Avian Flashcards

1
Q

List unique sphenisciforme (penguin) anatomy and physiology:

A
  • bifurcated trachea
  • lack of crop
  • bones are not pneumatic
  • feet associated with thermoregulation (prone to hypertermia during anesthesia)
  • salt glands - will atrophy in fresh water, salt supplementation not needed in captivity
  • DNA for sexing
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2
Q

What happens to penguin (sphenisciforme) weight before molt?

A

Can gain more than 25% -31% of weight before molt and can loose 41% of pick weight during. Appetite increases before (apr. 98%) and decreases dramatically (apr. 61%) during molt and increases after (apr. 29%). They loose all the feathers during molt.

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3
Q

What is the influence of feed, molt and egg laying on blood chemistry in penguin (sphenisciforme)?

A

Feed: postprandial increase of uric acid

Molt: HTC decreases 17%-24% and RBC decrease 12-17% during molt and start returning to normal 1-3 months after. Corticosterone decreases during molt and postmolt.

Egg laying: increase cholesterol, calcium, phosphorous, ALP

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4
Q

What are the main diseases in penguin (sphenisciforme)?

A

ASPERGILLUS: Profilatic antifungal can be used during stress.

MALARIA (Plasmodium relictum or elongatum): mosquitoes, bitting flies (vectors). Mortality in naive animals is high. Blood smear not very sensitive. Serologic test for black-footed penguin (Spheniscus demersus) may be used to other Spheniscid. Anemia, dyspnea, lethargy, innapetence, death. Tissue and blood phase. Treatment chloroquine, primaquine (also for profilaxis to mosquito).

WNV (flavivirus): Penguins being on of the most susceptible birds. Anorexia, weakness, vomiting, dyspnea, self isolation. vaccination recommended (equine vaccine).

EEE (alphavirus): Anorexia, lethargy, vomiting, bile-stained diarrhea, self isolation, ataxia, seizure. Hemagglutination serology test (rising titer 2-4 weeks apart). Some use horse vaccine.

PODODERMATITES: penguins should be encourage to swim.

GI foreign body, thiamine deficiency (stargazing, incoordination), metabolic bone disease

Chlamydophila psittaci afected an entire zoo coloni (n=63). Clinical sings were innapetence, lethargy, and light green urates. Treatment with doxy possible caused keratoconjunctites in 90% of birds. Infection possible via wild birds (gulls and pigeons).

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5
Q

List unique Podicipediformes (grebes), Gaviiformes (loons or divers), Procellariforme (albatrozes, petrels) anatomy and physiology:

A

Grebes: specialized, lobated digit (contracts or extends), used for propulsive locomotion in water. Predominance of non pneumatic bones and decreased air sac system. May ingest their own feathers (bulk to form pellets with undigestive items to be excreted).

Procellariforme: characteristic tubelike extention of the nares, well developed salt gland (dorsal to the orbit - can ingest salt water without need for fresh water), may acumulate gastric oil (except pelecanoididae) derived from diet (may excrete for defense, do not hold the beak close bird might aspirate). Prions (type of bird) are filter-feeders.

All: feed on aquatic animals (fish, invertebrates, carrion). supplement with thiamine and vit E.

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6
Q

What was shown to improve operative survival in wild western grebes (Aechmophorus occidentalis) for telemetry device?

A

Improved waterproofing, decreased communication into coelom, improved seal around protuding antenna by offsetting body wal from skin incision, applying tissue glue to the SC space, waterproof sealant to the skin, using porcine smal intestine submucosa at the site of the antenna egress.

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7
Q

What are the main diseases in Podicipediformes (grebes), Gaviiformes (loons or divers), Procellariforme (albatrozes, petrels)?

