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Presented ByDarshan Desai
Sem-VI
Roll No.:-08Pharmacology
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Eukaryotic (organized nucleus and cell
structure)
Non-motile Aerobic
Saphrophytic or parasitic
Cell wall contains glucan and chitin Cell membrane contains ergosterol
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Classified into four main types on the basisof their morphological and othercharacteristics:-
Yeasts (unicellular, budding)
Molds-yeast like fungi (hyphae, mycelia,spores)
Filamentous fungi with a true mycelium
Dimorphs (both)
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Fungal Disease Organism
Meningitis Yeasts (Cryptococcus neoformans)
Candidiasis Molds (Candida albicans)
Ringworm Filamentous Fungi(Epidermophyton floccosumTrichophyton spp.Microsporum spp.)
Pulmonary aspergillosis Filamentous fungi (Aspergillusfumigatus)
Histoplasmosis Dimorphic Fungi(Histoplasma capsulatum)
Coccidiomycosis Dimorphic Fungi(Coccidioides immitis)
Blastomycosis Dimorphic Fungi(Blastomyces dermatides)
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Organism: Cryptococcusneoformans yeast with a
thick polysaccharidecapsule
Habitat: bioterrorists (of a
sort), worldwide Pathogenesis: inhalation of
yeasts
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Pathophysiology:
Inhalation leads to
Transientcolonization
OR
Acute/chronic lung
disease OR
CNS invasion
Clinical Pneumonia OR Meningoencephalitis Acute or chronic Fever, headache, stiffneck, fever, delirium
Hydrocephalus
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Organism: Candida albicans etal (yeasts with hyphal forms)
Habitat: normal human flora
Pathogenesis:
Colonized areas: change inenvironment leads to
overgrowth Noncolonized areas: change in
immunity leads to invasion
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Pathogenesis of Candidainfections Primary host defenses:
Intact skin Intact mucosa withnormal pH and normalflora
Functioning lymphocytes Functioning neutrophils
Pathogenesis of localCandidainfections
Environmentalchanges Wet skin Changes in local flora
Hormones, foreignbodies Lymphocyte
dysfunction Immaturit
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Pathophysiology:- Surface molecules that
permit adherence of theorganism to otherstructures (eg, humancells, extracellular matrix)
Acid proteases andphospholipases that
involve penetration anddamage of cell envelopes
Ability to convert to ahyphal form (phenotypic
switching)
Clinical:-Granulomatousvasculitis
Diffuse cerebritiswith microabscessesMycotic aneurysmsMental status
changesFeverNuchal rigidity
ConfusionComa
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Organism:-Trichophyton,Microsporum,Epidermophyton floccosum
Habitat: soil, worldwide Pathogenesis: grow as
saprophytes on skin/nails;cause inflammation
below; introducedthrough skin by foreignbody, grow insubcutaneous tissues,spread via lymphatic
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Pathophysiology:-The fungus does not invade livingtissue but the fungus and itsmetabolic products cause
inflammation.Epidermophyton floccosumcauses athletes foot in humans
usually in the web area betweentoes and is common inshoewearingpeople because its favoured by
warm, humid conditions.
Clinical:Tinea crurisTinea corporis Tinea pedisTinea unguum Tinea capitis
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Organism: Aspergillusfumigatus and others
Mold without a yeastphase
Habitat: everywhere,worldwide
Pathogenesis: inhalationof spores
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Pathophysiology:-Spores in lung may: Elicit allergy
Grow in preexistingcavity Invade vasculature,disseminate with localand distant disease Neutrophils primedefenders
Clinical:- Allergicbronchopulmonary
aspergillosis Aspergilloma Invasive aspergillosi
with pneumonia, otheend-organ disease
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Organism: Histoplasma capsulatum
Soil dimorph (yeast in body, mold inenvironment)
Habitat: soils with high N content Ohio-Mississippi valley; Caribbean;
Central and S. America
Guano of bats, birds, poultry
(chicken coops and caves Pathogenesis: inhalation of spores
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Pathophysiology: Mold spores transform
into yeast in lung, elicitcellular immunity as perTB Hematogenousdissemination Skin test reactivity Walled off granulomata
Clinical:Mimics TB. Usually
latent disease, but may cause acute/chrocavitary lung disease
may disseminate afterinfection (infancy,immunocompromise) may reactivate years la
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Organism: Coccidioidesimmitis
Dimorph: mold in soil,
spherules and endospores inhost
Habitat: lower Sonoral lifezone (arid):Southwest US,
Mexico, Central and SouthAmerica
Pathogenesis: inhalation of
spores
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Pathophysiology:
Spores transformintospherules in lung, elicit
cellular immunity asper TB Hematogenous
dissemination Skin test reactivity Walled offgranulomas
Clinical:
Acute self-limited flu-likeseroconversion
syndrome(Valley fever) Acute or chronic lung
disease Dissemination(pregnancy, dark skin) Skin, Bone, CNS
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Organism: Blastomycesdermatiditis
dimorph: mold to yeast
Habitat: humid woodlands MidAtlantic zone
Beaver dams, peanut farms
Organic debris rather thansoil
Pathogenesis: inhalation ofspores
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Pathophysiology: Spores transform intoyeast in lung,
disseminate No good antigen testto define exposed
Population
Clinical: Acute or chronic lungdisease
(nodular/cavitary) Disseminateddisease:
Skin Bone Urinary tract in men
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1. H.P.Rang and M.M.Dale et al. 2007,Pharmacology (6thedition), churchilllivingstone elsevier,684-688
2. Principles Of Anatomy And PhysiologyBy-gerard J.Tortora,12th Edition Pg No-969-970
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