Galliformes Flashcards

1
Q

What are the 5 families in the order Galliformes? What species are in each of them?

A
  • 5 Families:
    • Phasianidae – Chicken, quail, partridges, pheasants, turkeys, peafowl, grouse.
    • Odontophoridae – New World quails
    • Numididae – Guineafowl
    • Cracidae – Chachalacas and curassows
    • Megapodiidae – Malleefowl, maleo, and brush-turkeys
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2
Q

Define the following poultry terms:

  • Pullet
  • Cockerel
  • Cock, rooster
  • Hen
  • Pollar
  • Broiler
  • Roaster
  • Chook
  • Capon
  • Alektrophobia
  • Cochins and Brahmas
  • Crest
  • Frizzle feathers
  • Saddle
  • Shank
  • Sex feather
  • Sickles
  • Snood
  • Pickout or peckout
  • Straight run
  • Spent
  • Fart egg, rooser egg, oops egg
A
  • Pullet – Young female chick
  • Cockerel – Young male chick
  • Cock, rooster – Adult male
  • Hen – Adult female
  • Pollar – Genetic female with male phenotype
  • Broiler – Meat chicken 5 lbs live weight at slaughter
  • Roaster – Meat chicken 6-8 lbs live weight at slaughter.
  • Chook – Australian term for chicken
  • Capon – Castrated male
  • Alektrophobia – Fear of chickens
  • Cochins and Brahmas – Feather-legged breeds
  • Crest – puff of feathers on heads of Houdan, Silkie, Polish breeds aka topkot.
  • Frizzle feathers – Curl rather than lay flat.
  • Saddle – part of back before tale.
  • Shank – Tarsometatarsus
  • Sex feather – Hackle, saddle, tail feather rounded in hen, pointed in rooster.
  • Sickles – long, curved tail feathers of some roosters
  • Snood – Turkey fleshy appendage behind nares.
  • Pickout or peckout – Cannibalism at vent.
  • Straight run – Clutch of newly hatched chicks that have not been sexed
  • Spent – Hen that is no longer laying
  • Fart egg, rooser egg, oops egg – small egg that passes through oviduct without reaching full size.
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3
Q

What is unique about the brain of the woodcock?

A

the cerebellum is ventral to the cerebrum and the foramen magnum is ventral to that

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4
Q

What is unique about the trachea of the Helmeted currasow?

A

It loops back to the cloaca before entering the lungs.

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5
Q

Describe the GI anatomy of galliform birds.

Describe the crop to ventriculus.

Do they have a gallbladder?

Do they have a cecum?

A

· GI

§ Distensible crop (except guana and chachalaca)

§ Muscular ventriculus

§ Well-developed ceca—all of them produce cecal droppings

§ Grit is not required for digestion

§ All species possess a gall bladder

· Feces – sulfur-colored droppings characteristic of histomoniasis. Cecal droppings are darker in consistency and occur at night.

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6
Q

What structures are unique to the galliform integumentary system?

A

· Integument

· Most species have spurs on their lower pelvic limbs

· Some species have portions of skin that is unfeathered, including the head, or ornamental structures

§ Snood = fleshy skin appendage near upper beak btwn the eyes

§ Prone to frost bite

· Since they are terrestrial, adaptation to be ground dwelling includes cryptically brown, black, gray—males may be brightly colored though

§ Not true of guineafowl, where both sexes are more drab colored

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7
Q

Describe the following musculoskeletal features in galliform birds?

How many cervical vertebrae do they have?

Is there any unique shoulder girdle anatomy?

What is their foot arrangement?

Are spurs attached to the bone?

A

· Musculoskeletal

· 16 cervical vertebrae

· Guineafowl have modified clavicles to hold elongated trachea

· Anisodactyl digits and commonly digit 4 is reduced in size

§ Phasianidae and Numidadae: digit 4 elevated, not in contact with the ground

§ Megapodiidae and Cracidae: digit 4 at same level as the ground

· Manus is shorter than, or about the same length, as antebrachium or brachium

· Sesamoid bone proximal to the carpus within the tendon of the tensor propatagialis muscle (see on rads)

· Spurs – composed of calcarial process ankylosed to the tarsometatarsus; removal is a surgical procedure.

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8
Q

Describe the reproductive anatomy & breeding strategy of Galliform birds.

A

· Reproduction:

· Functioning left ovary.

· Respiratory dz may predispose to oviductal impaction.

· Many exotic Galliformes are seasonal breeders, transition diet in early Feb.

· Guinea fowl form mating pairs, ratio of one male to 4-5 females recommended.

§ Eggs are tear-drop shaped (unique).

· Collect eggs once or twice daily depending on weather (more often if hotter).

· Infertile eggs can serve as source of bacterial growth (Pseudomonas) – remove from nest.

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9
Q

Describe the proper husbandry of galliform birds.

A
  • Housing:
    • Predator protection
    • Heating of buildings not required
    • Lack of adequate ventilation and retention of heat can result in resp disease.
    • Ammonia will build without proper ventilation.
      • Destroy cilia on trachea, allows for bacterial infection of lower resp tract.
      • Fans and misters can reduce heat in hot climates.
    • Additional heat can be provided by red heat lamps or heated floor mats for posthatch period, overheating and fire hazards are concern.
      • Birds will crowd away from source if overheated.
      • Sun exposure can cause feather color changes, result in disqualification for show.
      • Loud noises can be frightening, cause piling in corners and suffocation.
      • Heavy breeds can injure themselves jumping from perches.
      • Small birds may get trapped in corners.
      • Two next boxes for 3-5 hen flocks to reduce fighting.
      • Individual housing units per species recommended rather than mixing.
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10
Q

What breed generalities would you discuss with a client looking to get backyard chickens?

A
  • Choosing breeds:
    • Commercial broilers not recommended for backyard flocks, will grow rapidly without restricted feed resulting in musculoskeletal and cardiac issues.
    • Laying breeds tend to be lighter and more active.
    • Meat breeds tend to be larger and calmer, less aggressive.
    • Dual-purpose breeds are popular.
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11
Q

What are some common issues with hatching galliform chicks?

A
  • Common problems with hatching chicks:
    • Early deaths i.e. infertile eggs, improper storage prior to incubation, extreme temp fluctuation.
    • Late deaths, not pipped i.e. extreme temp fluctuation and poor humidity.
    • Pipped but dried and stuck to egg shell i.e. poor humidity in late incubation and hatching period, weakened embryos from temp fluctuations.
    • Pipped but drowned in fluids or malpositioned i.e. turning malfunction during incubation.
    • Once hatched, do not move until dry and fluffed.
    • Chicks that hatch without full yolk sac absorption should be euthanized.
    • Embryonated eggs euthanized by chilling.
    • All chicken chicks should be vaccinated for Marek’s dz within 24h post hatch.
    • Sex – when older, male chickens and turkeys have two dorsal papillae that can be observed after eversion of vent.

Speer

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12
Q

Describe the appropriate diet selection for chickens.

Describe the diets of the following galliform birds:

  • Pheasants
  • peacock pheasants and roul rouls
  • Argus hens
  • Koklass
  • Blood pheasants
  • Cracids
  • Grouse
  • Hoatzin
  • Willow Ptarmigan
A

· Chickens:

o Starter, finisher, meat builder and laying/breeding rations.

o Laying birds must have Ca supplementation and layer ration.

o Scratch only as a supplement after regular feed has been consumed.

o Anticoccidials recommended for backyard flocks.

· Pheasant species similar to requirements for domestic turkeys: 28-30% protein as chicks, decrease to 20-24% as growing/breeding, then 13-15% for maintenance—can use commercial poultry or game bird pellets

· Produce, insects as supplements

· Precocious chicks, so pecking must be encouraged

· Peacock pheasants and roul rouls need high protein supplements like meat or eggs

· Argus hens feed chicks for their first few days of life (so hens won’t be eating at that time)

· Koklass = strict vegetarians

· Blood pheasants eat moss, lichen, ferns, grass and conifer needle buds

· Cracids (Currasows, Guan, Chachalaca) are generally frugivorous, but do eat some insects

o There is a commercial diet for currasows

· Tetraonidae (grouse) are generally herbivorous as adults and have large ceca, although the woodcock each 60% earthworms and 40% insects

· (Hoatzins have such specialized plant requirements (much of the diet consists of arum plant) – no suitable captive diet is known)

· Willow ptarmigan have been known to develop Vitamin C deficiency in captivity → source in wild is unknown

· Eared pheasants, monals and cheer pheasants use the upper bill to search in the soil for food

o If proper substrate for this digging is not provided, they may require bill trims

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13
Q

What stimulates chickens to molt?

A
  • Molting:
    • 3-4 month molt period normal for backyard flocks.
    • Reduction of light period can stimulate molt. Important for hens to molt.
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14
Q

How can you tell if a given chicken is an active layer or not (assuming you haven’t seen which birds are laying the eggs)?

A
  • Laying:
    • Easiest way to determine lay is to palpate pubic bones, will have a 2-3 finger spread rather than meeting just below the vent as in nonlayer.
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15
Q

What is fipronil?

Is it legal to use in chickens?

Is it present in eggs?

What toxic effects have been documented?

A
  • Fipronil
    • broad-spectrum phenylpyrazole antiparasitic
    • interferes with activation of insect-specific GABAA receptors, resulting in neuronal hyperexcitation and death in fleas and ticks
      • can induce neurologic symptoms such as seizures, dizziness, sensory impairment, and agitation in humans by GABA receptor activity
    • major metabolites, fipronil sulfone and fipronil desulfinyl, have less selectivity for insect receptors, compared with the parent drug
    • repels insects from crops and homes
    • not approved for use in food-producing animals
    • no FDA approved fipronil products - pesticide regulated solely by EPA in US
    • High residues in tissues – lipophilic drug
      • long half life because of lipophilicity
    • can exert toxic effects following inhalation or ingestion
    • even fairly low concentrations of fipronil can cause mitochondrial injury by uncoupling phosphorylation, which can lead to cell death
      • murine models - toxic to repro system, causes thyroid enlargement, cancer, hepatocyte damage leading to hepatomegaly and hepatocellular carcinoma
      • dogs and mice - oral administration associated with neurologic damage, including developmental delays
  • pesticide products for flea and tick prevention that are formulated for oral administration are regulated by the FDA, whereas topical pesticide formulations are regulated by EPA
  • extralabel use of EPA-regulated products is expressly prohibited in the United States
    • extralabel use of fipronil, including inadvertent administration, to poultry is unlawful in the United States
  • FARAD may attempt to provide withdrawal interval recommendations in cases of accidental exposure or contamination

Consequences of fipronil exposure in egg-laying hens

JAVMA 2018 253(1) 57-60

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16
Q

How does lead affect backyard chickens?

Does lead move into eggs?

Are there any ways to reduce lead levels in backyard chickens?

A

Clinical signs:

· Lead toxicity in chickens - crop stasis to acute lethargy, diarrhea, ataxia, and marked weight loss, to more chronic progressive neurologic deficits due to axonal degeneration;

· symptomatic threshold for lead toxicosis in chickens, however, is not well established

o chickens may be relatively resistant to developing acute signs of lead toxicosis - early signs may be decrease in egg production

· BYCs would benefit from routine screening for lead

o presence of clinical signs are an unreliable indicator of exposure

· reduction in egg production is also documented in poultry that are intoxicated with lead

· chickens living in more densely populated areas had higher BLLs

· linear correlation between BLL of hens and the levels of lead in their eggs

· 1 study found that increased dietary calcium is correlated with lower liver and blood lead values

· 1 study found that supplementation with garlic reduces lead absorption

Subclinical Lead Exposure Among Backyard Chicken Flocks in Massachusetts

Daniel C. Mordarski, Jessica H. Leibler, Carolyn C. Talmadge, Gregory M. Wolfus, Mark A. Pokras, et. al.

Journal of Avian Medicine and Surgery, 32(3) : 185-193

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17
Q

A study investigated the effects of pathogens, parasites, and pesticide residues in Bavarian pheasants.

What did they conclude?

What pathogens were identified?

A
  • Concluded that the health risk for human consumption of Bavarian game birds is low (no Salmonella or Campylobacter was found).
  • Environmental toxins do not appear to be contributing to decline of game birds in Bavaria.
  • An infectious agent only found in one bird – Mycobacterium avium avium/silvaticum.
  • Some pheasants had tracheitis or bronchitis.
  • Parasites – heterakis, capillaria, eimeria, teichostongylus, syngamus.
  • E. coli most commonly cultured from liver, heart, lung. Considered normal contaminant.
  • No Campylobacter was detected.
  • Lead and promecarb toxicosis cause of death in two pheasants.

Schmitz, A., Kronthaler, F., Stein, K., Rinder, M., & Korbel, R. (2017). Decline of game birds (phasianus colchicus and perdix perdix) in bavaria: a survey on pathogenic bacteria, parasites, pesticide residues, and influence of set-aside land and maize cultivation. Journal of Zoo and Wildlife Medicine, 48(1), 18-30.

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18
Q

Describe an appropriate preventative medicine protocol for galliform birds.

A

· Biosecurity:

o Remove attractants for other birds or rodents.

o Remove carcasses immediately.

o Rodenticides and insecticides essential.

o Quarantine birds for 6 weeks. Three negative fecals at 2 week intervals.

· Quarantine

o For exotic Galliformes or domestic Galliformes destined for children’s zoo, minimum of 45-60 days

o Most diseases have 2 week incubation

o Serial testing for parasites—at least 3 negative fecals in a row, 2 weeks apart

§ Consider prophylactic treatment even if fecals are negative

· Perform exam

· Collect serum for Mycoplasma exposure, Newcastle disease, avian influenza

· Evaluate blood smears for hemoparasites

· Consider culturing feces for Salmonella while in quarantine

· Vaccination

Fowler 8

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19
Q

How long should galliformes be fasted for prior to anesthesia?

A

Four hours, to clear crop contents.

West

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20
Q

What complication can arise from intubation of currasows or guans?

A
  • Convoluted tracheal anatomy of currasows and guans may cause problems if secretions increase in response to intubation or if bird aspirates

West

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21
Q

Describe the use of local anesthesia in chickens.

A
  • Local Anesthesia
  • Two main groups:
    • Short acting – lidocaine and mepivacaine and long acting (bupivacaine)
    • Intrathecal injection of local anesthetic for spinal cord blockade not possible not feasible due to large blood vessels.
  • Birds are not more sensitive to side effects than mammals
    • Broiler chickens: lidocaine 6mg/kg IV – no adverse effects
    • Pharmacokinetics of lidocaine shown in chicken to be similar to mammals
    • Author (Darryl Heard) uses 10mg/kg for lidocaine and mepivacaine as upper limit and 2mg/kg or less for bupivacaine.

West

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22
Q

Describe the appropriate use of propofol in chickens.

What complications are common?

What is the safety margin like?

A
  • Propofol
  • Chickens: 4.5-9.7mg/kg followed by CRI 0.5-1.5mg/kg/min for 20 minutes, rapid induction – sometimes marked cardiopulmonary depression. – Single or multiple runs of premature ventricular complexes was observed in many birds. – one required lidocaine 0.5mg/kg IV for ventricular tachycardia.
    • Prop at 3 times the induction dosage was fatal in all birds
      • VERY narrow safety margin

WEst

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23
Q

Describe the use of alfaxalone in chickens. What doses are appropriate?

A
  • Alfaxalone
    • [JEPM 29(2019) pp119-122] Induction of anesthesia with intravenous alfaxalone in 2 chickens.
      • Poor quality at 5mg/Kg with period of excitement.
      • Relaxation occurred after 10mg/Kg and 15mg/Kg total dose
      • Individual variations including possible intrinsic differences in drug metabolism or differences in physiological status at time of surgery, and speed of administration of medication
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24
Q

What premeds have been shown to reduce MAC in chickens?

A

Morphine and methadone - West

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25
Q

What muscle relaxants have been used in chicken anesthesia?

A
  • Muscle Relaxants
  • Nondepolarizing short-acting muscle relaxant atracurium besylate (0.15 to 0.45mg/kg IV) can be used as an adjunct to inhalation anesthesia.
    • Chicken: 0.25mg/kg – 95% twitch depression in 50% of birds – lasts 35 minutes
      • 0.45mg/kg – 95% twitch depression in 95% of birds – lasts 50 minutes
      • Cardiopulmonary effects not significant

West

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26
Q

What is the predominant opioid receptor in the chicken midbrain and forebrain

A
  • opioid receptors
    • endogenous opioid system functions in central processing of nociceptive information, with endogenous opioids (b-endorphin and enkephalin) binding to opioid receptors to inhibit pain
      • chicken forebrain and midbrain - mu receptors most prevalent, detectable in chick embryos at 10 days old

West

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27
Q

Describe the use of morphine in chickens.

A
  • Morphine
    • Mu- agonist
    • studies in chickens have been conflicting on effects and required dosage, and may be breed/strain-dependent
    • Adult chickens 🡪 MAC-sparing effect
    • Pharmacokinetics in chickens: 2 mg/kg IV
      • Conflicting effects, dependent on breeds, clear faster than people or cats.

