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Human Microbial Diseases Block 1 > Bacterial Intracellular Pathogens > Flashcards

Bacterial Intracellular Pathogens Flashcards

1
Q

What are the cons of intracellular survival?

A
  • Must overcome host barriers
  • Must modulate innate immunity
  • Must modulate cell-mediated immunity
  • Must overcome bactericidal stress
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2
Q

What are the pros of intracellular survival?

A
  • Gain access to a protected / nutritious environment -> has a lot of carbon sources
  • Some protection from the immune response
  • Have time to adapt and modify the environment in the cell
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3
Q

How are intracellular pathogens grouped?

A
  • Facultative intracellular pathogens vs. obligate intracellular pathogens
  • Growth and survival in phagocytic cells after phagocytosis vs. growth and survival in non-phagocytic cells through induced uptake
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4
Q

Name some examples of facultative intracellular pathogens

A
  • Salmonella sp.
  • Legionella
  • Shigella sp. -> dysentry
  • Yersinia sp. -> plague / gastroenteritis
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5
Q

Name some examples of obligate intracellular pathogens

A
  • Mycobacterium sp.

- Chlamydia sp. -> pneumonia / genital infections

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6
Q

Name some examples of bacteria that grow and survive in phagocytic cells

A
  • Salmonella -> typhoid fever / gastroenteritis
  • Listeria monocytogenes -> listeriosis
  • Mycobacterium sp. -> TB / leprosy
  • Legionella pneumophila -> legionnaires disease
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7
Q

Name some examples of bacteria that grow and survive in non-phagocytic cells

A
  • Salmonella -> will infect gut epithelial cells
  • Shigella
  • Listeria
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8
Q

Describe the appearance of macrophages

A

Large mononuclear cells with granular cytoplasm

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9
Q

Where are Kupffer cells found?

A

Liver

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10
Q

Where are alveolar macrophages found?

A

Lungs

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11
Q

Where are osteoclasts found?

A

Bone

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12
Q

Where are microglia found?

A

Brain

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13
Q

What do macrophages require for activation?

A

IFN gamma

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14
Q

Where do macrophages migrate after killing?

A

Lymph nodes

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15
Q

Describe the appearance of neutrophils

A

Small with multilobed nucleus and granular cytoplasm

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16
Q

What do neutrophils do after killing?

A

Die at the site by apoptosis

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17
Q

What receptors do macrophages express for bacterial constituents?

A
  • Mannose receptor
  • LPS receptor
  • Glucan receptor
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18
Q

What type of bacteria does the LPS receptor detect?

A

Used for gram negative bacteria

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19
Q

What happens when bacteria bind to macrophage receptors?

A
  • Initiates the release of cytokines and small lipid mediators of inflammation -> particularly if TLR4 is bound
  • Internalisation of pathogen into the phagosome
  • Acidification of the phagosome
  • Fusion of the phagosome with lysosomes / granules containing antimicrobial compounds to form the phagolysosome
  • Oxygen and nitrogen species are generated
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20
Q

What pH does the phagosome reach when acidified?

A

3.5 - 4

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21
Q

What do TLRs recognise?

A

Pathogen-associated molecular patterns (PAMPs)

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22
Q

What does TLR binding on macrophages result in?

A

Cytokine production and cellular activation

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23
Q

Name the intracellular effector mechanisms of phagocytes

A
  • Acidification
  • Toxic oxygen-derived products
  • Toxic nitrogen oxides
  • Antimicrobial peptides
  • Enzymes
  • Competitors
24
Q

What enzymes help bacterial breakdown in phagocytes?

A
  • Lysozymes
  • Acid hydrolases
  • Collagenases
25
Q

What competitors are used in phagocytes?

A
  • Lactoferrin

- Vitamin B12-binding protein

26
Q

Compare the mechanisms of pathogen destruction that macrophages and neutrophils use

A
  • Both use phagosome acidification
  • Neutrophils use primary and secondary granules
  • Macrophages use lysosomes
  • Both use oxygen-dependent mechanisms and oxygen-independent mechanisms
  • Both use nitrogen-dependent mechanisms
27
Q

What are RNIs produced from?

A

L-arginine

28
Q

What enzyme is used to produce RNIs?

A

Inducible nitric oxide synthase (iNOS)

29
Q

How do intracellular bacteria avoid destruction by RNIs?

A

Break down L-arginine using arginases to prevent RNIs being formed

30
Q

What enzyme is used to produce ROIs?

A

NADPH oxidase

31
Q

What enzyme makes hypochlorous acid and singlet oxygen?

A

Myeloperoxidase

32
Q

What are the strategies for intracellular survival in phagocytes?

A
  • Avoid or prevent phagocytosis if unable to survive intracellularly
  • Internalised but able to proliferate in the vacuole -> disable / resist killing mechanisms
  • Internalised by phagocytosis but can escape the vacuole and survive in the cytoplasm
33
Q

How does Haemophilus Influenza avoid phagocytosis?

