Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MEDSCI 203 > Infection and Immunity > Flashcards

Infection and Immunity Flashcards

1
Q

Primary immune response

A

First encounter
Response is fairly weak and short lived but T and B memory lymphocytes are produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Secondary immune response

A

Subsequent encounter with the same organism
T and B memory lymphocytes enable much faster and stronger protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Immune hypersensitivity response

A

Primary response followed by secondary response harms the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Secondary response being harmful

A

Can cause harmful reactions, including tissue damage

Allergy to allergens

Tissue damage due to autoimmune reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are allergens detected by the immune system

A

Dendritic cells form the bridge between innate and adaptive immune responses

They are prototypic antigen-presenting cells of the immune system

Dendritic cells are critical for induction and regulation of adaptive immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do dendritic cells activate the adaptive immune system

A

Become activated and migrated to lymph nodes
Mature dendritic cells present antigen-derived peptides on cell surface MHC molecules to activate naive T cells with antigen receptors that recognizes the MHC/peptide combination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Neutrophil

A

12-15um
2-5 distinct nuclear lobes, abundant granules
Phagocytosis and degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Basophil

A

9-10um
2-3 nuclear lobes, many, large oval granules. Degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Monocyte

A

12-20um, round, oval notched, abundant granules
Phagocytosis and cytokine production in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Macrophage

A

15-80um
Elongated, indented or oval nucleus, many granule
Phagocytosis and cytokine production in the tissues, antigen presenting cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mature B and T cells

A

9-12um
round or slightly indented nucleus, few granules
Adaptive immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Plasma Cell

A

14-18um
round or oval nucleus, no granules
B effector cell, antibody production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NK cell

A

12-16um, round nucleus, many granules
Cytolysis and cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dendritic cell

A

Irregularly shaped cell and nucleus, many cellular projections
Phagocytosis and cytokine production, antigen presenting cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mast cell

A

5-25um non-segmented nucleus, many large granules
Degranulation and cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Antibody structure

A

2 heavy chains and 2 light chains held together by inter-chain disulfide bonds

2 antigen-binding sites
1 effector function-crontilling region

Effector functions e.g complement triggering, cell receptor binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Human heavy chain isotypes

A

1 of 5 possible heavy chain isotypes determine heavy chain isotype of Ig molecule

Receptors on leukocytes can bind Fc specific for Ab class

Called Fc receptors and are specific for Ab class

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Types of Ig molecule

A

IgM, IgD, IgG, IgE, IgA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which ig molecules mediate hypersensitivity

A

IgE, IgG and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Fc receptors and immune hypersensitivity reactions

A

Receptors for antigen-antibody immune complexes. They bridge humoral and innate immune systems. They are inflammatory mediators, do phagocytosis, degranulation and antibody-dependent cell-mediated cytotoxicity ADCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type 1 HS

A

IgE medited, allergy atopy
<1-30min

Allergens cross-link IgE bound on mast cells and basophils induce degranulation

Asthma, hay fever, eczema, hives, food allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an allergen

A

An antigen that generates an abnormal immune response that fights off a perceived threat that would otherwise be harmless to the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Atopic allergy

A

Grass pollen
Skin prick test
Immediate response (early phase reaction) with minutes
Late response (late phase reaction) a few hours later

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sensitization of Type 1 HS

A

Allergen breached tissue barrier
Phagocytosed by immature D cell
Travels to lymph node
Naive T cells recognise allergen derived pMHC on mature DC and become activated, differentiate into Th2 effector cells that help activate B cells. Activated B and Th2 cells leave the lymph node
Travel to where allergen entered body
Th2 cells produce cytokines that instruct plasma cells to produce IgE
IgE can bind directly to allergen or FCR on mast cells. Mast cells are sensitised for the effector stage
Excess IgE taken up by lymphatics
IgE encounters basophils in the blood and binds to FcRs to sensitise them
IgE encounters mast cells in other tissues and binds to FcRs to sensitise them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Effector stage of Type 1 HS (early stage)

A

Allergen enters tissue where sensitised mast cells are present
Allergen binds IgE molecules attached to mast cells via FcRs
Mast cells degranulate and secrete cytokines/chemokines
Breakdown of mast cells releases platelet-activating factor
Tissue-specfic symptoms of allergic response
Additional leukocyte recruited (eig eosinophils and sensitised basophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Differences of mast cell granulations due to route of allergen entry (Gastrointestinal tract)

