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OPPORTUNISTIC MYCOSES

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
Esophagitis Pulmonary inf. Cystitis Pyelonephritis

Peritonitis
Hepatosplenic Endophthalmitis Arthritis Osteomyelitis

Endocarditis
Myocarditis

Menengitis
Skin lesions

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 Amphotericin B Fluconazole, itraconazole 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 37C

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

Natural reservoir: air, soil

GENERAL FEATURES

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

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