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112 Cards in this Set

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Entomoeba histolytica

1. What is the related parasite that is almost morphologically indistinguishable? only way to tell?

2. How is this best distinguished from non pathogenic related species?

1. Entomoeba dispar; occasionally the classic RBC ingestion in cytoplasm is identified (not seen in any others)

2. E. coli: up to 8 nuclei in cyst w/ frayed ends on chromatid bar; in troph its non directional w/ eccentric nucleus

E. hartmanii: small size!! 5-10 micrometers rather than 25

1. How is E. hitolytica acquired> what are clinical sx?

2. Characteristic gross and microscopic findings? (shown in photo)

3. How are E nana and iodomoeba butschlii distinguished from E histolytica

1. ingestion of cysts in food or water --> protracted diarrhea due to colonic infestation and may cause extraintestinal amebic abscess in liver (most common site!) spleen or brain

2. amoebic abscess have anchovy paste material, colonic lesions have flask shaped ulcers especially in cecum, and protracted infections may mimic CA by causing napkin ring lesions (ameboma)

3. nana has large knobby "ball and socket" central karyosome (nucleus) in troph and cyst and cyst has no chromatoidal bodies; I butschlii cyst has prominent iodine staining vacuole, w/ similar karyosome to E nana


1. What is confirmatory test for Naegleria fowleri infection?

2. What are clinical sx/ acquisition?

3. What is are the clinical manifestations of acanthoemeba? histo appearence seen in culture photo?

1. culture on lawn if inactivated Escherichia coli reveals visible trail formed by ameba moving across the plate and ingestion of bacteria

2. fatal meningoencephalitis w/in days in kids swimming or diving in freshwater pools w/ infection of frontal lobe viaa cribriform plate

3. granulomatous amebic encephalitis and acantamoebic keratitis assoc w/ contact lenses; characteristic spiny acanthopodia

Giardia lamblia cyst on wet mount iodine stain

1. How can giardia trophozoites be diagnosed?

2. describe cysts and motility on wet mounts?

3. In stool samples, from what nonpathogenic organism must G. lablia be distinguished? how?

1. seen in stool specimens or small bowel biopsies viewed as kite/tear drop/ pear shaped from the top or as comma or spoon from the side

2. oval thick walled w/ 4 nuclei licated along central axostyle; demonstrate characteristic falling leaf motility

3. chilomastix mesnili; the cyst form has ONE nucleus near a safety pin shaped structure

Dientamoeba fragilis

1. characteristic features?

3. Clinical manifestations? common co-infection?

1. round binucleate w/ "fractured" central karyosome and single flagelleum attached to wall of organism at multiple points

2. occasional cause of diarrhea and anal pruritis in children; Enterobius vermicularis (pinworm)

Trichomonas vaginalis

1. characteristic appearance?

2. Clinical manifestations?

1. pear shaped w/ 2 nuclei in anterior end of central axostyle w/ undulating memrane extending 1/2 around oragnsim

2. sexually transmitted --> strawberry cervix and vaginitis

1. What is the differential for multiple tiny 2-5 micrometer organisms w/in histocytes?

2. What is the only way to diagnose leishmania oragnisms?

3. On what is are Leishmania cultured? what else?

4. What is the vector and describe clinical syndromes?

1. leishmania: distinct transverse bar like kinetoplast, exclusively intracellular

histoplasma capsulatum: budding

Toxoplasma: curved and mostly extracellular

Trypanaxoma cruzi: also have kinetoplast but in peripheral blood

2. tissue biopsy! usually of skin or bone marrow; amastigote is only form seen in human host (also donavoni in blood? FACT CHECK AND COMPARE KINETOPLAST)

3. Novy MacNeal Nicolle medium; trypanosoma spp

4. Sandfly Phlebotomus and Lutzomyia causing:

Solitary self limiting cutaneous lesions: New world spp in south america and texas is L. mexicana; Old world spp include L tropica, major and aethiopica usually in Mediterranean

Visceral leishmaniasis or kala azar: Old world L donovani w/ wide spread systemic dz w/ HSP and BM infections in africa, india, asia and middle east

Mucocutaneous: New world in south and central america caused by L braziliensis

1. List trypanosoma spp and describe respective dz manifestations?

1. T cruzi: Chagas dz, American trypanosomiasis, seen in aspirates of chagomas, LNs or infected tissue as C or S shaped; a leading cause of CHF in south and central america, and achalasia due to distal esophageal infection; acquired from Reduviid kissing bug that poops in sore (chagoma) or eye (Romana sign)

T brucei: African trypanosomiasis, sleeping sickness, seen as delicately curved w/ undulating flagellum along length an whip like tail; acute febrile illness often resulting in death acquired from tsetse fly

T cruzi

Balantidium coli

1. characteristic feature?

1. surface uniformly covered w/ cilia w/ large kidney bean shaped macronucleolus, large 50-70 micrometers

Cryptosporidium parvum

1. typical histologic appearance?