A

increased fluid secretion and peristalsis - diarrhoea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Differences of mast cell granulations due to route of allergen entry (Eyes, nasal passages and airways)

A

Decreased airway diameter, increased mucus secretion

Congestion and blockage of airways (wheezing, coughing phlegm) Swelling and mucus secretion in nasal passages. Ocular itching and sneezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Differences of mast cell granulations due to route of allergen entry (Blood vessels)

A

Increased blood flow, increased permeability
Increased fluid in tissues causing increased flow of lymph to lymph nodes, increased cells and protein in tissues, increased effector response in tissues. Hypotension potentially leading to anaphylactic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Determinants favouring atopy

A

Genetic determinants and environment determinants trigger events which leads to clinical atopy upon exposure to allergen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Type II HS

A

Direct antibody- mediated cytotoxic HS
Antibody (IgG or IgM)
5-8hr
IgM or IgM bind to cell-bound antigen, cell is destroyed by phagocytosis, complement activation or ADCC
Hemolytic anemias, Goodpasture’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Antibody-mediated cytotoxic hypersensitivity

A

Autoantibodies against cell surface Ag
Complement-dependent cell lysis
C3b-opsonised phagocytosis
FcR-mediated antibody-dependent cell-mediated cytotoxicity, ADCC (NK cells and macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Type III hypersensitivity

A

Immune complex-mediated HS
Antibody (IgG or IgM)
4-6 hr
Immune complexes trigger complement activation; phagocyte FcR engagement leads to release of lytic mediators
Arthus reaction, aspects of rheumatoid arthritis and systemic lupus erythematosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Immune complex-mediated hypersensitivity

A

Ab binds antigen in the blood (IC). Insoluble ICs form by cross-linking that lodge in small vessels. ICs enter tissues (kidneys, joints), drives local inflammation/tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is immunological tolerance?

A

Immunological tolerance is a state of unresponsiveness to an antigen

When a lymphocyte encounters an antigen it can either be activated, leading to an immune response, or inactivated/eliminated, lead to tolerance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Self reactive lymphocytes

A

Have the potential to respond to self antigens (or autoantigens) are called autoreactive lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens if immunological tolerance fails to remove self-reactive lymphocytes

A

Autoimmune diseases can occur if the resulting autoimmune response leads to tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Central tolerance

A

Deletion of strongly self-reactive T and B cells during their development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Where are lymphocytes developed

A

Primary lymphoid organs are sites in the body where lymphocytes develop

Thymus for T cells and bone marrow for B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Positive selection

A

Lymphocytes are positively selected based on their affinity of interaction with the self MHC complex expressed on cortical thymic epithelial cells. A T cell which does not recognise self at all will undergo death by neglect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Negative selection

A

Lymphocytes are negatively selected based on their affinity of interaction with self antigen-MHC complexes presented by dendritic cells, macrophages and cortical/medullary epithelial cells. A T cell which receives very strong signals will undergo apoptotic death

Autoreactive cells can escape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does pos and neg selection occur?

A

Positive selection occurs in the cortex when thymocytes are double positive for CD4 and CD8.
Thymic cortical epithelial cells mediate positive selection.
Developing T cells bearing antigen receptors that recognise self MHC with sufficient affinity survive.
T cells bearing TCRs that strongly recognise self peptide, self MHC are negatively selected.

DP cells express a successfully rearranged TCR with CD4 and CD8 on their surface

Positive selection rescues the T cell from default ‘death by neglect’

Those with high affinity interactions with dendritic cells presenting self MHC with self peptide undergo negative selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T cell education

A

Most thymocytes bear TCRs that fail to bind self MHC (80%)

Most thymocytes with TCRs that bind strongly to self peptide: MHC are removed by negative selection (20%)

Leaves 1-2% of positively selected thymocytes and ensures strongly autoreactive clones removed from T cell repertoire

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Education of B cells

A

Educated to not recognise self antigens during their development,
Developing B cells with BCRs strongly recognize multivalent cell-surface self antigen undergo selection

B cell precursor rearranges its immunoglobulin genes
Immature B cell bound to self cell-surface antigen is removed from the repertoire
Mature B cell bound to foreign antigen is activated
Activated B cells give rise to plasma cells and memory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What happens when an APC presents self-peptide

