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Parasitology > Protozoa > Flashcards

Protozoa Flashcards

1
Q

What is a Protozoa

A

A single cell eukaryotic organism

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2
Q

In terms of replication in a host how to Protozoa and worms differ

A

Protozoa can create tens of millions of oocysts just from ingesting one oocyst and in worms one ingested egg just becomes one worm

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3
Q

What Protozoa are flagellates

A

Giardia, tritrichomonas, trichomonas

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4
Q

How is giardia transmitted

A

Fecal-oral, in contaminated food or water that has cysts on or in it

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5
Q

How long is Giardia’s prepatent period

A

5-7 days

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6
Q

What type of life cycle does Giardia have

A

Direct

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7
Q

Can Giardia cysts survive in the environment and what does that mean clinically

A

No they can’t so when they are passed in the feces they are directly infective

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8
Q

What Protozoa has a trophozoite that is pear shaped/ sucking disk shape, with 2 nuclei and 2 axostyles, and 8 flagella

A

Giardia

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9
Q

Is Giardia zoonotic

A

Technically (potentially) yes but most genotypes (assemblages) are host specific so most human infections are not zoonotically acquired

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10
Q

How does Giardia cause clinical disease

A

The trophozoites adhere to the intestinal villi in the duodenum and disrupt them, shorten the microvilli, and cause enterocyte apoptosis–> malabsorption and mucoid diarrhea

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11
Q

Which is more common with Giardia, acute disease with deadly diarrhea or chronic disease with intermittent diarrhea

A

Chronic disease with intermittent diarrhea, especially in young animals

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11
Q

Which is more common with Giardia, acute disease with deadly diarrhea or chronic disease with intermittent diarrhea

A

Chronic disease with intermittent diarrhea, especially in young animals

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12
Q

What are the two best ways to diagnose Giardia

A

Zinc sulfate centrifugation to look for cysts or Fecal ELISA test

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13
Q

How do you treat for Giardia?

A

fenbendazole

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14
Q

What has a single nucleus and axostyle but has 3-5 flagella with one on the posterior end that looks like an undulating membrane

A

trichomonads

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14
Q

What has a single nucleus and axostyle but has 3-5 flagella with one on the posterior end that looks like an undulating membrane

A

trichomonads

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15
Q

What Protozoa lives in the genital tract of cattle

A

tritrichomonas foetus

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16
Q

What type of life cycle does tritrichomonas foetus have

A

direct

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17
Q

What does tritrichomonas do in cows and bulls?

A

it doesn’t cause any clinical disease in bulls and in cows it just causes abortions or pyometras as a result of the embryo dying and not being aborted

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18
Q

Will a cow positive with tritrichomonas ever be able to have a baby again

A

yes, she must go through 1 to 3 heat cycles and then she will be fertile again

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19
Q

What Protozoa May be found in a vaginal/prepuce wash

A

Tritrichomonas foetus

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20
Q

What must a cow have to be considered negative for tritrichomonas foetus

A

3 negative tests, 2 normal estrus cycles, or (bulls) be successfully bred to a virgin and she have a calf

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21
Q

Is there treatment for T.foetus

A

No just to do a breeding rest or use AI in the future and eliminate positive bulls

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22
Q

A cattery is having a problem of their cats having chronic diarrhea, what may be the cause

A

Tritrichomonas blagburni

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23
Q

What tritrichomonas is in dogs

A

Pentatrichomonas hominis

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24
Q

How many nuclei do ciliates have

A

2- a macro for vegetative function and a micro for reproduction

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25
Q

What is the replicative form and infective form of Balantidium coli and how do they replicate

A

Trophozoite is replicative, cyst is infective, and via binary fission

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26
Q

What is the biggest Protozoa

A

Balantidium coli

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27
Q

What is the host of Balantidium coli and is it zoonotic

A

Pigs and yes

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28
Q

What does an infection of Balantidium coli look like

A

Diarrhea because it invades intestinal mucosa (ciliates in it), but an animal can have large numbers of organisms with no clinical signs

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29
Q

How do you detect and prevent Balantidium coli

A

Direct fecal smear, float, or histology and try to prevent fecal contamination of water and practice good hygiene

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30
Q

Which Protozoa infects the skin, gills, and cornea of fish

A

Ichthyophthirius multifiliis

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31
Q

Which stage of Ichthyophthirius multifiliis is in the fish and which stage is released in the water

A

Trophont is attached to the skin of the fish and theront is in the water

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32
Q

What are treatments for ich and what stage of the Protozoa are they affective against

A

Increased salinity or temperature, chemical added to water, all work on theront

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33
Q

You go to a farm and find lots of ciliates in the feces of their horses and cattle. Are you going to treat these animals?

