Avian Parasitology

Question 1

What is the tracheal worm of Galliformes?

Answer 1

Syngamus tracheae

Question 2

What phylum are coccidian parasites in?

What three families of coccidian parasites affect birds?

Describe the effects of cryptosporidium in birds.

What is their lifecycle like?

What tissue tropism do these parasites have and what clinical signs result?

What are the four cryposporidium species that affect birds, what taxa to they affect, and what is their tissue tropism?

Answer 2

• Coccidia – single celled eukaryotic parasite
  
  • Phylum Apicomplexan
  • Characterized by apicomplast
  • Includes cryptosporidiidae, eimeriidae, and sarcocystiidae
• Cryptosporidiidae
  
  • Develop on apical surface of GI, respiratory, and urinary epithelium
  • Direct life cycles
  • Spores very stable in environment
  • Gastric vs enteric vs urinary vs respiratory tropism
    
    • Gastric – clinical signs usually decreased appetite, weight loss, chronic vomiting
    • Enteric – clinical signs usually weight loss and diarrhea
    • Urinary – can cause renal failure and gout
    • Respiratory – can cause respiratory distress, otitis, ocular disease
  • Some highly host specific while others broad host range
    
    • C. meleagridis – broadest host range, usually infects turkeys, enterotropic

Question 3

What are the three genera of eimeriid parasites that affect birds?

What is their typical lifecyle?

Describe the oocysts of caryospora, eimeria, & isospora.

What avian species are typically affected by caryospora? What clinical signs are present and how is this disease controlled?

How does eimeria typically present in birds? Give some example Eimeria species. What demographic is most susceptible?

How does Eimeria present in waterfowl? What Eimeria species do this?

How does Eimeria present in cranes? What species of Eimeria do this?

What species of isospora have extraintestinal stages in passerines?

Answer 3

• Eimeriidae
  
  • Clinically relevant genera – Caryospora, Eimeria, Isospora
  • Typically direct life cycle but can have facultative indirect life cycle
  • Caryospora
    
    • Oocysts – single sporocyst with 8 sporozoites
    • Carnivorous birds are definitive host with replication in the intestines
    • Direct and indirect life cycle possible
    • Causes enteritis in host
    • Management – disinfect, quarantine, feed prey free of caryospora
  • Eimeria
    
    • Direct life cycles
    • Oocysts – 4 sporocysts with 2 sporozoites each
    • Most species infect intestine but some species infect renal tubular epithelium
      
      • Cranes – disseminated visceral coccidiosis
        
        • E. reichenowi and E. gruis
        • Weakness, lethargy, oral granuloma, disseminated granulomas
          
          • Liver commonly affected organ
        • Oocysts produced in lungs and intestines
        • Oocysts disseminated via monocytes and can be seen on blood smear
    • Management – quarantine and disinfection
    • Often host specific
    • Intestinal tropic species – tend to cause more disease in young or compromised birds
  • Isospora
    
    • 2 sporocysts with 4 sporozoites each
    • Direct life cycle
    • Most replicate in intestinal epithelium but some have extraintestinal stages
      
      • Atoxoplasma in passerines – extraintestinal stage
        
        • Mononuclear leukocytes disseminate parasite
        • Lungs and liver most commonly affected
        • Fecal oral spread but arthropod vector also possible
        • Can cause significant mortality  Bali mynah

Question 4

What parasites in the family sarcocystiidae affect birds?

What do these oocysts look like?

What types of animals are the definitive hosts?

How do lesions differ between the definitive host and the intermediate host?

What two species of sarcocystis affect birds? What is their definitive host? What species are commonly affected?

What avian species typically show clincial disease with toxoplasma?

What avian species typically show disease with Neospora? What species are more resistant?

Answer 4

• Sarcocystiidae
  
  • Indirect life cycles
  • 2 sporocysts and 4 sporozoites
  • Carnivorous or omnivorous vertebrates are definitive hosts
    
    • Replication in intestines
    • Causes enteritis
  • Prey animals are intermediate hosts
    
    • Initial stages replicate in blood vessels and develop sarcocysts in tissue
      
      • Muscle common site
  • Management – separate definitive host and feces from intermediate hosts
  • Toxoplasma gondii
    
    • Facultatively indirect life cycle
    • Zoonotic
    • Cats are definitive hosts
    • Pigeons and canaries often exhibit clinical disease
      
      • Can resemble disseminated isosporosis of passerines
  • Neospora
    
    • Facultatively indirect life cycle
    • Quail resistant to infection
    • Can affect other bird species such as pigeons, wild parrots, passerines

Question 5

How are coccidial diseases diagnosed in birds?