A
  • Gaviiformes: Herpesvirus similar to infectious laryngotracheitis in common loon
  • Procellariforme:
    • poxvirus (transmission by mosquito, or by contact when feeding chicks)
    • Puffinosis (maybe coronavirus) on Manx shearwaters (Puffinus puffinus): genarally afects juvenile near fledging, high mortality after period of blisters on the feet and somethimes conjunctivitis
  • Clamidiosis: sea birds in general but more with Procellariforme
  • Aspergillus
  • Nematodes in grebes (intestinal, ventricular, and proventricular): Estrongylides tubifex, Contracaecum spp.
  • Oil spill, drowning by fish operations, ingestion of plastic by Laysan albatrosses
  • Mercury intoxication -reproductive effects
  • Domoic acid intoxication (biotoxin produced by algal bloom)
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8
Q

List unique Pelicaniforme (pelicans, tropic birds, cormorants, frigatebirds, anhingas, gannets) anatomy and physiology:

A
  • Most: large beak and gular (distensible) pouch on floor of the mouth (scoops water and prey, might be used as sexual display)
  • Extensive SC air sac diverticula between neek and breast, inflation controled by closing glottis, connected to respiratory system. Presumed to absorb shock when bird hits water and assit with floating. might difficult blood collection from jugular. Avoid nitrous oxide (cause significant expansion of SC air sac).
  • External nares are not patent in some birds (do not restraint beak close to prevent asphyxia)
  • Fish eating birds, but also crustaceans, amphibians, turtles, and ocasionally other birds
  • Supraorbital salt gland that might atrophy in fresh water
  • Some have a crista ventralis in the trachea
  • Mature white pelicans have a keratinized growth on dorsal maxilla during breeding
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9
Q

What special considerations should be taken when reparing the gular pouch in pellicaniformes?

A

Estabishing that subramal and ventral gular blood supply is intact as no anasthomose evidence between these vessels exist. The pouch should be repaired by separating the epithelial layers and suturing them separately (simple interrupted).

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10
Q

What are the main diseases in Pellicaniformes?

A
  • Aspergilosis
  • Pododermatitis
  • Endoparasites: typically ascarids. A study with American White pelican found 75 different species of parasites with little or no clinical signs.
  • Fenbendazole caused fatal enteritis and bone marrow damage in pin-backed pelicans, but was safe in low doses in brown pelicans.
  • WNV, New Castle, poxvirus
  • Avian influenza vaccination: mixed result. inactivated H5N2 vaccine elicited partial response in comorants nad no immune response in pelicans.
  • Brevetoxin and domoic acid (algi) intoxication.
  • Botulism
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11
Q

What are the clinical signs of brevetoxin and domoic acid (algi) intoxication in Pellicaniformes?

A
  • Brevetoxin in cormorants : ataxia, disorientation, intention tremors
  • Pelicans with domoic acid: slow, side-to-side head motion, fine motor tremors, scratching at the pouch, vomiting
  • Comorants with domoic acid: affected animals are usually docile when approached by humans
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12
Q

About 23 cases of postintubation tracheal obstruction in birds:

A
  • clinical signs were noted when between 50 -90% of the trachea was obstructed, average 16.6 days postintubation
  • Medical management was successuful in 3/9 mild cases
  • Tracheal ressection and anastomosis was successful in 4/9
  • Cases occurs in different neck lenght birds and with the use of different types of tubes
  • No cases in psittaciformes, falconiforms and coracciforms
  • Species with more acute narroing of the trachea might be more susceptible
  • Tracheotomy for debulking was unsuccessful
  • mortality rate of 70%
  • Avoid manipulation of head and neck and use humidified gases
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13
Q

About respiratory volume and lung density on CT of penguins:

A
  • Recumbency had a significant effect on air sac volume but not lung volume
  • Air sac volume was largest in conscious penguins in ventral recumbency
  • Air sac volume was lowest and lung density was highest in anesthetized penguins in dorsal recumbency. This position may not be recomended.
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14
Q

Effects of fresh water housing and fuid types on aquatic birds serum electrolyte concentrations

A
  • Western grebes (moves between waters of varying salinity) were able to maintain their electrolyte values
  • common murres and northern fulmars (holopelagic birds - spend entire life in the ocean) had serum electrolyte concentrations well below reference
  • Salt supplementation or salt water should be considered for holopelagic species
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15
Q

Ciconiiformes (Herons, Ibises, Spoonbills, Storks) unique anatomy/biology

A
  • Long lived (40-50 years)
  • most sexually monomorphic, but femeales are ussually smaller. Gender ID with DNA, but measurement of bill, tibio-tarsal and body length are successful
  • long necks (15 -20 vertebrae). Heron has a modified sixth cervical vertebra (holds in a S-shape during flight)
  • Storks lack syringeal musculature - most are mute, bill clattering is important form of communication
  • most are aquatic carnivors (fish, amphibians, insects, molluscs, small mammals, birds, reptiles)
  • Diet with fish: supplement with thiamine and vit E
  • synthetic canthaxanthin in pigmented birds (Roseate spoonbill and scarlet ibis). They have pink plasma.
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16
Q

