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Infectious Disease > Week 8 > Flashcards

Week 8 Flashcards

1
Q

3 yeasts

A

Candida
Cryptococcus
Pneumocystis

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2
Q

Hyaline Mould (1)

A

Aspergillus

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3
Q

Dimorphic fungus (6)

A 
Blastomyces
Histoplasma
Coccidioides
Candida
Sporothrix
Paracoccidioides
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4
Q

Mucorales (3)

A

Mucor, Rhizopus, Rhizomucor

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5
Q

Key features of fungi

A
  • Eukaryotic organisms
  • Consume oxygen via oxidative phosphorylation in mitochondria
  • Cell membrane and external cell wall
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6
Q

_______ makes up the cell wall of fungal membranes

2 enzymes important in the synthesis and drugs that mess with them

A

Ergosterol = major sterol of fungal cell membranes

Synthesis:
-Squalene epoxidase: squalene → oxidosqualene (targeted by allylamines)

-14 a-demethylase: lanosterol → ergosterol (targeted by azoles)

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7
Q

Polyenes

A

bind to synthesized ergosterol and disrupt interactions within cell membrane → increases membrane permeability

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8
Q

Fungal cell wall

A

external to cell membrane, made up of proteins and polysaccharides (mannan, glucan chitin)

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9
Q

Fungal cell wall contains _________ which interferes with DNA and RNA synthesis

A

cytosine deaminase

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10
Q

Mold

A

multicellular fungal colonies → HYPHAE = long tubular structures formed by multiple fungal cells lined up end to end
Hyphae grow towards a food source

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11
Q

Griseofulvin

A

inhibit fungal cell mitotic spindle → inhibition of mitosis and hyphae growth

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12
Q

Echinocandins

A

Glucan synthesized by 1,3 B-glucan synthase → inhibited by Echinocandins → cell wall instability

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13
Q

Yeast

A

single-celled fungus, replicate by budding

Pseudohyphae

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14
Q

Pseudohyphae

A

formed when buds fail to break off original yeast cell, forming long chains that resemble hyphae

present in yeast

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15
Q

Dimorphic fungi have what characteristics in the heat vs. cold?

A

mold in the cold, yeast in the heat (except Candida)

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16
Q 
Cryptococcus:
Main features (4)
A

Thick capsule, round
NOT dimorphic
Urease +
Yeast

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17
Q

Cryptococcus: Transmission

A

Transmission via inhalation - form soil and pigeon droppings

→ infect respiratory tract then disseminate hematogenously → localizes in CNS

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18
Q

Cryptococcus:

Host risk factors:

A

Opportunistic infection, but can cause disease occasionally in “normal” hosts
**AIDS
prolonged glucocorticoids, organ transplant, malignancy, sarcoid

**impaired cellular immunity*

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19
Q

Cryptococcus:

disease? (2)

A

1) Meningoencephalitis

2) Pulmonary cryptococcus

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20
Q

Meningoencephalitis

A

Due to hematogenous spread (typically from lungs)

Cryptococcus is NON INFLAMMATORY → many organisms, few PMNs→ obstruct CSF flow and increased intracranial pressure

Indolent course - 2 weeks of fever, malaise, headache

“Soap bubble” intraparenchymal lesions due to gelatinous pseudocysts that contain fungi

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21
Q

Pulmonary cryptococcus

A

asymptomatic or present with nonspecific symptoms (cough, hemoptysis, dyspnea, chest pain)

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22
Q

Cryptococcus:

Diagnosis (6)

A

1) Latex agglutination
2) India ink stain of CSF - shows polysaccharide capsule CLEAR under microscopy
3) Mucicarmine stain - specific for cryptococcus, appear pink
4) Culture on Sabouraud agar
5) Grows on Birdseed agar
6) CRAG = cryptococcal antigen test

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23
Q

cryptococcal antigen test (CRAG)

A

detects capsular polysaccharide
Highly sensitive, specific, cheap and fast

TEST OF CHOICE for cryptococcus

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24
Q

Treatment of cryptococcus

A

High mortality

Amphotericin B + Flucytosine (fungicidal) for meningitis + Fluconazole (fungistatic) for long term suppression in immunosuppressed patients

