Pelicaniformes/Suliformes

Question 1

What type of feet do pelecaniformes have?

Answer 1

Totipalmate

Question 2

Unique anatomical consideration of administering fluids SC to pelecaniformes?

Answer 2

 Subcutaneous air sacs known to connect with the resp system, inflated by closing of the glottis.
• Air pockets act as a shock absorber when hitting the water during dives and assists in floating.
• Boobies and gannets also have extensive SC air sacs.
• Male pelicans generally larger than females with longer bills.
• External nares not patent in brown pelicans, cormorants, boobies, gannets. Adaptation for diving.
• Gular pouch used for courtship display in frigatebirds, absent in tropicbirds.

Question 3

Unique anatomy of pelecaniformes?

Answer 3

o Totipalmate foot
o Presence of gular pouch
o Highly reduced tongue and hyoid structures
o Gular fluttering during open-mouthed breathing enables evaporative cooling
o Lack of brood patch
o Vestigial intestinal ceca
o Bilobed uropygial gland
o Skeletal pneumatization varies
 Anhinga (diving species) - apneumatic postcranial skeletons
 Cormorants - heavy-boned with pneumatization of only humeri or caudal cervical vertebrae
 Pelicans (soaring fliers) - extensive skeletal pneumaticity, except for femur
o Pelicans, gannets and boobies - diverticula extend from air sacs to form substantial cranioventral subcutaneous air cushion system
 Provide cushioning for water entry during diving from height
o Many Pelecaniformes have reduced (frigatebirds, pelicans) or obliterated (gannets, anhingas) external nostrils
 Breathing (and access to olfactory system) via open mouth or jugal operculum at commissure of bill (boobies, cormorants)
o Male frigatebirds - neck skin pouches with bare overlying skin that is inflated for display

Question 4

What are the different feeding approaches for brown pelicans, white pelicans, cormorants, boobies and gannets, frigates?

Answer 4

o Brown pelican feeds by diving.
o White pelican feeds by herding fish and dipping beaks into the water to scoop fish.
o Cormorants, anhingas surface divers and capture their prey under water.
o Tropicbirds, boobies, gannets are plunge divers.
o Frigates renowned scavengers, steal food from other birds.
o Birds in captivity need to adapt to dead fish, training may be required.

Question 5

Important restraint and handling considerations for pelecaniformes?

Answer 5

o As nares not patent in brown pelicans, cormorants, boobies, and gannets, beaks should be held slightly open during restraint to prevent asphyxia.
o May inflate SC air sac diverticulae when stressed, feels like crepitus.
o Wear eye protection, especially with anhingas.

Question 6

What bacteria has been associated with fatal enteritis in captive brown pelicans, suspected to have been from fish as source of infection?

Answer 6

Clostridium perfringens

Question 7

Effect of avian influenza vaccination on immune response in pelicans (F8)?

Answer 7

No immune response to domestic poultry vaccine. Partial response in cormorants.

Question 8

Clinical signs of west nile virus in pelicans and cormorants?

Histologic lesions

Answer 8

• Pelicans and cormorants - neurological signs common including head tilt, ataxia, disorientation
o Brain hemorrhage may be apparent
o Histo in cormorants - meningeal or neuropil hemorrhage; neuronal vacuolation; lymphohistiocytic myocarditis, mineralization, and hemorrhage; splenomegaly with lymphoid depletion, fibrinous splenitis, hemorrhage; renal and pancreatic lymphohistiocytic infiltrates; hepatocyte necrosis and intestinal crypt cell necrosis,
o Encephalitis or meningoencephalitis and myocardial necrosis or myocarditis are dominant lesions in American white pelicans
o Encephalitis and myocarditis in eared grebes

Question 9

Species of lice that causes severe hemorrhagic stomatitis and lives in gular pouch of pelicans and cormorants.

Answer 9

Piagetiella spp (pouch lice)

Question 10

What medication has been associated with fatal enteritis and bone marrow damage in pink-backed pelicans?

Answer 10

Fenbendazole!

o FATAL enteritis and bone marrow damage in pink-backed pelicans with fenbendazole admin.
 Found dead or in resp distress/death after presentation.
 Medicate birds individually or hand-toss medicated fish to individuals rather than treating an entire group with medicated fish in a pan.

