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CP Board Review - Microbiology > Mycology > Flashcards

Mycology Flashcards

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1
Q

Introduction – The Fungi

A

 Among the most abundant and widely
distributed of all organisms.
 ~ 1.5 million named and unnamed species,
2nd only to insects.
 All people continuously exposed to large
numbers of fungi.
 Only 12-15 fungi commonly cause serious
human diseases
– illustrates the effectiveness of our host
defenses.
 Serious fungal infections have increased
markedly in frequency in recent decades

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2
Q

The Rise of the Fungi

A

7th cause of deaths - rising

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3
Q

Basic characteristics

A 
 Eukaryotic (membrane-bound nucleus,
complex organelles)
 Energy and nutrition - parasitic or
saprophytic.
 Reproduce by budding, fission or spore
formation
 Cell walls (polysaccharide and
glycoproteins).
 Principal cell wall sterol is ergosterol
 Can grow as yeast-like cells or as molds.
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4
Q

Traditional Classification

A

 Zygomycetes (Rhizopus, Mucor, Absidia, Basidiobolus)
 Ascomycetes (Histoplasma, Blastomyces, some Candida)
 Basidiomycetes (Cryptococcus)
 Deuteromycetes (most pathogenic Candida species, pathogenic
Aspergillus species, Coccidioides)

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5
Q

Morphologic Classification

A

 yeast (Candida, Cryptococcus)
 molds (Aspergillus, Zygomycetes, many others).
 dimorphic fungi (Histoplasma, Blastomyces, Coccidioides, Paracoccidioides, Sporothrix)

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6
Q

Diagnosis of Fungal Diseases

A

 Culture causative fungus.
 Microscopic morphology
 Demonstrate specific host immune response
 Demonstrate fungal antigen(s)
 Demonstrate fungal nucleic acid sequence(s)
 Demonstrate distinctive fungal metabolite(s)

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7
Q

Culture

A 
 Culture
– Yeast-like fungi (Candida spp. and related)
 grow on routine bacterial media
– Filamentous fungi (molds)
 may grow on routine media
 should be cultured on mycologic media for
optimum recovery
 special requirements (M. furfur)
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8
Q

Mycologic Media

A

 Culture media for primary isolation): a
selective & non-selective agars, that can
include:
– Sabouraud’s glucose agar (SAB), non-selective
– Selective SAB, with chloramphenicol
– Selective SAB, with chloramphenicol plus
cycloheximide (Actidione)
– Blood Brain Heart Infusion (BBHI), non-selective
– BBHI with gentamicin (G) & chloramphenicol (C)
– Selective BBHI with G, C & Actidione
 Usually incubated at 30oC
– For possible dimorphs sub at 37 to convert to yeast

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9
Q

CanWe Do Fungal Blood Cultures?

A

 Yes!
 90% of the time looking for yeast fungemia;
usually from a urinary source
– Conventional blood culture is perfectly adequate
– Some conventional systems are insensitive for Cryptococcus
 Occasionally looking for fungemia with a mold or dimorph; Aspergillus, Fusarium,
Histoplasma.
– Special culture procedures
– Biphasic bottle
– Lysis-centrifugation (Isolator) system

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10
Q

Microscopy

A

 Microscopy
– budding yeast or mycelia are often
evident on Gram stains

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11
Q

Histopatholological stains

A

 GMS (Gomori/Grocott Methenamine Silver)
– Cell walls stain black, but so can collagen fibers, RBCs, etc.
Staining pattern plus morphology are indispensable.
 PAS (Periodic Acid Schiff)
– Cell walls stain pink/red. Other carbohydrate material & small lipid droplets may also take up the stain.
 Mucicarmine (Mayer’s or Southgate’s)
– Used to demonstrate the capsular material of C. neoformans, which stains pink/red. There are hypocapsular, or (rarely) acapsular isolates of C. neoformans
 H&E or tissue Gram stains most fungi, although some stain faintly. Not always dependable!

