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Pathogenesis of bacteria

Pathogenesis of bacteria. Original and development of Bacterial Infection. Infection ：. the invasion of a host organism's bodily tissues by disease-causing organisms, their multiplication, and the reaction of host tissues to these organisms and the toxins they produce. Pathogen:

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Pathogenesis of bacteria

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  1. Pathogenesis of bacteria

  2. Original and development of Bacterial Infection

  3. Infection： the invasion of a host organism's bodily tissues by disease-causing organisms, their multiplication, and the reaction of host tissues to these organisms and the toxins they produce.

  4. Pathogen: • A disease causing microorganism. • Nonpathogen: • A microorganism that does not cause disease. • Opportunistic pathogen: • A microorganism does not cause disease in normal conditions, • but is capable of causing disease under contain conditions.

  5. A bacterial infectious disease is a multi-factorial event which depends on: • Nature (virulence factors)of bacterial species or strain. • Immune status of bacteria invading hosts. • Environment conditions • Pathogenesisof microbial infection includes: • a) general process of infection • b) mechanisms of microbes causing disease transmissibility, adherence to host cells, invasion of host cells and tissues, toxigenicity, and ability to evade the host's immune system

  6. Pathogen--Pathogenicity The ability of a microorganism to cause disease • Factors that determine bacterial pathogenicity: • Virulence:The quantitative ability of a pathogen to cause disease that containing invasiveness and toxigenicity. • The amount of entry • The portal of entry

  7. LD50 (Lethal Dose, 50%) : • The number of pathogen required to cause lethal disease in half of the exposed hosts. • ID50 (Infective Dose, 50%) : • The number of pathogens required to cause disease or infection in half of the exposed hosts.

  8. Surface molecules on a pathogen, called adhesins or ligands, bind specifically to complementary surface receptors on cells of certain host tissues. E. Coli bacteria on human bladder cells Bacteria adhering to human skin • Adhesion (adherence, attachment): the process of microbes sticking to the surfaces of host cells. • Adhesion is a key initial step during infection (then invasion).

  9. Invasiveness: The process of microbes entering host cells or tissues as well as spread in the body. • Toxigenicity: The ability of a microorganism to produce toxins that contributes to the development of disease.

  10. intracellular bacteria: capable of living and reproducing either inside or outside cells Listeria monocytogenes Salmonella Brucella Mycobacterium Yersinia Neisseria meningitidis Cryptococcus neoformans • extracellular bacteria: capable of replicating outside of the host cells

  11. Source of infections • Exogenous infection • Infections caused by infectious agents that are come from the external environment or other hosts (patient, carrier, diseased animal or animal carrier). • “carrier”:individuals infected with infectious agents but no clinical signs or symptoms. • Endogenous infection • Infections caused by normal flora under certain conditions (opportunistic infection)

  12. Transmission of bacterial infection • Bacteria can be transmitted in airborne droplets to the respiratory tract, by ingestion of food or water or by sexual contact. • Specific bacterial species are being transmitted by differentroutes to specific sites in the human body: • Respiratory tract (Mycobacterium tuberculosis) • gastrointestinal tract (pathogenic E. coli) • Genitourinary tract (Neisseria gonorrhoeae) • Closely contact • Insect bite (Rickettsia) • Blood transfusion • Skin and other mucosa (eye)

  13. Common Diseases contracted via the Respiratory Tract • Common cold • Flu • Tuberculosis • Whooping cough • Pneumonia • Measles • Strep Throat • Diphtheria

  14. Mucus Membranes • Gastrointestinal Tract • microbes gain entrance thru contaminated food & water or fingers & hands • most microbes that enter the G.I. Tract are destroyed by HCL & enzymes of stomach or bile & enzymes of small intestine

  15. Common diseases contracted via the GastrointestinalTract • Salmonellosis • Salmonella sp. • Shigellosis • Shigella sp. • Cholera • Vibrio cholorea • Ulcers • Helicobacter pylori • Botulism • Clostridium botulinum

  16. Fecal - Oral Diseases • These pathogens enter the G.I. Tract at one end and exit at the other end. • Spread by contaminated hands & fingers or contaminated food & water • Poor personal hygiene.

  17. Mucus Membranes of the Genitourinary System Gonorrhea Neisseria gonorrhoeae Syphilis Treponema pallidum Chlamydia Chlamydia trachomatis HIV Herpes Simplex II

  18. Types of bacterial infection

  19. According to infectious state: • Inapparent or subclinical infection:The infection with no manifesting clinical signs and symptoms. • Latent infection or Carrier state:The infectionis inactive but remains capable of producing clinical signs and symptoms. • Apparent infection:The infection with manifesting clinical signs and symptoms.

