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Biology Year 2 > Parasitology > Flashcards

Parasitology Flashcards

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1
Q

Describe pinworm egg transfer

A

Adult female pinworms lay their eggs on the perianal skin

  • usually during the night
  • eggs are sticky and so adhere to skin

Eggs are easily transferred to the hands and mouth due to scratching of itchy area

  • eggs are then ingested when a person consumes contaminated food, drink or objects
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2
Q

Where do pinworms develop? Describe the process

A
  • Develop in the small intestine
  • after ingestion
  • eggs hatch in small intestine
  • release larvae
  • burrow into the wall of the small intestine
  • where they develop into adult pinworms
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3
Q

When do pinworms migrate to the large intestine?

A

When fully mature and ready to lay eggs

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4
Q

What is the Linnean rank of nematoda?

A

Phylum

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5
Q

How many moults are required for the pinworm to reach adulthood?

A

4

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6
Q

Are pinworms deoicious or monoicious?

A

Deoicious

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7
Q

What is a common diagnostic test for pinworms?

A

Sellotape test
- Tape across anus - place on microscope slide
- Worms or not - diagnostic

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8
Q

Are protozoa micro/macro parasites?

A

Micro

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9
Q

Are worms micro/macro parasites?

A

Micro

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10
Q

Macroparasites cannot generally replicate in the host - what does this mean for the level of infection? Give an example

A
  • levels of infection are determined by the number of infection events and number of infective stages e.g. gut nematodes
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11
Q

Microparasites replicate in the host - what does this mean for the level of infection? Give an example

A

Infection levels can rise rapidly after a single infection event (theoretically from one infectious stage)
- requires fast immune response to combat
- e.g. malaria

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12
Q

Describe the lifecycle of a parasite who is never exposed to the external environment?

A

Infective stage in host
- host eaten (predation or scavenging)
Development in new host
- Reproduction of parasite in host

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13
Q

What is an example of a parasite that’s entire life cycle is spent in internal environments

A
  • Trichinella spiralis (Trichinosis)
  • spiral threadworm (nematode)
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14
Q

Where is the infective stage of Trichinella spiralis (Trichinosis) – the spiral threadworm present?

A
  • Skeletal Muscle
  • Coiled up worm
  • Muscle larvae cyst (encysted larvae)
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15
Q

How does transmission of T. spiralis (Trichinosis) infection occur?

A

Ingestion of infected meat
- when raw or undercooked meat that contains encysted larvae

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16
Q

Where does T. spiralis (Trichinosis) develop?

A
  • Small intestine
  • after digestion larvae are released from their cysts
  • penetrate wall of the intestine to enter the bloodstream
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17
Q

Where does T. spiralis (Trichinosis) migrate after development in the small intestine?

A

Migration to skeletal muscle:

  • larvae travel through the bloodstream and enter the skeletal
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18
Q

What happens to T. spiralis (Trichinosis) after migration into the skeletal muscle?

A
  • Encyst
  • Remain dormant until consumption
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19
Q

Where does reproduction of T. spiralis (Trichinosis) occur?

A

Skeletal muscle cysts

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20
Q

Name the range of human symptoms of trichinosis?

A
  • Fever
  • Muscle pain
  • Gastrointestinal distress
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21
Q

Does T. spiralis (Trichinosis) release eggs or larvae?

A

L1 larvae

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22
Q

Describe the stages of the parasitic cycle which includes two or more host species and no contact with the external environment?

A
  • Reproduction of parasite in host
  • Production of stages infective to vector
  • Uptake of stage by vector
  • Development of infective stages in vector
  • Transmission of infective stages to new host as vector feeds
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23
Q

What is the definitive host?

A

Species where the parasite reaches sexual maturity

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24
Q

What is the intermediate host?

A

Species in which larval or non sexual stages develop

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25
Q

Briefly describe the disease cycle of Trichinosis?

A
  • Ingestion of infected meat
  • Development in the small intestine
  • Migration to skeletal muscle
  • Encyst and reproduce
  • Transmission to predator/scavengers via consumption of meat
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26
Q

In malaria what is the definitive host?

A

Female anopheles mosquito

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27
Q

When do female mosquitoes become infected in malaria (Plasmodium)?

A
  • Feed on the blood of plasmodium infected humans
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28
Q

What happens to plasmodium after ingestion by mosquitoes?

A
  • development in the mosquito gut
  • migrates to the mosquito’s salivary glands
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29
Q

How is plasmodium transmitted to humans?

A

Infected mosquito bites a human for a blood meal

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30
Q

Where does the development of plasmodium occur in humans and what does this cause?

A
  • Liver
  • Undergo a developmental transformation into liver stage parasites
  • Multiply rapidly and cause liver damage
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31
Q

What occurs after the liver stage of plasmodium development?

A

Invasion of red blood cells and multiple

  • Cause the red blood cells to rupture and release new parasites into the bloodstream
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32
Q

Briefly describe the 5 steps of plasmodium life-cycle

A
  • Infection of mosquito from bloodmeal
  • Development in the mosquito
  • Transmission to humans
  • Development in liver
  • Invasion of red blood cells
  • Cycle repeats
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33
Q

Describe direct parasitic life cycle

A
  • Reproduction of parasite in definitive
  • Release of infective stages (eggs/cysts) into outside environment
  • Reinfects into same host again
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34
Q

Describe features of parasites that have stages that are exposed to the outside environment

A
  • Free living forms relatively inert/inactive
  • Can be direct life cycle - one host species
  • Indirect life cycle - intermediate hosts
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35
Q

Describe how humans become infected by Ascariasis (Ascaris lumbricoides)?

A

Ingesting contaminated soil or food that contains eggs

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36
Q

Describe the development in the small intestines of humans by Ascariasis (Ascaris lumbricoides)?

A
  • Eggs hatch in the small intestine
  • Larvae burrow into the walls
  • Mature into adult worms
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37
Q

How long does maturation take and how large is an adult Ascariasis (Ascaris lumbricoides)?

A
  • Reach maturity after about 2-3 months
  • Up to 40 cm in length
  • Live in the human small intestine for up to 2 years
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38
Q

What happens to eggs produced by adult female Ascariasis (Ascaris lumbricoides)?

A

Passed out of the body in feces

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39
Q

How long does the development of larvae of Ascariasis (Ascaris lumbricoides) in the external environment take?

A
  • Eggs develop into larvae in the soil
  • Become infective after about 2-3 weeks
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40
Q

Briefly describe the life cycle of Ascariasis (Ascaris lumbricoides)

A
  • Egg ingestion from soil by human
  • Development in small intestine
  • Maturation of adult worms
  • Egg production and passing of the eggs in feces
  • Development of larvae in soil
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41
Q

Where do adult (Tapeworms/Cestodes - Taenia) live?

A

Intestines of the definitive host

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42
Q

How are (Tapeworms/Cestodes - Taenia) spread?

A

Eggs are passed out of the body in feces

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43
Q

Describe how Tapeworms/Cestodes (Taenia) enter the intermediate hosts?

A
  • Eggs develop into larvae in the environment
  • Ingested by intermediate hosts when they consume contaminated food or water
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44
Q

What are some examples of intermediate host of Tapeworms (Taenia)?

A

Cattle, pigs and fish

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45
Q

What is the cysticerci of Tapeworms/Cestodes (Taenia)?

A
  • Larvae develop into cycticerci once ingested by intermediate host
  • Cyst-like structures
  • Contain tapeworm larvae
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46
Q

How do Tapeworm/Cestode larvae (Taenia) enter the definitive host?

A
  • Ingestion of the infected intermediate host
  • Consumption of raw/undercooked meat
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47
Q

Describe the final stage of a Tapeworm infection - after the consumption of the intermediate host by the definitive host?

A
  • Larvae in the cysticerci are released in the intestine
  • Attaches to the wall of the intestine using scolex
  • Develop into adult tapeworms
  • Begins producing eggs
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48
Q

How do Tapeworms/Cestodes remain attached to the intestinal wall?

A

Hooks and Suckers - on scolex

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49
Q

Describe tapeworms reproductive strategy?

A
  • Both ovaries and testes
  • Capable of self fertilisation and cross fertilisation
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50
Q

Describe tapeworms egg laying?

A

Last section drops out with faeces
- bag of eggs

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51
Q

Where do tapeworms live in the intermediate host and how do they get there?

A
  • Penetrate intestinal wall of host
  • Live in muscle
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52
Q

Describe parasites which are active in external environment

A

Don’t bother

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53
Q

Describe the modes of transmission into the definitive host of parasites with a life strategy in which the parasite is active in the external environment

A
  • Ingestion of infective stages from environment
  • Penetration by infectious stages
  • Ingestion of infected intermediate host
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54
Q

Describe how water becomes contaminated with Schistoma (Blood flukes)?

A
  • excreted from the human host in the feces or urine and end up back in freshwater
  • eggs hatch in freshwater
  • miracidia released into water
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55
Q

How do Schistoma (Blood flukes) infect the intermediate host?

A

Miracidia penetrate the skin of snail intermediate hosts

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56
Q

What do Schistoma micadia (blood flukes) develop into?

A

sporocysts in intermediate snail host and multiply

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57
Q

How do Schistoma parasites (blood flukes) infect human hosts?

A

Infective cercariae penetrate the skin of humans in contact with contaminated water

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58
Q

Describe the events after a Schistoma parasites (blood flukes) enters a human host?

A
  • Cercariae enter the bloodstream
  • Mature into adults
  • Migrate to the blood vessels surrounding the intestines or bladder
  • Where they lay eggs
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59
Q

Briefly describe the lifecycle of Schistoma parasites (blood flukes)

A
  • Release of cercariae into environment from host
  • Infection of snail intermediate host in water
  • Release of infectious stage into water
  • Infection of human host
  • Development of adult parasites
  • Egg excretion
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60
Q

What is commensalism? Give an example

A
  • No metabolic dependance
  • e.g. clownfish and sea anemone
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61
Q

What is mutualism? Give an example

A

Obligatory relationship – both benefit
- e.g. oxpeckers on cattle in Africa

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62
Q

What is parasitism

A
  • One partner benefits
  • metabolic dependence
  • may cause harm to host
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63
Q

What are the theories for evolution of parasitism?

A

Loss of otherwise essential genes through mutualistic relationship with bacterial endosymbiont
- Gains traits that support manipulation of host
Horizontal gene transfer
- gain advantageous genes that allow organism to co-opt parasitic way of life
Parasitic features evolving under free living conditions
- the concept of pre-adaptation
- free-living traits co-opted for parasitic lifestyle

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64
Q

What is necromeny?

A
  • Consumption of dead organic matter as a primary food source.
  • necromenous animals do not actively kill their food source
  • considered a “halfway-house” between parasitic and free-living lifestyles
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65
Q

How many times has parasitism evolved in nematodes?

A

4 groups animal nematode parasites
3 groups of plant nematode parasites
- suggests some characteristic of nematodes that favours evolution of parasitism

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66
Q

Describe the loss of essential genes in Brugia malayi (Human filarial parasite)

A
  • loss of genes encoding enzymes required for essential biosynthesis pathways
  • no longer make vital compounds for survival
  • need external source (parasitism)
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67
Q

What are Meloidogyne incognita and M. hapla and what do they cause?

A
  • Plant parasites
  • Root-knot nematodes
  • Cause deformities in carrots
  • Severe infections result in reduced yields
  • Deformity impacts consumer acceptance
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68
Q

Describe horizontal gene transfer (HGT) in Meloidogyne incognita and M. hapla?

A
  • Produce cellulases and xylanases
  • not found in other animals
  • most similar to bacterial genes
  • Horizontal gene transfer from rhizobial bacteria in legume root nodules
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69
Q

What are Rhizobia?

A

bacteria that fix nitrogen after becoming established inside root nodules of legumes

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70
Q

Describe how a free living nematode in dung may be pre-adapted for animal parasitism

A

Conditions in pile of dung is similar to colon

  • Anaerobic
  • Toxic enzymes
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71
Q

Is there definitive proof of pre-adaptations in parasites

A
  • Nope, hypothetical concept
  • The pre-parasites of present-day parasites no longer exist
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72
Q

Describe how nematode associations with insects may represent pre-adaptation for parasitism

A

Development of
- Phoretic associations
- Necromenic associations
Neither yet parasitic – metabolic dependence on host develop later

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73
Q

What is phoresy?

A
  • Symbiotic relationship
  • Host organism used for transportation or dispersal purposes
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74
Q

What is dauer larvae?

A
  • Larva enters dormant phase
  • Non feeding stage
  • Specialised for survival and dispersal
  • Can survive harsh conditions
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75
Q

Do dauer stage larvae use phoresy?

A
  • Some do
  • Dauer uses insects for transportation
  • Means of dispersal and finding new food sources
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76
Q

Explain the connection between dauer stage larvae and insects

A
  • Dauer associates with insect host in species specific manner (particular beetle species etc)
  • wait for death then feeds on microbes growing on carcass
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77
Q

What features of a dauer larval stage?

A
  • Non aging
  • Doesn’t feed
  • Does not grow
  • Can survive for months
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78
Q

What is the evidence for pre-adaptation from dauer larval stage?

A
  • Both have specialised cuticle
  • Both cannot feed
  • Both can resume development to 4th larval stage
  • Where parasitic nematodes use an infective larvae its almost always 3rd stage
  • Dauer stage larvae are 3rd stage
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79
Q

What is the molecular evidence for dauer larval stage being a pre-adaptation for nematode parasitism?

A
  • Molecular similarities
  • conserved endocrine signalling mechanism involving dafachronic acid (DA) and DAF-12
  • controls formation of dauer and infective larvae
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80
Q

Describe C. elegans and its development into a the dauer stage

A
  • Free living nematode
  • L2 has to sense environment (eg temp.)
  • Can grow (become L3) or arrest (as a Dauer)
  • Development of dauer is default developmental behaviour
  • Specified when DAF-12 is not occupied by ligand (DA)
  • Under inducing conditions
  • Generate DA which binds to DAF-12 to produce non-dauer larvae
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80
Q

Describe Strongyloides papillosus and its development in context of the dauer stage

A
  • Parasitic nematode
  • Can switch between a free-living stage and a parasitic stage inside a vertebrate host
  • Halfway house between free living and parasitic lifestyle
  • During free-living stage
  • Choice between infective and non-infective larvae
  • Decision is driven by a signaling molecule called DA
  • Drives switch from infective to non-infective larvae
  • Equivalent to C. elegans where DA specifies non dauer larva
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81
Q

Where development of L3 is constitutive not facultative can DA turn off formation of infective larvae? What could the potential uses of this be

A
  • Yes, selective ligand modulators of DAF-12 might be used to stop L3 larvae progression
  • Can DA be used to control nematode transmission?
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82
Q

Describe the evidence Pristiochus pacificus provides for pre-adaptation

A

Necromenic species

  • Exposed to low oxygen and toxic host enzymes
  • Increase in detoxifying enzymes compared to C elegans
  • Not found in any other non-parasitic nematode
  • Intermediate type of association between C. elegans and true parasites?
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83
Q

What would an enlarged spleen suggest about an infection?

