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Queensland News

ADVANCINGVETERINARY SCIENCE

Australian Veterinary AssociationAugust 2009

Australian Veterinary AssociationAugust 2009

INSIDE THIS ISSUE:INSIDE THIS ISSUE:• Editor ’s Note

• Dogs and Cats in the Smart State

• Answers to some Frequently Asked Questions

• Survey of Wild Birds on Free Range Chicken Farms

• The Coughing Dog: Is it respiratory or cardiac disease? - Helpful diagnostic hints

• Common Household & Garden Plants & Fungi Poisonous to Pets in Queensland

• A Practical Guide To The Use Of Today’s Technology In Cardiac Patients

• AVA Members HR Advisory Service

• SHORT BITS…

AVA Queensland News - August 2009

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President’s Word

Congratulations and many thanks to the members of the Executive for their time and energy taken to implement and conduct the authorised implanting courses around the State.

It is also timely to remind members of the importance of reading material sent by the Government. The profession is taking on a serious responsibility and a leading role in correct animal identification and management for a civil benefit.

It has been somewhat mystifying that some members could not see past the placement of the transponders when the purpose is to gain an understanding of the Animal Management (Cats and Dogs) Act 2008. Proof of understanding the Act is part of the legislation’s requirements.

Our profession is well positioned to provide both the microchipping service and the education of cat and dog owners on the benefits and legal responsibilities for better pet management.

While referring to Government, there has been positive feed back from the Infectious Disease Control (IDC) Seminars. There is financial support from the State Government via the Department of Primary Industries and Fisheries and Queensland Health, including presentations by their staff which are duly appreciated.

It is important that veterinarians lead the way for continued revision of IDC because zoonotic diseases are on the rise and affecting global health.

Recently, the Queensland Division conducted a mail-out to lapsed members and we have been informed that the response was very encouraging, so a very warm thank you to those involved and welcome back.

The AVA president Dr Mark Lawrie and the National CEO Graham Catt are presently on a fact finding mission to the American Veterinary Medical Association and calling on the New Zealand Veterinary Association on the way home. We look forward to hearing about this trip at the forthcoming strategic planning weekend in Townsville. The Executive hopes to hear of ways to bring more benefits to our members.

On behalf of the Queensland Division, I would remind every one that at the Queensland office we appreciate beneficial input from colleagues – so, whether you are in government, industry, academia, the suburbs or the paddock, please keep those e-mails coming.

All the best for now.

Dr Bruce Pott

Editor’s NoteIn this issue, we are fortunate to have papers from Drs Brad Gavaghan on diagnosing the coughing dog and the situation on technology in cardiology, Ross McKenzie on poisoning of pets by common garden plants (and big hairy spiders), and from Bruce Remington on the surprising scarity of wild birds surveyed by the booming free range meat chicken industry.

Dr Gavaghan’s papers are sourced from the annual conference of the Division held at Yeppoon 20-22 March 2009. Those interested may obtain a copy

of the proceedings from the Divisional office. Drs McKenzie and Remington’s papers were given at meetings of the South East Queensland Branch.

The papers are reproduced in the News as a service to those members who were unable to attend the meetings and to give an idea of activities happening within the Division. If other Branches or Special Interest Groups would like articles published in the News you are cordially invited (exhorted) to send them in, whether they are technically or socially oriented. I am aware that many groups run their own newsletter. The News is an opportunity to extend information to the general membership.

Dr Bruce Pott - President


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Dogs and Cats in the Smart StateAnimal Management (Dogs and Cats) Act 2008

The following situation report is extracted from an email to Ms Amanda Pollard, PetPEP from Vanessa Young, Communication Officer, Communications and Marketing Branch, Department of Infrastructure and Planning.

On 1 July 2009 the Animal Management (Cats and Dogs) Act 2008 came into effect, and the Department of Infrastructure and Planning is working to educate the community and animal management professionals about the new laws and responsible pet ownership practices. To date the following initiatives have been implemented:

• a telephone hotline is operational on 1800 467 561, and staff are able to answer questions relating to the new legislation. Specific local government related questions, such as fees and amnesty periods are referred to the relevant local government contact.

• a dedicated website section is operational at www.dip.qld.gov.au/catsanddogs and explains the legislation and new requirements for pet owners, local governments and industry. It also has information about the Cat smart campaign, including its aims, an audio grab of the radio campaign, related media releases and electronic versions of the Cat smart poster and stickers.

• newspaper advertising of the new legislation is scheduled for late July to September, focusing on South East Queensland, where cat registration and microchipping provisions have first been introduced.

• ministerial media releases have been issued, and more are scheduled, to highlight significant events and milestones in relation to the implementation of the new legislation.

Coming up shortly will be a direct mail-out of information regarding the new legislation, and what it means for animal related businesses, animal welfare agencies, local governments and pet owners. Included in that mail-out will be some printed collateral to help spread the message of responsible pet ownership to the Queensland community.

This is in addition to the Cat smart poster and stickers, which will be distributed from the Department’s display at the Queensland Government pavilion during this year’s Brisbane Ekka.

The Department will supply Cat smart posters and stickers to AVA Queensland office.

Answers to some Frequently Asked Questions

Courtesy Mr Steve McMaster, Executive Officer, AVA Queensland Division.• Can a Pet Shop or Breeder sell a cat or dog before it is 8 weeks old? Yes, they can and consequently avoid

the need for microchipping the animal provided there are no local government regulations that specify the minimum age requirement for selling a cat or dog. The new owner should be notified of the requirement to microchip before the cat or dog reaches 12 weeks of age although this is not a requirement).

• Can an owner be forced to consent to their cat or dog having a microchip implanted? No, the role of the authorised implanter is not to enforce the legislation, they must obtain consent from the owner to implant a microchip. They can however advise the owner of the legal implications of non-compliance and if the owner still does not wish to proceed, it should be documented and signed by the owner.

• Can more than one microchip be implanted? Yes, under certain circumstances (e.g. export to country where a chip is non-compliant or if an existing chip is not functioning). It is however not permitted to remove an existing microchip.

