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Fungal infections of the oral cavity
This document discusses various fungal infections that can affect the oral cavity and respiratory tract, including candidiasis, aspergillosis, and zygomycosis. It describes the characteristics and morphology of fungi, including molds, yeasts, dimorphic fungi. It then covers the pathogenesis, clinical manifestations, diagnosis and treatment of the main opportunistic fungal infections.
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Overview of fungal infections specifically in the oral cavity.
Discussion on the evolution of medical mycology driven by factors like organ transplantation and HIV.
Fungi are eukaryotic and possess ergosterol, differing in cell wall composition from bacteria.
Fungal morphology includes molds, yeasts, yeast-like fungi, and dimorphic fungi with specific characteristics.
List of opportunistic fungal infections affecting the upper and lower respiratory tracts.
Common opportunistic mycosis, detailing its causes, manifestations, diagnosis, and treatment options.
Detailed information on Aspergillus species, including pathogenesis, clinical features, and treatment.
Discussion of Mucormycosis, its risk factors, manifestations, diagnosis, and high mortality treatment outcomes.
A case study summary involving a fungal infection in a diabetic patient, followed by investigative questions.
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Fungal infections of the oral cavity
- 1. Fungal infections ofthe oral cavity 1
- 2. Medical Mycology • Fungiwere discovered before bacteria & viruses • Most fungi cause skin or cosmetic infections while bacteria & viruses cause fatal diseases • Clinical Mycology has entered “Golden Age” in modern medicine due to: •Organ transplantation •Immunosuppressive drugs •Anticancer drugs •Broad-spectrum antimicrobials •HIV-disease Immunosuppression Opportunistic Fungal Infections 2
- 3. Fungi : GeneralCharacteristics • Are eukaryotic (possess a true nucleus with nuclear membrane & mitochondria) Cell membrane • Have ergosterol which is specific target for antifungal agents (cholestrol in mammalian cells) Cell Wall Lacks • Peptidoglycan • Techoic acids • Lipopolysaccharide Contains • Peptidomannan • Glycan (target for new antifungal agents) 3
- 4. Fungi Groups On thebasis of Morphology 1. Molds (filamentous fungi) • Most fungi are composed of filamentous (tubular) structures called hyphae. May be septated OR Aseptated Aseptate hyphae Septate hyphae 4
- 5. Types of Hyphae •Vegetative hyphae: penetrate the media and absorb food • Aerial hyphae : are directed above the surface of media • Reproductive hyphae : Aerial hyphae that carry different spores • Mycelium : A collection of hyphae Reproductive Hyphae & conidia Mycelium (thallus) Surface of media Aerial hyphae Vegetative hyphae 5
- 6. Fungi Groups On thebasis of morphology 2. Yeasts • Unicellular (rounded or oval) • Reproduce by budding • The only example of pathogenic yeast is Crptococcus neoformans 6
- 7. Fungi Groups On thebasis of morphology 3. Yeast-Like • Unicellular (rounded or oval) • Reproduce by budding but buds fail to detach and may form short chains of cells called pseudohyphae • Pseudohyphae are produced during infection and have diagnostic value • Example: Candida 7
- 8. Fungi Groups On thebasis of Morphology 4. Dimorphic Fungi • Able to grow in two different forms • As molds at room temperature • As yeasts on incubation at 370C & during infection in body “Mold in the cold, yeast in the heat” • Example: Histoplasma capsulatum 8
- 9. Opportunistic Infections ofthe URT& LRT • Candidiasis • Cryptococcosis • Aspergillosis • Zygomycosis ***ANY fungus found in nature may give rise to opportunistic mycoses *** 9
- 10. CANDIDIASIS • Most commonlyencountered opportunistic mycoses worldwide • Cellular immunity protects against mucocutaneous candidiasis, neutrophiles protect against invasive candidiasis • Endogenous infection. • Etiology: Candida spp. Most common: C. albicans C. tropicalis 10
- 11. Candida Morphologicfal Features • Micr.Budding yeast cells Pseudohyphae, true hyphae • Macr. Creamy yeast colonies (SDA) • Germ tube • Chlamydospore • Identification Germ tube 11
- 12. Sabouraud Dextrose agar Candidaalbicans Candida albicans Microscopic Morphology 12
- 13. Candida Pathogenicity • Attachment (Germtube is more adhesive than yeast cell) • Adherence to plastic surfaces (catheter, prosthetic valve..) • Protease • Phospholipase 13
