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55 Cards in this Set

  • Front
  • Back
Superficial mycoses
limited to DEAD skin and hair
DO NOT elicit a host cellular response
primarily cosmetic problem
-Tinea nigra and Tinea versicolor = infections of keratinized skin
-White and black piedra are infections of the hair
Cutaneous mycoses
infections taht are depper in the epidermis, but also infect hair and nails
-"ringworm" or Tinea - keratinophilic fungi (keratinases allow them to use keratin as substrate for growth)
*IMMUNO DEFICIENCIES exacerbate Tineas
Subcutaneous mycoses
involve the dermis and subcutaneous tissues, occur at sites of trauma where the organism is implanted into the tissue
-Lymphocutaneous sporotrichosis
Lymphocutaneous sporotrichosis
chronic subvutaneous mycoses, characterized by nodular and ulcerative lesions that devlop along the lymphatic glands that drain the primary site of inoculation
development of warty nodules that appear at sites of implantation of fungal elements
Tinea capitus is a problem of what population?
which tineas are more common in men than women?
Tinea pedis and cruris
Frequency of subcutaneous mycoses?
rare in the US and other highly dvpd countries
Malassezie furfur
lipophilic and grows around sweat glands
Tinia nigra is caused by:
a melanin-producing dimorphic fungus
Cladosporium (Exophilala) werneckii
Malassezia furfur and Cladosporium (Exophiala) werneckii are aquired from:
soil, animals or other people by DIRECT CONTACT
3 GENERA of DERMATOPHYTES causing cutaneous infections
Microsporum, Trichophyton and Epidermophyton
Classification of DERMATOPHYTES
GEOPHILIC (associated w/ soil)
ZOOPHILIC (associated w/ animals)
ANTHROPHILIC (associated w/ humans)
Sporotrhix shenkii
dimorphic fungus that causes sporotrichosis (type of subcutaneous infection)

found on decaying vegetation, grows as budding yeast at 37 degrees and hyphae at 25 degrees
Dematiaceous fungi
(fungi with brown to black melanin)
Dx of superficial and cutaneous mycoses depends on:
observing fungal elements in clinical specimens
-10% NaOH mount (carb cell wall of fungi preserved)
-spores and colony characteristics are useful
fungal elements INSIDE the hair shaft
fungal elements AROUND the hair shaft
Prevention/Tx of fungal infections
1) Topical and/or oral administration of various antifungal drugs
2) Azoles are useful for dermatophytes along with griseofulvin
3) surgical intervention may be required for subcutaneous fungal infections
most important human fungal pathogen in terms of frequency, # of types of diseases and severity
C. albicans
-frequent cause of diaper rash and thrush in infants
-frequent cause of severe infections in immunosupressed patients
-common cause of vaginitis
C. albicans
C. albicans is in the Fungi imperfecti (Deuteromycetes), meaning that...
sexual forms are unknown (recently have been shown to be capable of mating and cell fusion, but other aspects of repro unkown)
where is C. albicans found?

common inhabitant of the mucous membranes and GI tracts of humans
(normally peaceful coexistence with host)
NOT found free-living in nature
gram stain of C. albicans
stains GRAM positive (unlike most fungi)
C. albicans grows predominantly in what form?
on what type of media?
grows predominantly in BUDDING YEAST form

on usual laboratory media
colony morphology of C. albicans on most media
creamy white yeast colonies
under what conditions does C. albicans form vegetative hyphae?
forms vegetative hyphae...
beneath the agar surface
on rich media
at neutral pH
(does not form aerial hyphae)
What forms at the end of C. albicans hyphae under nutrient-limiting conditions?
what growth form predominants in tissue invading infections of C. albicans?
pseudohyphae and hyphae
Pathogenesis of C. albicans infections
C. albicans may invade upper cell layers of stratified squamous epithelium (lines oral cavity, tongue, esophagus and vagina) causing pathology
Oropharyngeal candidasis
inflammation of the mucosa or mucositis affects ~40% of patients receiving chemo
acute pseudomembranous candidiasis
= white patches on the mucosa
erythematous candidiasis
mild, reddening of mucosa
central papillary atrophy of the dorsal tongue
flattening of tongue papilli
angular cheilitis
invasion of the epithelium at corners of the mouth where upper and lower lips meet
esophageal candidiasis
invasion of the esophageal epithelium
primary host defense against oropharyngeal candidiasis
epidermis and the epithelium lining mucosal surfaces are primary defense

cationic peptides in secretions (eg histatin in saliva, defensins in epithelium) are active against C. albicans