A

DCs present self antigens derived from host cells, in the absence of pathogen attack

In the absence of pathogen attack the DC is not activated

DC encounters an autoreactive T cell that recognises the self MHC, self peptide combination it inactivates it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Suppression-regulatory T cells

A

Specialised autoreactive T cells
If Tregs encounter self antigen on APC they can inhibit surrounding autoreactive T cells by producing inhibitory cytokines like IL-10 and TGF-b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Ignorance-sequestered antigen release

A

Sympathetic ophthalmia
- Damage to an immunologically privileged site (eye)
- Release of sequestered eye antigens can result in an autoimmune response against eye proteins in both eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Requirements for autoimmune disease

A

Escape of autoreactive clones from central tolerance
Autoreactive clones encounter self-antigens
Peripheral tolerance failure
Autoreactive tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where does type II Hs act?

A

Organ-specific
Antibody - mediated (cytotoxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where does type III Hs act?

A

Systemic
Immune complex-mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Organ-specific autoimmunity diseases

A

Goodpastures syndrome
Myasthenia gravis
Pemphigus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Goodpasture’s syndrome

A

Antibodies against type IV collagen in basement membrane (glomeruli and alveoli)
Kidney dysfunction, bleeding in lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Myasthenia gravis

A

Antibodies block acetylcholine receptors
Muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Pemphigus

A

Antibodies against intercellular adhesion (desmogleins) between keratinocytes causing blisters
Can lead to fatal infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Thyroid autoimmune diseases

A

Graves disease
Hashimoto’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Graves disease

A

Autoantibodies bind the thyroid stimulating hormone receptor
Acts as agonist
Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Hashimoto’s disease

A

Autoantibodies against thyroglobulin and thyroid peroxidase
Complement activation and cytotoxic T cell - driven attack hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Systemic autoimmune disease

A

Soluble antigen and antibodies in optimal concentration
-> Precipitation
-> Vessel deposition (Type III hypersensitivity)
Kidneys - glomerulonephritis
Skin - rash
Joints - arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Systemic Lupus Erythematosus

A

Inflammation in the skin, joints, blood vessels, kidneys
Photosensitivity
Antinuclear autoantibodies, anti-DNA, anti-RNA, anti-nuclear proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Molecular mimicry

A

Some T and B cells may bear antigen receptors that recognise both the self epitope and the pathogen and epitope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Acute Rheumatic fever

A

Group A streptococcal post-infection complication
M proteins share epitopes with proteins in synovium, heart muscle, and hear valve. Antibody-mediated Type II hypersensitivity generates tissue damage and inflammation.
Arthritis and heart valve damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Factors influencing autoimmunity

A

Genotypes can be predisposed to autoimmunity

There are replacement and suppression treatments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How to do a gram stain

A

Heat-fixed slide stained with crystal violet (purple)
Stain attaches to peptidoglycan in bacterial cell wall.
Iodine binds to crystal violet and traps it in the cell
Add ethanol or acetone
-> Then stain with safranin or carbol fuchsin (pink)
-> Gram pos - retain crystal violet dye
-> Gram neg- doesn’t retain crystal violet dye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Gram negative

A

Outer membrane composed of lipopolysaccharides (LPS). Have an outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Gram positive

A

Thick peptidoglycan cell wall
Lack an outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Ziehl Neelsen stain

A

Carbol fuchsin (red) in phenol driven into bacilli with heat

For mycobacterium tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Motility of bacteria

A

Swarming
Twitching - use appendages, has pilus
Swimming
Gliding
Sliding - bind & unbinding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Aerotolerance

A

Obligate Aerobes -tolerant to oxygen. ATP production by aerobic respiration

Obligate Anaerobe - not tolerant to oxygen. ATP production by fermentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Biofilms

A

Sticky matrix - protection from immune system & antibiotics

Highly organized microbial communities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Genetic variability

A

Genetic material is in a chromosome or plasmid

Core + accessory genes = pan genome

There are big colonies and small colonies which evade immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Transformation of bacteria

A

Uptake of naked DNA from surrounding environment into the genome of the bacterial cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Transduction of bacteria

A

Bacteria DNA is transferred from one cell to another via bacteriophages (viruses) acting as vectors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Conjugation of bacteria