A

Not necessarily because it is normal to have commensal ciliates in the rumen and cecum in cattle and horses

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34
Q

Where is babesia found in a host and what hosts does it infect

A

In the erythrocytes of dogs especially and also horses, cattle, cats, and wildlife

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35
Q

How is babesia transmitted

A

Ticks mainly in the southeast but also blood transfusions, contaminated surgical instruments or needles, and maybe dog to dog directly (fighting)

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36
Q

What are signs of babesia

A

Hemolytic Anemia, fever, dark urine, depression, splenomegaly, and anorexia

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37
Q

Which stage of Babesia infects the red blood cell and is coming from the flea saliva

A

Sporozoites

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38
Q

Which stage of babesia is the growing stage and what is it called when they divide/what do they divide into

A

They grow as trophozoites and divide by merogony into merozoites

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39
Q

What groups of dogs have lots of Babesia

A

Greyhounds in Florida and fighting pit bulls

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40
Q

How do you diagnose Babesia

A

Via stained blood films, serology, or PCR

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41
Q

How do you treat Babesia

A

Azithromycin, Atovaquone and supportive care but it is unlikely you will completely eliminate the parasites so may need a blood donation

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42
Q

What is the best prevention of Babesia

A

In dogs isoxazolines (tick meds ex. Nexgard, bravecto) and in cattle acaricide washes

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43
Q

What are the two canine Babesia species

A

B. gibsoni (in SE not in FL) and B. canis vogeli which is most common in FL

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44
Q

What is the Babesia of cattle

A

B. bigemina

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45
Q

What causes equine piroplasmosis

A

Babesia caballi and Theileria equi

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46
Q

Can humans get Babesia from any “vet species”

A

No but it is zoonotic primary from rodent reservoir hosts

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47
Q

What Protozoa is found in cat macrophages and RBCs and has a tick vector

A

Cytauxzoon felis

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48
Q

Which state of Cytauxzoon felis is in macrophages and which in RBCs

A

The tissue stage is in macrophages and the prioplasms are in RBCs

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49
Q

What is the definitive/reservoir host for Cytauxzoon felis

A

North American bobcat, causes mild disease

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50
Q

Which tick transmits Cytauxzoon felis

A

The lonestar tick (Amblyomma americanum)

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51
Q

What is the pathogenisis of Cytauxzoon felis in cats

A

The infected phagocytes line the veins and occlude them which results in anorexia, dyspnea, lethargy, dehydration, jaundice, fever, progressing to hypothermia and coma, rapidly occurs in 5-7 days and is often fatal. Those that survive are persistently infected

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52
Q

How do you diagnose Cytauxzoon felis

A

Look for piroplasms on a blood smear or do a bone marrow or lymph node aspirate looking for infected macrophages or PCR

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53
Q

What is the TOC for Cytauxzoon felis

A

Atovaquone/azithromycin

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54
Q

What hosts is T. cruzi found in

A

in dogs, humans, raccoons, opossums, and armadillos across the south

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55
Q

What T. cruzi stage is founding the reduvid bug

A

Epimastigote

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56
Q

What stage of T. cruzi is found in the blood in an acute disease phase

A

trypomastigotes

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57
Q

What is the replicating form of T. cruzi in macrophages, cardiac, and smooth muscle cells

A

Amastigotes

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58
Q

When is peak parasitemia for T. cruzi

A

2-3 weeks

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59
Q

Will you be able to detect T. cruzi after a month of infection

A

no it would be undetectable by that point

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60
Q

What does acute T. cruzi cause

A

lymphadenopathy, fever, malaise, lethargy, splenomegaly, hepatomegaly, acute myocarditis, sudden death

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61
Q

What happens with chronic T. cruzi infection

A

Progressive myocardial degeneration

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62
Q

How do you diagnose T. cruzi

A

You can see it on a blood smear in the acute phase or for chronic phase you do serology. Also can see it on histology post-mortem (nests of amastigotes)