Ciconiiformes (Herons, Ibises, Spoonbills, Storks) considerations

A
  • many have crista ventralis in the center of glottis
  • capture myopathy is not uncommon
  • postintubation tracheal granulomatous obstruction has been reported
  • Trauma is the most common cause of surgery in captivity
  • fenbendazole toxicity has been reported in marabou stork
  • many storks defecate and urinate on legs for thermoregulation
  • Ht and hemoglobin increase with age. gender alteration to biochemical values.
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17
Q

What are the main Ciconiiformes (Herons, Ibises, Spoonbills, Storks) diseases?

A
  • Trauma is the most common non-infectious disease. Musculoskeletal abnormalities in growing chicks, foreign body, and pododermatitis due to inappropriate substrates.
  • Nutritional diseases: hypo E, hypothiaminosis, metabolic bone disease
  • free -ranging birds prone to toxicosis such as heavy metals, arsenic, pesticides.
  • Viral hemorrhagic disease enteritis (inclusion body diease): ciconid herpesvirus-1. fecal-oral. Dx-PCR, virus isolation, electron microscopy, Itranuclear inclusion bodies in GI tract and other tissues.
  • WestNile, EEE, Poxvirus, Aspergillus (pneumonia)
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18
Q

Anatomy and biology of Phoenicopteriformes (flamingos)

A
  • Adapted to extreme habitats (high salinity, alkalinity), long lived, nasal salt gland
  • plumage color - carotenoids (canthaxantin, astaxanthin, phoenicoxanthin) from diet and preen oils (uropygial gland)
  • Filter-feeders. Two groups according to diet 1) Phonicopterus - shallow beak, feed pn arthropods and mollusk 2) Phoenicoparrus and Phoeniconaias, deep beak, feed on algae and diatoms.
  • Sexual maturity, from gray plumage to pink (4-6 years)
  • Neck with 17 vertebrae
  • sex ID: tarsometatarsal lengh (in animal older than 1.5 years, male longer), PCR
  • canthaxantin-potent antioxidant accumuates in egg yolk and assumed to protect the embryonic sac
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19
Q

What are risk factors for pododermatitis in Flamingos and how to prevent?

A
  • Salt water pound increases existant foot lesions
  • Concrete, vinyl or rubber linning, and grass are inadequate
  • 10-cm fine granular sand (less than 1 mm) improves foot lesions in idoor and outdoor enclosures
  • Temperature below 15oC and indoor housing are a risk factor for pododermatitis
  • heated house with sand should be available in cold places
  • Hyperkeratosis, fissures, and nodular lesions develop in juvenile flamingos as early as 2-3 months. Papillomatous growths (fourth type lesion) where not seen before 5 months and is less often in animals less than 1 year.
  • Prevalence of nodular lesions with ulcerations increases in animals more than 4 kg, but no other lesions was aftect by body weight.
  • Low zinc was suspected to weaken the cornified epidermis and facilitate disease
  • No evidence of papilomavirus
  • The bacteria Arsenicoccus dermatophilus might be involved causing a primary inflammation
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20
Q

What are accepted methods for flying prevention in flamingos?

A

feather clipping, pioning and follicle extirpation. Pioned males have shown difficulties mantaining balance during mating.

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21
Q

What is the “crop milk” of flamingos?

A

Initially dark red and later pale red to yellow high energy containing cathaxanthin and white and red blood cells, produced by glands in the upper GI

22
Q

Phoenicopteriformes (flamingos) characteristics

A
  • Flamingos termoregulate by resting in one or both legs, so legs should not be pulled toward the body to mantain optimal perfusion and avoid hypertermia.
  • Bill impaction prevents accurate filtration - visible because of gular enlargment due to retrograde displacement of tongue
  • no closed septum between nares
  • PCV increases with age. Pink-orange plasma.
  • Cholesterol of flamingo chick is negatively correlated to body condition
  • Are able to fast for several days
23
Q

Diseases of Phoenicopteriformes (flamingos)

