Avian Gastroenterology

Question 1

What are the most common gastric neoplasms of psittacine species?

What speces are represented?

Answer 1

Gastric carcinomas and adenocarcinomas

Budgies, parakeets, lovebirds, cockatiels, conures, amazons

Terio Ch 32 - Psittaciformes

Question 2

Discuss teh GI anatomy of ratites.

Do they have a crop?

What is unique about the ostrich stomach anatomy?

What is unique about the cassowary ventriculus?

Describe the hindgut fermentation strategies of ratites?

What is unique about ratite excretion?

Do they have a bursa fo fabriius?

Do ratites have a gallbladder?

Answer 2

Ratites

• Lack a true crop.
• Ostriches, rheas – Small glandular patch in proventriculus, thick-walled ventriculus.
• Other ratites, proventriculus PV significantly smaller than V.
• Ostriches – Unique arrangement of the gastric compartments.
  
  • Thin, saclike PV, gizzard cranioventral.
• Rhea – enormous paired ceca for hindgut fermentation.
• Ostrich – voluminous colon and long rectum, small ceca.
  
  • Spiral folds within ceca increase SA.
• Emus, cassowaries – Large PV, diffusely glandular. V is small, lacks koilin in cassowary.
  
  • Paired vestigial ceca.
• Strong rectal-coprodeal sphincter results in separate defecation and voiding of urine and feces.
  
  • Feces stored in rectum, urine stored in proctodeum (acts as bladder).
  • Lack true bursa of Fabricius.
    
    • Forms integral part of dorsolateral wall of proctodeum.
    • Ostrich lacks a GB, present in other ratites.

Question 3

Do penguins have a crop?

What is unique about the penguin stomach?

Do they have a gallbladder?

Answer 3

Penguins

• Lack a crop.
• Large stomach, PV and V.
• PV stores food to feed chicks.
  
  • Consider before administering oral meds.
• RB settle in distal ventriculus, can appear towards cloaca on rads (misleading).
• Penguins have a gallbladder

Question 4

Describe the GI anatomy of Gaviiformes, Podicipediformes, and Procellariformes.

How do they handle dietary lipids from their meals?

How is this applicable clinically?

What is the benefit of ingesting feathers? Which group does this?

Answer 4

Gaviiformes, Podicipediformes, Procellariformes (Loons, Grebes, Petrels, Albatrosses)

Procellariformes except Pelecanoididae accumulate gastric oils in proventriculus.

• Concentrates lower volume, high caloric meals.
• Not secretory products, derived from dietary lipids and concentrated by regulating amount of lipid emptying.
  
  • Pylorus retains lipids while allowing water soluble ingesta to pass.
  • Lipid emulsifiers of intestinal origin may be reflexed retrograde to play a role in gradual lipid metabolism without entering intestine.
  • When handled, all spp may regurgitate gastric oils.
  • Northern fulmar can forcefully expel gastric oil as defense mechanisms.
• Podicipediformes routinely ingest own feathers.
  
  • Contribute bulk to bind undigested stomach contents, allow formation of uniform bound pellets to be extreted regularly.
    
    • May slow gastric transit time to max digestive efficiency and excretion of pellets may control gastric parasite loads.

Question 5

What is unique about the pelecaniformes GI tract?

Answer 5

Pelecaniformes (Pelicans, Tropicbirds, Cormorants, Frigatebirds, Anhingas, Gannets)

• Gular pouch – Drains water before swallowing prey. Courtship display. Absent in tropicbirds.
• Carnivorous, both PV and V are thin and extensible, relatively indistinguishable.
• Pylorus is very well muscled, may prevent FB and bones from entering SI.

Question 6

Describe the flamingo GI anatomy.

How does their bill shape reflect what they eat?

What is unique about their crop?

Answer 6

Phoenicopteriformes

• Phoenicopterus spp – Shallowbill, feed on arthropods and mollusks.
• Phoenicoparrus and Phoeniconaias spp – Deep bills, feed on algae and diatoms.
• Filter feed with bill upside-down.
• Spines on tongue act as a comb to clean internal horn lamellae on upper and lower beak.
• Crop produces crop milk

Question 7

Describe the GI anatomy of charadriiformes.

Answer 7

Charadriiformes

• Crop and gizzard simple and reduced.

Question 8

Describe the GI anatomy of accipitriformes & falconiformes.

What is the use of the tomial tooth?

Do all species have a crop?

What is a typical pH of the proventriculus?

Do they have a gallbladder?

Answer 8

Falconiformes (Falcons, Hawks, Eagles, Kites, Harriers, Buzzards, Ospreys, Caracaras, Sec Birds, Vultures)

• Tomial tooth on maxilla for severing neck of prey.
• All have a crop except bearded vulture.
• Simple stomach, pH ~1 capable of digesting bones.
• Ceca absent/vestigial.
• GB usually present.
• Small pancreas within duodenal loop.

Question 9

Describe the GI anatomy of gallinaceous birds.

What is their stomach like?

What about their ceca?

Answer 9

Galliformes

• Beak shape for picking up grains and small insects.
• Trauma may occur with wire housing.
• Granivorous, well-developed muscular ventriculus with striated muscle layers.
• Well developed ceca.

Question 10

Describe the anatomy of columbiformes.

What is unique about their crop?