  20. According to infectious sites: • Local infection: The infection is limited to a small area of the body. • Generalized or systemic infection: The infection is throughout the body, it can present as: • Bacteremia (菌血症):Bacteria enter bloodstream without propagation in • bloodstream (bloodstream only used as a channel tool for bacteria • to spread) • -Salmonella • Toxemia (毒血症): Exotoxins enter bloodstream but no bacteria in the blood. • - corynebacterium diphtheriae, clostridium tetani

  21. According to infectious sites: Endotoxemia (内毒素血症):Endotoxins enter bloodstream but no bacteria in the blood. - Shigella Septicemia (败血症):Bacteria enter bloodstream with propagation and release their virelent substances (e.g., toxins). - clostridium perfringens, Yersinia pestis Pyemia (脓毒血症)：Pyogenic bacteria enter bloodstream with propagation and release their virulent substances, and spread through bloodstream into the target organs to form pyogenic foci. - staphylococcus aureus

  22. Normal flora & Opportunistic infections &Hospital acquired infections

  23. All humans have bacteria (normal flora) that living on their external surfaces (skin) and their inner surfaces (Respiratory, Gastroenteric and Genitourinary tract mucosa). Normally due to our host defenses, most of these bacteria are harmless. • The infectious diseases that initiated in hospital are referred to as nosocomial infection(Hospital acquired infection ).

  24. Normal flora • Microorganisms that live on or in human bodies, and ordinarily do not cause human diseases

  25. Distribution of normal flora Skin Flora: Various environment of the skin results in locally dense or sparse microbial populations. Usually Gram-positive bacteria (e.g., Staphylococciand Micrococci ) are predominating. Oral and Upper Respiratory Tract Flora: Various microbial floras can be found in the oral cavity (e.g., anaerobic bacteria) and upper respiratory tract(e.g.,Neisseria, Bordetella and Streptococci ).

  26. Gastrointestinal Tract Flora: In normal hosts, flora in stomach are rare as well as transient, flora in duodenum and jejunum are sparse, and ileum contains moderately mixed flora. Flora in large bowel is dense (109-1011 bacteria/g of the content) and is predominantly composed of anaerobes.

  27. Urogenital Flora: Flora in vaginal (e.g., anaerobes and Lactobacillus) changes with the age of the individual, pH and hormone levels. Distal urethra contains a sparse mixed flora (e.g., Corynebacterium). Conjunctival Flora:Conjunctiva (eye) has few or no microorganisms. However, Haemophilus and Staphylococcus are frequently detected.

  28. Physiological Role of normal flora • Antagonism:a) Normal flora on skin and mucosa of hosts can form biolfilm (as a biological barrier) that acts as colonization resistance of exogenous pathogenic microbes; b) Normal flora may antagonize exogenous pathogens through the production of antibiotics. • Trophism: Normal flora in the intestinal tract synthesizenutrients that can be absorbed by human (e.g., vitamin K and vitamin B). • Immunoenhancement: Normal flora promotes the development of local lymphatic tissues (e.g., Peyer’s patches in the intestines).

  29. Conditions that opportunistic pathogens cause human diseases • Alteration of colonization sites • Declination of the host immunity defense • Dysbacteriosis -the state in which the proportion of bacterial species and the number of the normal flora colonizing in a certain site of a host present large-scale alteration

  30. Opportunistic infections (Infections caused by normal flora)

  31. “Opportunity” for opportunistic infection I. Low immunity of human body: Normal flora that usually don't cause disease in a person with a healthy immune system. If a person with a poor immunity, some of them can cause infection. II. Translocation of normal flora:Members of normal flora removed from the original inhabitancy into bloodstream or other tissues, these microbes may become pathogenic. III. Suppression of normal flora:When some numbers of normal flora are killed or inhibited, it creates a partial local void that tends to be filled by exogenous microbes or microbes from other parts of the body. Such microbes behavior as opportunists and some of them may be pathogens.

  32. Hospital acquired infections (Nosocomial infections)

  33. Hospital acquired infections specially indicate the opportunistic infections acquired during hospital stays. Formally, they are defined as infections arising after 48 hours of hospital admission. • Hospital acquired infections can be bacterial, viral, fungal or even parasitic. The most common pathogens include Staphylococci, Pseudomonas,Escherichia coli and Saccharomyces (fungus). • Most of microbes causing hospital acquired infections usually have a high resistance to antibiotics. • Prevention of hospital acquired infections includes personal hygiene (patients and hospital staff), a clean and sanitary environment in hospital, and complete sterilization of medical materials and equipments.

