Introduction to Microbial Pathogenesis

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 ntroduction

to

Microbial (thok kq ) 

Pathogenesis

(jksxtuu )

By: Rahul MalikJanuary, 2016

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Infectious Agent

• “A single [type] of micro-organism could beisolated from all animals suffering from anthrax;

• The disease could be reproduced in anexperimental host by infection with a pureculture of this bacterium; and

• The same [type] of micro-organism could

subsequently be reisolated from theexperimental host.” 

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Infectious Agents in Humans

• Prion - scrapie

• Viruses – HIV, influenza

• Bacteria – Mycobacterium tuberculosis• Fungi – Candida albicans

• Protozoa – Plasmodium falciparum

• Helminths – Schistosoma mansoni

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Normal Abnormal

Prion

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Virus

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Bacteria

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Fungi

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Protozoa

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Helminths

 Ascaris lumbricoides : human intestinal roundworm

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Barriers 

Physical barrier : Skin, Mucosal gel overlaying

epithelium (respiratory, gastrointestinal, urogenitary)

Microbiological barrier : Normal microbioflora

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Initiation of Disease

contact with pathogenic organism:

human to human, animal to human

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Transmission

•  Aerosols to respiratory mucosa

• Fomite to nasopharyngial or conjungtive

mucosa

• Fecal – Oral Route

• Mucosal surface to mucosal surface

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Transmission

Multiplication

Dissemination

Invasion

Breach of epithelium

Colonization of mucosa

Infectious Disease Cycle

or

 Attachment to target cells

To subepithelial or intracellular space

Evasion of

host defense

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Invasion

Bacterial Viral

•Transcytosis across superficial

epithelium to subepithilial space

•Induce engulfment by non-

phagocytic host cells

•Local reararrangement of host

cell cytoskeleton

•Phagocytosis

•Utilization of membranous cell

gateway

•Pass through plasma membrane

•Membrane invagination

•Clathrin

•Fusion with host cell plasma

membrane

•HIV gp120/41

•T lymphocyte CD4

•Macrophage CCR5

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Evasion/Manipulation of Host Defense

•  Modulation of innate/inflammatory response

•  Resistance to phagocytic killing in subepithelial space

•  Serum resistance

•  Antigenic variation

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Cell and Tissue Damage

•  Induction of apoptosis and necrosis

•  Virus-induced cytopathic effect

•  Induction of damaging host immune response