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CVSOH 4 > Avian Medicine > Flashcards

Avian Medicine Flashcards

1
Q

List 7 pathogens that cause disease in both animals and birds.

A

E.coli
Salmonella
Erysipelothrix
Aspergillus
Trichomonas Dermanyssus
Avian influenza
Newcastle disease

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2
Q

Which supplements are available to birds?

A

Grit, oyster shell, liquid calcium, meal worms, liquid vitamin supplements, essential amino acids, nucleotides, trace

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3
Q

Distinguish the role of prebiotics and probiotics in birds.

A

Prebiotics – promote normal bacterial flora

Probiotics – supply one or more normal gut bacteria

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4
Q

What are competitive exclusion products in avian medicine?

A

Undefined caecal bacteria, mix of anaerobes from healthy chickens fed back to chickens

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5
Q

How does temperature affect birds clinically?

A

If temperature is low = dying
High temperature = normal (41), make sure your thermometer can go up to 42

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6
Q

What are the general signs of sickness on clinical examination of a bird?

A
  • Increasing mortality and morbidity
  • Depressed
  • Quiet
  • Abnormal posture
  • Unkempt plumage
  • Locomotor and breathing difficulties
  • High or low <39˚C or >42.5˚C
  • Loss of condition
  • Empty crop
  • Sunken eyes
  • Pale or dark skin
  • Pale and small comb, wattles or snood
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7
Q

Describe how blood sampling is done in birds.

A
  1. Birds over 500g – 21 or 23g 5/8 needle and 2.5ml syringe. Under 500g – 23 or 25g 5/8 needle and 1ml syringe. 4 .
  2. Visualise brachial vein
  3. Tense skin with thumb and insert needle into vein just under skin
  4. Steadily withdraw 2ml blood. Careful not to collapse the vein.
  5. Laying hens can give fatty sera.
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8
Q

How is cytology of a bird’s liver section done?

A
  1. The liver section must be big enough to hold but small enough for the cut surface to fit on a glass slide
  2. Then blot dry
  3. A thick smear which when stained will be difficult to see through
  4. The reason being that the cut surface of the liver was not blotted dry enough
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9
Q

How are gut scrapes of the duodenum done in birds?

A
  1. Incise the intestine so that it opens and lays flat
  2. Remove excess contents or sample the contents
  3. Using a coverslip, carefully apply one edge to the mucosa and scrape along the surface
  4. Place the coverslip contents side down onto a slide and examine x10 then x40
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10
Q

How can mycoplasma capsule be killed?

A

Washing up liquid

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11
Q

What are some examples of tumours and immunosuppressive diseases in birds?

A
  • Marek’s disease virus (first vaccine ever produced against cancer)
  • Lymphoid leucosis/chick anaemia virus
  • Infectious bursal disease (bursa are a basis for immunology)
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12
Q

What are some examples of viral respiratory diseases in birds?

A

Infectious bronchitis virus
Newcastle disease virus
Avian influenza virus
Infectious laryngotracheitis

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13
Q

What are some examples of bacterial respiratory diseases in birds?

A

E.coli
Mycoplasma gallisepticum
Mycoplasma synoviae
Pasteurella multocida

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14
Q

Name a fungal and a parasitic example of respiratory disease in birds?

A

Fungi – aspergillus species

Nematodes – syngamus trachea

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15
Q

What are some examples of viral egg production diseases in birds?

A

Infectious bronchitis virus
Newcastle disease virus
Avian influenza virus
Infectious laryngotracheitis
Egg drop syndrome 76
Marek’s disease virus
Lymphoid leucosis

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16
Q

What are some examples of bacterial egg production diseases in birds?

A

Salmonella gallinarum
E coli
Mycoplasma gallisepticum
Mycoplasma synoviae

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17
Q

What are some examples of protozoal egg production diseases in birds?

A

Coccidia

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18
Q

What could be the pathogenic cause of plumage problems?

A

Mites, lice

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19
Q

What could be the pathogenic cause of gastrointestinal problems in birds?

A

Viruses – rotavirus

Bacteria – clostridia species, salmonella pullorum

Endoparasites – coccidia, worms

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20
Q

List the possible sources of flock infection in small holdings.

A
  • Staff
  • Visitors
  • Vehicles
  • Equipment
  • Replacement stock
  • Water
  • Feed
  • Air – blowers for feed lorries cross contamination
  • Bedding – can carry aspergillosis
  • Pigs, cattle, sheep
  • Insects – alphitobius beetle can eat litter and dead birds and can become contaminated with salmonella and be mechanical carriers of infection
  • Pets
  • Rodents – Pasteurella
  • Wild birds
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21
Q

What are the possible routes of infection in individual birds?

A
  • Through the eggshell
  • Through cuts in the skin or feather follicles
  • In the vent
  • Through the navel
  • In the nose
  • In the eye
  • Through the yolk
  • By mouth
  • In the ear
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22
Q

How is biosecurity implemented in flock holdings?

A
  1. Disease recognition
  2. Disease introduction – vertical, horizontal
  3. Hygiene, new birds, vaccination, worming, ectoparasites
  4. Medication when necessary
  5. Monitoring - bacteriology for salmonella and campylobacter, blood sampling for mycoplasma
  6. Action – slaughter of the flock
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23
Q

List 6 zoonotic diseases of birds.

A

Campylobacter jejuni
Erysipelothrix rhusiopathiae
Salmonella species
Chlamydophila psittaci
H5N1 avian influenza
Newcastle disease

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24
Q

How is campylobacter jejuni transmitted to people?

A
  • Ingestion of contaminated poultry
  • Water
  • Direct contact
  • Between people with faecal-oral route
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25
Q

How is erysipelothrix rhusiopathiae transmitted to people?

A

Puncture wounds

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26
Q

How are salmonella species transmitted to people?

A

Ingestion - faecal-oral route

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27
Q

How is chlamydophila psittaci transmitted to people?

A

Ingestion or inhalation of organism from birds

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28
Q

How is avian influenza H5N1 transmitted to people?

A

Aerosol
Direct contact

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29
Q

How is Newcastle disease transmitted to people?

A

Aerosol
Live vaccines

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30
Q

What is the protocol for notifiable diseases in birds?

A
  • Slaughter, movement restrictions, tracking and tracing
  • Trade ban on exports of live birds, eggs and poultry products
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31
Q

Name the 3 notifiable diseases in poultry.

A

Newcastle Disease of Poultry

Paramyxovirus 1 of pigeons – if this is in chickens they get Newcastle disease

Avian influenza (bird ‘flu) – H5Nx or H7Nx Poultry

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32
Q

What are the incubation periods of notifiable diseases?

A

Avian influenza = 3-14 days
Newcastle disease = 4-6 days
Paramyxovirus 1 = 4-6 days, shedding after 48h

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33
Q

What are the common clinical signs of Newcastle disease and avian influenza?

A
  • Mortality
  • Morbidity
  • Loss of appetite
  • Respiratory signs
  • Reduction in egg laying
  • Twisted necks the wrong way so can’t feed – starve
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34
Q

What are the systemic clinical signs of Newcastle disease?

A

High morbidity and mortality
Depression
Inappetant

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35
Q

What are the respiratory clinical signs of Newcastle disease?

A

Beak gaping
Gasping
Coughing
Gurgling
Rattling
Swelling of tissues in neck and around eyes

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36
Q

What are the nervous clinical signs of Newcastle disease?

A

Drooping wings
Dragging legs
Twisting of the head and neck
Circling
Complete paralysis
Apparent blindness

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37
Q

What are the enteric clinical signs of Newcastle disease?

A

Greenish watery diarrhoea

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38
Q

What are the reproductive clinical signs of Newcastle disease?

A

Partial/complete cessation of egg production
Misshapen eggs
Rough shelled
Loss of shell colour
Thin shelled
Watery albumin contained in eggs

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39
Q

What are the systemic clinical signs of paramyxovirus 1?

A

Green watery diarrhoea
Quiet
Relunctant to exercise
Lethargic
Depressed
Inappetant
Polydipsia
Occasionally sudden mortality

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40
Q

What are the nervous clinical signs of paramyxovirus 1?

A

May precede diarrhoea
Trembling wings and head
Tumble when landing
Inability to fly to perch
Drooping wing
Partial paralysis of wings and legs
Twisting of the neck/torticollis
Unable to pick up grain

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41
Q

How does paramyxovirus 1 differ in clinical signs between pigeons and chickens?

A

Pigeons with PPMV1 is more nervous signs opposed to chickens with PPMV1//Newcastle disease, which have mortality

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42
Q

How does incubation period of avian influenza differ between pathogenicity of strains?

A

HPAI = 9-14 days
LPAI = 3-14 days

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43
Q

What are the clinical signs of HPAI?

A

High morbidity and mortality (100%)
Lachrymation
Sinusitis
Oedema of head
Anorexia
Depression
Cyanosis of skin, comb and wattles
Diarrhoea
Drop in egg production

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44
Q

What are the clinical signs of LPAI?

A

Can be easily missed
Depression
Low by elevated mortality
Mild respiratory signs
Sinusitis
Egg production problems

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45
Q

What are the factors affecting flock vaccination?

A
  • Healthy chick
  • Nutrition – feed, water (too little or too many birds around drinker/feeder Is not good)
  • Environment – litter, atmosphere, lighting
  • Vaccine properties
  • Current epidemiology
  • Maternally derived antibody/MDA
  • Quality of administration
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46
Q

How do you know vaccination has worked?

A

Monitor vaccination using blue food grade dye. Broiler breeder given AE vaccine in the drinking water

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47
Q

Which medications are used in birds?

A
  • Anticoccidials – broilers, some rearing for replacement parents. Not for adults
  • Anthelmintics – Flubenvet (Solubenol) zero egg withdrawal
  • Antibiotics – only Aivlosin, Denagard and Tylan with a zero egg withdrawal
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48
Q

Which medications are no longer used in birds?

A
  • Anti-blackhead (Emtryl) – banned
  • Performance enhancers – growth promoters. No longer permitted
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49
Q

What are the possible aetiologies of sudden death in birds?

A
  • Virus – Avian influenza, Newcastle disease
  • Mycoplasma – M.gallisepticum
  • Bacteria – Erysipelothrix rhusiopathiae, Pasteurella multocida, Spotty Liver Syndrome/campylobacter
  • Fungi/yeast – Aspergillus fumigatus
  • Protozoa – Eimeria tenella, Histomonas meleagridis
  • Nematodes – Syngamus trachea (Gapeworm)
  • Mites – Red mite
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50
Q

What are the characteristics of Erysipelothrix rhusiopathiae bacteria?

A
  • Gram positive
  • Non-motile, non spore forming
  • Slender, slightly curved rods
  • Aerobic or facultative anaerobes
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51
Q

What are the clinical features of Erysipelothrix rhusiopathiae?

A

Large flocks
Found dead or may see sick fevered bird
Ruffled feathers
Lethargic
Anorexic
Scour
Decline in egg production

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52
Q

How is Erysipelothrix rhusiopathiae transmitted?

A

Lateral by ingestion from saliva, faces, carcasses and from contaminated soil

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53
Q

How is Erysipelothrix rhusiopathiae diagnosed?

A

Impression smears stained by gram method showing gram positive slender rods. Confirmed by bacterial culture

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54
Q

How is Erysipelothrix rhusiopathiae prevented?

