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NAVLE Exotic Exam Questions And Answers
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erythematous pruritic dermatitis of the chin that progresses to inguinal or perianal areas, brown crusts around face with nasal/ocular discharge, foot pad hyperkeratosis - ✔✔dermatologic clinical signs of canine distemper virus in ferrets fluorescent antibody testing or serum antibody titers - ✔✔diagnosis of canine distemper in ferrets very poor, 100% mortality - ✔✔prognosis of canine distemper in ferrets purevax D is the only USDA-approved distemper vaccine for ferrets, purevax is a recombinant canine vaccine - ✔✔prevention of canine distemper in ferrets middle aged to older ferrets, prevalence in US is 70%; most often caused by adrenal hyperplasia, resulting in uncontrolled release of sex hormones- NOT cortisol like in canine hyperadrenocorticism - ✔✔what is adrenal associated endocrinopathy in ferrets symmetric alopecia, sexually aggressive behavior, vulvar swelling, pruritis - ✔✔clinical signs of adrenal associated endocrinopathy in ferrets hyperestrogenism or seasonal alopecia - ✔✔differentials for adrenal associated endocrinopathy in ferrets occurs in intact females or caused by ovarian remnants - ✔✔hyperestrogenism in ferrets occurs in female and male ferrets during sexual activity - ✔✔seasonal alopecia in ferrets
blood levels of sex hormones (adrenal panel)- does not distinguish between intact female ferrets, remnant ovary, and hyperadrenocorticism; abdominal ultrasound; adrenal function tests will be normal - ✔✔diagnosis of adrenal associated endocrinopathy in ferrets adrenalectomy is treatment of choice, leuprolide which is a long-acting gonadotropin releasing hormone, deslorin which is long-acting gonadotropin releasing hormone - ✔✔treatment of adrenal associated endocrinopathy in ferrets good - ✔✔prognosis of adrenal associated endocrinopathy in ferrets non burrowing ear mites in rabbits - ✔✔what is Psoroptes cuniculi otitis with pruritis and often thick brown crusts or discharge, most commonly affects ear pinnae and canal, but can also cause dermatitis elsewhere on the body - ✔✔clinical signs of Psoroptes cuniculi in rabbits ear swabs and microscopic evaluation for mites - ✔✔diagnosis of Psoroptes cuniculi in rabbits miticides such as ivermectin, moxidectin, and selamectin- the mite can survive off host for 4- 21 days so sanitizing the environment is important - ✔✔treatment of Psoroptes cuniculi in rabbits larvae enter through nasal or oral openings and migrate to the skin, aberrant migrations are also possible such as the CNS - ✔✔lifecycle of cuterebra (in rabbits) subcutaneous cyst-like structure - ✔✔clinical signs of cuterebra in rabbits based on clinical signs - ✔✔diagnosis of cuterebra in rabbits extraction of the larvae, larvae must be extracted carefully without crushing because rupture may result in hypersensitivity reactions - ✔✔treatment of cuterebra in rabbits
mainly insect bites- wild rabbits serve as reservoirs - ✔✔transmission of myxomatosis in rabbits eyelid edema, lethargy, and pyrexia- death in about one week for pet rabbits, wild rabbits are very resistant - ✔✔clinical signs of myxomatosis in rabbits histopathology, virus isolation, and PCR - ✔✔diagnosis of myxomatosis in rabbits control vectors and vaccination - ✔✔prevention of myxomatosis in rabbits burrowing sarcoptic mite in guinea pigs - ✔✔what is trixacarus Caviae in guinea pigs severe pruritus resulting in dermatitis and alopecia - ✔✔clinical signs of trixacarus caviae in guinea pigs skin biopsy because skin scrapes are usually negative - ✔✔diagnosis of trixacarus caviae in guinea pigs topical selamectin/ivermectin - ✔✔treatment of trixacarus caviae in guinea pigs lack L-gluonolactone oxidase to synthesize ascorbic acid and must be provided with vitamin C - ✔✔vitamin C deficiency in guinea pigs cutaneous hemorrhage, delayed wound healing, and rough coat - ✔✔clinical signs of vitamin C deficiency in guinea pigs supplement with vitamin C - ✔✔treatment of vitamin C deficiency in guinea pigs burrowing mites in caged birds - ✔✔what is Cnemidocoptes
