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34 Cards in this Set
- Front
- Back
The type of host defenses encountered by pathogenic bacteria is influenced by what
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Both the site of infection and the life style of the bacteria
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What is the lifestyle of extracellular pathogens
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Remain attached to the outside of host cells, usually via pili or fimbriae. May cause disease via secretion of toxins (Vibrio cholerae)
Can be invasive via spread through tissue (between cells) (Pseudomonas aeruginosa) |
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Whis is the lifestyle of facultatively intracellular for epithelial, endothelial cells, or other non-professional phagocytes pathogens
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These may live within or outside of host cells
May provide a protected niche for bacterial replication or persistence If invasion is from cell to cell, bacteria can dodge extracellular defenses (Shigella spp) |
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What are two examples of obligate intracellular pathogens
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Chlamydia spp; Rickettsia
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What is the lifestyle of facultatively intracellular for phagocytes pathogens
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Avoid being killed by the host's first line of defense. Can utilize phagocyte to disseminate through the body (Salmonella, Legionella, Mycobacterium tuberculosis)
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Where are the common sites of infection
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Skin, Respiratory, Gastrointestinal, Urinary tract, reproductive tract, systemic
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What are host innate defenses
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Nonspecific inhibitory agents or physiological conditions encountered upon a pathogen's entry into the host (body-site dependent)
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Who are the resident phagocytes of monocyte/macrophage lineage in innate defense
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Alveolar macrophages, liver Kupffer cells, brain microglial cells, lymph node and splenic macrophages, kidney mesangial cells, synovial A cells
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How do innate defense cells uptake and kill bacteria
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Uptake of bacteria by resident phagocytes is via specific receptors.
Killing mechanisms include acidification of the phagolysosome; production of toxic oxygen species; nitric oxide; antimicrobial peptides |
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What is one of the most important functions of first line macrophages
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Release of cytokines and chemokines that initiate an inflammatory response. Signaling through TLRs causes secretion of pro-inflammatory cytokines
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What are two ways bacterial pathogens defend against the first-line macrophage defense
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Being facultatively intracellular for professional phagocytes (lyse the phagosome membrane, modify phagolysosomal environment, or inhibit acidification)
Inducing apoptosis which causes programmed death of phagocytes |
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What are the bacterial advantages of inducing apoptosis in phagocytes
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Inactivation of killing potential, Reduction in the number of defenders, No induction of normal cellular signaling processes of cytokine and chemokine signaling of necrotic death
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What is O2 independent killing by PMNs
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Release of lysosomal enzymes (collagenase, elastase) which damage tissue and enhance the inflammation process; also antimicrobial peptides
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What is O2 dependent killing by PMNs
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NADPH oxidase plus glucose results in superoxide anion
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What may happen if dead bacteria aren't degrade or removed
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Granulomas may occur, and more damage is inflicted on host tissue
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What are the pyogenic bacteria
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Pus forming bacteria that give rise to a strong inflammatory response, which does not immediately clear infection and thus results in pus
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What does complement do
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Opsonizes bacteria for PMN uptake and can directly kill gram-negative bacteria by direct lysis
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What are the alternative pathway and mannose-binding lectin pathway
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Pathways that are active early in infection, when specific antibody is not there
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What is the classical pathway
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Antibody is required bound to target for activation to occur
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Deposition of what is critical for uptake of bacteria by phagocytes
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C3b
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Which components form the membrane attack complex
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C5b, C6,C7,C8, and C9. The MAC can lyse gram-negative bacteria
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What do almost all principal bacterial pathogens that cause pneumonia and meningitis have in common
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Anti-phagocytic polysaccaride capsules. Nonencapsulated variants of these organisms are usually avirulent
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What is the M protein of Group A streptococci
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Sterically hinders complement from depositing on bacterial surfaces by binding fibrinogen and its breakdown product fibrin to its surface
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What do porins of Neisseria gonorrhoeae bind
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Host proteins that are negative regulators of complement activation (Factor H, C4bp)
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How do Neisseria sp, Haemophilus influenzae type b, and Streptococcus pneumoniae avoid antibodies
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They produces IgA1 protease
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What is a feature of the group B capsule of N. meningitidis
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It is poorly immunogenic, which challenges vaccine development
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What is the cause of gram negative shock
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Endotoxin
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What is endotoxin
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The lipid component of LPS that acts on macrophages. Nanogram amounts produce fever via release of Il-1 and TNF from macrophages
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What do large amounts of endotoxin produce
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The dramatic physiologic effects associated with inflammation (hypotension, decreased PMN and platelet counts, hemorrhage, DIC)
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When is endotoxin active
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Always, whether it is a free molecule, within cell wall fragments, or on intact gram-negative organisms
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What does LPS induced release of TNF-alpha by macrophages induce
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Protection at the local level, but catastrophic effect when released systemically
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What can endotoxin in the blood stream cause
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Rapid and irreversible shock. Venules in all tissues are simultaneously affected, which induces shock that can lead to organ failure and death
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What is important to remember about antibody to endotoxin
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It does not effectively neutralize endotoxin activity
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What can gram-positive bacterial infection lead to
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Septic shock due to the bioactivity of peptidoglycan fragments and other cell wall determinants, which leads to release of cytokines
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