Lecture 1: Exotics and Wildlife Flashcards
1
Q
What is an extremely common disease reptiles suffer from:
A
almost all with metabolic bone disease
2
Q
4 Goals for exotic nutrition
A
- Growth
- Health/longevity
- Decreased disease
- Breeding success
3
Q
4 Feeding strategies that we should strive for, for exotics?
A
- Nutritionally balanced
- Natural behaviour
- Consistently eaten
- Practical/economical
4
Q
What species does aflatoxicosis affect?
A
birds
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
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
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
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
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
10
Q
4 impacts of excess energy diets on rabbits
A
o Obesity
o Pododermatitis
o Urinary tract disease
o Dental disease
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
12
Q
How do cecotrophs differ from regular stool
A
- Cecotrophes = mucus
o High in vit B and K + 2x protein + ½ fibre
13
Q
What happens is coprophagy is prevented/inhibited
A
- Without coprophagy = abnormal stool
14
Q
What is a factor that increases coprophagy
A
- Highest cecotroph consumption when fed high non-digestible fibre diet
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
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
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
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)
19
Q
What is a common dietary related ferret disease
A
insulinoma
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)
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
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
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)
24
Q
4 Factors affecting Volume/Frequency of Feeding
A
- Age
- Reproductive status
- Season/daylight hours
- Temperature (hibernation/brumation)
25
What are 6 Common Nutritional Diseases affecting exotics?
Metabolic Bone Disease
Hypovitaminosis A
Vitamin E/Se Deficiency
Thiamin Deficiency
Vitamin C deficiency
Obesity
26
What are the 3 conditions of metabolic bone disease
ricketts
osteomalacia
fibrous osteodystrophy
27
What are the features of ricketts
* Rickets: young/growing animals – vit D or Ca deficiency
o Affects growth plates/physis of bone
28
What are the features of osteomalacia
* Osteomalacia: old – mineral loss = softening bone
29
What are the features of fibrous osteodystrophy
* Fibrous osteodystrophy: bone replaced with fibrous material
o Common – nutritional secondary hyperparathyroidism
30
3 factors affecting metabolic bone disease development
* Multifactorial
o Ca deficiency
o Ca:P imbalance (usually 2:1)
o Vit D deficiency
31
What are 3 sources of vit D? how does it differ for certain species (reptiles/birds)
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
What types of Vit D are utilized by the body? how does that change depending on species
* Vit D2: mammals can utilize
* Vit D3: utilized by new world primates/birds/fish (can’t use D2)
33
Clinical signs of metabolic bone disease
* 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
How is metabolic bone disease diagnosed
* 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
How to treat metabolic bone disease
* 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
How to prevent metabolic bone disease
* 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
How to prevent metabolic bone disease for insectivore reptiles
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
What common food items are deficient in Ca
o Ca deficient foods: seeds/muscle/organ/fruit/grain/insects
39
What are the uses of vit A in the body
* Vit A: used for cell replication/vision/bone remodelling/epithelium integrity/immune function
40
What foods are deficient in Vit A
* Vit A deficient food: all meat + seeds
41
What are the common clinical signs of hypovitaminosis A in birds
* 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
What are the common clinical signs of hypovitaminosis A in reptile
* 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
What are the common clinical signs of hypovitaminosis A in rabbits
* Clinical signs rabbits: neonates
o Hydrocephalus
o Still birth
44
What are the common clinical signs of hypovitaminosis A in all animals
* Clinical signs (common to all): poor fertility/growth rates/blindness
45
How to treat hypovitaminosis A
* Tx: vit A injection + dietary change (dark leafy green/liver/pellets)
o Tortoises = only dietary change required
46
How to prevent hypovitaminosis A
* Prevention: dietary retinol/beta carotene/carotenoids
o Supplement not required for animals fed whole prey
47
Function of Se/Vit E in boddy
* VitE/Se: reduce ROS, reproductive, MSK, circulation, nervous, immune
48
What species is vit E/Se def common?
* Deficiency common in: guinea pig, hamsters, fish, ruminants + some wildlife (E NA, AB)
49
What are the clinical signs of Vit E/Se deficiency
* 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
how to treat Vit E/Se def
* Tx: injections if mild, supportive care if severe (poor prognosis)
51
How to prevent vit E/Se def
* 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
What species does thiamine deficiency affect
* Common affect fish eater – pelican/penguin/marine mammal/snake/amphibian/fish
53
Why does thiamine deficiency occur
* Thiaminase activated after death in fish – enhanced by freezing
54
how does thiamine deficiency present clinically
* 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
How to treat thiamine deficiency
* Tx; dietary supplement
56
What species does vit C deficiency affect most
* Affecting: primates/bats/cavies/birds (some – swallow/bulbuls)/fish/cetaceans (some)
57
What does a lack of Vit C do?
* Lack enzyme that converts glucose to ascorbic acid
58
How does vitamin C def present clinically?
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
How to treat Vit C def
* Tx: fortified diets (feed within 90 days)
o If excess in fruit bat/lemurs = Fe toxicity (hemosiderosis or hemochromatosis)
60
What is the most common medical problem in captive animals
obesity
61
What does obesity predispose to?
o Predispose to
Dystocia
Hepatic lipidosis
Atherosclerosis (parrot)
Pododermatittis
Uroliths
Dental dz (rabbit)
62
How is obesity in rabbits linked to kidney dz?
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
What are the clinical signs of kidney dz in rabbits
Frequent urination/inappropriate urination/incontinence/stranguria
Hunched/bruxation
Urine sludge
Hematuria
Anorexia
64
What does rabbit dental dz clinically present as?
o Spurs/points/overgrown
o Slobbers
o Anorexia
o GI stasis/dysbiosis
o hepatic lipidosis
65
What common issue is rabbit dental dz related to
obesity
66
What type of diet is ideal for mature and young/lactating rabbits
* 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
List some reasons why hay is beneficial for rabbits
* 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
What common dz is obesity linked to in birds? What species of birds are most affected?
o Common; African grey/amazon
atherosclerosis
69
What are the risk factors of atherosclerosis in birds
o Risks: high fat/cholesterol diet, low activity, age, hepatic lipidosis, R-side heart fail
70
What are the clinical signs of atherosclerosis in birds?
o Clinically:
Death
Dyspnea
Lethargy
Paresis
