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Topics in Medicine and SurgeryTopics in Medicine and Surgery
Raptor Gastroenterology
Scott Ford, DVM, Dip. ABVP (Avian)raptor’s to
140
Abstract
Birds of prey have developed talons, a hooked beak, and a tongue and oral cavityreplete with pronounced hooks and papillae for prehending large boluses of food.The size of the proventriculus in relation to the ventriculus and weak musculatureof the ventriculus, combined with an extremely acidic luminal pH, are consistentwith a gastric digestive physiology maximized for protein digestion. The pyloricsphincter retains indigestible matter in the stomach, which is later compressed intoa pellet and egested. The ventriculus, pylorus, pancreas, and an elongated duode-num coordinate to maximize neutralization of acidic peptic juices and increase theefficiency of digestion and absorption. Raptors are susceptible to a variety ofinfectious and noninfectious diseases that affect the digestive tract. Diagnostictesting and treatment recommendations for raptor intestinal disease conditions arediscussed in this article. Copyright 2010 Elsevier Inc. All rights reserved.
Key words: bacteria; gastrointestinal; fungal; raptor; parasites; viral
Raptors serve an important role in the ecosys-tems in which they are found. These animalsare built to function in the top of the food
web, and as such have developed a gastrointestinaltract suitable for a carnivorous diet (Fig 1).
Anatomy and Physiology
Beak and oral cavity. The raptor beak is hookedand the tomia are very sharp over the rostral one halfto two thirds of its length. The pliability of the beakcommissures allows for insertion of fingers into thebeak for an oral examination or when administeringmedications. In most birds of prey, the opening andclosing strength of the beak is not significant be-cause the leg and neck muscles are primarily usedfor capturing and ripping the flesh of their prey. Themaxilla is hooked into the flesh of the prey item andthen pulled vertically to shred off boluses for swal-lowing. The palatine ridges, choanal borders, caudalborders of the tongue, and the glottal mound havecaudal-projecting epithelial projections that directfood into the esophagus (Fig 2). The mobility of a
ngue is greater than that found in parrot
Journal of Ex
species, in that the entire glottis can be projectedbeyond the oral commissure. Extreme tongue mo-bility in raptor species may help prevent suffocationwhen swallowing large food boluses. The epithelialprojections (hooks) located on the caudal border ofthe tongue can be utilized together with the lowerbeak to secure an endotracheal tube and preventretraction of the tongue and the incidence of spon-taneous extubation. The rostral portion of thetongue is generally thickened and keratinaceous.Because of the anatomic and physiologic composi-tion of the raptor tongue, application of a pulseoximetry transducer at this location is not recom-mended; however, the choanal entrance is still aviable choice for a reflectance probe.
From the Avian Specialty Veterinary Services of Alaska, Bre-merton, WA USA.
Address correspondence to: Scott Ford, DVM, Dip. ABVP (Avian),Avian Specialty Veterinary Services of Alaska, 13861 Hillcrest Dr.NW, Poulsbo, WA 98370. E-mail: [email protected].
© 2010 Elsevier Inc. All rights reserved.1557-5063/10/1902-$30.00
doi:10.1053/j.jepm.2010.05.004otic Pet Medicine, Vol 19, No 2 (April), 2010: pp 140–150
Ur, u
Raptor Gastroenterology 141
Ingluvies
All birds of prey possess an ingluvies (crop) exceptStrigiformes (e.g., owls).1,2 When distended, thecrop rests against the cranial edge of the clavicle.The raptor crop is fusiform-shaped and has a poorlydeveloped lower sphincter into the thoracic esoph-agus. Because a raptor may not be successful duringeach hunting attempt and the size of prey may bevariable, the crop allows the bird to consume largevolumes of food as quickly as possible. The speed ofconsumption is particularly important with smallerbirds of prey, which can be killed by other raptorsspecies, and piracy of hard-won prey is also avoided.The crop also allows slower, more complete diges-tion at a resting location of the bird’s choosing.3
Proventriculus and Ventriculus
The raptor proventriculus is consistently more devel-oped than the ventriculus when compared withPsittaciformes or other granivorous birds (Fig 3).
