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MMI 445 > Lecture 21- Leishmaniasis > Flashcards

Lecture 21- Leishmaniasis Flashcards

1
Q

What is leishmaniasis?

A

Morbid and potentially fatal protozoan parasitic infection

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2
Q

Leishmaniasis is classified as what type of disease?

A

Classified as a neglected tropical disease (NTD)

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3
Q

What are the three clinical manifestations of leishmaniasis?

A
  1. Visceral Leishmaniasis (VL)
  2. Cutaneous leishmaniasis (CL)
  3. Mucocutaneous/mucosal leishmaniasis (MCL/ML)
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4
Q

Species are ____ restricted and outcome is determined by _______

A
  • Geographically
  • Host factors
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5
Q

Leishmaniasis is transmitted by what?

A

Female phlebotomine (old world) and Lutzomyia (new world)

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6
Q

What is the class, order and genus?

A
  • Class = kinetoplastea
  • Order = Trypanosomatida
  • Genus = Leishmania
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7
Q

Who first described leishmaniasis in 1756?

A

Alexander Russell

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8
Q

The first species was describe by who?

A

Charles Donovan

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9
Q

What are the two important stages of leishmaniasis?

A
  1. Sandfly stage = promastigote
  2. Human stage = amastigote
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10
Q

Descibe the lifecyle of leishmaniasis

A
  • The promastigote form is the flagellated form
  • This stage is found in the sandfly
  • When the sandfly takes a blood meal it injects the promastigote through the skin
  • The promastigote gets phagocytised by the macrophages as part of the immune system
  • Once engulphed by these cells transform into an amastigote and they lose the flagella and become round bodies
  • Amastigotes is the stage found in human stage
  • The amastigotes multiply in number and cause the cell to burst and disseminate into a number of different areas in the body
  • The cycle repeats when sandfly takes its blood meal
  • It reverts back to the promastigote stage
  • They transform as they travel to the gut of the sandfly based on the nutrients present
  • They are injected to the next mammal or human when the sandfly takes a blood meal
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11
Q

Why is species knowledge useful?

A
  • Some go infect internal organs, some infect other areas of the skin
  • It depends on the species type, they have different predilections for different parts of the bodies
  • Different presentations are a result of different species
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12
Q

Why do you need to consider the role of the host immune response?

A
  • So you know whether or not the macrophages can actually get rid of the parasite
  • If immunocompromised, they can have more severe forms of the disease
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13
Q

What factors influence disease presentation?

A
  • Disease presentation is multifactorial
  • Species/geography
  • Host immune response
  • Virulence factors
  • Location of sandfly bite
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14
Q

What species cause VL?

A
  • L. donovani
  • L. chagasi (NW)/ L. infantum (OW)
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15
Q

Where are the majority of cases found for VL?

A

Brazil, Ethiopia, India, Somalia, and Sudan

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16
Q

What allows for the transmission of VL in densly populated areas?

A

Animal reservoirs (canine population)

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17
Q

What is Post kala-azar dermal leishmaniasis (PKDL)?

A
  • Complication of VL (6 months to 3 years) characterized by a maculopapular rash in patient previously recovered from VL caused by L. donovani
  • Reoccurance of the disease
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18
Q

What are the symptoms of VL?

A
  • Fever
  • Weight loss
  • Hepatosplenomagaly
  • Anemia
  • Thrombocytopenia
  • Hypergammaglobulinemia
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19
Q

What is the most common form of leishmaniasis?

A

CL

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20
Q

Where is CL common?

A

Afghanistan, Brazil, Iran, Peru, Saudi Arabia, Syria

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21
Q

What species causes CL?

A

Caused by members of both old and new world leishmania complex and Viannia subgenus

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22
Q

Only a small fraction of those infected will develop _______

A

CL disease

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23
Q

What is the first sign of CL infection?

A
  • Small erythematous papule
  • First nodules, develops into ulcer, generally self-healing
24
Q

What are some other forms/complications of CL?

A
  • Disseminated leishmaniasis (DL)
  • Diffuse CL (DCL)
  • Atypical CL (ACL)
25
Q

What is DL?

A

Macropapular skin lesions identified in 2 or more anatomical sites ranging from 10-300 in number

26
Q

What is DCL?

