Medical Bacteriology Flashcards
(158 cards)
1
Q
Types of pathogens?
A
- opportunistic
- primary pathogen
2
Q
define Opportunistic
A
normally non-pathogenic but can cause disease when opportunity arises
3
Q
define Primary pathogen
A
can cause disease in a host regardless of host immune or the resident microbiota
4
Q
To be a successful pathogen, you must…
A
Gain entry to the host
Access nutrients from the host to multiply
Evade host defences
Escape and colonise new host environments
5
Q
define virulence
A
the ability to cause disease.
6
Q
what is an example of high virulence?
A
Highly virulent: Streptococcus pneumoniae
- Just a few cells can establish an infection
7
Q
what is an example of low virulence?
A
Lower virulence: Salmonella typhimurium
- 1000+ cells must be ingested to establish infection
- Infection results in a self-limiting gastroenteritis in humans.
8
Q
define virulence factor
A
any aspect of a pathogenic microorganism that enables it to give rise to disease.
9
Q
define virulence gene
A
gene in a pathogenic microorganism which is responsible for its ability to cause disease.
10
Q
define virulence plasmid
A
bacterial plasmid that carries genes, e.g. toxin genes, that render its bacterial host pathogenic
11
Q
Some bacterial pathogens are successful due to
A
secretion of toxins
12
Q
Some bacterial pathogens are successful due to secretion of toxins – these include
A
Clostridium tetani which infects wounds from soil – it is slow growing but is virulent because of the release of a toxin.
13
Q
Some pathogens succeed by dividing and
A
overwhelming the host by their invasiveness (e.g. S. pneumoniae which evades host defences by means of encapsulating its cell with a polysaccharide capsule).
14
Q
Virulence factors can include
A
molecules that allow bacteria to avoid detection or factors that have an effect on the host allowing easier growth or access to nutrients
15
Q
Streptococcus pyogenes produces
A
streptokinase
16
Q
Streptococcus pyogenes produces streptokinase which dissolves
A
blood clots
17
Q
Streptococcus pyogenes produces streptokinase which dissolves blood clots – enabling the bacteria to
A
bypass the clotting system which normally limits infection
18
Q
Hyaluronidases that break down the extracellular matrix allowing
A
greater access to nutritents.
19
Q
Some of the best characterised virulence factors are
A
toxins that act upon cells (e.g. Murine toxin in plague).
20
Q
two kinds of immunity in your body:
A
innate
adaptive
21
Q
what does innate immunity provide protection against?
A
Protection against infection by fixed, relatively non-specific defence mechanisms
22
Q
innaate immunity is
A
non specific
23
Q
innate immunity examples
A
- Anatomical barriers (e.g. epithelium, mucus, tears, lysozyme)
- Inflammatory response
- Complement (works with adaptive immune response)
- Leukocytes: white blood cells
24
Q
the inflammatory response recruits
A
defence cells to the area
25
whats complement?
Cascade of proteins which destroy targeted cells
26
examples of leukocytes (white blood cells)?
- natural killer cells, mast cells, eosinophils, basophils
- macrophages, neutrophils, dendritic cells, T helper cells
27
what is the adaptive immune response?
Selective response mounted by immune system in which specific antibodies/cytotoxic cells are produced against an antigen recognised as foreign to the body.
28
adaptive immune response results in
long-lived and specific immunity against the pathogen.
29
vaccinrd exploit
the adaptive immune response.
30
After phagocytosis defence cells present antigens from the pathogenic bacteria at
the cell surface in association with major histocompatibility complex proteins (MHC) class II
31
After phagocytosis defence cells present antigens from the pathogenic bacteria at the cell surface in association with major histocompatibility complex proteins (MHC) class II and migrate to
the lymph node where it will interact with cells directing the adaptive immune response.
32
Complement aids in
the removal of bacteria
33
Complement aids in the removal of bacteria. One pathway is
to form of membrane attack complexes in bacterial membranes, punching them open.
34
Complement aids in the removal of bacteria. One pathway is to form of membrane attack complexes in bacterial membranes, punching them open.
