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micro module 3
fungi, protists, helminths, virology
| Question | Answer |
|---|---|
| def of mycology | the study of fungi |
| fungi we will study | molds and yeasts |
| characteristics of fungi: what are the 2 phases of the life cycle; are the colonies of mold visible or invisible to naked eye; are yeast unicellular are multicellular; | growth phase and reproductive phase; visible; unicellular; |
| characteristics of fungi: are molds multi or unicellular; molds grow in long tangled what; a filament is aka; many hyphae make the colony of mold what is the name for the colony; | multi; filaments; hypha; mycelium; |
| characteristics of fungi: dimorphic- what does this mean; why does this happen; | some forms of fungi can have a yeast and a mold phase; some diseases can have this and can be very serious |
| characteristics of fungi: most funi have what; def of aerial mycelium; areial mycelium give rise to __ structures; def of vegatative mycelium; why does vegatative anchor; | hyphae; they give rise to fruiting bodies and produce spores; reproductive; this mycelium is anchored to organic matter; to pull nutrients from the matter to grow mycelium; |
| characteristics of fungi:cell wall- what is it composed of;what is chitin made up of; this structure of cell wall provides what for the fungi; | chitin; a polysaccaride; rigitiy and strength to resist rupturing from increased internal pressure; |
| characteristics of fungi: def of a septa; when the fungi is divided into segments with septa what is this condition called; | divides the cytoplasm into separate cells; septate; |
| characteristics of fungi: def of coenocytic; what does it mean that all fungi are heterotrophic; most fungi are saprobes what does this mean; how do they break down organinc matter; | hyphae containing many nuclei; their carbon and energy source are from organic matter; they feed off dead decaying organic matter; they release enzymes to break it down |
| characteristics of fungi: are we heterotrophic; what are the positive aspects of fungi; what are the negative aspects of fungi; are most fungi beneficial; | yes, this presents a problem for tx; production of some antibiotics, certain foods, environmental decomposers; plant destruction, opportunistic pathogens; yes |
| influencing factors if fungal growth: how are nutrients taken up; are they aerobic or anaerobic; what temp do they grow best at; what pH do they grow best in; is increased carbs good or bad for them | through absortion; aerobic; room temp; acidic 5-6; good |
| what agar has the best growth for it | SDA |
| mold sporulation: occurs in what; asexual reproductive structures develop where on the hyae; what specialized hyphae does the asexual spores develop; def of spangium; what are the spores in the sporangium called; | fruiting bodies; the end; aerial hyphia; the sac that the asexial spores develop in; sporangiospores; |
| mold sporulation: what is the primary reproductive mode of fungi; def of conidia; how do the conidia develop'; | spores; these are free spores not enclosed by a spore bearing sac; by pinching off the tip of a special fertile hypha or by segmentation of preexisting vegatative hypha; |
| mold sporulation: what is the most common sexual spores; | conidia; |
| blastospore production: def; what happens after the blastospore is released | in budding a blastospore develps from the parent cell; a scar forms on the parent cell where the spore was released |
| def of athrospores; what type of hyphae is this located; | a rectangular spore formed when a septate hypha fragments at the cross walls; segmented; |
| true hyphae are in molds or yeasts; where are sudohyphae located; | molds; yeasts ; |
| can fungi produce sexually; def of sexual reporduction in fungi; what do the opposite fuse into; | yes; opposites come together and fuse; heterokaryon |
| taxonomic classification of fungi: fungi can be classified into how many phyla'; | 5; |
| sporulation- asexual reproduction: what is the function; what are the types of asexual mold spores; | reproduction, dissemination, protection of species- not are resistant as bacterial spores; conidiospores, sporangiospores, chlamydiospores; arthrospores; blastospores |
| conidiospores production: are these unprotected; they are freely exposed to what; are they light or heavy; are they resistant; why are they not resistant; do they cause disease; give example; def of conidia; | yes; the environment; light; no; b/c they are not in a sac ec; yes; penicillium sp; chain of conidiospores; |
| conidiospores production: what cell gives rise to the fruiting body; the conidia is on what; | the foot cell; the conidiophores; |
| conidiospores w/ columella: are they light weifht; are tehy unprotected; example; the conidiophore terminates into what; | yes; yes; aspergillus sp.; a columella |
| sporangiospores: are they resistant; what is the supporting stalk; what are the extenstions below they hypha; what is the membrane that surrounds they sporangiospores; example; these will cause disease in what type of patient; | yes; the sporangiophores; the rhizoid; the sporangium; Rhizopus sp.; immunocompromised; |
| chlamydospores: formed from what; what are they resistant to; the spherical conidium is formed by what; when is it released; | vegatative hyphae; heat, drying, freezing; the thickening of a hyphal cell; what the surrounding hypha is fractures; |
| arthrospores: are these resistants; why are they so resistant | yes; the thickening of the cell wall |
| blastospores: produced by what; mostly produced with what | buddding; yeast |
| yeasts: cells will not be equal in what; are they large or small; are they single or multicellular; are they larger or smaller than bacteria; are they produced asexually or sexually; how do they reproduce; what is their shape; | size; large; single; larger; asexually; by budding; shperical or oval ; |
| yeasts: def of psuedophypha; where is a scar formed; do new buds form in the scarred area | when they are produced bud- on bud and create a chain; where the bud is released; no |
| dimorphic fungi: this fungi grows as molds at what temp; the fungi transforms into yeasts at what temp; def of morphic; what is the infectious stage; what is the stage where it disseminates in tissues; is the yeast stage infectious; | room temp 24 degrees C; humna body temp 37 degrees C; change;the mold spore; the yeast stage; usually not; |
| most of the more dangerous human pathogenic guni are what | dimorphic |
| dimorphic fungi: how is this proven in the lab;why can we inhale them; what is the response in a healthy person; what state is communicable; what stage is not communicable;is it picked up from the environment; the genes are identified by what' | the temp of the culture is changes; b/c they are lightweight; flu; the mold spore stage; the yeast stage; yes; genetic probes (too dangerous to identify with dimorphisis; |