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63
Q

What is the treatment for T. cruzi

A

No good treatments in the US (Benznidazole but not available in the US)

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64
Q

What trypanosoma is nonpathogenic in cattle

A

trypanosoma theileri

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65
Q

What cells are Leishmania found in

A

macrophages

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66
Q

How is leishmania transmitted

A

sandflies but possible vertically and horizontally as well

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67
Q

what does leishmania cause disease in

A

dogs and humans

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68
Q

What are the clinical signs of Leishmania in dogs

A

cutaneous skin lesions, or visceral disease with chronic wasting, kidney failure, and generalized loss of body hair. Often asymptomatic infections are common and it may take months or years for dogs to show signs

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69
Q

How is Leishmania diagnosed

A

clinical signs and antibody assay like IFA or immunoassay. PCR. May also see amastigotes in smears from samples from bone marrow, lymph nodes, or affected skin.

70
Q

What is the treatment for Leishmania

A

Allopurinol but you can’t achieve a sterile cure, you can only achieve clinical remission

71
Q

What is the infective stage of coccidia

A

oocyte

72
Q

In a coccidia lifecycle what is the stage that infects cells, what is the replication stage, what is the sexual cycle, and what is the result

A

The sporozoite infects the host cells and then undergoes merogony to form merozoites, they infect new cells and initiate gametogeny (the sexual cycle)–> the micro/macrogametes undergo sexual reproduction to form the zygote which matures into the sporogony which forms oocysts

73
Q

How many coccidia oocysts can come from just one ingested oocyst and why is that concerning

A

23,040,000 oocysts, very concerning because one animal can quickly contaminate an environment

74
Q

What does the oocyst contain

A

sporozoites that are contained within sporocysts

75
Q

What are the Eimeria (coccidia) of cattle

A

Eimeria bovis and Eimeria zuernii

76
Q

What is the Eimeria life cycle location wise in a host

A

The oocysts are passed unsporulated and undergo asexual development in the small intestine and then in the cecum and colon. It has sexual stages in the cecum and colon

77
Q

What is the pre-patent period for Eimeria in cattle and will you see disease before then

A

14-21 days, and yes you will see clinical disease before the end of the pre-patent period (when they begin passing oocysts/detectable)

78
Q

When do you typically see disease in cattle from Eimeria

A

usually when there is a high infectious dose and you will see disease usually when the animal is stressed (overcrowding, unsanitary conditions, shipping, weaning, dietary changes)

79
Q

What does acute disease from Eimeria look like in cattle and who is usually infected

A

Bloody diarrhea, loss of appetite, fever, susceptible to secondary infections usually in cattle under a year. Sometimes can cause neurological signs (nervous coccidiosis or bovine winter coccidiosis)

80
Q

What does chronic Eimeria look like

A

poor preformance, reduced feed intake, unthrifty appearance, soiled rear, poor hair coats

81
Q

What Eimeria has the largest oocysts, and how many sporocysts and sporozoites

A

Bovis, has 4 sporocysts each with 2 sporozoites (just like other Eimeria)

82
Q

Why is Eimeria important in sheep and goats, what does it cause

A

it is economically important because it adds 3-4 weeks of feeding to get animals to the right weight and it causes watery diarrhea, dehydration, anemia, and rectal prolapse from straining

83
Q

What are some treatments for Eimeria

A

Lasalocid, decoquinate, monensin, amprolium (ELU in sheep and goats)

84
Q

Do horses get sick from Eimeria

A

No, most infections are silent

85
Q

What is distinct about the diagnosis of Eimeria in horses

A

they have large dark oocysts and they have globidia (macrogamonts) that are found in the small intestine

86
Q

What is the Eimeria of Camelids and what can it cause and where in the body are the macrogamonts

A

Eimeria Macusaniensis, it can range from subclinical shedding to severe enteropathy and death, you will find the macrogamonts in the small intestine

87
Q

Is Eimeria in chickens serious?