Additionally fragments ...
... signal to immune cells and act as signals to macrophages to phagocytose bacteria
35
The complement system can be activated by either
the adaptive immune response (by associating with antibody/antigen complexes on the surface of bacteria or by the recognition of bacterial wall components.
36
Invasive pathogens are generally
encapsuklated
37
Bacteria with capsules are more likely to
evade detection because their PAMPs are hidden (cloaked).
38
Host macrophages recognise
PAMPS
39
what are pamps
pathogen associated molecular patterns
40
exampels of pamps
lipopolysaccharide and flagellin
41
Bacteria evade detection by:
1) Invisibility
2) Provide a moving target
3) Mimicry
42
whats invisibility of bacteria?
Mask potential PAMPs under a capsule.
43
describe the moving targets of bacteria?
have variable external components which change regularly. Many capsule components are unique to particular strains and consist of a multiplicity of different repeating sugar moieties
44
Explain mimicry and what are some examples?
some bacteria (eg Group A Streptococcus) express glycoproteins that are identical to human cell glycoproteins (e.g. hyaluronan)
45
To invade or attack host cells, bacteria need to
attach to them.
46
Adhesion works via
recognition between proteins either at the tips of pili or within the cell wall and glycoproteins or glycans on the host cell surface
47
define endotoxins
integral components of bacterial cells, usually only released during damage.
48
Lipid A is an
endotoxin: induces host fever and other responses.
49
a high dose of endotoxin initiates
septic shock
50
Endotoxins: integral components of bacterial cells, usually only released during damage.
Remember lipopolysaccharide?
Lipid A is an endotoxin: induces host fever and other responses.
High dose: initiates septic shock.
Triggers...
... cascade of cytokines which damage host tissues.
51
exotoxin secreted by
bacteria
52
exotoxins may be specific or
general
53
Diptheria is a
toxin-mediated infectious disease. AB toxin causes inhibition of protein synthesis.
54
Secretion systems of various types:
-Release enzymes
-Assist host cell invasion
-Some inject components into host cells, changing their responses.
55
Type III secretion systems rely on ...
proteins similar to those forming the base of the flagellum – proteins are secreted through the pore via a ‘needle’ into a target cell
56
Type IV secretion systems are derived from
pilus proteins.
57
cholera is tradmitted by
vibrio cholerae
58
how is cholera transmitted
infection is transmitted via water contaminated by a sufferer or through shellfish
59
cholera causes
epidemics and has been responsible for many millions of deaths
60
whats the mode of action of Cholera toxin? [FULL]
- The AB exotoxin binds to gut epithelial receptor (GM1)
- Subunit A is internalised by endocytosis and activates G protein.
- G protein activates adenylyl cyclase (AC). Converts ATP to cAMP (a signalling protein).
- cAMP stimulates cystic fibrosis transmembrane conductance regulator pathway which makes the cell lose Cl- ions.
- Osmotic diarrhoea.
61
in the cholera toxin - mode of action, what does the AB exotoxin bind to?
gut epithelial receptor (GM1)
62
in the cholera toxin - mode of action, subunit A is internalised by...
... endocytosis and activates G protein
63
G protein activates
adenylyl cyclase (AC)
64
G protein activates adenylyl cyclase (AC). Converts ...
... ATP to cAMP (a signalling protein).
65
cAMP stimulates ...
... cystic fibrosis transmembrane conductance regulator pathway which makes the cell lose Cl- ions.
66
whAT is the secretion of V. cholerae ?
harpoon-like type VI secretion System
67
Adjacent cells –
punctured, toxic effector proteins delivered
68
what are the clusters of Vibrio cholerae genomes ?
Aux clusters 1, 2, and 4
69
Aux clusters 1, 2, and 4 share a
canonical hcp, vgrG, tap, effector, immunity gene organization
70
what is Hcp ?
Hemolysin-coregulated protein hexamers
71
Secreted VgrG proteins interact with ...
... toxic proteins (called effectors) to aid in their delivery.