PMNs phagocytize and kill C. albicans


Abs are present, but not associated w/ protection
how can one determine if CMI is compromised in patient iwth C. albicans infection?
DTH test with C. albicans antigens
why are hyphal and pseudohyphal forms of C. albicans more invasive than yeast forms?
Hwp1 (adhesin) is abundant on hyphae, mimics mammalian epithelial cell proteins that are substrate for TRANSGLUTAMINASE (cross-links epithelial proteins via glu and lys side chains)

C. albicans exploits the epithelial transglutaminase to attach hyphae to the mucosa
what type of molecules permit attachment of C. albicans to mucosal epithelial cells and to host proteins such as fibronectin?
ADHESINS (from ALS {agglutin-like sequence} gene family)
SAP's (secreted aspartyl proteinases), phosphatases and other enzymes facilitate C. albicans invasion by....
degrading host proteins
how might C. albicans might confer resistance to azole drugs
production of efflux pumps in presence of azole drugs may contribute to pathogenesis
C. albicans transmission
usually endogenous, but can be transmitted orall and sexually

person-to-person spread in hospitals where outbreaks may occur
How is C. albicans mucosal infection diagnosed?
demonstration of organism in infected lesion by KOH mount or gram stain or Histo stain where C. albicans appears to "graze" on the flattented cells that form the uppermost layer of stratified squamous epithelium
Factors that alter oral mucosal environment, predisposing individual to candidiasis
Xerostomia, Ab Rx, Poor oral hygiene, malnutrition, GI malabsorption, Iron, folic acid or vitamin deficiencies, carbohydrate-rich diets, heavy smoking, oral epithelial displasia
Factors that alter immune status of host and predispose individuals to candidasis
blood dyscrasias or malignancy, old age/infancy, radiation/chemo, HIV or other immunodeficiency, endocrin abnormalities, DM, hypothyroidism, hpyoparathyroidism, pregnancy, corticosteroid therapy, hypoadrenalism
Associations with increased rates of vaginal colonization and disease that predispose to candidiasis
pregnancy (3rd tri), high glycogen level, enhanced vaginal epithelial avidity, increased germ tube formation by estrogen, high estrogen content OC use, uncontrolle DM, attendance in STD clinics, antibiotic usage (broad spectrum), decreases levels of bacterial flora, lactobacillus levels reduced during candidiasis
lab eval & id of C. albicans
PRESUMPTIVE: germ tube formation in serum w/in 1-2 hours
DEFINITIVE: fermentation and assimilation of carbohydrates and other compounds
Treatment for mucosal C. alibcans infections
AZOLES (inhibit enzymes involved in ERGOSTEROL SYNTHESIS, prophylactic use may elicit drug resistance)

AMPHOTERICIN B for severe infections (binds to ergosterol)
drug resistance to azoles
has resulted from admin of low levels of drug

resistance mechanisms include mutation in the target enzyme as well as increased expression of efflux pumps
initially thought to be C. albicans, has been found in patients with HIV and is closely related to C. albicans, differing in repetitive DNA
C. dubliniensis
these two species account for approx 70-80% of yeast isolated from patients with invasive candidiasis
C. glabrata and C. albicans
why has C. glabrata recently become important?
has recently become important bc of:
its increasing incidence ww
it is intrinsically less susceptible to azoles and amphotericin B than C. albicans
these Candida species does not form germ tubes or pseudohyphae
C. glabrata
these Candida species forms germ tubes, but less frequently than C. albicans
C. dubliniensis