Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VETM 424 Parasitology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

What taxonomic group is common to both Leishmania and Trypsoma

A

Sarcomastigophora
* Kinetoplastidia: taxonomic group – contain kinetoplast (extranuclear replicating DNA at base of flagella)
o Both Leishmania and Trypanosoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is leishmania associated with

A
  • Tropical disease
  • Associated with low socioeconomic status (lack of screens/windows)
  • No vx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Types of leishmania

A

o Many species: L. infantum – infect dogs (also L. Mexicana or donovani)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What vector transmits leishmania

A
  • Vector: sandfly (in subfamily phlebotominae  phebotomus and Lutzomyia)

o No preference for specific mammals – transmission depends on the behaviour of the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is canine leishmaniosis found

A

L. infantum

Endemic in S. America, S. Europe, Africa, Asia
o Zoonosis
o Endemic in North American Foxhounds – but vectors not in NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

lifecycle of leishmanisis

A

o Life Cycle
1. Promastigote enter blood
2. Invade macrophage, become amastigote
3. Amastigote replicate
4. Amastigote burst host cell and re-invade naive macrophage
5. Infected macrophage goes into sandfly
6. Transform to promastigote and divide in sandfly gut
7. Migrate to probiscis and attach to epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pathogenesis of leishmaniosis

A

o Pathogenesis
 Infected macrophages spread in lymph and organs
 Can be clinical or subclinical – stress can trigger signs
 Incubation period: 3 months to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does leishmaniosis present (least to most severe)

A

o Clinically: dermal lesions (dry lesions/ulcers/alopecia), lymphadenopathy (fever/splenomegaly/uveitis), hyperglobulinemia (low albumin/anemia), kidney dz (poor prognosis)
 4 stages of disease (visceral = most severe, cutaneus = least severe)
 Varied signs depending on individual animal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How to diagnose leishmaniossiis

A

o Dx: detect parasite in lesions/lymph nodes
 PCR
 ELISA to detect antibodies but low sensitivity for non-clinical carriers/ can crosss react with T. cruzi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is an epidemiological problem with understanding leishmaniasis in dogss

A
  • Many carriers and only a few are clinical

difficult to detect without pcr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is leishmaniosis high in foxhounds

A

o Endemic in North American Foxhounds – but vectors not in NA
 Non-vector mediated transmission – not fully understood
* Vertical or horizontal (blood contact)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is leishmaniosis treated

A

o Tx: change depending on stage of disease
 Not usually curative
 Allopurinol long term
 Monitor with biopsy and histopathology/PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can we control the spread of leishmaniosis

A

 Reduce sandfly bites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does trypansoma infect

A
  • Affect many types of vertebrates (bird/amphibian/mammal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where is trypansoma located

A
  • Located: tropics, NA, USA
  • Restrain on cattle production Africa/SA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does trypansoma evade immune system

A
  • Immune evasion: variant surface glycoproteins on genetically same parasites = antigenic variation
    o Most express the same, but some express different – when immune system attacks main type, the other can replicate instead
16
Q

compare the 2 types of trypansoma

A
  • 2 forms (depend on species)
    1. Salavarian trypanosomes: via insect bite (via diptera flies)
    a. Highly pathogenic (except in wildlife)
    b. Sub-saharan africa
    c. Causes ‘Nagana’ in cattle
    2. Stercorarian trypanosomes: via mucus membrane contamination with feces/insect vector
    a. Non-pathogenic (except T. cruzi = chagas disease, in SA)
17
Q

what does t. cruzi cause and how is it transmitted?

A

o Causes American trypanosomiasis = Chagas disease in human/dog
o Transmitted by triatomine (various genera and species in this category)
 Blood feed at night
 Live in cracks in houses/under porches
 Transmit: contaminate mucus membranes, blood feeding (contaminate wound with feces) – shed in feces of bug

18
Q

Where is t. cruzi located

A

o Vector location: S USA (Arizona/Texas/Oklahoma/montana)