72
what is vertical gene transfer?
from parent to offspring
goes down the generations
73
what is horizontal gene transfer (HGT) ?
- Acquisition of genes by one species from another species.
- Can be called "lateral gene transfer"
- Gene goes "sideways"
- Common in bacteria (rare in eukaryotes)
74
what are the three mechanisms of horizontal gene transfer?
- Transformation
- Conjugation
- Transduction
75
whats transformation ?
DNA enters bacterial cell
76
whats conjugation?
bacterial equivalent of sex: conjugation tube forms between two cells and genetic material is exchanged.
77
whats transduction ?
genets transferred by carriage as part of bacteriophage
78
what are Pathogenicity islands?
Many virulence genes in compact distinct genomic (islands) (10-200kbp)
79
how are pathogenicity islands aquired?
Acquired by HGT
80
pathogenicity islands have a different G+C% content than
bacterial chromosome
81
many pathogens have which population structure?
Many pathogens have clonal population structure
1 clone may be responsible for widespread disease
82
Examples of pathogenicity island contents...
Iron uptake systems
Adhesins
Pore-forming toxins
Superantigens
Secreted lipases and proteases
Proteins transported by type I, III, IV and I secretion systems
Antibiotic resistance
83
Escherichia coli commensal bacterium, most strains..
... harmless
84
what strain of e.coli is harmless?
Escherichia coli commensal bacterium
85
Escherichia coli commensal bacterium assists with...
... food metabolism
86
Some strains of Escherichia coli commensal bacterium have acquired...
... genes by horizontal gene transfer, transforming into pathogens
87
Five categories of diarrheagenic E. coli recognised by
serotyping
88
Many virulence factors are derived from
bacteriophages, plasmids or transposons.
89
what are transposons?
DNA sequences that possess the property of inserting themselves elsewhere on the chromosomes by a process called transposition.
90
where do transposition occur?
Occur in prokaryotic and eukaryotic genomes.
91
the simplest bacterial insertion sequences carry only
gene necessary for their own transposition.
92
Larger transposons carry
other genes, e.g. antibiotic resistance.
93
what is Yersinia pestis ?
Gram-negative, facultative aerobe. Rod shaped, encapsulated.
94
what family does Yersinia pestis belong to?
Family Enterobacteriaceae
95
Yersinia pestis causes...
... Plague/the black death
96
the black death killed?
Killed up to 40% of population.
97
when was black death?
1347-1351 in Europe.
98
the black death caused...
... bleeding under the skin and necrosis - hence "black death".
99
the plague caused infection in 3 forms...
1) Bubonic
2) Septicemic
3) Pneumonic
100
bubonic plague effects?
infects lymph nodes causing them to swell into buboes. 70% mortality.
101
Septicemic in the
blood stream
102
Pneumonic: inhaled or reach lungs via
lymph or bloodstream
103
Pneumonic: inhaled or reach lungs via lymph or bloodstream. Few symptoms before
large amounts of bloody sputum.
104
pneumonic plague spreads from
person to person in the pneumonic stage
105
how is plague treated?
Treatable by antibiotics, e.g. streptomycin or gentamicin injection. Prompt treatment: 5% mortality.
106
Septicemic and pneumonic onset speed
so rapid that antibiotics are usually too late
107
Fleas circumvent the
skin barrier
108
Plasminogen activator function?
removes blood clots, allows infection to spread. Encoded on virulence plasmid.
109
Adhesin (YadBC) encoded on
chromosome
110
Type III secretion system for
Yop proteins
111
type III seceretion syste, inkjected into
host cells.
112
some Type III secretion system form...
... protein-lipoprotein complexes in cell wall to inhibit phagocytosis
113
Virulent strains secrete
Murine toxin
114
what is Murine toxin ?
a lethal respiratory inhibitor in mice, which also causes systemic shock and liver damage.
115
Yop proteins secreted into ...
... human target cells (e.g. macrophages) disrupt normal cellular activity and result in cell death
116
Plague is still endemic in
some areas, especially drier regions
117
plague is enzootic in
rodent populations
- Intermediate host: fleas
- Some rats carry chronic infections
118
when was plague imported to the united states?
