chap 15 Flashcards
basic steps of causing disease
- enter host
- penetrate/invade host defenses - using capsule, enzyme, and fimbriae/pili
- damage host - use toxins, intracellular pathogens
- exit host
portals of entry
mucous membranes - respiratory tract; GI tract;
genitourinary tract
skin - hair follicles, sweat glands, conjunctiva
parenteral route - deposition of microbes directly
under skin or mucous membrane
what is the preferred method of entry for pathogens?
respiratory tract and GI tract
ID50
infectious dose needed to cause symptoms in 50% of experimental hosts
LD50(lethal dose 50%)
dose of pathogen needed to kill 50% experimental animal hosts(measure potency)
how specifically do pathogens enter the host
- bind via adhesion/ligands on pathogen to cell membrane
biofilm formation
- microbial community contain in exopolysaccharide matrix
- adhere to surfaces
- very resistant
- dental plaque, catheters, ivs, heart valves
factors that allow for penetration of host defenses
- capsule - impairs phagocytosis by host cells
- cell wall comp: mycolic acids in some
M protien- for attachment,
antiphagocytic, inactive complement - extracellular enzymes
- antigenic variation - alter pathogen surface proteins;
possess alternate genes - opa protein - tight attachment for transcytosis
extracellular enzymes to penetrate host
- coagulases: clot blood, isolate bacteria from host
- kinases: destroy blood clots
- collagenase: digests collagen in connective tissue,
muscles, organs, tissues - protein A - make antibodies inactive
- proteases - destroy host proteins; IgA protease
process of opa protien(transcytosis)
- pilli anchor pathogen to epitheial cells
- opa protein attach for tight adherence
- pathogen travels through the cells to other cells and it keeps going
penetration into cytoskeleton
- penetrate using actin filaments in cytoskeleton
- invasions(salmonella) - pathogen surface proteins
that rearrange actin filaments
- make membrane ruffling(pathogen engulfed
into cell
pathogen damage to host cells
- use host’s nutrients: pathogen get host
siderophores(Fe chelators) - cause direct dmg in vicinity of infection: intracellular
pathogen(viral infection) - production of toxins: transported by blood, lymph
- inhibit protein synthesis
- disruption of membrane - induction of hypersensitivity reaction: overproduction
of cytokines - release of toxins
exotoxins
- types: a-b toxins, membrane disrupting, superantigens
- secreted into environment
- water soluble proteins(lot enzymes); most plasmid
based or in phages - antitoxins: toxoid forms to provide immunity
toxigenicity
ability for pathogen to produce substances that damage the host
toxemia
disease caused by spread of bacteria and its toxins in blood steam
a-b toxins
diphtheria toxin: inhibits proteins synthesis; phage
carries tox gene
botulism toxin: neurotoxin; prevents nerve impulses to
muscles; causes flaccid paralysis
tetanus toxin: neurotoxin tetanospasmin; blocks
inhibitory nerve impulses to muscles; cause
spasmodic contractions
vibrio enterotoxin: cholera toxin; causes cellular
secretion of fluids and electrolytes –> severe
diarrhea and dehydration
membrane - disrupting toxin
- cause lysis host cells by disrupting the plasma
membrane
- leukocidins: kill phagocytic white
- hemolysins: kill red blood cells
superantigens
- stimulate intense immune response of T cells
- t cells stimulated to produce cytokines; regulate
immune response
erythrogenic toxins: damage blood capillaries under
skin cause rash and scarlet fever
staphylococcal enterotoxin(s. aureus)
endotoxin
- lipid protein(A) of LPS of gram neg -> released when
cells die and lyse - stimulates macrophages release too much cytokines
- can activate blood clotting proteins and induce fever
- endotoxic shock: drastic drop in blood pressure
cytopathic effects
- visible effects of viral infection
cytocidal effect: results in cell death
- cytocidal viruses stop host biosynthesis and make
cell lysosomes release contents - syncytium formation
- granules formation
- virus infected cells form interferons(protects non-
infected cells) - antigenic changes on cell surface caused by virus
what is syncytium and how is it formed?
multinucleate infected cell
- virus entry(membrane fusion)
- viral replication(viral envelope on outside)
- noninfected cell fuses w infected
- syncytium forms are more cells get fused
what do oncogenic viruses do
transform cells into cancerous cells
portal of exit
secretion, excretion, discharges, tissue that is shed
- related to part of the body that was infected
- usually same portal entry and exit
