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CBI - UOE > Parasitic infection > Flashcards

Parasitic infection Flashcards

1
Q

parasites are

A

large, multicellular organisms

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2
Q

parasites dont generally

A

replicate within the mammalian host- passes through intermediate ghosts or through soil or water

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3
Q

parasites reproduce

A

sexually to create larval stages that mediate transmission

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4
Q

parasites consist of

A
  • nematodes
  • termtodes
  • cestodes
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5
Q

nematodes

A

roundworms

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6
Q

trematodes

A

flukes

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7
Q

cestodes

A

flatworms or tape worms

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8
Q

parasites cause what sort of infections

A

intestinal or systemic infection

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9
Q

where are parasites responsible for massive morbidity?

A

developing countries

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10
Q

vector of Schistosomiasis

A

water snail

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11
Q

parasite of Schistosomiasis

A

enters the body with the female wrapped inside the males

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12
Q

Schistosomiasis are the most important infections of

A

trematodes, or flukes in ihumans

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13
Q

how many species of Schistosomiasis

A

6

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14
Q

how many people affected by the species of Schistosomiasis

A

> 200 mill

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15
Q

where does Schistosomiasis occur

A

in fresh water contaminated with motile, fork-tails cercariae

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16
Q

life cycle of schistosomes

A

1) in fresh water eggs hatch to yield motile miraccidia
2) miracidia infect snails
3) in their intermediate snail hosts, the miracidia undergo maturation and multiplication to release many infectious cercariae

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17
Q

how do schistosomes penetrate host skin

A

shed their tails and use combination of proteases and muscular action of their oral suckers

18
Q

cercariae –>

A

schistosomula –> schistosomes

19
Q

immature schistosomula after penetration

A

1) after penetration, immature schistosomula migrate via the circulation to reach the liver microcirculation where they mature
2) worms do not multiply in the host- adult females reside intimately within a canal in the ventral body of the male
3) pairs migrate against portal venous blood flow (GI to liver) to release eggs into the veins draining the bladder and intestines
4) eggs elicit granulomatous inflammatory response which assist their transit into the intestines of bladder
5) excretion from the body in the stool or urine respectively

20
Q

parasite- protozoa

A

diverse group of unicellular pathogens that typically cause chronic infections, indicating high degree of evolutionary adaptation e.g. malaria

21
Q

what is a common theme that underlies the capacity of protozoa to persist in the host

A

antigenic variation

22
Q

protozoa parasites are divided into 2 groups

A

1) those introduced by bites or tissue injury

2) those introduced by ingestion of contaminated water

23
Q

vector fo Trypanosoma cruzi

A

kissing beatle

24
Q

what disease does Trypanosoma cruzi cause

A

trypanosomiasis - chagas disease

25
Q

stages of chagas disease

A

1) tritomine bug takes a blood meal, trypanastiogtes enter wound
2) metacyclic trypomastigotes penetrate various cells at bite wound site
3) inside cells they transform into amastiogtes
4) amastigotes multiply by binary fission in cells of infected tissues
4) intracellular amastigotes trasform into trypomastigotes then burst out of the cell and enter the blood stream
5) Triatomine bug takes a blood meal and ingests trypomastigotes
6) epimastigotes in midgut
7) multiply in midgut
8) metacyclic trypomastigotes in hindgut

26
Q

chagas disease also known as

A

trypanosomiasis

27
Q

kissing bugs also known as

A

Triatomine

28
Q

immune response to T.brucei (african sleeping disease)

A

1) initial response is by inflammatory cytokines
2) macrophages activation is hallmark of infection with trypanosomes (numbers and activities increase dramatically in tissues of trypanosome infected hosts)
3) VSG-specific, B cell responses associated with temporal (non-soluble i.e. not antibodies or complement) immunity to trypanosomes VAT arising during chronic infection
4) T cell dependent immune responses to invariant components of the VSG molecule associated with resistant hosts
5) sum of interaction of these immune responses thought to determine relative resistance and susceptibility of host and outcome of infection

29
Q

immune response to Schistosome eggs

A

granulomatous responses- via Th1 /2 cells

-characterised by tissues eosinophilia, elevated IgE and a Th2 pattern of cytokines

30
Q

the cardinal feature of schistosomiasis is

A

the presence of tissue granulomas surrounding eggs

31
Q

type 2 granulomatous responses to schistosome egss

A
  • granulomas are characterised by an organised circumferential infiltrate of Th2 cells, eonsiphils, macrophages and fibroblasts within a dense collagen-rich matrix
  • type 2 granuloma
  • transloacted into the intestinal lumen for excretion
  • eggs that are swept into the liver become trapped in the hepatic sinusoids
  • granulomas slowly dissipate m the collagenous scare coalesce and cirrhosis develops leading to obstruction of blood bow and the creation of aberrant vascular by pass channels cause varices
32
Q

granulomatous response sequesters

A

toxic egg antigens and kills the eggs

33
Q

bleeding varices leads to

A

death

34
Q

Trypanosome Variable Antigen Types

A

VAT

35
Q

in trypanosomes periods with few parasites (and few disease symptoms) are followed by

A

a large increase in parasite population

- this cycle continues until the host dies or becomes asymptomatic

36
Q

what mechanisms have trypanosomes evolved to escape obliteration by host defecne

A

antigenic variation- resulting in succesive dominate of each series of VAT overtime
- remission appear to result from generation of protective antibodies that destroy homologous trypanosomes

37
Q

each time the host antibodies are almost successfully eliminated..

A

the parasite eludes destruction by expression variant specific surface glycoproteins (VSG), thus becoming new VAT then rapidly multiplying

38
Q

expression of VATs

A
  • expression of VAT genes occurs in an imprecisely predictable order
  • when ingested by a test fly, the parasite loses VSG surface coat
  • expression continues when the trypanosome reach the emtacyclic state and are then able to infect the mammalian host
39
Q

the VAT phenomenon tis best known in

A

T.brucei

40
Q

VSG activation

A

VSG recognise day hosts immune system is released through flagellar reservoir and completely coverers the parasite as a surface coat

41
Q

how many genes do T.brucei possess coding for VSGs

A

1000- around 20% of genome

  • only one VSG will be expressed at any time
  • others are transcriptionally silent
42
Q

when are VSG genes expressed

A

when at the ends of the chromosome, in a special telomeric site called a VSG expression site

CBI - UOE (61 decks)

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