Do they have a gallbaldder?

What are their ceca like?

Answer 10

Columbiformes

• Prominent crop.
• Hyperplasia of crop mucosa with milk production in males in females, under influence of prolactin.
  
  • Semi-solid nutritious substance derived from desquamated crop epithelial cells.
• GB may be absent depending on species.
• Ceca are rudimentary.

Question 11

Describe the GI anatomy of Psittacines.

What is unique about their bills?

What is unqieu about Lories?

What about Cockatoos?

Answer 11

Psittaciformes

• Hooked bill with complex musculature.
• Upper mandible articulates with skull.
• Thick, muscular tongue.
• Loriinae – Tongue tip modified with erectile dermal papillae for gathering nectar and pollen.
• Superfamily Cacatuoidea distinguished by presence of GB.

Question 12

What is unique about juvenile cuculiformes oropharyngeal anatomy?

Answer 12

Cuculiformes (Cuckoos, Roadrunners)

• Juveniles have white to yellowish papillate patches in oropharyngeal caviy.

Question 13

Describe the GI anaomty of owls.

Do they have a crop?

What is the pH of their proventriculus? How does this affect them clinically?

Describe the function of their ceca.

Answer 13

Strigiformes

• No crop (unlike falconiformes).
• Ingested food passes into PV (glandular). pH ~2.5, unable to digest fur, feathers, bones.
• Ventriculus forms pellet of indigestible material, casted 10-13 hrs after meal.
• Paired secretory organs at juncture of ileum and colon – ceca.
• Fermentation of cellulose, water, Ca resorption and microbial action of benefit and pathogens occur in ceca.
  
  • Blind ended, product is brown, homogenous, odiferous.
  • Cecal contents eliminated when stressed.

Question 14

Describe the GI anatomy of caprimulgiformes?

What are their tongues like?

Do they have a crop?

What are their ceca like?

Answer 14

Caprimulgiformes (Nightjars, Allies)

• Vestigial, flaplike tongue contributes little to swallowing.
• No crop, large ceca present in all spp except owlet-nightjars.

Question 15

Describe the GI anatomy of turacos.

Do they have a crop?

What is the anatomy of their stomach like?

What about their ceca?

Answer 15

Musophagiformes

• Little or no ceca, distensible esophagus.
• No crop.
• Thick muscular PV and thin-walled ventriculus.
• Relatively large liver for body size.
• Regurgitation when stressed.

Question 16

Describe the GI anatomy of hummingbirds.

What is unique about their tongues?

Do they have a crop?

Do they have a gallbladder?

Do they have a cecum?

What is their GI emptying time?

Answer 16

Trochiliformes (Hummingbirds)

• Extendable tongue forms two parallel C-shaped grooves of keratinized membranes around rigid supporting rod with bifurcated end.
• Draws nectar via capillary action and traps fluid.
• Small crop, short intestinal tract.
• No cecum, no GB.
• Crop emptying time ~4 minutes.
  
  • Intestinal transit ~15 minutes.
  • 99% ingested glucose is absorbed.
• Liver highly metabolically active, highest levels of enzymes for lipid synthesis.

Question 17

Describe the GI anatomy of trogons.

What are their bills like?

What about their tongues?

Do they have a crop?

What is the stomach anatomy like?

What about their ceca?

Answer 17

Trogoniformes

• Cutting edges of maxilla, mandible, or both variably serrated.
• Decurved tip of bill.
• Short, triangular tongues with backward-pointing projections.
  
  • Cuban trogon exception – long tongue with bifurcate tip involved in nectar feeding.
• Short bills with unusually wide base for large gape to bill length.
• Long esophagus is thin walled, elastic, ringed by circular muscles important in regurgitation of large seeds.
• No crop.
• Expansible proventriculus, glandular tissue in closely packed hexagons.
• Large ventriculus, muscular.
• Paired ceca are well developed.

Question 18

Describe the GI anatomy of coraciiformes and bucerotiformes.

What is unique about their tongue anatomy? How does that affect their feeding style?

What is the purpose of the hornbill casque?

Why do they regurgitate so much?

Answer 18

Coraciiformes (Kingfishers, Motmots, Bee-eaters, Hoopoes, Hornbills)

• Lack stylohyoideus muscle, minimizes tongue mobility and affects feeding style and ceca.
• Hornbill casque air-filled chamber surrounded by keratin, purpose unknown.
  
  • Signaling mechanism.
  • Varies by species, gender, and age.
  • Buceros hornbills not found to have a connection between the casque space and maxillary sinus, unlike all other species.
  • All species assessed have a casque sinus between the casque and the calvarium.
• Many food items consumed whole.
• Pellets of indigestible material may be regurgitated, esp in bee-eaters.

Question 19

Describe the GI anatomy of piciformes.

What is unique about woodpecker tongues?

What is unique about toucan bills and their tongues?

Answer 19

Piciformes (Honeyguides, Barbets, Woodpeckers, Toucans)

• Woodpeckers have long tongues, sublingual glands produce sticky substance.
• Tongue muscles supported by extensive hyoid apparatus extending around back of skull and over the head.
• Toucan bills have serrated edges.
• Tongue is laminated along sides, brush-like toward tip.

Question 20

Describe the GI anatomy of passerines.

Do they have a crop?

What is their ceca like?