West

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28
Q

Describe the use of transdermal fentanyl patches in chickens.

A
  • Transdermal patch in chickens. Delaski et al. JAMS 1(1):6–15, 2017 (see abstract below)
    • Although maximum plasma fentanyl concentrations varied substantially by individual birds
    • mean of elimination half-life was 7.2 +/- 3.7 hours = less variation
    • In chickens, mu, kappa and delta receptors have been identified in the brains of chicks. Both mu and kappa agonists have reduced minimum alveolar concentration (MAC) in adult chickens
    • Morphine leads to more sedation in chickens than butorphanol does
    • Fentanyl reduced MAC in RTHA and HAP CRI
    • Patches tend to have variability in absorption due to fur (epilated vs clipped, thickness of skin, skin permeability and drug clearance)
    • Variability vs mammals may be due to increased metabolic rate, higher temperature, feathered skin.
    • Mean maximum concentration was 2.86ng/ml.
    • Elimination half-life was 7.2 h (in dogs it is 2 and in goats it is 5h)
    • Cockatoos 0.02mg/Kg had Cmax of 3.33ng/mL but no effects on analgesia
    • RTHA Cmax of 8.5-30ng.ml = reduced MAC
      • This study did not reach those levels to decrease MAC, unclear if it would.
    • Fentanyl patches 🡪 absorbed into skin acting as reservoir, absorbed slowly by first-order processs.
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29
Q

Describe the pharmacokinetics of meloxicam in chickens and its effect on eggs.

A
  • Chickens: (Souza et al. JAMS 32(1):8–12, 2018 see articles)
    • 1 mg/kg, chickens maintained a plasma concentration associated with analgesia in people for approximately 12 hours (0.5–1.5 ug/mL)
    • No residues detected in eggs at 8 days (yolks) and 3 days (whites) = 2 week withdrawal is enough
    • (Other studies: 5mg/Kg IM once = antinociceptive; 0.5-4mg/Kg = subjectively worked)
  • Pharmacokinetics and egg residues after oral administration of a single dose of meloxicam in domestic chickens (Gallus domesticus). JAMS 2017 31(4) 393
    • 1mg/Kg PO once.
    • drug was not detected after 4 days in egg whites and after 8 days in egg yolks
    • 1 mg/kg PO in chickens appears to maintain plasma concentrations equivalent to those reported to be therapeutic for humans for 12 hours.
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30
Q

There are several management related illness in managed chickens.

Describe the presentations and management of the following conditions:

  1. Cannibalism
  2. Bumblefoot
  3. Fatty Liver
  4. Caged Layer Fatigue
  5. Cloacal Prolapse
  6. Egg Binding & Dystocia
A
  • Cannibalism:
    • Chicks – unusual, usually due to not enough feed or diarrhea/soiled vents that attract pecking.
    • Control in older birds – reduce lighting, reduce number of birds, increase number of feeders, trim the beaks.
    • Spray superficial wounds with pruning tar for topical treatment and ID of which individuals are pecking. Red spectacles or contact lenses reduces the behavior in peckers.
  • Bumblefoot:
    • Soaking in Epsom salts twice daily for 10 minutes can help remove scabs.
      • Oral antibiotics may be warranted in infection. Prognosis declines with osteomyelitis.
  • Fatty liver [hemorrhagic liver syndrome]:
    • Extreme fat deposition, sudden drop in egg production, increased mortality.
    • Obese, pale combs and wattles, may be covered with dandruff.
    • Pets fed table scraps at risk. Mortality is from liver rupture and hemorrhage. Tx with prevention.
  • Caged layer fatigue (Osteoporosis):
    • Unable to stand, pathologic fractures, paralysis. Usually BAR.
      • Probably caused by vit D3, Ca, P deficiencies and/or imbalances.
      • May die acutely from spinal fracture, severed cords or recover following placement with easy access to food and water.
        • IM vit D3 or IV Ca may help.
        • Oyster shell added to diet ad lib for prevention. Needs to be retained in gizzard, don’t grind too fine.
      • Increased Ca in diet for too long can result in urolithiasis or permanent cessation of parathyroid gland activity.
  • Cloacal prolapse:
    • Stopping lay with reduced feed and decreased lighting, keeping vent clean in mild cases may help.
    • Chicks hatched in fall with increase of light in early spring can be prematurely induced into lay and they are predisposed to prolapse.
      • Controlling light extremely important.
  • Egg binding and dystocia:
    • Pullets too early in production or obese hens.
    • Eggs can be refluxed into the coelom, single or multiple in oviduct, or shell membranes/concretions in oviduct.
    • May be secondary to other reproductive disease.
    • Yolk coelomitis may occur.
    • Some salpingohysterectomized females can take on male characteristics (pollards).
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31
Q

Describe appropriate biosecurity for chicken operations.

A
  • Biosecurity:
    • Remove attractants for other birds or rodents.
    • Remove carcasses immediately.
    • Rodenticides and insecticides essential.
    • Quarantine birds for 6 weeks.
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32
Q

Describe the lesions seen in calcium or vitamind D deficient chickens at necropsy.

A
  • Ca/vit D deficiencies – rickets, osteomalacia.
    • Rickets – juveniles, enlargement or beading of the junctions of the ribs with sternum and vertebrae (rachitic rosary), bending of ribs with lateral flattening of thorax, pathologic fractures, lateral deviation of sternum and spinal deformities.
      • Histo – thickened zone of proliferation in growth plate of bones and enlarged parathyroid glands.
        • Phorphorus deficiency or calcium excess results in these changes in absence of parathyroid gland enlargement.

Terio

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33
Q

Describe the lesions associated with vitamin E deficiency in gallinaceous birds.

What age is most commonly affected?

A
  • Vit E deficiency – accumulation of peroxides and deficiency in antioxidants results in encephalomalacia, muscular dystrophy, exudative diathesis.
    • Encephalomalacia aka crazy chick disease.
      • 2-4 week old birds, damage to capillary walls result in edema, hemorrhage, malacia.
      • Swelling of cerebellum, petechial hemorrhage produces cherry red appearance.
      • Necrosis of cerebellar folia.
    • Muscular dystrophy – white streaks in muscle fibers. Can tx with addition of cysteine to feed.
    • Exudative diathesis – subcutaneous edema, hemorrhage, green-blue gelatinous appearance in ventral thorax and abdomen, periorbital. Add selenium to feed. Individual birds, vit E injection.
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34
Q

What vitamin is deficient in chickens with curled-toe paralysis?

What other lesions may be present on necropsy?

A
  • Curled-toe paralysis – vit B2 deficiency (riboflavin), required for myelin synthesis in peripheral nerves.
    • Generalized demyelinating polyneuropathy.
    • Sciatic, brachial, cervical, lumbar, large intramuscular nerves commonly swollen and soft.
      • Sciatic may be 5x larger than normal.

Terio

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35
Q

What lesions are observed in chickens with vitamin A deficiencies?

A
  • Hypovitaminosis A – Epithelial metaplasia and hyperkeratosis.
    • Thickening of mucosa of tongue, choana, salivary glands, esophageal glands, formation of pustule-like nodules due to hyperkeratosis and distension of ducts with cellular debris.
    • Conjunctiva, bursa of Fab, nasal passages, sinuses may have caseous exudate.

Terio

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36
Q

What nutritional deficiencies can lead to perosis?

A
  • Choline or manganese deficiency – perosis or chondrodystrophy.
    • Impaired endochondral bone growth.
    • Small for age.
    • Thickened, bent, twisted tarsometatarsi, deformed articular cartilage.
      • Gastroc tendon dislocation may occur.

Terio

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37
Q

What foods may predispose chickens to goiter?

A
  • Thyroid hyperplasia (goiter) – Dietary deficiency or excess of iodine, consumption of goitrogenic substances (spinach, cassava, peanuts, soybeans, kale, broccoli, brussels sprouts, cabbage, canola, cauliflower, mustard greens, radishes, rapeseed), goitrogenic drugs i.e. sulfonamides, and defective negative feedback control by the pituitary.

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38
Q

Describe the differences between acute and chronic gout in gallinaceous birds.

A
  • Gout
    • Urate accumulation in soft tissues or joints.
      • Uric acid end-product of protein and purine metabolism (uricotelic).
        • Acute (visceral) and chronic (articular) forms.
          • Urate deposition in joints can occur in both forms.
          • Acute urate deposition vs chronic urate deposition more appropriate terms vs visceral and articular gout.
          • Granulomatous inflammation observed in chronic cases.

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39
Q

In gallinaceous birds, exertional myopathy lesions are present in what muscles?

Broiler chickens are predisposed to what muscle lesions?

A
  • Exertional myopathy commonly affects wings and legs.
  • Deep pectoral myopathy – exertional compartment syndrome of the supracoracoid muscle characterized by ischemic necrosis in the absence of other muscular lesions.
    • Compartmental myopathy produces high levels of lactic acid and myonecrosis.
      • Complications include lactic acidosis, renal failure, arrhythmias, death.

Muscle turns green, dry, friable, necrotic.

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40
Q

Toxicities in chickens occur commonly from their pecking feeding behavior.

What are two of the most common toxicity types? What clinical signs would be seen?

A
  • Heavy metals.
    • Lead, zinc.
      • CS – wt loss, lethargy, depression, anemia, paralysis, head tremors, convulsions, death.
      • Demyelination of peripheral nerves, focal areas of vascular damage in cerebellum.
      • Differentiate from botulism.
      • Primary tx is removal of toxic metal.
  • Mycotoxicosis.
    • Aflatoxins, fusariotoxin.
    • High risk of exposure due to consumption of primary seed-based diets.
    • Cause immunosuppression, anemia, hemorrhage, hepatic degeneration, paralysis.
    • Fusariotoxins assoc with feed refusal, extensive necrosis of oral mucosa and skin, hyperplastic bone marrow.

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41
Q

Amyloidosis in gallinaceous birds is commonly associated with what chronic infections?

A
  • Amyloidosis.
    • In chickens, turkeys – commonly associated with chronic infections i.e. Mycobacterium avium, Mycoplasma spp, Enterococcus faecalis.

Teiro

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42
Q

What are the most commonly seen neoplastic lesions in chickens?

A
  • Neoplastic
    • Virus-associated most commonly observed.
    • Others – oral SCC, fibromas, lipomas, fibrosarcomas, leiomyomas in the mesosalpinx, leiomyosarcomas, rhabdomyomas, rhabdosarcomas, ovarian or oviductal adenocarcinomas with or without mets.
  • Xanthomas – nonneoplastic, white to yellow nodular masses that occur in skin, SQ, and internal organs.

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43
Q

Quail bronchitis is caused by what virus?

What clinical signs are present?

What gross and histologic lesions would be present on necropsy?

A
  • Adenoviruses – Aviadenoviruses
    • Quail bronchitis Virus
      • Resp dz, bobwhite and Japanese quail, < 4 wks age.
      • Older birds subclinical.
      • Gross – catarrhal tracheitis, corneal clouding, conjunctivitis, congestion in nasal passages and infraorbital sinuses.
      • Lymphoplasmacytic tracheitis, bronchitis, necrosis, large intranuclear inclusions (basophilic).
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44
Q

Inclusion Body Hepatitis in galliforms is caused by what virus?

What species are affected? Any age groups predisposed?

What other viruses may predispose them to IBH?

What lesions would be present on necropsy?

A
  • Adenoviruses – Aviadenoviruses
    • Inclusion body hepatitis – chickens, guinea fowl, turkeys.
      • Immunosuppressive viruses i.e. chicken anemia virus or infectious bursal dz virus may predispose.
      • 2-3 wk old birds or younger.
      • Gross – Enlarged, friable, pale liver, necrosis and hemorrhage.
        • Hydropericardium, hemorrhagic kidneys, intranuclear inclusions in hepatocytes and pancreas.
        • Dx – hepatocellular inclusions within lesions, virus isolation, immunofluorescence, PCR.

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45
Q

Hemorrhagic enteritis is caused by what virus in gallinaceous birds?

What lesions may be present on necropsy?

A
  • Hemorrhagic enteritis – Siadenovirus in turkeys, guinea fowl, partridges.
    • SI hemorrhage, friable enlarged spleen with reticuloendothelial cell hyperplasia.
    • Basophilic/amphophilic IN inclusions in RE cells.
    • Marble spleen dz – Siadenovirus in pheasants.
      • Spleen swollen, mottled, lungs congested and edematous.
      • IN inclusions in MP and lymphocytes and Kupffer cells in liver.
      • AGID or PCR can confirm.
    • Histo – variable degrees of lymphoid necrosis in bursa.
      • Lymphoid depletion in spleen, cecal tonsils, bone marrow.
      • IN and IC basophilic globular or characteristic botryoid inclusion bodies in MP and epithelial cells of bura.
      • May also be in thymus, spleen, cecal tonils, lungs, duodenum.
      • Nonenveloped, icosahedral viral particles loosely arranged or in paracrystalline array.
      • Dx – PCR (feces, tissues), ELISA, inclusion bodies in bursa and/or other organs.

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46
Q

Infectious Laryngotracheitis is caused by what etiologic agent in gallinaceous birds?

What species are primarily affected?

What lesions are present on necropsy?

A
  • Infectious laryngotracheitis ILT – Gallid herpesvirus 1 (GaHV1).
    • OIE reportable disease.
    • Primarily chickens, also pheasants, peafowl, turkeys.
    • Infects resp tract and conjunctiva.
    • Latency in trigeminal ganglia, reactivated in immunosuppressed birds.
    • Excess mucus, hyperemic mucosa, petechiae, intraluminal fibrinonecrotic material or hemorrhage.
    • May occlude laryngeal opening, cause suffocation.
    • Eosinophilic, IN inclusion bodies.
    • Syncytial cells may be present.
    • Dx – pathologic changes, VI, immunofluorescence, PCR.

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47
Q

Marek’s Disease is caused by what etiologic agent?

What species and age roups are typically affected?

How is this diseases transmitted?

A
  • Marek’s disease virus – Gallid herpesvirus 2 (GaHV2).
    • Quails, pheasants, turkeys, chickens.
    • Unvaccinated immature chickens 2-7 mos old, or any age.
    • Replicates in feather follicular epithelium, shed in dander.

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48
Q

Describe the four phases of pathogenesis in Marek’s Disease.

A
  • Marek’s disease virus – Gallid herpesvirus 2 (GaHV2).
    • Pathogenesis has four phases:
      • Early – inhalation of virus with feather dander infects resp epithelial cell and local MP followed by viremia with cytolytic viral replication in lymphocytes.
      • Latency phase in CD4+ T cells, systemic viral dissemination.
        • Cutaneous viral infection, replication, shedding.
      • Third – Reactivation in CD4+ T cells, late cytolytic stage and immunosuppression.
      • Final – reactivation of virus, neoplastic transformation of CD4+ T cells.

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49
Q

Describe the lesions associated with Marek’s Disease.

A
  • Marek’s disease virus – Gallid herpesvirus 2 (GaHV2).
    • Gross – bursal and thymic atrophy, tumor infiltration and enlargement of peripheral nerves, white discoloration of iris with dyscoria, nodular lesions in feather follicles, hepatosplenomegaly, pale white tumors in various organs.
      • Birds with visceral tumors may only be cachexic.
      • Enlarged crop may be present from paralysis of the vagus nerve. Ddx for crop impaction.
      • Peripheral nerve lesions – unilateral or bilateral, involve sciatic, brachial and vagus nerves and spinal root ganglia.
        • Type A and B lesions present in peripheral nerves, characterized by infiltration of neoplastic CD4+ T cells and mixed inflammation with edema, respectively.
        • PN lesions rare in quail and turkeys.
    • Histo – Cerebral perivascular lymphocytic cuffing, vasculitis, edema, gliosis, lymphocytic meningitis. Neoplastic and pleomorphic T lymphs in visceral organs.
      • Skin lesions surround feather follicles.
      • Eosinophilic IN inclusions may be present within feather follicle epidermis.
      • Lymphoma may be present in uvea, PN, brain.

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50
Q

How is Marek’s Disease diagnosed and managed?

A
  • Marek’s disease virus – Gallid herpesvirus 2 (GaHV2).
    • Viral detection along not confirmatory since MDV is ubiquitous.
    • Dx relies on characteristic lesions with detection of antigens (pp38 and meq) in tissues by IHC, VI, or PCR from feather tips, blood, or tissues.
    • Vx cannot be overdosed, is safe for clients to apply. In ovo or after hatch. Ddx avian leukosis.
    • Mortality is inevitable but sporadic, depopulation not recommended. All incoming birds must be vaccinated regardless of age.

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51
Q

What is the mechanism of epithelial cell hyperplasia with avian poxvirus?

A
  • Encodes a protein similar to epidermal growth factor, assoc with epithelial cell hyperplasia in infected tissues.