| def of mycoses; what is singular term | fungal diseases of humans; mycosis |
| def of genetic probes | known sequences of DNA that unknown organism are exposed to it to ID the species (used for labs that do not have a high classification |
| dimorphic fungi: when a fungal spore from the environement gain enterence to an animal what happens; the dimorphic fungi remain as a yeast where; when the yeast cells leave the animal host tand return to the environment they revert back to what state; | they germinate into yeasts; remain in this phase in the host; the sporulating hyphal state |
| dimorphic fungi: dimorphism is triggered by what | growth temp; |
| def of a true primary fungal pathogen | a species that can invade and grow in a healthy noncomprimised animal host |
| most fungal pathogens do not require a __ to complete their life cycle | host |
| where in environment do humans come across infectious funfi | air, dust soil |
| fungi enter the body mainly by what route | respiratory mucous, cuntaneous routes |
| why is fungi in the yeast form more invasive than when it is in the mold form | because they grow more rapidly and spread throughout the tissue and blood those with hyphae tend to localize along BV and LN |
| mycosis: cryptococcosis: yeast or mold; are they encapsulated; the encapsulation causes what; what happens to them in the environment; if they are dehydrated what can pick them up easily; how many deaths due to fungal diseases are caused by this | yeast; yes; slow phagocytosis by body; they dehydrate quickly; the wind; 25% |
| mycosis: cryptococcosis: shape; who is most likely to get disease; who is resistant; where in body does it mostly occur; where is second most likely place for it to occur; | spherical ovoid shape with small buds and a large capsule around it; debilitated patients; strong healthy humans; pulmonary infection; cutaneous infection |
| mycosis: cryptococcosis: what is the etiologic agent; what reservoir is it found in; what animal droppings is it associated with; what causes the yeast to be airborn; | cryptococcus neoformans; soil worldwide; birds; wind gusts; |
| mycosis: cryptococcosis: why does it proliferate in the bird droppings; what patients has the highest rate of occurances; s/s of AIDS pt | b/c of the high nitrogen content of the droppings; AIDS patients; severe form of meningitis |
| mycosis: cryptococcosis: what conditions predispose someone to having infection; where in world does it occur the most; | AIDS, steroid tx, DM, cancer; US; |
| mycosis: cryptococcosis: s/s in lungs; what happens if it reaches the brain; | most subclinical and infections resolve, but some have a fever, cough, nodules in lungs; HA, mental changes; coma, paralysis, seizures |
| mycosis: cryptococcosis: what is mortality rate; when is the mortality rate highest; transmission; who accounts for 85% of the cases in US; | >12%; in untreated cases ; inhalation of airborne yeast cells or basidiospores into the alveoli; HIV infected; |
| mycosis: cryptococcosis: sometimes it can become cutaneous how; how is it Dx; do the yeast cells look like pseudohyphae; | in a wound; negative staining of specimens to detect encapsulated budding yeast cells; no; |
| def of sequelae | the disease states the follow the primary |
| mycosis: cryptococcosis: what is the sequelae of the fungi; who is at risk; what is first s/s; tx for healthy people; tx for immunocomprimised | blood and meningitis; everyone; pulmonary infection; fluconazole; amphotericin B; |
| fluconazole- used for what; is it less or more toxic; who is it used for | fungal infections; less; healthy people |
| amphotericin B- who is it used for; used to treat what; is it toxic; what does it damage; people with damaged kidneys will often be what; | immunocomprimised; systemic fungal infections; yes; kidneys, bone marrow; anemic (b/c kidneys produce EPO |
| mycosis: candidiasis- what species is the major causes of candidiasis; microscopy of it; macroscopic look; transmitted how; where is there normal flora of it; who is not at risk; | candida albicans; budding cells that form elongate pseudohyphae and true hyphae; off- white pasty colony with yeasty odor; self infection, vaginal canal to newborn, STD; pharynx, genitalia, L. intestine, skin of 20% of humans; healthy; |
| mycosis: candidiasis- who is at risk; when is infection at increased risk; is it contagious; when is it contagious | extreme youth, pregnancy, drug therapy, immunodeficiency, trauma;any time that yeast is in contact with moist skin; usually no; nurseries, birth, surgery, sexual contact |
| mycosis: candidiasis- it is the most common what; where can it cause infection; when serious what can is disseminate into; where does infection take place most often; | fungal infection; mouth, pharynx, vagina, skin, lungs; the organs; mm and vagina; |
| mycosis: candidiasis- s/s; a pustula is a aka; what is the etiologic agent; is it a dimorphic fungus | itching, burning, reddening, swelling, discharge more or less, pustules, pain; white patch; Candida albincans; yes |
| mycosis: candidiasis- is it common for candida albicans to use its dimorphic abilities; when might it use its dimorphic abilities; when does someone get an infection | no; immune system is comprimised; when microbial population in body changes resulting in a overgrowth of yeast |
| mycosis: candidiasis- why is it considered an opportunistic infection;give example of immunocomprimed pt; | the yeast usually resides in these areas in body, but sometimes it can overgrow causing problems; DM- increased sugar and increased pH increases yeast; |
| mycosis: candidiasis- how do abx increase risk for this; def of thrush; who is most at risk for getting candida; | they wipe out bacteria and the yeast is able to overgrow; white adherent patchy infection affecting the membranes of the oral cavity or throat; immunocomprimised; |
| mycosis: candidiasis- what is the sequelae; do we see a secondary disease in healthy ppl; def of vulvovaginal candidiasis; treatment; | systemic candidiasis has 77% mortality rate; no; yeast infection the distrupts vaginal flora; fluconazole, nystatin; |
| mycosis: candidiasis- what is treatment for oral patients; what is given for systemic infection; s/s of vulvoganinitis; | swish and spit nystatin to destroy organism; ampiterricin B; white curd like growth; |
| mycosis: candidiasis- vulvovaginitis- why do antibiotics cause this; what is lactobacillus sp; | excessive abx may decrease protective bacteria in the vagina allowing C. albicans to flourish; a copetitive colonization the prevents the overgrowth of yeast vaginally; |
| mycosis: candidiasis- oral- what does it look like;cause; cause in newborns; | white curd liek growth on mucous membranes in mouth; immunosuppression, organism picked up during vaginal deleivery; |
| mycosis: candidiasis- onychia- def; who is at risk'; is it hard to treat; what is gram stain | involves the hardening, browning and distortion of fingernails; ppl with occupations that require their hands to be immersed in water; yes; positive |
| signs and symptoms; def of sign; def of symptom | something you can see; something that patient can only tell us |
| mycosis: candidiasis-why will it almost always return; what 2 areas usually result from abx use; | since it is an underlying infection that caused the overgrowth of candida, if it is not treated it will come back again; vaginal and intestinal |
| mycosis: candidiasis- cutaneous- where does it occur; s/s; give example' | pustules in irritated damp areas; painful inflamed tissue, clear discharge; diaper rash, axillary rash inquinal rash |
| mycosis: candidiasis- intestinal- def; s/s; | antibiotic use destroys the bacteria allowing yeast to overgrow; cramps, diarrhea |
| mycosis: dermatophytosis- where on body does it occur; what does it look like; does it disseminate; what does it look like; | infection of skin, hair and nails; a ring worm; rarely if ever; spreading legions that dries over time and becoems scaly looking at edges (red ridge); |
| mycosis: dermatophytosis- location of . . tinea pedis; tinea capitis; tinea barbae; tinea corporis; tinea cruris; the clinician will call this a ___ infection | athletes foot; scalp head; beard; body; groin; tinea; |
| mycosis: dermatophytosis- tinea is latin for what; all the tineas are subcategories for what; tinea capitis can cause loss of ____; tinea cruris is aka; | worm; dermatophytosis; hair; jock itch; |
| mycosis: dermatophytosis- def of tinea unguium; tinea unguium is aka; what is the etiologic agent of tinea; name the 3 genera; | the nail; onychomycosis; over thirty mold species belonign to 3 genera; trichopyton sp, microsporum sp, epidermophyton sp; |
| mycosis: dermatophytosis- what is the reservour; these molds feed off what; what is the infection called when we pick it up from our pets; | skin cells, pets or humans; the keratin of our dead skin cells; a zoonotic infection; |
| mycosis: dermatophytosis- why is there no sequale; how is it dx; why is potassium hydroxy used; what is abrev. for potassium hydroxy; how to dx with woods lamp; | b/c it does not move beyond the skin; potassium hydroxide used taking a skin scraping to see it on slide; the potassium kills our skin cells so only the mold is left to see; KOH: this has uv black lights and if it fluoresce than that means there is infect |
| mycosis: dermatophytosis- how is it transmitted; how is it transmitted by pets and humans; how is it transmitted in showers,floors cmbs and hats; | comming into contact with contaminated dead skin cells; the shedding of the cells; cells will be in those areas; |
| mycosis: dermatophytosis- what is the risk group; is the prognosis good; | damp irritated skin; yees; |
| mycosis: dermatophytosis- what is used for tx topically; what is tx orally; griseofulvin is used for what 2 tineas; what one has to be prescribed; | imidazoles; griseofulvin; scalp and nail infections griseofluvin; |
| imidazoles- what are they; it prevents what formation; | antifungal and antifungal agents; orcalsterol formation in fungal cell membranes and this kills the fungi (** does not effect us b/c we do not have this type of lipid) |
| histopalsmosis: aka; why is it called summer flu; if pt is healthy and comes in contact with organisms what are there cm; what are the s/s of a self limiting pulmonary infection; | darlings disease, summer flu, cave sickness; b/c high risk times are spring summer and fall; self limitign pulmonary infection; flue s/s or asymptomatic; |
| histopalsmosis: what are s/s of self limiting infection; are most of the cases self limiting or not; | fever, HA, cough, chest pain; yes; |
| histopalsmosis: 5% of the cases develop what;the chronic pulmonary infection mimics what; s/s of chronic; how can is disseminate; | chronic pulmonary infections; TB; granulomatous lesions deveop in lungs; the macrophages will engulf the yeast cell and spread organism to others organs |
| histopalsmosis: what is the etiologic agent; is it a dimorphic fungus; where is highest rate of occurance; what is the reservoir; | gistoplasma capsulatum; yes; eastern and central regions of U.S.; dry, dusty sail, ohia mississippi river valleys, caves chicken coops; |
| histopalsmosis: grows abbuntently in what type of soil; what dimorphic phase does pt get it; what phase is in lungs; once we are exposed to it what happens' | moist soil high in nitrogen content; mold spore phase; yeast phase; pt develops incomplete immunity; |
| histopalsmosis: def of incomplete immunity; can bats have the disease; how does it occur in chicken coops; | we will develop disease but it is not as severe first time; yes; chickens have it in their feces but they do not have the disease b/c it has a higher body temp |
| histopalsmosis: how are the spores dispersed; how can one see if they have partial immunity; | by wind through air; injection of the fungal extract injected into skin and monitored for allergic reaction |
| histopalsmosis: who is the sequelae; how is it transmitted; how long is the incubation time; who is at risk; tx | the immunocompromised become systemic; inhalation of mold spores into the lungs; 10 days; immunocomprimised; amphotericin B |
| histopalsmosis: how it given amphotericin B; what age group is most symptomatic; | those with severe lung infection and when dissemincaton occurs; chilren |
| mycosis: coccidioidomycosis: aka; is it a dimorphic fungus; what percent infected have asymptomatic pulmonary infection; what % have acute sympotomatic pulmonary infection; what are the s/s in acute symptomatic pulmonary; will individuals recover in acute | valley fever; yes; 50%; 45% of cases; flu like s/s, dry hacking cough, chest pain, fever; yes |
| mycosis: coccidioidomycosis: how long will we follow acute cases; why are they followed for 2 years in acute; s/s in acute; who usually gets pna; | 2 years; b/c they are at high risk for acute pulmonary infection; skin nodules and pna; immunocomprimised |
| mycosis: coccidioidomycosis: what % gets a chronic pulmonary infection; who is at risk for a chronic pulmonary infection; those with high risk have what s/s | 5-10%; immunocomprimised; cavities in lungs destroyed, dissemination of organism |
| mycosis: coccidioidomycosis: what is etiologic agent; is it a dimorphic fungus;reservior; what areas in us; how do animals cause disease; | cocciudioises immitis; yes; desert areas with cattle sheep;SWest us, northern mexico, S america; they deposit spores in soil |
| mycosis: coccidioidomycosis: how do railroads cause disease; how do earth quakes cause increased number of cases | trains disrupt the soil; the disruption of the soil causes an increased incidence |
| mycosis: coccidioidomycosis: what is the sequele; who is most likely to get the sequelae; is the mortality rate high in the sequelae;how is it transmitted; what develops in the lungs; | systemic infection in lungs, bones liver meninges skin; immunocomprimised; yes; inhaling the mold spores; yeast; |
