EXAM 1 Bacterial Pathogenesis Flashcards
bacterial interactions with human hosts can be ___ or ___
transient or permanent
what are the 3 bacterial interactions with human hosts?
- mutualistic symbiosis
- commensalism
- disease (pathogens)
- also…opportunists and pathobionts
what are opportunists and pathobionts?
an organism which, under normal circumstances, does not cause disease, but can be pathogenic under some conditions
the ___ microbiota is the largest and most studied in the body
gastrointestinal
what happens to the number and diversity of microbiota as you descend the GI tract?
it increases
GI microbiota help to extract ___ and ___ from food we eat
energy and nutrients
GI microbiota are required for proper ___ development
immune system
T or F
GI microbiota have no affect on metabolism of drugs
false
some drugs can be affected by GI microbes
GI microbiota protect against ___
pathogens
what is colonizing resistance?
microbiota inhibits colonization by newcomers
___ is a gram + anaerobe found in low abundance in the intestinal tract of 5% of humans
clostridium difficile
___ can be acquired in a hospital as spores (endospores) that are resistant to many stresses and long lasting
clostridium difficile
clostridium difficile only causes pathogenesis following antibiotic treatment that depresses the rest of the microbiota of the gut. describe.
- pseudomembranous colitis - severe ulceration of the colon
- first appeared in hospitals in 1970
- initially associated with use of clindamycin, now associated with other antibiotics including fluoroquinolones
GI microbiota have high ___, high ___, and high ___
- diversity
- density
- colonization resistance
- this all prevents incoming bacteria from colonizing, but if antibiotics are involved, it could wipe out a large number of the good GI microbiota, resuling in low diversity, density, and CR
antibiotic treatment allows c. difficile an opportunity for aggressive expansion
what happens with normal microbiota and no antibiotic?
no clostridium difficile infection risk
antibiotic treatment allows c. difficile an opportunity for aggressive expansion
what happens when there is a CDI risk, microbiota is disrupted, and an antibiotic is administered?
c. difficile that is resistant to the antibiotic has a selective advantage
antibiotic treatment allows c. difficile an opportunity for aggressive expansion
what happens where the microbiota is disrupted and no antibiotic is administered?
c. difficile that is resistant to the antibiotic has no advantage
what are the symptoms of pseudomembranous colitis?
diarrhea, abdominal pain, fever
____ antibiotic treatment alters normal gut microbiota, allowing for overgrowth of c. difficle, potentially causing ___
- broad spectrum
- pseudomembranous colitis
why can c. difficile survive antibiotics?
- resistance genes and mutations
- biofilm formation
- spore formation
unlike most pathogens, c. difficile produces a metabolically dormant spore that is excreted by ___. the infected spores can persist in the environment and are highly ___ to commonly used disinfectants and antibiotics
- infected patients
- resistant
c. difficile spores have multilayered protective coat consisting of what 5 things?
- cell membrane
- thick peptidoglycan mesh
- another cell membrane
- wall of keratin-like protein
- outer layer called exosporium
what two medically important bacteria form spores?
- anaerobic clostridium species and aerobic bacillus species
- both gram positive
c. difficile spores form when there is a shortage of ___
nutrients
c. difficile spores can remain dormant for ___
years
___ can stimulate c. difficile spore formation, creating a supershedding state that promotes ___
- antibiotic treatments
- dissemination of the pathogen
T or F
most antibiotics, hand sanitizers, or 60-95% isopropanol/ethanol will kill spores
false
what should be done to kill spores?
sterilize laboratory and hospital supplies by treating them with high pressure steam at sporicidal temperatures (autoclave)
what are 5 factors that facilitate bacterial infection and survival within a host?
- ability to outcompete commensals at many stages
- attachment to host cells and tissues via adhesins
- evasion of innate and adaptive responses
- acquisition of limiting nutrients
- dissemination within a host and transmission to new hosts
what are three ways bacterial pathogens deal with multiple host defenses?
- virulence factors prevent uptake and destruction by phagocytes
- some bacteria possess factors that promote survival in potentially inhospitable locations
- facultative intracellular bacteria regulate virulence factor expression
describe production of capsules that prevent phagocytosis as a survival strategy in extracellular environments
prevent complement depostion or mask deposited C3b from interaction with phagocyte receptors
as a survival strategy in extracellular environments, the ability of bacteria to vary surface exposed antigens allows what?
outgrowth of antigenically novel clones
describe secretion of molecules that interfere with host defenses as survival strategies within extracellular environments
- toxins that modify host cells
- enzymes that destroy defenses such as chemokines, slgA, and mucosal barriers
what are the bacterial pathogens that are resistant to reactive oxygen species and NO?
- superoxide dismutase, SOD
- staphylococci and salmonella
- suppression of host NO synthase expression
- listeria
many bacterial pathogens can neutralize phagolysozome contents via ___
secretion system effectors
what 2 bacterial pathogens can prevent phagolysozome fusion?
legionella and mycobacterium
what 3 bacterial pathogens can escape from the phagolysosome?
listeria, francisella, and rickettsia
listeria monocytogenes is the cause of ___
listeriosis, the 3rd leading cause of death due to foodborne illness
describe listeria monocytogenes
- gram positive facultative anaerobe
- mastered the ability to live within host cells
listerial internalins inlA and inlB engage surface receptors and trigger actin reorganization and signaling cascade activation. what is the result?
internalization of the bacteria by host cells that are not considered professional phagocytes (epithelial cells)
what are toxins?
virulence factors (excreted or not) that are toxic to human or animal or plant cells
___ cause aberrent activation of host inflammatory responses
toxins
___ bind and act at host cell surface, and can also act on host cell membranes
toxins
what are the A-B toxins?
include single chain (DT, and BoNT) and multisubunit toxins (cholera and anthrax toxins)
what toxin is encoded on large plasmid and has the following characteristics?
causes apoptosis/necrosis of host cells without inflammation or pain
causes buruli ulcers
necrotic lesions can cover up to 15% of body
eventually heal, leaving scars, but can cause death
mycobacterium ulcerans polyketide-derived mycolactone
a non-protein toxin
superantigens bind class ___ outside peptide cleft, recognized by less variant regions of TCR families. the superantigen forms a bridge between ___ and ___ and results in massive outpouring of ___. T cells become activated and then exhausted and die, which may be an advantage to bacteria
- class II MHC
- APC
- T cells
- cytokines
what promotes the dissemination of superantigens?
diarrhea
___ can cause food poisoning, bacteremia/sepsis, toxic shock syndrome, abscesses, and cellulitis
staphylococcus aureus
up to ___ the s. aureus population is colonized
1/3 (nasal)
___ can survive on skin, hospital gowns and gloves, neckties, and environment
s. aureus
what is HA-MRSA?
hospital acquired-methicillin-resistant s. aureus
transferred from staff to patient
what is CA-MRSA?
community acquired MRSA
daycare, wrestlers
together, how many deaths are HA and CA MRSA responsible for in the US?
about 20,000/yr (more than HIV)
what are some examples of molecules on the surface of s. aureus that interact with the host?
- adhesins
- capsule
- protein A
- MSCRAMMs (microbial surface components recognising adhesive matrix molecules)
what are some examples of toxic assets of s. aureus?
- toxic shock syndrome
- staph enterotoxins SEA-SEE
- exfoliative toxins
- leukocidins
- staphylokinase
- alpha-toxin
many of the virulence factors encoded by s. aureus are regulated by ___
quorum sensing