A

Has a polysaccharide coat that prevents the virus being taken up by phagocytosis

34
Q

Is Salmonella gram positive or gram negative?

A

Gram negative

35
Q

What cells does Salmonella infect intracellularly?

A

Phagocytes and non-phagocytic epithelial cells

36
Q

Where does Salmonella survive in phagocytes?

A

Survives and modifies the phagosome

37
Q

Does Shigella stay in the phagosome after being taken up by phagocytosis?

A

No, it escapes the phagosome

38
Q

Does Shigella have intracellular motility?

A

Yes, it can propel itself around the cytoplasm

39
Q

Name the diseases Salmonella can cause

A
  • Typhoid fever
  • Enteric fever
  • Non-typhoidal salmonellosis
40
Q

What Salmonella causes typhoid fever?

A

S. typhi

41
Q

What occurs in the first phase of typhoid fever?

A
  • Slow fever
  • Rose spots
  • Mild bacteraemia
42
Q

What occurs in the second phase of typhoid fever?

A
  • Organism reaches the gall bladder
  • Re-invasion of the intestine
  • Ulcers
  • Haemorrhage
  • Typhoid state
  • Muttering delirium or coma vigil
  • Death (20%)
43
Q

What Salmonella causes enteric fever?

A

S. paratyphi

44
Q

What Salmonella causes non-typhoidal salmonellosis?

A
  • S. typhimurium
  • S. enteriditis
  • S. heidelberg
  • S. newport
45
Q

What is the incubation period of non-typhoidal salmonellosis?

A

Usually 12-36 hours

46
Q

What are the symptoms of non-typhoidal salmonellosis?

A
  • Chills/fever
  • Nausea/vomiting
  • Abdominal pain
  • Diarrhoea
47
Q

How long does non-typhoidal salmonellosis last?

A

1-7 days

48
Q

How is Salmonella transmitted?

A
  • Chicken
  • Pork and beef products
  • Eggs
  • Some fresh produce
  • Some reptiles act as vectors
49
Q

When did the common ancestor of Salmonella exist?

A

25-40 million years ago

50
Q

What separated Salmonella and Escherichia lineages?

A

Acquisition of Salmonella pathogenicity island 1 and the ability to cause intestinal infections

51
Q

What are the 2 species of Salmonella?

A
  • S. enterica

- S. bongori

52
Q

What divided Salmonella into the 2 species?

A

Acquisition of SPI2

53
Q

How does Salmonella translocate the gut lumen?

A
  • Induces uptake into epithelial cells in the gut

- Can break down tight junctions between epithelial cells

54
Q

Describe the interaction between Salmonella and macrophages

A
  • Taken up by macrophages where it can survive and disseminate
  • Once taken into the phagosome it’s known as salmonella containing vesicle
  • Can induce apoptosis in macrophages inducing IL-1beta and inflammation
  • If released from macrophages can induce uptake into epithelial cells via the basolateral side
  • Ruffling occurs as the actin cytoskeleton of the macrophage is modified by the Salmonella
55
Q

Describe the mechanism of Salmonella invasion

A
  • T3SS translocates effectors into the host cytoplasm which activates host Rho GTPases
  • Effectors modulate the environment within the cell which leads to actin rearrangement (ruffling) and induction of mitogen-activated protein kinase paths destabilising tight junctions
  • Further changes in the actin cytoskeleton made via actin-binding proteins SipA and SipC leading to bacterial uptake
  • MAPK signalling activates host AP-1 and nuclear factor-kappaB causing the cell to release IL-8
  • SipB induces macrophage apoptosis and IL-1 and IL-18 release leading to further destabilisation of tight junctions allowing for more bacterial passage and brings more cells for the bacteria to infect
  • SptP leads to restoration of the actin cytoskeleton and down-modulating MAPK signalling and inflammation
  • SspH1 and AvrA also inhibit NF-kappaB
56
Q

How does Salmonella survive the macrophage?

A
  • Salmonella produces arginase II that breaks down L-arginine to prevent the production of RNIs
  • SPI-2 and PhoPQ are involved in the evasion of ROIs, SCV is also involved in this
  • Salmonella induces the TLR to create an activated state
  • Salmonella inhibits fusion of the lysosome with the SCV to prevent the breakdown of Salmonella
  • Salmonella pushes the macrophage to go to an M2 phenotype which produces more anti-inflammatory cytokines
  • Salmonella promotes pyroptosis, apoptosis, autophagy or necroptosis which are tyes of cell death the Salmonella can survive
  • Pyroptosis is caspase1 mediated and produces IL-1beta and IL-18
  • Necroptosis is characterised by IFNR and RIP 1,3
  • SipB promotes autophagy

Human Microbial Diseases Block 1 (7 decks)

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