Imported to United states in 1900s.
119
If rodent population crashes in urban setting, fleas can
switch hosts and transmit to humans.
120
Plague control?
- Good sanitary control
- Control rodent populations in urban centres.
- Monitoring and prompt response:
- Treatment
- Quarantine of exposed individuals
121
Colonisations of commensal bacteria starts after
birth
122
Colonisations of commensal bacteria starts after birth and includes
the skin, oral cavity, upper respiratory tract and gastrointestinal tract.
123
what do commensal nbacteria inhabit?
Inhabit mucosal and epidermal surfaces in humans, in the normal, non disease state
124
Microbiome plays an important role in
defence against pathogens.
125
what do microbiome act on?
Act on the host's immune system to induce protective responses that prevent colonisation and invasion by pathogens
126
the microbiome can directly ...
... inhibit the growth of respiratory pathogens for example by producing antimicrobial products/signals and competing for nutrients and adhesion sites
127
Microbiome refers to the
micro-organisms in a particular habitat
128
how many microorganisms in the gut microbiota ?
Approximately 100 trillion micro-organisms (most of them bacteria, but also viruses, fungi, and protozoa) exist in the human gastrointestinal tract
129
Microbiome can influence ...
... host’s fitness, phenotype, and health.
130
describe the Association between reduced diversity and disease.
Higher bacterial diversity = Indicator of Healthy Gut
Lower bacterial diversity = Reported in GI disease (IBD, Crohn’s)
131
human commensal bacteria in the mouth?
Mouth – Streptococcal spp.
132
human commensal bacteria in the stomach?
Gram +ve, Proteobacteria, Actinobacteria
133
human commensal bacteria in the small intestine
small intestine – Fusiform anaerobes
134
human commensal bacteria in the large intestine?
E. coli (facultative anaerobe), Clostridium, Bacteroides, Gram +ves, methanogens.
135
what is C. diff ?
a capsule-shaped bacterium that causes inflammation of the colon - colitis
136
what does c.diff produce?
produces two toxins - A and B
137
C. difficile that causes diseases is found...
... in the feces
138
spores can survive for
long periods in the environment (surfaces in a room)
139
spores can survive for long periods in the environment (surfaces in a room) and be spread by ...
... hands that touch conatimnated surfaces
140
how is c. diff transmitted?
person to person fecal-orally
141
is c.diff gram + or - ?
gram positive
142
is c diff aerobic or anaerobic ?
anaerobic
143
c diff is a commensal flora of
human intestines (2-5%)
144
c diff still has
pathogenicity
145
c. diff is extremely
antibiotic resistant
146
the c. diff genome consists of..
... a circular chromosome and a circular plasmid
147
c. diff is [..] forming
spore forming
148
what does c. diff stand for?
Clostridioides difficile
149
c diff is a bacterium whihc causes...
... an infection of th elarge intestine (colon)
150
c. diff infections symptoms?
Symptoms can range from diarrhoea to life-threatening colon damage.
151
illness frlom c diff typically after
use of antiboitoc medications
152
Illness from C. difficile typically after use of antibiotic medications - which
remove the commensal bacteria which keep C. difficile in check.
153
C. difficile can also secrete ...
...proline-based cyclic dipeptides that can inhibit gut bacteria, including commensal Clostridium species, maintaining its dominance.
154
who does c. diff commonly affect?
Commonly affects adults in hospital / long term care. Costly to health services.
155
Certain medical conditions or procedures may
make you more susceptible to a C. difficile infection
156
c diff sometimes cant be treated with
antibiotics
157
c diff sometimes cant be treated with antibiotics - cases of people with...
... recurrent / refractory disease
158
what is The Microbiome Treatment Centre (University of Birmingham) ?
First UK Medicines & Healthcare products Regulatory Agency licensed facility, providing FMT for clinical trials and for the treatment of patients with recurrent and refractory
Clostridium difficile infection.