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25
Q

Cryptococcus: Appearance

A

narrow-based yeast with unequal budding

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26
Q

Cryptococcus:

Virulence factors (2)

A

Capsule: inhibits phagocytosis

Melanin: strains without melanin production can’t cause disease → contributes to NEUROTROPISM

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27
Q

Candida:

Main features:

A

Opportunistic dimorphic fungus

Grows as budding yeast cells, pseudohyphae, true hyphae or spores

Mold at 37C, yeast (pseudohyphae + budding yeast) at 20 C

Part of our normal flora - mucous membranes of respiratory, GI, and female genital tracts

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28
Q

Candida:

Host risk factors:

A

Intensive medical care (indwelling catheters), TPN, abdominal surgery, broad spectrum abx

Immunocompromised hosts (premature infants, neutropenia, chemotherapy)

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29
Q

Candida:

Treatment: (3)

A

1) Nystatin mouthwash and oral fluconazole → thrush and esophagitis
2) Topical azoles or oral fluconazole for vaginitis
3) Oral fluconazole or IV echinocandins for disseminated (can also use Amphotericin B)

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30
Q

Candida:

A

1) Oral thrush
2) Vaginitis
3) Cutaneous candidiasis
4) Immunocompromised disease

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31
Q

Cutaneous candidiasis

A

beefy red rash with satellite pustular lesions in moist intertriginous areas (e.g. diaper rash)

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32
Q

Candida Vaginitis

A

(itching, copious cottage cheese clumps)

-Normal vaginal pH (pH<4.5)

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33
Q

Candida in immunocompromised patients

A

Disseminated candidiasis (can lead to endocarditis)

Candidemia → visceral disease (EYE**, kidney, brain, lung, skin, etc.)

**Endophthalmitis: fungal infection of eye typically

Esophagitis

Significant problem for nosocomial bloodstream infections (via catheters)

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34
Q

Candida: Diagnosis (3)

A

Blood cultures
Germ tube test: POSITIVE test strongly indicative of Candida
1,3-Beta-D Glucan Test

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35
Q

1,3-Beta-D Glucan Test

A

antigen present in most fungal cell walls

Sensitive, NOT specific to candida

Only effective when applied to select patients

Cross reacts with other environmental factors

Can also be used to identify Aspergillus infection

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36
Q

Aspergillus fumigatus (Aspergillosis):

Main features:

A

Usually does not cause disease
Very common in the environment

NOT dimorphic - only occurs as a mold (mats of hyphae, not a single-celled yeast)

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37
Q

Aspergillus fumigatus produces what toxin?

A

Produces Aflatoxin → carcinogen that causes hepatocellular carcinoma (found in peanuts, rice, cereal, grains)

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38
Q

Aspergillus fumigatus

Host risk factors:

A

NEUTROPENIA (e.g AML**), prolonged glucocorticoid use, advanced HIV, CGD, abnormal lung (e.g. COPD, old cavitary lung disease)

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39
Q

Aspergillus fumigatus

Disease

A

1) Allergic bronchopulmonary aspergillosis
2) Aspergilloma
3) Invasive aspergillosis
4) Sino-orbital aspergillosis

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40
Q

Sino-orbital aspergillosis

A

can present identical to mucormycosis, but occurs in neutropenic hosts (not diabetics)

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41
Q

Aspergilloma

A

fungus ball that develops in preexisting cavity in the lung (old TB site)
Can invade blood vessels → massive hemoptysis

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42
Q

Allergic bronchopulmonary aspergillosis

A

IgE mediated type I/IV hypersensitivity reaction → eosinophilia → inflammation of airways, mucus plugs in terminal bronchioles

Typically in patients with asthma or CF

Repeated attaches can lead to bronchiectasis

TX: corticosteroids

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43
Q

Invasive aspergillosis

A

invasion of lung tissue and bloodstream in immunocompromised host

Can occlude blood vessels and lead to PULMONARY INFARCTION

Can occur in patients with CGD

TX: voriconazole (mild) and Amphotericin B (Severe)

