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Bacteria and Immune Response Flashcards

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1
Q

what is the general structure of a prokaryote? (6)

A
  • no membrane-organelles
  • genetic information carried in double stranded circular molecule of DNA (nucleoid)
  • extrachromasomal DNA in plasmids
  • 70s ribosomes
  • prokaryote membrane (carries out other metabolic functions)
  • most have a complex cell wall
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2
Q

what are 3 structures that are present on some bacteria but not others? what are their functions?

A
  • capsule - adhesion, fluid absorption, protection from phagocytes
  • flagella - movement, ie. chemotaxis
  • pilli - common pilli attach to host cell membrane molecules, sex pilli allow horizontal gene transfer
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3
Q

what is the difference between the cell walls of Gram+ and Gram- bacteria?

A
  • G+: thick layer of peptidoglycan, teichoic acid anchors

* G-: thin layer of peptidoglycan, overlaid by outer membrane which is anchored by lipoproteins

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4
Q

what may cause a bacteria to be Gram-variable or Gram stain unreliable? (3)

A
  • too small
  • no cell wall
  • atypical life cycle
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5
Q

what are the 3 main bacteria shapes?

A
  • cocci - spherical
  • bacilli - rod
  • spirilla - helical
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6
Q

what are the 5 steps of Gram staining?

A

1 - fixation: eg. via heating
2 - crystal violet: complexes with peptidoglycans - stains +ve cells (-ve cells will appear purple at this point)
3 - iodine: allows CV to complex in +ve cells
4 - decolourisation: using acetone / alcohol solvent (-ve cells decolourised)
5 - counter-stain: safranin stains -ve cells pink

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7
Q

what are 2 examples of G+ cocci?

A
  • Staphylococcus aureus

* Streptococcus pneumoniae

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8
Q

what are 2 examples of G+ bacilli?

A
  • Listeria monocytogenes

* Corynebacterium diphtheriae

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9
Q

what is an example of a G- cocci?

A

Neisseria meningiditis

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10
Q

what are 2 examples of G- bacilli

A
  • Escherichia coli

* Salmonella species

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11
Q

describe the growth pattern of bacteria when introduced to a new environment (4)

A

lag-log

1 - initial lag: period of adjustment
2 - log: cell division occurs rapidly, exponential growth
3 - stationary: nutrients have depleted / toxins have built up
4 - death: enters a phase of decline

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12
Q

how do prokaryotes replicate their DNA?

A

unwinding of DNA, then each strand serves as a template for DNA polymerase

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13
Q

describe the process of conjugation in bacteria (2)

A

1 - a gene in conjunctive plasmids tell the cell to produce a sex pilus and replicate itself
2 - cytoplasmic bridge forms between 2 cells and allows conjunctive plasmid to be transferred

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14
Q

what are commensal bacteria?

A

bacteria that are not infectious and act as part of the body’s natural flora

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15
Q

what are 4 functions of commensal bacteria?

A
  • out-compete pathogenic bacteria for space and resources
  • produce by-products that prevent pathogen establishment
  • vitamins in gut are synthesised as end-products
  • stimulate immune system
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16
Q

where are the major flora communities? what are areas of the body with no bacteria in them called?

A
  • skin
  • mouth
  • large intestine
  • urinary tract
  • vaginal tract

sterile body sites

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17
Q

what are the 2 causes of bacterial infection?

A
  • commensal bacteria invades a sterile site

* pathogenic bacteria enter the body (non-commensal)

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18
Q

how can an infection be picked up? (3)

A
  • translocation from non-sterile to sterile areas
  • acquisition from animals / other humans
  • transmission from the environment
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19
Q

in what circumstances might an opportunistic infection be picked up? (3)

A
  • weakened immune system (eg. AIDS)
  • reduced flora community (decrease in competition)
  • breached surface barriers
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20
Q

what is a nosocomial infection?

A

an infection acquired while a patient is in hospital

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21
Q

what is a carrier?

A

an organism / individual that can transmit the pathogen but does not experience symptoms (transient or chronic)

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22
Q

what the 2 mains types of toxins produced by bacteria?

