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Microbiology Exam 2 > Intro to Fungi > Flashcards

Intro to Fungi Flashcards

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1
Q

What is mycosis?

A
  • a fungal infection in or on part of the body

- a disease caused by a fungus

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2
Q

Fungus: any of numerous ________ organisms in the kingdom Fungi which lack ______ and __________ and range in form from a single cell to a body mass of branched filamentous ________ that often produce specialized ___________. The kingdom includes ______, ______, and ________.

A
  • eukaryotic: have nuclei, usual organelles
  • chlorophyll and vascular tissue
  • hyphae
  • fruiting bodies
  • yeasts (unicellular). molds (multicellular) and smuts (fungal disease of flowering plants, and mushrooms)
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3
Q

Discuss fungi cell wall and membrane

A
  • rigid cell wall composed on chitin and glucan, NOT peptidoglycan like bacteria
  • cell membrane has ergosterol instead of cholesterol!!
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4
Q

Are bacteria or fungi larger? Who replicates faster?

A
  • fungi

- grow slower than bacteria which follows suite of their size

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5
Q

Describe yeast

A
  • unicellular
  • oval shaped or round
  • reproduce by budding or fission
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6
Q

Describe molds

A
  • multicellular
  • threadlike structures called hyphae** may be separated by septae
  • make spores
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7
Q

Describe dimorphic

A

-exist as mold in nature, but yeast in animals

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8
Q

All fungi can reproduce _________. Give examples.

A
  • asexually
  • molds release spores
  • yeast undergo binary fission
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9
Q

2 types of hyphae and which lifestyle of mold are hyphae associated with?

A
  • mold

- septated or coenocytic hyphae (hollow and multinucleated)

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10
Q

Where do molds grow or elongate? How do they “spread their seed”?

A
  • at their tips via apical extension
  • produce spores (conidia or sporangispores) that are easily airborne and germinate on suitable substrates giving rise to new hyphae
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11
Q

3 common ways to diagnose fungal infections in the lab

A
  1. culture of organism: most sensitive but takes time**
  2. direct microscopic examination: not sensitive, but fast (gram vs. silver stain)***
  3. Serologic testing for capsular polysaccharide for cryptococcus
    * * no molecular tests**
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12
Q

3 targets of antifungal therapy

A
  1. cell membrane: ergosterol vs. cholesterol
  2. DNA synthesis: compounds selectively activated by fungi and arrest DNA synthesis
  3. Cell wall
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13
Q

2 categories of antifungal drugs that act on cell membrane

A
  1. polyene antibiotics

2. azole antifungals

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14
Q

2 drugs that are polyebe antibiotics and what these drugs target

A
  1. Amphotericin B
  2. Nystatin (topical)
    * *target fungal cell wall by binding preferentially to ergosterol and forming ion channels that destroy osmotic integrity**
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15
Q

Amphotericin B: activity; fungicidal vs fungistatic; resistance; how it’s administered; side effects; alternative treatments; common uses

A
  • very broad activity, but poor penetration of joints and CNS
  • fungicidal since it forms pore
  • some resistance seen due to reduced levels of ergosterol in fungal membrane
  • administered IV
  • Very toxic: nephrotoxicity; fevers, chills, myalgias; hypotension; bronchospasm
  • can take lipid formulations that have less side effects but much more expensive
  • tends to be used for systemic and opportunistic mycoses
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16
Q

6 azole antifungals and which is most commonly used

A
  1. Ketoconazole
  2. Itraconazole
  3. Fluconazole**
  4. Voriconazole
  5. Miconazole. 6. Clotrimazole (and other topicals)
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17
Q

Compare mechanism of action between polyenes and azoles

A

-polyenes bind directly to ergosterol while azoles prevent its synthesis (indirect)

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18
Q

Enzyme targeted by azole drugs and what side effects are seen and why?

A
  • azoles bind lanosterol 14a-demethylase inhibiting production of ergosterol
  • some cross-reactivity seen with mammalian cytochrome p450 enzymes
  • drug interactions and hepatotoxicity: impairment of steroidneogenesis
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19
Q

Are triazoles funastatic or fungicidal?

