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MM Revision > Lung infections > Flashcards

Lung infections Flashcards

1
Q

Mechanical Factors against infections

A
  • Skin surface- epithelium
  • > desquamation of outerlayer (skin turnover process)
  • Cillia lining RT (respiratory tract) and GI tracts
  • As well as mucus lining- trapping effect
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2
Q

Chemical factors: Enzymes

A

Enzymes breaking down bacterial cell wall, membrane
* Tears- lysozyme, phospholipase
* Saliva in mouth
* Nasal secretions

Others
* Sweat- has fatty acids, inhibits bacterial growth
* >lowers pH, inhibit growth

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3
Q

Chemical factors: GI and RT

A
  • Defensins and proteins
  • antimicrobial property
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4
Q

Chemical factors: Lung

A
  • Surfactants
  • > stop lung tissue sticking to each other as it expands and contracts
  • > act as opsonins:promotoe phagocytosis, recruit phagocytic cells
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5
Q

Biological factor

A
  • Normal flora: GI and RT
  • Secrete toxic substance, competes with pathogenic bacteria for nutrients and attachment
  • Inhibiting colonisation
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6
Q

Why is alveoli attractive surface for pathogens?

A
  • High surface area for gas exhange
  • Surface for toxic particles to colonise
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7
Q

Mechanisms for alveolar pathogenic colonisation

A
  • Coughing
  • Alveolar macrphages: phagocytosis
  • mucocilliary escalator
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8
Q

What is meant by particle clearance is BIPHASIC

A

can either be
* fast:half life in mins - trachea and bronchi (tracheobronical mucocilliary clearance)
* slow: half life days to years- alveoli - alveolar clearance

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9
Q

Mechanism and rate of particle clearance depends on

A

Site of particle decomposition

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10
Q

Give me example of Alveolar Clearance

A

COVID
Deeper particle penetration
Slow process

If impaired - no clearance

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11
Q

Explain escalator effect in CF and Non CF patients?

A

Non CF
* Normal dept of pericilliary fluid
* Coordinated movement of cillia and mucus
* Mucus sit on top (island)
* Particle moved out of lung (coughing)

CF
* Poorly hydrated hypoxic environment
* Impaired cilliary function: Inhibits cillia beating
CF- impairs chloride transport system
* mucous not hydrated - turgid, thick
* not efficent clearance
* tissue disruption, mucus clog ->infections

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12
Q

CF later colonisers >10 years

A
  • Pseudomonas aerginosa (most damage)
  • Burkolderia cepacia (exacberates infection- co-infection)
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13
Q

CF microbial infection after birth

A
  • mucous stagnates in bronchioles

Early colonisers
* Staphylococcus aureus (+VE)
* Haemophilis influenza (+VE)

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14
Q

Pseudomonas aerginosa

A
  • gram negative rod
  • aerobic
  • Very large chromosome
  • > High functionality and survival
  • Survives in versatile environment
  • Opportunistic pathogen
  • > cause disease in susceptible individuals: CYSTIC FIBROSIS
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15
Q

Pseudomonas aerginosa produces virulence factors under what control?

A

Quroum sensing

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16
Q

How does cystic fibrosis affect compromised patient?

A

Compromised pateints- cancer, burn patients, immune system deficiencies

Problems/complications
* ventilator associated pneumonia
* dialysis catheter infections
* bacterial teratitis
* Otitis externa
* Burn wound infections

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17
Q

The toxic proteins produces P.aerginosa result in

A
  • Extensive tissue damage
  • Intefers immune system defense mechanism
  • Kill host cells near or at site of colonisation
  • Degrative enzymes- disrupt cell membrane, connective tissue in various organs
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18
Q

Virulence factors of Pseudomonas aerginosa

A
  1. Alginate and Rhamnolipids
    2.** Elastase and alkaline protease - destroys host immune system**
  2. Efflux pumps and modifying enzymes - antibiotic resistance
  3. Cytotoxicity
  4. Iron scavanging
  5. Flagella and Type IV pilli -motility
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20
Q