A
  • Pododermatitis
  • Capture myopathy - death due to massive myoglobinuris tubulonephosis and kidney failure
  • Trauma (28% of necropisies in 124 greater flamingos)
  • West Nile: vaccination of adult flamingos (killed horse vaccine) failed to produce antibody response or virus-neutralizing activity
  • Avipox (rapidly growing slightly bleeding skin tumors). Tx- surgical removal and famciclovir.
  • Artherosclerosis - collapses or death during stress and it was diagnosed 14% of 124 necropsies in greater flamingos. Afected animals wre 14-50 years old. Amyloidosis (6%), gout (4%), limb deformities (9%).
  • cyanobacterial toxins - hepato and neurotoxins
24
Q

Anseriformes families

A

Anatidae - ducks, goose, swan

Anhimidae - Screamers - lack webbed feet and have SC air sacs (may prduce a crackling sound when contracted ) and have pneumatic bones (even phalanges), may have keratinized tongues and are herbivorous

Anseranatidae - Australian magpie goose

Anseriformes may be more carnivorous, piscivorous, granivorous or herbivorous

Anseriforme males have a intromittent copulatory organ (spiral-shaped phallus) attached to the ventral cloaca

25
Q

Anseriformes characteristics

A
  • Some Anatidae undergo a postbreeding molt and all remiges or flight feathers are lost (in hours to days) and the bird is flighless for several weeks
  • neonatal ducklings’s down feathers are not waterproof and so they are susceptile to chilling
  • aneshetized animals with gas present “rollercoastering” (deep to moving), probably due to PCO2 chemoreceptors in the lung
26
Q

Studies in Anseriformes

A
  • Laser ablation (alternative to pinioning) showed swelling, edema, ulceration, and serosanguineous oozing, deemed minor side and resolved within 12 weeks, successfuly preventing feather regrowth in 65% of treated follicles (primary feathers).
  • Flunixin meglumine reduced COX-2 but was associated with muscle necrosis at the injection site in mallard ducks.
  • ketoprofen was associated with mortality in eider ducks, but has been used in studies with waterfowl
27
Q

Avian Bornavirus in anseriformes

A
  • Avian Bornavirus (non-enveloped RNA)
    • waterfowl appers to be the primary reservoir of ABV (first isolated in a wild Canada goose). low patogenicity to most waterfowl and long-term intermitent shedding in apparently healthy birds has been documented;
    • RT-PCR on brain of hunted killed waterfowl- 22 to 55% prevalence. on fecal swabs less or equal 10%
    • Fecal-oral route and vertical documented in domestic ducks
    • Infects central and enteric neurologic tissue, inducing inflammation and leading to neuronal and glial cell loss.
    • Histo: nonsuppurative encephalomyelitis and ganglioneuritis in clinical ill waterfowl.
    • Clinical sings: weak, unable to fly, neurologic, potential impacted upper GI.
    • PCR on freshly plucked contour feathers (calamus), crop biopsies, and rELISA on serum.
    • cloacal or fecal swabs noy recomended because of intermitent shedding
28
Q

Avian Influenza in Anseriformes

A
  • Family Orthomyxovirus, genus influenza A, enveloped RNA virus
  • Named for combination of surface glycoproteins, hemagglutinin (H) and neuraminidase (N), determining their virulence. H5 and H7 associated withincrease pathogenicity in birds.
  • Classified as low patogenic (LPAI) or high (HPAI)
  • LPAI in waterfowl - fecal-oral, with prevalence peaking in late summer and early fall in A. platyrhynchos (mallard duck) associated with premigration staging areas.
  • HPAI-H5N1 have been detected in asymptomatic wild waterfowl but more likely detected in affected birds. Mortality rate in chicken near 100% and has caused disease in atypical species (canids, felids, mustelids, viverids, suids, lagomorphs, and primates). Mortality in humans almost 60%.
  • HPAI - fecal-oral, through contaminated water sources and fomites but has a respiratory component and might spread by direct contact and respiratory secretions.
  • Clinical signs HPAI in poultry: decrease egg production, peracute death, GI and nervous systems (head tilt, paresis, paralysis, depression, head shake), characteristic respiratory rales, sinusitis, epiphora, edema of the head, cyanosis and hemorrhage of the wattles and comb.
  • Dx: virus isolation or RT-PCR on cloacal or pharyngeal swabs. H5 or H7 immediately notifiable to state and OIE.
29
Q

