Science Week Proceedings - Avian Health Chapter

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Science Week Proceedings - Avian Health Chapter
Science Week Proceedings
   Avian Health Chapter
Science Week Proceedings - Avian Health Chapter
2|SCIENCE WEEK 2019

Foreword from the Science Week
Scientific Program Convenor
Thank-you for joining us at ANZVCS Science Week 2019 at our new venue,
The Star – Gold Coast. This year, we are excited to present an innovative
and cutting edge scientific program and the inclusion, for the first time,
of centralised proceedings. The 2019 Science Week program consists
scientific programs from 20 Chapters, two College Plenary presentations
and the College Convocation. This represents an enormous team collaboration made possible by
contributions from College Council and Staff, the Science Week Committee, Chapter Science Week
Convenors and the Speakers.

I would like to personally thank the Chapter Science Week Convenors who have volunteered
significant amounts of their time towards Science Week 2019. Their enthusiasm, collegiality, and
tireless efforts throughout the past twelve months have ensured that the Chapter scientific
programs for 2019 are contemporary and state-of-the art. I am pleased that together, by producing
centralised proceedings and numerous multi-disciplinary Chapter collaborations, we have been able
to disseminate a great diversity of quality scientific knowledge. Once again, thank-you and I have
thoroughly enjoyed working with you all.

Thank-you also to the Speakers who represent a diverse range of the veterinary scientific community
including experts from human medicine, veterinary specialists, general practitioners, researchers,
members of industry, trainees, nurses and technicians. The contribution of your expertise and
knowledge to the scientific program is gratefully acknowledged.

Lastly, I would like to acknowledge and thank the team in the College office. Our Marketing, Events
and Membership officer, Mrs Thy Boskovic has worked tirelessly to deliver the organisational
infrastructure for this conference and she has been ably supported by the Assistant College
Manager, Ms Sharon Tinsley. I hope that you enjoy this year’s program and look forward to meeting
many of you at the conference.

Dr Wendy Goodwin
Scientific Program Convenor, Science Week
Science Week Proceedings - Avian Health Chapter
ANZCVS|3

Avian Health Chapter Science Week Convenor

On behalf of the Australian and New Zealand College of
Veterinary Surgeons (ANZCVS) Avian Chapter, I would like to
welcome everyone to Science Week 2019. This year we have a
full day of fascinating avian topics. Our avian stream is focused
on cutting edge research with an array of new and seasoned
presenters.

I would also like to extend a big thank you to all presenters and
participants for their contributions to the Avian Chapter.
Without your participation this day would not be possible. So again, Welcome to the avian stream
of Science Week 2019.

Dr Alexandr Mastakov
Avian Health Science Week Convenor
4|SCIENCE WEEK 2019

Table of Contents

Thursday 5th July
Foreword from the Science Week Scientific Program Convenor ...................................................... 2
Avian Health Chapter Science Week Convenor ................................................................................ 3
Table of Contents ............................................................................................................................ 4

Demystifying Lorikeet Paralysis Syndrome: a clinical investigation
  Dr Danny Brown .......................................................................................................................... 6
Avian anxiety: a holistic approach
  Dr Deborah Monks .................................................................................................................... 10
Birds on planes
  Dr Karen Dobson ....................................................................................................................... 19
The development of an electroencephalography model of nociception in domestic pigeons: some
trials and tribulations
   Dr Heidi Lehmann ...................................................................................................................... 20
Cervicocephalic airsac hyperinflation in domestic pigeons (Columbia livia) following halothane
anaesthesia.
  Dr Heidi Lehmann ...................................................................................................................... 21
Point of care diagnosis of Macrorhabdus ornithogaster
  Dr Hamish Baron ....................................................................................................................... 22
Juvenile Galah wasting syndrome – an update
  Associate Professor Bob Doneley .............................................................................................. 23
Induction of general anaesthesia using alfaxalone in the domestic chicken (Gallus Gallus
Domesticus)
  Dr Alexandr Mastakov ............................................................................................................... 27
Regional anaesthesia in birds
  Dr Akshata Taggers .................................................................................................................... 31
Management of a commercial avian disease outbreak
 Dr Rod Jenner ............................................................................................................................ 35
Backyard Poultry Session 1: Pharmacology of drug residues and related issues
  Dr Andrew Woodward............................................................................................................... 37
ANZCVS|5

Backyard Poultry Session 2: Clinical use of anti-microbial medications in backyard poultry
  Dr Deborah Monks .................................................................................................................... 40
Antimicrobial resistance in poultry: Pharmacological and clinical considerations
  Dr Stephen Page ........................................................................................................................ 47
6|SCIENCE WEEK 2019

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Demystifying Lorikeet Paralysis Syndrome: a clinical
investigation
Dr Danny Brown
Australia Zoo Wildlife Hospital, Beerwah, Queensland, Australia

Lorikeet Paralysis Syndrome (LPS) is traditionally defined as “a sudden onset of paralysis in both legs
(bilateral) and/or clenched feet”. This syndrome has been observed since the early 1970’s. The
condition has most commonly been described from affected birds in Sydney and the central New
South Wales coast area, south east Queensland and Victoria.1 The incidence of this classical form
LPS in our facility is approximately 5 %. This consistent with historical records showing between five
and ten percent of lorikeets rescued annually in south-east Queensland and coastal NSW are
presented with this syndrome.2

Recently, the definition of LPS has inadvertently evolved to include any lorikeet that is found on the
ground and is unable to fly and/or walk. This expansion has been partly brought about by a
misunderstanding of the original defined syndrome resulting in overdiagnosis coupled with the
routine use of the term by laypersons, particularly on social media. The end result is a belief that LPS
is currently in an epidemic form and is more common that previously described. The role of this
paper is to describe a clinical process that is actually affecting a large proportion of these birds but
is easily overlooked due to its cryptic nature.
ANZCVS|7

To understand the problem, we must redefine the clinical components of the syndrome.

