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Multisystems > Micro- Opportunistic Mycoses in AIDS > Flashcards

Micro- Opportunistic Mycoses in AIDS Flashcards

1
Q

What is the difference between primary and secondary prophylaxis?

A

Primary = antibiotic given prior to the onset of infection to vulnerable patients to prevent infection from developing

Secondary = antibiotic given AFTER a patient has developed an infection to prevent recurrence. [can be discontinued if immunosuppression is reversed.

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2
Q

Is Candida a yeast, mold or dimorphic fungi?
How do they appear in culture and in blood?
How do they look in tissue?

How quickly does it grow?
What does it look like with gram stain?

A

Candida grows solely as yeast form in culture.

In blood and culture :
3-5micron oval budding cells

In tissue:
branching pseudohyphae [incomplete separation of daughter yeast from mother cell yeast]

It grows rapidly [24-48hrs]
It stains G+ but is differentiated from bacteria by its size [5-10x larger]

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3
Q

What is the natural niche of Candida?

A

It is part of the normal flora of all humans and lives on:

  1. mucous membranes of GI tract and vagina
  2. moist intertriginous areas of axilla, groin, breasts
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4
Q

Candida usually causes mucosal infection. Invasive disease [candidemia and invasive candidiasis] are rare EXCEPT for what situations?
What negative sequelae arises when candida disseminates?

A
  1. central catheters
  2. foreign devices
  3. invasive procedures

Hematogenous embolic spread can lead to blindness as the result of endophthalmitis

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5
Q

Candidiasis occurs most commonly in AIDS patients with a CD4 count below what?

A

200

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6
Q

An AIDS patient with CD4 count below 200 presents with creamy, white curd-like patches on the tongue and oral mucosa that can be scraped off. What is this called?
What organism is responsible?
What other clinical manifestation is this person likely to have?

A

Thrush [oropharyngeal candidiasis] caused by Candida yeast infections.

Thrush is almost universally present in patients with esophageal candidiasis.

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7
Q

What are the 3 most common symptoms of esophageal candidiasis?

A
  1. odynophagia [pain swallowing]
  2. dysphagia [difficulty swallowing]
  3. retrosternal chest pain
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8
Q

How do you diagnose oropharyngeal/esophageal candidiasis?

A
  1. clinical presentation [presence of thrush; odynophagia, dysphagia]
  2. scrape thrush and use KOH or gram stain to look for yeast
  3. upper GI endoscopy to confirm esophageal candidiasis and to exclude CMV, HSV esophagitis

*culture is NOT useful because candida is part of normal flora

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9
Q

What are the 3 main causes of odynophagia in HIV/AIDS patients?
How do you confirm diagnoses?

A
  1. esophageal candidiasis
  2. HSV
  3. CMV
    [sometimes VZV]

Confirm with upper GI endoscopy

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10
Q

How is disseminated Candidemia diagnosed?

A

Positive blood cultures

[low sensitivity 50-70%]

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11
Q

What is treatment for oropharyngeal/esophageal candidiasis?

A
  1. topical therapy with clotrimazole, imidazole, troches, Nystatin for oral disease only
  2. Fluconazole = First line for esophagitis
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12
Q

Which 2 candida strains are intrinsically resistant to fluconazole?

Who does resistance normally occur in?
What are the 2 main reasons?
Why has resistance to fluconazole been going DOWN?

A

Resistant occurs in advanced AIDS in patients who were previously given fluconazole due to:

  1. natural selection for fluconazole resistant strains of albicans
  2. intrinsic resistance of krusei [100%] or glabrata [10-50]

Resistance has been going down because:
HAART makes oropharyngeal candidiasis less common so drugs are used less, making selection pressure for fluconazole resistance decrease

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13
Q

What drugs can be used for fluconazole-resistant candida?

What are the drawbacks?