| mycosis: coccidioidomycosis: what is the risk groups; what is the treatment in the lungs; who gets amphotericin B tx; | immunocomprimised everyone is at risk to some extent though; amphotericin B; systemic or high risk pt |
| mycosis: coccidioidomycosis: how long is tx; | one year; |
| mycosis blactomycosis: aka; most cases have what kind of recovery; who identified it; s/s; | gilchrist's disease; spontanious; a dermatologist Dr. gilchrists; contamination of cuts and abrasions and raised wart like lesions; |
| mycosis blactomycosis: pulmonary infection- what percent are asymptomatic; what percent are acute; when the infection is acute what does it mimic; s/s of a bacterial pna; | 50%; 50%; a bacterial pna; persistant cough, high fever, chest pains, muscle and joint pain, chils, sputum production; |
| mycosis blactomycosis: small % of acute infected do not recover and this turns into what' what does chronic infection mimic; what cancer does chronic mimic; what s/s are chronic; | chronic; TB; bronchogenic carcinoma; cavitation and nodular formation in the lungs; |
| mycosis blactomycosis: how can this be tested; is there a vaccine; what is etiologic agent; is it a dimorphic fungus | w/ blood test; yes; blastomuces dermatitidis; yes |
| mycosis blactomycosis: what is the 5 of ppl who develop immunity from vaccine; where is reservoir; where does it occur in U.S; do we know how the mold gets into the reserviors; | 60%; moist organic soil, rotting wood; mississippi river valley, north great lakes region, canada; no |
| mycosis blactomycosis: what is the sequelae; what type of cases usually disseminate; what is the transmission; how long is the incubation time; | dissemination to bone, organs, CNS skin lesions; chronic ones; mold spore inhalation; 30-45 days; |
| mycosis blactomycosis: who is at risk; who is treated; what is treatment for dissemination | everyone; all dx cases are treated to prevent dissemination risk; amphotericin B |
| mycosis: sporotrichosis: aka; s/s; what will the nodules look like; does this disseminate often; where does first nodule appear; what | rose thorn disease; cutaneous and subq nodule; necrosis and ulceration that are purple with pus and discharge; no; in abraded area of skin; |
| mycosis: sporotrichosis: what happens when organism enters subq layers; when it follows the lymphatic tract what do the nodules look like; what causes pt to seek tx | it follows the lymphatic tract; they will be a line of nodules; the ulcers are slow to heal |
| mycosis: sporotrichosis: is the fungus dimorphic; what is the etiologic agent; what is the reservior | yes; sporothrix schenchii; contaminated thorny plants, sphagnum moss, baled hay, wood |
| mycosis: sporotrichosis: why does it have to be thorny plants instead of all plants as a reservior;is there a sequelae; | the fungus needs a point of entry; dissemination is rare; |
| mycosis: sporotrichosis:is it treated easily; how is it transmitted; who is at risk; what is tx; what is tx for systemic | yes; the fungus enters through small cuts in usually hands and limbs;florests, farmers, forest employees; potassium iodine; amphotericin B |
| mycosis: pneumocystosis- this only occurs in what type of individual; what do they develop; pneumocystis carinii pneumonia is aka; | immunocomprimised; pneumocystis carinii pneumonia; PCP; |
| mycosis: pneumocystosis- s/s of PCP; where is the foamy liquid located; fluid in the alveoli causes the pt to what | severe inflammatory response in lungs with foamy liquid and cysts; in the alveoli; drown; |
| mycosis: pneumocystosis- why is the fungi called a cyst; what is the etiologic agent; | b/c they originally thought it was a protozoan;; pneumocystis jiroveci; |
| mycosis: pneumocystosis- what is the reservoir;are we all exposed to it; most chilren develop antibodies whaen; is it a pathogen in healthy ppl | everywhere, human source;yes; early on after exposure; no |
| mycosis: pneumocystosis- what is the sequelae; what is transmission; what is tx; the tx are what; what one is used in aids pt | pneumothorax and respiratory failure; organism is inhaled into the lungs; trimethoprim-sulfamethoxazole and pentamidine; prophylactic; pentamidine; |
| mycosis: aspergillosis- how does the mold enter the lungs; what etiologic agent; | it is inhaled and continues to grow as a mold in the lungs; aspergillus fumigatus; |
| mycosis: aspergillosis- why do ppl develop it in surguries; what can it cause in ear; what can it do to heart; | b/c it could be on equipment or in environment; otomycosis; heart valve issues; |
| aspergillus niger is used in what | beano |
| ergot toxin: ergotism- this is caused by what; what type of fungi is claviceps purpurea; this grows on what; s/s; why do ppl hallucinate; | claviceps purpurea; a mold; grains; numbness, hot burning cold sensations, seizures, paralysis, hallucinations, cardiac arrhuthmias; b/c it is a natural LSD |
| ergot toxin: ergotism- hypothesized that women in what trials had ergotism; what is a derivated of alkaloid in ergot; | salem witch trials; lysergic acid diethylamide (LSD) |
| ergot toxin: ergotism- tx | vasodilators, anticoagulants |
| mycotoxin- aflatoxin- aflatoxicosis- what is the atiologic agent; what can be contaminated; s/s; liver involvement can lead to what; common where | aspergillus flavus; peanuts, grains, cereal, corn in warm humid environments; vomiting, abdominal pain, pulmonary edema, convulsions, coma, fatty involvment of the liver kidneys and heart; liver cancer; in third world countries |
| mycosis: spores that germinate in the lungs into yeasts cells and produce an asymptomatic ____ infection | pulmonary |
| histoplasmosis: where is its primary location for growth; what does the yeast look like microscopically | the cytoplasm of phagocytes; yeast |
| what has the greatest virulence of all mycotic patheogens | coccidioidomycosis |
| what is the most common mycotic pathogen | canidia |
| protozoa: are they eukaryotes or prokaryotes, are the single or multicelled; do they have a plasma membrane; what is the common tx for protozoan infections | eukaryotes ; single; yes ; metronidazole |
| protozoa: how do they reproduce; by what process do they reproduce asexually; what is fission; what is shizagony; | asexual; fission, budding, shizagony ; divide into 2; dividing into multiple cells |
| protozoa: movement- what are the protozoa classified by; what doe the four types of movement | their movement;amoebas, flagellates, ciliates, sporozoa |
| protozoa: movement- def of amoebas; def of speudopods; def of flagellates; def of ciliates; ciliates are usually located where; | they utilize the pseudopod to move the cell; the extension of a cell that adheres to a surface and is pulled along; they move by flagella; they have small hairlike extensions that move the cell; water; there is no movement in t |
| protozoa: movement- def of sporozoa; when is there no movement in sporozoa | movement in the early stages; in adult stage |