Answer 20

Passeriformes (Songbirds, Perching Birds)

• Have a crop.
• Cecum is vestigial or absent in most.

Question 21

Describe potential lesions of the avian oral cavity.

List differentials for these signs.

Answer 21

• Oral cavity – Hyperemia, increased mucus, caseous plaques, swollen salivary glands other lesions.
  
  • CS – dysphagia, yawning, head shaking, food adherence to oral mucosa, exudate corners of mouth, extension of head if swallowing is painful.
  • Ddx – Candidiasis, trichomonas, capillaria, pox, gram negative infections, Helicobacter, hypovit A, trauma, oral papillomas, neoplasia.

Question 22

Describe potential clincial signs for a disease crop or esophagus in a bird.

What are some important differentials to consider?

Answer 22

• Crop and esophagus.
  
  • CS – regurgitation, fluctuant crop, matted head feathers, sour breath odor, stasis of crop, decreased contractions, fistulas at thoracic inlet.
  • Ddx – Gram neg infection, candidiasis, trichomoniasis, papillomatosis, thermal burns, trauma, GB, extraluminal obstruction, functional ileus, ingluvioliths

Question 23

What are the associated clinical signs with a diseased proventriculus or ventriculus in a bird?

What are some important differentials to consider?

Answer 23

• Proventriculus and ventriculus.
  
  • CS – vomiting, regurgitation, crop stasis, wt loss, passage of whole gains, diarrhea, melena.
  • Ddx – PVDD, neoplasia, Macrorhabdus ornithogaster, mycobacteriosis, candidiasis, papillomatosis, foreign body, functional ileus i.e. sepsis, lead, gram neg infections, parasites i.e. capillaria.

Question 24

What are some the expected clincial signs of intestinal disease in a bird?

What are some important differentials to consider?

What cecal diseases may affect birds?

Answer 24

• Intestinal disease.
  
  • CS – diarrhea.
    
    • Much less common than polyuria.
    • Other CS include pasting around the vent, mucus-laden stools, melena, hematochezia, abdominal pain.
  • Ddx – gram neg bacterial infections i.e. salmonella, clostridium, campylonbacter, chlamyophila, giardia, hexamita, coccidian, candidiasis, mycobacteriosis, intussusception, ileus
• Cecal coccidian, cecal worm i.e. Heterakis gallinarum

Question 25

What are common clinical signs associated with cloacal disease in birds?

How shoudl the normal cloacal mucosa look?

What are some important differentials to consider?

Answer 25

• Cloaca.
  
  • CS – tenesmus, frank blood in or on droppings, strong fecal odor, tissue protrusion, infertility.
  • Normal mucosa should be smooth, longitudinal folds around the orifice known as columns.
  • Ddx – cloacal papillomas, cloacal prolapse, cloacalithiasis, cloacitis (gm neg, anaerobes), paresis (neuro).

Question 26

Describe papillomatous disease of the avian cloaca.

How common is this?

what is the proposed etiology?

What are some potential complications of these papilomas?

What other organs may be affected?

What species are particularly susceptible?

How is disease diferent in Grey parrots?

Answer 26

• Papillomatous disease:
  
  • Most common neoplasia in the cloaca of New World psittacines.
  • Herpesviral etiology.
  • Most common in proctodeum.
  • May lead to partial obstruction of proctodeum.
  • Proliferation may extrude through vent lips.
  • Irregular ejection of urofeces, soiling around vent and feathers.
  • May have frank blood in urofeces.
  • Lesions of biliary and pancreatic ductular systems likely, cause of mortality long-term.
  • Amazons esp susceptible, high mortality from biliary and pancreatic duct carcinoma.
  • Confirmed in Grey parrots also.
    
    • May involve epithelium or mucous cells primarily.
    • Primarily mucous cells – adenomatous polyps more likely to become locally malignant as adenocarcinomas.
  • Tumor growth near entrance of ureters may lead to obstructive hyperuricemia.

Question 27

What is the most common form of cloacal prolapse in birds?

What species are particularly overrepresented?

Why does this occur?

How is it treated?

What are teh other two types of prolapse?

How are they treated?

Answer 27

• Cloacal prolapse:
  
  • Idiopathic coprodeal prolapse in cockatoos and other psittacines most common form of prolapse in pet birds.
    
    • Predominantly males.
    • Usually very attached to humans in the house.
    • Usually exhibit CS around time of sexual maturation.
    • Pushing and straining of the coprodeum leads to partial prolapse and reductions in vent tone with increase in vent width.
    • Progressively worsens, prone to opportunistic infections of hind gut, can die prematurely.
  • Tx via cloacopexy.
    
    • Usually continue to strain.
    • Research looking at behavioral intervention, hormones, chemical and surgical neutering, and ventplasty as options.
    • Prevention by rearing with conspecifics and following normal fledging procedures.
• Oviductal prolapse.
  
  • Should be surgically investigated and replaced.
  • +/- salpingohysterectomy.
• Rectal prolapse least common but most serious.
  
  • Intussusception of rectum is surgical emergency.
  • Endoscopy can ID origin of prolapsed tissues.
  • Sx exploration, reduction, and resection usually indicated.

Question 28

What are some common causes of cloacitis in avian species?

What fungal infection is likely to occur?

What helminths are likely to cause cloacitis? Are any species or groups particularly affected by these?