• Fenbendazole reported to be effective in brown pelicans at relatively low doses (22 mg/kg).

Question 11

Excess dietary supplementation of what vitamin lead to severe coagulopathy in pink-backed pelicans?

Answer 11

Vitamin E (hypervintaminosis E)

Question 12

List birds with reported fenbendazole toxicity.

Answer 12

Penguins, American white pelicans, pigeons, storks, vultures

 Stomatitis (pelicans), inconsistent hepatic, renal, or splenic enlargement, intestinal crypt cell necrosis, superficial mucosal necrosis, secondary bacterial colonization, nonspecific radiomimetic bone marrow suppression and splenic lymphoid depletion

Question 13

Mechanism of action of botulinum toxin?

Gold standard of diagnosis?

Answer 13

Inhibits neurotransmission by blocking acetylcholine secretion from peripheral cholinergic nerve terminals in motor and autonomic nervous systems.

Results in progressive paresis and paralysis

 Diagnosis
• Based on history, clinical signs, absence of other causes of paresis/paralysis
• Confirmation of botulinum toxin in blood or tissue
o Mouse bioassay - gold standard
o Antigen-capture ELISA testing of blood and serum for type C toxin used successfully
 Type C
• Large die-offs of free-ranging American white pelicans (and smaller numbers of brown pelicans) in S CA
• Pelicans, cormorants, grebes, and occasionally northern fulmar and Laysan albatross have contracted type C botulism
• Carcass-maggot cycle

Question 14

Algal biotoxins (general) produced by marine dinoflagellates and diatoms?

Freshwater cyanobacteria?

Answer 14

Dinoflagellates - brevetoxins, saxitoxins

Diatoms - domoic acid

Cyanobacteria - microcystins (also saxitoxins, anatoxins, dermatotoxic lyngbyatoxins).

Question 15

Describe special considerations for pouch repair in pelicans?

Answer 15

Pouch repair (F8)
	Special considerations include establishing that subramal and ventral gular blood supply is intact, as no evidence of anastomoses between these vessels exist and vascular damage can result in poor wound healing.
	Avoid full thickness suture patterns when repairing lacerations, avoid compressing the vascular layer.
	Repair pouch by separating the epithelial layers and suturing them separately using simple interrupted pattern.

MMWS Pelican Pouch Lacerations:

 Staples can be used temporarily so the bird can eat.
 Surgical repair ideally within 10 days.
 Keep anesthesia time < 3 hours, can do multiple procedures if necessary.
 Pouch tissue consists of inner and outer stratified squamous epithelium with central skeletal muscle.
• Split the inner and outer layers and close separately so no epithelium is sutured inside the closure.
• Tacking elastic tissue in place at several locations during the procedure can help prevent puckering.
• Horizontal mattress.
• Frequent small meals post-op. Limit access to water. Healing 10-14 days.
• Pouch skin can be sutured to bill keratin if tear is along the bill.

Question 16

Options for venipuncture in pelicans?

Answer 16

o Venipuncture via jugular or wing veins may be challenging in pelicans because the SC air pockets make visualization and palpation difficult.
o Medial metatarsal vein primary venous access.
 Pelicans also have accessible veins at medial side of digit 3, dorsal side of digit 2 at the foot joint crease, and the ventral mandible.
 Can use the ventral mandibular vein mid-mandible for IV cath.

Question 17

Normal ocular anatomy of pelicans?

What was the most abundant organism found on conjunctival PCR?

What is asteroid hyalosis?

Answer 17

OCULAR FINDINGS AND SELECT OPHTHALMIC DIAGNOSTIC TESTS IN CAPTIVE AMERICAN WHITE PELICANS (PELECANUS ERYTHRORHYNCHOS)
Matthew E. Kinney, Aaron C. Ericsson, Craig L. Franklin, Rebecca E.H. Whiting, and Jacqueline W. Pearce
Journal of zoo and wildlife medicine. 2017 Sep;48(3):675.

