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Parasitology 3rd year > Protozoa > Flashcards

Protozoa Flashcards

1
Q

The difference between giardia cysts and trophozoites

A

Cysts

  • have 4 nuclei
  • this is the infective stage
  • found in solid feces
  • small
  • needs to be stained in order to be seen

Trophozoites

  • tear shaped
  • have 8 flagella
  • found in loose feces
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2
Q

Giardia lifecycle

A
  1. giardia are transmitted by ingesting the cyst stage in contaminated food or water. Can survive for months.
  2. excystation occurs in teh duodenum
  3. replication via longitudinal binary vision (asexual repro)
  4. Encystment occurs in the lower intestinal tract - infective cysts passed in feces
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3
Q

Giardia duodenalis
Clinical signs

Giardia spp. Clinical signs

A
  • usually none

Giardia spp. Clinical signs:
If any, they will have blunting of intestinal villi leading to malabsorption and diarrhea from damaged enterocytes

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4
Q

Giardia duodenalis

Diagnosis

A

Fecal floatation - for cysts
- use zinc sulfate for detection

ELISA

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5
Q

Giardia duodenalis

Treatment

A
  • none approved
  • fenbendazole and metronidazole used in dogs and cats
  • treat once and everyone else in the household
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6
Q

Giardia duodenalis

Control and zoonosis

A

Control

  • bathe animals
  • removal of feces
  • difficult - resistant cysts

Zoonosis
Not sure if zoonotic, but treat it like it is

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7
Q

Trichomonas blagburni
What animal gets it?
Characteristics

A
  • cats
  • pseudocysts
  • longitudinal binary fission
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8
Q

Feline trichomoniasis

Clinical signs

A

Large-bowel disease

  • age of onset ~ 9 months
  • chronic diarrhea (blood and/or mucus)
  • tenesmus
  • Flatulence
  • irritated anus
  • fecal incontinence: main complaint from clients
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9
Q

Feline trichomoniasis

Transmission

A
  • fecal-oral route

- survival outside host: needs nutrient rich substance to survive (diarrhea or water)

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10
Q

Feline trichomoniasis

Diagnosis

A
  • direct fecal smear (a fecal would kill it; also super temperature sensitive)
  • culture
  • PCR
  • colonic biopsy
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11
Q

Feline trichomoniasis

Treatment and control

A

No approved treatment

  • ronidazole: watch for neuro signs as side effects though!
  • metronidazole or tinidazole
  • keep infected cats away from other cats
  • no litter box sharing
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12
Q

How to tell giardia trophozoites from tritchomonas trophozoites

A

Giardia move gracefully while tritrichomonas is spastic and unorganized

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13
Q

Name 3 non-pathogenic trichomonads

A
  1. Pentatrichomonas hominis - found in cecum and colon of mammals
  2. Tritrichomonas canistomae and T. Felistomae - found in the mouths of dogs and cats
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14
Q

Trypanosomes

  • in what species are they found?
  • how are they transmitted?
  • what does it cause/
A
  • found in blood and tissues of vertebrates
  • transmitted by blood feeding arthropods (ie flies)
  • mostly non pathogenic
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15
Q

Trypanosoma cruzi

  • what disease does it cause?
  • who is the DH
  • who are reservoir hosts
  • what vector does it use
  • where is it found
A
  • causes American Trypanosomiasis in dogs and cats; causes Chagas disease in humans
  • main DH: opossums and racoons
  • reservoir hosts/spills over into dogs, cats and armadillos
  • uses the reduviid bug (kissing bug) as a vector
  • found in Mexico, central and south america; rare in the US
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16
Q

Trypanosoma cruzi

Morphology

A

Uses a trypomastigote for the subterminal kinetoplast

Amastigote (pseudocyst)

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17
Q

Trpanosoma cruzi

Lifecycle

A
  1. Metacyclic trypomastigotes are the infective stage; passed in feces of IH. Enter host via bite wound, scratch, etc.
  2. Trypomastigoes found in blood; enter cells of spleen, liver, lymphatics and muscle
  3. Amastigotes replicate via binary fission form clusters in pseudocysts
  4. Cells rupture and trypomastigotes remain in circulation or reinfect
  5. Transform into epimastigotes - replicate via binary fission
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18
Q