 CLINICAL SYNDROME                                     DIFFERENTIAL DIAGNOSIS

 Unilateral or, more commonly, bilateral, flexed Classical LPS - non-suppurative encephalomyelitis,
 hocks and clenched feet and are unable to lead poisoning, thiamine deficiency, viral infections
 perch, usually resting on their hocks. A head tilt,
 intention tremor or voice change may also be
 present. Typically, there are no signs of trauma.
 Lateral recumbency, evidence of beak trauma, Trauma , particularly mid vertebral area
 bilateral legs in fixed extension with or without
 clenched feet. Usually unable to fly.
 Sternal recumbency or falls forward when Trauma, particularly lumbosacral vertebral area,
 attempts to move, may still have use of feet. pelvic injuries
 May have evidence of beak trauma. May be able
 to fly or use wings as support.
 Standing but wings in abnormal posture, Trauma – fractures of bones of the wings, usually
 evidence of trauma (bleeding, feather loss)           unilateral.
 Standing, evidence of beak trauma, attempts to Trauma – typically bones of the pectoral girdle
 fly but cannot gain height. Disorientation.           particularly coracoids +/- head trauma
 Standing but sometimes ataxic, +/-evidence of Trauma                 -   ????????
 beak trauma, unable to lift wings or attempt                         -   Head trauma/concussion
 flight.                                                              -   Intoxication

It is the latter subgroup of birds that I have been working towards finding a causative agent/condition
as this group of birds represents a large proportion of our clinical case load (30% of 195 cases
1/1/2019 – 1/5/2019). World Health Australia national wildlife health information system (eWHIS)
Surveillance Data shows 575 entries for Rainbow lorikeets of which 129 (22%) were entered as LPS.
8|SCIENCE WEEK 2019

Of these 129 birds, only 11% were described clinically as typical LPS with the remaining 89% being
typically described as “ataxic, unable to fly, and not blinking properly. No abnormality on x-rays”.

Clinically, these birds may be bright and alert or may show various degrees of neurological changes
consistent with concussive head trauma. The beak often shows evidence of keratin fractures
(pinpoint or linear) or haemorrhage. The legs and wings typically show no evidence of trauma and
the birds show no typical signs of Psittacine Circovirus changes in the feathers. Birds of all ages may
be affected. Radiographically, there are no obvious changes to be noted.

Based on clinical signs, it was assumed that the primary cause of the problem was likely to be related
to the head trauma but a large proportion of cases show no head trauma signs or improve
dramatically in their neurological clinical signs but remain unable to use their wings. In all cases, leg
functions, other than ataxic movements, were not affected.

Understanding the basis of a syndrome usually requires the identification of a commonality between
individuals with the same clinical picture. In early 2019, it was noticed that a characteristic palpable
difference existed between normal non-affected birds and those fitting the above syndrome. On
palpation of the cervical vertebrae of these birds when first anaesthetised and before manipulation
of the body, a common change was noted in the vicinity of the most caudal cervical vertebrae. The
second last cervical vertebrae, with the neck extended ventrally, was ventrally displaced. This allows
the sharp cranial edge of the last cervical vertebrae to be easily felt. When the neck is extended
dorsally whilst supporting the caudal cervical area, a distinct click is heard or obvious crepitus is felt
as the second last cervical vertebrae shifts dorsally into its correct orientation. Following this, the
sharp projection is then unable to be felt. The clinical perception is that what is being palpated is a
ventral subluxation of the caudal cervical vertebrae secondary to head/neck trauma.
Radiographically, this area is always overlaid and obscured by the condyles of the humerus so
abnormalities cannot be seen on plain radiographs.
ANZCVS|9

How does this affect the ability to fly? In the vicinity of the last two caudal cervical vertebrae is the
emergence point of the brachial plexus.3 My theory is that what we are seeing in these birds is a
simple brachial plexus crush injury brought about by a cervical vertebral luxation. Clinically, there is
still considerable work to be done with regards to the treatment implications of this injury.

References
1. Wildlife Health Australia, Rainbow Lorikeet Paralysis (clenched claw) Fact Sheet,
   https://www.wildlifehealthaustralia.com.au/Portals/0/Documents/FactSheets/Avian/Rainbow%20Lorikeet%20Par
   alysis%20Dec%202014%20(1.1).pdf , accessed 26th April 2019.
2. Booth RJ, Hartley WJ, McKee JJ. Polioencephalomyelitis in rainbow lorikeets (Trichoglossus haematodus). In:
   Veterinary Conservation Biology, Wildlife Health and Management in Australia. Proceedings of International Joint
   Conference, Martin A and Vogelnest L, editors. Sydney, 2001:157.
3. The Cornell Lab of Ornithology, All about Bird Anatomy, https://academy.allaboutbirds.org/features/birdanatomy/
   , accessed 27th April 2019
10 | S C I E N C E W E E K 2 0 1 9

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Avian anxiety: a holistic approach
Dr Deborah Monks
Brisbane Bird and Exotics Veterinary Service, Greenslopes, Queensland, Australia

With birds, anxiety disorders are often not considered as a diagnosis until the animal (or the owners)
is at crisis point and even then, treatment tends to focus on the clinical signs rather than the
underlying anxiety disorder.

What does an anxious bird look like?

Before pathological behaviour can be appreciated, clients and veterinary staff need to have a clear
understanding of normal avian behaviour, both generally and specific to that species. Most pet birds
are prey species, so fight/flight/freeze in response to perceived danger. Different bird species have
different temperament predispositions, and energy levels, and behaviour needs to be interpreted in
light of the previous experience of the bird, as well as the individual bird’s personality.

Indicators of an anxiety disorder in birds might include (adapted from Overall1):
    •   Excessive hiding. Anxious birds may not move around their environment confidently or
        regularly. They may spend more time obscuring themselves in foliage, in cage corners, in nest
        boxes. They may cling to an owner’s shoulder or neck or hide in longer hair.
    •   Hypervigilance. Being prey species (in general), it is normal for a bird to exhibit some
        vigilance. Hypervigilance, however, manifests as over-alertness, even in the absence of a
        specific threat. These animals generally are tense, with feathers held tightly against their
        bodies, and fixed, watchful facial expressions. They may fixate on normal items in their
        environments with watchful stares, refusing to approach. They may frequently ‘freeze’ in
A N Z C V S | 11

