Bug Parade 3 – Flashcards
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| Absidia biology |
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| Fungus Tissue sample: irregular broad hyphae, aseptate, 90* branching, ribonny Culutre: lid-lifter, sporangia with conidia inside, rhizoids between sporangia bases |
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| Absidia diagnosis and treatment |
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| Dx: Culture (lid-lift, sporangia with rhizoids between bases) Tx: treat underlying IMC, surgical debridement, AmpB + Caspofungin or prosaconazole + caspofungin |
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| Absidia disease |
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| Mucormycosis Rhinocerebral: DM with ketoacidosis Pulm/systemic: transplant pts |
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| Absidia virulence factors |
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| necrotic tissue around inflammation angioinvasive |
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| Acanthamoeba biology |
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| facultative parasite, small, free-living amoeba, soil and water |
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| Acanthamoeba diagnosis and treatment |
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| Dx: trophozoites in CSF, H&E in fixed tissue, Culture on water agar, Corneal scraping stains, Immunofluoro Ab Tx: combination Rx, problematic |
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| Acanthamoeba disease |
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| Eye entrance: severe keratitis Nasal entrance: granulomatous amebic encephalitis, disseminates in IMC Skin Entrance: granulomatous amebic encephalitis, dissem disease or skin lesion in IMC |
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| Acanthamoeba life cycle |
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| cysts mature in water to trophozoites, cysts or trophozoites can enter human (eye, nasal passage, or broken skin) |
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| Acylostoma caninum, Ancylostoma braziliense, Unicaria stenocephala biology |
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| Animal hookworm |
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| Acylostoma caninum, Ancylostoma braziliense, Unicaria stenocephala pathogenesis and presentation |
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| larvae wonder about in subcutaneous tissue Cutaneous larva Migrans Significant inflammation and painful swelling, itching that can lead to 2* infection |
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| Alternaria, Curvularia, Bipolaris biologies |
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| Dematiaceous fungi Pigmented (brown), septate hyphae, sometimes yeast, visible in H&E stain of tissue |
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| Alternaria, Curvularia, Bipolaris disease |
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| Sinusitis that can lead to brain abscesses If presents like aspergillis = poor prognosis (i.e. lung, liver or brain involvement with bloody sputum, vascular invasion, infarctions) |
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| Alternaria, Curvularia, Bipolaris epidemiology |
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| traumatic wounds and lacerations IMC |
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| Alternaria, Curvularia, Bipolaris virulence factors |
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| neurotropic!! |
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| Ancylostoma duodenale (Hookworm) biology |
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| Helminth, nematode, intestinal small, characteristic TEETH, multi-cell, visible to naked eye, cuticular, roundworm, extracellular |
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| Ancylostoma duodenale (Hookworm) diagnosis and treatment |
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| Dx: ID in feces Tx: Mebendazole or albendazole |
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| Ancylostoma duodenale (Hookworm) disease |
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| Asymp unless high number Ground itch: skin penetration, 2* infection Pulmonary: cough, wheeze, fever Intestinal: worms attach to mucosa and feed on blood, cont. move to new areas, exacerbated blood loss, iron deficiency |
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| Ancylostoma duodenale (Hookworm) life cycle |
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| lay egg (passed in feces), hatch in environment, larvae stage grow and shed cuticule layers, penetrate skin, larvae enter blood and go to heart, leave circulatory system in alveoli, larvae move up trachea and are swallowed, mature to adults in intestine, male and female mate, lay eggs, repeat |
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| Ancylostoma duodenale (Hookworm) transmission |
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| Trans: skin penetration, indiscriminate disposal of human waste |
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| Ascaris lumbricoides biology |
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| Helminth, nematode, intestinal Very large, ant. end has 3 lips, multi-cell, visible to naked eye, cuticular, roundworm, extracelluar |
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| Ascaris lumbricoides diagnosis and treatment |
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| Dx: ID in feces or larvae in sputum Tx: Mebendazole or albendazole |
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| Ascaris lumbricoides disease |
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| Asymp unless high number Pulmonary: cough, wheeze, fever, eosinophilia Children under 10: intestinal obstruction, fever, diarrhea, vomit, penetration of bile duct and liver by adult worms, peritonitis (perforation of intestinal wall) |
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| Ascaris lumbricoides epidemiology |
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| Most common parasitic helminth in world Assoc. w/ poor sanitation |
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| Ascaris lumbricoides life cycel |
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| male and female mate, lay eggs which embryonate in soil, larvae stages grow and shed cuticle layers, mature into adults, repeat Eggs are sensitive to sun but otherwise environmental resistant |
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| Ascaris lumbricoides pathogenesis |
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| infective eggs are swallowed, hatch in small intestine, L3 larvae migrate to hepatic portal, larvae enter lung and alveolar spaces causing cough, coughed up larvae are swallowed, larvae reach SI 2nd time, mature into adults and mate, lay unembryonated eggs, passed in feces, embryonate in soil, repeat |
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| Ascaris lumbricoides virulence factors |
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| Eggs can live in human for up to 2 years |
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| Aspergillis flavus biology |
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| Fungus Tissue sample: narrow septate hyphae, 45* branching Culture: grow at 25*C, 24-48hrs, narrow septate hyphae, few aerial, granular, "FRUITING HEAD"; yellow/brown, CONIDIA ARE CIRCUMFERENTIAL ON VESICLE |
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| Aspergillis flavus diagnosis and treatment |
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| Asthma: sputum culture, wheezing, infiltrates, eosinophils Fungus ball: chest X-ray or CT Disseminated: sputum culture |
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| Aspergillis flavus disease |
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| Allergic: IgE mediate Fungus ball: overgrowth in existing lung cavity, not invasive, tangled mass of hyphae Disseminated: IMC pts, spreads to lung/liver/brain/anywhere, vascular invasion and destruction, causes INFARCTIONS |
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| Aspergillis flavus treatment |
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| Voriconazole or AmpB, itraconazole or caspofungin |
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| Aspergillis flavus virulence factors |
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| Elastase - vascular invasion Aspiration can cause astham |
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| Aspergillis fumigatus biology |
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| Fungus Tissue sample: narrow hypahe, septate, 45* branching Cutlure: grow at 25*C, 24-48hrs, narrow septate hyphae, few aerial, granular; FRUITING HEAD (aspergillum), green/brown, conidia COVER ONLY 1/2 VESICLE; Killed by cyclohexamide (no mycobiotic culture growth) |
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| Aspergillis fumigatus diagnosis |
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| Allergic: sputum culture, wheezing, infiltrates, eosinophils Fungus ball: chest X-ray or CT Disseminated: sputum culture |
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| Aspergillis fumigatus disease |
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| Allergic: IgE mediated Fungus ball: overgrowth into existing lung cavity, not invasive, tangled mass of hyphae, BLOODY SPUTUM, most severe in IMC Disseminated Aspergillosis: IMC pts; spreads to lung/liver/brain/anywhere, vascular invasion and destruction, causes INFARCTION, bloody sputum |
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| Aspergillis fumigatus treatment |
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| Voriconazole or AmpB, itraconzole, caspofungin |
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| Aspergillis fumigatus virulence factors |
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| elastase - vascular invasion Aspiration can cause asthma |
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| Aspergillis niger biology |
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| Fungus Tissue sample: narrow septate hyphae, 45* branch Cutlure: grow at 25*C, 24-48hrs, narrow septate hyphae, few aerial, granular, FRUITING HEAD, black dots on white background, conidia are CIRCUMFERENTIAL |