| protozoa: def of trophozoite;def of cyst stage; when does it enter the cyst stage; what stage is resistant | the motile feeding stage; resting stage when the organisms is dormant; when the environmental conditions are not favorable; the cyst stage |
| protozoa: what develops on protozoa during cyst stage; def of encystation; def of excystation; do all protozoa have both stages; | a thick case around itself during environmental stress; the process of the organism changing from a trophozoite to a cyst ; morphin from cyststage to trohpozoite; no some just trophozoite |
| what is the second leading cause of death from parasitic disease; what is #1 parasitic disease; | amoebiasis; malaria |
| protozoa: amoebiasis- what is the etiologic agent; what is the transmission; s/s; tx; what does the metronidazole not effect; | entamoeba histolytica; fecal oral route; sharp abdominal pain, small amount diarrhea, bloodystools; metronidazole; the cyst stage; |
| protozoa: amoebiasis- how is it dx; what does histolytica mean; where does it occur; who is the primary host; | the cysts are in feces; destroy tissues; worldwide, often in tropics and travelers get it; humans; |
| protozoa: amoebiasis- is it multinucleid; how does the cyst get in body; since the cyst is resistant what is it able to get through; once the cyst gets to the jejunum what does it morph to; | yes; from intake of contaminated food and water into body; the stomach; the trophozoite stage through excystation |
| drug: metronidazole- brand name; tx what; what does it do; is the mode of action known; why is it toxic to parasites; what is shed in feces cysts or trophozoites | flagel; amebiasis; inhibits the DNA repair and acts in intestines; no; it interferes with hemoglobin metabolism in the food vacuole; cysts |
| protozoa: amoebiasis- when is in its active feeding form; what does the trophozoite feed off of; b/c the trophozoite is feeding off the wall what happnes; sometimes the feeding is so severe what can happen; | trohpozoite; the intestinal wall and what we are digesting; bloody diarrhea, ulcers; the trophozoite can eat through intestinal wall and perforate into perinoneal cavity casues peritonitois |
| protozoa: amoebiasis- what happens when the trophozoite enters the sigmoid; what is the process of morphing back into a cyst; the amoeba sectretes an enzyme that does what | it morphs back into the cyst stage; encystation; dissolves intestinal tissues and penetrates depper layers of the mucosa |
| protozoa- primary amoebic meningoencephalitis: aka; what is etiologic agent; what is the reservoir; how is it transmitted; | PAM; naegleria fowleri; warm frest water; nasal mucosa into the brain; |
| protozoa- primary amoebic meningoencephalitis: common where; how can we get it; s/s; what is mortality rate; is there a treatment; | anywhere freshwater is warm for a long period of time; by swimming or diving; nasal congestion, severe HA, high fever, death; 95%; no known effective tx |
| protozoa- giardiasis: etiologic agent; what is its movement; what is transmission; what can be contaminated; s/s; dx; tx; | giardia lamlia; flagellate; fecal oral route; the water and some foods; N, cramps, flatulence, foul smelling diarrhea; exam feces, enterotest capsule; metronidaxole; |
| protozoa- giardiasis: what is prevention; aka; what time of the year is it seen in michigan | protect water supply; adequate hygeine; giardia intestinalis; summer early fall; |
| protozoa- giardiasis: what stage of the organism do we ingest; how long does it take to incubate; where in body does excystation take place; does cysts or trophozoites shed in feces; where in intestines is trophozote located; how does it attach; | the cyst stage; 7 days; in the intestines; both duodenum and jejunum; via sucker device |
| enterotest capsule: how does it work | the capsule is swallowed it has a string attached and the capsule is left in place 2-4 hours and is then pulled up and it is examined for trophozoties |
| protozoa- giardiasis: some carriers can have no ss/s and shed cysts for years | |
| protozoa- trichomoniasis- etiologic agent; what is its movement; how long is it incubated; how is it transmitted; where is the reservoir in females; where is the reservior in males | trichomonas vaginalis; flagellate; 5-28 days; STD or fomite; vagina, urethra, urine; urethra, prostate sectretions, urine; |
| protozoa- trichomoniasis- s/s in females; s/s in males; how is it Dx; what does a wet prep show; tx; who is treated in STD | pruritis, vaginal frothy discharge, burning during urination; pain on urination and thin mucoid discharge; wet prep of discharge , sometimes picked up when screening urine; a jerky movement of flagellate; metronidazole (flagyl); all sex partners |
| protozoa- toxoplasmosis: etiologic agent; whatis the movement; what are the 3 stages it can be in; how is it transmitted; reservoir; how do cats tranmit to humans | toxoplasma gondii; sporozoan; cyst, trophocyte and oocyst; ingestion of cysts or oocysts; soil, animal, ingestion of undercooked beefpork lamb venison, birds, ordent, cat, gardening; contaminated cat feces; |
| protozoa- toxoplasmosis: when is it nonmotile; what are the 3 routes of transmission; who picks it up in the soil; how do we get it from soil; how does a cat give it to us; | in mature stage; soil; animals pick up cysts and th cysts develop in the muscle; we eat undercooked animals that have it; they kill a rodent who has it and there feces is contaminated when we clean their litter; |
| protozoa- toxoplasmosis: how do we get it from gardening; how long is incubation; it infects many places in the body, but what does it not infect; what % of population has been exposed to it but developed immunity; | we pass it from the soil to our mouths; 1-3 weeks; a RBC; 30%; |
| protozoa- toxoplasmosis: what stage do we ingestion; when does cyst turn into a trophozoite; s/s of healthy individuals; | cyst oocyst; when it is in the intestines; asymptomatic or mild symptoms and the recover easily; |
| protozoa- toxoplasmosis:s/s of immunocompromised ppl; why are pregnant women at risk; who is at higher risk; | fever, sore throat, liver, spleen or lymph node enlargement, eye damage, hearing loss, heart probs; they are not, the risk is to the unborn child; fetus, young children |
| protozoa- toxoplasmosis: how can the trophozoites enter the bloodstream; where in body is it dx; why is it dx in the blood; | they destroy the intestinal wall and enter the blood; in the blood; b/c the trophozoties can be seen in the blood, and antibodies are there in the blood; |
| protozoa- toxoplasmosis: why is it a risk for getus; what is the trophozoite called that crosses the placenta; what trimester is the most common time for the trophozoite to cross the placenta; what damage to fetus can occur; | the trophozoite can cross the placenta and damage the fetus;a torch agent; the 3rd trimetster; blindness, mental retardation; |