A
  • deals with blood-borne infections
  • potentially malaria
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84
Q

What is the malarial vector?

A
  • anopheles mosquito
  • Females drink blood (Males don’t bite)
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85
Q

How many plasmodium species can be transmitted to humans?

A

4

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86
Q

Which Plasmodium species is most widespread?

A

P. falciparum
- Tropical Africa, Asia and Latin America

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87
Q

What are factors that affect malaria distribution?

A
  • Temperature of >15°C
  • climate change affects range of malaria carrying mosquitoes
  • Cannot survive above 3000m
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88
Q

What are the 4 phases of the malarial lifecycle?

A

1 & 2. sexual phase and first asexual phase occur ONLY in Anopheline Mosquitoes.
3. second asexual phase is in the liver
4. Third asexual phase is in the blood (repeated many times)

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89
Q

What is the definitive host in malaria?

A

Anopheles mosquitos

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90
Q

What is the test for malaria?

A
  • Blood smear test
  • Count number of RBCs and infected cells
  • Calculate percentage parasitaemia
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91
Q

What occurs in the 3rd phase of malarial development and what is it called?

A
  • erythrocytic or blood stage
  • infected red blood cells rupture
  • releasing new malaria parasites
  • merozoites invade and infect new red blood cells
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92
Q

Describe the sexual phase of malaria

A
  • Anopheles mosquito ingests gametocytes
  • Activation male gametocyte
  • Releases osmophilic bodies into RBC
  • Disrupts RBC membrane
  • Causing swelling and rupture
  • Activated gametocytes undergo sexual reproduction
  • Form zygote
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93
Q

How many times is DNA replicated during the development of male gametocyte in malaria?

A
  • Replicated three times
  • Resulting in a nucleus with eight complete sets of DNA
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94
Q

How many kinetosomes are formed during gametogenesis in malaria?

A

Eight

  • in a microtubular organizing center during gametogenesis
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95
Q

What are kinetosomes?

A
  • Microtubule-based organelles
  • Crucial role in the generation of the whip-like movements
  • Base for the formation of cilia and flagella
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96
Q

What is the function of the kinetosome in malaria gametogenesis and how many are formed?

A
  • Base and growing point for the flagellum (axoneme) during gametogenesis in malaria
  • Eight are formed
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97
Q

What is exflagellation in malaria?

A
  • Activation of the male gametocyte and the subsequent release of the flagella in malaria
  • Can then fertilize the female gametes
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98
Q

What is the function of the flagellum in malaria?

A

Male gametocytes actively swims towards female gametocytes for fertilization

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99
Q

What happens after fertilization in malaria?

A
  • Zygote develops into an ookinete
  • Penetrates the inner gut wall of the mosquito
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100
Q

What is the next phase of the malaria life cycle after the ookinete stage?

A
  • First asexual phase
  • Ookinete develops into a sporozoite
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101
Q

What is an apicomplexan?

A
  • Group of parasitic protozoans that includes the malaria parasite
  • All apicomplexans have an apical complex
  • used for host cell invasion
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102
Q

What is a sporozoite? (malaria)

A
  • single-celled form of the malaria parasite
  • released from a sporocyst during the first asexual phase
  • migrates to the mosquito’s salivary glands
  • injected into the bloodstream of a new host
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103
Q

What is the ookinete? (malaria)

A
  • Product of fertilization between a male and female gametocyte
  • Enters the mosquito’s blood
  • Develops into single-cellular structure called a sporocyst
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104
Q

What and where does the oocyst feed on after development from ookinete? (Malaria)

A
  • Moves into the haemocoel (body cavity) of the mosquito
  • Feed on the haemoglobin of the mosquito’s blood meal
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105
Q

What are sporocysts? (malaria)

A
  • Formed inside the oocyst
  • Inside sporocysts, sporozoites undergo asexual replication
  • Contains thousands of daughter sporozoite cells
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106
Q

Sporozoites burst out of _____ and migrate to salivary gland of mosquito

A

Sporocysts

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107
Q

What cells does malaria enter after leaving the bloodstream? (malaria)

A

Kupffer cells which line liver capillaries

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108
Q

Where do sporozoites go after leaving Kupffer cells and what happens in these cells? (malaria)

A

Enter hepatocytes

  • sporozoites rapidly grow
  • become trophozoites
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109
Q

Does an infected person show symptoms during the merozoites phase? (malaria)

A

Nope

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110
Q

What is hypnozoite stage of P. vivax?

A
  • Trophozoites become latent hypnozoite stage (dormant)
  • Can cause relapses years later
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111
Q

What do trophozoites become when they divide? (Malaria)

A

Schizogony/schizonts - Merozoites

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112
Q

Briefly describe the third phase of malaria?

A

Asexual phase in RBCs

  • Merozoites burst out of hepatocytes and invade RBCs
  • Once inside - ingests haemoglobin
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113
Q

What are the two steps in Merozoites invasion of RBCs (malaria)?

A
  1. Receptor Recognition and Binding
  2. Erythrocyte Deformation
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114
Q

Describe RBC structure

A
  • Relatively rigid
  • Rigidity due to: Cytoskeleton
  • Difficult to disrupt
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115
Q

Describe entry into RBCs by malaria

A
  • Merozoite attachment – anywhere on red cell
  • Apical complex releases compounds that disrupt rbc membrane
  • Entry into cell
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116
Q

What is the role of MSP-1 in merozoite invasion? (malaria)

A

Causes parasite rolling around RBC surface for a while during merozoite invasion

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117
Q

What are AMA-1 and RON-2, and why are there two with almost identical roles? (Malaria)

A

Own receptors secreted which bind to RBC - assisting attachment
- redundancy (multiple proteins)

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118
Q

What is the role of PfRh5 in P. falciparum (malaria) RBC invasion?

A
  • Binds to Basigin
  • Blood group molecule on RBC surface
  • Essential for the invasion
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119
Q

What is the parasitophorous vacuole? (malaria)

A
  • Membrane-bound compartment
  • Formed around the parasite after invasion of host blood cells
  • Protective environment for the parasite to develop and replicate within the host cell.
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120
Q

What happens to the surface coat upon entry into RBC? malaria

A

THICK SURFACE COAT NOT ENGULFED
- Sloughed off

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121
Q

What are the components involved in the invasion of a red blood cell by a malaria parasite?

A
  • forms rhoptries and micronemes
  • only present in invasive stages.
  • structures are involved in the secretion of invasion molecules
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122
Q

How do rhoptries and micronemes help merozoites get into a cell? (malaria)

A
  • Secretion of invasion molecules e.g. RESA molecule
  • Enhanced fluidity of RBC membrane
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123
Q

What are the changes that occur in the RBC after the entry of the merozoite? malaria

A
  • Development of feeding stage - trophozoites
  • Production of enzymes that degrade haemoglobin
  • Development of novel transporter system - Maurer’s clefts

Changes in the shape and deformability of the RBC

  • formation of membrane “knobs”
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124
Q

What is the role of knobs that form on RBCs during malarial infection?

A
  • Important in the adhesion of parasitized RBCs to blood vessels (deep-seated capillary endothelium)
  • Knobs keep the parasitized cells away from the spleen, which is the main immune organ that controls malaria.
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125
Q

What are the fatal consequences associated with P. falciparum?

A

Cerebral malaria

  • sequestration of infected red blood cells in the small capillaries of the brain
  • Breakdown of BBB

Hydrostatic pressure changes

  • pressure on brain stem causes coma and death
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126
Q

What family is Toxoplasma?

A

Apicomplexa

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127
Q

What fraction of the human population does toxoplasma infect?

A

1/3 of the human population - very prevalent parasite

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128
Q

What types of organisms does toxoplasma infect?

A

Birds and mammals

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129
Q

What is the definitive host of toxoplasma?

A
  • Members of the CAT family are the DEFINITIVE host
  • can only sexually reproduce inside felines
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130
Q

Briefly describe toxoplasma

A

Obligate intracellular protozoan parasite
- only lives inside cells

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131
Q

How many strains of toxoplasma are there?

A

Three strains of Toxoplasma I, II, II

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132
Q

What is the primary route of infection for felines with the parasite Toxoplasma gondii?

A

Ingest tissues infected with bradyzoite cysts or oocysts containing sporozoites

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133
Q

What happens when bradyzoite cysts or oocysts are ingested by a feline? (toxoplasma)

A
  • Burst due to digestive system
  • Invade the intestinal epithelium of the feline
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134
Q

What can differentiate into male and female gametes in the definitive host and eventually become oocysts containing sporozoites? (Toxoplasma)

A

Both bradyzoite cysts and oocysts can differentiate into male either and female gametes

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135
Q

How are oocysts with sporozoites shed from the feline? (toxoplasma)

A
  • in its feces for up to three weeks
  • sheds several million oocysts per day
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136
Q

What can differentiate into male and female gametes and eventually become oocysts containing sporozoites in the definitive host? (toxoplasma)

A

Bradyzoites!

  • Oocysts are ingested by feline
  • Bradyzoites within oocysts can differentiate into male and female gametes
  • Leads to formation of new oocysts containing sporozoites
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137
Q

What do bradyzoite cysts develop from? (Toxoplasma)

A
  • Tachyzoites invade cells
  • Develop into bradyzoite cysts
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138
Q

What happens if a warm-blooded animal eats infected tissue containing bradyzoite cysts? (toxoplasma)

A

Bradyzoites are released into the intestine

  • differentiate into tachyzoites
  • disseminate throughout the body
  • become bradyzoite cysts again
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139
Q

What occurs when a bradyzoite cyst is ingested by a cat? (Toxoplasma)

A
  • invade the intestinal epithelium
  • differentiate into male and female gametes
  • become oocysts again
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140
Q

What are bradyzoites? (Toxoplasma)

A

Slow-dividing forms of the Toxoplasma parasite found in oocysts in infected muscle tissue

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141
Q

Where are toxoplasma cysts found in the body of infected animals?

A

Cysts are found in the muscle tissue of infected animals.

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142
Q

What are the potential risks for a pregnant woman if she is infected with Toxoplasma during the early trimester?

A
  • Parasites can cross the placenta and affect the developing baby
  • potentially causing developmental defects
  • potentially death
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143
Q

Who is at risk for reactivation of latent Toxoplasma infections?

A
  • Immunocompromised individuals
  • such as organ transplant recipients and HIV
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144
Q

What is the potential risk of Toxoplasma in HIV-positive patients?

A

Toxoplasma encephalitis as the infection can reactivate (from dormancy) and cause severe symptoms

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145
Q

What happens when Toxoplasma enters the latent phase?

A

the infection becomes dormant, and fever may subside

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146
Q

What is the rapidly dividing stage of Toxoplasma called?

A

Tachyzoite stage

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147
Q

What are some preventive measures to avoid Toxoplasma infection?

A
  • Avoid cat feces and soil where cats defecate
  • Cook meat thoroughly
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148
Q

What is the asexual stage of the T. gondii life cycle called?

A

Tachyzoites

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149
Q

Which hosts are considered intermediate hosts for T. gondii?

A

Various warm-blooded animals, including humans

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150
Q

Which cells can T. gondii tachyzoites target?

A

almost any nucleated cell in the body

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151
Q

What happens to tachyzoites when they are secreted into the bloodstream? (T. gondii)

A

tachyzoites actively penetrate into cells, replicate, and then burst out when the host cell die

  • acute disease
  • characterized by symptoms such as fever and cold-like symptoms
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152
Q

How is the growth of T. gondii tachyzoites limited?

A
  • limited by the immune response of the host
  • and tachyzoite transformation into cyst-forming bradyzoites.
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153
Q

What immune response is responsible for triggering the differentiation of T. gondii into bradyzoite cysts?

A

Th1 immune response
- Specifically the production of interferon-gamma (IFN-g)

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154
Q

How does the Th1 immune response contribute to controlling T. gondii infection?

A

Maintains it in a dormant state within bradyzoite cysts

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155
Q

What molecule secreted by T. gondii enhances the Th1 immune response?

A
  • Cyclophilin 18
  • establishment of a chronic infection within the host as it promotes dormancy in T. gondii
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156
Q

What can T. gondii bradyzoites cause in immunocompromised individuals?

A
  • T. gondii bradyzoites can cause acute encephalitis
  • inflammation of the brain
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157
Q

Where can sporulated oocysts contaminate? (Toxoplasma gondii)

A

water, soil, food and surfaces
- contact with feces

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158
Q

How stable are T. gondii oocysts in the environment?

A
  • Very stable
  • especially in warm and humid environments
  • enabling them to survive for extended periods outside of the host
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159
Q

Where does the sexual stage of T. gondii occur within the definitive host?

A

Intestine
Definitive host - cat

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160
Q

Why is the feline the only host that allows sexual reproduction of Toxoplasma?

A
  • Only mammal that lacks enzyme in their small intestines required to break down linoleic acid
  • Results in an excess of linoleic acid in their intestines
  • Allows Toxoplasma to develop sexually
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161
Q

How can the sexual life cycle of Toxoplasma be induced experimentally in other species?

A
  • Increasing the levels of free linoleic acid
  • Knocking out the gene for delta-6-desaturase (enzyme that breaks down linoleic acid)
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162
Q

What is the significance of inducing the sexual life cycle of Toxoplasma experimentally?

A
  • Study and research without the need for using cats
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163
Q

What does the parasite Toxoplasma use to move into host cells?

A
  • Apical complex
  • Rhoptries and micronemes
  • Releases chemicals that facilitate its movement into host cells
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164
Q

How do Toxoplasma parasites move through their environment?

A

Glide through the fluid in their environment using a molecular motor

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165
Q

How does the parasite Toxoplasma move without projecting pseudopod-like extensions?

A
  • Actomyosin motor system
  • Located beneath plasma membrane
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166
Q

What components are involved in the movement of Toxoplasma?

A

Actin and myosin - actomyosin motor
As well as special “gliding-associated proteins”

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167
Q

How does the actomyosin motor system facilitate the movement of Toxoplasma?