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| Aspergillis niger diagnosis |
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| Allergic: culture sputum, wheezing, infiltreates, eosinophils Fungus ball: chest x-ray or CT Diseeminated: sputum culture |
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| Aspergillis niger disease |
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| Allergic: IgE mediate Fungus ball: overgrowth in existing lung cavity, not invasive, tangled mass of hyphae Disseminated: IMC pts; spreads to lung/brain/liver/anywhere, vascular invasion and destruction causes IUNFARCTION |
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| Aspergillis niger treatment |
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| Voriconazole or AmpB, itraconazole, or caspofungin |
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| Aspergillis niger virulence factors |
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| Elastase - vascular invasion Aspiration can cause asthma |
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| Babesia microtti biology |
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| apicomplexan parasite, piroplasm |
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| Babesia microtti diagnosis and treatment |
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| Dx: parasites in blood smear Tx: clindamycin + quinine |
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| Babesia microtti disease |
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| 1-4wk incubation with malaise Occasional hemolytic anemia and renal failure |
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| Babesia microtti epidemiology |
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| Endemic in NE seaboard of US Increased risk: asplenia, IMC and elderly |
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| Babesia microtti vector |
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| Vector: deer tick Also blood transfusion transmission |
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| Blastomyces dermatitidis biology |
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| Dimorphic fungus Mold at 25* (nature), slow growth, LOLLIPOPS conidia Yeast at 37* (body) Intra or extracellular Thick cell wall, double refractile, BROAD-BASED BUD Mixed purulent PMNs and granulomas |
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| Blastomyces dermatitidis diagnosis and treatment |
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| Dx: PNA-FISH or PCR, broad based buds Tx: AmpB if disseminated, fluconazole, intraconazole |
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| Blastomyces dermatitidis disease |
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| Blastomycosis: cutaneous ulcers or pustules (may mimic melanoma), pulmonary disease with dissemination |
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| Blastomyces dermatitidis epidemiology |
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| probably water, soil, vegetation sources Endemic in Midwest and SE U.S. |
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| Blastomyces dermatitidis virulence factors |
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| reactivation possible with new IMC status |
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| Candida albicans biology |
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| Fungus White, round to oval hyaline, budding yeast, PSEDUOHYPHAE, Germ tubes Culture: grow at 25* or 37*C within 24hrs, grow on blood agar |
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| Candida albicans diagnosis |
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| KOH prep, silver stain, or blood culture PSEUDOHYPHE, germ tube (positive test does not mean this is the causitive agent) |
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| Candida albicans disease |
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| Mucocutaneous: thrush, oral and vaginal most common, relies on adherence to mucosa Cutaneous: common on skins of fat folds Systemic: multiple organ involvement, fungemia, mostly IMC pts |
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| Candida albicans epidemiology |
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| Pregnant with hx of yeast infection Cystitis with hx of bladder infection Increased risk: DM, cancer+chemo, braod-spec Abx, AIDS, urinary or vascular catheters 3rd most common cause of blood infection 1st or 2nd most deaths of blood infections |
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| Candida albicans treatment |
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| Superficial: topical clotrimazole or miconazole Oral: nystatin Life-threatening: AmpB, voriconazole, itraconazole Blood: FLUCONIZOLE |
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| Candida albicans virulence factors |
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| NF through GI tract (thus broad Abx creates opportuinity) |
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| Candida glabrata biology |
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| Fungus Tissue sample: round to oval hyaline, budding yeast, GERM TUBE Culture: grow at 37* or 25*C within 24hrs, grows on blood agar |
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| Candida glabrata diagnosis |
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| KOH stain, silver stain Germ tubes presence does not mean causative |
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| Candida glabrata disease |
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| UTI and torulopsis Can disseminate in IMC |
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| Candida glabrata treatment |
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| Superfiicial: topical clotrimazole or miconazole Oral: nystatin Life-threatening: AmpB, voriconazole, itraconazole Blood: MICAFUNGIN |
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| Cemix hemipterus biology and disease |
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| Ectoparasite Bed bugs |
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| Clonorchis sinensis biology |
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| Helminth, platyhelminth, trematodes/fluke, visceral multicell, extracell, visible to naked eye |
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| Clonorchis sinensis disease site |
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| Liver |
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| Coccidiodies immitis (posadasii) diagnosis and treatment |
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| Dx: DNA probe, Immunodiffusion, complement fixation, skin test (useless in endemic regions) Tx: AmpB, itraconazole, or voriconazole |
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| Coccidioides immitis (posadasii) biology |
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| Dimorphic fungus Mold at 25* (nature) Yeast at 37* (body) Tissue sample: spherules/sporangia that have endospores within Culture: slow growth at 25*, fluffly white or dermatophyte mold, BARREL-SHAPED artrhoconidia, No yeast grow-able in lab |
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| Coccidioides immitis (posadasii) disease |
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| Coccidioidomycosis: pulmonary is asymp in 60% of cases, 1-2% get disseminated disease A (-) skin test + high titer Abs -> poor prognosis |
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| Coccidioides immitis (posadasii) epidemiology |
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| Endemic in SW US (San Juan Valley, Phoenix) Dust storms, migrant workers, farmers, military Highly contagious in lab |
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| Coccidioides immitis (posadasii) virulence factors and transmission |
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| reactivation possible with new IMC status Endospores are the infectious agent Trans: aerosols of endospores, desert soil related |
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| Cryptococcus gattii biology |
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| Fungus Tissue sample: narrow-based budding yeast with halo, India ink, mucin stains wall/capsule, GMS and Giemsa Culture: slimey colonies, 48-72 hrs, killed by cyclohexamide, Urease(+), melanin produced on bird seed/niger seed agar |
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| Cryptococcus gattii diagnosis and treatment |
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| Dx: India ink, Latex agglutination Tx: AmpB or fluconazole or voriconazole; if meningitis: 5-FC b/c better CSF penetration |
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| Cryptococcus gattii disease |
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| Early: pulmonary, cough, weight loss Followed by: Fungemia Then: Meningitis w/ headache, vomit, nuchal rigidity (neck stiffness), 100% fatal w/o treatment Disseminates mostly in IMC pts |
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| Cryptococcus gattii epidemiology |
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| soil enriched with pigeon droppings |
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| Cryptococcus gattii virulence factors and transmission |
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| little tissue inflammation trans: aerosols, resp |
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| Cryptococcus neoformans biology |
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| Fungus Budding yeast with capsule (India Ink) Tissue sample: narrow-based budding yeast with halo, mucin stains wall/capsule, GMS and Giemsa stains Culture: slimey colonies 48-72hrs, killed by cyclohexamide, Urease(+), melanin production on niger seed/bird seed agar |
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| Cryptococcus neoformans diagnosis and treatment |
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| Dx: India Ink, Latex agglutination Tx: AmpB or fluconazole or voriconazole; if meningitis: 5-FC b/c better CSF penetration, keep txing until CSF is clear |
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| Cryptococcus neoformans disease |
