6.6 Protists 3 Flashcards

1
Q

what cells do leukocytozoon infect

A

erythrocytes

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2
Q

what transmits leukocytozoon and to what

A

blackflies transmit it to wild and domestic birds

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3
Q

locally, which birds are highly susceptible to leukocytozoon and which are resistant

A

domestic ducks susceptible and wild ducks, especially black ducks are resistant

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4
Q

what does leukocytozoon look like on a blood smear

A

the RBC nucleus is elongated and displaced to the side; females are blue and males are punk

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5
Q

when is transmission of leukocytozoon highest and in what population

A

spring; to ducklings shortly after they hatch

may get high mortality

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6
Q

for leukocytozoon, merogony occurs in ______________, gametogony occurs in ________________ and sporogony occurs in __________________

A

domestic ducks (in the liver and spleen); domestic ducks (in RBC); blackflies

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7
Q

what cells does haemoproteus infect and in what species

A

erythrocytes of wild and domestic birds, especially birds of prey in rescues

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8
Q

with haemoproteus, what stage in the host causes pathology and which is relatively benign

A

gametogony in the erythrocytes cause no damage but merogony in the endothelium, lung, liver, spleen, kidney causes problems

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9
Q

how can we differentiate haemoproteus from leukocytozoon on a blood smear

A

leukocytozoon displaces the nucleus of the RBC to the side but haemoproteus looks like purple granular material filling the RBC

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10
Q

what transmits haemoproteus and to what

A

midges and hippoboscid flies to wild and domestic birds (especially captive birds)

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11
Q

for haemoproteus, sporogony occurs in ___________, merogony occurs in ___________ and gametogony occurs in ______________

A

midges and hippoboscid flies; wild and domestic birds (endothelium, liver, spleen, lung, kidney); wild and domestic birds (RBC)

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12
Q

what is the name of the haemosporid apicomplexan parasites

A

Leukocytozoon and haemoproteus

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13
Q

some flagellates infect _________ and some infect _____________ (areas)

A

mucosal sites; blood

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14
Q

mucosal flagellate parasites generally _______________ and have ____________ life cycles

A

form cysts; direct

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15
Q

blood borne flagellate parasites generally infect hosts (how) and have __________ life cycles

A

using vectors; complex, multi-host

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16
Q

what are the 4 major groups of flagellate protists

A

diplomonads, trichomonads, amoeboflagellates, kinetoplastids

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17
Q

give examples of the following:
- diplomonads (2)
- trichomonads (1)
- amoeboflagellates (2)
- kinetoplastids (2)

A
  • diplomonads: giardia, hexamita
  • trichomonads: trichomonas
  • ameoboflagellates: histomonas, dientamoeba
  • kinetoplastids: trypanosoma, leishmania
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18
Q

what is the site of giardia infection

A

duodenum/upper small intestine

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19
Q

what is the structure of giardia

A

8 flagella, 2 nuclei prominent ventral disk

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20
Q

the giardia cyst is a rounded up ______________ with how many nuclei

what is a cyst synonymous with, if we were talking about apicomplexan parasites

A

trophozoite (2 squished together); 4 when mature

synonymous with an oocyst, we just call it a cyst now

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21
Q

how can you ID a giardia cyst

A

the contents shrink away from the cyst wall and it has 4 nuclei when mature

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22
Q

describe giardia life cycle

A

a cyst containing 2 trophozoites is ingested -> excysts in the host releasing the 2 trophozoites -> trophozoites divide by binary fission -> dehydration in the bowel triggers encystment -> cyst passed out in the feces

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23
Q

what is the main route of giardia infection

A

fecal-oral contamination with encysted forms

24
Q

does giardia have a monoxenous or heteroxenous life cycle

A

monoxenous

25
Q

what is the main clinical sign of giardia

A

malabsorptive enteritis with foul smelling, fatty diarrhea +/- blood

26
Q

does cross-transmission of giardia between hosts occur

A

controversial

27
Q

how can we diagnose giardia

A

fecal float; IFA; trophozoites seen in diarrhea if examined in saline directly; ELISA antigen tests

28
Q

what is the primary treatment for giardia

A

metronidazole and fenbendazole; used to be a vaccine but no longer available due to limited effectiveness

29
Q

where is trichomonas found in hosts?