19
Q

What animal reservoir does t. cruzi inhabit

A

o Wild animal reservoirs: racoons, oposssums, armadillos, domestic dog

20
Q

What is the life cycle of t. cruzi

A

o Life cycle
1. Triatomine bug takes blood meal
2. Infect macrophages and turn into amastigotes
3. Asexual reproduce
4. Burst into blood stream, turn into trypomastigotes
5. Trypomastigotes ingest by bug, infect organs
6. Trypomastigotes become epimastigotes in midgut of bug
7. Become trypomastigotes in hindgut and released via feces

21
Q

how does t. cruzi clinically present

A

o Clinically: acute and chronic phase
1. Acute: subclinical, fever, acute myocarditis
2. Chronic: cardiomyopathy/myocarditis (years)

22
Q

How to diagnose t. cruzi

A

o Dx: acute infection via trypomastigote blood smear, chronic via serology (parasite not always in blood/PCR (blood/LN aspirate)
 Usually diagnosed in chronic infection stage

23
Q

how to treat t. cruzi

A

o Tx: treat congestive heart fail
o Zoonotic – low risk of transmission (via blood contact)

24
Q

What type of trypansoma affects horses? Where is it located? clinical signs?

A
  • T. equiperdum - horses
    o Sexually transmitted
    o Clinically: dourine (swelling of genitalia + neurologic signs)
    o Location: Africa/Asia
    o Reportable in Canada
25
Q

What is the lifecycle of Sarcocystis

A
  • Lifecycle: predator prey life cycle (no vector)
    1. Definitive host (predator) consumes tissue from herbivore contaminated with bradyzoite
    2. Merozoite released and enter host cells in GI
    3. Host GI: Sexually reproduce via gamonts + gametes = zygote and oocyst formation = sporocyst (contain sporozoites) form
    4. Sporocysts released in feces
    5. Herbivore feeds in contaminated area
    6. GI tract: sporozoites released
    7. Morogeny and dissemination – 2 rounds asexual reproduction before merozoite formation
    8. Merozoite goes to muscle and forms sarcocyst aka bradyzoite (1 round of asexual reproduction)
    9. Merozoites may or may not release into blood
26
Q

What are some types of Sarcocystis

A

o S. cruzi/bovicanis aka. I. begemina
o S. hirsuta/bevifelis aka. I. begemina
o S. sp/neurona aka I. sp
o S. bovihominis aka. Isospora hominis

27
Q

What are the common cliinical signs of S. bovicanis? What animal does it affect? why is it relevant?

A

o S. cruzi/bovicanis aka. I. begemina: (+) pathogenic
 Common in cattle
 Mainly subclinical
 Clinical dz uncommon – due to heavy infection (morogeny in vascular endothelium)
* Lymphadenopathy/weight loss/submandibular edema = ‘dalmeny’ disease
 Cause carcass condemnation – when see cysts

28
Q

What dz does S. neurona cause?

A

 Equine protozoal myeloencephalitis (could also be cause by Neospora caninum/hughesi)

29
Q

Where is S. neurona found?

A

 Common in USA

30
Q

How is S. neurona transmitted? (common intermediate/definitive host/dead end host?)

A

 Definitive host; opossum (feed on intermediate host – scavange)
* Defecate near horses
 Intermediate host: nine banded armadillo, striped skunk, racoon, cats, sea otter
 Dead end host: equine

31
Q

What are the clinical signs of Equine protozoal myeloencephalitis

A

S. neurona

  • Varied incubation period (week to year)
  • Progressive severity – depends on part of CNS affected

 Clinically: ataxia/head tilt/facial nerve paralysis/dysphagia/weakness/atrophy

32
Q

What is the pathogenesis of Equine protozoal myeloencephalitis

A

S. neurona

 Pathogenesis: merozoites infiltrate CNS + cause inflammation = increase pressure/damage surrounding neuron = cell death + release merozoites into CNS/CSF

33
Q

How to diagnose Equine protozoal myeloencephalitis

A

 Dx: western blot/ELISA – difficult to detect in live horse (serotesting inadequate)
* Necropsy = characteristic CNS lesions

34
Q

How does the life cycle of S. neurona compare to other Sarcocystis

A

 Life cycle: no sarcocysts form – merozoites form meronts (asexual reproduction) in neurons

35
Q

How to treat Equine protozoal myeloencephalitis

A

S. neurona

 Tx; pyrmethamine + sulphonamide combo or Ponazuril

VETM 424 Parasitology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions