Unit 3 Bacterial Pathogenesis Flashcards Preview

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Flashcards in Unit 3 Bacterial Pathogenesis Deck (126):
1

Processes used by pathogens to produce disease

Pathogenesis

2

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

Virulence factors

3

Do all species have the same virulence factors?

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

4

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

Attachment factors

5

Is there only one attachment factors per microbe?

No there are many.

6

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

Fibronectin

The attachment proteins are fibronectin binding proteins

7

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

Fimbrae

Capsules, slime layers

S-layer, wall surface proteins

8

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

Fimbrae

Pili

9

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

Capsules

10

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.

Endotoxins

11

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

Exotoxins

12

These endotoxins are found on gram negative cells

Which part of it is the disease causing part?

Lipoplysaccharides (LPS)

Lipid A

13

These endotoxins are found on gram-positive cells.

Lipoteichoic acids (LTA)

14

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

Cytolysins

15

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

Superantigens

16

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-B toxins

17

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?

B binds to the receptor

A has negative action inside of the cell

18

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

Cytokines

19

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

Toxic Shock

20

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

Corynebacterium diptheriae

21

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-B toxin (exotoxin)

Endocytosis

Endosome

22

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?

Acidification

A channel

23

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

Translation factor EF2

Translation

Proteins

24

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

It can grow and block access of the airway

Pseudomembrane

25

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

Antitoxin

26

This is the causative agent of whooping cough

What type of toxin?

What type of proteins does it interrupt?

This releases too much_____, causing ______

Pertussis toxin

AB toxin, aerosol route

G proteins

cAMP

inbalanced water and ion concentration

27

Does the whooping cough vaccine ensure lifelong immunity?

Is it more deadly in adults or infants?

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

Infants.

28

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

Cholera toxin.

Stimulates G protein releasing cAMP causing H2O and ion imbalance

29

Where is cholera a problem?

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

30

What does cholera cause?

Diahrrea via hypertonic cells and dehydration.

31

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

Shiga Toxin

32

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

What occurred?

Dysentary

E. coli

Conjugation (copying over of plasmids)

33

Why is the shiga toxin dangerous?

What is it especially dangerous to?

Where does it cause harm?

It affects cells that line the endothelium (blood vessels)

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

Kidneys

34

Who is the shiga toxin especially deadly to?

Young and elderly

35

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

Clostidium botulinum

36

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

Acetylcholine

37

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

What does this cause?

SNARE proteins

Flaccid paralysis

38

Botulism and tetanus have what type of toxin?

What about cholera?

Diptheria, shiga are this type

Neurotoxin (interferes with nervous system)

Enterotoxin (interferes with digestive system)

Cytotoxins (they target cells)

39

How is botulism normally spread?

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.

40

This is a common soil microbe.

What does the vaccine protect us against?

It is also commonly called

Tetanus

The toxin, gives us inactivated version of it.

Lockjaw

41

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

Tetanus

42

What population usually dies from tetanus?

Infants, birthed in unsterile environments

43

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

Cytolysins

44

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 _____

Hemolysins

Iron

45

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

Alpha hemolysis

46

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

Beta Hemolysis

47

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

Gamma Hemolysis

48

Streptococcus pyogenes causes strep throat and has what lysis pattern?

Beta Hemolysis

49

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?

Alpha toxin

Staphylococcus Aureus

50

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?

PV leukocidin

Mitochondrial membrane

White blood cells (leukocydes)

51

What do dead white blood cells lead to?

Puss, also called pyogenic infection

52

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

Listeria monocytogenes

53

Listeria monocytogenes enters the shape and forms an

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

What activates it?

Endosome

Listeriolysin

Acidification

54

This bacterial toxin degrades phospholipids

These specifically degrade the lecithin phospholipid

Phospholipase cytolisins

lecithinasaes

55

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.

Clostridium Perfringens

56

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

Superantigens

57

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

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

What organism produces superantigens in her example?

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

Staphylococcus Aureus

Toxic Shock

59

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

Does it only occur this way?

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

No.

60

How can superantigens lead to food poisoning?

Food borne infection is different how?

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

Which is fast onset, food infection or food poisoning?

Food poisoning

Infection takes longer, onset is about 24 hours later

62

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

Capsule

63

Capsules block opsonization, interfering with

Phagocytosis

64

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

Opsonization

65

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

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

Capsules

66

The carbohydrates on capsules are the same as

Glycoproteins (self molecules)

67

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

Can bacteria use more than one?

Siderphores
Bacterial Transport Proteins
Low pH

Yes

68

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

Siderophore

69

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

Bacterial Transport Proteins

70

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

pH

71

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

Does this make it easier to get transported into cell?

More soluble under low pH

Yes

72

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

H+, acidic end products

73

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

Iron Binding Proteins

74

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

Hemolysins

75

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

Hemolysins

76

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

Streptococcus pyogenes

77

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

Opportunistic

78

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

No

79

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

Cellulitis and Erysipelas

80

This disease causes inflammation in tissues deeper under the skin

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

Cellulitis

Erysipelas

81

Can erysipelas progress to cellulitis if left untreated?

Yes

82

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

one affects the kidneys

Rheumatic heart disease/fever

Glomerulonephritis

83

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

Antibodies

84

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

Antibiotics

85

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

Acute Rheumatic Fever

86

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

Scarlet Fever

87

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.

Impetigo

88

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)

Necrotizing fascilitis

89

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

Puerperal Fever.

90

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

Pharyngitis/tonsilitis

91

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

Septicemia (Septic Shock)

Can be caused by other microbes, pyogens is just one

92

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

Toxic Shock Syndrome

Other bacteria can do this.

93

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

Pharynx

94

What attachment factors does S. pyogens have?

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

95

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

Microbiota (other microbes)

96

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

Physical damage to skin or mucosa

97

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

M protein

98

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

M Protein

Interferes with attachment, phagocytosis, and compliment activatation

99

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

Factor H (in later chapters)

100

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.

Hyaluronic Acid Capsule

101

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

C5a peptidase

102

These molecules of the immune system typically punch holes in membranes

Membrane attack complex (MAC)

103

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

DNase

104

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

Hyaluronidase

105

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

IdeS

106

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

Streptokinase

107

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.

Streptolysin S

Streptolysin O

108

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

SPE toxins

109

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

Mycobacterium tuberculosis

110

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

mycolic acids

111

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

Facultative intracellular colonizer

112

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

Mycolic Acids

113

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

Acid fast stain

114

Are there multi-drug resistant tuberculosis strains out there?

Yes

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

115

What is a common route tuberculosis spread by?

Aerosol (inhalation of them from infected individuals)

116

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

Phagosomes (white blood cells)

117

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

C3b and Mannose binding lectin

118

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

Lysosomes

liparabinomanna (LAM)

119

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

Superoxide dismutase and catalase

120

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

!

121

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

TNF-α

Granulomas

Note: reemergence occurs in some HIV infected patients

Occurs with asbestos too

122

Does everyone infected with TB have active TB?

What does it depend upon?

No, depends on our adaptive immunity (specific defenses)

123

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

Humoral response

Cell-mediated response

124

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

Cell mediated.

If activated early, doesn't allow bacteria to persist

125

How is the TB test administered?

A raised, hardened welt appears approximately ___ hours later

M. tuberculosis proteins are injected under the skin

72 hours

126

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

What follow up is done?

Individual is immunocompromised or recently infected

X-rays checking for granulomas