Parasites and Fungi Flashcards

(65 cards)

0
Q

What are examples of endoparasites?

A

Protozoa (one cell)

Helminths (worms - many cells)

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1
Q

What are examples of ectoparasites?

A

Lice
Bedbugs
Scabies
Mites

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2
Q

What are the different parasite types?

A

Obligate - cannot survive without a host

Facultative - able to survive outside a host (ex. Acanthamoeba)

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3
Q

What are the different types of parasite hosts?

A

Definitive - parasite reaches reproductive form
Intermediate - parasite grows but doesn’t reach reproductive form
Reservoir - can harbor parasite without showing ill effects

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4
Q

How are Protozoa acquired by people?

A

Fecal oral

Ingestion of contaminated food or water

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5
Q

How can Protozoa live inside humans?

A

Extracellular in blood (filariasis), intestine, urogenital system (schistoma)
Intracellular in tissue macrophages (leishmania) or RBCs (plasmodium)

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6
Q

How are Protozoa differentiated?

A

Size
Nucleus - clumped or dispersed, Maryland
Cytoplasm appearance
Organs of motility

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7
Q

What are the stages of Protozoa?

A

Trophozoite - actively feeding organisms in host niche - assimilation of organic nutrients using pseudopods, simple diffusion or active transport - various metabolic pathways
Cyst - metabolically inactive, able to survive under unfavorable conditions, resistant to chlorination and drying, integral for most

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8
Q

What is the spectrum of disease in giardia?

A

Asymptomatic carriage
Mild diarrhea
Severe malabsorption
Incubation period is 10 days

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9
Q

What are the possible organs of motility for Protozoa?

A

Simple cytoplasmic extrusions (pseudopods) - amoebae
Flagellates - giardia
Ciliates
Undulating membrane - sporozoa - obligate intracellular

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10
Q

How does protozoan reproduction work?

A

Asexual in humans

Sexual absent or restricted to insect vector

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11
Q

What is neurocysticercosis and what organism can cause it?

A

Cysts with organisms in it in brain

Taenia solium = pork tapeworm

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12
Q

What is a proglottid?

A

Tapeworm segment with male and female reproductive organs

Uterine branches fill with ova (eggs)

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13
Q

What is the basic life cycle of taenia coli or t. Saginata (beef)?

A

Pigs or cows (intermediate hosts) ingest proglottid
Eggs hatch in intestine and form cysts
Humans eat animal and then tapeworm develops and start to reproduce (humans are definitive host)
Human can become intermediate host if they eat proglottid instead of animal –> inf in brain

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14
Q

How does nutrition work in helminths?

A

Some have rudimentary digestive apparatuses, others directly absorb host nutrients
Most lack TCA cycle
Unable to use FFA or AA for energy
Fermentative

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15
Q

What is the only helminth that multiplies inside human host?

A

*s. stercoralis

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16
Q

What are the three broad categories of worms?

A

Nematodes - roundworms (intestinal or extraintestinal)

Platyhelminthes - flatworms (Cestodes - tapeworm, Trematode/flukes)

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17
Q

What medications can interfere with a stool sample?

A

Anti diarrheal
Antacids
Barium or bismuth
Oily laxatives

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18
Q

What do giardia trophozoites and cysts look like histologically?

A

Trophozoites - teardrop shape, two nuclei, suckers on bottom, picked up on trichrome stain, flagella, normally stay attached to intestine
Cysts - two trophozoites per, so four nuclei

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19
Q

What is a dfa test for giardia?

A

Direct fluorescent antibody
AB reagent specific for giardia with fluorescent tag - fluorescence indicates presence of giardia
Also detects cryptosporidium

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20
Q

What are other diagnostic methods for parasites?

