Endemic Mycoses Flashcards

1
Q

difference between dimorphic fungi and other fungi.

A

Dimorphic fungi exist as mold in environment and transform to yeast in human host

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2
Q

Describe how endemic mycoses are acquired.

A
  • all acquired by inhalation of spores
  • specific geographic locations
  • acute and/or reactivation disease (reactivation may occur outside of area of endemicity)
  • ranges of disease severity: can cause serious disease in normal hosts
  • H. capsulatum, C. immitis, and P.marneffei are major opportunistic pathogens
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3
Q

Histoplasmosis mode of transmission

A
  • Mold lives well in soil with high nitrogen content - areas contaminated with bird or bat droppings
  • Disturbance of soil results in aerosolization of microconidia.
  • Outbreaks associated with soil disturbance.
  • exposure to caves and bird roosts
  • excavation and demolition of old buildings
  • Ohio and Mississippi river valleys of the U.S.,
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4
Q

Histoplasmosis pathogenesis

A

Spores -> Lungs -> yeast form -> into macrophages -> RES
-Multiply within macrophages
-Travel to hilar and mediastinal LNs
-Spread thru entire reticuloendothelial system (lungs, lymph nodes, liver, spleen, bone marrow)
2-3 weeks after infection develop cellular immunity.
-Macrophages become fungicidal
-Develop necrosis with fibrous encapsulation (granuloma)
-Calcium deposition and, within a few years, calcified granulomas
-small #s of yeast remain viable within granulomas and can cause relapses of disease

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5
Q

Histoplasmosis Clinical Manifestations

A

-most infected individuals are asymptomatic
Pulmonary syndromes
-Acute
-usually mild, self-limited illness (Sxs 10-14d after exposure)
-more severe after heavy inoculum
-fever, sweats, cough, occ HA and GI complaints
-diffuse pulmonary infiltrates, +/- hilar or mediastinal LNs
Subacute – presents over weeks
-fever, sweats, cough, weight loss
-hilar or mediastinal lymphadenopathy
-possible focal or patchy pulmonary infiltrates
Chronic – inability to clear the infection
- F, cough, sweats, weight loss
-interstitial or consolidative infiltrates
+/- bullae, +/- calcifications
Mediastinitis
-frequent complication of pulmonary histoplasmosis
-can lead to acute pericarditis and cardiac tampanode
Progressive disseminated histoplasmosis
-patients with compromised cell-mediated immunity and patients on TNFα inhibitors
-fever, wt loss, sweats
-hepatosplenomegaly and lymphadenopathy (but less than 50%)
-hematologic abnormalities due to bone marrow involvement
respiratory distress
-possible GI, adrenal, CNS, and mucosal involvement
-Consider histoplasmosis whenever TB is being considered.

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6
Q

Histoplasmosis Diagnostic Tools

A
  • Culture:
    • good:“gold standard”
    • bad: 2-4 weeks to get results; low sensitivity
  • Fungal stain
    • Good: rapid
    • Bad: low sensitivity
  • Serology:
    • Good: rapid, high sensitivity
    • Bad: false – (immunocompromised &1st few weeks after exposure); false + (cross-reacts other fungi)
    • can’t differentiate active vs prior infxn
  • Antigen:
    • Good: rapid
    • Bad: low sensitivity in localized dz
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7
Q

Histoplasmosis Treatment

A
  • Primary self-limited: none
  • Moderate disease: Itraconazole
  • Severe disease: Amphotericin B
  • HIV pts may require lifelong suppressive Rx
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8
Q

Blastomycosis Mode of transmission

A
  • Mold grows in soil and leaf litter.
  • Disturbance of soil results in release of spores.
  • Dogs are 10x more susceptible than humans.
  • history of a pet dog recently ill may be a clue to the diagnosis
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9
Q

Blastomycosis Pathogenesis

A
  • Inhalation of conidia into alveoli.
  • Organisms change to the yeast form in the lungs.
  • Multiply by budding.
  • Hematogenous dissemination may occur before immunity develops.
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10
Q

