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Infection and immunity > 11 + 12. Emerging bacterial infections > Flashcards

11 + 12. Emerging bacterial infections Flashcards

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1
Q

what is an emerging infection?

A

an infection that is newly appeared in a population or previously existed but rapidly increasing in incidence or geographic range

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2
Q

what is a re-emerging infection?

A

infections that existed in the past but are now rapidly increasing in incidence or geographical or human host range

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3
Q

what are some misconceptions about infectious diseases?

A

that the period where they would be interesting or a problem is over and they are not worth research

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4
Q

what are some things that decrease the incidence of infectious diseases?

A

better housing
safer food and water
improved healthcare and immunisations
improved hygiene
better education

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5
Q

why are disease death rates slowly increasing again?

A

HIV and other diseases

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6
Q

what increases the incidence of emerging infectious diseases?

A

society getting older
more leisure time and travel
changes in technology
industrial food production
International travel
Complacency in public health and lack of funding
pathogens changing and adapting

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7
Q

what is tularaemia?

A

a bacteria disease classically associated with contact with infected animals or arthropod vectors

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8
Q

what are the different manifestations of tularaemia?

A

skin - lesions and flu like symptoms
ingestion - contaminated meat
inhalation - aerosol, 30% fatal

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9
Q

where is tularaemia normally found?

A

sub arctic northern hemisphere in remote areas

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10
Q

what type of infection is tularaemia?

A

zoonotic

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11
Q

where is tularaemia found that it was not previously thought?

A

in the southern hemisphere where it as differentiated into a number of branches

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12
Q

what bacteria causes tularaemia?

A

Francisella Tularensis

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13
Q

what is Francisella tularensis?

A

small
gram-negative
coccobacillus
intracellular pathogen

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14
Q

why is Francisella tularensis hard to culture?

A

normally intracellular so needs lots of supplements to be cultured

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15
Q

what is the natural reservoir of Francisella tularensis?

A

thought to rodents but they suffer so cannot be a reservoir
thought to be a protozoa amoeba

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16
Q

why does Francisella tularensis have a degraded genome?

A

intracellular so relies on host cells for most functions

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17
Q

why is the Francisella tularensis genome degraded?

A

10% of coding genes are non functional
insertion sequences
deletions
frameshifts

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18
Q

what functions can Francisella tularensis not do?

A

cannot Assimilate sulphur so cannot make cysteine
cannot make valine, isoleucine, theanine

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19
Q

what is the GC content of Francisella tularensis’s genome?

A

low GC content

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20
Q

how does Francisella tularensis change macrophage uptake mechanisms?

A

altered uptake of bacteria using pseudopod loops
altered uptake affects the next stages of degradation

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21
Q

what macrophage mechanism does Francisella tularensis inhibit?

A

the Reactive oxygen species burst which affects enzyme activation

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22
Q

what is the Francisella tularensis pathogenicity island?

A

a part of the genome with different GC content that massively contributes to pathogenicity
each genome can contain more then 1 copy

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23
Q

what does the Francisella tularensis pathogenicity island encode?

A

20 genes that encode a type 6 secretion system

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24
Q

what is a type 6 secretion system ?

A

a delivery system that injects effector proteins into host cells to disrupt phagocytosis

