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Parasitology 2 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Coccidia related vector borne agents

Agent, disease, IH, and DH

A
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2
Q

Life Cycle of Coccidia related vector borne agents

A

* iatrogenic- blood transfusions

* transovarial transmission in ticks for Babesia spp. only

* Sporozoite is infective phase–> injected into blood stream_-> merogony phase 1 & 2–> etc.

** Asexual phase is the pathogenic phase, remain in RBCs as macro and microgametes

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3
Q

Significance of Piroplasmosis

A
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4
Q

In Australia, what are the 3 main tick vectors that impact cattle and dogs?

A

Haemaphysalis (Bush tick), Rhipicephalus microplus (Cattle tick), Rhipicephalus sanguineus (Brown dog tick)

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5
Q

Distribution of Rhipicephalus microplus (cattle tick)

A
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6
Q

Global distribution of malignant theileriosis

A
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7
Q

Distribution of benign theileriosis- T. orientalis group

A

* compared to malignant forms it has mild pathogenecity (lucky for Australia!)- not always the case as it depends on immunity

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8
Q
A

Pathogenecity of coccidia vector borne?

* Haemolytic anaemia (hypoxia, organ damage)

  • direct RBC destruction- merogony
  • indirect- anti-RBC anti-bodies- splenomegaly

* Thrombocytopaenia

  • splenic sequestration of platelets
  • auto anti-platelet antibodies
  • consumptive coagulopathy- DIC, shock

* Cytoadhesion of RBC to capillaries of brain

  • cerebral babesiosis in Babesia bovis and Babesia caballi (horses)
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9
Q

What is unique about Theileria pathogenesis?

A

* Lymphadenopathy because body is trying to replace leukocytes

* Species and strain dependent on how pathogenic

* B. gibsoni would come between B. canis & B. vogeli

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10
Q
A
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11
Q

Immunity to piroplasms

A

* why in endemic areas you wouldn’t see Babesiosis- the main issue comes from naive animals exposed to ticks from introduction to a naive herd

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12
Q

Babesiosis in cattle

A
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13
Q

Canine babesiosis – name, vector, geography, and how pathogenic?

A
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14
Q

Babesiosis in dogs (Australasia)– what are the two genera? IHs? Clinical signs? Who?

A
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15
Q

Theileriosis in cattle- genera? What does it cause?

A

* cows in late pregnancy, early calving- cows are most susceptible to clinical forms

* might just see slight production loss, subclinical

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16
Q

Ante-mortem diagnosis of piroplasmosis

A

Has this dog always been in QLD?

* Cattle: Any new introductions to the herd? (especially in a tick free zone) OR have the cattle moved?

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17
Q

Post mortem diagnosis of B. bovis?

A

Impression smear of the brain due to massive numbers- capillaries of the brain are predilection site

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18
Q
A

Lymph node aspirate Schizont of T. annulata with merozoites in monocyte

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19
Q
A

Blood smear of cow infected with T. annulata

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20
Q
A

Babesia bigemina

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21
Q
A
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22
Q
A

Brain capillaries packed with infected erythrocytes parasitised by B. bovis

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23
Q
A

Normal capillary impression smear

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24
Q
A

Babesiosis

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25
Q
A

Differentials: Toxins (hepatotoxicity), Babesia bovis, Theileria orientalis complex, Babesia bigemini, Anaplasma (2 genera)

Live Samples: Whole blood- CBC, smear, stain, serology for exposure for Babesia, urine sample, rule out Theileria by FNA of lymph nodes, clotting times- blood that fails to clot

Dead samples: capillary impression smear of the brain, clotting times- blood that fails to clot

Findings: Regenerative anaemia - 0.14- 0.22- haemoglobinaemia

Found schizonts

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26
Q

How does Imidocarb dipropionate work? What does it treat?

A

Imidocarb dipropionate treats Babesiosis

* renders animal immune for 4 weeks- as it wears off slowly- ticks bite the animal and the animal gains exposure related immunity

27
Q

Treatment of Theileriosis in Australia?

A
28
Q

Controlling Tick Fever in Australia

A
29
Q

Malaria (plasmodium) significance

A
30
Q

Malaria (Plasmodium) Life Cycle

A
31
Q

What species of Plasmodium has dormant forms? How does this impact host? What species is the malignant form?