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44
Q

Aspergillosis Appearance

A

Narrow septate hyphae with acutely angled (45 degree) branching → differentiate with Mucormycosis (wide angled 90 degree non-septate hyphae)

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45
Q

Diagnosis of Aspergillosis (3)

A

1) Direct microscopy showing narrow hyphae septate that branch at 45-degree angles
- Angioinvasion and necrosis prominent

Serologic tests:

2) Aspergillus galactomannan antigen
3) B-D-Glucan antigen test (same one used for candida)

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46
Q

Mucormycosis:

Main features:

A

Ubiquitous fungi (bread mold) - found nature on decaying vegetation and in the soil BUT human infection is rare

Non-septate hyphae with broad angle branching (90 degrees)

Germinate in nasal passages → invade and proliferate in blood vessel walls → penetrate cribriform plate → enter brain

Growth stimulated in presence of high glucose and acid

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47
Q

Mucormycosis

Appearance?

A

microscopic hyphae, broad, ribbon-like nonseptate with 90 degree branching

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48
Q

Mucormycosis: Host risks for infection (6)

A

1) Diabetes mellitus (particularly with ketoacidosis)
2) AIDS
3) Neutropenic
4) Immunosuppressed (e.g. glucocorticoids)
5) Use of deferoxamine (chelates iron and aluminum - acts as siderophore, enhances Rhizopus growth and pathogenicity)
6) Iron overload

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49
Q

Diseases caused by Mucormycosis? (2)

A

Rhinocerebral mucormycosis

Pulmonary mucormycosis

50
Q

Rhinocerebral mucormycosis

A

necrotic ulcer on palate, orbit invasion, extension to cavernous sinus and brain

Almost only happens in patients with diabetes

Can cause cavernous sinus thrombosis

Can move extremely quickly

51
Q

Pulmonary mucormycosis

A

can present as slowly progressive nodule (looks like cancer) in “normal” hosts or rapid onset in IC hosts

52
Q

Treatment of Mucormycosis?

A

surgical debridement and high dose antifungal therapy (amphotericin B)

EMERGENCY

Manage underlying problems

53
Q

Pneumocystis Jiroveci

Main features

A

Opportunistic fungi - cysts containing dark oval bodies on microscopy

Fungal organism that lacks ergosterol

Transmission through inhalation of cysts

54
Q

Pneumocystis Jiroveci

Host risk factors:

A

HIV, solid organ transplant, stem cell transplants, ALL, lymphomas, chronic glucocorticoids

55
Q

Pneumocystis Pneumonia (PCP)

A

seen in HIV patients with CD4 < 200

Asymptomatic in immunocompetent

56
Q

Pneumocystis Jiroveci

Diagnosis

A

1) Silver stain of: induced sputum, bronchoalveolar lavage, lung biopsy
2) CXR: diffuse, bilateral infiltrates extending from perihilar region, “ground glass”

57
Q

Pneumocystis Jiroveci

Treatment and prophylaxis?

A

TMP/SMX or pentamidine

Prophylaxis: TMP/SMX, dapsone, atovaquone

58
Q

Blastomyces Dermatitidis:

Location?

A

Mississippi and Ohio River basins

59
Q

Blastomyces Dermatitidis:

Main features?

A

Dimorphic fungi (mold in the cold, yeast in the heat)

**Broad based budding organism on wet smear

60
Q

Blastomyces Dermatitidis:

Transmission?

A

Transmitted via inhalation of spores (conidia) typically from moist soil
→ spores phagocytosed and brought to RES → converted to yeast in tissue → survive and infect

61
Q

Blastomyces Dermatitidis:

Disease (2)

A

Pulmonary blastomycosis

Extrapulmonary disseminated disease

62
Q

Pulmonary blastomycosis

A

Acute pneumonia (uncommon) or chronic pneumonia (most common)

Acute or chronic pneumonia → granulomas in lung

63
Q

Extrapulmonary disseminated disease

A

(skin, bones)

Skin = verrucous lesion with irregular borders (mimics squamous cell carcinoma)

Bone = osteomyelitis, soft tissue swelling, chronic draining sinus tract

64
Q

Blastomyces Dermatitidis:

Diagnosis

A

culture with visualization of broadly based budding yeast cells in clinical specimens