• If a Pet Shop or Breeder has a cat or dog microchipped, do their details have to be recorded as the owner or can that part be left blank until the animal is sold? This is not permitted. The Pet Shop or Breeder must be listed as the owner and when they subsequently sell the animal, the new owner’s details will need to be submitted by the Pet Shop or Breeder.

• Are only cats or dogs that are sold requiring microchipping? No, all kittens and puppies and cats and dogs that change owners after July 1 (even if given away) must be microchipped and the appropriate details submitted.


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Continued from pg. 2

• If you have any additional questions or concerns, please let us know so we can find the answers and disseminate them to everyone.

Survey of Wild Birds on Free Range Chicken Farms Dr Bruce Remington [email protected]

This survey involves Free Range Meat Chicken Farms (not Egg Producing Farms) which all grow chickens for the larger producers. These producers are both National and State based. The farms operate under a number of different rules i.e. National and State government, the company that they grow for, and the Free Range certifying organization (Free Range Egg and Poultry Australia Inc. or FREPA).

The Free Range Chicken Meat industry has expanded rapidly over the past eight years, from a low base to over 32 million birds processed per year (compared to 14 million commercial egg layers and 2.7 million Free Range egg layers). This expansion has been driven by consumer demand and the economies in production offered by the larger poultry producers.

The impression that many have is that “there are large populations of Wild Birds Inhabiting Free Range Farms”. This may be due to reports from the northern hemisphere. However, the observation of Australian Free Range Farmers is that the number of wild birds landing on ranges is minimal. It was therefore decided by FREPA to try to quantify the “few wild birds” observation. The method was resolved to be a survey of FREPA members’ farms. At the time of the survey – 2004/2005 extending into 2006 – all FREPA chicken meat farms were in Southern Victoria and South East Queensland. Also all the 24 eligible farms were contracted to one of two major national chicken processors.

The survey needed to be conducted over twelve months to establish changes in season. It was also decided that the data of significance were the species or type of wild bird; the frequency of each species; and the numbers of wild birds sighted. The observations were to be made across a spectrum of bird watching skills. To aid in species recognition a survey form was produced which had a picture outline of the species along with the names of local types. Frequency of sightings of a particular species was reported as either daily, weekly, more than once a month, once in the month of recording. Numbers were also recorded at the same time in the categories of one, less than five, less than ten, more than ten.

Free Range Meat Chickens on the Range

Results1. Eight farms responded to the survey. Many of the non participants gave their reason as “not enough wild

birds to be worthwhile”.2. Numbers of birds seen were small, with an average of 32 reports/year.3. Variability between farms.4. Types of birds seen most often were:-

Flycatchers (Willie Wagtails) Swallows (although strictly speaking the survey was supposed to be of birds landing on the ranges, not flying over them) Magpies Mynahs Pigeons.

5. Frequency of Sightings:- Daily = 21% (mainly due to resident Magpies) Weekly = 18% <Weekly> Monthly = 13% Once a month = 48%.


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6. Sighting numbers in the month:- Less than 5 = 85% Less than 10 = 12% More than 10 = 3% (mainly Mynahs).

7. Problem species:- Pigeons: Two farms with fewer than 5 birds for one and two months Ibis: One farm with fewer than 5 for two weeks Parrots: One farm with fewer than 10 for less than a month (we speculate that there was a tree in fruit/flower).

Discussion

Of great interest are the reasons why only low numbers were observed. The following are some suggestions:

1. Different environment to the northern hemisphere, which is usually reported. Australia has a number of different habitats, most of which are different to those seen in the northern hemisphere. Also the type and numbers of migrating birds are different in Australia.

2. Broilers not layers. Maybe the information previously reported was on layer farms. Layer farms operate on a continuous production basis while the broiler farms surveyed operated on a batch basis where chickens are not on the range for significant periods.

3. No feed or water is allowed on the ranges of FREPA certified farms. This is probably the most important reason. If wild birds have no reason to be on the range, then they are not attracted. Feed is only provided in the connecting housing. Also no water, either drinking or as ponds, is allowed on the ranges.

4. The grass is always kept short for vermin control. Therefore there are no seeds or cover for wild birds. Studies at airports have found that birds are discouraged by short grass. Also the amount of mowing activity may disrupt the wild birds’ environment.

5. All ranges are fenced to protect the chickens from predators. This may deter some wild birds.

6. All of these commercial farms have almost constant human activity during daylight hours. The presence of people working in and around the facility may have a deterrent effect.

Conclusions

1. The situation in Australia with regard to wild birds is different to overseas reports.

2. Further work may be of benefit to find better ways to reduce wild bird intrusions. An example might be use of trees/bushes that do not attract wild birds but grow in specific environments.


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The Coughing Dog: Is it respiratory or cardiac disease? - Helpful diagnostic hints Dr Brad Gavaghan BVSc MACVSc FACVSc,Specialist Veterinary Cardiologist, Veterinary Cardiology Imaging79 Laidlaw St, Dayboro [email protected]

Many mitral valve disease patients are presented because of coughing. Geriatric, small breed dogs often have concomitant respiratory disease. Failure to alleviate the cough is a common cause of client dissatisfac-tion and frustration for the clinician .

Cough + loud mitral murmur = ??? If the cough is chronic more than one disease process may be present and it is important to identify all causes.

Possibilities include: • severe mitral regurgitation and secondary pulmonary oedema;

• severe mitral regurgitation, secondary pulmonary oedema and respiratory disease;

• compensated mitral regurgitation (e.g. no oedema) and left bronchus compression;

• compensated mitral regurgitation and unrelated respiratory disease, e.g. chronic small airway disease, tracheal collapse, pneumonia,

heartworm disease.

Helpful hints/how to avoid disasters when presented with a coughing, 10 year old poodle with a loud mitral murmur (a case study will be used to highlight the points discussed below )

In general: Patient history/clinical findings:• dogs with a chronic, frequent cough (e.g. > 3-4 months), not on diuretics, are unlikely (and of course there are exceptions!) to have

pulmonary oedema/heart failure as the cause of the long-term cough. That is, untreated pulmonary oedema does not typically wax and wane over a long period without progression to life-threatening decompensation.

• bright, alert, patients with a good appetite and exercise tolerance are more likely to have chronic airway disease than pulmonary oedema.