What time of day is best to collect a fecal sample?

What additional testing may be used for Cryptosporidium or Isospora?

What makes diagnosis of Sarcocystiss challenging?

What treatments are used for Eimeriidae or Sarcocystiidae parasites?

What about Cryptosporidium?

Answer 5

• Diagnosis of coccidial disease
  
  • Fecal float – good screening test for enteric coccidia
  • Afternoon fecal samples are best  circadian shedding
  • Cryptosporidium – acid fast positive, stain may increase detection
  • Gastrotropic cryptosporidium – gastric wash preferred over fecal
  • Toxoplasma, isosporosis in passerines, Eimeria in cranes – blood smear may aid detection
  • Diagnosis coccidia in indirect hosts is challenging
    
    • Necropsy
    • Sarcocysts in muscle – may see grossly but need histo to confirm
  • DNA-based methods are diagnostic of choice
    
    • PCR
• Treatment
  
  • Eimeriidae or sarcocystiidae – toltrazuril, ponazuril
    
    • Totrazuril – triazine anticoccidial drug, acts on apicoplast
  • Cryptosporidium – no drugs safe or effective for treatment
    
    • Monensin, salinomycin, alborixin, lasalocid, trifluralin, nicarbazin have shown some effect in vitro
    • Toltrazuril, spiramycin, halofuginone – used in stone curlew with C. parvum
    • Azithromycin – used in scops owl with C. baileyi

Question 6

Describe the transmission, clinical signs, and gross lesions of systemic isosporosis in passerine birds.

Answer 6

• Transmission is fecal-oral.
  
  • Asexual replication (merogony) within intestinal epithelium.
  • Followed by gametogony, fertilization, and shedding of unsporulated oocysts within feces.
  • Oocysts sporulate within environment and become infectious.
  • In species causing systemic (visceral) dz – extraintestinal meogony common within circulating MN cells and gametogeny may occur (rarely).
    
    • Circulating cells may serve as source for reinfection and shedding.
    • LC likely direct, vertical transmission suggested in some cases.
    • Potentially also insect vectors.
• Clinical Signs and Lesions:
  
  • May not show clinical signs.
  • CS – nonspecific, ruffled feathers, dyspnea, tachypnea, anorexia, hyporexia, wt loss, diarrhea, dehydration, death.
  • Juvenile and fledgling birds most susceptible.
  • Gross – splenomegaly*, foci of necrosis or inflammation in spleen and liver, thickened or dilated intestines, enlarged darkened liver, pale streaks within heart and skeletal muscle.
    
    • Darkened liver aka black spot because it can be viewed through body wall.
    • Dx – Impression smears of spleen, lung, liver may show lymphocytes and histiocytes or oval-shaped intracytoplasmic pale basophilic to eosinophilic merozoites surrounded by a colorless capsule (parasitophorous vacuole) that indents the nucleus.
  • Histo – vascular and perivascular inflammation and necrosis.
    
    • Spleen, liver, heart, lung, intestine.
    • Infected MN cells may adhere to blood vessel endothelium within lung.
    • Impression smears critical for diagnosis – difficult to see on histo.
    • Concurrent infections and stress may contribute to mortality.

Fowler 9

Question 7

How is systemic isosporosis definitively diagnosed?

Answer 7

• Gold standard – impression smears of visceral organs – spleen, liver, lung.
• May see larger single merozoites within a single parasitophorous vauole (waiting merozoite) and multiple smaller merozoites sharing a common parasitophorous vacuole (proliferative merozoites).
  
  • Merozoite within MN cells cause the characteristic appearance of indentation in the nucleus.
  • Not useful to screen live birds.
    
    • Cytology of whole blood and buffy coat smears may ID merozoites.
    • May ID organisms in feces if shed, but intermittent.
    • PCR.