American Trypanosomiasis: Dogs
(Trypanosoma cruzi)
Clinical signs

A

Acute stage: trypomastigotes in circulating blood

Chronic stage: no longer circulating

  • congestive heart failure
  • enlarged heart
  • arrhythmia
  • lethargy
  • respiratory difficulties
  • hepatomegaly
  • anemia
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19
Q

Trypanosoma cruzi

Diagnosis

A

Serological testing

- blood smear

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20
Q

Trypanosoma cruzi

Treatment

A
  • low efficacy against chronic disease
  • harsh side effects
  • treatment over 2 - 3 months: benznidazole, ravuconazole
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21
Q

Cystoisospora and Eimeria spp (coccidia)

  • in what species are they found
  • geography
  • how many hosts
A
  • very species specifc ie stenoxenous
  • worldwide
  • monoxenous - parasitize one host (DH)
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22
Q

Difference between cystoisopera and Eimeria eggs

A

Cystoisopera
- have 2 sporocysts and 4 sporozoites each

Eimeria
- have 4 sporocysts and 2 sporozoites each

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23
Q

Name 4 cystoisopora found in dogs

A

C. Canis
C. Ohioensis
C. Burrowsi
C. Neorivolta

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24
Q

Name 2 cystoisopora found in cats

A
  1. C. Felis

2. C. Rivolta

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25
Q

Cystoisopera

Lifecycle

A
  1. Undergo schizogony in feline small intestine
  2. Undergoes gametogony (sexual reproduction) in epithelial cells of cat
  3. Unsporulated oocyst then undergoes sporogony (asexual repro) to sporulated oocyst and makes it infective
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26
Q

Cystoisopora spp

Clinical signs and pathogenicity

A
  • occassional diarrhea and death
  • enteritis, colitis, weight loss, dehydration
  • not zoonotic (species specific)
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27
Q

Prevalence of canine coccidiosis

A

Younger animals will have highest incidence of infection

Older animals serve as carriers and reservoirs

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28
Q

Cystoisopora

Control

A
  • kennel sanitation; prompt feces removal
  • disinfectants with high ammonia concentrations
  • treatl all animals
  • use steam or heat with disinfectants
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29
Q

Coccidosis treatment in dogs and cats

A 
Sulfadimethoxine
Sulfaguanidine
Furazolidone
TMS
Sulfadimethoxine/ormetoprim
Quinacrine
Amprolium
Toltrazuril
Diclazuril
Ponazuril
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30
Q

Eimeria - is it a spurious parasite?

A

Yes; usually in dogs, sometimes in cats
Spurious = pseudoparasite.

When you see this its usually bc the dog ate another animal’s poop

NOT A TRUE PARASITE OF THE DOG/CAT

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31
Q

Cryptosporidium spp.

- seen in what animals? And in what location?

A
  • C. Canis = dogs small intestine
  • C. Felis = cats small intestine
  • C. Parvum = small intestine of cows

Its species specific, have to get reinfected with same speceis for immunity to kick in

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32
Q

Cryptosporidium life cycle

A
  1. Asexual reproduction in intestine of the host (schizogony0
  2. Then the merozoites undergo gametogony
  3. Oocysts are then passed in the feces or can reinfect the same host.
  4. If oocysts are passed in the feces they will be ingested and tehn excyst sporozoites and start all over
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33
Q

Cryptosporidium spp.

Transmission

A
  • direct contact with infective oocyst in feces
  • they are very hardy and spread very easily
  • contaminated food, equipment, fomites, etc.
  • water
  • large number of oocysts excreted and require only a low infective dose
34
Q

Cryptosporidium spp.
Oocyst resistance

What does not work?

A
  1. Physical disinfection: heat, freezing, UV irridiation
  2. Chemical disinfection: industrial strength chlorine and bleach, or hydrogen peroxide (let sit for 30 min)

Things that dont work: ethanol, isopropanol, lysol, formaldehyde, betadine, etc

35
Q

Cryptosporidiosis

Clinical signs

A

most infectious subclinical

  • profuse, watery diarrhea (distinct smell)
  • anorexia, dehydration, weight loss
  • villous atrophy, enteritis
  • healthy dogs/cat infections are usually self-limiting (get better on their own in 10 - 12 days)
  • persistent infections denote underlying cause such as distemper
36
Q

Cryptosporidiosis

Diagnosis

A

can do a fecal float but they are very hard to see

  • use an acid fast stain
  • will see a ton of them at the top of your fluid
37
Q

Cryptosporidiosis

Treatment

A
  • nitazoxanide: used for humans, kinda iffy

Drugs seen in literature:

  • paromoycin
  • tylosin
  • azithromycin
38
Q

Toxoplasmosis

  • what is it caused by
  • who is the DH
  • IH?
  • how is it transmitted
A
  • Caused by toxoplasma gondii: an obligate, intracellular parasite
  • DH = felidae family
  • IH = most mammals
  • transmission:
    Acquired = ingesting infective oocysts, consumption of undercooked meat
    Congenital = transplacental
39
Q

Toxoplasma gondii

Where are the various life stages found in the host?