What protozoa commonly affects Amazon parrots?

What mite can also cause crusting lesions of the vent in addition to its typical signs on the face?

Answer 28

• Cloacatis.
  
  • Bacterial uncommon.
    
    • Could be related to nutritional deficiencies, papillomatous dz, trauma, egg laying.
    • Venereal transmission of pathogenic bacteria has been reported.
  • Fungal.
    
    • Candida albicans most common.
    • Immunosuppression, diets high in sugars may contribute.
  • Parasitic.
    
    • Cloacotaenia megalops.
      
      • Cestode, waterfowl.
      • Primarily within coprodeum.
      • IM host ostracod.
    • Brachylaimid trematodes.
      
      • Cloaca and bursa in spp that consume snail IM host.
    • Urogonimus macrostomus digenic trematode, cloaca of temperate passerines.
    • Cryptosporidiosis in Amazons.
      
      • C. baileyi replicates in cloaca and bursa.
    • Knemidocoptes pilae infestation of cere and feet, also crusted lesions along vent.

Question 29

What are avian cloacaliths usually composed of?

What is the most common cause?

How do the urates become so hard and compacted?

Answer 29

• Cloacalith.
  
  • Uric acid.
  • Strong relationship to decreased or impaired coprodeal emptying, most often iatrogenic causes.
  • Sx of cloaca for papilloma removal most common cause.
  • Fibrosis in region of coprourodeal sphincter leads to prolonged retention of urates within coprodeum.
  • Digestion of mucopolysaccharide and protein matrix of excreted UA spherules by fecal bacteria and enzymes.
  • Facilitates UA crystallization and aggregation.

Question 30

What are the five main types of liver disease in birds?

Why do birds not have bilirubin?

What are some clincial signs of liver disease in birds?

What are some important differentials for liver disease in birds?

What enzyme activities may be increased with liver disease? Which are specific for liver disease in birds?

What is the only definitive way to diagnose liver disease in birds?

Answer 30

• Liver.
  
  • 5 categories of liver dz in birds:
    
    • Infectious, metabolic, toxic, neoplastic, congenital.
  • Biliverdin.
    
    • Green pigment formed through degradation of RBC.
      
      • Reptiles and birds lack biliverdin reductase and cannot form bilirubin.
  • Birds with overgrown beaks may have liver disease.
  • Urine of birds with liver dz usually hyposthenuric SG < 1.007.
  • Ddx – Pacheco’s dz, chlamydia psittaci, mycobacteriosis, other forms of hepatitis, toxins, hepatic lipidosis, hemochromatosis, neoplasia, chronic fibrosis.
  • Rads – liver should not extend outside a line drawn from scapular to greater trochanter of femur on VD.
    
    • Lateral – should not extend caudal to the end of the sternum.
    • Hepatometaly indicated by widening of liver shadow, loss of hourglass shape, caudal and dorsal displacement of ventriculus, alteration of shape of the liver.
    • Position of ventriculus helps distinguish false enlargement from true hepatomegaly.
  • Chemistry – elevated AST, LDH, BA; decreased glucose, TP, albumin.
  • AST – hepatocellular damage.
    
    • Als in muscle.
    • Evaluate in conjunction with CK.
    • AST longer half life vs CK.
  • GGT and GLDH specific for liver.
    
    • GGT increases with biliary damage or obstruction.
    • Marked elevations with bile duct carcinoma.
    • GLDH – mitochondrial enzyme, elevates with severe hepatic damage and necrosis i.e. Pachecos dz.
    • LDH not sensitive nor specific for liver dz.
    • ALP little value.
    • BA sensitive and specific for liver.
      
      • Functional capacity of liver.
      • Preferred to measure after 2-3 hours of fasting, but not necessary.
      • Does not have 100% correlation with hepatic dz.
    • TP, Alb may be reduced.
  • Rule out chlamydia in patients with liver dz.
  • Screen for toxins i.e. aflatoxins, lead.
  • Hepatic biopsy is the only way to definitively diagnose hepatic dz in birds.

Question 31

What are the clinical signs associated with pancreatic disease in birds?

What are the feces of a bird with exocrine pancreatic insufficiency like?

What are important differentials for pancreatic disease?

What enzyme has a high association with pancreatic disease in birds?

What is needed for definitive diagnosis?

Answer 31

• Pancreatic dz.
  
  • CS – malaise, anorexia, wt loss, vomiting.
  • Pancreatic exocrine insufficiency – polyphagia, wt loss, pale bulky droppings.
  • Ddx – pancreatitis, pancreatic necrosis, EPI, pancreatic neoplasia.
  • Elevated amylase has a high association with pancreatic dz in birds.
  • Dx depend son bx and histo.

Question 32

The septicemic form of avian pox is common in what avian species?

What are the typical histologic lesions?

Answer 32

• Avian pox – septicemic form common in canaries.
  
  • Proliferation of epithelial cells with ballooning degeneration and large eosinophilic, intracytoplasmic inclusions aka Bollinger bodies diagnostic.

Question 33

Avian papillomatosis commonly occurs in what species?

What anatomic sites are commonly affected?

How does the appearance of affected mucosa change?

What test can be done to confirm the tissue is papillomatous?

What is the proposed etiology?

What are some of the associated clinical signs?

