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parasites Flashcards

parasite 1 parasite 2 opportunistic antifungal therapy

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Biology 101 flashcards
1
Q

What fungi are, including their defining characteristics

A
  • eukaryotic, membrane-bound organelles
  • cell wall (diff from plants)
  • no photosynthesis
  • ergosterols in cytoplasmic membrane
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2
Q

The function and structure of the fungal cell wall

A
  • protects the cell (ex. lysis in hypotonic solutions)
  • long polysaccharides w/branches & cross-linking
  • 1,3 β-D glucan is found in the cell wall of some fungi, but not in host tissues
  • 1,3 β-D glucan is used in a diagnostic test for fungal infection, and that its synthesis is a drug target
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3
Q

The function of ergosterol in the fungal cell membrane

A
  • stabilize membrane
  • equivalent of cholesterol in us
  • don’t have in humans, so synthesis of ergosterols is a drug target
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4
Q

do distantly related fungi have similar morphology in tissue?

A

not necessarily so tissue morphology is not a reliable means of fungal classification

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5
Q

o Mold

A
  • multicellular fungi w/long thread-like filaments

- look fuzzy

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6
Q

o Yeast

A
  • unicellular fungi which are round or oval in shape
  • divide by budding
  • look smooth
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7
Q

o Hyphae

A
  • long thread-like filaments of molds
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8
Q

o Septum (as it refers to hyphae)

A
  • cell walls of hyphae that separate nuclei

- some have, others don’t

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9
Q

o Mycelium

A
  • mass of hyphae

- visible to eye w/o magnification = fuzz you see

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10
Q

o Dimorphic

A
  • yeast under some conditions (usually body temp) & mold under others (usually room temp)
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11
Q

• How to recognize a basic septate or aseptate hypha, a mold, and a yeast.

A
  • septate has septum separating nuclei
  • aseptate hypha look like multinucleated cells
  • mold looks fuzzy & stringy
  • yeast = smooth & circular
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12
Q

phyla of fungi are defined by

A

the method of sexual reproduction

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13
Q

fungi phyla that contain the fungi of medical importance

A

Mucoromycotina
Ascomycota
Basidiomycota

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14
Q

Mucoromycotina

A
  • zygospores (yoke-like struct btwn hyphae)
  • simple sugars as soure of energy
  • hyphae thin walled w/few septa
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15
Q

Ascomycota

A
  • ascospores (sac-like structs)
  • metabolize complex carbon sources
  • hyphae thick walled & septate
  • 1-3 beta-D glucan in cell wall
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16
Q

Basidiomycota

A
  • basidiospore (borne on projections or pedestals)

- metabolize complex carbon sources

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17
Q

dracunculosis

A

guinea worm, almost eradicated, worms go everywhere, mostly lower extremities, cause blisters that are painful & burning, immerse in water to relieve, female prolapse uterus & out comes babies, infect copepod, ppl drink unfiltered water, get worm; twirl on stick to pull F worm out
- control by filtering water & preventing ppl from going into water w/blisters

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18
Q

onchocerciasis

A

river blindness

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19
Q

echinococcal

A

cystic hydatid disease; actually dog tapeworm

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20
Q

The route of acquisition of Loa loa

A

bite of tabanid fly – night biting mosquito

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21
Q

loaiasis is mainly symptomatic in what kind of ppl?

A
  • newly infected people due to allergic response to worm
  • urticaria, pruritis, migratory angioedema
  • calabar swelling
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22
Q

The manifestations of loaiasis

A

o aSx – endemic pop
o death of adult worm -> toxin release -> granulomatous inflammation which then blocks lymph
o filarial fever – recurrent swelling from lymph obstruction, fever 7-10d
o chronic – obstructed lymph drainage -> damage from bacterial infection§ chyluria – white urine
o Tropical Pulm Eosinophilia – no obstruction, hyper-eosinophil response, earlier reaction to worms causes infiltrates in lung/gi but no edema, leads to fibrosis in lungs if untreated (due to immune response to dead worms)

