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27 Cards in this Set
- Front
- Back
Normal Flora
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10 to 13 human cells and 10 to 14th bacterial cells
Definition microorganisms that colonize the body but do not normally produce diseases Locations parts of the body that are exposed or communicate with the outside environment Semi-permanent acquired during and shortly after birth varies continuously throughout life Three types of symbiosis Commensalism Beneficial to one partner while the other is unaffected Mutualism Interactions between two organisms in which both organisms benefit Parasitism Beneficial to one partner while harmful to the other |
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Some important microorganisms of the normal flora and our interaction with these organisms.
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Skin: few residents in dry areas; large population in moister places
Mouth & nose: high microbial density Teeth: plaque = biofilm of bacteria Lungs: normally quite sterile Urethra: lightly colonized Vagina: extensive flora; age-related changes (lactobacillus) |
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What are the advantages and disadvantages of the normal flora.
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Advantage of Normal Flora:
• Antigenic stimulation Æ helps development of immune system • Preventing colonization by pathogens through microbial antagonism (i.e. competitive exclusion) by o competing with pathogens for nutrients & space o producing toxic factors or environmental conditions harmful to pathogens • Other: o production of vitamins B and K by gut flora Disadvantage of normal flora: • Harmful when overgrown or misplaced due to use of broad-spectrum antibiotics or when fecal flora are transferred to urinary tract |
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What are nosocomial infections and some of the major microorganisms causing nosocomial infections.
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Hospital-acquired infections (≠ community acquired infections)
Hospitals = major reservoir of opportunistic pathogens and antibiotic-resistant pathogens Compromised status of host, results from: invasive procedures (surgery, anesthesia) suppressed immune systems (drugs, radiations) Transmission routes person-to-person fomite (i.e. through non-living objects: e.g. needles, respiratory aids…) |
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1. Infection
2. Etiologic Agent 3. Pathogenesis 4. Predisposition factors |
Infection
colonization of body by pathogenic microbes may exist without symptoms of a disease Etiologic agent the cause of disease Pathogenesis how the disease develops Predisposition factors make the host susceptible to a disease e.g. gender, genetic background, geographical location, age, life style, immune status etc… |
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What bacterial pathogens are and the difference between opportunistic and primary pathogens.
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Strict pathogens
always associated with human diseases e.g. Mycobacterium tuberculosis (tuberculosis), Neisseria gonorrhoeae (gonorrhea)… Opportunistic pathogens take advantage of preexisting conditions that enhance susceptibility of patient to cause a disease or a more serious disease many of them are members of the patient’s normal microbial flora – e.g. Pseudomonas aeruginosa, Candida albicans |
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What are the mechanisms of bacterial pathogenesis
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Enter the environments (us)
Remain in the niche – colonization Gain access to food sources Escape clearance by host protective responses Problem Æ cause damage to human host |
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What are the portals of entry and exit?
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Natural openings
Respiratory tract – inhalation (e.g. Mycobacterium tuberculosis, S. pneumoniae) Gastrointestinal tract – ingestion (e.g. Salmonella, E. coli) Genitourinary tract – sexual transmission (e.g. Neisseria gonorrhoeae, Chlamydia trachomatis) Skin trauma (e.g. Clostridium tetani) arthropod bite (e.g. Rickettsia, Yersinia pestis) Exit from the host transmission to a fresh host shed in large numbers in secretions and excretions available in blood for uptake, e.g. blood-sucking arthropods or needles |
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What determines host suseptability?
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Organism factors overcome host factors!!!
Host Factors: Immune system Organism Factors: Dose and Virulence (ability to cause disease by host colonization, evation of host defenses and damage=disease) |
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What are the factors involved in colonization?
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Adhesion
to epithelial or endothelial cells of bladder, intestine, respiratory tract, blood vessels… major mechanisms pili adhesin proteins teichoic acid biofilm |
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Invasion
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After adhesion, invasive micro-organisms have the ability to penetrate the target tissue
Some invasive bacteria use normal phagocytic entry mechanisms to gain access Other invasive bacteria can enter host cells which are not naturally phagocytic, by specific attachment to the host cell production of surface proteins called invasins induction of local rearrangements of the cytoskeleton ð formation of pseudopod-like structures which engulf the pathogen into the host cell |
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Legionnaire’s Disease pathogenesis
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1) Attaches to alveolar macrophages Æ coiling phagocytosis
2) Prevents phagosome-lysosome fusion 3) Replication inside the phagosome 4) Lysis of phagocytes Hydrolytic enzymes Æ Lung damage & Inflammatory response |
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Salmonella enteric pathogenesis
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1. Adherence to mucosal surface induce changes in enterocyte or M cell Æ triggers surface ruffles
2. Ruffles = plasma membrane sites with filamentous actin cytoskeletal rearrangement 3. Uptake of organisms within host cell membrane-bounded vesicles |
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Evasion
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Bacteria have developed ways to avoid the major antibacterial defenses by inactivating or evading the host system and antibody
