TS8 - Parasites

Question 1

What are the three main classes of parasites?

Answer 1

Apicomplexa, Kinetoplastids, and Helminths.

Question 2

What defines a parasite?

Answer 2

An organism that lives on or inside another organism (host), benefits by gaining food and protection, and harms the host.

Question 3

What are some diseases caused by Apicomplexa?

Answer 3

Malaria (Plasmodium), Toxoplasmosis (Toxoplasma gondii), and Cryptosporidiosis (Cryptosporidium parvum).

Question 4

What is the primary challenge for parasites in the host?

Answer 4

Surviving the immune system rather than finding food.

Question 5

What is the role of the apical complex in Apicomplexa?

Answer 5

It contains organelles like rhoptries and micronemes used for host cell invasion.

Question 6

How is Plasmodium falciparum transmitted?

Answer 6

Through the bite of an infected Anopheles mosquito, which injects sporozoites into the human bloodstream.

Question 7

What are the symptoms of malaria caused by Plasmodium falciparum?

Answer 7

Severe anemia, cerebral malaria due to infected RBC adhesion, and metabolic acidosis.

Question 8

What is unique about Toxoplasma gondii’s host range?

Answer 8

It can infect most warm-blooded vertebrates and all nucleated cells, unlike Plasmodium, which is selective.

Question 9

How does Cryptosporidium parvum infect humans?

Answer 9

Through ingestion of fecally contaminated water containing oocysts, which release sporozoites to infect gastrointestinal epithelial cells.

Question 10

What are the two types of Kinetoplastids discussed in Lecture 2?

Answer 10

Extracellular (e.g., Trypanosoma brucei) and intracellular (e.g., Leishmania).

Question 11

What is the function of the kinetoplast in Kinetoplastids?

Answer 11

It contains mitochondrial DNA and is involved in energy metabolism.

Question 12

How does Trypanosoma brucei evade the immune system?

Answer 12

Through antigenic variation of its Variant Surface Glycoprotein (VSG) coat.

Question 13

What causes African Trypanosomiasis (sleeping sickness)?

Answer 13

Trypanosoma brucei gambiense and T. b. rhodesiense, transmitted by tsetse flies.

Question 14

What is the mechanism of host cell invasion by Trypanosoma cruzi?

Answer 14

It subverts host cell uptake processes, such as phagocytosis, to invade non-phagocytic cells.

Question 15

What disease does Trypanosoma cruzi cause?

Answer 15

Chagas disease, which can lead to chronic cardiac symptoms due to muscle invasion.

Question 16

How does Leishmania infect humans?

Answer 16

Through the bite of infected sandflies, which inject promastigotes that are phagocytosed by macrophages.

Question 17

What are the clinical forms of Leishmaniasis?

Answer 17

Cutaneous (skin sores), Mucosal (destroys mucus membranes), and Visceral (affects internal organs).

Question 18

What are Helminths?

Answer 18

Multicellular parasitic worms, such as Schistosoma mansoni (blood fluke) and Trichuris trichiura (roundworm).

Question 19

How does Schistosoma mansoni infect humans?

Answer 19

Through skin penetration by cercariae larvae released from freshwater snails.

Question 20

What is the pathology of Schistosomiasis?

Answer 20

Abdominal pain, diarrhea, blood in stool/urine, and chronic cases may lead to kidney failure or bladder cancer.

Question 21

How do Helminths like Trichuris trichiura infect humans?

Answer 21

Through ingestion of embryonated eggs, which hatch in the small intestine and mature into adults in the cecum.

Question 22

What are the advantages of an intracellular lifestyle for parasites?

Answer 22

Reduced immune detection and ability to remodel the host cell for survival.

Question 23

What are the challenges of intracellular parasitism?

Answer 23

Entering the host cell and remodeling it to create a suitable environment.

Question 24

How do Plasmodium merozoites invade erythrocytes?

Answer 24

Through active invasion using the apical complex, forming a moving junction with host cell receptors.