A
  1. intraconizole
    - capsule prep is poorly absorbed esp. with PPI/H2 blockers
    - swallow solution tastes terrible [poor compliance]
  2. echinocandins [caspofungin, micafungin, anidulafungin]
  3. amphotericin B
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14
Q

What is the treatment of choice for disseminated C. albicans infections?

A
  1. Fluconazole [1st choice]

Refractory:

  • echinocandins
  • voriconazole
  • amphotericin B
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15
Q

What is prevention for candidiasis?

A

HAART

*no antifungal prophylaxis is recommended

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16
Q

Is cryptococcus a yeast, mold or dimorphic fungus?
What is the structure?
How many days does it take to grow in culture?
What are the 2 main varieties important for human infections?
What are the 2 serotypes most common in AIDS patients?

A
  1. It is a yeast that has 4-6microns, round and has a polysaccharide capsule.
  2. 3-7 days to grow in culture
  3. neoformans, gatti
  4. A and D serotypes
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17
Q

What is the distribution of cryptococci regionally?
What is the niche?
What is the portal of entry into the human host?

A

It is worldwide

Niche = soil fertilized by pigeon/bird droppings

Portal of entry = lungs

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18
Q

What are the 2 major virulence factors of cryptococcus?

A
  1. polysaccharide capsule is antiphagocytic AND allows survival in macrophages
  2. Melanin
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19
Q

Cryptococcus infections are seen in AIDS patients with a CD4 count below what?

A

100

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20
Q

What are the 2 most serious clinical manifestations of cryptococcus?

A
  1. meningitis
    - worsening headaches/fever over weeks
    - NO photophobia or meningismus [like bacterial]
    - altered mental status
  2. pneumonia
    - asymptomatic OR
    - fever, chills, cough, SOB, lobar infiltrate OR
    - cryptococcoma = solitary pulmonary nodule in patients with HIGHER CD4 counts
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21
Q

Describe the CSF analysis for someone with cryptococcal meningitis.

A
  1. elevated or normal WBC with lymphocytic pleocytosis
    * more immunosuppressed = more normal WBC count
  2. Normal or decreased glucose
  3. Elevated protein [>1000]
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22
Q

For cryptococcal meningitis, what is the correlation between level of immunosuppression and WBC count?

A

More immunosuppressed will have a normal WBC count

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23
Q

For cryptococcal meningitis, what stain can give immediate diagnosis, but has low sensitivity and is rarely used in clinical practice anymore?

A

India ink

[you can also do gram stain because it is irregularly gram +]

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24
Q

What is the BEST test for cryptococcal meningitis and pneumonia?

A

Cryptococcal antigen in:

  1. CSF [95% sensitive]
  2. Serum [99% sensitive]

A positive blood titer in an immunocompromised person suggests dissemination to the lung even in absence of end-organ damage

For pneumonia, CXR with positive sputum confirms diagnosis.

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25
Q

What is the preferred initial treatment of cryptococcal meningitis?

A

Amphotericin B + flucytosine [5FC] for 14 day course followed by:
6-8 weeks of fluconazole

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26
Q

What is used as secondary prophylaxis for cryptococcal meningitis in patients with AIDS who have complete their amphotericin+ 5FC, fluconazole regimen? When should the prophylaxis be stopped?

A

fluconzole until CD4 count rises on HAART

27
Q

What are the 3 major toxicities of amphotericin B?

What is the major toxicity of 5-flucytosine?

A

Amphotericin B:

  1. renal toxicity/acute renal failure
  2. electrolyte abnormalities [hypo K and Mg]
  3. anemia

flucytosine:
1. bone marrow toxicity

28
Q

Why are echinocandins [caspofungin] NOT effective against cryptococcal meningitis?

A

Echinocandins act on the cell wall of fungi, but they cannot get to the cell wall due to crypto’s polysaccharide capsule

29
Q

What is the preferred treatment for severe cryptococcal pneumonia? Mild with no sign of cerebral disease?

