Endemic Mycoses Flashcards
(20 cards)
difference between dimorphic fungi and other fungi.
Dimorphic fungi exist as mold in environment and transform to yeast in human host
Describe how endemic mycoses are acquired.
- 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
Histoplasmosis mode of transmission
- 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.,
Histoplasmosis pathogenesis
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
Histoplasmosis Clinical Manifestations
-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.
Histoplasmosis Diagnostic Tools
- 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
Histoplasmosis Treatment
- Primary self-limited: none
- Moderate disease: Itraconazole
- Severe disease: Amphotericin B
- HIV pts may require lifelong suppressive Rx
Blastomycosis Mode of transmission
- 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
Blastomycosis Pathogenesis
- Inhalation of conidia into alveoli.
- Organisms change to the yeast form in the lungs.
- Multiply by budding.
- Hematogenous dissemination may occur before immunity develops.
Blastomycosis Clinical Presentation
-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
Blastomycosis Diagnostic Tools
- Histopathology
- Culture: colonization not believed to occur, so any culture + for Blastomycosis is considered pathogenic.
- Serology not particularly helpful for clinical diagnosis (poor specificity)
Blastomycosis Treatment
Mild disease: itraconazole
Severe disease: amphotericin B
Coccidioidomycosis Mode of Transmission and Pathogenesis
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
Coccidioidomycosis Clinical Presentationi
-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
Coccidioidomycosis Diagnostic Tools
- Direct microscopic evaluation of sputum or tissue
- Culture at 25°C (tell lab b/c v infectious)
- Serology (rising titers are bad prognostic sign)
Coccidioidomycosis Treatment
- Mild to moderate disease: fluconazole or itraconazole
- Severe: amphotericin B
Paracoccidioidomycosis Mode of Transmission
Mode of Transmission
-inhalation or traumatic inoculation of spores from soil
Pathogenesis:
Paracoccidioidomycosis Clinical Manifestations
- usually asymptomatic
- acute, subacute, or chronic pneumonia
- disseminated: lymphadenopathy, organomegaly, and bone marrow involvement
- chronic mucocutaneous ulcers
- meningitis
Paracoccidioidomycosis Diagnostic tools
- direct microscopy
- tissue biopsy
- culture
Paracoccidioidomycosis Treatment
- itraconazole is usual Rx
- amphotericin B for very severe cases
- TMP/SMX suppression in HIV+ pts
