Reptiles 4 Non-Infectious Diseases Flashcards
Most common presentation of pet reptiles
Anorexia
Anorexia in reptiles
- common?
- specificity?
> what should we check?
- Tx?
- Most common presentation of pet reptiles
<> - Non-specific:
- Any disease will cause anorexia
- Check husbandry
- Check the type of food offered
- Do general workup (i.e., physical examination, blood work, imaging, fecal testing)
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Treatment can be long - Supportive care
- Assisted feeding
> Esophagostomy tubes in chelonians
Metabolic Bone Disease
- categories we see
- Nutritional secondary hyperparathyroidism
- Renal secondary hyperparathyroidism
Metabolic Bone Disease
* Nutritional secondary hyperparathyroidism
> Causes
- Lack of UVB
- Improper Ca:P ratio (2:1) in diet
- Ca deficiencies
Reptile Vitamin D3 metabolism
- In most snakes, crocodilians, some chelonians, and some amphibians, a nocturnal lifestyle or ingestion of whole prey has allowed vitamin D3 to be primarily or completely obtained from the diet.
- However, diurnal, insectivorous, or herbivorous reptiles (particularly lizards, some chelonians, and some amphibians) require UVB exposure to activate the cholecalciferol pathway.
- Under natural conditions, reptiles synthesize vitamin D3 when exposed to sunlight.
- UV light in the spectrum (290–320 nm) reacts to convert cholesterol to the inactive
form of vitamin D3 in the skin; this vitamin D3 is then converted to 1,25-
dihydroxycholecalciferol (calcitriol) through the liver and kidneys. - Calcitriol is then used to facilitate the absorption of calcium from the intestinal
tract. - In captivity, an alternative to natural sunlight that mimics the spectrum of natural
light is required; these UV lights are often a poor replacement for natural sunlight,
and natural sunlight should be provided whenever possible. - When an animal cannot be provided with proper exposure to UV light, vitamin D3
supplementation can be considered; however, risks associated with hypervitaminosis D.
Metabolic Bone Disease
- signs
- Bone malformations
- Osteomalacia
- Fibrous osteodystrophy
- Pathologic fractures
- Stunting
- Neurological signs
- Muscular signs
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clinical cases of nutritional secondary hyperparathyroidism
> what happens / pathogenesis
> why do we see the signs that we do?
- In clinical cases of nutritional secondary hyperparathyroidism, excessive production of parathyroid hormone (PTH) from the parathyroid gland occurs in response to the diet or husbandry-related hypocalcemia.
- PTH increases blood calcium by stimulating bone resorption and renal tubular reabsorption of calcium; also stimulates the formation of 1,25- dihydroxycholecalciferol, which increases the absorption of intestinal calcium.
- Phosphorus excretion by the kidney is increased.
- Calcium deficiency can increase the threshold potential of nerves and muscles,
causing partial depolarization; spastic tremors and twitching of the digits.
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Signs - Bone malformations
- Osteomalacia
- Fibrous osteodystrophy
- Pathologic fractures
- Stunting
- Neurological signs
- Muscular signs
Metabolic Bone Disease diagnostics
- Total calcium
- Phosphorus
- Ionized calcium
- Radiographs
<><> - Also renal with the Ca:P ratio.
Metabolic Bone Disease Tx
Improve husbandry:
* UVB
* Dietary calcium supplementation
* Temperature
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Medical treatment
* Injectable calcium if iCa low (seizuring, tremors)
* Daily oral calcium
* Vitamin D3 weekly injections or oral supplementation
Metabolic Bone Disease
* Renal secondary hyperparathyroidism
- common in what animals?
> what do they need
- what is the problem with the kidneys here, and result?
- Common in chameleons
<> - Need high humidity
- Dripping water/misting/fogging for drinking
<> - Failing kidneys do not convert vitamin D3 to active form (calcitriol), and do not excrete phosphorus.
Hypovitaminosis A
- mostly in what reptiles? why? what do they require?
