Galliformes Journal Article Quick Review Flashcards
How was survivability in attwater’s prairie chicks affected by gavage feeding a diet high in fermentable carbohydrates?
How did medical treatment influence survivability/medical conditions?
REVIEW OF MORTALITY AND EFFECTIVENESS OF NEONATAL TREATMENT IN CAPTIVE ATTWATER’S PRAIRIE CHICKENS (TYMPANUCHUS CUPIDO ATTWATERI)
Mulreany L, Flanagan J, Molter C, Howard L, Tocidlowski M, Werre S, Vanhooser S, Morrow M.
Journal of Zoo and Wildlife Medicine. 2018 Sep;49(3):671-9.
Cause of death: yolk sac > maladaptation > musculoskeletal abnormalities > necrotic enteritis > mucoid enteritis
Most common pathogen in yolk sac infection = E. coli
Yolk sac infection associated with increased humidity and/or temperature
Most common pathogen with necrotic enteritis = Gram + rods
Mucoid enteritis etiology not determined
Gavage feeding highly digestible cereal grain diet → increased Clostridium shedding
Probiotics → decreased Clostridium shedding
Chicks that were gavage fed had:
Higher rate of necrotic enteritis, yolk sac infection
Lower rate of mucoid enteritis and maladaptation
Higher mortality in chicks receiving metronidazole or penicillin
Meloxicam increased survival in chicks with mucoid enteritis
Chicks that required medical treatment had a worse prognosis for survival.
Egg shell hygiene may be improved via washing, dipping, or spraying eggs with peroxide, UV exposure, or fumigation with formaldehyde.
Conclusions: Prairie atwater chicks die from yolk sacculitis from E. coli most commonly, which is associated with increased humidity and temperature.
What was observed regarding levels of lead in eggs of a chicken with lead toxicosis?
What are the toxic effects of lead? How is lead stored?
What are some chelation drug options? Is there a WDT for chelation?
Lead Levels in the Eggs of a Chicken With Lead Toxicosis
Lamb SK.
Journal of avian medicine and surgery. 2018 Sep;32(3):217-20.
FARAD requires 6-8 weeks of withdrawal time after chelation with CaEDTA
Lead storage: bones (94%) > blood (4%) > soft tissues (2%)
Blood holds 4% of lead, soft tissues hold 2% of lead and bones hold 94% lead
Toxic effects of lead:
Necrosis of GI tract, impaired GI motility
Increased RBC fragility leading → anemia
Competes with Ca and may substitute for Ca in bone
Mimics cells actions of Ca → cell death, cerebral edema
Chelation drug options: CaEDTA, D-penicillamine, and meso-2,3- dimercaptosuccinic acid
Rebound effect can occur when therapy is stopped and lead redistributes
May need many courses of treatment
Lead in eggs is highest in shell or yolk; levels in albumen generally negligible
Blood levels and egg levels of lead both decreased together with chelation therapy
Soil with high lead levels can lead to accumulation in chickens
Best to advise against eating eggs produced from hens that have been diagnosed with lead toxicity.
Conclusions: Chelation of lead toxicosis also reduces lead levels within eggs. Rebound effect may require multiple rounds of chelation, and it is unknown the effect on the egg if rebound should occur.
What are some risk factors associated with lymphoproliferative disease virus distribution in wild turkeys in NY?
What type of virus is lymphoproliferative dz virus?
Risk factors for and spatial distribution of lymphoproliferative disease virus (LPDV) in wild turkeys (Meleagris gallopavo) in New York State, USA
Alger K, Bunting E, Schuler K, Whipps CM.
Journal of wildlife diseases. 2017 Jul;53(3):499-508.
Lymphoproliferative disease virus (LPDV) = oncogenic retrovirus that causes neoplasia in wild and domestic fowl
Endemic in wild turkeys
LPDV causes internal and cutaneous tumors
Mass mortalities in domestic flocks
Rarely fatal in wild turkeys
Transmission: horizontal +/- vertical (seen in other retroviruses)
No vaccine available
Key Points:
Overall prevalence of LPDV in wild turkeys = 55%
Females > males
Adults > juveniles
Increased with increased agriculture:forest ratio
Prevent LPDV with adequate fencing around farms in areas of high prevalence
Uncertain if translocation affected distribution of the virus.