A
  • endotoxins (mainly G-): released after host cell lysis

* exotoxins (mainly G+): secreted from cell surface, dangerous as they can cause toxic shock syndrome

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23
Q

what factors affect infection? (6)

A
  • age, sex, ethnicity, diet
  • medical conditions / medication
  • immunocompromised
  • presence of foreign objects (bio films)
  • vaccination history
  • crowding, seasonal variation and public health measures
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24
Q

what is the natural course of infection? (7)

A

1 - entrance through breach of defences / barriers
2 - colonisation: adherence, adhesion, attachment
3 - multiplication and spread through the body
4 - invasion of host cells
5 - signs and symptoms: based on virulence and immune response
6 - resolution or chronic state occurs
7 - elimination / exit of pathogen

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25
what is a common infection of the respiratory system? what pathogens cause it? (2)
pneumonia * Steptococcus pneumoniae * Haemophilius influenza
26
what is a common infection of the gastrointestinal system? what pathogens cause it? (4)
food poisoning * Campylobacter * Salmonella * some E. coli * Shingella
27
what is a common infection of the CNS? what pathogen causes it?
meningitis • Neisseria meningitis
28
what is a common infection of bones / joints? what pathogen causes it?
osteomyelitis • Staphyloccocus aureus
29
what is a common infection of the skin / soft tissues?
cellulitis • Staphylococcus aureus
30
in what scenarios would an infection require empiric rather than targeted treatment? (7)
* infection of sterile site * meningitis, CNS infection, cerebral abscess * septic arthritis * deep ocular / periorbital infections (eye socket) * infections involving breach of the GI tract * any outbreak scenarios / public health risk * any infection in which the patient is septic
31
what characterises sepsis? (3)
* systematic loss of homeostasis + dysfunction of each organ * physiological demand requires increased cardiac output (tachycardia) * capillary leakage of plasma leading to tissue oedema
32
what are 4 lab tests used in the identification of bacteria?
* latex agglutination - find out antigens * indicator antibiotics * selective / differential media (eg. stool sample - only salmonella can grow on medium, commensal bacteria cannot) * chromogenic agar plate - automated with computer
33
what are the main differences between the innate and adaptive immune systems?
* innate: born with it - operates throughout life | * adaptive: changes in response to the pathogens it encounters
34
what are 2 features of the neutrophil cell?
* multi-lobed nucleus | * granular
35
where are neutrophils found outside of infection?
in blood circulation
36
in what 2 conditions do neutrophils undertake phagocytosis?
* direct contact with bacteria | * after bacteria have been opsonised
37
what 2 factors can be found in the granules of a neutrophil?
* bacteriostatic factors | * toxic factors
38
as well as phagocytosis? what other main function do neutrophils have?
release chemokines and cytokines
39
how are neutrophils directed to where a bacteria is?
* other cells release chemotactic factors | * move by chemotaxis towards bacteria
40
what must happen before neutrophils can enter tissues to tackle infection? (3)
* chemoattraction of neutrophil * rolling adhesion - neutrophil attach to endothelial cells * tight junctions are loosened
41
what is the difference between a monocytes and a macrophage?
monocytes are in the blood, macrophages are in tissue
42
what are 2 features of the monocyte cell?
* large | * kidney shaped nucleus
43
what is the function of macrophages? (4)
* phagocytose pathogens * clear cellular debris * release cytokines and chemokines * act as APCs
44
what is the main function of dendritic cells?
present antigens to T cells to activate the adaptive immune response
45
what are the 3 pathways that initiate the compliment cascade?
* classical - antigen:antibody complexes * alternative - pathogen surfaces * mannose-binding lectin: lectin -> pathogen
46
what are the 3 main effects of complement?
* inflammation - recruitment of inflammatory cells * lysis of pathogens * opsonisation - coating pathogens to make phagocytosis easier
47
what happens to T cells in the thymus? (2)
* maturation - acquire repertoire | * auto reactive cells are deselected
48
where do T cells travel to after leaving the thymus?
secondary lymphoid organs - spleen and lymph nodes
49
how are Th cells activated?
* a dendritic cell or macrophage with MHC call 2 presents pathogen antigen on cell surface * travels to lymphoid organs * the T cell corresponding to the pathogen complexes to the antigen and is activated
50
what are the effects of Th activation? (4)
* clonal expansion * some differentiate into memory cells * activate humoral response * activate cytotoxic T cells
51
how are cytotoxic T cells activated? (4)
* signal from Th cell activates the Tc cell * body cell infected with pathogen will present its antigen on cell surface using MHC class 1 * binds to the TCR on Tc cell * Tc cell then causes apoptosis
52
how do cytotoxic T cells cause apoptosis? (3)
