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Parasites and Disease > Apicomplexans > Flashcards

Apicomplexans Flashcards

1
Q

The Apicomplexans are otherwise known as the ______

A

Non-flagellated protozoans

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2
Q

What is phylum Apicomplexa characterized by?

A

Ultrastructural bodies called “apical complex”

Have transmissible “spore” stage. Rarely have pseudopodia and flagella only present in male gametes. Contains MALARIA

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3
Q

What is the zoonotic reservoir for “Babesiosis”?

A

Cattle

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4
Q

What is the causative agent of Babesiosis?

A

Hemoprotozoan parasites of the genus Babesia

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5
Q

Why is Babesiosis of interest to humans?

A

Very few types can infect humans, but when they do they are often misdiagnosed as Plasmodium (malaria).

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6
Q

What do Babesia parasites look like in erythrocytes?

A

Giemsa-stained smear shows circular purple (nucleus) area, or after that stage can undergo multiplication or reinvasion (multiple parasites per cell, not seen in Malaria)

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7
Q

Name and describe the 3 major life phases seen in the Apicomplexa

A

Merogony - Multiplication of trophozoites to form merozoites (some of which may become pre-gametogenic cells)

Sporogony - Formation of sporocyst, enclosing sporozoites within oocyst.

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8
Q

If sporogony occurs in an invertebrate, what occurs? How does this life cycle differ from that of Apicomplexans that undergo sporogony in the external environment?

A

Invertebrate - Becomes transmissible to vertebrate through something like a bite

External environment - Parasites will either be consumed by intermediate vertebrate, then zoites are produced and the intermediate vertebrate is consumed by the final host

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9
Q

Briefly describe the basic Apicomplexan life cycle

A

Alternates between haploid (spore) stage, diploid states. Spore is stable and resistant to the environment. Gametes are produced either directly or indirectly from spores, not directly by meiosis.

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10
Q

What is a “thin” blood smear?

A

Produced when a coverslip is dragged across a drop of blood to create a 1-cell thick layer of blood

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11
Q

How are Babesia gametes produced, describe how this is unique?

A

Tick feeds on blood containing pre-gametogenic cells. There is no oocyst or sporocyst, but developmental stages are otherwise typical.

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12
Q

Why is the Boophilus annulatus tick life cycle important for the transmission of Babesia

A

When a female who has fed on an infected cow lays eggs - the eggs are infected too (trans-ovarial transmission). Once the babies develop, they are already infected and can spread infection to another bovine animal

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13
Q

Describe the endopolyogeny of Apicomplexans that have no invertebrate host

A

Usually occurs in the intestinal tissues - sporocysts open to release sporozoites that infect epithelial cells.

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14
Q

Babesiosis differ from malaria in many ways. What are these?

A

No liver stage, no exo-erythrocytic stage.

They build up very quickly and cause a massive reduction in hematocrit.

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15
Q

Babesiosis results in a condition called “hemoglobinuria”. What is this and how can one tell it is happening?

A

A lot of free hemoglobin circulating in the blood stream as a result of burst red blood cells. Turns urine pink

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16
Q

_______ is the causative agent of relapsing or cyclical human diarrhea in immunocompromised hosts

A

Cyclospora cayatenensis

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17
Q

How is C. cayatenensis acquired and who is most likely to acquire it?

A

From contaminated tap water, fresh fruit, other sources. Usually only acquired by immunocompromised individuals (ex. HIV/AIDS)

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18
Q

How was Babesiosis eradicated in the southern US?

A

Ticks were killed using pesticides (Acaricides) by dipping cattle in pesticides before moving them elsewhere

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19
Q

C. cayatenensis is characterized by…?

A

2 sporocysts, each with 2 sporozoites. It fluoresces blue green under UV light

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20
Q

What is the appearance of a Cryptosporidium parvum parasite?

A

4 sporozoites in oocyst, no sporocyst

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21
Q

What are the clinical features of Babesiosis? Do people die of it?

