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BSC Zoology - Parasitology > 19. Protozoa (Leishmania) > Flashcards

19. Protozoa (Leishmania) Flashcards

1
Q

who is in the class kinetoplastida?

A
  • leishmania

- trypanosoma

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2
Q

what unique feature do kinetoplastids have?

A

the unique organelle, the kinetiplast

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3
Q

what is a kinetoplast?

A

a disk shaped mass of circular DNA inside a large mitochondrion that contains many copies of the mitochondrial genome

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4
Q

how does kinetoplast DNA look?

A

it is relatively abundant and is a tighly packed mass of DNA

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5
Q

the kinetoplastid genome is composed of ______.

A

ktDNA

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6
Q

the two types of ktDNA occur in a _________ and are called ______ and _______.

A

linked mass within the mitochondrion

mini-circles; maxi-circles

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7
Q

what do maxi circles encode?

A

mitochondrial genes and they are more or less equivalent to the mtDNA

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8
Q

mini-circles are ________ and rapidly evolving, and their function is less clear.

A

heterogenous

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9
Q

what do mRNAs expressed from maxi-circles require?

A

extensive RNA editing

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10
Q

what is RNA editing in maxi-circles mediated by?

A

several multi-protein complexes but the information comes from small guide RNAs that are encoded on mini-circles

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11
Q

what is special and novel about kinetoplastid DNA?

A

that there are 2 genomes in the mitochondrion, one of which contains sequence information that corrects errors in the other

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12
Q

how are the errors on the maxi-circles corrected?

A

they need to be edited

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13
Q

where does editing of the maxi-circles take place?

A

in the mitochondrion of kinetoplastids

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14
Q

what does the extent of editing correlate with?

A

the stage in the parasitic life cycle and the corresponding metabolic changes - such as aerobic/anarobic

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15
Q

what is mini-circle DNA used for in practice?

A

parasite detection and differentiating between various isolates

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16
Q

what is a glycosome?

A

a peroxisome-like organelle in which glycolysis occurs (conversion of glucose to pyruvate)

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17
Q

how many membranes does a glycosome have?

A

1

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18
Q

what does the glycosome change in comparison to other eukaryotic organisms?

A

it sequesters a large number of glycolytic enzymes that would otherwise be located in the cytosol

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19
Q

the glycosome of kinetoplastids shares some enzymes with _________ and __________ of other protists, plants and animals.

A

peroxisomes; glyoxysomes

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20
Q

what are the four major morphological forms of kinetoplastids, which are associated with the different life cycle stages in various species that cause disease in humans?

A
  • trypomastigote
  • amastigote
  • promastigote
  • epimastigote
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21
Q

where is the kinetoplast located in the trypomastigote?

A

on the posterior

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22
Q

where is the flagellum in a trypomastigote?

A

it emerges from the posterior end of the parasite (basal body, bb) and extends the length towards the anterior where the extension of the free flagellum emerges from the anterior end

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23
Q

how long is the undulating membrane in a trypomastigote?

A

it spans the length of the parasite

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24
Q

what is the use of the undulating membrane trypomastigote?

A

it functions like a fin and increases the motility of the organism

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25
Q

how does the amastigote look like?

A

spherical in shape and no free flagellum

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26
Q

the _____ and the ______ are present in the amastigote

A

basal body; base of the flagellum

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27
Q

what is the kinetoplast identified as in microscopy

A

a dark staining body near the nucleus

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28
Q

is the amastigote motile?

A

no

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29
Q

what is the morphology of the promastigote?

A

the kinetoplast is towards the anterior and a free flagellum with no undulating membrane emerges where it will pull the organism from

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30
Q

what is the morphology of the epimastigote?

A

The kinetoplast is more centrally located, usually just anterior to nucleus, and the flagellum emerges from the middle and forms a shorter undulating membrane than in trypomastigotes

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31
Q

who is noticeably more motile, epimastigotes or trypomastigotes?

A

trypomastigotes

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32
Q

what are the 4 types of leishmaniasis?

A
  • cutaneous leishmaniasis
  • mucosal leishmaniasis
  • visceral leishmaniasis
  • nodular post-kala-azar dermal leishmaniasis (PKDL)
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33
Q

how is Leishmania spp. transmitted

A

by the bite of certain species of sandflies

  • Phlebotomus (old world)
  • Lutzomia (new world)
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34
Q

most forms of Leishmania are only spread through ______ but some can be spread between humans

A

animals, as a zoonosis

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35
Q

how many species of Leishmania cause human infection

A

21/30 that can infect mammals

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36
Q

how are different species of Leishmania distinguished?

A

they are morphologically indistinguishable, they can be distinguished by isoenzyme analysis, DNA seq analysis, or monoclonal antibodies

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37
Q

which parasite causes visceral leishmaniasis?

A

L. donovani

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38
Q

which parasites cause cutaneous leishmaniasis?

A

L. tropica; (L. t. major, minor and ethiopia)

39
Q

which parasite causes mucocutaneous leishmaniasis?

A

L. braziliensis, also L. mexicana and L. peruviana

40
Q

what is visceral leishmaniasis also called?

A

Kala-azar, black fever, dum-dum fever

41
Q

what is cutaneous leishmaniasis also called?

A

oriental sore, Delhiulcer, Aleppo, Delhi or Baghdad boil

42
Q

what is mucocutaneous leishmaniasis also called?

A

espundia, Uta, chiclero ulcer

43
Q

how many countries is leishmaniasis found in?

A

88

44
Q

what kind of life cycle does Leishmania have?

A

a digenetic one; with 2 hosts

45
Q

what are the 2 morphological forms of Leishmania?

A
  • promastigote- in the sandfly vector

- amastigote- in the host (e.g. human)

46
Q

where is Leishmania found in cutaneous leishmaniasis?