65
Q

Blastomyces Dermatitidis:

Treatment

A

azoles, or amphotericin B

66
Q

Coccidioidomycosis

Main features

A

Dimorphic fungi

Yeast→ Large spherule containing endospores at body temperature

Mold → barrel-shaped arthroconidia

67
Q

Coccidioidomycosis

Transmission

A

inhalation of spores after dust exposure (e.g. after earthquakes, archeological excavations, desert military maneuvers)

68
Q

Coccidioidomycosis

Disease (2)

A

Pulmonary coccidioidomycosis

Extrapulmonary disease

69
Q

Coccidioidomycosis

Location

A

desert regions of western hemisphere (Arizona, CA, NM, Texas)

70
Q

Coccidioidomycosis

Risk factors

A

occupation, ethnicity, immune status

71
Q

Coccidioidomycosis

Diagnosis (2)

A

1) Spherules + alternating arthroconidia

2) Serology: antibodies indicate active disease
Early = immunodiffusion
> 1 month = complement fixation
Can be used to follow if someone is responding to treatment or predict extrapulmonary disease

72
Q

Pulmonary coccidioidomycosis

A

→ nodule or granuloma formation, possible erythema nodosum

73
Q

Extrapulmonary disease

A

due to disseminated disease or direct inoculation

Skin or subcutaneous soft tissue

Meninges

Skeleton

74
Q

Paracoccidioidomycosis: paracoccidioides brasiliensis

Main features

A

Thermally dimorphic fungus

Large, round or oval yeast cell surrounded by multiple, attached, narrow-necked budding daughter yeast cells that resemble a CAPTAIN’S WHEEL

75
Q

paracoccidioides brasiliensis

Location

A

Central and South America

76
Q

paracoccidioides brasiliensis

disease

A

Typically causes asymptomatic pulmonary infection (dry cough, dyspnea, fibrosis)

Classic triad: edentulous, cervical lymphadenopathy, chronic pulmonary disease

Can cause painful ulcer i

77
Q

Histoplasmosis

Main features:

A

DIMORPHIC yeast: mold at ambient temperature (20C) and yeast at body temperature (37C)

Mold → yeast conversion occurs in phagosomes after phagocytosis by macrophages

Facultative intracellular yeast inside macrophages

Hyaline septate hyphae with spherical thick-walled conidia and smaller microconidia

78
Q

Histoplasmosis: Location

A

endemic to Ohio, Missouri, and Mississippi River valleys

Lives in soil near bird and bat droppings

79
Q

Pulmonary histoplasmosis

A

Immunocompetent → granulomas appear as calcifications on XR
Immunocompromised → no granuloma formation

“SHOTGUN PNEUMONIA” = characteristic of histoplasmosis

80
Q

histoplasmosis

diagnosis (2)

A

Takes a long time to grow → blood culture not effective

Antigen detection test (some cross-reactivity)

81
Q

Sporotrichosis: sporothrix schenckii

Main features

A

DIMORPHIC yeast

CIGAR-SHAPED

Unequal budding yeast (human tissue) and mold form (plants - typically ROSE THORNS)

82
Q

sporothrix schenckii

causes what disease? (4)

A

“Rose Gardener’s disease”

1) Primary nodule that becomes necrotic and ulcerates
- -> Forms granulomas made up of histiocytes and giant cells

2) Lymphocutaneous sporotrichosis
3) Pulmonary sporotrichosis
4) Disseminated sporotrichosis → joint, bone, lung meninges

83
Q

Treatment of sporothrix schenckii

A

itraconazole, oral potassium iodide

84
Q

MOA amphotericin

A

Polyene
Bind plasma sterols (ergosterol) and form membrane pores → leakage of electrolytes

Fungicidal

85
Q

Mechanism of fungal resistance to amphotericin

A

Fungi produces less ergosterol or have thicker membranes that don’t form pores as easily

86
Q

Spectrum of use of amphotericin (6)

A

broad spectrum antifungal reserved for fungal meningitis, and serious, systemic mycoses

