ICL 4.1-4.3: Mycology Flashcards

Question

what's the pneumonic for which dimorphic fungi are commonly associated with clinical illness?

Answer 1

"body heat produces shape changes" B = blastomyces dermatitidis H = histoplasma capsulatum P = paracoccidioides brasiliensis/penicillium marneffei S = sporothrix schenckii C = coccidioides immitis

Answer 2

yeasts = round or oval, buds or pseudohyphae can be seen, colonies on agar are often smooth or flat molds = tubular structures with “fuzzy” appearance on cultures then diagnosis at the genus level can often be made by appearance (angle of branching, color of colonies, appearance of conidia, reaction to different types of stains, etc)

Answer 3

1. GMS stain 2. Mayer's mucicarmine 3. Masson-Fontana 4. periodic acid-Schiff stain (PAS) 5. calcafluor white 6. India Ink 7. gram stain 8. H & E

Answer 4

Gomori methanamine silver stain stains all fungal walls brownish/black and has a greenish background most sensitive stain for fungi of all types!!

Answer 5

helps distinguish cryptococcus from other yeast cryptococcus looks red; background is purple

Answer 6

stains fungal cell walls brown stains melanin helps to distinguish different types of molds, especially agents of phaeohyphomycosis

Answer 7

Stains polysaccharide elements in fungal cell wall red also stains the organism Tropheryma whipplei (causative agent of Whipple’s Dx), often described as “foamy macrophages”

Answer 8

stains chitin which then flouresces bright white under UV light you can use this stain on fresh clinical specimens! has largely replaced KOH

Answer 9

suspension of colloidal carbon particles useful for demonstrating the capsule on yeast in the CSF (cryptococcus species) looks like white circles on a black background

Answer 10

candida may occasionally pick up some dye in general, a routine gram stain will not show fungal elements

Answer 11

standard histology stain for tissues

Answer 12

many, but not all, pathogenic fungi can be recovered through culture on *selective media* some fungi can take up to 4 – 8 weeks to grow on routine culture media

Answer 13

when certain species of Candida grow for 3 hours at 37C for 3hours in human or sheep serum, it exhibits a specific pattern called germ tube formation only C. albicans and C. dublinensis exhibit germ tube formation there's mother cells with budding daughter cells (slide 37)

Answer 14

1. serology 2. B-D glucan 3. galactomannan

Answer 15

antibodies to fungal pathogens (usually dimorphic) are available eg histoplasmosis, blastomycosis and coccidioides lacks specificity/sensitivity

Answer 16

detects (1,3)-beta-D-glucan released into the circulation from the cell wall of certain fungi good for Candida and Aspergillus BUT ….cryptococcus, zygomcetes, mucor ssp, Rhizopus are not detected by this test

Answer 17

polysaccharide of the cell wall of Aspergillus can be detected by EIA in serum and BAL fluid

Answer 18

antibodies CF titers of > 1:32 are suggestive of acute infection H bands are positive in < 20% of patients with severe disease (specific, not sensitive) M bands are positive in most patients with histoplasmosis OR histoplasmosis antigen can be detected by EIA in urine, blood, BAL histoplasmosis = a type of lung infection; it is caused by inhaling Histoplasma capsulatum fungal spores -- these spores are found in soil and in the droppings of bats and birds

Answer 19

antibodies develop 1 – 3 weeks after infection they are specific, not sensitive for recent or active infection AB levels decrease with treatment AB can be detected by different methods like complement fixation, immunodiffusion, EIA (IgG of IgM)

Answer 20

cross-reacts with histoplasmosis antibody tests can get ID, CF, EIA antibodies DNA probes

Answer 21

1. polyene 2. azoles 3. echinocandins 4. pyriidine analog

Answer 22

amphotericin B

Answer 23

fluconazole itraconazole voriconazole posaconazole

Answer 24

1. caspofungin 2. microfungin 3. anidulafungin

Answer 25

5-flucytosine

Answer 26

eastern US minus florida "great lakes and ohio river valley" area

Answer 27

southwestern US and northern mexico

Answer 28

central US and the midwest

Answer 29

west coast = CA, oregon, washington

Answer 30

southern china and thailand

Answer 31

china and australia

Answer 32

south america!! super high in eastern south america

Answer 33

candida is a normal human commensal organism and it's only an opportunistic infection most infections are endogenous risk factors: 1. skin/mucosal disruptions 2. antibiotic use 3. IV/IVDA 4. hyperalimentation 5. neutropenia 6. GI tract surgery 7. burns 8. T-cell suppression