• an increased resting respiratory rate at rest or delayed recovery post-exercise is more common (again, there are exceptions!) in parenchymal lung disease (e.g. pulmonary oedema) than chronic airway disease.

• character of the cough, timing of the cough (e.g. nocturnal, post-exercise/excitement etc) can be poor indicators of cause, given the possibility of more than one cause of the cough being present.

Physical examination:• ability to elicit a cough by tracheal palpation does not exclude concomitant pulmonary oedema.

• murmurs less than grade IV/VI are less likely to indicate severe mitral regurgitation in non-obese, small or medium-sized patients.

• tachycardia (+/- arrhythmias) is more common in dogs with advanced cardiac disease versus respiratory disease patients.

• a strong femoral pulse, pink mucous membranes and a normal capillary refill time does not exclude advanced cardiac disease.

• a third of severe pulmonary oedema cases in humans have no crackles.

TIP: I see a reasonable number of respiratory disease patients with prominent inspiratory crackles without pulmonary oedema from their cardiac disease e.g`. must assess with thoracic radiographs.

Diagnostic tests:• radiography is the most sensitive indicator of the presence of pulmonary oedema versus other respiratory disease.

• thoracic radiographs are required before and after furosemide therapy if a diagnostic furosemide trial is undertaken (see below).

• NB: cardiac size may be normal in recent cases of chordal rupture with pulmonary oedema (ie insufficient time for the heart to eccentrically hypertrophy in response to the valvular disease) : require echo to assess for chordae rupture.

Trial therapy/response to therapy:


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• Reduction in cough frequency in response to furosemide therapy. False positive and false negative results are a concern.

• False (+) Anecdotal reports of temporary reduction in cough in chronic respiratory disease dogs in response to furosemide (dehydration = decreased secretion mobility = temporary decrease in cough??).

• False (-) Alternatively, cough may persist despite ‘successful’ resolution of pulmonary oedema due to concomitant respiratory disease.

TIP: Trial therapy with furosemide (e.g. 2 mg/kg bid or tid for 3-4 days) to assess for resolution of radiographic evidence of pulmonary oedema – this is an excellent diagnostic tool. If poor response, further cytological assessment (e.g. Broncho Alveolar Lavage, tracheal wash or fine-needle aspirate) is required.

Avoid trial responses to other cardiac meds for diagnosis (e.g. Angiotensin Converting Enzyme-I, pimobendan) as the effects are not able to be objectively measured (versus radiographs for diuretic trials). If cardiac disease is diagnosed based on the improvement in thoracic radiographs, then these other drugs can be added at that time.

Reduction in cough frequency in response to cough suppressants: • Successful cough suppression does not exclude the presence of concomitant pulmonary oedema.

• Cough suppression is warranted when the pulmonary oedema has resolved and frequent coughing of respiratory origin persists e.g. use of centrally-acting suppressants such as Actacode (codeine phosphate linctus 25 mg/5 mls) at 0.5-1.0 ml per 10 kg sid to tid as required or preferably treatment of the primary cause e.g. often cortisone and/or bronchodilators are administered via pediatric metered-dose inhaler spacer systems or nebulisers: examples include budesonide at 1 ml of 500 mcg/2 ml vial via saline nebulisation ( e.g. for 10-30 kg dogs), 5-10 mins sid to bid, or fluticasone via a metered-dose inhaler is often successful therapy. Where feasible, this therapy should be guided by bronchoalveolar lavage results and other respiratory disease diagnostic tests.



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Common Household & Garden Plants & Fungi Poisonous to Pets in Queensland Dr Ross A. McKenzie PSM DVScSpecialist in Veterinary [email protected]

Background

Queensland Health was concerned about the labeling of potentially harmful plants sold in nurseries. A broad-based committee was formed to assess the issue – with a particular focus on child health. Among other things, veterinary practices were surveyed to answer the question “How much plant poisoning actually happens in Queensland pet animals?”

Outcome: Self-regulation by Australian nursery industry; labeling guidelines issued to members. Available at http://www.ngia.com.au/

Acknowledgements

Advice on selecting surveyed practices: Aaron Palmer, Judy Seton.

Data from responding practices: Jocelyn Birch Baker, Mary Calder, Shannon Coyne, Adrienne Easton, Peter Gardiner, Tom Gradwell, Carmel Griffen, Amy Hehir, Tracy Holland, Melanie Irvine, Isobel Johnstone, Terri King, Terry King, Graham Lauridsen, Peter Lyons, Lisa Mason, Greg Muir, Dick Murray, Peter Noble, Rowan Pert, Paul Sheedy, Caroline Spelta, Angela Steenholdt, Philip Thomas, Mary Thompson, Rob van Drimmelen, Kurt Verkest, Laurie Wanstall.

Pet animal background data

Pet population, Queensland (calculated from ABS 1995, 2001 data)

Dogs = 0.5 millionCats = 0.4 millionPet birds = 0.2 million

Human population calculated as 4 million.

Pet Plant Poisonings

Fifty-three major veterinary practices were contacted in major cities/towns in Queensland in 2007 for plant poisoning of pets in the five years 2002-2006. Of these 25 (47%) responded.

Patient visits data: dogs: 500,000 = 100,000/yr, cats: 175,000 = 35,000/yr, birds: 24,000 = 5,000/yr.

Pet plant poisonings diagnosed: Dogs: 289 cases = 58/yr = 0.06% of patient visits. Birds: 7 cases = 1/yr = 0.03% of patient visits. Cats: 19 cases = 4/yr = 0.01% of patient visits.

