Opportunistic Fungal Infections Flashcards
cryptococcus neoformans, c. gatti epi
cause more life threatening infections than any other fungus
causes encephalitis
subsaharan africa and Latin america
neoformans- widely in nature, soil w/ bird droppings
gatti- trees
common in HIV
cryptococcus neoformans, c. gatti pathogenesis
polysaccharide capsule is distinguishing feature- composed of GXM that are necessary for virulence- prevents phagocytosis
urease positive
inhalation of spores cannot be eliminated. uses phenol oxidases to produce melanin from dopamine. the melanin protects it from oxidative damage
can spread from lungs to CNS in compromised individuals via microcappilaries
cryptococcus neoformans, c. gatti immunity
innate recepotrs TLR, CD14 recognize and activate cell mediated immunity Th1
cryptococcus neoformans, c. gatti clinical features
chronic meningioencephalitis
slow onset
headache, stiff neck, body aches, respiratory symptoms
cryptococcus neoformans, c. gatti diagnosis
presence of capsular Ag via plasma, urine CSF
CGB agar- turns blue
cryptococcus neoformans, c. gatti treatment
flucytosine, amphtericin B, fluconazole, itraconzaole
aspergillis epi
fumigatus and flavus- two major causes of disease
grow in mold form only (hyphae)- no dimorphism
easily airborne spores
inhalation causes disease in suppressed
fumigatus also can cause an allergic reaction
seen in hematopoietic stem cell transplants, organ transplants, chronic granulomatous disease, and HIV
aspergillis pathology
inhaled and germ tubes emerge to colonize cavity lesions with hyphae
quick dessemination is observed without therapy
aspergillis immunity
innate immune system critical- alveolar macrophages and neutrophils
Pentraxin 3, a soluble pattern recognition receptor, crucial
Th1 response important
aspergillis clinical features
cough, fever, chest pain, SOB
aspergillis diagnosis
biopsy
serum test
IgE Abs specific for aspergillis
aspergillis Abs
voriconazole, amphotericin B
mucor, rhizopus
grow in molds only, not dimorphic
however, grow in hyphae at right angles rather than Y shaped
spreads thru air
special population: diabetic ketoacidosis
mucor, rhizopus pathology
similar to aspergillis
spores germinate into hyphae and invade tissue
mucor, rhizopus immunity
need intact innate and adaptive systems, unknown else wise
mucor, rhizopus presentation
similar to aspergillis
looks like bacterial sinusitis, headaches and fever in frontal or retroorbital regions
mucor, rhizopus diagnosis/treatment
biopsy
surgical debridement and amphotericin B
pneumocystis jiroveci epi
CANNOT BE CULTURED
exists as a cyst of sporozoites that rupture and grow into trophozoite forms
animals are not a resevoir
asymptomatic infections are common
similar to parasites- sensitive to antiparasitic drugs
no ergosterol in membrane
pneumocystis jiroveci pathogenesis
loss of CD4 immunity leads to susceptibility
transmission via aerosols
inhaled cysts produce inflammation- causes plasma cells to produce “frothy exudate” that blocks O2 exchange and leads to pneumonia
pneumocystis jiroveci immunity
CD4 cells critical
killing of cells done by alveolar macrophages via PRRs
over activation of immune CD8 cells can cause significant damage
pneumocystis jiroveci symptoms
sudden onset fever, cough, dypnea, tachypnea,
x-ray = interstial pneumonia
pneumocystis jiroveci risk factors
low CD4
pneumocystis jiroveci diagnosis and treatment
stain w/ methanamine silver or fluorescent stain w/ Abs to diagnose
chemoprophylaxis in pts with CD4 deficits
trimethoprim-sulfamethoxazole is drug of choice
mold in the environment
emerging evidence that mold in the house hold should be avoided
inhalation of spores or mycotoxins can cause immune mediated responses that are damaging
causes a hypersensitive rxn associated with Th2
symptoms: nasal stuffiness, eye irritation, wheezing, skin irritation
people with asthma or chronic lung disease more at risk
indoor environment w/ high levels of moisture = more mold and more spores. more common in lower SES