Diseases in anseriformes other than influenza and bornavirus

A
  • lead toxicity: major cause of waterfowl mortality in the US
  • Pododermatitis: common in captivity.
  • Amyloid deposition: amyloid deposit secondary to chronic inflammatory conditions. Swans appear to be more sensitive. Pathology reviews of waterfowl: trumpeter and mute swans had high incidence of deposition in parenchymous organs (spleen, liver). in both studies diseases that caused significant chronic inflammation such as aspergilosis and pododermatitis were highly associated with amyloid deposition.
30
Q

biology and anatomy of falconiformes

A
  • each eye has two foveae, enabling two planes of vision (temporal fovea - binocular vison, central fovea-monocular vision). Andeam condors and black vultures have only a nasal fovea. Plumage is not sexually dimorphic, except on northern harrier, american kestrel, and merlin. vultures are dimorphic.
  • Most molt in symmetrical pairs, once year. Steppe buzzard exhibits boizarre molt, old world vultures may extend up to 2-3 years. Goshawk and eagles molt only partially each year, enabling to distinguishing second and third year birds (once riches adult plumage not possible to tell age). Induction of molting: manipulating photoperiod (18-20 h light/day after 4-6 weeks of less than 10h/day); use of thyroxine - very rapid molt; increase ambient temperature may speed molting and corticosteroids retard.
  • Bald eagle has fused adrenal glands; Savanna hawk has salt glands; Harris hawk is the only species of raptors that shows psychological feather plucking, and a temporary beak modification technique has been described to prevent self-mutilation.
  • All have crop, except bearded vulture. Ph of stomachis 1.0 in diurnal raptors (1.7 in hawks) and they are able to digest bones. ceca is absent or vestigeal.
  • many of the families Cathartidae (new worl vultures), Accipitridae (hawks, eagles, old world vultures, kites, harries, buzzard) and Falconidae (falcons, kestrels, merlins, caracaras) have two ovaries and two oviducts.
  • Accipter cannot be housed with other species and the sexes of merlins and northen goshawks (Accipter gentilis) should be housed separately (large female will kill male)
31
Q

Particularities of raptors feet

A
  • digital flexor tendons have unidirecional interlocking ratcheting mechanisms that resist digital extention when toes are clenched
  • Falconiformes are anisodactyl (three digits forward and one back), but Ospreys can swive all four digits to the rear (semi-zygodactylous)
  • third digid talon has specialized sharp edge for grooming
  • Non releasable if missing both second digits, one or both halluxes
  • The key for tendon repair is the use of a vascularized pedicle between the tendon and tendon sheath. waiting period of several weeks for vascularization of tendon.
32
Q

Nutrition in raptors

A
  • most vultures tend to have a Ca deficient diet (ingestion on viscera and meat mainly, large predators provide them with bone fragments)
  • Fatty-liver-kidney syndrome of merlins (fed day old chick)
  • small raptors (e.g. Accipter): hypoglycemia
  • Young secretary birds on standart raptor diet will have Ca/Phosp imbalance (they eat snakes in the wild)
  • Ospreys eat fish, thiamine deficiency - star gazing and neuro signs
  • Vit A and E deficiencies
33
Q

Anestesia/analgesia falconiformes

A
  • Propofol CRI in red-tailed hawks had minimal effects on blood pressure but effective ventilation was reduced. prolonged recovery with moderate-to-severe excitatory CNS signs.
  • Plasma buprenorphine concentrations were > 1 ng/mLfor 9 hours after both IM and IV administration in American kestrels.These results, in combination with those of a IM pharmacodynamic study (thermal antinociception), suggested that the analgesic effects of buprenorphine could last at least 6 to 9 hours in this species.
  • Rocurium bromide induces mydriasis without adverse effects in european kestrels
34
Q

Diseases falconiformes

A

Alspergillosis: lower serum prealbumin values in falcons. ELISA for Buteo species, PCR, and may increase beta and gama globulins.

Bumblefoot: degenerative, inflammatory condition. Abnormal pressure by improper perches. Inactivity, hypo A may play a role. Most common bacterium is S. aureus. Prevention: 1) good nutrition and preventing obesity; 2) perches of appropriate size, shape, cover; 3) adequate maneuvering space; 4) keeping talons at appropiate size and blunting tips (non hunting birds) 5) Exercise and monitring feet

Trauma: most common cause of presentation in rehabilitation. radio-ulnar synostosis (bony bridge between ulna nad radius) is common complication of external coaptation. Surgical excision of the bony union and application of a polypropylene mesh implant has restored function in mississippi kite.