A

intracellularly in macrophages in skin lesions

47
Q

where is leishmania found in visceral leishmaniasis?

A

in the mononuclear phagocyte system of blood, liver, lymph nodes, spleen

48
Q

what are the features of the promastigote stage of leishmania?

A
  • insect stage
  • motile
  • midgut
49
Q

what are the features of the amastigote stage of leishmanis?

A
  • mammalian stage
  • non-motile
  • intracellular
50
Q

where does sexual reproduction occur for Leishmania?

A

in sand flies, the natural vector of leishmania

51
Q

how is leishmania transmitted?

A

the bite of the infected female sandfly

52
Q

which stage do the sandflies inject into the host during their blood meals?

A

the infective stage - the promastigotes

53
Q

what part of the sandfly transmits the parasite?

A

the proboscis

54
Q

what happens to promastigotes that reach the puncture wound?

A

they are phagocytised by macrophages and other types of mononuclear phagocytic cells

55
Q

what do promastigotes transform into in the phagocytes?

A

into the tissuestage - the amastigotes

56
Q

how do amastigotes multiply?

A

by simple division

57
Q

what do amastigotes do after multiplying?

A

proceed to infect other mononuclear phagocytic cells

58
Q

what is the pathogenesis of leishmaniasis due to?

A

an immune reaction to the pathogen, particularly cell-mediated immunity

59
Q

what does lab examination of the blood show in leishmaniasis?

A
  • marked decrease in white blood cells
  • relative increase in monocytes and lymphocytes
  • reduced platelets
  • anemia
  • IgM and IgG levels are extremely elevated
60
Q

why are IgM and IgG antibodies extremely elevated?

A

due to both specific antibodies and polyclonal activation

61
Q

what is seen in clinical disease of cutaneous leishmaniasis?

A
  • it is generally self-healing
  • seen in skin
  • mucous membranes
62
Q

what is seen in the clinical disease of visceral leishmaniasis?

A
  • it is fatal, up to 90% if untreated
  • liver
  • spleen
  • bone marrow
63
Q

what causes cutaneous leishmaniasis in the old world?

A

L. tropica
L. major
L. ethiopia

64
Q

what causes cutaneous leishmaniasis in the new world?

A

L. mexicana

65
Q

which is the most common form of leishmaniasis?

A

cutaneous

66
Q

how is cutaneous leishmaniasis characterized?

A

one or more sores, papules, or nodules on the skin

67
Q

what are the sores of cutaneous leishmaniasis often described as?

A

a volcano with a raised edge and central crater

68
Q

what may be observed near the sores?

A

swollen lymph nodes

69
Q

where are the swollen lymph nodes if the sore is on the arm or the hand?

A

under the arm

70
Q

how long after the bite is a nodule produced?

A

2-8 weeks

71
Q

is the papule painful?

A

no, relatively painless

72
Q

the center of the papule _____ while _____ develop at the periphery

A

encrusts; satellite papules

73
Q

how long the the ulcer take to heal?

A

2-10 months - but leaves a scar

74
Q

which parasite causes mucocutaneous leishmanisis?

A

L. braziliensis

75
Q

what are the clinical features of mucocutaneous leishmaniasis?

A
  • the same as those of cutaneous leishmaniasis, except that in this disease the organism can metastasize and the lesions spread to mucoid tissues (oral, pharyngeal and nasal) and lead to their destruction and hence sever deformity.
76
Q

how long after the original skin lesion can the deformities occur in mucocutaneous leishmaniasis?

A

months to years after

77
Q

which parasite causes visceral leishmaniasis?

A
  • L. donovani and L. d. infantum in the old world

- L. donovani chagasi in the new world

78
Q

who does L. donovani infect?

A

people of all ages

79
Q

who does L. d. infantum infect?

A

young children as well as infants

80
Q

where is visceral leishmaniasis usually the least severe?

A

from the Middle East

81
Q

what is usually associated with visceral leishmaniasis?

A

fever, weight loss, and an enlarged spleen and liver

82
Q

why is there usually a delay in diagnosis of visceral leishmaniasis?

A

because the symptoms are not specific

83
Q

when should visceral leishmaniasis always be considered?

A

in patients with a chronic fever whom are from an endemic area

84
Q

what is the causative organism of New World visceral leishmaniasis?

A

L. d. chagasi

85
Q

why is there rarely a local lesion in visceral leishmaniasis?

A

because the L. donovani organisms are rapidly eliminated from the site of infection

86
Q

where do the parasites multiply in visceral leishmaniasis

A

in the mononuclear phagocytic cells of the spleen, live, lymph nodes, bone marrow, intestinal mucosa and other organs

87
Q

what are the symptoms 1-4 months after infection in visceral leishmaniasis?

A
  • occurrence of fever with a daily rise to 39-40°C, +chills and sweating
  • the spleen and liver progressively become enlarged
88
Q

what is the issue with chronic disease?

A

it renders patients susceptible to other infections

89
Q

what happens in untreated disease?

A

result is death

90
Q

what can happen to the hands/skin of a patient with visceral leishmaniasis?

A

jaundice

91
Q

how is diagnosis done for leishmaniasis?

A
  • based on a history of exposure to sandflies
  • synmptoms
  • isolation of the organisms from the lesion aspirate or biopsy, by direct examination or culture
92
Q

what is done in the laboratory?

A

the use of a biopsy, and examination of Giemsa stained slides of the relevant tissue is the most common technique

93
Q

what is antibody detection good for? what is it not useful for?

A

useful in visceral leishmaniases

limited value in cutaneous disease

94
Q

what methods exist for parasite detection/species identification?

A

biochemical (isoenzymes)
immunological (immunoassays)
molecular (PCR)

BSC Zoology - Parasitology (27 decks)

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