- 14. CANDIDIASIS Risk factors • Physiological.Pregnancy, elderly, infancy • Traumatic. Burn, infection • Hematological. Cellular immune deficiency, AIDS, chronic granulamatous disease, aplastic anemia, leukemia, lymphoma... • Endocrinological. DM • Iatrogenic. Oral contraceptives, antibiotics, steroid, chemotherapy, catheter... 14
- 15. Candidiasis Clinical manifestations 1. CUTANEOUSand SUBCUTANEOUS • a) b) c) Oral Pseudomembernous (thrush) Erythematous Hyperplastic • Vaginal • Dermatitis • Diaper rash 15
- 16. Candida albicans Granulomatous lesionsinvolving Candida diaper rash the hands. 16
- 17. Candida albicana The whitematerial are masses of the yeast 17
- 18. CANDIDIASIS Clinical manifestations 2.SYSTEMIC • Esophagitis •Pulmonary inf. • UTI( Cystitis) • Osteomyelitis • CNS (Menengitis) • Skin lesions • CVS 18
- 19. CANDIDIASIS Diagnosis • Direct micr.icexamination Yeast cells, pseudohyphae, true hyphae • Culture SDA, routine bacteriological media • Serology Detection of mannan antigen (ELISA, RIA, IF, latex agglutination) 19
- 20. CANDIDIASIS Treatment • CUTANEOUS Topical antifungal:Ketoconazole, miconazole, nystatin • SYSTEMIC Amphotericin B Fluconazole, itraconazole 20
- 21. Aspergillosis Causative Agent • Aspergillusfumigatus Systemic infection • Aspergillus flavus • Aspergillus niger- mostly local infection; otomycosis • Are molds that have septate hyphae with Vshaped branches (Fruiting body of Aspergillus) Source of infection • Widely distributed in environment • Transmitted by air-borne light spores • High environmental load is associated with sick building syndrome & contaminated AC system 21
- 22.
- 23. Aspergillosis Pathogenesis & Clinicalfeatures Aspergillus can colonize and invade: • Lungs • Wounds, burns • Cornea • External ear • Paranasal sinuses 23
- 24. Aspergillosis In lungs cancause: a) Hypersensitivity Reaction: Spores colonise RT without invasion and lead to allergic asthma, rhinitis, bronchopulmonary aspergillosis b) Aspergilloma (fungus ball): the spores colonise paranasal sinuses or a pre-existing cavity in lung (TB cavity) The radiological appearance may be similar to malignancy. c) Invasive Aspergillosis In immunocompromised can invade lungs causing hemoptysis & granuloma and disseminate to other organs Fatality rate 100% if not diagnosed and treated promptly. 24
- 25. Aspergillosis Lab Diagnosis Specimens :sputum, BM aspirate, biopsy Direct Microscopy • Shows branching septate hyphae Cultures : Microscopy shows radiating chains of spores Serology • In allergic condition: high levels of specific IgE • Galactomannan in invasive aspergillosis Treatment • Invasive aspergillosis Amphotericin B • Allergic conditions Steroids & antifungals 25
- 26. Zygomycosis Mucormycosis • Causative agents;saprophtic molds • Rhizopus, Mucor & Absidia • Have broad, hyaline aseptate hyphae • Have large no. of asexual spores inside a sporangium • Risk factors Diabetic ketoacidosis, immunosuppression • Pathogenesis Inhalation of sporangiospores • Infected tissue vascular invasion, thrombus, infarct, 26
- 27. 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 infection. • Skin inf. following burn or surgery 27
- 28. Zygomycosis Mucormycosis Diseases • Rhinocerebral zygomycosis oExtensive cellulitis of nasal mucosa, paranasal sinuses, orbit & brain o Rapidly fatal • Pulmonary & disseminated infections 28
- 29. Zygomycosis in adiabetic patient 29
- 30.
- 31. 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 appearance) 31
- 32. Image: Sporangia showingdifferent stages of sporangiospore development in the large sporangium, human nasal polyp, 32
- 33. Treatment • Surgical debridement •Amphotericin B ***High mortality rate 33
- 34. Case study • Ayoung Diabetic girl develops acute fatigue and fever. Her pediatrician discovers a leukemia and the girl is promptly treated with broad acting anticancer therapy. Two weeks after the therapy she started to developed a severe pneumonia which does not respond to antimicrobial antibiotics. A biopsy from the lung was taken and plated on Sabouraud dextrose agar containing antibacterial antibiotics. After incubation at 250C, a mold is seen. On further examination the girl is treated with amphotericin B and recover. The disease she had was 34
- 35. Questions • What isthe identity of the isolate ? • In what patient population does this organism normally cause infection? • How can you investigate the patient? 35