Card Set Information
micb 202 bac cards
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
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
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
shedding/ destruction of colonized host cells
How does N. Gonnorrhoeae bacteria evade the hosts adaptive immune response?
PicC protein is important as..
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
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...
Pro-inflammatory cytokine release
invasion of epithelial cells
SPI-2 ecodes a TTSS associated with
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