    response to unexpected noises. The degree of hypervigilance may begin to interfere with
    their social and environmental interaction.
•   Excessive reaction to stimuli. It is normal for a bird to startle in response to an unexpected
    noise, predator vocalisation (for instance, butcher birds and currawongs), strangers in the
    house, seeing threats (eg snakes). Anxious birds can startle so severely that they hurt
    themselves, flying into obstacles. They may vocalise repeated or excessive distress calls. In
    severe cases, they may ‘freeze’ for excessive periods of time.
•   Physical changes. Tremoring, tachycardia, tachypnoea can be seen.
•   Screaming. Inappropriate or excessive screaming is a common owner complaint, but not all
    screaming originates from pathological anxiety. Some birds vocalise loudly, as a normal
    behaviour. They can be calling to their owners or flock members; calling to wild birds (both
    forms of flock calling); admonishing other pets or humans within the environment; making
    appropriate alarm calls; or enjoying themselves (eg having a game, bath etc).
    The screaming associated with anxiety tends to be prolonged, associated with distressed
    posture and facial expression, and may seem without purpose. While separation anxiety
    screaming is correlated with the absence of the owner, and generally ceases upon their
    return, the screaming associated with generalised anxiety can occur independent of owner
    presence, foraging opportunities, removal of threats etc.
•   Feather damaging behaviour. This is often the presenting sign of an anxious bird, being very
    obvious to the owner. However, feather damaging behaviour is not pathognomonic of
    anxiety, nor is anxiety the only disorder that can cause feather damaging behaviour. Feather
    damaging can be the result of a complex interplay of factors - including genetic, social,
    environmental and neurochemical aetiologies, as well as a manifestation of underlying
    physical disease. When associated with anxiety, it has been compared to habitual, self-
    harming and other malfunctional behaviours in humans.2
•   Lack of self-directed behaviours. Many anxious birds are unable to engage in independent
    behaviour, which can manifest as overly ‘clingy’ behaviour with their owners, or a general
12 | S C I E N C E W E E K 2 0 1 9

       lack of interaction with their environment, despite foraging, environmental enrichment and
       other opportunities.

Diagnosing avian anxiety

Before diagnosing ‘anxiety’, a thorough physical assessment must be performed, followed by an in-
depth analysis of the home environment and bird’s specific owned, nutritional and behavioural
history. Often, a medical consultation is scheduled first, in order to do a physical examination, get
an initial history and run some baseline diagnostic tests. An example client questionnaire template
can be found here https://lafeber.com/vet/wp-content/uploads/Behav_Hx_Form_3.pdf. This can
be followed with a specific behavioural consultation, in which a much more detailed history is
obtained. Videos of the bird’s behaviour at home are useful, as is the presence of as many of the
bird’s regular carers as possible in the assessment consultation.

Ideally, veterinary staff will look below the physical manifestation of a problem (e.g. feather
damaging behaviour) and attempt to diagnose the underlying behavioural pathology.

A suggested list of abnormal behaviour required to diagnose avian anxiety could be:
At least one of:
   •   Severe or escalating withdrawal from interaction with people, conspecifics or environment
   •   Presence of seemingly pointless, repetitive behaviours with distressed body language. This
       can include screaming.
   •   Active feather damaging behaviour;

In association with at least two of the following:
   •   Hypervigilance
   •   Excessive startle response
   •   Hiding
A N Z C V S | 13

   •   Inability to calm/settle
   •   Tremoring, wing flicking, excessive muscle activity

The diagnosis of anxiety associated with specific triggers (e.g. separation anxiety) could include the
above but is also contingent on the presence of the trigger (e.g. removal of the owner from the
environment).

Does anxiety need to be treated?

Humans with anxiety disorders describe the suffering and poor quality of life that they experience
with these pathologies, and birds should be no different. By the time a bird is diagnosed with
anxiety, it is likely that the condition will have been present for some time, and that some of the
behaviour patterns may be less amenable to therapy. The impact on the affected individual, other
birds in the house (many birds are distressed by the distressed vocalisations or abnormal behaviour
of other birds), the owners, and other humans (e.g. neighbours) all argue for aggressive intervention
once the diagnosis is made.

When choosing a medication to use for anxiety, a common starting point is the modification of
serotonin levels within the brain.3 Fluoxetine and clomipramine have both been used in avian
species. Fluoxetine (at 2mg kg-1 q12h) is a selective serotonin reuptake inhibitor (SSRI) and increases
the serotonin levels by reducing its re-uptake within the neuronal synapse.2 Clomipramine (at 3mg
kg-1 q12h) is a tricyclic antidepressant, increasing levels of both norepinephrine and serotonin by
also reducing their re-uptake from the nerve synapse.2 In other species, these drugs are expected
to show effect 4-6 weeks after commencement, although this has not been definitively studied in
birds. As with all psychiatric disorders, not all individuals respond equally to medication, and
sometimes different or multiple medications need to be used.
14 | S C I E N C E W E E K 2 0 1 9

In dogs and cats, drugs such as trazadone, gabapentin and benzodiazepines are often used
situationally to manage acute crisis. While this has not been done routinely in birds, a recent paper
has demonstrated the use of trazadone at 30 mg kg-1 in pigeons.4 Trazadone is a serotonin 2A
antagonist/reuptake inhibitor (SARI) with an onset of action of 1-2 hours. Gabapentin has been
used in birds as both an analgesic and an anti-seizure medication5 and inhibits the release of
excitatory neurotransmitter. It could also be used just prior to stressful events. Benzodiazepines
are commonly used in birds for sedation and could also have application during acute crisis.

One of the problems treating anxious birds is the difficulty in administration of medication. The
drugs mentioned above are often unpalatable, even bitter, and birds are often not medication
trained. When coupled with baseline anxiety and perhaps hypervigilance, medication can be a
challenge! It can be difficult for owners to restrain birds to medicate them, and regular restraint can
be perceived as highly aversive by the bird, leading to an escalation in signs and damage to the
owner-animal bond.

This author has had some success using transdermal creams (e.g. clomipramine) with some owners
being able to massage the cream onto featherless areas of the body. Behind the crest is a good area.
The bioavailability of these drugs in transdermal formulations is unknown. Another route, recently
tried with fluoxetine, is using an ion-exchange resin as a taste-masking agent. The taste-masked
formulation allowed the medication to be administered on a favoured solid treat. Clients should be
advising avian clients to medication-train their animals, so that compliance is voluntary.

Medication alone is insufficient

As well as trying to rectify neurochemical imbalance, the treatment of avian anxiety must also
improve behavioural resilience. Resilience, a term used to denote the capacity to withstand stressful
events, is often reduced in the anxious individual. Additionally, anxious birds often lack the
behavioural skills to interact successfully with other humans, conspecifics or their environments.
A N Z C V S | 15

Improving their ‘skill-set’ is likely to provide more successful outcomes, and is more than simply
adding ‘enrichment and foraging opportunities’.

Providing more opportunities for self-directed behaviour, with the addition of toys, foraging and
enrichment items to the bird’s environment is desirable. In an anxious individual, unexpected
changes may cause significant distress, so new resources must be introduced with sensitivity and
keen observation. Some birds may be neophobic, and desensitization can be required. The aim is
never to increase the distress of the bird. Birds may need to be taught - with positive reinforcement
and small approximations – how to interact with and exploit new resources within their
environments. Owners may need to model appropriate behaviour. It is also important that owners
remain observant. An object is only enriching if the bird places a value upon it, and good owner
observation will ensure that appropriate items are used.

