Leshmaniasis Flashcards

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1
Q

What is the lector for Leishmania?

A

The sand fly

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2
Q

What are the two forms of Leishmania: when its in the vector vs when it’s in our cells? What’s the difference?

A

Vector form: promastigote Host form: amastigote.

Amastigote has kinetoplst. Promastigote has single flagellum and is motile.

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3
Q

What are the 3 main types of dz you get with Leishmania? What do we try to prevent in each one.

A

Cutaneous→ prevent morbidity
Mucosal→ prevent morbidity
Visceral → prevent mortality

Visceral is obviously the worst one.

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4
Q

In the Middle East we started having trouble with Leishmania during OIF and OEF. Describe what we saw

A

Lots of cutaneous leishmania (CL) from L. major and L. tropica.

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5
Q

How will you tell CL from Pyoderma, a pyogenic (pussy) bacterial skin infection?

A

CL: non painful papule, slow progression, ulcerates, rolled margins, induration around ulcer, no response to antibiotics

Pyoderma: painful/pruritic pustule, fast progression, ulcerates, non rolled margin, non indurated, responds to antibiotics

Basically, you know you’ve got pyoderma real quick because it hurts and comes on fast (doesn’t have time to have rolled margins or to indurate), and you’ll get rid of it quickly too because it responds to antibiotics

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6
Q

CL can also be seen outside the Middle East. What specifics of Leishmania causes it and what sx do you see.

A

L baziliensis

Also called a “pizza pie” lesion in lecture

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7
Q

How do you dx CL

A

Use multiple tests up front: Culture and PCR allow species ID.

Don’t use serology.

Must see kinetoplast to dx.

Hard to dx on skin biopsy.

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8
Q

Tx for CL?

A

Ranges based on the severity

Milder dz:

  • None
  • local liquid N2 or heat
  • paromomycin cream for tropicals
  • azoles

More serious dz:

  • miltefosine
  • antimonials
  • amphotericin B
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9
Q

What species usually causes mucosal leishmaniasis?

A

L. brazilliensis

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10
Q

What are the sx of mucosal leishmanisis

A

Starts with nasal stuffiness, inflammation→ ulceration of nasal mucosa.
Can involve lips, cheeks, palate, pharynx, larynx. Complications: disfigurement, aspiration, DEATH.

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11
Q

How do you dx ML?

A

PCR b/c of lack of parasites

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12
Q

Tx for ML?

A

Same as CL but give more

Monitor for 2 years

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13
Q

What causes visceral leishmaniasis and where do you get it?

A

L. donovonii common in India and Nepal, E. Africa.

L infantum in the Mediterranean and Brazil

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14
Q

What is the classic pentad of sx seen in VL known as the kala azar or black fever

A
  1. Fever (double quotidian fever–two peaks of fever per day)
  2. Weight Loss
  3. Hepatosplenomegaly
  4. Pancytopenia
  5. Hypergammaglobulinemia
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15
Q

How do you usually die from VL?

A

Bacterial and viral infections (pneumonia, measles, sepsis etc)

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16
Q

How do you dx VL??

A

seriology works here

17
Q

What’s the treatment for VL?

A

Liposomal amphotericin B

18
Q

Next cards are straight sketchy. Some might repeat the above info but repetition is the key to success, right? Right.

A

Huuhhhhhh

19
Q

Leishmania donovani. Describe the transmission involved here

A

Motile promastigtes infect macrophages and mature into amastigotes (non-motile). They replicate in macrophages and reticuloendothelial system

20
Q

Where do you find L. donovani?

A

Mediterranean, Middle East, Africa

21
Q

Sx of L. donovani?

A

black fever or kala-azar (visceral leishmaniases) → 100% fatal if untreated

  1. Hyperpigmented lesions
  2. Pancytopenia (bone marrow infection)
  3. Hepatosplenomegaly
  4. Fever, weakness
22
Q

Tx for L. donovani?

A

Amphotericin B

23
Q

Leishmania baziliensis. how do we dx this?

A

marrow, spleen, lymph node or lesion sample showing amastigote inside macrophages

24
Q

Sx of L. braziliensis?

A

Cutaneous leishmaniasis which presents as erythematous papule at the sand fly bite which expands and ulcerates “boils”. Can present in mucous membrane, skin and cartilage.

25
Q

Tx for L. braziliensis?

A

Stibugluconate