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23
Q

The route of acquisition of the lymphatic filariases

A

mosquito - mostly transmit Wucheria bancrofti

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24
Q

The mechanism of damage and manifestations of lymphatic filariasis

A
  • sheathed microfilaria that migrate into lymph & blood channels
  • toxin release when adult worms die, cause rxn & cause blockage due to immune response damage → granulomatous inflammation
  • early disease: recurrent painful inguinal swelling, watch for bacterial super infection
  • obstructive disease: can’t drain lymph & lots of edema in interstitial, elephantiasis from lymphedema, loss of skin elasitcity; chyluria when obstruction of renal lymph
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25
Q

role of Wolbachia bacteria in fertility of filaria

A

symbiotic relationship w/filaria, need for fertility, if kill bacteria, worms can’t reproduce

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26
Q

route of acquisition of Onchocerca volvulus

A

Blackfly bite

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27
Q

The manifestations of O. volvulus infection Cestodes

A
  • nodule where adult worms hang out & lay eggs = microfilaria
  • keratitis – microfilaria die in the eye -> inflammatory response causes cornea damage → blindness = river blindness
  • Microfilaria are killed all over the body -> hypopigmentation, dec. elasticity (from chronic inflammation)
28
Q

How infections of Taenia solium and Taenia saginata are acquired to infect the GI tract of humans (specific animals that are sources)

A
  • Eating beef/pork contaminated with oncospheres
  • adult tapeworm when eat larval stage (GI tract)
  • cysticercosis when eat eggs (everywhere else)
29
Q

How T. solium is acquired when it infects deep tissues of humans to cause cysticercosis

A

From food contaminated by eggs

30
Q

The manifestations of GI Taenia infection

A

adult worms latch onto SI & reproduce, release lots of proglottids that are pooped out & can get into animals when they eat it

31
Q

The manifestations of cysticercosis

A
  • oncospheres gain access to circulation
  • migrate everywhere, predominantly in muscle bc of biomass
  • Develop fluid filled bladders, can end in CNS → cysts cause seizures or focal neurological Sx
32
Q

The route of acquisition of Echinococcus granulosus

A

goats infected & canines eat, humans eat dog feces w/egg in it

33
Q

The route of invasion of E. granulosus

A

oncospheres hatch, penetrate intestinal wall, migrate everywhere, form cysts

34
Q

The manifestations of E. granulosus infection

A

hydatid cysts grow & push on things → symptomatic

35
Q

The route of acquisition of the schistosomes

A

water, penetrate skin into humans, back into water, into snails, into water

36
Q

Where schistosomes live in the body, and the route of exit

A
  • veins everywhere, most evolutionary successful places are liver, GI, bladder bc then can easily get into lumen & poop out
  • if not in those places, get trapped in tissue & cause granuloma formation which causes disease
37
Q

how schistosomes cause damage

A
  • inflammatory response to the eggs

- adults acquire host proteins & coat surface so immunologically silent

38
Q

The normal fungal flora

A

Candida albicans

39
Q

The sources of fungal infections

A

P2P, pets, environment

40
Q

Arms of immune system involved in responding to fungi

A
  • That neutrophils and T-helper cells are key in the immune response against fungi
  • neutrophils – phago yeast and kill, autolyse and release toxins on molds
  • T-helper – activate killing by PMN, MØ
41
Q

The body sites infected by dermatophytes

A

Infect just dead part of skin (stratum corneum), nails, hair, metabolize keratin

42
Q

The definitions of and manifestations of tinea corporis, tinea capitis, tinea cruris, onychomycosis (note that these are diseases, not species of fungi)

A

o Corporis – skin, body-wide; ringworm
o Capitis – scalp, hair loss; ringworm
o Cruris – crotch; jock itch
o Onychomycosis – nails, thickening and yellowing of nails usually toes

43
Q

Sporothirix schenkii type, source, spread

A
  • Ascomycota, dimorphic
  • environmental fungus worldwide on plants (hi in S. Amer), enters thru break in skin → nodule → ulcer
  • spreads along draining lymph → more nodules → ulcers
  • “rose handler’s disease”
44
Q

The manifestations of sporotrichosis

A

ulcerating nodules, traveling proximally

45
Q

That the endemic mycoses are caused by fungi which are

A
  • found in the environment in specific geographic areas
  • all Ascomycota
  • dimorphic (yeast form seen in tissue)
  • acquired in the same manner (inhalation of spores from environ)
  • more severe (e.g. dissemination) in immunocompromised, very young, or elderly people and in people who get a large inoculum of the fungus
46
Q