Figure 1. Basic gastrointestinal anatomy of first-year fledged baldproventriculus; lll, left liver lobe; rll, right liver lobe; vc, ventriculuscoiled loop adjacent to the pancreas); Re, rectum; Co, coprodeum;
The alternating thick and thin muscle areas noted in
the ventriculus of other birds are absent in raptorsbecause most animal protein requires relatively littlemechanical digestion but rather requires extensiveautoenzymatic digestion.2 Two types of glands existin the wall of the proventriculus: (1) tubular glandsfor the secretion of mucus and (2) gastric glands thatsecrete hydrochloric acid and pepsinogen.3 Pepsino-gen is activated to pepsin by hydrochloric acid orpreviously activated pepsin and has the ability tobreak down a wide range of tertiary structures ofprotein, exposing peptide bonds for additional di-gestion. The stomach pH of Falconiformes averagesapproximately 1.6 to 1.7 and in Strigiformes 2.4.2,3
The pellets of Strigiformes often contain incom-pletely digested remains (e.g., bones) and are mostlikely the result of a higher stomach pH.2 In contrastto most florivorous birds, the ventriculus is lackingmuscular development, has a relatively large lumen,and is more pliable. In addition, the proventricular-ventricular isthmus is not present so that the 2 or-gans form 1 large pear-shaped cavity in many birds ofprey. This lack of an isthmus and shape of the raptor
(Haliaeetus leucocephalus). Ce, Cervical esophagus; cr, crop; pro,rd); gb, gallbladder; p, pancreas; du, duodenum (this includes the
rodeum; Pr, proctodeum; Bu, cloacal bursa.
eagle(gizza
stomach allow space for larger pieces of prey and
142 Ford
decrease the time required for preparing food forswallowing.
Casting. Formation of gastric castings is not uniqueto birds of prey. It is also a daily activity in corvidsand some other Passeriformes and gulls, dependingon dietary intake. However, casting activity has beenprimarily investigated in birds of prey. Most species
Figure 2. Beak and oral cavity of a bald eagle. Note the soft commis-sures, papillae on the palatine ridges, choanal folds, laryngeal mound,and the pronounced papillae projecting caudally from the tongue. Thebird pictured at top has fishing line wrapped around the tongue base.
Figure 3. Stomach detail from a second-year bald eagle. Thethoracic esophagus is at right, proventricular mucosa at center, and
ventricular mucosa at left.of birds do not possess enzymes that can break downthe protein keratin, a common constituent of nails,hair, feathers, and scales.3 After digestion of a meal,the contractions of the ventriculus increase in am-plitude for about 12 minutes before pellet egestion,compacting the pellet and directing it to the cranialaspect of the proventriculus where it is then egestedby esophageal retroperistalsis in about 8 to 10 sec-onds.2 The meal-to-pellet interval is variable. Eges-tion of the pellet usually occurs in the morningunless food is ingested late the previous day. Presen-tation of a new meal to a hungry great horned owlwill delay pellet egestion to allow the bird to con-sume another meal, thereby producing a larger pel-let later.4 Field observations have suggested that owlsmay sometimes need to clear a pellet before ingest-ing the next meal.5 The pyloric region of the ven-triculus is located on the right side of this organ at a90° angle to the longitudinal axis of the proventric-ulus. A combination of interdigitating folds and asphincter control the exit of material from the stom-ach, favoring the passage of small, liquid, or softitems.3
Intestine, Liver, Pancreas
The raptor duodenum is relatively long and includessecondary loops in some species (e.g., sea eagles; seeFigs 4-6).1 Pancreatic and bile ducts empty into theascending loop of the duodenum (Fig 6).6 Birds ofprey possess a relatively large gallbladder. Bile saltsare important for lipid digestion in birds and arerecycled in the liver from the enterohepatic circula-tion.2,3 A unique trait of the avian digestive tract isthe periodic active reflux of digesta from the ileumand duodenum back into the stomach.2 Duke2 sug-
Figure 4. Digestive tract of a second-year bald eagle in situ.
gests this retroperistoltic action is an adaptation to
Raptor Gastroenterology 143
prolong digestion and increase digestive efficiencywithout increasing digestive tract size or feeding fre-quency. In raptors, the reflux of digesta from theintestine back into the stomach occurs approxi-mately every 30 to 60 minutes. Bicarbonate from thepancreas neutralizes the pH of digesta, which facili-tates the function of bile salts and enzymes in theintestine.3 The pancreas also produces trypsin, chy-motrypsin, and carboxypeptidase for reduction ofprotein to free amino acids and oligopeptides of 2 to6 amino acids in length. The free amino acids andoligopeptides are further hydrolyzed by enzymes em-anating from the brush border of intestinal villi.3
Klasing3 points out that Falconiformes that pursueaerial prey have intestines that are 20% to 40%shorter than those that hunt by soaring or pouncing.There may be a loss in digestive efficiency in birdswith a shorter intestinal tract, which may be compen-sated by a lighter body weight, increased aerial agil-ity, and greater hunting success.3
Ceca, Rectum, and Cloaca
The ceca are a pair of blind sacs emerging from theileocolic junction.1,3 In diurnal birds of prey, thececa are vestigial. In Strigiformes, the ceca are welldeveloped and appear to function primarily in waterresorption and nitrogen homeostasis. The ceca areperiodically emptied and produce a sticky, homoge-nous, particularly malodorous dropping at the rateof 2 to 3 per day in the domestic fowl. The large
Figure 5. Duodenum and pancreas of a mature bald eagle in situ.The descending loop is to the right, the secondary loops in thecenter, and the ascending loop proceeds off-image to the top center.A portion of the pancreas is visible just to the right of the ascendingloop.
