen M, Loh R, Greay T, Adlard R, Ryan U, Yang R. (2019) Further characterisation of Leucocytozoon podargii in wild tawny frogmouths

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Lederer R, Adlard RD, O’Donoghue PJ. (2002) Severe pathology associated with protozoal schizonts in two pied currawongs (Strepera graculina) from Queensland. Veterinary Record. 150, 520-522. doi: 10.1136/vr.150.16.520.

Reddacliff LA, Bellamy TA, Hartley WJ. Angiostrongylus cantonensis infection in grey‐headed fruit bats (Pteropus poliocephalus). Australian Veterinary Journal.

1999 77, 466-8.

Gelis S, Spratt DM, Raidal SR. (2011) Neuroangiostrongyliasis and other parasites in tawny frogmouths (Podargus strigoides) in south-eastern Queensland. Australian Veterinary Journal 0211;89: 47-50. DOI.org/10.1111 /j.1751-0813.2010.00660.

Centre for Veterinary Education

Ladds P. (2009) Pathology of Australian Native Wildlife. CSIRO Publishing, Melbourne.

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be administered instead of or in conjunction with oral fluids. Up to 10% of body weight can be administered subcutaneously. Some seabirds such as pelicans have subcutaneous air pockets and subcutaneous fluid administration should be avoided in these birds.

Robert Mills Moonee Beach Veterinary Surgery, PO Box 9012 Moonee Beach NSW 2450 e. rob@mooneevet.com.au C&T No. 6004 A multiparous beef cow was seen for dystocia, the farmer had called the vet out straight away and had not attempted to do anything.

Questions: 1. What is hanging out of the cow?

2. What is likely to be the diagnosis? i.e. what abnormality have we been presented with?

3. What is the very first thing that you are going to do?

4. What are your plans for management of this problem, what options will you give to the client before proceeding?

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Figure 1. Photo of the cow during parturition

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Control & Therapy Series – Issue 313 December 2023

Authors’ views are not necessarily those of the CVE

Contents

What's Your Diagnosis?

After-Hours Dystocia Case in a Multiparous Beef Cow

A DV E RTI S E M E NT

Contents

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Control & Therapy Series – Issue 313 December 2023

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For your dedication and commitment, especially when juggling study commitments with work and family, to complete this vigorous but rewarding continuing education. —CVE Tutors & Staff

Anaesthesia & Analgesia Tutors: Christina Dart & Eduardo Uquillas

—Compromised Patients Peter James Bell, NSW Amy Bullock, WA Xinyi Eunice Chan, Singapore Hilary Chok, QLD Shirley Chow, WA Jade Connolly, VIC Lucinda Foott, VIC Kirsty Fridemanis, QLD Charlotte Han, VIC Stephanie Harrop, ACT Andrea Khong, VIC Yip Bun Leung, NSW Yi-Hsien Lin, NSW Kate Phillips, VIC Nichola Richards, VIC Genevieve Shaw, NSW Samantha Spark, VIC Jill Teo, VIC Tiyaton Tuksaranupong, Thailand Zsófia Vass, Hungary Stephanie Wong, NSW

—Large Animals Melissa Ball, VIC David Brown, NSW Holly Dever, VIC Josephine Ginty, NSW Kate Hazeldene, VIC Lynley Johnson, SA Jerome Kalvas, SA Christine Powell, QLD Nicky Sheehan, NSW

—Unusual Pets Ramon de Armas, United States Josephine Ginty, NSW Catherine Hudson, NSW Chalitta Prasertwong, Thailand Holly Hyunjee Yang, WA

Beef Production Tutor: Paul Cusack Olli Beyer, SA Richard Bleckman, QLD Jessica Correa, QLD Jo Hoad, NSW Sharlet John, NSW Peter Nugroho, WA

Behavioural Medicine Tutors: Kersti Seksel, Debbie Calnon, Jacqui Ley, Barbara Lindsay, Sally Nixon, Isabelle Resch Vicki Brown, ACT Liam Brown, WA Joanna Chiang, Taiwan Eleanor Chipperfield, SA Angel Chu, VIC