A

Process of direct cell to cell transfer of genetic material mediated by conjugative plasmids (extrachromosomal DNA elements)

Found in guts or soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Pathogen

A

Microbe capable of causing damage to host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Infection

A

Colonisation/invasion of a host by a pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Sources of pathogens

A

Self and others
Food and drink
Environment, including soil, plants and water
Air
Inanimate objects
Insects and animals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Modes of transmission of disease

A

Airborne
Drinking and eating
Bodily fluids
Direct contact
Insect bite
Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Risk factors

A

Age
Existing/underlying medical conditions
Genetics
Hospitalisation/surgery
Medication
Contact

78
Q

How to cause an infection

A

Establish a foothold
Evade host defences
Proliferate
Cause damage

79
Q

Why do bacteria stick

A

Prevent being washed away and anchor at a preferred niche

80
Q

How do bacteria stick

A

Non-specific adhesion molecules (often reversible)

Specific adhesins - Gram-negative bacteria - Pili and Fimbriae. Outer membrane adhesins
Gram positive bacteria - cell wall proteins - Microbial surface components recognising adhesive matrix molecules

81
Q

Enteropathogenic E.Coli attachment

A

Initial contact with intestinal cells mediated through bundle forming pilus (BFP)

Attaching - effacing lesion
- characterised by effacement of brush border microvilli and intimate attachment of bacteria to cell.

82
Q

Locus of enterocyte effacement

A

Codes for Type III secretion system
Inject bacterial proteins into cell to change cell function

83
Q

Neisseria meningitidis

A

Pili attach to receptor on nasopharyngeal cell surface
Pili retract allowing adhesion of outer membrane adhesin to receptor on cell surface

84
Q

Staphylococcus aureus attachment

A

Lipoteichoic acids mediate initial attachment to cell surface

MSCRAMMS mediate stronger interaction with matrix proteins e.g fibrinogen, fibronectin, collagen

85
Q

Host defences

A

Skin, mucosal barriers
Antibacterial compounds in sections
Iron restriction
Complement
Phagocytes
Antibodies

86
Q

Invasion by Listeria

A

Entry
Lysis of the vacuole
Intracellular movement
Cell to cell spread
Lysis of the two-membrane vacuole

87
Q

Ways of resisting antimicrobial fluids

A

Altering surface charge so as to repel cationic peptides
Producing proteases e.g to cleave sIgA
Producing physical barrier e.g capsule, s-layer, outer membrane

88
Q

Evading the immune system

A

Using mask or hiding
Immune defense do not see the invader as NON-SELF

89
Q

Masking and hiding - capsule

A

Surface exposed protein antigens are recognised by antibodies. Complement deposited on surface of bacterium. Easily phagocytosed (opsonised) complement mediated lysis

Many vaccines composed of capsular polysaccharide so pathogen is easily recognised

90
Q

Masking and hiding - invading

A

Invades host cells like mycobacterium tuberculosis inside macrophages

Mimicking the host -appearing as SELF

91
Q

Mimicking

A

Antibodies recognise foreign antigens on surface of bacterium

Promotes destruction and disposal of pathogen

92
Q

Mimicking - binding Ig and Staph

A

Staph - Protein A binds to antibody Fc region
Inhibits the activation of complement, phagocytosis and ADCC
Cell now covered in layer of host proteins = recognised as self

93
Q

Mimicking - binding host proteins

A

MSCRAMMS bind to extracellular matrix proteins
Recognises as self

94
Q

Mimicking - binding factor H

A

If C3b forms on a cell it can target it for complement-mediated damage.

Serum factor H binds to our cells and degrades any C3b forming on the surface to protect us from damage

95
Q

Phagocytic killing

A

Attraction
Recognition and phagocytosis
Phagosome/lysosome fusion
To either bacterial killing or toxin production which leads to phagocyte death and bacterial survival

96
Q

Detoxifying the phagocyte

A

After formation of a phagosome, detoxified ROI or prevention of fusion means bacterial survival

97
Q

Complement factor proteolysis

A

Complement factor proteolysis refers to the cleavage or breakdown of complement proteins by proteolytic enzymes, which is a crucial step in the activation and regulation of the complement system.

