Microbiology-Leishmaniasis Flashcards

1
Q

Vector of leishmaniasis? Non-vector transmission of leishmaniasis?

A

Sand fly bite, this is why most transmission occurs in the summer. Blood transfusion, needle sharing, sexual transmission, lab and maternal transmission to fetus.

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2
Q

What would you expect to see on microscopy of this painless, chronic skin lesion after a sand fly bite in Africa?

A

Intracellular amastigotes with kinetoplasts (rod shape) indicating leishmaniasis. They like to live in macrophage phagolysosome and make superoxide dismutase. Note that in the sandfly gut it exists as promastigotes.

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3
Q

What are people with AIDS at higher risk for leishmaniasis in the Mediterranean?

A

Cell mediated immunity controls infection and wanes with immunosuppression. Note that immunity to reinfection develops because it is a persistent infection, but this increases risk for reinfection.

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4
Q

2 reservoirs of visceral leishmaniasis?

A

Humans (L. donovani) and dogs (L. infantum).

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5
Q

Where is cutaneous leishmaniasis endemic?

A

Tropics and mediterranean. Also present in Texas and Oklahoma with the wood mouse as the vector of (L. mexicana).

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6
Q

Where is mucosal leishmaniasis endemic?

A

Southern Peru, Bolivia, Brazil

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7
Q

Where is visceral leishmaniasis endemic?

A

Mediterranean, East Africa, India, Nepal, Brazil.

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8
Q

3 types of leishmaniasis? What species are involved in each type?

A

Cutaneous (most common): major, tropica, aethiopica, venezuelensis, mexicana, amazonensis. Mucosal (complication of cutaneous): brazillensis, peruviana, guyanesis, panamensis. Visceral: chagasi (same as infantum), donovani, infantum. If you see viana think mucosal.

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9
Q

Pathogenesis of leishmaniasis

A

Sand fly bites and injects anti-coagulant proteins -> Active factors elicit an immune response -> engulfed by phagocytes -> complement receptors permit entry to phagolysosome (molecular mimicry) -> low pH allows gathering of nutrients -> macrophages and T-cells eradicate infection.

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10
Q

Leishmaniasis that do not usually cause death?

A

Cutaneous and mucosal. Note that in the new world mucosal leishmaniasis is a complication of cutaneous leishmaniasis, but not in the old world.

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11
Q

Cause of spectrum of disease in visceral leishmaniasis?

A

Infectious dose variation, immune status, nutrition status and genetics determine if you will be able to control with granulomas or not.

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12
Q

Physical presentation of visceral leishmaniasis

A

Most are asymptomatic, however, some get Kala azar: hepatosplenomegaly (because the parasite disseminate throughout the reticuloendothelial system), fever, weight loss (IL-2 and TNF-alpha excess), pancytopenia and hypergammaglobulinemia.

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13
Q

Labs to check in a patient with suspect visceral leishmaniasis

A

Hct/Hgb (anemia), WBC (leukopenia), platelets (thrombocytopenia), liver enzymes (elevated from liver infection), hypoalbuminemia (from wasting) and polyclonal gammopathy.

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14
Q

Incubation period of leishmaniasis

A

Weeks to months, soldiers usually present toward the end of their tour or when they are back home.

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15
Q

Common causes of death of leishmaniasis?

A

Secondary bacterial or viral infections: pneumonia, measles, sepsis, Tb, dysentery. This is why you DO NOT biopsy the spleen in the US because of increased risk for infection, you biopsy the bone marrow then the liver.

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16
Q

Tx for leishmaniasis

A

AmphoB

17
Q

Most common sequelae of cutaneous leishmaniasis

A

Scarring

18
Q

Old world vs. new world cutaneous leishmaniasis?

A

New world is more wet and old world is more dry.

19
Q

Diagnosing cutaneous leishmaniasis?

A

Scrape under dry skin lesion, Giemsa stain, routine histopathology and PCR.

20
Q

Why are L. viannia species more likely to cause mucosal leishmaniasis?

A

The parasite is infected by Leishmania RNA virus 1 and can elicit a massive inflammatory response (Th1 and Th2) via TLR3.

21
Q

Presentation of mucosal leishmaniasis?

A

Skin lesions develop months to years after infection, starts with nasal stuffiness and inflammation that progresses to ulceration of the nasal septum. Lips, cheeks, palate, pharynx and larynx can also be involved. Airway compromise is most serious complication.

22
Q

Diagnosing leishmania

A

PCR (most sensitive, great for mucosal leishmaniasis), cultures and smears (need a lot of organisms to see it). You can only use serology (rK39) for visceral leishmaniasis. You can use a skin test in other places of the world.

23
Q

3 things to do to diagnose visceral leishmaniasis

A

rK39 serology, culture and bone marrow biopsy

24
Q

How do you determine treatment for visceral leishmaniasis?

A

By region (Nepal and India have resistance). Most tx with amphoB (IV) or oral miltefosine.

25
Q

How do you determine treatment for cutaneous leishmaniasis?

A

By species and simple or complex cutaneous leishmaniasis. Sometimes no therapy, sometimes freezing it off, topical azoles, topical paromomycin, miltefosine, and then IV amphoB or antinomials.

26
Q

How is immunity intentionally developed for leishmaniasis?

A

Leishmaniazation, intentionally inoculating to form a small scar instead of risking severe deformities later on.