Fowler 9

5 consecutive dialy fecal samples for PCR deteciton - Jaime’s paper

Question 8

Is there any seasonality to mortalities with Systemic Isosporosis?

Any physical examination abnormalities that may be identified?

What age groups are most commonly affected?

Answer 8

• 90% of birds died between Aug-Dec, seasonal
• Season had a significant effect with most deaths observed in autumn and winter
  
  • Molting occurs during that time; additional physiologic stressor - potential to suppress immunocompetence
• Most birds showed clinical signs before death. Hepatomegaly and pectoral muscle myositis
  
  • Significant correlation between liver silhouette measurement and the % of infected lymphocytes
• Most common postmortem: splenomegaly (100%), then hepatomegaly and multifocal foci in pectoral muscles and heart
• Histopath: lymphohistiocytic inflammation in organs with merozoites.
• Age predilection was seen with birds 1 - 4 years (most common 1-2 yrs) of age having the highest % mortality

Barbón, A. R., López, J., Jamriška, J., Thomasson, A., Braun, J., & Stidworthy, M. F. (2019). Clinical and pathological aspects of systemic Isospora Infection in Blue-crowned laughing thrushes (Garrulax courtoisi) at Jersey Zoo. Journal of avian medicine and surgery, 33(3), 265-277.

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Question 9

What is the effect of toltrazuril on systemic isosporosis.

Answer 9

PO toltrazuril 25 mg/kg may be effective in reducing shedding after one week (study not carried out further).

This study also suggested there may be transovarian transmission of systemic isosporosis.

Mohr, F., Betson, M., & Quintard, B. (2017). Investigation of the presence of Atoxoplasma spp. in blue-crowned laughingthrush (Dryonastes courtoisi) adults and neonates. Journal of Zoo and Wildlife Medicine, 48(1), 1-6.

Question 10

Describe the sensitivity of qPCR in detecting systemic isosporosis in passerine birds.

Answer 10

Submission of five consecutive daily samples has an diagnostic sensitivity of 0.86.

JZWM 2020. A qPCR assay and testing guideline for the molecular diagnosis of systemic isosporosis (formerly atoxoplasmosis) in passerine birds. Landolfi et al.

Question 11

Describe the morphologic characteristics of avian sprurids.

What is their typical life cycle?

Answer 11

• Spirurids – nematodes
  
  • characterized morphologically by the production of small, thick shelled, oval embryonated eggs in most genera, a variety of cuticular ornamentations in the cephalic area, lateral chords that can be large, and often an eosinophilic fluid in pseudocoelom
  • life cycle - ingested arthropod or crustacean intermediate host

Question 12

What are the characteristic features of Avian Acuariids?

What are the pathogenic genera of this family?

Where anatomically do they typically affect birds?

Answer 12

• Acuariids
  
  • characterized by cuticular cordons located in the cephalic/anterior portion or other cephalic ornamentations
  • include several of the most pathogenic spirurid genera in birds
  • usually infect the proventriculus, ventriculus, or upper digestive tract
  • Genera - Dispharynx, Echinuria, Acuaria, Streptocara

Question 13

What are the lesions typically associated with dispharynxosis in birds?

What are some secondary sequelae that may occur?

What species are typically affected?

Answer 13

• Dispharynxosis
  
  • diffuse proliferative or polypoid, adenomatous proventriculitis
  • complicated by exacerbated catabolism, aspiration pneumonia, and gastric bleeding
  • rarely associated with gastric neoplasia
  • psittacines often affected (Oceanian species especially)

Question 14

What is the target tissue of Streptocarta incognita?

What avian species are typically affected by this parasite?

Answer 14

• Streptocara incognita
  
  • Infects mucosa of ducks, swans, and flamingos
  • Target tissue – ventriculus, can infect other areas of upper GIT
  • Swans - severe necrotizing pharyngitis and esophagitis

Question 15

What avian species are typically affected by Gongylonema?

What are the lesions seen?

Answer 15

• Gongylonema
  
  • upper digestive tract disease
    
    • necrotizing stomatitis in scops owl fledglings
    • esophageal obstruction in horned owls

Question 16

What are the lesions seen with Echinuria uncinate infestation in birds?

What avian species are typically affected?