2. Clinical picture? shared by what other organism?

1. in small intestine biopsy sppears as basophilic dome shaped 8-10 micrometer structure adherent to enteric brush border (tho really intracellular in apical vacuole)

2. protracted diarrhea in immunocompromised hosts esp w/ AIDS; isospora belli


Isosopora belli

1. Histo description?

2. How do microsporidia appear in intestinal biopsy? what provides definitive diagnosis?

3. Where and when are cyclospora infections seen? acquisition, sx?

1. larger 15-30 micrometer thin elliptical structures interposed b/w enterocytes

2. numerous 1-1.5 micrometer intracellular organism at apex of enterocytes; electron microscopy

3. only seen in certain months, in nepal ,peru, haiti and guatemala, from ingestion of contaminated fruit and leafy veg, infecting small bowel w/ characteristic syndrome of several days of fever, severe watery diarrhea, extended anorexia and fatigue w/ significant weight loss


1. how is it acquired and what are the clinical manifestations?

2. characteristic appearacne?

1. beef or pork causing self limited gastroenteritis

2. hour glass shaped eggs w/ 2 sporocystes

Toxoplasma gondii

1. What form is shown in this photo? what other for is there?

2. Name a usfel diagnostic test and the most common?

3.How is this dz acquired? clinical presentation?

4. Give 2 situations of toxo infection that can have grave results?

1. bradyzoite (in the brain) which is a pseudocyt consisting of numerous organisms packed into cytoplasm of histiocyte; also tachyzoite which are free or extracellular small curved 3-5 micrometer forms

2. PCR in CNS and systemic infections, but serology based on EIA is used most commonly via anti-toxo IgM diagnostic of congenital and acute infections (keep in mind IgM persist for months so limited specificity)

3. ingestion of contaminated cat feces containing eggs --> mono like syndrome w/ fever and posterior cervical LAD

4. immunocompromised at great risk for CNS infection and if in infection occurs during 1st trimester there is risk of fetal loss while in 3rd trimester fetal CNS infection --> periventricular calcs and choriretinitis

1. What are the 4 plasmodium species that cause malaria?

2. Spread by? Describe clinical features common to all?

3. Group the species by fever spikes?

1. falciparum, vivax, ovale and malariae

2. anopheline mosquito; (lasting 6-12 hrs) paroxysmal fever/chills, correlateing w/ to intermittent intravascular hemolysis causing anemia and splenomegaly; hemosiderinuria and hemoglobinuria

3. q 48 hours: tertian; (benign) ovale vivax and (malignant) falciparum due to lethality and every other day fevers

q 72 hours: quartan; malariae

1. Which causes nephrotic syndrome?

2. Which has CNS involvement?

3. Which have TRUE relapse?

4. Discuss which erythrocytes are infected?

1. malariae

2. falciparum

3. vivax and ovale, all have recrudescence (revival)

4. ovale and vivax affect young RBCs; malariae infets old RBCs; and falciparum affects ANY

1. What may protect a person against malaria? which spp?

2. Describe stages and life cycle?

3. When are pts NOT at risk for TRUE relapse? differentiate from recrudescence?

4. When is the ideal time to obtain a specimen for malaria smears?

1. persons w/ HbS trait (HbSA) protected against falciparum; while Duffy negative are protected fom vivax which need FYa or FYb to mediate RBC attachment; GC6PD deficiency protects against all plasmodium spp

2. moquito sucks up infected blood and parasite matures into sporozoite (infective form) transmitted to human by bite where it goes to liver to proliferate (extraRBC schizogony) and release merozoites into blood to infect RBC (RBC schizogony); latent sporozoites in liver (hypnozoites) occur w/ ovale and vivax causing relapse

3. when infected by transfusion or transplacental spread; recrudescence is return of clinically undetectable levels

4. immediately antecedent to anticipated fever spike

double chromatin dot ring forms

1. Characteristic of ?

2. Why is it important to identify this species?

3. What are the only forms seen in PS of this species?

1. P falciparum

2. b/c it is potentially lethal

3. ring forms (trophozoites, can be multiple in 1 RBC, called applique if on periphery ) and gametocytes

banana shaped gametocyte

1. characteristic of what plasmodium species?

2. What are the features of P malariae on PS?

1. P falciparum

2. all stages seen, normal sized RBCs, no schuffner dots, only disitinct features are 6-12 nuclei in schizonts (vs 12-14 in vivax/ovale) and occasional band form trophozoites

schuffner dots

1. characteristic of what plasmodium species?

2. What other feature seen in this photo is characteristic of these same species?

3. What else differentiates these spp from falciparum?

1. vivax and ovale

2. RBC enlargment

3. all stages of developing organism can be seen (unlike falciparum, trophs and gametes onlu) AND gametocytes are amoeboid NOT banana shaped

bad form trophozoite of P malariae

babesia microti

1. What form is seen in photo?

2. differences from malaria?

3. location, arthropod and clinical sx?

