Pulmonary Fungal Infections 1 Flashcards
coccidioides organism
dimorphic: mold in soil, spherule in tissue. spores carried by wind, inhaled by humans. endemic in southwest US and latin america.
coccidioides pathogenesis
arthrospores are inhaled, infectious dose can be as low as a single infectious unit. high dosage more likely to cause symptoms. changes form to spherule in terminal bronchiole, and is filled with endospores. highly resistant to eradication. spherules and endospores are not infectious
coccidioides acute phase
innate immunity attempts to clear infection: often successful
coccidioides chronic phase
innate immunity inadequate for clearance, lymphocytes and histiocytes initiate granuloma and giant cell formation to contain. if person is healthy, usually contained in lungs. many patients have flulike symptoms. may appear as valley fever or desert rheumatism
coccidioides in immune compromised or in a high dose
disseminated infection by intracellular travel in macrophages and hematogenous spread. may affect any organ, mainly hits bones and meninges. induces immune anergy.
coccidioides exam
usually summer/autumn. obtain travel istory. PPD with coccidioidin or spherulin. positive if exposed with cleared or contained infection. negative if unexposed or disseminated infection
coccidioides contained infection
+PPD. often asymptomatic. may have influenza like illness. 50% have lung changes on xray. 10% develop erythema nodosum (adults) or multiforme (kids) or arthralgias (desert bumps)
coccidioides disseminated infection
most commonly affects meninges, bone, and skin/lymph node. dramatic sweats, dyspnea, fever, and weight loss. erythema nodosum is a good sign. may arise after prolonged incubation or reactivate after treatment.
coccidioides lab
take biopsies of relevant tissues. examine for spherules. culture on sabouraud’s agar. cultures are infectious. serology for exposure, titer spikes if disseminating (IgG). CSF: look for lymphocytic pleocytosis, elevated protein, hypoglycorrhachia, eosinophilia, IgG
coccidioides treatment
high morbidity but low mortality. no treatment for mild disease. must treat if predisposed to complications: immunosuppression, black/fillipino, cardiopulmonary disease, diabetes, pregnant. give amphotericin B for pregnant, and azoles for others. Amphotericin B and itraconazole in disseminated.
Histoplasma organism
most common systemic mycosis. thermally dimporphic: mold in soil, yeast in tissue. forms tuberculate macroconidia with thick walls and finger projections, and microconidia with smaller, thin, smooth walled, and infectious. endemic in patches worldwide: Ohio, missouri, mississippi, river valleys. African histoplasmosis is different
histoplasma pathogenesis
spores inhaled, healthy immunity kills a low dose but is overwhelmed by a high dose. spores may survive endocytosis and lysosomal fusion in macrophages by making bicarb and ammonia (raises pH and inactivates hydrolytic enzymes). converts to yeast in macrophages and replicates there. high dose can cause pneumonia with cavitary lung lesions, can cause tongue ulcers and pancytopenia in old and immunosuppressed
histoplasma exam
95% resolve at home. acute febrile respiratory illness. take good history. PPD not useful. mild cases have nonspecific flulike. spreading to lungs gives cough and chest pain. cavitary disease has characteristic sound on exam (amphoric breath sounds)
histoplasma disseminated disease
tongue lesions, granulomas in liver and spleen, weight loss, endocarditis, disrhythmia, lesions and masses in GI, scars in backs of eyes, mass lesions and meningitis,
histoplasma lab
culture from sputum, blood, bronchoalveolar lavage, CSF. tissue biopsy or bone marrow aspirate for histology: yeast cells inside macrophages. bloodwork shows pancytopenia in disseminated infection. thermally dimorphic culture: 25C is tuberculate macroconidia, 37C is yeasts. ELISA for histoplasma polysaccharide antigen in urine and serum. DNA probes. antibody titers can be useful but may cross react
histoplasma treatment
usually self limited. itraconazole for 6-12 weeks if in lungs. if disseminated, use amphotericin B. if kidney problems, use liposomal. if meningitis, fluconazole
blastomyces organism
dimorphic fungus: mold form is hyphae with small pear shaped conidia which are infectious. yeast form is round w/ doubly refractive wall and single broad based bud. endemic in eastern north america and great lakes region
blastomyces pathogenesis
inhalation of conidia. monocytes, macrophages, neutrophils kill conidia, but not yeast. yeast produce immune modulator BAD1 on cell surface. granulomatous response. bad if immunosuppressed
blastomyces exam
mild form: flulike illness. pneumonia. chronic illness: looks like TB
fast severe form: Acute Respiratory Distress Syndrome with fever
blastomyces lab
sputum microscopy. tissue biopsy stain with Schiff or silber. see yeast cells with single buds. culture from sputum or biopsy. exoantigen testing and DNA available. PPD and serology are inadequately specific
blastomyces treatment
symptomatic but not severe: itraconazole. severe: amphotericin B. fluconazole also appropriate for meningitis. surgical excision of loci
paracoccidioides organism
dimorphic fungus: mold = thin septate hyphae. yeast = thick walled w/ multiple buds. endemic to rural latin america
paracoccidioides pathogenesis
spores are inhaled, early lesions occur in lungs, asymptomatic infection common. more sever hits oral mucous membranes and lymph nodes. dissemination if immunosuppressed
paracoccidioides lab
pus/tissue samples: yeast cells with multiple buds. stain biposies with silver for yeast or granulomas. culture takes 2-4 weeks. serologic not good unless in endemic area. Skin test and CSF not helpful
paracoccidioides treatment
oral itraconazole. may use amphotericin B initially if severe. combine with correction of anemia, no smoking, improved diet, stop alcohol