Amyloidosis: associated with chronic infections. Serum test for falcon serum amyloid A.

Gout has recently been associated with C. perfringes infection.

Trash ingestion was the most important mortality factor in nestling California condor in the reintroduction program

Avian vacuolar myelinopathy: neurologic disease affecting bald eagles, american coots. Seasonal and appers to involve cyanobacteria (stigonematales). birds of pray acquire via ingestion of affected coots.

35
Q

Parasitic disease of Galliformes

A
  • Developed ceca, anisodactyl (three digits facing forward, one back), cecal dropping occur at night
  • Sulfur color droping - suggestive of histomoniasis
  • Chickens might be inapparent carries of the parasite Histomonas meleagris and might transmit to turkey and closely related Galliformes species. Dx intestinal scraping and clinical signs. depressed, craterlike lesions in liver and cecal cores.
  • Cappilaria (earthworm intermediate host), coccidiosis, Cryptosporidium
36
Q

Bacterial diseases of Galliformes

A
  • Avian tuberculosis: M. avium. Emaciacion. Transmission via ingestion of contaminated feed, water, feces. Wild birds might disseminate.
  • Avian cholera: Pastereulla multocida. Rodent control reduces incidence. chickens might serve as reservoirs but turkeys and related galliformes are often affected with unilateral or bilateral infraorbital sinusitis.
  • Necrotic enteritis: C. perfringens, mucoid and blood diarrhea.
  • Mycoplasma gallisepticum
  • **Bordetella avium: **inhalation, catarrhal rhinitis.
37
Q

Viral diseases of Galliformes

A
  • Avian influenza. Peafowl are less susceptible.
  • Avian pox: dry and wet forms (plaques within oropharynx and occlusion of trachea, higher mortailty.Vaccination and mosquito control.
  • Rotavirus: diarrhea and stunting.
  • Equine encephalitis: phesants and chukars. leg paralysis, torticolis, tremors. no gross lesions. vaccine without proven efficacy. mosquito control.
  • Laryngotracheitis: upper respiratory, herpesvirus. vaccination is not an option since it is live modified.
38
Q

Cuculiformes (cuckoos and roadrunners) biology/anatomy

A
  • Most are arboreal, diurnal, but many species vocalize only at night. not tolerant to cold.
  • sexual dimorphism in some, female is larger in 71% of species with parenteral care and males are larger in 84% of the brood parasitic species. Almost all parental species are monomorphic (95%), 41% of Old world brood parasitic and malkohas are dimorphic.
  • cuckoos are zygodactyly (two forward two back) and have a unique molt pattern: the odd numbered primaries are shed and regrow first, followed by the even numbered. Young have unique pattern of white and yellowish-tan papillate patches in the oropharinx.
  • Most cuckoos are solitary in nature and agressive (not haused in mixed exhibits).
  • cuckoos are carnivorous, with most being insectivorous, preying noxious insects such as carterpillars. they remove the toxic leaf products withing the intestines by beating them or wipping them first. they egest a pellet with indigestible parts. Other food items (specie dependant) are spiders, snails, frogs, snakes, mice, eggs, etc. Few Old world species are frugivorous. Roadrunners feed predominately on snakes and lizards during breeding season, beating prey against a rock.
39
Q

Cuculiformes (cuckoos and roadrunners) diseases

A
  • not exquisitely sensitive to infectious diseases
  • Avian poxvirus, aspergillus, Chlamydophila
  • Trauma is the most common noninfectious disease (agression)
  • neoplasia not common, but hepatic hemangioma and squamous cell carcinoma of ramphoteca
40
Q