direct contact - ✔✔transmission of cnemidocoptes in caged birds hyperkeratosis of face, legs, and beak - ✔✔clinical signs of cnemidocoptes in caged birds skin scrape - ✔✔diagnosis of cnemidocoptes in caged birds ivermectin - ✔✔treatment of cnemidocoptes in caged birds circovirus - ✔✔etiologic agent of psittacine beak and feather disease aerosol or fomites - ✔✔transmission of psittacine beak and feather disease immunosuppression of white blood cells leads to death by secondary infections- common in African Greys - ✔✔Clinical signs of acute psittacine beak and feather disease deformed beak and nails with feather color changes - ✔✔clinical signs of chronic psittacine beak and feather disease PCR on blood or feather pulp - ✔✔diagnosis of psittacine beak and feather disease supportive care, isolate - ✔✔treatment of psittacine beak and feather disease unhygienic conditions, infections, conditions leading to reduced mobility, improper perches - ✔✔predisposing factors of pododermatitis in caged birds plantar metatarsal pad or plantar digital pads are most commonly affected, lesions range from erythema and hyperkeratosis to ulceration - ✔✔clinical signs of pododermatitis in caged birds
feline panleukopenia, feline rhinotracheitis, mink virus enteritis, canine hepatitis, or canine parvovirus - ✔✔diseases that ferrets ARE NOT SUSCEPTIBLE TO Canine Distemper Virus (CDV) - ✔✔what is the etiologic agent of ferret distemper they are extremely sensitive to CDV, its virtually 100% fatal - ✔✔how sensitive are ferrets to CDV anorexia, mucopurulent ocular discharge, hyperkeratotic footpads and skin rash, death can occur 14 days after exposure to ferret CDV strains and 21 to 35 days after exposure to canine CDV strains - ✔✔common symptoms of ferret distemper include... CNS phase- hyperexcitability, muscular tremor, convulsions, excess salivation, coma - ✔✔ferrets that survive the catarrhal phase of distemper, may die during what phase vaccine available and labeled for use in ferrets are PUREVAX ferret distemper, passive immunity by maternal antibodies in the kit may prevent response to the first vaccine in the series, ferrets should receive only monovalent, or single agent, vaccines- DO NOT GIVE REGULAR CANINE VACCINE - ✔✔prevention of ferret distemper caused by a parvovirus that infects mink, ferrets, raccoons, skunks, and possibly other mustelidae
- ✔✔what is Aleutian Disease Virus/Aleutian mink disease caused by chronic progressive wasting disease, rear limb paralysis, muscle wasting, tremors, urinary incontinence, enlarged spleen, pallor, tarry feces - ✔✔classic symptoms of Aleutian milk disease no vaccine available; other parvovirus vaccines do not cross-protect - ✔✔prevention for Aleutian mink disease
very susceptible to several strains of human influenza (orthomyxovirus) - ✔✔how does human influenza affect ferrets by respiratory discharge from human to ferret - ✔✔transmission of human influenza virus to ferrets lethargy, fever, anorexia, and oculonasal discharge- non-fatal unless in compromised neonates - ✔✔symptoms of human influenza in ferrets symptomatic - ✔✔treatment of human influenza virus in ferrets susceptible, causing classic disease signs - ✔✔rabies in ferrets several vaccines available and labeled for use in ferrets including IMRAB 3 - ✔✔prevention of rabies in ferrets new, highly contagious disease of ferrets caused by a coronavirus - ✔✔epizootic catarrhal enteritis in ferrets most commonly diagnosed following new introduction of a ferret into a household or rescue facility - ✔✔when is epizootic catarrhal enteritis most commonly diagnosed green slime disease or green slime diarrhea - ✔✔what is epizootic catarrhal enteritis also called dark green slimy diarrhea, loss of appetite, lethargy - ✔✔symptoms of epizootic catarrhal enteritis in ferrets vaccine not available - ✔✔prevention of epizootic catarrhal enteritis in ferrets