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Kristie Clarke, ACT Bryana Clisby, United Kingdom Emma Crossland, VIC Lucian Currie, WA Jane Dunnett, TAS Anna Fenlon, NSW Gina Gainsborough- Waring, New Zealand Melissa Gosson, NSW Emma Gray, VIC Nicole Hillier, VIC An-Hsun Huang, Taiwan Jessie Johnson, WA Amy Kachurowski, Canada Justin Michaels, ACT Vienne Ng, SA Kaylee Onn, VIC Jessica Pickett, QLD Michelle Rassool, VIC Marissa Rosenbloom, United States Markéta Rybárová, Czech Republic Sophie Scott, SA Julia Smith, QLD Kirri Solly-Slade, VIC Hannah Steel, NSW Jennifer Wingham, NSW Jessica Yenson, ACT

Cardiorespiratory Medicine Tutors: Niek Beijerink & Mariko Yato Wasana Buayam, Thailand Siuyi Chia, WA Jenny Coonan, ACT Julie Cureton, VIC Jennifer Judd, SA Aomusa Kuaha, Thailand Krittinai Langputeh, Thailand Chun-han Lin, QLD Rutendo Mukandi, QLD Preawpailin Nakkarasin, Thailand Pattaranan Piyasart, Thailand Glenda Poon, NSW Kanyavee Premratanachai, Thailand Purich Sitmala, Thailand Thidawan Thumking, Thailand Komson Wongsommart, Thailand

Clinical Pathology Tutors: Sandra Forsyth & Karen Jackson Erin Allanson, VIC Brianna Caitens, QLD Charlie Camail-Pearce, WA Lauren Dowling, WA Jaclyn Fung, Hong Kong Michele Goh, SA Tuovi Joona, QLD Ryan Kotas, WA Andrew Laws, NSW Helen McLean, NSW Alexandra Meier, NSW Jennifer Millar, NSW Jessica Panozzo, NSW Emily Ryder, VIC

Control & Therapy Series – Issue 313 December 2023

Dieuwerke Schepers, VIC Avril Tsen, WA

Dermatology Tutors: Ralf Mueller, Sonya Bettenay & Stefan Hobi

—Advanced Sireetorn Apinuntanaphong, Thailand Thapanee Chuenngam, Thailand Heidi Furber, NSW Rachel Greenhill, QLD Jackrit Muensuwanwadee, Thailand Nuttawan Srifawattana, Thailand Ryan Tan, New Zealand Jessica Wallace, NSW Worapruch Wichachai, Thailand WORAWUT YAMGOSUM, Thailand

—Infectious Skin Disease Sireetorn Apinuntanaphong, Thailand Dylan Barber, VIC Grace Chapman, SA Liz Chmurycz, NSW Thapanee Chuenngam, Thailand Christine Clarke, SA Leonie Kwok, NSW Jackrit Muensuwanwadee, Thailand Fiona Smith, VIC Ryan Tan, New Zealand Worapruch Wichachai, Thailand Worawut Yamgosum, Thailand

—Pruritic Skin Disease Sireetorn Apinuntanaphong, Thailand Dylan Barber, VIC Emily Boshammer, QLD Anne-Marie Buden, VIC Vivien Cheok, NSW Siuyi Chia, WA Revathi G, VIC Rachel Greenhill, QLD Shanna Harris, WA David Hughes, NSW Jenny Ji, QLD Glenn Lee, Philippines Jackrit Muensuwanwadee, Thailand Mónica Pais, Mozambique Julie Ng Pangilinan, VIC Sarah Robinson, VIC Nutjira Sawatmongkol, Thailand Nuttawan Srifawattana, Thailand Worapruch Wichachai, Thailand Worawut Yamgosum, Thailand

Diagnostic Imaging —Abdominal

Tutor: Zoe Lenard Gaudiosa Berdon, Philippines Courtney Booth, NSW Rebekah Day, VIC Simone Dench, QLD

Authors’ views are not necessarily those of the CVE

Contents

Congratulations to the Distance Education class of 2023!