4. What coinfection is common?

1. the trophozoite tetrad due to multiple organisms w/in RBCs

2. extraerythrocytic forms are present (and none of the other life cycle forms)

3. eastern US, from Ixodes dammnini tick (same as Lyme dz) or Ixoces pacificus in western US --> nonperiodic fever and hemolysis, w/ leukopenia abnl LFTs

4. flavivirus and lyme disease

Pneumocystic jiroveci (carinii) NOW classified as FUNGUS was considered protozoan!!

1. What kind of stain is this? what is the giemsa and H&E appearance?

2. Acquisition and patient population?

3. Presentation?

1. GMS (showing classic concave disc), dont stain w/ giemsa so seen as negative space; also dont stain on H&E but have characteristic frothy exudates

2. airborne dissenimation in immunocompromised pts esp AIDS (MOST common defining illness!)

3. pneumonia w/ bilateral butterfly pulnonary infiltrates

1. List nematodes/roundworms w/ alternate nicknames? (10)

2. List tramatodes/flukes? (5)

3. List cestodes/tapeworms? (6)

1. Trichuris triciura/ whipworm

Ascaris lumbricoides

Necator americanus/


Ancylostoma duodenale/


Strongyloides stercoralis

Enterobius vermicularis/



Trichinella spiralis

Toxacara canis and cati


2. fasciola hepatica

fasciolopsis buskii

clonorchis sinesis

paragonimus westermoni


3. taienia saginata /beef

taenia solium/ pork

diphillobothrium latum/ fish

hymenolepsis nana/ dwarf

dipylidium caninum


Trichuris trichiura

1. Classic description of egg? worm?

2. Mode of infection and sx?

3. What is common dual infection?

1. Barrel w/ cork at both ends or tea tray; whip like anterior end and male has coil posteriorly

2. ingestion of eggs w/ cecal infestation and may be asymptomatic but heavy infections produce rectal prolapse in kids

3. Ascaris lumbricoides

ascaris lumbricoides

1. Worm and egg charachteristics?

2. infection, life cycle and clinical manifestations?

1. The work is HUGE up to 35 cm GROSS; egg is 60 micrometers, w/ rough bile stained mamillated exterior

2. ingestion of eggs that hatch intestine --> larvae that enter blood stream and travel to lungs to mature (Loeffler syndreom w/ transient pulmonary infiltrates and eosinophilia) and are swallowed to infest duodenum whihc may be asymtpomatic, cause pain, obstruction, cholangitis or appendiscitis, spontaneously expelled after 1 year UGHHHHHHHHHHHHH

Necatur americanus

1. distinguishing feature?

2. Eggs in feces are identical to ?

1. has cutting plates for mouthparts

2. Ancylostoma duodenale and Strongyloides stercoralis

Ancylostoma duodenale

1. distinguishing features?

2. How is this, necatur americanus and strongyloides stercoralis (one difference explained below) infections acquired?

3. Sx?

4. What is a similar spp w/ a different clinical syndrome?

1. has teeth for mouthparts

2. the larvae penetrate skin (dont go barefoot in sand yikes)

3. pruritic lesion on foot (ground itch), larvae enter circulation and trespass lungs (loffeler syndrome can result), then are expectorated and swallow to deposit in small bowel often causing iron deficiency anemia

4. Ancylostoma braziliense, it remains in skin resulting in cutaneous larva migrans

Strongyloides stercoralis

1. How is this distinguished from ancylostoma duodenale and necatur americanus?

2. What is unique about this egg?

3. With negative stool what diagnostic methods may be useful in ID?

4. What can happen in immunocompromised pts?

1. it has a short buccal groove and prominent genital primordium (they both have opposite and all the egg are the same)

2. They are not found in stool b/c they hatch in bowel, so rhabditoid larvae are seen in stool (which mature into filariform larvae to penetrate foot skin, as above)

3. duodenal aspirate or string test

4. autoinfection, where larvae mature w/in bowel and penetrate wall to circulation to begin life cycle again which can also lead to hyperinfection a deadly complication w/ wide dissemiation, pneumonia, gastroenteritis and sepsis

Enterobius vermicularis

1. Not routinely found in stool so what test is implemented?

1. cellophane tape test

Enterobius vermicularis

1. Characteristic feature?

2. Clinical manifestations and patient population?

1. Lateral ala

2. fecal oral ingestion of eggs w/ nocturnal migration of adults to lay eggs in periana region so may present w/ nocturnal anal pruritis, vaginitis or enuresis; appendicitis is occasional complication

1. What are the distinguishing features of filaria forms (microfilaria) in the peripheral blood? Besides occupation of peripheral blood what do the species on this card have in common?

