protozoa - apicomplexans - coccidia Flashcards

1
Q

apicomplexans morphology

A

unicellular, eukaryote, organelles

apical complex: organelle at anterior end, help penetrate host cell

some have micropyle (small opening) and micropyle cap

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2
Q

Cystoisospora host

A

dogs, cats, pigs

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3
Q

Cystoisospora morphology

A

infective form = oocyte
-must be sporulated to be infective
-sporulated oocyte contains: 2 sporocysts, each sporocyst has 4 sporozoites

small, ovoid shape, no locomotion structures – glides

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4
Q

Cystoisospora source

A

-feces: fecal-oral cycle
-ingestion of sporulated oocysts from feces of infected animal, feces-contaminated food/water, infected paratenic host
-oocysts are NOT sporulated in FRESH feces (it takes hours/<1 day for sporulation to occur

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5
Q

Cystoisospora clinical signs

A

-often asymptomatic
-diarrhea: higher risk if - very young, stress, immunosuppression, other underlying disease

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6
Q

Cystoisospora pathology

A

-disease = coccidiosis
-intracellular pathogen
-invades small intestinal epithelial cells
-stunted intestinal villi –> decreased absorptive surface
-diarrhea

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7
Q

Cystoisospora diagnosis

A

-fecal float
-shed intermittently (recommend >1 test)
-identify oocysts: unsporulated in fresh, sporulated if hours old

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8
Q

what do sporulated Cystoisospora oocysts contain?

A

two sporocysts
each sporocyst contains 4 sporozoites

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9
Q

Cystoisospora treatment and prevention

A

-medication
-supportive care (hydration, nutritional support)

-good sanitation
-prophylatic treatment (swine)
-clean environment: oocysts are very resistant
steam clean, 10% ammonia solution

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10
Q

Cystoisospora zoonotic?

A

no; coccidia are species-specific

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11
Q

coccidian life cycle

A

PPP: 4-14 days
oocysts can be shed for 1-3 weeks
very resistant

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12
Q

3 phase of coccidian life cycle

A
  1. schizogony - asexual phase
  2. gamogony - sexual phase
  3. sporogony - maturation phase
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13
Q

schizogony

A

-asexual phase
-host ingests oocyst
-sporozoites exit oocyst
-infect host cell –>schizont
-multiple division –> produce merzoites
-repeated numerous times

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14
Q

gamogony

A

-sexual phase
-merozoites infect host cell and differentiate: male- micro gametocytes, female-macro gametocytes
-microgametocytes develop flagella
-fertilize macrogametocytes
-produce thick-walled oocyst

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15
Q

sporogony

A

-oocyst maturation phase
-sporocysts develop within oocyst
-sporozoites develop inside sporocysts
-takes hours/<1 day
-for most species, this is completed outside host
-once sporulation occurs, oocyst is infective

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16
Q

Eimeria host

A

species-specific, basically everything BUT cats and dogs

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17
Q

Eimeria morphology

A

-infective form = oocyst
-must be sporulated to be infective
-oocyst contains: 4 sporocysts; each sporocyst contains 2 sporozoites

everything else same as cystoisospora

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18
Q

Eimeria source and transmission

A

fecal-oral (no paratenic hosts)

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19
Q

Eimeria pathology

A

infects small intestinal epithelial cells

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20
Q

Eimeria diagnosis

A

id oocysts on fecal float

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21
Q

Eimeria treatment

A

medication
supportive care

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22
Q

Eimeria prevention

A

good sanitation
prophylactic treatment for food-producing animals (does not prevent infection but allows host to build immunity)

23
Q

Eimeria zoonotic?

A

no

24
Q

Cryptosporidium host

A

mammals, birds, reptiles, humans

25
Q

Cryptosporidium morphology

A

-infective form = oocyst
-sporulate within host (immediately infection; auto-infection possible)
-sporulated oocyst contains: NO sporocysts, 4 sporozoites
-small
-spherical to oval
-no structures for locomotion

26
Q

Cryptosporidium clinical signs

A

asymptomatic or diarrhea

27
Q

Cryptosporidium source and transmission

A

fecal-oral
paratenic host

28
Q

Cryptosporidium patho

A

infects gastric or small intestinal epithelial cells

29
Q

Cryptosporidium diagnosis

A

PCR
acid-fast stain of fecal smear
ID oocysts on fecal float (difficult bc so small)

30
Q

Cryptosporidium treatment

A

medication - non approved
supportive care

31
Q

Cryptosporidium prevention

A

good sanitation
prevent ingestion of fecal-contamined food/water

32
Q

Cryptosporidium zoonotic?