- Mostlyin carnivorous/insectivorous reptiles
- Cannot convert β-carotenes to vitamin A
- Require supplement with pre-formed vitamin A
Hypovitaminosis A
- clinical signs
- Blepharedema, lachrymal and periocular gland distention
> Leopard geckos
> Red-eared sliders - Squamous metaplasia
- Gular edema in chameleons
- Immune suppression
Hypovitaminosis A
- properties of vitamin A
> functions
> forms
> enzymes for use?
> common in what animals? why?
- Vitamin A is a fat-soluble vitamin and an essential nutrient for humans. It is a group of organic compounds that includes retinol, retinal (also known as retinaldehyde), and retinoic acid. Vitamin A has multiple functions: it is essential for embryo development and growth, for maintenance of the immune system, and for vision, where it combines with the protein opsin to form rhodopsin – the light- absorbing molecule necessary for both low-light (scotopic vision) and color vision.
- Vitamin A occurs as two principal forms in foods: a) retinol (vitamin A1), found in animal-sourced foods, either as retinol or bound to a fatty acid to become a retinyl ester, and b) the carotenoids, alpha-carotene, β-carotene, gamma-carotene, and the xanthophyll beta-cryptoxanthin (all of which contain β-ionone rings), that function as provitamin A in animals which possess the enzymes that cleave and convert provitamin carotenoids to retinal and then to retinol.
- Herbivore and omnivore species possess this enzyme; some carnivore species lack this enzyme (but receive retinol in their animal-sourced diet).
- Vitamin A deficiency is common in all captive insectivorous reptiles, including leopard geckos, chameleons, and anoles. It is thought to result from dietary deficiency since a) it is unknown if insectivorous lizards can synthesize vitamin A from carotenoids in their diet, b) feeder insects are generally deficient in vitamin A and often receive vitamin A-deficient diets, and c) many food manufacturers omit vitamin A and substitute β-carotene in reptile multivitamins because of misinformation that vitamin A is toxic to insectivores.
Hypovitaminosis A Dx, Tx
Diagnosis:
* History
* Response to treatment
* Blood and liver vitamin A levels
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Treatment:
* Slow response
* Injectable (once) or oral vitamin A
* Be cautious about hypervitaminosis A
Hepatic Lipidosis
- is it common? in what animals?
- Very common
- Bearded dragons
- Female reptiles
Hepatic Lipidosis causes
- Accumulation of triglycerides in the liver
- Likely related to diet
- Estrogen-induced lipogenesis in lots of reptiles (like birds, but more extreme)
Hepatic Lipidosis Dx
Biochemistry:
* Unreliable
* Elevation in bile acids
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Imaging
* Hyperechoic liver on ultrasound
* Low density on CT
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Liverbiopsy
* Coelioscopy
Hepatic Lipidosis Tx
- Improve husbandry
- Improve diet
> Low fat invertebrates
> Switch to primary herbivorous - Chronic assisted feeding
- Drugs–currently being studied
> Gemfibrozil
> Carnitine
Constipation / Impaction
- common in what species? what causes this?
- Dx
- Tx
Common in all species
* Fecalith
* Undigested food
* Substrate, rocks
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Diagnosis
* Coelomic palpation
* Diagnostic imaging
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Treatment
* Enema
* Soaking
* Correct husbandry
* Vibration
* Enterotomy (uncommon)
Cloacal Prolapse
* What can be included in the prolapse?
- Cloaca (coprodeum)
- Rectum/colon
- Oviduct
- Phallus/hemipenes
- Bladder (chelonians)
Cloacal Prolapse
* Common causes
- Intestinal diseases
> GI parasitism
> Enteritis
> Fecalith/impaction - Husbandry (calcium)
- Improper diet
- Straining
- Coelomic disease
Cloacal Prolapse Tx options
Medical treatment
* Depends on the cause
* Reduction + transverse cloacal sutures
* Supportive care
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Surgical treatment
* Coeliotomy
> Colonic prolapse > intestinal resection and anastomosis, or reduction and pexy
> Oviductal prolapse > hysterectomy