2. Which two are acquired by mosquito bite? clincial manifestations?

3. Which by mango Chrysops fly? clinical manifestation?

1. based on presence or absence of a sheath and the pattern of nuclei in the tail; shed into and found in blood at periodic intervals espcially night so blood should be drawn b/w 2-4AM

2. wuchereria bancrofti and brugia malayi; both infest lymphatics --? lymphadenitis and lymphedema

3. loa loa; inhabits subcutaneous and conjunctival locations

1. Which microfilaria are NOT found in blood?

2. What is acquired from biting midge? clinical?

3. What is acquired from simulium black fly? clinical manifestations?

4. What is acquired from mosquito? clinical?

1. Mansonella perstans, onchocerca volvulus and dirofilaria immitis

2. Mansonella perstnas inhabits body cavities like plerua

3. Onchocerca volvulus, infects subcutaneous and conjunctival locations --> nodule formation and/or blindness, the microfilariae continuously migrate through skin and eye (rather than blood) causing dermatitis, keratitis, corneal opacity and is leading cause of blindness in central africa and central america

4. dirofilaria immitis infects lungs and can be found in granulomatous nodules

Trichinella spiralis

1. histo?

2. Acquisiton and sx?

1. encysted larvae, typically spiraled in sections of infected skeletal muscle

2.acquired by consumption of undercooked infected pork --> infection of skeletal muscle by encysted larvae causing myositis and weakness

1.What do Toxacara canis and to a lesser extent Toxacara cati cause?

2. patient population, mode of infection and clinical manifestations?

3. how is anisakiasis acquired and what are the clinical manifestations>

1. visceral larva migrans and

ocular larval micgrans

2. children who ingest soil contaminated w/ dog or cat feces and the organisms wander throughout various organs b/c they are incapable of completing life cycle in humans --> hypereosinophilia, HSM and pneumonitis

3. ingestion of raw fish, and organism penetrates GI tract and resides in bowel wall, endoscopic bx shows eosinophil rich granuloma w/ nematode

1. What is the only difference between Fasciola hepatica and Fasciolopsis buskii?

2. Describe egg, aquisition and clinical manifestation, common to both?

1. hepatica worm has conical cephalad and busckii worm has a pointed cephalad

2. largest egg in human parisitology, oval w/ thin shell and unshouldered operculum; acquired by eating freshwater plants in china (water cress), causes infestation of bile ducts w/ eventual biliary fibrosis

chlonorchis sinesis

1. what is adult cephalad appearance?

2. egg characteristics?

3. infection acquired where, by what and causes?

1. Snout like

2. small 10-20 micrometers w/ shouldered operculum w/ small aboperculer knob

3. orient, ingestion of undercooked fish w/ chronic biliary ftact infestations leading to fibrosis and is risk factor for cholangiocarcinoma

1. how is paragonimus westermani acquired and what are the clinical manifestations?

2. Egg appearance?

3. How are all schistosoma acquired? and in what circumstances and clinical manifestations?

1. ingestion of undercooked shellfish causing infestation of lung w/ pulmonitis

2. larger than clonorchis senesis but similar b/c oval w/ shouldered operculum (but noaboperculer knob) and smaller than fasciola and fasciolopsis

3. penetration of skin by free swimming fork tailed circariae found in snail infested water, they travel to mesenteric and pelvic blood vessels to deposit eggs which may cause systemic febrile illness due to immune complexes or reaction over type in tissue leading to visceral dysfunction

Schistosoma hematobium

1. geography?

2. Infects what organ w/ what increased risk and sx?

3. What is the best specimen for ID?

1. africa and middle east

2. infects veins of bladder w/ eggs deposited in bladder wall causing hematuria and irritative bladder sx --> SCC of bladder

3. terminal urine (last 10-20mL passed) best collected during increased shedding like mid day or after exercise

Schistosoma mansoni

1. geography

2. infects what location causing what sx?

1. africa esp nile delta

2. infects hepatic portal vasculature and inferior mesenteric vessels w/ eggs passed into intestine and periportal hepatic parenchyma causing pipestem fibrosis and eventual fibrosis

Schistosoma japonicum

1. geography?

2. Where does it infest and what sx?

1. philippines, china SE asia

2. also infects liver --> cirrhosis, b/c of its blunt spine it can also rarely travel to brain and spinal cord

Taenia saginata

1. How is this proglottid different from T solium?

2. Where is this organism common, how is it acquired and what does it cause?

3. Describe the egg and how is it morphologically different from solium?

1. saginata: >13 lateral uterine branches

solium: <13 branches

2. south and central america w/ ingestion of encysted organisms (cystercerci) in beef --> small bowel infestation by adult worm, eggs are NOT infectious to humans unlike solium

3. thick radially striated wall w/ 3 pair of hooks; egg is identical to solium

Taenia solium

1. How is scolex different from saginata?

2. Where is this organism common, how is it acqired and what does it cause?

3. name a key clinical manifestation and mode of infection NOT seen in saginata?

1. Saginata: smooth surface "unarmed " rostellum

Solium: many tiny hair like projections on surface "armed" rostellum; seen as double row of hhooklets that are acid fast and birefengent

2. rare in US only in "recent" immigrant , causes intestinal infection due to ingestion of measly pork containing encysted organisms (cystercerci)

3. Cystercercosis, condition in which cysts containing larvae are found in brain (neurocysticercosis) and other organs resulting from ingestion of eggs

Diphyllobothrium latum

1. main differential diagnosis? how is it distinguished?

