last lecture Flashcards
commensals
coexist (neutral relationship) however, the commensals are kind of beneficial when kept in check as they gobble up resources that would otherwise be used by more harmful bacteria
opportunists pathogens
pathogens that take advantage of breaks/disruption in the host defense system
primary pathogens
cause disease on their own
what environments are dental plaque found
fissures, approximal surfaces, gingival crevices
what are the nutrient sources for dental plaque found in fissures, ph, and redox potential
saliva and diet, neutral-acidic, positive
what are the nutrient sources for dental plaque found in approximate surface
saliva, diet GCF, neutral to acidic, slightly negative
what are the nutrient sources for dental plaque found in gingival crevice
GCF, neutral-alkaline, negative
biofilm
a community of bacteria attached to a surface that is encased in an extracellular polymer substances of “EPS”.
biofilm formation aids the participating bacteria by
1) providing protection against host defenses
2) limit the diffusion of nutrients
3) protection against antimicrobial substance
4) providing energy storage
5) quorum sensing
quorum sensing
a form of bacterial communication that allows a community of bacteria to coordinate gene expression in response to the size of the population or environmental cues
autoinducers
molecules released during quorum sensing. released by all members of a particular species. once enough of these molecules bind to transcriptional regulators on the cell surface, target gene expression is induced
threshold value
how many molecules needed for a specific particular transcriptional regulator in quorum sensing
what are the 4 virulence factors of s. mutant that contribute to dental caries
- acidogenic
- acid tolerant
- glycolsyltranferase (GTF)
- gluten binding proteins
acidogenic
ability to metabolize carbohydrates and produce acid
acid tolerant
ATR more tolerant to acid environment than commensal bacteria
glycosyltransferase
extracellular enzyme that forms polymers of glucose from sucrose, liberating fructose. BIOFILM formation
gluten binding proteins
surface proteins that bind to glucan
what are the three commensal bacteria that prevent dental caries
- S.oligofermentans
- S. australis
- S. Gordonil
how do S. oligofermentans help prevent dental caries
production of H2O2 from lactic acid which inhibit S. mutans
how do S. australis prevent dental caries
production of NH3 from arginine which will raise plaque pH
how do S. gordonii help prevent dental caries
production of a protease that degrades CSP and antagonizes S. Mutans
periodontitis
chronic inflammatory disease which affects the tooth- supporting tissue and increases risk for other disease like atherosclerosis, diabetes, and rheumatoid arthritis
virulence factors of Pg that contribute to periodontitis
- capsule- antiphagocyctic, down regulates cytokine production, encapsulated strains more virulent
- gingipains- degrades extracellular matrix components, cytokines, immunoglobulin and complaint factors. decreases fibrinogen which increases bleeding
- fimbriae- required for binding to host cells
- LPS- lipid A modification evade TLR4 interactions
sterilization
kills all forms of microbial life
1 Chemical: gas, formaldehyde vapor
2. physical: autoclave, hot air oven, incineration
disinfection
doesn’t kill all microorganisms (spores)
1. chemical: alcohol, h2o2, chlorine, chlorhexidine, formaldehyde
2 physical: boiling, filtration, pasteurization
antiseptics
can be used with living tissues h202
antimicrobials
used for treatment of infectious disease. derived from FUNGI or BACTERIA (penicillin, tetracyclines, sulfonamides)
Nosocomial infections
acquired in a hospital, symptoms may show during or after say
sources of nosocomial infections
- endogenous-patients own microbiota
2. exogenous- transmission from external environment
known nosocomial pathogens
MRSA and VRSA often caused by staphylococcus aureus that is commonly on the external skin layers but not within the body
drugs b-Lactams and non b_lactams target
cell wall. interfere with cross linking by lysing cell wall (penicillin, vancomycin)
ahminoglycosides, tetracylines, chloramphenicol and macrolides target
protein synthesis. prevent tRNA from itialitng or translocating or prevent ribosomes from completing task
quinolone, sulfonamides, metronidazole and rifampin
target nucleic acid synthesis . either DNA or RNA will be broken down and folate synthesis will stop
polymyxin b target
cell membrane. permeability lost and cellular material leaks out
things present in bacteria that are not present in host cells
bacteria cell wall, 70 s bacterial ribosome, folic acid synthesis
drug resistance
drug kill most bacteria and the surviving bacteria are resistant to drug. new bacteria can thrive. antibiotics creates selection for resistance
5 mechanisms of bacterial resistance
- efflux pump
- blocked penetration
- altered target
- enzymatic activation
- genetic resistance
efflux pump
happens at cell wall and btonrols what passes through
blocked penetration
happens at cell walll
altered target
some organisms have altered receptors preventing drugs from binding. MRSA modified so penicillin cannot bind
Enzymatic activation
- b-lactam ihibitors- where penicillin is inhibited because bacteria modify the shape of the b-lactam ring and open it up so its no longer effective
2 amino glycoside resistance- where a group of phosphates are removed from the drugs structure inactivating it and preventing it from binding
3 types of genetic resistance
- intrinsic
- acquired
- mutational
intrinsic resistance
structure provides a tolerance of certain drugs
acquired resistance
developing resistance over time
mutational resistance
resistance due to a genetic mutation
pathogen
a bacterial species that is able to cause disease when presented with favorable circumstances
extracellular pathogen
not able to invade host cells
facultative intracellular bacteria
can invade host cells but can survive in extracellular enviornment
obligated pathogens
requires host cell for survival
pathogencitiy
ability of any bacteria to cause damage in a susceptible human host
virulence
resumes pathogenicity, but allow expression of degrees from low to high
low virulence strain
streptococcus salvarious. universally presented in oropharyngeal flora of humans
moderate virulence strain
E. coli, universally found in colon but can cause bladder infection
high virulence strain
Bordetella pertussis (whopping cough) not found in normal flora
extremely high virulence
yersinia pestis causes plaque and highly infectious can lead to death in few days
3 stages of establishing infection
- adherence
- colonization
- bacteria are taken up in host vesciles
adherence
bacteria attach to host cell through specific pili, biofilms, fimbriae, or receptors. can bind to cell specific receptors mannose or fibronectin. first pili attachment brings organism closer to cell so second adhesion can occur (usually sugars teichoic acid) example. neisseria gonorrhoeae
colonization or invasion
what are the nutrient sources for dental plaque found ingram neg bacteria have special secretion system that injects proteins into host cells. EFFECTOR PROTEINS promote invasion and suppress host defense
bacteria taken up in host vesicle
take up through endocytosis in endosomes. endosomes fuse with lysosomes creating endolysosomes. invasive pathogens must disrupt normal cell vesicle trafficking or be able to escape the endosome and into the cytoplasm.