A

Serology - limited use in patients from endemic areas
Blood smears - plasmodium
Tissue biopsy - trichinella
Molecular testing

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21
Q

T. Cruzi

A

Hemoflagellate
Causes Chagas’ disease
Acute disease - no focal febrile syndrome
Late disease - cardiomyopathy, arrhythmia, death, mega colon, mega esophagus
*trypomastigote = infective in blood
*Amastigote = tissue form, binary fission
*epimastigote = binary fission

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22
Q
T. Cruzi
Intermediate host
Infection via...
Vector
Key terms
A

Bug
Bug poop
Yes
Cardiomyopathy, mud huts

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23
Q

Toxoplasma gondii

A
Sporozoan
Acute disease - similar to mono
Congenital
Re activation - multifocal lesions 
Cysts are full of bradyzoites
Oocyst - full of sporozoites
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24
``` T. Gondii Intermediate host Infection via... Vector Key terms ```
Everything including humans Multiple routes No HIV, pregnancy
25
Filariasis
W. bancrofti - near equator, most common, humans are definitive hosts, mosquito is intermediate, no reservoir B. malayi - Asia and Indonesia, less common, humans are definitive hosts, mosquitoes are intermediate, has reservoirs Mosquitos are also vectors Helminths
26
Fasciola hepatica
Sheep liver fluke Acute - larval fluke travel from intestines to bile duct and cause inflammation, reactions, bleeding, hives and cough, can kill sheep Chronic - larva mature into adults in bile ducts and pass eggs into feces, may be asymptomatic, may cause obstruction
27
``` F. Hepatica Intermediate host Infection via... Vector Key terms ```
Snail Watercress No vector Rancher, watercress
28
What are some common features of fungal infections?
*Most are chronic (indolent) Most are exogenous Few are communicable Several have characteristic ecological niche - *clue is patient exposure to these habitats
29
What are some differences between fungi and bacteria?
*Fungi are eukaryotes *cell wall has glucans and chitin instead of peptidoglycan Most in nature live on decaying material Do not need to colonize or infect tissues to perpetuate species
30
How does the fungal cell wall interact with drugs?
*beta 1,3-D-glucan is the target of echinocandins which inhibit glucan synthase and it is useful in diagnosis
31
What is the structure of fungal cell membrane?
Lipid bilateral Phospholipids *ergosterol - site of action of amphotericin b and azoles Functions to protect, regulate intake and secretion and cell wall synthesis
32
What is the fungal physiology?
Respire aerobically Metabolism is heterotrophic Slow growing
33
What are different fungal growth patterns?
Yeast - *single celled forms, reproduce by budding(bud=blastospore), pseudohyphae, colonies reaemble bacteria, candida and cryptococcus Molds - *grow as filamentous structures, *opportunists like aspergillus are monomorphic, hyphae, velvety granular appearance with pigment
34
What are dimorphic fungi?
Yeast form in mammalian host Filamentous mold form in soil or environment Perfect fungi have known sexual forms - s. cerevisiae, c. Neoformans Imperfect have no known sexual forms
35
Reproduction of fungi: conidiogenesis
Arthroconidia - Result from preexisting entire hyphae *break loose and initiate another cycle of reproduction by germination
36
Reproduction of fungi: blastoconidiogenesis
Most fungi especially yeasts Blastoconidia of yeast may continue to grow and elongate into *pseudohyphae Others may develop into *true hyphae that do not separate at maturity
37
Reproduction of fungi: macro/microconidia and sporangiopore
Some form large *macroconidia and/or small microconidia Others reproduce by cytoplasmic cleavage within structure called *sporangium Hyphae of the fungi are aseptate
38
Mycoses (fungal disease)
Ubiquitious Superficial and cutaneous grow on epidermis at 25 deg c and metabolize keratin - *caused by dermatohytes Rarely invade deeper that outer layers of skin, nail, or hair Subcutaneous Form deep, ulcerated, skin lesions involving extremities, caused by soil saprophytes and intro through trauma to hand, feet, or legs
39
Endemic mycoses
Systemic mycoses - *characteristic endemicity of fungi in certain geographic regions of the world *illness may occur in healthy individuals (primary infection) Portal of entry is lungs *endemic fungal pathogens all dimorphic Include histoplasmosis, blastomycosis, and coccidioidomycosis
40
What is an important risk factor for opportunistic mycoses?
*certain host gene defects
41
Cryptococcus neoformans
Encapsulated yeast Pneumonia *meningitis in AIDs if cd4<100
