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VETM 465 Nutrition > Lecture 1: Exotics and Wildlife > Flashcards

Lecture 1: Exotics and Wildlife Flashcards

1
Q

What is an extremely common disease reptiles suffer from:

A

almost all with metabolic bone disease

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2
Q

4 Goals for exotic nutrition

A
  • Growth
  • Health/longevity
  • Decreased disease
  • Breeding success
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3
Q

4 Feeding strategies that we should strive for, for exotics?

A
  • Nutritionally balanced
  • Natural behaviour
  • Consistently eaten
  • Practical/economical
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4
Q

What species does aflatoxicosis affect?

A

birds

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5
Q

What is aflatoxicosis caused by? What is its pathological mechanism? How to prevent?

A
  • Mycotoxin: Aspergillus spp.
  • Chronic ingestion from seeds/peanuts stored incorrectly
  • Path: hepatic fibrosis/cirrhosis + hepatic carcinoma
  • Prevent: storage (dry), use human grade products
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6
Q

What type of digester is a rabbit?

A
  • Monogastric hindgut fermenters/concentrate selectors (select high protein/energy food)
    o Bacteroides microbes
    o 40% ingesta in cecum
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7
Q

How can a rabbit’s diet affect the onset of respiratory disease

A
  • Diet can affect respiratory disease: ex. Pasteurellosis
    o Excess protein = excess ammonia = irritate nasal mucosa
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8
Q

What are 6 main impacts of a high forage diet for rabbits

A
  • High forage diet: essential for secretion/digestion/absorption/peristalsis/cell regeneration/excretion
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9
Q

5 impacts of a low forage diet on rabbits

A

o Barbering
o Trichobezoars
o GI stasis (secondary lipidosis)
o Lethargy/anorexia
o Death

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10
Q

4 impacts of excess energy diets on rabbits

A

o Obesity
o Pododermatitis
o Urinary tract disease
o Dental disease

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11
Q

How are cecotrophs created

A
  • Large and small fibres separated
    o Large particles = indigestible and excreted as fecal pellets
    o Small particles = digestible = reverse peristalsis back to cecum = ferment into cecotrophes
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12
Q

How do cecotrophs differ from regular stool

A
  • Cecotrophes = mucus
    o High in vit B and K + 2x protein + ½ fibre
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13
Q

What happens is coprophagy is prevented/inhibited

A
  • Without coprophagy = abnormal stool
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14
Q

What is a factor that increases coprophagy

A
  • Highest cecotroph consumption when fed high non-digestible fibre diet
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15
Q

Explain the physiology of a ferret and how does it relate to its diet

A
  • Obligate carnivores
  • Short GI tract = tube (no cecum/ileocolic valve)
    o Spontaneous secretion of HCl
    o Low gut flora
    o Few brush border enzymes
  • Small frequent meals (every 3hrs) – 10+ throughout the day
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16
Q

How does a ferret’s weight fluctuate seasonally? Why?

A
  • Daylight regulates food intake/weight
    o Gain weight in winter/seasonal obesity = normal
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17
Q

What are important characteristics of a ferret diet?

A

o High protein and fat: >35% protein + >20% fat
o Low carbohydrate and fibre: <5%
o 1st 3 ingredient should be animal protein

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18
Q

What foods should ferrets avoid? Why?

A
  • Avoid: dog/cat kibble
    o Excess carbohydrates/grain/fibre = urolithiasis via plant protein/struvite (dog food)
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19
Q

What is a common dietary related ferret disease

A

insulinoma

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20
Q

What is an insulinoma? How common of it is for ferrets?

A

o Insulinoma: B cell tumor (excess insulin production)
 25% all neoplasia
 High carb diet
 Uncommon in EU/Australia/New Zealand (better diets there)

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21
Q

Clinical signs of insulinoma in ferrets

A

 Clinically;
* Episodic hypoglycemia
* Lethargy
* Hind end ataxia/weakness
* Nausea (hypersalivation/pawing at mouth)
* Depression
* Seizure
* Star gazing

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22
Q

How to diagnose insulinoma in ferrets?

A
  • Low fasting blood glucose
  • Neurologic signs stop after meal
  • Imaging not required/helpful – tumor usually small
  • Biopsy and histo for definitive diagnosis
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23
Q

How to manage insulinoma in ferrets? What is the role of sx? What is the prognosis?

A
  • Glucocorticoids (prednisone) – first line tx
  • Diazoxide (inhibit pancreatic insulin release – expensive
  • Dietary change (high protein + low carb)
  • Client education: corn syrup for hypoglycemic events

 Sx
* Palliative
* Excise
* Will reoccur
* Rarely metastatic
 Survival 1-3 years (in dogs and cats = poorer prognosis)

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24
Q

4 Factors affecting Volume/Frequency of Feeding

A
  • Age
  • Reproductive status
  • Season/daylight hours
  • Temperature (hibernation/brumation)
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25
Q

What are 6 Common Nutritional Diseases affecting exotics?