1. paragonimus westermani has a shouldered operculum whereas D latum has UNshouldered operculum and small abopercular knob

Diphyllobothrium latum scolex

1. what is characteristic abou the proglottids?

2. Where and how is this infection acquired? sx?

1. they are characteristically much wider than long hand have coiled uterus

2. scandinavia, russia canada northern US and alska via ingestion of uncooked frewhwater fish --> intestinal infection, sometimes complicated by B 12 deficiency

1. What is the mosc common cestode recovered in US?

2. How is it acquired? sx?

3. Describe the egg?

1. hymenolepsis nana the dwarf tapeworm

2. ingestion of water or food contaminated w/ rodent droppings and person to person spreadd --> intestinal infection

3. inner and outer shell w/ two polar thickening pair of filaments that look like tiny bows WTF

1. How is Echinococcus acquired and what are the sx?

1. ingesting food contaminated w/ eggs from poop of infected dog (definitive host) sheep and cattle are intermediate host, causes cysts in various organisms especially the liver which can be uni/multilocular or polycystic depending on spp and may give rise to pulmonary cysts if they rupture

1. List 4 pair of common dual infections?

2. Falling leaf motility?

3. Progressive motility?

1. ascaris & tricuria

Enterobius and D fragilis

Babbesia, lyme dz & flavivirus

lepromatous leprosy &

strongyloides hyperinfection

2. G lamblia

3. E hitolytica

1. Amoebae culture?

2. hemoflaggelate culture?

3. Eat T solium cysts get? eggs get?

4. What two organisms cause skin/eye infections?

5. what two organisms are capable of human to human spread?

1. bed of Escherichia coli

2. novey Mac Neil nicolle medium

3. cysts --> intestinal infection

eggs --> cysticercosis

4. Loa loa and onchocerca volvulus

5. enterobius and H nana

1. In contrast to other parasites what is the immunodeficiency basis for G lamblia infection?

2. splenectomy increases severity of what infection?

1. B cell/ humoral deficiency

2 .babesiosis

calcoflour white

1. For what is this used and briefly explain process?

2. Based on morphology hat general clinical assumpions can be made?

1. a flourochrome that binds selectively to cellulose in fungal walls, screening technique for fungus, specimen is breifly digested in 10% KOH then calcoflour white is added before examination under flourescence scope

2. hyphae indicative of clinical infection while yeast may be normal flora unless obtained from sterile sites

cryptococcus neoformans

1.what is a classic method to ID this? esp in what specimen?

2. What 3 general purpose fungal culture media are used, temp length?

1. india ink in CSF, sensitivity 50%

2. brain heart infusion agar, sabouraud agar and inhibitory mold agar at 25-30C for 4-6 wks



1. What are general differences in microscopic and colony morphology of yeasts and molds?

2. What are the 4 major categories in fungal diff dx?

3. What

1. yeast: small creamy "bacterial like" colonies; unicellular organisms displaying budding

mold: large fuzzy colonies; multicellular organisms forming hyphae

2. hyaline septate molds, pigmented septate molds (dematiaceous, supposedly the only ones seen on H&E), aseptate molds and dimorphics

1. What is a dimorphic fungi and how do they present to lab?

2. What are the general steps of fungal ID in lab?

1. one that converts to yeast form, presents to lab in mold form

2. exclude dimorphic (it converts to yeast or w/ exoantigen test) then look at 4 major characteristics: rate of growth , type of hyphae (septate vs aseptate), pigmentation (dematiaceous or non pigmented hyaline), type of sporulation (basis for instant pattern recognition)

1. Broadly what do very rapidly and very slowly growing molds suggest?

2. List pathogenic fungi notorious for rapid growth?

3. What growth pattern suggests contaminant?

4. What drug is used in isolation media and what pathogens inhibited by it?

1. rapid: zygomycetes (aseptate, ribbonlike)

slow: Dimorphics, dematiacious, require >1 week to make visible colonies

2. C immitis, aspergillus spp, scedosporium apiospermum, zygomycetes "lid lifters'

3. if rapid growth is seen AFTER a prolonged incubation

4. Cycloheximide inhibits zygomycetes aspergillis and C neoformans

1. For what is the phenol oxidase test used? explain

2. The urease test? explain

1. aid in ID of Cryptococcus neoformans which can oxidize diphenolic compounds (caffeine, dopamine dopa) --> pigment production

2. Also used to ID C. neoformans (which produces urease and is pathogenic vs candida whcih may be contaminant and does not produce urease) as well as differentiate species of trichophyton from one another (metagrophytes produces urease rubrum does not); basically fungi w/ urease produce ammonium which changes Ph and an indicator in the agar has color change

1. how is fungal dimorphism demonstrated in lab?

2. Which two dimorphics need special agar conditions and what are they?

3. What has largely replaced yeast conversion, give brief explanation?

4. Serologic tests available for what fungi?

1. Temp change; molds grow at 25-30C while yeast grow at 37C body temp (the tissue form!!!)

2. Histoplasma capsulatum needs BHI w/ blood and Blastomyces dermatitidis needs BHI or cottonseed agar for conversion; while coccidoides immmitis is almost NEVER converted

3. exoantigen test done for fungal antigens on culture material (NOT clinical specimen) where extract is

prepared from isolate and reacted w/ species spp antisera

4. dimorphic and aspergillus

Histoplasma capsulataum

1. characteristic histologic appearance?

2. Where is this infection prevalent?

3. Clinical findings?

1. often in necrotizing gramulomas w/ organisms in histiocytes seen as 2-5 micrometer narrow based budding yeast w/ bundling that gives them a pseudocapsule

2. ohio and mississippi river valleys found in soil contaminated by chicken or bat poop

3. pulmonary nodules, chronic sclerosing mediastinitis, HSM, LAD, acquired though inhalation (like most dimorphics); disseminated often involves reticuloendothelial system and dx is easy on BM bx

Histoplasma capsulatum

1. describe culture appearance?

1. hyaline hyphae w/ spiked macroconidia that are more frequent/well developed in mature cultures, so early on they may mimick T rubrum or B dermitidis w/ lollipop appearance



coccidoides immitis

1. Describe culture appearance and time?

2. Where is this prevalent and what does it cause clinically?

1. grows easily in ~7 days seen as mycelia formed of easily separated barrel-shaped arthroconicdia (like histo is difficult to convert to yeast)

2. california san Joiquin desert causes Valley Fever via inhalation involving lungs w/ dissemination to skin >> viscera; immunocompromised, blood group B, filipinos, african americans and 3rd trimester pregnancies at increased risk for dissemination

Coccidoides immitis

1. Describe histology, ddx and differences?

1. seen w/in granulomata as giant 50-200 micrometer spherule w/ thick hyaline walls enclosing hundreds of tiny 1-5 micromter endospres; may be confused w/

Rhinosporidium seeberi: presents as exophytic nasal lesion

Prototheca wickerhami: presents as olecranon bursitis

Histoplasma capsulatum: these have budding



Blastomycoses dermatitidis

1. appearance in tissue sections?

2. Where is this infection acquired and from what animal?

3. infection and dissemination?

1. fairly uniform 8-12 micrtometer broad based budding yeast

2. ohio and mississippi river valleys (like histo but not in bats and chickens) in dogs

3. infects lungs and can disseminate to skin and bone

blastomycoses dermatitidis

1. culture appearance?

2. What 4 other spp must be distinguished from this?

1. hyphae w/ intermitttent lollipoplike smooth conidia

2. other forms that make similar lollipops: paracoccidoides, scedosporium and chyrosporium (which looks identical)

sporothrix schenkii

1. culture appearance?

1. hypate w/ daisy head like conidia

sporothrix schenkii

1. appearance in tissue sections?2. Acquisiton in contrast to other dimorphics?

3. Clinical manifestations?

1. 2-5micrometer long cigar shaped yeast w/ narrow based budding in background of purulent inflammation

2. NOT by inhalation but by trauma to the skin, often hand or arm and classically via rose thorns, b/c it is a saprophyte of dead plant material

3. it causes local infection w/suppuration --> local lymphangitis w/ chain of nodules proceding up the extremity; lymphocutaneous sporotrichosis; can disseminate to bone in immunocompromised patients

paracoccidoides braziliensis

1. tissue section appearance?

2 culture mold appearance?

3. geography, acquisition and clinical manifestations?

1. 10-15 micrometer yeast w/ circumferential budding looking like a mariners wheel

2. indistinguishable from blastomycoses dermatitidis

3. in south and central america due to inhalation --> pneumonitis w/ disseminated infection involving the reticuloendothelial system, bowel, and liver

reverse side of trychophyton rubrum w/ red pigment that diffuses into agar

1. Histologically these spp are differentiatated by micro and macroconidia? list 3 examples in each group?

1. macro:

microsporum canis:

microsporum gypseum:

Epidermophyton floccosum:


trychophyton rumbrum:

trychophyton mentagrophytes:

trychophyton tonsurans:

microsporum canis

spindle shaped macroconidia w/ pointed upturned ends and transverse septae

T rubrum

tear shaped microconidia spaced alonghyphae "birds on a wire"

microsporum gypseum

macroconidia are oval shaped w/ blunt ends and transverse septae

epidermophyton floccosum

club shaped macroconidia w/ transverse septae

trychophyton mentagrophytes have grape like clusters of microconidia and occasional spiral hyphae

1. What is special about these infections?

1. they can penetrate hair shafts (endothrix) unlike T rubrum

Trichophyton tonsurans has marked size and shape variability in microconidia

1. What is a way to rapidly diagnose a dermatophyte infection that does NOT speciate them?

2. List forms of dermatophyte infection?

1. KOH stained scrapings

2. tinea capitis

tinea corporis (ring worm)

tinea cruris (jock itch)

tinea pedis

tinia unguium (onychomycosis)

Aspergillius spp

1. characterizing features in tissue?