scabies, ringworm, rabies, bacterial fecal pathogens like salmonella - ✔✔zoonotic diseases ferrets can get hyperadrenocorticism or hyperestrogenism - ✔✔adrenal associated tumor diseases in ferrets bilateral alopecia, swollen vulva and vaginal discharge, stump pyometra in spayed jill, urinary blockage or dysuria in males, excessive mounting behavior and aggression in both sexes- signs are secondary to hyperestrogenism due to adrenal tumor - ✔✔common signs of hyperadrenocorcticism or hyperestrogenism (adrenal assocaited tumors) in ferrets NO because ferrets have elevated ESTROGEN, whereas dogs have elevated cortisol - ✔✔is ferret hyperadrenocorticism similar to canine hyperadrenocorticism anemia, bone marrow suppression, muscle wasting, posterior weakness and lethargy - ✔✔things that can happen in chronic cases of hyperadrenocorticism in ferrets most effective treatment is adrenalectomy of affected gland, but this is sometimes difficult due to close proximity to vena cava; alternative treatments include lupron which is an estrogen reducing GnRH, lysodren which is an adrenal toxic agent proved to be effective in dogs but is not safe or effective in ferrets so cannot be recommended in this species - ✔✔treatment of hyperadrenocorticism in ferrets tumor of the pancreas derived from beta cells secreting insulin - ✔✔what is insulinoma beta cells normally secrete insulin in response to increases in blood glucose; increased insulin lowers blood glucose to normal levels - ✔✔what is normal job of beta cells they secrete unregulated amounts of insulin resulting in hypoglycemia - ✔✔what do insulinomas do
very common in ferrets > 5 years of age - ✔✔insulinomas in ferrets glucose levels < 60 mg/dL (normal 80-120) are suggestive but insulin secretion may be inconsistent - ✔✔what is suggestive of an insulinoma in ferrets hypoglycemia and neurologic signs - ✔✔most common symptoms of insulinomas in ferrets surgical removal of the affected pancreas is commonly performed, but recurrence rates are high- 40% over 10 month post-op scan - ✔✔treatment of insulinoma low fasting glucose level, neurologic signs typical of hypoglycemia, relief of symptoms with administration of glucose or feeding - ✔✔Whipple's triad for insulinoma in ferrets that is DIAGNOSTIC juvenile lymphosarcoma in ferrets < 2 years old and adult lymphosarcoma in ferrets > 4 years old
- ✔✔two forms of lymphoma/lymphosarcoma in ferrets fast growing, aggressive lymphoblastic disease - ✔✔behavior of juvenile lymphosarcoma in ferrets slow-growing, chronic lymphocytic disease - ✔✔behavior of adult lymphosarcoma in ferrets poor, <10% response to chemotherapy, short-term palliative relief may be achieved with administration of prednisone - ✔✔prognosis of lymphoma/lymphosarcoma in ferrets generally cutaneous, visceral involvement is rare - ✔✔mast cell tumors in ferrets single or multiple raised, well-circumscribed, hairless nodules from 2 mm to 1 cm - ✔✔what do mast cell tumors typically look like in ferrets
be needed to confirm diagnosis of AC like with PCR analysis of blood, feces, and/or respiratory fluids, several serologic assays are available; complement fixation, latex agglutination, elementary body agglutination, immunofluorescence antibody; CULTURE IS THE GOLD STANDARD OF TESTING MODALITIES BUT IS DANGEROUS AND ONLY CARIED OUT BY LICENSED LABORATORIES; post-mortem examination of tissues is diagnostic - ✔✔diagnosis of avian chlamydiosis oral or injectable doxycycline is the drug of choice and treatment generally lasts for 45 days due to the life cycle of this intracellular organism; high dietary sources of calcium may inhibit the absorption of tetracyclines such as doxycycline so that should be removed during standard treatment of adult birds- if the patient is a young growing bird where a source of daily dietary calcium is necessary, the doxycycline and calcium supplement should be given 4-6 hours apart - ✔✔treatment of avian chlamydiosis use common sense personal and pet hygiene practices, test and quarantine newly acquired birds, avoid purchasing birds from avian fairs or poorly managed aviaries, vaccines are not yet available
- ✔✔prevention of avian chlamydiosis birds have a high vitamin A requirement - ✔✔vitamin A requirement in birds hypovitaminosis A - ✔✔one of the most common deficiencies in pet birds important for the differentiation of epithelial cells and immune system function - ✔✔what is vitamin A important for sinus infection, blunted choanal papillae, squamous metaplasia of epithelial tissues, poor skin condition- hyperkeratosis - ✔✔clinical signs of vitamin A deficiency in birds calcium deficiency - ✔✔the most common mineral deficiency in pet birds egg shell production (deficiency can lead to egg binding), bone formation, blood clotting, neuromuscular and cardiac function - ✔✔calcium is important in birds for...
