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SD IV: Block 3 Week 2 > Infectious Disease 02 > Flashcards

Infectious Disease 02 Flashcards

1
Q

What is the organism that causes candidiasis?

A

C. albicans

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2
Q

Thrush is caused by what organism and what area of the body does it affect?

A

C. albicans

superficial infection on mucosal surfaces of the oral cavity

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3
Q

What is severe disseminated candidiasis?

A

in neutropenia due to leukemia, chemotherapy, or hematopoietic stem cell
transplantation, may cause shock/DIC

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4
Q

Pathogenesis of candidiasis?

A

adhesins, enzymes that contribute to invasiveness, ability to grow as biofilms

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5
Q

Morphology of candidiasis? (histological appearance)

A

can appear as yeast, pseudohyphae, true hyphae (Routine H&E, Special stains - Gomori methenamine-silver, Periodic acid-Schiff)

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6
Q

What are come C/F of candidiasis?

A

Candida vaginitis

Infection of nail proper (onychomycosis), nail folds (paronychia), hair follicles (folliculitis), -intertriginous skin - armpits or webs of fingers and toes (intertrigo), penile skin (balanitis)

Diaper rash

Esophagitis

Myocardial Abscesses and Endocarditis - most common fungal endocarditis in prosthetic heart -
valves or intravenous drug abusers (tricuspid valve)

Brain Microabscesses and Meningitis

Endophthalmitis

Hepatic Abscesses

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7
Q

What are the organisms that can lead to cyrtococcosis?

A

C. neoformans and C. gattii (encapsulated yeasts)

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8
Q

What is the treatment which immunocompromised individuals receive which makes them susceptible to cryptococcosis?

A

high-dose corticosteroids, a major risk factor

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9
Q

Where is cryptococcus neoformans typically present?

A

in soil and in bird (particularly pigeon) droppings

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10
Q

What does melanin produced by Cryptococcus do to evade the body’s immunity?

A

(catalyzed by Laccase in the yeast): antioxidant, decreases antibody-mediated phagocytosis, counteracts
antifungal agents, binds iron and provides cell wall integrity

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11
Q

What is an important enzyme produced by crytococcosis that produces mannitol leading to osmotic edema and inhibits killing of yeast by neutrophils and reactive O2 species?

A

mannitol dehydrogenase

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12
Q

What is the morphology of Cryptococcosis?

A

“soap-bubble lesions”

India ink preparations on CSF

stains intense red with periodic acid-Schiff and mucicarmine in tissues

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13
Q

What is Aspergillosis caused by (what pathogen)?

A

aspergillus fumigatus

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14
Q

What are some C/F of Aspergillosis?

A

allergic bronchopulmonary aspergillosis

serious sinusitis, pneumonia and invasive disease in immunocompromised persons

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15
Q

What is the predisposing condition to get aspergillosis?

A

neutropenia and use of corticosteroids

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16
Q

What is a carcinogen produced by Aspergillosis?

A

aflatoxin

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17
Q

What area of the body does aspergillosis have a tendency to invade?

A

blood vessels

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18
Q

Describe gross presentation of aspergillosis in the body.

A

Fungus in pulmonary cavities with minimal/no invasion of tissues

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19
Q

C/F of aspergilloma?

A

patients have recurrent hemoptysis

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20
Q

What kind of people does invasive asperiollosis typically infect?

A

opportunistic; infection immunosuppressed hosts

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21
Q

Where are the primary lesions of aspergillosis?

A

usually found in lung

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22
Q

How does Aspergillosis typically appear on a histological slide?

A
  • Fruiting bodies (usually in lung cavities) and septate filaments, 5 to 10 μm thick, branching at acute angles (40 degrees)
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23
Q

What type of lesions are found in the lungs in those with primary invasive aspergillosis infection?

A

Target lesions

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24
Q

What is another name for Zygomycosis?