Cryptococcus
Blastomyces
Coccidioides
Histoplasma
Candida
Mucor
87
Q

Pharmacokinetics of amphotericin

A
  1. NOT absorbed orally - IV only
  2. Good distribution but does NOT enter CSF or bone
  3. Liver and renal excretion
88
Q

Toxicities of amphotericin

A

“amphoterrible”
1. Infusion reaction - Fever/Chills, Hypotension
2. NEPHROTOXICITY
3. ANEMIA (decreased EPO synthesis due to nephrotoxicity)
4. ELECTROLYTE ABNORMALITIES (hypomagnesemia, hypokalemia,
hypocalcemia)
5. ARRHYTHMIAS (from hypokalemia)
6. IV PHLEBITIS
7. **Hydration can decrease nephrotoxicity
8. **K+ and Mg2+ should be supplemented due to alteration of renal
tubule permeability with amphotericin B

89
Q

MOA azoles

A

inhibit cytochrome P450 enzyme sterol
14-demethylase → block ergosterol production (essential for fungal plasma
membrane)
1. → hyperpermeability of fungal plasma membrane → cell lysis and
death
2. Typically fungistatic

90
Q

Mechanism of fungal resistance to azoles

A

resistance can develop rapidly with

mutations in targeted enzymes

91
Q

Azoles spectrum of use

A

local and less serious systemic fungal infections

aspergillosis, candidiasis, candidemia

92
Q

Two different subclasses of azoles

A
  1. Imidazoles

2. Triazoles

93
Q

Imidazoles

A

Ketoconazole : used for topical fungal infections, Cushing
syndrome (inhibit GC synthesis), Prostate cancer
(antiandrogenic)

Clotrimazole, Miconazole : topical agents used for cutaneous
fungal infections (e.g. pregnant women with vulvovaginitis)
94
Q

Triazoles

A

newer and safer
a. Fluconazole → used for chronic suppression of cryptococcal
meningitis in AIDS patients and candidal infections of all types
i. *Drug of choice for Cryptococcal meningitis and
Coccidioidal meningitis
ii. Orally available
iii. Distributes well (EVEN CSF)
iv. Renal excretion
v. Most frequently used -azole
b. Itraconazole → local blastomycosis, coccidiomycosis, and
histoplasmosis infections
c. Posaconazole, Voriconazole

95
Q

Azole toxicity

A
  1. Inhibition of P450 enzymes → many drug-drug interactions
  2. Inhibition of steroid synthesis ( gynecomastia )
  3. GI distress
  4. Hepatotoxicity → monitor liver function
  5. QT prolongation
  6. **Contraindicated in pregnancy = TERATOGENIC
96
Q

3 echinocandins

A

Caspofungin , Micafungin, Anidulafungin

97
Q

MOA echinocandins

A

inhibit fungal enzyme 1,3-B-D-glucan synthase →
prevent synthesis of B-glucan (part of fungal cell wall) → fungal cell loses
resistance to cell lysis → fungal cell death

98
Q

Echinocandins spectrum of use

A

Aspergillus and Candida species

  1. Caspofungin : used for RACE
    a. Refractory invasive aspergillosis
    b. Azole-Resistant Candida strains
    c. Candidemia
    d. Empiric treatment in febrile neutropenic patient
  2. Micafungin : used for candidemia, esophageal candidiasis, prophylaxis
    for patients undergoing hematopoietic stem cell transplant
  3. Anidulafungin : used for esophageal candidiasis and systemic Candida
    infections
99
Q

Echinocandins pharmacokinetics

A
  1. Metabolized by LIVER - DO NOT induce or inhibit CYP450

2. Given IV, not orally absorbed

100
Q

Host factors and echinocandins

A

Must change dosage if pt taking drugs that induces/inhibits

CYP450

101
Q

Toxicities of echinocandins (4)

A
  1. Infusion hypersensitivity reactions (histamine-mediated flushing and
    delirium, hypotension, bronchospasm, phlebitis
  2. GI symptoms
  3. Asymptomatic LFTs
  4. Fever
102
Q

MOA Flucytosine (5-FC)

A
  1. 5-FC metabolized to 5-FU in fungal cells by cytosine deaminase
  2. 5-FU inhibits fungal DNA and RNA synthesis selectively → less toxicity
    to humans
  3. Synergistic with amphotericin
103
Q

