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Microbiology 350 > Unit 3 Bacterial Pathogenesis > Flashcards

Unit 3 Bacterial Pathogenesis Flashcards

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1
Q

Processes used by pathogens to produce disease

A

Pathogenesis

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2
Q

These are pathogen products that enhance bacteria’s ability to cause disease

A

Virulence factors

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3
Q

Do all species have the same virulence factors?

A

No. Different species have different virulence factors. Depends upon genome

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4
Q

Some of the first virulence factors that a host will encounter are

A

Attachment factors

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5
Q

Is there only one attachment factors per microbe?

A

No there are many.

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6
Q

Attachment factors on bacteria bind to these large plasma glycoprotein in the plasma and extracellular matri

A

Fibronectin

The attachment proteins are fibronectin binding proteins

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7
Q

These are attachment factors with a specialized pili that has an adhesive tip (tips are specific, pili not)

These are various surface associated molecules

There are also specialized proteins for attachment

A

Fimbrae

Capsules, slime layers

S-layer, wall surface proteins

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8
Q

These attachment factors are short and numerous

These attachment factors are long and there are just one of them, allowing them to attach to each other

A

Fimbrae

Pili

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9
Q

Which help prevent phagocytosis in addition to aiding in attachment, capsules or slime layers?

A

Capsules

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10
Q

These type of virulence factors are part of the cell wall structure and induce inflammatory responses after cell death. Not protein. They typically require high amounts to cause harm.

A

Endotoxins

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11
Q

These virulence factors are proteins that are released outside of the producing cell.

A

Exotoxins

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12
Q

These endotoxins are found on gram negative cells

Which part of it is the disease causing part?

A

Lipoplysaccharides (LPS)

Lipid A

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13
Q

These endotoxins are found on gram-positive cells.

A

Lipoteichoic acids (LTA)

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14
Q

This type of exotoxin acts on cell membranes, typically punching holes in it causing fluid to rush in and bursting.

They can also be enzymes which digest phospholipids, destroy membrane and cause lysing

A

Cytolysins

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15
Q

This type of exotoxin nonspecifically stimulate T cells to secrete large amounts of cytokines

A

Superantigens

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16
Q

This type of exotoxin has 2 subunits, one which binds the the host cell and the other that has a negative action inside of the cell by having enzymatic activity

A

A-B toxins

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17
Q

Which subunit of the A-B toxins binds to the host cell receptor? It only goes in the host cell if it triggers endocytosis, otherwise it doesn’t

Which has a negative action inside of the cell?

A

B binds to the receptor

A has negative action inside of the cell

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18
Q

These are communication chemicals whose release is triggered by superantigens. Causes too much information, interference occurs, causing inflammation (fever/ shock)

A

Cytokines

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19
Q

This is one example of shock that occurs in vagina via staphylococcus aureus

A

Toxic Shock

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20
Q

This bacteria is the cause of diptheria, respiratory illness that sprends via the aerosol route

A

Corynebacterium diptheriae

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21
Q

What type of toxin is Corynebacterium diptheriae?

How does it enter the host cell via the receptor (which are plentiful on the cell because they are in the heart and kidney)

This forms a ___

A

A-B toxin (exotoxin)

Endocytosis

Endosome

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22
Q

In the endocytosis of diptheria bacteria, how is the B subunit recept released from the the receptor in the endosome?

What forms, which the A subunit ultimately goes through?

A

Acidification

A channel

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23
Q

What does corynebacterium diptheriae inactivate by release of A subunit into the cytoplasm?

What does it abolish?

So the cell can’t make ____ in the heart and kidneys

A

Translation factor EF2

Translation

Proteins

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24
Q

What is the white stuff that forms on tonsils in diptharia?

It can grow and block access of the airway

A

Pseudomembrane

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25
Q

What is used to treat diptharia (antibodies which bind the toxin before it binds the cell)?

A

Antitoxin

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26
Q

This is the causative agent of whooping cough

What type of toxin?

What type of proteins does it interrupt?

This releases too much_____, causing ______

A

Pertussis toxin

AB toxin, aerosol route

G proteins

cAMP

inbalanced water and ion concentration

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27
Q

Does the whooping cough vaccine ensure lifelong immunity?