Answer 34

``` C. albicans** C. krusei C. parapsilosis C. lusitaniae C. glabrata ```

Answer 35

it's pretty drug -resistant and it's rapidly spreading there are some strains that are resistant to all 3 available classes of antifungals it can cause outbreaks in healthcare facilities and common healthcare disinfectants are less effective at eliminating it it can be carrier on patients skin without causing infection which allows spread to others...

Answer 36

1. local mucocutaneous infections: oral, esophagitis, vulvovaginitis, baanitis, chronic mucocutaneous candidiasis 2. disseminated infection = candidemia, hepatosplenic candidiasis 3. focally invasive infections urinary tract, bone/joint, endocarditis literally causes white pupils....and thrush and CMG

Answer 37

1. hematologic malignancies 2. transplant 3. HIV 4. CVC 5. hyperalimnetation 6. ATB 7. GI surgery

Answer 38

1. from the gastrointestinal tract mucosal barrier 2. from an intravascular catheter 3. from a localized focus (eg pyelonephritis)

Answer 39

no so if you see it in the blood it means you've been infected Candida in the blood is NEVER contaminant it either came from the GI tract, IVs, and focal source if CVC (central venous catheter) is suspected as the source, it needs to be removed you also need to rule out dissemination to make sure it didn't go to the heart, eye, spleen or liver

Answer 40

GI tract = major source with neutropenia IV = major source with non-neutropenia

Answer 41

candidemia in neutropenic hosts (WBC <1000) has some differences than in non-neutropenic hosts ophthalmological findings for chorioretinitis are minimal until the neutropenia resolves source of the candidemia is usually GI tract > CVC in this setting GI tracts mucositis from chemotherapy can lead to release of endogenous flora (bacteria and fungi like candida) into the bloodstream resulting in neutropenic fever and dissemination

Answer 42

urinary tract involvement can occur through hematogenous dissemination to the kidneys or entry into the lower GU tract = bladder: cystitis there is also the potential ascent to the upper GU tract (kidney – pyelonephritis) candiduria can represent infection or colonization --> most patients with indwelling foley catheters and candiduria are colonized, not infected, and do not develop candidemia from this source persistent candiduria/ symptomatic candiduria warrants imaging of the kidneys

Answer 43

1. C. neoformans ubiquitous in guano contaminated soil 2. C. gattii eucalyptus trees these two are *encapsulated* yeasts that are urease positive!!

Answer 44

route of infection is inhalation then there can be hematogenous dissemination it's found in the soil and pigeon droppings!

Answer 45

immunocompromised hosts like with T-cell defects!! rarely seen in immunocompetent hosts can infect lungs, skin, but has a predilection for the CNS (meninigitis)!! skin = bumps all over your face lungs = patchy infiltrates, pneumonia

Answer 46

CD4 <200 (usually < 100) can see fever, malaise, headache, stiff neck, photophobia developing over a 1 – 2 week period "soap bubble" lesions in the gray matter of the brain it's really bad and can lead to permanent neural deficits or be lethal

Answer 47

1. cryptococcal Ag + blood or CSF 2. recovery of crypto 3. India stain: you'll see white cells with halos around them and a dark background (negative stain) 4. latex agglutination test that detects repeating polysaccharide capsule

Answer 48

amphotericin +5FC (flucytosine) for 2 weeks followed by fluconazole

Answer 49

histoplasma capsulatum

Answer 50

found in the midwestern US, Southeastern US, Central/South America -- along the ohio and mississippi river specifically indiana for indiana jones (sketchy) but cases of histoplasmosis have been reported in patients with no known travel history to endemic areas

Answer 51

portal of entry is inhalation of the conidia (spores) spores enter lungs and travel to alveolar spaces where immune cells trap them and they're ingested by macrophages bird or bat droppings! think of this with people in caves or farmers immune cells transport sporse through the lymph system to mediastinal lymph nodes where they multiply and if not eliminated, enter your blood-stream and spread through your body if inoculum is large or macrophages cannot ingest/kill the fungi, disease can develop

Answer 52

T-cell deficits = HIV, transplant, anti-TNF agents when an immunocompromised person gets histoplasmosis it often becomes disseminated and effects the liver and spleen = hepatosplenomegaly and calcification on the organs this is because histoplasmosis targets reticuloendothelial system which has lots of macrophages which are prevalent in the liver and spleen

Answer 53