  34. Generally, infection process caused by a bacterial pathogen involves the four steps as the following: I. Adhesion II. Penetration and spread III. Survival and propagation in the host IV. Tissue injury Any bacterial factors involved in the four steps determine the virulence of bacteria.

  35. i. Bacterial virulent factors (Implying of Natureof bacterial species or strain) In step I: Adhesion

  36. BACTERIAL VIRULENCE FACTORS Environmental signals often control the expression of the virulence genes. Common signals include: Temperrature/Iron availability/low ion/ Osmolality/Growth phase/pH/Specific ions

  37. The fist step of bacterial infection is the adhesion to a specific epithelial surface of the host. • Adhesion is a specific interaction and then a specific combination between adhesins (virulent factors) of bacteria and their receptors on the surface of host cells. • Adhesins include lipoteichoic acid (for G+), some of outer membrane proteins (for G-), ordinary pilus (for both) and so on.

  38. receptor Type 1 Bacterium adhesin mannose P Epithelium lipoteichoic acid F-protein • galactose • glycolipids • glycoproteins fibronectin Adhesion E. coli fimbriae

  39. i. Bacterial virulent factors In step II: Penetration and spread

  40. After the adherence, the bacteria may entered into host cells. • Invasion is commonly used to describe the entry of bacteria into host cells, implying an active role for the organisms and a passive role for the host cells. • Invasion often occurs in mucosa of intestine, urinary tract and respiratory tract, and much less in skin.

  41. 1. reside on epithelial surface for a few of bacteria (e.g. Vibrio cholerae) 2. penetrate the epithelial barrier and invade host cells but remain in local tissues for a few of bacteria (e.g. Shigella spp.). 3. pass into the bloodstream and/or from there spreadinto systemic sites including internal organs for many of bacteria (e.g. Salmonella typhi spread into spleen and liver through bloodstream).

  42. Invasive pathogen reach epithelial surface pathogen produce hyaluronidase Pathogens invade deeper tissues

  43. Degradative enzymes • Collagenase:to destroy collagen. There are a lot of collagens in soft tissue including connective tissue. • Hyaluronidase:to destroy hyaluronic acid which is a major component in the matrix of connective tissue. • Coagulase:to coagulate fibrinogen in tissue fluid and plasmainto fibrin. (to protect bacteria from damage by many agents) • Streptokinase/fibrinolysin:The former activatesfibrinogenase to thrombin, which results in the degradation of fibrin. And the latter directly lyse fibrin. • Streptodornase:it is a DNase. • Cytolysins:1)hemolysins (to dissolve red blood cells) • 2) Leukocisins (to kill leukocytes or tissue cells )

  44. i. Bacterial virulent factors In step III: Survival and propagation in the host

  45. After bacteria enter hosts, they must have anti- phagocyte ability for surviving. Surviving is a basis for further propagation of bacteria. • In human body fluids, there are phagocytes, antibody, complement and lysozyme, which can destroy extracellular bacteria. • Some of bacteria can produce anti-phagocyte factors. • Propagation: is the aim of bacteria entering hosts. On the other hand, only certain number for a bacterium can cause disease!!!

  46. Antiphagocytic Substances 1. Polysaccharide capsulesof S. pneumoniae, Haemophilus influenzae, Treponema pallidum ; B. anthracis and Klebsiella pneumoniae. 2. M protein and fimbriaeof Group A streptococci 3. Surface slime(polysaccharide) produced as a biofilm by Pseudomonas aeruginosa 4. O polysaccharideassociated with LPS of E. coli

  47. Antiphagocytic Substances 5. K antigen(acidic polysaccharides) of E. coli or the analogousVi antigenof Salmonella typhi 6.Cell-bound or solubleProtein Aproduced by Staphylococcus aureus. Protein A attaches to the Fc region of IgG and blocks the cytophilic (cell-binding) domain of the Ab. Thus, the ability of IgG to act as an opsonic factor is inhibited, and opsonin-mediated ingestion of the bacteria is blocked.

  48. PHAGOCYTE r r r Fc receptor BACTERIUM Protein A Protein A inhibits phagocytosis immunoglobulin M protein inhibits phagocytosis Complement fibrinogen M protein peptidoglycan

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