Answer 16

• Echinuria uncinate
  
  • proventricular disease in young ducks and swans
  • Lesions - proventricular thickening due to glandular hypertrophy and dilatation, parasitic granulomas

Question 17

What is the target tissue for Acuaria skrjabini infestation in birds?

What species are typically affected?

What clinical signs occur as a result of infestation?

Answer 17

• Acuaria skrjabini
  
  • targets the ventriculus in finches
  • pathogenic in passerine birds
  • burrow between the koilin and ventricular gland
  • can cause weight loss, anorexia, diarrhea, and ventriculitis, with koilin degeneration and thickening, ulceration, hemorrhage, secondary bacterial and fungal infections

Question 18

What are the clinical signs of Procyrnea species in birds?

What avian species are commonly affected?

What clinical signs and lesions occur as a result of infestation?

Answer 18

• Procyrnea spp. (Habronematidae)
  
  • pathogenic in passerine birds, can also affect nonpasserine species such as woodpeckers and toucans
  • burrow between the koilin and ventricular gland
  • can cause weight loss, anorexia, diarrhea, and ventriculitis, with koilin degeneration and thickening, ulceration, hemorrhage, secondary bacterial and fungal infections

Question 19

What are three genera of pathogenic tetramerids in birds?

What tissue do they typiclaly affect?

What clincial signs and lesions occur as a result?

Answer 19

• Tetramerids
  
  • Sexual dimorphism
  • numerous species in the genera Tetrameres and Microtetrameres, as well as a few species of Geopetitia (in particular, G. aspiculata) can cause disease
  • infect the proventriculus of wide range of avian hosts
    
    • Geopetitia - also targets esophagus and ventriculus
  • Tetrameres and Microtetrameres - burrow within lumen of proventricular glands
  • Geopetitia - encysts on the serosal surfaces
  • Can cause anorexia, weight loss, diarrhea anemia, and proventriculitis
  • Lesions - raised, red foci in the proventricular mucosa that may resemble hemorrhage

Question 20

What nematodes commonly affect the ocular adnexa of birds?

What sites do they infest and what lesions do they produce?

Answer 20

• Oxyspirura, Thelazia, and Ceratospirura (family Thelaziidae)
  
  • target conjunctival sac, eyelid, Harderian gland, nasolacrimal duct
  • cause mainly conjunctivitis, corneal opacity or ulceration, and Harderian adenitis

Question 21

How are filarid parasites transmitted?

What are three genera that produce disease in birds?

What are the lesions associated with Sarconema eurycerca?

What are teh lesions associated with Pelecitus? What species are commonly affected by this parasite?

What are the lesions and clincal signs are typically associated with Chandlerella quiscali? What species are commonly affected by this parasite?

Answer 21

• Filarids
  
  • transmitted by hematophagous arthropods
  • most nonpathogenic
  • onchocercids Sarconema, Pelecitus, Chandlerella, and Paronchocerca have been associated with disease
    
    • Sarconema eurycerca - myocarditis, vasculitis, fibrinoid necrosis, and hemorrhagic tracts in the heart with intralesional adult filarids and microfilariae
    • Pelecitus - causes inflammation of periarticular soft tissues in psittacine birds and toucans
    • Chandlerella quiscali
      
      • widely distributed in common grackles and other passerine birds
        
        • adults live in the cerebral pachymeninges
      • emus – can cause torticollis and ataxia due to encephalitis
      • granulomatous encephalomyelitis due to this parasite reported in a northern crested caracara

Question 22

What are the air sac parasites of birds?

What are three species of Serratospiculum and where do they occur?

What are the most common clinical signs and lesions?

How are these diagnosed and treated?

Answer 22

• Diplotriaenoid spirurids
  
  • air sac parasites
  • adults produce ova with fully differentiated first-stage larvae in air sacs  ova coughed up and swallowed
  • intermediate host often arthropods
  • Serratospiculum - main diplotriaenoid of birds
    
    • affects mostly falcons, but also other raptors and crows
    • S. tendo - usual species in Europe
    • S. seurati - Middle East
    • Serratospiculoides amaculata – USA
  • Most common signs - dyspnea and reduced fitness on flight
  • Causes air sacculitis and hyperplasia, may cause pneumonia as well
  • Tx - melarsomine and ivermectin
  • Diagnosis – fecal exam

Question 23

What are the three parasites that produce hemosporidiosis in birds?