Normal anatomical findings in pelicans:

Blue to brown iris (blue to tan in breeding season)

Ellipsoid pupil (similar to black skimmers)

No filoplumes

Conjunctival hyperemia

Abnormal findings:

Asteroid hyalosis: degenerative condition → small, white, refractile opacities in the vitreous

Mycoplasma sp. Was most abundant organism found on conjunctival PCR

Conclusions: Pelicans have an ellipsoid pupil consistent with other nocturnal/crepuscular animals.

Question 18

What was observed in rehabbed juvenile heron and egret chicks fed capelin?

Most common bone?

Most common location?

Additional lesions?

Answer 18

CLINICAL AND PATHOLOGIC FINDINGS OF AN OUTBREAK OF VITAMIN D3–RESPONSIVE METABOLIC BONE DISEASE IN HERON AND EGRET (FAMILY ARDEIDAE) CHICKS FED CAPELIN (MALLOTUS VILLOSUS)
Horgan M, Duerr R, Murphy B.
Journal of Zoo and Wildlife Medicine. 2021 Jan;51(4):958-69.

In rehabbed juvenile heron and egret chicks with metabolic bone disease:

Fed capelin (low in vitamin D)

Most common bone affected = tarsometatarsus (folding fractures and angular deformities)

Similar to red-legged seriema (Kozel 2016)

Most common location affected = proximal third of long bones

Enlarged, hyperplastic parathyroid glands (red arrows in photo)

Incidence of MBD lowered after vitamin D supplementation

Conclusions: Metabolic bone disease (most commonly affecting the proximal tarsometatarsus) can occur in growing piscivorous fish fed only capelin, so you should supplement vitamin D.

Question 19

What was observed in brown pelicans infected with a mixed clostridial infection (clostridium sordellii and clostridium perfringens)?

Answer 19

Unusual Outbreak of Fatal Clostridiosis in a Group of Captive Brown Pelicans (Pelecanus occidentalis).
Lueders I, Ludwig C, Kasberg J, Baums CG, Klimke K, Dorner MB, Ströse D, Schmidt V.
J Avian Med Surg. 2017 Dec;31(4):359-363.

Cases:
4.2 brown pelicans developed neurologic signs (weakness, pharyngeal paralysis, ataxia)

One died within 3 days, and the remaining birds died over 38 days

Treatment was attempted with erythromycin

Multiple Clostridium spp. were cultured from cloacal swabs but no botulinum toxin was detected via PCR

Detected hemolysin sordellilysin (sdl), which lyses cells and can disrupt hemostasis

Detected alpha-toxins from C. perfringens

Necropsy showed myositis and ulcerative diphtheroid inflammation of the colon and rectum in most birds

Isolated multiple Clostridia from environment, especially from the exhibit pool

Key Points:
Clostridia are anaerobic, Gram-positive, spore-forming bacteria

Spores can persist in the environment for years

Clostridial toxins (none of these toxins were found in these cases):

Botulinum neurotoxins (BoNT) is produced by C. botulinum and produces flaccid paralysis

Lethal toxin (TcsL) is the sole product of C. sordellii

C. sordellii has been shown to cause necrotic enteritis in birds, but it is rare in pelicans

Common lesions are hematomas and myonecrosis in breast and leg muscles in humans

Clindamycin is an antibiotic that can suppress toxin synthesis

Bactericidal antibiotics are contraindicated because they cause massive toxin release

Tilapia and other fish species can be a source of C. botulinum and type C botulism in wild brown and white pelicans

Conclusions: A mixed clostridial infection caused an extended course of clinical disease in captive brown pelicans.

Question 20

What occurred in white ibis experimentally infected with AIV?

Answer 20

EXPERIMENTAL INFECTIONS AND SEROLOGY INDICATE THAT AMERICAN WHITE IBIS (EUDOCIUMUS ALBUS) ARE COMPETENT RESERVOIRS FOR TYPE A INFLUENZA VIRUS
Bahnson CS, Hernandez SM, Poulson RL, Cooper RE, Curry SE, Ellison TJ, Adams HC, Welch CN, Stallknecht DE.
Journal of Wildlife Diseases. 2020 Jan 2.

Key Points:
Experimentally-infected shed two strains of AIV for several days with no clinical signs

Peak shedding on day 6 from oropharyngeal contents

Cloacal shedding was in lower quantities

White ibis co-housed with infected ibises also shed virus (likely acquired from water)

Wild white ibis have antibodies to lots of AIV variants, but not able to isolate virus

Conclusions: White ibises could be a part of maintaining avian influenza by being asymptomatic shedders.

