Protozoan and Helminth Parasites

Question 1

What are obligate parasites?

Answer 1

required to spend at least part of their life cycle in a parasitic relationship

Question 2

What are facultative parasites?

Answer 2

generally free living but can become parasitic if they enter a suitable host

Question 3

What is a definitive host?

Answer 3

the host in which the parasite reaches sexual maturity

Question 4

What is an intermediate host?

Answer 4

a host that is required for parasite development but no sexual development takes place

Question 5

What is an incidental host?

Answer 5

a host that can be infected but does not play a role in the parasite’s life cycle
often a ‘dead-end’ host

Question 6

What is a paratenic host?

Answer 6

no development takes place but the parasite remains alive and infective to another host

Question 7

How do parasites typically enter a host?

Answer 7

through broken skin, mouth or elsewhere
Arthropod vectors (mosquito, tsetse fly…)

Question 8

What are helminths?

Answer 8

term used to refer to parasitic worms

1. nematodes (roundworms)
2. cestodes (tapeworms)
3. trematodes (flukes)

Question 9

What type of disease is malaria?

Answer 9

an acute disease
Severe anaemia
Coma
Hypoglycaemia
Acidosis
Organ failure
Respiratory distress
Pregnancy complications

after multiple infections severity usually decreases

Question 10

What is the causative agent of malaria?

Answer 10

Plasmodium spp.

Question 11

What are apicomplexan parasites?

Answer 11

parasites that contain an apical complex, a specialised structure consisting of various organelles that allow for invasion of host cells

use gliding motility to infect host cells
Substrate dependent as doesn’t involve flagella or shape shifting

eg plasmodium falciparum moves in corkscrew fashion to move into host cell
(Other eg: Cryptosporidium spp, Toxoplamsma gondii)

Question 12

What is African Trypanosomiasis?

Answer 12

transmitted by tsetse fly (definitive host)
causative agent of sleeping sickness in humans and nagan in domestic livestock
proliferates extracellularly in the host bloodstream
moves into the nervous system at lager stages of infection

parasites are coated in variant surface glycoprotein (VSG)
shields parasite by hiding invariant proteins
these proteins are hidden in pockets that antibodies cannot easily reach

Question 13

What type of organism is Plasmodium?

Answer 13

a protozoan parasite

Question 14

What is PfEMP1?

Answer 14

allows infected red blood cells and other uninfected red blood cells to stick to blood vessel walls and each other
this is to avoid being filtered out by the spleen
but creates blockage in the blood vessel
present in Plasmodium

Question 15

Why are African Trypanosomes so hard to get rid of?

Answer 15

1500-2000 VSG genes in trypanosome genome
~15 expression sites in the genome
only 1 expression site is active at a time

when immune system combats 1 VSG it switches to another

trypanosomes have an inexhaustible repertoire of antigenic variants
→ can establish long term chronic infection

Question 16

What mechanisms do African Trypanosomes use to switch between different VSGs?

Answer 16

1. gene conversion
2. segmental gene conversion
3. telomere switch
4. transcriptional switch

Question 17

Pathology of intestinal helminths?

Answer 17

Abdominal pain
Diarrhoea
Malnutrition
Protein deficiency
Iron deficiency
Growth reduction
Neurological problems
Susceptibility to other infections

Question 18

Challenges of combatting helminth infections?

Answer 18

Good at evading and suppressing host immunity
-large size makes them difficult to kill/dislodge
-takes decades to develop immunity and protective memory
-long lived (can live 3-10yrs in host)

Helminth Co evolved with humans for long time, good at manipulating immune system

Question 19

Hygiene hypothesis?

Answer 19

Low or absent helminth burden present in westernised populations
Lack of helminths to suppress immune system
Increased immune responses from helminth vacuum (more allergies)

Question 20

What is cysticercosis?

Answer 20

Taenia solium - species of tapeworm
Eggs ingested
Develop into larvae in gut, penetrate into intestinal wall and encyst in muscle and CNS
Can cause brain and spinal cord pathologies (dizziness, seizures, epilepsy)

Question 21

What is Schistosoma spp.?

Answer 21

Trematode

Question 22

Kinetoplastid parasites?

Answer 22

Human African trypanosomes
Trypanosoma cruzi
Leishmania spp

Vector borne with insect definitive hosts
Can be intra or extracellular

Question 23

Advantages and disadvantages of trypanosomes proliferating in bloodstream?

Answer 23

Adv:
Glucose and nutrient rich
Readily accessible to insect vector

Disadv:
Fully exposed to immune system
Proliferative stages cannot survive in tsetse fly gut (stumpy form can tho)

Question 24

Advantages and disadvantages of intracellular life in a blood cell?

Answer 24

A:
Nutrients from host cell
Shield from immune system
Erythrocyte host cells readily available and accessible to mosquito vector - transmission efficient

D:
Parasite needs to convert terminally differentiated erythrocytes into cells with nutrient uptake systems
Remodelling of membrane by parasite increases cell rigidity- may be detected and removed by spleen

Question 25

Parasitaemia?

Answer 25

Detectable levels of parasite in blood (like viraemia)

Question 26

How do trypanosome parasites avoid antibody action?

Answer 26

Variant surface glycoproteins cover surface and shield invariable proteins from antibody binding (eg flagella components)

Highly variable N terminal sequence
Conserved C terminus anchored in PM

Question 27

What happens at high trypanosome density?

Answer 27

Slender form proliferates until high density
Increase in parasitaemia
Increases concentration of sif (stumpy induction factor)
Causes some parasites to differentiate into non-replicating transmissible stumpy forms

Example of Quorum Sensing to maximise transmission opportunities while maintaining infection

Question 28

Downside of stumpy form?

Answer 28

Not replicating
No new production of different VSG types
Host immune system can catch up to them (that’s why only some differentiate from replicating slender forms)