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Parasitology 1 > 6.4 Protists 1 > Flashcards

6.4 Protists 1 Flashcards

1
Q

Protists; overview; basic body structure, movement, repro

A

*all are single‐celled, eukaryotic organisms
*ancient group of organisms
*may or may not have a sexual process
*some use flagella or cilia for locomotion

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2
Q

Parasitic Protists; general overview; where they infect; life strategies

A
  • parasitic protists infect virtually all sites in the body either intracellularly or extracellularly
  • both simple and highly complex life cycle strategies
  • some possess resistant stages to pass from host to
    host
  • others use intermediate and/or paratenic hosts to move from one definitive host to the next
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3
Q

Parasitic Protists; Major Groups (6)

A
  • Apicomplexa
    (enteric and ‘tissue’ coccidia, malaria, piroplasms)
  • flagellates
    (kinetoplastids and trichomonads)
  • ciliates
  • amoebae
  • Microsporidia
  • Myxosporidia
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4
Q

Phylum Apicomplexa; General Life Cycle

A

Oocysts containing sporozoites
> Merogony >
Meronts (=schizont) containing merozoites
> Gametogony >
Gametes
-macrogametes: female
-microgametes: male
-fuse to form a zygote
> Sporogony >
Oocysys containing sporozoites

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5
Q

Eimeriorina is a suborder of phylum:

A

Apicomplexa

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6
Q

Eimeriorina ‘True’ Coccidia; families and their members

A

Family Eimeriidae
* Eimeria, Isospora, Caryospora spp.

Family Sarcocystidae
* Sarcocystis, Toxoplasma, Neospora, Cystoisospora

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7
Q

Eimeriorina also known as

A

‘True’ Coccidia

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8
Q

Eimeriorina ‘True’ Coccidia; which are primarily enteric parasites?

A

Family Eimeriidae
* Eimeria, Isospora, Caryospora spp.

Family Sarcocystidae
* Cystoisospora

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9
Q

Eimeriorina ‘True’ Coccidia; which are primarily ‘tissue coccidia’?

A

Family Sarcocystidae
* Sarcocystis, Toxoplasma, Neospora

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10
Q

Eimeriorina; General Characteristics; where it lives, types of life cycle, site of infection

A
  • obligate intracellular parasites
  • both monoxenous (Eimeria, Cystoisospora, etc.) and heteroxenous (Toxoplasma, Sarcocystis, etc.) life cycles
  • parasites of the digestive tract of the definitive host but many other tissues of the intermediate host
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11
Q

Apicomplexan parasites; do what to host cells

A

actively penetrate host cells
-pull cell membrane around themselves, form parasitophorous vacuole

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12
Q

Eimeria spp.; develop where

A
  • intestinal development in specific vertebrates
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13
Q

Eimeria spp.; oocyst appearance

A

Sporulated oocysts have:
* sporocysts with Stieda bodies
* sporozoites with refractile bodies

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14
Q

Eimeria species ‐ Life Cycle

A

Endogenous Stages 1
* sporozoites invade epithelial cells
* merogony (=schizogony) gives rise to multinucleate meronts (=schizonts) within host cells which finally produce merozoites
* merozoites usually reinvade cells to start a second (or more) round(s) of merogony

Endogenous Stages 2
* merozoites eventually enter cells and begin gametogony (formation of gametes)
* microgamonts each give rise to many microgametes (males)
* macrogamonts give rise to a single macrogamete (female) ‐ macrogametes possess characteristic wall‐forming bodies

Endogenous Stages 3
* biflagellate microgametes (males) are motile and search out macrogametes (female) which they fertilize
* the resulting zygote is an unsporulated oocyst
* the unsporulated oocyst passes from the host in the feces to begin the cycle again

Exogenous Stages
* the unsporulated oocyst undergoes sporulation
* requires oxygen, moisture and warmth
* meiosis and then asexual division gives mature (sporulated) oocyst
* ONLY sporulated oocyst is infective to next host.