Conclusions: Lymphoproliferative disease virus is endemic in wild turkeys in New York.
What disease was of high prevalence in a survey of wild turkeys in Canada?
Detection of lymphoproliferative disease virus in Canada in a survey for viruses in Ontario wild turkeys (Meleagris gallopavo).
MacDonald AM, Jardine CM, Bowman J, Susta L, Nemeth NM.
Journal of wildlife diseases. 2019 Jan;55(1):113-22.
Lymphoproliferative disease virus = oncogenic virus in wild and domestic turkeys
Endemic in wild turkeys → subclinical disease
Key Points:
LPDV was common (65% prevalence) in wild turkeys
Males > females
Strain was similar to North American strain.
No LPDV in other bird species tested
Wild turkeys with proliferative skin lesions were likely to test positive for avian poxvirus
Few cases of reticuloendothelial virus coinfection with LPDV (both can manifest as multiorgan lymphoid neoplasia).
No cases of avian influenza
Conclusions: Wild turkeys in Canada have a high prevalence of lymphoproliferative disease virus.
What was the most common mycoplasma spp isolated in a survey of free-ranging turkeys in Ontario?
HIGH PREVALENCE OF MYCOPLASMA AND EIMERIA SPECIES IN FREE-RANGING EASTERN WILD TURKEYS (MELEAGRIS GALLOPAVO SILVESTRIS) IN ONTARIO, CANADA
Amanda M. MacDonald, Claire M. Jardine, Evelin Rejman, John R. Barta, Jeff Bowman, Hugh Y. Cai, Leonardo Susta, Nicole M. Nemeth
J. of Wildlife Diseases, 55(1):54-63 (2019)
Most common Mycoplasma = M. gallpavonis
M. meleagridis (turkey, quail, peafowl) → respiratory disease, poor growth, bone deformation in juveniles
M. synoviae (chicken, turkey) → synovitis, resp disease - domestic chicken, turkey
M. iowae (turkey) → embryonic mortality, joint-related growth abnormalities, mild air sacculitis
M. gallisepticum (house finches, chukar partridges, ring-necked pheasants)
Eimeria → emaciation, lethargy, hemorrhagic diarrhea, death (rare)
Transmission: Ingestion of oocysts from environment
Key Points:
Non-pathogenic mycoplasma and Eimeria found in almost all turkeys
Most common Mycoplasma = M. gallpavonis
Poultry pathogens were rare (M. meleagridis, iowa, synoviae)
Most common Eimeria:
E. meleagrimitis = E. adenoeides > gallopavonis
Conclusions: Nonpathogenic Mycoplasma and Eimeria were extremely common in wild turkeys in Ontario.
What parasite caused mortality in captive-bred bobwhite quail and what is the vector?
HAEMOPROTEUS (PARAHAEMOPROTEUS) SPP. IN CAPTIVE-BRED BOBWHITE QUAIL (COLINUS VIRGINIANUS) IN SOUTHERN UTAH, USA
E. Jane Kelly, Thomas J. Baldwin, David D. Frame, April L. Childress, James F. X. Wellehan
J. of Wildlife Diseases, 54(4):726-733 (2018).
Haemoproteus → serious disease in pigeons, quail, and turkeys (high mortality)
Transmission: Culicoides (biting midges; parahaemoproteus) and Hippoboscid flies (haemoproteus)
Parasitemia highest in summer and fall, in habitats that support the insect vector
Key Points:
Parahaemoproteus subgenus = major cause of death in bobwhite chicks - vector likely Culicoides spp
Clinical signs: depression, ruffled, difficulty walking, or dead
Necopsy: pale skeletal muscle w/ multifocal hemorrhage, petechiae on air sacs/serosal surfaces
Histo: schizonts in live and spleen
Example of a virulent infection resulting from a complete life cycle of the protozoa - schizont stage in liver, merozoites in RBCs (infection not abortive; merozoites in sinusoids of the liver suggest asexual reproduction was successful).
Conclusions: Parahaemoproteus found as cause of mortality in managed bobwhite quail chicks.
Describe the path of avian cardiac depolarization and how it differs from mammals.
