pathophys exam pt 2

factors of infection

communicability/transmissibility, infectivity, pathogenicity, virulence, toxigenicity, immunogenicity

infectivity

how effectively does it establish infection

pathogenicity

how likely is infection going to produce disease

virulence

how severe is the disease

toxigenicity

does toxin production contribute to disease

immunogenicity

how effectively does it stimulate an immune response

how do most pathogens infect

enter through digestive tract but also enter via direct contact, inhalation, ingestion, bites of an animal or insect

what determines tropism

host receptor availability, intracellular environment and route of entry

main defense against bacteria

neutrophils, complement, antibodies

major host defense against viruses

type i ifns, nk cells, cd8 t cells

virus key biological feature

obligate intracellular replication

fungi biological feature

eukaryotic

major defense against fungi

neutrophils, macrophages, th17

protozoa major biological feature

eukaryotic parasites

helminths key biological feature

multicellular parasites

major host defense against helminths

th2, igE, eosinophils

how do pathogens avoid immune system

avoid recognition, avoid, phagocytosis, survive after phagocytosis, disable immune responses, escape antibodies

how pathogens avoid recognition

antigenic variation, intracellular residence, latency

how do pathogens avoid phagocytosis

capsules and biofilm

toxin secreted bacteria

highly specific cell targets, disrupts signaling, protein synthesis or membrane integrity

how do pathogens survive after phagocytosis

block phagosome-lysosome fusion

how do pathogens disable immune responses

interfere with interferon signaling, complement evasion, alter antigen presentation

how do pathogens escape antibodies

antigenic variation

endotoxins

Lipopolysaccharides (Lipid A inflammatory component) contained in cell walls of gram neg organisms released during cell destruction, does not become an issue until you kill them

direct pathogen damage

toxins, cell lysis, nutrient competition, tissue invasion

host mediated damage in due to pathogen

cytokine excess, neutrophil enzymes, fibrosis from chronic inflammation