Plant Poisonings Of DogsLife-threatening poisonings (descending order of occurrence):Brunfelsia spp. (francisia, yesterday-today-and-tomorrow) fruits [36 cases]Onions (Allium cepa) [34]Cycad seeds (Cycas revoluta) [28]Duranta erecta (golden dewdrop, cv. Sheena’s Gold, cv. Geisha Girl, cv. Alba) [12]Cardiac glycoside-containers (oleanders etc.) [8] Grapes/raisins (Vitis vinifera) [3 cases]Lilium spp. (lilies) [3]Cyanobacteria [2]Tobacco (Nicotiana tabaccum) [2]Stinkhorn fungi (Order Phallales) [2]Avocado (Persea americana) [1]Rhododendron [1]Melia azedarach (white cedar) fruit [1]


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Plant Poisonings Of CatsLife-threatening poisonings (descending order of occurrence):Lilium spp. (lilies) [13 cases]Brunfelsia spp. fruits [2]Cycad seeds [1]+ Duranta erecta [1 – Scanlan et al. 2006]

Minor poisonings:Aroids [2]Cannabis sativa [1]

Plant Poisonings Of BirdsLife-threatening poisonings (descending order of occurrence):Avocado (Persea americana) [6]Oleander (Nerium oleander) [1]+ Duranta erecta [3 – Scanlan et al. 2006]

Minor poisonings (very small or no threat to life, descending order of occurrence:Macadamia kernels [83 cases]Cannabis sativa (marijuana) [62]Aroids (Dieffenbachia, Zantedeschia, etc.) [5]Other plants [4]



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Summary by Major Poisonous Plants and Toxins, Life-Threatening Poisonings:

Brunfelsia spp. PoisoningBrunfelsia spp. (about 40 species; South American origin; Family Solanaceae).Known toxic species Brunfelsia australis (francisia, yesterday-today-and-tomorrow) in Australia, Brunfelsia pauciflora in North America & Australia, Brunfelsia latifolia in Australia.Conditions of poisoning: Fruits are toxic. Dogs attracted to ripe fruit will eat large amounts (April-June), fatal cases have had 40-100 fruits in stomach.Clinical signs: vomiting, diarrhoea, urination, ataxia, muscle tremor, convulsions (extensor rigidity, opisthotonus). Signs may also include excitement, nystagmus, stomatitis, haematuria.Pathological signs: gastroenteritis, fruits in faeces/stomach.

Organosulphur compoundsAllium cepa (onion) toxic doses reported for dogs: 600-800 g raw onion (single dose) = 3-5 large onions (each large bulb weighs about 170-200 g); or 15 + g raw onion/kg (400 + g for a 25 kg dog = 2 large onions) daily for 2-3 days causes anaemia of sudden onset; or 11 g raw onion/kg (275 g for a 25 kg dog = about 1.5 large onions) daily for several days causes anaemia of gradual onset. Cooking does not destroy toxicity.

Allium cepa (onion) toxic doses reported for cats: 28 g raw onion/kg (112 g for a 4 kg cat = about 1 medium-sized onion) once daily for 3 days.

Allium sativa (garlic) toxic doses reported for dogs: diet containing 7% raw garlic toxic to dogs; fed for 50 days; time to onset of anaemia not stated.

Sources: kitchen and barbecue scraps; human meal residues; Chinese cuisine, pizza; baby food (onion powder).

Syndrome: Heinz body haemolytic anaemia, haemoglobinuria.

Cycad Seed PoisoningToxicant: Methylazoxymethanol (MAM), a glycone of cycad glycosides cycasin and macrozamin.Sources: any coning female cycad (dioecious taxa). Syndrome: Liver and alimentary necrosis.

Duranta erecta Poisoning (Garden Or Hedge Shrubs)Dogs, cats, birds, cattle, kangaroos, humans.Fruits, leaves.Toxin unknown: large amounts required for toxicity.

Dogs - clinical signs: depression (drowsiness, drooped eyelids), gum pallor; excessive salivation, bradycardia, melenic diarrhoea + plant fragments, tetanic convulsions from external stimuli, ± coma & death.

Dogs - clinical pathology (2 dogs): no liver or kidney dysfunction.Dogs - necropsy (1 pup): plant material (fruits, leaves) in gastro-intestinal tract, stomach haemorrhage.

Cardiac Glycoside PoisoningNerium oleander toxic dose: Dog: fresh leaf fatal at 50-220 mg/kg; cat: fresh leaf fatal at 40-50 mg/kg (1 fresh leaf = 1.5 g); 20 kg dog fatal dose = 1-3 leaves, 4 kg cat fatal dose = << 1 leaf.

Syndrome: sudden death, vomiting, diarrhoea ± blood, cardiac arrhythmias, pre-renal azotaemia.

Grape poisoningSmallest reported toxic doses for a 20 kg dog = 40 g grapes, 60 g raisins, or 120 g sultanas.Toxicant unknown.Syndrome: nephrosis.


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Clinical signs continue for several days to 3 weeks after ingestion, vomiting within hours of ingestion in all cases: vomitus contained partly-digested grape/raisin, anorexia (60% of cases), diarrhoea (50%), oliguria or anuria with or without isosthenuria (50%), lethargy (40%), signs of abdominal pain (30%), ± ‘uraemic’ odour of exhalations.

Lilium (lily) & Hemerocallis (day lily) poisoningToxicant unknown, possibly 3-methoxy-2(5H)-furanone. Sources: all parts of the plants (including flowers); gardens, potted plants, cut flowers.Toxic dose: Cat: < 1 leaf.Syndrome: nephrosis.Clinical signs: vomiting and hypersalivation, onset 0-3 hours after ingestion and may persist 4-12 hours, anorexia and depression continue and intensify 24-72 hrs after ingestion, ± polyuria; evident 12-30 hours after ingestion, ± anuria in untreated cats 24-48 hours after ingestion.Untreated cases die within 5 days.Tremors and seizures were reported in 8 (36%) of 22 cats ingesting Hemerocallis spp.

Cyanobacterial toxinsMany algal blooms are non-toxic to animals, but all should be considered potentially toxic. Gene probes are being developed to differentiate toxic from non-toxic Microcystis. Cyanobacterial Peptide PoisoningSources: Microcystis aeruginosa and others.Syndrome: acute liver necrosis.

Cyanobacterial Alkaloid NeurotoxinsToxicants (Australian cyanobacteria): paralytic shellfish toxins = sodium channel blockers. Anatoxin-a and homoanatoxin-a are post-synaptic depolarising neuromuscular blocking agents which mimic acetylcholine; act at both nicotinic and muscarinic receptors. Toxicity causes paralysis of skeletal muscle and paralysis of breathing.Sources: Anabaena spp. and others.Syndrome: sudden death ± dyspnoea.

Stinkhorn fungus poisoningSyndrome is variable – range of signs have included: vomiting and diarrhoea (± blood), ± miosis (pin-point pupils), ± clotting defects (transient), ± liver damage (increased AST), collapse, respiratory and circulatory depression, cyanosis.

Death cap fungus poisoningToxicants: amatoxins (bicyclic octapeptides).Sources (Australia): Amanita phalloides under oak trees, some other Amanita species, Galerina, Lepiota.Syndrome: acute liver necrosis.

Avocado poisoningToxicant: persin.Sources: All avocado parts except seeds; all cultivars in Australia.Toxic doses: Budgerigar ripe fruit lethal dose 50-100 g/kg (Hass & Fuerte) or 3-6g/bird (60g adult). Canary ripe fruit lethal dose 100 g/kg (Hass); 2.5g/bird (25g adult). Syndrome: cage birds - sudden death; dogs – cardiac dysfunction (large repeated doses only).

Azalea poisoningToxicant: andromedotoxin (grayanotoxin).Sources: Rhododendron species, other plants in Family Ericaceae.Toxic dose: lethal dose of leaves is as little as 0.2% body weight.


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Syndrome: emesis, cardiac dysfunction.Clinical signs: drooling saliva, vomiting, retching, diarrhoea, tenesmus, abdominal pain, cardiovascular effects (bradycardia, hypotension through vasodilation, atrioventricular block), ± sudden death, ± dyspnoea, ± paresis/semi-paralysis.

Meliatoxin (white cedar fruit) poisoningSyndrome: dog (1 Australian case): lethargy, mild ataxia, increasing muscle weakness, recumbency, jaw paresis (mouth open, tongue protruding, difficulty lapping fluids), recovered slowly over 48 hours. Syndrome: dogs (North America): vomiting, hypersalivation, abdominal pain, diarrhoea, bradycardia, seizures.

Ricin poisoningSource: Ricinus communis (castor oil plant) seeds.Toxic dose: dog ricin oral lethal dose = 1 ± g/kg. One R. communis seed = 0.25 g and contains about 0.25 mg ricin, therefore 1 seed is potentially lethal.Syndrome: severe enteritis ± dysentery.

Summary of Major Poisonous Plants which Pose Very Small or No Threat to Life:

Cannabis PoisoningToxicant: Tetrahydrocannabinol.Toxic dose: dog: lowest toxic dose = 84.7 mg/kg. Death from Cannabis is not expected (dog oral lethal dose > 3g/kg).Syndrome: central nervous system depression.Clinical signs: onset usually within 1-3 hr; duration 30 min to 36-48 hr with a maximum of 96 hr; first 6-8 hours most intense for dogs, depression (somnolence) (60% of cases), ataxia / incoordination and sudden falling (58%), rapid arousal to normal from somnolence common, anxiety manifest as being “head shy” is common, ± behavioural disorders.

Macadamia kernel poisoning - raw or roasted kernelsToxin: unknown.Toxic dose (Australian clinical cases): 0.7 – 4.9 g/kg (mean 3.0 g/kg), 5-40 kernels for a 20 kg dog. US experimental reproduction of toxic signs with 20 g/kg.Clinical signs: posterior paresis, ataxia, muscle tremor (weakness), depression, recumbency, ± joint pain and swelling, vomiting, hyperthermia.Spontaneous recovery in 12-24 hours.

Aroid poisoning‘Toxicant’: calcium oxalate raphide (needle-shaped) crystals.Syndrome: buccal irritation, transient.

Addendum:Theraphosid spider venomSources: barking, whistling, bird-eating spiders or “tarantulas”.Animals affected: dogs.Mode of action: neurotoxic.Poisoning circumstances: undescribed for dogs.Main effects: flaccid paralysis; death within hours in all dogs known to have been bitten. Pathology, diagnosis, therapy: undescribed.Prevention: prevent access if possible.


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A Practical Guide To The Use Of Today’s Technology In Cardiac Patients Dr Brad Gavaghan BVSc MACVSc FACVSc (cardio) Veterinary Specialist Services Cnr Logan and Lexington Roads, Underwood, Brisbane Q [email protected]

The following discussion will cover those topics below:

1. SpO2 - Pulse oximetry2. Blood pressure assessment - Doppler3. Central venous pressure assessment4. End-tidal gas analysis - capnography5. Urine output6. Electrocardiography

1. How to record an ECG 2. Systematic ECG assessment techniques 3. The normal ECG 4. Recognition of some common arrhythmias.

1. SpO2 - Pulse Oximetry

The pulse oximeter measures the percentage saturation of haemoglobin with oxygen. It works by emitting two wavelengths of light and measuring the amount of light that is reflected. The probe is usually placed on unpigmented mucosa (eg lip), or, in anaesthetized patients, it is placed on the tongue.

Valuable information is given about both cardiac and respiratory function. If the patient’s ventilation is compromised enough (e.g. pulmonary oedema), or if the percentage of inspired oxygen drops (poor oxygen cage set-up), this will be reflected in a drop in SpO2. Equally important however is the fact that if the cardiac output drops and the tissues continue to remove oxygen at a constant rate, the SpO2 will drop.

The pulse oximeter continually displays the SpO2 as well as the pulse rate. The SpO2 should remain > 93%.

2. Blood Pressure Assessment - Doppler

Definitions and pathophysiology In humans, systemic arterial hypertension (SAH) may be defined as either:an increase in systemic arterial blood pressure (BP) above normal rangeor a BP that results in clinical or pathological sequelae.

There is insufficient data in veterinary patients to define a strict ‘cut-off’ BP that accurately separates normal versus abnormal patients, particularly with reference to the likelihood of clinical sequelae, therefore when assessing the clinical relevance of a blood pressure reading, it is important that the clinician takes into account the:• patient’s age, breed, species, body condition• physiological state – agitated versus calm• presence of predisposing systemic disease (e.g. renal disease)• presence of clinical sequelae (e.g. ocular manifestations).