A

Up to a month after infection fever, chills, sweating, myalgias, fatigue, anemia. People don’t die of Babesiosis unless they are immunocompromised. Sometimes they have to have spleen removed

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22
Q

How is Babesiosis found?

A

Antibody detection, PCR, Giemsa smears

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23
Q

How is Babesiosis treated in humans?

A

Quinine (anti-malarial), azithromycin, clindamycin

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24
Q

What is the main reservoir for Toxoplasma gondii infection?

A

Cats - Felidae

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25
Q

_____ are in-tissue cysts produced by Apicomplexans

A

Bradyzoites

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26
Q

Describe the life cycle of Toxoplasma gondii

A

Cats typically eat zoite infected prey, bradyzoites released into intestine. Invade epithelial cells of the small intestine.
They undergo asexual replication then gametogony (sexual). The oocyst sporulates within 1-5 days and is consumed by intermediate host.

27
Q

_____ are female generating cells in Apicomplexan parasies, whereas _____ are male generating

A

Macrogametocyte,

microgametocyte

28
Q

How do humans become infected with Toxoplasma gondii?

A
  1. Ingestion of undercooked infected meat
  2. Ingestion of the oocyst from fecally contaminated hands/food
  3. organ transplant/blood transfusion
  4. Transplacental
29
Q

How is Toxoplasma gondii infection treated?

A

Anti malarial drugs

30
Q

How come we don’t have malaria in Manitoba? Is it possible that we will in the future?

A

We have a mosquito free season. However, we do have one species of Anopheles mosquito that could be a malaria vector if climate change affects us much more

31
Q

Who is credited (won a nobel prize) with the first demonstration of malaria transmission by mosquitos?

A

Ronald Ross

32
Q

The causative agent of malaria is the genus _____

A

Plasmodium

33
Q

Most human malaria victims are ______

A

Children and pregnant women

34
Q

Malaria deaths per year are on par with that of ____ and ____

A

HIV/AIDS and TB

35
Q

What is the easiest way to determine whether a mosquito is of the Anopheles group?

A

Lifts posterior up when feeding

36
Q

How is malaria diagnosed?

A

Microscopy, seroconversion (look for rise in antibodies), enlarged spleen/liver, fever, vomiting, muscle aches, anemia, coma
PCR and antigen (ELISA) tests

37
Q

What are the three primary malaria-transmitting mosquitos and what do they all have in common?

A

Anopheles darlingi, Anopheles gambiae, Anopheles stephensi. What they have in common is that they prefer humans, and do very well in disturbed habitats around humans

38
Q

What is a “catholic feeding pattern” when it comes to mosquitos?

A

Don’t prefer any particular host

39
Q

Which parasite accounts from over 90% of human malarial deaths?

A

Plasmodium falciparum

40
Q

Which parasite is the most common cause of malaria (though not the most deadly)

A

Plasmodium vivax

41
Q

_______ protein is a protein that allows malaria sporozoites to bind to the liver cell membrane. Why is this protein significant?

A

Circumsporozoite protein. People can develop antibodies against this protein as a type of immunity

42
Q

What type of antibodies do people in malaria endemic areas develop? How long does this immunity last?

A

They develop partial resistance to trophozoites in the blood. This immunity goes away after living far away from malaria-endemic areas for >6 months.

43
Q

What does it mean if an area is hyper-endemic for malaria?

A

Everyone in the area gets at least 1 case of malaria per year.

44
Q

What kind of resistance do humans in hyper-endemic malaria areas develop?

A

The person who has the disease doesn’t develop immunity, but they can develop antibodies against the gametocytes. When gametocytes are transferred from the blood into the mosquito, the antibodies can affect the gametes and prevent fusion of macro and microgametes.

45
Q

What type of infection does Plasmodium vivax produce?

A

Usually produces periodic fevers and chills. Has a very slow buildup of schizonts in the blood - cannot enter red blood cells of certain ages

46
Q

What type of infection does Plasmodim falciparum produce? How does it differ from P. vivax?