No, they may only contain ~20% of the required amounts - ✔✔are seed diets sufficient in calcium requirements in birds conures and African Grey parrots - ✔✔birds that may have increased susceptibility to calcium deficiency avoid by either feeding high calcium foods such as cabbage, kale, watercress, or by supplementation with mineral blocks, ground oyster shell, or "cuttlebone" - ✔✔how to avoid calcium deficiency in pet birds seed diets as well as most grains, fruit, and vegetables - ✔✔what food sources in birds contain protein of low biologic value and can therefore lead to essential amino acid deficiency cockatoo species - ✔✔what bird species are particularly susceptible to essential amino acid deficiency anemia and decreased muscle mass - ✔✔common clinical signs of essential amino acid deficiency in birds macaws, amazons, cockatiels, and budgies - ✔✔birds that excessive dietary fat is most commonly a problem in hepatic lipidosis progressing to hepatic failure, development of xanthomas/lipomas - ✔✔what can excessive dietary fat in birds lead to sweets such as pastries or large amounts of sweet fruits can result in fermentation of simple sugars, leading to an anaerobic intestinal environment that promotes growth of Clostridium perfringens and can result in life-threatening infection - ✔✔what can excessive sugars to in birds two variants of circovirus which is a single stranded DNA virus- circovirus-1 with is the original PBFD virus with high morbidity and mortality; circovirus-2 is specific to lories and is less severe
nerve supply to proventriculus, ventriculus, and small intestines are destroyed causing inability to digest food properly leading to regurgitation, vomiting, progressive weight loss, passage of undigested food, abdominal and crop distention, neurologic disease with ataxia, tremors, seizures; classic signs is severely dilated thin wall of the proventriculus which can be seen radiographically- most frequently a fatal neurotropic disease - ✔✔clinical signs of PDD presumptive diagnosis can be made from clinical signs and radiographs, antemortem biopsies of intestine sometimes helpful, histology is most reliable revealing a lymphoplasmocytic ganglioneuritis, necropsy reveals dilated gastrointestinal tract - ✔✔diagnosis of PDD only treatment is supportive, including NSAIDs, since disease seems inflammatory; place exposed birds in isolation, they may live normally for years - ✔✔treatment of control of PDD herpesvirus- double stranded DNA virus, several variants - ✔✔etiologic agent of Pacheco's disease highly contagious with high morbidity and mortality that can affect all ages of psittacines, most common in multiple bird homes and aviaries, transmission is by direct contact with infected feces or ocular/nasal discharge, birds can be asymptomatic carries, any bird surviving an outbreak is likely a latent carrier of the virus - ✔✔pathogenesis and epidemiology of Pacheco's disease birds with sudden death in aviaries are highly suspect, lethargy, anorexia, diarrhea, green urates (indicative of liver damage), sinusitis, conjunctivitis, and neurologic signs, enlarged liver/spleen/kidneys, acute viral hepatitis with liver necrosis - ✔✔clinical signs of Pacheco's disease PCR of blood and cloacal swab for herpesvirus DNA, diagnosis is usually made on postmortem- virus isolation and characteristic histopathology including hepatic inclusion bodies; reliable serologic test NOT available, consider Pacheco's disease in ANY psittacine that dies suddenly with no previous signs of illness - ✔✔diagnosis of Pacheco's disease a killed virus vaccine is available but its effectiveness and use is controversial, PCR testing to determine whether of not birds are infected then remove, acyclovir is effective against some strains
of Pacheco's but may cause kidney damage, generally untreatable so supportive care is important
- ✔✔treatment and control of Pacheco's virus avain polyomavirus- double stranded DNA virus, originally described in budgies, hence the historical name Budgerigar fledgeling disease - ✔✔etiologic agent of polyomavirus in birds latent carrier state is common with adult birds appearing clinically normal until they undergo stress, significant disease of aviculturists worldwide especially young birds, extensive host range; transmitted by direct contact with infected material via feather dust, feces, aerosols, and parenteral feeding of chicks, thought to spread vertically (via egg) as well - ✔✔pathogenesis of polyomavirus in birds high mortality in young psittacine birds, lethargy, anorexia, delayed crop emptying, regurgitation, diarrhea, feather abnormalities, petechiae, acute death can occur, acute and chronic forms are seen