Is it more deadly in adults or infants?

A

No. Wears off over time. Have to get it again.

Infants.

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28
Q

This bacteria works similarly to pertussis but in the digestive tract.

A

Cholera toxin.

Stimulates G protein releasing cAMP causing H2O and ion imbalance

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29
Q

Where is cholera a problem?

A

Where there is no sewage or water treatment (fecal matter gets into water supply)

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30
Q

What does cholera cause?

A

Diahrrea via hypertonic cells and dehydration.

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31
Q

This toxin stops protein synthesis differently than diptheria, causes breakdown of RNA component of the ribosome

A

Shiga Toxin

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32
Q

Shiga toxin was long associated with _____ then became associated with ______

What occurred?

A

Dysentary

E. coli

Conjugation (copying over of plasmids)

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33
Q

Why is the shiga toxin dangerous?

What is it especially dangerous to?

Where does it cause harm?

A

It affects cells that line the endothelium (blood vessels)

Capillaries, which are one layer thick, repair can’t occur, hemorrhages occur

Kidneys

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34
Q

Who is the shiga toxin especially deadly to?

A

Young and elderly

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35
Q

This bacteria produces botulism, usually via contaminated food for adults.

A

Clostidium botulinum

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36
Q

Botulism interferes with chemical messaging that causes our muscles to contract, what neurotransmitter does it affect?

A

Acetylcholine

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37
Q

The A part of botulism interferes with what proteins which cause the secretion of acetylcholine?

What does this cause?

A

SNARE proteins

Flaccid paralysis

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38
Q

Botulism and tetanus have what type of toxin?

What about cholera?

Diptheria, shiga are this type

A

Neurotoxin (interferes with nervous system)

Enterotoxin (interferes with digestive system)

Cytotoxins (they target cells)

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39
Q

How is botulism normally spread?

A

Food (canned food) where they grow anaerobically (don’t eat weird cans)

Also can be spread via honey, never give it to infants. Oil too.

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40
Q

This is a common soil microbe.

What does the vaccine protect us against?

It is also commonly called

A

Tetanus

The toxin, gives us inactivated version of it.

Lockjaw

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41
Q

This disease works by preventing the release of inhibitory GABA and glycine NTs, resulting in spastic paralysis (overstimulation)

A

Tetanus

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42
Q

What population usually dies from tetanus?

A

Infants, birthed in unsterile environments

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43
Q

These exotoxins are made by the bacteria and work and the plasma membrane of cells, often forming pores or degrading phospholipids

A

Cytolysins

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44
Q

These are a classic example of cytolysins, they lyse red blood cells.

They are produced if a microbe lacks a particular nutrient, which in this case is _____

A

Hemolysins

Iron

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45
Q

This lysis pattern has greenish tinge around the colony, means there is an incomplete breakdown of red blood cells

A

Alpha hemolysis

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46
Q

This lysis pattern has bright areas around the colonies, signifies complete breakdown

A

Beta Hemolysis

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47
Q

This lysis pattern has nothing happening around the colonies, no lysis at all

A

Gamma Hemolysis

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48
Q

Streptococcus pyogenes causes strep throat and has what lysis pattern?

A

Beta Hemolysis

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49
Q

This bacterial toxin is a pore forming cytolysin that binds to a membrane and forms a pore for calcium influx. It triggers apoptosis.

Whats a mircobe example of this?

A

Alpha toxin

Staphylococcus Aureus

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50
Q

This additional toxin of staphylococcus aureus forms pores for the entry of toxin.

What type of cell does it target in our bodies?

What does it disrupt, leading to apoptosis?

A

PV leukocidin

Mitochondrial membrane

White blood cells (leukocydes)

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51
Q

What do dead white blood cells lead to?

A

Puss, also called pyogenic infection

52
Q

This bacteria is associated with food borne illness. Processing causes microbes of it to get onto the food and it is capable of growing in the fridge

A

Listeria monocytogenes

53
Q

Listeria monocytogenes enters the shape and forms an

What is the toxin that cuts the endosome/membrane sac?

What activates it?