ELECTROCARDIOGRAM ANALYSIS OF THE GOLDEN (CHRYSOLOPHUS PICTUS) AND SILVER (LOPHURA NYCTHEMERA) PHEASANTS
H. Hassanpour, H. Zarei, L. Nasiri and P. Hojjati
Journal of Zoo and Wildlife Medicine. 49 (4): 881-886, 2018.
Avian heart conduction:
Purkinje fibers follow coronary arteries
Wave of excitation arrives at left ventricle rapidly
Depolarization = subepicardium → myocardium → endocardium
Mammals start at endocardium and move outward
Ventricular depolarization sequence = R apex → R base → L base → L apex
Unique features of avian ECGs:
Negative mean electrical axis
Alterations in MEA helpful in diagnosing heart disease in turkeys/chickens
Ta waves in some specie (pigeon, Andean condor, muscovy ducks, laughing dove, European kestrel)
No Ta wave in griffon vulture, little owl, Eurasian eagle owl, rook
Golden and silver pheasants do not have Ta waves
Conclusions: Golden and silver pheasant ECGs have a negative mean electrical axis (like all birds) and no Ta waves (like some birds.
What is the recommended withdrawal time for chickens receiving oral meloxicam?
Pharmacokinetics and egg residues after oral administration of a single dose of meloxicam in domestic chickens (Gallus domesticus)
Souza MJ, Bergman JB, White MS, Gordon KI, Gerhardt LE, Cox SK.
American journal of veterinary research. 2017 Aug;78(8):965-8.
After meloxicam 1 mg/kg PO once:
No drug was detected in egg whites after 4 days and in yolks after 8 days.
Half-life shorter than Hispaniolan Amazon, red tailed hawks, or great horned owls
tMax was shorter than Hispaniolan Amazons and great horned owls.
Maximum plasma concentration higher than Amazons (both given 1 mg/kg). Also higher than owls or red tails
Conclusions: Withdrawal period of 2 weeks is recommended after a single dose of meloxicam in chickens.
Pharmacokinetics and Egg Residues of Meloxicam After Multiple Day Oral Dosing in Domestic Chickens
Souza MJ, Bailey J, White M, Gordon K, Gerhardt L, Cox SK.
Journal of avian medicine and surgery. 2018 Mar;32(1):8-12.
Meloxicam at 1 mg/kg PO q12h does not accumulate
Persists longer in yolk
No adverse effects
Withdrawal time of 14 days
Conclusions: Meloxicam withdrawal time for multidose course of meloxicam in chickens is 14 days.
Describe the PK and egg residues following Clavamox in domestic chickens. How does the PK differ from blue fronted parrots?
Pharmacokinetics and Drug Residue in Eggs After Multiple-Day Oral Dosing of Amoxicillin-Clavulanic Acid in Domestic Chickens
Leah Shannon, Sherry K. Cox, Joan Bailey, Chelsea Fortner, Rebecca Davis, Lillian Gerhardt, Marcy J. Souza
J. of Avian Medicine and Surgery, 34(1):3-8 (2020)
Amoxicillin did not reach therapeutic levels
Absent from plasma after 2 h
Absent in eggs after 4 days
Clavulanic acid absent from plasmas after 8 h
Never detected in eggs
Conclusions: Clavamox at 125mg/kg PO q12h in chickens did not reach therapeutic levels.
In blue fronted parrots, this dose led to plasma concentrations considered to be therapeutic ~ 6hrs.
Describe difference in PK between Wyandotte hens vs Leghorns dosed with meloxicam.
Souza, M. J., Gerhardt, L. E., Shannon, L., Fortner, C., Davis, R., Condon, M., … & Cox, S. K. (2021). Breed differences in the pharmacokinetics of orally administered meloxicam in domestic chickens (Gallus domesticus). Journal of the American Veterinary Medical Association, 259(1), 84-87.
Detection in egg whites in both were similar, but egg yolk significant (longer in Wyandotte).
Wyandote longer terminal half life, slower elimination, greater area under the curve.
Similar Cmax and tmax.
Overall slower metabolism in Wyandote.
Conclusion: Wyandotte hens should be dosed every 24h, Leghorns every 12 hrs.
WDT of 2 wks recommended for both following meloxicam tx.
Describe PK of single oral dose of ponazuril in the indian peafowl.
