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PARA424 > lecture 16- protozoa, kinetoplastids > Flashcards

lecture 16- protozoa, kinetoplastids Flashcards

1
Q

what unique organelle do kinetoplastids have?

A

kinetoplast

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2
Q

kinetoplast = …

A

a disk-shaped mass of circular DNA inside a large mitochondrion genome

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3
Q

kinetoplastid DNA is relatively …

A

abundant

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4
Q

what kind of DNA makes up the kinteoplastid genome?

A

ktDNA

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5
Q

what organelle is ktDNA within?

A

the mitochondria

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6
Q

what are the two types of ktDNA?

A
  1. maxi-circles: encode several mitochondria genes and are more or less equivalent to the mtDNA
  2. mini-circles: heterogenous and rapidly evolving; DNA encode guide RNAs responsible for RNA editing
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7
Q

what is true about mRNAs expressed from maxi-circles?

A
  • they require extensive RNA editing, done by several multi-protein complexes with information coming from small guide RNAs (gRNAs)
  • gRNAs serve as the template for editing
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8
Q

what can mini-circle DNA be used for?

A

parasite detection and differentiating isolates

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9
Q

what is the glycosome and its function?

A

a peroxisome-like organelle in which glycolysis occurs

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10
Q

what are the four major morphological forms found in kinetoplastids that cause human disease?

A
  1. trypomastigote
  2. amastigote
  3. promastigote
  4. epimastigote
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11
Q

leishmania

A

zoonotic protozoan parasites that cause a disease known as leishmaniasis

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12
Q

how is leishmania transmitted?

A

by the bite of certain species of sandflies

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13
Q

how many species of leishmania infects humans?

A

21 out of 30 species

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14
Q

different species of leishmania are …

A

morphologically indistinguishable

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15
Q

L. donovani causes …

A

visceral leishmaniasis

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16
Q

L. tropica causes ..

A

cutaneous leishmaniasis

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17
Q

L. braziliensis causes …

A

mucocutaneous leishmaniasis

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18
Q

how many countries has leishmaniasis been found in?

A

88 countries

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19
Q

where is L. donovani most prevalent?

A

Asia and Africa

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20
Q

where is L. tropica most prevalent?

A

Asia, Africa and Mediterranean

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21
Q

where is L. braziliensis most prevalent?

A

Central and South America

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22
Q

more than 90% of the world’s cases of visceral leishmaniasis are in …

A

India, bangladesh, nepal, sudan and brazil

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23
Q

what kind of life cycle does Leishmania acquire?

A

digenetic life cycle

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24
Q

what are the 2 morphological forms of Leishmania?

A
  1. promastigote, found in the sandfly vector

2. amastigote, in the host (humans)

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25
Q

what is the pathology of Leishmaniasis?

A

pathogenesis is due to an immune reaction to the pathogen, particularly cell mediated immunity

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26
Q

what does a laboratory examination of leishmaniasis mark?

A

a marked decrease in white blood cells with relative increase in monocytes and lymphocytes, reduced platelets and anemia

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27
Q

in leishmaniasis, …. are extremely elevated in a first infection

A

IgM and IgG levels

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28
Q

What parts of the body do cutaneous leishmaniasis affect?

A
  • generally self-healing
  • skin
  • mucous membranes
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29
Q

what parts of the body do visceral leishmaniasis affect?

A
  • fatal
  • liver
  • spleen
  • bone marrow
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30
Q

cutaneous leishmaniasis

A
  • the most common form of leishmaniasis
  • characterized by one or more sores/ulcers, papules or nodules on the skin
  • organism multiplies locally producing a skin nodule 2-8 weeks after the bite
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31
Q

what species of leishmania causes mucocutaneous leishmaniasis?

A

L. braziliensis

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32
Q

why is mucocutaneous leishmaniasis so dangerous?

A
  • unlike cutaneous leishmaniasis, it can metastasize causing the lesions to spread to mucoid tissues (oral, pharyngeal and nasal) , which lead to severe deformity
  • may occur months to years after original skin lesion
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33
Q

what species of Leishmania cause visceral leishmaniasis?

A

L. donovani, L. donovani infantum (old world), L. donovani chagasi (new world)

34
Q

what are the epidemiological features of L. donovani?

A

affect people of all ages, L. donovani infantum affects young children and infants

35
Q

…. leishmaniasis is the most severe form of leishmaniasis and may be fatal if left untreated

A

visceral

36
Q

patients with … should be considered for visceral leishmaniasis

A

chronic fever

37
Q

why is there rarely a local lesion in visceral leishmaniasis?

A

L. donovani organisms in VL are rapidly eliminated from the site of infection. They localize and multiply in the mononuclear phagocytic cells of spleen, liver, lymph nodes, bone marrow, intestinal mucosa and other organs

38
Q

symptoms of visceral leishmaniasis

A

splenomegaly, swollen abdomen, severe muscle wasting, and jaundiced hands

39
Q

how is leishmaniasis diagnosed?

A
  • evaluation of the history of exposure to sandflies
  • biopsy is required
  • examination of Giemsa-stained slides of the relevant tissue (most commonly used to detect the parasite)
40
Q

what is the treatment for Cutaneous/mucocutaneous leishmaniasis?

A

sodium stibogluconate - antimony containing drug with many serious side effects

41
Q

what is the treatment for visceral leishmaniasis?

A

liposomal amphotericin-B - an antifungal medication

-causes severe and potentially lethal side effects

42
Q

what are ways to prevent leishmaniasis?

A
  1. suppress the reservoir - dogs, rats, gerbils, other small mammals and rodents
  2. suppress the vector- sandfly, control measures involve house spraying
  3. prevent sandfly bites
    - most important at night
    - wear protective clothing
    - use insect repellant
    - use permethrin treated bed nets
43
Q

What disease is trypanosomes responsible for?