A

It can be! there can be very severe outbreaks because it has a very short direct lifecycle

88
Q

What are the clinical signs of Eimeria in chickens

A

Ruffled feathers, depressed, may have bloody diarrhea, loss in egg production, and can have mortality within hours of first signs

89
Q

How do you diagnose Eimeria in chickens

A

look for the oocysts in the mucosal surface of the ceca

90
Q

What Eimeria in chickens is the most pathogenic and what can it cause

A

Eimeria tenella and it causes bloody feces and rapid death, will see a ceca dilated with blood

91
Q

Is there a vaccine for Eimeria in chickens

A

yes but the development of immunity is dependent on reinfection and it is really only useful in chickens that live longer or are grown longer

92
Q

What are two programs used in chickens to decrease drug resistance with Eimeria

A

Shuttle- change in drug in the grow-out period
Rotation complete change of drugs

93
Q

What is a common zoonotic coccidia that is a major problem and expense in the diary industry and is zoonotic

A

cryptosporidium

94
Q

How are cryptosporidium oocysts passed and what is unique about the oocysts

A

passed sporulated and the oocysts are very thin walled and they can cause an auto-reinfection within the animal

95
Q

What are the clinical signs of cryptosporidium in cattle

A

typically in 5-15 day old calves, yellow to white putty-like feces with profuse diarrhea, depression, anorexia, abdominal pain

96
Q

What is the pre-patent period of cryptosporidium

A

3-12 days

97
Q

How do you diagnose crypto

A

flotation with sugar but oocysts are very small, can use a special stain or IFA or ELISA. You can also see the oocysts with a histopath from necropsy

98
Q

Many genotypes of protozoa are species limited? How about the crypto of cattle and its ability to spread to humans

A

Humans can be infected with C. parvum from cattle but we also have our own specific species C. hominis

99
Q

what is the treatment for cryptosporidium

A

there isn’t one, just try to reduce stress and practice good sanitation (but disinfectants aren’t effective against crypto oocysts)

100
Q

How is a Isosporoid oocyst different than Eimeriid

A

When they are fully sporulated the Isosporoid has 2 sporocysts each with 4 sporozoites while the Eimeriid has 4 sporocysts each with 2 sporozoites

101
Q

What is a common cause of piglet diarrhea and is ubiquitous in confined farrowing environments

A

Isospora suis

102
Q

What is the type of life cycle of Isospora suis, and the pre-patent period, and how long is it patent for. Are the oocysts directly infective?

A

it has a simple direct life cycle, PPP of 5-7 days and is patent for 1.5-3 weeks. Once shed the oocysts only take a day to sporulate in warm temperatures, but no they are not directly infective when they are shed in the feces

103
Q

where do the sporozoites of Isospora suis invade

A

the jejunal and ileal enterocytes

104
Q

What are the clinical signs of Isospora suis

A

Nursing pigs often affected with nonhemorrhagic diarrhea that is unresponsive to antibiotics, piglets become dehydrated and fail to gain weight

105
Q

How do you prevent Isospora suis

A

Clean the crates before farrowing (can kill oocysts with steam) and you can give Toltrazuril for prevention in piglets

106
Q

What are the signs of cryptosporidium in pigs

A

usually asymptomatic but can have nonhemorrhagic diarrhea and unthriftiness

107
Q

How does a cat get Cystoisospora

A

it ingests the oocyst either directly from environment or the monozoic cysts in the tissues of an infected prey animal (like a mouse) OR the cat can be reinfected from itself from extra intestinal cysts

108
Q

How do you diagnose Cystoisospora in a cat

A

Flotation, and they will sporulate quickly (but are passed unsporulated

109
Q

What way of infection has the shortest PPP in cystoisospora cysts

A

Ingestion of the tissue cyst

110
Q

Does age help with cystoisospora immunity

A

yes

111
Q

Does cystoisospora cause disease in the intermediate/paratenic hosts and are those hosts obligatory

A

no, only in the definite host (ex. cat or dog), and no the route of infection is primarily fecal/oral

112
Q

What is the PPP of cystoisospora when ingested fecal-oral route and what is the patent period

A

7-10 days and 1-3 weeks

113
Q

What are the large oocysts of cystoisospora in dogs

A

Isospora canis

114
Q

What cystoisospora are referred to as the ohioensis complex

A

Isospora ohioensis, I. neorivolta, I. burrowsi

115
Q

Do dogs get good immunity after cystoisospora infection

A

yes, they have good immunity to shedding the oocysts

116
Q

What does clinical cystoisospora in dogs look like

A

common in young animals however can be in stressed adults/immunosuppressed, diarrhea that is mucoid or bloody, dehydration, anemia, anorexia, vomiting, abdominal pain