The shared manifestations and pathophysiology of endemic mycoses

A
  • often asymptomatic
  • Sx of acute infection may be mild or resemble influenza or acute pneumonia
  • Sx of chronic infection resembles TB
  • dissemination of fungi leads to extrapulmonary manifestations
47
Q

Acute pulmonary infection may be asymptomatic or have flu-like, or pneumonia-like symptoms

A
  • Chronic pulmonary infection often has tuberculosis-like symptoms
  • Disseminated infection can have many manifestations
48
Q

The approximate geographic distributions for H. capsulatum, B. dermatitidis, C. immitis

A
  • H. capsulatum - ohio and mississippi river valley US (construction)
  • B. dermatitidis, - ohio river valley of eastern US
  • C. immitis - southwest USA (inc by dry summer following wet winter), construction
  • construction stirs up soil
49
Q

The manifestations of H. capsulatum infection, and the risk factors for the specific manifestations

A
  • acute asymptomatic or Mild: self-limited dry cough, fever, malaise; pulm granuloma, rheumatologic and dermatologic complications in 5% (healthy)
  • acute severe histoplasmosis= rales (high inoculum)
  • cavitary lung histoplasmosis = low-grade fever, productive cough, dyspnea, wt loss (underlying lung prob like emphysema), growth in bullae, destruction, expansion & coalescene of bullae → cavitation
  • disseminated histoplasmosis → HSM, pancytopenia (bone marrow), skin (ulcers, nodules) (infants, elderly, immunocompromised)
50
Q

How the immune system responds to H. capsulatum

A

Mo phagocytose, capsulatum replicates within Mo bc increase pH so doesn’t get killed, Th1 respond (2wk post) rel. TNFa→ killing by Mo

51
Q

The manifestations of B. dermatitidis infection, and the risk factors for the specific manifestations

A
  • 50% asymp (otherwise healthy)
  • acute pulmonary blastomycosis: fever, malaise, mild chest discomfort, dry cough
  • chronic: productive cough with blood (again like TB)
  • extrapulmonary blastomycosis: when disseminate, skin most common: raised, heaped up lesion or ulcerative
52
Q

The manifestations of C. immitis infection, and the risk factors for the specific manifestations

A
  • acute asymptomatic or mild: fever, malaise, mild chest discomfort, dry cough (healthy)
  • acute severe cocci (high incolum)
  • cavitary lung (underlying lung disease, diabetes)
  • disseminated cocci: skin, joints, bones; meningitis - worst case scenario (infants, elderly, immunocompromised)
53
Q

The morphology of the endemic mycoses in tissue (not in culture)

A

all grow as yeast in body

54
Q

Ectoparasite

A

infestation bc superficial (ie. scabies, lice)

55
Q

endoparasite

A

infection bc deep w/in

56
Q

protozoa

A

unicellular, usually replicate within host

57
Q

helminths

A

multicellular, develop outside host

58
Q

arthropod

A

invertebrate animal that have an exoskeleton, segmented body & jointed appendages

59
Q

definitive host

A

host in which parasite if it has a sexual life form will complete it

60
Q

intermediate host

A

host in which asexual division occurs

61
Q

mechanisms by which parasites lead to disease

A
  • mechanical obstruction – hydatid cyst of liver, intestinal block, small vessel obstruction
    o killing of host cells - myocarditis
    o competition for nutrients – hookworm: Fe, Fish tapeworm: B12
    o eliciting an inflammatory response – myocarditis, chorioretinitis
62
Q

immune response associated with helminth infections

A

eosinophilic response

63
Q

The defining characteristic of flagellates

A

o That flagellates usually have a trophozoite and cyst form
o Asexual, Have flagella (duh)

64
Q

symptoms of giardiasis

A

o Chronic diarrhea, weight loss, malabsorption

o Foul smelling diarrhea, malaise, anorexia

65
Q

route of acquisition of Giardia lamblia

A

o Fecal/oral, P2P, contaminated food/water, highly infective

66
Q

The pathogenesis of G. lamblia

A

o Attach to brush border, non-invasive, cause damage to epithelium

67
Q

How nitroimidazoles and nitazoxanide kill anaerobic parasites (note that they can kill anaerobic bacteria the same ways)

A

does something to DNA I think….

Microbiology (8 decks)

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