Opportunistic Fungi Flashcards
You think your patient has a systemic endemic mycosis. What do you do first?
Serum 1,3-β-D-glucan test
Candida family
- Primarily exist as yeasts, but may form hyphae in invasive infections
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Candida albicans is the most common human pathogen among them
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Candida albicans in blood
Source of Candida infection
- Most derived from host’s normal flora (endogenous)
- Typically colonize the GI tract from mouth to rectum, vagina, and skin
Candidiasis risk factors
- Neutropenia
- Broad-specturm antibiotics (opens niche)
- Renal failure requiring dialysis
- Venous catheters
- Parenteral nutrition
Many risk factors associated with ICU patients.
Candida-mediated disease
Superficial:
- Adherent white plaques on mucocutaneous surfaces (thrush)
- Not painful
- Those in warm, moist areas such as armpits, groin, under breasts: intertriginous candidiasis
- Those in babies: diaper rash
- Underlying tissue not damaged, no long-term consequences
Disseminated:
- May present as fever, sepsis, organ dysfunction
- Microabscesses may develop in organs, resulting in organ-specific disorders: meningitis, chorioretinitis, hepatosplenic abscess, vertebral osteomyelitis
- Endocarditis common when prosthetic heart valves are involved
Diagnosis of candidiasis
Mucosal candidiasis: Swipe and culture. Fast and effective
Invasive candidiasis: Blood culture works, but not as sensitive. Biopsy works, but is invasive. Tissue culture more sensitive and specific, same deal. 1,3-β-D-glucan serology is always helpful.
Treatment of candidiasis
Mucosal/intertrigonous candidiasis: Local antifungal cream or powder (often nystatin)
Disseminated candidiasis: Systemic antifungal agent. Usually fluconazole or an echinocandin, liposomal amphotericin B for really bad infections.
Prevention of candidiasis
Mucosal infections in AIDS patients are so common that prophylaxis is indicated, but resistance often develops.
Patients at highest risk, like neutropenic patients or HSC transplant patients, are treated prophylactically with an azole during periods of highest risk.
Cryptococcus neoformans
Environmental yeast which reproduces by budding. Surrounded by an atypically huge polysaccharide capsule when in tissues (but not when in the environment), which prevents phagocytosis.
Source of Cryptococcus infection
- Found worldwide in soil contaminated with bird excrement
- Inhaled into alveoli, then multiplies in lung, often asymptomatically
- Infects 20% immunocompetent, 80% immunodeficient individuals
Cryptococcus neoformans-mediated disease
- May begin as mild lung symptoms, usually in immunosuppressed individuals
- Followed by nervous system symptoms, meningitis, worsening headaches, fever, cranial nerve palsies, mental status changes
- Further non-neuronal dissemination may occur in AIDS patients, who may display diffuse pulmonary infection, skin lesions, and widespread visceral infection
Cryptococcus neoformans-mediated damage
- C. neoformans begins producing its capsule once inside the lung
- Capsule also interferes with Th1 mediators
- Displays substantial neurotropism on second wave replication after migrating through blood
- Further dissemination almost exclusively in AIDS patients, and may appear in visceral organs or skin
Diagnosis of cryptococcal meningitis
- Lumbar puncture and CSF examination by India ink stain
- Latex agglutination test on CSF or serum is highly sensitive and specific
- VERY IMPORTANTLY, cryptococci do NOT express 1,3-β-D-glucan
Treatment of cryptococcosis
- Cryptococcal meningitis:Liposomal amphotericin B and flucytosinefor several weeks,wean to flucytosine alone for several months
- Patients with T-cell defects may require flucytosine for life following infection
- Pulmonary cryptococcosis: Flucytosine alone