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52
Q

Describe the lesions associated with avian pox in gallinaceous birds.

How is this disease transmitted?

How is it diagnosed?

Is there a vaccine?

A
  • Avian poxvirus – fowlpox, quailpox, turkeypox.
    • High morbidity, low mortality.
    • Encodes a protein similar to epidermal growth factor, assoc with epithelial cell hyperplasia in infected tissues.
    • Gross – proliferative tan nodules, primarily on unfeathered head, feet.
    • Nodules ulcerate, become brown and hemorrhagic as a result of local trauma.
    • Wet/diphtheritic form characterized by proliferative and ulcerative lesions with diphtheritic membranes in mouth, tongue, esophagus, conjunctiva, upper resp tract. Both forms may occur together.
    • Histo – Irregular acanthosis, spongiosis, ballooning degeneration with brightly eosinophilic, intracytoplasmic inclusions (Bollinger bodies) in skin.
    • Bollinger bodies typically considered diagnostic; molecular testing also available.
    • Transmission – ocular, GI, resp routes, exposure to contaminated environments, food, water, mosquito bites break skin and facilitate infection. Inc 4-10 days, all ages.
    • Dx – VI, PCR, EM support histo.
    • Vx – stab stick through wing web. Turkeys – apply to drumksticks; otherwise can get infections on head from sleeping with head under wing in contact with ‘take’ sites of vaccines on wing.
53
Q

Describe the presentation of low path versus high path influenza in gallinaceous birds.

What HA & NA subtypes are present in high path?

How is this disease confirmed?

What are the natural reservoirs?

A
  • Avian influenza virus – Influenza A viruses.
    • Anseriformes, Charadriiformes natural reservoirs.
    • Classified by hemagglutinin (HA) and neuraminidase (NA) surface glycoproteins.
    • Two pathotypes – low and highly pathogenic AIV.
      • All AIVs reportable to the OIE for domestic spp, only HPAI reportable for wild birds.
      • Wide range of CS depending on host species, age, immunity.
      • LPAIV may be subclinical or assoc with resp, GI, urinary, and repro tracts.
      • Virus is usually limited to mucosal epithelium of resp and GIT due to requirement for trypsin-like enzyme for cleavage of HA protein.
      • Circulation of H5 and H7 subtypes LPAIV in poultry may result in acquisition of multiple basic AA in the HA protein cleavage site and emergence of high path.
    • HPAIV – high mortality in chickens and turkeys.
      • CS include depression, paresis, paralysis, mortality.
      • Edema, cyanosis of head and comb, hemorrhages, necrosis.
      • Dx – VI, antigen capture immunoassays, rtPCR or qRTPCR in oropharyngeal (chicken) and cloacal swabs (waterfowl), feces, organs.
        • Rapid dx by screening oropharyngeal swabs using matrix gene for influenza A by qRTPCR and testing of positive samples with H5 and H7 subtype-specific qRTPCR.
      • Flocks positive by screening tests must have samples sent to accredited lab for PCR confirmation; if H7 or H5, sent to National Veterinary Services Laboratories NVSL; all flocks confimed positive for either low or high path will be depopulated. No vx permitted in US without permission from USDA.

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54
Q

What is the etiologic agent of Newcastle Disease?

What are the three forms? How do they vary in virulence?

What is the pathogenesis?

What lesions are present on necropsy?

A
  • Newcastle disease virus – Avian paramyxovirus 1.
    • OIE notifiable.
    • Forms
      • Velogenic – highly virulent. Aka exotic Newcastle, not in US.
        • Severe nervous and resp dz, high mortality up to 100%.
      • Mesogenic – moderately virulent.
        • Primarily affect egg production, produce mild respiratory disease and cause low mortality.
      • Lentogenic – nonpathogenic.
        • Usually asymptomatic in adults, may cause resp dz in young.
    • Pathogenesis – viral replication in mucosal epithelium of resp and GIT, viremia, viral dissemination to multiple organs and brain.
    • Gross lesions – facial edema, ventricular and/or proventricular hemorrhage, necrosis and hemorrhage of intestinal mucosa (especially cecal tonsils and Peyer’s patches), splenomegaly with congestion and mottling.
      • Histo – nonsuppurative encephalitis, disseminated vasculitis, necrosis in lymphoid tissues, hemorrhage of conjunctiva, trachea, GIT.
      • Low virulence NDV – mild conjunctivitis, rhinitis, tracheitis, pneumonia, airsacculitis.
    • Dx – VI, RTPCR, DNA sequencing support histo.
    • Intracerebral pathogenicity index ICPI test determines the virulence of the virus.

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55
Q

Eastern Equine Enceaphalitis causes neuro signs in what gallinaceous birds?

What is the family of the etiologic agent?

What lesions are commonly observed?

A
  • Eastern equine encephalitis – EEE (Togaviridae, Alphavirus) – zoonotic, causes neuro signs and encephalitis in ring-necked pheasants, chukar partridges, turkeys.
    • High mortality, young birds most susceptible.
    • Pale focal areas in heart and enlarged mottled spleen.
    • Histo – lymphocytic meningoencephalitis with perivascular cuffing, gliosis, neuronal degeneration, satellitosis.
      • Myocardial necrosis, lymphocytic myocarditis, lymphoid depletion.

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56
Q

Highlands J Virus is what type of virus?

What gallinaceous birds does it affect?

What lesions are associated with it at necropsy?

A
  • Highlands J virus (HJ) – Alphavirus (togaviridae) infection of turkeys and chukar partridges.
    • N and S America.
    • Splenomegaly, myocardial pallor, necrotizing myocarditis, intestinal serosal hemorrhage, enteritis with necrosis of gut-associated lymphoid tissue, lymphocytic meningoencephalitis, lymphoid necrosis.

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57
Q

What is the etiologic agent of infectious bronchitis in galliformes?

What species/age groups are commonly affected?

What methods of control are available?

A
  • Infectious bronchitis virus IBV (Gammacoronavirus)– resp disease, young chicks, coronavirus. Chicks may have permanent damage to repro tract resulting in false layers (inability to lay eggs when older).
    • Live and killed vaccines available, usually not used unless chicken is going to a show.

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58
Q

What avian pneumoviruses commonly affected gallinaceous birds?

Which species does each affect and what clinical signs are associated?

A
  • Pneumoviridae, metapneumovirus
  • Turkey rhinotracheitis TRT and swollen head syndrome SHS – highly contagious resp dz caused by avian metapneumoviruses.
    • TRT primarily dz of turkeys.
      • TRT – watery mucoid exudate in nasal passages and trachea, periorbital and infraorbital edema, polyserositis with airsacculitis, pericarditis, salpingitis, oophoritis.
        • Small eosinophilic intracytoplasmic inclusions in acute dz, nasal turbinates and trachea.
        • Dx – VI, RT-PCR on upper resp tract tissues, swabs, mucus.
    • SHS primarily dz of chickens.
      • SHS – swelling of sinuses, SQ of mandible, neck, wattles due to accumulations of yellow gelatinous caseous material.
    • Viruses infect and replicate in epithelium of resp tract causing ciliostasis, secondary bacterial ifnections.
59
Q

Avian encephalomyelitis is caused by what etiologic agent in gallinaceous birds?

What clinical signs and lesions are present?

How is the disease diagnosed and managed?

A
  • Avian encephalomyelitis virus – Genus Tremorvirus.
    • Neuro signs in 1-3 wk old birds.
    • Infection of intestinal epithelium followed by viremia, viral dissemination to organs, muscle, brain.
    • Pale muscular layers of ventriculus may be only gross lesion.
    • Survivors may develop cataracts. Chicks from infected hens may be blind.
    • Dx – CS include spinning/torticollis/seizure, disseminated nonpurulent inflammation of CNS, ID of characteristic central chromatolysis in neuronal cell bodies in brain stem.
      • VI on brain samples confirms, fluorescent Ab can be performed on tissues for antigen.
      • No tx; Vx for prevention. After 8 wks of age, at least 4 wks prior to production. Can be co-applied with stab stick during pox virus vx.

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60
Q

Lymphoid leukosis in gallinaceous birds is caused by what etiologic agent?

What clinical signs does it cause?

What lesions are present on necropsy?

A
  • Lymphoid leukosis LL - Family Retroviridae, Genus Alpharetrovirus, Avian Leucosis Sarcoma virus
    • Older chickens, avian leucosis sarcoma viruses.
    • 10 subgroups – A-J.
      • Variety of tumors – lymphoid leukosis, soft tissue sarcomas, epithelial cell tumors (renal), tumors of endothelial origin (hemangioma, hemangiosarcoma).
        • Lymphoid leukosis most common.
          • Bursa of Fabricius is the target organ for neoplastic transformation in chickens with LL.
          • ALVs cause insertional activation of c-myc in transformed follicles by placing this gene under control of viral LTR which causes maturation arrest and proliferation of bursal stem cells.
        • Gross – hepatosplenomegaly, grayish soft tumors in various organs i.e. liver, spleen, bursa.
          • Large lymphocytes efface normal tissue, compress adjacent parenchyma.
          • Lymphoma in bursa has an intrafollicular growth pattern.
          • Dx difficult, similar CS to Marek’s and reticuloendotheliosis virus.
          • IHC for B cell and IgM surface markers, VI from peripheral WBC and tumor homogenates, standard PCR for confirmation.
          • Viral detection alone not confirmatory due to ubiquitous ALV.
61
Q

Reticuloendotheliosis virus in gallinaceous birds causes what signs?

What is the etiologic agent?

A
  • Reticuloendotheliosis.
    • Primary dz of chickens and turkeys.
    • Retrovirus in Gammaretrovirus genus. Reticuloendotheliosis Virus
    • Causes lymphoma, acute reticular cell sarcoma aka reticuloenddotheliosis, various nonneoplastic lesions.
    • CS – poor BCS, reduced reproductive performance, increased flock mortality.
    • Lesions with VI and PCR from blood and tumor diagnostic.
62
Q

Lymphoproliferative Disease in gallinaceous birds is caused by what etiologic agent?

What species is most commonly affected?

What lesions are seen on necropsy? How is this disease diagnosed?

A
  • Lymphoproliferative dz LD.
    • Turkeys in Israel and Eu (domestic), wild turkeys in NA.
    • Multifocal tan, raised, firm skin nodules – lymphoid cells mixed with palsma cells in unfeathered skin.
    • May affect spleen, liver, other organs. Common in wild turkeys in US but lesions assoc with infection and rare.
    • Dx with histo, most sensitive is molecular detection of BM, but whole blood, visceral organs and spleen may also be used. Transmission unknown.
63
Q

Where is Escherichia coli typically present in galliformes? Where is it considered pathogenic?

What clinical signs and lesions are present?

A
  • Colibacillosis – Localized or systemic infection caused by E. coli.
    • E. coli normally present in intestine of birds, excreted in feces.
    • Primary or secondary pathogen.
    • CS – may be absent, or lethargy, anorexia, peracute death.
      • Chronically infected birds stunted and unthrifty.
      • Colisepticemia or systemic E. coli most common pathogenic presentation.
    • Localized infections – omphalitis in hatchlings, salpingitis in laying hens, cellulitis of skin wounds, synovitis, airsacculitis, pericarditis, [erihepatitis.
    • Chronic granulomas aka coligranulomas aka Hjarre’s dz.
    • Attaching and effacing E. Coli has been reported.

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64
Q

Which two salmonella serotypes are of particular concern in gallinaceous birds?

What clinical signs are present with those diseases?

What are teh clinical signs of other salmonella serotypes?

A
  • Salmonella.
    • S. enterica subsp enterica serotypes Pullorum and Galinarum – pullorum disease and fowl typhoid, respectively.
    • Nonmotile, generally host specific, reportable to OIE.
    • Egg transmitted, diarrhea in young chicks and poults, high mortality, adults asymptomatic.
    • S. gallinarum (fowl typhoid) similar to pullorum, mature birds do show clinical signs.
      • PT (pullorum/typhoid testing) can be conducted via small blood drop from wing vein onto plate agglutination test right on the farm.
        • If positive on plate test, test serum via accredited vet diagnostic lab for confirmation.
    • CS – anorexia, dehydration, huddling, depression, diarrhea, death.
    • Depression, reduced feed consumption, decreased egg production, fertility, hatchability.
      • Swelling of joints, dyspnea, blindness may occur.
      • Histo – fibrinoheterophilic inflammation, multiple organs.
    • Other serotypes in S. enterica subsp. Enterica are motile and nonhost specific, dz caused by these bacteria are aka paratyphoid salmonellosis.
      • Public health concern.
      • CS usually in young or immunosuppressed birds.
      • Mortality within first few weeks of age or at onset of laying, adults typically not clinical.
        • Bacteria localized to intestine or GB of carriers, intermittently shed in feces.
    • S. enterica subsp arizonae causes arizonosis in young turkeys.
      • Egg-transmitted infection.

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65
Q

Describe the clinical signs of yersiniosis in galliformes?

How is this disease transmitted?

What lesions are present in the acute versus chronic forms?

What is an important differential?

A
  • Yersinia spp ubiquitous to environment and water, multiply at low temps.
    • Y. pseudotuberculosis most important for septicemic dz in birds.
      • Chronic dz more common – nonspecific clinical signs, sudden death.
      • Wt loss, swollen joints, paresis.
      • Acute – swelling of liver and spleen, bloody to fibrinous exudate in coelom.
      • Chronic – granulomas in organs and skeletal muscle.
        • Resembles avian mycobacteriosis.
    • Histo – coagulative necrosis of hepatocytes, fibrin, heterophillic infiltration with intralesional gram negative bacilli/giant cell granulomas.

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66
Q

What is the etiologic agent of Fowl Cholera?

What lesions are typically present?

What species are particularly susceptible?

What preventative measures can be put in place?

A
  • Pasteurella multocida – fowl cholera.
    • Acute septicemia, high mortality and morbidity.
      • All birds may be susceptible. Most severe in turkeys.
      • Chronic infection in joints, abscesses of head, oviduct, resp tract.
      • Infection includes cannibalism of sick and dead birds.
      • Carriers may harbor organism in choana, contaminating feed, water, environment.
      • Vaccines available; variable success with abx, tetracyclines with citric acid added to drinking water and reduction of calcium use will increase efficacy of the antibiotic.

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67
Q

What is the etiologic agent of Infectious Coryza?

What are teh typical clinical signs?

How is this disease transmitted?

What lesions are typically present?

A
  • Infectious coryza – Avibacterium paragallinarum.
    • Acute respiratory disease.
    • Transmission via direct contact, aerosol, contamination of drinking water.
    • Recovered birds may become carriers.
    • Upper resp clinical signs, nasal discharge, sneezing, swelling of face.
    • Drop in egg production.
    • Sinusitis, rhinitis, conjunctivitis, tracheitis, bronchitis, airsacculitis.
    • Histo – epithelial hyperplasia, edema, infiltration of inflammatory cells.

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68
Q

What are the clinical signs of galliformes affected with Ornithobacterium rhinotracheale?

Which birds are more affected?

A
  • Ornithobacterium rhinotracheale – Gram negative, acutely highly contagious resp dz.
    • Mild in young birds.
    • Older birds can have acute pneumonia, high mortality.
    • Paralysis through arthritis, osteitis, osteomyelitis.

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69
Q

What are the clinical signs of bordetellosis in galliformes?

What species are particulary susceptible?

A
  • Bordetellosis – Highly contagious upper respiratory tract disease.
    • Young turkeys, quail, partridges.
    • Bordetella avium.
      • Conjunctivitis, sneezing, moist tracheal rales in young birds, dry cough in older birds.
    • Dyspnea, OB. Deformation of tracheal rings.

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70
Q

What are the four clostridial diseases of importance in gallinaceous birds?

A
  • Clostridium.
    • Gram positive, spore-forming, catalase negative, anaerobic bacilli.
      • Environmental, pathogenicity via toxins.
      • Four clostridial diseases of importance in gallinaceous birds:
        • Ulcerative enteritis – C. colinum.
          • Acute, young birds, multiple ulcers throughout GIT, hepatic necrosis.
          • GI perforation and peritonitis may occur.
          • Survivors will shed in feces.
        • Necrotic enteritis – C. perfringens type A and C.
          • NetB toxin (NOT alpha-toxin), critical to pathogenesis.
          • Severe fibrinonecrotic enteritis, diphtheric pseudomembrane, high mortality.
        • Gangrenous dermatitis – C. perfringens or C. septicum.
          • Peracute, fatal, occurs in warm environments.
          • Bacteria introduced through cutaneous wounds.
          • Found dead with gangrenous skin, emphysematous or serosanguinous cellulitis.
        • Botulism – C. botulinum.
          • Progressive flaccid paralysis in captive pheasants and sometimes chickens.
          • Warmer months.
          • Of 8 known toxin types, type C most common in gallinaceous birds.
            • Lack characteristic gross or microscopic lesions.
            • Dx with detection of toxin in serum, crop, GI contents of moribund birds.
            • Can be found in gut of normal chickens, toxin can be produced post mortem.
              • Finding the toxin in tissues of dead birds does not confirm botulism.

