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Host and Defense > EXAM 1 Bacterial Pathogenesis > Flashcards

EXAM 1 Bacterial Pathogenesis Flashcards

1
Q

bacterial interactions with human hosts can be ___ or ___

A

transient or permanent

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2
Q

what are the 3 bacterial interactions with human hosts?

A
  • mutualistic symbiosis
  • commensalism
  • disease (pathogens)
  • also…opportunists and pathobionts
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3
Q

what are opportunists and pathobionts?

A

an organism which, under normal circumstances, does not cause disease, but can be pathogenic under some conditions

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4
Q

the ___ microbiota is the largest and most studied in the body

A

gastrointestinal

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5
Q

what happens to the number and diversity of microbiota as you descend the GI tract?

A

it increases

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6
Q

GI microbiota help to extract ___ and ___ from food we eat

A

energy and nutrients

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7
Q

GI microbiota are required for proper ___ development

A

immune system

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8
Q

T or F

GI microbiota have no affect on metabolism of drugs

A

false

some drugs can be affected by GI microbes

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9
Q

GI microbiota protect against ___

A

pathogens

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10
Q

what is colonizing resistance?

A

microbiota inhibits colonization by newcomers

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11
Q

___ is a gram + anaerobe found in low abundance in the intestinal tract of 5% of humans

A

clostridium difficile

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12
Q

___ can be acquired in a hospital as spores (endospores) that are resistant to many stresses and long lasting

A

clostridium difficile

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13
Q

clostridium difficile only causes pathogenesis following antibiotic treatment that depresses the rest of the microbiota of the gut. describe.

A
  • 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
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14
Q

GI microbiota have high ___, high ___, and high ___

A
  • 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
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15
Q

antibiotic treatment allows c. difficile an opportunity for aggressive expansion

what happens with normal microbiota and no antibiotic?

A

no clostridium difficile infection risk

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16
Q

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?

A

c. difficile that is resistant to the antibiotic has a selective advantage

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17
Q

antibiotic treatment allows c. difficile an opportunity for aggressive expansion

what happens where the microbiota is disrupted and no antibiotic is administered?

A

c. difficile that is resistant to the antibiotic has no advantage

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18
Q

what are the symptoms of pseudomembranous colitis?

A

diarrhea, abdominal pain, fever

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19
Q

____ antibiotic treatment alters normal gut microbiota, allowing for overgrowth of c. difficle, potentially causing ___

A
  • broad spectrum
  • pseudomembranous colitis
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20
Q

why can c. difficile survive antibiotics?

A
  • resistance genes and mutations
  • biofilm formation
  • spore formation
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21
Q

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

A
  • infected patients
  • resistant
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22
Q

c. difficile spores have multilayered protective coat consisting of what 5 things?

A
  • cell membrane
  • thick peptidoglycan mesh
  • another cell membrane
  • wall of keratin-like protein
  • outer layer called exosporium
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23
Q

what two medically important bacteria form spores?

A
  • anaerobic clostridium species and aerobic bacillus species
  • both gram positive
24
Q

c. difficile spores form when there is a shortage of ___

A

nutrients

25
Q

c. difficile spores can remain dormant for ___

A

years

26
Q

___ can stimulate c. difficile spore formation, creating a supershedding state that promotes ___

A
  • antibiotic treatments
  • dissemination of the pathogen
27
Q

T or F

most antibiotics, hand sanitizers, or 60-95% isopropanol/ethanol will kill spores

A

false

28
Q

what should be done to kill spores?

A

sterilize laboratory and hospital supplies by treating them with high pressure steam at sporicidal temperatures (autoclave)

29
Q

what are 5 factors that facilitate bacterial infection and survival within a host?

A
  • 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
30
Q

what are three ways bacterial pathogens deal with multiple host defenses?

A
  • 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
31
Q

describe production of capsules that prevent phagocytosis as a survival strategy in extracellular environments

A

prevent complement depostion or mask deposited C3b from interaction with phagocyte receptors

32
Q

as a survival strategy in extracellular environments, the ability of bacteria to vary surface exposed antigens allows what?

A

outgrowth of antigenically novel clones

33
Q

describe secretion of molecules that interfere with host defenses as survival strategies within extracellular environments

A
  • toxins that modify host cells
  • enzymes that destroy defenses such as chemokines, slgA, and mucosal barriers
34
Q

what are the bacterial pathogens that are resistant to reactive oxygen species and NO?

A
  • superoxide dismutase, SOD
    • staphylococci and salmonella
  • suppression of host NO synthase expression
    • listeria
35
Q

many bacterial pathogens can neutralize phagolysozome contents via ___

A

secretion system effectors

36
Q

what 2 bacterial pathogens can prevent phagolysozome fusion?

A

legionella and mycobacterium

37
Q

what 3 bacterial pathogens can escape from the phagolysosome?

A

listeria, francisella, and rickettsia

38
Q

listeria monocytogenes is the cause of ___

A

listeriosis, the 3rd leading cause of death due to foodborne illness

39
Q

describe listeria monocytogenes

A
  • gram positive facultative anaerobe
  • mastered the ability to live within host cells
40
Q

listerial internalins inlA and inlB engage surface receptors and trigger actin reorganization and signaling cascade activation. what is the result?

A

internalization of the bacteria by host cells that are not considered professional phagocytes (epithelial cells)

41
Q

what are toxins?

A

virulence factors (excreted or not) that are toxic to human or animal or plant cells

42
Q

___ cause aberrent activation of host inflammatory responses

A

toxins

43
Q

___ bind and act at host cell surface, and can also act on host cell membranes

A

toxins

44
Q

what are the A-B toxins?

A

include single chain (DT, and BoNT) and multisubunit toxins (cholera and anthrax toxins)

45
Q

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

A

mycobacterium ulcerans polyketide-derived mycolactone

a non-protein toxin

46
Q

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

A
  • class II MHC
  • APC
  • T cells
  • cytokines
47
Q

what promotes the dissemination of superantigens?

A

diarrhea

48
Q

___ can cause food poisoning, bacteremia/sepsis, toxic shock syndrome, abscesses, and cellulitis

A

staphylococcus aureus

49
Q

up to ___ the s. aureus population is colonized

A

1/3 (nasal)

50
Q

___ can survive on skin, hospital gowns and gloves, neckties, and environment

A

s. aureus

51
Q

what is HA-MRSA?

A

hospital acquired-methicillin-resistant s. aureus

transferred from staff to patient

52
Q

what is CA-MRSA?

A

community acquired MRSA

daycare, wrestlers

53
Q

together, how many deaths are HA and CA MRSA responsible for in the US?

A

about 20,000/yr (more than HIV)

54
Q

what are some examples of molecules on the surface of s. aureus that interact with the host?

A
  • adhesins
  • capsule
  • protein A
  • MSCRAMMs (microbial surface components recognising adhesive matrix molecules)
55
Q

what are some examples of toxic assets of s. aureus?

A
  • toxic shock syndrome
  • staph enterotoxins SEA-SEE
  • exfoliative toxins
  • leukocidins
  • staphylokinase
  • alpha-toxin
56
Q

many of the virulence factors encoded by s. aureus are regulated by ___

A

quorum sensing

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