Unit 3 Bacterial Pathogenesis Flashcards
1
Q
Processes used by pathogens to produce disease
A
Pathogenesis
2
Q
These are pathogen products that enhance bacteria’s ability to cause disease
A
Virulence factors
3
Q
Do all species have the same virulence factors?
A
No. Different species have different virulence factors. Depends upon genome
4
Q
Some of the first virulence factors that a host will encounter are
A
Attachment factors
5
Q
Is there only one attachment factors per microbe?
A
No there are many.
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
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
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
9
Q
Which help prevent phagocytosis in addition to aiding in attachment, capsules or slime layers?
A
Capsules
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
11
Q
These virulence factors are proteins that are released outside of the producing cell.
A
Exotoxins
12
Q
These endotoxins are found on gram negative cells
Which part of it is the disease causing part?
A
Lipoplysaccharides (LPS)
Lipid A
13
Q
These endotoxins are found on gram-positive cells.
A
Lipoteichoic acids (LTA)
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
15
Q
This type of exotoxin nonspecifically stimulate T cells to secrete large amounts of cytokines
A
Superantigens
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
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
18
Q
These are communication chemicals whose release is triggered by superantigens. Causes too much information, interference occurs, causing inflammation (fever/ shock)
A
Cytokines
19
Q
This is one example of shock that occurs in vagina via staphylococcus aureus
A
Toxic Shock
20
Q
This bacteria is the cause of diptheria, respiratory illness that sprends via the aerosol route
A
Corynebacterium diptheriae
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
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
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
24
Q
What is the white stuff that forms on tonsils in diptharia?
It can grow and block access of the airway
A
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
