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Dipendra ShresthaKDCH
Histoplasma capsulatum
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CHARACTERISTICS (CONT.)
Dimorphic fungus Mycelium at 25-30º C - Sexual multi-cellular
saprophyte, septate, form microconidia and macroconidia
Yeast at 37º C - Asexual unicellular intracellular parasite, white, thin walled, oval
Mycelial form is most commonly found in the environment
Reservoir is soil enriched with droppings of birds or bats
Human, many domestic animals, bats are infected by ingestion of spores 2
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PATHOGENESIS
Infection begins with inhalation of microconidia or hyphal fragments
Mycelial form transforms into yeast form Triggered by elevated temperatures and
increased cysteine levels
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PATHOGENESIS (CONT.)
Yeast cells are phagocytized by host immune system
H. capsulatum is able to survive phagocytosis Apoptosis of infected macrophages allow H.
capsulatum to spread Infection is usually self-limiting in
immunocompetent individuals, Cell mediated immunity arises in 15 days
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HISTOPLASMOSIS 2 major forms of histoplasmosis
Pulmonary and disseminated
Pulmonary histoplasmosis Conidia or mycelial fragments are inhaled and
lodge on the mucous membranes of the respiratory tree or in the alveoli of the lungs, where they encounter macrophages and are phagocytosed.
Form lesions in lungs nodes The patient may feel fever, chest pains, a
general ill feeling, and a dry cough. Distinct patterns may be seen on a chest x-ray. Chronic lung disease resembles tuberculosis and
can worsen over months or years.
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PULMONARY HISTOPLASMOSIS
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PULMONARY HISTOPLASMOSIS
Chronic pulmonary histoplasmosis (1/100,000)pre-existing structural lung
defect, i.e. COPD, emphysema (damage of alveoli resulting less O2 supply)
chronic pneumonia or infection in cavities, increased sputum
reactivation or reinfectionMediastinal granulomatosis and fibrosis
Fibrosis, occlusion of mediastinal structure
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PULMONARY HISTOPLASMOSIS
Chronic fibrocavitary histoplasmosis
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MEDIASTINAL GRANULOMATOSIS
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DISSEMINATED HISTOPLASMOSIS
Occurs primarily in immunocompromised individuals where H. capsulatum is able to spread from the lungs into other organs
Patients display fever, malaise, and occasionally petechiae or skin lesions (cutaneous histoplasmosis)
Tests often reveal mucous membrane ulcerations, simultaneous enlargement of the liver and spleen, and enlarged lymph nodes
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DISSEMINATED HISTOPLASMOSIS (CONT.)
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DISSEMINATED HISTOPLASMOSIS (CONT.)
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Defects in host immunity Infants, immuncompromised, HIV
Acute, subacute, chronicFailure of macrophages to kill fungusDiffuse spread throughout MPS
Oropharyngeal ulcers Hepatosplenomegaly Adrenal GI Endocarditis Meningitis Brain abscess Lymphadenopathy Coagulopathy Bone marrow suppression (pancytopenia)
PROGRESSIVE DISSEMINATED HISTOPLASMOSIS
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ORAL HISTOPLASMOSIS
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DIAGNOSIS
1. Obtain appropriate specimenssputum bone marrowblood lesion scrapingsurine biopsy specimens
2. Direct Examination Tissue Specimens
stains for fungi – Giemsa, Wrightroutine histology - H & E- small yeast (2-4 ) intracellular in
macrophages- Sputum - KOH or calcofluor
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BLOOD THIN SMEAR
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CALCOFLUOR STAIN X400
Narrow-neck bud
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H&E MOUTH BIOPSY
Yeast in macrophages
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GIEMSA STAINING OF LUNG BIOPSY
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HISTOPLASMOSIS (DIAGNOSIS CONT.)
3. CultureSabouraud’s agar with cycloheximide and cholramphenicol, 25º C for 2-6 weeks give white cottony mycelium
White - brown mould
Typical microscopic morphology
Mould at RT in SDA
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MICROSCOPIC MORPHOLOGY
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MICROSCOPIC MORPHOLOGY
macroconidia and microconidia
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HYPHAL TO YEAST CONVERSION AT 37ºC
Yeast-like colonies
Yeast cells
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DIAGNOSIS (CONT.)
Histoplasmin Skin testCulture filtrate (histoplasmin) is inoculated
to observe cell mediated immunity. Serology
Complement fixation test Precipitation and agglutination
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TREATMENT
Treatment is not required in most cases Itraconazole and/or amphotericin B in more
serious cases No effective treatment for fibrosing
mediastinitis
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Itraconazole
Amphotericin B