A

-fungostatic

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20
Q

2 most commonly prescribed azole drugs and their similarities and differences

A

-fluconazole and voriconazole
-both can be given orally or via IV, both have good absorption
F: used against Candida, Cryptococcus, Histoplasma, Coccidioides, NOT Aspergillus
V: primary treatment for invasive Aspergillus

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21
Q

Category and drug that act on fungal cell wall

A
  • Echinocandins

- Caspofungin is most important drug

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22
Q

Enzymatic target of Echinocandins; are they fungostatic or fungicidal?

A
  • inhibit B1,3 glucan synthesis (polymer of glucose)

- damage to the cell wall results in osmotic fragility thus they tend to be fungicidal

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23
Q

Caspofungin: how is it administered? What is it used for? Common side effects?

A
  • IV only
  • used for invasive candidiasis or invasive aspergillosis refractory to other therapies
  • side effects are infusion related: IV site irritation; fever, headache, rash, flushing, erythema due to infusion; symptoms consistent with histamine release–usually not bad enough to be discontinued
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24
Q

Category and drug of antifungal therapy that is DNA synthesis inhibitors

A
  • Pyrimidine analogues

- Flucytosine

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25
Q

Flucytosine: mechanism, resistance, and side effects

A
  • actively transported across fungal membrane where it is converted to 5-flurouracil by cytosine deaminase; further modified and inhibits thymidylate synthase
  • resistance arised readily
  • side effects with prolonged use: bone marrow suppression, hair loss, abnormal LFTs
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26
Q

Most fungal pathogens do NOT require a host to complete their lifecycles and infections are NOT _______.

A

-communicable

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27
Q

What are the fungi that naturally inhabit the human body?

A
  • dermatophytes that cause cutaneous infections

- candida sp.

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28
Q

What are true fungal pathogens and what are the 2 examples of them?

A
  • fungi that can cause infection in normal hosts
  • they are distributed in a predictable geographical pattern
  • Histoplasmosis (Ohio Valley Fever)
  • Coccidiomycosis (San Joaquin Valley Fever)
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29
Q

All fungal pathogens, aside from the true pathogens, are _______.

A

-opportunistic

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30
Q

Pathogenesis of fungi: portals of entry; virulence factors; how our body gets rid of them

A
  • primary mycoses: respiratory portal; inhaled spores
  • subcutaneous: innoculated skin; trauma
  • Cutaneous and superficial: contamination of skin surface
  • VF: thermal dimorphism, toxins, capsules and adhesion factors, hydrolytic enzymes, inflammatory stimulants
  • antifungal defenses are integrity of barriers and respiratory cilia
  • most important defenses are cell-mediated immunity, phagocytosis, and inflammation
31
Q

4 different patterns of mycoses infections

A
  1. superficial: affect skin, hair, nails; ringwork, jock itch, athlete’s foot
  2. Subcuteanous mycoses (tropical): affect muscles and CT immediately below skin
  3. Systemic (invasive) mycoses: involve internal organs; due to primary or opportunistic in immunocompromised
  4. allergic mycoses: affect lungs or sinuses; patients may have chronic asthma, CF, or sinusitis
32
Q

2 primary (true) fungal pathogens

A
  1. histoplasma capsulatum
  2. coccidiodes immitis
    * both dimorphic*
33
Q

What causes Histoplasmosis: Ohio Valley Fever? Describe this pathogen.

A
  • Histoplasma capsulatum: most common true fungal pathogen
  • dimorphic
  • produce conidia (spores) that are inhaled
  • ONLY intracellular fungus
34
Q

Distribution and growing conditions of Histoplasma sp.

A
  • worldwide but most prevalent in eastern and central US

- grows in moist soil high in nitrogen content: associated with bird and bat droppings which have high N2

35
Q

Histoplasma pathogenesis

A
  • inhalation of spores from disturbed soil
  • spores germinate to yeast in lung
  • may stay localized or spread via lymphatics within monocytes
  • intensity of exposure and immune status are important determinants of pathogenesis
  • seen in MACROPHAGES, causes granulomatous inflammation
  • reactivation in immunocompromised
36
Q

What cells is Histoplasma seen in and what type of inflammation does this cause?

A
  • macrophages

- granulomatous inflammation

37
Q

Clinical Presentations of Histoplasma

A
  • Acute: typically acute, self-limited fu-like syndrome and recover in 1-2 weeks
  • rarely progressive pulmonary develops with cavitary fibrosis
  • can sometimes cause chronic disease and like TB can remain in lungs and be reactivated later; forms granulomas but unlike TB, are not caseating; diffuse
  • disseminated hematogenous spread can present with overwhelming shock, disseminated intravascular coagulation, respiratory distress, and high mortality
38
Q

Histoplasma lab diagnosis

A
  • microscopic/histologic identification of intracellular yeast
  • culture can take 2-3 weeks
  • urine antigen to polysaccharide antigen (best if disseminated)
39
Q

Treatment of Histoplasma

A
  • usually self-limited so don’t treat
  • Amphotericin for acute disease
  • Long-term Itraconazole for immune compromised, such as AIDS patients
40
Q

What causes Coccidiomycocis: Valley Fever? Describe the pathology and transmittance of pathogen.

A
  • Coccidiodes immitis
  • block-like arthroconidia in the free-living stage and spherules containing endospores in the lungs
  • spherules rupture and release spores which starts process again
  • arthrospores inhaled from dust, creates spherules and nodules in lung
41
Q

What environments and regions is Coccidioides found?

A
  • alkaline soils in semiarid, hot climates

- endemic to SW U.S.

42
Q

Coccidiomycosis symptomatic vs. asymptomatic

A
  • 60% asymptomatic
  • reportable disease in CA
  • if symptoms, typically self-limited, flu-like
  • 1% get disseminated disease
43
Q

Clinical presentation of Coccidiomycosis

A
  • determined by degree of dust exposure
  • Valley Fever is self-limited: 7-21 days after exposure develop cough, fever, joint pain; somtimes get hemoptysis or erythema nodusum (painful nodules on shins); can see eosinophilia
  • chest film shows infiltrates with lymphadenopathy; diffuse nodules may be seen and are a more specific finding
  • disseminated disease is rare and may involve almost any organ, esp. meninges if untreated
44
Q

Immunity and Coccidiomycosis

A

-infection confers immunity and a positive skin test

45
Q

Coccidiomycosis Diagnosis and treatment

A
  • often missed bc nonspecific symptoms
  • Sputum culture (takes weeks, lab hazard)
  • Microscopic: look for spherules in tissue/sputum
  • self limited infection= no tx
  • disseminated disease or patients with risk factors get Amphotericin B plus an Azole, treat with Azole for a year
46
Q

What is the most important and frequent opportunistic pathogen?

A

-Candida albicans aka Candidiasis

47
Q

Morphology of Candida

A

-yeast, but can form hyphae so not uncommon to see both in clinical specimens

48
Q

Why is culture of Candida difficult?

A

-frequently found as normal flora in mouth, gut- makes culture interpretation difficult

49
Q

Candida is the 4th most common _________. What is its associated mortality?

A
  • bloodstream infection
  • 35% mortality
  • Candida in the blood is NEVER just a contaminant, always a pathogen
50
Q

Generally describe the variability of Candida albicans infections

A
  • can be short-lived, superficial skin irritations to overwhelming, fatal systemic diseases involving any organ
  • *local or systemic**
51
Q

Superficial infections due to Candida albicans

A
  • accounts for 80% of nosocomial fungal infections and 30% of deaths from nosocomial infections
  • Thrush: thick, white adherent growth on mucous membranes of mouth and throat
  • Vulvovaginal yeast infection: painful inflammatory condition of female genital region that causes ulceration and whitish discharge
  • Esophageal candidiasis
52
Q

Risk factors, typical clinical features, and treatment of Candida albicans invasive infections

A
  • RF: immunosuppression, neutropenia, IV catheters, TPN, antibiotics, surgery
  • CF: fever (even on Abx), skin lesions, retinitis, endocarditis, microabscesses in any organ
  • Tx with Fluconazole or Amphotericin B
53
Q

How can on tell is abscess is from cancer or infection?

A

-inflammated, red rim if from infection, not cancer

54
Q

What causes Cryptococcosis? Describe its morphology

A
  • Cryptococcus neoformans
  • widespread encapsulated yeast that inhabits soil and is enriched around pigeon roosts
  • oval cells surrounded by halo which is polysaccharide capsule
55
Q

What patients commonly get Cryptococcosis?

A

-AIDS, cancer, or diabetes

56
Q

How is Cryptococcus neoformans transmitted and clinically present?