42
Pneumocystis jiroveci
*pneumonia in AIDs if cd4<200 | Adhesion by surface glycoproteins
43
Aspergillus
Ubiquitous environmental mold Inhale spores Causes pneumonia Extra pulmonary spread Bone marrow transplant, liver transplant, chemotherapy patients, CGD Adhesion by complement receptors and hydrophobins
44
What is the pathogenesis of fungal infections?
Neutrophils actively recruited and destroy fungal hyphaes | *invasive fungal diseases like aspergillosis and candidemia develop in patients with severe neutropenia
45
What modifications do cryptococcus and histoplasma show during invasion process?
Increased metabolic rate Modified metabolic pathways Modified cell wall structure
46
How are macrophages involved in the pathogenesis of fungal infections?
Activated ones control multiplication of intracellular yeast Granulomatous inflammation which can lead to calcified fibrinous granulomas, a characteristic pathology Cytokine response lead to clinical manifestations - fever, fatigue, weight loss
47
What stains fungal cell walls?
Giemsa | Silver stain reveals organisms when giemsa not optimal
48
What is am common mycological agar?
*sabouraud dextrose Ph less than 6 C-source Inhibitory agents are cycloheximide, penicillin, streptomycin
49
What can be detected using direct antigen detection in blood and CSF?
Galactomannan - component of aspergillus cell wall | Beta 1,3 D glucan
50
How are intracellular parasites controlled?
By macrophages activated by parasite specific th1 cells
51
How does immunity to schistosomes work?
Dominant mechanism involves th2 cells, IgE, mast cells and eosinophils Directed to prevention of reinfection - Adult worms reside in blood vessel lumen and resist immunologic mechanisms Concomitant immunity - cercariae is form that penetrates skin - turns into schistosomula which is the stage vulnerable to attack (must happen within 48-72 hrs!) --> ADCC
52
What is concommitant immunity?
Mammalian host resists reinfection with skin stage worms yet is incapable of eradicating adult worm ADCC is primary mechanism
53
How does immunity to toxoplasma work?
``` Obligate intracellular - sequestered from immune elements Dormancy and latent infections in immunocompromised Primary mechanism involves phagocytic killing by activated macrophages Sterile immunity rare - brain and eye cells lacking class 1 MHC hold latent inf ```
54
How does immunity to malaria at sporozoite stage work?
Sporozoites enter liver cells AB promotes opsonization and complement mediated lysis, blocks binding and penetration of liver cells Extracellular - ignored by CTL
55
How does immunity to malaria in liver stage work?
Intracellular - hidden from antibody Express antigens on MHC 1 CTL kills and produce IFNgamma which promotes NO
56
How does immunity to malaria in the erythrocytic stage work?
No MHC - escape CTL | AB opsonizes and promotes removal by RES, also prevent binding and penetration by extracellularly merozoites
57
How does immunity to trichinella work?
Gut phase --> tissue migratory phase --> intramuscular Adult worms in GI lumen is stage most vulnerable to attack Rapid expulsion - IgE leads to growth of gut mast cells, goblet cells, prevents re-infection without affecting muscle larvae More mucus increases gut motility and hampers parasite foothold Parenteral involves ADCC of larvae Intramuscular in larvae capsules - eventually calcify and die
58
What is an example of a parasite that uses antigenic variation to avoid immune system?
Trypanosomes
59
Where is antigenic mimicry best developed?
Schistosomes
60
How are different Th cells active in infections?
1 - protozoan, protect against leishmaniasis 2 - helminth, leads to lethal leishmaniasis 3 - bacteria
61
How does immunity to leishmania work?
Obligate intracellular parasite Resides in RES utilizes complement receptor on macrophages to gain entry - inhibits ROS thrives in acid of lysosome Infected macrophages become resistant to activation
62
What is the hygiene hypothesis?
Parasitic infections especially worms induce generation of t reg cells that down regulate allergic diseases Not a result of a th1 response that cross regulates th2 response
63
How does immunity to schistosomiasis work?
Eggs in liver invoke immune response and cause pathology Early th1 response followed by late th2 response to egg antigens in liver cause granuloma formation and eventual liver fibrosis Culminates in ascites
64
How does immunity to onchocerciasis work?
Nematode infection Th2 response to larval antigen creates chronic inflammation of ocular surface Eosinophils and neutrophil infiltration Leads no river blindness