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15
Q

only form of the Eimeria life cycle that is infective to the next host

A
  • ONLY sporulated oocyst is infective to next host.
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16
Q

Eimeria species; Pathogenesis/Lesions/Clinical Signs

A
  • enteritis, may be bloody depending on species
  • inflamed, congested mucosa with mucosal sloughing in serious cases
  • villar atrophy results from death of enterocytes
  • malabsorptive diarrhea
  • decreased production parameters
    (increased water intake and reduced feed conversion efficiency)
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17
Q

Eimeria spp.; which domestic animals do they infect

A

-cattle
-sheep
-goats
-poultry
-horses

18
Q

Eimeria spp. of cattle

A

E. bovis *
E. zuernii*

E. auburnensis
E. alabamensis, etc.

19
Q

Eimeria spp. of sheep

A

E. ahsata*

E. ovina

20
Q

Eimeria spp. of goats

A

E. ninakohlyakimovae*

E. arloingi

21
Q

Eimeria spp. of poultry

A

Many Eimeria spp.*

22
Q

Eimeria spp. of horses

A

E. leukarti

23
Q

Eimeria spp of Cattle; most pathogenic and life cycle character

A
  • Eimeria bovis and E. zuernii most pathogenic
  • Life cycles have two generations of merogony followed by gametogony
  • First generation meronts are huge
24
Q

Bovine Coccidiosis in Canada; general; source of infection, who gets infected, outcomes, disease geography

A
  • environmental oocysts source of infection
  • infection of immunologically naïve animals (usually calves)
  • infected animals develop immunity to further infection (do not shed parasites)
  • distinctly different diseases in eastern Canada (e.g. Ontario) and western Canada (e.g. Saskatchewan)
25
Q

Bovine Coccidiosis in Canada; Eastern Canada; summer and winter environment, consequences

A

SUMMER
* Environment: lush, wet, warm pastures
* Host: susceptible calves on pasture
* Agent: high reproductive potential

Consequences
‐ relatively high stocking density (productive pasture)
‐ good oocyst survival (wet, warm, protected)
‐ high parasite density (good survival and many susceptible hosts in a confined area)
>Disease: Coccidiosis in naïve calves

WINTER
* Environment: confined barn environment
* Host: most calves immune now
* Agent: high reproductive potential

Consequences
‐ hosts are numerous and crowded
‐ good oocyst survival (wet, protected)
‐ low parasite density (good survival but most hosts are immune to infection)
>Disease: No Coccidiosis in immune calves

26
Q

Bovine Coccidiosis in Canada; Western Canada; summer and winter environment, consequences

A

SUMMER
* Environment: dry, hot, sparse pastures
* Host: susceptible calves on pasture
* Agent: high reproductive potential

Consequences
‐ relatively low stocking density (pasture not very productive)
‐ very poor oocyst survival (dry, hot, UV radiation)
‐ low parasite density (combination of poor survival and few susceptible hosts spread over a large and inhospitable area)
>Disease: Little or no coccidiosis in naïve calves

WINTER
* Environment: confined barn environment
* Host: most calves susceptible
* Agent: high reproductive potential

Consequences
‐ hosts are numerous and crowded
‐ good oocyst survival (wet, protected)
‐ high parasite density (good survival and most calves are susceptible to infection)
>Disease: Coccidiosis in naïve calves

27
Q

Eimeria spp of domestic poultry

A

Apicomplexa: Coccidia

In chickens
-E. acervulina
-E. maxima
-E. necatrix
-E. tenella

In turkeys
-E. adenoeides
-E. meleagrimitis

Hosts: species‐specific coccidia

28
Q

Eimeria spp of domestic poultry; site of infection

A

Site: throughout intestinal tract, species‐specific

29
Q

Eimeria spp of domestic poultry; Pathogenesis

A
  • each species infects a particular region of the intestinal tract
  • all species can be pathogenic IF sufficient numbers of oocysts are ingested by a susceptible host
  • immune status of host with respect to that particular species is a critical determining factor if animal is going to become clinically ill
30
Q

