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![Page 1: Prof. Khalifa Sifaw Ghenghesh Dept. of Medical Microbiology, Faculty of Medicine, Tripoli University, Tripoli-Libya بسم الله الرحمن الرحيم BACTERIAL PATHOGENESIS.](https://reader035.fdocuments.in/reader035/viewer/2022070412/56649ee15503460f94bf240e/html5/thumbnails/1.jpg)
Prof. Khalifa Sifaw GhengheshDept. of Medical Microbiology,
Faculty of Medicine, Tripoli University,
Tripoli-Libya
الرحيم الرحمن الله بسم
BACTERIAL PATHOGENESIS
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The Pathogen:• A Disease Producing Microorganism.
Pathogenicity: • Capacity to Initiate Disease.
Virulence: • Capacity to Harm the Host.• Refer to Degree of Pathogenicity.
Opportunistic Pathogens: • Common or Non Pathogenic Microbes. e.g.
Normal Flora of the Body.
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Infection: • The Lodgement and Multiplication of a
Parasite in or on the Tissues of a Host.
Disease: • A Rare Consequence of Infection.
Measurement of Virulence:• The Median Lethal Dose (LD50) is Used.
• Number of Microorganisms or Micrograms of Toxin Required to Kill 50% of Infected Animals.
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Koch's Postulates
Isolated• diseased not healthy people
Growth• pure culture
Induce disease• susceptible animals
Re-isolated• susceptible animals
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Virulence factors (Determinants of pathogenicity)
Number of initial organisms
Immune status
PATHOGENICITY
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VIRULENCE FACTORS
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Virulence factors help bacteria to: • Invade the host,
• Cause disease, and
• Evade host defenses.
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1 .Toxigenicity
Tissue injury:• Exotoxins:
• Include several types of protein toxins and enzymes produced and/or secreted from pathogenic bacteria.
• Include cytotoxins, neurotoxins, and enterotoxins.
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• Endotoxins:• Lipopolysaccharide • Gram-negative bacteria• Endotoxic (Septic) Shock:
• Hypotension (tissue pooling of fluids)• Disseminated intravascular coagulation• Fever• Lack of effective oxygenation• Overall system failure
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Differentiation of Exotoxins and Endotoxins.
Exotoxins Endotoxins----------------------------------------------------------------------------------------Excreted by living cells. -Released after death of
bacteria.-Relatively unstable. -Relatively stable.-Highly antigenic; -Do not stimulate formation stimulate the formation of antitoxin. of high-titer antitoxin.-Converted into antigenic, -Not converted into toxoids. nontoxic toxoids.-Highly toxic. -Weakly toxic.-Do not produce -Often produce fever fever in host. in host.
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2 .Invasiveness
Capacity of a pathogen to spread in the host tissues after establishing infection.
Surface components that allow the bacterium to invade host cells can be encoded on plasmids, but more often are on the chromosome.
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Penetration and spread
Vibrio choleraeVibrio cholerae
SalmonellaSalmonella enteritidisenteritidis
SalmonellaSalmonella typhityphi
EpitheliumEpithelium
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3. Capsules
Antiphagocytic structures
Polysacchride
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The Relatively Stable, Irreversible Attachment of Bacteria to a Surface.• Fimbrial Adhesins
• Nonfimbrial Proteinaceous Adhesins.
4 .Adhesion
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adhesinadhesin
EPITHELIUMEPITHELIUM
receptorreceptor
BACTERIUMBACTERIUM
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E. coli with fimbriae (Pili)
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5. Siderophores
Iron-binding factors that allow some bacteria to compete with the host for iron, which is bound to hemoglobin, transferrin, and lactoferrin.
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6. Other Aggressions
Mainly Enzymes:• Hyaluronidase >> Spreading Factor.
• Coagualse >> Thrombin - Like Enzyme.
• Fibrinolysin >> Streptokinase.
• Proteases >> Hydrolyse Immunoglobulins.• Others