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| Early: pulmonary, cough, weight loss Followed by: Fungemia Then: Meningitis w/ headache, vomit, nuchal rigidity (neck stiffness), 100% fatal w/o treatment Disseminates mostly in IMC pts |
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| Cryptococcus neoformans epidemiology |
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| soil that is enriched with pigeon droppings |
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| Cryptococcus neoformans virulence factors and transmission |
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| little tissue damage Trans: aerosols, resp. |
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| Cryptosporidium parvum biology |
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| Apicomplexan parasite, zoonotic, intracellular/extracytoplasmic, asexual and sexual repro, oocysts are product of sexual (GI tract) and are infectious agent |
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| Cryptosporidium parvum diagnosis and treatment |
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| Dx: oocysts in stool, Kinyoun acid fast stain, IMF microscopy, PCR for species Tx: Otherwise healty-support, rehydrate; IMC-nitazoxanide (also for otherwise healthy kids), paromomycin (high tox) and HAART |
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| Cryptosporidium parvum disease |
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| 3-10d incubation Otherwise healthy: freq. watery diarrhea, nausea, vomit, abdominal cramps, low-grade fever, last 1-2wks IMC pts: severe, persistent diarrhea (life-threatening), disseminates to liver and pancreas (cholangiohepatitis/cholecysitis/choledocthitis/pancreatic); profound disruption of mucosal surfaces -> fibrosis/cellular infiltration/crypt abscessation |
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| Cryptosporidium parvum transmission, virulence factors and pathogenesis |
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| Trans: antrhoponosis (daycare, nosocomial, fecal-oral); zoonosis (deer, swine, cat, dogs, fecal-oral); waterborne (swimming pool, resist chlorine); foodborne VFs: large number oocysts in feces Path: live in brush border of intestine |
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| Diphyllobotrhrium latum biology |
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| Helminth, platyhelminth, cestode/tapeworm multicell, extracell, visible to naked eye proglottids and scolex |
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| Diphyllobotrhrium latum cycle |
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| embryos ingested, develops to adult hood, adult can live for several decades, eggs and gravid proglottids released in feces, eggs hatch in water, embryos eaten by FISH and develop to larval stages, FISH ingested by human |
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| Dracunuculus biology |
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| Helminth, nematode, tissue multi-cell, extracell, roundworm, visible with naked eye, cuticular |
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| Dracunuculus life cycle and transmission |
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| male and female mate, lay eggs, hatch to larvae, larvae grow and shed layer, mature to adults, repeat trans: ingestion |
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| Entamoeba histolytica biology (type, motility, reproduction) |
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| Amitochondridate parasite, amoeba no mitochondria, motile, shape shifters Cysts and trophozoites |
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| Entamoeba histolytica disease |
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| Amebiasis: intermittent diarrhea with blood and mucus, vomit, cramps, ulcers, colitis, colon perforation Extraintestinal amebiasis: penetration of muscularis mucosa, 2* lesions anywhere (mostly liver abscess), fasting growing, acute or chronic, gradual or sudden onset, risk of rupture, responds well to drugs |
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| Entamoeba histolytica dx and tx |
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| Dx: identify cyst or trophozoites in stool or tissues, serology in invasive disease Tx: Asymp - iodoquinol, Mild to severe - MNZ followed by iodoquinol |
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| Entamoeba histolytica transmission and pathogenesis |
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| Trans: contaminated food/water, anthropoeisis (only humans) Path: colonize colon, reproduce, trophozoites invade mucosa, grow lengthwise due to muscularis mucosa blocking, can invade past sometimes and get to liver, encystation in colon |
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| Entamoeba histolytica virulence factors |
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| adhere to host cell membranes, contact-dependent cytotoxicity can live in environment for 9-30days fairly resistant to chlorine |
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| Enterobius vermicularis (Pinworm) biology |
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| Helminth, nematode, intestinal Multi-cell, visible to naked eye, cuticle, extracellular, roundworm |
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| Enterobius vermicularis (Pinworm) diagnosis and treatment |
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| Dx: ID in feces, Scotch tape test Tx: Mebendazole or pyrantel pamoate; treat whole family, clean bedding and house |
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| Enterobius vermicularis (Pinworm) disease |
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| Asymptomatic unless high number Anal itching, irritability, insomnia, 2* rashes and infection Vaginitis and vaginal discharge if migrate to vagina Rare cases lead to appendicitis |
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| Enterobius vermicularis (Pinworm) epidemiology |
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| Most common worm infection in US Most common in kids (daycare/schools) Re-infection and cure rates are both high |
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| Enterobius vermicularis (Pinworm) life cycle |
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| male and female adults mate in colon, females come out of anus at night and lay eggs, larvae stages grow and shed cuticle layers, mature into adults, repeat |
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| Enterobius vermicularis (Pinworm) prevention |
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| hygiene, hand-washing |
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| Enterobius vermicularis (Pinworm) transmission |
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| Trans: ingestion req. indiscriminate disposal of human waste, fecal egg contamination of soil/foodstuff/animal food/hands/etc.; autotransmission |
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| Epidermophyton floccosum biology |
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| Fungus Uses keratin as nitrogen source Macroconidia in pairs/triplets, large, club-like, thin-walled Sabouraud's culuture (w/ cyclohexamide) Killed by refrgeration |
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| Epidermophyton floccosum diagnosis and treatment |
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| Dx: KOH prep (macoconidia in pairs/triplets, thin-walled, club-like, large) Tx: Oral terbinafine |
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| Epidermophyton floccosum disease |
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| Lesion: outer area is red, inner area pale Groin: cruris Feet: pedis, Athlete's foot Dermatophytosis: groin and feet |
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| Epidermophyton floccosum virulence factors |
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| Minimal to moderate inflammation deep invasion is RARE |
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| Fasciola hepatica biology |
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| Helminth, platyhelminth, trematodes/fluke, visceral multicell, extracell, visible to naked eye |
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| Fasciola hepatica disease site |
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| liver |
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| Fasciolopsis buski biology |
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| Helminth, platyhelminth, trematodes/fluke, visceral multicell, extracell, visible to naked eye |
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| Fasciolopsis buski disease site |
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| Intestinal tract |
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| Fusarium biology |
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| Fungus Macroconidia are sickle-shaped and contain many cells Macrocondiia are the infectious agent |
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| Fusarium disease |
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| Fusariosis/hyalohyphomycosis: keratitis, disseminated infection burn unit, |
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| Giardia lambia biology (type, stages) |
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| Amitochondridate parasite (lack mitochondria) Extracellular Trophozoite - motile, two nuclei, adhesive ventral disk, divides by binary fission Cyst - 2 trophozoites encysted, protected against heat and disinfected; infectious agent |
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| Giardia lambia diagnosis and treatment |
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| Dx: cyst or trophozoite in stool, Ag detection, UGI aspirates/biopsy, endoscopy Tx: MNZ or nitazoxanide |
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| Giardia lambia disease |
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| Giardiasis 1-2wk incubation, most cases asymp Diarrhea (sudden, explosive, malodorous, greasy, floats), flatulence, sulfuric-belch, cramps, nausea, weight loss, prolonged symptoms |
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| Giardia lambia epidemiology |