A
  • Generates force and pulls itself into host cells
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168
Q

What structure does Toxoplasma form to protect itself from the host cytoplasm?

A
  • Forms a parasitophorous vacuole
  • Acts as a safe compartment for the parasite
  • Regulating its access to nutrients and waste
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169
Q

How does Toxoplasma move by interacting with the extracellular matrix (ECM)?

A
  • Moves by forming and breaking specific interactions with the ECM
  • When the front of the parasite breaks its attachment, it springs forward
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170
Q

Can Toxoplasma be transmitted through blood transfusions?

A

Yes

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171
Q

Who is particularly at risk from Toxoplasma infection?

A
  • dangerous for immunocompromised individuals
  • fetus of pregnant women
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172
Q

Describe the steps in toxoplasma entry into cells

A
  1. Apical structures: rhoptries and micronemes involved in attachment process
  2. Moving junction formation: The rhoptries and micronemes form moving junction (MJ)
  3. Invasion: tachyzoite enters the host cell through the MJ
  4. Rear dragging and front surging: spring-like motion
  5. Parasite repeats the cycle of attachment, movement, and release, propelling itself forward
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173
Q

What is the rhoptry bulb in apicomplexa?

A
  • Specialized secretory compartment (organelle)
  • Located at the apical end of the parasite
  • Contains proteins that are discharged during invasion
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174
Q

What is the significance of IgM antibodies in Toxoplasma infection?

A
  • first type of antibodies produced in response to an infection
  • presence indicates a recent or ongoing infection.
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175
Q

What is the recent trend of toxoplasma infection numbers?

A

substantial rise in the number of people infected

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176
Q

What is one factor that has contributed to the high number of toxoplasma infections, particularly in France?

A

Consumption of rare or undercooked meat is one of the factors that has led to a high number of infections

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177
Q

How does Toxoplasma infection influence sex ratios in humans?

A

Women who are seropositive for Toxoplasma (have antibodies) tend to have more sons than uninfected women

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178
Q

Where does Toxoplasma rest in the body?

A
  • Forms microscopic cysts in the brain
  • Remains in dormant state
  • These cysts act as a long-term reservoir for the parasite
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179
Q

What are the common treatments for Toxoplasma infection?

A
  • Combination of sulfonamides and pyrimethamine
  • Inhibits growth and replication
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180
Q

How is congenital transmission of Toxoplasma reduced?

A

Spiramycin

  • often used during pregnancy to reduce the risk of congenital transmission
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181
Q

Is there a vaccine available for humans to prevent Toxoplasma infection?

A

No, currently there is no vaccine available for humans to prevent Toxoplasma infection.

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182
Q

Why is it challenging to target encysted bradyzoites with drugs? (Toxoplasma)

A

Dormant state less susceptible to drug action

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183
Q

What could be a potential side effect of targeting bradyzoite cysts in the brain?

A
  • may lead to the release of toxic components
  • triggering a harmful inflammatory response in the body
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184
Q

What are the regions included in the “Old World” for sandflies?

A

Old World includes Middle East, Europe, Asia, Africa

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185
Q

Which regions are considered part of the “New World” for sandflies?

A

South America, Central America

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186
Q

Describe the transformation of Leishmania parasites after injection of metacyclic promastigotes into the host by sandfly

A
  • Invade macrophage
  • Transform into amastigotes
  • Amastigotes multiply until lysis
  • Releasing more parasites that can invade additional macrophages
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187
Q

What happens when a sandfly bites an infected host and takes up amastigotes in their bloodmeal? (Leishmania)

A

Transform into the infective metacyclic promastigotes

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188
Q

Why do leishmania parasites produce a substance to block the sandflies mouth

A
  • Sandfly will have to regurgitate to remove the plug
  • Potentially transmit the parasites to a new host during feeding
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189
Q

How do parasites in the midgut create a plug in the fly’s mouthparts?

A
  • Produce a proteoglycan gel
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190
Q

Describe the morphology of the leishmania parasites in sandflies.

A
  • Promastigote
  • Single-celled

Flagellated organisms

  • Aids in their movement
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191
Q

What is the characteristic feature of cutaneous leishmaniasis?

A
  • Lesions on the surface of the skin
  • Occurring at sites with a high concentration of infected macrophages
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192
Q

What is the infective stage of the parasite in Leishmania?

A

flagellated metacyclic promastigote

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193
Q

What is Lipophosphoglycan (LPG) and what is its role in Leishmania?

A
  • Inositol lipid anchor
  • Used for adhesion and invasion
  • Component of glycocalyx
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194
Q

What are Glycosylphosphatidylinositol (GPL) anchored glycoproteins and what is their role (Leishmania)

A
  • Surface proteases
  • Increase in levels during infective metacyclic forms
  • Helps the metacyclic promastigotes in establishing an effective interaction with host cells
  • Degrade host immune factors
  • Degrade components of the extracellular matrix
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195
Q

What is the function of complement in opsonization?

A

Involves coating pathogens with complement proteins

  • complement-coated pathogens attract immune cells
  • such as phagocytes
  • engulf and eliminate them more efficiently
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196
Q

What is the function of complement in cell lysis?

A

formation of a lytic sequence
- process involves the buildup of an attack complex that creates pores in the pathogen’s membrane
- leading to osmotic shock and death

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197
Q

What is the function of the complement system in chemotaxis and inflammation?

A
  • Small fragments act as chemoattractants
  • Attract more immune cells
  • such as neutrophils and macrophages, to the site of infection or inflammation
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198
Q

What is the function of the complement system in chemotaxis and inflammation? - oops did this one twice dont bother

A

babadook

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199
Q

Are complement functions antigen-specific or non-specific?

A

Non-specific
- rapid and generalized immune response

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200
Q

What is the role of opsonization in phagocytosis?

A
  • Complement proteins bind to pathogens.
  • Complement fragments (C3b) act as opsonins.
  • Opsonins attract phagocytes and macrophages.
  • Phagocytes and macrophages have receptors for C3b.
  • Recognition of C3b enhances phagocytosis.
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201
Q

How do macrophage-infecting pathogens like Leishmania exploit opsonization and phagocytosis?

A

Attach to the surface of host cells (macrophages)

  • using molecules like GP63
  • pathogens aim to be pulled inside the host cell
  • glycocalyx allows complement to stick to it
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202
Q

How does the thickness of the surface glycocalyx of Leishmania change during complement interaction and why?

A
  • layer thickens
  • acts as a protective barrier against the host’s immune system
  • protects against complement-mediated lysis
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203
Q

What are strategies deployed by leishmania to survive within host cells?

A

Thickening of the glycocalyx
Shedding of some Lipophosphoglycan (LPG) from surface
- removes complement components
Increased expression of GP63 (surface protease)
- inhibiting the destruction of the parasite by macrophages

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204
Q

How does the parasitophorous vacuole of leishmania act on pH to assist in survival with macrophages?

A

Vacuole maintains a slightly acidic pH

  • inhibits the activity of lysosomal enzymes
  • surface protease GP63 functions more efficiently in acidic pH
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205
Q

What are scavenger enzymes (leishmania)?

A

Amastigote form of the parasite produces scavenger enzymes

  • Help neutralize reactive oxygen species (superoxide and nitric oxide) produced by the macrophage
  • Protecting the parasite from oxidative damage
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206
Q

How does leishmanias inhibition of Protein Kinase C (PKC) benefit the parasite?

A

PKC - enzyme involved in generating toxic macrophage metabolites

  • Parasite’s Lipophosphoglycan (LPG) inhibits its action
  • Preventing production of these toxic metabolites
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207
Q

What is the first cell type that floods into a wound when the skin is wounded and what is their function?

A

Neutrophils

  • Phagocytosis
  • don’t necessarily move in antigen specific way
  • as likely to take up bead as parasite
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208
Q

What happens when neutrophils take up Leishmania parasites?

A
  • Leishmania survives digestion
  • Undergo apoptosis
  • Releasing the parasites into the environment
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209
Q

What is the Trojan Horse route of infection?

A
  • Pathogens enter neutrophils and await macrophages for further infection.
  • macrophages take up apoptosing neutrophils cells as clearance mechanism
  • take up parasite as well
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210
Q

Briefly describe the leishmania lifecycle?

A
  • Sand fly blood meal - takes up amastigote
  • Transforms into infectious metacyclic promastigote
  • Sandfly bites and passes promastigote to new host
  • M. Promastigote taken up by macrophage
  • Transform into amastigotes
  • Grow and multiply in macrophages
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211
Q

How many people are estimated to be infected with Chagas Disease?

A

Estimated that 16-18 million people

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212
Q

How many people die each year from Chagas Disease?

A

Approximately 50,000 people die annually

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213
Q

What is the vector that transmits Chagas Disease?

A

Triatomine bugs
- also known as kissing bugs

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214
Q

What are the two ways to combat vector-borne parasites?

A
  • Control the vector (e.g., through insecticide use, habitat modification)
  • Treat individuals to kill the parasite (e.g., through medication, vaccines)
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215
Q

What is Romana’s sign?

A

Marker of acute Chagas disease infection
- Swelling and redness that occurs around the eye when a person is infected

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216
Q

What happens to the parasite when it is inside the cells of the body? (Chagas Disease)

A

Parasite loses its flagellum and transforms into amastigote stage

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217
Q

What structure binds the flagellum to the surface of a protozoan (trypanosome)?

A
  • Undulating membrane
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218
Q

What is the infective stage of Trypanosoma cruzi?

A

Metacyclic trypomastigote stage

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219
Q

What happens when Trypanosoma cruzi enters a cell in the wound site?

A
  • metacyclic amastigotes move into cells and transform into amastigote form
  • multiplies
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220
Q

What happens after the amastigotes burst out of the cells? (Leishmania)

A
  • Transform into trypomastigotes
  • Flagellated form
  • Re-infect phagocytes or uptake by sandflies
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221
Q

How do Trypanosoma cruzi infect other cells? dont bother

A

The trypomastigotes infect other cells and transform back into amastigotes. bipbop

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222
Q

Where does the multiplication stage of Trypanosoma cruzi occur in the kissing bug and what is the next stage of development?

A

Occurs in the midgut

  • Formation of metacyclic trypomastigotes
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223
Q

How are Trypanosoma cruzi parasites transmitted by the kissing bug?

A

Triatomine insects excrete the parasites in their hindgut

  • the infection can enter the body through rubbing the bug excrement into the eye or through mucosal surfaces
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224
Q

Briefly describe the cycle of Trypanosoma cruzi

A

Triatomine bug takes blood meal

  • ingests trypomastigotes
  • transforms into epimastigote
  • transforms into metacyclic trypomastigote
  • takes bloodmeal and defecates
  • passes metacyclic trypomastigote into bite wound or mucosal membrane
  • M. trypomastigote penetrates various cells at bite site
  • transforms into amastigotes
  • transform into trypomastigotes then burst out of cell
  • ready for uptake by kissing bug or reinfection of cells
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225
Q

When do chronic symptoms of Chagas disease typically develop?

A

Chronic symptoms usually develop after approximately 10-40 years

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226
Q

What are some early symptoms of Chagas disease?

A

Early symptoms may include fever and general malaise.

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227
Q

What happens during chronic Chagas disease?

A

Parasite multiplies in the body over time

  • Can cause an enlarged heart and may lead to cardiac arrest
  • (thinning of blood vessel walls and the risk of rupture)
  • can lead to the enlargement of the esophagus
  • can cause complete loss of tissue integrity in colon
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228
Q

What does molecular analysis suggest about Chagastic patients with parasites in different organs?

A

Bip bop dont stop!

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229
Q

What is the role of Gp85 in T. cruzi attachment and what prevents them from rapid destructions?

A
  • stage-specific surface glycoprotein
  • Multiple forms of Gp85 are expressed on the surface of the parasite
  • providing variability to avoid immune destruction while maintaining the ability to attach to host cells
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230
Q

What is the function of trans-sialidases in T. cruzi?

A

Role in the attachment process

  • Can chop or move sialic acid residues on the surface of the parasite
  • Allowing it to interact with and attach to host cells
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231
Q

How does the variability in Gp85 contribute to T. cruzi’s ability to invade cells?

A

Antigenic variability in Gp85 among different clones of T. cruzi

  • allowing the parasite to evade the host immune response
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232
Q

What is the role of the parasitophorous vacuole in T. cruzi invasion?

A

Resides in it during invasion of host cells

  • provides a protected environment for the parasite to survive and replicate
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233
Q

How does T. cruzi differ from other protozoans (such as Leishmania) in terms of its invasion mechanism?

A
  • Does not rely on actin-mediated phagocytosis for invasion
  • Parasitophorous vacuole is not derived from the plasma membrane of the host cell
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234
Q

What is the source of the membrane for the parasitophorous vacuole in T. cruzi?

A

Lysosomal membranes

  • unlike other protozoans that may use host cell’s plasma membrane or surface molecules for vacuole formation
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235
Q

Does T. cruzi spend its entire life cycle within the parasitophorous vacuole?

A

No, while it initially resides in the vacuole, the parasite eventually escapes and replicates in the cytoplasm of the host cell.

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236
Q

What molecules does T. cruzi attach to on the cell surface during invasion?

A
  • Receptor Tyrosine Kinases
  • Protein receptor (TGFβRII)
  • Act as attachment points for the parasite
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237
Q

How does T. cruzi trigger a cellular increase in cellular calcium and the repair process in the host cell?

A

Attaches to the cell surface
Secretion of oligopeptidase B

  • binds to G protein coupled receptors and activates phospholipase C (PLC)

Secretion of Cruzipain

  • which cleaves kininogen into kinins
  • bind to cell surface kinin receptors and activate PLC

Triggers an increase in intracellular calcium concentration
Signals the host cell to initiate a cellular repair process

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238
Q

How does T. cruzi deceive the host cell into initiating a cellular repair process?

A

Attaches to specific molecules on the cell surface

  • Lysosomes are attracted to the site where T. cruzi attaches to the host cell
  • Triggers a response in the host cell to repair the “wound”
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239
Q

What happens after lysosomes accumulate under the site of T. cruzi attachment?

A

Lysosomal membranes fuse and create a membrane for the parasitophorous vacuole

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240
Q

How does T. cruzi enter the cell during the fusion of lysosomal membranes?

A

Combination of parasite movement and the “pulling/recovery” of lysosomal membranes along microtubules

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241
Q

What triggers the differentiation of T. cruzi from trypomastigote to amastigote?