When adding foraging to the bird’s behavioural repertoire, it is important to ensure that the bird
understands how to forage. This may need to be taught. Some birds lack foraging skills and will
cease to look for food if they cannot see it in the normal place. Sometimes, birds will withdraw if
foraging difficulty is increased too rapidly. Regular weighing of the bird is advisable.

Providing more opportunities for empowerment is a powerful tool in the maintenance of
psychological health. In the avian context, this includes providing the opportunity for flight (rather
than having trimmed wings). Flighted birds have more choice than clipped birds, although birds that
are poor fliers may need to have flying or landing lessons to improve their skills. Birds that have
never learned to fly can be encouraged to build up their wings using training to begin wing flapping
as a rewarded and elicited behaviour.

Bird training can be very empowering for the patient, and can encompass tricks (fetch, turn around
etc.); medication training (taking water out of syringe etc.); exercise (recalling to shoulder etc.); or
improved communication (the bird might be trained to call for human interaction or attention by
16 | S C I E N C E W E E K 2 0 1 9

ringing a bell or whistling, rather than screaming). It is also possible to reinforce – and request –
‘calmer’ behaviour, which can be beneficial.

For any individual, an unpredictable environment is likely to feel insecure. Predictability can be
added to a pet bird environment by having a regular schedule (for instance, regular-outside-of-cage
time; regular bedtime regimen); having a regular environment (no sudden changes in the cage, the
household, the husbandry etc.). In cases where a very predictable schedule is not possible, adding
cues to the owner interaction with the bird may help. For instance, using words or phrases that
signal ‘you won’t get out of your cage’; ‘now is cage-free time’; ‘the blender is about to make a noise’
etc. may improve the bird’s understanding of the environment, and provide a greater sense of
control.

Once an anxious bird is responding to treatment, it is worth considering whether small, controlled
changes can be introduced to the schedule or environment, in order to encourage better resilience.
The purpose of this is NOT to cause a relapse in the bird’s clinical signs of anxiety, but to improve the
bird’s robustness. It must be done with very great sensitivity and observation, and in miniscule
increments. These changes might eventually grow to incorporate semi-regular boarding at a facility,
occasional change in the human carer, introduction of new toys/cage furniture, or larger scale cage
changes. For instance, with a plan such as this, a bird may be comfortable staying in a boarding
establishment while the owner is away on holiday, with minimal or only mild increase in anxiety
levels.

Behaviour is dynamic, and owners of anxious birds should be trained themselves to be on a
permanent path of observation, analysis and change. Although it may become easier for owners to
respond to flares in anxiety signs with time, these birds may have permanent neurochemical
pathology. Their responses to stressors and change may never be ‘normal’, so owners may need to
commit to long-term management.
A N Z C V S | 17

Prevention

Given the complexity of treatment, the prevention of avian anxiety would be ideal. This could be
achieved with:
   •   Better selection of breeding birds so that less anxious parents are bred. There is likely a
       heritable component to avian anxiety, based on the work done in other species. Certainly,
       feather damaging behaviour appears to be heritable.2
   •   There has been work done on avian personality traits, with more extraverted Orange-Winged
       Amazon individuals exhibiting more resilience when faced with environmental deprivation.6
       Better temperament matching of individuals with their likely environments (while not really
       possible at the moment due to a lack of temperament measurement tools) may result in less
       suffering.
   •   Allow parent-rearing and an extended juvenile bird interaction time (flocking) so that birds
       develop emotional and social skills. Van Zeeland et al2 in their review, cite maternal
       deprivation, the lack of development of social skills, and social isolation as being implicated
       in malfunctional behaviour. It is not difficult to see how this may be intertwined with anxiety
       in predisposed individuals, nor to see how this is exacerbated by current industry standards.
   •   Provide good enrichment opportunities and a complex but navigable environment. Having
       control over the environment and choices is empowering.
   •   Allow birds to be flighted if at all possible. If not, provide structures to allow choice of
       movement (eg ladders)
   •   Avoid boredom by providing foraging and exercise opportunities.
   •   Train resilience.
18 | S C I E N C E W E E K 2 0 1 9

References
1. Overall K. How to Deal with Anxiety and Distress Responses: Dogs In: Proceedings Atlantic Coast Veterinary
   Conference. 2001.
2. van Zeeland Y, Spruit BM, Rodenburg B, et al. Feather damaging behaviour in parrots: A review with consideration
   of comparative aspects. App Anim Behav Sci 2009; 121:75-95.
3. Radosta L. Behavioural Pharmacology Update. In: Proceedings New York Vet Show. Nov 9-10. 2017
4. Desmarchelier MR, Beaudry F, Ferrell ST, Frank D. Determination of the pharmacokinetics of a single oral dose of
   trazodone and its effect on the activity level of domestic pigeons (Columba livia). Am J Vet Res. 2019
   Jan;80(1):102-109.
5. Beaufrère H et al. Diagnosis of presumed acute ischemic stroke and associated seizure management in a Congo
   African grey parrot. J Am Vet Med Assoc 2011;239:122–128
6. Cussen VA, Mench JA The Relationship between Personality Dimensions and Resiliency to Environmental Stress in
   Orange-Winged Amazon Parrots (Amazona amazonica), as Indicated by the Development of Abnormal Behaviors.
   PLoS ONE 2015; 10(6): e0126170

Bibliography
Arikian, Steven R. and Jack M. Gorman. A Review of the Diagnosis, Pharmacologic Treatment, and Economic Aspects of
Anxiety Disorders Prim Care Companion J Clin Psychiatry 2001; 3(3): 110-117.
Horwitz, D. Anxiety in Dogs. In: Proceedings Western Vet Conference, 2012.
Tynes V & Sinn L. Abnormal repetitive behaviors in dogs and cats: a guide for practitioners. Vet Clin North Am Small
Anim Pract May 01 2014 Volume 44, Issue 3, Pages 543-64
A N Z C V S | 19

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Birds on planes
Dr Karen Dobson
Railway Row Veterinarians, Emu Plains, New South Wales, Australia

A 23 gram, male, 14 week old hand reared blue mutation of Forpus corlestis (Pacific Parrotlet) was
presented. He arrived in Sydney the previous afternoon via air freight delivery from Brisbane. The
International Air Transport Association provides documentation for Live Animal Regulations when
freighting birds. Quarantine is the time where new birds may be observed over 4 - 6 weeks to help
identify illness and prevent its introduction into a healthy flock. Veterinarians have a key role to
assist the aviculturist in early disease recognition and initiation of specific therapeutics to ensure a
better outcome for the birds. The diagnostic work up and therapy are discussed.
Other contributing factors are discussed. Histopathology showed acute, multi focal ransom cellular
necrosis of the liver, with intralesional bacilli consistent with a haematogenous Distribution of an
infectious agent. There were florid colonies of short bacilli implicating sepsis as the cause of death.