| protozoa- toxoplasmosis: torch diseases- def; in TORCH each letter stands for what; what soes TORCH stand for; what is included in other | those that are blood born and it can cross the placenta; a disease; toxoplasmosis, other, rubells, cytomegalovirus, herpes simplex O; syphilis |
| protozoa- toxoplasmosis: who is at high risk; what is tx; what age is most at risk; | immunocomprimised, nonimmunepregnant women, children; sulfonomide drugs; 10-24 months |
| helminths: are they multicellular or unicellular; def of ovum; what is the 2 egg stage; def of larva; are these infections comon in humans; | multi; this is the egg stage; ova; immature stage between the ovum and the adult; yes |
| helminths: what are general s/s of all helminths infections; | abdominal cramping, diarrhea may or may not be present, lung involvment w/ coughing, inflammation in pathways, sometimes there are not s/s; |
| helminths: platyhelminths- what type of worm; what does it mean that they are hermaphrodites; what is a cestode; | flat worm; they have both male and female organs and they can produce their own offspring; this is a platyhelminth class of flat worm; |
| helminths: platyhelminths- what does the worm look like; def of scolex; def of proglottid; what part is filled with egges | long segmented with suckers; this is the head and the suckers and hooks are located here; this is the segmented body sections; the proglottid |
| helminths: platyhelminths- the segment causes the worm to be what; if the proglottid is filled with ova what is it now called; name for pork tapeworm; name for deeg tapeworm; what is tx; does beef or pork have hooks; does beef or pork have suckers; | really long; the gravid proglottid; taenia solium; taenia saginata; praziquantel; pork; beef |
| helminths: platyhelminths- what is an intermediate host; def of definative host; | an animal where the worm lives in its immature state; the host has the matture adult worm; |
| drug: praziquantel- used for what; what is its action; | tape worms; it interferes with worm metabolism; |
| helminths: platyhelminths- how do humans get infection; where does the larvae develop into adults in the human; where do the adult tape worm shed ova in a human; | the undercooked pork or beef is ingested and they ingest the T. slium, the larvea; in the intestine; in the feces |
| helminths: platyhelminths- when human feces shed ova what can pick this ova up from the soil; when animals ingest the ova what happens; when larvea mature in the muscle of animal what is this called; what eats undercooked muscle; | animals; the larvae leave the ova and the migrate to muscle walls; cysticerci; humans |
| helminths: platyhelminths- cysticercosis- how is this diffferent; does this happen with taenia solium or taenia saginata; after the larvea hatch where do they migrate to; once they migrate what do they develop into; | humans ingest the eggs; taenia solium; the muscles, brain, liver heart; a cysticerci |
| helminths: nematodes- aka; what % of the world population is infected with these; | round worms; 30%: |
| helminths: nematodes- pinworm diease: it is the most prevelent what; is it easy or hard to treat; what is the etiologic agent; is it a small or large worm; | helminthic infection in Us; easy; enterobius vermicularis; small |
| helminths: nematodes- pinworm diease: who is the definative host; who is the intermediate host; how do humans ingest this; after ova is ingested what happens; where does it mature; at night what happens; why does it migrate to perianal area | humans; there is not one; from fecally contaminated material; larvea leave ova and matures into adult pinworm; in the cecum; the adult will migrate to perianal area; to lay eggs |
| helminths: nematodes- pinworm diease: how long do the ova stay in perianal area before they are infective; so when individual wakes up what happens; | 4-6 hours; they itch area and reinfect themelves or contaminate sheets others, clothing; |
| helminths: nematodes- pinworm diease: what is treatment; how is it dx; what is a tape prep; | mebendazole; identifiing ova in feces; they parent at night take a tong depresser with tape around it and put it on slide for physician |
| drugs: mebendazole: what is one mode of action; | it prevents uptake of glucose from worm and starves it; |
| helminths: nematodes- whip worm disease: etiologic agent; where in world is it most comon; how does one becomce infected; where do ova hatch; after it becomes an adult where does it migrate to; | trichuris trichiura; topics; they ingest contaminated food with infected ova; GI tract; cecum and ascending colon; |
| helminths: nematodes- whip worm disease: in cecum what does adult worm produce; do we infect others; why don't we infect others; does it have the general CM; what is tx; | 1000s ova/ day for a year; no; as we release the ova in our feces they have to mature in warm damp soil for 3-6 weeks so we do not infect others; yes; mebendazole |
| helminths: nematodes- round worm disease- etiologic agent; how long is the mature worm; how do humans become infected; where do larvae leave the ova; in the L. intestines what do the larvae do; | ascaris lumbricoides; one foot; the ingest the eggs; in the large intestines; they penatrate the intestinal wall; |
| helminths: nematodes- round worm disease- after the larvae leave the intestinal wall where do they migrate to; where do larvae mature; in the lungs what are s/s; what happens to the larvae in the lungs; when they are swallowed again they go where for 2nd | the lung;the lungs; inflamation and mucous production with coughing; they are coughed up and swallowed again; GI tract |
| helminths: nematodes- round worm disease- once in GI tract for second time what happens; do they cause many s/s/; sometimes what serious thing can happen; how is it Dx; tx | they mature into and adult and the adult produces ova to be expelled into the feces; no; humans can have a high worm load and they can create a bowel obstruction ova in feces and intact worms; mebendazole |
| helminths: nematodes- round worm disease- is it common; how does it exit body; what happens when it blocks bili area; | yes; anal, nasal, oral; gall stones s/s; |
| helminths: nematodes- trichinosis- etiologic agent; who are the cysts shed from; once the cysts are in soil what ingests them; what happens when they in pigs; | trichinella spiralis; the human feces; pigs; the larvae emerge from ova in intestine track |
| helminths: nematodes- trichinosis- after the larvae hatch what do they penetrate; where do the larvae migrate to after penetration; what forms once larveae are in muscle; | they penetrate the intestinal wall; they migrate to muscle; a cyst |
| helminths: nematodes- trichinosis- humans ingest undercooked pork and eat what; after we ingest pork what happens ; what does it do in muscles; when is it fatal; is it comon in use; | the cysts; they larvae emerge and migrate to muscle; it encysts; when heart and brain are infected; |