A

Low pH

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242
Q

What molecule is produced in response to low pH and what is its role? (T. cruzi)

A

Tc-Tox

  • disrupts the parasitophorous vacuole and releases the parasite into the cytoplasm of the host cell
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243
Q

What molecule does tc-tox resemble in the complement system?

A

C9 - used by immune system to punch holes in cells

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244
Q

Where does T. cruzi replicate within the host cell?

A

Parasites multiply in cytosol - not synchronous

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245
Q

Describe T. cruzi development within host cells

A
  • Trypomastigotes differentiate into Amastigotes
  • these divide and multiple
  • then differentiate into intracellular epimastigotes
  • Before transforming back into trypomastigotes
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246
Q

How does T. cruzi spread to new cells or enter the bloodstream? Useless don’t bother

A

bipdopscripscrop

247
Q

What are key features of trypomastigotes in T. cruzi?

A
  • Found in blood
  • C shaped
  • Flagellated
  • Surface proteins essential for pathogenesis
248
Q

What are key features of amastigotes in T. cruzi?

A
  • Intracellular in tissues (esp. muscle)
  • Rounded
  • Flagellum not visible, low motility
249
Q

What are the two groups of platyhelminthes?

A
  • Cestodes
  • Trematodes
250
Q

What are some cestode groups?

A
  • Tapeworms
  • Planarians
251
Q

What are some trematode groups?

A

bip bop bad luck

252
Q

What is the common name for the parasitic disease caused by blood flukes?

A

Schistosomiasis

253
Q

What is the characteristic feature of trematodes (flukes) that distinguishes them from other parasites?

A
  • Trematodes have two prominent suckers
  • An oral sucker and a ventral sucker
254
Q

What size are blood flukes (trematodes)?

A
  • too big to live inside cells
  • can reach sizes of about 1 centimeter
255
Q

What is the vector for Schistosomes?

A

Water snail

256
Q

How do humans become infected with Schistosomes?

A

Contact with water inhabited by the appropriate species of infected snail

257
Q

Where do Schistosomes mature and reproduce in the human body?

A

Particularly around the liver

258
Q

How are Schistosome eggs released from the human body?

A
  • Female Schistosomes release eggs into the lumen of blood vessels
  • Passed out of the body through urination or defecation.
259
Q

What happens to Schistosome eggs in water?

A

hatch in the water, releasing miracidia, which are free-swimming larvae.
- enter water snails

260
Q

How do cercariae, the infective stage of Schistosomes, enter the human body?

A

Penetrate the skin

261
Q

How are cercariae released from the snail into the water? (Schistosomiasis)

A
  • Released from the snail through physical and enzymatic digestion
  • Released induced by light shining on snail
262
Q

What happens to the tail of cercariae during penetration? (Schistosomiasis)

A

Cast off

263
Q

What is the result of incomplete cercarial penetration? (Schistosomiasis)

A

In some cases, cercariae die in the skin

  • leading to dermatitis known as “swimmers itch.”
  • occurs when schistosomes of one species try and penetrate the wrong host
264
Q

What do the acetabular glands of cercariae do during penetration? (Schistosomiasis)

A

Secrete proteases and are involved in the shedding of the glycocalyx

  • Shed via microvilli
  • New double unit membrane is formed from membranous vesicle
265
Q

What attracts cercariae to human skin? (Schistosomiasis)

A
  • Gradients of fatty acids released from the skin and L-arginine
  • As well as warmth
266
Q

How long do schistosome relationships last?(Schistosomiasis)

A

Mate for life

267
Q

What cues the discharge of the acetabular glands in cercariae? (Schistosomiasis)

A

Fatty acids which predominate at deeper sites in the skin

  • Proteases are secreted to help burrow deeper
268
Q

What types of proteases dominate in the secretions of the acetabular glands? (Schistosomiasis)

A
  • Cercarial elastases (serine proteases)
  • Degrade skin molecules
269
Q

How do we know that acetabular glands are important in invasion? (Schistosomiasis)

A
  • Cercariae without tails can still invade when injected percutaneously
  • But cercariae without acetabular glands cannot
270
Q

What is the function of enzymes that are released by cercariae when nearing blood vessels? (Schistosomiasis)

A

Thioredoxin peroxidase and superoxide dismutase

  • help counteract reactive oxygen species found in the cells of the skin at this level
271
Q

What are two strategies schistosomiasis uses to assist in entry in the bloodstream

A

Apoptosis of host cells in the skin - may assist in entry

Secretion of enzyme that degrades C1 inhibitor

  • which control vascular permeability
  • degradation increases permeability
  • making entry into bloodstream easier
272
Q

What is the characteristic behavior of adult male and female schistosomes in the blood vessels?

A

Male curls up around the female

  • groove holds female parasite
  • female releases eggs
273
Q

In schistosomiasis what would blood in urine suggest about the infection?

A

Heavy schistosomiasis infection

  • eggs can pass through the bladder wall
  • leading to the presence of blood in the urine.
274
Q

What is the role of schistosome eggs in causing pathology?

A

Can cause damage as they migrate and get lodged in the liver

  • leading to inflammation and fibrosis
275
Q

How does the host respond to schistosome eggs?

A
  • Tries to wall off the eggs
  • leading to inflammation and the formation of granulomas
276
Q

What are the long-term effects of schistosome eggs trapped in the body?

A

Chronic schistosomiasis

  • Persistent pathology due to the presence of trapped eggs
  • Ongoing inflammation and fibrosis
277
Q

What are schistosome miracidium?

A
  • Hatch from eggs on contact with water
  • Penetrate the snail host
  • Transform into a sporocyst stage
278
Q

How do schistosome miracidia move?

A

Swim using cilia

279
Q

What triggers the cessation of swimming in schistosome miracidia?

A

Changes in salt concentration

280
Q

What do miracidia schistosomes differentiate into?

A

Sporocysts

  • Undergo asexual reproduction
  • Produce more daughter sporocysts
281
Q

Where do schistosome cercariae develop?

A

Form within sporocysts

282
Q

Why do hookworms stunt growth in children?

A

Drink blood - cause anaemia

283
Q

What is the response of hookworm L3 larvae to thermal gradients?

A

Migrates to the cutaneous surface of mammals through thermotaxis

284
Q

Where are hookworm larvae typically found in the skin?

A

Cracked skin, wounds, and hair follicles

  • they follow the path of least resistance
285
Q

What enzymes do hookworm (Ancylostoma duodenale and Necator americanus) (L3) larvae secrete to help penetrate the skin?

A
  • Secrete hyaluronidase out of their mouthparts
  • Helps them penetrate the skin by breaking down hyaluronic acid
286
Q

What is the response of hookworm larvae to host-derived chemoattractants?

A

Move toward the venules (small veins) within the host’s circulatory system

287
Q

Where do the larvae of hookworms (Ancylostoma duodenale and Necator americanus) get trapped in the host’s body and what does it cause?

A

Lung capillaries

  • leading to formation of microhemorrhages in the lung tissue
288
Q

How do hookworm larvae pass through the basement membrane to reach the microvasculature?

A
  • Secrete an alkaline protease
  • Attacks the basement membrane
289
Q

What do hookworms use to latch on to the small intestine?

A

Hooks

290
Q

How do hookworms stop clotting during feeding

A

Secretion of proteases (anticoagulants)

291
Q

What is the function of the efficient pharynx in hookworms?

A

Constantly drinks blood and pumps out enzymes

292
Q

Where does the final development to adulthood occur in hookworms?

A

small intestine

293
Q

What is esophageal pumping in hookworms?

A

Rapid and coordinated contractions of the esophageal muscles

  • draws in and swallow large amounts of fluid
294
Q

How many people are estimated to be infected with hookworm worldwide?

A

Approximately 500 million people

295
Q

What is the target of the new hookworm vaccine being developed?

A

Hookworm aspartic hemoglobinase

  • a protease that cleaves host hemoglobin
  • stimulates the production of antibodies against the hookworm aspartic hemoglobinase
  • leads to starving of the worms
296
Q

What are the stages of infection?

A

1) Entry into the body
2) Replication and spread
3) Disease manifestation
4) Exit from the body to infect others.

297
Q

What are some of the body’s barriers to infection?

A

Physical barriers

  • skin
  • mucous membranes

Mechanical barriers

  • movement of mucus by cilia

Chemical barriers

  • low pH
  • enzymes

Microbiological barriers

  • normal microbiota
298
Q

What is the difference between cells of the innate and adaptive immune system?

A

Innate immune system

  • macrophages and neutrophils
  • respond quickly to infections but do not have memory

Adaptive immune system

  • B cells and T cells
  • respond more slowly but possess memory
  • respond faster upon reinfection
299
Q

What is the common lymphoid progenitor pathway?

A

Gives rise to B cells and T cells

300
Q

What is the myeloid and granulocyte progenitor?

A

Gives rise to innate immune cells

  • Dendritic cells
  • Macrophages
  • Granulocytes (neutrophils, eosinophils, and basophils)
301
Q

What are the main functions of macrophages?

A

Phagocytosis

  • activation of bactericidal mechanisms
302
Q

What are the main functions of dendritic cells?

A
  • Antigen uptake in peripheral sites
  • antigen presentation in lymph nodes
303
Q

What are the main functions of neutrophils cells?

A

Phagocytosis

304
Q

What are the main functions of Eosinophils cells?

A

Killing of antibody-coated parasites

305
Q

What are the roles of phagocytes in the innate immune system?

A
  • act as effector cells to actively remove infection
  • Also act as Antigen Presenting Cells (APCs)
  • contain proteases to create an inflammatory response
306
Q

What are the steps of phagocytosis?

A
  • Attachment of the pathogen to the phagocyte
  • Ingestion of the pathogen into a phagocytic vacuole
  • Killing of the pathogen
  • Degradation of the pathogen
307
Q

What are the key characteristics of the adaptive immune response?

A
  • Acquired (develops after exposure to a pathogen)
  • Specific (tailored for a particular pathogen)
  • Memory (the second response is bigger and faster than the first)
308
Q

What are the two main types of lymphocytes in the adaptive immune system, and where are they produced?

A

B lymphocytes (B cells)

  • which are produced in the bone marrow

T lymphocytes (T cells)

  • produced in the thymus
309
Q

What are the surface receptors on B cells and T cells called, and what do they recognize?

A

B cells have (BCRs) antibodies or immunoglobulins (Ig)

T cells have T cell receptors (TCR)

Both BCRs and TCRs recognize foreign molecules

310
Q

What are antigens and antigenic epitopes?

A
  • typically large molecules (usually proteins) that can be recognized by antibodies
  • parts of antigens recognized by antibodies are called “antigenic epitopes”
311
Q

Describe the structure of an antibody

A
  • Shaped like a ‘Y’ and is made up of two heavy chains and two light chains
  • Both light and heavy chains have constant and variable regions
  • Constant region of the heavy chains is called the Fc portion
  • Antigens bind at the variable end of the antibody
312
Q

How does the shape of the antigen-binding site contribute to antibody function?

A
  • Different antibodies have differently shaped antigen-binding sites
  • gives antibodies their specificity
313
Q

What are the effector functions of antibodies in the humoral immune response?

A
  • secreted by plasma cells
  • can neutralize pathogens and toxins
  • promote phagocytosis (opsonization)
314
Q

How does Antibody Dependent Cell mediated Cytotoxicity (ADCC) work?

A

Antibodies bind to antigens on the cell surface

  • Cells with Fc receptors (NK (neutral killer) cells or macrophages) can bind to the Fc region of these antibodies
  • Interaction mediates extracellular killing but not phagocytosis
315
Q

What is opsonization?

A

Opsonins (antibodies and other things) coat pathogen, mark it for destruction and make it easier to engulf

316
Q

How do T cell receptors interact with antigens?

A

Unlike antibodies, T cell receptors don’t recognize antigens directly

  • Antigens presented to them via Major Histocompatibility Complex (MHC)
  • Large proteins are broken down into peptides inside cells through a process called antigen processing
  • these peptides are then associated with MHC molecules inside the cell and expressed on the cell surface
317
Q

What is the Major Histocompatibility Complex (MHC) and what role does it play in antigen presentation?

A

Unlike antibodies, T cell receptors don’t recognize antigens directly

  • Large proteins are broken down into peptides inside cells - antigen processing
  • MHC molecules associate with antigenic peptides inside cells and then display these peptides on the cell surface for recognition by T cells.
318
Q

What are Class I MHCs?

A

presents intracellular antigens (e.g., from viruses) to CD8 cells

319
Q

What are Class II MHCs?

A

Presents extracellular antigens (e.g., from worms) to CD4 cells

320
Q

What is the difference between MHC class I and class II molecules in terms of their expression and the type of antigens they present?

A

MHC class I molecules are found on most nucleated cells

  • present peptides derived from intracellular pathogens

MHC class II molecules are expressed on antigen-presenting cells like macrophages, dendritic cells, and B cells

  • they present peptides from extracellular pathogens.
321
Q

How do CD4 and CD8 T cells interact with MHC molecules?

A
  • T cell receptor binds to both the MHC molecule and the antigenic peptide
  • Necessary to trigger an immune response
322
Q

What is the role of cytotoxic CD8 T cells in the immune response?

A

Recognize and kill cells that are infected with pathogens

  • cells infected with viruses, malaria parasites, or Toxoplasma
  • Upon recognition, they deliver a death signal to the infected cell
323
Q

How do innate and adaptive immunity cooperate for effective protection?

A

Antigen-presenting cells of the innate immune system, such as dendritic cells

  • Pick up antigens from an infection site and activate T cells in the lymph nodes
  • Activated T cells then return to the site of infection and control innate effector responses through the local secretion of cytokines.
324
Q

What are cytokines?

A

Cell signalling molecules

  • Aid in cell-to-cell communication in immune responses
325
Q

What are CD4 T cell subsets and what roles do they play?

A

Cells can differentiate into several subsets, including Th1, Th2, Th17, and Treg cells, each with its own function.

326
Q

What is the role of Th1 cells?

A

Produce interferon gamma
- which activates macrophages

327
Q

What is the role of Th2 cells?

A

Produce interleukin 4

  • activates cells like eosinophils and basophils
328
Q

What is the role of Th17 cells?

A

Role in neutrophil activation and inflammatory responses

329
Q

What is the role of Treg cells?

A

Help suppress the immune response to prevent damage to the body’s own cells.

330
Q

What are the key cytokines that drive Th1 cell development?

A

Interleukin-12 (IL-12)

331
Q

What are the key cytokines that drive Th2 cell development?

A

Interleukin-4 (IL-4)

332
Q

what are signature cytokines of Th2 response?