Blastomycosis Clinical Presentation

A

-Most cases probably asymptomatic/subclinical
-Most common clinical manifestations
1. pulmonary
2. cutaneous
3. bone
4. genitourinary
Pulmonary disease
-Acute pneumonia
-frequently presents as atypical pneumonia with alveolar
-infiltrates that doesn’t respond to usual antibioticss
-mass-like lesions frequently misdiagnosed as cancer
Subacute and chronic pneumonia
–fever, sweats, fatigue, weight loss
Radiology: varied
-alveolar infiltrate, mass-like lesion, multiple nodules
-lobar infiltrates, and cavitary lesions can be seen
Non-pulmonary manifestations of blastomycosis
-COMMON
1.cutaneous lesions: verrucous w/ raised border or ulcerative
2.GU tract infection – prostatitis and epididymoorchitis
3.osteomyelitis (up to ¼ of extra-pulmonary cases)
-LESS COMMON
-septic arthritis
-laryngeal and orpharyngeal nodules
-ocular infection
-meningitis
-intracerebral abscesses

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11
Q

Blastomycosis Diagnostic Tools

A
  • Histopathology
  • Culture: colonization not believed to occur, so any culture + for Blastomycosis is considered pathogenic.
  • Serology not particularly helpful for clinical diagnosis (poor specificity)
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12
Q

Blastomycosis Treatment

A

Mild disease: itraconazole

Severe disease: amphotericin B

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13
Q

Coccidioidomycosis Mode of Transmission and Pathogenesis

A

Mode of Transmission
-people acquire infection by breathing in arthrocondia

Pathogenesis

  • Fungus grows in sandy soils of southwest
  • Grows wing like chains caused Mycelia that allow it to become airborne
  • Living spores take flight w/ wind and other disturbances
  • Once airborne, spores are easily inhaled
  • In the lungs the spores become spherules that begin replicating and filling the lung
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14
Q

Coccidioidomycosis Clinical Presentationi

A

-A spectrum of disease: 50-70% of patients with asymptomatic infection
-Most common presentation: Self-limited pneumonia 1-3 wks after exposure
-Symptoms: fever, cough, chest pain, fatigue, shortness of breath, chills,
-muscle and joint aches, night sweats, weight loss
-these can last for several months.
-5-10% have persistent pulmonary symptoms
-develop residual pulmonary sequelae such as nodules or peripheral thin-walled cavities.
Eosinophilia in about 25% of patients
Extrapulmonary coccidioidomycosis
Dissemination to skin, bone, and meninges most common
Very uncommon in immunocompetent hosts
- 0.5% of infxns within persons of Caucasian ancestry

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15
Q

Coccidioidomycosis Diagnostic Tools

A
  • Direct microscopic evaluation of sputum or tissue
  • Culture at 25°C (tell lab b/c v infectious)
  • Serology (rising titers are bad prognostic sign)
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16
Q

Coccidioidomycosis Treatment

A
  • Mild to moderate disease: fluconazole or itraconazole

- Severe: amphotericin B

17
Q

Paracoccidioidomycosis Mode of Transmission

A

Mode of Transmission
-inhalation or traumatic inoculation of spores from soil

Pathogenesis:

18
Q

Paracoccidioidomycosis Clinical Manifestations

A
  • usually asymptomatic
  • acute, subacute, or chronic pneumonia
  • disseminated: lymphadenopathy, organomegaly, and bone marrow involvement
  • chronic mucocutaneous ulcers
  • meningitis
19
Q

Paracoccidioidomycosis Diagnostic tools

A
  • direct microscopy
  • tissue biopsy
  • culture
20
Q

Paracoccidioidomycosis Treatment

A
  • itraconazole is usual Rx
  • amphotericin B for very severe cases
  • TMP/SMX suppression in HIV+ pts