Lecture 1: Exotics and Wildlife Flashcards
What is an extremely common disease reptiles suffer from:
almost all with metabolic bone disease
4 Goals for exotic nutrition
- Growth
- Health/longevity
- Decreased disease
- Breeding success
4 Feeding strategies that we should strive for, for exotics?
- Nutritionally balanced
- Natural behaviour
- Consistently eaten
- Practical/economical
What species does aflatoxicosis affect?
birds
What is aflatoxicosis caused by? What is its pathological mechanism? How to prevent?
- Mycotoxin: Aspergillus spp.
- Chronic ingestion from seeds/peanuts stored incorrectly
- Path: hepatic fibrosis/cirrhosis + hepatic carcinoma
- Prevent: storage (dry), use human grade products
What type of digester is a rabbit?
- Monogastric hindgut fermenters/concentrate selectors (select high protein/energy food)
o Bacteroides microbes
o 40% ingesta in cecum
How can a rabbit’s diet affect the onset of respiratory disease
- Diet can affect respiratory disease: ex. Pasteurellosis
o Excess protein = excess ammonia = irritate nasal mucosa
What are 6 main impacts of a high forage diet for rabbits
- High forage diet: essential for secretion/digestion/absorption/peristalsis/cell regeneration/excretion
5 impacts of a low forage diet on rabbits
o Barbering
o Trichobezoars
o GI stasis (secondary lipidosis)
o Lethargy/anorexia
o Death
4 impacts of excess energy diets on rabbits
o Obesity
o Pododermatitis
o Urinary tract disease
o Dental disease
How are cecotrophs created
- 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
How do cecotrophs differ from regular stool
- Cecotrophes = mucus
o High in vit B and K + 2x protein + ½ fibre
What happens is coprophagy is prevented/inhibited
- Without coprophagy = abnormal stool
What is a factor that increases coprophagy
- Highest cecotroph consumption when fed high non-digestible fibre diet
Explain the physiology of a ferret and how does it relate to its diet
- 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
How does a ferret’s weight fluctuate seasonally? Why?
- Daylight regulates food intake/weight
o Gain weight in winter/seasonal obesity = normal
What are important characteristics of a ferret diet?
o High protein and fat: >35% protein + >20% fat
o Low carbohydrate and fibre: <5%
o 1st 3 ingredient should be animal protein
What foods should ferrets avoid? Why?
- Avoid: dog/cat kibble
o Excess carbohydrates/grain/fibre = urolithiasis via plant protein/struvite (dog food)
What is a common dietary related ferret disease
insulinoma
What is an insulinoma? How common of it is for ferrets?
o Insulinoma: B cell tumor (excess insulin production)
25% all neoplasia
High carb diet
Uncommon in EU/Australia/New Zealand (better diets there)
Clinical signs of insulinoma in ferrets
Clinically;
* Episodic hypoglycemia
* Lethargy
* Hind end ataxia/weakness
* Nausea (hypersalivation/pawing at mouth)
* Depression
* Seizure
* Star gazing
How to diagnose insulinoma in ferrets?
- Low fasting blood glucose
- Neurologic signs stop after meal
- Imaging not required/helpful – tumor usually small
- Biopsy and histo for definitive diagnosis
How to manage insulinoma in ferrets? What is the role of sx? What is the prognosis?
- 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)
4 Factors affecting Volume/Frequency of Feeding
- Age
- Reproductive status
- Season/daylight hours
- Temperature (hibernation/brumation)
What are 6 Common Nutritional Diseases affecting exotics?
Metabolic Bone Disease
Hypovitaminosis A
Vitamin E/Se Deficiency
Thiamin Deficiency
Vitamin C deficiency
Obesity
What are the 3 conditions of metabolic bone disease
ricketts
osteomalacia
fibrous osteodystrophy
What are the features of ricketts
- Rickets: young/growing animals – vit D or Ca deficiency
o Affects growth plates/physis of bone
What are the features of osteomalacia
- Osteomalacia: old – mineral loss = softening bone
What are the features of fibrous osteodystrophy
- Fibrous osteodystrophy: bone replaced with fibrous material
o Common – nutritional secondary hyperparathyroidism
3 factors affecting metabolic bone disease development
- Multifactorial
o Ca deficiency
o Ca:P imbalance (usually 2:1)
o Vit D deficiency
What are 3 sources of vit D? how does it differ for certain species (reptiles/birds)
- Absorb directly via diet
a. Many reptiles cannot injest adequate amounts – require UVB/heat - Sunlight/UVB + heat source = vit D precursor production on skin > liver > kidney
a. Heat and UVB must be associated/simultaneous - Birds: uropygial gland creates Vit D3 precursors which are activated by UVB (ingested when they preen)
- Reptiles have endolymphatic sacs in back of mouth – can see on radiograph
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)
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
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
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
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)
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)
What common food items are deficient in Ca
o Ca deficient foods: seeds/muscle/organ/fruit/grain/insects
What are the uses of vit A in the body
- Vit A: used for cell replication/vision/bone remodelling/epithelium integrity/immune function
What foods are deficient in Vit A
- Vit A deficient food: all meat + seeds
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
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
What are the common clinical signs of hypovitaminosis A in rabbits
- Clinical signs rabbits: neonates
o Hydrocephalus
o Still birth
What are the common clinical signs of hypovitaminosis A in all animals
- Clinical signs (common to all): poor fertility/growth rates/blindness
How to treat hypovitaminosis A
- Tx: vit A injection + dietary change (dark leafy green/liver/pellets)
o Tortoises = only dietary change required
How to prevent hypovitaminosis A
- Prevention: dietary retinol/beta carotene/carotenoids
o Supplement not required for animals fed whole prey
Function of Se/Vit E in boddy
- VitE/Se: reduce ROS, reproductive, MSK, circulation, nervous, immune
What species is vit E/Se def common?
- Deficiency common in: guinea pig, hamsters, fish, ruminants + some wildlife (E NA, AB)
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
how to treat Vit E/Se def
- Tx: injections if mild, supportive care if severe (poor prognosis)
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
What species does thiamine deficiency affect
- Common affect fish eater – pelican/penguin/marine mammal/snake/amphibian/fish
Why does thiamine deficiency occur
- Thiaminase activated after death in fish – enhanced by freezing
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
How to treat thiamine deficiency
- Tx; dietary supplement
What species does vit C deficiency affect most
- Affecting: primates/bats/cavies/birds (some – swallow/bulbuls)/fish/cetaceans (some)
What does a lack of Vit C do?
- Lack enzyme that converts glucose to ascorbic acid
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
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)
What is the most common medical problem in captive animals
obesity
What does obesity predispose to?
o Predispose to
Dystocia
Hepatic lipidosis
Atherosclerosis (parrot)
Pododermatittis
Uroliths
Dental dz (rabbit)
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
What are the clinical signs of kidney dz in rabbits
Frequent urination/inappropriate urination/incontinence/stranguria
Hunched/bruxation
Urine sludge
Hematuria
Anorexia
What does rabbit dental dz clinically present as?
o Spurs/points/overgrown
o Slobbers
o Anorexia
o GI stasis/dysbiosis
o hepatic lipidosis
What common issue is rabbit dental dz related to
obesity
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
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
What common dz is obesity linked to in birds? What species of birds are most affected?
o Common; African grey/amazon
atherosclerosis
What are the risk factors of atherosclerosis in birds
o Risks: high fat/cholesterol diet, low activity, age, hepatic lipidosis, R-side heart fail
What are the clinical signs of atherosclerosis in birds?
o Clinically:
Death
Dyspnea
Lethargy
Paresis