A
  • tachyzoites: rapidly dividing, found in liver, lungs, spleen, LN
  • bradyzoites: slowly dividing, found in heart, skeletal muscle, eye, brain
  • oocysts: found in feces of cat
40
Q

Toxoplasma gondii

Lifecycle

A
  1. Cat ingests a sporulated oocyst, or a tachyzoite (transplacental), or a bradyzoite (from an IH). If the cycle starts with an IH, they contrac the parasite thru sporulated oocysts.
  2. Parasite undergoes schizogony + gametogony in intestine or tachyzoites can migrate thru body of cat and infect anything except a RBC.
  3. If parasite went to intestine, then they will develop oocysts that will pass in feces. If tachyzoite started migrating, then they could be transported thru placenta to fetus or host immunity can develop and they will develop into bradyzoites and develop as cysts in host tissue.
41
Q

Toxoplasma gondii

What is unique about the DH and IH of this parasite?

A

Cats are the DH, but they can act as both a DH and an IH because they can form bradyzoites and if something were to eat the cat, they would become infected.

42
Q

Toxoplasma gondii

When do oocysts sporulate? What effect does this have on human control of the parasite?

A

Once released in feces, they will sporulate every 1 - 5 days.

So if you clean the litter box every day, the oocysts will not be infective and you can eliminate exposure.

43
Q

Toxoplasma gondii

Name the 3 ways a DH can become infected

A
  1. Ingesting sporulated oocysts
  2. Ingesting tissue cyst (bradyzoite)
  3. Tachyzoites (congenital - transplacentally)
44
Q

Toxoplasma gondii

How does shedding in cats work?

A
  • no confirmed oocyst shedding in clinically ill cats.
  • infected cats seroconvert 2 - 3 WEEKS after infection so by the time they are clinically ill, they have already shed their oocysts
  • cats shed ONCE in their lifetime unltess they get reinfected
45
Q

Toxoplasma gondii

Describe disease in cats

A
  • fever, anorexia, jaundice, hepatitis, pancreatitis, neuro problems, respiratory interference, death
46
Q

Toxoplasma gondii
Diagnosis
Whats important to realize about some of these tests?

A

fecal exam
Biopsy
PCR
serological tests: IFA, ELISA
- important: one positive serum sample only indicates past infection!
- a 16-fold rise in titer in serum taken 2 - 4 weeks after 1st positive indicates acute aquired infection

47
Q

Toxoplasma gondii

Treatment in cats

A
  • sulfonamide+pyrimethamine
  • clindamycin hydrochloride
  • TMS (trimethoprim-sulphonamide)
  • supportive care
48
Q

Toxoplasma gondii
Control
Zoonotic?

A
  • do not feed raw meat
  • keep cats indoors to prevent hunting

zoonotic!! Can cause neuro disease and birth defects, stillbirth

  • cook meat thoroughly (can be found in pork)
  • change litter box daily
  • wear gloves when gardening
49
Q

Neospora caninum

  • DH?
  • IH?
  • geographic distribution
  • transmission: aquired or congential?
A
  • DH = dogs and coyotes
  • IH = cattle, sheep, goats, deer, many mammals and birds
  • world wide
  • trasmission:
    Acquired = ingesting oocysts, consumption of raw meat
    Congenital = transplacental
50
Q

Neospora caninum
name its 3 Lifestages and where they are found
When do oocysts sporulate?