A handout has been compiled indicating measures that may be used by vendors and purchasers to
maximise outcomes for birds travelling by air freight.
20 | S C I E N C E W E E K 2 0 1 9

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

The development of an electroencephalography model of
nociception in domestic pigeons: some trials and
tribulations
Dr Heidi Lehmann
Massey University, Palmerston North, New Zealand

Electroencephalography (EEG) in lightly anaesthetised animals has been used successfully utilised as
an ethical model of nociception in numerous mammalian species undergoing noxious procedures
(e.g. castration).1 Many such endeavours have been in the aim of improving animal welfare in
livestock industries in Australia and New Zealand. Previous work at Massey University with chickens
has tried to apply both surface and depth electrode recording to a similar avian model.2,3 Whilst level
of consciousness and anaesthesia have been recorded satisfactorily, no EEG response was able to be
detected to noxious stimuli. Current theory, of which my PhD is centred on, is to try and elaborate
this model in another avian species, rock pigeons, with the concept that a technical problem has
thus far prevented signal detection. Factors including the electrode placement, EEG recording and
analysis techniques, plus the potential use of fMRI for depth target location will be examined in my
project. Given my background in anaesthesia, this component’s attenuating effects on the EEG signal
will also be examined.

References
1. Murrell JC, Johnson CB. Neurophysiological techniques to assess pain in animals. J Vet Pharmacol Ther
   2006;29:325–335.
2. Trebilcock P. Investigating the electrical response of the brain of the domestic chicken (Gallus gallus domesticus) to
   nociception through the use of depth electroencephalography (dEEG) [Masters thesis]. [Palmerston North, New
   Zealand], Palmerston North, New Zealand, 2015.
3. McIlhone AE, Beausoleil NJ, Johnson CB et al. Effects of isoflurane, sevoflurane and methoxyflurane on the
   electroencephalogram of the chicken. Vet Anaesth Analg 2014;41:613–620.
A N Z C V S | 21

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Cervicocephalic airsac hyperinflation in domestic pigeons
(Columbia livia) following halothane anaesthesia.
Dr Heidi Lehmann
Massey University, Palmerston North, New Zealand

Eight feral population domestic pigeons were started on a cross-over controlled study assessing the
differences of anaesthetic agent on electroencephalographic (EEG) baseline values. Each bird was
anaesthetised with halothane in oxygen for a baseline agent effect on EEG response at three
different minimum anaesthetic concentration (MAC) values (1.0, 1.5 and 2.0). Five minutes of EEG
recording was taken following a 15 minute stabilisation period at each anaesthetic depth. One to
two birds were anaesthetised each day. Following recovery from the halothane anaesthesia, the
birds were recovered and returned to their conspecifics housing. A washout period of seven days
prior to the next agent, isoflurane, was completed. Following the first two birds of the next agent
assessment being successfully anaesthetised, it was noted that the next two birds had slight neck
region swelling, diagnosed as cervicocephalic air sac hyperinflation in the morning, which
progressed rapidly with marked severity over the next 18 hours. Four birds developed the same
symptoms, including signs of dyspnea. Needle drainage was attempted and repeated at four to eight
hourly intervals as required, with one resolving completely. The original bird noted to have
cervicocephalic hyperinflation deteriorated rapidly and was markedly dyspneic 24 hours following
original detection of the condition. Following euthanasia on humane grounds, the remaining four
birds were showing signs of continued inflation. All birds were consequently euthanased. Post-
mortem examination showed no abnormalities consistent with possible causes (trauma, infectious
agent). The aim of this presentation is to discuss the timeline and occurrence of this cervicocephalic
airsac hyperinflation, and clarify possible causes.
22 | S C I E N C E W E E K 2 0 1 9

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Point of care diagnosis of Macrorhabdus ornithogaster
Dr Hamish Baron1,2, Dr David Phalen2
1
    The Unusual Pet Vets, Mornington Peninsula, Victoria, Australia
2
    The University of Sydney, Sydney, New South Wales, Australia

Macrorhabdus ornithogaster is an ascomycete yeast that grows at the isthmus of the ventriculus and
proventriculus of birds. Antemortem diagnosis has traditionally involved direct visualisation of
organisms on wet-mount or Gram stain preparations. However, point-of-care diagnostic modalities
have never been compared to establish a recommended diagnostic tool for the identification of M.
ornithogaster. We compared five diagnostic modalities; Gram stain, direct fecal wet preparation,
fecal suspension technique, fecal suspension with Gram stain and fecal suspension with methylene
blue. Each technique was performed on 96 fecal samples collected during the treatment of M.
ornithogaster infected budgerigars with water-soluble amphotericin B. The fecal suspension
technique produced statistically higher organism counts than all other techniques and was always
estimated to have the largest detection probability. It was also demonstrated as having 100%
specificity and sensitivity when M. ornithogaster counts were high, with a decrease in sensitivity
when birds infected with low numbers of the organism were sampled. We recommend that the fecal
suspension technique be implemented as the most sensitive and specific modality for point-of-care
diagnostics of Macrorhabdus ornithogaster.

Keywords: Macrorhabdus ornithogaster, diagnosis, cytology, feces
A N Z C V S | 23

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Juvenile Galah Wasting Syndrome – An Update
Associate Professor Bob Doneley, Ms Pia Saavedra Diaz, Dr Helen Owen, Dr Stephanie Shaw
The University of Queensland, Gatton, Queensland, Australia

Abstract
In the last 20 years the author has observed a syndrome in free-living juvenile galahs (Eolophus
roseicapillus) in south-eastern Queensland characterised by severe weight loss, mucoid diarrhoea
and high mortality. Investigative work revealed two enteric pathogens accounting for the clinical
signs, Macrorhabdus ornithogaster and Spironucleus spp. Since the initial reports, the species range
affected by this syndrome has extended to include juvenile Little Corellas (Cacatua sanguinea) and
the geographic distribution now includes Queensland, New South Wales, the ACT and Western
Australia. The role of other pathogens, perhaps immunosuppressive, in the pathogenesis of this
disease has been investigated.

