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MBIO 1010 > Lecture 12: Medical Microbiology > Flashcards

Lecture 12: Medical Microbiology Flashcards

1
Q

_______: The collection of all the microorganisms living in association with the human
body (microflora, microbiota)

A

human microbiome

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2
Q

T/F: microorganisms outnumber our human cells, and have wayyyy more genes

A

true!
outnumber us 10^14>10^13
20000<20000000

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3
Q

T/F: Colonization begins immediately after birth

A

true!

colonized through vaginal canal and breastfeeding

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4
Q

T/F: Every exposed area in/on the surfaces of the body are colonized with bacteria

A

true
skin and mucous membranes

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5
Q

T/F: Internal tissues should be free of microbes

A

true

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6
Q

what are some examples of internal tissues that should be free of microbes?

A

peritoneum, pericardium, pleura, blood, muscles, organs

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7
Q

what is the beneficial product that E. coli produces for us?

A

vitamin K in our colon

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8
Q

T/F: most bacteria in/on our body are harmless commensals (that can always turn bad) and many contribute to our health

A

true

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9
Q

T/F: Different areas of the skin vary in chemical composition and moisture
content

A

true

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10
Q

what are the three different microenvironments of the skin?

A

dry, moist, sebaceous

each have different microbial populations

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11
Q

_______ (skin microbiota):
Forearms, hands
* High numbers of Betaproteobacteria
* Known from 16 rRNA genes
* Rarely cultured and their role isn’t known
* Second highest is corynebacteria
* Most are harmless commensals
* Some may cause skin infections
* Ex) Corynebacterium diphtheriae
* Can cause non-healing ulcers of the skin: cutaneous diphtheria

A

dry skin

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12
Q

where do we have high numbers of Betaproteobacteria

also corynebacteria

A

dry skin

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13
Q

______ (skin microbiota):
Armpits, nostrils
* High numbers of corynebacteria and staphylococci
* Most are harmless commensals
* Ex) Staphylococcus epidermidis
* Most frequently isolated from skin
* Some are important pathogens
* Ex) Staphylococcus aureus
* Cause of boils, abscesses, wound infections

A

moist skin

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14
Q

where are there high numbers of corynebacteria and staphylococci

A

moist skin
armpits and nostrils

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15
Q

_____ (skin microbiota):
Sebaceous skin
* Oily skin around the nose, on the upper chest and back
* High numbers of propionibacteria
* Anaerobic Actinobacteria that produce propionic acid as an end-product of
fermentation
* Ex) Propionibacterium acnes
* Lives in hair follicles, and eats oil secreted by skin (sebum)
* Overgrowth can trigger inflammation
* Inflammatory acne

A

sebaceous skin

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16
Q

where do we have high numbers of propionibacteria (species: acne)

A

on our sebaceous skin (oily skin)

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17
Q

_____ are anaerobic actinobacteria that produce propionic acid as an end-product of fermentation

A

propionibacteria

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18
Q

_______ has antimicrobial enzymes:
* Lysozyme
* Lactoperoxidase
* Catalyzes production of superoxide radicals O2
-
* Oxidative damage to invading microbes

A

Saliva

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19
Q

_______: Catalyzes production of superoxide radicals O2-
* Oxidative damage to invading microbes

A

lactoperoxidase

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20
Q

The mouth is home to a complex microbial community including
_________

A

aerobes and anaerobes

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21
Q

______ mucosa:
* Aerobic
* Lives on mucous membranes like the tongue

A

Neisseria mucosa

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22
Q

_________:
* Aerotolerant anaerobe
* Produces a sticky dextran slime layer that lets it
stick to surfaces
* Forms biofilms in crevices around the teeth
* Produces lactic acid as an end-product of
fermentation
* Degrades tooth enamel
* Dental carries (cavities)
* Can lead to inflammation along the gum line:
* Gingivitis

A

Streptococcus mutans

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23
Q

Low pH and proteolytic enzymes make the ______ inhospitable to most
microbes
* Some bacteria do colonize the _______

A

stomach

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24
Q

_________: Cause of stomach ulcers
* Colonizes surface of the mucous membrane
* Membrane is protected from stomach acids by mucous
* Has a number of virulence factors:
* Urease neutralizes surrounding acidity
* Exotoxin: kills cells of the mucous membrane
* Endotoxin: triggers an inflammatory response
* Treated with antibiotics – tetracycline

A

helicobacter pylori

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25
Q

helicobacter pylori produce both exo- and endo-toxin… what do they both do?