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12
Q

Host antibody responses

A 
 More useful in endemic than opportunistic mycoses
 Cross-reactions between fungi very
common
 Recombinant fungal protein antigens
may be useful
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13
Q

Diagnostically-useful fungal antigens

A 
 Commonly Used
– Cryptococcus neoformans galactoxylomannan
–Histoplasma capsulatum surface antigens
 Used in specific/complex situations
– Candida albicans enolase
– Aspergillus fumigatus galactomannan.
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14
Q

Outline

A

Molds; Aspergillus, the zygomycetes,
and others
 Yeasts; Candida and Cryptococcus
 Dimorphic and endemic fungal infections

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15
Q

Aspergillosis: Microbiology

A

 Pathogenic species
– A. fumigatus
– A. flavus
– A. niger
 Common features
– narrow septate hyphae that branch at 30-
45 degrees in tissue (acute-angle branching)
– produce asexual spores in environment and in cultures, but not in mammalian tissues

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16
Q

Aspergillosis: Epidemiology/ecology

A

 Ubiquitous environmental saprophytes (dust, soil, on plants, etc).
– Everyone is exposed to spores every day.
 Disease when natural defenses break down.
– Neutropenia or phagocyte dysfunction (eg, CGD) is the key risk factor for invasive aspergillosis.
– T-cell immunity is less important.
– Environment influences incidence -  with filtered air, increase with construction and demolition.

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17
Q

Aspergillosis Allergic Bronchopulmonary

Disease

A 
 hypersensitivity leads to allergic pneumonitis or allergic bronchopulmonary
aspergillosis (ABPA).
 allergic aspergillosis
– bronchospasm
– fleeting pulmonary infiltrates
– tends to be chronic or recurrent
 refractory asthma
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18
Q

Aspergillosis Pulmonary colonization

A 
 saprophytic colonization - usually no
symptoms, but hemoptysis can result
from local invasion
 saprophytic colonization of preexisting
lung lesions > superficial invasion >
hemoptysis
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19
Q

Invasive Aspergillosis

A

 Invasive aspergillosis:
– infection via inhalation of airborne spores.
– spores survive and germinate (produce hyphae) if local phagocytes are absent or dysfunctional.
– hyphae invade locally and spread via blood vessels.
– dissemination to distant organs via bloodstream.
– vascular invasion and occlusion produces extensive tissue necrosis and infarction.
 Pulmonary
 Sinusitis
 Other and disseminated disease

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20
Q

Aspergillosis Diagnosis

A

 Diagnosis is difficult
 Cultures
– blood negative, even with disseminated
disease
– sputum/respiratory - colonization vs invasion
 Biopsy & microscopy - KOH of fresh tissue or histopathology
 Antibody testing seldom useful
 Immunologic detection of cell surface antigens
– Galactomannan test becoming more
available, often used for screening at-risk
patients
 PCR of rDNA
sequences in blood and/or bronchial fluids
 All limited in availability and data to support use
 MORPHOLOGY

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21
Q

Aspergillus fumigatus

A 
 The most common pathogen
 A. fumigatus has a dark-green colony
 Flask-shaped vesicle with conidia swept
away from stalk 
 Single row of phialides (uniseriate)
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22
Q

Aspergillus flavus & niger

A 
 A. flavus
– Biseriate
– Yellow colony
– Phialides surround vesicle
 A. niger
– White base with densely black conidia
– Dark, rough conidia
 Also potential pathogens
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23
Q

Mucormycosis (Zygomycosis) Microbiology

A 
 Pathogenic species -- Zygomycetes
– Rhizopus sp.
–Mucor sp.
– Absidia sp.
 Common properties
– broad, aseptate hyphae, branching at
90 degrees in tissue
– produce sexual and asexual spores in
the environment and in cultures, but not
in mammalian tissues.
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24
Q

Mucormycosis Epidemiology/ecology

A

 Ubiquitous environmental molds (decaying
organic matter, fruits, etc).
 People are regularly exposed to spores of
these fungi.
 Disease develops when natural defenses are deficient. Major risk factors include:
– diabetic ketoacidosis, other metabolic acidoses (eg, uremia)
– organ transplantation and abnormal CMI
– neutropenia
– burns
– iron chelation therapy

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25
Q

Mucormycosis Rhinocerebral

A

 Rhinocerebral
– rapidly progressive necrotizing pansinusitis
– spreads into cranium via blood vessels if
untreated.
– can disseminate to distant sites via bloodstream

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26
Q

Mucormycosis Pulmonary and other

A

 Pulmonary
– necrotizing pneumonitis with secondary blood vessel invasion, thrombosis & infarction
– Dissemination to distant organs is common
 Cutaneous
– complication of extensive burns or other wounds
 Gastrointestinal (rare)
– invasion of gastrointestinal mucosa in malnourished children in developing countries.