A

Can induce cerebra malaria (malaria in the brain) - causes coma.
DifferenceL Merozoites produced by schizogony can reproduce in red blood cells of any age - induces intense anemia. P. viviax has to infect red blood cells of a particular age.

47
Q

What are “hypnozoites” - in reference to malaria infection

A

Occurs with P. vivax and P. ovale. These are dormant forms of malaria parasites in the liver. They may not cause symptoms until months or years after infection when they are reactivated in a procesws called “Recrudescence”

48
Q

What type of infection does P. malariae produce

A

Develops extremely slowly - so slowly that it is referred to as “latent malaria”

49
Q

What happens when mosquitos have large amounts of sporozoites in the salivary glands?

A

They become hyper aggressive, going after a meal with ferocity

50
Q

Fully mature schizonts of P. falciparum can have between __ and ___ parasites inside

A

8 and 30

51
Q

What are ways in which malaria can be prevented?

A

Vector control - environmental management and insecticide treatment.
Interrupting contact - don’t go outside at night, mosquito-proofing houses, repellents, bednets

52
Q

How did air conditioning reduce mosquito-human contact in the US?

A

People stopped going outside at night, closed windows, generally spent more time indoors

53
Q

What is one of the biggest success stories in malaria control in children?

A

Bed nets! Especially ones coated with permethrin, which provides a vapour barrier as well

54
Q

How is malaria treated and what do the drugs target?

A

Drugs typically target schizonts in erythrocytes (Called schizonticides).

55
Q

Describe the antimalarial drug “quinine”

A

Historically important as a natural medicine. Aboriginals in south america knew about it and pulled barks from the Peruvian “Cinchona” plants. Before 1930 it was the only effective antimalarial - new ones needed to be developed during WWII because the Japanese cut off the supply by invading SE asia. Highly toxic - can cause jaundice and destroy the kidneys.

56
Q

Describe the anti-malarial drug “Atebrin”

A

Developed during WWII as alternative to quinine. Can result in blindness

57
Q

Describe the anti-malarial drug “Chloroquine”

A

Very effective and completely synthetic. Very low cost and used from the 40s until about the 90s. Very few side effects, even after long use (years of use). Widespread underuse (not taking it for the full 2 weeks) of chloroquine led to most strains of P. falciparum and some of P. vivax becoming resistant.

58
Q

Describe the anti-malarial drug “Primaquine”

A

The only one that is effective against the hepatic stage of malaria. Used to be used as a prophylactic because it would stop it at the liver stage. Can destroy even hypnozoites of P. vivax and P. ovale. Has little effect on P. falciparum.
Toxic to individuals who have low levels of Glucose-6-phosphate dehydrogenase - people who are deficient will die (about 15% of asian people). People must be screened before taking primaquine

59
Q

Describe the anti-malarial drugs “Proguanil”, “Pyrimethamine”, “Atovaquone”

A

Anti-folates.

Proguanil - Folate antagonist, binds to enzyme dihydrofolate reductase. Sometimes used as a prophylactic.

60
Q

Describe the anti-malarial drug “Malarone”

A

Mixture of two anti-folates (proguanil + Atovaquone). 95% effective against drug resistant P. falciparum. So far free of side effects (unless pregnant. folic acid is very important to developing fetus)

61
Q

Describe the anti-malarial drugs “Maloprin” and “Fansidar”

A

Both made of two chemically similar anti-folates. Resistance is widespread - neither are recommended

62
Q

Describe the anti-malarial drug “Mefloquine/Lariam”

A

Quinoline methanol derivative, which is structurally similar to quinine. Long half life (only need 1 pill per week), schizonticide. Can cause “acute brain syndrome” - people can go crazy (strange dreams, paranoia)
Developed to replace chloroquine as resistance spread. Resistance is now developing.

63
Q

Describe the anti-malarial drug “Artemisinins”

A

Group of products that come from a wormwood shrub developed in China. Always known as anti-fever drugs, now used to treat malaria. We don’t know how, but we do know that sometimes it doesn’t help treatment, just symptoms

Parasites and Disease (11 decks)

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