How are papillomas treated?

Answer 33

• Papillomatosis.
  
  • Oral cavity, esophagus, crop, proventriculus, or cloaca.
    
    • Most common in macaws, hawk-headed parrots, Amazons.
    • Roughened surface/mass or granular appearance to mucosa.
    • Application of 5% acetic acid to mucosa enhances visualization of papillomatous tissue.
    • Cloaca most common site.
    • Association between papillomas and neoplasias of liver and pancreas (esp Amazon spp).
    • Cloacal carcinoma may result from malignant transformation.
    • Herpesvirus etiology proposed.
    • Appears transmissible.
    • May cause dyspnea or wheezing depending on location.
    • Tenesmus and infertility can occur with cloacal papillomas.
    • Tx – Surgical removal, laser, chemical cautery.
      
      • Chemical cautery with silver nitrate sticks repeated several times at weekly intervals.
    • Bleeding can be minimized by application of barium to the mucosa.

Question 34

What is the etiologic agent of proventricular dilatation disease?

What are the lesions this virus produces?

Will all positive birds develop disease?

What are the classic features on radiographs?

How is this disease definitively diagnosed?

How is it treated?

Answer 34

• Proventricular dilatation disease.
  
  • Aka macaw wasting dz, PDD.
  • Not reported in budgerigars.
  • Splanchnic ganglion neuropathy.
    
    • Commonly affects nerves supplying PV and V.
    • Ocular lesions i.e. choroiditis and optic neuritis have also been described.
  • Avian bornavirus.
    
    • Unstable in environment.
    • Clinically normal birds test positive.
    • Autoimmune responses may play a role in development.
  • Dx – CS, characteristic GI changes on rads, biopsy.
    
    • Rads – the presence of gas, enlargement of the proventriculus, or changes in shape or position are common.
    • Barium series can differentiate PDD from proventricular masses, FB, other luminal defects.
    • Dx – biopsy of affected GI.
    • Mucosal bx via endoscopy are nondiagnostic since lesions are in the muscular tunic.
    • Full-thickness PV bx recommended in older references, but assoc with high mortality.
    • Crop biopsies are low risk, preferred.
      
      • Can be segmental, random biopsy may provide false-negative results.
  • Tx – celecoxib (COX2) reported to suppress clinical signs and reduce pathologic changes.
  • Tepoxalin, combo of COX 1, 2, and 5-lipoxygenase (LOX) inhibitor may have improved effects.
  • Addition of amantadine may improve therapeutic success.
  • Metoclopramide in severe cases.
  • Isolate from other birds, strict sanitation, control of pests.

Question 35

What is the etiologic agent of Pacheco’s disease?

What are the typical clinical signs?

What lesions are found on necropsy?

What is the typical therapy? Does it stop the disease?

Answer 35

• Pacheco’s disease:
  
  • Herpesvirus. (PsHV-1)
  • Severe, acute, systemic dz of psittacines.
  • Liver most severely affected.
  • Found dead.
  • Nx – hepatosplenomegaly.
  • Generally in aviaries following intro of new birds.
  • Acyclovir may help during outbreaks to prevent onset.
    
    • Limits viral replication, not virucidal.

Question 36

What species of mycobacteria commonly affect birds?

What lesions typically occur?

What are teh typical clinical signs?

How is this disease diagnosed?

How is this disease treated?

Answer 36

• Avian mycobacteriosis.
  
  • M. genavense, M. avium.
  • Zoonotic.
  • Systemic granulomas.
  • Wt loss, good appetite, chronic diarrhea, lethargy.
  • Skin lesions may be seen.
  • Ubiquitous in soil, resistant to disinfection.
  • Shed in feces.
  • Dx may include cbc/chem/EPH, rads, fecal acid-fast, PCr, biopsies (liver).
    
    • May have extremely high WBC.
    • Rads – dilated or thickened bowel loops, hepatosplenomegaly, granulomas, lytic bone lesions.
    • Acid-fast organisms may be in feces, cytology, biopsies, necropsy.
    • Nonstaining, clear ghost-like rods on routine cytology.
    • Intermittent shedding. Pool fecal samples over 1 week.
  • Tx usually not recommended.
    
    • For large collections, quarantine exposed birds and disinfect.
    • Zoonotic risk for owners, long course of tx with abx if pursued.
      
      • Ethambutol, cycloserine, clofazimine, clarithromycin, rifabutin, aminoglycosides, floroquinolones.

Question 37

Gram negative microflora in avian (non-carnivore) GI tracts can result in what lesions?

How is this diagnosed? What specific bacteria should you be concerned with?

How is this treated?

Answer 37

• Gram negative pharyngitis, ingluvitis, enteritis.
  
  • Can cause erosive dz or granulomatous lesions.
  • Dz – cytology, culture.
  • PCR for salmonella spp.
  • Tx with abx and probiotics.
    
    • Avoid abx unless high organism load or high potential for dz.

Question 38

Bacterial hepatitis in avian species is typically caused by what kind of bacteria?

What are some typical clinical findings in birds with this disease?

What is a good antibiotic of choice with culture is not available?

Answer 38

• Bacterial hepatitis.
  
  • Gram negative bacteria predominate.
  • May result in high elevation of EBC, hepatomegaly, elevated AST, elevated bile acids.
  • Enrofloxacin DOC when culture not available, good penetration into hepatic tissue.