117
Q

What are the cystoisospora in cats and do they get good immunity after infection

A

Isospera felis (large oocyte) and Isospera rivolta (small oocyte) and they do not get complete immunity and they can reshed oocysts if they are challenged/stressed

118
Q

What is the treatment for cystoisospora

A

in dogs only sulfadimethoxine is approved or ELU of ponazuril, diclazuril, and toltrazuril, there is no approved drug in cats

119
Q

What is the definitive and intermediate host of Toxoplasma gondii

A

Felids are the definitive host and any vertebrate is the intermediate host

120
Q

How can hosts be infected with toxoplasmosis

A

ingestion of oocysts or tissue cysts or transplacental transmission

121
Q

What form causes clinical toxoplasmosis (acute infection), is this form also responsible for transplacental transmission?

A

the tachyzoite and yes it is

122
Q

what produces toxoplasmosis oocysts

A

cats only

123
Q

What toxoplasmosis form is the slow growing/ tissue cyst form

A

the bradyzoite

124
Q

What do bradyzoites do in intermediate hosts

A

They will invade enterocytes, transform to tachyzoites, and initiate the extra-intestinal cycle

125
Q

What do bradyzoites do in cats

A

They invade enterocytes and begin first round of merogony

126
Q

In cats what is the difference in life cycle when they ingest toxoplasma tissue cysts vs. oocysts

A

With tissue cysts they undergo the enteroepithelial cycle and become oocysts (standard coccidia replication in intestine)
Ingesting oocysts they being the extra-intestinal cycle–> develop into tachyzoites then into bradyzoites then tissue cysts or back into tachyzoites and initiate the enteroepithelial cycle to form oocysts

127
Q

After ingesting the tissue cysts how long is the PPP and the patency in cats

A

PPP 4-10 days and patentcy 1-3 weeks

128
Q

Will being reinfected with Toxoplasma affect the shedding of a cat

A

they will shed fewer oocysts upon reinfection

129
Q

What causes clinical toxoplasmosis in cats

A

the extraintestinal cycle (ingested oocyst) and disease is from the tachyzoites replicating and transforming to bradyzoites and forming tissue cysts–> common to find cysts in pulmonary, cardiac, hepatic, and ocular tissues

130
Q

What are the clinical signs of toxoplasmosis in a cat

A

fever, dyspnea, icterus, ocular lesions common

131
Q

Are you likely to see toxoplasma oocysts on a fecal

A

No because there is a very short patent period

132
Q

You do antibody titers for toxoplasmosis on 2 cats, one has high IgG and one had high IgM. What do these results tell you

A

The cat with IgG was infected with toxoplasma in the past and the cat with high IgM has a recent infection of toxoplasma

133
Q

Is there an approved treatment for toxoplasmosis

A

No

134
Q

What are the best ways to prevent toxoplasmosis in a cat

A

keep them inside, don’t allow them to hunt/scavenge, don’t feed them raw/rare meats

135
Q

Name 4 ways humans get toxoplasmosis (not from cats)

A

From undercooked/raw meat (ingestion of tissue cysts), especially pork, from unwashed fruits or vegetables (ingestion of oocysts), from the soil (ex. gardening) (ingestion of oocysts), transplacentally/transfusion/transplant

136
Q

What does toxoplasmosis cause in sheep

A

abortions, stillborns or weak lambs, only if infected for the first time during pregnancy, and if lambs survive they will be born uninfected

137
Q

What are clinical signs of toxoplasmosis in dogs

A

mostly in dogs under a year of age, fever, dyspnea, diarrhea, vomiting, ocular involvement less common. Can also see neurologic signs like asymmetrical hindlimb paresis in older dogs

138
Q

Should zoos be concerned about toxoplasmosis in their monkeys

A

Definitely! Can be a very deadly disease

139
Q

What does toxoplasmosis cause when a fetus is infected early in pregnancy

A

Retinochoroiditis, intracranial calcifications, hydrocephalus

140
Q

What does toxoplasmosis cause when a fetus is infected late in pregnancy

A

eye deficiencies (retinochortitis, blindness, visual impairment), deafness

141
Q

If a woman is already seropositive for toxoplasma and gets pregnant is her baby at risk?