A

* Immunosuppressed impacted by P. vivax if lay dormant

* P. falciparum- malignant, cerebral form

* black water- aka haemoglobinuria

32
Q

Malaria (Plasmodium) Control

A

* Wolbachia Sterile male release- makes the females infertile

33
Q

Haemosporidians in birds

A

* Malaria like

34
Q

What phylum are Flagellates in?

A
35
Q

For flagellates, what are cysts? Trophozoite? Promastoigote? Amastigote?

A
36
Q

Life Cycle of Giardia

What is the most likely source?

A

* Ingest a cyst–> trophozoites come out–> divide by binary fission–> colon–> form cyst wall

** most likely source– person to person OR between kid and dog OR contaminated food and water

37
Q

Significance of Giardiosis

A

Endemic * Adults- subclinical carriers– kids as well

Naive –> end up with full blown acute diarrhoea, if you’re not treated you become a subclinical carrier too

38
Q

Species of Giardia

A

Only one we need to know

39
Q

What are the two genotypes of G. duodenalis that infect humans?

A
40
Q

Pathogenesis of Giardia

A

* literally physically preventing nutrients from entering the blood stream- “carpet”

41
Q

Typical presentation of Giardia

A

Fatty, Floaty, Flatulence

42
Q

Diagnosis of Giardia, Dog in the house?

A

Treat the dog- 3 days of febantel (drontal)

* fresh faeces- fresh faecal smear

* in house SNAP test

* research purposes always use PCR- because most sensitive

43
Q

Treatment and control of Giardia

A
44
Q

Trichomonads Features

A

* Simple direct life cycle– faecal oral (close contact, wet environment), venereal transmission (not very enviornmentally resistant)

* no cysts- just live in trophozoite form

* 3-6 Flagella– one of which forms an undulating membrane

* Single nucleus

45
Q

Trichomoniosis– in humans, cattle, cats, and pigeons, doves, fowl and other birds

A
46
Q

Feline intestinal trichomoniosis

A

Relatively new pathogen of cats

* Agent- Tritrichomonas foetus

Typically:

* Large bowel diarrhoea (mucoid, tenesmus)

* Waxes and wanes

* Chronic diarrhoea (weeks) cats up to 2 years of age

* Cattery outbreaks

* Asymptomatic shedding common

47
Q

Diagnosis and treatment of feline tritrichomoniosis

What’s the difference between giardia and tritrichomoniosis in faecal smear?

A

** in faeces: Giardia– looks like a falling leaf motion VS. Tritichomoniosis- goes in a straight line

48
Q

Bovine tritrichomoniosis

A

* Agent: Tritrichomonas foetus

* Venereal disease- STD- mating/ coitus +/- iatrogenic

* Infertility and early embryonic death

* costs to endemic herd- culling, replacement herd, vet fees

* endemic in the NT extensive cattle farming- uncontrolled mating

49
Q

Tritrichomoniosis Presentation in a bull

A
50
Q

Tritrichomoniosis Presentation in a cow

A
51
Q

Tritrichomoniosis presentation in a herd

A
52
Q

Diagnosis in Trichomoniosis

A
53
Q

Control of tritrichomoniosis in bulls

A

* you don’t treat bulls, you cull!

* with replacement heifers, they take a few months to get over infection 3-4 months– retain cows if they continue to test negative- if they continue to test positive– cull them too

* notifiable!!

** vaccine only increases fertility, does not cure

54
Q

Avian Trichomoniosis- signficance

A
55
Q

Avian Trichomoniosis Transmission, who is normally affected?

A

** direct route- not faecal oral, mother to baby

56
Q

Avian Trichomoniasis- Presentation

A
57
Q

Diagnosis, Treatment and control of Avian Trichomoniosis

A
58
Q

Histomoniosis significance in birds– what does it cause? Who? morbidity and mortality?

A
59
Q

Life cycle of Blackhead (Histomonas meleagridis+ co infection with E. coli)

A

* Blackhead Stored in cecal worm egg–> earthworm eats eggs–> chickens eat earthworms–> flagellated trophozoites get in they quickly invade cecal muscosa, lose tail, become amastigote forms–> some enter circulation enter liver or other organs–> bird can become a carrier or get sick and die

** Cloacal drinking is another means of transmission: birds sitting in wet litter sucking it up

60
Q

Presenation of Histomoniosis in a bird

A
61
Q

Diagnosis of Histomoniosis

A
62
Q

Control of Histomoniosis diagnosis

A
63
Q
A

Parasitology 2 (13 decks)

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