Fungi part A Flashcards
Fungi are single or multicell?
spores?
cholorphyll?
Eukaryotes
Spore-forming
No chlorophyll
Fungi O2 use?
Most fungi are aerobic
some facultative and strict anaerobes
fungi cell walls usually have?
Cell walls usually contain chitin
polysaccharide containing N-acetylglucosamine (NAG)
possible fungi growth forms?
- filamentous (molds)
2. unicellular (yeasts)
filamentous growth
septate vs. coenocytic?
threadlike filaments =hyphae>mycelium = mass of hyphae
septate vs. coenocytic hyphae (with and without crosswalls between cells)
grow by extension of tip and branching
unicellular growth
single cells (ovoid or spherical)
reproduce asexually by cell division (budding)
sexually by cell fusion and spore formation
fungi possible reproductive means
sexual and asexual
asexual reproduction
a. cell division= budding/ transverse division
Some yeast-form fungi perform asexual cell division by budding, other by transverse division (fission).
b. spore formation= spores released
sexual reproduction, morphologies?
involves production of “sexual spores” by meiosis of a diploid cell
Anamorph: form producing asexual spores, often mold-like growth form
Teleomorph: form producing sexual spores, typically a fruiting body
dimorphism of fungi
ability to grow as yeast form or mold form
many pathogenic fungi are dimorphic
most likely fungal form in human body? exception?
yeast form more typical at human body temperature
Candida is exception to this
both forms of Candida exist inside and outside the body
candida forms (hyphae/ growth?)
Candida actually forms pseudohyphae and pseudomycelia pseudohyphae -
hyphal growth is a modified budding where newly budded cells remain attached to mother cell
non-dimorphic pathogenic fungi
Aspergillus - mold from only
Cryptococcus neoformans - yeast form only
Mycoses -
fungal infections Classified by affected area of body Superficial Cutaneous Subcutaneous Systemic
Primary mechanisms for fighting fungi:
Neutrophil phagocytosis and killing
T cell-mediated immunity
Superficial mycoses
types
regions they occur
keratinized outer layers of skin, hair, and nails
Mild infections/minimal inflammatory response
Easy to treat or clears without treatment
Piedras and Tineas
mostly occur in tropics
Piedras
common agents?
infections of hair shaft
Trichosporon beigelii and white piedra
Tineas
infections involving outer layers of skin, nails, and hair Malassezia furfur (skin) and Pityriasis versicolor
most common superficial mycoses agents
Pityriasis versicolor and white peidra
Pityriasis (tinea) versicolor found where? sign? in the environment? transmission?
Disease found worldwide
Pigmented macules - not elevated but altered color
M. furfur not found in the environment
Human-to-human transmission
Cutaneous mycoses
keratinized outer layers of skin, hair, and nails
Skin infections: no invasion beyond stratum corneum (outermost layer of epidermis)
BUT a more apparent host response is elicited (unlike superficial mycoses)
genuses causing cutaneous mycoses
trophism/ effect on this tissue?
“Dermaphytes”
Microsporum
Trichophyton
Epidermophyton
Keratinophilic and keratinolytic
Cutaneous mycoses cause what kind of fungal disease?
Cause tineas (”ringworm") Tinea pedis = athlete's foot Tinea cruris = jock itch Characterized by inflammation-ring of inflammatory scaling
Cutaneous mycoses transmission
soil?
animals?
Diagnosis?
Person-to person transmission
Some are soil organisms
Others are zoonoses
Diagnosis by microscopy of samples
Subcutaneous mycoses
response to chemotherapy?
treatment?
dermis and subcutaneous tissue
Do not respond well to antifungal chemotherapy
Need to excise
Sporotrichosis cause? spp?
from what source?
tx?
subcutaneous mycoses- Sporothrix schenkii
Thorns and splinters
Responds to oral potassium iodide
Systemic mycoses
caused by?
saprobes?
invade internal organs
caused by endemic dimorphic fungal pathogens
saprobe - organism living on dead or decaying matter
possible agents of systemic mycoses
forms?
diseases?
all can be mold/mycelial in environment form or yeast form in our body, except Coccidioides immitis, this forms spherules in body
Histoplasma capsulatum= Histoplasmosis
Blastomyces dermatitidis= Blastomycosis
Coccidioides immitis= Coccidioidomycosis
Spherule
100s of endospores, characteristic of Coccidioides immitis
Histoplasma capsulatum from where/ how acquired?
Bird or bat droppings (high nitrogen content)
Acquire fungus by inhalation of conidia (asexual spores)
Histoplasma capsulatum in macrophages
Organism remains viable within macrophages
modulate pH of phagolysosome
Histoplasma capsulatum immunity
Ab? CMI?
Antibody plays no role in resolution
Cell-mediated immune system of CD4 T lymphocytes and activated macrophages are important for immunity
Histoplasma capsulatum symptoms intially? progression? reactivation?
Primary infections most often asymptomatic
Granulomas develop in lung with caseous necrosis (plus calcification)
reactivation infection can occur years later
Histoplasma capsulatum treatment
3-12 months of antifungal agent
Histoplasma capsulatum environment vs tissue forms
environment: mold
tissue: yeast
Blastomyces dermatiditis
found where?
how acquired?
Found in decaying matter (e.g leave litter)
Acquire fungus by inhalation of conidia (asexual spore)
Blastomyces dermatiditis immunity
Cell-mediated immune system of CD4 T
lymphocytes and activated macrophages
are important for immunity
Blastomyces dermatiditis primary infection symptoms?
progression? reactivation?
hallmark of disease?
Primary infections symptomatic in <50% of patients
Granulomas develop with caseous necrosis (plus calcification)
reactivation infection can occur years later
Cutaneous lesions are a hallmark of disease, heaped up borders and small, central
microabscesses
Blastomyces dermatiditis diagnosis/ treatment length
histopathological examination (thick-walled yeasts with single broad-based bud) antifungal agents for 6-12 months
Coccidioides immitis found where
Southwestern USA = lower Sonoran life zone
Huge “blooms”
Coccidioides immitis targets
Lung is primary target but the fungus spreads through
the circulatory system and infects many organs
Coccidioides immitis symptoms
large amount innoculate?
common name of dx?
dissementation?
Usually no symptoms - cell-mediated immunity
Sometimes with large amount of innoculate: acute pulmonary infection, arthralgias and skin lesions
“desert rheumatism” or “valley fever”
Disseminated coccidioidomycosis= chronic meningitis -fatal if not treated (lifelong)
Coccidioides immitis diagnosis/ treatment length
presence of spherules
treated over 12-24 months