A

Endosome

Listeriolysin

Acidification

54
Q

This bacterial toxin degrades phospholipids

These specifically degrade the lecithin phospholipid

A

Phospholipase cytolisins

lecithinasaes

55
Q

This organism’s alpha toxin is a lecithinase associated with gas gangrene in wounds. Or it can lead to temporary stomach illness if in the digestive tract.

A

Clostridium Perfringens

56
Q

These are exotoxins that act on helper T cells, causing them to release many nonspecific cytokines and eventually causes systemic inflammatory response

A

Superantigens

57
Q

How do superantigens trigger the release of more cytokines than normal antigens?

A

Any CD4+ T cell can be linked (forming a bridge) and activated by a superantigen, rather than just specific T cells.

In other words, it causes a less focused immune respone

58
Q

What organism produces superantigens in her example?

What to superantigens sometimes lead to via inflammation? It causes fever and changes blood pressure

A

Staphylococcus Aureus

Toxic Shock

59
Q

What must be done to prevent toxic shock via tampons in the past?

Does it only occur this way?

A

Changing them frequently. There was a special long lasting kind, made with polyacrylamide component that caused it.

No.

60
Q

How can superantigens lead to food poisoning?

Food borne infection is different how?

A

Enterotoxins produced by strains of S. aureus. The toxin is in the food and you eat it, aka intoxication.

You ingest bacteria, not a toxin.

61
Q

Which is fast onset, food infection or food poisoning?

A

Food poisoning

Infection takes longer, onset is about 24 hours later

62
Q

This aspect of bacterial pathogens is an extracellular loose matrix of polysaccharides (sugar) that provide attachment and immune evasion mechanisms for the pathogens

A

Capsule

63
Q

Capsules block opsonization, interfering with

A

Phagocytosis

64
Q

A process preventing antibodies and/or complements that have attached to a pathogen from binding to white blood cell receptors for phagocytosis

A

Opsonization

65
Q

These also can reduce entry into the endocytic pathway by lessening antigen presentation

They mimic ‘self’ molecules, preventing stimulation of antibody/compliment responses

A

Capsules

66
Q

The carbohydrates on capsules are the same as

A

Glycoproteins (self molecules)

67
Q

What are the three mechanisms that bacteria normally have to obtain iron from our bodies?

Can bacteria use more than one?

A

Siderphores
Bacterial Transport Proteins
Low pH

Yes

68
Q

This is made inside bacterial cell and released outside of it, it has an affinity for iron, it competes with our iron binding proteins and grabs iron and brings it back into bacterial cell

A

Siderophore

69
Q

This is produced by bacteria and binds the hosts iron binding transport protein and the iron itself, bringing it to the surface of the plasma membrane where it can go into cell

A

Bacterial Transport Proteins

70
Q

iron comes in different forms and different solubilities depending upon the ___

A

pH

71
Q

Under low pHs (acidic conditions), is the iron more soluble or less soluble?

Does this make it easier to get transported into cell?

A

More soluble under low pH

Yes

72
Q

What do bacteria that lower the pH release around the cell?

A

H+, acidic end products

73
Q

If you have an infection, the body ups the amount of ______ to starve the bacteria responsible for the infection

A

Iron Binding Proteins

74
Q

How do SOME bacteria respond to iron starvation caused by the increase of iron binding proteins by the immune system?

A

Hemolysins

75
Q

These have the ability to destroy the red blood cell to get at iron within Hb

A

Hemolysins

76
Q

This is an opportunistic pathogen that produces a variety of disease, as it possesses numerous virulence factors. Many strains along with varying host conditions allow the disease to occur

A

Streptococcus pyogenes

77
Q

These type of pathogens become problems when host defenses are down, and the bacteria are in our normal flora but go elsewhere and grow.

A

Opportunistic

78
Q

Does removing one virulence factors preven’t the pathogenicity of streptococcus pyogenes?

A

No

79
Q

These are two inflammation disease produced by streptococcus pyogenes, causes bright red and warm spots on the body. Usually swollen and painful. Caused by immune system activity trying to remove infection

A

Cellulitis and Erysipelas

80
Q

This disease causes inflammation in tissues deeper under the skin

This disease causes inflammation on the dermis (closer to the surface) of the skin

A

Cellulitis

Erysipelas

81
Q

Can erysipelas progress to cellulitis if left untreated?