Emergency Medicine Tutors: Yenny Indrawirawan, Sophia Morse Carmen Ali, NSW Ella Bartolovic, SA Doris Cho, Hong Kong Lauren Fahler, VIC Georgina Frazer, VIC Alice Liaw, Singapore Kate McIntyre, TAS CHITASUDA OUNPRASERT, Thailand Tiana Park, VIC Yun Ting Peng, Taiwan Warangkana Promsatit, Thailand Nicole Rutledge, QLD Kevin Verhoeven, QLD Peter Wood, WA Nelson Zhang, Singapore

—Musculoskeletal Tutor: Xander Huizing Amelia Allen, QLD Jenny Andrew, VIC Stephen Baumberg, New Zealand Francesca Black, VIC Georgina Champion De Crespigny, SA Wan Shan Choi, NSW James Collison, NSW Jacqueline Letondeur, NSW Elissa Marriott, VIC Emily McKee, VIC Pooja Mishra, ACT Claude Patrick Monet, NSW Madison Newton, QLD Louisa Poutsma, NSW Teagan Rainford, QLD Wesley Simek, VIC Philippa Simms, WA Elizabeth Sorensen, VIC Ye Swe, Myanmar Yanling Tan, Singapore Briar Thornburrow, NSW Christiana Willenborg, NSW

Feline Medicine Tutors: Rachel Korman, Lara Boland, Katherine Briscoe, Michael Linton, Katie McCallum, Myles McKenna, Carolyn O’Brien, Kerry Rolph, Ashlie Saffire, Samantha Taylor & Jane Yu Geneviève Alidarso, Netherlands Fiona Anderson, VIC Michael Auld, QLD Christina Ball, United States Annie Baltz, Ireland Jorge Baron, VIC Martina Boberova, Slovakia Ken Brunson, United States Magdalena Budzinska, United Kingdom Jasmine Champagne, United States Jirassa Champaiboon, Thailand Thea Chan, NSW Fu Ming Chan, NSW Charlotte Chen, United States Siuyi Chia, WA Victoria Cole, VIC Simone Cooper, NSW Matthew Cox, NSW Lalida Damrongchonlatee, Thailand Patricia de Mello Pimentel, VIC Mariana do Nascimento, United Kingdom Nattamon Ekkanan, Thailand

—Thoracic

Tutor: Belinda Hopper Ali Ashrafi, ACT Dylan Barber, VIC Tom Bowden, VIC Mitchell Edwards, NSW Ross Evans, QLD Erin Gagliano, QLD Kathy Gillies, VIC Elly Jackson, VIC Chi Yan Kan, QLD Prabkirat Kaur, Singapore Rebecca Kelly, TAS Xiaotong Liang, QLD

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Rockey Fong, Singapore Styfany Foo, WA Anna Giles, New Zealand Shawn Han, Taiwan Laura Hartman, Canada Emma Hoolihan, SA Olivia Hsieh, Taiwan Donglei Huang, VIC Tiffany Jacobs, WA Suzanne Jenkin, New Zealand Yvette Jevons, QLD Noppadol Kanjananupradit, Thailand Marloes Keijzer, Netherlands Alyson Keir, United States Juthamas Khodthong, Thailand Denyse Khor, Singapore Eloise Koelmeyer, NSW Tula Laongam, Thailand Fiona Le Surf, NSW Tina Lee, TAS Hailey MacDonald, Canada Jennifer Magee, United States Samantha Millette, United Kingdom Anna Minoli, United Kingdom Spiridon Mkheiber, United Kingdom Evangelia Moutevelidi, United Kingdom Karina Mužilová, Czech Republic Pamela Newman, United Kingdom Victoria Poore, United Kingdom Maja Puc, Slovenia Ivanna Juliana Raminhos, Portugal Suzana Ruscanu, France Kasamyra Sainsbury, VIC Manassanant Sangpithak, Thailand Rebecca Sawyer, United States Jessica Shelley, QLD Olga Sjatkovskaja, Estonia Petra Smit, Netherlands Catharina Stopik, Germany Malin Sundh, Sweden Pawish Suranunt, Thailand Tereza Tahboub, Israel Polina Tan, NSW Amelia Tennent, NSW ELIZABETH THOMAS, New Zealand Gabriele Valyte, Lithuania Kevin Verhoeven, QLD Jane Vine, NSW Ashley Wagner, United States Lois Wakelin, United Kingdom Pakteema Wanithanont, Thailand Stacey Woodland, QLD Wai Fong Yim, Hong Kong Valeria Zamora, Chile