A

Nope! In fact that provides immunity and prevents transplacental transmission

142
Q

What can toxoplasmosis do in an immunocompromised person

A

cause encephalitis and disseminated toxoplasmosis

143
Q

What is unique about Sarcocystis life cycles

A

They have an obligate two host life cycle

144
Q

What is the definitive host for Sarcocystis

A

Canids

145
Q

Who sheds the Sarcocystis oocysts

A

The definitive host (must be carnivore or omnivore)

146
Q

Where are Sarcocystis tissue cysts found and who are they infective to

A

Tissue cysts only found in Intermediate host and are infective to the definitive hosts

147
Q

What is the PPP of Sarcocystis

A

7-14 days in definitive host

148
Q

Fill in the blank- this is in terms of sarcocystis
_______ are tissue cysts that are filled with _____, which are _______ for the definitive host

A

Sarcocysts are tissue cysts that are filled with bradyzoites which are infective for the definitive host

149
Q

How many dog and cats shed sarcocystis oocysts and how many swine, cattle, and sheep are infected

A

Only about 5% dogs and cats shed oocysts and over 50% of cattle, swine, and sheep

150
Q

Is there any pathogenesis in the definitive host of sarcocysts

A

No

151
Q

There are some cases for the Intermediate hosts where Sarcocystis can be clinically severe. What are these species

A

S. cruzi in cattle, S. tenella in sheep, and S. neurona in horses (aberrant host)

152
Q

What are the clinical signs of Sarcocystis in cattle

A

Anorexia, fever, anemia, lethargy

153
Q

Prevention of Sarcocystis

A

Don’t feed raw never frozen meat to dogs and prevent contamination of pastures and feedstuffs

154
Q

Equine Protozoal myeloencephalitis only causes clinical disease in how many horses

A

0.5-1% of horses but there is over 50% seroprevalence in some areas

155
Q

What is the causative agent of EPM

A

Sarcocystis neurona

156
Q

What is the definitive host of Sarcocystis neurona and are they the only animals to pass the oocysts

A

Virginia opossum and yes

157
Q

What are the intermediate hosts and aberrant host of Sarcocystis neurona

A

Armadillo, raccoon, skunk, and the dead-end/aberrant host is a horse

158
Q

What are the only stages of Sarcocystis neurons in a horse

A

the meronts and merozoites in the CNS, no cyst stages evident in tissue

159
Q

What are clinical signs of EPM/ sarcocystis neurona

A

focal or multifocal signs of neurological disease- dyspnea, abnormal airway function, lameness (often in hindlimbs), seizures. You will always see a progression and the most common early sign is a training problem

160
Q

What is the pathology of EPM

A

multifocal lesions in the CNS, especially in the spinal cord

161
Q

How do you diagnose EPM

A

antibody tests, a PCR test is not definitive (poor sensitivity- you can trust a positive though)

162
Q

Can you believe a negative antibody test for EPM

A

not always, if the case is acute it may be too early to see antibodies

163
Q

What is the basis for treating EPM and what do you treat with

A

Often do presumptive treatment if a horse is showing clinical signs, so diagnosis by treatment, you treat with Ponazuril, Diclazuril
Early diagnosis and treatment is the key to recovery!

164
Q

How do you prevent EPM

A

reduce access of opossums to horse feed, clean up spilled grain, keep it covered

165
Q

What is the definitive host of Neospora caninum and the intermediate host

A

dogs- DH and cattle- IH

166
Q

How is neospora caninum transmitted

A

vertically in both cattle and dogs

167
Q

what does neospora caninum cause in cattle (especially dairy cattle)

A

abortions

168
Q

What passes Neospora caninum oocysts

A

dogs

169
Q

what animal(s) will form tissue cysts of Neospora caninum

A

the IH and the DH so dogs and cattle (and sheep, goats, horses, deer, and wild canids)

170
Q

What are clinical signs of Neosporosis in dogs

A

progressive ascending paralysis, most severe in pups infected in utero

171
Q

How do you treat Neospora caninum in dogs

A

Need to treat early with Pyrimethamine, sulfonamides, and clindamycin

172
Q

What happens if a seropositive cow for neospora caninum keeps having babies

A

In the subsequent pregnancies she is less likely to abort but the calves will be born infected via vertical transmission

173
Q

What disease causes abortion storms or sporadic to clustered abortions in Dairy farms

A

Neospora caninum

Parasitology (2 decks)

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