evading recognition and killing by phagocytes growing inside cells to hide from these host responses Ways to evade complement or antibody response: Intracellular growth (e.g. Mycobacteria, Chlamydia) Antigenic variation, mimicry or masking (e.g. Neisseria gonorrhoeae) Inactivation of antibody or complement (e.g. IgA-specific protease) Capsule and Biofilm - prevents antibody and complement from reaching the bacteria Protection of the membrane from attack (e.g. LPS O antigen prevents; M protein in S. pyogenes) Ways to escape phagocytosis: Preventing contact with phagocyte (e.g. capsule) Preventing opsonization Production of enzymes capable of lysing phagocytes streptolysin produced by S. pyogenes α-toxin produced by C. perfringens Ways to evade phagocytic killing: Inhibition of phagolysosome fusion; Resistance to lysosome products; Escape from phaogosome and propagation into cytoplasma |
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Mechanisms of Host Damage
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1. By-products of bacterial growth – tissue destruction
acids or gas from fermentation 2. Degradative enzymes break down host tissues & facilitate development of infection and spread into the tissue phospholipase, collagenase, protease, hyaluronidase... 3. Toxins directly harm tissue or trigger destructive biologic activities endotoxins: cell wall components freed when cells die and break up. exotoxins: soluble proteins released by living bacterial cells 4. By inducing hypersensitivity reactions |
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Endotoxins
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• Endotoxins: cell wall components freed when cells die and break up
o gram(-) lipopolysaccharide = endotoxin o in gram(+): teichoic and lipoteichoic acids – endotoxin-like effects o peptidoglycan and its breakdown product • Lipopolysaccharide (LPS) activates almost every immune mechanisms as well as the clotting pathway • Low concentrations Æ fever, vasodilatation, and activation of immune and inflammatory responses • High concentrations o Æ excessive response – shock & death |
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Exotoxins
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• Proteins released by living bacterial cells
• Local effect or effect at sites distant from the site of infection • Often receptor-binding proteins that alter a function and/or kill the cell • Toxin genes often on plasmid or lysogenic phage • Cytolysins: enzymatic lysis and pore forming |
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How do intracellular-acting toxins access their substrates with the host cells?
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• AB toxins
• released into the host environment • may act locally or diffuse to act distally • B subunit = binding component; interacts with receptors on the cell membrane & promotes entry • A subunit = active component • Targets: ribosomes, transport mechanisms, intracellular signaling (cAMP production, G protein function) • Direct injection of toxins through flagella or pilus into host cells by Type III or IV secretion systems, respectively • Finally, Bordetella adenylate cyclase toxins directly enter the cytosol from the plasma membrane |
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Examples of intracellular-acting toxins
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1. Diphtheria toxin
2. Cholera toxin 3. Neurotoxins |
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Diphtheria toxin
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• Inhibition of protein synthesis
• Inactivation of elongation factor-2 Æinactivates transfer of amino acids from tRNA to the polypeptide chain during translation of mRNA by ribosomes • Infection of mucosa of oropharynx • Multiplication of bacteria and production of toxin • Exotoxin activity Æ death of surrounding cells • È • Inflammatory reaction leads to collection of a gray exudate which evolves into thick pseudomembrane • This coating adheres strongly to mucosa and may extend into larynx/trachea ð obstruction and suffocation |
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Cholera toxin
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• Hyperactivation
• A1 portion ADP-ribosylates a regulatory molecules involved in production of cAMP Æ increase in intracellular cAMP |
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Neurotoxins
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• Both are AB toxins
• Tetanus toxin: • blocks release of inhibitory neurotransmitters Æ unopposed firing of the motor neurons Æ constant contraction • Botulinum toxin: • blocks release of acetylcholine from peripheral nerves Æ preventing contraction Æ flaccid paralysis |
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Superantigens
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• Bind to the external regions of the T-cell receptor and the major histocompatibility complex class II (MHC II) on macrophage
• nonspecific interact • Æ massive release of cytokines • E.g. S. aureus TSST-1 (Toxic Shock Syndrome Toxin) |
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S. aureus and Toxic Shock Syndrome
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• Often associated with use of tampons, but can result from focal infections at any body site by toxin-producing S. aureus
• The organism does not disseminate; the toxin does and is responsible for the clinical features***** • Sudden onset: fever, vomiting, diarrhea • Then: red rash resembling a sunburn and desquamation 1-2 wks later • Hypotensive shock, impaired renal and hepatic functions, occasional deaths • 3% of all cases are fatal |
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Important Bacterial Virulence Mechanisms
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1. Colonization
• Adherence • Biofilm 2. Damage • By-products of growth (gas, acid) • Endo/Exotoxins • Degradative enzymes • Cytotoxic proteins • Superantigens 3. Evading host defence • Evasion of phagocytic and immune clearance • Capsule / Biofilm • Intracellular growth 4. Resistance to antibiotics |
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Classify infectious diseases
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• Epidemic diseases: Infectious diseases that attacks many people at the same time in the same geographical area.
• Endemic diseases: Diseases that constantly present in a local population, e.g. Malaria • Pandemic diseases: Worldwide occurrence, e.g. plague, AIDS |
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Koch’s Postulates
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• Purpose: to establish the etiology (cause) of an infectious disease.
• Experimental procedures: • Same pathogen must be present in every disease case. • The pathogen is isolated from the diseased host and grown in pure culture. • The pathogen from the pure culture is inoculated into a susceptible animal and must be shown to reproduce the same disease. • The pathogen must be isolated from the animal and be shown to be the same as the original organism. • Exceptions to Koch's Postulates • Pure culture cannot be obtained using artificial media, e.g. Treponema pallidum (syphilis). • No experimental animal (so Step 3 and 4 cannot be carried out). |