parasites Flashcards
parasite 1 parasite 2 opportunistic antifungal therapy
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
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
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
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
5
Q
o Mold
A
- multicellular fungi w/long thread-like filaments
- look fuzzy
6
Q
o Yeast
A
- unicellular fungi which are round or oval in shape
- divide by budding
- look smooth
7
Q
o Hyphae
A
- long thread-like filaments of molds
8
Q
o Septum (as it refers to hyphae)
A
- cell walls of hyphae that separate nuclei
- some have, others don’t
9
Q
o Mycelium
A
- mass of hyphae
- visible to eye w/o magnification = fuzz you see
10
Q
o Dimorphic
A
- yeast under some conditions (usually body temp) & mold under others (usually room temp)
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
12
Q
phyla of fungi are defined by
A
the method of sexual reproduction
13
Q
fungi phyla that contain the fungi of medical importance
A
Mucoromycotina
Ascomycota
Basidiomycota
14
Q
Mucoromycotina
A
- zygospores (yoke-like struct btwn hyphae)
- simple sugars as soure of energy
- hyphae thin walled w/few septa
15
Q
Ascomycota
A
- ascospores (sac-like structs)
- metabolize complex carbon sources
- hyphae thick walled & septate
- 1-3 beta-D glucan in cell wall
16
Q
Basidiomycota
A
- basidiospore (borne on projections or pedestals)
- metabolize complex carbon sources
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
18
Q
onchocerciasis
A
river blindness
19
Q
echinococcal
A
cystic hydatid disease; actually dog tapeworm
20
Q
The route of acquisition of Loa loa
A
bite of tabanid fly – night biting mosquito
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
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)
23
Q
The route of acquisition of the lymphatic filariases
A
mosquito - mostly transmit Wucheria bancrofti
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
25
role of Wolbachia bacteria in fertility of filaria
symbiotic relationship w/filaria, need for fertility, if kill bacteria, worms can’t reproduce
26
route of acquisition of Onchocerca volvulus
Blackfly bite
27
The manifestations of O. volvulus infection Cestodes
- 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
How infections of Taenia solium and Taenia saginata are acquired to infect the GI tract of humans (specific animals that are sources)
- Eating beef/pork contaminated with oncospheres
- adult tapeworm when eat larval stage (GI tract)
- cysticercosis when eat eggs (everywhere else)
29
How T. solium is acquired when it infects deep tissues of humans to cause cysticercosis
From food contaminated by eggs
30
The manifestations of GI Taenia infection
adult worms latch onto SI & reproduce, release lots of proglottids that are pooped out & can get into animals when they eat it
31
The manifestations of cysticercosis
- 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
The route of acquisition of Echinococcus granulosus
goats infected & canines eat, humans eat dog feces w/egg in it
33
The route of invasion of E. granulosus
oncospheres hatch, penetrate intestinal wall, migrate everywhere, form cysts
34
The manifestations of E. granulosus infection
hydatid cysts grow & push on things → symptomatic
35
The route of acquisition of the schistosomes
water, penetrate skin into humans, back into water, into snails, into water
36
Where schistosomes live in the body, and the route of exit
- 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
how schistosomes cause damage
- inflammatory response to the eggs
| - adults acquire host proteins & coat surface so immunologically silent
38
The normal fungal flora
Candida albicans
39
The sources of fungal infections
P2P, pets, environment
40
Arms of immune system involved in responding to fungi
- 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
The body sites infected by dermatophytes
Infect just dead part of skin (stratum corneum), nails, hair, metabolize keratin
42
The definitions of and manifestations of tinea corporis, tinea capitis, tinea cruris, onychomycosis (note that these are diseases, not species of fungi)
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
Sporothirix schenkii type, source, spread
- 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
The manifestations of sporotrichosis
ulcerating nodules, traveling proximally
45
That the endemic mycoses are caused by fungi which are
- 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
The shared manifestations and pathophysiology of endemic mycoses
- 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
Acute pulmonary infection may be asymptomatic or have flu-like, or pneumonia-like symptoms
- Chronic pulmonary infection often has tuberculosis-like symptoms
- Disseminated infection can have many manifestations
48
The approximate geographic distributions for H. capsulatum, B. dermatitidis, C. immitis
- 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
The manifestations of H. capsulatum infection, and the risk factors for the specific manifestations
- 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
How the immune system responds to H. capsulatum
Mo phagocytose, capsulatum replicates within Mo bc increase pH so doesn't get killed, Th1 respond (2wk post) rel. TNFa→ killing by Mo
51
The manifestations of B. dermatitidis infection, and the risk factors for the specific manifestations
- 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
The manifestations of C. immitis infection, and the risk factors for the specific manifestations
- 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
The morphology of the endemic mycoses in tissue (not in culture)
all grow as yeast in body
54
Ectoparasite
infestation bc superficial (ie. scabies, lice)
55
endoparasite
infection bc deep w/in
56
protozoa
unicellular, usually replicate within host
57
helminths
multicellular, develop outside host
58
arthropod
invertebrate animal that have an exoskeleton, segmented body & jointed appendages
59
definitive host
host in which parasite if it has a sexual life form will complete it
60
intermediate host
host in which asexual division occurs
61
mechanisms by which parasites lead to disease
- 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
immune response associated with helminth infections
eosinophilic response
63
The defining characteristic of flagellates
o That flagellates usually have a trophozoite and cyst form
o Asexual, Have flagella (duh)
64
symptoms of giardiasis
o Chronic diarrhea, weight loss, malabsorption
| o Foul smelling diarrhea, malaise, anorexia
65
route of acquisition of Giardia lamblia
o Fecal/oral, P2P, contaminated food/water, highly infective
66
The pathogenesis of G. lamblia
o Attach to brush border, non-invasive, cause damage to epithelium
67
How nitroimidazoles and nitazoxanide kill anaerobic parasites (note that they can kill anaerobic bacteria the same ways)
does something to DNA I think....