Question 39

What is the etiologic agent of pseudotuberculosis in avian species?

What are the typical sources of infection for pet birds?

What are the typical clinical signs?

What lesions are typically seen?

Answer 39

• Pseudotuberculosis.
  
  • Yersinia pseudotuberculosis.
    
    • Rodents and wild birds infection source for pet birds.
    • Diarrhea, malaise, pneumonia, high mortality.
    • Granulomatous.
    • Bacterial culture for dx.

Question 40

What bacteria causes pharyngitis in small psittacines?

What species are typically affected?

What are the typical clinical signs?

How is this diagnosed?

How is it treated?

Answer 40

• Helicobacter pharyngitis.
  
  • Small psittacines.
  • Resides in palatine salivary glands.
  • Cockatiels and lovebirds.
  • Hyperemia pharyngeal mucosa most prevalent sign.
  • Signs of oral pain – head shaking, yawning, dysphagia, retching.
  • May have nasal discharge.
  • Dx – spiral-shaped gram neg bacteria on pharyngeal swabs. PCR.
  • Tx with oral doxycycline or enrofloxacin generally successful.

Question 41

What bacteria causes necrotizing enteritis and cloacitis in birds?

What are the typical clinical signs?

How is this diagnosed?

How is it treated?

Answer 41

• Clostridium.
  
  • Necrotizing enteritis, cloacitis.
  • Strong odor to feces.
  • C. perfringens type C or C. tertium.
  • Toxins may lead to shock and death.
  • Sporulated bacteria on gram stains.
  • Anaerobic culture.
  • Tx with penicillins, i.e. clavamox, macrolides, metro.

Question 42

What pet bird species is commonly affected with campylobacter?

What are the typical clinical signs?

How is it diagnosed?

How is it treated?

Answer 42

• Campylobacter.
  
  • Chronic diarrhea.
  • Finches most common.
  • Diarrhea, amylorrhea, high mortality in young birds.
  • Dx with wet-mount or cytology/gram stain.
  • Potentially zoonotic.
  • Tx with macrolides or fluoroquinolones for min 3 wks.
  • Strict sanitation.

Question 43

What is the etiologic agent of psittacosis?

How is it transmitted?

What are the typical clinical signs?

How do signs differ between neotropical and old world psittacines?

How is this disease diagnosed? What are the best tests?

How is it treated?

Answer 43

• Avian chlamydiosis.
  
  • C. psittaci.
    
    • Fecal, urine, and respiratory shedding.
    • Zoonotic via inhalation.
    • Resp and hepatic signs predominate.
    • CS – serous oculonasal discharge, conjunctivitis, pneumonia, air sacculitis.
    • Wt loss, green watery urine (liver dz), diarrhea.
  • Neotropical psittacines classical signs with resp dz, green urine, leukocytosis.
  • Australian, Pacific, Asian psittacines more chronic dz.
  • African psittacines i.e. lovebirds appear most resistant.
  • Dx – gold standard is culture.
  • Obligate intracellular pathogens, requires tissue culture, chicken embryos, or mouse inoculation.
    
    • Only positive if bird is shedding.
    • ELISA and PCR are specific and sensitive if shedding.
    • Several serologic tests available.
    • Latex agglutination and elementary body agglutination useful to detect infected subclinical carriers.
      
      • Titers drop more rapidly with recovery than complement fixation.
  • Tx – 45 day course of tetracycline (doxy).
    
    • Biweekly rechecks recommended for complications assoc with tx.
    • Birds in contact with the affected animal must also be treated. Medicated feeds available.

Question 44

What fungal disease commonly affects the pharynx of young birds?

Is there a species particularly prone to this disease?

Are there any risk factors for developing this disease?

What are the typical clinical signs?

How is this diagnosed?

How is it treated?

Answer 44

• Candidiasis.
  
  • Candida albicans.
    
    • Young birds, esp cockatiels.
    • Sugary diets may promote yeast growth.
    • Cs – thickened crop wall, delayed emptying, regurgitation.
    • Foul-smelling droppings.
    • Dx – gram stain from swab of crop, fecal smear.
    • Budding yeast.
    • Tx – nystatin prophylactically when abx prescribed for young birds.
      
      • Will not be effective with deeper tissue invasion.
      • Most azoles usually effective.

Question 45

What is the etiologic agent of avian gastric yeast?

Where in the GI tract is this organism typically found?

What clinical signs are typical with this disease?

How is it diagnosed?

How is it treated and prevented?

Answer 45

• Avian gastric yeast.
  
  • Macrorhabdus ornithogaster.
    
    • Limited to proventriculus but also GIT may be infected.
    • Globular mucinous cysts at isthmus between proventriculus and ventriculus.
    • CS – wt loss, regurgitation, vomiting, melena, passage of whole seeds.
    • Dx – finding organism in feces or from crop sample or proventriculus.
    • May be found in some clinically normal birds.
    • PCR.
    • Affected birds have elevated proventricular pH, acidification of drinking water may improve survival.
    • Oral amphotericin B is the most successful tx, may alleviate CS and reduce shedding.
      
      • Will not typically eliminate the yeast from stomach.
      • 30 day course.
      • Avoid aspiration, irritating to resp membranes.
        
