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describe housing
enclosures made of synthetic nonporous material, sealed wood, plexiglass
vertical for arboreal species, horizontal for terrestrial species
larger enclosures are better
provide basking light reaching maximum temperature of 100-105 degrees
recommended humidity for tropical species 80-90%, desert species require 30-50%
UVB lighting necessary for vitamin D synthesis and calcium absorption
substrates: newspaper, artificial turf, aspen bedding, cypress, mulch
nutrition for herbivores (lizards)
grasses, leaves, vegetables and fruit
moderate to high fiber and moderate to low fat and protein
alfalfa to provide protein source, fed in moderation
don’t feed dog and cat food
avoid parsley, spinach and chives (may reduce calcium level)
nutrition for carnivores (lizards, snakes)
prey, small mammals, birds, or other reptiles
high protein diet with moderate fat and low fiber
immature rodents should be coated with a calcium supplement
avoid feeding live prey, may cause injury to reptile
nutrition for insectivores (lizards)
crickets, mealworms and waxworms
insects must be fed a nutrient rich diet for up to 2 days before being offered to the reptile
gut loading
nutrition for omnivores (lizards)
plant and prey items
water: depending on the species water may be offered in a dish, misting, or dripping system
restraint/handling in lizards
restrain head first
secure the head by placing the index finger and thumb around base of mandible; use free hand to hold rear legs and tail
do not grab the tail; some lizards lose the distal part of their tail as a defense mechanism
calming trick: some species calm down when both eyes are covered (use cotton balls or gauze) and warp around head with bandaging material; produces vagal stimulation
venipuncture sites: ventral coccygeal (tail) vein; jugular vein; ventral abdominal vein
restraint and handling in chelonians (turtles and tortoises)
nonaggressive: safe handling by grasping both sides of shell
restrain head by grasping base of skull at the mandible with index finger and thumb; use gentle traction to extend head and neck; excessive pressure may lead to injury of cervical spine
venipuncture sites: jugular vein, subcarapacial venous sinus (just above the head and underneath shell at midline), dorsal coccygeal vein
handling and restraint in snakes
restrain by grasping head at level of mandible, support body with the other hand
needs to be an additional handler for every 3-4 feet of snake to support the snake’s spine
never drape snakes over a persons neck
who should not receive ivermectin since it is toxic?
chelonians, indigo snakes, or debilitated snakes
toxicity leads to neurologic defects and often death
diseases in lizards
metabolic bone disease
renal disease
urinary calculi
gout
parasites
bacterial (gram negative most common)
fungal
zoonotic diseases (salmonella)
viral (adenovirus, west nile virus, herpes virus)
metabolic bone disease in lizards
malnutrition and lack of exposure to UVB light leads to decreased synthesis of vitamin D3 which is essential for calcium absorption and metabolism
clinical signs: weakness, lethargy, stunted growth, muscle fasciculations, abnormal gait or posture, fractures, soft mandible
without treatment and correct husbandry this condition is fatal
parasites in lizards
ticks, mites
trematodes, cestodes (tapeworm), nematodes (roundworm)
oxyurids: often present in low numbers without causes disease
Entamoeba invadens: may cause severe GI disease
Cryptosporidium: when associated with disease, does not respond to therapy and fatal
blood parasites: usually do not cause disease, rarely anemia in some patients
fungal disease in lizards
localized and systemic infections have been associated with Aspergillus, Candida, Cryptococcus, and Chrysosporium
salmonella in lizards
normal inhabitant of reptile gut flora, intermittently shed in feces
no successful technique to eliminate shedding of these organisms
may result in severe GI disease in humans
adenovirus in lizards
nonspecific clinical signs (neurologic, poor body condition, death)
transmission though to be fecal oral route; no treatment currently available
west nile virus in lizards
recently identified in crocodiles, unsure role of reptiles in route of transmission
herpes virus in lizards
may cause wart like growths on skin, associated with stomatitis, disease in the liver, lung, or spleen
no treatment
diseases in snakes
malnutrition
obesity
parasitic
bacterial: opportunistic gram negative bacteria
fungal dermatitis
viral
cancer
zoonotic diseases (salmonellosis)
parasites in snakes
ticks, snake mites (may lead to anemia)
Cryptosporidium serpentis: either asymptomatic carrier or gastroenteritis; antibiotics reduce shedding
Coccidian parasites: treatment is sulfonamides
Entamoeba invadens: fecal-oral transmission; clinical signs include HGE, dehydration, muscle wasting, death
inclusion body disease in snakes
suspect cause retrovirus
causes neurologic disease, weight loss, abnormal shedding, and secondary infections
no treatment
transmission suspected association with snake mites
herpes virus in snakes
isolated from lesions in liver, pancreas, kidney, and adrenal cortex
no treatment
adenovirus in snakes
associated with liver damage
Paramyxovirus in snakes
transmission through contact with contaminated respiratory secretions
clinical signs: nasal discharge, pus and blood tinged discharge from glottis, neurologic disease
no treatment
Campylobacter in snakes
bacteria naturally harbored by snakes
may cause disease in humans
wear gloves when cleaning cages and clean with sodium hypochlorite
common snake mite
can bite people leading to dermatitis
does not stay on humans
diseases in chelonians
Hypovitaminosis A
metabolic bone disease
gout
hepatic lipidosis
accelerated growth or early maturity
zoonotic diseases: Salmonella, Mycobacterium, Campylobacter, Chlamydia, Yersinia, Vibrio, Aermonas, and E.coli
hypovitaminosis A in chelonians
vitamin A deficiency
many clinical signs associated with degeneration of epithelial surfaces
gout in chelonians
increased production of uric acid results in ingestion of excessive protein
decreased excretion of uric acid may be due to dehydration or kidney disease
hepatic lipidosis in chelonians
normal physiologic process during hibernation or during egg formation
lipidosis can also be a pathologic process in obese or anorexic chelonians
clinical signs: obesity, lethargy, weight loss, infertility, abnormal feces, anorexia
accelerated growth or early maturation in chelonians
occurs in juveniles or hatchlings fed high protein diets
associated with renal disease, skeletal deformities and high mortality