A
  1. Bradyzoite - found in CNS, can remain viable in dead tissue for 7 - 10 days
  2. Tachyzoite - any tissue
  3. Oocyst - sporulates within 24 hours
51
Q

Neospora caninum

Lifecycle

A
  1. Dog ingests bradyzoites and it invades intestinal epithelium
  2. Schizonts develop - schizogony occurs
  3. Merozoites released - reinvade as 2nd schizont OR gamont develops
  4. Gamonts undergo gametogony produce zygote which devlops into unsporulated oocyst which is passed in feces
  5. Oocyst picked up by IH and sporulates to allow sporozoites to invade intestinal epithelium as tachyzoites
  6. Tachyzoites encyst mainly in muscle, CNS or travel to placenta
52
Q

Neospora caninum

Describe disease in dogs

A

Most severe in congenitally infected puppies: they have limb paralysis with hind limb extenstion. But will only infect a couple pups in a litter; don’t know why.

Will have generalized disease in some pups and older dogs. Will show CNS involvement, myocarditis, hepatitis and pneumonia.

Death if untreated.

53
Q

Neopsora caninum

Diagnosis

A

Just like toxoplasma

  • fecal exam (oocysts)
  • serological exam: IFA and ELISA (rise in titer in serum taken 2 - 4 weeks after 1st titer indicates acute acquired infection)
  • biopsy
  • PCR
54
Q

Neospora caninum

Treatment

A
  • variable prognosis with treatment: better with adult dogs, nothing kills tissue cysts
  • clinical improvement unlikely if rapidly ascending paralysis present
    Adults/older puppies; TMS and pyrimethamine or clindamycin
    Puppies 9 - 13 weeks: clindamycin
55
Q

Neospora caninum

Control

A
  • limit oocyst contamination food/water
  • remove dead animals or aborted fetuses
  • do not breed bitches infected with N. Caninum
  • do not breed pups from infected bitches
  • do not feed raw meat
56
Q

Hammondia spp.

  • phylum
  • what other parasite does it look like? What is the difference?
  • what type of lifecycle does it have?
  • how is it transmitted?
A
  • Apicomplexa
  • looks JUST like neospora and toxoplasma but Hammondia is not really pathogenic
  • it has an obligatory 2 host lifecycle
  • transmitted to DH via ingested bradyzoites and transmited to IH via ingested oocysts
57
Q

Hammondia hammondi
DH?
IH?
Is it pathogenic?

A 
DH  = cats
IH = rordents, pigs, dogs

Non-pathogenic!

58
Q

Hammondia heydorni
DH?
IH?
Pathogenic?

A 
DH = dogs, coytoes
IH = catle, buffalo, sheep, moose, goats, dogs

It may cause diarrhea

59
Q

Hammondia spp

Lifecycle

A
  • no congenital transmission

DH: ingest bradyzoites

  • schizogony and gametogony in intestine
  • oocysts sporulate outside DH
  • no extraintestinal stages = no tachyzoites, no cysts

IH: ingest oocysts
- tachyzoites and bradyzoite cysts in skeletal muscle, lungs, LN, occasionally brain

60
Q

Hammondia spp.

Diagnosis

A
  • looks JUST like neospora and toxoplasma
  • fecal floatation
  • serology for neopora or toxoplasma
  • experimental PCR
61
Q 
Sarcocystis spp
Phylum?
DH?
IH?
Geography?
Transmission?
A
  • apicomplexa
  • DH: carnivore
  • IH: herbivore
  • worldwide
  • transmission: predator-prey relationship
    DH = consuming IH containing sarcocysts
    IH = ingesting food contaminated with sporocysts
62
Q

Sarcocystis spp.

Lifecycle

A
  1. Gametogony occurs in the intestine of the DH
  2. Sporocysts released in feces
  3. Schizonts form in cells of IH and will burst releasing sarcocysts in skeletal and cardiac muscle of IH.
63
Q

Sarcosporidiosis

Diagnosis and control

A
  • fecal float (sporulated sporocysts) DH
  • biopsy
  • western blot (Ab in serum or CSF)
  • PCR
  • history

Control

  • bury/incarcerate dead livestock
  • cover stored grain
  • keep carnivores out of animal housing facilities
64
Q

Cytauxzoon felis

  • phylum? What thingy under phylum is it? Not a coccidia…
  • DH?
  • IH? Vector?
  • reservoir host?
  • geography
A
  • apicomplexa. Its a piroplasm; a protozoan parasite
  • DH = domestic cats
  • IH/vector = ticks: dermacentor variabilis and Ambylyomma americanum
  • reservoir host = bobcats
  • geography: emerging disease in N. America
65
Q

Cytauxzoon felis

Epidemiology: where is it found? What season?