A

exotoxin: kills cells of the mucous membrane

Endotoxin: triggers an inflammatory response

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26
Q

because the helicobacter pylori produces endotoxin it must be…

A

a gram negative

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27
Q

helicobacter pylori produces ____, which neutralizes the surrounding pH to 7, which degrades the bicarbonate/mucous wall of the stomach that protects membrane from stomach acid…. causing stomach ulcers (considered a carcinogen!)

A

urease

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28
Q

______: Area of rapidly changing pH
* As pH becomes slightly alkaline the quantity and variety of bacteria found
in the gI tract substantially increases

A

small intestine

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29
Q

T/F: As pH becomes slightly alkaline the quantity and variety of bacteria found
in the gI tract substantially increases

A

true! more types can survive in higher pH

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30
Q

_______:
* Genus of Gram positive lactic acid bacteria
* Opportunistic pathogen
* Frequent cause of nosocomial infections
* Example: blood borne infection
* Develop antibiotic resistance readily
* Vancomycin resistant ____
* Spread resistance genes on to other Gram positive bacteria
* Horizontal gene transfer

A

Enterococcus

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31
Q

what does horizontal gene transfer mean?

A

genes transfer buddy-buddy, instead of passing down through daughter cells

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32
Q

_______: pH is neutral
* Environment is anoxic
* Enormous number of microbes ~ 10^11 cells/g of feces
* Mostly anaerobes and facultative aerobes

A

large intestine

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33
Q

why are most of the bacteria in the large intestine anaerobes/facultative aerobes?

A

because oxygen is super lucrative! only a little bit even makes it through, so then its used super fast!!

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34
Q

______: Most cultured bacterium from feces
* Indicator of fecal contamination
* Most strains are non-pathogenic
* May stimulate the immune system
* Produce vitamin K

A

E. coli

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35
Q

T/F: 16S rRNA gene sequences reveal that E. coli
probably makes up < 1% of bacteria in the large
intestine

A

true

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36
Q

Largest group of bacteria in large intestine are strict anaerobes
from the genera _______

A

Bacteroides and Clostridium

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37
Q

explain how high numbers of methanogens in the gut have led to obesity (mouse studies)

A

Studies compared normal mice with germ
free mice:
* Germ free mice had 40% less body fat
Inoculated germ free mice with microbes
from healthy mouse intestines
* Inoculated mice quickly gained weight
Compared the microbiomes of normal weight
mice to genetically obese mice
* Genetically obese mice had fewer
Bacteroidetes, more Firmicutes and way
more methanogens
* Suggested that methanogens use up H2
which promotes bacterial fermentation
* Bacterial fermentation makes
nutrients available to the host

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38
Q

which bacteria are more present in lean mice? less?

A

more: bacteroidetes
less: firmicutes, methanogens

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39
Q

which bacteria are more present in obese mice? less?

A

more: firmicutes, methanogens
less: bacteroidetes

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40
Q

how does the presence of methanogens affect obesity?

A

they use up H2 which promotes bacterial fermentation… which makes more nutrients available for absorption… increases caloric intake

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41
Q

T/F: Changing the microbiota of the large intestine
can affect human health

A

true! if antibiotics are taken and normal flora is wiped out, opportunistic pathogens can take over

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42
Q

what happens with Antibiotic associated colitis?

A

Clostridium difficile grows
* Inflammation of the colon results

Treatment:
* Further antibiotics
* Probiotics
* “Transpoosition”

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43
Q

______: Home to a variety of bacteria including Staphylococci,
Streptococci and Corynebacteria
* Some people harbor pathogens among their normal
microflora
* Carriers
* Ex. Staphylococcus aureus

A

upper respiratory tract

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44
Q

________
* No resident microflora
* Mucous, lysozyme, ciliated cells, Secretory IgA,
alveolar macrophages

A

Lower respiratory tract

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45
Q

what three types of bacteria do we have in our upper respiratory tract?

A

staphylococci
streptococci
corynebacteria

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46
Q

______: kidneys, bladder
* Normally free of microorganisms (should be mostly sterile)

A

Upper urinary tract

47
Q

Some members of the normal microbiota can act as opportunistic pathogens when transferred to urinary tract… like?

A

E. coli
most common pathogen that causes UTIs

48
Q

the ______ in the reproductive/urinary tract is home to some Gram neg. bacteria

A

urethra

49
Q

why are men less likely to get UTI’s compared to women?