A

Severe:
Amphotericin B

Mild symptoms, no evidence of cerebral disease:
High dose fluconazole

30
Q

What is prevention for cryptococcal meningitis?

A

Improving CD4 count via HAART

*antifungal prophylaxis is NOT recommended

31
Q

Is histoplasmosis yeast, mold or dimorphic fungi?
Describe its structure.
How long does it take to grow in culture?

A

Dimorphic:

25 degrees/soil = mould

37 degrees/body tissue = oval budding yeast [2x4micron] present intracellularly in phagocytic cells

It takes 4 weeks to grow in culture

32
Q

What is the common regional distribution of histoplasma?
What is the niche?
How does infection occur?

A

It is common in :
Ohio River Valley
SouthEAST
Northern/Eastern Texas

Niche is soil fertilized by bird/bat guano

Infection is by inhaling spores after aerolization. In endemic areas nearly everyone is infected.

33
Q

Histoplasma disseminated disease infections usually occurs when the CD4 count is below what?
Are infections usually primary, or due to reactivation?

A

CD4 below 100

It is usually a reactivation from a prior infection

34
Q

How does diffuse histoplasma infection present?

A
  1. fever, weight loss, weakness
  2. cough, SOB
  3. diffuse lymphadenopathy, pancytopenia
  4. miliary pattern on CXR
35
Q

What 2 dimorphic fungal infections can be difficult to distinguish from miliary TB on CXR?

What dimorphic fungal infection presents mimicing community acquired pneumonia?

A

Miliary:
Histoplasma
Coccidiodomycosis

Pneumonia:
Blastomycosis

36
Q

How is diagosis of disseminated histoplasmosis made?

A
  1. histo antigen urine test [95% sensitive]

2. cultured out of blood, stained with silver stain [GMS]

37
Q

How do diagnostic techniques differ for histo when the patient is immunocompetent vs. compromised?

A

Competent:
1. Fungal Ab Panel [not sensitive for disseminated]

Compromised:
1. Histo antigen urine test [ not sensitive for lung only]

38
Q
  1. What is the drug of choice for moderate to severe histoplasmosis?
  2. Mild to moderate / maintenance doses in relapse?
A
  1. amphotericin B

2. itroconzaole > fluconazole

39
Q

What is prevention for histoplasmosis disseminated infection?

A
  1. avoid travel to endemic areas
  2. HAART
  3. secondary prophylaxis with low CD4 and history of disseminated histo with itroconazole
40
Q

Is coccidioides immitis yeast, mould, or dimorphic?
Describe the structure.
How long does it take to grow in culture?
What is unique about this organisms growth?

A

Dimorphic:

25/soil = mould
37/body tissue = yeast “endosporulating spherules”

It grows in 5-10 days [much faster than histo]
It is EXTREMELY infectious so special precautions must be taken by lab personnel.

41
Q

What are the endemic regions of the US for coccidiodes?
What is the organisms niche?
When are they infectious?

A
  1. desert southWEST
  2. West Texas –> California
  3. Sonoran Life zone [border of mexico, US]

They grow in the soil. After rainy season or dust storms, the mycelia of mould form form arthroconidia which become aerolized and infectious.

42
Q

Patients with a CD4 count below ______ tend to have more severe disease and disseminated disease for coccidiodes.

A

100

43
Q

What are the 3 main features of disseminated disease for coccidioides infections in HIV patients?

A
  1. diffuse pneumonia [miliary]
  2. osteomyelitis
  3. meningitis
44
Q

What is the most useful/diagnostic method of choice for diagnosing coccidiomycosis?

A

Serology:

  1. immunodiffusion
  2. complement fixation [IgG] 1:32 is diagnostic for disseminated disease
    - eosinophilic pleocytosis

This is done to monitor progression of disease and is diagnostic for CSF in meningitis

45
Q

What is treatment of choice for coccidioides pneumonia?

