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Parasitology > Parsitology - Lecture 16 (Protozoa) > Flashcards

Parsitology - Lecture 16 (Protozoa) Flashcards

1
Q

Discuss the breakdown of Protozoa into its basic categories

A
  • ciliates
  • amoeba
  • apicomplexa
  • flagellates

we are only gonna focus on flagellates and apicomplexa

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2
Q

When considering flagellates, what species fall under this category

A
  • Giardia
  • Tritrichomonas
  • ## lesihmania
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3
Q

When consdiering Giardia, discuss the basics

A
  • Simple life cycle: trophozoite in intestine rounds up into a cyst which is excreted into the environemnt
  • Cyst is ibfective –> fecal-oral transmission
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4
Q

Discuss the lcinical signs of Giardia

A
  • almost always asymptomatic (giardia is commonly found in healthy animals but dissease is usally in young, immunosupressed animals
  • young affected animals: malabsorption syndromel chronic diahhrea; no fever and no blood loss in feces
  • ## In ooder animals, ddiahhrea can be acute, intermittent, or chronic
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5
Q

Discuss the diagnosis of Giardia

A
  • dirrect fecal smear or diahhreic feces (both trophozoites and cysts can be detected)
  • fecal float: cysts are detected on floatation
  • ELISA SNAP test for antigen in feces
  • Diagnosis can be difficut as shedding of cysts is intermittent
  • -
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6
Q

which protozoa is seen in the image

A

oardia trophozites in fecal smear

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7
Q

What is the treatment for Giadria?

A
  • **Fenbendazole –> 3-5 days is most effectuive*
  • Metronidazole –> treatment failures are more common with this

Prevention: 1) clean up dog poop immediately 2) bathe animals oon last day to remove cysts

Giardia is not as zooonotic as once thought

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8
Q

Discuss the basics of trichomonas blagburni in cats

A
  • lives in the **large intestine ** of cats
  • Only exists in troiphozoite form –> replicates by binary fission
  • Can cause chronic large bowel diahhrea
  • Transmission is fecal oral route
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9
Q

Discuss the diagnosis of Trichomonas blagburni in cats; also diuscuss treatment and control

A
  • Diagnosis: Direct fecal smear; PCR (best method)
  • ## Treatment: Ronidazole
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10
Q

Note that I left Leishmania slides out of flashcard set

A

So check to make sure leishmania is not going to be on the exam

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11
Q

Discuss the classes in which apicomplexa is broken down into

A

Apicomplea is broken donw into two categories:
1) Coccidia –> includes Toxoplasma gondii, Neospora caninum, and Cytoisospora
2) Hemoprotozoa –> Cytauxzoon and Hepatozoon

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12
Q

Discuss the basics of apicomplexa

A
  • obligate intracelluklar parasites
  • Complex life cycles:
    - stages that invade cells are called zoites
    • sexual and asexual replication occurs

Life cycle:
- view picturre

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13
Q

Discuss toxoplasma gondii in cats and the basics

A
  • Extremely broad intermediate host range but only one definitive host
  • capable of infecting nearly any nucleated cell
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14
Q

Discuss the life cycle of Tixipolasma gondii in cats

A

1) Cats arew the definitive host: a) sexual replication occurs ion the intestinal epithelial cells. b) oocysts are produced and shed in cat feces
2) The oocyst sporuylates in the enviribment
3) The sporulated oocyst can be ingested by a variety of iintermediate hosts
4) Asexual replicationoccurs in intermediate hosts resulting in tissue cysts
5) Ingestion of bradyzoite tissue cysts results in infection

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15
Q

what are the different ways in which an animal can get infected with toxoplasma gondii

A

Three ways in which animals get ingected:
1) ingest a spoprulated oocyst
2) Ingest a bradyzoite tissue cyst
3) Transplacental transmission

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16
Q

When considering toxolpasma gondii, discuss the life cycle iin relation to the “ingestion of an oocyst” (1 of 3 modes for infection of an animal)

A

Route 1: Ingestion of an oocyst:
- oocysts are excreted by cats only
- oocysts sporulate in the enviornment
- When the sporulated oocyst can infect any mammalian or avain host

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17
Q

When considering toxolpasma gondii, discuss the life cycle iin relation to the “Ingest a bradyzoite tissue cystt” (1 of 3 modes for infection of an animal)

A

Route 2: Ingestionof a bradyzoite tissue cyst
- sporuylated oocyst is ingested –> zoites break out of the oocysts and inavde and proliferate in tissues throughout the boddy; this stage is refrrred to as the tachyzoite stage
- Tachyzoites stimulate a strong immunerepsonse (and cause clinical disease)
- The immune response forces the parasites to slow down adn encyst; this cyst is refrred to as the bradyzoite

NOTE that Tachyzoites are not infectious while bradyzoite tissue cysts are infecvtious just like the oocyst

18
Q

When considering toxolpasma gondii, discuss the life cycle iin relation to the “transplacental infection” (1 of 3 modes for infection of an animal)

A

Route 3: Transplacental infection
- fetal death
- HUmans: fetal deatH, STILL DEATH, birth defects

Main poiint is that: ONLY the tachyzoite is capable of passing through the placenta to the fetud

  • The course of infection is determined by immunity
19
Q

Discuss the differences in infection with a naive host when compared to an immune host

A
  • in short, oretty much a naive host is going to experience the infection and ewhat not but the immune host is not affected when the oocyst or bradyzoite cyst si ingested by host
20
Q

When considering a toxoplasma gondii infection, discuss how an infection by this parasite in a cat differs from that of any other ammallian host

A

For cats and any other mamallain host, the life cycle is the same

EXCEPT that sexual replication and oocyst prodyction only occurs in cat intestine

21
Q

Discuss toxoplasma gondi and specifically explain the thing about oocysts and feces

A

Immune reopsonses are good at preventing reinfection so rarely see oocyst in cat feces because cats shed for ,30 days ONCE in their luives

22
Q

Discuss the oathologic effects of toxoplasma gondii in cats

A
  • infection in cats is almost always ASYMPTOMATIC

Oocysts or tissue cysts are ingested:
- Tachyzoites develop and disperse throughout the body
- Immune system respo nds strongly –> tachyzoites are forced to form bradyzoite cysts
- Immune repsonse is usually efficient and sufficent enough to prevent any ill effects

  • Cliical signs usually develop if a cat is ummunosupressd –> immune system cant control the proliferating tachyzoites ……… this can happen either : 1) after ingestion of oocyst or bradyzoite tissue cyst 2) upon reactivation
    of tissue bradyzoite cysts
  • Clinical signs depend on where the tachyzoites establish anmf replicate, and the degree of inflammatory response:
    - commonly affect lymph noodes, liver, lung, CNS, and eye
    - Causes hemoorhage and necrosis
    - May manifest clinically as fever, weifght loss, lethargy, neurologic signs, sight abnromalities
23
Q

Discuss toxoplasma gondii in terms of diagnosis

A

Diagnosis can bevery difficult

  • Missing infomration I didnt write down but

Main point is that for a serologic diagnosis: remember that a positive titer is only evidence of past infection …………Also, presence of anitbodies ONLY tells you that the cat had been infected and harbors bradyzoite tissue cysts. Therefore, this does not confirm an active infection

Evidence of active infection via:
- demonstarte IgM titer
- Demmonstrate a four-fold or greater increase in IgG titer over time
- Clinical signs that arent attritutable to other diseases
- Positive response to treatment

24
Q

Discuss toxoplasma gondii in terms of treatment and control

A
  • Treatment of acute toxoplasmosis - “TCP” ……. called this because Trimethaprim sulfa; Clindamycin; and Pyrimethamine

There is no treatment that eliminates bradyzoites

Control: clean litter boxes daily; do not feed cats undercooked meat; yada yada yada

25
Q

Now, consider toxoplasma gondii in dogs, discuss the pathologic effects

A
  • Infection in dogs is almost always asymptomatic
  • Usually associated with pronounced imunosupression –> especially with co-infection with canine distemper virus
26
Q

Discuss the similarities and diffferent between Neospora caninum and Toxoplasma in terms of the life cycle

A

Similar life cycle to toxoplasma except:
- dogs are the only defintive hosts –> only dogs produce oocysts
- Cattle are the intermediate host
- Dogs become infected by eating tthe bradyzoite issue cyst from cattle tissues
- NOT ZOONOTIC –> no human infections have been reported

27
Q

Discuss the neospora caninum life cycle

A
  • Dog definitive host –> produces oocysts that contaminate ruminant feed/water –> cattle bradyzoite tissues cysts
  • after infection, dogs undergo tachyzoite and bradyzoite development
  • Bradyzoites can reactivate in dogs and releases tachyzoites which can transmit transplacentally –> reuslts in neonatal canine neosporosis
28
Q

Discuss the pathologic effects of neospira caninum

A

Neonatalk canine neosporosis:
- manifests between 3-9 weeks of age
- more than one puppy in the littter wil develop hind limb paralysis with hyperextension
- Muscle weakness and contracture dvelop
- Dysphagia and eventually death

  • Clinical disease can manifest at any age in dogs –> due to tachyzoites disseminating throughout the tissues
  • porgnosis is poor
  • most infections are symptomatic because the majority od dogs are seropositive
29
Q

Discuss the treatment, control, and diagnosis for neospora caninum

A
  • Diagnosis: mostly presu,tpive:
    • clincial signs anf history + positive serology (with increasing IgM or IgG titer)
    • also, oocysts are raely seen in fecal floats
    Treatment –> TCP (Trimethoprim sulfa + clindamycin + pyrimethamine

Prevention:
- prevent dogs from eating raw tissues
- prevent contamination of cattkle feed with dog feces
- do not breed bitches that have neopsorosis or have whelped pippies tha have developed neopsorsis

30
Q

Discuss Cytoisospora - Coccidiosis

A
  • intestinal coccidia; very host specific; multiple spcies in each host

Life cycle: Direct life cycle
- Dog or cat sheed oocysts into the envionmrnet in feces
- oocysts must sporulate to become infectious
- dog/cat eats a sporulated oocyst
- Asexual replicationoccurs in intestinal epithelial cells –> huge increasse in parasite nunbers
- Sexual replicationoccurs in intestinal epithelial cells
-

Can also be transmitted through a paratenic host
- sporulated oocyst are eaten by rodent
- sporozoites come out of oocysts and **encyst ** in the tissues of rodent
- rodent eaten by cat/dog

31
Q

what eggs are these from on a fecal floatation

A

Cytoisipora

32
Q

Discuss the pathologic effects and treatment of cytoisospora

A
  • Clinical signs: usually asymptomatic; in young animals, diahhrea, wieght loss, dehydrartion

Treatment: Sulfadimethoxine —> approved and labeled for coocidiosi in dogs;
Also, Trimethoprim sulfa could be siccessful

Control: good sanitation!!

33
Q

What species fall under the categoryof Hemprotozoa

A
  • Cytauxzoon
  • Babesia
  • Hepatzoon
34
Q

disuss the baiscs of tick born apicomplexans

A
  • dfinitive host = the tick; also ote that sexual replication (porduction of oocysts/sporzoites) occurs in the tick
  • Asexual reproductionoccurs in the dog or cat internmediate host –> Note that this results in th eproductionof gametes
  • Gametes are picked up by the tuck during a bloood meal –> note the fusionof gametes = sexual reproduction
35
Q

Discuss the basics of Heptazoon americanum

A
  • Emerging disease in dogs in the southern US
  • transmitted by Amblyomma maculatum
  • Life cyclk: 3 host tick
    • hosts: broad host range

Life cycle: Infection begins when dog **ingests ** an infected tick or paratenic host that ate a tick
- sexual reproduction occurs inb dog muscle and forms “onion skin” cysts and pyogranulomas
- Gamonts appear in leukocytes in peripheral blood
- Tock ingests gamonts when they feed - sexual replication and productionof oocyst occurs

36
Q

Discuss the pathogenesis of hepatozoon americanum

also discuss the lcnical signs and note about diagnosis stuff

A
  • asexual replication in dog muscle tissue

For diagnosis, note that the Gamonts in circulating leukocytes are not a reliable diagnostic technique

Diagnosis: muscle biopsy to find cysts
PCR

Treatment: meant to improve quality of life and is NOT CURATIVE; also do the TCP treatment

Prognosis: poor

Prevention: acaracides, prevent exposure to ticks
Clinical signs:
- muscle atrophy, soreniss, stifniss, and weakness
- neutrophilic leukocytosis
- mucupurulent ocular discharge
- periosteal bone proliferation

37
Q

Now, discuss Cytauxzoon species in Cats

A
  • emerging disease in cats
  • Transmiited by Amblyomma americanum
  • Life cycle: 3 host tick
    - Hosts: broad host range
    - Bobcats are reservoirs of cytauxzoon

In cats:
- cat is bitten by infected Amyblomma americanum
- Aexual reproduction begins with endothelial associated macrophages which fomr huge schizonts –> causes clinical disease
- Pirplasms invade erytrhocytes
- Ticks pick up parasites from infected cat amd devlopment of oocyst occurs in ticks (definitive host)ly the erythrocytic stage (piroplasm) is transmitted and no schizonts develop –> making it much less pathogenic

Note that: cats can also get this htorguh blood trans fusions, cat bites, but only the erythrocytic stage (piroplasm) is trabsnmitted and no schizonts dveelop –> much less pathogenic

38
Q

Discuss the clinical signs for cytauxzoon species

A

Cats usally get severe disease and >50 % mortality:
- high fever
- anemia, jaundice
- DIC and shock
- depression, lethargy,m anorexia, and drhydration

39
Q

Discuss the diagnosi of Cytauxzoon spp and also discuss the treatment

A

Diagnosis:
- piroplasms in blood smear
- schizonts in macrohages in splenic, lymph node or bone marrow aspirate
- PCR

40
Q

Discuss the basics of Diagnosis for tick borne apicomplexans

A
  • Serology kinda sucks ass
    • Antibodies used in serological test for prtozoa have alot of cross reactivity between protozoal infections and are NOT VERY SPECIFIC …
    • serology is ONLY infornative if you are looking at the dynamics of the titers
  • PCR is cream of the croop because it is sensitive and specific and is beocming more widely used

Parasitology (20 decks)

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