Virulence factor pf Pseudomonas aerginosa

Alginate

A
  • Adhesion to surface
  • Biolfim growth and formation
  • Biolfim: complex of exopolysaccharide
  • Protection: macrophages,biocides, antibiotics, bacteriophages
  • > limits treatment options
  • chronic inflammation response
20
Q

Virulence factor of Pseudomonas aerginosa

Cytotoxicity

A
  • Produces pyocyanin (green on agar plate)
  • Type 3 secretion system (T3SS) - pumps proteases -> host cell
  • Exotoxin A
  • HCN
21
Q

Virulence factor of Pseudomonas aerginosa

Iron Scavenging

A
  • High affinity
  • Siderophores- pyochelin, pyoverdine
  • Proteases
22
Q

Pseudomonas aerginosa is an example of what type of pathogen?

A

Extracellular pathogen

23
Q

IntrAcellular pathogens involve

A
  • ALL virus- oligate viruses
  • Plasmodium genus parasite- Malaria diease
  • > lives and replicated in the cytsol and endosomal compartments of cell
  • Some bacteria
  • Certain Protozoa and Fungi
24
Q

Legionaires disease is caused by what pathogen?

A

Legionella pneumophila
Intracellular pathogen
Motile at low temperatures
water-borne spread (water systems relatively cool)

25
Q

Whats the difference between Legionnaires disease and Pontac fever?

A

Legionnaires disease
* Acute fulminating pneumonia
* low attack rate

Pontac fever
* mild, non-pneumonic febrile infection
* High attack rate

26
Q

Legionella sources

A
  • Man made water distribution systems
  • > warm storage tanks, pipes, AC cooling towers, shower heads
  • even potting compost (Austrailia)
  • bacteria multiple
  • released as water droplets (aerosols)
27
Q

Prevention of Legionella pneumophila spread

A
  • chlorinate water
28
Q

Key feature of Legionnaires disease

A
  • Infects lung macrophages
29
Q

As legionella favours water environmments it does what co-naturally?

A
  • Colonises within Biofilms
  • Access to nutrients from other biofilm species for its growth
30
Q

Importance of Ameobal cyst

A
  • Legionella pneumophila found inside ameobal cyst
  • evolved to survive within in
  • Using the same strategy it has adopted to survive within macrophages
  • Intefering with host immune clearance
31
Q

Explain the invasion process of Legionella pneumophila

A
  • L.pneumophila enters macrophage
  • Via phagocytosis using ICM/DOT proteins
  • Resides within permissuble vacuole resistant to lysosymal activity - prevents lysome and phagosome from fusing
  • No enzymatic activity, free-radical release
  • Thus, establishes replication within phagosome
  • Averts macrophage function
32
Q

L.pneumophilla

How is the permissible vacuole controlled?

A
  • Controlled ICM/DOT genes
  • Encodes for secretion apparatus related to Type IV conjugation system
  • Pump effector proteins -> host vacuole
33
Q

How does it invade the macrophage

Virulence determinants of L.pneumophila

A
  1. Flagella expression
    >fla mutants less infective for macrophages/amoebae
  2. Pillin genes
    >attachment to host cells (+biofilm)
    >intracellular growth (inside host vacuoles)
  3. Type IV secretion Dot/Icm complex
  4. Macrophage infectivity protein (Mip protein)
  5. Kat A (periplasm) and Kat B (cytosol)
34
Q

Virulence determinants of L.pneumophila

Type IV sectrion Dot/ICM complex

A
  • Complex of Dot/Icm proteins
  • Span across bacterial and host membrane
  • To translocate effector molecules ->host cell
  • Required ATP energy provided by Dot B protein
  • Changes in Dot A/B does not affect invasion in amoeba - A.castellani (Host organism)
35
Q