Question 21

What unique lesions were observed in pelicans with microcystin toxicosis?

Answer 21

MYONECROSIS AND DEATH DUE TO PRESUMED MICROCYSTIN TOXICOSIS IN AMERICAN WHITE PELICANS (PELECANUS ERYTHRORHYNCOS)
McCain S, Sim RR, Howerth EW, Aschenbroich S, Kirejczyk SG, McHale B, Jerry C, Kottwitz JJ, Wilson AE, McManamon R. Myonecrosis and death due to presumed microcystin toxicosis in american white pelicans (pelecanus erythrorhyncos). Journal of Zoo and Wildlife Medicine. 2020 Jun;51(2):407-15.

Cyanobacterial toxin = Microcystin

Typically causes depletion of vita E and acute hepatic failure

In pelicans with microcystin toxicosis:

Diet: capelin (low vitamin E)
Signs: inability to stand, anorexia, wt loss
Clin path: Increased WBC and heterophils
Histo: severe chronic, diffuse rhabdomyofiber degeneration and necrosis
No evidence of acute hepatic failure or hemorrhage

Conclusions: Microcystin toxicity can cause inability to stand and muscle necrosis, but not hepatic failure, in American white pelicans.

Question 22

What is the primary storage site for lead in the body?

What changes were observed in waldrapp ibis RBCs following lead toxicity?

Answer 22

Diagnosis and Treatment of Heavy Metal Toxicosis in Six Waldrapp Ibis (Geronticus eremita).
Guthrie AL, Jayson SL, Strike TB, Sparrow SJ, Flach EJ, Szladovits B.
Journal of Avian Medicine and Surgery. 2020 Dec;34(4):371-80.

Cases: Adult Waldrapp ibis with lead toxicity (emaciation, wing droop, lethargy, reluctance to fly)after paint chip ingestion

1 died, others were treated with chelation with calcium EDTA IM

Most were anemic with RBC changes (hypochromic polychromatophils, dacrocytes, D cells, basophilic stippling)
Increased CK, AST, +/- GDH

Key Points:
Lead toxicity primarily affects the hematopoietic and nervous systems

Signs of lead toxicity in birds = lethargy, weakness, mental dullness, ataxia, paresis, paralysis, seizures, green urates, diarrhea, crop stasis and impaction, regurgitation

Droopy wings is from demyelination of nerves of the brachial plexus

Ingested lead is more toxic than embedded lead because gastric acid dissolves lead

Lead is primarily stored in bone (half-life of 20-30y)
In blood, leads to erythrocyte fragility

Often see fine basophilic stippling in RBCs

Zinc toxicity affects exocrine pancreas and causes lethargy, PU/PD, diarrhea, regurgitation

Conclusions: Waldrapp ibises with lead toxicity were successfully treated with Ca EDTA injections.

Question 23

Describe the effects of migratory flight on hematologic parameters of northern bald ibises?

Of the following, which increased and which decreased? HCT, TWBCs, lymphs, eos, het:lymph ratio, hets, basos.

Answer 23

The effects of migratory flight on hematologic parameters in northern bald ibises (Geronticus eremita).
Stanclova G, Schwendenwein I, Merkel O, Kenner L, Dittami J, Fritz J, Scope A.
Journal of Zoo and Wildlife Medicine. 2017 Dec;48(4):1154-64.

Background:
Critically endangered northern bald ibis were taught via Human-Led Migration to travel from Morocco to Europe
Sample pre-flight, immediately post-flight, and 1 day post-flight

Key Points:

Compared to pre-flight, the immediate post-flight data found:

Decreased HCT, TWBCs, lymphocytes, eosinophils

Increased heterophil:lymphocytes, heterophils, basophils

One-day post-flight was very similar to immediately post-flight

Potential causes for decreased HCT: water conservation, decreased erythropoiesis, less blood viscosity

Similar leukogram changes compared to:

Pigeons: decreased eosinophils, monocytes; increased heterophils

Conclusions: After migration in northern bald ibises, hematocrit, white blood cells (from a decrease in lymphocytes and eosinophils) decreased, while heterophils and basopils increased.