Cuculiformes (cuckoos and roadrunners) reproduction

A
  • recognized by brood parasitic reproductive behavior but 2/3 bild their own nests and have different parenteral care
  • nonparasitic cuckoos lay white eggs but many brood parasitic lay colored eegs that resemble the host’s eggs. other lay dark “cryptic’ eggs. The female cuckoo will often push the eggs to lay her own. The young usually hatches and grows first and in most cases evicts the eggs or young of the host species.
41
Q

biology/anatomy of columbiformes

A
  • anisodactyl feet (3 forward, one back)
  • waterproofing relies on powder since uropygial galnds is rudimentary or absent
  • both sexes incubate eggs. Crop milk: cheesy, semi solid, nutricious substance derived from desquamated crop epithelia cells under influence of prolacting causing hyperplasia in both genders. Primary food for the first 7-10 days of life. halocrine secretion consisting of 50% protein (cells), 45% fat (lipid droplets), and negligible carbs (no lactose). Easily digestible and source of immunoglobulins. Responsible for rapid growth and short fledling times (10-40 days).
  • vascular cervical plexus: sexual and territorial display, thermoregulation and possible facilitation of nutrient and enzyme deposition during lactation
  • ceca is rudimentary and gall bladder i absent in many genera
  • granivorous, occsional invertebrates, fruit doves
  • drink water via suction with beak in the water
  • can drop contour feathers when handling
42
Q

Colubrid anesthesia

A
  • Medetomidine alone or combined may yield variable results and profound bradicardia and bradypnea
  • ketamine, alone or with diazepam or xylazine IM, IV, IO has been reported
43
Q

Infectious disease columbiformes

A
  • free-ranging Columba liva carries C. psittaci but most prevalent genotype has a low virulence and zoonotic potential
  • susceptible to fatal Salmonella enterica Typhimurium var. Copenhagen strain of S. enterica is a major disease in pigeons.
  • Candida albicans, Aspergillus, Cryptococcus (granuloma)
  • zoonotic potential pigeon guano: Cryptococcus, Histoplasma, Blastomyces, Candida
  • susceptible to Newcastle and a distinct paramyxovirus type 1, causing severe neuro signs in columbiformes and only mildly pathogenic to poultry
  • Pigeonpox (transmitted by arthropods)
  • Herpesvirus: conjunctivitis, respiratory signs, pharyngitis, esophagitis
  • PIGEONS APPEAR TO BE RESISTANT TO WEST NILE AND BOTH HIGH AND LOW PATHOGENIC AVIAN INFLUENZA
44
Q

disease columbiformes

A
  • Trichomonas gallinae
  • Sarcocystosis: may cause acute fatal pneumonia in Old World columbids. protect birds from contact with roaming opossums and their feces.
  • T. gondii, Cryptosporidium, Leucocytozoon
  • trauma is very common, since columbids are agressive
  • benzimidazole anthelmintics (albendazole, fenbendazole) should be use cautiously if used at all. toxicosis is dose related: damage to developing feathers, weight loss, intestinal mucosa damage, bone marrow hypoplasia, leukopenia, death.
  • all-in, all-out quarantine practices (min 45 days). screening for Chlamydophila and Trichomonas
45
Q

Gruiformes (Cranes, coots, bustards) biology/anatomy

A
  • Many are vulnerable or endangered
  • cranes have perforated nares and are long lived (50 years)
  • adult crane (except African crowned cranes) have long convoluted trachea encosed withing the bones of the keel (producing lloud bugling call). Swans are the same.
  • Omnivorous, including grains, fish, amphibians, mollusks, rodents, insects.
  • hemolysis with EDTA, use heparin
  • Both parents share brooding and chick care. Chicks are agressive with siblings. Monogamus for life. cryopreservation of semen and artificial insemination were successful.
46
Q

Gruiformes (Cranes, coots, bustards) anesthesia

A
  • cranes are susceptible to dose dependent isoflurane-induced respiratory depression and hypotension, particularly under spontaneous ventilation. multimodal aproach with controlled ventilation is recommended.
  • cranes have larger tracheal dead space and inadequate ventilation and hypercapnia are frequently accompanied by bradycardia.
  • filed work: ketamine and xylasine, K and diazepan IM, or propofol (bolus or CRI). Alphaxolone and alphadolone IV have been used successfully for short procedures.
  • Alpha-chloralose (in corn) has been used to capture wild and scaped cranes. ingested dose is variable and increased risk of capture myopathy.
47
Q

Gruiformes (Cranes, coots, bustards) infectious diseases

A
  • Infectious diseases appear to be mainly bacterial and sporadic and occur mainly in birds predisposed to environmental or population stress
  • Eye infection in chicks is caused by P. aeruginosa (use antibiotics)
  • M. avium and salmonelosis are frequently associated with crowding, contaminated environment or both
48
Q

Gruiformes (Cranes, coots, bustards) infectious diseases

A
  • Inclusion body disease of cranes (gruid herpesvirus tipy 1 disease): nonspecific clinical signs. Outbreaks in North America and other continents. Antibody response in surviving cranes lasts several years and the animals should be considered carries. A survey of wild cranes in Wisconsin and Indiana did not find any exposure. Study showed absence of vertical transmission in a pair of seropositive black-necked cranes.
  • Eastern equine encephalitis: arbovirus transmitted by vector mosquito Culisetta melanura. Acute death or depression, lethargy, ataxia, paresis, abnormal postures with head and neck. Whooping crane exhibit mainly the viscerotropic form with minimal neural involvment while Mississipi crane have been diagnoses withthe neurotropic form.
  • West Nile virus: arbovirus, flaviviridae, transmited by Culex sp. significant mortality in Mississipi and Florida crane chicks. Adult seemed resistant and experimental infection failed to induce death in sandhill crane despite viremia. Lethargy, weakness, ataxia, weigt loss, inappetence. Mortalities are rare even without vaccine.
  • Infectious bursal disease: arbirnavirus, birnaviridae, acte oncet thattargets the lymphoid tissue of the bursa, resulting in immunosuppresion. Highly contagious in young chickens. Seropositivity to IBD was associated with the deaths of captived raised and released whooping cranis in Florida, and virus shown to be endemic in the region.Housing cranes near chickens or turkeys should be avoided.
  • **Avian pox, Newcastle **
  • Vaccines for EEE, WNV (once a year, killed horse vaccine). One study failed to demonstrate seroconversion (EEE vaccine) in sandhill cranes. However this species seems resistant to clinical disease. WNV killed vaccine shown to protect young sandhill and wooping cranes (IM, 3 doses series), however sandhill cranes did not seroconvert.
49
Q

Gruiformes (Cranes, coots, bustards) parasitic disease

A
  • coccidia (Eimeria): important cause of mortality in captive. Disseminated visceral coccidiosis: E. reichenowi infection may become systemic with widespread extraintestinal dissemination. Multifocal nodules in many organs, GI, lung, air sac, trachea, nares. Apprpriate countermeasures: parasite surveillance, pen rotation, separation by age classes.
  • Capillaria, Eucoleus, Ascaridia, Syngamus
50
Q

Gruiformes (Cranes, coots, bustards) noninfectious disease

A
  • Trauma due to intraspecific aggression, including disruption on the social order and somethimes parents to chicks.
    • Trauma to the beak (pen fencing), trauma resulting in ruptured air sac (SC emphysema). Neck fractures in captivity (flight response).
    • Trauma is the leading cause of mortality in wild and reintroduced cranes and bustards, specially from collision with power lines. birds are essentially blind in the direction of flight while scanning the terrain below.
    • Predation significant in wild and reintroduced cranes
  • Capture Myopathy: Exertional rhabdomyolysis observed after manipulation and immobilization of cranes and bustards. peracute death from cardiac failure, pain, stiff movements, swollen, hard muscles warm to touch.
51
Q

Gruiformes (Cranes, coots, bustards) disorder in chicks

A
  • **Leg disorders: **hand raised cranes are predisposed - deformities in the proximal ends of tibiotarsus and tarsumetatarsus, distal end of tibiotarsus and intertarsal and tibio-femoral joints. Result from rapid weight gain (first 4 weeks) combined with insufficient limb strengh. may also be nutritional deficiency, improper handling, or combination. Exercise is known to reduce the incidence (walking, swimming several times/day). If weigh gain exceeds 10% - feed withholding.
  • Crooked toes common - splinting at first sign.
  • Natural incubation (hatching and rearing parent or foster) appears to reduce leg and toe abnormalities.
  • Diets containing low methionine or sulfur-contaning amin acids reduces chick growth rates.
52
Q

Gruiformes (Cranes, coots, bustards) noninfectious disease

A
  • Arthitis: joints of legs. trauma (most common cause), septic, secundary to congenital or developental, immune-mediated.
  • Fracture of long bones: serious problemes due to high rate of cmplications and subsequent death. prosthetics have been used.
  • Toxins: lead, C. botulinum (progressive paralysis), Famphur (organophosphate anticholinesterase inseticide) in wild crane sin GA. 9500 sandhill cranes died in Texas and New Mexico because of Fusarium (contaminated peanut) - inability to hold head straight while flying or standing. Neurotoxic cyanobacteria.