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71
Q

What are the four species of mycoplasma of concern to gallinaceous birds?

What clinical signs are present?

How is this disease diagnosed and treated?

A
  • Mycoplasma spp.
    • Chronic respiratory disease.
    • Lack cell wall, related to gram positive bacteria.
    • Host-specific.
    • Vertical or horizontal transmission.
    • M. gallisepticum.
      • Prevalent in domestic turkey flocks.
      • Resp signs, swelling of infraorbital sinus.
      • Coinfection with other resp pathogens common.
    • M. synoviae – pale comb, stunted growth, lameness, swollen joints, breast blisters.
    • M. meleagridis and M. iowae in turkeys, lower egg production with minimal to no resp signs.
    • Dx with isolation on culture or PCR. On-farm plate test available.
    • Tylosin approved for 1 mo treatment.

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72
Q

What are the clinical signs of Erysipelas rhusiopatheae in gallinaceous birds?

A
  • Erysipelas rhusiopatheae
    • Turkeys, pheasants, rarely chickens.
    • Sudden onset, serosal, cutaneous, and muscular hemorrhage and splenomegaly.
    • Chronic form characterized by endocarditis and polyarthritis.
    • Zoonotic infection.

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73
Q

Staphylococcus aureus infection in gallinaceous birds produces what lesions?

How is this disease transmitted?

A
  • Staphylococcus aureus.
    • Arthritis, tenosynovitis, osteomyelitis, endocarditis, omphalitis.
    • Skin injuries point of entry i.e. pododermatitis. Also resp tract.

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74
Q

How does mycobacteriosis present in gallinaceous birds?

What species are highly suceptible? Which are more resistant?

How is this disease managed?

A
  • Mycobacterium avium.
    • Chickens, partridges highly susceptible.
    • Pheasants, guinea fowl, domestic turkeys less susceptible.
    • Bacteria can survive for 4 years in environment.
    • Marked leukocytosis due to monocytosis.
    • Abnormal gait or paralysis with joint infection, dull feathers.
      • Lesions in liver, spleen, intestine, lung, BM.
      • Granulomatous inflammation.
        • Acid-fast stains highlight large numbers of bacteria within cytoplasm of MP and MN giant cells.
          • Rule out salmonella infections, coligranuloma, fowl cholera. Culture and PCR.
      • No tx; Cull infected flocks.

Terio

75
Q

What is the etiologic agent of brooder pneumonia in chickens?

How is this disease transmitted?

What risk factors predispose birds to this disease?

What lesions are present?

How is this disease diagnosed and managed?

A
  • Aspergillosis – A. fumigatus, A. flavus, A. niger.
    • Pathogenesis
      • Inhalation of spores result sin infection.
      • Strong inflammatory response.
      • Seeds into the coelomic cavity and pneumatized bones.
      • Systemic spread via macrophages or due to hematogenous spread.
    • Risk Factors
      • Aka brooder pneumonia – More severe in younger birds 7-10 days after hatch, assoc with immunosuppression.
      • Poor husbandry, moldy feed or litter, damp bedding, high stocking densities, poor ventilation, increased species, breed susceptibility.
    • Gross – Thickening of air sacs and pleura, white exudate (mycelia) or green powdery-like (conidia) material. Poor BCS. Plugs of caseonectoric material within trachea or syrinx, ascites.
    • Osteomyelitis.
      • Keratoconjunctivitis with caseous plaques below the nictitating membranes with topical exposure (chickens) vs hematogenous spread resulting in posterior ophthalmitis or panopthalmitis in turkeys.
    • Histo – giant cell granulomas, septate, branching hyphae with parallel walls with dichotomous 45 deg angle and branching. Stains with GMS, PAS.
      • With ocular lesions, granulomas within pectin and hyphae within vitreous humor and retina.
    • Dx – combo of PCR with galactomannan assays can increase reliability of molecular results.
      • Tracheal washes can be cultured, visualized via cytology. ELISA for Ab.
      • Rads may suggest asper.
    • Tx – itraconazole/voriconazole can be used for tx; ketoconazole variable success. Copper sulfate in water or sprayed on ground may help reduce transmission.

Terio

76
Q

How does Candida albicans present in gallinaceous birds?

What lesions are appreciated on necropsy?

A
  • Candida albicans.
    • Mortality in young birds.
    • Ulcerative and proliferative white plaques aka Turkish towel appearance; pseudomembranes; lesions in oral cavity, crop, esophagus. May cause ulceration and hemorrhage in proventriculus and ventriculus.
    • Systemic, dermatologic, and comb infections have been reported.
    • Oval candida spp yeast with parallel septate hyphae; pseudohyphae include chains of elongated yeast. GMS, PAS positive. Gram positive.

Terio

77
Q

How do Eimeria spp affect gallinaeous birds?

Which ages are most susceptible?

How is this disease controlled?

A
  • Eimeria
    • Direct LC, fecal-oral transmission.
    • GIT of poultry, kidney in geese.
    • Age
      • Young birds 1-4 mos old.
      • Birds < 1 wk do not have chymotrypsin and bile salts for breaking down oocysts and are not susceptible to disease.
    • CS - Diarrhea, sometimes hemorrhagic.
    • Control
      • Yards should be rototilled monthly after tx with dilute bleach or lime.
      • Coccidiostats in feed for prevention.
        • Not in organic feed, monitor those flocks closely.
      • Outbreaks tx with amprolium or with sulfadimethoxine (Albon) off-label.
        • Sulfa drugs should not be used in laying hens.
        • Overdoses with amprolium lead to hemorrhagic diathesis and death, narrow safety margin.
        • Vaccines in large flocks in ovo or at hatch.
        • Pooled fecal sample annually for screening recommended.

Terio

78
Q

What is the etiologic agent of blackhead in Turkeys?

What intermediate hosts are required for transmission of this parasite?

What galliformes are carriers? Which are susceptible?

What lesions are present on necropsy?

A
  • Histomonas meleagridis
    • Causes blackhead in turkeys; CS – yellow droppings, depression, death.
    • Incubation 7-10 days.
    • Recovered birds can harbor histomonads in ceca.
    • Bloodwork – low UA and hgb, rise in BG, increased AST and LDH common.
    • Multifocal necrosis sof liver with bulls-eye appearance, necrotizing typhlitis with necrotic cecal cores.
    • Chickens can carry without CS; other galliformes susceptible.
    • Arthropod IM host – nematode Heterakis gallinae. Transmission via earthworms, flies, grasshoppers, sowbugs, crickets.
    • Prevention by avoiding housing turkeys on ranges inhabited previously by chickens or other game birds, control earthworms.

Terio

79
Q

What blood parasites affect gallinaceous birds?

How are they transmitted?

A
  • Hemosporidia
    • Apicomplexan, include Plasmodium, Hemoproteus, Leucocytozoon transmitted by mosquitoes.
    • LC – sporogony in insects, schizogony (merogony) and gametogony in tissues or blood cells, respectively, of vertebrate host.
    • Culicidae moswuitoes – Plasmodium.
    • Biting midges (Ceratopogonidae), louse flies (Hippoboscidae) – hemoproteus.
    • Blackflies (Simuliidae) – Leucocytozoon.

Teiro

80
Q

What ectoparasites affect gallinaceous birds?

A
  • Lice – Specific, transmission by direct contact; feed on feathers or debris from feather surfaces, eggs laid along feather at base of shaft.
  • Mites – Not host specific, two groups; mange (feed on skin cells), blood sucking mites.
    • Two most common mites of poultry – northern fowl mite (ornithonyssus sylviarum) and red mite (Dermanyssus gallinae).
    • Scaly leg mites – (Knemidocoptes mutans) most common in birds.
      • Burrow, can be severe.
    • Depluming mite – Knemidocoptes laevis aka Neocnemidocoptes gallinae – severe pruritus and feather pulling from burrowing.
    • Dermanyssus gallinae – red mite; blood sucking.
      • Feeds at night, results in wt loss, anemia, death.
      • Does not live on the host. Can be found in seams of bedding areas as salt-and-pepper or fuzzy white appearance.
      • Do NOT use carbaryl powder (Sevin) on birds or premises.
      • Tx ivermectin and other OTC insecticides. Rotate to prevent resistance.
      • Can bite humans.
  • Fleas – Stick-tight flea aka Echidnophaga gallinacean.
    • Females remain embedded in skin of host, males mobile. Feed on blood.
  • Fowl ticks – soft ticks, heavy infestations can cause anemia or paralysis. Vectors for Borrelia anserine (spirochetosis).
  • Bed bugs (Cimex lectularis) – reddish brown, size of ticks, cloacal irritation, feather loss, anemia, decreased egg production.

Terio

81
Q

Describe the reproductive strategies of gallinaceous birds?

A
  • General
    • Generally mate in pairs, lots of male displays—dancing, booming (grouse, curassow, guan), high flying (woodcock)
    • Guinea fowl should have 1 male to 4-5 females
  • Estrous cycles
    • Seasonal breeders
  • Anatomical features
    • Functioning left ovary
    • Guinea fowl eggs tear drop shaped!
  • Maternal care
    • Females provide most of incubation
    • Brush turkeys don’t incubate their eggs—depend on geothermal sunlight and heat from decomposing vegetation

Fowler

82
Q

Describe the nesting and keeping of galliform eggs.

A
  • Gestation/parturition
    • Nest boxes easily accessed by staff for egg collection/artificial incubation
      • 18 inches long x 12 inches high x 12 inches wide with 3-4 inch lip to keep straw in
    • If want synchronous hatch, can keep eggs in fridge for up to 5-7 days
    • Chick development best confirmed 4-5 days after start of incubation
    • Guinea fowl require high humidity, higher temp due to thicker shell—usually incubated with waterfowl eggs
    • Nidifugus downy young
      • Nidifugus = leave nest shortly after birth
    • Young are called chicks
    • Young guineafowl = keets
    • Dimorphic almost from hatching
83
Q

What are the most common presentations of backyard chickens to the ER?

A
  • Trauma (n=25) – predators (11 – 6 were dogs/foxes, 3 were raptors), some accidental (3) or flock-mate induced (2). 12/25 were euthanized. 6/13 non-euthanized birds received sedation or anesthesia for wound care.
    • Survey found curbing predation was biggest challenge for owners – review enclosure information
  • Nonspecific signs (n=11) – variety of different diagnoses (coelomic mass, salpingitis, ovarian carcinoma, renal disease, egg binding)
  • Reproductive disease (n=10 on presentation, n=17 21.8% confirmed with visit) – cloacal prolapse (5), egg-binding (3), 4 euthanized, 1 died
    • Pullets begin laying eggs at 18-21 weeks, some breed not until 6 months
  • 45% were discharged from the hospital, 41% were euthanized, 2 died
  • Marek’s disease
    • Marek’s disease virus – alphaherpesvirus
    • Vaccination in commercial chicks at 1 day of age of in ovo at 18-days – reduces incidence of MDV-induced lymphoma but replication and infection still occurs
    • Typically affects chickens 10-20 weeks
    • Forms – classic (paresis, paralysis) or vague signs with lymphoma, ocular form (lymphocyte infiltration of iris) and cutaneous form with feather follicle changes
    • Difficult to differentiate from avian leukosis virus induced lymphoid changes
      • Rarely signs < 14 weeks of age
      • Vertical & horizontal transmission (only horizaontal transmission w/ Marek’s)
      • No effective vaccine
  • Respiratory diseases – Avibacterium, Mycoplasma, Pasteurella, E. coli, Pseudomonas, Newcastle, influenza, ILT
  • Crop abnormalities – ileus more likely than obstruction (test lead)
  • Abnormal droppings – diarrhea (Salmonella, Clostridium, Campylobacter) v renal issues (gout)
  • Remember these are food animals…FARAD and such…the baytril was bad
    • Fluoroquinolones, cephalosporins, metronidazole, chloramphenicol, clenbuterol, glycopeptides, nitroimidazoles, nitrofuranes prohibited for use
84
Q

Describe the neonatal medical management of attwater’s prairie chicken.

A

Yolk sac infection was the most common cause of death (21%; n = 73) followed by maladaptation (19%; n = 68), musculoskeletal abnormalities (19%; n = 66), necrotic enteritis (13%; n = 44), and mucoid enteritis (11%; n = 39).

  • Yolk sac infections most commonly caused by Escherichia coli – exposure of chick naval, less commonly contamination of egg shell or vertical transmission (reproductive infection)
  • Incubator settings – 37.5 C, 55-65% humidity
  • Orthopedic disorders – perosis (chondrodystrophy) due to nutrient deficiencies, splay leg (spraddle leg) associated with slick floors or high humidity in incubators
  • Mucoid enteropathy etiology unknown
  • Necrotic enteropathy likely due to Clostridium perfringens, shedding increased with diets high in easily digestible cereal grains

Take Home: Diets low in fermentable carbohydrates reduce risk of necrotic enteritis, egg & incubator sanitation reduces risk of yolk sac infection

Mulreany, L., Flanagan, J., Molter, C., Howard, L., Tocidlowski, M., Werre, S., … & Morrow, M. (2018). Review of mortality and effectiveness of neonatal treatment in captive Attwater’s prairie chickens (Tympanuchus cupido attwateri). Journal of Zoo and Wildlife Medicine, 49(3), 671-679.

85
Q

Descrbie the absorption and pathogenesis of lead in chickens?

Where in the egg does lead deposit?

A
  • Acidic pH of proventriculus and ventriculus allow lead to be solubilized.
    • Lead then absorbed into blood through small intestines.
    • 90%+ absorbed lead binrds RBCs, distributed to tissues.
    • Blood and well-vascularized organs hold onto 4% lead burden, soft tissues will have 2%, bones will have 94%.
    • GIT – lead causes necrosis of epithelium and impairment of GI motility.
    • Lead can alter hematologic system by interfering with heme synthesis and increasing RBC fragility, leads to anemia.
    • Liver degeneration and necrosis can also occur.
    • Lead may substitute for calcium in bone, can mimic or inhibit cellular actions of calcium, which can lead to necrosis, impairment of neuronal differentiation, cerebral edema.
    • Also interferes with cellular metabolism in mitochondria and inhibits P-450 enzymes.
  • Lead in eggs.
    • Can be deposited into shell, yolk, and albumen of an egg.
    • Shell usually highest, some studies shows yolk higher.
    • Within the contents of the egg, yolk usually highest, albumen levels low to negligible.
    • Yolk and albumen usually tested together because that is what we consume.
    • Mechanism of how lead gets into lead unknown.
      • Could be when Ca is mobilized form bones for eggshell formation, lead is able to use the same path for Ca deposition into the shell.
      • Ovarian tissue has been found to have lead, could pass into yolk and albumen.
    • In this case – as lead levels decreased in blood, a linear reduction of lead in yolk was likely.
  • Valid concerns have been raised for humans consuming eggs or meat from birds that have lead toxicosis.
    • Half-time and withdrawal time unknown.
    • Children and pregnant women particularly susceptible.
    • Developing CNS thought to be more vulnerable to lead’s toxic effects.
    • An adult would have been required to consume 6 eggs at the concentration found in this study to be in the level above daily limit for people.
    • Best to advise against eating eggs produced from hens that have been diagnosed with lead tox, even if they no longer have detectable lead in blood or eggs following chelation.

Lamb, S. K. (2018). Lead Levels in the Eggs of a Chicken With Lead Toxicosis. Journal of avian medicine and surgery, 32(3), 217-220.

86
Q

A recent study evaluated the prevalence of lymphoproliferative disease virus adn reticuloendotheliosis virus in canadian turkeys.

How prevalent were those diseases? Were any other pathogens identified?

A

Reticuloendotheliosis virus was detected in 4% (5/119) of LPDV-positive Wild Turkeys. Grossly evident skin lesions from five Wild Turkeys tested positive for poxvirus, and all turkeys tested negative for AIV. This study provides evidence of LPDV circulation in Canada and provides a baseline for comparison with future Wild Turkey pathogen surveillance and monitoring in Ontario and elsewhere. Key words: Avian influenza virus, avian poxvirus, Canada, lymphoproliferative disease virus, Ontario, reticuloendotheliosis virus, surveillance,

Wild Turkey.

  • Wild turkeys reintroduced to Ontario in 1980s
  • Lymphoproliferative disease virus is an oncogenic virus that can cause disease in both wild and domestic turkeys
    • High prevalence in eastern US
    • Infections typically subclinical but development of lymphoid tumors can be fatal
  • No animals positive for LPDV had evidence of associated disease
  • Possibility of cross-border transmission of disease from other wild turkeys
  • 4% coinfected with REV and LPDV- can both manifest as multiorgan lymphoid neoplasia
  • Prevalence in Canada contrasts with absence of reported LPDV cases in domestic turkeys In North America
  • No reports of AIV exist in wild turkeys; pox is not currently considered a major concern in domestic poultry

MacDonald, A. M., Jardine, C. M., Bowman, J., Susta, L., & Nemeth, N. M. (2019). Detection of lymphoproliferative disease virus in Canada in a survey for viruses in Ontario wild turkeys (Meleagris gallopavo). Journal of wildlife diseases, 55(1), 113-122.