Question 24

What blood parameters increased with transport od dalmation pelicans?

Answer 24

The Effects of Capture, Restraint, and Transport on Hematologic, Plasma Biochemical, and Blood Gas Values in Dalmatian Pelicans (Pelecanus crispus).
Kinney ME.
J Avian Med Surg. 2018 Jun;32(2):95-101.

Background:
Dalmation pelicans were bled for CBC, plasma biochemsitry, and venous blood gas

Immediately after manual capture in exhibit
~74 minutes later following transport to hospital

Key Points:
Parameters that increased with transport:
Heterophil to lymphocyte ratio
CO2, bicarbonate, TCO2, base excess, PCO2

Parameters that decreased with transport:

Total WBCs
Absolute lymphocytes, eosinophils, monocytes
TP, lactate, phosphorus
Oxygen saturation, PO2, TWBC

Parameters that did not change:
PCV, absolute heterophils, absolute basophils
Glucose, sodium, chloride, potassium, total calcium
AST, ALP, LDF, CK, cholesterol
pH

Conclusions: Capture and transport of Dalmatian pelicans can cause a relative leukopenia, lymphopenia, monocytopenia, eosinopenia, elevated H:L ratio, and unchanged venous blood gas, despite a mild respiratory acidosis and compensatory metabolic alkalosis

Question 25

What is unique about meloxicam pharmacokinetics in brown pelicans? What psittacine spp is similar?

Answer 25

Pharmacokinetics of a Single Dose of Oral Meloxicam in Rehabilitated Wild Brown Pelicans (Pelecanus occidentalis)
Molly D. Horgan, Heather K. Knych, Sharon E. Siksay, Rebecca S. Duerr
J. of Avian Medicine and Surgery, 34(4):329-337 (2020).

Anecdotal reports of meloxicam toxicity in pelicans = visceral gout, GI ulceration, coagulopathy

Pelicans adminstered meloxicam 0.2mg/kg PO once had:

Longest half life of any avian species (36 h!)

Bimodal peak = enterohepatic recirculation

Also seen in african grey parrots and loggerhead sea turtles

African grey parrots also have a long PO meloxicam half-life (33 h)

Conclusions: Brown pelicans a very long half life for meloxicam, even at low doses (0.2mg/kg).

Question 26

What type of antibiotic is ceftiofur crystalline-free acid?

Describe its pharmacokinetics in Cattle Egrets.

Answer 26

Pharmacokinetics of a Single Intramuscular Injection of Long-Acting Ceftiofur Crystalline-Free Acid in Cattle Egrets (Bubulcus ibis).
Waldoch JA, Cox SK, Armstrong DL.
J Avian Med Surg. 2017 Dec;31(4):314-318.

Background:
Ceftiofur crystalline-free acid (CCFA) is a time-dependent, bacteriocidal, third generation cephalosporin
Time-dependent antibiotic efficacy is determined by the amount of time above MIC

Key Points:

Subcutaneous CCFA administration has disadvantages:

In American black ducks, SC CCFA lasted shorter than IM administration

In American flamingos, less consistent PK values with SC CCFA compared to IM

CCFA time of efficacy (time above MIC) in other species:
Cattle: 6 days
Horses: 10 days (with 2 doses)
Swine: 8 days
CA sea lions: 5 days
Asian elephants: 7 to 10 days
Bearded dragons: 12 days
Ball pythons: 5 days
Rhesus macaque: 7 days

Conclusions: Ceftiofur crystalline-free acid administered at 20 mg/kg IM in cattle egrets provides antimicrobial treatment above MIC of 1 mcg/L for 72 hours.

Question 27

What topical products are effective in removing polyisobutylene rubber polymers from herons?

Answer 27

Use of Margarine for the Successful Removal of Polyisobutylene in an Anhinga (Anhinga anhinga) and Great Blue Heron (Ardea herodias)
Ratliff CM, Hernandez A, Watson CB, Bergbreiter DE, Schmalz S, Rech R, Heatley JJ.
Journal of Avian Medicine and Surgery. 2020 Mar;34(1):70-7.