A

Hygiene
Vaccination
Amoxycillin

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55
Q

What are the post mortem findings of Erysipelothrix rhusiopathiae?

A
  • Petechial haemorrhages on the heart
  • Abdominal fat
  • Congestion and miliary white pinpoint foci in the liver
  • Sticky mucus in intestinal tract
  • Generalised septicaemia – bloody discolouration of the abdominal contents
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56
Q

What are the characteristics of pasteurella multocida?

A
  • Gram negative
  • Non-motile, non-spore forming
  • Aerobic or anaerobic
  • Classified according to capsular antigens - A, B, D, E and F
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57
Q

How is pasteurella multocida transmitted?

A

Lateral spread through saliva and faeces
Rodents are an important source of infection

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58
Q

How is pasteurella multocida diagnosed?

A

Impression smears stained with methylene blue to show safety pin appearance and confirmed by bacteriological culture

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59
Q

How is pasteurella multocida prevented?

A

Amoxycillin, tetracyclines and fluoroquinolones

Autogenous vaccines

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60
Q

What are the clinical signs of acute pasteurellosis in birds?

A
  • Respiratory distress
  • Fevered
  • Cyanosis
  • Ruffled feather
  • Anorexia and lethargy may be seen
  • Reddening and cyanosis of skin of head, mucus from the beak
  • Closed eyes or froth in the inner canthus of the eye
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61
Q

What are the post mortem findings of acute pasteurellosis?

A
  • Petechial haemorrhages on the heart
  • Abdominal fat
  • Consolidated pneumonia
  • Congestion and miliary white pinpoint foci in the liver
  • Sticky mucus in intestinal tract
  • Generalised septicaemia – bloody discolouration of the abdominal contents
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62
Q

What are the clinical signs of chronic pasteurellosis?

A
  • Swollen wattles and swelling between the wattles
  • Occasionally torticollis due to a meningitis
  • Infectious arthritis of legs and wings
  • Tracheal râles
  • No specific egg abnormalities in either acute or chronic forms in laying flocks
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63
Q

Name and describe the bacteria that causes spotty liver disease in birds.

A

Campylobacter hepaticus

  • Gram negative
  • S shaped bacterium
  • Microaerophilic at 37˚C
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64
Q

What are the clinical signs of spotty liver disease?

A

Found dead
Fevered looking hen with ruffled feathers
Anorexia and lethargy
A drop in egg production

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65
Q

How is spotty liver disease diagnosed?

A

No bacteria seen on impression smears, failure to isolate Pasteurella or erysipelas on routine culture

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66
Q

How is spotty liver disease prevented?

A

Amoxycillin, tetracyclines, furazolidone

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67
Q

What are the post mortem findings of spotty liver disease?

A
  • Yellow excess pericardial fluid
  • Splenomegaly
  • Pale kidneys
  • Sticky mucus in intestinal tract
  • Generalised septicaemia – bloody discolouration of the abdominal contents can also occur
  • Bacteriology = negative
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68
Q

What are the clinical signs of red mites?

A
  • Can kill hens
  • Mite infestation associated with poor egg production, poor quality eggs, reduced fertility and hatchability
  • Mites will bite egg collectors and are associated with allergic reactions
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69
Q

What are some behavioural causes of sudden death?

A

Aggression, cannibalism, pecking at crop or vent, smothering

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70
Q

What are some metabolic causes of sudden death?

A

Acute death syndrome, ascites, visceral gout

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71
Q

What are some traumatic causes of sudden death?

A

Predation, drowning, egg bound, fly strike, foreign bodies, mating damage, prolapse cloaca or oviduct, starvation, suffocation

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72
Q

What are some environmental causes of sudden death?

A

Chilling, frost bite, heat stress

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73
Q

What are some nutritional causes of sudden death?

A

Crop full of feed, impactions, intussusception, overgrown beak, poisoning, vitamin deficiency

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74
Q

What are the causes of cannibalism and pecking?

A

Boredom
Over stocking
Mating
Sodium deficiency
Lack of animal protein
Ascarid infections

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75
Q

What are the clinical signs of cannibalism and pecking?

A
  • Watch for general signs of aggression or aberrant investigative pecking
  • Damage to ears, eyes, nostril, wattles and comb, toes and wings, crop, tail and vent
  • Blood on eggs may indicate vent damage
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76
Q

How is cannibalism and pecking treated and prevented?

A

Rectify management deficits
Dim lights
Insert orange or red bulbs
Beak tipping
CD’s
Vegetable stalks
Sodium bicarbonate

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77
Q

What are the post mortem findings for acute cannibalism and pecking?

A
  • Anaemia – very pale carcass, pale liver, lungs pink and fat white)
  • Feed in the crop
  • Blood clot in abdomen
  • The kidneys will be pale
  • Missing cloaca
  • Usually the proventriculus, gizzard, duodenum and ovary remain with the rest of the intestines and oviduct missing, large follicles on the ovary are also missing
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78
Q

What are the post mortem findings of chronic cannibalism and pecking?

A

Necrotic swellings due to trauma followed by infection

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79
Q

How is cannibalism and pecking differentiated from pecking after death?

A

Unlikely to be any blood clots in the abdomen and the carcase is not so pale

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80
Q

What is smother?

A

Sudden fright
Abnormal crowding behaviour – ones on the bottom asphyxiate

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81
Q

What is acute death syndrome?

A

Spontaneous ventricular fibrillation possibly associated with acidosis due to increased blood lactate

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82
Q

What are the clinical signs of acute death syndrome?

A
  • Associated with rapidly growing broilers particularly the male
  • Birds flip over onto back and flap before dying
  • They are often found on their back with legs extended
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83
Q

How is acute death syndrome diagnosed?

A

History of rapidly growing flock above target weight and post mortem findings

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84
Q

How is acute death syndrome prevented?

A
  • Lower energy intake, through management of lights, feed restriction and change from pellets to mash
  • Light patterns seem to be the most useful practically
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85
Q

What are the post mortem findings of acute death syndrome?

A

Pale carcase
Some lung congestion

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86
Q

What does ascites cause in birds?

A

Cause increased blood pressure secondary to pulmonary insufficiency associated with high altitude (decreased oxygen tension), poor ventilation (too dusty) and respiratory disease

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87
Q

What are the clinical signs of ascites in birds?

A

Dyspnoea
Stunting
Sudden death
Recumbent
Open mouthed breathing
Panting
Eyes closed
Cyanosis
Distended and turgid abdomen

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88
Q

How is ascites prevented?

A
  • Control respiratory diseases thereby preventing lung damage, avoid genetic predispositions
  • Can be alleviated by attention to temperature fluctuations, lighting, ventilation and feed control
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89
Q

What is visceral and articular gout is birds?

A

Kidney damage that results failure to excrete urates resulting in hyperuricaemia

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90
Q

What are the infectious and non-infectious causes of visceral and articular gout?

A

Infectious - nephrotropic strains of infectious bronchitis virus or avian nephritis virus, the cause of baby chick nephropathy

Non-infectious - vitamin A deficiency, calcium excess, feeding high protein rations and mycotoxins such as ochratoxin, citrinin and aflatoxin

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91
Q

What are the clinical signs of visceral and articular gout?

A
  • An increase in mortality, depression, low feed intake and lethargic
  • Lameness with swollen joints
  • White urates may be visible in the joints
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92
Q

What are post mortem findings of visceral and articular gout?

A
  • Deposition of monosodium urate crystals
  • Articular gout – the periarticular tissue is white with a thick white fluid in the joint
  • Visceral gout (broiler breeder chick left) – chalky white papery deposits of urates on the heart, viscera, pale swollen kidneys, urates in the ureters
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93
Q

Where is the position of the heart in birds?

A

Heart is between the lungs in birds

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94
Q

What aspects of history and husbandry affects appearance of disease?

A
  • Vaccinated or not
  • Presence of pathogen
  • Husbandry failures - poorly vaccinated, over stocked, mixed ages, failure to quarantine
  • Inadequate environment
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95
Q

When does carbon monoxide poisoning occur in poultry?

A

Gas brooders produce carbon monoxide if not working or cleaned properly and can cause carbon monoxide poisoning in the birds

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96
Q

Why does grit need to be put down?

A

So they can put it in the crop which they use to grind down food so they don’t get impactions

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97
Q

What are the presenting signs of respiratory diseases?

A
  • Coughing or voice change
  • Sneezing, nasal discharge, head shaking or sinusitis
  • Dyspnoea, panting, tail bobbing or cyanosis
  • Haemoptysis
  • Abnormal breathing sounds
  • Coughing up blood
  • Morbidity and mortality
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98
Q

What are the hosts of gapeworm?

A

Pheasants and partridges but not chickens

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99
Q

What is avian metapneumovirus?

A

Also known as Avian Rhinotracheitis (ART). Turkey Rhinotracheitis (TRT) and Swollen Head Syndrome

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100
Q

What are the clinical signs of avian metapneumovirus?

A
  • Depressed
  • Lethargic with a high morbidity but low mortality
  • Oedema around the eye and back of the head
  • Closed eyes
  • Froth inner canthus of eye
  • Lachrymation
  • Conjunctivitis
  • Rhinitis
  • Open mouthed breathing
  • Uni-or bilateral infraorbital sinusitis
  • Torticollis
  • Drop egg production and hatchability
  • Pale thin shelled eggs
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101
Q

How is avian metapneumovirus transmitted?

A

Aerosol, dust and droplets, close contact

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102
Q

How is avian metapneumovirus diagnosed?

A

Clinical and PM findings with confirmatory serology, brain histology, virus isolation, PCR

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103
Q

How is avian metapneumovirus prevented?

A
  • Prevention using live and inactivated vaccines
  • Control secondary with antibiotics
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104
Q

What type of pathogen causes infectious bronchitis?

A

Delta coronavirus

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105
Q

What are the clinical signs of infectious bronchitis in susceptible birds?

A

Depressed
Inappetent
Polydipsia
Wet litter
Poor growth rates
Rhinitis
Lachrymation
Facial oedema
Snicking
Head shaking
Coughing
Urate scour associated with nephrotropic strains
Mortality due to kidney damage
Damage the oviduct > cystic oviduct or blind layers

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106
Q

What are the clinical signs of infectious bronchitis in eggs?

A

Reduction production
Loss of shell colour
Abnormal ridging of shell
Thin shells
Watery white
Infection in young = secondary colisepticaemia
Laying adults = egg peritonitis

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107
Q

How is infectious bronchitis transmitted?

A

The air
Faeces
Faecal contamination of eggs
Water bedding and equipment
Virus can be shed for up to 8 weeks in faeces

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108
Q

How is infectious bronchitis diagnosed?

A

Clinical and post mortem findings confirmed by antibody tests ELISA, HI, virus neutralisation, RT PCR and histology

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109
Q

How is infectious bronchitis prevented and treated?

A
  • Prevention using live and inactivated vaccines
  • Treatment is aimed at controlling secondary infections which may include E.coli vaccines or antibiotic therapy
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110
Q

What is the pathogen causing infectious laryngotracheitis?

A

Gallid herpes 1 virus which can become latent

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111
Q

What are the clinical signs of infectious laryngotracheitis?

A

Cyanosis of the face and wattles
Froth in the inner canthus of the eye
Rhinitis
Lachrymation
Conjunctivitis
Facial oedema
Head shaking
Extension of the head and neck and tracheal rales
Haemoptysis

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112
Q

How is infectious laryngotracheitis transmitted?