A

their anatomy! much harder for bacteria to survive when urine is constantly flushing them out
plus urinary tract is so much further from rectum

50
Q

______ in the vagina
produces lactic acid from glycogen
* Lowers pH and prevents growth of other
microbes (kills bacteria and STIs)

A

Lactobacillus acidophilus

51
Q

T/F: If normal microbiota is disturbed secondary
to a course of antibiotic therapy
* Yeasts can overgrow and cause yeast
infections

A

true! because yeasts are eukaryotic they aren’t targeted by antibiotics, opportunistic growth!

52
Q

______: growth of microbes that are not normally present in the host
(regardless of whether or not the host is harmed)

A

Infection

53
Q

______: damage or injury that impairs regular host functions

A

Disease

54
Q

______: a microbe that is able to cause disease

A

Pathogen

55
Q

________: a microbe that causes disease only in the
absence of normal host resistance

A

Opportunistic pathogen

56
Q

Streptococcus pneumoniae and E. coli are both ______

A

Opportunistic pathogens

57
Q

________: the ability to cause disease

A

Pathogenicity

58
Q

_______: the severity of the disease that is caused

A

Virulence

59
Q

whats the LD50 value?

A

Number of pathogenic cells or dose of a toxin that will cause death in 50%
of inoculated animals

60
Q

if the LD50 value is lower is it more or less virulent?

A

more virulent… less cells needed to cause 50% deaths

61
Q

_______: the process by which a disease develops

A

Pathogenesis

steps that lead to an infection and tissue damage

62
Q

_______: genetically encoded traits that contribute to a
pathogen’s ability to cause disease

A

Virulence factors

63
Q

______: The ability of a pathogen to stick to a surface and begin colonization

A

adherence

64
Q

what are two non-covalent adherence factors?

A

capsules and slime layers

65
Q

_______ uses slime layer to stick to teeth and form a biofilm

A

Streptococcus mutans

66
Q

______ uses capsule to stick to cells in the lungs

A

Streptococcus pneumoniae

67
Q

how do capsules protect cells from phagocytes?

A

phagocyte can’t recognize bacteria in capsule, can’t destroy it

68
Q

what is the other adherence factor?

A

adhesins

69
Q

_____: specific surface molecules that allow
selective adherence to particular cell types

A

Adhesins

70
Q

Strains of enterotoxigenic E.coli produce
_____ allowing specific adherence to
enterocytes in the intestine (adhesin)

A

fimbriae

71
Q

Neisseria gonorrhoeae produces _____
that allow it to attach to mucosal epithelial
cells (adhesin)

A

fimbriae

72
Q

how does neisseria gonorrhoeae bring itself closer to enterocyte membrane?

A

retracts its fimbriae, then opas proteins can specifically attach to certain receptors on the host cell

73
Q

T/F: Some pathogens can colonize and grow on the surface of tissues, others need to invade tissue

A

true

74
Q

______: the ability of a pathogen to enter into host cells or spread
through tissues

A

Invasiveness

75
Q

what are some virulence factors that promote invasiveness?

A

siderophores
exoenzymes
invasins

76
Q

what are siderophores?

A

iron binding molecules
* Host proteins transferrin and lactoferrin sequester iron, making it
unavailable for microorganisms
* Limit the growth of invaders
* Siderophores rip iron out of tissues to be used by bacteria (competes with us for growth!)

77
Q

why is bacteria that are invasive so bad?

A

they’re no longer localized!! can’t target them as efficiently

78
Q

what are exoenzymes?

A

proteins that are excreted by bacteria to degrade host
tissues

79
Q

what are the five types of exoenzymes?

A

hyaluronidase
collagenase
proteases, nucleases, lipases
fibrinolysin
coagulase

80
Q

_______: hydrolyzes hyaluronic acid (a connective tissue component
that holds animal cells together)
* Allows pathogen to spread between cells

A

Hyaluronidase

81
Q

_______: degrades collagen (extremely abundant connective tissue in
animals)
* Allows pathogen to spread through tissues

A

Collagenase

82
Q

_______:
* Degrade host macromolecules

A

Proteases, nucleases and lipases

83
Q

______: dissolves fibrin clots

A

Fibrinolysin

84
Q

______: induces fibrin clots

A

Coagulase

85
Q

why does Streptococcus pyogenes makes streptokinase (a fibrinolysin)?

A

to escape clots that try to trap them

86
Q

Staphylococcus aureus produces coagulase to protect it from phagocytes, why?

A

if it can induce clots to surround it, it can hide from immune system!

