Transcript SİSTEMİK MİKOZLAR

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
Esophagitis
Hepatosplenic
Pulmonary inf.
Cystitis
Pyelonephritis
Endocarditis
Myocarditis
Endophthalmitis
Arthritis
Osteomyelitis
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 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