A

Signature cytokines IL-4, IL-5, IL-9, and IL-13

333
Q

What are signature cytokines of Th1 response?

A

Gamma interferon - IFN-gamma

334
Q

What is the Thp cell?

A

Unpolarized CD4+ T cell

  • Can differentiate into either a Th1 or Th2 cell
  • depending on the cytokines it encounters
335
Q

What is the role of dendritic cells (DC) and macrophages (Mo) in the Th1/Th2 cell development model?

A

Dendritic cells and macrophages are antigen-presenting cells

  • They uptake, process, and present antigens to T cells, along with the appropriate cytokines
  • Drive the differentiation of the T cells
  • IL-12 produced by these cells can stimulate Th1 cell development, while IL-4 can stimulate Th2 cell development
336
Q

How does the immune response change in chronic vs acute infection according to the Th1/Th2 cell development model?

A

Acute infection

  • the immune response tends to be dominated by Th2 cells
  • activate cells like eosinophils and basophils

Chronic infection

  • the immune response tends to be Th1-dominant
  • activates macrophages and promotes inflammation.
337
Q

Briefly describe T. muris - resistant and susceptible host immune response?

A

T. muris is a gut-dwelling nematode parasite

  • partially invades intestinal epithelial cells

In a resistant host

  • leads to a Th2 response and acute infection

Susceptible host

  • Th1 response is elicited, leading to chronic infection.
338
Q

What are filarial nematodes?

A

Tissue dwelling nematode parasites

339
Q

What are the two main types of Filariasis?

A
  • Lymphatic filariasis (caused by Wuchereria bancrofti or Brugia malayi)
  • Onchocerciasis (caused by Onchocerca volvulus).
340
Q

What is the pathology of Onchocerciasis?

A
  • Dermatitis
  • “river blindness”
  • damage to cornea in eye.
341
Q

What is the most common feature of Lymphatic filariasis?

A

Hydrocele

  • Worms like lymphatics around the scrotum leading to fluid accumulation
  • In endemic areas, 40-60% of adult males have hydrocoeles
342
Q

How does Onchocerciasis affect the skin and eyes?

A

Adult worms live over bony prominences

  • larvae circulate in the skin
  • causing damage to elasticity, itching, aging, and depigmentation.
  • If larvae migrate across the cornea, they can cause opacity leading to blindness.
343
Q

Where do the parasites lodge in Lymphatic filariasis?

A

Lymphatic system

344
Q

How long do the parasites live and what do they produce in Lymphatic filariasis?

A
  • several years within the human lymphatic system.
  • produce immature larvae called microfilariae
  • circulate in the bloodstream and lymphatic vessels
345
Q

What is the life cycle of the parasites in Lymphatic filariasis?

A

Adult females release microfilaria larvae which circulate in blood

  • Microfilaria is taken up by the mosquito vector
    penetrates the thoracic muscles of the mosquito
  • Develops from 1st to 3rd stage larvae in the mosquito
  • The 3rd stage is released into the human host upon biting
346
Q

Where is Lymphatic filariasis a problem?

A

Large parts of South America, Africa, and Asia.

347
Q

What is produced by the parasites in Lymphatic filariasis?

A

millions of microfilariae which circulate in blood.

348
Q

What is the vector of Onchocerciasis?

A

Simulium (black fly)

349
Q

What causes the suffering and disability in Lymphatic filariasis?

A

Pathology

  • adult worms living in lymphatics/sinuses of lymph node causing dysfunction and inflammatory damage

Dilation of lymphatics

  • Thickening of vessel walls, incompetent lymph valves, ultimately blockage of lymphatics (especially on death of the worm)
350
Q

What conditions are caused by filariasis pathology?

A
  • Hydrocoele
  • Elephantiasis of arms and legs
  • Local inflammation of lymph nodes (filarial fever)
351
Q

What is the global burden of Lymphatic filariasis?

A

Total number afflicted is around 120,000,000

352
Q

How does elephantiasis manifest in Lymphatic filariasis?

A
  • Legs become swollen due to dysfunction of lymphatics leading to fluid accumulation
  • skin becomes cracked
  • allowing bacteria and fungi to flourish
353
Q

What is chyluria in the context of Lymphatic filariasis?

A

Worms living in and damaging the lymphatic system

  • result of hidden internal damage to kidneys and the lymphatic system
  • intermittent discharge of lymph into urine
354
Q

What is the treatment approach for Lymphatic filariasis?

A

Interrupt transmission

  • Eliminate microfilariae from the bloodstream
  • with drugs (ivermectin)

Control morbidity

  • assisting lymph flow and preventing secondary infections
355
Q

What are the eye manifestations of Onchocerciasis?

A

Microfilariae migrate to the eye
- where they die
- causing inflammation, scarring, impaired vision, and potentially blindness
- Onchocerciasis is the second leading cause of blindness of infectious origin

356
Q

What are the skin manifestations of Onchocerciasis?

A

Chronic dermatitis

  • intense itching
  • subcutaneous inflammatory response due to dying microfilariae
  • thickened “lizard skin”
  • lax skin due to destruction of elastic fibers
  • potential loss of pigment “leopard skin”
357
Q

What are the levels of antigen-specific IgG and IgE in filariasis?

A
  • Endemic normals make low levels of antibodies across all isotypes.
  • Elephantiasis individuals produce high levels of antibodies across each isotype.
  • Microfilaraemics produce high levels of IgG4 and very little IgE
  • not sure this flashcard is helpful but hay ho
358
Q

Why is the IgG4/IgE ratio important in the immune response in Lymphatic filariasis?

A
  • High IgG4 levels may reduce some pathology
  • If IgE is needed to get rid of the worm
  • Excessive IgE-mediated ADCC can contribute to tissue damage and worsen the pathology (antibody-dependent cell-mediated cytotoxicity)
359
Q

What is the role of IgG4 in immune response to lymphatic filariasis?

A
  • high levels of IgG4 antibodies can compete with IgE for binding to the same antigens.
  • “blocking” of the antigen
  • preventing IgE-mediated immune response triggering a strong inflammatory reaction
  • limiting tissue damage
360
Q

What is the characteristic of T cell response in MF+ individuals in lymphatic filariasis?

A

Poor T cell response

  • resulting in hyporesponsiveness
361
Q

What is the difference between MF- and MF+ individuals?

A
  • MF- individuals do not have microfilariae (larval stage) in their blood
  • while MF+ individuals do have microfilariae present
362
Q

What do reduced IFN-gamma and intact IL-4 responses to microfilaria suggest about an MF+ individual?

A

Reduced IFN-gamma response:

  • MF+ individuals show a reduced production of interferon-gamma (IFN-gamma)
  • associated with Th1 immune responses.
  • suggests an impaired cellular immune response against the filarial parasites

Intact IL-4 response:

  • cytokine associated with Th2 immune response.
  • IL-4 is involved in promoting antibody production, particularly IgE
  • plays a role in the immune response against microfilariae.
363
Q

Which type of cytokine is inhibited in MF+ individuals filarial infections?

A

IFN-gamma - Th1 cytokine response

364
Q

What is the effect of drug treatment on the responsiveness of immune cells in filarial infections?

A

restore responsiveness to some extent in filarial infections

365
Q

Give an example of a drug used in treatment of filarial infections?

A

Diethylcarbamazine - kills parasites

  • partially restores both T cell responses and IFN-gamma production
366
Q

What is the cellular response observed in asymptomatic microfilaraemic individuals with lymphatic filariasis?

A

Reduced T cell responses

  • high levels of IL-4, IL-10, and TGF-beta
  • low levels of IFN-gamma
367
Q

What is the effect of DEC (diethylcarbamazine) treatment on T cell responses and IFN-gamma production in lymphatic filariasis?

A

EN (endemic normals) and individuals with elephantiasis tend to have low worm numbers but higher IFN-gamma levels.

368
Q

What are the characteristics of Tregs (regulatory T cells) in lymphatic filariasis?

A

can dampen both TH1 and TH2 responses.
They are associated with high levels of IL-10 and TGF-beta.

369
Q

How can the action of activity of Tregs in lymphatic filariasis be countered?

A

Blocking IL-10 can partially restore proliferation

370
Q

What is a challenge in treating neglected tropical Intestinal dwelling nematodes with drugs?

A
  • developing single nucleotide polymorphisms (SNPs) that confer resistance to the available drugs
  • leaving few effective options for treatment
371
Q

What are the main species causing human intestinal nematode infections?

A
  • Trichuris trichiura (whipworm)
  • Ascaris lumbricoides (roundworm)
  • Necator americanus (hookworm)
  • Ancylostoma duodenale (hookworm)
372
Q

What is the life cycle of Ascaris lumbricoides (roundworm) and Trichuris trichiura (whipworm)?

A
  • Adults in intestine lay eggs
  • Develop outside the host (Ascaris - infective L2 stage larvae) (whipworm - infective 1st stage larvae)
  • ingested by host
  • larvae hatch in the intestine
  • migrate through tissues to the lungs
  • move up trachea then swallowed
  • Mature into adults in the intestine
373
Q

What is the difference in the life cycle of the Hookworms Necator americanus and Ancylostoma duodenale?

A

Necator americanus

  • obligate skin-penetrating hookworm

Ancylostoma duodenale

  • alternate route
  • infective third-stage larvae (L3) can be swallowed and passed directly to the gut
374
Q

According to WHO, what is the global burden of soil-transmitted helminth infections? What percentage of infections occur in the developing world?

A
  • More than 1.5 billion people (24% of the world population) are infected with soil-transmitted helminths
  • 70% developing world
375
Q

Why do children born in endemic areas harbor worms for most of their lives? (Intestinal nematode infections)

A

Repeated exposure and an inability to develop protective immunity against them

  • Even though immune recognition and attack
  • Parasites survive
  • Evolved mechanisms to combat host defence ie. evade/modulate host attack
376
Q

What are the biological features of intestinal nematode infections?

A
  • Long-term persistence
  • Elicit immunity only after years, or even decades, of exposure
  • Show an overdispersed distribution
377
Q

What is the common pattern of intestinal nematode infections distribution in communities?

A

Aggregated (overdispersed) distribution

  • meaning certain areas carry a higher worm burden
378
Q

What are the clinical syndromes associated with high-intensity intestinal nematode infections?

A
  • Anaemia
  • Abdominal pain, colitis, diarrhea, dysentery
  • Growth stunting

Rarely

  • finger clubbing
  • rectal prolapse
379
Q

Describe the trend in prevalence of intestinal nematode infections in a population?

A

Reaches 90% and stabilises

380
Q

What is the intensity of infection in the context of helminth infections and what does it tell us?

A
  • Measurement of the number of parasite eggs or worms per gram of feces
  • provides information about the parasite burden within an individual
381
Q

What can the intensity of infection indicate?

A
  • provides information about the parasite burden within an individual
  • insights into morbidity and disease severity
382
Q

Explain why the convex age intensity profile is often during childhood (intestinal nematode infections)?

A

Influenced by
Acquired Immunity: resulting from years of exposure to the parasite

  • repeated exposure lead to development of protective response

Differences in Exposure: Children may have higher rates of exposure

  • due to factors such as environmental conditions, behavior, or cultural practices (hygiene practices & behavioral differences)

Susceptibility: due to their developing immune systems

  • individuals reach adulthood, their immune system matures
  • leading to decreased susceptibility
383
Q

What does the convex age intensity profile indicate?

A

Characterized by a peak in infection intensity during a specific age group, often children, indicates several potential factors at play

  • Children may be more susceptible to infection due to their developing immune systems and reduced ability to mount an effective immune response
384
Q

What is the relationship between worm burden and reacquisition of infection?

A
  • Individuals with high worm burden tend to reacquire high worm burden after treatment, suggesting a predisposition for a specific infection level.
  • Wormy individuals tend to reacquire similar worm burdens faster compared to those who are less predisposed.
385
Q

Describe typical field study structure for intestinal nematode infections

A

Select population for study

  • typically 100-200 people divided into age cohorts.
  • Estimate current intensity of infection via eggs/g faeces +/or counting worms after anthelmintic treatment
  • Take blood samples pre and post-treatment
  • Assess reinfection levels over 1-2 years and take new blood samples

Analyse peripheral IRs in relation to

  • Infection intensity, reinfection levels, worm fecundity +/or weight and look for negative correlations
386
Q

What are potential issues during field studies for intestinal nematode infections?

A

Compliance – teenagers
Compliance – need all stool samples within a certain time period to accurately estimate wb

387
Q

What is the prevalence of Trichuris trichiura infection in the human population?

A

Approximately 1 in 5 individuals in the human population

388
Q

What is the relationship between IgE levels and infection intensity in Trichuris trichiura infection?

A
  • IgE levels are negatively correlated with infection intensity
  • High levels of parasite-specific IgE suggest a strong immune response
  • associated with Th2 immunity
389
Q

What is the evidence for acquired immunity in human trichuriasis?

A

As infection intensity decreases with age, IgE levels continue to rise

  • High levels of parasite-specific IgE suggest a strong immune response associated with Th2 immunity
390
Q

What is the role of IL-4 in controlling IgE production (Trichuris trichiura)?

A

IL-4 is a cytokine associated with Th2 immune responses

  • very important for making IgE
391
Q

What is a serum biomarker for in Trichuris trichiura?

A

Th2 immune response - IgE and IL4

392
Q

How many people worldwide are infected with hookworm? and which species is most common?

A

Approximately 1.3 billion people worldwide

  • predominantly Necator americanus
393
Q

What is the average worm load in hookworm (Necator americanus and Ancylostoma duodenale) infection?

A

Approximately 40 worms per infected individual

394
Q

How much blood loss occurs per day due to hookworm infection?

A

estimated 5.1 million liters of blood loss per day worldwide

394
Q

How much blood loss occurs per day due to hookworm infection?

A

hookworm infection leads to an estimated 5.1 million liters of blood loss per day worldwide.

395
Q

What cytokine is associated with resistance to hookworm (Ancylostoma duodenale and Necator americanus) reinfection?

A
  • presence of IL-5
  • type 2 response
  • Promotes activation of eosinophils
396
Q

Why do we need laboratory models of intestinal nematode infection?

A

understand the basis of chronic infection and resistance to infection

  • provide controlled conditions, defined infection history, and manipulable systems, allowing researchers to study the immune response and effector mechanisms involved in these infections.
397
Q

What are the common features in resistance to intestinal nematode infection?

A
398
Q

What is the lifecycle of Trichinella spiralis?