Question 25

What is the role of the PTEX complex in Plasmodium?

Answer 25

It exports parasite proteins across the parasitophorous vacuole membrane into the host erythrocyte.

Question 26

How does Plasmodium remodel the infected erythrocyte?

Answer 26

By creating knobs for adhesion, altering the cytoskeleton, and forming new nutrient transport pathways.

Question 27

What is the function of PfEMP1 in malaria?

Answer 27

It mediates cytoadhesion of infected erythrocytes to blood vessels, avoiding spleen clearance.

Question 28

How does antigenic variation help parasites evade immunity?

Answer 28

By switching surface proteins (e.g., VSG in Trypanosomes, PfEMP1 in Plasmodium) to escape antibody recognition.

Question 29

What is the role of RIFINs in Plasmodium?

Answer 29

They bind inhibitory immune receptors (e.g., LILRB1) to suppress NK cell killing of infected erythrocytes.

Question 30

How do Trypanosomes clear bound antibodies?

Answer 30

Through rapid endocytosis at the flagellar pocket and hydrodynamic flow generated by swimming.

Question 31

What is the mechanism of ApoL1 in killing Trypanosomes?

Answer 31

It forms pores in the parasite's membrane after being endocytosed via the HpHb receptor, causing lysis.

Question 32

How do human-infective Trypanosomes resist ApoL1?

Answer 32

Through SRA protein (T. b. rhodesiense) or TgsGP (T. b. gambiense), which inhibit ApoL1 pore formation.

Question 33

What is the complement system's role in immunity?

Answer 33

It opsonizes pathogens, recruits immune cells, and forms membrane attack complexes (MAC) to lyse pathogens.

Question 34

How does Leishmania evade complement-mediated lysis?

Answer 34

By elongating lipophosphoglycan (LPG) on its surface to prevent MAC insertion and cleaving C3b to iC3b.

Question 35

What is the hygiene hypothesis?

Answer 35

The idea that reduced exposure to parasites like Helminths increases susceptibility to allergies and autoimmune diseases.

Question 36

How do Helminths modulate host immunity?

Answer 36

By secreting molecules (e.g., HpARI) that inhibit inflammatory cytokines like IL-33, suppressing type 2 immune responses.

Question 37

What are the genetic adaptations in humans to combat parasites?

Answer 37

Sickle cell trait (malaria resistance), ApoL1 variants (Trypanosome resistance), and unusual antibodies (e.g., LAIR1-containing).

Question 38

What are the drawbacks of genetic adaptations like sickle cell trait?

Answer 38

Homozygotes suffer from sickle cell anemia, and ApoL1 variants increase kidney disease risk.

Question 39

How is schistosomiasis controlled?

Answer 39

Through praziquantel treatment, snail control, sanitation, and health education.

Question 40

What are the strategies to reduce malaria transmission?

Answer 40

Insecticide-treated bed nets, indoor residual spraying, and eliminating mosquito breeding sites.

Question 41

What is the mechanism of action of artemisinin?

Answer 41

It is activated by haem to form free radicals that alkylate parasite proteins, killing Plasmodium.

Question 42

How does chloroquine resistance occur in malaria?

Answer 42

Mutations in the PfCRT transporter prevent chloroquine accumulation in the digestive vacuole.

Question 43

What is the target of the RTS,S malaria vaccine?

Answer 43

The circumsporozoite protein (CSP) on Plasmodium sporozoites, formulated with Hepatitis B surface antigen and adjuvant AS01.

Question 44

What is the efficacy of the RTS,S vaccine?

Answer 44

Approximately 36% protection over 4 years in children aged 5-17 months.

Question 45

Why is PfRH5 a promising blood-stage malaria vaccine candidate?

Answer 45

It is essential for erythrocyte invasion via basigin binding, and antibodies against it block parasite replication.

Question 46

What are the challenges in developing parasite vaccines?

Answer 46

Antigenic variation, redundancy in invasion pathways, and the complexity of parasite life cycles.