Internal Medicine: A Problem Solving Approach Tutors: Jill Maddison, Sue Bennett & Susan Carr Linda Bradbury, VIC Julie Brown, QLD Candibyani Candibyani, Singapore Yun Han Chen, QLD Sharline Cheng, VIC Sum Yau Cheung, Hong Kong Michelle Chin, VIC Anitha Chumkam, Thailand

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Emma Macintosh, NSW Cassandra MacPherson, NSW Pooja Mishra, ACT Bess Morgan, TAS Katherine Morgan, QLD Elizabeth Parsons, NSW Philip Perring, VIC Natasha Pesce, NSW Louisa Poutsma, NSW Melissa Psaila, NSW Jamie Russell, QLD Jacinta Schembri, TAS Felicia Tam, NSW Yanling Tan, Singapore Tanat Tatchanachai, Thailand Elanore Waldon, NSW Christiana Willenborg, NSW Chun Fung Wong, NSW Mayumi Yoshino, QLD

Raymond Gates, NSW Jane Gibbs, VIC Brooke Gordon, VIC Tal-Petra Guse, WA Jennifer Hall, QLD Hester Huang, SA Jessie Lonergan, NSW Iris Ma, Hong Kong Cassandra MacPherson, NSW Pooja Mishra, ACT Khin Swe Mon, Myanmar Nandini Mudeliar, United States Champika Nissanka, QLD Michelle Pepper, VIC Louisa Poutsma, NSW Jack Robinson, TAS Yustina Roman, NSW Run Sakulsirajit, Thailand Philippa Simms, WA Sharrbitra Sivakumar, Malaysia Tamara Stegeman, QLD Aislinn Stokes, NSW Yanling Tan, Singapore Amy Underwood, NSW Christiana Willenborg, NSW Chun Fung Wong, NSW Reiko Yamazaki Lai, NSW

Internal Medicine: Keys to Understanding Tutors: Darren Merrett, Steve Holloway & Jen Brown Sarah Carter, VIC Vivian Chan, VIC Cheryl Chan, NSW Korarit Chanritisen, Thailand Emma Cook, NSW Samantha Coomes, QLD Jodie Donovan, NSW Aninca Jordaan, WA WARANYA KITSASON, Thailand Pak Chun Kwong, VIC James Le, NSW Tahlia Ling, TAS Vanessa Low, United Kingdom Katherine Macmillan, VIC Catherine McDonough, VIC Felicity Miller, VIC Karlien Penning, VIC Srisuda Promdan, Thailand Rebecca Ryan, VIC Udita Saxena, NSW Rachel Simidgi, WA Wendy Smith, QLD Sirada Tayayouth, Thailand Bronte Turner, SA Nicole Whitehouse, NSW

Clinical Neurology Tutors: Laurent Garosi & Simon Platt Agnieszka Adamiec-Dygus, United Kingdom Lynda Bonning, VIC Sabine Broekaart, Netherlands Alicja Czerwiec, Poland Elizabeth Duhs, NSW Supattra Janchome, Thailand Wan-Ju Jao, SA Patimaporn Kalerum, Thailand Nuntapob Lertchaiprasert, Thailand Salisa Lertsrimongkol, Thailand

