Opportunistic Mycoses

 General futures
 Serous infection
 Caused by fungi regarded nonpathogenic
 List of fungi causing disease increased
 Based on clinical setting
 Patient has impaired host defense
 Secondary underline diseases
 Malignancy and AIDS
 Alteration in normal flora
 Candidiasis, Aspergillosis
 Cryptococcosis
 Mucoromycosis
 Candidiosis or Candidiasis
 Most commonly encountered
opportunistic mycoses worldwide
 Cellular immunity protects against
mucocutaneous candidiasis
 Oral , vaginal, skin,
 neutrophils protect against invasive
candidiasis
 Lung, spleen, liver and so on
 Normal flora
 Endogenous inf.
 MOST COMMONLY ISOLATED
CANDIDA SPECIES

 C. albicans
 C. tropicalis
 C. parapsilosis
 C. kefyr
 C. glabrata
 Mycology or morphology
 Macro
 Creamy yeast colonies (SDA)
 Micro
 Yeast cell reproduce by budding
 Produce either pseudo or true hyphae
 Only Candida glabrata produce yeast only
 Germ tube, fermentation and assimilation
reactions
 PATHOGENICITY

 Attachment (Germ tube is

more adhesive than yeast
cell)
 Adherence to plastic
surfaces (catheter,
prosthetic valve..)
 Protease
 Phospholipase
 Risk factors
 Physiological.
 Pregnancy, elderly, infancy
 Traumatic.
 Burn, infection
 Haematological.
 Cellular immune deficiency,
 AIDS, chronic granulomatous disease,
 aplastic anaemia, leukaemia, lymphoma...
 Endocrinological
 DM, hypoparathyroidism, Addison disease
 Iatrogenic.
 Oral contraceptives, antibiotics,
 steroid, chemotherapy, catheter...
 Clinical manifestations-I
 Cutaneous and Subcutaneous
 Oral
 Vaginal
 Onychomycosis
 Dermatitis
 Diaper rash
 Balanitis
Clinical forms of candidiasis
 Clinical manifestations-II

 Systemic
 Esophagitis Peritonitis
 Hepatosplenic
 Endophthalmitis , Arthritis
 Osteomyelitis, Meningitis
 Skin lesions, Pulmonary infection
 Cystitis, Pyelonephritis
 Endocarditis, Myocarditis
 Clinical manifestations-III

 Chronic mucocutaneous
 Candida inf. of skin and mucous
membranes
 Verrucose lesions
 Impaired cellular immunity
 Autosomal recessive trait
 Hypoparathyroidism, iron deficiency
 Laboratory diagnosis
 Direct microscopic examination

 Yeast cells, Pseudohyphae, true

hyphae
 Culture
 SDA, routine bacteriological media
 Serology
 Disseminated candidosis
 Detection of mannan antigen
(ELISA, RIA, IF, latex agglutination
Lab Diagnosis refer to lab practical for more details
 Treatment
 Cutaneous
 Topical antifungal
 Ketaconazole, Miconazole, nystatin
 Systemic
 Amphotericin B
 Fluconazole, itraconazole
 Chronic mucocutaneous
 Amphotericin B
 Fluconazole, itraconazole
 Transfer factor
Cryptococcosis
 Etiologic agent
 Cryptococcus neoformans
 Mycology
 Monomorphic (yeast at 25Ć and
37Ć)
 Possess mucoploysaccaride capsule
 Epidemiology and Ecology

 World wide
 Roosts and droppings of pigeons
 Exogenous infection
 Four serotypes
 A-D (most frequently A)
 B-C isolated from AIDS patients in
Africa
 Underlying cellular
immunodeficiency
 (AIDS, lymphoma)
 Pathogenicity factors

 Capsule
 Diphenol oxidase (+) (Bird seed
 agar/caffeic acid medium)
 Ability to grow at 37°C

 Clinical diseases
 PULMONARY
 Asymptomatic
 flu-like/hilar lap/cavitation
Clinical diseases cont.
 Disseminated
 **Meningitis (acute/chronic) in AIDS
 Cryptococcoma
 Skin lesions
 Other

 Laboratory Diagnosis
 Samples
 CSF, sputum,
 aspiration from skin lesion
Diagnosis cont.

 Direct exam
 India ink
 Culture
 SDA, Niger seed agar
 Canavanine –glycine bromothymol
blue
 Serology***
 Detection of capsule antigen in CSF
and serum by latex agglutination test
 Treatment

 Amphotericin B + flucytosine
 Life-long fluconazole
prophylaxis following primary
treatment (in AIDS patients)
Aspergillosis
 General characteristic
 Purely an opportunistic infection
 Infection Depend on host immunity
 Cause abortion in sheep and cattle
 Pulmonary in birds
 Carcinogenic in animals
 Aspergillus spp.( most common: A.
fumigatus)
 Risk factors and pathogenesis

 Immunosuppression, DM..
exogenous inf. (inhalation of
spores)
 Inhalation of spores by atopic host
Hypersensitivity reactions (allergy)
 Ingestion of products contaminated
with Aspergillus toxins 
Mycotoxicosis / hepatocellular and
colon carcinoma
 General futures
 Natural reservoir
 air, soil
 Pathogenicity factors
 hypha, phospholipase
 Infected tissue
 vascular invasion, thrombus, infarct,
bleeding
 Macroscopic
 powdery mould colonies
(colour of the spores varies from one
species to other)
 Microscopic
 septate hyphae (dichotomous branching),
vesicula, phialides, microconidia
 Diseases associated with
Aspergillus
 Clinical manifestations-I
 Mycotoxicoses
 Allergic aspergillosis
1. Asthma (Type I)
2. Allergic bronchopulmonary
aspergillosis (Types I, III)
II. Non-invasive local colonization
 Aspergiloma (Fungus ball) (lungs,
 paranasal sinuses)
 Otomycosis (external otitis)
 Onychomycosis
 Eye inf. (conjunctival, corneal,
intraocular)
 Clinical manifestations-II

IV. INVASIVE ASPERGILLOSIS

1. Pulmonary
2. Disseminated
 GIT, brain, liver

 kidney, heart, skin, eye

 Laboratory 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)
 Diagnosis of Aspergillosis
Asp. In the lung

ASPERGILLOMA

Colony appearance of Aspergillus

Structure of Aspergillus
 Treatment
 Allergic
 Steroid
 Aspergiloma

(if symptomatic) Surgery
 amphotericin B
 Local and superficial infections

Nystatin
 Invasive infection
 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
 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
 Laboratory diagnosis
 Samples
 Sputum, BAL
 biopsy of paranasal sinuses..
 Direct exam
 Nonseptate
 ribbon-like hyphae which branch at
right angles, sporangium
 Culture
 SDA (cotton candy appearance)
Clinical and lab diagnosis
 Treatment

 Surgical debridement
 Amphotericin B

 ***High mortality rate