Meningitis?

A

Pneumonia:

  1. amphotericin B for severe miliary
  2. fluconazole for lobar/mild pneumonia

Meningitis:
1. fluconazole for better CNS penetration

46
Q

What is unique about treatment of coccioides caused meningitis?

A

Life-long maintenance therapy with fluconazole is required for ALL patients regardless of HIV status

47
Q

What is prevention of coccidioides infection?

A
  1. avoid endemic areas/exposure

2. HAART

48
Q

Is blastomyces dermatitidis yeast, mold or dimorphic?

What is the structure?

A

Dimorphic:

25/soil = mold
37/ body tissue = Broad-Based Budding yeast with refractile walls

49
Q

What is the geographic distribution of blastomyces?

A
  1. southEAST/ southCENTRAL that border Mississippi
  2. ohio river
  3. GREAT LAKES
50
Q

What are the 2 ways initial infection with blasto can occur?

A
  1. inhalation of conidia into the lungs

2. direct inoculation through the skin

51
Q

What clinical syndromes are associated with people with AIDS and blastomycosis?

A
  1. Pulmonary
    - mimics community acquired pneumonia
    - chronic alveolar infiltrates, fibronodular infiltrates
  2. Extrapulmonary
    - Cutaneous
    - osteomyelitis
    - genitourinary disease
    - CNS disease [meningitis, mass lesions]
52
Q

How is blastomycosis diagnosis made in patients with pulmonary disease?
Disseminated disease?

A

Pulmonary Disease:

  1. cultured out of sputum
  2. KOH or PAP stain

Disseminated:
1. antigen testing for urine and blood

53
Q

What is the drawback of antigen testing of urine for diagnosing blasto?

A

cross-reactivity with histoplasma

54
Q

What is treatment for severe blastomycosis? Mild to moderate/prevention of relapse?

A

Amphotericin B = severe

Itroconazole = mild/moderate/relapse

55
Q

Is sporotrichosis yeast, mold or dimorphic?
Describe the structure.
How fast does it grow?

A

25/soil = mold

37/tissue = cigar shaped yeast [1-3x 3-10]

It grows in 1 to 2 weeks in culture

56
Q

What typically causes infection with sporotrichosis?

A
  1. Contact or traumatic injury with moss or thorny plants [roses]
  2. inhalation [rarely]
57
Q

What are the cutaneous manifestations of sporotrichosis?

A

Centripetal spread via lymphatics.

Red, painless papules that slowly enlarge and are violaceous.

58
Q

Disseminated disease with sporotrichosis occurs in patients with advanced AIDS. What is the mortality even WITH appropriate therapy?

A

70-90%

59
Q

What is diagnosis for sporotrichosis?

A

Culture

60
Q

What is treatment for sporotrichosis?

A

Itroconazole

[amphotericin B is reserved for severe/disseminated]

61
Q

What is prevention for sporotrichosis?

A
  1. avoid trauma with moss/roses and inhalation

2. HAART

62
Q

Is penicilliosis yeast, mold or dimorphic?
Describe the structure.
Where is it endemic?

A

Dimorphic:
25 = mold with finger-like projections that carry infectious spores, red pigment in culture
37 = yeast that is elongated with transverse septum

Endemic in Southeast Asia and Southern China.

63
Q

A patient presents with fever, chills, cough, hemoptysis, night sweats and weight loss.
He has lymphadenopathy, hepatosplenomegaly, and pancytopenia.
His skin and mucous membranes demonstrate umbilicated lesions.
You do a smear from lymph node biopsy and see extracellular elongated yeasts with transverse septums. You also see intracellular yeasts in phagocytes.
In culture, a soluble red pigment diffuses into the agar.

What is the pathogen?
What is treatment of choice? How long should maintenance therapy last?

A

Penicillium marneffei

Treatment is amphotericin B and maintenance should be for life.

Multisystems (29 decks)

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