| helminths: nematodes- trichinosis- are they small or large; s/s if muscles are infected with cysts; treatment for larvae; what is hard to treat; how are muscles treated | small; kill cysts in pork prior to consuming by freezing or cooking; muscle aches, swelling around eyes; mebendazole; cysts; remove part of muscles that have cysts |
| helminths: nematodes- hookworm disease- what does it infect; what is the etiologic agent; who is the host; the hooks are imbedded where; how do the hooks do once imbedded in tissue | the upper intestines; ancylostoma duodenale and necator americanus; the human; in the intestinal tissue; they suck blood |
| helminths: nematodes- hookworm disease- what is tx; s/s from the sucking of blood; how do ova enter soil; once in soil what emerges; what does the rhabditiform larvae mature to; what is immature larvea; what is noninfective larvea | mebendazole; anemia; from human feces; rhabditiform larvae; the filaform larvae; phabditiform; rhabditiform; |
| helminths: nematodes- hookworm disease- what is the mature larval stage; what does the filariform attach to in soil; how does filariform enter humans; how does it enter through skin; | filariform; blades of grass; through skin in infected soil; the filariform secretes enzymes that break down tissue and it can then enter the bloodstream |
| helminths: nematodes- hookworm disease- when the larvea enter blood stream what is s/s on skin; where do the larvae travel once in blood stream; s/s in lungs; | reddened inflamed, itching area on place of penetration; to the lungs; coughing increased mucous production; |
| helminths: nematodes- hookworm disease- the larvae is coughed up and what happens; s/s in intestinal tracts; when does larvae mature; when does anemia occur; how dx; tx; prevention; | it is swallowed and infects the intestines; anemia, cramping, in the intestinal tract; when worm load is high; seeing hookworm ova in ntestinal tract; medandazole; be careful where you walk barefoot |
| Metronidazol (flagyl): action | This drug is absorbed by the organism and inhibits nucleic acid synthesis by disrupting the DNA and finally killing the organism. |
| virology: when did this study start; how did viruses get their name; are they more abundant than bacteria; what is size of virus | late 1800s;b/c virus means poisen; yes; 250 nm- 20 micrometers |
| virology: scientists- iwanowsky- when; what did he notice about the tobacco plant; what did he do; what happened to the healthy leaf; what was conclusion; | 1892;that it became brown and liquid; he took a tobacco leaf, ground it up and filtered the juice and he put it on a healthy leaf; it became diseased; stated there was something smaller than bacteria causing this b/c he could not see it on a scope |
| virology: scientists- beijerink- when; what did he do; what else did he do; what do we know now what model they were working on; | 1898; reapeated iwanowsky's experiment and got same results; he noted that boiling destroyed the infectious agent; the tobacco mosiac model |
| virology: what should viruses be described as other then an organism; how should they be described rather then alive or dead; | infectious particles; active or inactive |
| virology: when were we able to see the electron microscope; | in the 1940s in military; |
| virology: how are they an obligate intracellular parasite | that they cannot multiply unless it invades a specific host cell and instructs its genetic and letabolic machinery to male and release new virus |
| virology: scientists- edward Jenner- when; what was occupation; what virus Hx did he describe; what is cowpox virus; what did milk maids not develop b/c of this; why did they not develop small pox; | late 1700s; english physician; cowpox virus; this disease occured on the utters of cows, they were vescicles and would harm dairy cows, milk maids also got virus on their hands; small pox; since they were exposed cowpox, the viruses similar they didn't ge |
| virology: scientists- edward jenner- this discovery made it possible for the extermination of what; when was last known case of small pox; when did WHO declare world free of endemic smallpox; where do we still have it | smallpox; 1977; 1980; russia and us b/c we have a sample of it |
| virology: do viruses have cells; vrial replication in a cell does what; does it independantly fulfill the charecteristics of life; | no; causes death or loss of function of that cell; no |
| virology: scientists- edward jenner- he removed pus from where and placed it where; what happened to boy; what did he do to the boy later; what country was doing this same work earlier | fresh cowpox scars on milkmaids and placed it into scratches he made on boys arm; he developed cowpox and recovered; inoculated the boy with pus from a smallpox pt and boy lived; china |
| virology: inactive macromolecules outside host cell are only active when; | inside host cell; |
| virology: scientists- pasteur- what vaccine did he use; who did he inoculate; what was modified in vaccine; when | rabies; a boy; it was attenuated (weakened); 1885 |
| virology: scientists- stanley- when; what debate did he bring forth | 1935; whether viruses are alive or not |
| virology: properties of a virus- what is the genome; when are viral components synthesized; is it capable of independent metobolic reactions; what is a virion; what is it called outside a cell; | DNA or RNA; within a host cell; no; infectious virus; innert ; |
| virology: properties- all viruses have a ___ range; why do they have a host range; what is HIV host range; what does HIV bind to | host range; b/c of a protein coat around their strucutre they can only bind to certain protein receptors on cells and cause disease; primates and humans; CD$ positive cells |
| virology: Viral symmetry- what does symmetry mean; name the 3 types;helix def; | shape; helix, icosahedron, complex; they have coiled rod shaped capsomers that form hollow discs that resemble a bracket; tobacco mosaic, rabies, measles; |
| virology: ex of CD4 positve cells; | T helper lymphocytes (HIV binds to this and destroys them; |
| virology: properties- viruses contain DNA or RNA, can they contain both; when is a virus is considered infectious; | no; when it binds to a protein and enters the cell; |
| virology: Viral symmetry- def of ocosahedron; examples; def of complex; example; | 3D 20 sided polyhedron, herpes, parvovirus, polio; combo of above structures more introcate in structure; bacteriophages, smallpox |
| virology: strucural components- genome- does they virus always have this; what 2 can it be; can it be both; what is function; contains what instructionsl; what surrounds it | yes; DNA & RNA; no; it expressed genetic info; how to reproduce the virus; the capsid |
| virology: strucural components- capsid- it is the most prodominent what; made primarily of what; these protein are subunits called what; how many capsomers; this determines what (function); is it in every virus | geometric figure when magnified; proteins; capsomeres; thousands; host range, tissue tropism, aids in host cell attachment; yes |