A
  • usually found in feral cats (access to more ticks)

- most often seen in the summer

66
Q

Cytauxzoon felis

Life cycle

A
  1. Tick feeds on infected host and ingests the piroplasm (infective stage) in RBCs
  2. Asexual development - merozoites migrate to salivary glands of tick
  3. Infected tick feeds on DH (cat). Merozoites enter macrophage, schizogony occurs in macrophages. Merozoites released when macrophage ruptures and enters RBCs where they develop into piroplasms.
67
Q

Cytauxzoon felis

What type of Transmission can occur

A

Transstadial transmission can occur. = tick can pick it up at any life stage and will pass with it as it molts and develops

68
Q

Cytauxzoon felis

Pathogenicity: 2 forms

A

Fatal form:
- fever, depression, lethargy, anorexia, jaundice, death

Non-fatal form:
- similar signs as fatal form but may also be asymptomatic and have persistent parasitemia

69
Q

Cytauxzoon felis

Which phase is most destructive?

A

Schizogenous phase most destructive

When macrophages are infected with schizonts and block blood vessels

70
Q

Cytauxzoon felis

Diagnosis and control

A

Giemsa stained blood smears
PCR
Biopsy

Control: keep cats indoors, tick control, promptly remove ticks

71
Q

Cytauzxoon felis

Treatment

A

Supportive care
Atovaquone and azithromycin
Heparin as needed

72
Q

Babesia spp.
Phylum - what thingy under phylum?
Geography
DH?

A
  • apicomplexa: invasive stage = piroplasm
  • worldwide
  • DH = dogs
73
Q

Babesia

Lifecycle

A
  1. On RBC of dog, piroplasms divide by binary fission.
  2. Piroplasm (infective stages) ingested when tick ingests RBCs
  3. Undergoes schizogony in larval tick.
  4. Experiences transstadial transmission where schizont stays with tick as it molts and undergoes 2nd generation schizogony
  5. Then undergoes gamogony to develop into a motile zygote and moves to salivary glands of the tick.
  6. Motile zygote undergoes sporogony and develops to sporulated oocyst.
  7. Sporozoites released and enter vertebrate host during blood meal.
74
Q

What forms of transmission can Babesia spp. Undergo?

A

Both transstadial and transovarial transmission:
Transstadial = motile zygote moves to salivary glands
Transovarial = motile zygote enters ovary of adult female, enters developing egg and moves into salivary glands of developing tick larva

75
Q

Name 2 species of Babesia and their vertebrate host and associated vector:

A

Babesia canis

  • vertebrate host: dogs, wolves, jackels
  • arthropod host: ixodid ticks = rhipicephalus sanguineus or dermacentor spp.

Babesia gibsoni

  • vertebrate host: canids
  • arthropod host: suspect rhipicephalus sanguineus in US
76
Q

Babesia canis
Who usually carries it?
Who exhibits clinical signs?
How is it transmitted?

A
  • adult dogs are usually the carriers with unapparent disease
  • puppies experience severe disease
  • transmitted via ticks
77
Q

Babesia gibsoni

  • who usually experiences disease?
  • where did it come from?
  • how is it transmitted?
A
  • adults and puppies get same disease, at any age
  • introduced in US in 70s -80s; endemic in Africa, Middle east, Asia
  • transmitted in US via fighting, ear cropping, tail docking, blood transfusions and transplacentally
78
Q

Babesia spp.

Clinical signs

A

Anemia, pale mm, fever, amber/brown urine, splenomegaly, thrombocytopenia

79
Q

Babesia spp

Diagnosis

A
  • blood film: piroplasms only visible if clinically ill.
  • IFA: not good; lots of false negatives/positives, titers >1:80 significant
  • PCR: will detect carriers, differentiate between species
80
Q

Babesia canis and Babesia gibsoni

Treatment

A

Babesia canis

  • no therapy required
  • relapse possible
  • imidocarb dipropionate (imizol)

Babesia gibsoni

  • azithromycin and atovaquone (combo treatment)
  • supportive care
  • relapse more likely
  • does not respond well to imidocarb dipropionate
81
Q

Giardia spp.
Hosts
Geographics
Lifecycle type - indirect or direct

A
  • hosts: mammals, birds, amphibians
  • world wide
  • direct

Parasitology 3rd year (6 decks)

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