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34 Cards in this Set

  • Front
  • Back
The type of host defenses encountered by pathogenic bacteria is influenced by what
Both the site of infection and the life style of the bacteria
What is the lifestyle of extracellular pathogens
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)
Whis is the lifestyle of facultatively intracellular for epithelial, endothelial cells, or other non-professional phagocytes pathogens
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)
What are two examples of obligate intracellular pathogens
Chlamydia spp; Rickettsia
What is the lifestyle of facultatively intracellular for phagocytes pathogens
Avoid being killed by the host's first line of defense. Can utilize phagocyte to disseminate through the body (Salmonella, Legionella, Mycobacterium tuberculosis)
Where are the common sites of infection
Skin, Respiratory, Gastrointestinal, Urinary tract, reproductive tract, systemic
What are host innate defenses
Nonspecific inhibitory agents or physiological conditions encountered upon a pathogen's entry into the host (body-site dependent)
Who are the resident phagocytes of monocyte/macrophage lineage in innate defense
Alveolar macrophages, liver Kupffer cells, brain microglial cells, lymph node and splenic macrophages, kidney mesangial cells, synovial A cells
How do innate defense cells uptake and kill bacteria
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
What is one of the most important functions of first line macrophages
Release of cytokines and chemokines that initiate an inflammatory response. Signaling through TLRs causes secretion of pro-inflammatory cytokines
What are two ways bacterial pathogens defend against the first-line macrophage defense
Being facultatively intracellular for professional phagocytes (lyse the phagosome membrane, modify phagolysosomal environment, or inhibit acidification)
Inducing apoptosis which causes programmed death of phagocytes
What are the bacterial advantages of inducing apoptosis in phagocytes
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
What is O2 independent killing by PMNs
Release of lysosomal enzymes (collagenase, elastase) which damage tissue and enhance the inflammation process; also antimicrobial peptides
What is O2 dependent killing by PMNs
NADPH oxidase plus glucose results in superoxide anion
What may happen if dead bacteria aren't degrade or removed
Granulomas may occur, and more damage is inflicted on host tissue
What are the pyogenic bacteria
Pus forming bacteria that give rise to a strong inflammatory response, which does not immediately clear infection and thus results in pus
What does complement do
Opsonizes bacteria for PMN uptake and can directly kill gram-negative bacteria by direct lysis
What are the alternative pathway and mannose-binding lectin pathway
Pathways that are active early in infection, when specific antibody is not there
What is the classical pathway
Antibody is required bound to target for activation to occur
Deposition of what is critical for uptake of bacteria by phagocytes
Which components form the membrane attack complex
C5b, C6,C7,C8, and C9. The MAC can lyse gram-negative bacteria
What do almost all principal bacterial pathogens that cause pneumonia and meningitis have in common
Anti-phagocytic polysaccaride capsules. Nonencapsulated variants of these organisms are usually avirulent
What is the M protein of Group A streptococci
Sterically hinders complement from depositing on bacterial surfaces by binding fibrinogen and its breakdown product fibrin to its surface
What do porins of Neisseria gonorrhoeae bind
Host proteins that are negative regulators of complement activation (Factor H, C4bp)
How do Neisseria sp, Haemophilus influenzae type b, and Streptococcus pneumoniae avoid antibodies
They produces IgA1 protease
What is a feature of the group B capsule of N. meningitidis
It is poorly immunogenic, which challenges vaccine development
What is the cause of gram negative shock
What is endotoxin
The lipid component of LPS that acts on macrophages. Nanogram amounts produce fever via release of Il-1 and TNF from macrophages
What do large amounts of endotoxin produce
The dramatic physiologic effects associated with inflammation (hypotension, decreased PMN and platelet counts, hemorrhage, DIC)
When is endotoxin active
Always, whether it is a free molecule, within cell wall fragments, or on intact gram-negative organisms
What does LPS induced release of TNF-alpha by macrophages induce
Protection at the local level, but catastrophic effect when released systemically
What can endotoxin in the blood stream cause
Rapid and irreversible shock. Venules in all tissues are simultaneously affected, which induces shock that can lead to organ failure and death
What is important to remember about antibody to endotoxin
It does not effectively neutralize endotoxin activity
What can gram-positive bacterial infection lead to
Septic shock due to the bioactivity of peptidoglycan fragments and other cell wall determinants, which leads to release of cytokines