A

Horizontally as an aerosol and by mechanical vectors, possibly windborne

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113
Q

How is infectious laryngotracheitis diagnosed?

A

PM, serology, histopathology, IN viral inclusion bodies, PCR, virus isolation

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114
Q

How is infectious laryngotracheitis prevented?

A

Continued vaccination to avoid cross infection

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115
Q

How is infectious laryngotracheitis treated?

A
  • Broad spectrum antibiotic therapy - control secondary bacterial infections
  • Supportive –sodium salicylate
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116
Q

What are the post mortem findings of infectious laryngotracheitis?

A
  • Died in good condition
  • Glottis obstructed by caseous plug
  • Papillae on caudal aspect of laryngeal mound
  • Trachea and glottis opened to show caseous plug moulded to inner aspect of the glottis and a mild tracheitis
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117
Q

What are the clinical signs of mycoplasma gallisepticum?

A

Conjunctivitis
Frothy exudate in eye
Tracheal râles
Nasal discharge
Coughing
Open mouthed breathing
Depressed appetite
Weight loss
Lowered egg production
Loss of shell colour
Exacerbated by intercurrent infections
Ammonia

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118
Q

How is mycoplasma gallisepticum transmitted?

A

Egg transmitted through vertical transmission
Aerosol from direct contact with infected birds
Laterally through fomites

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119
Q

How is mycoplasma gallisepticum diagnosed?

A

Confirmed by culture of the mycoplasma, PCR or blood samples from live b9irds (RSA, HI and ELISA tests)

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120
Q

How is mycoplasma gallisepticum prevented?

A

Live and dead vaccines are available
Controlled but not eliminated by antibiotics

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121
Q

What is avibacterium paragallinarum?

A

Facial oedema that could be associated with infectious coryza

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122
Q

What are the clinical signs of avibacterium paragallinarum?

A
  • Sinusitis
  • Serous to mucoid nasal discharge
  • Facial oedema
  • Conjunctivitis
  • Froth in anterior canthus of eye
  • Gurgling sounds
  • Foul odour from beak if infection is chronic or complicated with secondary infections
  • Diarrhoea
  • Reduced feed
  • Water consumption
  • Uncomplicated cases generally high morbidity and low mortality
  • Egg production drops
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123
Q

How is avibacterium paragallinarum transmitted?

A

Chronic or healthy carriers introduce infection which spreads by direct contact, aerosol or on fomites

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124
Q

How is avibacterium paragallinarum diagnosed?

A

Bacteriological culture, factor V required and low oxygen tension, serology

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125
Q

How is avibacterium paragallinarum prevented?

A
  • Vaccination, good hygiene, single age flocks
  • Tetracyclines, Quinolones and macrolides can be used to treat
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126
Q

What are the clinical signs of mycobacterium avium?

A
  • Cachexia
  • Birds look dull, depressed, lethargic, fluffed up, prominent sternum, pale skin and comb which may be small shrunken
  • Lameness associated with bone infection
  • Diarrhoea with soiling of the vent feathers
  • Go out of lay
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127
Q

How is mycobacterium avium transmitted?

A

Close contact with the live or dead bird, ingestion of faeces or faecal aerosols, contaminated ground and equipment

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128
Q

How is mycobacterium avium diagnosed?

A

Clinical and post mortem findings with confirmatory bacteriology – Ziehl-Neelsen staining of impression smears and culture

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129
Q

How is mycobacterium avium prevented?

A

There is no specific treatment and avian mycobacteria are particularly antibiotic resistant

Control is by testing birds – PCR on faeces, tuberculin test (wattle in the chicken), agglutination and ELISA tests, with the removal of carriers and good hygiene and management

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130
Q

What are the post mortem findings of mycobacterium avium?

A
  • Poor condition with tubercular granulomata
  • Irregular grey to white nodules that can be found in the liver, spleen, intestine and bone marrow
  • Granulomas are firm, with pale yellow caseous centres, sometimes bile stained in the liver and intestine
  • Miliary white caseous nodules in the spleen and nodules in the bone
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131
Q

What is the pathogen involved in respiratory aspergillosis?

A

Aspergillus fumigatus and other fungi. The spores are found in mouldy hay, straw and grain

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132
Q

What are the clinical signs of respiratory aspergillosis?

A
  • Gasping, outstretched necks, within a few days or birds can be affected over several weeks
  • Increased mortality, morbidity in neonates and juvenile less in adults
  • There may be weight loss due to a failure to eat because of the breathing difficulty
  • Torticollis if brain affected
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133
Q

How is respiratory aspergillosis diagnosed?

A

Clinical and PM findings, impression smears, culture

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134
Q

How is respiratory aspergillosis prevented?

A
  • Do not use mouldy hay
  • Nebulisation of antifungal products
  • Supportive care
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135
Q

What are the findings on post mortem of respiratory aspergillosis?

A

Multiple white nodules, sometimes with dark green centres, in various organs most commonly lungs and abdominal viscera

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136
Q

What are the clinical signs of trichomonas gallinae?

A

Yellow caseous lesions in the mouth
Inappetent
Hunched up
Fluffed up
Gaping
Swallowing
Dyspnoea
Cachexic
Foul smell from mouth

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137
Q

How is trichomonas gallinae transmitted?

A

Pigeons via crop milk, feed and water

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138
Q

How is trichomonas gallinae diagnosed?

A

Throat and crop swabs reveal motile protozoa
History
Clinical signs
Post mortem
Histology

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139
Q

How is trichomonas gallinae prevented?

A
  • Prevention regular cleaning of feeders and drinkers, using water sanitisers
  • Fowl – prevent access of pigeons to feeders and drinkers
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140
Q

What are the clinical signs of syngamus trachea?

A
  • Hear the birds snicking
  • Birds seen to be going back, ill thrift and some found dead
  • Gaping with neck extended, snicking (sneezing) and anaemic
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141
Q

How is syngamus trachea diagnosed?

A

History, clinical signs, gross PM lesions, trachea or intestinal smears to look for worm eggs

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142
Q

How is syngamus trachea prevented?

A

Regular worming with flubendazole in feed

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143
Q

What are the presenting signs of alimentary disease in birds?

A
  • Morbidity and mortality
  • Loss of appetite, picking at feed, litter eating
  • Faeces and urates adherent to feathers
  • Enlarged crop
  • Bad smell from beak
  • Beak deformities
  • Failure to gain weight, poor growth
  • Increased water consumption, thirsty
  • Wet, damp, sticky or greasy litter
  • Pungent, sickly smell, rancid
  • Dirty eggs
  • Regurgitation
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144
Q

What changes can occur in the faeces due to alimentary disease?

A

Abnormal colour
Abnormal consistency
Undigested feed
Liquid urates

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145
Q

What are the presenting signs of reproductive disease in commercial flocks?

A
  • Morbidity and mortality
  • Failure to come into lay
  • Drop in egg production
  • Reduced hatchability
  • Infertility
  • Increased number of floor eggs
  • Any eggshell changes
  • Any internal egg changes
  • Low flock water intake
  • Low flock feed intake
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146
Q

What are the presenting signs of reproductive disease in backyard flocks?

A

Egg bound
Prolapse
Not laying
Failure to come into lay
Thin shells
Abnormal shells
Abnormal material

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147
Q

What is a blastodisc?

A

Infertile, small dense white area on top of yolk, 2mm diameter. White arrow on yolk

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148
Q

What is a blastoderm?

A

Fertile, small doughnut shaped white area on top of yolk, 4-5mm diameter –white arrow

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149
Q

What are the respiratory clinical signs of colibacillosis and colisepticaemia?

A

Open mouthed breathing
Panting
Lachrymation
Rhinitis
Snicking
“E.coli “scream
Depression
Diarrhoea
Inappetence
Mortality

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150
Q

How is colibacillosis and colisepticaemia transmitted?

A

Inhalation of aerosol droplets and dust

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151
Q

How is colibacillosis and colisepticaemia prevented?

A
  • Ventilation and drinker management
  • Vaccination requirements
  • Amoxicillin, potentiated sulphonamides and tetracyclines
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152
Q

What are the post mortem findings of colibacillosis and colisepticaemia?

A
  • Pericarditis
  • Perihepatitis
  • Peritonitis
  • With/without air sacculitis
  • Septicaemia
  • Dehydration
  • Congestion of the liver, kidneys, lungs and spleen
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153
Q

What is cellulitis in birds secondary to?

A

Secondary to mating or peck damage

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154
Q

How is cellulitis diagnosed?

A

At slaughter in meat type birds, history and clinical signs in parent flocks

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155
Q

How is cellulitis prevented?

A

Antibiotics
House temperatures - effect on feathering
Immunosuppressive disease

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156
Q

What are the post mortem findings of cellulitis?

A

Yellow parchment like pus subcutaneously on the ventral abdomen extending downwards from the vent

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157
Q

What is coligranuloma?

A
  • This is most often a pathological curiosity which could be confused with Avian TB.
  • There are no specific clinical signs but hard yellow granulomas are seen in the intestine, mesentery and sometimes liver of adult chickens on post-mortem.
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158
Q

What are the clinical signs of salmonella?

A
  • Can be subclinical
  • Depression
  • Pasty vent feathers
  • Lameness and unevenness
  • Slight drop in egg production
  • Slight loss of condition - combs are smaller and paler
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159
Q

How is salmonella diagnosed?

A

Clinical signs, PM lesions, microbiology monitoring, serology

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160
Q

How is salmonella prevented?

A

Competitive exclusion products
Vaccination
Amoxycillin, enrofloxacin, tetracyclines

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161
Q

What are the post mortem findings of salmonella?

A

Neonate inflamed yolk sacs, septicaemia, pericarditis, white caseous typhlitis

Juvenile – Se pericarditis, perihepatitis and retained infected yolk sac. Joint infections

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162
Q

What is the pathogen of pollorum disease?

A

Salmonella Pullorum

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163
Q

What are the clinical signs of pullorum disease?

A
  • Mortality up to 100%
  • Increase in dead in shell
  • Deaths shortly after hatching, depression
  • Respiratory signs
  • Inappetence
  • White sticky droppings on vent feathers
  • Lameness
  • Swollen joints
  • Poor growth
  • Shrunken combs
  • Reduced egg production
  • Infertility
  • Poor hatchability
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164
Q

How is pullorum disease transmitted?

A

Vertically, only a small percent eggs infected. Infected chick hatches, laterally as fluff from chick heavily contaminated, as dries spread through incubator. Persist in environment for many months

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165
Q

How is pullorum disease diagnosed?

A

History, clinical signs, PM lesions, microbiology, serology

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166
Q

How is pullorum disease prevented?

A

Serological testing and culling
Good hygiene
Amoxycillin, enrofloxacin, tetracyclines
Vaccination

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167
Q

What is the acute presentation of salmonella gallinarum?

A
  • Increase in mortality, inappetence, drop in egg production
  • Depression, respiratory distress and a watery to mucoid yellow diarrhoea
  • Loss of condition, anaemia, shrunken pale combs and wattles
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168
Q

What is the subacute presentation of salmonella gallinarum?

A

Sporadic mortality, weakness, yellow pasty droppings, increase dead in shell, mortality in newly hatched chicks

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169
Q

How is salmonella gallinarum transmitted?

