CANDIDIASIS
By: Sanam Soroudi Michelle Duong
Bryan Houlberg Colby Smith
Candida is Present in Everyone
Normally resides in the skin, mouth, GI tract, and
vagina
Overgrowth is prevented by other
microorganisms
Carriers experience few or no symptoms
At least 75% of all women will experience
Candidiasis at some point in their lives
Clinical Features
Acute Pseudomembranous Candidiasis
(Thrush):
– White, cheesy, creamy, loose patches that can be
easily rubbed off.
– Underlying mucosa is erythematous and easily
bleeds.
Clinical Features
Chronic Hyperplastic Candidiasis
– White plaque that does not rub off
– Commonly found on buccal mucosa along
occlusal line in V-shape and widening as it
approaches commissure.
Clinical Features
Atrophic (Erythematous) Candidiasis
– Smooth and flat, red and raw. Generalized red
area of atrophic tissue.
– Common on hard and soft palate due to ill
fitting dentures; or dorsum of tongue.
Diagnostic Testing
Generally diagnosed by clinical appearance
Culture
– Usually swab lesion and grow on agar medium
Superficial Smear w/ PAS Staining
Diagnostic Testing
Barium Swallow
– Pt swallows thick Barium
mixture, take radiograph
– For visualizing esophageal
candidiasis
Newer Diagnostic Avenues
PCR
Monoclonal Antibody
Rapid Latex Agglutination (RLA)
Many Factors Can Cause
Candidiasis
Increased incidence with:
–
–
–
–
Diabetes Mellitus
Immuno-compromised
Pregnancy
Burn patients
Other causes:
–
–
–
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Oral contraceptives
Antibiotics
Sexually transmitted
Hormone replacement therapy
Pathogenesis 1
Adhesion is an important determinant of
Candida’s virulence
– Candida produces a large number of
adhesins that mediate adherence to host
epithelial and endothelial cells
– Strains with faulty adhesins are avirulent
Pathogenesis 2
Candida produces many enzymes that
contribute to its pathogenicity
– Produces 9 proteinases involved in invasion
of tissues by degredation of extracellular
matrix proteins
– Produces adenosine which blocks neutrophil
degranulation, thus impairing phagocytosis
Pathogenesis 3
Candida adapts rapidly to changes in host
environment
– Shifts between phenotypes in a reversible and
random fashion
– Produces genetically altered variants at a high rate
– This adaptation makes it difficult for host defenses to
attack and eliminate infection
Histology
ACUTE:
-Neutrophils in the Stratum Corneum is
characteristic
-Diffuse inflammatory infiltrates
-Fungal elements
are sparse
CHRONIC:
-Hyperkeratosis and
pseudoepitheliomatous hyperplasia
-Compact orthokeratosis
-Spores and hyphae are identifiable
-Ill-defined granulomas
Treatment
ANTI-FUNGALS:
-Topical- localized candidiasis in patients
with normal immune function.
-Systemic- disseminated disease or in
patients that are immune-compromised
Medications
Nystatin (swish and swallow)
Clotrimazole (troche)
-Topical treatment for Pseudomembranous
Candidiasis and Chronic Hyperplastic
Candidiasis
Ketoconazole
Fluconazole
Itraconazole
-Systemic tablets for treatment of
Pseudomembranous and Chronic Hyperplastic
Candidiasis.
Nystatin ointment
Miconazole, Clotrimazole, Ketoconazole creams
-Treatment of Chronic Atrophic Candidiasis
Amphotercin B
-Treatment of invasive Candidiasis
Multiple Choice Questions
Which of the following is NOT an appropriate
treatment for Oral Candidiasis?
a. Ketoconazole
b. Nystatin
c. Penicillin
d. Clotrimazole
Multiple Choice Question 2
A fungal infection characterized by white
lesions that rub off is:
a.
b.
c.
d.
Acute Pseudomembranous Candidiasis
Histoplasmosis
Chronic Hyperplastic Candidiasis
Coccidiomycosis