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Bacteria capable of harming a "normal" host
Degree of pathology caused by the organism (quantitative)
Why can't Transient microbiota remain in the body for extended periods of time?
- Competition from resident microbes
- Immune elimination
- Chemical changes that discourage growth
How can bacteria provide nutritive benefits to a host?
- Synthesis of vitamins (own needs)
- steroid metabolism (bile acids)
- organic acid production (acetic acid)
- glycosidase reaction (sugar fermentation)
where is the vast majority of normal flora?
- Coordinated chemical sensing between cells
- autoinducers = signalling molecules
Why are biofilms antimicrobial resistant?
- EPS mesh barrer
- Nutrient barrier (slow growth= antibiotic resistance)
- Persistor cells (repopulation
Why might it be harder for an antibiotic to treat a gram-negative bacterial infection?
Gm-'ve outer membrane can be selectively permeable.
iron-binding protein that acts as an immediate antimicrobial defence
enzyme that generates singlet oxygen to kill bacteria. antimicrobial.
forms a fibrin clot around the "wall" of a damaged host cell for infection localization
List possible antibiotic resistance mechanisms of bacteria.
- mutations in target
- efflux pump removal
- degrading enzymes
- decreased cell-wall permeability
iinjecting of pre-formed antibodies raised agains a specific bacteria into an infected person. (not common)
Koch Postulate #1 ; problem with this?
- Suspected pathogenic organism should be present in all cases of the disease and absent from healthy animals.
- ; Individuals can carry pathogens, but not get disease
Koch postulate #2; problem?
- Suspected pathogen should be grown in pure culture
- ; some pathogens cannot be grown in pure culture (viruses)
Koch's postulare #3? ; problem?
- Cells of the pure culture of the suspected pathogen should cause the same disease in a healthy animal.
- ; Pathogens can cause disease in one species but not another
Koch's postulate #4? ; problem?
- Pathogen must be re-isolate from the diseased animal and show to be identical to the original suspected pathogen
- ; Pathogen may not grow in pure culture (virus)
low continual frequency of disease
worldwide epidemic (sporadic outbreaks between continual low level)
Two component system
- Virulence genes are regulated by a sensor and a regulator.
- autophosphorylation, phosphate transfer for transcription activation
What does the host response to N. Gonorrhoeae consist of?
- anti-microbial peptide production
- antibody production
- shedding/ destruction of colonized host cells
How does N. Gonnorrhoeae bacteria evade the hosts adaptive immune response?
- Antigenic variation
- Phase variation
PicC protein is important as..
- an adhesin
- proper assembly of pilus (adhesion, DNA uptake)
- N. Gonorrhoeae adhesin protein
- important for neutrophils to phagocytose
How can pilE loci of the pilC be expressed while pilS loci are silent?
pilE contains the portion that codes for the conserved N-terminus of the protein
the process of turning on or off the expression of a particular gene product (Opa proteins in N. Gon)
Antigenic variation occurs prominently in the _-terminal region of pilin.
C-terminal (N-terminal region of pilin is highly conserved)
how does the S. Pneumoniae polysaccharide capsule prevent phagocytosis?
- Prevents deposit of antibody or peptidoglycan on bacterial surface
- prevents the formation of C3b complex (complement pathway opsonization)
- proteins secreted by Gm+ & Gm- bacteria
- may cause damage far from bacterial colony site
- heat sensitive
- type of exotoxin
- affects cells lining the GI tract, causing massive fluid secretion
Why cant a vaccine be used to treat endotoxin shock? (fluid leak, inflammation, coagulation)
- edotoxins are non-protein molecules
- and are not very immunogenic
SPI I encodes TTSS that is associated with...
- Cell invasion
- Pro-inflammatory cytokine release
- macrophage apoptosis
- invasion of epithelial cells
SPI-2 ecodes a TTSS associated with
- intracellular survival
- replication (mice)
- macrophage cytotoxicity (mice)
- systemic disease (mice)
How does SPI-2 avoid phagosome-lysosome fusion?
Injects proteins and modifies membrane of vacuole it is inside.
What are the TOP 4 diseases of bioterrorist threats