What is their typical life cycle?

What avian species are susceptible?

What is the geography of infection?

What is the morbidity and mortality associated with these species?

Is there a seasonality to infestation?

What are the typical signs?

How are the three parasites transmitted?

What lesions typiclaly occur?

How is this parasite controlled?

Answer 23

Hemosporidiosis

• Etiology: PROTOZOAN. Plasmodium, Haemoproteus, Leucocytozoon
• Synonym: Avian malaria
• Life Cycle: Insect-sporozoites in salivary gland, invade tissues of bird 1, reproduce to merozoites, go to blood. Vector 2 bites bird 1, sexual reproduction in vector’s midgut; oocysts rupture in salivary gland, infect bird 2
• Susceptible Species: Numerous. Many are carriers.
• Geography: Depends on habitiat preference of birds and vectors.
• Morbidity & Mortality: Infection common, morb.mort not as common.
• Seasonality: Absolutely-onset of warm weather (maybe year round in warm places)
• Clinical Signs: Emaciation, loss of appetite, resp difficulty, weakness, lameness. Anemia. Some are carriers and have no clinical signs.
• Transmission: Vector-borne
  
  • Haemoproteus ceratopogonidae (culicoides aka biting midge or no-see-ums), hippoboscidae
  • Plasmodium: culicidae (culex, aedes; aka mosquitoes)
  • Leucocytozoan: simulidae (black flies)
• Pathology: Hepato/splenomegaly, thin watery blood. Hemosiderosis (haemoproteus and plasmodium only)
• Diagnosis: Blood smear examination. Leucocytozoon cause dramatic changes in cell shape. In turkeys-pectoral muscles look like sarcocystis (white streaks and bloody spots). Plasmodium: must see schizonts in cells.
• Control: Reduce vector populations.

Question 24

Compare and contrast the appearance of the three avian hemosporidia on blood smear.

Answer 24

Question 25

What is the etiologic agent of Trichomoniasis? What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 25

**Trichomoniasis** * Etiology: PROTOZOAN. *Trichomonas gallinae* * Synonyms: Canker (doves and pigeons), **frounce (raptors)** * Life Cycle: Direct. * Susceptible Species: Young doves, pigeons (80-90% affected) due to pigeon 'milk' during feeding. Raptors. Some song birds. Turkeys and chickens too. * Geography: Wherever pigeons are. The U.S. got it from imported pigeons/doves. * Morbidity & Mortality: Most no M/M. Morb 4% mortality 3% with respiratory and intestinal infection in ducklings to four weeks old. * Seasonality: Year-round but concentration in late spring/summer, fall. * Clinical Signs: Asymptomatic in most. Fatal in some 4-18 days after infection. Wt. loss, listless, ruffle, caseous material from beak, eyes, nares. Face appears puffy and distended. * Transmission: Oral to oral. Direct. * Pathology: Cream yellow spots on oral mucosa. These can progress to be masses that block the upper GI. Can penetrate tissue. * Diagnosis: Fresh (within 30-60 minutes) oesophageal smear, infraorbital sinus exudate or GI contents: isotonic saline for highly motile protozoa with undulating membrane and flagella. Staining (Liu's method). Pear shaped, 12-20µm by 8-12µm, with nucleus, four anterior flagellae, backward-directed trailing flagellum, a pelta, clearly visible axostyle, and an undulating membrane

Question 26

What are the etiologic agents of intestinal coccidiosis in avian species? What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 26

**Instestinal coccidiois** * PROTOZOAN. Coccidia: *Eimeria sp* (herbivores mostly), Isospora in carnivores * Coccidiosis, coccidiasis. * Complex, but direct. 1-2 wk life cycle. Oocysts shed in feces, become infective in environment. Ingestion. Invade intestines. * Not a big problem with free ranging birds. Sandhill cranes: DVC (disseminated visceral coccidiosis) occurs from normal flora. Lesser scaup (females): *E. aythyae*. * Worldwide. * Variable. Dose dependent. Host dependent. * None. * Not reported from free ranging. Captive: inactivity, anemia, wt. Loss, unthrifty, watery diarrhea-greenish and bloody. * Feco-oral. * Variable. Hemorrhagic gastroenteritis. Dry crust on internal mucosa. DVC: \<5mm light granulomas esophagus, but really any surface, Light patches on heart and liver. * Fecal not worthwhile (disease develops before large numbers of cysts are in feces). * Cocciodiostats. Good hygiene. * Self-limiting usually.

