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Microorganisms + Disease > Mechanisms of Pathogenesis L4 > Flashcards

Mechanisms of Pathogenesis L4 Flashcards

1
Q

what are the groups that pathogens are divided into

A

opportunistic pathogens

primary pathogens

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2
Q

what are opportunistic pathogens

A

Only cause serious disease when host defences are impaired

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3
Q

what are primary pathogens

A

Capable of causing disease in absence of immune defects

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4
Q

what do bacterial groups possess

A

virulence determinants which contribute to their ability to cause disease

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5
Q

if a pathogen has a single virulence is it pathogenic

A

Rarely is possession of a single virulence determinant sufficient to make a bacterium pathogenic
Virulence is Multifactorial relies on several things that the bacteria makes

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6
Q

what is the bacterial surface composition importance

A

mediates initial interactions with mammalian tissues and other surfaces
how the organism causes disease - bacterial virulence

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7
Q

what is the capsule

A

usually a polysaccharide layer, generally covers the whole bacterial surface

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8
Q

what is adhesion

A

fimbrae and pili are rod shape structures involved in sticking bacteria to surfaces

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9
Q

what are the envelope proteins for

A

some involved in adhesion, others involved in nutrient uptake, getting nutrient into the bacteria to grow

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10
Q

what contains lipopolysaccharide

A

only in gram negative bacteria

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11
Q

what is the function of lipopolysaccharide

A

Is important in immune invasion particularly complement invasion
Acts as a toxin, can induce damage

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12
Q

what happens between healthy to diseased

A

modulated by host immune responses

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13
Q

what happens when pathogen enters our tissues

A

immune system tries to remove
Bacteria can respond to get over the immune response
Dynamic equilibrium between the the bacteria and the immune system, depending which is ‘winning

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14
Q

what are the bacterial disease processes

A
  1. colonisation (adhesion, nutrient acquisition)
  2. tissue invasion
  3. avoidance of host defences
  4. tissue damage
  5. transmission
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15
Q

what is colonisation

A

First stage of disease process

Definition - Establishment of a stable population of bacteria in the host

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16
Q

where is bacteria available for colonisation

A

Source of bacteria is the environment, infected individuals or normal flora

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17
Q

what is the first interaction of bacteria in colonisation

A

Frequently on mucosal surface e.g respiratory tract (breathe organisms in), gastrointestinal tract (ingestion) or urogenital tract (sexual contact)

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18
Q

what is colonisation resistance caused by

A

Combination of host and bacterial factors which prevent colonisation by potential pathogens

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19
Q

examples of host factors that cause colonisation resistance

A
  • low gastric pH
  • bile
  • proteases
  • peristalsis
  • salivary and mucous flow
  • immunoglobulin A production
  • macrophages
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20
Q

bacterial factors that cause colonisation resistance

A

Include competition by normal flora for space, nutrients and receptors and production by bacteria of fatty acids and bacteriocins

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21
Q

why are lactobacilli important in colonisation

A

Lactobacilli in breast milk colonise gut in new born babies and prevent infection by E.coli
In the vagina, Lactobacilli metabolise glycogen, resulting in a low pH, limits colonisation by potential pathogens

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22
Q

what can occur if interfere with colonisation resistance

A

disruption of normal bacterial flora may result in removal of competition and overgrowth of normal flora
in low amounts they are ok, but overgrowth can cause disease

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23
Q

can antibiotics help with interference with colonisation resistance

A

Treatment with antibiotics may lead to overgrowth of Clostridium difficile and Staphylococcus aureus in the gut and Candida albicans in the mouth
act as opportunistic pathogens

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24
Q

what could allow colonisation of organisms not usually found in a particular site