87
Q

A recent study investigated the prevalence of mycoplasma and eimeria in eastern wild turkeys (Meleagris gallopavo).

A

At least one Mycoplasma spp. was isolated from 98.7% (150/152) of EWTs, with six species identified. Mycoplasma gallopavonis was identified most commonly in 96.7% (147/152), followed by Mycoplasma gallinaceum in 23.7% (36/ 152).

  • Potential poultry pathogens (Mycoplasma meleagridis, Mycoplasma iowae, and Mycoplasma synoviae) were isolated from swabs of five (3.3%) EWTs. Coinfections with up to three Mycoplasma spp. were detected in 36.8% (56/152) of EWTs.

Most EWTs tested positive for Eimeria spp. oocysts (75.6%; 99/131).

  • A subset of positive samples (n¼16) were characterized by PCR, which detected the following species: Eimeria meleagrimitis (93.8%), Eimeria adenoeides (93.8%), Eimeria gallopavonis (56.3%), and Eimeria meleagridis (12.5%).
  • Important game species in Ontario with close interface between EWT and poultry flocks
  • Skewed toward males due to hunter-harvest regulations
  • Potential for economic losses from Mycoplasma and Eimeria infection of poultry as well as poor biosecurity in farms
  • Pathogenic Mycoplasma species in this study was rare (M. meleagridis, M. synoviae and M. iowae)

TAKE HOME: High % of non-pathogenic Mycoplasma and Eimeria species in EWT

  • Overall Eimeria oocyst prevalence 75.6%

MacDonald, A. M., Jardine, C. M., Rejman, E., Barta, J. R., Bowman, J., Cai, H. Y., … & Nemeth, N. M. (2019). High prevalence of Mycoplasma and Eimeria species in free-ranging eastern wild turkeys (Meleagris gallopavo silvestris) in Ontario, Canada. Journal of wildlife diseases, 55(1), 54-63.

88
Q

Describe the surgical extraction of hen follicles for IVF.

A
  • Follicle was identified on US – preovulatory follicles (diameter > 10 mm) in hens observed as anechoic ovals, with the presence of concentric rings and narrow anechoic limits, similar characteristics to those observed in mammalian preovulatory follicles.
  • Left lateral celiotomy and extraction of follicles:
    • Incision left paralumbar region, form last rib to pubic tailbone.
    • Femoral artery and vein retracted dorsally.
    • External, internal oblique and transverse abdominal muscles incised.
    • Entered abdominal air sac.
    • Intestines and uterus were retracted towards the coelomic wall to expose ovary and follicles.
      • Each follicle was isolatedand slight traction applied until the follicle separated from the ovary.
      • Then inspected site for bleeding, repeated to obtain the highest possible number of follicles with different degrees of maturity without damaging the ovary.
      • Placed into PBSE medium. Total 30 follicles obtained.
      • Closed routinely. Post-op supportive care, pain management.
  • Fertilized each follicle with IVF protocol from other studies. Incubated.
    • Observed for presence of blastomeres; only 16% total success of IVF.
  • Percentage rate of IVF success is low. About 60% in this study were suitable for IVF, and 16% successful.
  • The end result of assisted reproduction is to increase the reproductive efficiency, resolve reproductive problems, and improve genetics of domestic animals as well as animals in zoos and collections.
  • Surgical procedure in this study considered successful in obtaining viable follicles.
  • No adverse effects.

Perez-Rivero, J. J., Lozada-Gallegos, A. R., & Herrera-Barragán, J. A. (2018). Surgical Extraction of Viable Hen (Gallus gallus domesticus) Follicles for In Vitro Fertilization. Journal of avian medicine and surgery, 32(1), 13-18.

89
Q

What is a significant parasite in bobwhite quail (Colinus virginianus) leading to a significnat mortality event?

Describe the pathogenesis of the disease. How is it transmitted?

A
  • Haemoproteus:
    • Transmitted by arthropods, infect mammals, reptiles, amphibians, birds.
    • Two subgenera – Haemoproteus, Parahaemoproteus, with different vectors.
      • H – Hippoboscids.
      • PH – Culicoides (biting midges).
    • Haemoproteus is the most common avian hemoparasite.
    • Traditional view that infections are largely nonpathogenic.
    • Can cause serious disease in pigeons, quail, turkeys.
    • Abortive haemoproteus spp infections in nonadapted avian hosts tend to be more severe.
    • Parasitemia highest in summer and fall, in habitats that support the insect vector.
    • Younger birds are more susceptible.
  • High mortality captive-bred Bobwhite quail on ranch in Utah (400 died).
    • 9 birds necropsied.
    • CS – depression, ruffled appearance, difficulty walking, or simply found dead.
    • Hemosporidian molecular analysis on pooled liver, lung, and trachea.
    • Gross necropsy – most prominent lesions pale skeletal muscle with multifocal hemorrhages and petechiae in air sacs and on serosal surfaces of most organs.
    • Moderate to severe degenerative myositis with intramyofiber schizonts and minimal lymphoplasmacytic infiltrates in the proventriculus, ventriculus, heart, and skeletal muscle.
    • Fibrinoid to heterophilic vasculitis in multiple organs with intraendothelial or intravascular merozoites and scattered thrombosis.
    • Liver and spleen multiple degenerative schizonts.
    • Mild, subacute, lymphocytic, histiocytic interstitial pneumonia.
    • Blood smears showed Haemoproteus spp in erythrocytes.
  • Molecular dx – subgenus Parahaemoproteus.
    • Closely related to forms found in Columbiformes, Passeriformes, and Strigiforme.
    • Vector was likely to be a Culicoides spp.
    • In Bobwhite Quail in southern Utah, death was attributed to infection with Parahaemoproteus and the vector was likely to be a Culicoides spp.
  • This is an example of a virulent infection resulting from a complete life cycle of the protozoa.

Kelly, E. J., Baldwin, T. J., Frame, D. D., Childress, A. L., & Wellehan, J. F. (2018). Haemoproteus (Parahaemoproteus) spp. in captive-bred bobwhite quail (Colinus virginianus) in southern Utah, USA. Journal of wildlife diseases, 54(4), 726-733.

90
Q

Describe the sites used for ultrasonographic imaging of galliform species.

A
  • Sites:
    • ventromedian site - most useful, transducer positioned midline immediately caudal to sternum
    • caudal parasternal site - second approach, most poultry large enough to have sufficient space between last rib and pelvic bones
      • probe is placed on right side of bird with the leg being pulled either backwards or forwards to avoid disturbance from ventriculus
      • apply pressure to compress air sac
    • cranial parasternal site - may be used from both sides of the body, mainly for echo
      • medial and lateral sternal notch provide extra windows not present in other avian species
      • position 1-2cm dorsal to ventral midline, just in front of the stifle joint and angled steeply cranially
    • intracloacal ultrasonography
      • applicable in birds >2 kg
      • enhanced images of normal kidney and gonads
    • transesophageal ultrasonography – use phased-array ultrasound transducer for echo

Radiography and Ultrasonography in the Backyard Poultry and Waterfowl Patient

Maria-E. Krautwald-Junghanns, Torsten Moerke-Schindler, Susanne Vorbrüggen, and Kerstin Cramer

Journal of Avian Medicine and Surgery Vol. 31, Issue 3 (Sep 2017). 189-197

91
Q

Describe the imaging of the cardiovascular system in galliform birds.

A

Cardiovascular:

  • Radiographic signs of cardiac disease often are nonspecific
    • alterations in cardiac shape, radiographic density, and visibility of the great vessels
  • Echocardiogram
    • Gold standard for diagnosing heart disease
    • Do not pluck aquatic bird if possible
    • established examination for avian structural and functional cardiac measurements mainly is B-mode (2-D) echocardiography, using the ventromedian and parasternal coupling sites
    • M-mode measurements described in commercial turkeys, broilers, and Leghorn chickens, some waterfowl species (obtained by transesophageal access)
      • ability to get transverse images using cranial parasternal approach
    • Most common findings in backyard birds - hydropericardium and hypertrophy or dilation of the right ventricle, often caused by right-sided CHF
    • rate of inflow as well as outflow of blood can be determined by using the spectral Doppler function - depicted in a 2D-curve against time

Radiography and Ultrasonography in the Backyard Poultry and Waterfowl Patient

Maria-E. Krautwald-Junghanns, Torsten Moerke-Schindler, Susanne Vorbrüggen, and Kerstin Cramer

Journal of Avian Medicine and Surgery Vol. 31, Issue 3 (Sep 2017). 189-197

92
Q

Describe the imaging of the hepatic system in poultry species.

A
  • hepatomegaly
    • common causes include infectious (bacterial, viral) and hepatic lipidosis
    • Rads - broadened radiographic outline of the liver and proventricular displacement in lateral view
      • Traumatic air sac rupture can make liver margins appear very distinct
  • Ascites
    • Rads contraindicated because dorsal recumbency can cause respiratory compromise
      • May see decreased serosal detail and widened shape of the abdominal serosal sac
    • US – modality of choice
      • Can perform coelomocentesis US guided
  • Parenchymal disease
    • US – can evaluate hepatic parenchyma for disease/congestion
      • Can perform US guided tissue sampling
      • imaging will be impeded if surrounding organs enlarged or if the GIT is full – common problem in chickens
  • Most poultry have a gallbladder
    • positioned caudal to the right liver lobe

Radiography and Ultrasonography in the Backyard Poultry and Waterfowl Patient

Maria-E. Krautwald-Junghanns, Torsten Moerke-Schindler, Susanne Vorbrüggen, and Kerstin Cramer

Journal of Avian Medicine and Surgery Vol. 31, Issue 3 (Sep 2017). 189-197

93
Q

Describe the imaging of the gastrointestinal system and spleen in poultry species.

Any useful techniques?

A
  • US – few indications with GI disease
    • Can often visualize intestinal loops
      • Look for peristalsis to identify intestine
      • duodenum - located easily on cross-section due to its U-shape
      • intestines can be examined only with transducers featuring frequencies of at least 10 MHz in birds <1kg
        • luminal contents and different layers in intestinal wall can be recognized to some degree
        • can sometimes see granulomatous lesions
    • Oral administration of water as a contrast medium at 20 mL/kg before US exam can improve image quality
    • Esophagus and crop may be examined in large poultry
    • ventromedian and caudal parasternal coupling sites provide good views of the ventriculus
      • marked by hypoechoic, round to oval muscular layer with adjacent hyperechoic koilin lining
      • koilin layer itself is assessed best at transducer frequencies >12 MHz
    • exam of proventriculus is successful in large birds or if the organ is enlarged
      • cross-section usually images as round structure of medium echogenicity with hyperechoic contents
    • cloaca - imaged by tilting the transducer caudally from the ventromedian coupling site
      • cloacal wall is hyperechoic, narrow, and regular in appearance, surrounding cloacal contents with different levels of echogenicity
      • flush out fecal material and instill water to improve diagnostic picture quality of cloacal wall in poultry
  • Rads – better than US for assessing GI and spleen in most cases
  • galliform birds can have very full crops
  • waterfowl may ingest foreign objects, often metal and commonly seen in GI on rads
  • can perform contrast study with barium sulfate, esp to differentiate proventricular dilation from hepatomegaly
    • waterfowl can get PDD
    • ddx – parasitism (Amidostomum species or tapeworms), candida infection
  • ventriculus – obvious in granivorous birds because of grit
    • excessive grit intake can suggest calcium-deficient nutrition in egg-laying hens or GI malfunction, such as infection (enteritis due to varying causes, most commonly parasites)
    • presence of grit distal to the ventriculus in intestine is considered pathologic
    • presence of intestinal gas considered normal in some waterfowl and game birds
    • FB obstruction of intestines in birds is not commonly accompanied by gas distention as in mammals
  • spleen rarely seen on rads in healthy poultry and, if so, only on lateral view
    • can be enlarged and visualized on VD and lateral in cases of infection or neoplasia

Radiography and Ultrasonography in the Backyard Poultry and Waterfowl Patient

Maria-E. Krautwald-Junghanns, Torsten Moerke-Schindler, Susanne Vorbrüggen, and Kerstin Cramer

Journal of Avian Medicine and Surgery Vol. 31, Issue 3 (Sep 2017). 189-197

94
Q

Describe the imaging of the renal and reproductive systems in galliformes.

A
  • Rads:
    • enlargement of renal silhouette commonly indicates generalized infection and rarely noninfectious causes (kidney cysts, neoplasia)
    • Can see gonadal enlargement – pathologic vs normal reproductive activity
    • Cannot diagnose salpingitis on rads
    • Can see hyperostosis which indicates repro activity
  • US:
    • ventromedian and parasternal coupling sites are applicable
    • kidney size and texture - evaluated when renomegaly present
      • reflection of waves and reduced homogeneity of tissue may indicate renal calcification or deposition of uric acid crystals within parenchyma
    • testes and ovary also can be visualized in sexually active poultry
      • serial ultrasound helps in the diagnosis of follicle retention
      • US can be used as a second imaging modality if rads inconclusive for dystocia cases with a fully developed egg present
    • US - modality of choice to differentiate soft tissue opacities (also seen with egg-related peritonitis), especially in egg binding without a calcified shell
      • May also allow differentiation of egg within uterus vs loose in coelom
      • Can help diagnose salpingitis and egg yolk peritonitis
95
Q

Describe the imaging of the respiratory tract of poultry.

A
  • Recognize unique tracheal anatomy of various species
    • Black swan - trachea forms a loop/coil
    • Trumpeter swan - elongated and distended trachea situated partly in sternum
    • Magpie goose - externally convoluted trachea, small simple syrinx in both sexes
    • Male ducks (subfamily Anatinae, some species of Anserinae) - balloon-like, irregular distension of the syrinx (bulla syringealis or tympaniform bulla)
  • Rads:
    • increase in density or localized areas showing a loss of the normal reticular pattern may indicate pneumonia
    • Air sac walls may become thickened, increasingly visible with airsacculitis
      • often a sequela of E. coli septicemia in chickens
    • evaluating the air sacs radiographically in backyard poultry can be challenging
      • often food filled GI and reproductive activity
    • significant species variation in appearance of extrathoracic clavicular air sac diverticula which are visible in pectoral muscle mass around proximal end of humerus in healthy poultry
96
Q

Describe the imaging of the musculoskeletal system in poultry.

A
  • species variation
    • shortened tibiotarsus and chondrodystrophic bones in the Japanese bantam, silkie, and Chabo chickens
    • development of helmet-like structure in Polish chicken and crested duck
    • polydactyly in Faverolle chickens
    • metatarsal spur of male game birds
    • Physiologic mineralization of extensor and flexor digitorum longus tendons of the hind limbs can be seen in domestic chickens and is normal
  • pathology more common in long bones of legs than wings
    • Indian runner ducks often have limb abnormalities
      • primarily joint alterations and osteolysis - consequence of pododermatitis given their erect posture and resulting overload of their hind limbs
  • conditions commonly found in backyard poultry and waterfowl seen in rads:
    • metabolic bone disease (rickets)
    • osteoporosis
    • arthritis (often with concurring hepatomegaly in cases of salmonellosis)
    • neoplasia
      • predominantly osteolytic nature in birds
    • osteolytic lesions, surrounded by sclerosis and focal opacities in long bones, also develop commonly in cases of mycobacteriosis
      • frequently with hepatomegaly, splenomegaly, and thickened intestines
97
Q

A recent study attempted to validate biochemical reference intervals in domestic chickens.

What limitations exist for the VetScan rotor?

Which tests were validated (to thelevel of ClSI) based on what’s been published?

A
  • This study showed that only NA, K, and GLOB intervals in the Exotic Animal Formulary could be properly validated and suitable for use in adult laying hens.
  • Consider the Ca and BA limitations of the avian VetScan rotor when sampling laying hens.

Other findings:

  • GLU decreased with age.
    • BA was below the dynamic range of the rotor in 91% cases, accuracy of this value unknown.
      • BA produced and recycled by hepatocytes.
      • Indicator of liver function – high BA reflect impaired ability of hepatocytes to extract them from portal circulation.
    • BA was positively correlated with UA.
      • UA excreted by kidneys, primary indicator of renal function in birds as it is the primary means of nitrogenous waste excretion.
      • Starvation, gout, renal dz, nephrocalcinosis (vit D excess), dehydration, and chronic hypovitaminosis A may cause changes in the uric acid concentration.
      • UA levels can show variability between spp and will vary with dietary protein level, total food intake, bodily requirements for AA.
      • Laying birds generally have lower levels of UA than nonlaying birds.
    • Could not determine the lower limit for calcium.
      • Hypocalcemia can lead to loss of muscle condition, muscle twitching, clonic and tonic muscle spasms, seizures.
        • May also result in uterine inertia and subsequent egg binding and egg-related coelomitis.

