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51 Cards in this Set
- Front
- Back
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Pathogenicity
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Ablitly to cause disease
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Virulence
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Degree of ability to cause disease
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Number of microbes
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ID 50
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Microbe virulence
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LD50 Lower number means higer virulence
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Encoded by the genome
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Virulence factor
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Con of Virulence
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Enable microbe to establish itself on host, enhance microbes potential to cause disease
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Pro of Virulence
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Often antigenic, may be used serologically, may be inactivated, preventing infection
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Adhesin virulence
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Pili Flagella
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Invasins act
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extracellularly like digestive enzymes
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Capsules
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resist phagocytosis
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Exotoxins
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secreted
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Toxin transporters
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get toxins into host cells
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Endotoxins
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not secreted, gram negative, LPS---> shock
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Obligate parasites/pathogens
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Have to invade a host
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Opportunistic parasites/pathogens
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Invade a host if it is available, but its not required
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Primary Pathogens
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cause disease upon infection, Not normally associated with host eg Plague, flu virus
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Opportunistic Pathos
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Cause dieseas under some circumstances, are somtimes members of normal flora, pseudomonas, candida
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Modern approach to Koch's pstulates "molecular postulates
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Not enough to just ID the microbe, you must describe the strain's virulence factors and genes
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Purpose of normal flora
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Prevent colonization by potential pathogens
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Free Living Gram Positive
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Cocci- S. Aureus, S. Epidermis, Strep Pyogenes
Spore bacilli- clostridium Non spore forming bacilli |
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Free Living Gram Neg
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Cocci: N. meningitidis
Bacilli: E. coli |
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Free Living Acid Fast
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Mycobacterium
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Normal Flora Fungi
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Candida Albicans
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Non Flora microbes must
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colonize and defeat body defenses
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Opportunistic infections cause disease in people with
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Immunodeficiency, Immunosuppression, Flora being out of place, distubance in normal flora balance
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Steps to pathogenesis
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1. Entry 2. Invasion and Infection. 3. Adherance and Colonization 4. Inflammation and Toxins 5. Non specific and specific immune response 6. Pregression 7. Exit
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Entry and transmission can be
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Horizontal and/or Vertical
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Chronic carrier
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Someone who cannot be infected but can spread the disease. OR someone whos has not shown symptoms but spreads the disease
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Methods of invasion
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Zippering, or ruffleing
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Cell Wall components
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teichoic acids, avoid complement and antibodies
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Stealth Tactics
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Avoid antibodies, antigenic variation, intracellular life: invasins
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Enzymes
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degrade tissue, promote tissue invasion, these are not toxins
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Cell Wall Fc receptors
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Bind antibody at "dangerous end" (constand region) so that it cant bind to macrophages
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Antigenic variation
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alteration of antigens, mimicking host self antigens
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Viruses are
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OIPS
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Exotoxins
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Gram positive, secrete proteins
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The proteins that exotoxins secrete are
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very potent, soluble, heat liable, PLASMID ENCODED,
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Superantigen
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extoxin that doesnt get presented normally. resulting in hyperstimulation of Th cells, excess inflammatory cytokines IL1, SHOCK
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Endotoxins
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LPS of gram neg. LPS Not protein, not secreted genes are chomosomal
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Lipid A
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component of LPS, Toxic in the blood stream, massive immune stimulation, induce fever and shock, coagulation
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Antigen O
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serotypes, antigenic
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Lipid A activates Macro which leads to
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Inflammatory Cytokines> fever and hypotension
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Lipid A activates Complement which leads to
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Promotion of histamine release > hypotension
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Disease reservoirs
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sources of ongoing infection
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Examples of reservoirs
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Human, carriers
Animal, zoonoses nonliving, soil and water |
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Contact Transmission
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Direct, Indirect, droplets
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Direct Contact Transmission
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Acquired by physical contact with infected person or animal, rabies, herpes
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Indirect Contact Transmission
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Aquired from contact with a contaminated material, fomite/surface.Tetnas, cold, ringworm
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Droplet Contact Transmission
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Aquired by mucus membrane contact with contaminated droplets. short range, cold
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Vehicle transmission
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aquired by exposure to contaminated water, air, food. Long distance air, fecal oral food
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Vector transmission
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acquired by saliva feces from an insect arthropod animal carrier
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