A

Metabolic Bone Disease
Hypovitaminosis A
Vitamin E/Se Deficiency
Thiamin Deficiency
Vitamin C deficiency
Obesity

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26
Q

What are the 3 conditions of metabolic bone disease

A

ricketts
osteomalacia
fibrous osteodystrophy

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27
Q

What are the features of ricketts

A
  • Rickets: young/growing animals – vit D or Ca deficiency
    o Affects growth plates/physis of bone
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28
Q

What are the features of osteomalacia

A
  • Osteomalacia: old – mineral loss = softening bone
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29
Q

What are the features of fibrous osteodystrophy

A
  • Fibrous osteodystrophy: bone replaced with fibrous material
    o Common – nutritional secondary hyperparathyroidism
30
Q

3 factors affecting metabolic bone disease development

A
  • Multifactorial
    o Ca deficiency
    o Ca:P imbalance (usually 2:1)
    o Vit D deficiency
31
Q

What are 3 sources of vit D? how does it differ for certain species (reptiles/birds)

A
  1. Absorb directly via diet
    a. Many reptiles cannot injest adequate amounts – require UVB/heat
  2. Sunlight/UVB + heat source = vit D precursor production on skin > liver > kidney
    a. Heat and UVB must be associated/simultaneous
  3. Birds: uropygial gland creates Vit D3 precursors which are activated by UVB (ingested when they preen)
  4. Reptiles have endolymphatic sacs in back of mouth – can see on radiograph
32
Q

What types of Vit D are utilized by the body? how does that change depending on species

A
  • Vit D2: mammals can utilize
  • Vit D3: utilized by new world primates/birds/fish (can’t use D2)
33
Q

Clinical signs of metabolic bone disease

A
  • Clinically:
    o Lameness
    o Bone deformities
    o Fractures/bone softening
    o Swollen jaws/tooth loss
    o Hypocalcemic tetany
    o Deformed shells - turtle
    o Paralysis - lizards
    o Poor feathering/deformed eggs
    o Reluctance to climb
34
Q

How is metabolic bone disease diagnosed

A
  • Dx: via hx and clinical signs
    o Facial/long bone swelling (primate/carnivore) + osteodystrophy
    o Radiographs
    o Ionized Ca (total serum Ca not useful – regulated by body)
    o Plasma VitD
35
Q

How to treat metabolic bone disease

A
  • Tx:
    o Acute: calcium gluconate IV (if seizures)
    o Chronic: dietary Ca:P supplement + vit D supplementation (ensure not using products with high vit A – toxicosis risk)
    o Euth
36
Q

How to prevent metabolic bone disease

A
  • Prevention: balanced diet/supplements
    o Pre-killed + properly stored (freeze <6months, thawed properly – don’t exceed 40C)
    o Access to UVB (290-315nm)
     Careful of expiration dates/distance from animal/basking/measure levels/mesh (will cut out UV rays)/ plastic vs glass
    o Stay in preferred optimal temperature/humidity zone (POTHZ)
37
Q

How to prevent metabolic bone disease for insectivore reptiles

A

o Insect diets:
 gut loading insect diets (24-48 hours before) AND dusting in Ca – must eat quickly (or else not humane)
 variation in diet: earthworm/captive hornworm as treat/cricket/crustacean (pill bugs)

38
Q

What common food items are deficient in Ca

A

o Ca deficient foods: seeds/muscle/organ/fruit/grain/insects

39
Q

What are the uses of vit A in the body

A
  • Vit A: used for cell replication/vision/bone remodelling/epithelium integrity/immune function
40
Q

What foods are deficient in Vit A

A
  • Vit A deficient food: all meat + seeds
41
Q

What are the common clinical signs of hypovitaminosis A in birds

A
  • Clinical signs birds: common in parrots
    o White plaques in mouth/esophagus
    o Blunting of choanal papilla
    o Conjunctivitis/sinusitis
    o Respiratory infection
    o Poor growth
    o Ataxia
    o Gout
    o Occlusion of uropygial gland = abnormal feathers
    o Squamous metaplasia of salivary glands
42
Q

What are the common clinical signs of hypovitaminosis A in reptile

A
  • Clinical signs reptile: common in red eared slider/leopard gecko
    o Short-tongue syndrome – plugged mucus gland
    o Lethargy
    o Weigh loss/wasting
    o Conjunctival swelling
    o Dermal and bone lesions
43
Q

What are the common clinical signs of hypovitaminosis A in rabbits

A
  • Clinical signs rabbits: neonates
    o Hydrocephalus
    o Still birth
44
Q

What are the common clinical signs of hypovitaminosis A in all animals

A
  • Clinical signs (common to all): poor fertility/growth rates/blindness
45
Q

How to treat hypovitaminosis A

A
  • Tx: vit A injection + dietary change (dark leafy green/liver/pellets)
    o Tortoises = only dietary change required
46
Q

How to prevent hypovitaminosis A

A
  • Prevention: dietary retinol/beta carotene/carotenoids
    o Supplement not required for animals fed whole prey
47
Q

Function of Se/Vit E in boddy

A
  • VitE/Se: reduce ROS, reproductive, MSK, circulation, nervous, immune
48
Q

What species is vit E/Se def common?