98
Q

Complement disruption

A

Complement disruption refers to the interference or inhibition of the complement system, a crucial component of the immune system involved in host defense, inflammation, and the clearance of pathogens

99
Q

Antigenic variation

A

Invading population mutates and is not recognised by immune system

100
Q

Outer membrane blebs

A

Blebs of outer membrane containing lipopolysaccharide and outer membrane proteins released as immune decoys

101
Q

Iron resources

A

Transferrin in blood
Function in enzymes
Stored as ferritin in cells
Siderophores
Specific binding proteins

102
Q

Peptic ulcer disease

A

Break in the lining of stomach/small intestine
Symptoms: Upper abdominal pain
Belching
Vomiting
Weight loss
Bleeding

103
Q

H. Pylori prevalence

A

From asymptomatic to deadly
Gastritis (80-90%)
Peptic ulcer (10-20%)
Gastric cancer (1-2%)
MALT lymphoma (<1%)

Estimated that 50% of world’s population is infected

104
Q

H. pylori: transmission

A

Gastro-oral
Fecal oral
Sexually?

105
Q

H pylori: disease progression

A

Infection
Superficial gastritis (Days - weeks)
Chronic gastritis (Months - years)
Antral gastritis, pangastritis, chronic active gastritis (Decades)
Duodenal gastric metaplasia, Atrophy intestinal metaplasia, chronic active gastritis (decades)
Duodenal ulcers
Gastric cancers & ulcers
MALT lymphoma

106
Q

Flagellum

A

H. pylori uses it to swim fast to mucus layer

107
Q

Helical shape

A

Gives ‘screw-like’ movement which allows it to penetrate mucus

108
Q

H. pylori acid resistance

A

Uses urease to produce a ‘cloud’ of ammonia to neutralise acid

109
Q

H. pylori: mucus ‘de-gels’

A

H. pylori raises ph, mucin de-gels

110
Q

H. pylori gastric coloniser

A

Attaches to gastric epithelium via Lewis b carbohydrate receptor with BabA adhesin

111
Q

Chronic infection: Immune evasion

A

Evade host defense
LPS = poorly recognised by TLR4 -> low levels of cytokine production

Flagellum subunits = poorly recognised by TLR5 -> low levels of cytokine production

Vacuolating toxin A (VacA)
Inhibits phagosomal maturation. T/B cell proliferation, iNOS generation

Coating with plasminogen and cholesterol -> mimic host

112
Q

Chronic infection and inflammation

A

Loss of function of cells in the inflamed area

113
Q

Ulcers

A

a lesion found on the mucous membrane

114
Q

Peptic ulcer

A

ulcer in the lining of the stomach or duodenum, where hydrochloric acid and pepsin are present

115
Q

Gastric ulcer

A

in stomach

116
Q

Duodenal ulcer

A

in duodenum

117
Q

Stomach acid production

A

Food/thought of food
G cells produce gastrin
ECL cells produce histamine
Parietal cells produce acid

118
Q

H. pylori infection of antrum

A

Inflammation
Loss of function of somatostatin cells
Increased gastrin production and acid production
Acid enters duodenum
Inflammation of duodenum
Duodenal ulcer & acid hypersecretion

119
Q

H. pylori infection of corpus

A

Inflammation
Loss of function of parietal cells
Loss of acid production
Intestinal-like cells in stomach
Inflammation
Gastric ulcer & acid hyposecretion

120
Q

H. pylori and genetic instability of epithelial cells

A

Irregular AID expression
Double-strand DNA breaks
Impaired DNA mismatch repair
Irregular DNA methylation
miRNA regulation

121
Q

cag pathogenicity island

A

Region of DNA involved in pathogenicity
>30kb
28 genes
T4SS
cag pathogenicity island correlates with increase virulence and disease severity in humans

122
Q

Intimin

A

Attachment to host cells
Formation for attachment and effacement lesions on surface of host cells

123
Q

H. pylori CagA

A

Phosphorylated in gastric cell
CagA-P stimulates phosphorylation cascades, apoptosis, morphological change, cytokine production, cell proliferation

Promotes release of ROS from mitochondria. Stimulates oncogenic pathways

124
Q

H. pylori virulence factors

A

Flagella - bacterial mobility & chemotaxis to colonise under mucosa
Urease - neutralize gastric acid. Gastric mucosal injury by ammonia
Lipopolysaccharides - adhere to host cells inflammation
Outer proteins - adhere to host cells
Type IV secretion system - pilli-like structure for injection for effectors
Exotoxins - vacuolating toxin (vacA) gastric mucosal injury
Secretory enzyme - mucinase, protease, lipase - gastric mucosal injury