A

Upon digestion of the meat by the new host

  • larvae are released
  • Rapid development (L1-L4) and molting occur in the intestine

Viviparous females lay live larvae (L1)

  • muscle larvae then penetrate the intestine
  • enter blood vessels then migrate to the muscles
  • where they encyst
  • muscle larvae develop within the nurse cell complex
  • muscle larvae remain dormant until the host is eaten
399
Q

How has the key role of CD4+ helper T cells in resistance to Trichinella spiralis been demonstrated?

A
  • Adoptive transfers and in vivo depletions of T cells
  • shown that mice without CD4+ T cells become susceptible to infection
400
Q

What study on in whipworm showed the importance of T cells in immunity?

A

Mouse model infected with whipworm (Trichuris muris) showed that nude mice

  • which lack T cells
  • unable to expel the parasite
401
Q

What are the CD4+ T helper cell subsets and their regulatory mechanisms?

A

Th1 cell development

  • driven by IL-12
  • produces interferon gamma (IFN-gamma)

Th2 cell development

  • driven by IL-4
  • involved in antibody production and inflammation
402
Q

Why is the lab model of Trichuris muris considered useful?

A

Mouse whipworm

  • shares similarities with the human parasite Trichuris trichiura
  • allows investigation of immune responses involved in both acute infection (resistance) and chronic infection (susceptibility)
403
Q

What is the life cycle of Trichuris muris in mice?

A
  • Ingestion: eggs typically present in contaminated food and water
  • Egg Hatching: inside intestines, the eggs hatch, releasing larvae
  • Penetrate the intestinal wall and migrate to the colon where they develop
  • Larvae mature into adult whipworms within the cecum and colon of the mouse
  • Produce eggs, passed in the mouse’s feces into the environment
404
Q

What response is seen in susceptible mice to Trichuris muris?

A

Type 1 immune response

  • characterized by production of IFN-gamma
405
Q

What cytokine responses are associated with resistance to Trichuris muris infection?

A

Th2 immune response

  • characterized by production of cytokines such as IL-4, IL-5, IL-9, and IL-13.
406
Q

What is the role of IgG1 and IgG2a antibodies in Trichuris muris infection?

A

Th2 response

  • leads to the production of IgG1 antibodies
  • resistant

Th1 response

  • switch to IgG2a antibodies controlled by gamma interferon
  • susceptible
407
Q

Which cytokines are associated with rapid expulsion of Trichuris muris in BALB/c mice?

A

Production of IL-4, IL-9, and IL-13 in the mesenteric lymph nodes.

408
Q

What happens when IL-4R is blocked in BALB/c mice infected with Trichuris muris?

A

Inhibition of the Th2 immune response

  • no expulsion of the parasite
409
Q

What happens when IL-4 is knocked out in mice on a resistant background during Trichuris infection?

A

Susceptible

  • unable to produce Th2 responses.
410
Q

What happens when IL-13 is knocked out in mice on a resistant background during Trichuris infection?

A

Delayed Th2 responses

  • become susceptible to infection
411
Q

What type of T cell response is associated with susceptibility to Trichuris infection?

A

TH1 type response

  • lead to chronic infection
412
Q

Which nematode species exhibit a protective immune response involving IL-4 and Th2 cells?

A

Trichinella, Trichuris, and Heligmosomoides polygyrus

413
Q

What are the common effector mechanisms associated with intestinal helminth infections?

A

Eosinophils and IgE

  • Type 1 hypersensitivity response
  • Their direct role in resistance is difficult to demonstrate
414
Q

Is IL-4 essential for resistance to Nippostrongylus infection?

A

IL-4 is not essential for resistance to Nippostrongylus infection

  • there are IL-4 independent mechanisms of expulsion that exist
415
Q

Are eosinophils essential for the expulsion of parasites?

A

Not essential for the expulsion of parasites.

  • Depletion of eosinophils or the absence of eosinophils in genetically deficient mice does not prevent the expulsion of parasites
416
Q

Does IL-5 play a role in eosinophil development?

A

IL-5 is critical for eosinophil development

  • Depletion of IL-5 leads to a lack of eosinophils.
417
Q

What is the role of mast cells in intestinal helminth infections?

A
  • Non-specific inflammatory responses
  • Create hostile environment with their proteases
418
Q

What evidence suggests mast cells are not essential for getting rid of helminth worm infections?

A
  • mice depleted of mast cells can still expel Nippostrongylus and Trichuris parasites
419
Q

Are mast cells important in the resistance to Trichinella infection?

A

Play a role in the resistance to Trichinella infection

  • suggesting their potential importance in this particular helminth infection.
420
Q

What is mastocytosis?

A

Characterized by abnormal accumulation and proliferation of mast cells in various tissues of the body

421
Q

What are Antibody’s role in resistance to intestinal helminths?

A

No evidence to support the importance of antibody in resistance.

422
Q

Describe immune serum as a method of producing helminth immunity

A

Blood serum obtained from individuals who have developed a robust immune response against helminth infections

  • contains high levels of antibodies specific to the parasite
  • passively transfer resistance to naïve individuals by administering large volumes of serum
  • temporary immunity against helminth
423
Q

Describe Interleukin-4 (IL-4) and Interleukin-13 (IL-13)

A

Th2-type cytokines

  • can act as effector molecules in immune response against helminth infections.
424
Q

Direct effects of IL-4 and IL-13 on gut epithelial cells

A

Increase fluid secretion, contractility, and epithelial cell turnover

  • Effects inhibit feeding and make it harder for helminths to survive in the gut
  • constantly being expelled along with the shedding of epithelial cells
425
Q

Describe goblet cell hyperplasia

A

Controlled by Th2 cytokines

  • promote the expansion and activation of goblet cells
  • leading to increased mucin production and mucus secretion
  • defense mechanism against the invading pathogens, trapping and expelling the parasites from the body.
426
Q

What is the significance of Muc5ac in the expulsion of intestinal helminths?

A

Muc5ac-deficient mice are unable to expel these parasites

  • crucial role of this mucin in the protective immune response
427
Q

Describe the effector Mechanisms in Protective Immunity to Intestinal Nematodes

A

Antigen Presentation

  • Worms burrow in gut epithelial cells and secrete/excrete antigens
  • Antigens are picked up by antigen-presenting cells (APCs)

Antigen Processing and T Cell Activation:

  • Antigens are processed by APCs and presented to T cells in draining lymph nodes
  • T cells are exposed to parasitic antigen peptides and become polarized into Th1 or Th2 cells depending on cytokine milieu

T Cell Homing and Migration:

  • T helper cells circulate using homing receptors to follow chemotactic signals and reach the site of infection

Cytokine Release:

  • Th2 cells release IL-13, which can increase gut epithelial cell turnover and facilitate the expulsion of worms from the gut
428
Q

What are the two species of Trypanosoma causing African Trypanosomiasis?

A
  • Trypanosoma brucei gambiense
  • Trypanosoma brucei rhodesiense
429
Q

Which species of Trypanosoma causes a chronic infection?

A

Trypanosoma brucei gambiense

430
Q

Which species of Trypanosoma causes an acute infection?

A

Trypanosoma brucei rhodesiense

431
Q

What is the term for African Trypanosomiasis when found in cattle?

A

Nagana

432
Q

Which animals have been shown to harbor Trypanosoma brucei rhodesiense?

A

Bush pigs, zebras, hippos, and warthogs. - wild mammals

433
Q

Which animals have Trypanosoma brucei gambiense been found in?

A

Cattle and pigs.

434
Q

How are african trypanosomes transmitted to humans?

A

Tsetse fly bite

  • genus Glossina
435
Q

How many new cases of trypanosomiasis are reported each year?

A

300,000 new cases.

436
Q

What factors have contributed to the increase in sleeping sickness cases?

A

Independence of many countries, civil war, and changes in health policies.

437
Q

Which form of sleeping sickness is more prevalent in West Africa?

A

The chronic form - Trypanosoma brucei gambiense

438
Q

Is the East African form (Trypanosoma brucei rhodesiense) of sleeping sickness increasing or declining?

A

Declining

439
Q

What are the initial clinical signs of sleeping sickness?

A

Fever, weakness, headache, swollen lymph nodes, joint pains.

440
Q

What are the symptoms in the advanced stages of sleeping sickness?

A

Anaemia, heart problems, oedema, central nervous system invasion leading to concentration difficulties, lethargy, coma, and death.

441
Q

What is the current drug in use for treating sleeping sickness?

A

Melarsoprol

  • Arsenic-based drug with serious side effects
  • 1000 die each year from arsenic encephalopathy

DFMO - also known as eflornithine

  • safer and more efficacious
442
Q

What are the two morphologies of African trypanosomes in blood smears?

A

Slender form and stumpy form

443
Q

Do African trypanosomes invade cells?

A

No, they do not invade cells unlike T. cruzi

444
Q

What are the characteristics of African trypanosome morphology?

A
  • free-swimming single-celled protozoans
  • long, thin body, a flagellum, and an undulating membrane.
  • kinetoplast at the front
445
Q

What is the role of the stumpy form of African trypanosomes?

A
  • stumpy form is taken up by the tsetse fly and transmits the infection
  • undergoes development to become the infective metacyclic form in the salivary glands of the tsetse fly
446
Q

What is the infective stage of African trypanosomes?

A

Metacyclic trypomastigote

447
Q

What happens when a tsetse fly bites an infected mammalian host?

A

Only the stumpy forms of trypanosomes survive in the tsetse fly

  • differentiate into procyclic trypomastigote
  • epimastigote
  • ending up in the salivary glands as infective metacyclic trypomastigote
448
Q

Different stages in the lifecycle of African Trypanosomes:

A
  • Procyclic stage: Ingested by the tsetse fly and multiplies in the midgut.
  • Epimastigote stage: Attached to the midgut wall of the tsetse fly vector.
  • Metacyclic stage: Infective stage in the salivary glands of the tsetse fly.
  • Slender form: In the bloodstream of the mammalian host, actively dividing.
  • Stumpy form: Non-dividing, pre-infective form in the bloodstream
449
Q

What is the surface molecule responsible for antigenic variation in Trypanosomes?

A

Variable Surface Glycoprotein (VSG)

450
Q

What is the composition of VSG in Trypanosomes?

A

VSG makes up approximately 10% of the dry weight of the organism.

451
Q

What type of forms are dominant in the bloodstream of a mammalian host in African trypanosomes?

A

Slender forms are the majority, while a few stumpy non-dividing forms are also present.

452
Q

What is the effect of antibodies on trypanosomes expressing the dominant VSG?

A

kill 99.999% of trypanosomes expressing the dominant VSG

  • complement fixation and opsonization
453
Q

Why doesn’t antibody-mediated killing eliminate all African trypanosomes?

A

Altering expression of VSG coat

  • unrecognizable by antibodies
  • allowing them to continue multiplying
454
Q

How can a slight change in the amino acid isomer on an epitope prevent antibody interaction? (African Trypanosomiasis)

A

Changing the isomer of an amino acid on an epitope

  • enough to eliminate antibody interaction with the trypanosome
455
Q

How do antibodies interact with complement to combat trypanosomes? (African Trypanosomiasis)

A

Antibodies can interact with complement to punch holes in trypanosomes, leading to their destruction.
- also cause agglutination, clumping the trypanosomes together, which can then be phagocytosed by macrophages

456
Q

What is the difference between homotype and heterotype in trypanosome VSG expression? (African Trypanosomiasis)

A

Most slender trypanosomes express one type of VSG
- referred to as homotype
A small proportion (about 1 in 10,000 to 100,000) have switched to express a different VSG, known as heterotype.

457
Q

Is VSG switching triggered by antibody production? (African Trypanosomiasis)

A
  • No, VSG switching is not caused by antibody production.
  • It is a timed switch of VSG expression that can occur independently of antibody-mediated immune responses
458
Q

What is the estimated repertoire of VSGs in trypanosomes? (African Trypanosomiasis)

A

approximately 2,000 to 2,500 different types

459
Q

What is the role of the first 20-30 amino acids in the VSG protein? (African Trypanosomiasis)

A

constitute a signal peptide that is involved in the movement of the new VSG across the parasite membrane.

460
Q

What is the significance of the next 360 amino acids in the VSG protein? (African Trypanosomiasis)

A

VSG protein are highly variable between different VSGs and contribute to antigenic variation

461
Q

What is the role of the last 120 amino acids at the C-terminal end of the VSG protein? (African Trypanosomiasis)

A

relatively conserved and are typically involved in anchoring the protein to the membrane

462
Q

What is the function of the GPI signaling molecule in the VSG protein? (African Trypanosomiasis)

A

responsible for anchoring the VSG protein into the membrane.

463
Q

Why is there a common structure at the bottom of the VSG? (African Trypanosomiasis)

A

allows for the efficient removal of the fatty acids by a single enzyme, facilitating the exchange of different VSG variants.

464
Q

How does the trypanosome express one VSG at a time? (African Trypanosomiasis)

A
  • has an expression-linked copy (ELC) of the VSG gene, which is duplicated and translocated to a specific site on the chromosomes called the expression site.
  • Only the copy of the gene located in the expression site is transcribed, allowing for the expression of a single VSG variant
  • unique mechanism among single-celled organisms.
465
Q

Where are the expression sites typically located in the trypanosome genome? (African Trypanosomiasis)

A

usually found near telomeres, preserving the original VSG gene while allowing for the expression of a specific variant.

466
Q

How is the switch from one VSG gene to another achieved? (African Trypanosomiasis)

A

degradation of the existing copy of the gene
- opens up the expression site for a new VSG gene to be copied and translocated

467
Q

Are all VSG genes expressed by duplicating and translocating them to expression sites near telomeres? (African Trypanosomiasis)

A

Those already located near telomeres

468
Q

How do trypanosomes achieve a large number of telomeres despite having a relatively normal amount of DNA? (African Trypanosomiasis)

A
  • more telomeres than usual by having an array of different-sized chromosomes
  • arrangement provides them with numerous telomere sites for the placement of VSG genes and enables the expression of a large repertoire of VSG variants.
469
Q

How can recombination contribute to the generation of variation in VSG genes?(African Trypanosomiasis)

A

Recombination can occur between telomere-linked genes that code for different segments of a VSG gene
- leads to the “joining” of these segments, resulting in the generation of a VSG gene with combined characteristics
- novel VSG gene combinations.