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25
what is IgIC?
part of the type 6 secretion system
26
what does IgIC do?
it plays a massive role in inducing apoptosis in cells
27
why can lactate dehydrogenase be used as a marker for apoptosis?
it is released on cell death
28
why does tularaemia have potential to be a biological weapon?
very very transmissible thought to have used in Stalingrad invasion
29
what is bacillus anthracis?
large gram-positive rods that associate in chains form vegetative spores
30
why are vegetative spores dangerous?
allows for long periods of surivial aerosol infection easy to store and distribute
31
where is anthrax endemic?
Central Asia and USA several African countries associated with the soil
32
does anthrax have outbreaks?
natural sporadic outbreaks
33
what are the 3 types of anthrax infection?
Cutaneous skin infection ingestion Inhalation - the most serious and fatal contact with spores and bacteria
34
Cutaneous anthrax
associated with lesions and oedema in infected areas antibiotic treatment is effective if given quickly
35
how does anthrax infect cells?
disable innate macrophage response using lethal and edema factor
36
what type of toxin is lethal and edema factor?
AB toxins 7 protective antigen subunits that bind and are taken up by the macrophage LF/EF bind to the subunits and enter the macrophage forms a channel to excrete the toxins into the cytosol
37
what does edema factor do?
is an adenyl cyclase causes water efflux and swelling (edema)
38
what does lethal factor do?
a Zn Metal-protease 3 domains - protective antigen binding, substrate recognition and catalytic portion degrades Mitogen-Activated Protein (MAP) kinase kinase
39
what do MAP kinase kinases do?
Involved in a signalling phosphorylation cascade to induce changes in gene expression
40
how does lethal factor target MAP kinase kinases?
on multiple kinase kinases there is a specific sequence for the enzymes to bind to
41
what else does lethal factor do?
cytoskeletal rearrangements in non macrophage cells
42
Why should melioidosis be considered a high burden neglected tropical disease?
its burden is under-recognised and cases are under-reported due to non-specific symptoms
43
who are most likely to be infected with melioidosis?
Agricultural workers in SE Asia to be exposed and have repeated contact US soldiers bought it to the west in the Vietnam war
44
what is the melioidosis burden?
165,000 cases a year 89,000 deaths both are very under reported endemic in 45 countries high mortality ~40%
45
what causes melioidosis?
Saprophyte B. pseudomallei
46
where are most melioidosis cases reported?
Thailand so we get most data from here
47
why is melioidosis a problem?
not much investment compared to similar diseases like Dengue
48
where geographically are melioidosis cases mostly located?
large clusters in SE asia and Thailand Northern Australia South America these have similar environments and soil conditions
49
why do we find B. pseudomallei in south america?
same strains and genomes as Africa starting to appear after the slave trade
50
what is the main way melioidosis spreads through SE asia?
spreads along and around the Mekong river
51
why is melioidosis an emerging disease?
anthropogenic spread Environmental dispersal increased susceptible population type 2 diabetes increasing antibiotic resistance
52
why is increasing type 2 diabetes a problem for melioidosis?
it is a risk factor for melioidosis and massive increases the risk of death from melioidosis
53
when was melioidosis first discovered?
1911 in Malaysia by army doctor Whitmore
54
how does melioidosis manifest?
skin lesions with abscesses on the skin, liver, lungs, spleen
55
how do you get infected with melioidosis?
mainly farmer worker through the skin in like cuts and scraps
56
why is melioidosis called the great mimicker?
it can manifest in a number of ways and causes a fever which is very common for tropical diseases
57
what is prognosis for lung melioidosis?
1/3 dead after a month 1/2 dead after a year
58
what is latent melioidosis?
Asymptomatic and latent form can go undetected for decades the longest example is 29 years lesions in the lungs only positive cultures when very sick
59
what is Burkholderia pseudomallei?
gram-negative rods lone or in clumps complex so several different species associated with the disease
60
what are Burkholderiae in general?
gram-negative, motile, aerobic, non-spore forming plant pathogens and opportunistic human pathogen Facultative intracellular parasite large genomes but split into 2 chromosomes
61
how is B. pseudomallei active in the cytoplasm?
manipulate the actin cytoskeleton induce fusion between infected cells and new cells forms distinct multinucleated giant cells
62
why is the formation of multinucleated giant cells important for B. pseudomallei pathogenesis?
crucial for the ability to form abscesses but different from TB as not surrounded by T cells
63
what is the difference between B. pseudomallei abscesses and other disease abscesses?
the abscess is caused by the pathogen not the immune system
64
how does B. pseudomallei subvert macrophage function?
B. pseudomallei triggers low levels of IFNb so less ROS are generated resist degradative enzymes in the phagosome
65
where is B. pseudomallei taken into in non phagocytic cells?
the cytoplasm
66
how does B. pseudomallei escape the complement?
using a polysaccharide capsule the membrane attack complex cannot reach the binding sites or binds far away to cause damage
67
what are the 2 secretion systems B. pseudomallei has?
type 3 SS to escape endosome type 6 SS for cell fusion
68
what are secretion systems used for?
to take material from the cytoplasm of the bacteria through the host membrane and into the host cell
69
how can we prove type 6 SS causes cell fusion?
use Flucytosine to block the type 6 SS and we don't see any cell fusion or multinucleated giant cells form
70
how does B. pseudomallei use BimA to move around the cell?
for actin motility and remodelling of the cytoskeleton actin is used to push the bacteria around the cell (comet tails) this is important for multinucleated cell formation
71
what treatments are available for B. pseudomallei?
IV ceftazidime (b-lactam) 10-14 days Extended treatment possible meropenem reserve agent oral trimethoprim or sulfamethoxazole
72
how are B. pseudomallei intrinsically resistant to many antibiotics?
membrane bound efflux pumps to remove antibiotics before they cause damage modified pores in membranes to prevent antibiotic entry B-lactamase enzymes like PenA
73
how can B. pseudomallei acquire resistance?
mutations and plasmids

Infection and immunity (22 decks)

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