Question 27

What is the etiologic agent of renal coccidiosis in birds? What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 27

**Renal coccidiosis** * PROTOZOAN. Coccidia: Eimeria sp. esp ***E. truncata*** * Same * Matures and reproduces in the kidney only and in the cloaca at the junction of the ureters. Unk how they get to the kidney. * All ducks. Most asymptomatic. * Worldwide. * Mort in geese, eider ducklings and cormorants * During dense aggregation: breeding, feeding. * None * Feco-oral. * Emaciation. Renomegaly: pale with white foci. * Histopathology.

Question 28

What is the etiologic agent of rice breast disease? What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 28

**Sarcocystis** * PROTOZOAN. *Sarcocystis rileyi* * Rice breast disease, sarcosporidiosis * Indirect. Paratenic host (bird)=sporozoites, merozoites. Definitive host: carnivore. * Dabbling ducks, wading birds. Grackles. * No. Amer. So. Africa. Australia, Canada, Mexico. * Mort rare in waterfowl. * Year-round, observed during hunting season. * Usually none. Severe: loss of muscle=weakness, lameness, paralysis * Feco-oral. * Grains of rice running in parallel streaks in the muscle tissue, usually breast, +/-cardiac * Lesions. Histo.

Question 29

What are the Eustrongyloides species that affect birds? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 29

**Eustrongylidosis** * *NEMATODE. Eustrongyloides tubifex, E. ignotus, E. excisus* * Verminous peritonitis. * Indirect. 2 intermediates required. L1-feces of bird. Eaten by oligochaete worms become L2, L3. Fish eat, become L4. Then get consumed by fish, birds, reptiles, amphs. * Wading birds (young) most common: herons, egrets, loons, cormorants. Birds of prey. * US species: *Eustrongyloides tubifex, E. ignotus* others worldwide * Infection common in some regions, occasional epizootics fish-eating birds * Year-round. Morts in spring/summer (young birds) * Variable. Dysphagia, dyspnea, anorexia. * Oral ingestion of intermediate host. * Tortuous raised tunnels on serosa of GI. Fibrinoperitonitis. Large worms: 151mm. * Lesions. Speciation of worms. * Difficult. Fish and worms infected \>1yr. * Penetrate ventriculus within 3-5 hrs of ingestion. Shed10-17 days post infection. * Gastritis and intestinal perforation by consuming uncooked fish with larvae.

Question 30

What are the two tracheal worms that infest birds? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 30

**Tracheal worms** * *Cyathostoma bronchialis, Syngamus trachea* * Gape worm, syngamiasis, gapes. * Indirect: Adults in trachea, eggs in GI, then feces or vomitted. Invertebrates eat eggs: slugs, earthworms, snails, fly larvae. Consumed, penetrate GI, get into bloodstream (then travel this way to lungs). * Ducks, geese, swans: *Cyathostoma bronchialis*. Land birds: *Syngamus trachea.* Starlings. * Worldwide. More common in UK. * Not commonly reported in free rangin g US birds. Morb 80% mort 20% in goslings has been reported * Year-round. * None usually. Smaller birds have narrower tracheas, may see resp signs. Coughing. Anemia. * Ingestion of intermediate host. * Worms in trachea. * ID worm. Classic "Y" shape: male and female attacehd permanently. * Not feasible. * Live 3.5 years in inverts. * None.

Question 31

What is the heartworm of anseriform birds? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 31

**Heartworm: swans and geese** * NEMATODE. *Sarconema eurycerca.* * Filarial heartworm, sarconema * Indirect: microfilarids in bloodstream of bird, biting louse feeds on bird, L1,L2, L3 develop here. Louse bites other bird, L3 infects go to myocardium. * Swan, geese. * Wherever the birds are. * Prevalence of infection with microfilariae has been reported as high as 22.4%. Low mortality. * Highest on breeding grounds. * Usually none. Other disease may debilitate. * Vector: biting louse: *Trinoton anserinum.* * Heart may be enlarged.Thread like worms under epicardium. * Lesions. Speciation of worms.