A

Mucormycosis

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25
What is Zygomycosis typically caused by?
opportunistic infection caused by bread mold fungi
26
What are some major predisposing factors of Zygomycosis?
neutropenia, corticosteroid use, diabetes mellitus (Rhinocerebral mucormycosis), iron overload and breakdown of cutaneous barrier (burns, surgical wounds, or trauma
27
What is the morphological features of zygomycosis?
non-septate hyphae
28
What is the name of the organism that causes malaria? (severe cerebral malaria)
Plasmodium falciparum (cause of severe cerebral malaria)
29
Pathogenesis of Malaria?
Release of merozoites induces the host cells to produce cytokines such as TNF that cause fever
30
What are some mutations conferring selective advantage over malaria?
Mutations conferring selective advantage: 1. Point mutations in globin genes: HbS, HbC disease 2. Globin deficiencies: α- and β-thalassemia 3. Mutations affecting RBC enzymes: G6PD deficiency 4. RBC membrane defects: absence of DARC (Duffy surface blood group), band 3, spectrum
31
What is the organism P. falciparum mainly able to infect in the body?
RBCs
32
Pathogenesis of P. falciparum
Causes infected red cells to clump together (rosette) and stick to endothelial cells lining small blood vessels (sequestration), which blocks blood flow * Several proteins, including P. falciparum erythrocyte membrane protein 1 (PfEMP1), associate and form knobs on the surface of red cells
33
What is a diagnostic test for P. falciparum?
giemsa staned peripheral blood smears
34
What are some major complications of P. falciparum infection?
splenomegaly cerebral malaria (malarial or Durck granulomata)
35
What does Babesios in blood smears resemble? (infection by what other organism)
P. falciparum ring stages
36
What is a common histological feature of Babes micro infection?
Maltese cross appearance
37
How is Leishmaniasis spread?
through the bite of infected sandflies
38
What is the difference between the promastigote and amastigote types of Leishmaniasis infection?
* Promastigote: develops and lives extracellularly in the sandfly vector * Amastigote: multiplies intracellularly in host macrophages
39
what are the different types of Leishmaniasis infection?
Visceral disease cutaneous disease Mucocuatenous disease?
40
What is the type of organism mainly causing leishmaniasis visceral disease?
Leishmania donovani
41
C/F of visceral Leishmaniasis?
Kala-azar: hyperpigmentation of the skin in individuals of South Asian ancestry
42
C/F of cutaneous leishmaniasis?
relatively mild, localized ulcers on exposed skin
43
C/F of mucocutaneous leishmaniasis?
ulcerating, or non-ulcerating lesions in nasopharynx
44
C/F of diffuse cutaneous leishmaniasis?
begins as a single skin nodule, which continues spreading until the entire body is covered by nodular lesions
45
What are some defenses that Leishmaniasis causing parasites use to evade the immune system?
Lipophosphoglycan forms a dense glycolysis that activates complement (leading to C3b deposition on the parasite surface_ and inhibits complement action (preventing MAC insertion into the parasite membrane) Gp63 is a zinc-dependent proteinase that cleaves complement and some lysosomal antimicrobial enzymes
46
What organism causes African Trypanosomiasis?
Trypanosoma bruceli rhodesiense
47
What is the type of dysfunction caused by African Trypanosomiasis?
sleeping sickness
48
What vector typically spreads African Trypanosomiasis?
Tsetse flies
49
Trypanosoma brucei rhodesiense is covered by a single, abundant, glycolipid-anchored protein called what?
variant surface glycoprotein (VSG)
50
What is a characteristic feature found in the cells of one infected with Trypanosoma Bruce rhodesiense?
Mott cells: globules filled with immunoglobulins
51
What is the pathogen causing Chugs disease?
Trypanosoma cruz - American trypanosmiasis
52
How is Chugs disease spread?
through triatomine bugs or (kissing bugs)
53
What is the organism being shown?
Left: T. brucei Right: T. cruzi
54
What are some C/F of Chagas disease?
1. Lethalacutemyocarditis-clusters of amastigotes causing swelling of individual myocardial fibers and intracellular pseudocysts, major cause of sudden death due to cardiac arrhythmia in endemic areas
54
What are some C/F of Chagas disease?
1. Lethalacutemyocarditis-clusters of amastigotes causing swelling of individual myocardial fibers and intracellular pseudocysts, major cause of sudden death due to cardiac arrhythmia in endemic areas
54
What are some C/F of Chagas disease?
1. Lethal acute myocarditis-clusters of amastigotes causing swelling of individual myocardial fibers and intracellular pseudocysts, major cause of sudden death due to cardiac arrhythmia in endemic areas Chronic chagas: myocardial inflammation GI: damage to myenteric plexus causes dilation of the colon(megacolon) and secondary achalasia)
55
Treatment from Chronic Chagas leading to heart involvement?
cardiac transplantation
56
Strongyloidiasis is caused by what organism?
Strongyloides stercoralis
57
Pathology of Strongyloidiasis?
The worms live in the soil a◦nd infect humans when larvae penetrate the skin, travel in the circulation to the lungs, and then travel up the trachea to be swallowed
58
Where do the adult worms, larvae, and eggs of those infected with Strongyloid stercoralis live?
crypts of duodenum and ileum
59
Taenia solium is transmitted in what two ways?
1. Larval cysts (cysticerci) ingested in undercooked pork attach to intestinal wall, develop into mature adult tapeworms producing mild abdominal symptoms. Life cycle is completed and cysticercosis does not develop 2. eggs ingested in food or water: contaminated human feces, larvae hatch and penetrate gut then disseminate giving rise to cysticerocis
60
Taenia saginata is also called what?
beef tapeworm
61
Diphyllobothrium is also called what?
fish tapeworm
62
Another name for tapeworm?
cestodes
63
How does one get hydatid disease?
ingestion of eggs of echinococcal species
64
Host of echinococcus granulosus? the intermediate?
definitive host -dog, intermediate -sheep
65
Host for infection of Echinococcus multiocularis? intermediate?
definitive - fox , intermediate – rodents)
66
What organs are Cysticerci commonly involved with?
brain, muscles, skin, and heart
67
Encystment in the brain of those with Cysticerci would cause what?
neurocysticerosis convulsions, increased intracranial pressure, and other neurologic disturbances may occur
68
Describe the cysts caused by cysticerci.
Cysts : ovoid and white to opalescent, often grape-sized, and contain an invaginated scolex with hooklets that are bathed in clear cyst fluid
69
Another name for E. granulosus?
hydatid cyst
70
Where do 2/3rd of E. granulosus cysts reside in the body?
liver
71
Describe features of hydatid cysts.
* Outer opaque non-nucleated layer, inner nucleated germinative layer and opalescent fluid, Daughter cysts often develop within the large mother cyst fine, sand-like sediment within the hydatid fluid (hydatid sand)
72
The offending pathogen causing trichinosis.
* T. spiralis, T. nativa, or T. britovi
73
Transmission of Trichinosis is caused by what?
ingestion of larvae in undercooked meat from infected animals
74
How does trichinosis affect the heart?
patchy interstitial myocarditis
75
Where does T. spirals normally reside in the body?
Preferentially encysts in striated skeletal muscles with the richest blood supply (diaphragm, deltoid, etc)
76
What is the pathogen leading to Schistosomiasis?
S. mansoni
77
Schistosomiasis infections can lead to chronic granulomatous bladder inflammation via infection with what?
S. haematobium
78
What is the pathology of Schistosomiasis?
penetrate human skin with the aid of powerful proteolytic enzymes that degrade the keratinized layer

SD IV: Block 3 Week 2 (8 decks)

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