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Fungal Infections PowerPoint Presentation

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Description : Check out this medical presentation on Skin Inflammation, which is titled "Fungal Infections", to get an overview of fungal infections.

Tags : Skin Inflammation, Fungal Infections

Published on : Jul 05, 2021 | Views : 1902 | Downloads : 4

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Slide 1-

Fungal Infections Once exotic and rare Now increasingly common Fungi are not “virulent” But they are good at taking advantage “Opportunistic”
Slide 2-

Fungal biology Eukaryotes Non-motile Aerobic Saprophytic or parasitic Cell wall contains glucan and chitin Cell membrane contains ergosterol
Slide 3-

Fungal cell structure Yeasts (unicellular, budding) Molds (mycelial, spores) Dimorphs (both)
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Pathogenesis Toxins: produced but not relevant to human infections Disease from: Bulk of organisms Immune response to them or their byproducts
Slide 5-

Overview of fungal infections Superficial (skin or mucosa) Subcutaneous Systemic: “True pathogens” – infect healthy hosts, although disease worsens with immunocompromise “Opportunists” – disease almost exclusively in immunocompromise
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Superficial Fungal Infections Dermatophytes: Molds producing keratinase Saprophytes on skin/nails; inflammation below Diseases: tinea corporis tinea capitis tinea cruris tinea pedis tinea unguum
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Superficial fungal infections Malassezia furfur Lipophilic yeast Disease: Tinea versicolor (itch, pigment changes) Occasionally, fungemia with lipid infusions
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Subcutaneous fungal infections Pathogenesis: introduced through skin, grow in subcutaneous tissues, spread via lymphatics. May reach distant organs especially bone, joints in path. Most common in nonindustrialized world (“Madura foot”)
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Subcutaneous: sporotrichosis Organism: Sporothrix schenkii Dimorphic soil organism Worldwide distribution Pathogenesis: splinters or thorns inoculate organism into subcutaneous tissues
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Sporotrichosis Pathophysiology: Yeast travel along lymphatics Elicit mixed pyogenic/ granulomatous reaction Clinical: Gardners and persons of sport Ulcerating nodules along hard cord Bone and joint destruction Occasional dissemination
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Systemic fungal infections: the “true pathogens” Histoplasmosis, Coccidioidomycosis and Blastomycosis Dimorphic Respiratory acquisition Restricted geographic distribution Infect normal hosts Disease reminiscent of TB
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Histoplasmosis Organism: Histoplasma capsulatum Dimorphic soil organism Habitat: soils with high N content Ohio-Mississippi valley; Puerto Rico, Central and S. America Guano of bats, birds, poultry (chicken coops and caves) Pathogenesis: inhalation of spores
Slide 13-

Histoplasmosis Pathophysiology: Spores transform to yeast in lung, elicit cellular immunity as per TB Hematogenous dissemination skin test reactivity (histoplamin) Clinical: mimics TB May disseminate early (infancy, immunodef.) May cause acute nodular/cavitary lung disease May reactivate years later
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Coccioidomycosis Organism: Coccoides immitis Dimorphic soil organism with spherules and endospores in host Habitat: the lower Sonoran life zone (arid) Southwest US, Mexico, Central and South America Pathogenesis: inhalation of spores
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Cocci Pathophysiology: Spores transform to spherules in lung, elicit cellular immunity as per TB Hematogenous dissemination Skin test reactivity (coccoidin) Clinical: Acute self-limited flu-like seroconversion (Valley fever) Dissemination (pregnancy, dark skin, immuno-compromised) Skin Bone CNS
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Blastomycosis Organism: Blastomyces dermatitidis Dimorphic soil organism Habitat: humid woodlands MidAtlantic countryside Beaver dams, peanut farms Organic debris Pathogenesis: inhalation of spores
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Blastomycosis Pathophysiology: Spores transform into yeast in lung, disseminate. No good antigen test to describe exposed population Clinical: Acute or chronic lung disease (nodular/cavitary) Disseminated disease skin bone urinary tract
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Systemic fungal infections: the “opportunists” “True pathogens” geographic restriction Dimorphic Infection by inhalation Pyogenic/granulo-matous host response Similar to TB Infection ~= immunity “Opportunists” Omnipresent Yeasts or molds Varies routes Host response varies Widely variable No lasting immunity
Slide 19-

Cryptococcosis Organism: Cryptococcus neoformans yeast with thick polysaccharide capsule Habitat: Bioterrorism of a sort, worldwide Pathogenesis: inhalation of yeast
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Cryptococcosis Pathophysiology: transient colonization OR acute/chronic lung disease OR CNS invasion Clinical: Meningoencephalitis acute or chronic fever, headache, stiff neck, loss of vision complicated by hydrocephalus cryptococcal antigen for diagnosis
Slide 21-

Candidiasis Organism: Candida albicans et al Habitat: normal human flora Pathogenesis: colonized areas: overgrowth noncolonized areas: invasion
Slide 22-

Candidiasis Pathogenesis: Breach in Skin or mucosal integrity Normal bacteriologic flora Neutrophil function or CMI Clinical settings: Moisture, antibiotics, pregnancy HIV infection Intravenous catheters Chemotherapy or marrow ablation
Slide 23-

Candidiasis Diagnosis: Gram stain may help Infection and colonization may be difficult to distinguish Treatment: Remove the breach in defenses, if possible
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Aspergillosis Organism: Aspergillus fumigatus and others Mold without a yeast phase Habitat: everywhere, worldwide Pathogenesis: Inhalation of spores
Slide 25-

Aspergillosis Pathophysiology: Spores in lung may elicit allergy grow in preexisting cavity invade vasculature, disseminate (neutrophils key) Clinical: Allergic broncho-pulmonary aspergillosis Aspergilloma Invasive, with pneumonia, other end-organ disease
Slide 26-

Mucormycosis Organism: species of Mucorales, genera Rhizopus and Mucor Mold without a yeast phase Habitat: Everywhere, worldwide Pathogenesis: Inhalation of spores
Slide 27-

Mucormycosis Pathophysiology: Alveolar MPH/PML clear organisms BUT Acid Sugar Neutrophil dysfunction May enable relentless growth Clinical: The most acute and fulminant fungal infection known Pneumonia progressing to infarction Sinusitis progressing to brain abscess