Question 32

What are the nematodes that infest the gizzard of birds? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 32

**Gizzard worms** * NEMATODE. *Amidostomum sp. a*nd *Epomidiostomum sp.* * Stomach worm, ventricular nematodiasis. * Direct. L0-L1 in environment (molt to L2, L3 in 24-72h). Ingestion, burrow to gizzard--become become adult. Some indirect--but not really discussed. * Ducks, **geese**, swans, coots, grebes, pigeons. Canvasback ducks hi % infection. * None reported. * Infection common. Hi % infection but mort is low * None * None in most. Poor growth. Interferes with digestion-emaciation. * Oral ingestion. * Gizzard lining sloughs, hemorrhagic, worms in denuded surfaces. * Fecal examination. Histopathology.

Question 33

Describe the effects of acanthocephalan infestation on birds. ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 33

**Acanthocephaliasis** * THORNY HEADED WORMS Phylum-acanthocephala * Thorny-headed worms. * Indirect. Intermediate hosts: crustaceans (amphipods, isopods, decapods). Fish, snakes, frogs: paratenic host. * Ducks, geese, swan (esp cygnets), passerine birds. * Worldwide * Sometimes epizootics; may cause high mortality * Year-round. * Lethargy, non-specific. * Oral ingestion of host. * White nodules on serosal surfaces. Intestinal mucosa has white to orange colored parasites firmly attached. * Fecal exams-not definitive but indicative. ID organism.

Question 34

What are the nasal leeches that affect ducks? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 34

**Nasal leeches** * *Theromyzon sp.* * Duck leeches * Puddle ducks, swans. Diving ducks. * Northern areas (north of 30th parallel)-coldwater adapted. * Spring/summer * Leeches on eyes or nares. Head shaking. Labored breathing. * Direct. * Ocular damage. Nasal passages blocked by engorged leeches. Extensive damage to nasal lining. * 10-45mm long. Amber or olive. 4 pairs of eyes. * Tough to control --they are also a food item of many species so controlling them can be damaging.

Question 35

What is the etiologic agent of histomoniasis? ## Footnote What is the life cycle? What are the susceptible avian species? Where geographically is this parasite located? What is the morbidity and mortality? Is there seasonality to this parasite? What are the clinical signs? How is this parasite transmitted? What is the associated pathology? How is this parasite diagnosed? What prevention or treatment is available? Are there any human issues?

Answer 35

**Histomoniasis** * PROTOZOAN Histomonas meleagridis * Blackhead (reduced hemoglobin=cyanosis) * Cecal worm: *heterakis gallinarum* (nematode) is the vector. Earthworms can carry the cecal worm larvae, but don't have to * Gallinaceous birds (grouse, chicken, partridge). Geese and wild turkeys too. * Lethargy, unthrifty. Sulfur yellow feces * Chickens are carriers of the cecal worm. The earthworm does not have to be involved. * Don't put partridges and quail where you keep wild turkeys. Or chickens either

Question 36

What is the scientific name of the Fowl Tick? What clincial signs does it cause? What is the scientific name of the pelican louse? What about the scaley leg mite?

Answer 36

Ectoparasites * Fowl Tick – Argasidae – Affects Chickens, Causes paralysis, can cause death * Pelican louse – Piagtella * Knemidocoptes - mange

Question 37

A recent study evaluated the gastrointestinal parasites of booth managed and free-ranging birds in a zoo environment. How prevalent were parasites in the managed birds? What about the positive birds? Were parasites similar or different across teh two groups? What were the most common parasites seen?