Systolic arterial blood pressure is determined by the combined influences of :• diastolic arterial blood volume (ie fluid intake versus secretion, i.e. via influences of anti-diuretic hormone,

angiotensin II)• amount and rate of flow into that space with each beat (i.e.stroke volume, contractility, preload, afterload

etc)• arteriolar vascular resistance (ie vasodilation vs vasoconstriction)• aortic compliance (influenced by age, disease, autonomic innervation and hormones e.g. angiotensin II).


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Given that diastolic blood pressure is more difficult to measure in our patients, it is fortunate that isolated diastolic hypertension is not thought to be common in veterinary patients.

Aetiology

Systemic Arterial Hypertension may be divided into: • essential (primary) hypertension (common in humans)• secondary hypertension (common in veterinary patients).

The most common causes of SAH are:In dogs: renal disease (↑ BP in 60%); In cats: renal disease (↑ BP in 61-73%) and hyperthyroidism (↑ BP in up to 87%).

Other causes include: hyperadrenocorticism (↑ BP in 60% dogs); diabetes mellitus (↑ BP in 50-70% dogs); pheochromocytoma (episodic ↑ BP in 50% dogs); acromegaly; hypothyroidism (atherosclerosis); hyperaldosteronism; obesity; chronic anaemia; polycythemia; hypergammaglobulinaemia (ie increased viscosity).

Diagnosis

This statement supports the balanced clinical approach to the diagnosis of hypertension, rather than only treating a BP measurement, taken on only one occasion.

What is normal BP?

Dog: By consensus, a systolic BP between 160-165 mmHg and a diastolic BP between 90-95 mmHgare considered to be the upper thresholds for normotension in the dog.The Veterinary Blood Pressure Society (VBPS) proposed a mild elevation (systolic/diastolic mmHg) at > 150/95, moderate elevation > 160/100 and severe elevation at 180/120. Sighthounds tend towards higher normal pressures at approx 145-150 mmHg (systolic).

Cat: Similar to the dog, but perhaps 5 mmHg less. For adequate perfusion of the central organs BP must be above:Direct: systolic >70 mmHg, mean >50 mmHg;Indirect: systolic > 90 mmHg, mean > 70 mmHg.

Moderate hypotension is: Indirect: systolic 80-90 mmHg, mean 60-70 mmHg

Severe hypotension is: Indirect: systolic < 75 mmHg, mean < 60 mmHg

Measurement TechniquesDirectDirect arterial puncture – with measurement via either an aneroid manometer or a pressure transducer.

IndirectDoppler – (e.g. Parks Medical)Oscillometric – (e.g. Dinamap)Plethysmography – (e.g. Finapress).

The clinical diagnosis of hypertension should never be established on the basis of a single blood pressure measurement in the absence of overt clinical disease consistent

with the diagnosis (Cowgill LD, ACVIM 2001)


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This discussion will mostly look at the Doppler technique as this is the most popular ‘in practice’ method of BP measurement.

Doppler

Uses a piezoelectric crystal to send and receive an ultrasound signal that detects blood flow in an artery distal (usually superficial palmar or plantar arterial arch or the coccygeal artery e.g. tail in cats) to an inflatable cuff.

Accurate assessment requires:• good, repeatable operator technique• correct cuff size (cuff width to be 40% of circumference of limb [dog], or 30-40% of circumference [cat])• calm patient.

Averaging of approx 5 measurements is ideal.

Only reliably measures systolic BP (not diastolic BP).

Oscillometric – (e.g. Dinamap)

Measures the magnitude of arterial pulsations produced in an air-filled cuff: these are inaccurate with patients that are moving, have arrhythmias, hypotension or bradycardia.

3. Central venous pressure (CVP) assessment

CVP is a simple way to evaluate right ventricular function.CVP is a measure of the right atrial pressure, which is the chamber of the heart into which venous return from the all of the body (except the lungs) occurs.This is measured via the placement of a long catheter into the entrance of the right atrium, via the jugular vein.CVP is particularly useful for regulating the volume and rate of IV fluids that are administered to a patient. If the CVP is low despite fluid therapy, the rate of fluid therapy can be increased, provided there is no left heart failure. If the CVP is elevated, fluid therapy can be discontinued and possibly re-commenced at a slower rate when the CVP is at an acceptable range.

Procedure: extension tubing is attached to the CVP/jugular catheter, then a water manometer is attached to the extension tubing via a 3 way stopcock. An administration drip set and bag of fluids is attached to the other port of the three way tap. The manometer can be attached to the cage with the zero marking at the left of the right atrium (i.e. at approximately the point of the shoulder in sternal recumbency, or mid-sternum in lateral recumbency).

Normal range is 3-7 cm of water.Some reasons for a high CVP: occlusion of the jugular vein; over-administration of fluids; right ventricular heart failure.If the CVP is low, patient has reduced blood volume.

4. End-tidal gas analysis – capnography

A capnograph measures infra-red absorption to determine the concentration of CO2 (carbon dioxide) in expired gases. It gives a digital report of the inspired and expired CO2 concentrations during each ventilatory cycle.It is therefore only of use in the anaesthetized patient.It can assist in rapidly diagnosing airway and breathing failure.In patients breathing supplemental oxygen the capnograph can detect ventilation problems earlier than a pulse oximeter. It measures the CO2 directly at the endo-tracgheal tube through an adaptor.Normal peak CO2 expiratory is 30-50 mmHg.


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5. Urine output

Provides indirect information regarding cardiac output and the overall state of the circulation.Adequate kidney perfusion = adequate urine production ie 1-2 mls/kg/hr = likely to have adequate whole body perfusion.Bladder catheterization is indicated if patient cannot be moved or is unable to urinate (e.g. spinal patients).A closed collection system is preferred, with the urine weighed for accuracy (ie 1 gm=1ml).The urine specific gravity may also provide information regarding hydration status ie Urine Specific Gravity < 1.008 if overhydrated, USpG > 1.030 if underhydrated. Other factors such as systemic disease (e.g. Cushings Disease), renal disease etc can alter these measurements.

6. Electrocardiography

6.1 How to record an ECG

Place the patient in right lateral recumbency, with the proximal limbs perpendicular to the body/trunk.The patient should be placed on a blanket or rubber matting to reduce interference with metal tables.Depending on the country, 50 or 60 Hz (cycle) interference is the most likely artifact affecting ECG recordings. This alternating current (AC) may come from electrical supply in the room, including supply to the ECG.