470
Q

Why are telomeres considered recombination hotspots in trypanosomes? (African Trypanosomiasis)

A

highly repetitive stretches of DNA, including short tandem repeats
- prone to recombination events

471
Q

What is the significance of the Expression Site Body in trypanosomes? (African Trypanosomiasis)

A

specialized compartment found in the nucleolus of trypanosomes
- site where the expression of a single Variant Surface Glycoprotein (VSG) gene occurs at any given time
- sequesters all the necessary molecules required for gene expression, ensuring that only one VSG is expressed
- unique feature observed only in African trypanosomes

472
Q

What enzyme is involved in the transcription process within the Expression Site Body and why is it surprising? (African Trypanosomiasis)

A

RNA polymerase I (Pol I)
- Pol I is typically associated with the transcription of ribosomal RNA rather than protein-coding genes.

473
Q

How do trypanosomes control the balance between stumpy and slender forms? (African Trypanosomiasis)

A
  • quorum sensing
  • population of healthy slender forms reaches a certain threshold
  • release peptidases that break down host and parasite-derived proteins into oligopeptides.
  • oligopeptides are reabsorbed by the slender forms
  • triggering their transformation into the stumpy form.
474
Q

What is the initial step of Leishmania infection in macrophages?

A

promastigote form of the parasite invades macrophages
- subverts the process of phagocytosis to establish a parasitophorous vacuole
- provides a protected niche for the parasite to survive and replicate within the host cell

475
Q

What are the two major groups of lymphocytes involved in the adaptive immune response?

A

T cells and B cells

476
Q

Why are inbred strains of mice used in experiments with Leishmania infection?

A
  • represent a genetically identical population.
  • better control of host genetics when studying immune responses
  • facilitates tissue transplantation between animals without rejection.
477
Q

How was the basis for the difference in controlling early Leishmania infection investigated?

A
  • by conducting backcrossing experiments between a resistant strain and a susceptible strain of mice
  • F1 generation was backcrossed onto the resistant strain, and animals that remained susceptible were selected and further backcrossed
  • process was repeated several times until mice with all resistant strain genes except for one, which conferred susceptibility, were obtained
  • response to Leishmania infection in these mice was analyzed and compared to the original resistant strain
478
Q

What was the main finding regarding the control of early Leishmania infection based on the backcrossing experiments?

A
  • control of early Leishmania infection is primarily governed by a single genetic locus
  • susceptibility or resistance to the infection in mice can be attributed to specific genetic factors.
479
Q

Describe Genetic Susceptibility Study in Leishmaniasis using Backcrossing Experiments

A
  • Select mice: Inbred mouse strains are selected based on their genetic background
    Infect mice: by injection into the footpad or by exposure to infected sandflies.
  • Monitor infection: signs of infection, such as swelling of the footpad, weight loss, and parasite load in tissues.
  • Determine susceptibility: most susceptible strains will show more severe disease symptoms and higher parasite loads than the least susceptible strains.
    Backcrossing: To study the genetic basis of susceptibility, backcrossing experiments
  • breed susceptible mice with mice that have a known genetic resistance to leishmaniasis
  • The resulting offspring will have a mixed genetic background, but will inherit the resistant genes from the resistant parent
480
Q

What is the gene called that controls susceptibility to Leishmania and other macrophage-infecting pathogens?

A

Lsh (Leishmania susceptibility gene) or N-ramp (natural resistance associated macrophage protein).

481
Q

What is the function of the N-ramp gene? (Leishmania)

A

encodes a divalent ion transporter molecule, although its exact function is not fully understood.

482
Q

How was the N-ramp gene identified? (Leishmania)

A

genetic analysis and backcrossing experiments with congenic mice, researchers identified mutations in the N-ramp gene in strains that varied in their ability to control Leishmania infection.

483
Q

What other macrophage-infecting pathogens are controlled by the N-ramp gene? (Leishmania)

A

implicated in controlling susceptibility to other pathogens, such as Salmonella and Mycobacteria

484
Q

What is the major pathway used by macrophages to deal with intracellular parasites? (Leishmania)

A

nitric oxide pathway is the major pathway used by macrophages to combat intracellular parasites.

485
Q

How is nitric oxide (NO) produced in macrophages? (Leishmania)

A

use oxygen and nitric oxide synthase to produce nitric oxide, as well as nitrites and nitrates.

486
Q

What is the role of nitric oxide in killing intracellular pathogens? (Leishmania)

A

toxic to organic molecules in its vicinity and is used by macrophages to kill intracellular pathogens, along with superoxide.

487
Q

How does nitric oxide enter the parasitophorous vacuole to kill the parasite? (Leishmania)

A

readily diffuse across lipid membranes

488
Q

How does N-ramp contribute to killing parasites? (Leishmania)

A
  • N-ramp concentrates nitrite ions in the parasitophorous vacuole
  • converted into nitric oxide (NO) in the acidic pH.
  • Nitric oxide is toxic to parasites and helps in their elimination.
489
Q

What is the structure of N-ramp? (Leishmania)

A
  • transmembrane molecule with N-terminal and C-terminal regions.
  • embedded in the membrane and functions as an ion transporter.
490
Q

How can a mutation in N-ramp affect the control of early Leishmania infection?

A

Certain mutations, such as a glycine to aspartic acid substitution, can alter its ability to transport ions

491
Q

hsah

A

gj

492
Q

How does the transport activity of Nramp-1 depend on pH? (Leishmania)

A

faster transport rate observed in more acidic environments

493
Q

What is the role of Nramp-1 in transport? (Leishmania)

A
  • divalent cation transporter
  • ability to extrude manganese (Mn2+), iron (Fe2+), and zinc (Zn2+) from macrophages at a faster rate in Nramp-1 positive macrophages
  • starves the parasite of vital cofactors and introduces toxic nitric oxide (NO)
  • killing of the parasite.
494
Q

What activates macrophages to become effective killers? (Leishmania)

A
  • IFN-γ is produced by CD4+ T cells, specifically Th1 cells.
  • Interferon-gamma (IFN-γ) activates macrophages
495
Q

Are CD4+ T cells important in leishmaniasis?

A
  • orchestrate aspects of adaptive immunity through cytokine secretion
  • including the production of IFN-γ, which activates macrophages.
496
Q

What is adoptive transfer of immunity and what can it be used to gain insight into? (Leishmania)

A
  • involves transferring immune cells (such as lymphocytes) from resistant mice into naïvemice to evaluate their impact on infection control
  • Adoptive transfer of immunity can be tested to understand the importance of specific genes or immune cells.
497
Q

What are the benefits of using inbred mice strains during adoptive transfer studies? (Leishmania)

A
  • done without fear of tissue rejection
  • allows for the precise investigation of the impact of transferred immune cells on infection outcomes.
498
Q

What were the findings of adoptive transfer studies in leishmaniasis?

A
  • adoptive transfer of CD4+ T cells into naïve animals resulted in faster healing and disease control.
  • In contrast, recipient animals that received random CD4+ T cells from uninfected mice showed disease progression similar to normal
499
Q

What happened in adoptive transfer studies using BALB/c mice? (Leishmania)

A
  • BALB/c mice, which are poor at controlling leishmaniasis, exhibited worsened disease outcomes in adoptive transfer studies.
  • CD4+ T cells from infected BALB/c mice were transferred to naïve mice, the infection progressed more rapidly.
500
Q

What is the underlying reason for the difference in adoptive transfer outcomes between C3H and BALB/c mice? (Leishmania)

A
  • attributed to the immune response bias of BALB/c mice
  • have Th2 bias, which is effective in expelling the gastrointestinal parasite Trichuris muris but ineffective in controlling leishmaniasis
501
Q

What cytokines are produced by Th1 cells? (Leishmania)

A

Th1 cells produce large amounts of Interferon-gamma (IFN-γ) and IL2. They do not produce IL4, IL5, IL6, IL9, and IL10.

502
Q

What Th1 and Th2 responses both produce? (Leishmania)

A

IL3 and GM-CSF
- mainly remember IL3 not sure where GM-CSF has come from

503
Q

What cytokines are produced by susceptible mice in response to Leishmania infection?

A
  • high levels of IL4 and low levels of Interferon-gamma (IFN-γ)
  • also produce cytokines such as IL5, IL6, IL9, and IL10.
  • Characteristcs of Th2 response
504
Q

What cytokines are produced by resistant mice in response to Leishmania infection?

A

high levels of Interferon-gamma (IFN-γ) and low levels of IL4. Their response is characterized by a Th1 immune profile.

505
Q

How do Interferon-gamma (IFN-γ) and IL4 interact in the immune response to Leishmania?

A

counter-regulate each other. An Interferon-gamma dominant response suppresses the generation of a Th2 response.

506
Q

What is the effect of neutralizing IFN-γ with antibodies? (Leishmania)

A

Neutralizing IFN-γ leads to non-cure and exacerbation of the disease.

507
Q

What is the effect of neutralizing IL-4 with antibodies? (Leishmania)

A

leads to cure and protection against the infection.

508
Q

What does the size of the lesion indicate in the resistant and susceptible mice? (Leishmania)

A

size of the lesion is larger in susceptible mice compared to resistant mice.

509
Q

Why is it difficult to study Leishmania in humans?

A
  • researchers can only obtain peripheral tissues (e.g., blood) for analysis
  • individuals may have other infections or illnesses
  • challenging to assess the number of times a person has been infected and when these infections occurred.
510
Q

What immune parameters can be measured to assess the immune response to Leishmania in humans?

A
  • Delayed type hypersensitivity (DTH) skin tests, which are indicative of Th1 responses, can be performed
  • presence of strong anti-Leishmania antibody responses in individuals tends to be associated with worse disease
  • although antibodies themselves do not play a direct role
  • The antibody response can serve as a proxy for Th2 response, encouraged by interleukin-5 and interleukin-6
511
Q

What type of immune response is associated with mucosal leishmaniasis?

A

Strong Th1 response.

512
Q

What is associated with a strong Th1 response in mucosal leishmaniasis?

A

associated with more severe disease manifestations in mucosal leishmaniasis.

513
Q

What is the significance of a balanced response in cutaneous leishmaniasis?

A

associated with better control of the infection and milder disease symptoms in cutaneous leishmaniasis

514
Q

Diffuse cutaneous leishmaniasis

A

A severe form of cutaneous leishmaniasis where the infection spreads extensively throughout the skin.

515
Q

Antibody - describe its relevance in leishmania response

A

Proteins produced by B cells that play a limited role in combating leishmaniasis.
In some cases, a strong antibody response may worsen disease outcomes.

516
Q

Which of these is associated with severe diffuse cutaneous leishmaniasis?
- Antibodies / DTH (Delayed Type Hypersensitivity)
- Parasite Load / Th1 response
- Cytotoxicity / Il-10

A

Antibodies
Parasite Load
Il-10

517
Q

Which of these is associated with severe mucosal leishmaniasis?
- Antibodies / DTH (Delayed Type Hypersensitivity)
- Parasite Load / Th1 response
- Cytotoxicity / Il-10

A

DTH (Delayed Type Hypersensitivity)
Th1 response
Cytotoxicity

518
Q

What is DTH (Delayed Type Hypersensitivity)? (Leishmania)

A
  • immune response that plays a role in cutaneous leishmaniasis.
  • indicative of a Th1-type response and is characterized by the recruitment of immune cells to the site of infection
  • localized inflammation and tissue damage
519
Q

What is the vector responsible for transmitting schistosomiasis?

A

water snail

520
Q

How are humans infected with schistosomiasis?

A

come into contact with water containing cercariae, which penetrate the skin.

521
Q

What is a fluke?

A

Trematode worm
- Flukes have complex life cycles and often require multiple hosts, including snails and vertebrates.
Schistosomes are flukes

522
Q

How many suckers do flukes have?

A

2

523
Q

Which animals are commonly used as laboratory models for studying schistosomiasis?

A

Mice, rats, baboons, rhesus monkeys, and cattle.

524
Q

Do animal models show evidence of immunity against schistosomiasis?

A

Yes, these animal models show evidence of immunity.
- Rhesus monkeys exhibit strong immunity to reinfection
- rats can terminate primary infection and develop resistance to reinfection

525
Q

Why is it difficult to establish good models of schistosomiasis in the laboratory?

A

Schistosomes are not natural parasites of rodents, and they have a longer lifespan than mice

526
Q

In early experiments with Rhesus Monkeys infected with S. mansoni, what were the results regarding immunity? (Schistosomes)

A
  • able to destroy worms from a second infection
  • but did not destroy the adults that had established from the first infection.
  • Despite this, immunity could be stimulated by both larval and adult stages of the parasite
527
Q

How was immunity stimulated in the monkeys during the experiments? (Schistosomes)

A

stimulated by either large numbers of irradiated cercariae (which die before maturity) or by transplantation of adult worms.

528
Q

What is the term used to describe the observed immune response in the monkeys? (Schistosomes)

A
  • referred to as “concomitant immunity.”
  • appears to operate most effectively against larval stages
  • all stages of the parasite can stimulate immunity
529
Q

What is the structure of the schistosome’s tegument?

A

consists of inner and outer plasma membranes. It is represented by two lipid bilayers covering the surface of the schistosome cells.

530
Q

What changes occur in the body surface of the schistosome when it transitions from water to the host body?

A
  • change in its body surface
  • loses its protective glycocalyx
531
Q

What is the name of the larval stage of the schistosome?

A

schistosomulum formed from cercariae

532
Q

How do adult schistosomes survive in the host?

A
  • decreased antigenicity
  • acquire molecules from the host, including blood group antigens, into their tegument.
  • camouflage and evade recognition by the immune system
533
Q

What was observed in the experiment involving young and older schistosomula and antibodies?

A

young and older schistosomula were incubated with antibodies specific to host red blood cell (RBC) molecules or schistosome molecules

534
Q

What were the key findings of the experiment on the acquisition of host blood group molecules by schistosomula?

A
  • young schistosomula had schistosome identity on their surface
  • older schistosomula acquired host blood group molecules onto their surface membranes.
  • demonstrated young schistosomula initially displayed schistosome molecules on their surface
  • as they matured over 4 days, they acquired host blood group molecules onto their surface membranes
535
Q

Briefly describe the experiment that showed the importance of host-specific antigens in schistosome infection and its findings

A
  • worms from a mouse were transferred to a normal monkey
  • worms covered in mouse molecules that were recognized by the monkey’s immune system.
  • camouflaging allowed the worms to evade the immune response
  • However, when the monkey had pre-formed immunity against the mouse molecules, the worms were killed
536
Q

What are the mechanisms involved in anti-larval immunity against schistosomes?

A

action of Antibodies, specifically IgG and IgE and cell-mediated cytotoxicity.

537
Q

How are antibodies involved in killing schistosomula?