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27
Q

Mucormycosis - Diagnosis

A

 Cultures often negative, even in
specimens containing visible fungal forms
 Direct microscopy
(KOH preps or histology) is most important diagnostic modality.
 No reliable serologic tests for antibodies or
antigens, no DNA tests at this time.

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28
Q

Zygomycetes in Culture

A

 Wooly, rapidlygrowing mold

 Large, distinctive sporangium

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29
Q

Mucormycosis - Treatment

A 
 Multiple treatment modalities are
essential
– correct underlying host defense
abnormality
– surgical debridement/removal of necrotic
tissues is essential
– amphotericin B, ? Newer azoles
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30
Q

Other Important Molds

A

 Pseudallescheria boydii, Penicillium marneffei, Fusarium spp. can all
cause invasive disease in compromised hosts
 A variety of fungi (the dermatophytes)
cause skin infections
 Many rare/unusual syndromes caused by a
variety of organisms

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31
Q

Fusarium

A

 Opportunistic pathogen, esp in
neutropenic patients
 Common in fungal keratitis
 Most commonly F. solani complex
 Fusiform macroconidia; microconidia produced as well
 Fluffy, white or colored colonies in culture

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32
Q

Dermatophyte infections

A 
 Taenia whatever…
– Capitis; head and hair
– Corporis, cruris, pedis; skin of body, groin, or feet
 Onychomycosis – nail infections
 Three major genera
– Trichophyton
– Epidermophyton
– Microsporum
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33
Q

Trichophyton

A

 Colonies
– Slow to moderately rapid growth
– Waxy, glabrous to cottony.
– Front, white to bright yellowish beige or red violet.
– Reverse pale, yellowish, brown, or reddish-brown
 Microscopic
– Microconidia, macroconidia, and arthroconidia
 Miroconidia numerous; onecelled and round or pyriform in shape.
 Macroconidia are multicellular smooth-walled and cylindrical, clavate or cigar-shaped.
Produced in very few numbers or not at all.

34
Q

Epidermophyton

A

 Colonies
– Grow moderately rapidly (10d or so)
– Front: brownish yellow to olive gray or khaki
– Reverse: orange to brown with an occasional yellow border.
– Flat and grainy initially; then radially grooved and velvety.
 Microconidia are typically absent.
 Macroconidia (10-40 x 6-12 μm), thin walled, 3- to 5- celled, smooth, and clavate-shaped with rounded ends

35
Q

Microsporum

A

 Colonies
– Glabrous, downy, wooly or powdery.
– Growth variable
– Color varies depending on the species
 Front: white to beige or yellow to cinnamon.
 Reverse: yellow to red-brown.
 Microconidia
– Unicellular, solitary, oval to clavate in shape, smooth, hyaline and thin-walled.
 Macroconidia
– hyaline, echinulate to roughened, thin- to thickwalled, typically fusiform and multicellular, often with an annular frill.

36
Q

The Dermatophytes Compared

A

 Trichophyton differs from Microsporum and
Epidermophyton by having cylindrical, clavate to cigar-shaped, thin-walled
or thick-walled, smooth macroconidia.
 Epidermophyton is differentiated from
Microsporum and Trichophyton by the
absence of microconidia.
 Microsporum differs from Trichophyton and
Epidermophyton by having spindle-shaped
macroconidia with echinulate to rough walls

37
Q

Candidiasis Microbiology

A 
– Causative agents
Candida albicans
Candida tropicalis
Candida parapsilosis
Candida glabrata
Candida krusei
 Others
– Properties
 All yeast-like fungi that reproduce by
budding
 All except C. glabrata also produce
pseudohyphae and/or true hyphae.
38
Q

Candidiasis Epidemiology/ecology

A 
 Most Candida species colonize normal
humans
– C. albicans, C. tropicalis and C. glabrata
- GI and female GU tract
– C. parapsilosis and others - skin
 Some also present in soil, plant
matter.
 High carriage on skin of HCW
 Disease occurs when normal host defenses break down
 Skin and mucosal barriers
 Cell-mediated immunity
 Granulocytes
 Person-to-person transmission can
occur,
 Frequency of serious Candida infections increased >10-fold from 1980-89
39
Q