A

impairment of normal physiological functions

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25
how may bacterial overgrowth in mouth occur
Dehydration may reduce salivary flow
26
what must bacteria be able to do in mucosal surfaces
mucosal sites are physiologically flushed e.g saliva in the mouth, peristalsis in the gut bacteria must adhere to cell surfaces Some bacteria adhere to other surfaces
27
what are the adherence stages
attachment adhesion Subsequent stages may result in aggregation to produce a biofilm - associated with biomaterials e.g catheters
28
what may happen to biofilms in adherence
Biofilms may disperse and seed new sites of infection
29
what happens in the attachment stage
non-specific physicochemical properties of the bacterium and the target surface - charge and hydrophobicity Bacterial and mammalian cell surfaces usually both have a nett negative charge, only allows bacterium to approach cell surface within approx 10nm
30
what is the attachment phase like
reversible and mediated by weak ionic interaction such as hydrogen bonding and Van der Waal’s forces
31
what occurs in adhesion stage
involves specific interactions between bacterial surface components (adhesins) and mammalian cell surface receptors Interaction allows bacterium to become intimately associated with cell surface - overcoming repulsive forces associated with charge effects
32
what is adhesion like
usually considered to be an irreversible process
33
what is the biofilm made up of
composed of bacteria and associated molecules form a matrix in which the bacteria are embedded made up of bacterial cells and an extracellular matrix made of proteins, polysaccharide and DNA
34
what are bioflims
Once attached, some bacteria continue to grow in association with the surface to form a multi-layered biofilm
35
can biofilms be removed by antibiotics
antibiotics may not penetrate or work on all cells in the biofilm
36
how do biofilms cause infection throughout the body
Biofilms may also disperse – and cause infection at other body sites
37
how do phagocytic cells ingest bacteria in the biofilm
Phagocytic cells cannot easily ingest bacteria in a biofilm
38
what are conditioning films
biomaterials are implanted into tissue, they very quickly become coated with host proteins e.g fibrinogen, fibronectin coating of host proteins is referred to as a conditioning film
39
what do the conditioning films do
bacteria can adhere to “bare” biomaterials in vitro, in tissues the conditioning film components probably act as the major receptors to which bacteria adhere
40
adhesin examples
Fimbriae - rod like protein adhesins e.g E. coli | Polysaccharide adhesins e.g oral streptococci
41
receptor examples
Blood group antigens | Extracellular matrix proteins (stick cells altogether) e.g fibronectin, collagen
42
what is essential for bacterial growth
iron
43
how much iron is available in our body for bacteria
Levels of free iron ion our tissues are very low (low as can be toxic to us) not enough iron for need of bacteria
44
how do bacteria get enough iron for growth
bacteria express high affinity iron uptake systems two main systems: 1. Siderophores 2. Direct binding of host iron transport proteins
45
what happens in the siderophore system
Bacteria sense not much iron available, switches on set of genes produce a siderophore, has a very high affinity of molecules with Fe3+ (ferric) Siderophore interact with host tissue, has a higher affinity for the ferric than it does for the host tissue Siderophore releases host tissue back into circulation, it uptakes the ferric Goes to specific bacterial receptor on the surface, siderophore binds to receptor, is internalised into cell, iron is reduced to Fe2+ Fe2+ has lower affinity for siderophore, so is released and the bacteria can use it Siderophore reused
46
what happens in the transferrin binding receptor mechanism
Bacterium makes a receptor on the surface that specifically recognises transferrin Transferrin in circulation with the ferric attached binds to the bacterium receptor Transferrin cant be taken into cell as too big, iron removed from surface and taken into cell and transferrin released
47
how is the Transferrin binding receptor mechanism limited
Only binds human transferrin – limits this organism
48
when are high affinity iron uptake systems in use
Only expressed under conditions of iron limitation e.g in mammalian tissues
49
what controls the expression of mechanisms for iron uptake
Expression controlled genetically by an iron dependent gene regulator called Fur Fur = ferric uptake regulator (controls amount of iron taken up as too much iron is also toxic for bacteria
50
what happens when there is a lot of iron in the body
Fur protein ferric uptake regulator binds to iron that available in cell forms a dimer – dimerisation Binds to specific dna sequence Bound to promoter blocks transcription of gene
51
what happens when there is not a lot of iron in body
deficient no binding occurs so gene can be transcribed to obtain iron from tissues
52
what is invasion
Some bacteria are able to penetrate into, through or between cells
53
why may invasion occur
may aid in survival and their spread to other body sites
54
where do bacteria invade
some bacteria can invade epithelial cells others invade phagocytic cells adhesion to specific receptors usually first stage in invasion
55
what are adhesins called
invasins
56
what do complements do
kills many Gram-negative bacteria | Complement and antibodies target bacteria for destruction, promoting phagocytosis and killing
57
what do cytokines do
allow cells to communicate with each other, can generate both antibody and phagocytic responses
58
