Infectious Disease -- Parasite Packet #2 Flashcards

1
Q

Babesiosis method ot transmission

A

Deer Ticks

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2
Q

Symptoms of Babesiosis?

A

Fever + Hemolytic Anemia

Mild unless patient is asplenic/IC

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3
Q

African Sleeping Sickness is caused by what organism…

A

Trypanosome rhodesiense

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4
Q

Symptoms of African Sleeping Sickness?

A

Proliferation of Kinetopastid form of RBCs
Intermittent fevers, lymphadenopathy, Splenomegaly
Progressive Brain Dysfunction (Leptomeningtis), Cachexia, Death

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5
Q

Trypanosome rhodesiense is transmitted by…

A

Tsetse Fly

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6
Q

What is Cachexia?

A

Wasting of the body due to chronic illness

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7
Q

What causes the fever spikes seen in African Sleeping Sickness?

A

Immune-mediated killing of large numbers of organisms. Genetic rearrangement allows for escape of some organisms for another round of infection.

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8
Q

Counterintuitive components of the African Sleeping Sickness/Host Immune response relationship

A

Interferon gamma production by CD8 cells stimulates parasite growth.

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9
Q

Tissue destruction in African Sleeping Sickness is caused by…

A

Antigen-Antibody complex deposition

Release of lysosomal enzymes form degenerating phagocytes

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10
Q

Dermatological symptoms in African Sleeping Sickness?

A

At site of inset bite, a large, red, rubbery chancre

Ulcer+mononuclear inflammatory infiltrate

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11
Q

Chagas’ disease is caused by…

A

Trypanosma Cruzi

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12
Q

Chagas’ disease is transmitted via…

A

Kissing Bugs

They feed on sleeping inhabitants and pass infection via feces

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13
Q

Erythematous site of entry in Chagas’ disease?

A

Chagoma

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14
Q

Chagas’ disease is an infection of what cell type?

A

Primarily Macrophages
It avoids killing by moving from lysosome into the cytosol
Can also get muscle cells

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15
Q

How do Trypanosma get back out of macrophages in Chagas’ disease?

A

After they develop flagella, they burst the macrophage to infect other cells

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16
Q

Symptoms of acute Chagas’ disease?

A

Cardiac Damage/Failure
Fever
Generalized Lymphadenopathy/Splenomegaly

17
Q

Symptoms of Chronic Chagas’ disease?

A

Autoantibodies and T cells cross react with host myocardial, nerve, lymphocyte, and extracellular proteins.
Dilated cardiomyopathy and cardiac arrythmias.

18
Q

Pathology in Acute Chagas’ myocarditis?

A

Formation of intracellular pseudocysts
Focal myocardial cell necrosis
4 chamber dilation

19
Q

Pathology in Chronic Chagas’ disease myocarditis

A

Dilated heart with mural thrombi
Interstitial and perivascular infiltrates (mono,lympho, plasma)
Cardiac Cell necrosis and interstitial fibrosis

20
Q

How is Toxoplasmosis spread?

A

Cat feces, undercooked pork/lamb

21
Q

Normal Pathogenesis of Toxoplasmosis?

A

Parasite enters thru gut, spreads systemically
Cysts containing bradyzoites remain dormant for years
Controlled by T cell mediated response

22
Q

How do AIDS patients typically develop Toxoplasmosis?

A

Reactivation of dormant organisms from cysts

23
Q

Effects of Toxoplasmosis on 1st trimester fetus?

A

Destroy developing heart, brain, and lungs

Can also cause chorioretinitis

24
Q

Pathology of Toxoplasmosis (normally)?

A

Lymphadenopathy

Follicular Hypertrophy

25
Q

Pathology of neonatal toxoplasmosis?

A

Destructive lesions of the CNS of microglial nodules
Extensive CNS necrosis, vascular thrombosis
Intense Inflammation
Necrosis of liver, heart, lung, Adrenals

26
Q

How is Leishmaniasis spread?

A

Released into skin by sandfly

27
Q

Cellular pathogenesis of Leishmaniasis

A

Leishmaniae phago. by macrophages
Transform to round amaztigotes w/ kinetoplast
Divide in phagosomes
Rupture m.phage to infect others

28
Q

Three forms of Leishmaniasis?

A

Cutaneous
Mucocutaneous
Visceral

29
Q

How is Leishmaniasis spread determined?

A

Temperature requirements of the specific parasite

30
Q

How is severity of Leishmaniasis lesions determined?

A

Host Reponse
Cellular Response – Granulomas
Anergic host – widespread disease

31
Q

How do Leishmaniasis parasites avoid immune destruction?

A

Alter phagolysosome environment
Resistant to C5-C9 complex
Scavenges Oxygen Radicals

32
Q

Pathology of Visceral Leishmaniasis?

A

Spread through RES – Severe systemic disease
Hep.spl.megaly, lymphodenopathy, pancytopenia, fever, weight loss. Eventually, Liver becomes fibrotic and lesions develp in the lungs, GI, kidneys, pancreas, and testes.

33
Q

Usual cause of death in Leishmaniasis?

A

Bacterial infections

34
Q

Pathology of cutaneous Leishmaniasis?

A

Localized disease

Single ulcer with surrounding granulomatous inflammation

35
Q

Pathology of mucocutaneous form of Leishmaniasis?

A

Moist, ulcerating/nonulcerating lesions which may be disfiguring
May involve larynx, nasal septum, anus, or vulva

36
Q

What do you need to know about nagleria?

A

Parasitic Meningitis from water source
Through the Cribiform plate
Death in 5-16 days
Caused by ameobae in CSF

37
Q

What do you need to know about Acanthamoeba?

A

Parasitic meningtisi in immunosuppressed individuals
Entry though nasal mucosa, lung, or skin
Sense of taste, smell altered
Treat with Ampho. B