Introduction
Galahs (Eolophus roseicapillus) and Little Corellas (Cacatua sanguinea) are widely distributed around
the country. Over the 20 years, a syndrome associated with severe weight loss, mucoid diarrhoea
and high mortality rates has emerged as a common clinical presentation in these free-living birds in
south-east Queensland, New South Wales, the ACT and Western Australia (Hamish Baron and David
Phalen, personal communications). The syndrome mostly affects juveniles during the spring and
summer, the breeding season for these species. Although the cause(s) of this syndrome have not
been elucidated, two pathogens were identified in a two-year study conducted with free-living
emaciated galahs, namely Macrorhabdus ornithogaster and Spironucleus spp.1
24 | S C I E N C E W E E K 2 0 1 9

Although both these pathogens produce weight loss and diarrhoea, there is not a clear correlation
between the detection of the pathogens in faecal samples and the diagnosis of disease. It is therefore
not clear if they are primary pathogens, or secondary to underlying diseases and pathology.

Methods and materials
A total of 25 wild birds (galahs and corellas) from south-east Queensland were examined over a 6
month period. Seventeen of these birds were diagnosed ante-mortem with extreme weight loss; the
other eight (the control group) were euthanased for unrelated problems (e.g. road accident trauma).
All birds were euthanased, necropsied and tissues collected for PCR (Spironucleus) and
histopathology (PBFD, Chlamydia psittaci, and other diseases).

Results
The clinical and pathological findings in these birds are summarised below.

                                    Affected group (17 birds)        Control group (8 birds)
Weight (averaged)                        Galah (4): 219g                 Galah (5): 309g
                                         Corella (2): 237g               Corella (1): 350g
Diarrhoea                                  14/17 (82%)                      2/8 (25%)
Macrorhabdus positive                       3/17 (18%)                      1/8 (12%)
Spironucleus positive                       8/15 (53%)                      1/8 (12%)
PBFD                                        3/17 (18%)                          Nil
Chlamydiosis                                 1/17 (6%)                          Nil
Other diseases                              5/17 (29%)                     8/8 (100%)

   •      Two birds in the affected group were not tested for Spironucleus
   •      Of the 3 in the affected group that were positive to Macrorhabdus, 1 had PBFD
   •      Of the 8 in the affected group that were positive to Spironucleus, 1 had septicaemia, 1 had
          chlamydiosis, 1 had air saculitis (cause unidentified), and 1 had PBFD.
   •      One of the affected group had both Macrorhabdus and Spironucleus
A N Z C V S | 25

Discussion
Weight loss syndrome in wild juvenile galahs and little corellas is positively correlated with the
presence of M ornithogaster and Spironucleus spp. In the majority of affected birds, these pathogens
were associated with other conditions such as Psittacine Beak and Feather Disease, chlamydiosis,
septicaemia, air saculitis of unknown origin, or concomitant infection with both M ornithogaster and
Spironucleus spp.

Histopathology may lack sensitivity in the detection of diseases such as Macrorhabdus (Baron,
personal communication), Chlamydiosis, and PBFD when compared with PCR, so it appears likely
that the actual incidence of these diseases in the affected birds may be higher than indicated in this
study.

These findings agree with those of David Phalen (personal communication) in New South Wales and
Brice, in Western Australia.2 Both reported high incidences of PBFD in galahs and corellas presented
with weight loss and confirmed as having Macrorhabdus and/or Spironucleus infections.

It appears that these concurrent immunosuppressive diseases make treating these cases difficult.
Although amphotericin B has been recommended as a treatment for Macrorhabdus infection,
recurrence is common. Spironucleus is difficult to treat with nitroimidazoles such as metronidazole
and ronidazole. With the addition of PBFD in the patient at the same time, it results in a poor
prognosis for the majority of these cases.

It seems likely that the ‘Juvenile Galah Wasting Syndrome’ is multifactorial, difficult to treat, and
may be grounds for euthanasia of affected birds on presentation to veterinary clinics.
26 | S C I E N C E W E E K 2 0 1 9

References
1. Doneley B. Weight loss syndrome in juvenile free-living galahs (Eolophus roseicapilla). In: Proceedings Annual
   Conference Australasian Association of Avian Veterinarians and Unusual and Exotic Pet Veterinarians, 2012. p. 9-
   11.
2. Brice B. The Avian Gastric Yeast Experience. https://kanyanawildlife.org.au/wp-content/uploads/The-AGY-
   experience.pdf. Accessed on 29/04/2019
A N Z C V S | 27

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Induction of general anaesthesia using alfaxalone in the
domestic chicken (Gallus Gallus Domesticus)
Dr Alexandr Mastakov, Mrs Rebecca de Gier, A/Prof Joerg Henning, A/Prof Bob Doneley
The University of Queensland, Gatton, Queensland, Australia

Introduction
Alfaxalone is a synthetic neuroactive steroid that acts centrally on the gamma aminobutyric receptor
subtype A (GABAA)1. Alfaxalone produces anaesthesia by binding with the receptor and causing and
influx of chloride ions. This results in hyperpolarisation of the postsynaptic cell membrane and
inhibition of neuronal impulse transmission.1 Alfaxalone has been on the market since 2001 in
Australia and is available for off label use in birds. The drug has numerous advantages over
traditional inhalant anaesthetics including rapid induction time, reduced requirement for manual
restraint and ability to administer the drug through multiple routes (SC, IM, IV, IO). Published
literature for alfaxalone use in birds is limited and is only available for a few species including
Bengalese finches, domestic chickens, flamingos, budgerigars and mute swans.2-6 The findings within
these studies have been inconsistent with a significant variation in the dose required to achieve
general anaesthesia. This experimental study examines the quality of anaesthesia and the dose
required for induction of general anaesthesia in domestic chickens (Gallus Gallus Domesticus) for
intravenously administered alfaxalone.

Materials and methods
Alfaxalone (Alfaxan® Multidose, Jurox Pty Ltd, Australia) was administered to 10 domestic healthy
adult ISA brown hens in two unpremedicated and three premedicated anaesthetic trials over a
period of 4 weeks. In the unpremedicated trials chickens were only given alfaxalone IV (Alfaxan®
28 | S C I E N C E W E E K 2 0 1 9

Multidose, Jurox Pty Ltd, Australia). In the premedicated trials, chickens were given butorphanol 2mg
kg-1 IM (Torbugesic®, Zoetis Inc, Australia) and midazolam 0.5mg kg-1 IM (Hypnovel®, Roche Products
Pty Ltd, Australia), 15 minutes prior to administration of alfaxalone IV. Doses of alfaxalone (Alfaxan®
Multidose, Jurox Pty Ltd, Australia) used in unpremedicated trials were 5mg kg-1 and 7.5mg kg-1.
Doses of alfaxalone used in premedicated trials were 3.2 mg kg-1, 4mg kg-1, 5mg kg-1. Induction of
general anaesthesia was achieved by IV administration of alfaxalone (Alfaxan® Multidose, Jurox Pty
Ltd, Australia) over 60 seconds. The chickens were classified as anaesthetised if endotracheal
intubation was able to be achieved successfully and with ease. The duration of anaesthesia, quality
of anaesthesia, quality of recovery, time to sternal recumbency, time to standing and time to normal
feeding and preening behaviours was recorded.