how do gram negative bacteria avoid complement
cause sepsis are complement resistant Resistance due to lipopolysaccharide (LPS) on the bacterial surface Polysaccharide side chains of LPS sterically hinder access of activated complement components to the bacterial membrane
59
how can bacteria be complement resistant
Side chains prevent the membrane attack complex in the membrane
60
what happens if bacteria is not complement resistant
membrane attack complex insert through bacterial membrane and forms a pore, internal contents of bacteria seep, loss of bacterial contents will kill the bacteria
61
can capsules aid avoidance of complements
prevent complement deposition or activation at an appropriate site e.g E.coli Some bacteria also produce proteins which interfere with complement function - chemoattractant protect against direct contact with complement
62
avoidance of antibodies using a bacterial capsule
prevent antibody binding or are weakly antigenic, so prevent efficient phagocytosis (so not recognised doesn’t initiate response to clear them) Many different capsular types may be produced
63
avoidance of antibodies using antigenic variation
used by some bacteria to avoid binding of antibodies Genetic mechanism allows it to change New variant of protein is not recognised – avoid recognition Why can be repeatedly infect
64
avoidance of antibodies using antigenic mimicry
Some bacterial capsules are identical to mammalian tissue molecules so are not recognised as foreign Structure similar to structures in our tissues Not to recognise self If can coat in host tissue wont recognise
65
avoidance of antibodies using enzymatic digestion of antibodies
e.g Neisseria meningitidis produces an IgA protease degrades IgA antibody on mucosal surfaces and prevents it from agglutinating bacteria Produce enzymes – proteases that chop IgA, so antibody not functioning prevents the agglutination of antibodies also
66
how do bacteria avoid phagocytes
Some bacteria produce toxins which kill phagocytes or inhibit their migration to sites of infection Inherent physical properties of some bacterial capsules inhibit phagocytosis
67
how is the interaction of bacteria and phagocytes reduced further
hydrophilic capsule - phagocytic capsule like hydrophobic
68
affect of alpha toxins
High conc of alpha toxins kills | Low conc of alpha toxins inhibits their migration
69
how can some bacteria modify their response to cytokines
Some bacteria can modify normal cytokine responses and alter the immune response in favour of bacterial survival Can interfere with direction immune response is directed – interfere with the cytokine response
70
how can tissue damage occur
1. Direct effects of bacterial toxins 2. Indirect effects of bacterial toxins 3. Induction of autoimmune responses(own cells attack by own immune system) bacterium contains proteins and antigens, some are nearly identical to some in our body
71
what are the two types of bacterial toxins
``` exotoxins endotoxins (LPS) ```
72
what do exotoxins do
actions selective for specific biochemical targets
73
what do endotoxins do
activates many biochemical pathways - effects mediated by triggering of cytokine release from mammalian cells
74
what do cytokines do
released include TNF –α (stimulate further tissue damage) | High concentrations cause cell/tissue damage
75
what are exotoxins made by
gram +ve and -ve
76
what are endotoxins made by
gram -ve
77
what is an exotoxin
protein
78
what is an endotoxin
lipopolysaccharide
79
how are exotoxins released
secreted by living bacteria
80
how are endotoxins released
cell lysis
81
what happens to exotoxins and endotoxins when heated
exotoxins usually heat labile - proteins will denature | endotoxins usually heat stable
82
what toxoids (vaccines) are there for exotoxins and endotoxins
exotoxins - toxoids available | endotoxins - no toxoids
83
how lethal are exotoxins and endotoxins
exotoxins - potentially | endotoxins - lethal (higher conc)
84
how are bacterial exotoxins classified
molecular mode of action
85
what do type 1 exotoxins do
Bind to mammalian surface proteins and trigger transmembrane signals
86
what do type 2 exotoxins do
Pore or channel forming toxins
87
what do type 3 exotoxins do
Bind to surface receptors and translocate active component into the cell
88
where are exotoxins generally located
cytoplasm of bacterial cell
89
where are endotoxins generally located
outer membrane (surface layer of gram -ve bacteria)
90
what makes up lipopolysaccharide
lipid A core oligosaccharide o-polysaccharide
91
how is a pore formed in the membrane
Receptor on mammalian cell surface Pore forming toxin bind Aggregates to form multimer that forms a pore in the membrane
92
what is the lipid A function in LPS
anchors molecules into outer membrane – very hydrophobic
93
what is the o polysaccharide function
stop complement getting to bacterial membrane, also stimulate an immune response (can sometimes be protective)
94
what are some properties of LPS
- pyrogenic (gives you a fever) - potentially lethal - activates complement cascade (tissue damage) - activates clotting cascade - induces TNF - alpha production - induces interelukin 1 production
95
what is transmission
Spread from host to host maintains bacterial pathogens in the population – otherwise they would die out if the infected host dies
96
what is horizontal transmission
via direct contact, air, food, water, insect vectors
97
why are spores able to survive in a lot of environments
survive in soil and water etc don’t dry out
98
what is vertical transmission
mother passing on infection to neonates in utero

Microorganisms + Disease (16 decks)

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