50/60 cycle interference and other artifacts can be reduced: • by good contact between electrode and patient, including wetting of the site with alcohol or ECG pastes

and the use of clean/free-of-rust alligator clips (ideally a pair of pliers can be used to flatten the alligator teeth to improve patient comfort);

• avoid excessive wetting of the electrode site; • turn-off flourescent lights, unplug unnecessary appliances; • use the most ‘ECG-friendly’ room in the clinic; • insulation under the patient as mentioned above; • avoid clips touching each other;• avoid clips touching more than one site on the patient;• correct use of in-built ECG filters;• ensure ECG machine has a grounding electrode;• close animal’s mouth if necessary for 3-4 seconds to record each lead if panting/respiratory motion is

a problem.

Electrodes should be placed on both stifles and elbows, according to the colour or letter code for the system.The limb leads (three electrodes plus a grounding electrode), will allow the recording of 6 leads (or traces) in the frontal plane. These are the bipolar leads I, II, III and the unipolar or augmented leads (aVR, aVL, aVF).In addition to these frontal plane leads, electrodes can be placed directly onto the chest wall, resulting in explorer or V (voltage ) leads. In real terms, this allows ‘viewing’ of the electrical signal from a different viewing angle. This is helpful with assessment of mean electrical axis (MEA), particularly as it pertains to right ventricular enlargement and for detection of ‘p’ waves (especially with the left-sided chest leads) and other deflections in more complex arrhythmia presentations.

The three most commonly used V leads are:CV 5RL : (V1) fifth right intercostal space near the edge of the sternumCV6LL : (V2) sixth left intercostal space near the edge of the sternumCV6LU : (V4)sixth left intercostal space near the costocondral junction.

6.2 Systematic ECG assessment techniques

In order, assess:• Heart rate• Heart rhythm• Measure complexes and intervals.



Heart rate

If rhythm is regular, use: Divide 3000 by the number of small boxes (each represents 20 ms at a 50 mm/sec paper speed) within the R-R interval (or 1500 divided by number of small boxes if using the 25 mm/sec paper speed) (see Figure 1)Or use a heart rate calculator ruler.

If rhythm is irregular:Count how many complexes (or R-R cycles) occur within a 6 or 10 second time frame as marked on the paper. e.g. 9 complexes in 6 seconds, multiply this number by 10 (ie 6s x 10 = one minute) to calculate the rate per minute (e.g. 9 x 10 = 90 bpm).

Heart rhythmGeneral inspection:Is it a normal sinus rhythm? Are any deviations from normal occurring in a repetitive sequence? (e.g. respiratory sinus arrhythmia); are they occasional, frequent or continuous? Regular (some forms of ventricular tachycardia) or irregular (e.g. atrial fibrillation).

P wave identification: Are they present, are they regular or irregular?

QRS complex recognition:Are all QRS complexes uniform in appearance? Are they likely to be ectopic ventricular complexes (wide and bizarre) in origin or are they derived from a supraventricular mechanism (normal in appearance)?

Figure 1: Normal canine P-QRS-T complex.Time intervals areas for a paper speed of 50 mm/sec.Amplitude as for 1 cm= 1 mV

Relationship between P wave and QRS complexes:

Usually a long lead II rhythm strip is used. Use calipers or a card with marks placed on it to record the duration of P-P wave intervals, P-QRS intervals, and QRS-QRS intervals for evidence of rhythm abnormalities.

Measuring Complexes and IntervalsUse the lead II rhythm strip.Measurements are made in terms of width or interval length measured in milliseconds (ms) or seconds (sec) by measuring the number of small boxes, with each box measuring 20 ms (or 0.02 sec) at a paper speed of 50 mm/sec.


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The height of each deflection is measured in millivolts (mV). The ECG machine will have a calibration switch that will demonstrate the height of a 1mV deflection. This is usually set at 1 cm = 1 mV.

6.3 Some examples of common arrhythmias: Figure 2: Supraventricular Premature Complexes (SVPCs). P denotes the premature complex. Each sinus complex is followed by a premature complex, in a bigeminal rhythm.

Figure 3: Atrial FibrillationThis rhythm is present in a dog with dilated cardiomyopathy. The ventricular rate has been slowed to an average of 160 bpm with digoxin.

Figure 4: Ventricular Premature Complexes (VPCs)This ECG is from a dog with pancreatitis and associated myocarditis. The second complex is a VPC, the fifth complex is a fusion complex.

Figure 5: Ventricular Tachycardia (VT)Multiform VT at 180 bpm from a dog with gastric dilation.

Acknowledgements:

Thanks to Dr Fiona Campbell, Anita Parkin VN, Michelle Kleinschmidt VN, Penny Murphy VN, Rebecca Smart VN for assistance with preparation of these notes. ECG Traces from Tilley: Essentials of Electrocardiography of the Dog and Cat.


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19

AVA Members HR Advisory ServiceProviding Members with expert advice and support on

employment mattersHR Matters

AVA Members HR Advisory Service

Serious Misconduct and Termination

Practice owners are often faced with a level of conduct from an employee that justifies instant dismissal rather than giving a written warning or following standard disciplinary procedures. There is no strict definition of what constitutes serious misconduct, however instances of serious misconduct can be described as follows;

• Theft from the business

• Fraud

• Assaulting someone in the workplace

• Being intoxicated or under the influence of drugs at work

• Severe breaches of OH&S legislation

• Conduct that poses serious risk to the reputation, viability or profitability of the business.

Serious misconduct is generally wilful or deliberate behaviour and consists of one single incident where severe misconduct was present as opposed to the cumulative effects of a number of actions by the employee over time. When an employee is terminated for reasons of serious misconduct they forfeit the applicable notice of termination period contained in their industrial instrument.If you feel an employee has committed serious misconduct and you are looking to terminate them, please contact one of the HR Hotline team to discuss the matter first. Given the lack of clear definition as to what is and is not serious misconduct it is best to be entirely sure that the dismissal is justified otherwise the employee may be able to access remedies such as unfair dismissal as the onus of proof is on the employer to prove that the misconduct was serious enough to warrant an instant dismissal.