* release perforin and granzymes when T cell attaches to cell receptor * perforin creates a tube between cells * granzymes enter and trigger apoptosis
53
what are membrane-bound immunoglobulins? (2)
* on B cell surface | * act as antibody and receptor
54
what happens after a B cell is activated?
* clonal expansion * differentiation into plasma cells * release antibodies
55
what are the 3 most significant types of antibodies? give their shape and function
* Ig A - dimer, involved in mucosal immunity * Ig D - monomer, native B cell receptor * IgM - pentamer, made first, antigen receptor and involved in complement activation
56
what are 3 modes of antibody action on pathogens?
* neutralisation - clump bacteria, easier for phagocytosis * opsonisation * complement activation
57
what are the 2 goals of inflammation?
* expel foreign body / infection | * cause structural and functional repair
58
what are the 5 characterisations of inflammation? what causes these signs?
* heat (calor) - vasodilation * redness (rubor) - increased blood flow (vasodilation and fever) * swelling (tumor) - fluid in extracellular matrix * pain (dolor) - stretching of tissue (oedema), mediators stimulate pain receptors * loss of function (function laesa) - inhibited by pain and swelling
59
what are 3 positive aspects of inflammation?
* isolates damaged area * mobilises effector cells / molecules * promotes healing and repair
60
what are 3 negative aspects of inflammation?
* response may be out of proportion to threat * may cause more damage to body than agent would have * chronic inflammation (eg. allergies / autoimmune conditions)
61
what must inflammation do to localise inflammatory cells and molecules? (2)
* exudate fluids and proteins | * concentrate cells of blood in damaged tissue using cytokines
62
what happens during the initiation stage of inflammation? (3)
* changes in microvasculature * extravasated - discharge of blood into tissues * leukocytes emigrate across tight junctions into tissues
63
what happens at the progression phase of inflammation?
cytokines and cellular inflammatory systems are activated and amplified
64
what happens in the resolution phase of inflammation?
specific inhibition and dissipation of cytokines / mediators
65
how do neutrophils perform phagocytosis? (2)
* isolates pathogen in phagocyte | * granules containing digestive / destructive enzymes fuse with phagosome and destroy pathogen
66
what are Toll-like receptors, PAMPs, and DAMPs? which cells have Toll-like receptors?
* TLRs bind to PAMPs and DAMPs to induce a response from the leukocyte cell * PAMPs (pathogen associated molecular patterns) are expressed by bacteria on their cell surface, and allow leukocytes to recognise them as dangerous * DAMPs (damaged associated molecular patterns) are expressed by cells what are dying (or tumour cells) - not always associated with infection • mostly innate immune cells - macrophages, monocytes and dendritic cells (also sometimes fibroblasts and epithelial cells)
67
how do macrophages perform phagocytosis?
fuse phagosome with lysosome (rather than granules)
68
describe how lymph leaves the blood and enters the lymphatic system (5)
1 - fluid moved out of capillaries at arteriole end due to hydrostatic pressure 2 - (most) proteins and blood cells remain inside, so blood becomes more concentrated in the capillary 3 - osmotic pressure draws fluid back into circulation at venue end 4 - some proteins do escape however, and allow some fluid to be retained in tissues 5 - blind ending lymphatic capillaries draw excess fluid and proteins from tissue into lymphatics
69
what condition is causes by a failure of the lymphatic system to reabsorb fluid from tissues? what are some common causes? (3)
* lymphoedema | * usually caused by lymph node damage after an accident, surgery or radiotherapy
70
what are the 2 ways in which lymph can enter the lymphatic capillary?
* flow into lumen through gaps between specialised epithelium (valve) * absorbed by plasma membrane via pinocytosis and then released in lumen
71
how is the lymphatic capillary held open?
anchoring filaments
72
what is the route of lymph after it enters at the capillary? (5)
* increasingly larger lymphatic vessels * through lymph nodes * collecting ducts * lymphatic trunk * either the right lymphatic duct or the thoracic duct
73
what parts of the body does the right lymphatic duct and thoracic duct drain from?
* RLD - upper right limb and above (right side) | * thoracic - lower limbs, upper left limb and above (left side)
74
where does lymph re-enter circulation? why here?
* subclavian veins running beneath collar bones | * blood is under the lowest pressure here
75
other than lymphocytes, what other leukocytes are found in the lymph node?
macrophages, dendritic cells
76
what is the function of reticular tissue in the lymph node?
connective tissue acting as stroma
77
in what parts of the lymph node are T, B and dendritic cells housed?
* B cells - cortex follicles | * T cells + dendritic cells - paracortex
78
what are the primary lymphoid organs? what are the secondary lymphoid organs? what are their broad functions?
* 1º - bone marrow and thymus * generate lymphocytes * 2º - lymph nodes and spleen * maintain native lymphocytes and initiate adaptive immune response

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