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

11 + 12. Emerging bacterial infections Flashcards

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
Q

what is IgIC?

A

part of the type 6 secretion system

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26
Q

what does IgIC do?

A

it plays a massive role in inducing apoptosis in cells

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27
Q

why can lactate dehydrogenase be used as a marker for apoptosis?

A

it is released on cell death

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28
Q

why does tularaemia have potential to be a biological weapon?

A

very very transmissible
thought to have used in Stalingrad invasion

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29
Q

what is bacillus anthracis?

A

large
gram-positive rods that associate in chains
form vegetative spores

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30
Q

why are vegetative spores dangerous?

A

allows for long periods of surivial
aerosol infection
easy to store and distribute

31
Q

where is anthrax endemic?

A

Central Asia and USA
several African countries
associated with the soil

32
Q

does anthrax have outbreaks?

A

natural sporadic outbreaks

33
Q

what are the 3 types of anthrax infection?

A

Cutaneous skin infection
ingestion
Inhalation - the most serious and fatal
contact with spores and bacteria

34
Q

Cutaneous anthrax

A

associated with lesions and oedema in infected areas
antibiotic treatment is effective if given quickly

35
Q

how does anthrax infect cells?

A

disable innate macrophage response using lethal and edema factor

36
Q

what type of toxin is lethal and edema factor?

A

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
Q

what does edema factor do?

A

is an adenyl cyclase
causes water efflux and swelling (edema)

38
Q

what does lethal factor do?

A

a Zn Metal-protease
3 domains - protective antigen binding, substrate recognition and catalytic portion
degrades Mitogen-Activated Protein (MAP) kinase kinase

39
Q

what do MAP kinase kinases do?

A

Involved in a signalling phosphorylation cascade to induce changes in gene expression

40
Q

how does lethal factor target MAP kinase kinases?

A

on multiple kinase kinases there is a specific sequence for the enzymes to bind to

41
Q

what else does lethal factor do?

A

cytoskeletal rearrangements in non macrophage cells

42
Q

Why should melioidosis be considered a high burden neglected tropical disease?

A

its burden is under-recognised and cases are under-reported due to non-specific symptoms

43
Q

who are most likely to be infected with melioidosis?

A

Agricultural workers in SE Asia to be exposed and have repeated contact
US soldiers bought it to the west in the Vietnam war

44
Q

what is the melioidosis burden?

A

165,000 cases a year
89,000 deaths
both are very under reported
endemic in 45 countries
high mortality ~40%

45
Q

what causes melioidosis?

A

Saprophyte B. pseudomallei

46
Q

where are most melioidosis cases reported?

A

Thailand so we get most data from here

47
Q

why is melioidosis a problem?

A

not much investment compared to similar diseases like Dengue

48
Q

where geographically are melioidosis cases mostly located?

A

large clusters in SE asia and Thailand
Northern Australia
South America
these have similar environments and soil conditions

49
Q

why do we find B. pseudomallei in south america?

A

same strains and genomes as Africa
starting to appear after the slave trade

50
Q

what is the main way melioidosis spreads through SE asia?

A

spreads along and around the Mekong river

51
Q

why is melioidosis an emerging disease?

A

anthropogenic spread
Environmental dispersal
increased susceptible population
type 2 diabetes increasing
antibiotic resistance

52
Q

why is increasing type 2 diabetes a problem for melioidosis?

A

it is a risk factor for melioidosis and massive increases the risk of death from melioidosis

53
Q

when was melioidosis first discovered?

A

1911 in Malaysia by army doctor Whitmore

54
Q

how does melioidosis manifest?

A

skin lesions
with abscesses on the skin, liver, lungs, spleen

55
Q

how do you get infected with melioidosis?

A

mainly farmer worker through the skin in like cuts and scraps

56
Q

why is melioidosis called the great mimicker?

A

it can manifest in a number of ways and causes a fever which is very common for tropical diseases

57
Q

what is prognosis for lung melioidosis?

A

1/3 dead after a month
1/2 dead after a year

58
Q

what is latent melioidosis?

A

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
Q

what is Burkholderia pseudomallei?

A

gram-negative rods lone or in clumps
complex so several different species associated with the disease

60
Q

what are Burkholderiae in general?

A

gram-negative, motile, aerobic, non-spore forming
plant pathogens and opportunistic human pathogen
Facultative intracellular parasite
large genomes but split into 2 chromosomes

61
Q

how is B. pseudomallei active in the cytoplasm?

A

manipulate the actin cytoskeleton
induce fusion between infected cells and new cells
forms distinct multinucleated giant cells

62
Q

why is the formation of multinucleated giant cells important for B. pseudomallei pathogenesis?

A

crucial for the ability to form abscesses
but different from TB as not surrounded by T cells

63
Q

what is the difference between B. pseudomallei abscesses and other disease abscesses?

A

the abscess is caused by the pathogen not the immune system

64
Q

how does B. pseudomallei subvert macrophage function?

A

B. pseudomallei triggers low levels of IFNb so less ROS are generated
resist degradative enzymes in the phagosome

65
Q

where is B. pseudomallei taken into in non phagocytic cells?

A

the cytoplasm

66
Q

how does B. pseudomallei escape the complement?

A

using a polysaccharide capsule the membrane attack complex cannot reach the binding sites or binds far away to cause damage

67
Q

what are the 2 secretion systems B. pseudomallei has?

A

type 3 SS to escape endosome
type 6 SS for cell fusion

68
Q

what are secretion systems used for?

A

to take material from the cytoplasm of the bacteria through the host membrane and into the host cell

69
Q

how can we prove type 6 SS causes cell fusion?

A

use Flucytosine to block the type 6 SS and we don’t see any cell fusion or multinucleated giant cells form

70
Q

how does B. pseudomallei use BimA to move around the cell?

A

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
Q

what treatments are available for B. pseudomallei?

A

IV ceftazidime (b-lactam) 10-14 days
Extended treatment possible
meropenem reserve agent
oral trimethoprim or sulfamethoxazole

72
Q

how are B. pseudomallei intrinsically resistant to many antibiotics?

A

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
Q

how can B. pseudomallei acquire resistance?

A

mutations and plasmids

Infection and immunity (22 decks)

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