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| Worldwide, endemic in US Most common non-bacterial diarrhea cause in US Most common protozoan disease in US Assoc. with backpacker, hikers, and daycares |
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| Giardia lambia pathogenesis |
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| ingest cyst trophozoites excystate in small intestine and attach via suction and cytoskeleton rearrangement, reproduction and proliferation encystation in colon and desposit in feces can cause malabsorptioin in high number |
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| Giardia lambia prevention |
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| boil drinking water or filter |
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| Giardia lambia virulence, reservoirs, transmission |
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| VF: as symptoms improve, become more infectious b/c more cyst formation and deposition in stool; resistant to chlorine; adhere to membrane of host cells, contact-dependent cytotoxicity Reservoirs: domesticated cats and dogs Trans: ingesting cyst, fecal-oral, STD (oral/anal sex) |
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| Histoplasma capsulatum biology |
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| Dimorphic Fungus Mold at 25* (nature): aerial hyphae, silky, slow growth, tuberculate/spikey macroconidia Yeast at 37* (body): intracellular, no capsule, found in sputum/lung wash/biopsies, very small with hint of halo but NO CAPSULE, GMS stain good |
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| Histoplasma capsulatum diagnosis and treatment |
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| Dx: Skin test (useless in endemic regions), Abs (useless unless in urine which indicates active disease), DNA probe for definitive Tx: Asymp-no tx; Dissem-voriconazole, itraconazole; Life-threatening-AmpB via IV |
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| Histoplasma capsulatum disease |
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| 90-95% minor cold symptoms 5% severe flu-like, dosage is factor in the severity, causes clusters of cases 1-5% get dissemination, mostly IMC 1& get chronic pulmonary disease (cough, fever, wt. loss) |
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| Histoplasma capsulatum epidemiology |
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| AIDS, IMS, corticosteroids pts Mississippi River Valley, Indianapolis Black birds, chicken, bats, geese 80-85% of Midwest population has positive skin test |
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| Histoplasma capsulatum virulence factors |
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| Reactivation possible with new IMC status Multiplies within macrophages and sometimes PMNs Granulomatous inflammation, similar to TB |
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| Hortaea werneckii biology |
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| fungus Brown pigmented branched septate hyphae, budding yeast Culture with cyclohexamide |
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| Hortaea werneckii diagnosis and treatment |
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| Dx: KOH prep (brown, branched, septate hyphae, budding yeast) Tx: Selenium (dandruff shampoo) |
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| Hortaea werneckii disease |
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| Tinea nigra: dark brown or black patches on soles of hands or feet; superficial infection only |
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| Hortaea werneckii virulence factors |
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| does not invade skin, little to no inflammation, easily treated |
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| Leishmania cutaneous disease |
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| Cutaneous leishaminiasis Starts 1mo after infection, remains localized to skin, chronic but self-limiting; Dry, painless ulceratin; occaissionally satellite lesions Granuloma forms and heals leaving a depressed scar Assoc. w/ major and aethiopica = oriential sore Assoc. w/ Mexicana and braziliensis = bay sores |
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| Leishmania diagnosis |
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| Cutaneous - ulcer smear or biopsy Visceral - bone marrow or liver biopsy, clinical signs |
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| Leishmania diffuse cutaneous disease |
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| rare, chronic, non-healing, non-ulcerating nodules all over body, Assoc. with Mexicana and aethicopica Due to lack of CMI |
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| Leishmania mucocutaneous disease |
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| localized to skin initially, then metastasizes to mucosa Initial cutaneous ulcer that heals spontaneously, spreads via lymph/blood to nasal and buccal mucosa (up to 16yr post infection) Assoc. w/ braziliensis |
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| Leishmania new and old world species |
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| New: Mexicana, braziliensis Old: aethicopica, donovani, major, tropica |
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| Leishmania sp. biology (type, motility, reproduction) |
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| Kinetoplastid parasite, protozoa Cork-screw like movements, single flagella, divide by binary fission |
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| Leishmania sp. pathogenesis |
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| injected (via bite) as promastigotes, phagocytosed by macrophages, mature to amastigotes, repro by fission, rupture host cell, infect neighbor cells |
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| Leishmania sp. vector and reservoir |
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| Vector: sandfly Reservoirs: dog, sloth, fox, hyrax |
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| Leishmania treatment |
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| Cutaneous - AmpB, cryosurgery Mucocutaneous - AmpB, cryosurgery Visceral - pentavalent antimony |
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| Leishmania visceral disease |
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| Visceral leishaminiais (kala azar) infects reticuloendothelial cells (mostly macrophages) Assoc. w/ donovani only Parasite in blood, spleen, nodes and liver High fever oscillates every 48hrs Abdominal swelling, progressive and drastic weight loss High mortality w/o tx 2* post-kala-azar dermal leishmaniniasis |
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| Loa Loa (filarial worm) biology |
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| Helminth, nematode, tissue multicell, extracell, visible to naked eye, cuticular, roundworm |
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| Loa Loa (filarial worm) disease |
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| Loiasis |
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| Loa Loa (filarial worm) life cycle |
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| male and female mate, lay eggs, hatch to larvae, grow and shed cuticle layers, mature to adults, repeat L1 form in humans, arthropod takes up L1 and deliver L3 |
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| Loa Loa (filarial worm) transmission and pathogensis |
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| Trans: skin penetration via insect Path: most due to release of symbiotic bacteria from dead worm |
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| Loa Loa (filarial worm) treatment |
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| Ivermectin or diethylcarbamazine |
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| Malassezia furfur (flobus) biology |
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| Fungus "Spaghetti and meatballs" Req. olive oil to grow and Cyclohexamide |
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| Malassezia furfur (flobus) diagnosis and treatment |
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| Dx: KOH prep (short curved, unbranched hyphae, spherical yeast; spaghetti and meatballs Tx: Selenium (dandruff shampoo) |
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| Malassezia furfur (flobus) disease |
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| Tinea versicolor: hypo or hyperpigmented patches on skin, superficial infection only |
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| Malassezia furfur (flobus) virulence factors |
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| interferes with melanin production, does not invade skin, little to no inflammation, easy to treat |
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| Microsporum audouinii biology |
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| Fungus Uses keratin as nitrogen source Macroconidia are spindle-shaped, pitted walls Grows on Sabouraud's and mycobiotic cultures |
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| Microsporum audouinii diagnosis and treatment |
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| Dx: KOH prep (spindle shaped, pitted walls) Tx: topical imidazole |
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| Microsporum audouinii disease |
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| Dermatophytoses Lesion: red outer, inner pale RARE IN HUMANS, more in soil |
question
| Microsporum audouinii virulence factors |
answer
| minimal to moderate inflammation deep invasion is RARE |
question
| Microsporum canis biology |
answer
| Fungus Uses keratin as nitrogen source Macroconidia have thick/rough walls, 8-15cells, curved tip Sabourauds and mycobiotic (cyclohexamide) growth Fluffy granule colones and bright yellow on reverse |
question
| Microsporum canis diagnosis and treatment |
answer
| Dx: KOH prep (thick/rough walls, 8-15cells, curved tip) Tx: topical imidazole |
question
| Microsporum canis disease |
answer
| Dermatophytoses Lesion: outer is red, inner pale area (healing) Capitis (head), corpus (body, ringowrm), Pedis (food, Athlete's), cruris (Groin), barbae (beard), unguium (nail, onychomycosis) |