87
Q

_____: proteins that allow bacteria to invade and enter directly into
host cells

A

Invasins

88
Q

_______:
non-lactic acid, non-spore forming
psychrotolerant member of the Firmicutes
* Can be found in unpasteurized dairy products, improperly packaged
processed meats
* Produces invasins that promote phagocytosis by macrophages
* Hijacks the cytoskeleton to escape the phagolysosome
* Spreads from cell to cell avoiding the
humoral immune response

A

Listeria monocytogenes

89
Q

_____: bacteria in the blood

A

Bacteremia

can be carried to different organs and tissues

90
Q

______: bacteria multiplying in the blood

A

Septicemia

Can lead to Sepsis
* Widespread systemic inflammation
* Septic shock
* Can be caused by Gram negative bacteria (Ex: Gram negative
sepsis)
* Also by Gram positives: Staphylococci and Enterococci

91
Q

why do we never want bacteria in our blood?

A

blood has perfect conditions for growth… and can take the bacteria EVERYWHERE in our body!

92
Q

why can septic shock be caused by any gram negative bacteria?

A

because they produce the endotoxin

93
Q

which gram positives cause septic shock?

A

staphylococci and enterococci

94
Q

______: Proteins released by growing bacteria
* Inhibit host cell function or kill host cells
* Usually heat labile
* Can be extremely toxic

A

exotoxins

95
Q

Bacillus anthracis releases…

A

exotoxin

has several virulence factors:
* Capsule, exoenzymes and the anthrax toxin
* Interferes with the immune response and kills macrophages

96
Q

what are the three categories of exotoxins?

A

Cytoxins, AB toxins, Superantigens

97
Q

______, a type of exotoxin, Disrupt cytoplasmic membrane integrity
* Cell lysis and death

A

cytotoxins

98
Q

what are the three types of cytotoxins?

A

hemolysins
Lecithinase or phospholipase
Leukocidins

99
Q

_______:
* Lyse many cells (not just red blood cells)
* Ex. Streptococcus pyogenes
* Produces streptolysin: attacks sterols in the cell membrane

A

Hemolysins

100
Q

__________:
* Dissolves membrane lipids
* Ex. Clostridium perfringens
* α-toxin (gas gangrene)

A

Lecithinase or phospholipase

101
Q

_____: destroy white blood cells
* Ex) Staphylococcus aureus: staphylococcal α-toxin
* Toxin subunits insert into the membrane and oligomerizes to form a heptamer
* A membrane spanning pore
* Cell contents leak out and the cell dies

A

Leukocidins

102
Q

what are the two subunits of AB toxins?

A

Two subunits: Active subunit and Binding subunit

103
Q

__________ (Corynebacterium diphtheriae)
* Subunit B: specifically binds to a protein on animal cells
* Subunit A: moves across the membrane
* Interferes with protein synthesis
* Gene for diphtheria toxin is not encoded on the chromosome, but instead on
a virus

A

Diphtheria toxin

104
Q

T/F: Gene for diphtheria toxin is not encoded on the chromosome, but instead on
a virus

A

true!
gene is delivered to bacteria, but cannot be passed down to daughter cells

105
Q

what are three other examples of AB toxins?

A

tetanus, botulism and cholera toxins

106
Q

_______: Activate T cells to elicit an extreme immune response

A

superantigens

107
Q

_______: Bind to MHC molecules and TCRs outside the antigen binding sites
* Bridge the gap and mimics proper antigen presentation
* Huge number of T cells can be activated
* T cells produce cytokines
* Extreme immune response
* Extreme fever, systemic inflammation, shock, death

A

superantigens

108
Q

Staphylococcus aureus cause _____, when super antigen exotoxin builds up over time

A

toxic shock
syndrome toxin (TSST)

109
Q

______: Lipopolysaccharide from the Gram negative outer membrane
* The toxic part is: Lipid A
* Only released when cells die
* Generally considered less toxic than exotoxins
* A lot is needed to cause symptoms

A

endotoxin

110
Q

which kind of bacteria has endotoxin?

A

gram negative

111
Q

______- colonizes the intestine and multiplies producing a huge number of
bacteria
* As these bacteria die they release endotoxin
* Causes fever, diarrhea, generalized inflammation

A

Salmonella

112
Q

when is Lipid A released from gram negative bacteria?

A

when they die- and lipopolysaccharides breakdown

113
Q

Gram negative sepsis is an example of _____ release

A

endotoxin

Gram negative bacteria multiply in the blood
* Killed by immune system, releasing endotoxin
* Massive inflammation leads to septic shock and death

MBIO 1010 (12 decks)

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