Subsequent Pregnancies and Eligibility for Parental Leave

Question: We have an employee who is currently on maternity leave with two months to go until she returns. She has recently called and advised that she has fallen pregnant again. Although she will still be returning to work, she will be in the workplace for around 6 months before she goes on maternity leave again.

I have looked at the Standard and it says that an employee must have completed 12 months continuous service with the employer prior to going on leave.

Does this mean that she does not receive a second lot of parental leave?

Answer: In short, the answer is no. An employee must have completed the initial 12 month qualifying with the employer before being entitled to take unpaid leave, after this point the employee is able to claim unpaid parental leave at any time provided the employee complies with the necessary notice and documentation requirements.

Question: Our employee has just gone on parental leave. She is now pregnant again; this means that the employee will give birth before her expected return to work date.

Answer: In these circumstances, provided the employee complies with the notice and evidentiary requirements, it is possible for the employee to claim a second period of unpaid maternity leave without having to return to work.

For more information, contact the team at the AVA Members HR Advisory Service on1300 788 977 or email [email protected].

The Hotline is open from 8.30am – 5.00pm Mon – Fri AEST.


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SHORT BITS…

Stupeed, Breed or Deed

The Scottish Parliament is considering a Bill which will make it an offence by the “proper person” to allow any dog to be dangerously out of control, anywhere in Scotland. In summary, a dog is defined as dangerously out of control if (1) it is not being kept under control effectively and consistently and (2) its behaviour, size or power give rise to reasonable alarm and apprehension on the part of any individual.

Dr Andrew Easton kindly drew the article reporting the Bill (in the Veterinary Record, 4 July 2009:2) to the attention of the News. Those wishing to read the Bill may visit www.scottish.parliament.uk/s3/bills/29-dogControl/index.htm

It certainly is sensible for legislation to address the “proper person”, because it seems reasonable to expect that such persons are able to read, and that the dogs can not.

Smart but Forgetful State?

The Queensland Horse Council is amazed that the Department of Primary Industries and Fisheries is considering terminating the position of Horse Industry Development Officer, created after the serious outbreak of Equine Influenza less than two years ago.

In the June 2009 eQuiNEWS, the Council also draws the attention of members to halting the spread of Class 2 plant pest Fireweed. Fireweed has small, yellow, daisy like flowers about the size of a $2 coin. It contains an alkaloid which is toxic for herbivores, causing liver damage and other signs. The toxin can cause sudden death or cumulative toxicity.

Divisional Strategy

On 29 and 30 August, Division and Branch representatives will meet in Townsville to draw up a Strategic Plan for the coming year. National AVA will be represented and the strategic plan will dovetail with the national strategy. The meeting is an annual event and is being held in Townsville to spread the ease of representation.

The strategy will have the following broad aims: develop and improve member benefits; advocate policy solutions to government, industry and veterinary schools; engage branches; communicate Division achievements to members and non-members.

Members’ inputs are welcomed and encouraged. Please address any comments to the Queensland office or your Branch representative.

Arthritis

Our tireless Executive Officer, Mr Steve McMaster, has brought to the attention of the News a press release by the Australian National Kennel Council dated 21 July 2009. A new type of stem cell technology is being used successfully in dogs in Australia to relieve painful joint problems such as arthritis.

The technology is called Regenerative Stem Cell Technology and involves harvesting fat cells from the dog, processing and purifying them, and re-injecting them into the affected joint. Improvement in quality of life and in movement of the joint is claimed to be as high as 80 percent.

The technology has been practised in Australia for less than 12 months. Readers interested in following up this Short Bit may contact Dr Peter Higgins at [email protected]

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Deposit Facilities • Asset Finance • Commercial Property Finance • Goodwill & Practice Purchase Loans • Home Loans • Income Protection & Life Insurance • Professional Overdraft

Investec Experien Pty Ltd ABN 94 110 704 464 (Investec Experien), Investec Bank (Australia) Limited ABN 55 071 292 594 (Investec Bank). Deposit products are issued by Investec. Before making any decision to invest in these products, please contact Investec Experien, a division of Investec, for a copy of the Product Disclosure Statement and consider whether these products suit your personal financial and investment objectives and circumstances. We reserve the right to cease offering these products at any time without notice.Deposits made with Investec are guaranteed by the Australian Government as part of the Financial Claims Scheme for amounts up to AUD$1 million per client. Amounts in excess of AUD$1 million are also eligible to be guaranteed on application under the Australian Government Guarantee Scheme for Large Deposits and Wholesale Funding. The terms of the government guarantee may change in the future and Investec reserves the right to amend these terms accordingly.The interest rate of 5.25% p.a, inclusive of the 1% p.a. bonus interest, is current as at 1 June 2009 and we reserve the right to change the interest rates in relation to this product at any time without notice. The extra 1% interest rate is only available on new d-POD or POD+ accounts opened by qualified Medical or Accounting professionals with Investec Experien from 5 June to 31 August 2009, with online access activated. The bonus interest will apply to the variable interest rate for 90 days from the date the account is opened. Bonus interest only applicable on deposit facilities with a maximum investment of $500,000. All finance is subject to our credit assessment criteria. Terms and conditions, fees and charges apply. Income Protection/Life Insurance is distributed by Experien Insurance Services Pty Ltd (Experien Insurance Services) which is an authorised representative of Financial Wisdom Limited AFSL No. 231138 (AR No. 320626). Experien Insurance Services is part owned by Investec Experien.

Join the AVA and see the difference

The vision of the Australian Veterinary Association is for a global community that respects and values the benefits of enhanced animal health, welfare and production.

The Queensland Division mission is to be the state organisation representing and serving the interests of the veterinary profession in Queensland to act and speak with a single voice on matters of importance to our members. Why not spread the word about the benefits of AVA membership to your non member colleagues?

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With added benefits such as:◊ GE Money CareCredit Client Finance Plans

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◊ British Veterinary Association Journals – In Practice and The Veterinary Record

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For more information contact AVA member services on 1300 137 309

or email [email protected]

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