Types and Pa Tho Physiology of Fungal Disease

8/2/2019 Types and Pa Tho Physiology of Fungal Disease

1/21

Presented ByDarshan Desai

Sem-VI

Roll No.:-08Pharmacology


2/21

Eukaryotic (organized nucleus and cell

structure)

Non-motile Aerobic

Saphrophytic or parasitic

Cell wall contains glucan and chitin Cell membrane contains ergosterol


3/21

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)


4/21

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)


5/21

Organism: Cryptococcusneoformans yeast with a

thick polysaccharidecapsule

Habitat: bioterrorists (of a

sort), worldwide Pathogenesis: inhalation of

yeasts


6/21

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


7/21

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


8/21

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


9/21

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


10/21

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


11/21

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


12/21

Organism: Aspergillusfumigatus and others

Mold without a yeastphase

Habitat: everywhere,worldwide

Pathogenesis: inhalationof spores


13/21

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


14/21

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


15/21

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


16/21

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


17/21

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


18/21

Organism: Blastomycesdermatiditis

dimorph: mold to yeast

Habitat: humid woodlands MidAtlantic zone

Beaver dams, peanut farms

Organic debris rather thansoil

Pathogenesis: inhalation ofspores


19/21

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


20/21

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


21/21

Documents

Types and Pa Tho Physiology of Fungal Disease