A
  • Deficiency common in: guinea pig, hamsters, fish, ruminants + some wildlife (E NA, AB)
49
Q

What are the clinical signs of Vit E/Se deficiency

A
  • Clinically: species dependent
    o White muscle disease
    o Stiffness/paralysis – skeletal muscle necrosis + mineralization
    o Cardiomyopathy = sudden death if stressed
    o Ill thrift/lethargy (guinea pig/deer)
    o Conjunctivitis (Guinea pig)
    o Neurologic/opisthotonos (birds) – encephalomalacia
    o Steatites (reptiles) – inflame/mineralization of fat
50
Q

how to treat Vit E/Se def

A
  • Tx: injections if mild, supportive care if severe (poor prognosis)
51
Q

How to prevent vit E/Se def

A
  • Prevention: dietary requirement met – species variation
    o Fish/high fat supplement
    o Measure serum Vit E
    o Follow expiry on dry food
    o Neonatal hoofstock – supplement injection within 1-2 days in deficient area
52
Q

What species does thiamine deficiency affect

A
  • Common affect fish eater – pelican/penguin/marine mammal/snake/amphibian/fish
53
Q

Why does thiamine deficiency occur

A
  • Thiaminase activated after death in fish – enhanced by freezing
54
Q

how does thiamine deficiency present clinically

A
  • Clinically
    o Anorexia/weight loss
    o Ataxia/limb paralysis
    o Tremor/seizure
    o Stargazing
    o Cardiac fail
    o Loss of equilibrium/edema/poor fish growth
55
Q

How to treat thiamine deficiency

A
  • Tx; dietary supplement
56
Q

What species does vit C deficiency affect most

A
  • Affecting: primates/bats/cavies/birds (some – swallow/bulbuls)/fish/cetaceans (some)
57
Q

What does a lack of Vit C do?

A
  • Lack enzyme that converts glucose to ascorbic acid
58
Q

How does vitamin C def present clinically?

A

o Poor coat/skin
o Lameness
o Stomatitis
o Broken back disease (fish)
o Long bone swelling (epiphysis)/fractures
o Susceptible to dz
o Anorexia
o Diarrhea

59
Q

How to treat Vit C def

A
  • Tx: fortified diets (feed within 90 days)
    o If excess in fruit bat/lemurs = Fe toxicity (hemosiderosis or hemochromatosis)
60
Q

What is the most common medical problem in captive animals

A

obesity

61
Q

What does obesity predispose to?

A

o Predispose to
 Dystocia
 Hepatic lipidosis
 Atherosclerosis (parrot)
 Pododermatittis
 Uroliths
 Dental dz (rabbit)

62
Q

How is obesity in rabbits linked to kidney dz?

A

o Obesity and kidney dz linked
o Risk of uroliths
o Risk factors; obesity/low exercise/alfalfa/over supplemented with vit/mineral
o Ca regulation: serum Ca not narrowly regulated/excrete in urine = sludge

63
Q

What are the clinical signs of kidney dz in rabbits

A

 Frequent urination/inappropriate urination/incontinence/stranguria
 Hunched/bruxation
 Urine sludge
 Hematuria
 Anorexia

64
Q

What does rabbit dental dz clinically present as?

A

o Spurs/points/overgrown
o Slobbers
o Anorexia
o GI stasis/dysbiosis
o hepatic lipidosis

65
Q

What common issue is rabbit dental dz related to

A

obesity

66
Q

What type of diet is ideal for mature and young/lactating rabbits

A
  • Rabbit diet:
    o Growing/lactating: high protein (16-18%) + >16% fibre, grass/legume hay
    o Adults: timothy hay (high fibre/low fat)
    o <15% fibre = diarrhea/anorexia
67
Q

List some reasons why hay is beneficial for rabbits

A
  • Why is Hay good for rabbits
    o Benefit Ca:P ratio
    o Behavioural enrichment
    o Reduce aggression/excessive grooming/barbering
    o Inappropriate chewing
    o Reduce obesity/pododermatitis
    o Reduce urolith/dental/infectious dz
68
Q

What common dz is obesity linked to in birds? What species of birds are most affected?

A

o Common; African grey/amazon

atherosclerosis

69
Q

What are the risk factors of atherosclerosis in birds

A

o Risks: high fat/cholesterol diet, low activity, age, hepatic lipidosis, R-side heart fail

70
Q

What are the clinical signs of atherosclerosis in birds?

A

o Clinically:
 Death
 Dyspnea
 Lethargy
 Paresis

VETM 465 Nutrition (4 decks)

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