question
| Microsporum canis virulence factors |
answer
| minimal to moderate inflammation deep invasion is RARE |
question
| Microsporum gypseum biology |
answer
| Fungus Uses keratin as nitrogen source Macroconidia are ellipsoidal, round ends, thin walls, 2-7cells Grow on Sabourauds and mycobiotic cultures Powdery cinnamon colored colonies, orange/brown |
question
| Microsporum gypseum diagnosis and treatment |
answer
| Dx: KOH prep (ellipsoidal, thin walls, round ends, 2-7 cells) Tx: topical imidazole |
question
| Microsporum gypseum disease |
answer
| Dermatophytoses Lseion: outer red, inner pale area (healing) Capitis (head), corpus (body, ringworm), pedis (foot, Athlete's), cruris (groin), barbae (beard), unguium (nail, onychomycosis) |
question
| Microsporum gypseum virulence factors |
answer
| minimal to moderate inflammation deep invasion is RARE NO HIAR PERFORATION |
question
| Mucor biology |
answer
| Fungus Tissue sample: irregular, BROAD hyphae, aseptate, 90* branching, ribonny Culture: slimey, lid-lifter, SPORANGIA with conidia inside, NO RHIZOIDS |
question
| Mucor diagnosis and treatment |
answer
| Dx: culture (lid-lift, sporangia with conidia inside, no rhizoids) Tx: treat underlying issue of IMC, sugical debridement, AmpB + caspofungin or prosaconazole + caspofungin |
question
| Mucor disease |
answer
| Mucormycosis Rhinocerebral: nasal sinus infection that rapidly spreads to brain, DM with ketoacidosis Pulm/Systemic: transplant patients |
question
| Mucor virulence factors |
answer
| necrotic tissue around inflammation angioinvasive |
question
| Naegleria fowleri biology |
answer
| facultative parasite, free living amoeba |
question
| Naegleria fowleri disease |
answer
| Primary Amebic Meningioencephalitis: swimming in contaminated water/in Neti pot; consumes brain cells; rapid course; headache, fever, stiff neck, unusual taste/smells, acute hemorrhagic brain abscess, invade vessel walls, purulent CSF with motile trophozoites, convulsions, coma, death in 5-6days persistent seizures = 95% death rate |
question
| Naegleria fowleri life cycle |
answer
| cysts mature to trophozoite or flagellated-form in water bodies, penetrate nasal mucosa of humans, migrates to brain via olfactory nerve |
question
| Naegleria fowleri treatment |
answer
| AmpB and other RX |
question
| Necator americanus (Hookworm) life cycle |
answer
| lay egg (passed in feces), hatch in environment, larvae stages grow and shed layers, larvae penetrate skin, access blood and travel to alveoli, larvae crawl up trachea and are swallowed, larvae mature to adults in intestine, mate, lay eggs, repeat |
question
| Necator americanus (Hookworm) biology |
answer
| Heminth, nematode, intestinal small, characteristics PLATES for teeth, multi-cell, extracellular, visible to naked eye, cuticular, roundworm, |
question
| Necator americanus (Hookworm) diagnosis and treatment |
answer
| Dx: ID in stool Tx: mebendazole or albendazole |
question
| Necator americanus (Hookworm) disease |
answer
| Asymp unless high number Ground itch - skin penetration, 2* infection Pulmonary: cough, wheeze, fever Intestinal: worm attach to mucosa and feed on blood, cont. move to new area, exacerbated blood loss, iron deficiency |
question
| Necator americanus (Hookworm) transmission |
answer
| Trans: skin penetration, indiscriminate disposal of human waste |
question
| Onchocerca volvulus (filarial worm) biology |
answer
| Helminth, nematode, tissue multicell, extracell, visible with naked eye, cuticular, roundworm |
question
| Onchocerca volvulus (filarial worm) disease |
answer
| River blindness, onchocerciasis |
question
| Onchocerca volvulus (filarial worm) life cycle |
answer
| male and female mate, lay eggs, hatch to larvae, grow and shed layers, mature to adult, repeat L1 form in humans Arhtropod takes up L1 and deliver L3 |
question
| Onchocerca volvulus (filarial worm) transmission and pathogenesis |
answer
| Trans: skin penetration by insect Path: mostly from release of symbiotic bacteria from dead worms |
question
| Onchocerca volvulus (filarial worm) treatment |
answer
| Ivermectin or diethylcarbamazine |
question
| Paracoccidioides brasiliensis biology |
answer
| dimorphic fungus Mold at 25* (nature): small lollipops Yeast at 37* (body): large, MARINER'S WHEEL, |
question
| Paracoccidioides brasiliensis disease |
answer
| Lung infection that can disseminate widely Quiescent infection can be activated by new IMC status |
question
| Paracoccidioides brasiliensis epidemiology |
answer
| Rare in US Assoc. with agricultural immigrants from Brazil or other endemic area |
question
| Paracoccidioides brasiliensis virulence factors |
answer
| reactivation possible with new IMC status |
question
| Paragonimus westermani biology |
answer
| Helminth, platyhelminth, trematodes/fluke, visceral multicell, extracell, visible to naked eye |
question
| Paragonimus westermani disease site |
answer
| Lungs |
question
| Pediculus humanus biology and disease |
answer
| Ectoparasite Body or head louse |
question
| Penicillum marneffei biology |
answer
| Dimorphic fungus Mold at 25* (nature) Yeast at 37* (body): fission style budding |
question
| Penicillum marneffei diagnosis, treatment, and prevention |
answer
| Dx: fission budding, hx of SE Asia, IMC Tx: AmpB, for IMC has to life-long Prevent: Fungal prophylaxis for HIV pts |
question
| Penicillum marneffei disease |
answer
| Pulmonary infection that mimics TB/cryptococcosis; disseminates to skin via blood Skin lesions: similar to molluscum contagiosum, eventually become BLACK AND NECROTIC |
question
| Penicillum marneffei epidemiology |
answer
| Rare in US Endemic in SE Asia |
question
| Penicillum marneffei virulence factros |
answer
| Reactivation possible with new IMC status Reservoirs: soil, bamboo rats |
question
| Phthirus pubis biology and disease |
answer
| Ectoparasite Pubic or crab louse |
question
| Piedriae hortae biology |
answer
| Fungus must be culture with cyclohexamide |
question
| Piedriae hortae disease |
answer
| Black piedra: black hair spots |
question
| Piedriae hortae virulence factors |
answer
| does not invade skin, little to no inflammation, easily treated |
question
| Plasmodium falciparum biology |
answer
| amicoplexan parasite, protozoa |
question
| Plasmodium falciparum diagnosis |
answer
| Travel hx, Giemsa stain, can have multiple trophozoites in one cell, gametocytes are banana-shaped Schizont = large number of merozoites |
question
| Plasmodium falciparum disease |
answer
| General Malaria: 7-21d inc, 48hr cyclic fever Complicated Malaria: severe anemia, resetting from clumping RBCs, renal and hepatic disease, blackwater fever (dark urine), splenomegaly, dysenteric malaria Erythrocytic Schizogony: infection of blood cells with ring form undergo trophic phase (ingests Hb and grows dark), division via schizogony, lyses the RBC to release merozoities, 48hr periodid cycle, high fever and anemia Cerebral Malaria: impaired consciousness, w/ or w/o seizures; due to blocking blood flow from inflammation to parasitized and lysed RBCs; rapidly progressive to coma and death; RETINAL WHITENING Pregnancy Malaria: maternal anemia, increased risk of miscarriage/stillbirth/low birth weight, due to damage of vessels and tissues from blood cell defects |
question
| Plasmodium falciparum epidemiology |
answer
| 3rd most common microbe killer 90% of deaths are in Africa Most severe of plasmodium sp. and responsible for almost all deaths Sickle-cell is protective G6PD Deficiency is resistant |
question
| Plasmodium falciparum pathogenesis/life cycle |
answer
| mosquito bites and injects sporozoites from a rupture oocyst; sporozoites infect liver cells and multiply; ruptures liver cell and infects blood cells -> ring form; matures in blood cell and then ruptures it; continues ring form can also form gametocytes in blood cells; can be picked up by mosquito and united (male/female) in mosquite -> oocyst-> rupture -> sporozoites |
question
| Plasmodium falciparum prevention |
answer
| Insecticiees, larvicides, mosquito nets |
question
| Plasmodium falciparum treatment |
answer
| Central America: chloroquine Pyrimethamine and sulfadiazine Artemisin Atavaquone/proguanil(malarone) Doxycycline Mefloquine (ok for preggers) Primquine (not in G6PD deficient pts) |
question
| Plasmodium falciparum vector and virulence factors |
answer
| Vector: anopheline mosquito (females, night feeding) VFs: PfEMP (membrane protein, attaches to epithelial cell receptors), antigenic variation of PfEMP |
question
| Plasmodium malariae biology |
answer
| amicoplexan parasite, protozoa |
question
| Plasmodium malariae diagnosis |
answer
| Travel history, Giemsa stain Parasitized RBCs are smaller than normal |
question
| Plasmodium malariae disease |
answer
| General Malaria: inc. 3+wks, initially flu-like, can be sudden and severe, intermittent fevers every 72hrs, anemia, jaundice, splenomegaly incomplete tx -> low persistent parasitemia |
question
| Plasmodium malariae epidemiology |
answer
| most persistent but least severe sp. of plasmodium |
question
| Plasmodium malariae pathogenesis |
answer
| mosquito bites and injects sporozoites from ruptured oocyst, infect liver cells and multiply, rupture host cell and infect blood cell, ring form stage, mature in blood cell and rupture it ring stage can also form gametocytes, which when picked up by mosquitos can mate and form oocyst |
question
| Plasmodium malariae prevention |
answer
| larvacides, insecticides, mosquito nets |
question
| Plasmodium malariae treatment |
answer
| Central America: chloroquine (ok for preggers) Pyrimethamine and sulfadiazine Artemisin Atavaquone/proguanil(malarone) Doxy Mefloquine (ok for preggers) Primquine (not for G6PD deficiency) |
question
| Plasmodium malariae vector and virulence factors |
answer
| Vector: anopheline mosquito (female, night feeding) VF: can survive up to 20yrs in peripheral blood |
question
| Plasmodium ovale biology |
answer
| amicplexan parasite, protozoa |
question
| Plasmodium ovale diagnosis |
answer
| Travel history, Giemsa stain, Infected RBC's with ring stage and Schuffner's dots, Oval RBCs |
question
| Plasmodium ovale disease |
answer
| General malaria: 15d-4yr incubation, initially flu-like, sudden and can be severe, intermittent fever (every 48hrs), anemia, jaundice, enlarged spleen, relapses due to latent form Relapsing Malaria: can occurs years after initial infection, latent form = hypnozoite, often in liver |
question
| Plasmodium ovale epidemiology |
answer
| least prevalent of plasmodium sp. |
question
| Plasmodium ovale pathogenesis |
answer
| mosquito bites and injects sporozoites (from rupture oocyst), infect liver cells and multiply, ruptures hepatocytes and infects blood cells (ring stage, immature), matures and ruptures blood cell can also form gametocytes after ring stage, then picked up by mosquito and male/female gametocytes can mate and mature to oocyst filled with sporozoites |
question
| Plasmodium ovale prevention |
answer
| larvicide, insecticide, mosquito nets |
question
| Plasmodium ovale treatment |
answer
| Central America: Chloroquine (ok for preggers) Pyrimethamine and sulfadiazine Artemisin Atavaquone/proguanil(malarone)) Doxy Mefloquine (ok for preggers) Primquine (not for G6PD deficiency) |
question
| Plasmodium ovale vector |
answer
| Vectors: anopheline mosquito (female, night feeding) |
question
| Plasmodium vivax biology |
answer
| amicoplexan parasite, protozoa |
question
| Plasmodium vivax diagnosis |
answer
| Travel history, Giemsa stain, RBCs with ring stage and Schuffner's dots Parasitized RBCs are larger than normal |
question
| Plasmodium vivax disease |
answer
| General Malaria: 15d-9mo incubation, initially flu-like, can be sudden and severe, intermittent fever (every 48hrs), anemia, jaundice, splenomegaly, relapse due to reactivation of latent form; only infects Duffy(+) people Relapsing Malaria: can occur years after initial infection, latent form = hynozoite, often in liver |
question
| Plasmodium vivax epidemioloy |
answer
| Duffy(-) people are immune |
question
| Plasmodium vivax pathogenesis |
answer
| mosquito bites and injects sporozoites (from ruptured oocyst), infect liver cells and multiply, rupture host cell, infect RBCs, ring stage form, mature and rupture blood cell ring stage form can also make gametocytes, which when picked up by mosquito can mate and form oocyst filled with sporozoites |
question
| Plasmodium vivax prevention |
answer
| larvacides, insecticides, mosquito nets |
question
| Plasmodium vivax treatment |
answer
| Central America: chloroquine (ok for preggers) Pyrimethamine and sulfadiazine Artemisin Atavaquone/progaunil(malarone) Doxy Mefloquone (ok for preggers) Primquine (not for G6PD deficient) |
question
| Plasmodium vivax vector |
answer
| Vector: anopheline mosquito (female, night feeding) |
question
| Pneumocystis jiroveci (carinii) biology |
answer
| Fungus Giemsa stain on lung fluid show trophozoites in cysts (up to 8 cells) Cysts only seen with GMS |
question
| Pneumocystis jiroveci (carinii) epidemiology |
answer
| AIDS, post-transplant, IMS and chemo+leukemia pts |
question
| Pneumocystis jiroveci (carinii) treatment |
answer
| TMP-SMX = 1* pentamide = 2* |
question
| Pneumocystis jiroveci (carinii) virulence factors |
answer
| does not grow on fungal media in lab |
question
| Rhizopus biology |
answer
| Fungus Tissue sample: irregular, broad hypahe, aseptate, 90* branching, ribonny Culture: lid-lifter, sporangia with conidia inside, rhizoids at base of sporangia |
question
| Rhyzopus diagnosis and treatment |
answer
| Dx: culture, lid-lift, sporangia with rhizoids at base Tx: treat underlying IMC issue, surgical debridement, AmpB + caspofungin or prosaconazole + caspofungin |
question
| Rhyzopus disease |
answer
| Mucormycosis Rhinocerebral: nasal sinus infection rapidly progresses to brain; DM with ketoacidosis Pulm/systemic: transplant patients |
question
| Rhyzopus virulence factors |
answer
| necrotic tissue around inflammation angioinvasive |
question
| Sarcotes scabiei biology and disease |
answer
| Ectoparasite Itch mite, scabies in humans, mange in animals |
question
| Schisotosoma haematobium prevention |
answer
| no human waste in water bodies and reservoirs, snail control |
question
| Schisotosoma haematobium treatment |
answer
| Early and intermediate stages" antihistamines, steroids, +/- praziqantel |
question
| Schistosoma haematobium biology |
answer
| Helminth, platyhelminth, trematode/fluke, blood extracell, multicell, visible to naked eye |
question
| Schistosoma haematobium diagnosis |
answer
| Eosinophilia common, Anemia, luekopenia, thrombocytopenia Skin test postive for 1-2months Serologic tests Recovery of eggs in urine |
question
| Schistosoma haematobium disease |
answer
| Initial: local dermatitis Migrate: in blood, toxic reaction, pulm congestion, fever, sweating Acute: 1-2mo after infection, may last 3mo; fever, chills, bloody stools, hematuria, lymphadenopathy; due to eggs moving through intestine and bladder Chronic: 1-2yrs after initial infection; most serious, fatigue, severe intestinal/hepatic/renal inflammation and scarring, vascular obstruction, granuloma; REDUCED bladder capacity, URETHRAL OBSTRUCTION, renal stones, BLADDER CALCIFY, genital granulomas, carcinoma of the bladder |
question
| Schistosoma haematobium epidemiology |
answer
| East Africa, Nile Valley, Middle East |
question
| Schistosoma haematobium life cycle |
answer
| eggs in feces, hatch in water environment, larvae penetrate snail tissue, mature to cercariae, released by snail into water, cercariae are free-swimming, penetrate human skin (lose tail in process), access blood, migrate to portal system, infect and mature in liver, pair up (mate for life), migrate to venous plexus of bladder, lay eggs, passed in urine, repeat |
question
| Schistosoma japonicum biology |
answer
| Helminth, platyhelminth, treamatode/fluke, blood multicell, extracell, visible to naked eye |
question
| Schistosoma japonicum diagnosis |
answer
| Dx:Eosinophilia, anemia, leukopenia, thrombocytopenia Skin tst (+) for 1-2mo Serology REcover eggs in stools |
question
| Schistosoma japonicum disease |
answer
| Initial: local dermatitis Migrate: in blood, toxic reaction, pulm congestion, fever, sweating Acute: 1-2mo after infection, fever chills, bloody stools, hematurnia, lymphadenopathy, egg passing through intestine and bladder; 3 mo duration Chronic: 1-2yrs after initial infection, most severe; fatigue severe intestinal/hepatic/renal inflammation and scarring, vascular obstruction, granuloma; liver CIRRHOSIS, ASCITES, pronounced KATYAMA SYNDROME |
question
| Schistosoma japonicum epidemiology |
answer
| China, Japan, Phillippines |
question
| Schistosoma japonicum life cycle |
answer
| Egg in feces, hatch in water environment, penetrate snail tissue, mature, cercariae released by snail into water, cercariae are free swimming, penetrate skin of human (lose tail in process), access blood, migrate to portal sys, mature to adults in liver, pair up (mate for life), migrate to mesenteric venules, lay eggs, shed in stool, repeat |
question
| Schistosoma japonicum prevention |
answer
| no human waste in water bodies and reservoirs, snail control |
question
| Schistosoma japonicum treatment |
answer
| Early to intermediate stages: antihistamines, steroids, +/- praziqantel |
question
| Schistosoma mansoni biology |
answer
| Helminth, platyhelminth, trematode/fluke, blood multicell, extracell, visible with naked eye |
question
| Schistosoma mansoni diagnosis |
answer
| Eosinophilia, Anemia, Leukopenia, Skin test: positive for 1-2mo Serology tests Recovery of eggs in stool |
question
| Schistosoma mansoni disease |
answer
| Initial: localized dermatitis Migration: parasite in blood, toxic reaction, pulm congestion, fever, sweating Acute: 1-2mo after infection, fever, chills, bloody stools, hematuria, lymphadenopathy, last 3mo; eggs in intestine and bladder Chronic: 1-2yrs after initial infection; fatigue, sever intestinal/renal/hepatic inflammation and scarring, vascular obstruction, granuloma; hepatosplenomegaly -> abdo pain, diarrhea, bloody stools, giant splenomegaly, right heart failure, immune complex neuropathy |
question
| Schistosoma mansoni epidemiology |
answer
| Africa, Middle East, parts of S. America, West Indies, Puerto Rico |
question
| Schistosoma mansoni life cycle |
answer
| eggs in feces, hatch in water environment, penetrate snail tissue, mature, cecariae released by snail into water, free-swimming, penetrate skin of human (in process, loses tail), accesses circulation, migrate to portal blood and liver, mature into adults, pair up (mate for life), migrate to mesenteric venules, lay eggs, eggs circulate to liver and are shed in stool |
question
| Schistosoma mansoni prevention |
answer
| no human waste in water bodies and reservoirs, snail control |
question
| Schistosoma mansoni reservoir and pathogenesis |
answer
| Reservoir: humans, live in mesenteric venules Path: cecariae enter by direct penetration, loses tail to become schistosomulae, enter circulation, move to liver and lungs, adults mate and move to colon |
question
| Schistosoma mansoni treatment |
answer
| Early-intermediate stages: antihistamines, steroids, +/- praziqantel |
question
| Schistosoma presentation in US |
answer
| From ducks and other animals (humans 2* host) Burrows into skin, cercarial dermatitis, multiple exposure will elicit allergic reaction Tingling, burning, itching, small redish pimples or small blisters |
question
| Sporothrix schenckii biology |
answer
| Dimorphic fungus Mold at 25* (nature) Yeast at 37* (body): CIGAR-SHAPED, small budding, LONG NARROW NECK on bud, STOVEPIPE BUD, rapid growth, 48-72hrs, FLOWERETTES/ROSSETTES/DAISY conidia |
question
| Sporothrix schenckii disease |
answer
| Sporotricosis: 1*-non-healing ulcer on finger/arm/or leg; 2*-linear series of nodules/ulcers along lymphatic drainage path, puss Pulmonary form is RARE |
question
| Sporothrix schenckii epidemiology |
answer
| Worldwide Farmers, gardeners, florists, horticulturists Brazilian cat-lovers |
question
| Sporothrix schenckii treatment |
answer
| AmpB IV for dissemination Voriconazole, itraconazole used to use potassium iodide |
question
| Sporothrix schenckii virulence factors |
answer
| reactivation possible with new IMC status |
question
| Strongloides stercoralis (Threadworm) biology |
answer
| Helminth, nematode, intestinal multi-cell, extracelluar, visible to naked eye, cuticular, roundworm |
question
| Strongloides stercoralis (Threadworm) diagnosis and treatment |
answer
| Dx: ID in feces or intestinal aspirates, Marked eosinophilia Tx: Ivermectin or albendazole |
question
| Strongloides stercoralis (Threadworm) disease |
answer
| Asymp unless high number Skin: raised red serpiginous lesions, recur at irregular intervals, common on lower back/butt Pulmonary: cough, wheeze, fever Intestinal: abdo pain/tender, flatulence, nausea, vomit, diarrhea, malabsorption, weight loss, intestinal obstruction, UC, intestinal perforation Hyperinfection: IMC or debilitated pts, dissem through body, encephalitis, hemorrhagic pneumonia, death |
question
| Strongloides stercoralis (Threadworm) life cycle |
answer
| male and female adults mate, lay eggs, larvae hatch, grow and shed cuticle layers, mature to adults, repeat |
question
| Strongloides stercoralis (Threadworm) transmission and pathogenesis |
answer
| Trans: skin penetration, indiscriminate disposal of human waste Path: female worm lives in intestine and lays eggs, eggs hatch and are passed in feces as larvae [auto-infection], lives independently in soil, access through skin penetration, disseminates in blood, exits at alveoli, coughed up, swallowed, mature into adults in intestines, repeat |
question
| Taenia saginata biology |
answer
| Helminth, platyhelminth, cestode/tapeworm multicell, extracell, visible to naked eye prolgiottids and scolex |
question
| Taenia saginata diagnosis |
answer
| "Proglottid in feces, visible to naked eye Eggs in feces, with 100x Scotch tape test" |
question
| Taenia saginata life cycle |
answer
| embryos ingested, develops to adult hood, adult can live for several decades, eggs and gravid proglottids released in feces, CATTLE ingest eggs, eggs develop to onocosphere (embryo with 4 hooks), human ingest BEEF |
question
| Taenia solium biology |
answer
| Helminth, platyhelminth, cestode/tapeworm multicell, extracell, visible to naked eye Proglottids = segments, mature ones grow off end and shed into feces Scolex = head |
question
| Taenia solium diagnosis |
answer
| Proglottid/egg in feces; Scotch tape test Biopsy of cysts X-ray show calcified cysts Serology Eosinophilia |
question
| Taenia solium disease |
answer
| Cystercosis: autoinfection, eggs passes through intestine lumen, penetrates tissues, migrates to muscles and brain, encystation and can live up to 5yrs, causes inflammation -> symptoms Muscle cyst: fever, pain Eye cyst" impaired vission Brain cyst: neurocystercosis, epilepsy, look like tumors, mental problems, personality changes and seizures |
question
| Taenia solium epidemiology |
answer
| Neurocysticercosis is major causes of epilepsy in endemic countries |
question
| Taenia solium life cycle |
answer
| Embryos ingested, matures to adult, can liver for several decades in body, eggs and gravid proglottids shed in feces, ingested by PIG, eggs develop to onchospheres, humans ingest PORK and contract onchospheres |
question
| Taenia solium prevention |
answer
| Avoid autoinfection via fecal-oral route |
question
| Taenia solium treatment |
answer
| Niclosamide (usually only one dose) Praziquantil Recheck after tx Cystericercosis: Albendazole + praziquantel, +/- corticosteroids, sometimes surgery |
question
| Toxocara canis (Roundworm) biology |
answer
| Helminth, nematode, tissue Multi-cell, extracell, visible with naked eye, cuticular |
question
| Toxocara canis (Roundworm) diagnosis and treatment |
answer
| Dx: symptoms, history of dog contact, blood tests Tx: Mebendazole |
question
| Toxocara canis (Roundworm) life cycle and transmission |
answer
| male and female adults mate, lay eggs, hatch to larvae, grow and shed layers, mature to adults, repeat Trans: ingestion |
question
| Toxocara canis (Roundworm) pathogenesis |
answer
| contact with feces or ingesting worm cysts in other host tissue, ingested eggs hatch and penetrate intestinal wall, move to lots of tissues (lungs/brain/eyes), does not develop past larvae stages, causes local inflammation and severe disease (hemorrhagic, necrosis, eosinophil infiltration) |
question
| Toxocara canis (Roundworm) reservoirs and epidemiology |
answer
| nematode of dogs Neglected infection of poverty trans: ingestion |
question
| Toxocara canis disease |
answer
| Visceral larva migrans: convulsions, neurological symptoms, myocarditis Ocular larva migrans: most common at age 7-8, exudative endophthamitis, retinoblastoma |
question
| Toxocara cati (Roundworm) biology |
answer
| Helminth, nematode, tissue multicell, extracelluar, roundworm, cuticular, visible to naked eye |
question
| Toxocara cati (Roundworm) diagnosis and treatment |
answer
| Dx: symptoms, history of cat exposure, blood tests Tx: mebendazole |
question
| Toxocara cati (Roundworm) disease |
answer
| Visceral larva migrans: convulsions, neurological symptoms, myocarditis Ocular larva migrans: most common at age 7-8, exudative endophthalmitis, retinoblastoma |
question
| Toxocara cati (Roundworm) pathogenesis |
answer
| contact with feces or ingesting worm cysts in host tissue, ingested eggs hatch, larvae penetrate wall of SI, move to tissues (lung/eye/brain), does not develop past larvae, causes local reaction (hemorrhagic, necrosis, eosinophil infiltration) |
question
| Toxocara cati (Roundworm) transmission |
answer
| ingestion |
question
| Toxoplasma gondii biology |
answer
| apicomplexan parasite, obligate pathogen, intracellular, protozoa |
question
| Toxoplasma gondii diagnosis |
answer
| Serology: not reliable in AIDS pts PCR: amniotic fluids Clinical features and response to tx |
question
| Toxoplasma gondii disease |
answer
| IMC Toxoplasmosis: reactivation of cysts or 1* infection can lead to encephalitis, headache, confusion, ataxia, hemiparesis, blurred vision; can get brain lesion visible on CT Congenital Toxoplasmosis: 1* infection during pregnancy, 1st or 2nd tri most fatal; hydrocephalus, calcifications in brain, hepatosplenomegaly, jaundice, fever, anemia, pneumonia, blindness; can cause neuro, chorioretinitis or intellectual problems after birth (normal); might be assoc. with schizophrenia |
question
| Toxoplasma gondii epidemiology |
answer
| 15-30% infected in US, up to 80% in France IMC at risk for severe disease 1st and 2nd trimester 1* infections are more likely to show symptoms in infant |
question
| Toxoplasma gondii hosts, virulence factors, and pathogeneis |
answer
| Shedoocysts in feces of definitive host Def host: felines Intermediate hosts: rodents, sheep, humans, birds VF: broad host range, infect any nucleated cell, high prevalence, chronic infection Path: competent immune system will maintain oocyst form, IMC -> more severe |
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| Toxoplasma gondii transmission |
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| Undercook/raw meat (pork, lamb, goat), unwashed veggies contaminated with oocysts, contaminated water, inhale/ingest oocysts in cat litter or gardens, CONGENITAL |
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| Toxoplasma gondii treatment |
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| Sulfadiazine + pyrimethamine or Clindamycin + pyrimethamine or Atavaquone |
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| Trichinella spiralis biology |
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| Helminth, nematode, tissue INTRACELLULAR, multi-cell, cuticular, visible with naked eye, roundworm |
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| Trichinella spiralis diagnosis and treatment |
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| Dx: Ab test, muscle biopsy Tx: Steroids fro severe symptoms, Mebendazole or Albendazole (esp. if still in intestinal phase) |
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| Trichinella spiralis disease |
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| 1-2d after ingestion: diarrhea, vomit, abdo pain 5-7d later: facial edema, splinter hemorrhage under nails, fever After 2wks: muscle-assoc. symptoms appear; headache, fever, fatigue, chills, cough, aching joints, muscle tender and pain, itchy skin, death (rare) due to myocarditis/encephalitis CNS damage/or pneumonia |
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| Trichinella spiralis epidemiology |
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| 2% mortality in clinical cases 10% mortality if CNS involved |
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| Trichinella spiralis life cycle |
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| male and female adults mate, lay eggs, hatch to larvae, grow and shed cuticle layers, mature to adult, repeat |
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| Trichinella spiralis transmission and pathogenesis |
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| Trans: raw/undercooked pork or wild game (carnivorous or omnivorous) Path: larvae stage invades striated muscle, parasite then secretes angeogentic cytokines, blood vessels grow to parasitized cell, conversion of host cell to NURSE CELL |
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| Trichomonas vaginalis biology (type, O2 req., motility, repro) |
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| amitochondirate parasite, extracellular pathogen, binary fission division (when in UG epi), anaerobic, flagella, protozoa |
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| Trichomonas vaginalis complicatins |
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| Sterility in men and women (due to chronic inflammation and tissue destruction) Endometriosis or cervical cancer in women (from constant damage and repair) Increases chances of miscarriage, premature, low birth wt, and infant mortality Lesion facilitate HIV infection and increase viral shedding |
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| Trichomonas vaginalis diagnosis and treatment |
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| Dx: discharge, strawberry cervix, parasites in vaginal secretions Tx: oral MNZ, tinidazole if resistant to MNZ |
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| Trichomonas vaginalis disease in men |
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| Usually asymp Urethritis or prostatitis Recently assoc. with prostate cancer |
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| Trichomonas vaginalis disease in women |
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| 50% begin asymp, symp w/in 6mo Vaginitis - redness, irritation, burning, vaginal discharge and odor; Acute - diffuse vulvitis, yellow-green discharge, hemorrhagic spots on vaginal mucosa (strawberry cervix) Chronic - mild symp with pruritis, vaginal discharge mixed with mucus |
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| Trichomonas vaginalis epidemiology |
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| Endemic in US, but worldwide distribution Most common non-viral STD |
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| Trichomonas vaginalis prevention |
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| prevent reinfection by treating sexual partners and using condoms til tx completed |
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| Trichomonas vaginalis transmission and pathogenesis |
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| Trans: STD Path: only has trophozoite form, resides in lower UG of women and urethra/prostate of men |
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| Trichomonas vaginalis virulence factors |
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| adhere to cell membrane (cell-contact-dependent cytotoxity) often asymptomatic in men -> spread w/o knowing infected can survive up to 24hr in urine, semen, and water rod-like axostyle stabs cell, 5 flagella target glycoproteins, laminins, and fibronectin |
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| Trichophyton mentagrophytes biology |
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| Fungus Uses keratin as nitrogen source Microconidia are grape-like clusters Sarbourauds and mycobiotic cultures downy colonies (from feet), granular colonies (from animals) Urease(+) |
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| Trichophyton mentagrophytes diagnosis and treatment |
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| Dx: KOH prep (grape-like clusters) Tx: oral griseofulvin |
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| Trichophyton mentagrophytes disease |
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| Dermatophytoses: feet and nail Lesion: red outer, pale inner |
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| Trichophyton mentagrophytes virulence factors |
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| minimal to moderate inflammation deep invasion is RARE CAN PERFORATE HAIR |
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| Trichophyton rubrum biology |
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| Fungus Uses keratin as nitrogen source Microconidia are tear drop and bird on a fence Sarbourauds and mycobiotic cultures white fluffy/granular colonies, CHERRY RED ON REVERSE Urease (-) |
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| Trichophyton rubrum diagnosis and treatment |
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| Dx: KOH prep (tear drops, birds on a fence) Tx: oral griseofulvin |
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| Trichophyton rubrum disease |
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| Dermatophytoses: feet and nail Lesion: outer red, inner pale |
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| Trichophyton rubrum virulence factors |
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| minimal to moderate inflammation deep invasion is RARE NO HAIR PERFORATION |
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| Trichophyton tonsurans biology |
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| Fungus Uses keratin as nitrogen source MICROconidia are elongated balloons or stretched teardrop shaped Sabourauds and mycobiotic cultures Wrinkled/cratered colonies Growth enhanced by THIAMINE |
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| Trichophyton tonsurans diagnosis and treatment |
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| Dx: KOH prep (microconidia, tear drop shaped) Tx: oral griseofluvin |
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| Trichophyton tonsurans disease |
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| Dermatophytoses: feet (pedis, Athlete's) and nail (unguium, onychomycosis), capitis (head) Lesion: outer red, inner pale #1 cause of tinea capitis |
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| Trichophyton tonsurans virulence factors |
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| minimal to moderate inflammation deep invasion is rare |
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| Trichosporin beigelii biology |
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| Fungus must be cultured with cyclohexamide |
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| Trichosporin beigelii disease |
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| White piedra: white hair spots |
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| Trichosporin beigelii virulence factors |
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| does not invade skin, little to no inflammation, easily treated |
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| Trichuris trichiura (Whipworm) biology |
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| Helminth, nematode, intestinal Multi-cell, visible to naked eye, extracellular, roundworm, cuticular outer layer |
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| Trichuris trichiura (Whipworm) diagnosis, treatment, and prevention |
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| Dx: ID in feces Tx: Mebendazole Prevent: Sanitary disposal of human waste |
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| Trichuris trichiura (Whipworm) disease |
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| Asymp unless high number Abdominal pain, diarrhea and weight loss w/ moderate to heavy burder Rectal prolapse in heavily parasitized children along with diarrhea, cramps, urgency and tenemus |
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| Trichuris trichiura (Whipworm) life cycle |
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| Male and female adults attach to mucosa in cecum and mate, lay unembryonated egg, shed in feces, embryonate in soil, ingested by human, larvae grow and shed layers (before and after ingestion), larvae hatch in SI, larvae mature into adults, repeat cycle |
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| Trichuris trichiura (Whipworm) tranmission |
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| Trans: ingestion req. indiscriminate disposal of human waste, fecal egg contamination of soil/foodstuff/animal feed/hands/etc. |
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| Trypanosomatidae brucei biology (type, motility, reproduction) |
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| Kinetoplastid parasite, protozoa Cork-screw like movements, single flagella, divide by binary fission |
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| Trypanosomatidae brucei disease |
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| African sleeping sickness |
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| Trypanosomatidae cruzi biology |
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| Kinetoplastid parasite, protozoa Cork-screw like movements, single flagella, divide by binary |
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| Trypanosomatidae cruzi disease |
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| Chagas: 7-14day incubation, lasts 1-2wks; restlessness, sleeplessness, increasing exhaustion, bone and muscle pain, fever, enlarged spleen/liver/nodes, diffuse myocarditis, possible pericarditis and endocarditis Children - meningioencephalitis and coma Death due to CNS involvement or chronic infection Chronic: low level in blood, but nerve degeneration; cardiomyopathy; megaesophagus; megacolon |
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| Trypanosomatidae cruzi dx and tx |
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| Dx: symptoms, blood smear (could be too low or be a non-path cousin), ELISA, PCR Tx: Acute - bidzimidazole or nifurtimox; Chronic - no drugs, manage symptoms |
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| Trypanosomatidae cruzi epidemiology |
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| South and Central America Frong roofs and mud walls Occasionally in TX |
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| Trypanosomatidae cruzi life cycle and reservoirs |
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| develop and divide in gut of vector, deposited in feces, scratching causes penetration of human skin, divides intracellularly, proliferate locally, 10days later in blood Reservoirs: monkeys, armadillos |
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| Trypanosomatidae cruzi pathogenesis |
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| inject via bite as promastigotes, phagocytosed by macrophages, mature to amastigotes, reproduce by fission, rupture host cell, infect neighboring cells |
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| Trypanosomatidae cruzi transmission |
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| Kissing bug (triatoma infestans) Bites sleeping people on face Also: blood transfusion, congenital, breast feeding, ingest contaminated food/drink |
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| Wucheria sp. (filarial worm) biology |
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| Helminth, nematode, tissue multicell, extracell, visible with naked eye, cuticular, roundworm |
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| Wucheria sp. (filarial worm) disease |
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| Lymphatic filariasis, elephantitis |
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| Wucheria sp. (filarial worm) life cycle |
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| male and female mate, lay eggs, hatch to larvae, grow and shed cuticle layers, mature to adults, repeat L1 form in humans; Arthropod takes up L1 and delivers L3 |
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| Wucheria sp. (filarial worm) transmission and pathogensis |
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| Trans: skin penetration via insect Path: most due to release of symbiotic bacteria from dead worms |
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| Wucheria sp. (filarial worm) treatment |
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| Ivermectin or diethylcarabamazine |