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Suzie Mauger, SA Marlene Møller-Nissen, Denmark Zoe Munro, NSW Vitthanan Natepoo, Thailand Pakkakorn Panyathip, Thailand Akkarawoot Sararat, Thailand Vickie Saye, ACT Jutamat Thamkitja, Thailand Julie Waring, NSW Theresa Yenen, Netherlands

Ophthalmology Tutors: Robin Stanley Harry Bartram, VIC Susan Bilbow, WA Peter Brunsdon, NSW Kei Suet Chan, Hong Kong Jessica Grice, VIC Shona Hay, QLD Kanokpich Imcharoon, Thailand Bruce Krumm, NSW Luana Nieman, VIC Keri Rheinberger, QLD Farzin Sahebjam, TAS Ana Santiago, VIC Pitchaya Sattayaveewattanakul, Thailand Bethany Staples, NSW Lai Man Ting, Hong Kong

Surgery Tutors: Chris Tan, Mark Newman, Bronwyn Fullagar & Wendy Archipow Courtney Baker, VIC Loriana Cassarino, VIC Martin Cossey, WA Ed Dakin, New Zealand Cerdy Deloso, Philippines Duncan Durie, VIC Kathryn Elliott, QLD Michael Franklin, VIC Amy Hewitt, VIC Tuovi Joona, QLD Kylene Kelbe, VIC Amy Lee, NSW Shi Min Lee, QLD Sheryl Lim, VIC Paul McCosker, QLD Chloe McDonald, VIC Justin Mergl, Canada Hannah Mitchell, NSW Samuel Morgan, TAS Laeticia Oon, VIC Fei Wern Pang, VIC Aaron Park, NSW Bryce Philpott, NSW Victor Poon, Hong Kong Bethany Richards, NSW David Riordan, NSW Nyssa Ross, NSW Vivian Samuel, NSW Courtney Streeter, ACT Maithreyi Sundaresan, NSW Emily Suthern, ACT Aun Shun Tan, Malaysia Joshua Tannen, VIC Jean Teoh, Malaysia Steve Tran, VIC

Control & Therapy Series – Issue 313 December 2023

Chantelle van der Lingen, QLD Yvonne Vesty, VIC Panyawat Wachirapongpakorn, Thailand Jordan Wainwright, SA Wister Wang, NSW Clara Wilkins, ACT Rou Feng Yau, VIC

And to DE participants who passed the 2023 ANZCVS exams Small Animal Medicine Sarah Nicholls See Mun Tsang

Small Animal Surgery John Barrett Matthew Coombs Joyce Hung Danae Noitakis Si Chia Teoh Viola Wynne-Hoelscher

Veterinary Behaviour Daphne Ee Lian Ang Liam Brown Si Ying Erika Chan Elizabeth Davis Chantelle McGowan Bronwyn Sharman

Veterinary Emergency and Critical Care Suzanna Mauger Yanzhi Zhang

Veterinary Radiology (SA) Charlotte Gibson Amy Graham Pascal Urlings

Early Bird Lucky Draw Congratulations to winner Dr Emily Gray from Perth Vet Emergency who won $1,000 off her course enrolment fee.

2024 Distance Education enrolments still open! cve.edu.au/distance-education

Contents

Rianna Dinon, SA Olivia Fong, Hong Kong Amy Freestone, QLD Kaela Hall, NSW Lydia Herbert, NSW Leah King, WA Huirin Lee, VIC Amber Leonard, QLD Alvin Liu, ACT Kate Luk, VIC Zachary Lynch, NSW Kelly McKenzie, New Zealand Briar Morton, ACT Mari Roberts, WA Emma Shepherd, SA Cyrus So, NSW Belinda Stone, SA Julia Thompson, VIC Lilliana Thornton, NSW JueJun Wang, VIC Christophorus Widjanarko, Indonesia Natalie Wood, ACT Laura Zane-Todd, VIC

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