| virology: strucural components- what is the term nucleocapsid; def of naked virus; | the genome = + the capsid; the virus only has the nucleocapsid |
| virology: strucural components- spikes- do all viruses have this; made of what; they genetically match what; function; they are the functional envelopse what; | no; post cell membrane lipids and proteins; host; attaches ; projections that contain enzymes that aid in attachement; |
| virology: strucural components- enevelope- do all viruses have this; part od what;function | no; host cell memrane and viral componenets;and aids in penetration of host cell |
| virology: strucural components- genome enzymes- do all viruses have this; function; example | no; aids in genome replication; has an enzyme that helps replicate b/c we do not have that enzyme |
| virology:life cycle of animal virus- what type of virus; what does it first do the they cell; | dna containing enveloped virus; it attaches |
| virology:life cycle of animal virus- what are five components; attachment- what happens; | attachment, penetration, uncoating of viral nucleic acid, release of virions from host cell;the spikes,capsids or envelope attach to the host cell surface receptors |
| virology:life cycle of animal virus- penetration; what happens; whole virus or envelope fuses with what; | proteins on surface of virus bind to proteisn on surface of host cell; cell membrane |
| virology:life cycle of animal virus- uncoating of viral nucleic acid- what happens | genome now released into the cell; |
| virology:life cycle of animal virus- replication, suntheiss and assembly of viral structures- what happens; what does it inhibit in host cell; replication of what; synthesize of what; reassembly of what; | free viral nucleic acid exertscontrol over the host's synthetic and metabolic machinery and the cell synthesizes components of new virus ; protein synthesis; DNa; protein; viral structures |
| virology:life cycle of animal virus- replication, suntheiss and assembly of viral structures- what is unusual of this; | viral DNA replication takes presidence and host cell is inhibited |
| virology:life cycle of animal virus- release of virions- what 2 ways does this occur; def of lysis; def of budding; why does host cell die if it buds too long; | lysis of the cell or budding; rupturing t hrough the nucleus; expcytoses; b/c cell cannot survive b/c it is killing cell wall ; |
| virology: viral replication in DNa protein synthesis- DNa is transcribed into what;mRNa is translated into what; after translation what happends | mRNa; viral proteins; it is reassembled into virions |
| virology:RNA virus replication- positive RNA virus- example; what does it mean that it is positive; aka; | polio virus; it is mRNA and makes sense to host cell; sense RNA virus; |
| virology:RNA virus replication- positive RNA virus- to a host cell it is ready for what; what is translated into what; | translation; viral proteins and more positve RNA viruses |
| virology:RNA virus replication- negative RNA virus- aka; to go through protein synthesis what has to occur first; what does transcription produce; why does it produce positve RNA; after transcription process is same as what; example | nonsense RNA virus; transcription; positve RNA;b/c that is what the host cell can read; positive RNA; measles virus |
| virology:RNA virus replication- where does it occur; | cytoplasm and nucleus; |
| virology:RNA virus replication- what are the 3; | positive, negative and retrovirus; |
| virology:RNA virus replication- retrovirus RNa virus- it has what around its genome; ex; what is name for enzyme; what is formed; name for double stranded DNA; provirus becomes part of what; what occurs after provirus becomes part of host DNA; | enzyme; HIV; transcriptase; double stranded DNA; provirus; host DNA; proteins synthesis; |
| virology:RNA virus replication- retrovirus RNa virus- The rna enters and what is first event; what does first event produce; name for viral double stranded DNA; provirus is transcribed into what; translated into what | the viral RNA has to be reversed transcribed using transcriptase; double stranded DNA; reverse transcriptase; MRNA; viral proteins; |
| virology- cytopathic effect (CPE)- def; where can they be seen; example of a test used to see these effects; changes in what surface | host cell changes due to viral infection, it alters microscopic appearance; in viral cell cultures and in natural infections of cell; pap smear; cell surface |
| virology: naming and c lassification- what is the order general to most specific; HIV example: what is family, what is genus, what is species; what is another way to name;what is classification based on; is it a binomial system; | family, genus species; retroviridae, letivirus, human immunodeficiency virus; name of disease followed by a virus; type of nucleic acid, morphology tissue affected; no; |
| virology:interferon: abrev; what is it; viral DNA stimulates the host to synthesize what; the cell being attacked by virus stimulates others to produce the interferon to protect other cells; what are the 3 types;interferons surround what; | INF; a natural antiviral agent; interferon; alpha, beta gamma; uninfected cells; |
| virology:interferon: the interferons from infected cell stimulate the uninfected cell to produce what; the antiviral proteins block what; | antiviral proteins; the viral protein sunthesis and thus interferes with viral replication; |
| viruses and cancer: what % of viruses causes cancer; def of oncogenic viruses; example of oncongenic viruses; epstein barr causes what cancer; human T-cell leukemia virus causes what cancer; HPV causes what | 20%; they act as a carcinogen and transform normal cells into cancerous cones; epstein barr; burkitss lymphoma; leukemia;cervical and penile cancer |
| the oncogene theory: our normal protooncogene DNA can be activated by what; proto-oncogenes control what; what are proto-oncogenes; what happens when a proto oncogene turns into an oncogene; if cancer cell occurs it is not what | carcinogens; growth/metabolism of the cell; small sections of our genome; uncotrolled growth and metobolic reactions occur and tumor cells develop; regulated |
| can antibodies enter cells | no |
| the oncogene theory: when a cell reaches a certain size when proto oncogenes are in control what happnes; oncogenes- each cell is what type of cell; | it stops growing; a tumor cell; |
| definitions- viroid; prion; ex of prion; do all prions produce disease; what will not destroy these; nanobe; | virus like particle but is naked nucleic acid fragment that is known to causes disease in plants only; infectious abnormal protein that can induce disease; mad cow disease; no; NORMAL PROCESSING cooking, autoclaving; newly identified particle 20 nm, |
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