A

Yes

82
Q

Inflammatory sequela (caused by previous infection) diseases caused by streptococcus pyogens, one effects the heart. They are autoimmune.

one affects the kidneys

A

Rheumatic heart disease/fever

Glomerulonephritis

83
Q

Rheumatic heart disease/fever and glomerulonephritis are autoimmune because they cause the release of a lot of ______ causing cross-reactivity with the heart and kidneys

A

Antibodies

84
Q

What lowers the amount of crosslinking in RHD/RHF and glomerulonephritis these days

A

Antibiotics

85
Q

Which causes more mild and temporary damage to the heart valves, RHD or acute rheumatic fever? It’s not permanent.

A

Acute Rheumatic Fever

86
Q

This disease is caused by a different strain of streptococcus pyogens that can produce a toxin. Produces red discoloration throughout the body. Less localized than RHD, acute rheumatic fever and glomerulonephritis. Cross linking to other diseases can occur

A

Scarlet Fever

87
Q

A streptococcus pyogens disease commonly seen in children, has characteristic crusty scabs on top of inflammation. Begins with a small wound. Also caused by S. aureus. Gram positive. No permanent scarring.

A

Impetigo

88
Q

This streptococcus pyogens disease causes destruction of tissues that causes damage to deeper tissue layers like connective tissue coverings and muscles themselves. Flesh-eating bacteria. Starts with another pyogens disease like cellulitis (inflammation causing)

A

Necrotizing fascilitis

89
Q

A rare disease today caused by s. pyogens, handwashing/hygiene decreased it in hospitals. Leads to death, starts by infection during childbirth

A

Puerperal Fever.

90
Q

The common form of s. pyogens, infects throat causing inflammation and redness. Lead to puss forming (pyogenic) as well. Usually cleared up by immune system (self limitingg) but faster with antibiotics

A

Pharyngitis/tonsilitis

91
Q

This disease caused by s. pyogens is an infection that has gained access to the blood stream and colonize it (growing and dividing). Can lead to shock, aka high fever, drop in blood pressure, clotting cascades

A

Septicemia (Septic Shock)

Can be caused by other microbes, pyogens is just one

92
Q

A disease caused by s. pyogens that is a different strain, caused by over-reactive immune response, usually due to wound infections.

A

Toxic Shock Syndrome

Other bacteria can do this.

93
Q

S. pyogens is opportunistic, meaning it is part of our normal flora. Where is its primary residence?

A

Pharynx

94
Q

What attachment factors does S. pyogens have?

A

Fimbrae, other surface components (gram positive) that attach to fibronectin and collagen

95
Q

S. pyogens is normally kept in check by ________ but if things change it may expand its population

A

Microbiota (other microbes)

96
Q

What might allow direct access to deeper tissues for s. pyogens?

A

Physical damage to skin or mucosa

97
Q

This is another attachment factor (virulence factor) that also contributes to the establishment of microcolonies on the skin and pharynx

A

M protein

98
Q

This virulence factor of s. pyogens is highly negatively charged, helps it adhere to our cells

Additionally, any antibodies don’t bind in properly, causes increased chance of autoimmunity because antibodies are floating around more

A

M Protein

Interferes with attachment, phagocytosis, and compliment activatation

99
Q

The M protein can interact with this in the serum so it can’t interact with complement proteins

A

Factor H (in later chapters)

100
Q

This discourages complement fixation, the chemical of it is in tight junctions and prevents fluids going between cells. Considered part of the body’s self because it’s so prevalent. Antibodies therefore don’t bind it.

