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19 Cards in this Set
- Front
- Back
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pathogenesis of bacteria depends on
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virulence factor: pilli, adherence surface(teichoic acids, adhesion, IgA proteases) exotoxins or endotoxins capsule if they survive in stomach acid |
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bacteria can cause disease in 2 major mechanisms
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toxin production invasion and inflammation |
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toxin can be endotoxin or exotoxin
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exotoxin are polypeptides released by the cell endotoxin: are LPS which form an integral part of the cell wall. GRAM NEGATIVE |
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animal source disease
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cat scratch fever (bartonella hensalae) insect vector - lyme disease, rock mountain spotted fever animal excreta- ecoli hemolytic - uremic syndrome fomite source- staphylococcal skin infection |
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disease in fetus or neonate
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transplacental: treponema pallidum- congenital syphilis listeria monocytogenes: neonatal sepsis and menigitis cutomegalovirus- congenital abnormalities parvovirus B19- hydrops fetalis toxoplasma gondii- toxoplasmosis |
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withing birth canal/ at time of birth
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streptococcus agalactiae(group B)--neonatal sepsis and meningitis Ecoli- neonatal sepsis and meningitis chlamydia trachomatis- conjunctivitis or pnemonia Neisseria gonorrhoeae- conjunctivitis herpes simplex type 2- skin CNS or disseminated infection(sepsis) |
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enzymes secreted y invasive bacterial: collagenase and hyaluronidase |
degrade collagen and hyaluronic acid allowing bacteria to spread through subcutaneous tissue importat in cellulitis caused by streptococcus pyogenes |
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coagulase
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produced by staphylococcus aureus accelerates the formation of a fibrin clot from fibrinogen this clot may protect the bacterial from phagocytosis by walling off the infected area and coating the organisms with a layer of fibrin |
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IgA protease
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degrade IgA, allowing the organism to adhere to mucous membrane and is produced chiefly by NLGONORRHOEAE, haemophlus influenza, and streptococcus pneumoniae
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leukocidins
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can destroy both neutrophilic leukocytes and macrophages
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biofilms adhesins |
protect the bacteria from antibodies molecules that mediate adherence to cell surface |
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intracellular pathoges
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bacteria has intracellular survival, which enhances their ability to cause disease they also cause granulomatous lesion |
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examples of intracellular pathogens
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mycobacterium, legionella, brucella and listeria
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mechanisms that intracellular pathogens use to survive
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1. inhibitionof the fusion of the phagosome with the lysosome, which allows the organism to avovid degradative enzymes in the lysosome ( 2. inhibition of acidification of the phagosome which will reduce the activity of the lysosomal degratdative enzyme (mycobacteria, legionella) 3. escape from the phagosome into the cytoplasm where there are no degradative enzymes (S. sonnei listeria sp) |
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exotoxins encoded by bacteriophage dna are
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diphtheria toxin, cholera toxin, and botulinum toxin
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exotoxin polypeptides when treated with formaldehyde or acid or heat
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are now called toxoid are good antigen and induce th synthesis of protective antibodies called antitoxins eg botulism and tenaus are use for protective vaccines because they retain their antigenicity but no toxicity |
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endotoxin activates macrophages
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IL 1-- FEVER TNF-- FEVER and hypotension NITRIC OXIDE: hypotension |
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endotoxin activates complement
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C3a: hypotension edema C5a: neutrophil chemotaxis |
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endotoxin activates Hageman factor
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coagulation cascade- DIC
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