Results
The minimum IV alfaxalone dose required to achieve general anaesthesia consistently and
predictably in unpremedicated and premedicated chickens was 5mg kg-1 and 4mg kg-1 respectively.
The duration of anaesthesia ranged from 1 minute 32 seconds to 3 minutes 20 seconds and was
increased with the use of premedication and with higher doses of alfaxalone. Premedication
increased the time it took for the chickens to stand after anaesthesia and return to normal feeding
and preening behaviours. The ease of intubation, quality of anaesthesia and recovery improved
when premedication was used. Most chickens within the premedicated and unpremedicated
experimental trials exhibited excitation episodes upon anaesthetic induction and recovery. These
episodes were characterised by dorsoflexion of the head, generalised tremors, wing flapping and
rigid extension of limbs. The excitation episodes were less frequent, less severe and shorter in
duration in the premedicated chickens where alfaxalone was used at doses of 4mg kg-1 and 5mg kg-
1
    . Heart rate and respiratory rate remained stable throughout each experimental trial with no post
induction apnoea. No anaesthetic mortalities occurred.
A N Z C V S | 29

Conclusions/Relevance to Avian Practice
Alfaxalone is a safe and effective anaesthetic induction agent in the domestic chicken. The duration
of anaesthesia, quality of anaesthesia and quality of recovery are positively influenced by
premedication and the dose of alfaxalone used. Excitation is common on anaesthetic induction and
recovery but can be controlled using appropriate premedication. Based on the findings of this study
alfaxalone can be used at a dose rate of 4 – 5 mg kg-1 IV in well sedated chickens to provide rapid
loss of consciousness and induction of general anaesthesia enough for endotracheal intubation.
Additional studies are required into pharmacokinetics and pharmacodynamics of alfaxalone, dose
safety margins, and efficacy in additional bird species.

Acknowledgements
I would like to acknowledge Jurox and Dr Brad O’Hagan for providing the alfaxalone (Alfaxan®
Multidose, Jurox Pty Ltd, Australia) used in this study and for acting as a knowledgeable point of
contact during the study design process. I would also like to thank Dr Vicki Baldrey for allowing me
to use the quality of anaesthesia and recovery scoring system that she developed for her alfaxalone
study in mute swans.

Ethical Animal Research
This study was approved by the Animal ethics committee, University of Queensland (UQ), Gatton,
QLD, Australia (Approval number: AE44693).
30 | S C I E N C E W E E K 2 0 1 9

References
1. Riviere JE, Papich MG. Veterinary pharmacology and therapeutics. Tenth edition edn. Wiley Blackwell, 2018:267-
   269.
2. Perrin KL, Nielsen JB, Thomsen AF, Bertelsen MF. Alfaxalone anesthesia in the bengalese finch (lonchura
   domestica). J Zoo Wildl Med 2017;48:1146-1153.
3. Baldrey V. Alfaxalone as an anaesthetic induction agents in mute swans (Cygnus olor). British Veterinary Zoological
   Society Proceedings of the Autumn Meeting 2014, Lancaster University Management School and Blackpool Zoo,
   UK, 7-9 November 2014 Invertebrates and Megavertebrates - Veterinary Advances 2014:37.
4. Villaverde-Morcillo S, Benito J, Garcia-Sanchez R, Martin-Jurado O, de Segura IAG. Comparison of isoflurane and
   alfaxalone (alfaxan) for the induction of anesthesia in flamingos (Phoenicopterus roseus) undergoing orthopedic
   surgery. J Zoo Wildl Med 2014;45:361-366.
5. Escalante GC, Balko JA, Chinnadurai SK. Comparison of the Sedative Effects of Alfaxalone and Butorphanol-
   Midazolam Administered Intramuscularly in Budgerigars (Melopsittacus undulatus). BIOONE, 2018:279-285,
   277.
6. White DM, Martinez-Taboada F. Induction of anesthesia with intravenous alfaxalone in two isa brown chickens
   (gallus gallus domesticus). J Exot Pet Med 2019;29:119-122.
A N Z C V S | 31

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Regional anaesthesia in birds
Dr Akshata Taggers, Dr Alexandr Mastakov
The University of Queensland, Gatton, Queensland, Australia

Introduction
Multimodal analgesia is recommended for soft tissue and orthopaedic procedures involving the
avian thoracic and pectoral limbs. Regional anaesthesia has been shown to be effective for
prevention of surgical pain and works by altering neuronal signal conduction in a reversible manner
to prevent electrical impulse transmission.1 Local anaesthetics reversibly bind to voltage gated
sodium channels in cell membranes and limit the ability of sodium entry into nerve cells. This
prevents the cell from depolarising and producing a nerve impulse.1 There are significant advantages
to using local anaesthetics including their reversibility, MAC sparing effects and the ability to limit
drug effects to an anatomical region without affecting the animal’s consciousness or impairing CNS
function.1-4 There are several published studies of local anaesthetic (bupivacaine and lidocaine) use
in birds however the findings among the studies have been inconsistent.5-9 The two main regional
blocks that have been investigated in birds are the sciatic femoral-block and brachial plexus block.

Procedure
To administer a local nerve block effectively and improve the chance of success a nerve stimulator
is required. The nerve stimulator is initially set to provide a current of 1.0 mA, applied for 0.1 ms
with a 1 Hz frequency.10 The feathers are plucked, the skin aseptically prepared and a ground
electrode is placed within 5 cm of the insulated stimulating needle entry point. The stimulating
needle is advanced towards a desired nerve and if the location of the needle is close to the desired
32 | S C I E N C E W E E K 2 0 1 9

nerve, then there will be a targeted motor response that leads to contraction of the associated
muscle groups.10 Proximity to the nerve is judged as optimal when a current of 0.4mA is enough to
elicit muscle contraction.10 Local anaesthetic is infiltrated once the appropriate site has been
identified. The nerve block is deemed effective once muscle contractions have ceased in the
presence of electrostimulation.