A

Nodular, non ulcerative lesions on the face, limb and back

27
Q

What is ACL?

A
  • In those who are immunocompromised
  • Unusual crusted, lupoid, sporotrichoid or verrucous ulcers
28
Q

Where is VL commonly identified?

A

Latin America (Brazil, Peru, and Bolivia)

29
Q

What is MCL/ML?

A

Sequela of the initial CL infection affecting mucous membranes of the upper respiratory tract

30
Q

How does it get to the mucous membrane in MCL?

A

Through the lymphatic or haematogenous pathway

31
Q

MCL is caused by what species?

A

Viannia subgenus

32
Q

What plays a role in MCL infection?

A

Species, host immune response and endosymbiont Leishmania RNA virus-1/2 thought to play a role

33
Q

What are the signs of MCL infection?

A
  • First signs = nasal inflammation/stuffiness at first
  • Followed by ulcerationof the nasopharyngeal mucosa
  • Lastly, perforation of the septum
  • Susceptible to secondary bacterial infections
34
Q

What is the difference between old world and new world?

A
  • Old world = found in Asia, Africa, Middle East
  • New world = Viannia subgenus
35
Q

What is Th1?

A

Pro inflammatory response

36
Q

What is Th2?

A

Anti inflammatory response

37
Q

What type of Th response does MCL have?

A
  • Th1 response
  • Low parasite burden
  • Severe disease
38
Q

What type of Th response does DCL have?

A
  • High parasite burden
  • Th2 response
  • Severe disease
39
Q

Describe the relationship between Th1 and Th2 response and disease severity

A
40
Q

What markers are involved with Th1 response?

A

IFN-y, TNF-a, IL-12, IL-23, IL-27 (overexpression)

41
Q

What markers are involved with a Th2 response?

A

IL-4, IL-6, IL-13, IL-10

42
Q

What are some key virulence factors?

A
  • Kinetoplastid membrane protein -11 (kmp-11)
  • Lipophosphoglycans
  • Heat shock proteins (HSPs)
  • Cysteine peptidase (CPs)
  • Host factors
  • A2 protein
43
Q

What is the virulence factor Kinetoplastid membrane protein -11 (kmp-11)?

A
  • Modulate host immune response, reducing NO production
  • Parasite uses it to its benefit to reduce the amount of NO produced within the macrophages to prevent it from being killed and allowing it to survive better
44
Q

What is the virulence factor Lipophosphoglycans?

A
  • Involved in sandfly stage for attachment, differentiation and growth
  • Heavily in the promastigote stage
  • They are upregulated in the sandfly to allow them to grow better
45
Q

What is the virulence factor Heat shock protein (HSP)?

A
  • Provide thermotolerance during differentiation phase
  • Allow to tolerate changes in temperature
  • Sandfly temperature 22-26C and the human body is 36C
  • Increases when a promastigote enters the human body
46
Q

What is the virulence factor Cysteine peptidase (CP)?

A
  • Expressed during amastigote stage
  • Involved in evading the immune response, prevent the killing of the parasite
47
Q

What is the virulence factor host factors?

A
  • MMP-9 involved in adherence for migration (allowing to stick to skin), phosphoprotein phosphatases (PPS), metal dependent protein phosphatases (PPMS) involved in producing antileishmanial molecules
  • Allow to enter the host
48
Q

What is virulence factor A2 protein?

A
  • Only found in visceralizing species (protection against temperature stress)
  • Believed to have a role in developing those more severe clinical manifestations
  • Evaluated as a vaccine target now for VL
49
Q

True or False? There is a difference in the number of chromosomes for new world and old world leishmaniasis

A

True

50
Q

Are microscopic examinations available?

A

Yes for biopsies, aspirates, scrapings, impressions or cultures

51
Q

What are the three stains available for microscopy?

A
  1. Giemsa stain
  2. Amastigotes
  3. Promastigotes
52
Q

Serology is limited to?

A

VL

53
Q

What types of serology tests are available for VL?

A
  • ELISA/EIA
  • IFA
  • DAT
54
Q

Treatment is complicated and limited to _____

A

Expensive drugs with substantial toxic effects

55
Q

What is recommended in addition to therapy?

A

Wound care

56
Q

Clinical resolution does not equal _______

A

Parasitological cure (can remain dormant)

MMI 445 (26 decks)

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