5-FC spectrum of use

A
  1. Systemic fungal infections in combination with amphotericin B (e.g.
    cryptococcal meningitis)
  2. Orally available, distributes in CSF
104
Q

Toxicities of 5-FC

A

Bone marrow suppression

105
Q

MOA terbinafine

A 
interferes with ergosterol synthesis by inhibiting
squalene epoxidase (fungicidal)
106
Q

Terbinafine spectrum of use

A

systemic treatment of superficial skin, hair,
and nail infections (NOT deep infections)
1. Not absorbed well orally, but accumulates in keratin precursor cells

107
Q

MOA griseofulvin

A

inhibits fungal growth by binding microtubules and
disrupting mitotic spindles
1. Human microtubules are less sensitive

108
Q

Griseofulvin spectrum of use

A

systemic treatment of “superficial’ skin, hair, and nail
infections (NOT deep infections)
1. Not absorbed well orally, but accumulates in keratin precursor cells

109
Q

Picornaviruses

Main features

A

Main features: icosahedral capsid, nonenveloped, linear (+)ssRNA

Acid STABLE → fecal-oral transmission → replicate in intestinal tract

110
Q

Picornaviruses

Replication

A

Replicate exclusively in cell CYTOPLASM - NO replication proteins in virus particles (only protein shell + ssRNA)

Contain protease that cleaves one large polypeptide into multiple functional viral proteins

111
Q

Picornaviruses include what 5 viruses

A

Poliovirus

Echovirus

Rhinovirus (NOT fecal oral, is fomit-hand or aerosol)

Coxsackie virus

Hepatitis A virus

112
Q

Immune response to picornavirus includes what two mechanisms?

what defines host serotypes?

A
  • IgA and IgG
  • Maternal antibodies

Epitopes on capsid proteins recognized by antibodies that neutralize infectivity DEFINE HOST SEROTYPES

113
Q

Picornavirus: Pathogenesis of infection:

A

Primary infection at mucosal surfaces → Viremia to infect target organs

Neutralizing IgM and IgG antibodies in the blood will block viremia

Neutralizing IgG antibodies block disease but will NOT block infection

IgA antibodies necessary at mucosal surfaces to block infection

114
Q

Poliovirus

causes what 4 possible diseases

A

1) Paralytic poliomyelitis
2) Non-paralytic poliomyelitis (aseptic meningitis)
3) Abortive poliomyelitis (sore throat, malaise) - minor URI
4) MOST individuals asymptomatic → can circulate unnoticed

115
Q

Paralytic poliomyelitis

A

Poliovirus destroys motor neurons in anterior horn → LMN disease (decreased DTRs, respiratory insufficiency)

116
Q

Poliovirus: Replication

A

poliovirus ingested → replicates in lymphatics of GI tract (e.g. Peyer patches) → viremia → enter CNS, cross BBB → aseptic meningitis or paralytic poliomyelitis

117
Q

Poliovirus:

Killed vaccine

A

SALK - only one used in USA because NO RISK for developing actual disease

Disadvantage: only IgG immunity, limited mucosal immunity

118
Q

Poliovirus:

Live (attenuated) vaccine

A

Live (attenuated) vaccine = SABIN
Taken orally, induces IgA (local) immunity

Virus shed in feces, providing group immunity with person-to-person contact

Used in developing countries

Can get vaccine associated paralytic poliomyelitis

**Do not want to give to anyone with B cell dysfunction

119
Q

Echoviruses:

2 diseases

A

aseptic meningitis and URI’s

120
Q

Coxsackie A:

6 diseases

A

Aseptic meningitis

Paralysis

URI’s

Herpangina (mouth blisters)

Acute hemorrhagic conjunctivitis

Hand-foot-and-mouth disease

121
Q

Coxsackie B: 7 diseases

A 
Aseptic meningitis
Paralysis
URI’s
Myocarditis (dilated cardiomyopathy)
Pericarditis
Bornholm disease
Hepatitis
122
Q

Hepatitis A:

transmission and disease

A

Transmission: fecal-oral
Disease: acute viral hepatitis

Infectious Disease (9 decks)

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