Board, M. M., Crespo, R., Shah, D. H., & Faux, C. M. (2018). Biochemical Reference Intervals for Backyard Hens. Journal of avian medicine and surgery, 32(4), 301-306.

98
Q

What is different about avian compared to mammalian coagulation?

A

Missing some intrinsic factors - XI, XII

Thrombocytes adhere and spread in a monolayer over a damanged area - in mammals there are 3D aggregates - this may contribute to longer bleeding times in birds.

Rodenbaugh, C. I., Lyon, S. D., Hanzlicek, A. S., Kanda, I., Payton, M. E., Rizzi, T. E., … & Brandão, J. (2019). Dynamic viscoelastic coagulometry of blood obtained from healthy chickens. American journal of veterinary research, 80(5), 441-448

99
Q

Describe dynamic viscoelastic coagulometry.

What are the ideal sample for its use in chickens with suspected coagulopathies?

A

· Viscoelastic coagulation:

o Large range of results reported w/ thomboelastography in Amazon parrots and other species; no current reference standard and limits

o DVC = Dynamic viscoelastic coagulometry; vertical oscillating probe in cuvette containing whole blood and coagulation activator and measures resistance to oscillation as viscosity that changes w/ clot formation

Dynamic viscoelastic coagulometry feasible in chickens, use whole blood as citrated blood resulted in hypocoagulability and variable results

Rodenbaugh, C. I., Lyon, S. D., Hanzlicek, A. S., Kanda, I., Payton, M. E., Rizzi, T. E., … & Brandão, J. (2019). Dynamic viscoelastic coagulometry of blood obtained from healthy chickens. American journal of veterinary research, 80(5), 441-448.

100
Q

Describe the ECG of golden and silver pheasants.

What is unique about avian electrocardiophysiology?

A

Hassanpour, H., Zarei, H., Nasiri, L., & Hojjati, P. (2018). Electrocardiogram analysis of the golden (chrysolophus pictus) and silver (lophura nycthemera) pheasants. Journal of Zoo and Wildlife Medicine, 49(4), 881-886.

Abstract: The aim of this study was to describe normal electrocardiogram patterns and values in two species of conscious pheasants (golden and silver). The standard bipolar and augmented unipolar limb leads electrocardiograms were recorded in the birds. The wave forms were analyzed in all leads at 50 mm/sec and at 10 mm = 1 mV to determine PR, QRS, ST, and QT durations and P, net QRS complex, and T amplitudes. The polarity of each wave form was tabulated in all leads. The mean electrical axis for the frontal plane, calculated using leads II and III, was mostly negative in two species (-43 ± 28.08 in golden and 92 ± 10.08 in silver pheasant). The P wave was predominantly positive in most of the leads. The pattern of wave forms of the QRS complexes were different (Rs, QS, rS, R, RS, QR, qR). The T wave was almost positive in leads I, II, III, and aVF. The heart rates of the birds were mean (± SD) of 320 ± 36 beats/min (golden) and 314 ± 31 beats/min (silver). Description of normal electrocardiogram parameters will facilitate a better understanding of electrocardiogram changes of unhealthy birds.

  • Perkinje fibers of birds follows the path of coronary arteries
  • Depolarization sequence – right ventricle apex, RV base, LV base, LV apex
  • P wave polarity varies in birds
101
Q

What is the most frequently observed leukocyte of the black-fronted piping guan?

A

de Aquino Goulart, M., Locatelli-Dittrich, R., Vaz, F. F., Lange, R. R., de Oliveira Koch, M., & de Queiroz Castilhos, B. (2019). Hematological reference intervals of endangered captive black-fronted piping-guans (aburria jacutinga) in the state of paraná, brazil. Journal of Zoo and Wildlife Medicine, 50(1), 199-204.

  • Black-fronted piping-guan (Aburria jacutinga)
    • From Brazil, northeastern Argentina, & oriental Paraguay
    • Endangered
  • Results found were within expectations and reflect good clinical health on individuals
  • Hemoglobin concentration may be decreased due to fasting
    • As an iron porphyrin protein complex - synthesis is affected by deficient nutrition
    • However, hematologic values suggest adequate nutritional status of birds
  • Lymphocytes were most observed cells in WBC differential
  • H:L ratio similar to means reported for other bitds (0.5-3.0)

TAKE HOME: Lymphocytes most observed.

102
Q

What is the predominant leukocyte of the bobwhite quail?

What leukocyte quantification method worked best?

A

Journal of Avian Medicine and Surgery34(2):132–141, 2020

Complete Blood Cell Count and White Blood Cell Counting Method Comparison in 49-day-old Bobwhite Quail (Colinus virginianus)

Ian Kanda, RVT, VTS (Exotics), Jessica Robertson, DVM,James Meinkoth, DVM, PhD, Dipl ACVP,and Joa ̃o Branda ̃o, LMV, MS, Dipl ECZM (Avian)

Abstract: The northern bobwhite quail (Colinus virginianus) is a game bird experiencing decline throughout much of its range. There are limited species-specific and age-specific hematologic data for bobwhite quail. Complete blood cell counts in eighteen 49-day-old captive-raised quail of unverified sex were used to contribute data to reference intervals for the species as juvenile animals. Values for packed cell volumes, total solids, red and white blood cell counts, and white cell differential calculations were recorded for each animal. Bobwhite quail of this age were found to be primarily lymphocytic, but considerable variability was observed. White blood cell counts were obtained by estimates from blood smears and Phloxine B stain. White blood cell counts performed with x1000 magnification did not compare well with other white blood cell methods, including Phloxine B stain.

Key Points:

  • Northern bobwhite quail – near threatened, primarily due to hunting. Birds are captive bred and released to maintain hunting populations
  • Methods
    • WBC differential – 500 leukocytes counted at 1000x, 10 fields at 400x, and phloxine B method
    • Ideally 40 birds of each sex would have provided stronger reference data
  • Bobwhite quail are lymphocytic – consistent with other Galliformes
    • They start out heterophilic after hatching but transition to predominately lymphocytic by 2 weeks old
  • 10 fields at 400x matches with phloxine B method, the 1000x 500 leukocyte method was not as reliable

Take Home: WBC/RBC indices available for clinical use; bobwhite quail are a lymphocytic species

103
Q

Meloxicam, given at a dose of 1 mg/kg, maintained therapeutic concentrations for how long in domestic chickens?

How long was the drug present in eggs following a single dose?

A

Pharmacokinetics and egg residues after oral administration of a single dose of meloxicam in domestic chickens (Gallus domesticus)

JAMS 2017 31(4) 393

Abstract:

OBJECTIVES: To determine the pharmacokinetics of meloxicam in domestic hens and duration and quantity of drug residues in their eggs following PO administration of a single dose (1 mg of meloxicam/kg).

ANIMALS 8 healthy adult White Leghorn hens.

PROCEDURES Hens were administered 1 mg of meloxicam/kg PO once. A blood sample was collected immediately before and at intervals up to 48 hours after drug administration. The hens’ eggs were collected for 3 weeks after drug administration. Samples of the hens’ plasma, egg whites (albumen), and egg yolks were analyzed by high-performance liquid chromatography.

RESULTS The half-life, maximum concentration, and time to maximum concentration of meloxicam in plasma samples were 2.8 hours, 7.21 µg/mL, and 2 hours, respectively. Following meloxicam administration, the drug was not detected after 4 days in egg whites and after 8 days in egg yolks.

CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that meloxicam administered at a dose of 1 mg/kg PO in chickens appears to maintain plasma concentrations equivalent to those reported to be therapeutic for humans for 12 hours. The egg residue data may be used to aid establishment of appropriate drug withdrawal time recommendations.

Summary:

  • Meloxicam - a safe and effective medication for analgesia in chickens
  • Study objective: determine the PK of meloxicam in hens and duration and quantity of drug residues in eggs following PO admin of single dose at 1mg/kg

Results/discussion

  • mean terminal half-life, maximum concentration, and time to maximum concentration were 2.79 ± 1.01 hours, 7.21 ± 3.29 µg/mL, and 2.0 ± 0.92 hours
  • PO administration of meloxicam 1 mg/kg to chickens should maintain therapeutic plasma concentrations for 12 hours
  • meloxicam present for longer period in egg yolks than in egg whites
  • data suggests that 2-week withdrawal time should be adequate to avoid residues for single PO 1mg/kg of meloxicam
104
Q

What is the egg withdrawal for meloxicam, administered orally at a dose of 1 mg/kg q12h for a week?

Is that different from administered at just a single dose?

A

Pharmacokinetics and Egg Residues of Meloxicam After Multiple Day Oral Dosing in Domestic Chickens

Souza, Marcy J., Bailey, Joan, White, Molly, Gordon, Kristen, Gerhardt, Lillian, et. al.

Journal of Avian Medicine and Surgery, 32(1):8-12

Abstract:

With increased ownership of backyard poultry, veterinarians must treat these birds appropriately and take into consideration drug withdrawal times for eggs meant for consumption. Few studies have examined the pharmacokinetics or egg residues for medications commonly used in avian medicine. This study determined the pharmacokinetics of meloxicam in domestic chickens (n¼8) after oral dosing at 1 mg/kg q12h for a total of 9 doses (5 days). Additionally, the presence of meloxicam residues in eggs was determined. The terminal half-life, maximum concentration, and time to maximum concentration were 3.02 6 1.15 hours, 7.14 6 1.54 lg/mL, and 1.6 6 0.52 hours, respectively. No drug was detected in yolks and whites after 8 days and 3 days, respectively. On the basis of these results, a 2-week withdrawal time should be adequate to avoid drug residues in eggs meant for consumption.

Summary:

  • Eight adult, white leghorn hens - meloxicam 1mg/kg PO administered every 12 hours for a total of 9 doses
    • Blood collected from each hen on day 5 just before administration of the ninth dose
    • Blood collected at 10, 20, and 30 minutes, and at 1, 2, 4, 8, 12, 24, and 48 hours after the ninth dose
    • Eggs collected for 3 weeks starting the first day after meloxicam administration was discontinued
    • PK parameters do not appear to differ between single and multiple doses of meloxicam in domestic chickens
    • Meloxicam 1mg/kg maintained a plasma concentration associated with analgesia in people for ~ 12 hours
    • drug residue found in yolk up to 8 days after and in white up to 3 days after meloxicam was discontinued
    • withdrawal time of 2 weeks should be adequate to avoid meloxicam residues in eggs
105
Q

Does amoxicillin-clavulanate administered at a dose of 125 mg/kg in domestic chickens reach therapeutic concentrations? If so, how long?

What sort of withdrawal is expected in eggs?

A

Shannon, L., Cox, S. K., Bailey, J., Fortner, C., Davis, R., Gerhardt, L., & Souza, M. J. (2020). Pharmacokinetics and Drug Residue in Eggs After Multiple-Day Oral Dosing of Amoxicillin-Clavulanic Acid in Domestic Chickens. Journal of avian medicine and surgery, 34(1), 3-8.

  • Takeaway: Clavamox 125 mg/kg PO Q12H did not reach therapeutic plasma concentrations. No clavulanic acid detected in eggs, amoxicillin only detected for 4 days after discontinuation.
106
Q

Describe the procedure for intravenous and intraosseous regional limb perfusion in the domestic chicken?

Which method with ceftiofur sodium provided the highest concentrations?

A

Knafo, S. E., Graham, J. E., & Barton, B. A. (2019). Intravenous and intraosseous regional limb perfusion of ceftiofur sodium in an avian model. American journal of veterinary research, 80(6), 539-546.

  • IVRLP procedure:
    • Penrose drain used as a tourniquet around the selected leg at mid tibiotarsal level
    • 25g catheter put into the metatarsal vein → dose of ceftiofur diluted with sterile saline (0.9% NaCl) solution total volume of 3 mL, which was then injected through the catheter followed by 0.3 mL (the volume of the butterfly catheter) of sterile saline
    • IVC removed, bandage placed and tourniquet left on for 10 minutes
  • IORLP procedure:
    • Lidocaine injected into the periosteum of the proximal tibiotarsal bone
    • Penrose drain was used as a tourniquet around the mid femoral level
    • IO catheter placed (Sterile 22-gauge, 1.5-inch spinal needle) into the proximal aspect of the tibiotarsal bone
    • (indwelling- so secured with tissue glue and tape tabs that were sutured to the skin)
    • Dose of ceftiofur was diluted with sterile saline solution for a volume of 3 mL, which was injected through the catheter followed by 0.3 mL of heparinized saline solution to ensure that the entire dose was administered and to keep the catheter patent
    • Tourniquet was left in place for 10 minutes to allow the drug to perfuse into the tissues distal to it
    • Tourniquet was removed, and the leg wrapped with a bandage to protect the indwelling IO catheter which was left for 6 days during the entire tx period
  • Only adverse effects were bruising from the IVRLP, none from the IORLP or IM treatment groups
  • IVRLP resulted in a significantly greater concentration of ceftiofur in the synovial fluid of the ipsilateral tibiotarsal-tarsometatarsal joint of chickens than either IORLP or IM administration of the same dosage of the drug
  • Following IVRLP, the synovial fluid ceftiofur concentration was several times that in plasma
  • Results of the present study indicated that ceftiofur concentrations believed to be therapeutic against most bacterial pathogens could be achieved in synovial fluid samples obtained from the tibiotarsal-tarsometatarsal joint of chickens following IVRLP and IORLP of ceftiofur (2.2 mg/kg) once daily for 6 consecutive days
107
Q

Did antifungal implants in Japanese quail manage to reach therapeutic concentrations?

A

Souza, M. J., Redig, P., & Cox, S. K. (2017). Plasma concentrations of itraconazole, voriconazole, and terbinafine when delivered by an impregnated, subcutaneous implant in Japanese quail (Coturnix japonica). Journal of avian medicine and surgery, 31(2), 117-122.

During the course of the study, targeted terbinafine concentrations were achieved in some birds at various time points, but concentrations were inconsistent. Itraconazole and voriconazole concentrations were also inconsistent and did not reach targeted concentrations. Currently, the implant examined in this study cannot be recommended for treatment of aspergillosis in avian species.

  • Aspergillus fumigatus – 95% of infections, Aspergillus flavus is next
  • Frequent handling for treatment (q8h needed for voriconazole in RTH) may contribute to negative outcomes
  • Implants failed to release sufficient plasma levels – terbinafine was slightly better
108
Q

What advantages do hydrogels provide in the administration of drugs in avian species?

How did sodium salicylate hydrogels in chickens perform?

A

Booty, S. J., Harding, D. R., Whitby, C. P., Gater, M., Chambers, P., & Singh, P. M. (2018). Sustained-release injectable hydrogel formulations for administration of sodium salicylate in broiler chickens. Journal of avian medicine and surgery, 32(4), 294-300.

Results of the pharmacokinetic study indicated that NaSA concentrations remained above the minimum effective concentration (MEC) for analgesia in humans for 24 ± 8.9 (LALG) to 26 ± 4 (HALG) hours for the hydrogel formulations compared to 10 ± 5.6 hours for the aqueous formulation. These hydrogel formulations may have potential in providing long-term analgesia in avian species, but need further evaluation with pharmacodynamic or pharmacokinetic/ pharmacodynamic modeling studies.

  • Higher avian metabolisms result in more rapid elimination of drugs
  • Repeated handling to accommodate faster elimination results in increased stress
  • Hydrogels can be loaded with different drugs
  • More cross-linking results in smaller pores and slower drug release
  • Alginate formulations are water like and can be injected with a needle

Take Home: Hydrogel formulations may allow for less frequent drug administration in avian species

109
Q

What is the current engagement of veterinarians seeing backyard poultry?

A

Take Home: Periurban agriculture is increasing; companion animal vets are starting to see these species but may not have the training to do it well

J Am Vet Med Assoc 2020;257:196–209

Assessment of veterinarians’ engagement with backyard poultry and small-scale livestock operations in four western states

Alda F. A. Pires dvm, mpvm, phdAmos Peterson dvm, mscJerome N. Baron dvm, mscRagan Adams ma, dvmDale A. Moore dvm, mpvm, phd

Abstract:

OBJECTIVE: To assess veterinarian engagement with owners of poultry and livestock in urban and peri-urban areas (UPAs) of 4 western states, to evaluate the knowledge and experience of veterinarians in UPAs for treating domestic poultry and livestock, and to identify barriers to the provision of veterinary services to backyard poultry and small-scale livestock operations.

SAMPLE: 880 veterinarians in UPAs.

PROCEDURES: 2,400 members of the veterinary medical associations of California, Colorado, Oregon, and Washington who worked in metropolitan areas with a population > 5,000 people were randomly selected and invited to participate in a needs assessment survey. Response data were analyzed with univariable logistic regression and multiple correspondence analysis.