Eimeria spp of domestic poultry; Treatment/Prevention:

A
  • numerous licensed compounds
  • continual prophylactic anticoccidial usage the norm
  • management (litter) supplements prophylaxis
  • live vaccines useful for breeders/layers and being used increasingly in broiler flocks or in operations wishing “organic” (e.g. RWA) product
31
Q

Eimeria spp of domestic poultry; Anticoccidial Usage considerations

A
  • Anticoccidial resistance is a widespread problem
    -continuous and shuttle programs; within a flock
    -rotation programs; between flocks
  • Rarely are these compounds used therapeutically and most do not have label claim against these parasites for treatment
32
Q

Cystoisospora spp.; General Characteristics; who they infect, hosts, site

A
  • Infect – carnivorous/omnivorous mammals, or birds of prey
  • infections in young dogs, cats and particularly swine of regional interest
  • each Cystoisospora sp. is host‐specific
    (humans have their own species, Cystoisospora belli)
  • infect cells of the intestinal mucosa (Note: exceptions)
33
Q

Cystoisospora spp.; life cycle

A
  • unsporulated oocysts occur in feces
  • sporulation occurs to form sporulated oocysts
  • sporulated oocysts each contain 2 sporocysts with 4 sporozoites within each sporocyst
  • sporulated oocysts are infective to the next host

> ingestion and digestion of sporulated oocyst cyst
excystation
endodyogeny
merogony
gametogony
fertilization
unsporulated oocyst
sporulated oocyst (Infective)

OPTION for Cystoisospora only:
>ingestion of sporulated oocyst by paratenic host
>excystation
>sporozoites leave intestine
>monozoic cyst in extraintestinal tissue
>digestion of cyst….

34
Q

Cystoisospora spp.; sporulated oocysts each contain

A

2 sporocysts with 4 sporozoites within each sporocyst

35
Q

Cystoisospora spp.; Pathogenesis and Clinical Signs

A
  • like most coccidia, Cystoisospora spp. causes disease in young (neonatal) animals
  • direct damage to epithelial cells
    (destroyed as the parasites leave the cells after dividing)
  • immune‐mediated enteritis
  • results in diarrhea as the main clinical sign
36
Q

Cystoisospora spp.; Diagnosis

A
  • 4 species infect dogs and 2 infect cats
    ‐ these vary in their ability to cause disease
  • distinguish species on the basis of:
    a) location and cells infected in gut
    b) details of endogenous development c) size of oocyst and sporocysts within
    (Note: little clinical relevance, ID to genus only)
37
Q

Cystoisospora spp.; Treatment

A
  • usually self‐limiting disease if small numbers of oocysts caused the infection
  • control of oocyst numbers is preventative
    (surface disinfection in a timely manner – remember sporulation time)
  • watch for dehydration because of diarrhea
  • can treat with sulfa drugs (inhibit folic acid biosynthesis) or off‐label toltrazuril (Baycox )
38
Q

Cystoisospora suis; disease; when/where is it seen, PPP, sporulation time, pathogenesis

A

Neonatal coccidiosis in swine
* Almost always seen clinically in pigs less than 4 weeks of age
* PPP = 4‐6 days; sporulation time = 3‐5 days
* Destruction of villar epithelium principal cause of diarrhea – may lead to sloughing of entire epithelium
* Extensive destruction may occur during PPP

39
Q

Prepatent period

A

the period between infection with a parasite and the demonstration of the parasite in the body especially as determined by the recovery of an infective form (as oocysts or eggs) from the blood or feces.

40
Q

Cystoisospora suis; clinical signs

A
  • Clinical signs include profuse pale yellow diarrhea, failure to gain weight, runting, death

Parasitology 1 (8 decks)

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