A

Primarily lateral in the faeces but egg transmission is possible

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170
Q

How is salmonella gallinarum diagnosed?

A

History, clinical signs, post-mortem lesions, microbiology, serology

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171
Q

How is salmonella gallinarum prevented?

A
  • Good hygiene
  • Amoxycillin, enrofloxacin, tetracyclines may alleviate but not cure the disease
  • Vaccines
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172
Q

What are the clinical signs of coccidiosis?

A

Hunched up
Fluffed up
Eyes closed
Pale skin
Inappetent
Polydipsic
Lethargic
Faecees may contain blood (Et) or have an orange colour

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173
Q

How is coccidiosis diagnosed?

A

History, clinical signs, faecal examination, post mortem lesions

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174
Q

How is coccidiosis prevented?

A
  • Disinfectants that kill oocysts at clean-out
  • Vaccine for chicken coccidia, in feed anti-coccidials
  • Treat with Amprolium or Toltrazuril
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175
Q

What are the post mortem findings of coccidiosis?

A

Haemorrhagic typhlitis
Anaemic carcass
Sudden death
Note the gizzard is full of feed

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176
Q

What are the clinical signs of histomonas meleagridis?

A

Lethargy
Yellowish diarrhoea (far left)
Weakness
Egg peritonitis
Caseous typhlitis

177
Q

How is histomonas meleagridis transmitted?

A

Most infections indirect oral/faecal route via the worm, Heterakis gallinarum or earthworm

178
Q

How is histomonas meleagridis diagnosed?

A

History, clinical signs, PM confirmed by histopathology

179
Q

How is histomonas meleagridis prevented and treated?

A

Regular worming to control caecal worms

No specific treatment but the tetracyclines and herban may help

180
Q

What are the post mortem findings of impaction?

A
  • Gross distension of the intestinal tract
  • Emaciation
  • Presence of foreign body
181
Q

How is impaction prevented?

A
  • Feeding practices – timing feed and water, grit
  • Brooding environment
  • Removal FB’s
182
Q

What are the differential diagnoses for impaction?

A

Avian TB, tumours, malnutrition

183
Q

What are the clinical and post mortem signs of pendulous crop?

A

Sporadic, foul acid smelling fluid

PM – emaciation, distended fluid filled crop

184
Q

What are the clinical and post mortem signs of intussusception?

A

Depressed, hunched, vent pecking, mortality

PM – good condition, invagination of ileum into rectum

185
Q

What are the clinical and post mortem signs of volvulus?

A

Emaciation, lethargy, mortality, lameness, abdominal distension

PM – congested, twisted and dilated small intestine

186
Q

What is egg peritonitis?

A
  • Ovum that is released into the abdomen naturally as the pullets come into lay or secondary to another infection (IB, ND, AI) or non-infectious stress.
  • The ovum may remain sterile or become infected. If the latter then commonly with E.coli resulting in a marked peritonitis
187
Q

What are the clinical signs of egg peritonitis?

A
  • Increased mortality
  • Depression
  • Distended and purple discolouration of the abdomen
  • Dyspnoea
  • Diarrhoea and urate staining at vent
  • Eggshell abnormalities
188
Q

How is egg peritonitis diagnosed?

A

History, clinical signs, PM lesions, microbiology, laparoscopy, ultrasound, radiographs

189
Q

How is egg peritonitis treated?

A
  • Identify the original stressor
  • Antibiotic treatment against Gram negative bacteria
  • Vaccination of the replacement flock in rear and live vaccines have been given in lay
  • Pet hen – fluid therapy, abdominal flushing with antibiotic
190
Q

What are the post mortem findings of egg peritonitis?

A
  • “Scrambled egg” around the intestines
  • Offensive smell
  • Inspisated (yellow plaque like) or white fluid exudate in the abdomen
  • Generalised septicaemia
  • Congestion of the viscera and the ovary
  • Large regressing ova
191
Q

How is salpingitis transmitted?

A

Associated with vent pecking, parasitism, respiratory infections

192
Q

How is salpingitis diagnosed?

A

History, clinical signs, PM lesions, microbiology, laparoscopy, ultrasound, radiography

193
Q

How is salpingitis prevented and treated?

A
  • None in commercial birds, hysterectomy possible in pet birds
  • Attempt to identify the cause and remove it
  • Antibiotic therapy may keep the pet hen alive but she will probably never lay again
  • Hysterectomy
194
Q

What are the post mortem findings of salpingitis?

A
  • Emaciation
  • Dehydration
  • Grossly enlarged impacted oviduct with caseous yolk material laid down in concentric rings
  • Impacted oviduct with caseous yolk material laid down in concentric rings
195
Q

What are the pathogens involved in neonatal septicaemia?

A

E.coli and Pseudomonas aeruginosa

196
Q

How is neonatal septicaemia transmitted?

A

Through the eggshell, in aerosols or by injections

197
Q

How is neonatal septicaemia diagnosed?

A

History, clinical signs, post-mortem lesions, microbiology

198
Q

How is neonatal septicaemia prevented and treated?

A
  • Determine source of infection
  • Cull affected chicks and medicate, if necessary, with a suitable antibiotic
199
Q

What are the post mortem findings of neonatal septicaemia?

A

If they take longer to die then congestion of peritoneum, subcutaneous oedema, pericarditis and perihepatitis may be seen

200
Q

What are the clinical signs of yolk sac infections?

A

Depressed chicks with swollen, turgid distended abdomens, inflamed navels (omphalitis) and eggy smell

Rot quickly

201
Q

How are yolk sac infections diagnosed?

A

History, clinical signs, post mortem lesions, microbiology

202
Q

How are yolk sac infections prevented?

A

Sort out egg hygiene and culling

203
Q

What is the cause of non-starters?

A

Failure of chick to find food and water

204
Q

What are the clinical signs of non-starters?

A

Small weak chicks
No food in the crop
Moribund
Seen from 3-5 days

205
Q

What is the presentation of musculoskeletal disease in birds?

A

Morbidity and mortality (fell off perch)
Reluctant to move
Staggering
Falling over, falling off perch
Limping
Wing drooping
Swollen joints and tendons
Muscle weakness
Not perching
Not flying

206
Q

What is the presentation of nervous disease in birds?

A

Shaking/trembling
Twisted neck
Circling
Head tilt

207
Q

What are the causes of bumblefoot?

A

S.aureus, sometimes E.coli, M.synoviae and nutritional or mechanical damage

208
Q

How is bumble foot diagnosed?

A

History, clinical signs, PM lesions, histopathology

209
Q

How is bumblefoot prevented commercial and backyard flocks?

A

Commercial – litter quality, perch design and nutrition

Backyard – poultice, surgical debridement, x-ray and antibiotic cover

210
Q

What is scaly leg?

A

Knemidocoptes mutans

Raised scales on the toes, feet and legs
Bird ceases to feed and drink and then dies

211
Q

How is knemidocoptes mutans transmitted?

A

Mites are highly contagious and are picked up from the ground. Female mites burrow into the skin. The entire life cycle is completed in 17 –21 days

212
Q

How is knemidocoptes mutans diagnosed?

A

History, clinical signs, PM lesions, skin scrapings

213
Q

How is knemidocoptes mutans treated and prevented?

A
  • An acaricide should be applied to the affected area every 10 days
  • The house should be cleaned and sprayed with an acaricide - Exzolt contains fluralaner and has a zero egg withdrawal
214
Q

What is the aetiology of tendon rupture?

A
  • Trauma
  • Reovirus infection
  • Mycoplasma infection
  • Chronic debilitating disease – coccidiosis and Marek’s disease
  • Poor skeletal development early in rear
215
Q

What are the clinical signs of tendon rupture?

A
  • Limping or snatchy gate
  • Loss of condition
  • Swelling and thickening of the tendon above the hock with or without heat and pain depending on the age of the lesion
216
Q

What is the pathogenesis of tendon rupture?

A

If infectious vertical and horizontal spread. Weakening of the gastrocnemius tendon with rupture and haemorrhage. Green discolouration of the skin above the hock

217
Q

How is tendon rupture treated?

A

Cull the affected birds, try to identify the cause of the problem

218
Q

What is the aetiology of femoral head necrosis?

A

S.aureus, Enterococcus sp., sometimes S.hyicus, E.coli

219
Q

What are the clinical signs of femoral head necrosis?

A
  • The bird is reluctant to walk and may use its wings when doing so, may sit back on its hocks or lie on one side
  • Severely lame
  • When moved, screeches
220
Q

How is femoral head necrosis treated and prevented?

A
  • Affected birds should be culled on welfare grounds
  • Tylan may help prevent infection. Ensure that the drinker lines are clean
221
Q

What is the aetiology of infectious arthritis?

A

S.aureus, sometimes S.epidermidis, Pasteurella multocida, Erysipelothrix rhusiopathiae, Mycoplasma synoviae, E.coli and S.Typhimurium

222
Q

What are the clinical features of infectious arthritis?

A

Lameness, limping, swollen knees, hocks and tendons, heat in the joint, depression

Pigeon – wing lameness and reluctance to fly, just about feel slight swelling in the shoulder joint

223
Q

How is infectious arthritis transmitted?

A

Through the eggshell, aerosol and oral

224
Q

How is infectious arthritis diagnosed?

A
  • History, clinical signs, post-mortem lesions (swelling, pus in joint), microbiology, histopathology
  • PM revealed excess yellow fluid in the shoulder joint
  • Unable to culture S.Typhimurium, this lack of confirmation is a common problem
225
Q

How is infectious arthritis prevented?

A

Check management practices stocking densities, feeder space, drinker systems and water sanitisation, lighting regimes and vaccination practices

226
Q

Explain the aetiology of deep pectoral myopathy.

A
  • Ischaemia of the supracoracoid muscle, which elevates the wing
  • It lies between the sternum and pectoral muscles which do not allow for muscle swelling
  • Wing flapping will increase the demand for oxygen and increase the blood supply to this muscle
  • The swelling compresses the capillaries blocking them which results in muscle cell death
  • This can occur when heavy birds are frightened, chased and handled. More likely, in free range flocks
227
Q

What are the clinical signs of deep pectoral myopathy?

A

No signs. The damage to the supracoracoid muscle does not lead to any clinical signs

228
Q

How is deep pectoral myopathy diagnosed?

A

History, clinical signs, PM lesions, histopathology, microbiology

229
Q

How is deep pectoral myopathy prevented?

A

No treatment. Ideally identify affected birds during processing so that they do not enter the food chain. This can be done by shining a light into the body cavity.

230
Q

How is rickets prevented?

A
  • Identify whether this is due to low calcium or phosphorus
  • Vitamin D3 or 25-hydroxy vitamin D in the drinking water will help in the cases of hypocalcaemia but may exacerbate hypophosphataemia
  • Change the feed
231
Q

What is the pathogen for nervous encephalomyelitis

A

Picornavirus infection, also known as epidemic tremors

232
Q

What are the clinical signs of nervous encephalomyelitis in parents and chicks?

A

Parents – drop in egg production, white shelled eggs, reduced hatchability

Chicks – ataxia, depression, failure to thrive, fine tremors

233
Q

How is nervous encephalomyelitis transmitted?

A

Vertically through the egg and horizontally through faeces

234
Q

How is nervous encephalomyelitis diagnosed?

A

History, clinical signs, no specific post-mortem lesions other than failure to eat, dehydration and loss of condition, serology, virus isolation, histopathology of brain and pancreas. No lesions in peripheral nerves

235
Q

How is nervous encephalomyelitis prevented and treated?

