Pathogenesis Flashcards
parasite
consumes host resources at expense of host
pathogenesis
disease
pathogenicity
microbes ability to cause disease
virulence
quantitative measure of pathogenicity (degree and efficiency)
primary pathogen
causes disease in healthy individual
opportunistic pathogen
doesn’t harm healthy individual, but when host environment changes (like becomes immunocompromised), disease occurs
e.g. toxoplasma
human exposed surfaces
- GI tract, mouth, respiratory tract, urogenital tract
- sterile environments: blood and organs
how does the skin defend against pathogens
- secrete lipids to prevent drying
- lactic acid and lysozyme
- e.g. propionibacterium acnes causes acne
how does mucous membranes protect against pathogens
- physical barrier: tightly lined epithelial cells
- chemical barrier: mucus secretes solubles with antimicrobial activities
what is plaque and what bacteria cause it to form
- large biofilm
1. streptococcus colonizes which causes plaque
2. filamentous fusobacterium thicken plaque
3. anaerobic actinomyces grow in thick plaque
how does tooth decay occur
- pathogenesis is a shift to bad bacteria
- streptococcus mutans is bad bacteria which begins to colonize
bacteria associated with ulcers
- h.pylori
- lophotrichous and uses flagella to invade mucus
- secrete urease to alter local pH
- cleared with antibiotic treatment
5 things that make a successful pathogen
- access to host and appropriate tissue
- evade host defenses
- establish a niche
- replicates through host nutriet acquisition
- damage to host
7 common features of infection
- exposure
- adherence (using pili or glycocalyx)
- invasion
- growth and dissemination
- virulence factors (measured by LD50 and attenuation is when virulence is reduce - problems with any of the other steps or loss of virulence factor)
- evade host damages
- host cell damage
how can we find virulence gene
- virulence assay (mutant transponson assay)
- genome comparison between similar pathogenic and non-pathogenic species
4 type of toxins
- endotoxin (LPS) cell associated with gram (-) and cause systemic fever and inflammation
- exotoxins secreted into environment:
- cytotolytic toxins (pore formers or phospholipases): cause cell lysis
- AB toxins: two subunits - B binds to host receptors and A enters cytoplasm
- Superantigen toxins: simulate significant immune response
AB toxin in cholera
- B binds to host receptor GM1
- A delivered to cytoplasm and interferes with cAMP pathway
- ion movement is disrupted and move to lumen rather than blood
- water follows ions into lumen and out of the body causing diahrea
- cholera that are pathogenic have a toxin co-regulated pili that were orginally to recieve bacteriophage
trypanosome life cycle
- in the gut of tsetse fly
- transferred to bloodstream and CNS of human host
- vector borne parasite
how to trypanosome fight against adaptive immunity?
- adaptive immune system makes antibodies
- typanosome goes through antigenetic variation after each cycle, expressed antigens change
- this gives waves of fever and parasite count
- they create this variation by switching what telomere expression sites are on or by recombination
immunofluorescence assay
- similar to FISH
- attaches fluorescence onto antibody and when antibody binds to antigen, a signal is produced
how to trypanosome fight against innate immunity?
- innate immune system: lytic factor in our serum
- certain trypanosomes show resistance to this serum