Polyisobutylene (PIB)= sticky, hydrophobic rubber polymer

Is not removed from birds with with canola oil or Dawn alone

Successful PIB removal = Pre-wash with Dawn, cover in margarine, second wash with Dawn
All types of margarine work because of high lecithin content that forms a stable emulsion
Mineral oil should also work for PIB

Conclusions: Margarine and mineral oil are effective in removing polyisobutylene from bird feathers.

Question 28

Pharmacokinetics of danofloxacin in brown pelicans?

What make danofloxacin an appealing antibiotic choic?

Answer 28

Schmitt, T. L., Nollens, H. H., Simeone, C. A., & Papich, M. G. (2019). Population Pharmacokinetics of Danofloxacin After Single Intramuscular Dose Administration in California Brown Pelicans (Pelecanus occidentalis californicus). Journal of Avian Medicine and Surgery, 33(4), 361-368.

• Danofloxacin is an appealing antibiotic drug for exotic and wildlife species because it has a broad spectrum, a long half-life, and low protein binding
• No adverse effects noted
• The absorption was rapid (T1⁄2 = 0.4 hours) and was shorter than the elimination (T1⁄2 = 2.76 hours). Rate of absorption was highly variable among the birds
• The pharmacokinetic parameters in this study indicated that danofloxacin produced a peak concentration of approximately 2.5 lg/mL. The targeted pathogens in cattle (Mannheimia haemolytica and Pasteurella multocida) have low 90% MIC (MIC90) values of 0.06 lg/mL.
• Breakpoint for susceptibility testing indicates that ‘‘susceptible’’ bacteria from cattle have MIC values of <0.25 lg/m L
• The concentrations for danofloxacin administered to the brown pelicans intramuscularly reached therapeutic targets for low MIC values cited for bovine pathogens.
• The typical Cmax value from this study was 2.5 lg/mL, which would be sufficient for bacteria with MIC values <0.25 lg/mL, at a target Cmax of 10x the MIC.

Question 29

Prognosis for pelicans treated for oiling?

Answer 29

POSTRELEASE SURVIVAL OF CALIFORNIA BROWN PELICANS (PELECANUS OCCIDENTALIS CALIFORNICUS) FOLLOWING OILING AND REHABILITATION AFTER THE REFUGIO OIL SPILL
JWD 2021 57(3) 590-600

• Oiled and released birds survived an average of 251 + 93.7 days, compared to average of 240.3 + 85.6 days for control birds
• no significant difference in survival between oiled and control birds at either 6 mo or 1 yr
o survival rates in both groups ~75% at 6 mo
• limitations – difficult to determine mortality definitively using transmitters
• oiled and rehabbed birds had higher TP
• control birds had higher eosinophil counts

Conclusion: California Brown Pelicans that were oiled during Refugio oil spill and captured, cleaned, rehabilitated, and instrumented with PTT satellite tags did not have higher mortality in year following release compared to unoiled pelicans that were captured and similarly instrumented

• Most oiled and rehabilitated pelicans can survive for 6 mo - 1 yr+ following release

Question 30

Describe the unique anatomy of pelicans:
- Do they have a salt gland?
- Do they have a crop?
- What are the two main functions of the gular pouch?
- Do they have a tongue?
- Where is the trachea located?
- Where does breathing occur in this species?
- What is unique about their shoulder anatomy?

Answer 30

Unique Anatomy of Pelicans
* Diurnal, globous-shaped eyes with flat corneal surface and nictitating membrane that moves up to protect cornea
* Lack of periocular skin feathers and supraciliary ridge likely predisposes them to ocular sun damage, provide shade and glare reduction
* Salt gland of brown pelicans helps maintain osmolar balance
* Absent crop, instead large gular pouch attached to mandible
* Pouch used in hunting and for thermoregulation via eversion through the oral cavity
* Traumatic injury to gular pouch can compromise survival, minimal anastomosis of pouch vasculature results in poor tissue healing of thin, distensible epithelium
* Most blood to head and pouch supplied by left carotid artery
* Absent tongue
* Highly mobile glottis at base of puch- trachea courses down right side of next, ventral to the esophagus
* Lack of a strong esophageal sphincter facilitates regurgitation and endoscopic or manual removal of foreign objects from esophagus, proventriculus or ventriculus
* vestigial/absent nasal passages within bill restrict air movement into the lower airways through the mouth- bill is maintain open during physical restraint
* Air cavities occur within pneumatic long bones and a system of SQ air sacs along the ventral and cervical regions
* As in other avian species- pneumatic bones are humerus and femur should NOT be used for I/O catheters
* SQ airsacs may increase in volume during stress and handling, not mistake for SQ emphysema
* Fusion of sternum and clavicles result in rigid pectoral girdle and allows to soar

Question 31

Describe the feeding and nutrition of pelicans:
- What is their typical diet?
- What are some nutritional deficiencies that are common in this species and how do they present?
- Supplementation with what vitamins are recommended?

Describe the ideal housing of pelicans?
- What type of pools do they need?
- What type of water do they need?

Answer 31

Feeding and Nutrition of Pelicans
* Predominately piscivorous
* Opportunistic hunters and feed on wide variety of fish species, crustaceans and amphibians
* Predation other avian species, chicks/nestlings
* Rec feed minimum of three species fish in managed care
* Vitamin E deficiency results from degradation in stored fish.
– Develop skeletal and cardiac muscular degeneration, liver necrosis, anemia, impaired repro, death may occur acutely or associated with capture/restraint
– Pale-streaked skeletal muscle and myocardium, fatty liver at necropsy
* Supplementation vitamins A,D,B1, E recommended
* Hypervitaminosis E- associated with coagulopathy in pink-backed pelicans based on interferences with vitamin K function

Housing of Pelicans
* Large, open pools at least 1 meter deep and large flat areas for roosting,loafing
* Grasses/shrubbery provide privacy, create barrier
* Protect from harsh temps
* Fungal infections spread easily within flocks
* Water quality management impt for brown pelicans, salt gland may atrophy if inadequate salinity

Question 32

Describe the noninfectious diseases of pelicans.

What are common causes of traumatic injury?

What are the significant toxins pelicans may be exposed to?
- What are the effects of oil spills on these birds?
- HOw do they present with heavy metal toxicity?
- How do they present with brevetoxin or cyanotoxins? How are these treated?

Is neoplasia common in these birds?

Answer 32

Traumatic Injury of Pelicans
* Common reason for presentation
* Collision, wind turbines, fishing line entanglement, fish hooks, lacerations, constrictive injuries, fractures

Toxin Exposure in Pelicans
* Heavy metals, pesticides, oil, algal blooms, environmental contaminants
* Oil contamination as they will dive through floating oil in pursuit of prey
* Oil interferes with feather’s ability to provide water repellency, insulation and buoyancy
* Internally, oil ingestion or inhalation results in hemolytic anemia, kidney/liver failure, pneumonia, immunosuppression
* Heavy metal- regurgitation, weight loss, ataxia, blindness, seizures, death - lead or zinc- fluid therapy, metal chelation
* Brevetoxins from dinoflagellates, cyanotoxins from cyanobacteria and domoic acid from algae- pelicans become affected after ingestion of contaminated fish or shellfish- toxin bioaccumulate in body fat
– CLinical signs from brevetoxin/DA include neurologic signs of loss of palpebral reflex, anal tone, inability to stand or lift head, disorientation, ataxia and seizures.
– Brevetoxine detected in whole blood or feces via ELISA
– Cyanotoxins have cytotoxic effects on liver, nervous system and skin
– Dalmatian pelican mortality- cyanotoxicosis ingestion of contaminated fish
– Treatment- supportive care, gavage feeding, fluid therapy, Benzodiazepines may control seizure activity

Neoplasia of Pelicans
- uncommon

Question 33

Describe the infectious diseases of pelicans.

What are important bacterial diseases of these birds?

What are the viral diseases that lead to significant mortality?

What is teh most common nematode of these birds?

What is the sea bird tick?

What is the pouch louse?

What are some complications with the use of antiparasitics in these birds?