Sciatic-femoral block
The sciatic nerve is located caudomedial to the femur and parallel to the ischiadic artery.10 The sciatic
nerve supplies sensation to the skin of the foot as well as the entire lower leg, dividing into the tibial
and fibular nerve proximal to the stifle joint. The tibial nerve innervates extensors of the intertarsal
joints and the digital flexors, and the fibular nerve innervates flexors of the intertarsal joint and
digital extensors of the leg.11 The sciatic nerve block landmarks are the greater trochanter (GT) of
the femur and the ischiatic tuberosity (IT). Electrostimulator needle entry is approximately one-third
of the distance along an imaginary line drawn from the GT-IT.10

The femoral nerve provides sensory input to the skin of the upper thigh and inner leg. Additionally
it provides motor function to the anterior compartment of the thigh and the extensor muscles of the
knee.11 The femoral nerve is blocked by placing the bird in lateral recumbency, the limb to be blocked
is abducted by 90 degrees and extended caudally.10 The nerve is located cranial to the femoral artery
which can be palpated to confirm its position. The electrostimulator needle is inserted into the
quadriceps femoris muscle, cranial to the femoral artery.10

Brachial plexus block
The brachial plexus provides sensory and motor innervation to the wing and pectoralis muscle.9, 11
The dorsal section of the plexus divides into the radial and axillary nerves that allow for flexion of
the wing.9, 11 The ventral section divides into the pectoralis trunk and terminates as the median and
ulnar nerves which control extension of the wing.9, 11
There are two main approaches to the brachial plexus block:
A N Z C V S | 33

Dorsal approach
The dorsal approach is performed by identifying and palpating the depression between the last
cervical and the first thoracic vertebrae.6 The wing is extended and adducted towards the body and
the scapula identified laterally. The brachial plexus is located beneath the scapula and cranioventral
to the spinal depression.6 The electrostimulation needle is inserted cranioventrally beneath the
scapula to access the brachial plexus.6

Axillary approach
For the axillary approach the brachial plexus is located subcutaneously and craniodorsally in a
triangular depression formed by the medial edge of the pectoralis muscle, the cranial edge of the
bicep brachii muscle and the dorsal aspect of the serratus ventralis muscle.6 The wing to be blocked
is abducted 90 degrees and the electrostimulator needle is inserted into the triangular depression
of the associated landmarks in a craniodorsal direction and adjusted until maximal muscle
contraction is observed during electrostimulation.6

Conclusions
The studies evaluating the efficacy of the brachial plexus block indicate that the response can be
variable and is associated with a high failure rate.5, 6, 9 Similarly only one experimental study has been
undertaken to evaluate the efficacy of the sciatic-femoral block.10 Clinically within our hospital we
have observed a noticeable benefit from local anaesthetic blocks intraoperatively and
postoperatively for orthopaedic and soft tissue surgeries involving the thoracic and pectoral limbs.
Additional experimental studies examining the efficacy of these blocks, required local anaesthetic
dose and evaluation of peripheral nerve anatomy differences among bird species is warranted.
34 | S C I E N C E W E E K 2 0 1 9

References
1. Riviere JE, Papich MG. Veterinary pharmacology and therapeutics. Tenth edition edn. Wiley Blackwell, 2018:267-
   269.
2. Latney L, Runge J, Wyre N et al. Novel Technique for Scapulohumeral Amputations in Avian Species: A Case Series.
   Isr J Vet Med 2018;73:35-45.
3. Futema F, Fantoni DT, Auler JO, Jr. et al. A new brachial plexus block technique in dogs. Vet Anaesth Analg
   2002;29:133-139.
4. Lee A, Lennox A. Sedation and local anesthesia as an alternative to general anesthesia in 3 birds. J Exot Pet Med
   2016;25:100-105.
5. da Cunha AF, Strain GM, Rademacher N, Schnellbacher R, Tully TN. Palpation- and ultrasound-guided brachial
   plexus blockade in Hispaniolan Amazon parrots (Amazona ventralis). Vet Anaesth Analg 2013;40:96-102.
6. Brenner DJ, Larsen RS, Dickinson PJ et al. Development of an Avian Brachial Plexus Nerve Block Technique for
   Perioperative Analgesia in Mallard Ducks. BIOONE, 2010.
7. Cardozo LB, Almeida RM, Fiúza LC, Galera PD. Brachial plexus blockade in chickens with 0.75% ropivacaine. Vet
   Anaesth Analg 2009;36:396-400.
8. Brenner DJ, Larsen RS, Pascoe PJ et al. Somatosensory evoked potentials and sensory nerve conduction velocities
   in the thoracic limb of mallard ducks (Anas platyrhynchos). Am J Vet Res 2008;69:1476-1480.
9. Figueiredo JP, Cruz ML, Mendes GM et al. Assessment of brachial plexus blockade in chickens by an axillary
   approach. Vet Anaesth Analg 2008;35:511-518.
10. d’Ovidio D, Noviello E, Adami C. Nerve stimulator-guided sciatic-femoral nerve block in raptors undergoing surgical
    treatment of pododermatitis. Vet Anaesth Analg 2015;42:449-453.
11. Koenig HE, Korbel R, Liebich H-G, Klupiec C. Avian Anatomy : Textbook and Colour Atlas (Second Edition). 5m
    Publishing, Sheffield, 2016.
A N Z C V S | 35

Avian Health Chapter
Coolangatta Room 2, July 4, 2019

Management of a commercial avian disease outbreak
Dr Rod Jenner
Rosetta Management Pty Ltd, Cornubia, Queensland, Australia

Commercial poultry veterinary medicine is a highly unique stream of veterinary science and has a
very strong focus on preventative medicine. Infectious disease outbreaks are invariably the result of
a break in biosecurity (as per the definition of biosecurity) – not always preventable but should never
be unexpected. Biosecurity in this context is more than quarantine – also includes vaccination,
preventative medication, good nutrition, genetics, husbandry and management.

Veterinary modalities used in a diagnostic workup – ethology, gross pathology, histopathology,
epidemiology, microbiology (virology, bacteriology), serology, immunology, pharmacology,
therapeutics, veterinary public health.

Treatment regimens are limited to flock-based treatment protocols rather than individual bird. It is
cost-prohibitive to consider hospital pens in large-scale operations, but feasible in the smaller niche
farms, or with high value stock (rare, severe shortage or genetically superior). Even then high value
stock is largely replaceable so it would be unusual to individually treat a commercial bird. Treatment
options are severely limited by availability of suitable therapeutics due to availability of drugs and
food safety considerations, putting more emphasis on preventative measures. Nonsteroidal anti-
inflammatory drugs are never used in poultry medicine, so therapeutic treatments are limited to
antimicrobials.
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