Bacteriology

Front 1

Major points:
Disease result of -
"classic" dimorphism =
Protective Host immune response -
Latency -
Determine exposure by -
Disease more severe when?
Transmission ISN'T -
Lab mold cultures -

Back 1

spore inhalation

Environmental form = mold
Tissue form = yeast or specialized

Cell mediated immunity - CD4 cells generated against fungus -> activate phagocytic cells -> macrophages activated to fuse and "wall off" fungi (granuloma formation) THEREFORE: immune compromised host may not wall off infection and fungi will spread

Infection may become latent and by the formation of granulomas (like TB)

DTH skin test

In the presence of HIV infection

transmission is NOT person to person

these cultures are very hazardous

Front 2

Histoplasma capsulatum
Clincal significance: (distribution, endemic areas, severity of infection)

Back 2

wide distrib - temperate, subtropical and tropical

highly endemic to Ohio and Mississippi valley regions

<1% become progressive and require therapy

Front 3

Pathogen Properties
growth:
structural characteristics:
Virulence factor:

Back 3

dimorphic growth - environment hyphal/mycelial form, infected tissue yeast form

Hyphae - septate, branching, spores (microconidia and macroconidia)
Yeast - ovoid, found within macrophages, capsular appearance is just an artifact of staining

Virulence - can grow inside macrophages, surviving in phagocytic vacuole

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Pathogenesis:

Back 4

Inhaled spores (micro) -> small brochioles or alveoli -> germinate after 2-3 days -> proliferate within macrophages -> migrate to mediastinal lymph nodes, spleen, liver -> prolif for 9-15 days -> onset host immune response

yeast usually found inside macrophages, can be found extracellularly and in epithelial cells

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Infections:

Back 5

Acute pulmonary histoplasmosis - in immunocompetent hosts

Disseminated histoplasmosis - rare and severe, found with AIDS

Chronic Pulmonary Histoplasmosis - opportunistic, often mistaken for tuberculosis

Colonization in abnormal pulmonary spaces - allowed by Lung structural defects

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Diagnosis:

Back 6

Histoplasmin skin test indicated exposure to organism, not necessarily infection

Fungal stain of tissue, ID in lab cultures on special media, demonstrated dimorphism and tissue form, exoantigen tests to demonstrate specific Ags to mycelial cultures
Wright stain blood smear - look for intracellular yeasts in macroph
Chest X-ray, CF test, sputum culture, wright stain of sputum contribute to diagnosis of chronic pulmonary histo

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Prevention:

Treatment:

Back 7

avoid envir exposure

antifungal therapy for disseminated disease

Front 8

Blastomyces dermatitidis

Clinical significance:

Back 8

mainly occurs as sporadic infection in immunocompromised hosts
Epidemics and cases noted in AIDS patients and immunocomp hosts
Cell-mediated immunity vital to control growth
Commonly infects dogs in endemic zones - severe or lethal

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Properties:
growth form

Back 9

Filamentous hyphae with aerial spores
Colonies appear cottony
Produced in lab cultures at room temp
Grows as yeast at 37C, smooth colonies
Single buds and broad base

Front 10

Pathogenesis:

Back 10

inhalation of spores from hyphae in soil -> Bad1 (blastomyces adhesin 1) promotes uptake by macrophages -> at 37C spores turn into yeast -> multiply in lung -> acute influenza-like pulmonary infection (may resolve or progress) -> yeasts disseminate via blood and lymph to visceral organs -> macrophages may carry yeast to other organs -> replicate in macrophages until they are activated by cytokines from T cells -> over several weeks, host develops acquired cell immunity (DTH appearance, T cell proliferation, circulating Abs) -> Cell med immunity leads to protection from infection

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Environmental distribution:

Risk factors:

Diagnosis:

Back 11

hard to ID because cross reactive DTH test with H. capsulatum - may be mississippi and ohio river basins and the carolinas

Recreationala activity in wooded areas

grows only in yeast form in host, detect with KOH mount or fungal stains of tissue
Also, immunodiffusion test for paitent Abs to A Ag produced from culture filtrates

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Coccidioides immitis
aka:
Clinical significance:

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Valley fever

40% infections - lower resp infection and/or systemic illness symptoms, lasts 2-6 weeks
Small # cases progress to chronic pulmonary form (*cavity formation)
Disseminated disease - more common in immunosuppressed

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Structure (envt and host):

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Envt - mycelial phase - barrel shaped arthroconidia, (arthospores hazardous to lab workers) easily fragmented, highly infectious, hazardous when cultured in lab

Host - large, thick walled spherules with numerous endospores

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Pathogenesis:

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Inhaled arthroconidia -> lodge in alveoli -> develop to spherules in tissues -> spherule rupture -> release endospores into tissue -> endospores develop into spherules

Host response:
Initially macroph and PMNs (fungi resist killing by PMNs) -> onset of CMI leads to protection from infection

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Epidemiology:
Where?
Who?

Back 15

Where?
Fungus has been isolated from soil

endemic to certain areas of N, S, and C America (e.g. central texas)

Fungus grows in "Lower Sonoran Life Zone" - arid, hot, low altitude, alkaline soil, sparse flora

Almost all of 100,000 annual infections are in SW US

Who? common in men of dark skin and especially Filipino

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Diagnosis:

Back 16

ID spherules with KOH mount or fungal stain of infected tissue

Culture organism on special media - demonstrate dimorphism and tissue form

Skin test positive 1-4 wks post onset of primary symptoms (remains + for life)
*dissem infect can cause anergy

Serologic tests - monitor disease progress
-IgM precipitating Ab positive within first three weeks
- IgG complement fixing Abs develop later (titers increase as disease disseminates)
- Abs disappear with disease resolution, persist with continued infection

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Prevention:

Treatment:

Back 17

avoid env't exposure

Antifungal therapy for disseminated

Front 18

Paracoccidioides brasiliensis:

Back 18

wagon wheel appearance of yeasts found in tissues (due to circular budding)