ways bacteria can avoid being killed after entering cell
modify endosome to facility survival, escape endosome and replicate in cytoplasm, block endosome and lysosome fusion
ways bacteria is killed once it enters cell
endolysosome digests bacteria, acidification
transmission
long term survival of bacteria is dependent on ability to replicate, survive and be transmitted to another host
modes of transmission
airborne, food borne, vector borne, water borne, blood borne
inducible innate immunity
PAMPs, DAMPs AMPs, IgA, complement, phagocytes
non inducible innate immunity
lysozyme, cilia of trachea, stomach acid, mucus, intact skin, commensal bacteria, flushing action of urinary tract, sequestration of iron
many bacteria have ____ attachment mechanisms
multiple; pili or fimbriae and biofilm formation
_____ is secreted into mucus; it helps prevent pathogens from adhering to mucosal surfaces aiding in bacterial clearance
sIgA
sIgA protease
enzyme that pathogens have that can degrade that immunoglobulin. it cleaves sIgA in the hinge region to release the Fc portion from the Fab portion
extracellular tissue fluid contains ____ that breaks down cell wall of gram + bacteria
lysozymes
the _____ of ____ bacteria prevents penetration of lysozyme
outer membrane; gram -
siderophores
pathogenic bacteria can produce siderophores which compete with human proteins for available iron, allowing for bacterial growth
3 strategies for bacteria to avoid detection by immune system
- invade and survive inside host cell like macrophages
- avoid contact wth phagocytes
- inhibit phagocytic engulfment
major infections caused by facultative intracellular bacteria
Mycobacterium tuverulosis (tuberculosis),, mayobacterium leprae (leprosy)
major human infections caused by obligate intracellular bacteria
rickettsia rickettsia (rocky mountain spotted fever) rickettsia prowazekkii (endemic typhus)
_____ bacteria have special secretion systems that inject proteins into host cells
gram negative (effector proteins)
effector proteins function
promote invasion of host cells or suppress host cell defense
how can bacteria avoid inducible innate host defenses
avoid phagocytosis by macrophages and PMN (polymorphonuclear leukocytes) by using a capsule
capsules bind to ____ present in serum
factor h. this degrades complement protein C3b preventing its deposition on bacterial cell surface
if the bacteria is able to avoid inducing a ______ then the host is unable to focus phagocytotic defense
inflammatory response
inhibition of phagocyte chemotaxis
streptococcal kills phagocytes and suppresses neutrophil chemotaxis
some bacteria can avoid engulfment though ____adaptions
specialized surface adaptions
PAMSP are recognized by?
TLRs toll-like receptors
Lipid A affects ____ of bacteria preventing antimicrobial peptides from attacking
surface charge
how do bacteria avoid innate PAMPs antibodies and adaptive immunity
antigenic variation; varying surface antigens presents PAMPs from being recognized
varying ____ prevents PAMPs form being recognized
sufrace antigenen
some pathogens can activate _____ in cells and kill them
apoptotic pathways; decreases number of defenders and prevents alarm bells form osunding
exotoxin a activates ____ to kill cells
apoptotic pathway
in order for bacteria to survive they must not only survive dost defuse but also _____
distrust host function
ways bacteria cause injury to host
exotoxins endotoxins hydrolytic enzymes superantigen inflammation
exotoxins
bacterial secreted proteins; have host cell specificity and bind to specific receptors. can have local and systemic effects depending on distribution. toxins can be
endotoxins
lipid A proteins of LPS of Gram - cavteria. stimulates cytokine release (inflammation); induces fever through release of IL-1 and TNF from macrophages
hydrolytic enzymes
facilitate tissue invasion (collagenase amor hyaluronidase)
superantigen exotoxin
stimulate massive cytokine secretion
inflammation
prolonged immune response to bacteria can damage host tissues (periodontal disease)
3 things exotoxins can be
- inhibitory
- stimulatory
- fatal
a-b exotoxins
b subunits bind host cell surface receptor glycoproteins or glycolipids. A (active)subunit gets transported by direct fusion or endocytosis into host cell and act son target protein
membrane active exotoxins
create pores in host cell membranes. E coli or S. aureus. causes loss of cell integrity and leakage through DAMPs
Parts of the endotoxin
- O antigen polysaccharide side chains
- core polysaccharide
- lipid a (toxin)
lipid a toxin
phospholipid with glucosamine instead of glycerol located on outer membrane
superantigen
polyclonal stimulator of t cells. binds to MMCH II and causes t cells to release cytokines
staphylococcus aurees and group a strep
toxic shock syndrome
pulmonary alveoli filled with OMNs and macrophages due to inflammation cant
absorb oxygen