125
Q

Bacteria migration

A

Bacteria migrate most between corpus and fundus

126
Q

Low acid production

A

Pangastritis - atrophic gastritis - gastric cancer

127
Q

H. pylori leads to

A

Chronic gastritis

128
Q

High acid production

A

antral-predominant gastritis - peptic ulcer disease

129
Q

Treatment

A

First line therapy = one-week “triple therapy”. Proton pump inhibitor such as omeprazole + antibiotics such as clarithromycin and amoxicillin

130
Q

Disease action

A

Pathogen establishes a niche on/in host’s body
Pathogen causes disease (e.g aided by toxins)
= infectious disease

131
Q

Intoxication action

A

Pathogen produces a toxin ex vivo
Person ingest toxin & toxin causes disease
= microbial intoxication

132
Q

Microbial intoxication

A

May result from eating food where bacteria have previously grown and produced a toxin

Staphylococcal food poisoning
Botulism

133
Q

Staphylococcal food poisoning

A

Produces a family of related toxins
Heat and protease resistant
Able to survive harsh conditions of the stomach
Very quick onset - few hours
Vomiting, diarrhoea & stomach cramps
Quick recovery 1-2 days
No treatment
Molecular mechanisms unknown

134
Q

Sources of Staphylococcal

A

Animal products
Lack of hygiene

135
Q

Cholera

A

Infection of small intestine with Vibrio cholerae
Faecal-oral route
Eating/drinking food/water contaminated with faeces

136
Q

Cholera facts

A

Highly infectious
Incubation period
No or mild symptoms
20% - rice water diarrhoea
Cholera toxin

137
Q

Cholera rice water

A

Fluid loss severe - 40L a day
Dehydration and electrolyte imbalance

138
Q

Cholera toxin AB5 familiy

A

A subunit - bind to stimulatory G protein after golgi and ER modification

B-subunit - binds to ganglioside receptor which allows entry into cell

139
Q

Guanine nucleotide-binding (G) proteins

A

Binding of hormone produces a conformational change in receptor.
Receptor binds to G protein
Binding induces a conformational change - GDP is replaced by GTP.
Gs dissociates from rest of G
Gs binds AC synthesis of cAMP; hormone dissociated
Hydrolysis of GTP to GDP causes Gs to disassociate from AC and bind to the rest of G

140
Q

Cholera toxin mechanism

A

Locks G protein cause NAD+ -> ADP-ribose
ADP-ribosylation of Gsa causes constant activation of cyclase, resulting in increased levels of cAMP.
This activates Protein Kinase A
causes active secretion of chloride ions via CFTR and loss of water by osmosis

141
Q

Cholera review

A

Toxin mediated disease
AB5 and acts intracellularly 5xB subunits: binding and entry
1xA subunit: enzymatic activity
Causes chloride secretion
Profuse diarrhoea
No physical damage and reversible.
Up to 40L a day

142
Q

Cholera resurgence

A

Climate change - cyclones, flooding, drought
Political
Limited healthcare and availability of vaccine
Ongoing health emergencies

143
Q

Enterohaemorrhagic E. coli

A

Type 3 secretion system
Produces Shiga-like toxin
Faecal oral route
3-8 days
Severe, bloody diarrhoea and abdominal cramps

144
Q

Haemolytic uremic syndrome

A

7 days after symptoms
Anaemia caused by destruction of RBC (haemolytic anaemia)
Acute kidney failure (uremia)
Low platelet count (thrombocytopenia)
5-10% mortality and in children

145
Q

Shiga toxins

A

STx: Shiga toxin from Shigella dysenteriae

STx1: Shiga-like Toxin 1 from E.coli - 1 amino acid difference from STx

STx2: Shiga-like Toxin 2 from E.coli - 56% identity from STx and STx1. Most common cause of human disease

146
Q

Enteropathogenic

A

Acute diarrhoea (children)

147
Q

Enterohaemorrhagic

A

Bloody diarrhoea
Haemolytic uraemic syndrome (anaemia and kidney failure)