2. Characterizing feature from culture for all spp?

3. On what kind of media is Aspergillus grown and what is the characteristic colony appearance?

1. hyaline septate molds w/ 45 degree dichotomous branching but NOT specific

2. Fruting head (swollen vesicle)

3. grow on Czapek agar w/ distinct margins w/ white aprons

A fumigatas

single row of phialides giving rise to chains of conidia covernig only the top of the vesicle

1. appearance of colonies?

1. lue green w/ distinct white apron

A flavus

circumferential phialides resembling lollipop

A niger

heavily pigmented conidia

1. culture appearance?

1. blackened surface but reversei yellow/gray; vs dermatiaceous molds that have pigment in front and back

A terreus

two rows of phialides

1. culture appearance?

1. cinnamon buff to orange

1. Which aspergillus is most common human isolate?

2. List disease manifestations?

1. A fumigatus

2. commonly pulmonary:

aspergilloma: fungus ball in old cavitary lesion (eg Tb) in otherwise immunocompetent patient

Allergic bronchopulmonary aspergillosis: colonizes airway w/out invasion eliciting marked allergic response w/ mucus impaction peripheral eosinophilia and reactive airways may --> bronchiectasis and increased incidence in CF patients, dx supported w/ serum anti-aspergillus IgE; A flavus is also common cause

Allergic sinonasal aspergillosis: aka allergic fungal sinusitis

semi-invasive pulmonary aspergillosis: aka chronic necrotizing pulonary aspergillosis w/ colonization of cavitary regions in emphysematous parenchyma / wuperficial invasion seen in pts getting steroids for lung dz

invasive bronchopulonary aspergillosis: seen in immunocompromized invased lung parenchyma and has angioinvasion

charcot leydin crystals in mucin of allergic fungal sinusitis w/ abundant eos in background

1. list forms of allergic sinusitis?

2. What is a more spp characteristic histologic finding assoc w/ aspergillus infection? describe?

3. What other fungal spp has angioinvasion?

1. Similar to lung dz, fungal sinusitis >> fungus ball, chronic invasive, acute/fulminant invasive

2. calcium oxolate, envelope shaped

3. mucormycosis (mucor rhizopus, absidia, cunninghamella)

1. What are the general characteristics of hyalinohyphomyces?

2. What separates these spp? list spp in each category?

1. hyaline-septate molds that cause invasive fungal infections

2. conidia morphology

clusters: acremonium, gliocladium, fusarium

branching chains: penicillium, paecilomyces, scopulariopsis,

singly:scedosporium beuveria sepedonium chryosporium

Acremoium w/ long hair like conidiophores and clusters of tiny conidia

gliocladium highly distincitve branching phialides w/ clusters of spherical condia resembling goffball at end of out- streched fingertips

1. culture?

1. lawn of green growth withOUT an apron

fusarium macroconidia

1. With what other fungal spp may this be confused on H&E and what can help?

2. What clinical manifestation is uniquely common w/ disseminated infections of fusarium?

1. may resemble dichotomous branching organism like aspergillus but fusarium has hyphae branch at 90 degree right angles

2. fungemia, high frequency of positive blood cultures


1. most common clinically significant spp? describe shared morphology

1. P marneffei; broom like arrangement of branching phialides giving rise to chains of conidia which may resemble A fumigatas



1. What are general features used to differentate dermatiaceous pigmented molds?

2. List 3 main groups and spp w/in each?

1. characteristic front and back pigmentation of colonies

2. fast growers, conidia w/ transverse septa: bipolaris, drechslera, exserohilum, helminthosporum,


fast growers, transverse and logitudinal septa: alternaria, ulocladium, stemphilium

slow growers: cladosporium carrionii, phialophora, fonsacaea pedrosi, exophila jeanselmei and wangiella dermatitidis (indistinguishable) aureobasidium pullulans, phaeoannellomyces wernickii




fonsacaea "wooden coat rack"


1. Describe histo?

2. what species are the 3 main causes?

1. sucutaneous mycosis assoc w/ prominent pseudoepitheliomatous hyperplasia of overlying epidermis w/ characteristic pigmented hyphae, yeasts that are septated in > 1 plane --> medlar bodies or copper pennies

2. phialophora cladosporium carrionii, and fonsecaea

1. What are 3 aseptate molds? characteristic culture finding?

2. to what 2 diagnostically useful structures do these give rise?

1. zygomycetes, rhizopus, mucor and absidia that grow so rapidly w/o borders called "lid lifters"

2. rhizoids and sporangia


1. characteristic appearance?

2. What is the main visual difference from absidia?

3. Mucor?

4. Classic infection of mucor?

1. makes rhizoids and nodal sporangiophores (arise directly over rhizoids) which are full of tiny spores that collapes when mature looking like "collapsed umbrella"

2. Absidia has internodal sporangiophores (b/2 rhizoids)

3. Mucor does not produce rhizoids

4. rhinocerebral in person w/ diabetic ketoacidosis; all these spp also invade vessel walls like aspergillus

1. What characterizes ID of candida yeast? be spp for one species

2. What yeast spp do arthroconidia characterize?

3. What yeast form NO hyphae? and how are they distinguished?

1. formation of pseudohyphae on cornmeal tween 80 agar; C albicans has chlamydospore formation

2. geotrichum or trichosporon (urease +)

3. cryptococcus: urease and phenoloxidase +

rhodotorula: urease +

saccharomyces: both tests inert

germ tube test

1. describe procedure and purpose?