Answer 33

INFECTIOUS DISEASES OF PELICANS

Bacterial and Fungal Diseases
* Clostridium botulinum - common cause of mortality in American white pelican since 1980
– One of largest die-offs occurred in 1996 in Salton Sea- contaminated tilapia
– Neuro signs predominant- weakness, ataxia, flaccid muscle, paralysis, dysphagia
* Clostridium perfringens, E. coli, Proteus spp., Campylobacter- other bacterial infections and causes of bacterial enteritis
* Pododermatitis secondary to reduced exercise, abnormal weight bearing on injured extremities, poor nutrition, suboptimal housing
– Medical management challenging
– Antibiotic perfusion with ampicillin/sublactam used to treat digital lesions and pododermatitis
– Uncommon, asper caused mortality of Dalmatian, brown and white pelicans

Viral Diseases
* Newcastle Disease
* West Nile Virus
* Avian Influenza Virus
* Avian Poxvirus
* Hundreds of American white pelican deaths attributed to virulent Newcastle virus- neuro signs of wing droop, leg paralysis/paresis, neck droop, inability to move
* Pelican chicks particularly susceptible to WNV- likely cause of chick mortality in breeding colonies of American White pelicans- encephalitis, head tilt, disorientation, tremors, paralysis.
* Diagnosis confirmed via serology or viral isolation from CNS lesions
* Pelicans likely reservoirs and vectors for AI- may lack clinical signs
* Vaccination with commercially available poultry vaccine did not work
* Pox virus- skin lesions- mucosal pathology of digestive and upper respiratory tracts

Parasitic Infection
* Contracaecum spp. - nematode most commonly reported. Can cause hemorrhage and ulceration of esophagus, proventriculus, and ventriculus
* Others- trematodes, cestoes, nematodes
* Sea bird tick Carios (Ornithodorus) capensis infests nests of brown pelicans, associated with nest abandonment
* Piagetiella peralis heavy infection with pouch louse- gular pouch hematomas and erosive stomatitis
* Antiparasitics use cautiously- fatal enteritis and bone marrow damage after fenbendazole in pink-backed pelicans and American white pelican have occurred
* Brown pelicans successfully treated with lower doses of fenbendazole
* Ivermectin, pyrantel, prazi considered

Question 34

A recent study evaluated the causes of morbidity and mortality in three ibis species.

What is the scientific name of the northern bald ibis, african sacred ibis and the scarlet ibis?

What was the most common morbidity identified?
- Did this vary by species?

What was the most common cause of mortality?
- What viral disease is important to consider in these birds?
- What species was more commonly affected by aspergillosis?

What bacteria was commonly cultured on post-mortem examinations?

Answer 34

Journal of Zoo and Wildlife Medicine, 54(1) : 94-101
A RETROSPECTIVE ANALYSIS OF THE MORBIDITY AND MORTALITY OF CAPTIVE NORTHERN BALD IBIS (GERONTICUS EREMITA), AFRICAN SACRED IBIS (THRESKIORNIS AETHIOPICUS), AND SCARLET IBIS (EUDOCIMUS RUBER) HOUSED AT THE LONDON ZOO FROM 2000 TO 2020

Key Points:
- Most common morbidity was pododermatitis followed by trauma and undetermined
– Pododermatitis signif more prevalent in SCI than NBI or ASI; whereas trauma (to wing most common followed by beak) was more common in ASI
– Toxicosis was the main cause of morbidity in NBI 🡪 lead, history of 6 animals placed into a temporary enclosure
– Nestlings had greater odds of nutritional morbidity than adults; Females had greater odds of undetermined morbidity than males (manifested primarily as thin BCS in female ASI and SCI
- Most common cause of mortality was trauma followed by infectious (primarily vegetative valvular endocardiosis and aspergillosis)
– Trauma predominantly caused by impact collisions w/I habitat (most commonly wing, head & legs). Ibis at risk of beak trauma when managed in hard-walled enclosures.
– No VVE cases dx antemortem – clinical signs of VVE included weakness, poor plumage, poor BCS, and cardiac murmur (absence of a murmur does not preclude dz)
– 5/13 ibises that had VVE had concurrent pododermatiis
– Majority of aspergillosis cases were in ASI
– Trauma was most common COD in nestlings (fell out of nest w/o an identifiable cause)
- Camplyobacter isolated in 25% of post mortem bacterial cultures – infections were subclinical but should be considered d/t zoonotic concern.