A

yes, but many are species specific

33
Q

Toxoplasma gondii host

A

definitive = cats
paratenic = mammals

34
Q

Toxoplasma gondii morphology

A

infective form = sporulated oocysts
-leaves host unsporulated
-must be sporulated to be infective (sporulates in 1-5 days)
-sporulated oocyst contains: 2 sporocysts, each sporocyst contains 4 sporozoites
-spherical shape

35
Q

Toxoplasma gondii life cycle

A

3 important life stages
1. oocysts: shed in cat feces, develop in definitive host ONLY, infective after sporulating

  1. tachyzoites: within all hosts; multiply quickly; responsible for clinical signs
  2. bradyzoites: within cysts in all hosts; multiply slowly; infective if ingested
36
Q

Toxoplasma gondii life cycle - paratenic/intermediate hosts

A

-schizogony: tachzoites – spread to tissues; bradyzoites – in tissue cysts
-no gamogony
-no sporogony

37
Q

Toxoplasma gondii life cycle - definitive host

A

-schizogony: tachyzoites – spread to tissues; bradyzoites – in tissue cysts
-gamogony (sexual)
-sporogony (oocyst sporulation)

38
Q

Toxoplasma gondii source

A

-oocysts: in feces of infect cats; fecal-contaminated water, food, soil
-tissue cysts: in tissues of infected paratenic host
-infected mother: transmitted to fetus

39
Q

Toxoplasma gondii transmission

A

-ingestion: direct ingestion of sporulated cysts; indirect ingestion of paratenic host with tissue cysts containing bradyzoites
-transplacental: infection of female during pregnancy –> tachyzoites invade placenta, fetus

40
Q

Toxoplasma gondii clinical signs

A

-diarrhea
-can disseminate via lymphatic and portal system to many organs and tissues:
brain –> encephalitis, CNS signs
lungs –> pneumonia
liver –> hepatitis
muscle –> muscle pain, stiffness
eyes –> inflammation, ocular disease
fetus –> abortion, CNS disease

41
Q

Toxoplasma gondii pathology

A

acute disease
-GI signs, diarrhea: tachyzoites multiplying in intestinal cells
-tachyzoites invade other organs and tissues

chronic phase
-bradyzoites form tissue cysts: due to immune pressure from host
-few to no clinical signs
-tissue cysts may remain for life
-if host immune system wanes: tissue cyst can rupture; bradyzoites become active tachyzoites; disease recurs

42
Q

Toxoplasma gondii diagnosis

A

-serology: measuring 2 antibody types - IgM and IgG
-fecal float: oocysts
-histopathology: biopsy - bradyzoites in tissue cysts; postmortem
-PCR

43
Q

Toxoplasma gondii treatment

A

-medication
-supportive care

44
Q

Toxoplasma gondii prevention

A

-prevent ingestion of sporulated cysts from cat feces
-prevent ingestion of bradyzoites: prevent predation, cook meat thoroughly

45
Q

Toxoplasma gondii zoonotic?

A

yes

46
Q

neospora caninum host

A

definitive - dogs
intermediate - many, like cattle, sheep, horses, goats

47
Q

neospora caninum predilection site

A

definitive host - intestinal mucosa, CNS
intermediate host - repro system, nervous system

48
Q

neospora caninum clinical signs

A

dogs: neurologic signs
cattle: major cause of abortions

49
Q

sarcocystis host

A

definitive: carnivores
intermediate: herbivore (horses, cattle, sheep, goats)

50
Q

sarcocystis predilection site

A

definitive host: GI tract
intermediate host: skeletal muscle

51
Q

sarcocystis clinical signs

A

definitive host: myostits, GI, or neurologic signs
intermediate: usually asymptomatic

exception in horse: severe neurologic disease

52
Q

hematozoon host

A

definitive: dogs
intermediate: ticks

53
Q

hematozoon clinical signs

A

musculoskeletal- periosteal bone proliferation, joint and muscle pain

chronic wasting, death