Candidiasis
Clinical and pathologic features –
Thrush and esophageal disease

A 
 Skin and mucosal surfaces involved when
CMI is abnormal
– ulcerations with surrounding inflammation
– thrush
– esophagitis
– gastrointestinal ulcers
 Usually C. albicans
 HIV infection, inhaled steroids
40
Q

Candidiasis

Clinical and pathologic features, other mucosal disease

A

 Vaginitis – a common disease
– Edema, pruritis, thick discharge (sometimes thin or scanty)
– Extension to vulva/perineum common
– Diabetes, antibiotic therapy, pregnancy
– ?Oral contraceptives
– 75% lifetime incidence, some with no identifiable risk
– Local or systemic azole therapies
– KOH prep to diagnose – office procedure
 Diaper rash
 Skin & nail infections

41
Q

Candidiasis
Clinical and pathologic features –
Organ system and nosocomial

A 
 Urinary tract infections
– Most common with Foley catheters
 Intravenous catheterrelated infections
 Pneumonia quite rare, but a frequent
colonizer
42
Q

Candidiasis

Clinical and pathologic features – disseminated disease

A 
 Hematogenous infections
– no characteristic syndrome, depends on
organ or organs involved and host’s
ability to respond
 Some species tend to attack particular hosts (eg, C. glabrata in diabetics, C. tropicalis in neutropenic patients)
 Blood cultures may be negative; repeated
cultures and empiric therapy in at-risk
patients
43
Q

Candidiasis Diagnosis

A

 Culture (blood cultures may be neg in patients with disseminated infection)
 Direct microscopy (yeast and/or
pseudohyphae demonstrable by KOH
preparation, Gram stain, histology)
 Antibody responses seldom useful.
 Immunologic detection of distinctive antigens, PCR rarely used.

44
Q

Candidiasis

A

 The germ tube test
– Grow yeast in serum 2h
– Separates C. albicans and other Candida
species
 C. albicans is generally fluconazole susceptible
 Other Candida include species with a higher frequency of resistance.

45
Q

Candida Species – ID

A

 Biochemical tests
– API, others
 Correlate to morphology on cornmeal
agar

46
Q

Candida albicans

A

 Budding spherical to ovoid blastoconidia

47
Q

Candida glabrata

A

 No pseudohyphae – also seen with
Cryptococcus, but capsule usually evident as
space surrounding cell for Crypto.

48
Q

Candida parapsilosis

A

 Short, curving pseudohyphae with round to

oval blastoconidia

49
Q

Candida tropicalis

A

 Multibranched pseudohyphae, blastoconidia borne singly or in chains from along pseudohyphae

50
Q

Candida lusitaniae

A

 Short, curved pseudohyphae with

blastoconidia at or between septae

51
Q

Candida krusei

A

 Branching pseudohyphae with elongated

blastoconidia

52
Q

Candidiasis Treatment

A

 azoles (fluconazole, ketoconazole,
itraconazole),
– Resistance in C. glabrata and C. krusei
 Caspofungin & other echinocandins
 amphotericin B
 Some Candida species resistant to specific
antifungals (e.g. C. lusitaniae & Ampho B)
– Susceptibility testing increasingly important
 Germ tube test used for C. albicans
– C. albicans most common pathogen, usually susceptible to all agents

53
Q

Cryptococcosis Microbiology

A

 Cryptococcus neoformans
 Properties
– budding yeast-like cells in culture and in tissues
– polysaccharide capsule
– ‘perfect’ stage - Filobasidiella neoformans
– 2 varieties: neoformans and gattii

54
Q

Cryptococcosis Epidemiology/ecology

A

 worldwide distribution
 var. neoformans associated with pigeon
droppings and soil.
 var. gattii associated with Eucalyptus trees
in Australia and Southern California;
current epidemic evolving in British Columbia and Pacific Northwest
 >80% of infections in people with serious
abnormalities of cell-mediated immunity
(eg, AIDS, transplantation, others).