A

Hyaluronic Acid Capsule

101
Q

This virulence factor actually breaks down complement proteins which act as opsonization factors, leaving a trail for white blood cells (phagocytes) to migrate towards infection site, prevents MACs killing bacteria

A

C5a peptidase

102
Q

These molecules of the immune system typically punch holes in membranes

A

Membrane attack complex (MAC)

103
Q

This virulence factor breaks down connective tissues, liquefies them, spreads through pus and the breakdown of these tissues

A

DNase

104
Q

This virulence factor breaks down hyaluronic acid in tight junctions and connective tissues, breaking down tissue barriers

A

Hyaluronidase

105
Q

This virulence factor breaks down IgG antibodies which act as an opsonization factors

A

IdeS

106
Q

This virulence factor breaks down fibrin clots that are made to seal off infection from rest of body, aka staphlokinase in staphococcus aureus

Enzymes like the one above are also used medically

A

Streptokinase

107
Q

These two virulence factor are a cytolitic toxins that form pores and lyse the cell , specifically white blood cells. This one is oxygen stable

This one is not oxygen stable.

A

Streptolysin S

Streptolysin O

108
Q

These are a family of superantigens that produce toxic shock via inflammation, fever, etc by overstimulating T cells to release too many cytokines

A

SPE toxins

109
Q

This bacteria causes tuberculosis, which is characterized by the destruction of lung tissue.

It can occur in other areas of the body, like the brain

A

Mycobacterium tuberculosis

110
Q

All members of the mycobacterium tuberculosis genus have an unusual cell wall containing ____, which is waxy and therefore hydrophobic making it difficult to cross that cell wall

A

mycolic acids

111
Q

Mycobacterium can live inside other cells, including white blood cells, but also outside blood cells. What is the term for this?

A

Facultative intracellular colonizer

112
Q

These help mycobacterium resist common staining methods, interfere with antibiotics (other things have to be used to get past it), some induce other disease states (like M. Leprae), all of them use similar tactics to induce disease

A

Mycolic Acids

113
Q

To stain mycolic acids, what type of stain do you use?

A

Acid fast stain

114
Q

Are there multi-drug resistant tuberculosis strains out there?

A

Yes

People stopped taking their antibiotics early, some financial issues (it’s a few months long treatment)

115
Q

What is a common route tuberculosis spread by?

A

Aerosol (inhalation of them from infected individuals)

116
Q

The mycobacterium tuberculosis replicates inside ____ of lung macrophages, which protects the cells from complent mediated lysis and antibodies because it is a membrane sac

A

Phagosomes (white blood cells)

117
Q

Mycobacterium tuberculosis actually encourages phagocytosis via opsonization with complement proteins ___ and _______ by things on its surface to get into the phagosome

A

C3b and Mannose binding lectin

118
Q

Mycobacterium tuberculosis prevents phagosome fusion with ___ to stay alive in lung macrophages

Bacteria also produce and surround themselves with ___, which downregulalates oxidative burst and neutralizes toxic oxygen species

A

Lysosomes

liparabinomanna (LAM)

119
Q

These can also be produced by mycobacterium tuberculosis to protect it from oxidative damage

A

Superoxide dismutase and catalase

120
Q

Additionally, mycobacterium tuberculosis can be dumped by a phagocyte but since it is undamaged it can still spread

A

!

121
Q

When macrophages can’t eliminate the mycobacterium tuberculosis microbed elevated ____ levels occur

Chronic inflammation results in a walled off _______, which corrals the bacteria with white blood cells, connective tissue and calcification but damages lung tissue

A

TNF-α

Granulomas

Note: reemergence occurs in some HIV infected patients

Occurs with asbestos too

122
Q

Does everyone infected with TB have active TB?

What does it depend upon?

A

No, depends on our adaptive immunity (specific defenses)

123
Q

There are two adaptive immunity responses

This one is primarily involved in making antibodies, good for bacteria that are outside of cells

This one comprises immune system cells that kills infected body cells

A

Humoral response

Cell-mediated response

124
Q

Which adaptive immunity response is protective against TB? Humoral or cell-mediated?

A

Cell mediated.

If activated early, doesn’t allow bacteria to persist

125
Q

How is the TB test administered?

A raised, hardened welt appears approximately ___ hours later

A

M. tuberculosis proteins are injected under the skin

72 hours

126
Q

If there is no hardened welt, what does that say?

What follow up is done?

A

Individual is immunocompromised or recently infected

X-rays checking for granulomas

Microbiology 350 (13 decks)

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