intestine of raptors is short and linear, except in the
kestrel, which is noted for possessing an unusuallylong large intestine (believed to augment water con-servation).3 The mucosa of the large intestine hasvilli, though not to the degree of the small intestine,and is an important site for water resorption fromboth feces and urinary products.1-3 Urine enters thelarge intestine by active retroperistalsis from the uro-deum of the cloaca. Because of the high nitrogencontent of a protein-rich diet, birds of prey producelarge amounts of nitrogenous waste.3 The extra liq-uid necessary to excrete and transport the largeamounts of nitrogenous waste is recovered efficientlyby the ceca (in Strigiformes), cloaca, and large in-testine. The process can be so efficient that manybirds of prey do not require water beyond that pro-vided in their prey, although water should still beprovided to these birds in captivity.
Additional Digestion Considerations
The digestive and metabolic strategies of birds ofprey are optimized for a diet high in protein and lowin carbohydrates. Relatively few studies have investi-gated protein accretion, gluconeogenesis, and fattyacid synthesis in faunivorous birds relative to omniv-orous (e.g., poultry) or florivorous (e.g., parrots)birds. Raptors generally have lower plasma insulinlevels relative to chickens, although it was deter-mined that insulin is more responsive to glucoselevel in kestrels than in chickens.7 However, it ap-pears that insulin is not the only significant factorinvolved in the regulation of glucose in kestrels.7
Barn owls were found to take longer to absorb orallydelivered glucose and to clear blood glucose thanchickens.7 Delayed insulin clearance is believed toresult from a decreased ability to downregulate glu-coneogenesis from lactate or threonine, possibly be-cause these substrates, particularly threonine, areconsistently abundant in the natural diet (whereasthey vary from insufficient to excessive in the diet ofomnivores).7 Delayed insulin clearance could be animportant consideration when selecting an appro-priate gavage diet for chronic inanition.
Parasitic Diseases
Protozoa
Trichomoniasis. Trichomonas gallinae is the caus-ative organism of trichomoniasis, also known as“frounce” by falconers (or “canker” among pigeonfanciers). Lesions associated with trichomoniasis in-
fections are caseous, diphtheritic, painful, vascular,
144 Ford
and occur in the respiratory and upper digestivesystems.8 Confirmation of a T. gallinae diagnosis ismade by microscopic visualization of flagellated pro-tozoans on a fresh saline solution mount of lesionmaterial.8 The organism can still be recovered fromwarmed saline solution preparations of samples col-lected from lesions even after several days of carcassrefrigeration. The organism is largely adapted toColumbiformes, so that even apparently healthy in-dividuals can be subclinical carriers. Some falconersavoid pigeon meals for their birds altogether, or atleast practice freezing and thawing of pigeon car-casses along with removal of the crop, cervical esoph-agus, and head because of the possibility of exposingtheir birds to this parasite.9 Because trichomonadscan be present in other tissues of a diseased bird,simply removing the upper gastrointestinal tractalone will not completely eliminate risk of bird ex-posure. Direct transmission of T. gallinae betweenraptors has been reported.9 Treatment with metro-nidazole at 30 to 50 mg/kg every 24 hours for 5 to 7days or carnidazole (Spartrix; Wildlife Pharmaceuti-cals, Inc., Fort Collins, CO USA) at 30 mg/kg every12 hours for 3 days is usually effective to treat birdsinfected with T. gallinae.8 Birds that have severe oral,esophageal, or ingluvial lesions may require paren-teral fluid support, gavage feeding, or placement ofa pharyngostomy tube for feeding. Pain and thepotential for secondary bacterial infection shouldalso be addressed by treating the patient with butor-phanol (1-2 mg/kg orally [PO]/intramuscularly[IM] every 8-12 hours as needed).10
Coccidiosis. Eimeria spp., Cryptosporidium spp., Fren-
Figure 6. Duodenum of a mature bald eagle in situ. Red arrowsdenote the pancreatic duct that empties into the aborad portion ofthe ascending duodenum.
kelia spp., Sarcocystis spp., Caryospora spp., and Toxo-
plasma gondii have all been represented in raptors.8
Most coccidian infections are nonpathogenic in rap-tors, but significant clinical disease may occur inyoung birds, in large or mixed collections, and inanimals with compromised immunity.11 Clinicalsigns of coccidiosis in birds of prey include lethargy,depression, anorexia, salivary gland inflammation,regurgitation, enteritis, cloacitis, conjunctivitis,sneezing, diarrhea, and death.8,11,12 The most com-mon pathogenic genus of coccidia diagnosed in rap-tor species appears to be Caryospora spp., particularlyin merlins.9,13 Oocysts are sporulated in Sarcocystisspp. and nonsporulated in Caryospora spp. whenidentified on microscopic fecal examination.9 Tis-sue cysts of Sarcocystis spp. are found in some birdsof prey and may not be associated with clinicaldisease.14 In the case of cryptospordia, a definitivediagnosis can be achieved through cytological exam-ination of mucosal swabs or feces, using direct mi-croscopy and staining techniques.11 Published treat-ments for avian coccidiosis include sulfadimethox-ine (Albon; Pfizer Animal Health, Exton, PA USA) at25 to 55 mg/kg PO every 24 hours for 3 to 7 days,pyrimethamin (Daraprim; Catalytica Pharmaceuti-cals, Inc., Greenville, NC USA) at 0.5 mg/kg PO every12 hours for 14 to 28 days, toltrazuril (Baycox; Bayer,Leverkusen, Germany) at 7 mg/kg PO every 24 hoursfor 2 to 3 days, paramomycin (for Cryptosporidium spp.)at 100 mg/kg PO every 12 hours for 7 days, or ampro-lium at 15 to 22 mg/kg PO every 24 hours for 4 to 6days (supplementation of thiamine may be recom-mended).11,13,15 Forbes has investigated the develop-
Figure 7. Cloacal urolith removed from a bald eagle.
Raptor Gastroenterology 145
ment of a vaccine to decrease the transmission of Caryo-spora spp., which can be particularly important in facil-ities housing mixed species.16
NematodesCapillariasis has been documented in free-livingNorth American raptors.17,18 Many infections arelikely subclinical, but overt disease signs includeemaciation, depression, diarrhea, dysphagia, oral le-sions, and death.8 The oral and esophageal lesionsmay resemble those associated with trichomoniasis.Gastrointestinal ascarids include Ascaridia spp., Por-rocaecum spp., and Contracaecum spp., and clinicalsigns, if present, may resemble capillariasis. Diagno-sis of nematodes in the gastrointestinal tract is ac-complished by microscopic analysis of feces, digesta,or mucosal impressions. Because prey may also con-tain parasite ova, care must be taken to differentiatethe source of exposure when a bird has been diag-nosed with capillariasis. To determine the exactsource of exposure, and because ova may be shedinconsistently, examination of serial diagnostic sam-ples is recommended.19 Ivermectin, fenbendazole,levamisole, mebendazole, and piperazine have beenprescribed for the treatment of nematodes. Caremust be taken when treating birds with fenbenda-zole because it has been reported that this antipar-asitic agent may cause death in some avian spe-cies.8,20
Other HelminthsTrematodes may infest the bile ducts and duodenumof raptors and, in most cases, are not consideredpathogenic, even in large numbers, although lethalcases are reported.19,21,22 Clinical signs of trematodeinfestation can include weight loss, diarrhea, anddeath. A sedimentation technique is recommendedfor concentrating trematode ova from feces for mi-croscopic identification.9 Treatment with rafoxanide(Ranide, MSG AGVET; Merck & Co., NJ USA) orpraziquantel (Droncit; Haver Lockhart, KS USA) hasbeen described for raptors diagnosed with trema-tode infestations, although one author notes thatpraziquantel may only decrease transmission and noteliminate the parasite in nonraptor species.19,23
Cestodes are uncommon and rarely cause dis-ease in raptors.19 Clinical signs, if present, mayinclude mild diarrhea and weakness. Diagnosis of acestode infestation is usually made by visualization ofproglottids in the feces or around the vent. Praziquan-tel is the treatment of choice for raptors diagnosedwith cestodes. Acanthocephalans are rarely reported inraptors and are generally considered nonpathogen-
ic.17,19,21,24 If present, acanthocephalans are usuallylocated in the aborad small intestine, but unfortu-nately there are no published treatments for raptorspecies.19
Bacterial/Fungal Diseases
Cooper lists Escherichia coli and Proteus spp. as normalbacterial flora within a raptor’s lower intestinaltract.9 In addition to these, Staphylococcus aureus, Ba-cillus spp., and Corynobacterium spp. are commonlycultured from the pharyngeal area of birds of prey.9
The bacterial organisms Lamberski describes as nor-mal intestinal flora of red-tailed and Cooper’s hawksin California include Staphylococcus/Micrococcus spp.,Corynebacterium spp., Pasteurella spp., Streptococcusspp., Salmonella spp., and Bacillus spp.25 Bacteria thatoriginate from or infect the gastrointestinal tract ofraptors that may be pathogenic include E. coli, Proteusspp., Pasteurella multocida, Salmonella spp., Klebsiella spp.,Pseudomonas aeruginosa, Shigella spp., and Clostridium botu-linum.8,26,27 In a survey of falcons in the United ArabEmirates, E. coli, Chlamydia psittaci, Pseudomonas spp.,and Clostridium perfingens are the most common bac-terial pathogens.28 Clinical signs of disease, ifpresent, of gastrointestinal infection with these or-ganisms listed above are often nonspecific (e.g., slowcrop emptying, weight loss, regurgitation, diarrhea,lethargy, death). Initial treatment should be basedon the patient’s history, clinical signs, and cytologi-cal results of gastrointestinal/fecal swabs. Adjust-ments to the treatment regimen may be modifieddepending on organism isolation, antimicrobial sen-sitivity testing, and response to therapy. Most gastro-intestinal infections of raptor species usually involveGram-negative and anaerobic organisms, therefore theauthor’s preferences for immediate antibiotic therapyinclude trimethoprim sulfadimethoxazole (Bactrim;Roche, Nutley, NJ USA) at 48 mg/kg PO every 12hours, ciprofloxacin (Bayer, Shawnee Mission, KSUSA) at 20 mg/kg PO every 12 hours, Clindamycin(Antirobe; Pharmacia and Upjohn, Kalamazoo, MI) at50 to 100 mg/kg PO every 12 hours, or amoxicillin/clavulanate (Clavamox; Pfizer, New York, NY USA).10
Pasteurella multocida is a Gram-negative aerobethat infects raptors either through consumption ofinfected waterfowl or from the bites of domesticfelids.15,29,30 Infection can originate from crop inju-ries or abscesses associated with prey ingestion. Clin-ical signs associated with a P. multocida infectioninclude weakness, animal bite lesions, weight loss,oculonasal discharge, infraorbital swelling, dyspho-nia, synovitis, neurological signs, peripheral edema,and whitish plaques of the oral cavity and esopha-
gus.30,31 Infected birds can die suddenly or over a
146 Ford
period of time, depending on the pathogenicity ofthe organism and the health and species of bird.30
Histologic lesions of an avian P. multocida infectionare consistent with septicemia and include dissem-inated intravascular coagulation, serositis, and mi-croabscessation. Diagnosis can be accomplished byculture of the organism from lesions.32 Treatmentshould include fluid support and antimicrobial ther-apy that may include cefotaxime (Claforan; Hoechst-Roussel/Intervet Inc., Sommerville, NJ USA) 100mg/kg IM every 12 hours or piperacillin/tazobac-tam (Zosyn; Wyeth, Madison, NJ USA) 200 mg/kgIM every 12 hours.10
A necrotizing gastroenteritis associated with Clos-tridium perfringens infections has been described inraptors, although raptors seem resistant to infec-tion.8,29 Diagnosis of C. perfringens is based on cytolog-ical examination of the fecal material, and, if con-firmed, a recommended treatment is trimethoprimsulfadimethoxine at 48 mg/kg every 12 hours for 7 to10 days.
Pseudomonas spp. infections will cause clinical dis-ease in raptor species and has been reported as acontributing infectious organism in falcon stomatitiscases from which Trichomonas spp. were isolated.33
Mycobacterium avium has been the most frequentlyreported mycobacterial species isolated in raptors,although other species and subspecies of mycobac-teria (e.g., M. avium paratuberculosis) are emerging asmolecular diagnostic techniques improve and theiruse increases.29,34-36 Mycobacteriosis most commonlyaffects the gastrointestinal tract and liver, causingformation of granulomatous tubercles and thicken-ing of the intestinal wall. However, other tissues andorgans can be infected including meninges, joints,subcutis, skin, spleen, lung, and bone.35,36 Becausemany tissues can be affected, clinical signs are gen-erally nonspecific but may include muscle wasting,swollen and painful joints, subcutaneous nodules,and depression. A complete blood count will usuallyreveal a significant leukocytosis (20,000/�L up to200,000/�L white blood count) with a concurrentheterophilia and monocytosis.35,37 A diagnosis of my-cobacteriosis can be supported by acid-fast stainingof fecal smears (least sensitive method) or polymer-ase chain reaction testing or culture of feces orlesions.37 A definitive diagnosis of mycobacteriosiscurrently requires culture, which involves special lab-oratory conditions and precautions. Treatment pro-tocols for mycobacteriosis-infected companion birdscan be found in the literature, but no controlledtreatment studies have been performed in these spe-cies. Treatment is not generally recommended for
wild birds because the duration of treatment may lastat least 12 months or more and there is potential forhuman infection and recurrence. However, it maybe possible to treat mycobacteriosis in permanentlycaptive birds.
Candida albicans infections occur in raptors, par-ticularly falcons. Samour cites that immunosuppres-sion (e.g., stress, malnutrition [hypovitaminosis A],medical treatment) is usually involved in raptorsdiagnosed with candidiasis.38 Candida albicans infec-tions usually involve the oral cavity, crop, or esoph-agus, with affected birds exhibiting dysphagia, cropstasis, regurgitation, and depression.15 Palpation ofthe crop may reveal thickening and roughening ofthe ingluvial wall. Lesions consist of white or grayplaques and a “turkish towel” appearance to themucosa. Stained cytological preparations from swabsof lesions or fecal material may reveal abundantbudding yeast. Published treatments include the useof nystatin, ketaconazole, itraconazole, fluconazole,or miconazole.38
Viral Diseases
HerpesvirusGeographically, avian herpesviruses is a global dis-ease. Herpesvirus has been identified in pigeons anddoves on every continent except Antarctica, and inowls, falcons, and eagles in North America and Eu-rope.39 Herpesviruses tend to be adapted to a spe-cific host species and become widespread within thefree-living populations of this species. Infections inhealthy, natural hosts are generally mild, subclinical,and become latent.39-41 More severe or lethal diseasefrom host-adapted herpesviruses occurs most oftenwith young birds or in older birds that are immuno-compromised with concomitant illness or injuries.41
Herpesviruses are spread mainly by activities thatrequire direct contact (e.g., consumption, mating,feeding of young or mates, fecal-oral routes).39,42
There are no published reports of herpesviruses be-ing vertically transmitted.39 Consumption of pigeonslatently infected with Columbid herpesvirus (CHV)is most likely the primary route for herpesviral infec-tion and disease in falcons.43-47 In these nonadaptedhosts, the virus causes greater morbidity and mortal-ity (up to 100% flock mortality). One authority sus-pects that falcons traditionally from regions that arefree of common pigeons may be more susceptible todisease from CHV (Dewey Savell, falcon breeder,Oakley, CA, personal communication, September2007).
Gross lesions associated with a herpesvirus infec-tion include hepatomegaly and splenomegaly, usu-
ally with multifocal pale necrotic foci throughout the
Raptor Gastroenterology 147
parenchyma. Pseudomembranous lesions may alsobe found in the oral cavity and any point within thegastrointestinal tract, the bronchioles, thymus, thy-roid, kidneys, and gonads.44 Histologically, herpesvi-rus infections produce intranuclear inclusion bodiesin affected cells.48 Birds are typically lethargic, weak,experience slow crop emptying, and exhibit biliver-dinuria.43 The disease may progress rapidly in ex-tremely susceptible birds, and they will usually diewithin 1 to 3 days of infection.39,42-44
Treatment for avian herpesvirus is rarely reward-ing and focuses on aggressive supportive care (e.g.,parenteral fluids, supplemental heat, removal ofcrop contents in the event of crop stasis). Antiher-pesviral drugs such as acyclovir have appeared toanecdotally benefit infected birds but will not clearthe infection (W. Ferrier, oral communication, Jan-uary 2007). Prevention of herpesvirus infections cen-ters mainly on careful inspection of pigeons used forraptor food or total avoidance of this type of bird asa dietary choice. Closed aviary concepts applied toboth the feeder pigeon flock and to the raptorsthemselves are also important and should be a cor-nerstone to the husbandry practices of that facility.Other avian herpesviruses, such as isolates associatedwith Pacheco’s disease, have been addressed by vac-cination. A CHV vaccine has been successfully testedin challenge trials with gyrfalcon hybrids but is stillnot widely available.49 Herpesviruses generally donot remain active for long outside of the host, there-fore they are spread mainly by activities that requiredirect contact (e.g., mating, feeding of young ormates, fresh fecal contamination and consump-tion).39,42 Because herpesviruses have not beenshown to have vertical transmission, herpesvirus-freecollections of birds can be created if eggs are re-moved and incubated either artificially or under asurrogate hen.
PoxPoxviruses have been identified in a number of rap-tor species around the world.39,50 Poxvirus lesionsprimarily occur on the face, feet, legs, conjunctiva,oral cavity, or vent. Birds may be unable to feed iflesions mechanically obstruct the oral cavity or obstructvision. Generally, birds that clear the infection areconsidered immune, but recurrence has occurred inrecovered birds undergoing stressful events, suggestingthat some birds may remain latently infected.39 Con-trol of biting insects (e.g., mosquitoes), quarantineof infected birds, and good facility hygiene are im-portant preventative measures. A commercial vac-cine to obtain immunity against poxvirus infections
has been used in falcons.51AdenovirusFalcon adenovirus appears to be host-adapted andwidespread among peregrine falcons but can alsocause disease in nestling aplomado, teita, and teita �peregrine falcon hybrids.52,53 One case report de-scribes adenovirus in a Harris hawk, Bengal eagleowl, and Verreaux’s eagle owl.54
Botulism
Toxins produced by Clostridium botulinum, which maybe present in carrion or affected waterfowl prey, areparticularly potent.8 Clinical signs associated withbotulism toxicosis include flaccid paralysis of neck,limb, pharyngeal, and respiratory muscles. Diagnosisis based largely on history and clinical signs but canbe confirmed by mouse inoculation neutralizationassay or with toxin analysis of frozen kidney or liverfrom the affected bird. Treatment of botulism toxi-cosis includes supportive care (e.g., parenteral flu-ids, nutritional support, supplemental heat) and ad-ministration of C. botulinum type A or C antitoxin(0.05-1.0 mL/d).8
Lead Intoxication
Lead is ingested as fragments from fishing tackle,bullets, or other projectiles that are embedded orcontained in the gastrointestinal tract of carrion orlive prey.55,56 Lead intoxication is commonly diag-nosed in raptor species and is a worldwide concern.Neurological effects (e.g., depression, paresis, inten-tion tremors, hyperesthesia, seizures), anorexia, biliv-erdinuria, and anemia are common clinical signs ob-served in lead-intoxicated birds.55-57 There appears tobe some species variability regarding the disease se-verity associated with lead intoxication.56 Affectedbirds may also experience gastric hemorrhage and enter-itis with resultant melena or hematochezia. Radiographsand blood lead level will confirm the diagnosis of leadtoxicosis. Recommended treatment includes the use ofchelators such as CaNa2 EDTA (Calcium DisodiumVersenate; 3M Pharmaceuticals, Northridge, CA USA)35 mg/kg IM every 12 hours.10 After stabilizing thepatient, removal of any lead foreign body within thegastrointestinal system via gastric lavage, endoscopicretrieval, or proventriculotomy is indicated.55,58
Sour Crop
Ingluvial stasis can result from obstruction or disease
of the gastrointestinal tract (e.g., trichomoniasis,
148 Ford
candidiasis), from overfeeding, or from systemicconditions such as severe dehydration or inanitionfollowed by feeding.9,59 In addition to crop stasis, thebird may regurgitate, and the regurgitant may have afetid odor because of fermentation of crop contents,whereby the animal becomes depressed and pro-duces small mutes consisting of bile and urates. Aconcurrent bacterial infection can ultimately causecrop edema and endotoxemic shock.38 Treatmentfor ingluvial stasis includes removal of food, eitherorally or by ingluviotomy, followed by oral antibiot-ics, such as trimethoprim sulfadimethoxazole at 48mg/kg PO every 12 hours or clindamycin at 50 to100 mg/kg PO every 12 hours until clinical signsresolve. Some authors also lavage or gavage dilutedantiseptics (e.g., chlorhexidine) into the upper gas-trointestinal tract after removal of fermented cropcontents.38 Radiographic images and other diagnos-tic tests are recommended to identify and addressthe underlying cause of ingluvial stasis. Food shouldslowly be reintroduced in conjunction with fluidtherapy.