148
Q

Shiga-toxin producing and verotoxin-producing

A

Haemolytic uraemic syndrome

149
Q

Shiga-like toxins

A

Toxins that cause cell death
Bind to Gb3 in digestive tract = bloody diarrhoea
and kidney = HUS (kidney failure)

150
Q

Cattle, swine and deer

A

Don’t have receptor
Carry bacteria without any toxic effect, while shedding them in their faeces

151
Q

Mechanisms of action of Shiga toxins

A

B subunits bind to Gb3 in cell membrane
A subunit transported to ER
Subunit cleaved by protease to make enzymatically active
Removes a single adenine from 28s rRNA = irreversibly inactivates ribosome inhibiting protein synthesis
Results in cell death

152
Q

Alternative mechanism of action of shiga toxin

A

B subunits bind to Gb3 in cell membrane
Inactivates ADAMTS 13
Accumulate multimers of Von Willebrand’s Factor on endothelial surface, leads to clumping of platelets

153
Q

Alternative Alternative mechanisms of action. Shiga toxin

A

Bind to Factor H
Prevent inactivation of C3b
Persistent C3b activity
Increased alternative pathway complement activation, leads to increased endothelial inflammation

154
Q

Shiga-like toxin

A

Toxin mediated disease
Shiga-like toxin belongs AB5 family
5xB subunits: binding and entry
1xA subunit: enzymatic activity
Transported from cell surface to cytosol via Golgi and ER
Stops protein translation
Inflammation of intestinal epithelium and apoptosis, loss of barrier function
Physical damage
Digestive tract = bloody diarrhoea
Kidney = HUS

155
Q

Cytolysins

A

Form a pore through the cell membrane
Results in cell death or induction of apoptosis
Haemolysis - cytolysins that destroy RBC

156
Q

Why destroy host cells?

A

Spreading: destruction of tissue allows bacteria to move
Immune evasion: killing immune cells helps bacteria escape immune response
Nutrition: cells full of useful nutrients

157
Q

Exoenzymes

A

Proteins secreted by microorganisms
Lipases
Proteases
DNAse
Hyaluronidase

158
Q

Lipases

A

Staphylococcus aureus b toxin/Shingomyelinase C - immune evasion factor, destroys leukocytes

Clostridium perfringens Zn-metallophospholipase C - spreading factor, involved in invasive disease (myonecrosis)

Clostridial myonecrosis - Gas gangrene

159
Q

Proteases

A

Pseudomonas aeruginosa elastase - degrade collagen, elastin and other host proteins e.g IgG, complement, chemokines

LasA = serine protease (nicks proteins)
LasB = Zinc metalloprotease (fully degrades nicked proteins)

160
Q

Burn wound infections

A

Elastases causes damage leading to acute inflammation & work with other toxins and enzymes leading to tissue necrosis

Degradation of tissue allows spread of the bacteria and the disease (septicaemia)

161
Q

DNAses & NETS

A

Bacteria destroy NETS using DNAse which helps spreading and immune evasion

162
Q

Pus

A

Bacteria and leukocytes
Release of chromosomal DNA from leukocytes increases viscosity
Bacterial DNases cleave DNA and decrease viscosity
Facilitates bacterial spreading

163
Q

Tissue damage

A

Chemical change in interstitial fluid leads to mast cells releasing histamine and heparin. Dilation of blood vessels, increased blood flow, increased vessel permeability. Leads to area becoming red, swollen, warm and painful and clot formation

164
Q

Tissue repair

A

Histamine and heparin attract phagocytes, especially neutrophils. Specific defenses and removal of debris by neutrophils and macrophages, stimulation of repair lead to tissue repair

165
Q

Inflammation & infection

A

Bacteria enter wound
Platelets release wound clotting proteins at wound site
Mast cells secrete factors that mediate vasodilation and vascular constriction
Increased delivery of blood plasma & cells to injured area
Neutrophils secrete factors that kill and degrade pathogens
Neutrophils and macrophages remove pathogens by phagocytosis
Macrophages secrete cytokines (IL-8)
More immune cells attracted activates cells involved in tissue repair

166
Q

What does tissue damage/infection lead to?