A
  • Vaccination in rear
  • Cull affected chicks or they die from an inability to reach feed and water
236
Q

What are the clinical signs of Marek’s disease/transient paralysis?

A
  • Ataxia, paresis – acute form of marek’s looks like botulism
  • Associated with non-neoplastic vasogenic oedema
  • Some may recover if separated and given ready access to feed and water
237
Q

What are the differential diagnoses of Marek’s disease/transient paralysis?

A

Femoral head necrosis
Spinal osteomyelitis
Kinky back
Botulism

238
Q

What are the aetiology of avian encephalomalacia?

A

Vitamin E deficiency – α-tocopherol

239
Q

What are the clinical signs of avian encephalomalacia?

A

The chicks are in good condition, muscular weakness, ataxia, torticollis, spasmodic incoordination and death

240
Q

How is avian encephalomalacia diagnosed?

A
  • History, absence of egg production drop in the parents, minimal gross lesions, little or no food in the digestive tract
  • Examination of the brain will reveal cerebellar oedema and petechial haemorrhages in some
  • Confirmation by histopathology
241
Q

How is avian encephalomalacia prevented?

A

Check that vitamin E inclusion level in the feed and give extra in the drinking water

242
Q

What is the aetiology of Marek’s disease?

A

Gallid alphaherpesvirus with predilection for nerves. Virus is ubiquitous

  • Serotype 1 – pathogenic oncogenic and attenuated strains
  • Serotype 2 – naturally non-pathogenic strains
  • Serotype 3 – non-oncogenic MDV related virus from turkeys
243
Q

What are the clinical signs of Marek’s disease?

A
  • Seen from 4 weeks of age in unvaccinated and 14 weeks in vaccinated birds
  • There are 4 recognised forms
  • Transient paralysis – rare in broilers from 4 weeks of age
244
Q

How is Marek’s disease transmitted?

A

horizontal through desquamation of cell associated virus in epithelial cells from feather follicles that are inhaled

245
Q

How is Marek’s disease diagnosed?

A

History, gross post-mortem lesions, histopathology and virology (PCR, virus isolation)

246
Q

How is Marek’s disease prevented?

A
  • Day old vaccination
  • Disinfection is critical between flocks of rearing birds to ensure that they are not subjected to high levels of challenge before immunity develops at 2 weeks of age
  • No treatment, supportive care
247
Q

What is the post mortem feature of Marek’s disease?

A

Enlarged nerves in pelvic plexus

248
Q

What are the clinical signs of fowl paralysis?

A
  • Paralysis legs and wings, one leg back, one forward
  • Torticollis
  • Dyspnoea
  • Diarrhoea, scouring, emaciation
249
Q

Describe lesions caused by Marek’s lymphomas.

A

Nervous –enlargement of peripheral nerves, loss normal striations and loss of white colour

Visceral – enlargement of liver, spleen, gonads, heart, stomach, lungs

250
Q

How is Marek’s disease caused by lymphomas diagnosed?

A
  • PCR
  • Cytology, histopathology (pleomorphic cells)
  • Virus isolation
251
Q

Describe the transmission and pathogenesis of Marek’s disease lymphoma.

A

Feather follicle dander gets into atmosphere > breathed in> viraemic and some lodged in feather follicles, some lodged in organs. In hatcheries, can vaccinate, no adults or juveniles so no spread here, and then they can go on to other flocks. But can die 12 weeks onwards if not vaccinated

252
Q

What is the pathogen of lymphoid leucosis?

A

Alpharetrovirus

253
Q

What are the neoplastic and non-neoplastic clinical signs of lymphoid leucosis?

A

Neoplastic – sporadic mortality, inappetence, cachexia, weakness and a scour

Non-neoplastic – poor egg production, slow into lay, fewer eggs, smaller eggs and reduced fertility and hatchability. Hatched chicks may show a depressed growth rate

254
Q

How is lymphoid leucosis transmitted?

A

Vertically through egg, horizontally through saliva, faeces and feather debris

255
Q

How is lymphoid leucosis prevented and treated?

A

Eradication in the breeding programmes

256
Q

Name 2 primary immunosuppressive diseases of birds.

A

Gyrovirus – chicken anaemia virus

Birnavirus – infectious Bursal Disease (Gumboro)

257
Q

Name 4 secondary immunosuppressive diseases of birds.

A

Tumours – Marek’s, leucosis
Malnutrition
Mycotoxins
Mycoplasmas

258
Q

How are immunosuppressive diseases managed in birds?

A
  • Vaccination
  • Ventilation – rate, CO2, CO, NH3, O2
  • Nutrition – e-, protein, form
  • Management – lighting, litter, drinkers, housing
  • Combination of diseases – IBD, CAV, MD, 1 predisposing another
  • Temperature, RH%, dust
259
Q

What is the pathogen of chicken anaemia?

A

Gyrovirus of the family Circoviridae

260
Q

What are the clinical signs of chicken anaemia?

A
  • Chicks from infected flocks show an increased mortality (10%) from 7 days with a gangrenous dermatitis like disease being seen at 14 days
  • Horizontal infection in maternally immune flocks is subclinical
261
Q

How is chicken anaemia transmitted?

A

Vertically through the egg but horizontal spread is more important through the oral faecal route

262
Q

How is chicken anaemia prevented and treated?

A

Vaccination of parents, antibiotic treatment for secondary infections in progeny, good hygiene

263
Q

What are the post mortem findings of chicken anaemia?

A
  • Atrophy of the thymus in the chick on the left
  • Anaemia and pale bone marrow can be found in the femur
  • The spleen is pale and the Bursa of Fabricius may be atrophied
  • The immunosuppression predisposes the chicks to secondary bacterial infections which manifest as gangrenous dermatitis of the legs and wings
264
Q

What is the pathogen of infectious bursal disease?

A

Birnavirus serotype 1

265
Q

What are the clinical signs of infectious bursal disease?

A

Depression
White watery droppings
Soiled vents
Anorexia
Thirst
Prostration
Subclinical

266
Q

How is infectious bursal disease diagnosed?

A

History, post-mortem lesions, histopathology, serology, virology

267
Q

How is infectious bursal disease prevented and treated?

A

Prevention by vaccination

Giving electrolytes in the drinking water and raising house temperature by 1 –2oC may aid recovery in some

268
Q

What are the post mortem findings of infectious bursal disease?

A
  • Dehydration, petechial haemorrhages in thigh muscles
  • Pale swollen kidneys, splenomegaly
  • Enlargement of the Bursa of Fabricius, oedematous and firm, haemorrhage on the serosal and mucosal surfaces. The depopulation of B cells causes immunosuppression
269
Q

Describe avian skeletal anatomy.

A
  • Skeleton reduced/fused – adaptation to flight
  • Sternal vertebrae fused to form sternum (keel)
  • Some vertebrae fused to the pelvis and pygostyle (tail)
  • Bones have thin brittle cortices and wide medullas
  • May be pneumatised eg humerus – light and strong
  • Network of air spaces – sinuses in skull, such as infraorbital sinus
270
Q

What are some examples of when iris colour may differ in birds?

A
  • Change with age/vary between sexes
  • African grey eyes turn from black when young to yellow when adult
  • Male cockatoos will have black iris and females will have red/brown iris
271
Q

What is the ventriculus/gizzard?

A

Muscular grinding organ (seed eaters) grinds up food and goes back and forth between gizzard and proventriculus

272
Q

Describe the anatomy of the kidneys and gonads.

A

Kidneys – cranial, middle and caudal divisions

Gonads – paired testes in male, left ovary only in female (few species have two)

273
Q

Describe the anatomy of the upper respiratory system.

A
  • No epiglottis
  • Tracheal rings complete – do not ETT as there is no give in trachea due to complete rings
  • Syrinx at base of trachea before bifurcation (sound production)
274
Q

Describe the anatomy of the avian lungs.

A
  • Parabronchi open into atria which are connected to air capillaries (site of gas exchange
  • Lungs rigid and non-collapsible; no diaphragm
  • Lungs connected to air sacs – air drawn into lungs by inflating air sacs
275
Q

How are the air sacs connected to the pneumatic bones?

A

Cervical/cervicocephalic/interclavicular connected to humerus

2 x Cranial thoracic air sacs; 2 x Caudal thoracic air sacs; 2 x Abdominal air sacs; connected to femurs

276
Q

How does air get through the avian respiratory system?

A

2 breaths

277
Q

Name the 3 glands in birds.

A

Uropygial (preen), aural and vent gland

278
Q

What are pterylae and apterylae?

A

Feather follicles arranged in tracts = pterylae
Featherless skin in between = apterylae

279
Q

Name and describe the types of feathers.

A
  • Contour = external plumage (flight and body feathers) including wing (primary and secondary) and tail feathers
  • Down – fluffy insulating feathers
  • Powder down – barbs break to produce powder (keratin flakes), such as African greys, cockatoos
  • Semi-plume – found below contour feathers, insulation, courtship
  • Filoplume – sensory function
  • Bristle – round beak and eyes – sensory/tactile, protective function
280
Q

Distinguish primaries and secondaries.

A

Primaries – attached to periosteum of metacarpus
Secondaries – attached to periosteum of ulna

281
Q

What happens if blood feathers are damaged?

A

They can bleed a lot. Ligating or pulling feather out will stop this bleeding

282
Q

Which birds moult continuously?

A

Psittacines

283
Q

What is the consequence of masking phenomenon in birds?

A

Sick birds often in critical condition – need to be seen immediately

284
Q

What does clinical examination of droppings indicate?

A
  • 3 parts – clear urine (no bladder), white urates, formed green/brown faeces
  • Polyuria – increase in urine (differential diagnosis stress)
  • Diarrhoea – loose (unformed) faeces
  • Green/yellow urates – biliverdinuria (liver disease)
  • Haematuria/haemoglobinuria (Pb poisoning, renal disease), melaena (GIT bleeding)
  • Undigested food
285
Q

How are birds handled?

A
  • Parrots – beak more dangerous than the feet restrain head/neck first. Raptors – restrain feet first
  • Don’t restrict sternal movements
286
Q

How is clinical examination of the body done?

A
  1. Palpate crop
  2. Weight and assess BCS
  3. Auscultate heart, lungs dorsally, air sacs ventrally
  4. Assess hydration status – venous refill time > 2 secs >7% dehydration
  5. Palpate ‘abdomen’ – mass/egg/fluid/hernia
  6. Examine vent
  7. Wings and legs – palpate, flex and extend joints
  8. Examine feet and nails constrictions, joint swelling (gout), missing digits
  9. Pododermatitis (bumblefoot) – erosion, erythema, ulceration, swelling of plantar surface
287
Q

How is blood collection done in birds?

A
  • May be easier and safer under GA in small, wild or very sick birds
  • Right jugular vein (larger than left)
  • Ulnar vein (medial elbow) – prone to bleeding/haematoma formation
  • Median metatarsal vein – larger birds
288
Q

What are the injection sites in birds?

A
  • Subcutaneous – inguinal fold, interscapular region
  • Intramuscular – distal third pectoral muscles
  • Intravenous – jugular veins, ulnar/basilic veins, metatarsal veins
  • Intraosseous – ulna or tibiotarsus
289
Q

What are the sites of intraosseous fluid therapy?

A

Distal ulna, proximal tibia, avoid pneumatised bones

290
Q

How is crop tubing done to give nutritional support to sick birds?

A
  • Use largest diameter tube so no worry about going down airway – metal for parrots
  • Extend neck and pass tube into left side of mouth, over tongue and into oesophagus
  • Palpate right side base of neck to confirm tube in crop (feel separate trachea)
  • Every 2-8 hours
291
Q

Why is wing clipping rarely indicated?

A

Can lead to sternal injury from crash landing, psychological problems, feather plucking/chewing

292
Q

When is wing clipping useful?

A

Can be useful temporarily while training dominant/aggressive bird

293
Q

How is wing clipping done?

A

Various techniques – better for vet to do rather than owner at home but should be stressed that this is generally not a good idea

If done should be bilateral – so at least bird can still glide to the floor, always leave 2-3 primaries to support new blood feathers that will come through eventually

294
Q

Describe haematology in birds.

A

Heparin or EDTA suitable for haematology in most species (but blood of some species eg penguins, hornbills, flamingos, crows, cranes will lyse in EDTA)

Avian erythrocytes nucleated automated counts unreliable. Manual method needed to determine white cell count and differential

295
Q

How is in patient care for birds?

A
  • Away from predators (sight, sound, smell)
  • Quiet, well lit and warm (30 ° C) – will not eat in the dark
  • Tail guard for raptors
  • Pond/water for waterfowl
  • Baths for other species
296
Q

How does treatment for birds differ than in small animals?

A
  • Birds have high metabolic rate therefore require increased doses and frequency compared to mammals
  • Putting treatments in water not reliable and may result in bird not drinking
  • May not voluntarily take meds in food either – crop tubing / direct administration preferable
297
Q

Which household hazards pose threat to birds?

A
  • Teflon fumes (non-stick pans) do not affect people but cause birds to die suddenly
  • Cigarette smoke, aerosols
  • Heavy metal objects
  • Fans, open windows
  • Salt, chocolate, avocado, milk, alcohol
298
Q

What are the clinical signs of nutritional disorders in birds?

A
  • Malnutrition
  • Frequent/incomplete moult, retained feather sheaths, flaky, dry, pruritic skin, pododermatitis
  • Long, friable/splitting, deformed, secondary infections
  • Obesity/emaciation, regurgitation/vomiting, loss of appetite, ileus, diarrhoea
  • Respiratory signs
299
Q

Why are seed based diets bad for birds?

A
  • High in fat and calories
  • Deficient in vitamins and minerals
  • Poor calcium : phosphorus ratio
  • Deficient in essential amino acids
  • May be contaminated with fungal spores
  • Mya be contaminated with aflatoxins
300
Q

What are the consequences of hypovitaminosis A?

A
  • Leads to squamous metaplasia/keratinisation of epithelial surfaces oropharynx, respiratory, urogenital and gastrointestinal tract, skin
  • Secondary bacterial/fungal respiratory infections, sinusitis, rhinitis, diarrhoea
  • Rhinoliths, blunted choanal papillae, salivary gland abscesses
  • Poor feather/skin quality
  • Poor reproductive performance
301
Q

What are the causes of gastrointestinal disease in birds?

A
  • Infection – fungal, bacterial, viral
  • Parasites – nematodes, cestodes, protozoa
  • Heavy metal toxicity – lead and Zinc
  • Malnutrition – hypovitaminosis A
  • GIT obstruction – neoplasia, FBs
  • Crop burns (hand-reared parrots)
302
Q

How does gastrointestinal disease present at clinical examination?

A
  • Weight/body condition
  • Dysphagia
  • Crop enlargement/impaction
  • Vomiting/regurgitation matting of feathers on head, head bobbing
  • Assess faeces – diarrhoea, presence of undigested seeds
303
Q

What are the diagnostic techniques used in avian gastrointestinal disease?

A
  • Faecal smears for cytology
  • Crop/proventricular wash for cytology
  • Faecal flotation for endoparasites
  • Culture and sensitivity
  • PCR/serology – for avian bornavirus, C.psittaci
  • Radiography – barium contrast studies useful, 20ml / kg
  • Fluoroscopy – to assess gastrointestinal motility in proventricular dilatation disease
  • Endoscopy
304
Q

How is gastrointestinal disease treated medically in birds?

A
  • Nutritional support
  • Fluid therapy
  • Prokinetics – metoclopramide, cisapride
  • Antibiotics/antifungals
  • Anthelmintics/antiprotozoal drugs
305
Q

What are some possible disorders of the crop?

A
  • Ingluvitis
  • Crop stasis – hand-reared birds or secondary to systemic disease
  • Crop burns lead to necrosis and crop fistula, either under or over the skin. Surgery when extent of necrosis is apparent so wait 5-7 days before surgery
  • Crop impaction
  • Fermentation of crop contents = ‘sour crop’ – endotoxic shock and death
306
Q

How are emergency crop disorders treated?

A

Empty crop via gavage or surgical incision, IVFT, supportive care

307
Q

What are the clinical signs of avian gastric yeast infections?

A
  • Progressive weight loss, ‘going light’, weakness
  • Polyphagia or ‘sham’ eating
  • Regurgitation/vomiting – staining round beak/feathers
  • Undigested seeds in faeces
  • High morbidity, occasionally death
308
Q

How is avian gastric yeast diagnosed?

A

Faecal cytology – but shed intermittently
Proventricular wash for cytology

309
Q

What are the post mortem findings of avian gastric yeast?

A

Dilated proventriculus
Mucosal ulceration at isthmus
Organism in mucosal scrapings

310
Q

How is avian gastric yeast treated?

A
  • Amphotericin B 30 days
  • Good clinical response but organism not eliminated
  • Consider birds life-long carriers
  • Reduce stress – overcrowding
  • Improve diet
311
Q

What is the cause of proventricular dilatation disease? What is its transmission and incubation period?

A

Avian Bornavirus
Transmission faecal-oral
Incubation period 2-3 years +

312
Q

What are the clinical signs of proventricular dilatation disease?

A
  • Carriers asymptomatic
  • Chronic progressive weight loss, lethargy, vomiting/regurgitation, undigested food in faeces
  • Sudden death
313
Q

How is proventricular dilatation disease diagnosed?

A
  • ABV PCR (cloacal/choanal swab or feathers) and serology
  • Crop biopsy for histopathology –include blood vessel with adjacent nerve
  • Lymphoplasmacytic ganglioneuritis on PM
314
Q

What are the post mortem findings of proventricular dilatation disease?

A
  • Distended/ruptured proventriculus with/without duodenum
  • Non-suppurative lymphoplasmacytic ganglioneuritis
  • Perivascular cuffing CNS and peripheral nerves
315
Q

How is proventricular dilatation disease treated?

A
  • No cure
  • Easily digestible food
  • Supportive care including antibiosis for secondary infection, prokinetics
  • Celecoxib (COX-2 inhibitor) to reduce inflammation around nerves
316
Q

What are some disorder of the skin and feathers?

A
  • Nutritional disease
  • Infectious disease parasitic, viral, bacterial, fungal
  • Neoplasia
  • Feather damaging behaviour
317
Q

What are the clinical signs of nutritional diseases?

A
  • Hypovitaminosis A – dry flaky, pruritic skin, hyperkeratosis, impaction of uropygial gland
  • Malformed feathers
  • Abnormal moulting
  • Colour change
  • ‘Stress/fret marks’
318
Q

What are feather cysts?

A
  • Swollen follicle containing ingrown feather
  • Can be quite painful, leading to self trauma and secondary infection
319
Q

How are feather cysts treated?

A
  • Incise and remove feather and keratin debris
  • Surgical removal of follicle if they recur
320
Q

How are cnemidocoptes mites diagnosed?

A

Scrape for microscopy

321
Q

How are cnemidocoptes mites treated?

A

Ivermectin topically weekly 2-3 times
Treat in contacts too

322
Q

Distinguish dry and wet pox?

A

Dry pox – crusty/scabby lesions eyelids and around beak

Wet pox – diphtheritic lesions in oropharynx

323
Q

What are the clinical signs of polyomavirus?

A
  • Feather dystrophy in young birds see SC haemorrhages, loss of wing/tail feathers ‘runners’
  • Sudden death in other parrots
324
Q

What is the pathogen of psittacine beak and feather disease, its incubation period and transmission?

A
  • Circoviruses
  • Virus shed in feather dust, faeces, crop fluids
  • Incubation period 3 weeks – years
325
Q

What are the clinical signs of acute psittacine beak and feather disease?

A

Young birds die rapidly from immunosuppression and secondary infections such as aspergillosis

326
Q

What are the clinical signs of chronic psittacine beak and feather disease?

A
  • Feather loss/dystrophy
  • Retained feather sheaths
  • Deformed feathers
  • Colour change
  • Beak lesions/lack of powder down – usually beak colour is dark grey due to the power down on the feathers from grooming, but in these birds there is no powder down
327
Q

How is psittacine beak and feather disease diagnosed?

A
  • PCR on blood and/or feathers
  • Histopathology – characteristic inclusion bodies in feather follicles/bursa of Fabricius
  • Haematology – anaemia and severe leucopaenia
328
Q

How is psittacine beak and feather disease treated?

A
  • Unlikely to be successful in acute cases – chronic cases are more likely to have success but will be prone to more repeated infections
  • Supportive care, avian interferon, blood transfusion, treat secondary bacterial and fungal infections
329
Q

Distinguish primary and secondary bacterial and fungal dermatitis?

A
  • Often secondary to trauma – feather damaging behaviour or neoplasia
  • Primary bacterial dermatitis – Staph, Mycobacterium spp
330
Q

How is bacterial and fungal dermatitis diagnosed?

A

By cytology, biopsy or culture - fungal dermatitis Candida, Malassezia, dermatophytes

331
Q

Name and describe 3 cancers in birds.

A
  • Lipomas all seed diets
  • Xanthomas – deposition of cholesterol with secondary inflammation. Friable, vascular masses often on distal wing
  • Neoplasia of uropygial gland – SCC
332
Q

What is feather damaging behvaiour?

A
  • African greys, cockatoos – in more intelligent species
  • More common in females
  • Condition of captivity – important welfare issue
  • Distinguish between feather plucking/picking, feather chewing and self trauma/mutilation
333
Q

What are the possible medical causes of feather damaging behaviour?

A
  • Malnutrition
  • Mites, lice
  • Giardia in cockatiels
  • PBFDV, polyomavirus
  • Bacterial/fungal dermatitis/folliculitis/pulpitis
  • Allergic dermatitis/primary inflammatory skin disease
  • Hepatopathy
  • Air sacculitis, aspergillosis
  • Gastrointestinal disease eg PDD
  • Pancreatitis
  • Reproductive disease eg yolk coelomitis
  • Focal pain/discomfort eg arthritic joint, neoplasia (underside of wing, uropygialgland)
  • Wing clipping
    chronic low level zinc (or lead) toxicity
334
Q

Why might a bird be malnourished when causing feather damaging behaviours?

A
  • Hypovitaminosis A, hypocalcaemia
  • Hyperkeratosis of epidermis/feather follicles
  • Squamous metaplasia of uropygial gland
  • Poor quality brittle feathers, dry flaky, pruritic skin
335
Q

How is feather damaging behaviour managed?