A

GI, urogenital organs, crop of birds

30
Q

how does trichomoniasis differ from giardia

A

no cysts formed -> direct transmission

31
Q

what is the structure of giardia

A

3-5 flagella, 1 nucleus, undulating membrane

32
Q

what is the life cycle of trichomoniasis

A

direct transmission of trophozoites -> divide by binary fission in the host

33
Q

describe the pathogenesis of trichomonas in the following species:
1) cattle
2) pigs
3) horses
4) birds

A

cattle: venereal disease (vaginitis, early abortions)

pigs: non-pathogenic

horses: infects cecum and colon

birds: severe infections of crop and esophagus (also lower GI)

34
Q

how do you diagnose trichomoniasis

A
  • direct smears looking for trophozoites
  • culture
35
Q

what bird species is highly susceptible to oral trichomoniasis and why? what does it resemble? how can we differentiate?

A

pigeons -> feed young using exfoliated crop epithelial cells (crop milk)

resembles thrush (Candida albicans) - differentiate by how easily it comes off when you try to remove it

36
Q

what is the Histomonas meleagridis life cycle

A

divides by binary fission, no cyst, transmitted within Heterakis (cecal nematode eggs) as a paratenic host

37
Q

how does histomonas work its way up the food chain

A

trophozoites ingested by Heterakis (cecal nematodes) -> escape GI and invade the ovaries and uterus -> multiplies within nematode eggs and larvae -> ingested by earth worm -> ingested by birds

38
Q

what is the life cycle of histomonas once ingested by the bird host

A

divide in the cecae -> trophozoites penetrate the mucosa -> enter blood -> go to liver -> rapid multiplication of trophozoites in the liver

39
Q

what bird species is highly susceptible to Histomonas meleagridis

40
Q

what are the lesions of Histomonas meleagridis infection (2)

A
  • edematous cecum
  • yellow-green liver necrosis and lesions
41
Q

what are the clinical signs of Histomonas meleagridis infection

A

droopiness, ruffled feathers, hanging wings

yellowish diarrhea

42
Q

how do we treat Histomonas meleagridis

A

metronidazole, management, remove soil contact, anthelmentics to remove Heterakis host

43
Q

what bird operations are most susceptible to Histomonas meleagridis infection and why

A

free-ranging due to soil contact and exposure to Heterakis (cecal nematode) which acts as the paratenic host

44
Q

what is the appearance of ciliates

A

have cilia, usually arranged in rows

45
Q

how do ciliates divide

A

binary fission; some genetic exchange by conjugation

46
Q

T/F some ciliates form cysts

47
Q

what are the two ciliate protists that cause disease in veterinary species

A

Balantidium coli and Ich multifiliis

48
Q

Balantidium coli:
- where is it located
- does it form cysts? if yes, appearance
- replication

A
  • mainly large bowel as a trophozoite
  • yes; has a curved, dense nucleus, and thick cyst wall
  • binary fission
49
Q

what species does Balantidium coli infect? is it a zoonotic risk?

A

swine; yes (ingestion of cysts)

50
Q

what are the clinical signs of Balantidium coli

how can we treat it

A
  • diarrhea
  • dysentery
  • abdominal pain
  • weight loss

Tetracyclines

51
Q

Ich multifiliis host

A
  • fish in aquaria
52
Q

what is the life cycle of Ich multifiliis

A

cysts containing tomites on the skin of the host -> tomite penetrates the skin and grows within the epithelium -> tomont encysts and divides forming tomites within the cyst -> cyst opens releasing tomites

53
Q

what is the infective form of Ich multifiliis

54
Q

where does microsporidia cause infection

A

GI tract or other MM

55
Q

what is the structure of microsporidia

A

single-celled spore with a coiled filament (extrusive tube)

56
Q

describe the microsporidia life cycle

A

spore ingested (?) by host -> infects GI tract and MM -> polar filament penetrates host cells -> asexual mitotic divison gives rise to sporoplasm -> sporoplasm divides into spores -> spores mature