Lecture 7 - Vector Parasite Interactions Flashcards

1
Q

What are the four stages in the life cycle of mosquito?

A

Eggs > larvae > pupae > mosquitoes.

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2
Q

When do mosquito eggs hatch into larvae?

How many times do larvae shed their skin?

What happens during pupal stage?

What do newly emerged adult mosquitoes do first?

A
  • Most eggs hatch into larvae within 48 hours.
  • Larvae shed their skins four times, growing larger after each shedding.
  • The pupal stage is a resting, non-feeding stage of development, but pupae are mobile.
  • The newly emerged adult rests on the surface of the water for a short time to allow itself to dry and all its body parts to harden.
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3
Q

What is the difference between mosquitoes laying eggs and sand flies laying eggs?

When do eggs hatch in sand flies?

How many larva instar forms are they?

A
  • Sand flies lay 30-70 eggs at a time and mosquitoes lay one egg at a time.
  • Sand fly eggs hatch after 4-20 days.
  • There are 4 larva instar forms.
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4
Q

What kind of feeders are triatomine bugs?

In which disease are they vectors?

Do nymphs transmit parasites as well?

How are the parasites transmitted?

A
  • Triatomine bugs are blood-feeders.
  • They are vectors of Chagas disease (South American Trypanosomiasis).
  • Nymphs transmit parasites as well.
  • Parasites are transmitted through the faeces.
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5
Q

How do parasites enter the host?

What is the percentage of bugs infected? And what is this inside of houses?

A
  • Via eyes, mucous membranes and abraded skin (80% of transmission).
  • Up to 50% of bugs infected (70% of the houses).
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6
Q

Factors influencing transmission to humans:

  • Bugs are ‘…’ – single most important factor.
  • … defecation
  • Bugs infest … housing and … roofs
  • Rodent/possum enters … cycle.
  • … consumption of bugs
  • Bugs infected for … (nymphs and adults) – adult bugs have … infection rates
  • Up to …% of bugs infected (70% of houses)
  • Biting nuisance: 20 bites per night – … ml blood. No pain with bite.
A

Factors influencing transmission to humans:

  • Bugs are ‘domesticated’ – single most important factor
  • Early defecation
  • Bugs infest poor housing and thatched roofs
  • Rodent/possum enters domestic cycle.
  • Mistaken consumption of bugs
  • Bugs infected for life (nymphs and adults) – adult bugs have higher infection rates
  • Up to 50% of bugs infected (70% of houses)
  • Biting nuisance: 20 bites per night – 3 ml blood. No pain with bite.
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7
Q

South American Trypanosomiasis (Chagas’s disease) is caused by which parasite?

Where do the parasites multiply in triatomine bugs?

How is infection acquired?

A
  • Trypanosoma cruzi.
  • They multiply in the hindgut of the bug as epimastigotes and develop into metacyclic trypanosomes.
  • Infection is acquired by rubbing faeces of the bug into a wound or conjunctiva.
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8
Q

What happens with the parasites once they enter the host?

A
  1. In the host trypomastigotes multiply at the site of the bite, enter the bloodstream and a variety of tissues, particularly neuroglia and muscle cells.
  2. Parasites develop as intracellular amastigotes and form pseudocysts.
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9
Q

What happens when the pseudocysts (developed by amastigotes) rupture?

Are pathological effects chronic?

A

Rupture of these pseudocysts causes inflammation, tissue damage and further dissemination.

Most pathological effects are chronic, probably related to a combination of tissue damage, neuronal loss and autoimmune response.

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10
Q

Describe characteristics of Acute Chagas’ disease (4).

A
  • Most common in children
  • 1/3 are symptomatic (fever, fatigue, body aches, headache, rash)
  • Acute phase lasts 1-3 months and resolves spontaneously.
  • 15-40% will develop chronic disease.
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11
Q

Chronic Chagas’ disease occurs 10-20 years after initial infection. Describe classical manifestation.

A
  1. Cardiac disease: biventricular cardiomyopathy or cardiac rhythm disturbance (heart block).
  2. Mega-oesophagus or megacolon: intramural nerve damage. Presents as aspiration pneumonia and abdominal distention.
  3. Similar mega disorders of other hollow muscular structures such as small bowel and ureter.
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12
Q

How is Chagas diagnosed (4)?

A
  1. Microscopy
  2. Culture
  3. Xenodiagnosis (letting uninfected bugs feed on patients)
  4. Biopsy for amastigotes
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13
Q

How is Chagas’ treated? Is there a difference between acute and chronic treatment?

A

Nifurtimox and benznidazole suppress parasitaemia and prevent acute neurological and myocardial complications.

Chronic treatment is more difficult: benznidazole and pacemakers.

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14
Q

Name three species where males and females feed on plant carbohydrates and only females feed on blood.

A
  • Mosquitoes (malaria)
  • Blackflies (filariasis)
  • Sand flies (leishmania)
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15
Q

Name two species where both sexes are obligate blood feeders.