asymptomatic infection occurs in >95% of patients symptoms: 1. pulmonary = subacute, acute diffuse, fibrosing mediastinitis 2. extrapulmonary = skin lesion, CNS infection, adrenal gland involvement, primarily

Answer 54

1. subacute pulmonary infection weeks to months after inhalation of microconidia mild symptoms = fever, chills, headache, cough, chest pain can occur CXR with focal infiltrates, hilar lymphadenopathy; usually resolves without treatment 2. acute disease diffuse or localized; can see severe illness with progression to respiratory failure or dissemination if ICH or large inoculum dose 3. chronic pulmonary histoplasmosis fever, night sweats, productive cough, dyspnea, chest pain, fatigue (can look like TB) 4. fibrosing mediastinitis rare, but it represents excessive fibrotic response to histoplasmosis you'll see cough, dyspnea, occasional hemoptysis fibrosis results in invasion/entrapment of heart and great vessels -- no good treatment available....

Answer 55

1. serology with complement fixation titers of >1:32 indicative of active disease H band signifies active disease: M band cannot distinguish between recent and remote infection 2. urinary antigen test performs better than serum antigen as a diagnostic tool and can monitor response to therapy 3. histopathology (macrophages filled with histoplasma) 4. cultures

Answer 56

mild disease = no treatment moderate disease = itraconazole severe disease (acute pulmonary) = amphotericin

Answer 57

can occur from re-infection or reactivation immunosuppression is key risk factor extra-pulmonary manifestations commonly seen --> up to 70% of patients may also have pulmonary involvement as well with interstitial infiltrates or nodules urinary and serum antigen testing is useful in diagnosing active disseminated histo --> but a negative test does not rule out histo infection

Answer 58

treatment is amphotericin B ( 2 weeks if non-CNS, 6 weeks if CNS) followed by at least one year of itraconazole

Answer 59

causes disease in ICH (AIDS/other T-cell deficiencies) in endemic areas suspected route of infection is inhalation

Answer 60

fever, weight loss, skin lesions, anemia, HSM, cough

Answer 61

amphotericin B for 2 weeks, then oral itraconazole

Answer 62

relatively non-virulent organism and infection in non-ICH usually only involves the skin/subcutaneous tissues papule develops at inoculation site; fungus is introduced from trauma from a rose thorn or something lymphatic spread proximal to papule (sporotrichoid spread or nodular lymphangitis) over days; *ascend up the lymphatics from the site of infection miminal pain and/or systemic complaints

Answer 63

inoculation of organism through gardening (roses, classically) or soil "rose gardener disease"

Answer 64

clinical picture or culture culture looks like cigar shaped yeast

Answer 65

itraconazole til 2 – 4 weeks after lesions resolved

Answer 66

inhalation of conidia leads to infection inhalation of aerosolized spores

Answer 67

asymptomatic in the majority of cases with control at alvelar level by macrophages/neutrophils blastomycosis has a virulence factor BAD-1which allows conversion from mold to yeast phase cell mediated immune system deficits associated with clinical illness acute or chronic pneumonia can also develop hematogenous dissemination often follow symptomatic infection --> skin, bones, GU sites commonly affected gross looking lesions

Answer 68

diagnosis is primarily through culture but fungal elements seen on histopathology have a characteristic appearance can also do urine antigen test

Answer 69

itraconazole for mild disease amphotericin for moderate/severe disease

Answer 70

Paracoccidioides brasiliensis and P. lutzii

Answer 71

asymptomatic infection common <5% of people develop symptoms symptomatic primary infection usually seen in children, young adults if it disseminates to reticuloendothelial system = fever, weight loss, lymphadenopathy, HSM, anemia/aplastic anemia

Answer 72

inhaled into lungs with control of infection via macrophages and neutrophils in the alveoli --> granulomas can form in the lungs (source for potential reactivation) respiratory droplets

Answer 73

happens when there's reactivation from a granuloma in the alveoli! can see pulmonary infiltrates, mucosal involvement

Answer 74

1. culture yeast form in the lungs looks like a captain's wheel; literally 2. serology

Answer 75

generally extended duration of trimethoprim-sulfamethoxazole (at least 2 years) or 6 – 12 months itraconazole amphotericin for severe infections

Answer 76

1. abscesses on the forehead and clavicular region resulting in osteoarticular involvement 2. abscess formation originating in the lymph nodes 3. inguinal lymphadenopathy 4. abdominal lymphadenopathy with ascites and hepatosplenomegaly usually see it in kids

Answer 77

1. cutaneous lesions of the face resulting from hematologic dissemination lesions are paplar and ulcerating 2. perioral and chin lesions (super bad....) 3. cervical and submandibular lymphadenopathy with fistulization 4. verrucous lesion with irregular borders in the perianal region

Answer 78

1. Coccidioides immitis | 2. C. posadasii

Answer 79

caused by coccidioides inhalation of a singe athroconidium is sufficient to start infection in the alveoli, the fungal cell develops into a spherule --> after several days, the spherule ruptures releasing endospores infection is usually contained by the immune system at this point but primary Coccidial pneumonia may develop if not contained = chest pain, cough, fever associated with soil/dust in specific geographic locations

Answer 80

night sweats, weight loss, severe fatigue, arthritis/arthralgia (“desert rheumatism”), erythema nodosum (painful red nodules on the shins) erythema nodosum is only seen in healthy patients because it means it's a robust immune response pulmonary nodes, cavities, and/or progressive fibrosis may develop extrapulmonary manifestations = skin, bone, joint, CNS most common sites of spread

Answer 81

HIV, transplant, lymphoma, chemotherapy, steroids, pregnancy (especially 3rd trimester) more likely to see dissemination to the bone and the meninges to cause meningitis on top of the normal symptoms

Answer 82

1. potential exposure in an endemic area with new onset LRTI or arthralgia or rash consistent with erythema nodosum 2. isolation of coccidioides it's never a contaminant/colonizer and isolation of the organism is consistent with infection culture poses a threat to lab personnel so let the micro lab know ahead of time if cocci suspected 3. antibody tests

Answer 83

primary coccidioides usually resolves without treatment sequalea may be difficult to manage residual nodules may require resection; surgical debridement may be needed itraconazole or fluconazole for mild disease amphotericin B for more severe disease

Answer 84

infection generally confided to lungs probably transmitted by the airborne route with asymptomatic infection common usually just causes symptoms in immunocompromised individuals (it's an AIDS defining illness) ex. pneumocystis carinii

Answer 85

diffuse interstitial pneumonia = cough, fever, dyspnea extrapulmonary manifestations rare

Answer 86

recovery of the organism (induced sputum or BAL) with identification through silver stains or NAATs CXR will show whispy "ground glass" infiltrates

Answer 87

Bactrim +/- steroids for hypoxia (paO2 <70) or pentamidine if sulfa allergy

Answer 88

aspergilla A. fumigatus A. flavus A. terreus A niger

Answer 89

1. allergic reactions 2. bronchopulmonary disease after inhalation 3. cutaneous infections 4. disseminated disease

Answer 90

inhalation of spores relatively common BUT....disease/invasion relatively uncommon

Answer 91

if inhaled conidia begin to germinate into hyphae, they secrete cell wall components like beta-D-glucan and are then cleared by resident alveolar macrophages neutrophil recruitment and the activation of cellular immunity occurs and microbial clearance results

Answer 92

neutropenia, steroids, T-cell suppression (AIDS, organ transplant)

Answer 93

fungal elements gain access to the host via inhalation in lungs or sinuses; rarely via cutaneous or GI routes on histopathology, see vascular invasion with tissue necrosis/infarction --> fungal cell surface components bind to blood vessel wall components = angio-invasive!! classic presentation = fever, pleuritic chest pain, hemoptysis in a neutropenic patient you can also see other disease manifestations like tracheobronchitis in HIV, lung transplant patients and multi-organ system dissemination = skin, CNS, eyes, sinus (rhino-cerebral/rhino-ocular), liver, kidneys, CT scan: nodules with surrounding ground-glass infiltrates (the halo sign) = ring enhancing lesions

Answer 94

1. Culture/stains of clinical specimens | 2. Galactomannan, B-D-glucan assays

Answer 95

Voriconazole +/- an echinocandin +/- surgical debridement

Answer 96

aspergilloma is a clump of mold which exists in a body cavity such as a paranasal sinus or an organ such as the lung caused by aspergillus genus so people with TB or Klebsiella are susceptible because they have cavities in their lungs that could easily be colonized by aspergillus aka fungus ball

Answer 97

when pre-existing pulmonary cavity (from old TB, COPD, etc) gets colonized with Aspergillus spp fungal ball consists of hyphae, fibrin, mucus, debris within the cavity (usually A. fumigatus) asymptomatic aspergilloma usually refers to a single fungal ball with stable serial CXR appearance and no evidence of angio-invasion aka an aspergilloma

Answer 98

1. chronic cavitary pulmonary aspergillosis it's a subacute process that happens in immunocompetent hosts with expansion of pulmonary cavities without tissue invasion 2. chronic fibrosing pulmonary aspergillosis progression of chronic cavitary pulmonary aspergillosis with extensive fibrosis 3. chronic necrotizing pulmonary aspergillosis ICH with tissue invasion

Answer 99

symptom complex depends on degree of tissue invasion, expansion of the fungal ball, presence of other infections, host immune system symptoms = fever, cough, dyspnea, hemoptysis, fatigue/malaise, productive cough, chest pain

Answer 100

Radiologic evidence of rounded mass in a pulmonary cavity Aspergillus IgG + with or without + culture

Answer 101

treatment decisions are complex and depend on the host and the stage of disease options include the following, alone or in combination = observation, surgical resection, antifungal therapy

Answer 102

allergic bronchopulmonary aspergillosis

Answer 103

a type I hypersensitivity reaction to airway colonization with Aspergillus (usually fumigatus) it's seen in patients with underlying asthma or cystic fibrosis fungi do not invade the mucosa, but can trigger mucoid production/impaction --> this can lead to fibrosis and potential respiratory compromise clinically, can see recurrent asthma features, eosinophilic mucous plugs

Answer 104

no specific diagnostic criteria just suspect ABPA in the following setting: 1. history of asthma or CF 2. + IgE levels against Aspergillus fumigatus or + Aspergillus skin test 3. elevated serum IgE levels 4. CXR consistent with ABPA (eg, central bronchiectasis)

Answer 105

steroids and antifungal therapy (usually itraconazole)

Answer 106

1. Rhizopus* 2. Mucor* 3. Rhizomucor 4. Cunninghamella 5. Absidia mucormycosis is acquired when spores produced by the mold are inhaled or, much less commonly, when they enter the body through a cut or other break in the skin. The infection causes pain, fever, and sometimes cough and can destroy structures in the face

Answer 107

causes mucormycosis increased growth with high glucose, acidic conditions due to enzyme, ketone reductase (diabetics in DKA are at high risk for this fungus infection) serum from healthy individuals inhibits growth of Rhizopus but serum from individuals in diabetic ketoacidosis stimulates growth deferoxamine chelates iron and can be used to treat patients with iron overload BUT it increases fungal iron uptake = stimulates fungal growth and leads to tissue invasion

Answer 108

inhalation of spores with angioinvasion in the right clinical setting infarction of infected tissues is a hallmark of invasive disease orbital = pussy eyelid with necrosis; literally looks like a dying eyeball so gross cutaneous = bad purple black bruise spot rhinocerebral = black necrotic looking nose

Answer 109

a chronic subcutaneous fungal infection of the skin/soft tissue after inoculation of spores usually in the lower extremity (foot) from a thorn or splinter slow, painless growth of lesions swelling, sinus tracts, discharge of ‘grains’ from the sinus tracts (clusters of organisms) --> may extend over time into muscle, bone, and lymphatic vessels/can have secondary bacterial infections legit looks like a super swollen foot with pussy blisters all over

Answer 110

treatment is prolonged antifungal therapy (often itraconazole) with adjuvant surgery

Answer 111

a chronic, indolent infection of the skin caused by cutaneous inoculation of spores from ‘black molds’ starts as erythematous papules with slow growth to large verrucal lesions can be associated with tissue fibrosis, lymphedema, squamous cell carcinoma diagnosis is confirmed by finding muriform cells on biopsy

Answer 112

treatment by surgical removal, long-term antifungal therapy, usually with itraconazole

Answer 113

fungal infections of the skin, hair, nails the fungi metabolize keratin in the skin, hair, and nails may have itching if on the skin or hair, often annular, may have erythema, occasionally scattered vesicle ex. tinea pedis = athletes foot ex. tinea cruris = groin = jock itch ex. tinea unguium = fungal toenails ex. tinea capitis = scalp

Answer 114

1. Trichophyton spp* 2. Microsporum spp, 3. Epidermophyton spp they're dermatophytes that all live on the skin

Answer 115

clinical appearance, KOH scapings, culture

Answer 116

topical antifungal agents azoles!

Answer 117

1. superficial disease (immunocompetent hosts) 2. disseminated infection occurs in patients with prolonged neutropenia /T-cell immunodeficiency /bone marrow transplant patients with severe graft-versus-host disease you'll see cutaneous lesions and positive blood cultures -- may have lung or sinus involvement uniformly fatal in neutropenic patients with disseminated disease

ICL 4.1-4.3: Mycology Flashcards

(142 cards)