Answer 37

Carrera-Játiva, P. D., Morgan, E. R., Barrows, M., & Wronski, T. (2018). Gastrointestinal parasites in captive and free-ranging birds and potential cross-transmission in a zoo environment. *Journal of Zoo and Wildlife Medicine*, *49*(1), 116-128. Abstract: Gastrointestinal parasites are commonly reported in wild birds, but transmission amongst avifauna in zoological settings, and between these captive birds and wild birds in surrounding areas, remains poorly understood. A survey was undertaken to investigate the occurrence of gastrointestinal parasites in captive and free-ranging birds at Bristol Zoo Gardens between May and July 2016. A total of 348 fecal samples from 32 avian species were examined using the Mini-FLOTAC flotation method. **Parasites were detected in 31% (45/145) of samples from captive birds and in 65.5% (133/203) of samples from free-ranging birds.** Parasites of captive individuals included ascarids (Heterakis spp. and other morphotypes), capillarids, oxyurids, strongyles, a trematode, and protozoans (Eimeria spp., Isospora spp., Caryospora sp., and Entamoeba spp.). Parasites of freeranging birds included ascarids (Ascaridia spp., Porrocaecum spp., and other morphotypes), capillarids, oxyurids, strongyles (Syngamus spp. and other morphotypes), cestodes (Choanotaenia spp., Hymenolepis spp., and other morphotypes), a trematode, and protozoans (Eimeria spp., Isospora spp., Entamoeba spp.). **Similar types of parasites were detected in captive and free-ranging birds, but capillarid ova morphology was similar only between closely related species, eg in corvids (captive azure-winged magpies [Cyanipica cyana] and wild jackdaws [Corvus monedula]) and between wild columbids (collared doves [Streptopelia decaocto], rock doves [Columba livia], and wood pigeons [Columba palumbus]).** The prevalence and intensity of nematodes and coccidia in birds housed outdoors did not differ statistically from species housed indoors. **Results indicate that captive and free-ranging birds may share parasites when closely related, but this would need to be confirmed by the study of adult specimens and molecular tests**. Determining which parasites are present in captive and free-ranging species in zoological parks will support the establishment of effective husbandry practices to maintain the health status of managed species. * Goals - determine presence, prevalence, and intensity of GI parasites of both captive and free-ranging birds, investigate potential cross-transmission by establishing morphological similarity between parasite ova * Captive birds - 31% positive for GI parasites * Strongyles, capillarids, and Isospora spp. common both indoor and outdoor enclosures * Free-ranging birds – 66% positive for GI parasites * Coccidia most common followed by ascarids * Captive and free-ranging birds had 6 similar parasites - capillarids, oxyurids, strongyles, Isospora spp, Eimeria spp, Entamoeba spp * Passeriformes, columbiformes, galliformes in captive and free-ranging conditions 🡪 high prevalence (\>55%) of infection * Capillarids and coccidia most prevalent * No statistical differences in prevalence or intensity of nematodes and coccidia between birds in indoor and outdoor enclosures * Substrates used in enclosures (indoor and outdoor) supported transmission of parasites * Only capillarids of corvids azure-winged magpies (captive) and jackdaws (free-ranging) showed morphological similarity suggesting parasite sharing

Question 38

A recent study investigated the gastrointestinal parasites of birds in an ornithological garden. What orders had the highest incidence of GI parasites? What parasite type was most common? What was the most common nematode type?

Answer 38

**A Cross-Sectional Survey of Gastrointestinal Parasites in an Ornithological Garden**. Salavati A, Khalilzade-Houjaqan M, Haddadmarandi M, Arabkhazaeli F, Madani SA. Journal of Avian Medicine and Surgery. 2022;36(4):380-7. Key Points: - Presence of fecal parasites was most common in Anseriformes and Galliformes - Protozoan parasites most frequent (apicomplexans - Crypto, Eimeria, Isospora; trichomonads, and histomonas) -- Flagellates were most frequently observed protozoal parasite, more likely to be found in Anseriformes; second most frequent was apicomplexans -- Eimeria were most commonly identified in Galliformes and free-ranging birds -- Eimeria and histomonas more likely to be detected in pooled samples - Most nematode eggs were strongyle type -- Most common in free-ranging Anseriformes and Pelecaniformes -- Most likely to be found in pooled samples vs individual - Multiparasitism seen in 10%, not associated with any order - Very few ectoparasites recovered Conclusions - Captivity may predispose birds in a closed aviary to parasites due to maintenance in the environment and may predispose to clinical disease with commensal organisms due to high density, stress, inadequate sanitation, or impaired preventative programs