A
  • Tsetse flies (sleeping sickness)
  • Triatomine bugs (chagas)
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16
Q

Life cycle of Trypanosoma cruzi in host:

  1. An infected triatomine bug takes a blood meal and releases … in its faeces near the site of the bite wound. … enter the host through the wound or through mucosal membranes.
  2. The trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular … .
  3. The amastigotes multiply and differentiate into … .
  4. The trypomastigotes are released into the blood stream and go to new infection sites and transform into … again.
A
  1. An infected triatomine bug takes a blood meal and releases trypomastigotes in its faeces near the site of the bite wound. Trypomastigotes enter the host through the wound or through mucosal membranes.
  2. The trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes.
  3. The amastigotes multiply and differentiate into trypomastigotes.
  4. The trypomastigotes are released into the blood stream and go to new infection sites and transform into amastigotes again.
17
Q

Life cycle of Trypanosoma cruzi in triatomine bug:

  1. The triatomine bugs becomes infected by feeding on human/animal blood that contains circulating … .
  2. The ingested … transform into … in the vector’s midgut.
  3. The parasites multiply and differentiate into … in the hindgut.
A
  1. The triatomine bugs becomes infected by feeding on human/animal blood that contains circulating parasites.
  2. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut.
  3. The parasites multiply and differentiate into trypomastigotes in the hindgut.
18
Q

Is it possible for triatomine bugs to feed on plants?

Would there be any advantage to the bugs? Would there be a disadvantage?

A
  • Yes, they can feed on plants.
  • Advantages: more opportunity to get nutrients, carbohydrates, fitness advantage.
  • Fitness disadvantage: more likely to take up pathogens.
19
Q

Chagas disease can be a foodborne illness. Examples of parasites enhancing transmission to the next host:

A
  • Alteration of mosquito behaviour –longer feeding time
  • Blockage of sand fly gut to promote regurgitation
20
Q

Effect of Plasmodium infection on the feeding persistence of Anopheles stephensi throughout the sporogonic cycle:

Vector-borne parasites such as malaria have been shown to modifythe feeding behaviour of their invertebrate hosts so as to increase the probability of transmission. How?

A

Feeding persistence of female Anopheles stephensi towards a human host is decreased in the presence of Plasmodium yoelii nigeriensis oocysts (which cannot be transmitted), but increased when the malaria has developed into transmissible sporozoites in the salivary glands.

21
Q

Transmission of Leishmania:

Explain the mechanism of PSG (gel-like matric secreted by promastigotes in sand flies with mature infections.

A

Gut blockage by Leishmania promotes feeding and transmission.

Fly feeds with difficulty and regurgitates parasites into wound.

22
Q

Leishmania infantum/L. major life cycle:

  1. The sand flies inject the … from their proboscis during blood meals.
  2. Promastigotes in bloodstream are … by macrophages. Promastigotes transform into … .
  3. Amastigotes multiply and infect other … cells.
  4. Sand flies become infected by … the infected cells during blood meal.
  5. In sand flies amastigotes transform into promastigotes in …, and migrate to … .
A
  1. The sand flies inject the promastigotes from their proboscis during blood meals.
  2. Promastigotes in bloodstream are phagocytized by macrophages. Promastigotes transform into amastigotes.
  3. Amastigotes multiply and infect other phagocytic cells.
  4. Sand flies become infected by ingesting the infected cells during blood meal.
  5. In sand flies amastigotes transform into promastigotes in midgut, and migrate to proboscis.
23
Q

Dengue virus life cycle:

  1. Virus will fuse with skin cell through … formation.
  2. Once in the cell, the virus will release the dengue viral … .
  3. The viral RNA hijacks the host cell’s machinery to … itself.
  4. Viral RNA enclosed with C-proteins uses rough ER to get enclosed with …. proteins.
  5. It travels through the Golgi complex, where the viruses is converted into its … form.
  6. Mature dengue is released and can … other cells.
A
  1. Virus will fuse with skin cell through endosome formation.
  2. Once in the cell, the virus will release the dengue viral RNA.
  3. The viral RNA hijacks the host cell’s machinery to replicate itself.
  4. Viral RNA enclosed with C-proteins uses rough ER to get enclosed with M- and E-proteins.
  5. It travels through the Golgi complex, where the viruses is converted into its infectious form.
  6. Mature dengue is released and can infect other cells.
24
Q

Lymphatic Filariasis (Wuchereria bancroft) life cycle:

  1. Mosquito introduces … filarial larvae onto the skin of human host.
  2. They develop in adults that commonly reside in … .
  3. Adults produce … , which migrate into lymph and blood channels moving actively.
  4. Mosquito ingests microfilariae during blood meal. After ingestion microfilariae lose their … and some move to … muscles.
  5. In thoracic muscles microfilariae will develop into … larvae and subsequently into third-stage larvae.
  6. Third-stage larvae move to mosquito … .
A
  1. Mosquito introduces third-stage filarial larvae onto the skin of human host.
  2. They develop in adults that commonly reside in lymphatics.
  3. Adults produce microfilariae, which migrate into lymph and blood channels moving actively.
  4. Mosquito ingests microfilariae during blood meal. After ingestion microfilariae lose their sheaths and some move to thoracic muscles.
  5. In thoracic muscles microfilariae will develop into first-stage larvae and subsequently into third-stage larvae.
  6. Third-stage larvae move to mosquito proboscis.