Zec, S. H., Papich, M. G., Oehler, D. A., Hills, K., Schmid, S., Huth, K., … & Paré, J. A. (2021). Pharmacokinetics of a single oral dose of ponazuril in the Indian peafowl (Pavo cristatus). Journal of Zoo and Wildlife Medicine, 52(2), 548-554.
Single dose of oral ponazuril was absorbed, detectable at 20 and 40 mg/kg.
All negative for coccidial shedding 1 week after the second trial.
Ponazuril was slowly eliminated, with an elimination half-life 200h for each dose (~8 days).
What was observed with IV limb perfusion of ceftiofur sodium vs intraosseous limb perfusion?
Intravenous and intraosseous regional limb perfusion of ceftiofur sodium in an avian model
Sophie Emmanuelle Knafo DVM1; Jennifer E. Graham DVM1 and Bruce A. Barton PhD
American Journal of Veterinary Research June 2019, Vol. 80, No. 6, Pages 539-546
IV regional limb perfusion of ceftiofur sodium (compared to intraosseous RLP) had:
Higher synovial levels (21-27x higher!)
Lower plasma levels
Mild phlebitis/bruising IV
No difference between plasma levels of IV RLP and IM injection
AST increased in all groups, but the highest in IV RLP group
Conclusions: IV RLP with ceftiofur sodium in chickens created a significantly higher synovial concentration of drug compared to IO RLP or IM administration, but IO RLP had significantly higher plasma concentration.
What was observed in a comparison of anesthetic efficacy of lidocaine and bupivacaine in spinal anesthesia in chickens?
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.
No epidural space in birds - Well developed arachnoid space in the synsacral spinal cord.
Bupivacaine had significantly delayed onset vs lidocaine.
All groups had a decreased cloacal temp except bupivacaine at the lowest dose.
Some chickens in the high dose bupivacaine group became ventrally recumbent.
Lidocaine and bupivacaine produced effective anesthesia in caudal coelomic area, delayed onset and lasted longer with bupivacaine.
What galliform species is highly susceptible to WNV?
WEST NILE VIRUS INFECTION IN RUFFED GROUSE (BONASA UMBELLUS) IN PENNSYLVANIA, USA: A MULTI-YEAR COMPARISON OF STATEWIDE SEROSURVEYS AND VECTOR INDICES
Nicole M. Nemeth, Lisa M. Williams, Angela M. Bosco-Lauth, Paul T. Oesterle, Matt Helwig, Richard A. Bowen, Justin D. Brown
J. of Wildlife Diseases, 57(1):51-59 (2021).
West Nile virus: zoonotic, mosquitoborne flavivirus
Ruffed grouse are highly susceptible to WNV
40% severe CS in experimental infections (oftencardiac pathology and encephalitis)
Corvids are also highly susceptible to WNV
Key Points:
Low WNV seroprevalence (14%) in Ruffed Grouse in Pennsylvania
Vector index was negatively correlated with seroprevalence (high proportions of infected mosquitoes concurrent with high WNV infection rates and low survival of those grouse).
Nobuto strips for the detection of anti-WNV antibodies was validated in samples but with decreased sensitivity
Authors recommend storing at -20C
Conclusions: Ruffed Grouse are highly susceptible to WNV-associated mortality.
How was a vaccine protocol for juvenile greater sage grouse modified and why?
Vaasjo, E., Black, S. R., Pastor, A., & Whiteside, D. P. (2021). Assessing the humoral response to and safety of a commercially available equine west nile virus vaccine in a zoo-based conservation breeding population of endangered greater sage-grouse (centrocercus urophasianus). Journal of Zoo and Wildlife Medicine, 52(2), 732-736.
All chicks vx 3 times (2-3 wk apart) starting between 1-3 wks age and then boostered annually.
All samples from juvenile birds were negative for antibody detection.
Of adults, 35% had a positive Ab response.
Only two cases of vx reaction overall.
Vaccination with a commercial equine killed WNV vaccine commonly used in zoo spp failed to produce a detectable humoral response in juvenile greater sage grouse after a 3 vx protocol. There was a variable response in adults that had been vaccinated annually for several years.
Cell mediated immunity may be of greater importance. No WNV assoc deaths even with confirmed cases.
Vx protocol since refined to include only 2 doses of vaccine before annual boosters, cost saving significant.