1. yeasts suspended in serum and incubated at body temp (37C) for 3 hours then wet mount is made to look for formation of germ tubes (hyphae forming directly from wall of yeast, which have no constriction at juncture w/ yeast cell unlike pseudohyphae); identifies C albicans w/ 90% sensitivity and 100% specificity

1. urease test performed on what agar?

2. Which fungi are positive for urease?

3. Describe phenol oxidase test and what yeast does it identify?

4. what are the specific culture requirements for Malassezia furfur?

1. christensen

2. cryptococcus, rhodotorula, candida crusei and trychophyton mentagrophytess

3. it's an enzyme that converts amine (in cekk wall of cryptococcus) to pigment melanin; organisms are incubated on bird seed (niger seed) agar that contains caffeic acid which cryptococcus can turn into pigment melanin

4. incubated at 35C and overlaid w/ olive oil as a source of long chain fatty acids

1. What is notworthy in Candida albicans colonies? and why is this important?

2. What form does colonization by C albicans usually take?

1. formation of filamentous extensions "feet" or "spider colonies" around the edges of older colonies; b/c its by far the most common candidal isolate

2. Asymptomatic!

candica albicans

1. what are the characteristic morphological features and on what agar?

2. What are the most common infections and in what setting are they seen?

3. Describe an inherited condition related to Candida?

1.blastoconidia and chlamydospores are diagnostic on cornmeal agar

2. mucocutaneous > UTI > visceral, in diabetic, pregnancy,immunosupression or pts on broad spectrum antibacterials

3. chronic mucocutaneous candidiasis, w/ candida spp immunodeficiency characterized by protracted superficial infections of skin, nails, oral cavity and pharynx often w/ endocriopathies like hypoparathyroidism, adrenal insufficiency

cryptococcus neoformans

1. What kind of stain is this? list 3 other stains with which this organism reacts and describe why?

2. What is the key histologic feature of cryptococcus?

1. mucicarmine (shown) and alcian blue: positive due to polysacharide rich capsule

Fontana-Masson: positive due to phenoloxidase enzyme in capsule (also basis for phenol oxidase test)

india ink: cannot penetrate capsule so gives organism "budding ghost" appearance especially in CSF, 80% sensitivity in HIV pts, only 40% in non HIV

2. the size variability (3-15 micrometers)

1. What lab test can be sed to ID cryptococcus and on what specimens?

2. Name a characteristic culture feature?

3. how is this organism acquired?

4. Same for Cryptococcus gatti? what is notable about infection w/ this organism?

1. cryptococcal polysaccharide antigen in serum or body fluids like CSF, latex particles coated w/ Ab to capsular antigen for basis of test which is >95% sensitive and specific

2. capable of growth at 37C

3. inhalation of infected soil contaminated w/ chicken or pigeon poo

4. C. gatti assoc w/ trees especially eucalyptus; it can cause infection in immunocompetent hosts!

1. What kind of infection do cryptococcus spp cause?

2. where does cryptococcus disseminate?

3. what is the common patient population?

1. usually primary pulmonary infections forming well defined single or multiple nodules and ranging from mild to penumonia

2. brain and bone

3. HIV patients but has decrased w/ AART therapy and now is seen increasingly in organ transplant recipients or other immunocompromised

1. How are trichosporon and geotrichum differentiated?

2. What kind of infection do these cause?

1. trichosporon: hockey stick pseudohyphae; urease positive

geotrichum: rabbit ears pseudonhyphae; NOT pos for urease

2. white piedra, hair shaft infection EWWWWWW

rhodotorula characterized by red colonies

Malassezia furfur

1. buzz word and morphologic appearance?

2. Growth requirements?

3. Causes what clinical syndromes?

1. spaghetti and meatballs or meatballs and franfurturs seen on KOH prep or histology due to short hyphae and spherical yeast

2. Sabouraud media at 35C overlaid w/ olive oil

3. tinea versicolor and TPN related sepsis

1. What fungus has a beer like odor?

2. substrate in and enzyme detected in birdseed agar?

3. What 3 species have red pigmented colonies?

4. Two species causing angioinvasion and parenchymal infarction?

1. Saccharomyces

2. contains caffeic acid and dectects phenol oxidase

3. rhodotorula, penicillium marneftii, fusarium

4. aspergillus and zygomyosis

prototheca wicherhamii

1. What is unique about this infection? describe histology?

2. Describe infection w/ loboa loboi?

1. it's the only alge that causes human infection; distinctive endosporulating cysts looking like hub cap following penetrating skin trauma w/ cutaneous infection adn olecranon bursitis

2. fungus doesnt grow in culture --> enlarging veruccous skin lesion tx w/ excision w/ histologic appearance of string of beads yeast in dermis