RESULTS: 880 (37%) invitees completed or partially completed the survey. Most respondents self-reported working in UPAs (686/825 [83%]) and companion animal only (n = 551) or predominant (211) practices. Although most (656/863 [76%]) respondents perceived an increase in backyard poultry and livestock in their practice areas, few were actively treating such animals primarily because of a lack of facilities, interest, or experience. Most respondents believed veterinarians have an important role in ensuring public health and preventing zoonotic disease.

CONCLUSIONS AND CLINICAL RELEVANCE: Backyard poultry and livestock are increasing in popularity in UPAs of 4 western states, and veterinarians are needed to provide services to such animals. Further research and continuing education are necessary to encourage practitioners in UPAs to engage with owners of backyard poultry and livestock to ensure the health and welfare of those animals and guard public health.

Key Points:

  • Urban and peri-urban agriculture has increased 30-40% from 1988-2007
    • This has lead to an increase in backyard poultry and small ruminants with less understanding and biosecurity for preventing disease
    • Outbreaks of Newcastle disease, Marek’s, and the 2015 HPAI outbreak have been traced to backyard poultry flocks
    • Previous survey of owners indicated a desire for greater access to veterinary care by properly trained individuals
  • Goal of this study was to establish what is known of the veterinary populations ability to see these animals
    • In the last six months, 25% had examined > 2 poultry patients, 20% >2 small ruminant patients, 11% >2 cattle patients, 11% > 2 swine patients, 9% >2 camelid patients
    • Most were companion animal only or predominant practitioners
    • Most said they had little knowledge to answer husbandry or medical questions in regards to poultry, with little interest in the other species
110
Q

What infectious diseases or toxins are playing a role in the decline of game birds in Bavaria?

A
  • Discussion:
    • Significant effect of land usage on pheasants and partridges in Bavaria.
      • Reduction in set-aside and less-distinct areas, and an increase in maize cultivation areas coincided with decline of game bird numbers.
    • Heterakis most commonly detected parasite.
    • Partridges appear to be especially susceptible to capillariosis.
    • Only one bird with parasites showed clinical signs, so they concluded parasites have not directly contributed to decline in pheasant numbers in Bavaria.
    • Concluded that the health risk for human consumption of Bavarian game birds is low (no Salmonella or Campylobacter was found).
    • Environmental toxins do not appear to be contributing to decline of game birds in Bavaria.

Anna Schmitz, Franz Kronthaler, Katrin Stein, Monika Rinder, and Rüdiger Korbel “DECLINE OF GAME BIRDS (PHASIANUS COLCHICUS AND PERDIX PERDIX) IN BAVARIA: A SURVEY ON PATHOGENIC BACTERIA, PARASITES, PESTICIDE RESIDUES, AND INFLUENCE OF SET-ASIDE LAND AND MAIZE CULTIVATION,” Journal of Zoo and Wildlife Medicine 48(1), 18-30, (1 March 2017). https://doi.org/10.1638/2014-0126.1

Abstract: Due to a Europe-wide decline of grey partridge (Perdix perdix) and pheasant (Phasianus colchicus) populations, this study was conducted focusing on the county of Bavaria, south Germany. The aim was to assess the health status of game birds and identify possible causes of decline. For this purpose 203 pheasants and 11 partridges were examined during the 2011 hunting season. Pathologic examinations were conducted including examinations for parasites and bacteria. Due to public health significance, a screening for Salmonella sp., as well as real-time polymerase chain reaction examinations for Campylobacter sp. and Mycobacterium avium ssp. avium, were done. Because pesticides and land-usage can possibly influence bird numbers, the birds were screened for environmental toxin residues, including neonicotinoid insecticides, and land-usage data were correlated with the hunting bags. The result was a very-strong positive correlation of set-aside areas and a less-strong negative correlation of maize cultivation acreage. More than 90% of the birds had a good health status; only individuals showed pathologic alterations. For example, avian tuberculosis was found in two pheasants and a severe capillariosis in two partridges. A possible role of female reproductive disorders has to be confirmed in further investigations. In conclusion, results suggest the decrease of set-aside areas could be a possible reason for decline.

111
Q

How do avian macrophages function compared to mammalian macrophages?

A

Jin, X., Zhang, X., Li, J., Yu, W., & Chen, F. (2018). Activation of chicken macrophages during in vitro stimulation and expression of immune genes. American journal of veterinary research, 79(12), 1306-1312.

Abstract:

OBJECTIVE To characterize activation and expression of immune genes of chicken macrophages after in vitro stimulation with lipopolysaccharide (LPS) and mouse erythrocytes.

ANIMALS Five 15-day-old chickens and 2 BALB/c mice.

PROCEDURES Macrophages were extracted from chicken bone marrow or peripheral blood and then stimulated with cytokines secreted from cell lines L929 and HD11. Stimulated chicken macrophages were further cocultured with LPS or mouse erythrocytes, and gene transcription of some distinctive cytokines was detected by use of a real-time PCR assay.

RESULTS Morphological features and phagocytic function of macrophages were characterized. Activated macrophages had an elongated shape with a large cell nucleus, and they had phagocytic function. Distinctive genes encoding the surface marker gene CD11b were identified; high quantities of CD11b were transcribed. Relative transcription of chicken genes BF and BL in mature cells cocultured with both stimuli was lower than for control cells. However, the quantity of genes encoding M1- or M2-distinctive cytokines (interleukin [IL]-1β, IL-10, IL-12, inducible nitric oxide synthase, tumor necrosis factor-α, and transforming growth factor-β) that were transcribed differed significantly between stimulation with LPS and mouse erythrocytes.

CONCLUSIONS AND CLINICAL RELEVANCE Chicken macrophages were differentially stimulated by LPS and mouse erythrocytes, which suggested that in vitro stimulation can distinctly influence the transcription and expression of immune genes of chicken macrophages.

  • CD11b gene is a distinctive gene for macrophages – no phenotypic difference between mammalian and avian macrophages

Take Home: Avian macrophage activation is similar to mammalian processes

112
Q

What are the typical smooth muscle biomarkers of avian leimosarcoma?

A
  • Smooth muscle markers – SMA & vimentin

Zordan, M. A., Garner, M. M., Smedley, R., Neelis, D., & Sánchez, C. R. (2017). Leimyosarcoma of the Wing in a Vieilott’s Fireback Pheasant (Lophura rufa). Journal of avian medicine and surgery, 31(2), 152-155.

Abstract: A 15-year-old, female Vieilott’s fireback pheasant (Lophura rufa) presented with a 2- day history of a drooping right wing. Examination revealed severe soft tissue swelling in the area extending from the right shoulder to the humeral-radioulnar joint with associated bruising and feather loss. Results of a complete blood cell count revealed marked heterophilia and lymphocytosis, and results of serum biochemical analysis showed severe increases in creatine kinase and aspartate aminotransferase activities, hypoproteinemia, and hypoalbuminemia. Radiographs revealed osteolytic lesions of the right humerus with pathologic fractures and circumferential soft tissue swelling. Although surgical wing amputation was successful, the bird died the next day while being treated. The mass was diagnosed histologically and immunohistochemically as a leiomyosarcoma. This is the first neoplasia of any kind reported in this species, to our knowledge, and one of the very few reports of smooth muscle neoplasms affecting the limb of a bird.

113
Q

Describe the process of adminstering spinal anesthesia in avian species. How is the anatomy different in birds versus mammals?

What effect does lidocaine and bupivicaine have when administered for spinal anesthesia in chickens. Any differences between the two?

A
  • Spinal cord of chickens – 3 meningeal layers:
    • Pia mater, arachnoid, dura mater.
    • No epidural space caudal to thoracic region of the coelom (general attachment of the vertebral periosteum to the dura mater).
    • In contrast, arachnoid space is well developed in the synsacral spinal cord.
    • Epidural injection not possible in LS area of chickens, but spinal injection is easily performed.

Takeaways: Lidocaine 2 mg/kg or bupivacaine 0.5 mg/kg produced effective anesthesia in the caudal coelomic area for approximately 20 and 55 minutes, respectively. No adverse effects. Sedation recommended first.

Khamisabadi, A., Kazemi-Darabadi, S., & Akbari, G. (2021). Comparison of Anesthetic Efficacy of Lidocaine and Bupivacaine in Spinal Anesthesia in Chickens. Journal of Avian Medicine and Surgery, 35(1), 60-67.

Abstract: Lidocaine is used for epidural and spinal anesthesia in various animal species. The ideal drug for epidural and spinal anesthesia should have a long effective duration in addition to a fast onset of action, and adequate analgesia and muscle relaxation. Despite the delayed onset of action, bupivacaine provides a longer duration of anesthesia than lidocaine. The purpose of this study was to compare the onset to effect and duration of action between lidocaine and bupivacaine for spinal anesthesia in broiler chickens. Thirty-two, 8-week-old, female Ross broiler chickens were randomly divided into 4 groups of 8: 1) 2 mg/kg lidocaine (L); 2) 0.1 mg/kg bupivacaine (B0.1); 3) 0.25 mg/kg bupivacaine (B0.25); and 4) 0.5 mg/kg bupivacaine (B0.5). After aseptic preparation, a 23-gauge spinal needle was inserted into the synsacrococcygeal space of the chickens with correct needle placement confirmed by a sudden loss of resistance. Spinal anesthesia was performed with the aforementioned doses of lidocaine and bupivacaine. The respiratory rate and cloacal temperature were measured every 10 minutes in each chicken until the anesthetic effect was no longer present. The onset to effect and the duration of action were calculated for each bird based on the pinch test at predetermined time intervals. The results are demonstrated as mean ± SD. The onset of action for bupivacaine (9 ± 1.41, 4.33 ± 1.15, and 3.33 ± 1.23 minutes in B0.1, B0.25, and B0.5 groups, respectively) was significantly delayed compared with that of lidocaine (1.37 ± 0.52 minutes). The duration of action of B0.5 (54 ± 6.08 minutes) was significantly longer than that of any other group (17.87 ± 3.18, 11 ± 1.41, and 18 ± 4.36 min in L, B0.1, and B0.25 groups, respectively). The results showed that a spinal injection of 0.5 mg/kg bupivacaine produces approximately 55 minutes of spinal anesthesia in these broiler chickens, which is much longer than the 18 minutes of anesthesia provided by 2 mg/kg lidocaine. Considering the various disease conditions that affect the cloacal area of birds, one can use each of these anesthetic drugs for either short-term or long-term spinal anesthesia in chickens and possibly other avian species.

Key Points:

  • Salpingohysterectomy, cloacopexy, cloacoplasty, other caudal coelomic surgical procedures may benefit from regional anesthesia.
  • Bupivacaine has a delayed onset vs lidocaine but produces longer anesthetic effect.
  • No systemic or local adverse effects in this study.
  • All 3 bupivacaine doses onset significantly delayed vs lidocaine.
  • Bupivacaine at highest dose had a significant difference in duration of action vs all other groups.
  • Decreased cloacal temps in all groups except B0.1 over time. Vasomotor tone and body shivering cease with sympathetic and somatic nerve block, respectively.
  • Lidocaine group RR increased after 20 min, B0.25 and B0.5 RR decreased. Not statistically significant.
  • Local anesthetic drug of choice should have a fast effective onset, long duration of action, and provide appropriate analgesia and muscle relaxation.
  • 50% chickens in B0.5 group became ventrally recumbent, suggests anesthetic effect on ischiadic nerve within the sacral plexus.
114
Q

In chickens with induced fractures and bone-cement spacers, how did the masquelet-induced membranes develop?

What would be the ideal time for second stage reconstructive surgery?

A

Journal of Avian Medicine and Surgery, 35(1) : 51-59

Masquelet-Induced Membrane Characteristics in Chicken Radii Bone Defects

Luis O. B. Cueva, DVM, MSc, Sheila C. Rahal, DVM, MSc, PhD, Carlos E. Fonseca-Alves, DVM, MSc, PhD, Shayra P. Bonatelli, DVM, MSc, Maria J. Mamprim, DVM, MSc, PhD, Camila C. D. A. Francia, MSc, PhD, Caio H. P. Burini, DVM, MSc, PhD, and Luciane R. Mesquita, DVM, MSc, PhD (Reviewed by AJC)

  • In birds, instability, infection and the presence of metallic implants near or at the fracture site are the primary factors that may delay or inhibit bone fracture healing.
    • Reconstruction of diaphyseal bone is challenging to establish the strength and function
    • Have previously used bone transport with circular external fixator in tibiotarsal defect in a parrot
  • Masquelet-induced membrane allows bone reconstruction in 2 stages
    • First, is soft tissue and bone debridement, inserting a cement spacer and stabilizing the limb
    • Leave this in for 4-8 weeks to form the induction membrane, then incise the membrane, remove the spacer and fill the cavity with graft or biomaterials
  • Aim of this study was to evaluate the formation of the Masquelet-induced membrane created by creation of segmental bone defects in the radii of healthy chickens.
  • Masquelet-induced membranes have a greater thickness at 21 and 30d post-sx than the 15d sample
    • Formation of induced membrane occurs in shorter period (15-30d) in chickens compared to 4-8wk in humans
    • None of the bone spacers dislocated, but the majority have some degree of displacement of the fracture ends
      • Recommend that these fractures should be stabilized in clinical cases for alignment
    • Rare cases of bone resorption at the fracture ends (n=2)
    • 15d post-sx, 3 distinct zones seen: cell layer in contact with bone cement, layer with collagen fibers, and layer in contact with muscle
      • Induced membrane had significant angiogenesis and organized collagen fibers at this time point
      • Considered optimal histologic characters for the membrane and that second stage for bone reconstruction was possible at this time
    • Occurrence of bone formation at fracture extremities seen at 30d post-sx
    • Membranes did not adhere to bone spacer, but there was membrane penetration into the cement surface irregularities

Take home:

  • Formation of masquelet-induced membrane was observed in the chicken bone defect sites at all period (15,21,30d) but optimal histologic characteristics for second stage bone reconstructive surgery were detected at 15 days post-sx

References:

N/A

115
Q

Describe the oxidative stress response in domestic chickens and magpies.

Are there any environtal influences?

What about sex?

A

Evaluation of Oxidative Stress in Blood of Domestic Chickens and Eurasian Magpies (Pica pica)

Journal of Avian Medicine and Surgery 35(1):28–36, 2021

Abstract: A physiological equilibrium exists between pro- and antioxidant factors. When the oxidant factors exceed the capacity of their removal or inactivation, oxidative stress (OS) occurs. The OS levels were assayed in plasma obtained from 2 bird species. Blood samples were collected from 20 healthy domestic chicken hens, 10 living in an intensive farming environment and 10 freerange, and from 18 healthy Eurasian magpies (Pica pica; 7 females and 11 males, with an estimated age of .1 year of age). For OS biomarker assessment, the determinable reactive oxygen metabolites (d-ROMs) were measured, and the plasmatic antioxidant test (PAT) was performed; the OS index (OSI) was then calculated (d-ROMs/PAT 3 1000) as a parameter of overall oxidative stress. Moreover, lipid peroxidation was assessed by measuring plasmatic malondialdehyde (MDA) levels. A hematological evaluation was also performed on each bird with a hemocytometer, on which a blood sample was placed to obtain both a total and differential white blood cell (WBC) count. In hens, OSI and MDA levels were significantly higher (P ¼ .04, and P ¼ .004) in subjects from intensive farming (14.7 6 7.1 and 27.2 6 10.4 nmol/mL) than in those bred in rural conditions (5.6 6 10.3 and 8.2 6 13.3 nmol/mL). In magpies, a positive correlation between the total WBC count and OS was found, and both d-ROMs and OSI were significantly higher (P ¼ .03) in subjects with a total WBC count greater than the median value (20.4 3 103 cells/lL) with respect to those with a total WBC count less than the median value. The results generated from this study indicate that higher OS levels occurred in hens bred in an intensive indoor farm environment compared with outdoor free-range conditions. Possibly the higher OS levels could be related to the higher stocking density and dust levels found in the indoor facility. Additionally, the correlation between OS biomarker levels in magpies and total WBC count suggests that OS level is influenced by immune response, in agreement with previous studies. Collectively, present data seem to be promising for the application of OS measurement in avian medicine for health and animal welfare monitoring

Discussion

· Significantly higher OSI values and lipid peroxidation levels in chickens maintained in a high-density indoor environment compared with similar birds living freely outside

· Significantly lower RBC and PCV values were observed in the chickens from G1 evaluated in this study with respect to G2. A possible reason for this difference could be the damaging action by ROMs on erythrocyte membranes and hematopoiesis, because it was previously observed that oxidative stress can exacerbate hemolytic anemia

· Significantly higher PAT levels were found in male magpies with respect to females; this result is in agreement with that previously observed in the zebra finch (Taeniopygia guttata), in that males showed higher levels of overall antioxidant defenses with respect to females

· The correlation between OS biomarker levels in magpies and total WBC count suggests that OS level is influenced by immune response

· UA does not appear to influence OS biomarkers

· The data obtained from this study indicate that the use of OS biomarkers as a tool to detect and monitor health problems or evaluate the welfare condition in bird species may be possible

116
Q

What effect does West Nile Virus have on wild Ruffed Grouse (Bonasa umbrellus) populations?

A

They may be highly susceptible to the disease - more work is needed

WEST NILE VIRUS INFECTION IN RUFFED GROUSE (BONASA UMBELLUS) IN PENNSYLVANIA, USA: A MULTI-YEAR COMPARISON OF STATEWIDE SEROSURVEYS AND VECTOR INDICES

Journal of Wildlife Diseases, 57(1), 2021, pp. 51–59

ABSTRACT: Eastern populations of Ruffed Grouse (Bonasa umbellus) have been in a decades-long decline across the mid-Atlantic and southern Appalachian Mountains of the US. West Nile virus (WNV), which first arrived in the US in 1999, is suspected to have contributed to these declines based on decreased population indices since the arrival of WNV in Pennsylvania as well as on high, experimentally induced WNV-associated morbidity rates. A 3-yr statewide survey was conducted across Pennsylvania to measure flavivirus (i.e., WNV) seroprevalence among hunter-harvested grouse. The overall seroprevalence from 2015–17 was 14.4% (81/563); annual seroprevalence ranged from 2.8% (4/145) in the 2017 hunt year to 22.6% (52/230) in 2016–17. We analyzed the effects of numerous variables (i.e., Ruffed Grouse age and sex, hunt year, WNV vector index [VI], and region of Pennsylvania) on WNV serostatus by logistic regression. While there was no significant difference in WNV seroprevalence between sex and age group, there was significant variation in seroprevalence between geographic regions of Pennsylvania and across hunt years. Additionally, there was a negative correlation between WNV seroprevalence and VI. Low seroprevalence rates among Ruffed Grouse corresponded to years with a high VI, supporting experimental findings that Ruffed Grouse may be highly susceptible to WNV-associated disease. Additional strategic research efforts are essential to more effectively measure the effects of WNV on Ruffed Grouse and other vulnerable avian species

Intro

· Ruffed Grouse populations are declining, WNV may be playing a role

· We determined statewide flavivirus (i.e., WNV) seroprevalence of Ruffed Grouse over multiple hunt years

M&M

· 3 year statewide sero-survey across Pennsylvania (2015-2017)

· The presence and titer of antibodies to WNV were determined by plaque-reduction neutralization test (PRNT)

· Also evaluated vector index (VI). The VI as described in Jones et al. (2011) provides an estimate of the abundance of infected mosquitoes by combining the average number of mosquitoes collected per trap and the estimated WNV infection rate of all individuals of the tested mosquito species

Results and discussion

· The overall flavivirus (i.e., WNV) seroprevalence among Ruffed Grouse sampled during the three hunt years (excluding pilot study year of 2014–15) was 14.4% (81/563), which included 42 of 67 Pennsylvania counties.

· Seroprevalence in three consecutive sampling periods was 13.3% (25/188) in 2015–16, 22.6% (52/230) in 2016–17, and 2.8% (4/145) in 2017

· West Nile virus seroprevalence in Ruffed Grouse and WNV VI were negatively correlated

· There was no difference in WNV seroprevalence between sex (P¼0.149) or age group

· Results from our 3-yr study reveal that flavivirus (i.e., WNV) seroprevalence was variable but generally low (range 3–23%) in hunter-harvested Ruffed Grouse in Pennsylvania.

· This low seroprevalence is similar to that detected in other highly susceptible species such as the American Crow (Corvus brachyrhynchos), Fish Crow (Corvus ossifragus), and Greater Sage-grouse

· The low WNV seroprevalence in Ruffed Grouse in Pennsylvania has multiple potential explanations, one of which is low virus exposure rates via WNV-infected, ornithophilic mosquitoes.

· An alternative explanation to the low seroprevalence is that Ruffed Grouse are highly susceptible to WNV-associated mortality, and thus low numbers of infected birds survive to the subsequent fall or winter

· The negative correlation between VI, which incorporates average mosquito density and estimated infection rate in a given area, and flavivirus (i.e., WNV) seroprevalence in Pennsylvania Ruffed Grouse further support the possibility that there were high proportions of infected mosquitoes concurrent with high WNV infection rates and concurrent low survival of grouse

117
Q

Describe the use of a vessel and tissue sealing device (Ligasure) for ovariectomy in domestic chickens.

Is it recommended?

A

Take Home Message: Vessel Sealing Device for ovariectomy resulted in significant hemorrhage and incomplete ovary excision.

Sullivan, J. L., Wakamatsu, N., Yin, J. H., Roberts, T., & Bennett, R. A. (2021). Assessment of a vessel and tissue–sealing device for ovariectomy in chickens to evaluate the potential application of the procedure to other avian species. American Journal of Veterinary Research, 82(4), 310-317.

Abstract: OBJECTIVE: To assess the feasibility of a novel technique involving a vessel and tissue– sealing device (VTSD) for ovariectomy in chickens to evaluate the potential application of the procedure to other avian species.

ANIMALS: 20 domestic laying hens (Gallus domesticus), of which 10 were immature (< 4 months old) and 10 were adults (> 18 months old).

PROCEDURES: Ovariectomy was performed with a VTSD through a left lateral celiotomy. Birds were allowed to recover for 14 days after the procedure and then were euthanized for necropsy. A board-certified veterinary pathologist performed complete necropsies, with particular attention to identifying any remaining ovarian tissue.

RESULTS: All birds survived the procedure. For the mature and juvenile birds, the mean ± SD durations of anesthesia (interval from intubation to extubation) were 67.2 ± 7.6 minutes and 50.5 ± 5.1 minutes, respectively, and mean durations of surgery were 45.3 ± 8.5 minutes and 31.6 ± 5.1 minutes, respec- tively. Three birds had severe hemorrhage during ovariectomy. At necropsy, ovarian tissue was present grossly in 2 mature birds and histologically in 6 additional birds (2 mature and 4 juvenile birds), indicating incomplete excision in 8 (40%) birds.

CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that the evaluated VTSD can be used to successfully perform ovariectomies in both juvenile and mature chickens, although the procedure was associated with major hemorrhage and incomplete excision of ovarian tissue in some cases. Use of this VTSD for ovariectomy in birds of other species, particularly birds with reproductive tract disease, should be investigated.

Key Points:

  • Most female birds, with few exceptions, have only L side of the repro tract – ovary, oviduct, uterus or shell gland.
  • Right side atrophies during embryonic development
  • L ovary is adhered to the Cd vena cava, common iliac, and L kidney
  • Mesovarium is wide and short, little distance between the ovary and vasculature/L kidney
  • Usually if lift ovary to ligate ovarian vessel- damage to larger vasculature → severe hemorrhage.
  • Indications for ovariectomy: Neoplasia, ovarian cysts, oophoritis, bacterial yolk sac coelomitis, behavioral disorders with hormonal component. Ovariectomy for sterilization of birds is not recommended owing to the risk of fatal hemorrhage (salpingohysterectomy performed instead but may result in ovulation into the coelom and coelomitis).
  • Incomplete ovariectomy may result in follicle production and hormone secretion.
  • Hemorrhage most common complication, often life-threatening, always occurred dorsal to the ovary after the jaws of the VTSD were opened. Originated from the CdV and CIV, not the ovarian artery.
  • It was not possible to completely remove the ovary in any bird with 1 application of the VTSD.
  • Air sacculitis secondary to sepsis is a risk associated with celiotomy
118
Q

A recent study infestigated the effects of high-dose repeated meloxicam administration in Rhode Island Red Chickens.

What is the scientific name of the chicken?

What dose was used in this study?

What was the mortality rate of the treatment group?

What lesions were seen on necropsy?

What is the mechanism of meloxicam renal toxicity in birds?

What were the indicators of acute tubular injury in the affected hens?

A

Journal of Avian Medicine and Surgery, 36(2): 128-139
Clinicopathologic, Gross Necropsy, and Histopathologic Effects of High-Dose, Repeated Meloxicam Administration in Rhode Island Red Chickens (Gallus gallus domesticus)
Houck, Emma L., Petritz, Olivia A., Chen, Laura R., Fletcher, Oscar J., Thomson, Andrea E., et al.

Key Points:
- Trauma is reported to be the most common presenting complaint for backyard poultry
- Single doses of high dose meloxicam (3 and 5 mg/kg) reduced hyperalgesia to thermal nociception
– No previous reports of adverse effects in avian species at studied dosages including up to 20 mg/kg
– Recommended for livestock in regions with avian scavengers (Gyps spp - vultures)
- Objectives 0 characterize clinical, clin path, and histo findings of meloxicam based on upper dose range of the single dose studies demonstrating analgesic effect (5 mg/kg PO BID x 5 days)
- ~ 40% premature mortality rate noted in the treatment group
– All had peracute (sudden lethargy) or no clinical signs. No weight loss.
– All birds had renomegaly and lesions consistent with renal and visceral gout
- Gross necropsy findings in meloxicam group included renomegaly, renal gout, and visceral gout (most commonly on liver, serosal surfaces, hear and lungs)
– 60% of birds in meloxicam group had evidence of renal gout on histo and 40% had severe acute tubular injury (ATI) (cortical tubular ectasia, tubular necrosis
- Hematologic changes not clinically relevant - Meloxicam group had greater heterophil percentage, and H:L ratio.
– UA increased with ATI score, but was not significantly different from the control group
– UA useful to confirm severe ATI and renal failure but may not be sensitive for mild-moderate renal pathology
– UA also increased with ovulation
- Lethargy, increased UA, grossly visible visceral gout, and histologic ATI with intratubular urate tophi are similar to toxic diclofenac and ketoprofen lesions seen in other birds. No all birds in meloxicam group developed ATI.
- Mechanism of toxicity is different from mammals – thought to be toxic to renal tubular epithelium by increasing reactive oxygen species and interfering with p-amino-hippuric acid channels.
– Also suspected to be due to zero order pharmacokinetics and accumulation from saturation of metabolic processes.

Take-Home Message:
- Repeated dosing of 5 mg/kg meloxicam has the potential to induce peracute renal and visceral gout and subsequent mortality from meloxicam induced acute tubular injury and is NOT recommended in chickens.
- Meloxicam induced renal toxicity led to 40% mortality in chickens in this study.
- Clinical signs of illness, changes in body weight, and changes in clinicopathologic data were not sensitive indicators of ATI in hens given meloxicam at the toxic dose used in this study.

119
Q

A recent study investigated the pharmacokinetics and egg residues of meloxicam in Bantam Cochin chickens.

The plasma concentrations remains above therapeutic thresholds for how long?
- What is the recommended dosing and interval?
- How does that differ from Leghorns and Columbian Wyandottes?

What is the recommended egg withdrawal?

A

JAMS 2022 36(2) 140-144
Pharmacokinetics and Egg Residues of Oral Meloxicam in Bantam Cochin Chickens

Key Points:
- No adverse effects
- Bantam Cochin hens demonstrated a significantly longer mean apparent terminal half-life, greater area under the curve, smaller elimination rate constant, and longer egg residue times compared with white leghorn hens.
- These findings suggest that bantam Cochin hens, similar to Columbian Wyandotte hens, exhibit a larger drug distribution with slower metabolism and clearance
- Ok results from the bantam Cochin hens did not significantly differ from those reported for the Columbian Wyandotte hens.
- No PD studies done in chickens thus far
- Plasma concentrations in the current study remained above thresholds in other species for 20 hours (humans) and 8 hours (parrots)
- Based on these results, we recommend the same dose previously recommended for Columbian Wyandottes be used in bantam Cochins (1 mg/kg PO q24h) until pharmacodynamic studies can be performed to identify the therapeutic plasma concentration range.
- This dose is less frequent than that recommended for white leghorn hens because of the slower metabolism and clearance of the drug in bantam Cochins.
- Egg withdrawal of 2 weeks should be sufficient based on these and previous results

120
Q

A recent study evaluated the potential nephrotoxic effects of amikacin administered via intravenous limb perfusion in chickens.

Why is this a potential concern?

How did uric acid values change over the course of repeated RLP?

What lesions were associated with its use?

A

JAMS 2022 36(2) 187-191
Clinicopathologic Findings in Chickens (Gallus gallus domesticus) Administered Amikacin Through Intravenous Regional Limb Perfusion

Key Points:
- Regional limb perfusion (RLP) is commonly used with amikacin
- Potentially nephrotoxic drugs, such as amikacin, may increase the risk of nephrotoxicity with RLP because of the presence of the renal portal system and direct venous blood flow from the pelvic limbs to the kidneys
- The objective of this study was to evaluate the safety of amikacin administered by RLP in healthy chickens following repeated administration at the published dose of 20 mg/kg (q24h x 3 days)
- Plasma uric acid concentrations increased over time in both groups and did not differ significantly between control and treatment groups at any time point before or after RLP
– The difference in values between the time points was also not considered clinically relevant, and all uric acid concentrations remained within published reference intervals at all time points
- None of the birds had grossly appreciable pathology at the postmortem examinations.
- There were no significant differences in histologic renal pathology scores between the 2 groups or between the left and right kidneys within each group

121
Q

A recent study investigated IM alfaxalone and midazolam versus midazolam and butorphanol for sedation of rhode island red hens.

How did the two protocols compare?
- Which had faster onset of sedationg?
- Which resulted in better sedation (more likely to achieve positioning for radiography)?
- Which had lower HR & RR
- Which had the faster recovery

What were some side effects noted with the alfaxalone group?

A

Journal of Avian Medicine & Surgery 36(3):287-294;2022
EFFECTS OF INTRAMUSCULAR ALFAXALONE AND MIDAZOLAM COMPARED WITH MIDAZOLAM AND BUTORPHANOL IN RHODE ISLAND RED HENS (GALLUS GALLUS DOMESTICUS)
Kyra A. Knutson, DVM, Dipl ACZM, Olivia A. Petritz, DVM, Dipl ACZM, Andrea Thomson, BS, RVT, James Robertson, MA, and Julie A. Balko, VMD, Dipl ACVAA

Key Points:
- Alfaxalone-midazolam: faster onset of sedation, higher sedation score, longer duration of action, and more likely to achieve radiographic positioning
- Lower HR and RR wit butorphanol-midazolam but faster recovery
- Some hyperexcitability and opisthontonos with alfaxalone group

122
Q

A recent study conducted a pathogen survery and discussed predictors of lymphoproliferative disease virus in wild turkeys in Maine.

What is lymphoproliferative disease virus?
- What lesions does it cause?
- Is it documented in the wild?
- What factors are associated with it?

What are the effects of reticuloendotheliosis virus?

What about Salmonella pullorum?

What about Mycoplasma gallisepticum?

How prevalent are these diseases in Maine?
- Is there a sex or season predilection to them?

A

JWD 2022 58(3):537-549
Pathogen Survey And Predictors Of Lymphoproliferative Disease Virus Infection In Wild Turkeys (Meleagris gallopavo)
Shea SA, Gonnerman M, Blomberg E, Sullivan K, Milligan P, Kamath PL

Key Points:
- Lymphoproliferative disease virus (LPDV) = avian oncogenic retrovirus
– Can cause lymphoid tumors and mortality in domestic turkeys
– In 2009, LPDV was identified in Wild Turkeys in the US
– Higher LPDV prevalence in NE USA vs. southern and western regions
– Increased LPDV transmission at the species’ northern range limit could be driven by increased interactions due to limited nutrient sources during winter months
– Wild turkeys can show nonspecific clinical signs (e.g., lethargy, ataxia)
– Age has been identified previously as a predictor of LPDV infection
- Reticuloendotheliosis virus (REV) -> runting, immunosuppression, and tumor growth in poultry
- Salmonella pullorum -> mortality in young poultry or reduced reproductive output in adults
- Mycoplasma gallisepticum (infectious sinusitis)
– One of the costliest diseases in the commercial poultry industry
– Causes air sacculitis and reduce egg production, fertility, and hatchability in turkeys

TLDR:
- High prevalence of LPDV and M. gallisepticum in wild turkeys in Maine.
- Females and adults were significantly more likely to be infected with LPDV.
- Higher LPDV prevalence in the spring compared to winter.

123
Q

What was the novel Avibacterium species identified in turkeys in Colorado?

What is the scientific name of the turkey?

What lesions were associated with this disease?

A

NOVEL AVIBACTERIUM SPECIES ASSOCIATED WITH SINUSITIS AND CONJUNCTIVITIS IN A MERRIAM’S WILD TURKEY (MELEAGRIS GALLOPAVO MERRIAMI) FLOCK IN COLORADO, USA
Jayne S. Ellis, Christopher A. MacGlover, Kerry S. Sondgeroth, Derek Brown, Joshua B. Daniels, and Karen A. Fox
Journal of Wildlife Diseases, 58(4), 2022, pp. 725–734

Take Home: Novel avibacterium (Avibacterium gallopavo) identified in a clinically affected Meriams Wild Turkey with periocular swelling and skin crusting and was identified in turkeys from the same flock without clinical signs