A
  • organisms is inhaled and amount of inoculum is important
  • often relatively asymptomatic or with nonspecific symptoms
  • infection of lungs leads to cough, fever, and lung nodules
  • can spread via blood to most any organ, but the brain and meninges are favorite targets
57
Q

What is a favorite target of disseminating Cryptococcus? What are these conditions called?

A
  • brain and meninges
  • Cryptococcal meningitis/encephalitis
  • can be fatal
58
Q

Cryptococcal meningitis/encephalitis: who gets it? what are symptoms and outcomes?

A
  • most often in AIDS patients with CD4<50
  • high burden or organisms or poor inflammatory response
  • indolent meningitis:stiff neck, photophobia uncommon
  • initial exam unimpressive, but can progress to mental status changes, visual, hearing, CN findings
  • can be chronic, but invariably fatal if not treated
59
Q

Cryptococcus diagnosis and treatment: what is method of choice?

A
  • direct microscopic examination: india ink preps of CSF
  • detection of cryptococcal antigen is method of choice
  • systemic infection: Amphotericin B and flucytosine for 2 wks, thenby 8 weeks fluconazole
  • AIDS patients can take fluconazole as prophylaxis
60
Q

What is the method of choice for Cryptococcus and what is it looking for?

A

-detection of cryptococcal antigen of polysaccharide capsule that breaks off

61
Q

What is the first opportunistic infection recognized in AIDS patients?

A
  • Pneumocystis pneumonia

- infection only in immunocompromised

62
Q

What does X ray of Pneumocystic pneumonia look like? What causes it? What life forms does it have? How do you treat it?

A
  • diffuse, bilateral infiltrates; looks more like viral than bacterial pneumonia
  • Pneumocystic jiroveci
  • trophozoites and cysts
  • treat with bactrim
63
Q

If you stained Pneumocystic with silver stain, what would you see?

A

-the cysts

64
Q

Aspergillus is a ubiquitous _________ fungus. It can cause _________.

A
  • airborne soil

- allergic hypersensitivity

65
Q

Aspergillis morphology

A
  • mold

- acutely branching hyphae with septae with fruiting bodies

66
Q

Differentiate Aspergillis from Mucor

A
  • A: mold with acutely branching, SEPTATED hyphae with fruiting bodies
  • M: mold with NON-SEPTATED hyphae, with right angle branching
67
Q

Where does Aspergillus infect usually? What if it is invasive?

A
  • usually infects lungs; can colonize sinuses, ear canals, eyelids, and conjunctiva
  • invasive: produce necrotic pneumonia and infection of brain, heart, and other organs
68
Q

Aspergillus spores germinate and form ________. What are these? Why are they a tx obstacle?

A
  • fungal balls/aspergilloma
  • noninvasive fungus balls in a cavity
  • usually seen with preexisting lung disease like sarcoid or TB
  • often asymptomatic, can cause hemoptysis, chest pain, SOB
  • drugs are ineffective bc cannot access fungi, so need resection is hemoptysis (expel blood in sputum)
69
Q

Invasive Aspergillosis

A
  • very destructibe
  • angioinvasive, leading to infarction and necrosis
  • lung infection is most common but can spread elsewhere
  • early diagnosis is essential bc high mortality
70
Q

How does one diagnose invasive aspergillosis? Treatments?

A
  • tissue needed to visualize fungus bc culture is usually not effective
  • Amphotericin and Voriconazole
71
Q

Cutaneous mycoses are infections strictly confinded to what area and why? What is their common name? Natural reservoirs?

A
  • keratinized epidermis
  • fungi feed on keratin
  • ring worm
  • humans, animals, soil
72
Q

Cutaneous mycosal infections are facilitated by ____________. They usually have a long infection period followed by?

A
  • moist, chafed skin

- localized inflammation and allergic reactions to fungal proteins

73
Q

Cutaneous mycoses: infections elicit what response type and what is the result of this? How does one indicate site? KOH preps show what? How does one treat this?

A
  • cellular response leading to inflammed, outward spreading lesions
  • Tinea + modifier indicate sites
  • branching, septate hyphae seen on KOH preps
  • Topical azole antifungals, nystatin
74
Q

Dermamycoses are caused by fungi that are ______ and _______.

A

-closely related and morphologically similar

Microbiology Exam 2 (11 decks)

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