        • Fatal tracheitis may occur if aspirated.
        • Sodium benzoate in drinking water may show promise in large groups of birds.

Question 46

What birds are commonly affected by trichomonas?

What are the typical clinical signs?

How is this diagnosed and treated?

Answer 46

• Trichomoniasis.
  
  • Upper GIT.
  • Oral cavity, esophagus, crop.
  • Wild birds – Columbiformes, raptors.
  • Dx saline wt mount of lesions or crop wash.
  • Tx – metronidazole, carnidazole, ronidazole.

Question 47

What age group of birds are most affected by coccidiosis?

What are the typical clinical signs?

How is this diagnosed and treated?

Answer 47

• Coccidiosis.
  
  • Direct LC.
  • CS most severe in young birds – wt loss, diarrhea, fecal-pasted vents, death.
  • Dx – oocysts in fecal float.
  • Tx sulfonamides, amprolium, ponazuril, toltrazuril.

Question 48

How common is cryptosporidium seen in birds?

What are teh typical clinical signs?

How is it diagnosed and treated?

Answer 48

• Cryptosporidium.
  
  • Seldom diagnosed in birds unless immunosuppressed.
  • CS – enteritis, diarrhea, vomiting.
  • Organisms in feces with acid-fast or PCR.
  • Histo – enteritis or proliferative proventriculitis.
  • Tx not usually helpful.

Question 49

What bird is commonly affected by giardia?

What are teh typical clinical signs?

How is this diagnosed and treated?

Is this zoonotic?

Answer 49

• Giardia psittaci.
  
  • Common in budgerigars.
  • Most clinically healthy.
  • Young birds may have diarrhea, dehydration, poor growth.
  • Lugol’s iodine solution – oocysts.
  • Consider zoonotic.
  • Tx – metronidazole.

Question 50

What is the other name of hexamita?

What birds are commonly affected?

How is this differentiated from giardia?

What are the typical clinical signs?

How is this treated?

Answer 50

• Hexamitiasis aka spironucleosis.
  
  • Common in cockatiels and game birds.
  • Trophozoites are smaller vs giardia and move more erratically.
  • Most are subclinical, may show polyuria or diarrhea.
  • Feather-damaging behavior in some cockatiels.
  • Tx is challenging, failure is common – can try metro, ronidazole, carnidazole.

Question 51

What is the most common microsporidian disease of birds?

What speices are commonly affected?

What risk factors are associated with infection?

What are the typical sites of infection?

Answer 51

• Encephalitozoonosis – Encephalitozoon hellum.
  
  • Microsporidium, intestinal.
  • Small psittacines i.e. lovebirds and budgies.
  • Immunosuppression thought to be a factor.
  • Strong association with psittacine beak and feather disease.
  • May involve intestine, liver, kidneys.
  • Dx usually on necropsy.
  • Potentially zoonotic.

Question 52

What bird species are commonly affected by cochlosoma?

What are the typical clinical signs?

How is it diagnosed and treated?

Answer 52

• Cochlosomiasis.
  
  • Cochlosoma spp – flagellated protozoans.
  • Nestling mortality in finches (also seen in ducks and turkeys)
  • Can be carried by adults without CS.
  • Society finches may be resistant to disease, will expose other spp.
  • Dx wet mount of feces.
  • Tx metro or ronidazole.

Question 53

What nematodes commonly affect the upper GI of pet birds?

What about the ventriculus?

What about the intestines?

Tapeworms are seen in which wild caught parrots fairly frequently?

Answer 53

• Nematodes.
  
  • Upper GI – capillaria, spiruroidea.
  • Ventriculus – Acuaria.
  • Intestines – Ascaridia spp, Capillaria obsignata.
  • Tx ivermectin or pyrantel.
• Tapeworms.
  
  • Wild-caught African greys and cockatoos.
  • Wt loss, enteritis, eosinophilia.
  • May see proglottids in droppings.
  • Tx praziquantel.

Question 54

Ingluvioliths are typically composed of what?

What causes them?

How are they treated?

How is recurrence prevented?

Answer 54

• Ingluvioliths.
  
  • Stones within crop – smooth, usually uric acid with concentric layers.
  • Consumption of urates usually plays role (coprophagy).
  • Tx with ingluviotomy.
  • Housing birds in caged without access to droppings may minimize reoccurrence.

Question 55

What is the most common GI neoplasm of psittacines?

Where does it typically occur?

Answer 55

• Gastric neoplasia.
  
  • Reported in several spp.
  • Majority dx post-mortem following acute hemorrhage caused by ulceration of the mass.
  • In all psittacines, cases reported neoplasia in the isthmus between the proventriculus and ventriculus.
    
    • Majority proventricular adenocarcinomas.
    • Should be a ddx for older birds with vomiting, wt loss, passage of whole seeds.
  • Can do a barium study. Endoscopic bx risk of perfing stomach.
  • Metastases uncommon, sx resection can be curative but is not reported. Sucralfate may be helpful.

Question 56

What avian neoplasia is commonly associated with cloacal papillomas?

What avian species is commonly affected?

How is liver disease supported in birds?

Answer 56

• Liver neoplasia.
  
  • Amazon parrots – biliary adenocarcinoma strongly assoc with cloacal papillomas.
    
    • Liver should be evaluated in birds with papillomatous disease.
    • Lymphoma also reported in liver.
    • Milk thistle, lactulose may be supportive in liver dz.

Question 57

What is the most common clinically evident nutritional deficiency in avian pets?

What are teh typical clinical signs?

How is this confirmed cytologically?

Answer 57

• Hypovitaminosis A.
  
  • Most common clinically evident nutritional deficiency of avian pets.
  • Oral caviry – swollen salivary glands, keratin cysts, blunted and thiccckened choanal papillae, redness in throat, increased susceptibility to infection.
  • Hyperkeratosis may be seen.
  • Heavily cornified squamous epithelial cells on cytology.

Question 58

What sort of damage can occur to the crop with improper feeding?

What are the sequelae to these wounds?

How should the crop be closed surgically?

Answer 58

• Crop trauma, burns, and fistulae.
  
  • Improper hand feeding or tube feeding.
  • Food can leak into SQ tissue.
  • Cellulitis can occur around the pharynx or SQ space.
  • Thermal burns progress from edema to necrosis.
    
    • Results in fistula.
    • May progress to endotoxemia.
  • Up to 50% crop wall can be dissected without significant impact.
    
    • Crop and skin should be closed separately.

Question 59

What avian species are commonly affected by hepatic lipidosis?

Is this typically associated with anorexia?

What are the typical clinical findings?

How is this treated?

Answer 59

• Hepatic lipidosis.
  
  • Excessive fat between liver cells.
  • Budgies, amazon parrots.
  • Not usually associated with anorexia (unlike cats).
  • Typically chronic, low-grade liver dz.
  • Polyuria, hypoproteinemia, elevated AST and bile acids, enlarged liver, lipemia, normal CBC, overgrown beak, coagulopathies.
  • Dx with liver biopsy.
  • Tx low-fat, balanced diet.
    
    • Gradually change diet over 3-4 wks.
    • Adding L-carnitine for otherwise appropriate diet may be required.
    • Silymarin/antioxidants.

Question 60

What avian species are commonly affected by iron storage disease?

What organs are most commonly affected?

How is this disease definitively diagnosed?

How can this disease be managed?

Answer 60

• Hemochromatosis
  
  • Iron storage disease.
  • Deposition of iron-containing pigments into viscera.
  • Originally believed to be assoc with excessive dietary iron, now attributed to the bird’s inability to process generally acceptable levels of dietary iron.
    
    • Mynahs, toucans, birds of paradise, tanagers.
    • Rarely psittacines.
  • Liver primary target.
    
    • In mynahs – more chronic, heart and liver failure resulting in ascited and pulmonary edema.
  • Resp distress, abdominal swelling common in generalized cases.
  • Toucans – acute presentation, found dead.
  • Hematology usually unremarkable.
    
    • Even with severe organ damage.
  • Serum iron, iron binding capacity, serum ferritin, and other blood tests of questionable usefulness.
  • Definitive dx liver biopsy.
    
    • Hepatic iron levels also diagnostic.
  • Clinical improvement may be seen with dietary iron restriction and phlebotomy.
    
    • Weekly removal of 1% body wt of blood (1 mL/100 g) until resolution of CS and then monthly.
    • Deferoxamine – iron binding agent may slow iron absorption.
    • Px for long-term survival guarded.
    • In predisposed spp, low iron diets highly recommended with iron content of the food product < 150 ppm.
    • Citric acid enhances iron absorption, limit citrus fruit.

Question 61

Aflatoxins are produced by what organisms?

What clinical signs are typically seen?

How lesions are present histologically?

How is this disease managed?

Answer 61

• Aflatoxicosis.
  
  • Biologically active mycotoxins.
    
    • Liver toxicity.
  • Toxins occur in animal feeds, corn, cottonseed, peanuts.
    
    • Increase during drought or insect damage facilitating invasion of aspergillus flavus and A. parasiticus.
  • Acute – hepatitis, icterus, hemorrhage, death.
  • Pets – chronic more common.
    
    • Subtle signs i.e. cachexia, anorexia, wt loss, biliverdinuria.
    • Suppression of CMI, reduced phagocytosis, depressed complement and interferon production.
  • Histo – acute centrilobular necrosis or mild inflammation/fibrosis.
  • Tx – removing source of aflatoxin, supportive care, liver protectants, control secondary infections.

Question 62

What avian species is suceptble to acute pancreatic necrosis?

What are the typical clinical signs?

What clinicopathologic findings are observed?

Answer 62

• Acute pancreatic necrosis.
  
  • Obese quaker (monk) parrots appear particularly susceptible.
  • Cause unknown, improvement in nutrition has reduced incidence.
  • Severe depression, anorexia, polyuria, diarrhea, vomiting.
  • WBC and amylase usually elevated, glucose may be very high as well.
  • Usually die within few days of signs.

Question 63

How common is exocrine pancreatic insufficiency in birds?

What are the typical clinical signs?

How can this disease be diagnosed?

Answer 63

• Pancreatic exocrine insufficiency.
  
  • Rare in birds.
  • CS – polyphagia, wt loss, pale bulky droppings.
  • Feces can be mixed with iodine to determine if there is undigested starch present.
  • Amylase may be normal in these cases.
  • Tx using pancreatic enzymes to predigest food may improve signs.
  • May spontaneously resolve.