A

Activation of mast cells
Mast cells release heparin and histamine
Vasodilation and increased permeability of blood vessels
Leukocytes extravasate from blood and migrate to site of injury/infection
Migration guided by chemokine interleukin-8 (IL-8) produced by activated macrophages

167
Q

Bacterial triggering of inflammation

A

Immune cells recognise conversed structures on bacteria
-PAMPS
- LPS on Gram Negative
-LTA on Gram positive
Flagellin - protein part of bacterial flagellum
Peptidoglycan - polymer of peptides and sugar forming bacterial cell wall
Bacterial DNA

168
Q

Endotoxin

A

Alternative name for LPS but also refers to LOS (lipooligosaccharide)
Anchored in outer membrane
Not secreted like exotoxins

169
Q

Lipooligosaccharide

A

No O-antigen
Limited to 10 saccharide units
Major glycolipids expressed on mucosal Gram negative bacteria

170
Q

Sepsis

A

Life threatening complication of an infection
Inflammation triggered throughout the body
Can lead to organ damage and multiple organ failure

171
Q

Endotoxins & sepsis

A

Infection
Bacteria in bloodstream (bacteremia)
Cell lysis - release of endotoxin
Cytokine storm - sepsis

172
Q

TLR signalling

A

LPS binding protein binds to LPS/LOS, delivers to CD14 then to TLR-4 which induces pro-inflammatory cytokines (IL-1B, TNF-a)

173
Q

IL-1B

A

Macrophages are activated and release cytotoxic effectors (ROS, enzymes)

Vasodilation blood vessels
Hypotension
Intravascular coagulation

174
Q

TNF-a

A

Brain - increased body temp and loss of appetite

Vasodilation blood vessels
Hypotension
Intravascular coagulation

175
Q

Bacterial infections resulting in strong inflammatory response

A

Meningococcal disease
Superantigen-triggered toxic shock

176
Q

Meningococcus

A

Enter through nasal pharyngeal route
Have LOS and capsule

177
Q

Meningococcal disease

A

Meningococcemia or meningitis

178
Q

Meningococcemia

A

Blood infection
Bacteria enters through the nose & throat
Purplish rash
Cold hand and feet
Breathing fast
Limb, joint and muscle pain

179
Q

Meningitis

A

Spinal cord/brain infection
Passage through blood-brain barrier
Severe headache & stiff neck signal infection
Bacteria in spinal cord & brain membranes
Sensitivity to bright light
Seizures
Severe headaches
Stiff neck

180
Q

Lipid A of LOS

A

Causes extensive inflammatory response
Causes most damage and symptoms

181
Q

Outer membrane blebs

A

Bacteria also releases blebs out outer membrane
Contain LOS
Acts as immune decoy

182
Q

Meningococcal disease

A

Very sleepy and vacat
High sleepy and vacat
High fever
Confused and delirious
Vomiting

183
Q

Immune damage of meningococcal disease

A

Alteration of coagulation pathways
Intravscular coagulation
Weakened epithelium
Bleeding under skin
Phagocytic cells release ROI and enzymes
Extensive tissue damage and necrosis
Treatable with antibiotics
Multiple organ failure
No vaccine protects against all types

184
Q

Super antigen-triggered toxic shock

A

Caused by exotoxins
No enzymatic activity but instead causes huge systemic inflammatory response
Can result in multiorgan failure

Mortality:
S aureus 40-50%
S pyogenes 50-70%

185
Q

T cell activation

A

Antigen-presenting cell presents antigen specific to T-cell. Activated T-cell produces cytokines
<0.01% activated

186
Q

Superantigens

A

Activates 2-30% of T cell population
Massive production of proinflammatory cytokines
No enzymatic activity
Act from outside cell by binding to MHC class II on APC and TCR on non-specific T cells
Systemic acute inflammation, toxic shock syndrome

187
Q

Autoimmunity

A

Antibodies produced in response to infection cross-react with host antigens

188
Q

Bacterial infection leads to…

A

Innate immune response
Adaptive immune response (generation of antibodies)
Antibody cross reacts with human antigen (molecular mimicry)

189
Q

Acute Rheumatic fever

A

Group A Streptococcus leads to pharyngitis/skin infection. Generation of antibodies against proteins in joints/heart muscle. Acute rheumatic fever is inflammation and leads to rheumatic heart disease.

190
Q

Migratory polyarthritis

A

Most common symptom in ARF patients
Inflammation (pain) starting in one joint
After a time, inflammation reduces and start in another joint. Caused by auto-reactive antibodies against collagen in joints

MEDSCI 203 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions