Bacterial mechanism 5
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Bacterial mechanism 5

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Bacterial mechanism 5 Bacterial mechanism 5 Presentation Transcript

  • LOGO BACTERIAL MECHANISMS OF PATHOGENICITY VETERINARY MEDICINE BRAWIJAYA UNIVERSITY
  • PATHOGENICITY1 VIRULENCE2
  • disease Metabolite production/ toxigenicity Damage the host tissue Penetrate / no penetration Evade host defenses Adhere to host tissue HOW MICROORGANISMS ENTER A HOST Transmissibility Evade the host Immune system
  • Transmission Direct: sexual contact, contact with patient lesion Indirect: By vector (mechanic & biologic) Via contaminated materials: air, water, food, equipment, etc
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  • Mucous Membranes -Respiratory tract: inhaled into the nose or mouth influenza, pneumonia, tuber- culosis, etc -Gastrointestinal tract Most microbe HCl & enzymes in the stomach or small intestine or by bile Pathogens are eliminated from the host with feces Transmitted via food, water, contaminated finger Poliomyelitis, hepatitis A & E, shigellosis, amoebic dysentery, salmonellosis, etc -Genitourinary tract Most as sexually transmitted disease (STD) herpes, warts, etc -Conjunctiva Most by contaminated fingers Secreted via discharge conjunctivitis PORTALS OF ENTRY Skin -The largest organs of the body - Is a important defense mechanism against pathogens -Unbroken skin impene- trable by the most m.o -Enter by opening skin (hair follicles, sweat gland ducts), injury The parenteral route -If the pathogen directly into the tissues beneath the skin or mucous membrane when the barriers are penetrated or injured -Via punctures, injection, bites, cuts, wounds, surgery & splitting due to swelling or drying -Hepatitis virus, gangrene, tetanus, rabies, etc. HOW MICROORGANISMS ENTER A HOST
  • THE PREFERRED PORTAL OF ENTRY Entered the body cause disease???? The occurrence of disease depends on several factors  Many pathogen have a preferred portal of entry  Number the organism  The presence of normal flora  Host condition (immune system)
  • Enzymes Tissue-degrading Enzymes  lecithinase, collagenase degrade the major protein of fibrous connective tissue invasion  coagulase work conjunction with serum factor fibrin wall around the bacteria lesions persist in the tissue & protect them from phagocytosis, antibody & drugs  Hyaluronidase hydrolyze hyaluronic acid ground substance of connective tissue  Streptokinase (fibrinolysin) dissolve coagulated plasma, fibrin clots
  •  Cytolysin hemolysins/streptolysins, leucosidins  IgA1 Proteases  Produce some bacteria causing disease  Split IgA1 at specific proline-threonine or proline-serine bonds in hinge region IgA1 (antibody) inactivation
  • Antiphagocytic factors Some pathogens evade phagocytosis or leukocytes microbicidal  Staphylococcus aureus , has surface protein A binds to Fc of IgG  Streptococcus pneumoniae polysaccharide capsule  Streptococcus pyogenes (group A) protein M  Mostly show much antigenic heterogeneity  > 90 capsular polysaccharides  > 80 protein types
  • Intracellular Pathogenicity Some m. o. live and grow in the hostile environment , in polymorphonuclear cells, macrophages, or monocytes  Prevent phagolysosomes fusion and live in cytocol of the phagocyte cells  Or may be resistant to lysosomal enzymes & survive in phagolysosome Resistant to phagocyte killing mechanism Difficult reached by antibody and by drugs
  • Antigenic Heterogeneity The surface structure of bacteria have considerable antigenic heterogeneity Antigenic drift Antigenic shift Antigenic changes
  • Iron requirement Iron is essential nutrient for the infectious process Iron has a wide oxidation-reduction potential important for variety of metabolic function The host’s iron metabolism denies pathogenic bacteria an adequate source of iron for growth Bacteria have developed several methods to obtain sufficient iron for essential metabolism  Siderofor catechol (phenolate): enterobactin hydroxamate The availability of iron affects the virulence of pathogens
  • The role of biofilm Exopolysaccharides produces by the bacteria Mucilagenous layer  Adhere to hard surface  Bind between bacteria Produces by one species bacteria or more than one species Difficult reached by immune system Difficult reached by some antimicrobial drugs
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