Microbial Mechanisms Of Pathogenicity

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Microbial Mechanisms of Pathogenicity

I. Portals of Entry - avenues where pathogens gain entrance to the body of other hosts. A. Mucous Membranes - Penetration through the lining mucous membrane (respiratory, ,GIT,GUT) - Easiest, most frequent route

-Cold, pneumonia, TB Typhoid, hepatitis, Amoeba, Gonorrhea, Syphillis, AIDS B.Skin - through openings - boring through - grow in the skin

hair follicles hookworm fungi

c. Parenteral – direct deposition through injury puncture, cuts Surgery 

Once entry has been accomplished, most microorganisms have mechanisms of Host attachment( Adherence ) - necessary for virulence & infection(glycocalyx,pilus)

 Adhesions/Ligands

on host cells – – – –

Glycocalyx Fimbriae M protein Opa protein gonorrhoeae – Tapered end pallidum

bind to receptors

Streptococcus mutans Escherichia coli Streptococcus pyogenes Neisseria Treponema

How do Pathogens penetrate Hosts Defenses? 1.Presence of Capsules

impairs phagocytosis

- Streptococcus pneumoniae

2.Components of the Cell Wall *M Protein – Streptococcus pyogenes - Heat & Acid resistant - resists phagocytosis * Fimbria - Neisseria gonorrhea - for attachment * Waxes – Mycolic acid - M. tuberculosis - allows bacteria to grow inside macrophages

3. Production of Enzymes Kinases Digest fibrin clots Hyaluronidase Hydrolyses hyaluronic acid Collagenase Hydrolyzes collagen IgA proteases Destroy IgA antibodies Siderophores Take iron from host ironbinding proteins Coagulase Coagulate blood

4. Antigenic Variation - process by which infectious organisms alters its surface protein to evade the immune system. - can occur through three broadly defined genetic processes: gene mutation recombination switching - consequence of antigenic variation is antigenic escape. 5. Penetration into the host cell cytoskeleton * Invasins – Salmonella strains & E.coli - rearrages actin filaments

How do pathogens damage Host cells? 1. Using the Host’s nutrients Fe(Iron) – used by most pathogens -pathogens release siderophores that take iron away from iron transport proteins in host. 2. Direct damage Engulfed bacteria Host cell raptures multiplies inside releasing more Host cell bacteria

3. Production of Toxins Toxin – poisonous substances produced by microorganisms. - about 220 bacterial toxins are known. Toxicity – degree to which a toxin is poisonous Toxigenicity – capacity of organism to produce toxins.







Toxemia – presence of toxins in the blood Toxins may be produced during a local infection but are released & do their damage systemically. Only small amounts of toxins are enough to cause disease. Recovery from a toxin-induced disease does not necessarily confer immunity.

Toxin induced damage may include: 1. Fever 2. Cardiovascular disturbance 3. Destruction of blood vessels 4. Diarrhea 5. Disruption of the Nervous System 6. Plasma membrane disruption 7. Inhibition of protein synthesis 8. Shock

Types of Toxins: A. Exotoxins B. Endotoxins A. Exotoxins - Proteins (enzymes) - produced inside cells & do their damage upon release - harmful even in small amts - mostly seen in Gram +



A-B toxins or Type III toxins

Types of Exotoxins based on target sites: a. Cytotoxins – disrupts host cells - gas gangrene diphtheria, scarlet fever b. Enterotoxins – disrupts the lining of the GI tract - food poisoning diarrhea

c. Neurotoxins – disrupts nerve cells - botulism, tetanus Antitoxin – antibodies that binds & inactivates toxins Toxoid – physically or chemically inactivated exotoxin - vaccines

Exotoxins

B. Endotoxins – Lipid A portion of LPS - weak in terms of Host damage induced except when given in large quantities. - associated exclusively with Gram- negative bacteria - exerts their effect only upon release from cell envelope(lysis)

Endotoxin





Bacterial cell lysis is the consequence of the action of some antibiotics and thus a temporary worsening of symptoms may accompany upon initiation of antibiotic therapy. Most of the time all endotoxins produce the same symptoms. - consequence of the body reacting to the endotoxins rather than the endotoxins exerting specific effect on the host.



Host responses to endotoxins: 1. Fever 2. Chills 3. weakness 4. Aches 5. septic shock 6. death

Cytopathic Effects of Viruses

Pathogenic Properties of Fungi   







Fungal waste products may cause symptoms Chronic infections provoke an allergic response Tichothecene toxins inhibit protein synthesis Fusarium Proteases Candida, Trichophyton Capsule prevents phagocytosis Cryptococcus Ergot toxin Claviceps





Aflatoxin Aspergillus Mycotoxins Neurotoxins: Phalloidin, amanitin

Pathogenic Properties of Protozoa   

Presence of protozoa Protozoan waste products may cause symptoms Avoid host defenses by - Growing in phagocytes - Antigenic variation

Pathogenic Properties of Helminths   

Use host tissue Presence of parasite interferes with host function Parasite's metabolic waste can cause symptoms

Portals of Exit: - related to the part of the body that has been infected - microorganisms may use the same portals of entry & exit secretions excretions discharges shed tissue - Respiratory GIT, GUT

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