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OPPORTUNISTIC MYCOSES
Sevtap Arikan, MD
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OPPORTUNISTIC MYCOSES General features
CAUSATIVE AGENTS Saprophyte in nature/found in normal flora HOST Immunosupressed /other risk factors
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OPPORTUNISTIC MYCOSES
Candidiasis Cryptococcosis Aspergillosis Zygomycosis Other: Trichosporonosis, fusariosis, penicillosis…… ***ANY fungus found in nature may give rise to opportunistic mycoses ***
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CANDIDIASIS Most commonly encountered opportunistic mycoses worldwide
Cellular immunity protects against mucocutaneous candidiasis, neutrophiles protect against invasive candidiasis Endogenous inf. Etio: Candida spp. Most common: 1. C. albicans 2. C. tropicalis
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MOST COMMONLY ISOLATED CANDIDA SPECIES
C. albicans C. tropicalis C. parapsilosis C. kefyr C. glabrata C. krusei C. guillermondii C. lusitaniae
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Candida MORPHOLOGICAL FEATURES
Micr. Budding yeast cells Pseudohyphae, true hyphae Macr. Creamy yeast colonies (SDA) Germ tube (C. albicans, C. dubliniensis) Chlamydospore (C. albicans, C. dubliniensis) Identification Germ tube, fermentation and assimilation reactions
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Candida PATHOGENICITY
Attachment (Germ tube is more adhesive than yeast cell) Adherence to plastic surfaces (catheter, prosthetic valve..) Protease Phospholipase
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CANDIDIASIS Risk factors
Physiological. Pregnancy, elderly, infancy Traumatic. Burn, infection Hematological. Cellular immune deficiency, AIDS, chronic granulamatous disease, aplastic anemia, leukemia, lymphoma... Endocrinological. DM, hypoparathyroidism, Addison disease Iatrogenic. Oral contraceptives, antibiotics, steroid, chemotherapy, catheter...
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CANDIDIASIS Clinical manifestations-I
1. CUTANEOUS and SUBCUTANEOUS Oral Vaginal Onychomycosis Dermatitis Diaper rash Balanitis
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CANDIDIASIS Clinical manifestations-II
2. SYSTEMIC Peritonitis Hepatosplenic Endophthalmitis Arthritis Osteomyelitis Menengitis Skin lesions Esophagitis Pulmonary inf. Cystitis Pyelonephritis Endocarditis Myocarditis
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CANDIDIASIS Clinical manifestations-III
3. CHRONIC MUCOCUTANEOUS Candida inf. of skin and mucous membranes Verrucose lesions Impaired cellular immunity Autosomal recessive trait Hypoparathyroidism, iron deficiency
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CANDIDIASIS Diagnosis
Direct micr.ic examination Yeast cells, pseudohyphae, true hyphae Culture SDA, routine bacteriological media Serology Detection of mannan antigen (ELISA, RIA, IF, latex agglutination)
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CANDIDIASIS Treatment
CUTANEOUS Topical antifungal: Ketoconazole, miconazole, nystatin SYSTEMIC Amphotericin B Fluconazole, itraconazole CHRONIC MUCOCUTANEOUS Transfer factor
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CRYPTOCOCCOSIS Underlying cellular immunodeficiency (AIDS, lymphoma)
Exogenous inf. Pathogenesis Inhalation of yeasts Etio. Cryptococcus neoformans
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Cryptococcus neoformans General properties
Natural reservoir Soil, bird droppings Micr. Encapsulated yeast (India ink) Macr. Creamy, mucoid colonies (SDA) Serotypes A-D (most frequently A) Pathogenicity factors a. Capsule b. Diphenol oxidase (+) (Bird seed agar/ caffeic acid medium) c. Ability to grow at 37°C
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CRYPTOCOCCOSIS Clinical manifestations
1. PULMONARY Asymptomatic/flu-like/hilar lap/cavitation 2. DISSEMINATED **Meningitis (acute/chronic) Cryptococcoma Skin lesions Other
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CRYPTOCOCCOSIS Diagnosis
Samples CSF, sputum, aspiration from skin lesion Direct exam. India ink Culture SDA Serology*** Detection of capsule antigen in CSF and serum by latex agglutination test
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CRYPTOCOCCOSIS Treatment
Amphotericin B (+ flucytosine) Life-long fluconazole prophylaxis following primary treatment (in AIDS patients)
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ASPERGILLOSIS Etio: Aspergillus spp.(most common:A. fumigatus)
Risc factors and pathogenesis 1. Immunosupression, DM..exogenous inf. (inhalation of spores) 2. Inhalation of spores by atopic host Hypersensitivity reactions (allergy) 3. Ingestion of products contaminated with Aspergillus toxins Mycotoxicosis / hepatocellular and colon carcinoma
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Aspergillus GENERAL FEATURES
Natural reservoir: air, soil Pathogenicity factors: hypha, phospholipase Infected tissue: vascular invasion, thrombus, infarct, bleeding Macr: powdery mould colonies (color of the spores varies from one species to other) Micr: septate hyphae (dichotomous branching), vesicule, phialides, microconidia
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ASPERGILLOSIS Clinical manifestations-I
I. ALLERGIC ASPERGILLOSIS 1. Asthma (Type I) 2. Allergic bronchopulmonary aspergillosis (Types I, III) II. NONINVASIVE LOCAL COLONIZATION 1. Aspergilloma (Fungus ball) (lungs, paranasal sinuses) 2. Otomycosis (external otitis) 3. Onychomycosis 4. Eye inf. (conjunctival, corneal, intraocular)
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ASPERGILLOSIS Clinical manifestations-II
III. INVASIVE ASPERGILLOSIS 1. Pulmonary 2. Disseminated: GIT, brain, liver, kidney, heart, skin, eye IV. MYCOTOXICOSIS
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ASPERGILLOSIS Diagnosis
Samples Sputum, BAL, tissue... Direct exam. Septate hyphae and conidia in sputum; intravascular hyphae in tissue Culture SDA (without cycloheximide) (should grow at least in 2 cultures !) Serology Allergy (detection of specific IgE in serum--RAST) Invasive inf. (detection of galaktomannan antigen in serum--ELISA)
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ASPERGILLOSIS Treatment
ALLERGIC Steroid ASPERGILLOMA (if symptomatic) Surgery, amphotericin B LOCAL, SUPERFICIAL INF. Nystatin INVASIVE INF. Surgical debridement Amphotericin B, itraconazole ***High mortality rate
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ZYGOMYCOSIS Causative agents Rhizopus, Rhizomucor, Mucor...
Natural reservoir Air, water, soil Risk factors Diabetic ketoacidosis, immunosuppression Pathogenesis Inhalation of sporangiospores Infected tissue vascular invasion, thrombus, infarct, bleeding
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ZYGOMYCOSIS Clinical manifestations
I. RHINOCEREBRAL Nose, paranasal sinuses, eye, brain and meninges are involved Orbital cellulitis II. THORACIC Pulmonary lesions, parenchymal necrosis III. LOCAL Posttraumatic kidney inf. Skin inf. following burn or surgery
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ZYGOMYCOSIS Diagnosis
Samples Sputum, BAL, biopsy of paranasal sinuses.. Direct exam. Nonseptate, ribbon-like hyphae which branch at right angles, sporangium Culture SDA (cotton candy appearence)
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ZYGOMYCOSIS Treatment
Surgical debridement Amphotericin B ***High mortality rate
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