55
Q

Cryptococcosis Clinical manifestations

A 
 pulmonary (self-limited or progressive)
 CNS (subacute - chronic) meningitis or
meningoencephalitis, mass lesions rare
 extraneural disseminated disease
(skin, bone, etc)
56
Q

Cryptococcosis Diagnosis

A

 Culture
 Direct microscopy (India ink, Gram stain)
 Test for polysaccharide antigen.

57
Q

Cryptococcal Histopathology

A

 Mucicarmine +
• Purulent, granulomatous or inert inflam. reaction
• If granulomatous, could be either caseating or “sarcoid” type granulomas

58
Q

Malasessia furfur

A

 A lipophilic yeast associated with catherter
infections, typically in neonates on extended
courses of parenteral lipid.
– Also seen in adults with severe immunocompromise
 Fever, signs of sepsis, catheter blockage.
 Diagnosis requires lipid in culture; alert lab.
 Treated by catheter removal and D/C lipids
if possible.

59
Q

Sporotrichosis Microbiology & Epidemiology

A 
 Sporothrix schenckii
– dimorphic (hyphae at ambient temp,
round to cigar-shaped yeast at 37C and
in tissues
– natural habitat: soil and plant matter
–Worldwide distribution
– Most frequent in gardeners or others
exposed to plant material.
60
Q

Sporotrichosis Pathogenesis and clinical

features

A

 Pathogenesis
– inoculation via trauma (thorns or splinters
common) > local inflammation > spread
via lymphatics
– Clinical and pathologic features
 lymphocutaneous disease in normal hosts
 extracutaneous (bone, lung, meninges)
 disseminated disease in compromised hosts (rare).

61
Q

Sporotrichosis Diagnosis and treatment

A 
 Diagnosis
– culture
– microscopy of aspirates or biopsy
 Treatment
– iodides
– amphotericin B
– ?azoles.
62
Q

Sporothrix in Culture

A

 Black mold with ‘florettes’ of conidia

63
Q

Histoplasmosis

A 
 Histoplasma capsulatum
– dimorphic (hyphae at ambient to 30 degrees C; small budding yeast at 37 degrees C and in tissues)
– present in soil (especially if heavy
bird or bat droppings) throughout the
world
– prevalence highest in Midwestern USA.
64
Q

Histoplasmosis Pulmonary Disease

A

 Most infections are asymptomatic
 M:F 4:1
 Primary pulmonary infection
– usually self-limited
– severe diffuse pneumonia with large inoculum
 Chronic pulmonary infection
– Histoplasmoma
– Cavitary (resembles TB)
– Mediastinal fibrosis
 Disseminated (primary or recrudescent infection)
– severe and rapidly progressive in AIDS patients, other immunocompromised
hosts and infants
 Fever, malaise, anemia, hepatosplenomegaly
– subacute but progressive in normal adults (mucosal ulcerations common); more common in older patients
 GI, CV, CNS involvement
 Histoplasmomas

65
Q

Histoplasmosis Diagnosis

A

 culture (may take 2-4 weeks)
 direct microscopy (tissue sections, periph blood)
– epithelioid granulomas, tuberculoid, caseating
– can also produce noncaseating granulomas
– old histoplasmomas (“fibrocaseous or
fibrocalcific lesions”): yeasts dead or dying
 skin testing (epidemiology only)
 serum antibodies (CF or ID to H or M antigens)
 immunoassay for antigens in urine, serum, CSF.

66
Q

Histoplasma capsulatum at 30C:

A

fluffy mold with TUBERCULATED MACROCONIDIA (spiny large spores)

67
Q

Histoplasma capsulatum at 37C

A

dry, coral-like colony with small budding yeasts, 2-4 uM, narrow neck

68
Q

Leishmania vs. Histoplasma

A

Leishmania Discrete organisms with nucleus and kinetoplast PAS(-)

Histoplama Yeast, often budding Parent and bud not within a discrete membrane PAS(+)

69
Q

Blastomycosis (North American)

A 
 Blastomyces dermatitidis
– dimorphic fungus: hyphae at ambient to
30 degrees C highly refractile yeast with broad-based budding at 37 degrees C or in
tissues
– soil fungus in Eastern US and Africa
– M:F ratio approx 10:1.
70
Q

Blastomycosis Pathogenesis

A

 Infection is by inhalation
– Pulmonary disease most common
– Dissemination via bloodstream
 Control via specific T-cell mediated
immunity, but little increase in frequency or severity in patients with CMI deficiency
 Histopathology - acute inflammation and granuloma formation.

