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
Pathology of neonatal toxoplasmosis?
Destructive lesions of the CNS of microglial nodules Extensive CNS necrosis, vascular thrombosis Intense Inflammation Necrosis of liver, heart, lung, Adrenals
26
How is Leishmaniasis spread?
Released into skin by sandfly
27
Cellular pathogenesis of Leishmaniasis
Leishmaniae phago. by macrophages Transform to round amaztigotes w/ kinetoplast Divide in phagosomes Rupture m.phage to infect others
28
Three forms of Leishmaniasis?
Cutaneous Mucocutaneous Visceral
29
How is Leishmaniasis spread determined?
Temperature requirements of the specific parasite
30
How is severity of Leishmaniasis lesions determined?
Host Reponse Cellular Response -- Granulomas Anergic host -- widespread disease
31
How do Leishmaniasis parasites avoid immune destruction?
Alter phagolysosome environment Resistant to C5-C9 complex Scavenges Oxygen Radicals
32
Pathology of Visceral Leishmaniasis?
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
Usual cause of death in Leishmaniasis?
Bacterial infections
34
Pathology of cutaneous Leishmaniasis?
Localized disease | Single ulcer with surrounding granulomatous inflammation
35
Pathology of mucocutaneous form of Leishmaniasis?
Moist, ulcerating/nonulcerating lesions which may be disfiguring May involve larynx, nasal septum, anus, or vulva
36
What do you need to know about nagleria?
Parasitic Meningitis from water source Through the Cribiform plate Death in 5-16 days Caused by ameobae in CSF
37
What do you need to know about Acanthamoeba?
Parasitic meningtisi in immunosuppressed individuals Entry though nasal mucosa, lung, or skin Sense of taste, smell altered Treat with Ampho. B