- ✔✔clinical signs of polyomavirus in birds DNA PCR probe test of feces and blood is good but will only catch birds actively shedding and NOT latent carriers, serology is unreliable in most psittacines and only IDs exposure and not actively shedding birds; histopathology with viral intranuclear inclusion bodies in the liver, spleen, kidney, heart, and feather follicles - ✔✔diagnosis of polyomavirus in birds closed breeding aviaries are recommended, cloacal swab on all birds leaving an aviary and all newly acquired birds before being introduced into a collection, APV vaccine appears encouraging in certain situations but usefulness is controversial but is not indicated in all psittacines - ✔✔treatment and control of polyomavirus in birds non-stick cookware releases an odorless vapor when heated above a critical temperature ( degrees) which accumulates in the avian lung and results in fluid accumulation, impairing gas exchange, sudden death may be seen within minutes- oven liners and hair curling iron can also be a source of teflon vapors - ✔✔how are teflon vapors toxic to birds the toxic agent is persin a phytochemical found in avocado - ✔✔toxic agent of avocado for birds
the avian liver is particularly sensitive to alcohol, birds often like the taste of beer, but even the levels of alcohol found in beer can be very toxic - ✔✔alcohol toxicity in birds green iguana - ✔✔the most common of all reptile pets in the US intestinal salmonella - ✔✔estimated up to 90% of pet iguanas harbor what zoonotic disease often implicated as an asymptomatic, zoonotic disease reservoir- assume that ALL iguanas are potential sources of infection - ✔✔salmonellosis in iguanas young, old, and immunocompromised individuals are at greater risk of infection - ✔✔who are at greatest risk of zoonotic transmission of disease from pet iguanas washing hands before and after handling, maintaining clean cages, immediate and safe removal of feces - ✔✔proper hygiene for handling iguanas campylobacter, Klebsiella, Aeromonas - ✔✔other bacterial fecal-oral organisms capable of causing zoonotic enteritis that iguanas can harbor cryptosporidia - ✔✔protozoal fecal-oral organism that iguanas may harbor that can cause zoonotic enteritis decreased activity, inappetence, seeking heat, isolation, subtle skin color changes (dull or dark), abnormal shedding (dysecdysis), changes in color of feces and urates - ✔✔general signs of disease in iguanas a number of disorders related to imbalance of vitamin D3, calcium, and phosphorus- these substances are needed for bone growth and maintenance, and blood coagulation - ✔✔what is metabolic bone disease
nutritional metabolic bone disease and renal metabolic bone disease - ✔✔types of metabolic bone disease improper diet or inadequate lighting - ✔✔causes of nutritional metabolic bone disease chronic kidney disease - ✔✔cause of renal metabolic bone disease boney protuberances in long bones- vertebral column of the back and tail, lower jaw; possible softening of these bones leading to pathologic fractures; muscle weakness, lethargy, and reluctance to move - ✔✔clinical signs of metabolic bone disease usually based on clinical appearance and investigation of husbandry practices - ✔✔diagnosis of metabolic bone disease provide proper diet, provide calcium supplementation, provide optimal temperatures, provide appropriate UV light - ✔✔treatment of metabolic bone disease more common in snakes and chelonians than in iguanas - ✔✔ulcerative stomatitis (Mouth rot) in reptiles usually due to poor husbandry - ✔✔usual cause of ulcerative stomatitis in iguanas chronic trauma/excoriations to rostrum from persistent rubbing on caging materials; secondary bacterial infection results in inflammation, ulceration, or abscessation - ✔✔cause of ulcerative stomatitis in reptiles plaque formation, erythema of gingiva, increased salivation, may progress to septicemia and pneumonia - ✔✔clinical signs of ulcerative stomatitis (mouth rot) local debridement, systemic antibiotics, improving patient's environment - ✔✔treatment of ulcerative stomatitis (mouth rot) in reptiles