A
  • Treat underlying condition
  • Improve diet, vitamin A supplementation
  • Extra warmth, analgesia
  • Allergy
  • GnRH agonists
  • Collars if self traumatising
  • Steroids contraindicated
336
Q

What are the behavioural causes of feather plucking?

A
  • Inadequate socialisation in young parrots
  • Boredom
  • Attention seeking
  • Sexual frustration
  • Tool for coping with stress
337
Q

How is behavioural modification if feather plucking done?

A
  • Enrich environment
  • Should be accustomed to change and new experiences at a young age
  • Introduce foraging/working for food
  • Train, teach a cue and reward it
  • Don’t reinforce unwanted behaviour
  • Psychotropic drugs only once medical causes excluded
338
Q

What are the predisposing factors of egg binding?

A
  • Malnutrition (hypocalcaemia), obesity
  • Excessive egg production
  • Can be life-threatening due to compression of pelvic and renal vasculature/nerves/ureters metabolic disturbances and shock
339
Q

What are the causes of egg binding in birds?

A
  • Oviduct muscle dysfunction (hypocalcaemia)
  • Salpingitis/metritis
  • Abnormally large/malformed eggs
  • Oviduct neoplasia, torsion
  • Systemic/concurrent disease
  • Lack of appropriate nesting site
340
Q

What are the clinical signs of egg binding?

A

-Depression, lethargy, weakness, reduced activity
- Straining, wide-based stance
- Dyspnoea
- Leg paresis
- Decreased frequency of defaecation
- Coelomic distension

341
Q

How is egg binding treated?

A
  • Fluid therapy, nutritional support
  • Provide warmth, dark, quiet, oxygen
  • Oxytocin controversial – may help, would only work if sphincter was well dilated already
  • Intra-cloacal prostaglandin E2 gel increases uterine contractions and relaxes uterovaginal sphincter
342
Q

How is ovocentesis and egg collapse used to treat egg binding?

A

Pass needle through cloaca (safest) or ventral coelomic wall and collapse egg with digital pressure

343
Q

When is coeliotomy and surgical removal done to treat egg binding?

A

Obstructive dystocia/oviduct torsion

344
Q

What can excessive egg laying predispose to?

A

Hypocalcaemia and egg binding

345
Q

What are the causes of excessive egg laying?

A

Inappropriate human ‘mate’ providing sexual stimulation, constant light (lack of diurnal rhythm), readily available high fat food

346
Q

How is excessive egg laying prevented?

A
  • Decrease daylight to 8 hours initially
  • Remove nest site/move cage
  • Behavioural training/client education to establish platonic relationship
  • Leave eggs in nest /replace with dummies
  • Provide pelleted diet – remove fruit
  • Introduce foraging behaviour
  • Hormonal manipulation – GnRH agonists, suprelorelin implant
347
Q

What are the clinical signs of egg yolk coelomitis?

A

Depression
Anorexia
Weakness
Weight loss
Abdominal distension
Decreased egg production

348
Q

How is egg yolk coelomitis diagnosed?

A
  • Leucocytosis on haematology
  • Increased fibrinogen, increased calcium, lipaemia
  • Ultrasound – fluid distension of coelom
  • Coeliocentsis – yellow/pink fluid with WBC and yolk globules
349
Q

How is egg yolk coelomitis treated?

A
  • Supportive care – analgesia, fluid therapy, nutritional support
  • Long-term antibiotics based on culture and sensitivity
  • Surgery – lavage and salpingohysterectomy and/or ovariectomy
350
Q

Which tumours are common in budgies?

A

Renal/ovarian/testicular tumours

351
Q

What are the clinical signs of renal, ovarian and testicular tumours in budgies?

A

Weight loss
Coelomic distension
Leg paresis (sciatic nerve compression)
PUPD
Excessive sexual behaviour
Cere colour changes

352
Q

What are the causes of respiratory disease?

A
  • Tracheal obstruction
  • Inhaled toxins
  • Infectious – bacterial, fungal, viral
  • Parasitic
  • Allergic/pulmonary hypersensitivity – macaws
  • Pulmonary tumours
  • Compression of trachea or air sacs - hepatomegaly, ascites, obesity, egg binding
353
Q

How is the upper respiratory tract assessed in clinical examination?

A
  • Nasal/ocular discharge
  • Swellings – palpate periorbital area (sinuses)
  • Conjunctivitis
  • Sneezing
  • Rhinoliths
354
Q

What are the clinical signs of lower respiratory tract disease?

A

Cough
Dyspnoea
Voice change
Weight loss
Lethargy
Tail bob
Anorexia
Cyanosis

355
Q

What are the predisposing factors to sinusitis/rhinitis?

A

Hypovitaminosis A
Inhaled irritants
Low humidity

356
Q

What are the clinical signs of sinusitis/rhinitis?

A
  • Nasal or ocular discharge, sneezing
  • Exophthalmos, bilateral periocular swelling (infraorbitalsinus)
  • Conjunctivitis, shaking/ rubbing head, matting / loss of feathers around eye
  • Rhinoliths
357
Q

How is sinusitis/rhinitis treated?

A
  • Antimicrobial treatment
  • Nebulise – F10 diluted
  • Debridement/removal of exudate within sinuses eg nasal/sinus flushing, trephination
358
Q

What are the predisposing factors of aspergillosis?

A

Immunosuppression
Stress
Hypovitaminosis A
Long term prophylactic antifungals

359
Q

What are the clinical signs of aspergillosis?

A

Voice change
Dyspnoea
Weight loss
Anorexia
Lethergy
PUPD
Biliverdinuria

360
Q

How is aspergillosis diagnosed?

A
  • Radiography
  • Haematology – leucocytosis, heterophilia, monocytosis, anaemia
  • SPE – increased ß-globulins with/without γ-globulins, decreased A:G ratio
  • Endoscopy
  • Tracheal/sinus washes for cytology/culture
  • Cytology/biopsy/culture – septate branching hyphae
  • ELISA
361
Q

How is aspergillosis treated?

A
  • Surgical debulking of granuloma(s)
  • Topical and nebulised (droplets)
  • Systemic antifungals
362
Q

What are the clinical signs of chlamydophila psittaci?

A
  • Fluffed up, depressed, anorexia
  • Conjunctivitis, rhinitis, sinusitis, ocular/nasal discharge, dyspnoea
  • Biliverdinuria
  • Anorexia, weight loss, diarrhoea, polyuria, sudden death
  • None – subclinical carriers
363
Q

What are the clinical signs of chlamydophila psittaci in ducks?

A

Sinusitis
Rhinitis
Diarrhoea

364
Q

What are the clinical signs of chlamydophila psittaci in raptors?

A

Often chronic weight loss
Diarrhoea
Dyspnoea

365
Q

What are the clinical signs of chlamydophila psittaci in pigeons?

A

Conjunctivitis (‘one-eyed cold’)
Dyspnoea
Green urates/diarrhoea
PUPD

366
Q

What pathogens are involved in chlamydophila psittaci?

A

Disease often occurs in combination with other pathogens eg paramyxovirus, mycoplasma, trichomonas spp

367
Q

How is chlamydophila psittaci diagnosed?

A
  • Leucocytosis, heterophilia, monocytosis, anaemia, increased liver enzymes
  • Radiography – hepatomegaly, splenomegaly, thickened air sacs, loss of parabronchial detail in lungs
  • PCR – pooled faecal samples or conjunctival/choanal/cloacal swab
368
Q

What are the post mortem findings for chlamydophila psittaci?

A

Splenomegaly
Hepatomegaly
Air sacculitis
Pneumonia
Myocarditis
Pericarditis

369
Q

How is chlamydophila psittaci?

A
  • Doxycycline
  • Tetracyclines inhibit Chlamydia protein synthesis
  • Consider prophylactic antifungal treatment
370
Q

What are the causes of liver diseases?

A
  • Infection
  • Metabolic/nutritional - lipidosis, iron storage disease
  • Toxicosis eg aflatoxicosis
  • Amyloidosis
  • Neoplasia
371
Q

What are the clinical signs of liver disease?

A
  • Fluffed up, lethargy, weight loss or gain, sudden death
  • Biliverdinuria – yellow/green urates
  • Poor feather quality/colour change
  • Beak overgrowth/flaking
  • Respiratory compromise – ascites, hepatomegaly
  • Hepatic encephalopathy
372
Q

How is liver disease treated?

A
  • Dietary change
  • Hepatoprotectants
  • Lactulose – hepatic encephalopathy
  • Removal of ascitic fluid
  • Antibiotics/antifungals
373
Q

What are the pre-anaesthetic considerations for avian anaesthesia?

A
  • Chronic underlying illness common
  • Often sicker than owners realise
  • Stabilise before GA for surgery
  • Visual assessment and history
  • Brief physical examination
  • Body condition and weight
  • Blood samples – PCV, TP, glucose measured before hand
374
Q

How often are passerines fed in hospital?

A

High metabolic rate, especially passerines – quickly use up energy reserves feed every 1-2 hours if they are a very small bird

375
Q

What analgesia is used in bird anaesthesia?

A
  • Opioids – butorphanol, duration unlikely to be more than 2-4 hrs (methadone is like half hour)
  • NSAIDs – meloxicam, care if dehydrated, hypotensive or in shock
  • Local anaesthetics – lidocaine or bupivacaine. Birds more sensitive to LA toxicity than mammals – rapid systemic uptake
376
Q

Why is immobilisation of bird limbs done?

A

Immobilisation prevents further soft tissue damage – prevent closed fracture becoming an open fractures. Figure of 8 wing bandage

377
Q

How is premedication done in avian anaesthesia?

A
  • Midazolam IM, SC or intranasal
  • Can be sufficient alone for non painful procedures
  • Useful to calm birds in respiratory distress
  • Reverse with flumazenil
378
Q

How is pre-anaesthetic fasting done in birds?

A
  • Short fasting times to decrease chance of regurgitation but minimise hypoglycaemia
  • Aim is to empty crop
  • 2-4 hours parrots; 30 minutes budgies
  • Large raptors up to 12 hours
379
Q

How is gas induction done in birds?

A
  • Masks for induction and short procedures
  • If procedure > 30mins reduce iso/sevo % over time as plane of anaesthesia often deepens due to recirculation of gases within air sacs
380
Q

How are birds intubated?

A
  • Uncuffed tubes to prevent pressure necrosis (complete tracheal rings)
  • Provides patent airway, decreases dead space, protects against aspiration, allows IPPV
381
Q

What is post-intubation stenosis?

A
  • Intubation can (rarely) cause tracheal mucosal damage and strictures
  • Present with worsening dyspnoea up to 14 days post GA
  • As a precaution, if see blood on tube give dose of meloxicam
382
Q

How are waterfowl induced in anaesthesia?

A
  • Use of face mask in waterfowl can cause apnoea and bradycardia due to stimulation of trigeminal receptors around beak and nares
  • Dive reflex
383
Q

How are birds positioned under general anaesthetic?

A
  • Lateral recumbency best
  • Ventilation may be decreased in dorsal recumbency (especially larger birds) so have to do IPPV if in this position for long
383
Q

When is air sac perfusion done in avian anaesthesia? Where is this done?

A
  • Useful for head surgery or as emergency procedure in tracheal obstruction and can breathe through these tube directly into air sacs
  • Into left caudal thoracic air sac, behind last rib
384
Q

Why is heart rate difficult to monitor in avian anaestesia?