71
Q

Blastomycosis - Clinical manifestations

A 
 Pulmonary - progressive pneumonia, can be severe
 Extrapulmonary - necrotic skin ulcers
most common
– Subcutaneous nodules
– also bones, joints and other organs.
– GU disease in men
72
Q

Blastomycosis Diagnosis

A

Diagnosis
– culture sputum, skin lesion, etc (may take 2- 4 weeks)
– look for broad-based budding yeast by
microscopy (stained sections or KOH preps)
– antibodies to crude B. dermatitidis antigens cross-react with other fungi, but antibodies to recombinant protein
antigen (WI-1) are specific – not widely
available

73
Q

Blastomyces morphology

A

 Microbiology Culture at 30°C:
– Fluffy, white-buff mold, “prickly stage”
– Pear-shaped (“pyriform”) conidia, resembles Chrysosporium, P. boydii. “Lollipops”.
 Convert to yeast – broad-based budding is more diagnostic

74
Q

Coccidioidomycosis (Valley Fever)

A

 Coccidioides immitis
– dimorphic fungus hyphae that produce
arthrospores at ambient to 30 degrees C
endosporulating spherules in tissues
– Soil fungus in lower Sonoran life zone (California, Texas, Arizona, Baja Calif, etc)
– Variable acquisition rates depending on weather, earthquakes, etc.
– most dangerous fungus in laboratory.

75
Q

Coccidioidomycosis

A

 Pulmonary
– Most cases are asymptomatic
– Symptomatic pneumonia occurs
 usually self-limited
 can progress to severe necrotizing/cavitary pneumonia
 Extrapulmonary
– more likely if CMI is abnormal (AIDS, imunosuppressive drugs, pregnancy) and in African-Americans and Filipino racial groups
– many tissues can be involved, including bones, joints, kidneys, meninges
– hypersensitivity reactions (Erythema nodosum in 5%)

76
Q

Coccidioidomycosis Diagnosis

A

 culture sputum, material from extrapulmonary lesions, etc BE CAREFUL!
 demonstrate spherules by histology
 skin test (negative in disseminated disease)
 antibody tests (high titers of serum antibodies in progressive or disseminated
disease, antibodies disappear with effective therapy)

77
Q

Coccidiomycosis in Culture

A

 Fluffy white mold

 Thick-walled barrel-shaped hyphae

78
Q

Coccidioides Histopathology

A
  • Thick-walled spherules (10-80 μM, ave. 50 μM), with endospores; look for all stages of development in acute lesions, & fragmented spherules in old lesions
  • Granulomatous inflamm., with caseation. Pyogenic Rx at areas where endospores are discharged
  • Fibrocaseous/fibrocalcific coccidioidomas with calcification
79
Q

Penicillium marneffii

A

 Endemic to SE Asia
 Causes disease in HIV-infected patients.
– Pulmonary, disseminated, and cutaneous disease
– Found in blood and bone marrow in
disseminated disease
 Yeast phase in tissue with cross-wall in a
single cell.
 Colony with diffusible orange pigment

80
Q

Paracoccidioidomycosis (S. American blastomycosis)

A 
 Paracoccidioides brasiliensis
– dimorphic fungus hyphae at ambient to 30 degrees C large yeast with multiple buds at 37 degrees C
– Central and S. America only
 ? soil or plants
 more cases in rural than urban areas.
81
Q

Paracoccidiodomycosis Pathogenesis & Clinical Manifestations

A

 Pathogenesis - little is known except
that T-cell immunity is important for
control and that lesions are granulomatous
 Clinical manifestations - pulmonary, lymph
nodes, skin, oral mucosal lesions most common

82
Q

Paracoccidiodomycosis Diagnosis

A 
 Culture
– Slow, white-buff fluffy mold
– Pyriform conidia, like B. dermatidis
or P. boydii (thus, like Blasto at 30C:
not fully pathognomonic)
 Direct microscopy 
– yeast form with multiple buds
– Also seen in culture at 37 degrees C

CP Board Review - Microbiology (6 decks)

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