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43 Cards in this Set
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- Back
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Normal microbiota (flora)
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microbes that inhabit particular sites in human host without causing serious harm
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Where can you find normal flora
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growth limited to surface of skin and mucous membranes
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Normal flora are co-adapted for maximal stability and minimal harm
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Commensalism - microbe benefits with neutral effect on host
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Syngergistic - both microbe and host benefit
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How are normal flora protective to host?
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compete with pathogens for attachment and nutrients
produce bacteriocins (toxic peptides that kill closely related species) prime immune system |
produce vitamins and other beneficial substances (E. coli and vitamin K)
aid in digestion of food |
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How can normal flora cause disease?
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weakened host defenses
transferred to a part of body that they don't normally inhabit opportunistic pathogen usually does not cause disease but can under certain circumstances |
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Pathogencitiy
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ability of microbe to gain entry to host tissues and bring about change
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Virulence
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degree of pathogenicity
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Virulence Factors
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microbe produced factors that enable invasion
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Pathogenicity islands
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clusters of genes encoding virulence factors
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avirulent strains lack these segments of the genome
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Disease process
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Exposure with infections agents
Colonization Entry Evasion of host defenses Causing damage to host Exit |
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Exposure with infectious agents (endogenous vs exogenous)
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Endogenous infection caused by an agent present on or in one's body
Exogenous infection caused by agents encountered outside one's own body |
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Exposure - What are the reservoirs of infection? Define and give the three reservoirs)
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living or non-living continual source of infection
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Humans, animals (zoonoses), and environment (soil or water)
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Types of Human reservoirs
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communicable disease (person to person)
symptomatic carrier (active case of disease) asymptomatic carrier (not active case of disease) |
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Animal reservoirs
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zoonotic disease (zoonoses)
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Environment reservoirs
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includes non-communicable diseases also, like tetanus
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Exposure - Transmission to new host
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Direct contact and indirect contact
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Transmission via direct contact
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horizontal transmission (person to person or animal to person) via touching or exchange of body fluids
vertical transmission (mother to unborn child) like HIV and gonorrhea |
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Transmission via indirect contact (fomites, vehical transmission, and vectors)
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fomites are contaminated inaminate objects (bed lining, syringes)
vehical transmission from contaminated food, water, or aerosoles vectors are living intermediate carries agent from reservoir to new host (ex - arthropods) |
vectors can be mechanical (passive transport) or biological (replicates in vector)
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Colonization (determining factors)
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infectious dose is number of invading microbes
capabilities of infectious agents - infectivity is ability to attack and multiply and adhesins are microbial proteins that bind to receptor on host cell enabling attachment (usually on pili) |
immune competence of host
health of membrane or normal microbiota - primary infection is inital infection of healthy host and secondary is when there's another infection by different microbe |
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Entry - Invasiveness
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non-invasive - grows on surface
invasive - penetrates cells or tissue |
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Entry - Dissemination (localized and systemic infections)
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localized infection - limited to small area
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systemic infection - toxemia is toxin in blood stream and septicemia is when microbes are in blood (bacteremia, viremia)
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Entry - Cellular entry is facilitated by...
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phagocytosis and invasins which are bacterial proteins that induce uptake by non-phagocytic cells
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Entry - Dissemination factilitated by exoenzymes
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Hyolurinidase - digest hyaluronic acid in ECM
Collegenase - digest collagen in ECM Streptokinase - dissolves fibria clots |
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Evasion of host defenses - Innate
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Capsules not recognized by TLR's/concealed complement activators
Resists phagocytosis cont. on next |
resists engulfment - capsule; coagulase forms blood clot from fibrinogen
leukocidins which are secreted proteins that kill phagocytes survives within phagocytes by escaping from phagosome to cytoplasm or preventing fusion of lysosome with phagosome |
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Evasion of host defenses - Acquired Defenses
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Antigenic variation, destroy/inactivate Ab, block MHC I signaling pathway
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Antigenic variation
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change surface Ag to limit effectiveness of Ab and TCR (TLR?)
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Destroy or inactivate the Ab
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Ig Protease - cleaves Ab molecule
Fc receptor - binds to Fc portion of Ab |
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Block MHC Class I signaling pathway
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Inhibits killing by CTL (killer T cell)
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Causing damage to the Host (Toxins)
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Exotoxins or Endotoxins
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Toxins - Exotoxins
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proteins secreted by bacterial cells
produced by Gram positive and negative |
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Exotoxins are varied, can have specific effect on particular cell, what are two that we covered?
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Enterotoxins - acts on intestinal tract
Nuerotoxins - acts on nervous system |
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Many exotoxins are Ab toxins, what are the two subunits?
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A subunit - toxic component (enzymatic activity harms host cell)
B subunit - delivery component (binds to a receptor on target cell) |
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Are exotoxins toxic only at high concentrations?
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No
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Which is more toxic, exo or endotoxins?
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Exo
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What is the endotoxin, and when is it released?
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Lipid A component of LPS in gram negative outer membrane is released when it is lysed
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What does the Lipid A endotoxin cause?
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Fever and decreased blood pressure (activates complement)
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Where does the pathogen exit?
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Portal of exit usually same as portal of entry
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What is clinical syndrome?
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Array of signs and symptoms associated with a disease.
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What is the difference between a sign and a symptom?
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A sign is measurable/observable change in body function and a symptom is what the patient experiences, something not observable.
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Acute infection
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short incubation period, short duration
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Chronic disease
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longer incubation, much longer duration
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Recurrent disease
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becomes active again following a period of inactivity
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Latent infection
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infectious agent persists in a non-replicating form
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