Normal Microbiota Locations and Predominant Microbes Normal by benbenzhou

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									     Normal Microbiota: Locations and Predominant Microbes                                                 Normal Microbiota: Benefits and Detriments
                                                    Predominant Microbes                      Benefits
Skin                           Staphylococcus epidermidis, Micrococcus, Corynebacterium
Eye (conjunctiva)              Staphylococcus epidermidis, Propionibacterium acnes            • Compete with pathogens for attachment sites and resources.
Oral cavity                    Oral cavity                                                    • Stimulate cross-reactive antibodies.
     Teeth                          Streptococcus mutans, Streptococcus sanguis
     Subgingiva                     Anaerobic bacteria (e.g., Actinomyces)                    • Antagonize potential pathogens through the production of antimicrobial
Respiratory Tract              Respiratory Tract                                                chemicals.
     Nostrils                       S. epidermidis, Corynebacterium, Staphylococcus aureus
     Sinuses                        Usually sterile                                           • Synthesize vitamins (K, B12, other B vitamins) and energy.
     Upper respiratory tract        Many (non-Beta hemolytic streptococci, Neisseria)
     Lower respiratory tract        Sparse
Gastrointestinal Tract         Gastrointestinal Tract                                         Detriments
     Upper GI Tract                 Helicobacter pylori
                                                                                              • Dental caries and gingivitis.
     Small Intestine                Sparse (Lactobacillus, Micrococcus)
     Large Intestine                G- coliforms, G+ enterococci, Clostridium, methanogens    • Opportunistic pathogens
Urogenital Tract               Lactobacillus acidophilus, S. epidermidis, Enterococcus
                                                                                                   o Normal microbes in the wrong place
                                                                                                   o Normal microbes with additional genes (plasmids or prophage)
                                                                                                   o Immunocompromised individuals




                               Steps to Pathogenicity                                                                           Transmission
                                                                                             Direct contact Indirect contact (spread by fomites)

                                                                                                                                       Droplet contact (airborne within 1 meter)
                                   1. Transmission


                                           2. Colonization


                                             3. Evasion from host defenses

                                                                                             Vehicle Transmission
                                                     4. Toxicity                             (food, water, airborne > 1M)       Mechanical vector
                                                                                                                                                             Biological vector
                                    Colonization                                                                       Evasion of Host Defenses
                                     Bacterial Cell
                                                 1a. Nonspecific adhesion due to          Evading phagocytosis
                                                     hydrophilic interactions,                Invading tissues where phagocytes do not patrol
                                                     Brownian motion, van der
                                                     Waals forces.                            “Hiding” in host antigens (staphylococcal coagulase, Treponema fibronectin)
                                                                                          Evasion of phagolysosome digestion
                                        1b. Specific adhesion due to binding of
                                                                                              Inhibition of lysosome action (Salmonella, Mycobacterium, Chlamydia)
                                            bacterial adhesins (e.g., surface proteins,
                                            lipoteichoic acid, lipopolysaccharide) to         Escape from phagosome (Ricketssia)
                                            host cell receptor sites.
                                                                                          Killing phagocytes (hemolysins)
                             2.    Secretion of Invasins which are proteins that allow
                                   bacteria to invade host tissues and/or cells.          Induction of ineffective antibodies

                                  Hyaluronidase and Collagenase which break down          Antigenic variation
                                   hyaluronic acid and collagen (which connect host
                                   cells together)
                                  Bacterial Kinases prevent clotting of blood.
       Host Tissue                Neuraminidase destabilizes host cell membrane and
                                   enhances intracellular invasion.




                                  Bacterial Toxins                                                                              Exotoxins


                                                                                                                                                                Lysogenic
                                                                                                                                          Exotoxin
                                                                                                                                                                conversion
                                                                                                                                  A-B toxin. Inhibits protein
                                                                                            • Corynebacterium diphtheriae                                            +
                                                                                                                                    synthesis. Cytotoxin.

Source               Gram– Source                       Mostly Gram+ (but also G-)
                                                                                            • Streptococcus pyogenes
                                                                                                                                    Membrane-disrupting.
                                                                                                                                                                     +
                                                                                                                                       Erythrogenic.
                            Metabolic product           By-products of growing cell
Metabolic product    LPS (Lipid A) of cell wall
                                                                                            • Clostridium botulinum                 A-B toxin. Neurotoxin            +
Chemistry            Lipid        Chemistry             Protein

                             Fever?                     Various but specific                • C. tetani                             A-B toxin. Neurotoxin
Symptoms             Fever, Shock, Inflammation
                             Neutralized by             Yes                                 • Vibrio cholerae                      A-B toxin. Enterotoxin            +
Toxoid Formation     No
                             antitoxin
LD50                         LD50
                     Relatively large                   Small                               • Staphylococcus aureus               Superantigen. Enterotoxin.
                          Extent of Host Involvement                                                                  Classifying Infectious Diseases

•   Local infection        Pathogens limited to a small area of the body                      Communicable disease         A disease that is spread from one host to another.

•   Systemic infection     An infection throughout the body
                                                                                              Contagious disease           A disease that is easily spread from one host to another.
•   Bacteremia             Bacteria in the blood
•   Septicemia             Growth of bacteria in the blood                                    Noncommunicable disease A disease that is not transmitted from one host to another.
•   Toxemia                Toxins in the blood
                                                                                              Endemic disease              Disease constantly present in a population.
•   Viremia                Viruses in the blood
•   Primary infection      Acute infection that causes the initial illness                    Epidemic disease             Disease acquired by many hosts in a given area in a
•   Secondary infection    Opportunistic infection after a primary infection                                               short time.

•   Subclinical disease    No noticeable signs or symptoms (inapparent infection)             Pandemic disease             Worldwide epidemic.


                                                                                              Herd immunity                Immunity in most of a population.




                            The Stages of a Disease                                                           Nosocomial (Hospital-Acquired) Infections

                                                                                                Are acquired as a result of a hospital stay
                                                                                                5-15% of all hospital patients acquire nosocomial infections
                                                                                                Why are nosocomial infections so prevalent?
                                                                                                    Pathogenic microbes present in health care settings
                                                                                                    Immunocompromised patients present in health care settings
                                                                                                    Multiple modes of transmission (air, puncture wounds, direct contact)
                                                                                                Why are nosocomial infections so dangerous?
                                                                                                    Multiply antibiotic resistant strains


                                                                             Sequela




                                                                                Figure 14.5

								
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