A
  • bind to the surface of schistosomula, allowing white blood cells (eosinophils and macrophages) to attach to the parasite
  • release of cytotoxic granules onto the schistosome surface kills parasite
538
Q

What is the role of cell-mediated cytotoxicity in anti-larval immunity against schistosomes?

A
  • Instead of phagocytosing the large schistosome parasite
  • white blood cells release cytotoxic granules onto the schistosome surface
  • effectively killing the parasite
539
Q

How do eosinophils contribute to the killing of schistosomes?

A
  • When schistosomula are mixed with eosinophils and schistosome-specific IgE antibodies
  • the eosinophils attach to the parasite’s surface and release cytotoxic granules
  • The chemicals from these granules destroy the parasite by causing the membranes to bleb and disrupt.
540
Q

What evidence suggests the presence of acquired immunity in schistosome infection?

A
  • higher prevalence of schistosome eggs in the urine of children compared to adults suggests the acquisition of immunity over time
  • important to consider factors such as water exposure, as schistosome infection occurs through contact with contaminated water
541
Q

What is the purpose of re-infection studies in investigating resistance to schistosomiasis?

A
  • Re-infection studies are conducted to assess the level of resistance or susceptibility to schistosomiasis in individuals who have previously been treated with praziquantel, the drug used to clear the parasites.
  • By re-infecting individuals after treatment, researchers can evaluate the effectiveness of the drug and monitor the level of re-infection
542
Q

What need to be controlled and what other factors need to be measured in re-infection studies carried out on schistosomiasis?

A
  • controlling for exposure to water, as water contact is a common mode of transmission for schistosomiasis.
  • measure snail and cercarial densities
543
Q

What drug is used to treat schistosomiasis?

A

praziquantel

544
Q

What were the findings of the re-infection study regarding acquired immunity in different age groups? (Schistosomiasis in the Gambia)

A
  • Young individuals tend to reacquire infections at similar levels as before treatment.
  • As individuals get older and develop immunity, they produce more IgE antibodies and have elevated eosinophils.
  • Children may have antibodies, but they may not effectively activate the cells required to kill the parasites.
  • Antibody-mediated resistance takes time to develop
545
Q

Which of these is associated with lower re-infection rates in schistosomiasis?

A

IgE!!
- High IgE can decreased re-infection by 10 times
- High IgG4 increased re-infection by 10 times

546
Q

What is the main pathogenic stage of schistosomes?

A

Eggs

547
Q

What happens when schistosome eggs are present in host tissues?

A
  • release histolytic secretions
  • antigens present on the eggs are recognized by T helper cells (TH)
  • release lymphokines
  • leading to the recruitment of inflammatory cells into the granuloma
  • immune response results in the formation of granulomas around the eggs
548
Q

What are the consequences of severe granuloma formation in S. mansoni infections? (Schistosomes)

A
  • particularly when eggs are washed back into the liver
  • can lead to hepatosplenomegaly, esophageal varices, and ultimately death
549
Q

What are the consequences of S. haematobium damage to the bladder and ureter? (Schistosomes)

A

Damage to the bladder and ureter in S. haematobium infections can result in renal failure and ultimately death.

550
Q

How do schistosomes modulate immune responses?

A

producing eggs that induce granuloma formation and inflammation. The adult worms themselves do not cause illness.

551
Q

What are the chronic issues associated with egg clearance in schistosomiasis?

A

can lead to the accumulation of granulomas, liver and spleen enlargement, impaired blood flow, increased blood pressure, and the development of complications such as oesophageal varices and renal failure.

552
Q

What is the purpose of the granuloma response? (Schistosomes)

A

serves to wall off the schistosome eggs and contain the infection.
- protective mechanism aimed at reducing pathology and preventing further dissemination of the parasite.

553
Q

How does the immune response to schistosome eggs change over time?

A
  • immune response produces large granulomas in an attempt to contain the eggs
  • However, as the infection progresses, the immune response is downregulated, resulting in a decrease in the size and intensity of the granuloma response
  • mechanism to balance the need to contain the eggs with minimizing chronic disease and tissue damage.
554
Q

Where do adult cestodes live in their definitive host?

A

Adult cestodes live in the intestine of their definitive host
- usually a vertebrate animal including humans.

555
Q

How do cestodes attach to the gut of their host?

A

suckers or hooks located on their scolex (the small head of the tapeworm).

556
Q

What are proglottids?

A
  • Body segments of cestodes
  • The mature proglottids, known as gravid proglottids, contain eggs and break off from the end of the worm to be passed out of the host’s gut into the environment.
557
Q

What are oncospheres?

A

larval stage of tapeworms that are released from the eggs
- penetrate intestinal wall and circulate to musculature
- characterized by a six-hooked structure

558
Q

What are cysticerci?

A

larval stage of tapeworms found in the tissues of intermediate hosts. They form cyst-like structures

559
Q

What is the definitive host for adult tapeworms?

A

Humans

560
Q

How do cattle and pigs become infected with tapeworms?

A

Cattle and pigs become infected with tapeworms by ingesting eggs - containing oncospheres

561
Q

What happens to the oncospheres after they hatch from the eggs? (Cestode)

A

burrow through the gut wall, invade striated muscle, and develop into cysticerci, where they can remain for several years.

562
Q

How do humans become infected with tapeworms?

A

consuming infected meat containing cysticerci. The tapeworms then develop into adults in the human intestines over a period of two months.

563
Q

What is cysticercosis and where can it occur in the human body? (Cestode)

A
  • condition caused by the encysted larvae of T. solium in humans.
  • cysticerci can localize in various body organs, including the eye, liver, and brain.
    In some countries, up to 20% of all neurological cases are attributed to cysticercosis, such as in Mexico.
564
Q

What percentage of neurological cases are attributed to cysticercosis in Mexico? (Cestode)

A

Up to 20%

565
Q

What causes hydatid disease?

A

Echinococcus - cestode

566
Q

What is the smallest tapeworm and how long is it?

A

Echinococcus
- only 3-9mm long
- has only 3 proglottids.

567
Q

What are the definitive hosts of Echinococcus?

A

Carnivores - e.g. dogs, foxes etc.

568
Q

What is the distribution of Echinococcus?

A

Common in Asia, Australia, East Africa, Southern Spain, S America, Northern parts of N. America and Wales!

569
Q

How does the hydatid cyst evade the host immune response? (Echinococcus)

A
  • laminated layer of the cyst becomes coated with Factor H, a complement inhibitory factor from the host
  • prevents complement from working and helps the metacestode evade immune recognition.
570
Q

What is the life cycle of hydatid disease? (Echinococcus)

A

Infection occurs when eggs are ingested, and oncospheres hatch in the gut, enter circulation, and migrate to various organs.
- develop into cysts, producing protoscolices and daughter cysts, which can grow very large over months or years.

571
Q

What was the cause of sudden death during a football game due to a hydatid cyst? (Echinococcus)

A

rupture of a hydatid cyst in the liver during a football tackle caused the fluid from the cyst to move into the tissues, triggering a massive allergic reaction that led to the teenager’s sudden death.

572
Q

What are the characteristics of the metacestode stage in hydatid disease? (Echinococcus)

A
  • bound by a thin cellular layer called the germinal layer (GL)
  • fills with fluid to form a cyst
  • GL buds on the inside to give rise to brood capsules and protoscoleces
  • outside of the GL forms an acellular extracellular matrix known as the laminated layer
  • helps maintain the physical integrity of the metacestode and evades the immune response
573
Q

What are brood capsules? (Echinococcus)

A
  • develop within the metacestode stage of certain cestode parasites
  • budding structures that form on the inner surface of the germinal layer
  • contain a cluster of protoscoleces
574
Q

What are protoscoleces? (Echinococcus)

A
  • larval forms of cestode parasites found within the brood capsules of the metacestode stage
  • small, invaginated structures that have the potential to develop into adult worms
  • equipped with structures such as hooks or suckers that allow them to attach to the intestinal wall of the definitive host upon ingestion.
575
Q

How does the metacestode develop into the adult stage? (Echinococcus)

A

metacestode develops into the adult stage when it is ingested by the definitive host (carnivore)
- attaches to host gut mucosa
- develops into adult

576
Q

What is the composition of the laminated layer in Echinococcus metacestodes?

A

rich in carbohydrates, particularly mucin-like molecules

577
Q

What is the size of Hymenolepis nana?

A

also known as the dwarf tapeworm
measuring less than 40mm in length.

578
Q

How do humans become infected with Hymenolepis nana?

A

ingesting embryonated eggs from contaminated food, water, or hands.

579
Q

Why are parasite vaccines difficult to develop?

A

complexity of parasites, their eukaryotic nature, and their intricate life cycles and antigens.

580
Q

How many vaccines are currently available against human parasites?

A

only one vaccine available against a human parasite.

581
Q

What are some different types of parasite vaccines?

A
  • live vaccines
  • attenuated vaccines
  • dead vaccines
  • extracts
  • purified antigens
    recombinant antigens
    DNA vaccines
  • RNA vaccines.
582
Q

What factors need to be considered when developing a parasite vaccine?

A
  • target population (e.g., definitive host, disease-bearing host)
  • type of immunity desired (sterile immunity or disease-controlling immunity)
583
Q

What is sterility immunity?

A
  • complete protection against infection
  • prevents the infection from establishing in the host
  • characterized by the complete elimination of the pathogen or its replication within the host
584
Q

What is disease-controlling immunity?

A
  • aims to minimize the severity of the disease rather than completely preventing infection
  • individual may still become infected, but the immune response induced by the vaccine helps control the infection and reduce the severity of symptoms
585
Q

Which parasite vaccine was the first to be developed and what was it for?

A
  • Dictyocaulus viviparus
  • a lungworm infection in cattle that causes husk
  • major problem in the farming industry
586
Q

Can you describe the life cycle of Dictyocaulus viviparus?

A
  • eggs hatching in the host
  • releasing larvae that pass out with host feces.
  • larvae are then ingested by the host during feeding
  • undergo two molts to become infective
  • migrate to the lungs
  • moult to juvenile and then to adults
  • causing infection and disease.
587
Q

How is the lung worm vaccine produced to prevent full infection?

A

Irradiate L3 larvae
- development into L4 then die
- prevents them from reaching the lungs
- prevents development to adulthood

588
Q

What is the bottleneck to Huskvac production?

A

Live larvae must be harvested from feces of infected cattle
- then washed, and irradiated.

589
Q

Are there human vaccines available for taeniid infections?

A

No

590
Q

What is the target of immunity (vaccination) against Taenia in the animal model and why?

A

Target is the onchosphere (great because it is before it gets to muscle).

591
Q

How is immunity achieved in the animal model of taenia?

A

antibody-mediated

592
Q

Can immunity be achieved by injecting oncosphere antigens alone?

A

Yes

593
Q

What is the challenge in vaccinating sheep against T. ovis? (Taenia)

A

Cannot obtain enough oncospheres to vaccinate all the sheep

594
Q

How did researchers overcome the challenge of vaccinating against T. ovis? (Taenia)

A
  • Recombinant antigens were generated using mRNA from oncospheres
  • cDNA
  • expressed in E. coli
  • screened with antibodies from immune sheep - pick correct antigens
  • Vaccinate
595
Q

What is T. ovis and why is it significant?

A

species of tapeworm that infects sheep. It is significant because it was the first-ever recombinant parasite vaccine developed. However, it is not currently in commercial use.

596
Q

Describe use of irradiated sporozoites in malarial vaccination

A

Irradiated Sporozoites
- confer sterile protective immunity in humans

597
Q

How many children does malaria?

A

400,000 in sub-Saharan

598
Q

Why did it take six years to sequence the Malaria genome?

A

biased base composition
- Plasmodium, the parasite that causes malaria, more than 80% of the bases are either adenine (A) or thymine (T)
- challenging to determine the overlapping regions

599
Q

Describe the use of immunoglobulin in malaria

A

Immunoglobulin from immune donors can transfer protection to non-immune people

600
Q

Who are short term immunity vaccines designed for?

A

Tourists and Soldiers: For short-term protection during travel or deployment to malaria-endemic regions, vaccines aim to provide disease blocking and reduce the risk of infection.
- Cost and storage are typically not major concerns in this context.

601
Q

Who are long term immunity vaccines designed for?

A

Residents of Endemic Areas: vaccines are designed to confer life-long immunity to individuals living in malaria-endemic regions
- need to address challenges related to storage, transport, stability, and ease of use.

602
Q

Describe merozoite antigens as a potential vaccine target - what are the antigen targets

A
  • responsible for the symptomatic blood-stage infection
    Vaccines targeting merozoite antigens
  • such as Merozoite Surface Protein 1 (MSP-1) and Apical Membrane Antigen 1 (AMA-1)
  • aim to elicit an immune response against these antigens to prevent or reduce the severity of the disease.
603
Q

What does the RTS,S/AS01/2 do?

A

Malarial vaccine
- induces high levels of CS repeat specific antibody and IFN-γ production (i.e. a Th1 response)

604
Q

What did trials for RTS,S/AS01/2 vaccine find?

A
  • Recipients of the vaccine were 30% less likely to show fever or early signs of the disease at 6 months
  • Recipients of the vaccine were 60% less likely to show severe symptoms of disease at 6 months
  • Fourth dose of the vaccine was crucial to maximize its benefits.
  • Vaccine did not work sufficiently well in younger infants.
  • Vaccine rollout initiated in areas with high malaria transmission.
605
Q

What is the modified RTS,S vaccine called?

A

R21.

606
Q

What is the main protein targeted by the R21 vaccine?

A

circumsporozoite protein (P. falciparum) in Plasmodium falciparum malaria.

607
Q

Describe an indirect life-cycle

A

Reproduction of parasite in definitive
Release of infective stages (eggs/cysts) into outside environment
reinfects into same host again
- Uptake of stages by intermediate host
- Development of infective stages in intermediate host
- Transmission to final host by ingestion of infective stages or of intermediate host
Cycle continues

608
Q

What causes Lymphatic filariasis?

A

Wuchereria bancrofti or Brugia malayi

609
Q

What causes Onchocerciasis?

A

Onchocerca volvulus

610
Q

What is latin name for whipworm?

A

Trichuris trichiura

611
Q

What is the latin name for roundworm?

A

Ascaris lumbricoides

612
Q

Name two hookworms

A
  • Necator americanus
  • Ancylostoma duodenale
613
Q

What are trematodes?

A

Class of flatworms known as flukes

  • obligate internal parasites
  • requiring at least two hosts
  • includes blood flukes such as schistosomes

Biology Year 2 (4 decks)

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