Avian Parasitology Flashcards
What is the tracheal worm of Galliformes?
Syngamus tracheae
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?
- 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
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?
- 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
- Cranes – disseminated visceral coccidiosis
- 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
- Atoxoplasma in passerines – extraintestinal stage
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?
- 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
- Initial stages replicate in blood vessels and develop sarcocysts in tissue
- 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
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?
- 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
- Eimeriidae or sarcocystiidae – toltrazuril, ponazuril
Describe the transmission, clinical signs, and gross lesions of systemic isosporosis in passerine birds.
- 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
How is systemic isosporosis definitively diagnosed?
- 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
Is there any seasonality to mortalities with Systemic Isosporosis?
Any physical examination abnormalities that may be identified?
What age groups are most commonly affected?
- 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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What is the effect of toltrazuril on systemic isosporosis.
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.
Describe the sensitivity of qPCR in detecting systemic isosporosis in passerine birds.
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.
Describe the morphologic characteristics of avian sprurids.
What is their typical life cycle?
- 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
What are the characteristic features of Avian Acuariids?
What are the pathogenic genera of this family?
Where anatomically do they typically affect birds?
- 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
What are the lesions typically associated with dispharynxosis in birds?
What are some secondary sequelae that may occur?
What species are typically affected?
- 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)
What is the target tissue of Streptocarta incognita?
What avian species are typically affected by this parasite?
- 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
What avian species are typically affected by Gongylonema?
What are the lesions seen?
- Gongylonema
- upper digestive tract disease
- necrotizing stomatitis in scops owl fledglings
- esophageal obstruction in horned owls
- upper digestive tract disease
What are three genera of pathogenic tetramerids in birds?
What tissue do they typiclaly affect?
What clincial signs and lesions occur as a result?
- 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
What nematodes commonly affect the ocular adnexa of birds?
What sites do they infest and what lesions do they produce?
- Oxyspirura, Thelazia, and Ceratospirura (family Thelaziidae)
- target conjunctival sac, eyelid, Harderian gland, nasolacrimal duct
- cause mainly conjunctivitis, corneal opacity or ulceration, and Harderian adenitis
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?
- 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
- widely distributed in common grackles and other passerine birds
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?
- 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
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?
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.
Compare and contrast the appearance of the three avian hemosporidia on blood smear.