Trauma and Foreign Bodies
Because of the anatomic and physiologic pyloricfunction in birds of prey, ingested foreign bodiesshould be confined to the upper alimentary tractand stomach.3 Fishhooks and other fishing tacklecan be a serious disease concern in bald eagles,ospreys, and other piscivorous birds of prey. In somecases, the hook does not actually perforate the gas-trointestinal tract, and consequently the birds areable to regurgitate this foreign body or they can becarefully retracted and removed under anesthesia.Occasionally, the removal of hooks can be accom-plished by pressing them through the mucosa andsurface epithelium to expose the barbs (if present),at which time the tip of the hook is cut off, and theremainder, with any attached line, is orally retracted.Often, surgical removal via ingluviotomy or proven-triculotomy is necessary. Hooks in the crop or cra-nial thoracic esophagus are usually accessed via aningluviotomy incision, whereas hooks lower in thegastrointestinal tract require a left lateral approachinto the proventriculus. Survey radiographic imagesof the entire upper gastrointestinal tract should betaken after removal of the known foreign body(s) toensure all objects (e.g., tackle, hooks, sinkers) havebeen extracted. Birds affected by heavy metal intox-ication may not be able to cast or otherwise regurgi-tate all of the ingested lead fragments from theventriculus. Because of the absence of a constricted
proventricular-ventricular isthmus, compact denseparticles, such as lead fragments or fishing sinkers,may be removed by gastric lavage via an ingluvi-otomy incision. If a gastric lavage is unsuccessful,endoscopic retrieval via an ingluviotomy or proven-triculotomy incision is indicated.38
Severe trauma or disease (e.g., trichomoniasis) ofthe crop wall may result in devitalization of this tissueand the overlying surface epithelium, resulting inthe formation of a fistula or granuloma.9,58 Suchdefects must be surgically debrided and closed in 2layers (crop wall and skin). Ingluvial obstruction dueto a concentration of bones from prey (food) is arelatively common gastrointestinal emergency pre-sentation among falconry birds. Frequently, the ob-struction is the neck of a quail or other avian preyitem. Preventative measures include offering necksonly if they have been cut into several pieces, partic-ularly when feeding birds that demonstrate a ten-dency to quickly gulp their food. Reduction of abird’s tendency to quickly eat its food can be man-aged by increasing the bird’s flying weight slightly orby increasing the bird’s sense of security when feed-ing (i.e., feeding them indoors or out of sight fromother perceived competitors). When ingluvial ob-structions occur, the bird may make frequent, un-successful motions to “put over” their crop (a motioninvolving alternately extending the neck and shrug-ging the shoulders to force food from the crop intothe thoracic esophagus). Resolution of ingluvial ob-struction is accomplished by performing an ingluvi-otomy. The dependent ventral midline region of thecrop is a relatively avascular area and easily accessiblepoint of entry, and consequently is the recom-mended site for surgical entry. To perform an inglu-votomy, longitudinal skin and matching crop inci-sions are made, whereby the surgeon enters the croplumen. After removal of the ingesta, a blunt instru-ment or endoscope should be used to inspect thecervical and thoracic esophagus for remaining ob-jects that may be perforating the wall or blocking thelumen. The crop and skin are closed in 2 layers withmonofilament suture in a simple interrupted pat-tern.9,58
Lower gastrointestinal traumatic or obstructiveconditions are rare in birds of prey. However, uroli-thiasis does occur in chronically or severely dehy-drated individuals. Disabled free-living birds of preymay suffer from uroliths during severe water- andfood-deprivation because of the efficiency of waterresorption in the rectum and cloaca. The presenceof uroliths will cause visible and audible strainingduring attempts to defecate. The urate concre-tions are easily detected as a gritty sensation when
gently probing the cloaca with a thermometer. An
Raptor Gastroenterology 149
enema or mechanical reduction and retractionwith thumb forceps will usually result in an un-eventful removal of the uroliths (Fig 7).59
Nutritional Concerns
Provision of a whole-prey, wholesome diet is importantto the long-term health of raptors. When feedingwhole prey is not possible, the use of a vitamin supple-ment intended for birds of prey (e.g., Vitahawk; DBScientific, Oakley, CA USA) is recommended. Wholeprey provides all essential amino acids in their cor-rect proportions for sustaining life, while hair andfeathers should assist in casting.3
Reintroduction to spontaneous alimentation aftergastrointestinal stasis, chronic inanition, or othersevere disease should be accomplished carefully withparticular attention to hydration and type of metab-olizable energy provided. Fluid therapy is a primaryconcern because a raptor’s digestive processes in-volve abundant secretion. Digestion is also energyintensive, so a critical care diet’s energy sourcesshould be easily absorbed. As mentioned earlier,raptors are particularly well-adapted to metabolizingamino acids to meet their energy needs. This processcan also aid in the metabolization and elimination oflactic acid, which generally accompanies inanitionand chronic debilitation. Therefore, use of carbohy-drate-rich gavage diets may not be as helpful as dietsrich in fat and protein, particularly when these con-stituents are reduced to short chains or amino acidsthat are easily absorbed by the intestinal mucosa.
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