OPPORTUNISTIC MYCOSES Sevtap Arikan, MD
OPPORTUNISTIC MYCOSES General features CAUSATIVE AGENTS Saprophyte in nature/found in normal flora HOST Immunosupressed /other risk factors
OPPORTUNISTIC MYCOSES Candidiasis Cryptococcosis Aspergillosis Zygomycosis Other: Trichosporonosis, fusariosis, penicillosis…… ***ANY fungus found in nature may give rise to opportunistic mycoses ***
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
MOST COMMONLY ISOLATED CANDIDA SPECIES C. albicans C. tropicalis C. parapsilosis C. kefyr C. glabrata C. krusei C. guillermondii C. lusitaniae
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
Candida PATHOGENICITY Attachment (Germ tube is more adhesive than yeast cell) Adherence to plastic surfaces (catheter, prosthetic valve..) Protease Phospholipase
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...
CANDIDIASIS Clinical manifestations-I 1. CUTANEOUS and SUBCUTANEOUS Oral Vaginal Onychomycosis Dermatitis Diaper rash Balanitis
CANDIDIASIS Clinical manifestations-II 2. SYSTEMIC Peritonitis Hepatosplenic Endophthalmitis Arthritis Osteomyelitis Menengitis Skin lesions Esophagitis Pulmonary inf. Cystitis Pyelonephritis Endocarditis Myocarditis
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
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)
CANDIDIASIS Treatment CUTANEOUS Topical antifungal: Ketoconazole, miconazole, nystatin SYSTEMIC Amphotericin B Fluconazole, itraconazole CHRONIC MUCOCUTANEOUS Transfer factor
CRYPTOCOCCOSIS Underlying cellular immunodeficiency (AIDS, lymphoma) Exogenous inf. Pathogenesis Inhalation of yeasts Etio. Cryptococcus neoformans
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
CRYPTOCOCCOSIS Clinical manifestations 1. PULMONARY Asymptomatic/flu-like/hilar lap/cavitation 2. DISSEMINATED **Meningitis (acute/chronic) Cryptococcoma Skin lesions Other
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
CRYPTOCOCCOSIS Treatment Amphotericin B (+ flucytosine) Life-long fluconazole prophylaxis following primary treatment (in AIDS patients)
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
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
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)
ASPERGILLOSIS Clinical manifestations-II III. INVASIVE ASPERGILLOSIS 1. Pulmonary 2. Disseminated: GIT, brain, liver, kidney, heart, skin, eye IV. MYCOTOXICOSIS
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)
ASPERGILLOSIS Treatment ALLERGIC Steroid ASPERGILLOMA (if symptomatic) Surgery, amphotericin B LOCAL, SUPERFICIAL INF. Nystatin INVASIVE INF. Surgical debridement Amphotericin B, itraconazole ***High mortality rate
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
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
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)
ZYGOMYCOSIS Treatment Surgical debridement Amphotericin B ***High mortality rate