A
  • Can be difficult as some birds have a HR of 300-400bpm.
  • HR should not drop below 100 bpm in parrots/raptors
385
Q

Which capnographer is used and and why is capnogrpahy used in avian anaesthesia?

A
  • Side stream units with low sampling rates best for small birds
  • Birds susceptible to hypercapnia – assisted ventilation advisable
386
Q

What are the possible complications in avian anaesthesia?

A
  • Hypoventilation and apnoea common - 100% oxygen/turn off isoflurane, check ET tube patency
  • IPPV – don’t over-inflate, as this may rupture air sacs)
  • Cardiac arrest quickly follows apnoea and is very difficult to reverse
  • Chest compressions at min 60-80/minute
387
Q

When should birds first eat after recovering after GA?

A

Must eat quickly - within 30 minutes if<100g

388
Q

Why might birds recover slowly from GA?

A
  • Pre-anaesthetic medication
  • Hypothermia
  • Hypovolaemia
  • Hypoglycaemia
  • Haemorrhage – give colloids/blood
  • Pain
389
Q

What are the principles of avian surgery?

A
  • Atraumatic tissue handling
  • Meticulous haemostasis – small birds can’t afford to lose lots of blood
  • Preservation of blood supply
  • Magnification
  • Small instruments
  • Minimal tissue tension
  • Closure of dead space
390
Q

What are the nursing considerations for avian surgery?

A
  • Pluck (don’t cut) feathers – remove minimum number (can tape out of the way)
  • Care with alcohol when preparing op-site – overdoing this will lead to hypothermia
  • Bird skin very thin – so plucking can tear the skin so be careful
391
Q

How can skin be surgically closed on the limbs and digits in birds?

A

Simple interrupted or everting mattress sutures on thicker skin on limbs and digits

392
Q

How do abscesses in birds differ?

A

Abscesses contain caseous pus (like reptile pus) s0 can’t lance it and let it come out you have to dig it out

393
Q

How are liver biopsies done in birds?

A
  • Skin tented and incised immediately caudal to edge of sternum
  • 1-2cm horizontal incision through skin
  • Blunt dissection through muscle to coelomic cavity
  • Wedge biopsy of caudal edge of liver
394
Q

How is a ventral midline coeliotomy done in birds?

A
  • Skin tented and incised midline caudal to sternum
  • Linea alba tented and incised to enter coelom
  • Lateral flaps can be made along edge of sternum or along pubis caudally if needed
395
Q

How do you do chlamydia testing in birds?

A

Combined conjunctival, choanal and cloacal swab for PCR. Can also send of faeces from 3-5 days for a pooled sample for PCR

396
Q

What is done for a bird with hypocalcaemia?

A

Do not change diet from seeds to pellets while ethe bird is sick immediately – do this long term after well. Cannot add supplement to seeds as they will crack open the seeds and to husk/shell and supplements fall to the floor. So give calcium directly to the bird. Zolcal D is the liquid calcium and vitamin supplement, fairly palatable.

397
Q

What is the most likely cause of heterophilia in birds?

A

Bacterial or fungal infection. Stress and inflammation would have a mild heterophilia but not this high. Toxic changes indicate bacterial and fungal.

398
Q

Why might a chlamydia PCR come back negative?

A

The bird has been on enrofloxacin for 2 weeks – has not treated chalmydia if it has chamlydia but would stop shedding, so can do serology instead in light of being on baytril for 2 weeks. False negatives common due to intermittent shedding.

399
Q

Serology came back positive for chlamydia. How are you going to treat the bird?

A

Doxycycline 45 days oral PO or long acting doxycycline injection that lasts about a week (can no longer get in UK so have to import)

400
Q

What are the differential diagnoses for paresis?

A

Hypovitaminosis A, hypocalcaemia, trauma, arthrosclerosis (cholesterol deposits narrow arteries in vessels around the heart and legs), egg binding, CNS lesions, neoplasia putting pressure on the sciatic nerve, renal disease/enlargement, lead poisoning

401
Q

What is the normal appearance is the lungs on radiographs?

A

Honey comb pattern

402
Q

How do you check if a bird is positioned straight on radiographs?

A
  • Check with sternum and spine overlapping each other if straight
  • Hourglass shape of heart and liver
403
Q

What might a consequence of an enlarged liver in birds be?

A

Compresses air sacs

404
Q

How is hepatic lipidosis treated?

A
  • Supportive care - warmth, fluids, nutritional support
  • Diet change from seeds to pellets - carbohydrates replace fat as calorie source
  • Liver support - milk thistle
  • L-carnitine (decrease blood triglyceride and fatty acid levels)
405
Q

Why do you have to do a ventral midline approach for an exploratory coeliotomy in birds?

A

Have to go midline to avoid cutting into air sacs

406
Q

What are the differential diagnoses for dyspnoea?

A
  • Aspergillosis (more chronic than acute, birds quite thin)
  • Chlamydia
  • Allergy
  • Inhaled toxins if in homes
  • Tracheal obstruction
  • Hepatomegaly or ascites squashing air sacs but these may be more chronic than acute
407
Q

How are air sac tubes placed?

A
  1. Quick prep
  2. Behind last rib
  3. Into caudal thoracic air sac
  4. Tube with hole in side as well as end
  5. Secure through muscle and skin
  6. Can maintain GA through tube to allow endoscopy to visualise the lesion
408
Q

In abattoirs, how can you inspect poultry at 180 birds per minute?

A
  • Practice
  • By never looking directly in front – moving at 3/s so by the time you spot it, its gone
  • Because in a wall of normality and uniformity, deviation is easy to spot
409
Q

What are the FSA rejection conditions for poultry reported back to vets and farmers?

A

Abnormal colour/fevered
Ascites/oedema
Bruising or fractures
Cellulitis
Contamination
Dead on arrival
Death other than slaughter
Dermatitis
Emaciation
Hepatitis
Joint lesions/arthritis
Machine damage
Overscald
Pericarditis
Perihepatitis and peritonitis
Respiratory disease
Runts
Salpingitis
Tumours and nodules

410
Q

What information is sent to the producer of the plant before birds arrive at abattoir?

A

Age of birds, date of placement, number of chicks placed, mortality at 14 days, mortality to date, medication given and at what date, details any disease diagnosed, list other tests

411
Q

Why is a spike in mortality seen at 14 days in poultry?

A

Get a spike in mortality at 14 days as takes 14 day for litter to work properly

412
Q

What is the welfare problem with collection of birds for sending to abattoirs?

A

Problem with collection is that small amount of people sent in to get a large amount of bird in a short period of time. Turning upside down (no diaphragm so fallen air sacs), picking up by 1 leg or 1 wing, can cause a large proportion of the birds to be damaged before arrival. Welfare problem and economic problem.

413
Q

What is the welfare issue at arrival of abattoirs?

A

Transport issues with heat stress

414
Q

What are the welfare at lairage?

A
  • No access to water, not fed for 12 hours before slaughter, so stress levels are already high
  • Purpose is to keep abattoir going, a magazine
  • If birds at the bottom are panting, birds at the top will be dying
  • If birds are wet, more electricity in stunning will be needed as will just go round the bird in the moisture instead of through them
415
Q

What happens at shackling in abattoirs?

A

Hung upside down alive and electrical stunning. Will flap when put in and it is painful. Can only be hung like this by law for 1 minute

416
Q

How is electrical stunning done in small abattoirs and halal abattoirs?

A
  • Bath of water with electrode in it, when head is put in, current goes through bird to the shackle
  • Can have 20-40 birds in the bath at once. Induces epilepsy electrically to overstimulate brain function, so animal cannot process pain or any other sense in stunning
  • This is done before pain occurs, takes about 100ms
  • Right amount of current these birds cannot feel pain
417
Q

What happens in bleeding at abattoirs?

A
  • Needs to be done while still unconscious, it will be unconscious for 60-90s
  • Cut both carotid and jugulars, dead in 17s. Knife or automatic neck cutters
  • Blood pressure drops heart still beating. Isoelectric brain death
  • Must have licensed slaughter person after to make sure every bird is cut
  • Have to bleed for 90s by law to make sure they are dead
418
Q

What happens in scalding at abattoirs?

A
  • Tank of hot water
  • Loosen feather follicles
  • 220,000 birds a day, water not replaced – stops being water after a while
  • Will kill most pathogenic bacteria but not all
  • This area is hot, feathers and faces put into the air – definitely getting campylobacter
419
Q

What do pluckers do at abattoirs?

A

Rubber fingers attached to discs that spin to beat all the feathers off

420
Q

What is the purpose of whole bird inspection at abattoir?

A

Allowed to use trained, qualified and supervised by OV vet plant staff. First chance to remove any obviously diseased birds. Peri-cloacal cellulitis – one side of the vent is slightly more yellow than the other, men can’t see this, women are so much better at seeing this.

421
Q

What is the purpose of the venter and eviscerator at abattoir?

A

Carousel makes a cut and pulls this out in a vacuum and eviscerate pulls this out. Offal hangs off a clip with corresponding bird. In an enclosed area for health and safety.

422
Q

Name and describe the final stages at poultry abattoirs.

A
  • Offal inspection
  • Crop removal – manually or by machine
  • Neck cracker – there is always the possibility of contamination of necks with crop contents. Machine made meat – pet food, chicken nuggets
  • Lung sucker – removes any remaining lung tissue by application of a vacuum whilst scraping internal cavity
423
Q

What is the only thing allowed to remain in poultry carcasses?

A

Kidneys

424
Q

What is colisepticaemia in post mortem inspection?

A

Polyserositis, all serosa get inflamed and fill with pus, older the lesion the more flaky it will be. Organs are full of pus

425
Q

What is the result of birds with ascites at abattoir?

A

Birds with ascites can drown as they stand, can cook in their own fluid, liver hardens

426
Q

What is green leg disease at post mortem inspection?

A

Haemorrhaging as an older lesion

427
Q

What is peri-cloacal cellulitis on post mortem inspection?

A

Slightly yellower on 1 side of the vent. Unfit for human consumption. Very easy to miss os gets through the system a lot. Coliform infection. Selling it = breaks the law

428
Q

How are uncut birds a huge welfare issue?

A

Uncut birds in electrical abattoirs – massive welfare issue. Bird has recovered from epilepsy and conscious for scalding.

429
Q

What is scabby hip on post mortem inspection?

A

Necrotic pus below the skin

430
Q

What is necrotic dermatitis on post mortem inspection?

A

Clostridial infection, looks cooked in this area. Causes gangrene in humans

431
Q

What is focal hepatic necrosis on post mortem inspection?

A

Clostridial perfringes produces specific pattern, happens because we withdraw food from the birds and bacteria proliferate.

432
Q

How is jaundice distinguished from corn fed poultry?

A

Jaundice will have liver enlargement

433
Q

What is oregon disease on post mortem inspection?

A

Supracoracoideus muscle lifts the wing up, has a membrane over this. Muscle expands if flapping madly, crushes against membrane and muscle dies off

434
Q

How quickly can pericarditis be developed in poultry?

A

24h

435
Q

What is the appearance of traumatic peritonitis by a metal object in poultry post mortem inspection?

A

Black inside

436
Q

What is the result of poultry with tumours?

A

Unfit for human consumption

437
Q

What are craters on the skin indicative of in poultry post mortem inspection?

A

SCC/avian kertaocanthoma = unfit for human consumptions

CVSOH 4 (25 decks)

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