A

trypanosomiasis - sleeping sickness

44
Q

what do trypanosomes mainly infect?

A

most types of domestic livestock, many wild animals and man

45
Q

what kind of fly are trypanosomes transmitted in?

A

tsetse fly, of the genus Glossina

46
Q

what species of trypanosomes cause West African sleeping sickness

A

trypanosoma brucei gambiense

47
Q

what species of trypansomes cause East African sleeping sickness?

A

trypanosoma brucei rhodesiense

48
Q

what animal does Trypanosoma brucei brucei infect?

A

antelopes and other african ruminants (cattle, horses, camels)

49
Q

what is the disease T. brucei brucei cause?

A

nagana - a type of sleeping sickness in animals

50
Q

what is the affect of nagana in African ruminant animals?

A

reduce the growth rate, milk productivity, and strength of farm animals, leading to eventual death of the infected animals

51
Q

the trypanosomes of equines and of camels are transmitted not by tsetse flies, but by..

A

direct blood contact during copulation or by biting insects such as horse flies that probe several animals one after the other

52
Q

how many cases a year of trypanosomiasis are there?

A

about 300,000 new cases each year

53
Q

humans are the main reservoir for what species of trypanosomes?

A

T. brucei gambiense

54
Q

who are the main reservoirs for T. brucei rhodesiense?

A

wild game animals and cattle

55
Q

how can T. brucei be transmitted in humans?

A
  1. mother to child infection
  2. blood transfusion
  3. sexual contact (rare)
  4. laboratories: accidental infections, although this is uncommon
56
Q

Where is T. b. gambiense found?

A

central and western Africa

57
Q

what is the effect of T. b. gambiense infection?

A

causes a chronic conditions that can extend in a passive phase for months or years before symptoms emerge

58
Q

what species of T. b. gambiense chronic infection, is responsible for the acute form?

A

T. b. rhodesiense

59
Q

where is T. b. rhodesiense found?

A

southern and eastern Africa

60
Q

how is the infection of T. b. rhodesiense different from T. b. gambiense?

A

its infection emerges in a few weeks and is more virulent and faster developing

61
Q

what is unique about African trypanosome’s life cycle?

A

the whole life cycle has extracellular stages

62
Q

how does trypanosoma avoid the host’s immune response?

A

using antigen variation

63
Q

what is antigen variation?

A

the process of a parasite changing its surface protein. in the case of trypanosomes, antigen variation is used by variation of the variant surface glycoproteins (VSGs)

64
Q

what do Trypanosomes do with the VSGs during antigen variation?

A

parasite produces and covers its own plasma membrane with VSGs. as host’s antibodies attack the parasite, it changes its expression to the new VSGs and masks itself from the body’s natural defence mechanisms against foreign particles

65
Q

T. brucei gambiense invades the …

A

CNS initiating a chronic, sleeping-sickness

66
Q

T. brucei rhodesiense affect on humans?

A

rapid weight loss, heart involvement, and death

67
Q

what is the diagnosis on african trypanosomiasis?

A

demonstrating trypanosomes by microscopic examination of lymph node aspirates, blood, bone marrow or, in the late stages of infection, cerebrospinal fluid

68
Q

how are motile trypanosomes found in diagnosis?

A

using a wet preparation, fixing a smear stained with Giemsa and examined under the microscope

69
Q

what is the treatment for African Trypanosomiasis?

A

the drug regimen depends on the infecting species and the stage of infection.

  1. pentamidine and suramin are used to treat the hemolymphatic stage of West and East African Trypanosomiasis
  2. Melarsoprol is the drug of choice for late disease with CNS involvement
70
Q

what is the prevention/control for african trypanosomes?

A
  1. attempts to control the tsetse fly vectors
  2. tracking of wild game animals
  3. selective breeding of cattle
71
Q

what is Chagas disease?

A

caused by the protozoan parasite Trypanosoma cruzi. a zoonotic disease that can be transmitted to humans by blood-sucking triatomine bugs

72
Q

trypanosoma cruzi can be transmitted through …

A
  1. blood transfusions
  2. organ transplantation
  3. transplacentally
  4. lab accidents (rare)
73
Q

where does chagas disease (american trypanosomiasis) occur?

A

exclusively in the Americas particularly in poor, rural areas of Mexico, Central America, and South America

74
Q

what is the vector for Trypanosoma cruzi

A

the triatomine bug

75
Q

what is the pathology of infection of american trypanosomiasis?

A

chagas manifests in all hollow organs. infected individuals typically remain infected for life

76
Q

what is the most recognized marker of acute Chagas?

A

the Romana’s sign, which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited

77
Q

what are symptoms like in the early stage of American trypanosomiasis?

A

symptoms are mild and usually produce no more than local swelling at the site of infection

78
Q

what happens as American trypanosomiasis progresses?

A
  • serious chronic symptoms can appear, such as heart disease and malformation of the intestines
  • if untreated, the chronic disease can be fatal
79
Q

both … and …. stages are found in humans (American trypanosomiasis)

A

amastigotes and trypomastigote stages

80
Q

what is the treatment for American trypanosomiasis (chagas disease) ?

A
  • the drug of choice is benzimidazole

- currently no vaccine

81
Q

how is American trypanosomiasis prevented/controlled?

A
  • prevention focused on fighting the vector by using sprays and paints containing insecticides and improving housing and sanitary conditions in rural areas
  • mosquito nets are recommended
  • testing of blood donors since blood transfusion is the second most common transmission route of chagas disease
82
Q

what protozoan species are kinetoplasts?

A

Trypanosoma and Leishmania (Flagellata genus)

PARA424 (12 decks)

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