Virulence determinants of L.pneumophila

Kat A (periplasm) and Kat B (cytosol)

A
  • produces catalase/peroxidase activity -> detoxifies it
  • why> maintain criticallu low H2O2 levels
  • To prevent host from mounting oxidativr burst defense
  • Compatible w/phagosome trafficking mediated by typr IV secretion apparatus
36
Q

L.pneumophila pathogenesis and exit

A
  • Ingested by phagocyte->phagosome
  • > isolated from endosomal pathway
  • Bacteria->replicative form
  • > resistant to acidic environment and fusion block remobed
  • Fuses with lysosome - privide niche environment for replication
  • Nutrients deplete (amino acids) , and second messenger molecule ppGpp triggers cascade of regulatory events
  • Enters stationary phase and recruit proteins
  • > Let A, Let S, Let E, Rpos, FliA
  • These proteins coordinate transition of bacteria to exit of host cell membrane
  • Express motilty
  • Produce IcmT proteins meduate exit by forming pores in membrane
  • Zinc metalloprotease (Msp) - degrades host vacuole and outmembrane, explored and mutlplied bacteria swims out
  • Starts infection cycle again
37
Q

Mycobacteriem tubercolosis

A
  • Weakly gram-negative
  • Strongly acid fast aerobic rod
  • Multi-lobed appearance
  • 24-30 hoour doubling time
38
Q

What distinguishes mycobacterium?

A

Unusual cell wall

39
Q

How does TB spread?

A

Spreads person to person by infectious aerosol

40
Q

Mycobacterium tubercolosis cell wall

A
  • **CMN groups **
  • Lipid rich cell wall of mycolic acids
  • Resistant to biocides, detergents and antibiotics

Structure: cytoplasm >cytoplasmic membranes>peptidoglycan layer> CMN groups. lipid rich cell wall

41
Q

Infection of M.tubercolosis: three stages

A

Bacilliary growth= growth of rod-like bacteria
Prevention of dissemination= stop spread of disease
Hematogenous dissemination= spread into bloodstream
Primary acute infection= aggressive form

42
Q

What is the gramnuloma and how is it formed when TB enters lungs?

A

Granuloma is formed to protect bacteria from spreading. Surrounded by necrotic tissue.
> organises aggregates
> surrounds areas of tissues infected by mycobacterium tubercolosis
> act as a barrier that contains the infection
> preventing the bacteria from spreading to other parts of the body
> containment limit the infection’s progression.

Recruitment of
* epitheliod cells (type of immune cell)
* multinucleated giant cells -specialized cells that form when multiple individual cells fuse together, resulting in a single cell with multiple nuclei.
* activated macrophages
* CD4+ T lymphocytes
* CD8+ T lymphocytes

43
Q

Progression of pulmonary Tubercolosis

A
  • Bacterium= Tubercle bacilli
  • inhale implants on to bronchioles/alveoli
  • engulfed by macrophage/neutrophils -> phagocytosis
  • multplies intracellulary
  • > spreads to lymph nodes, bloodstream and distant organs

After 2 weeks
* Granuloma forms
* Lymphocystes surround it =Ghon Tubercle
* Central portion of Ghon tubercle undergoes necrosis “cheesy appearance”

  • Necrotic tissue breaks down - fluid-like subsance
  • sloughs into bronchus
  • forming cavity
  • entry into tracheal broncheal system
  • infectious - spread to other areas via coughing and sneezing (airborne transmission)
  • Macrophages try to contain and clear infection = Healing by resolution
  • Some cases cannot be completely cleared -> scar tissue/fibrosis calcification
  • > created distinctive structure = Ghon complex
44
Q

Wht Mycobacterium tubercolosis such a successful pathogen?

A
  • Evades destruction from pahgocytosis
  • Dusrupts phagosome maturation
  • So no bacterial degredation by lysosome
  • Persist and survive in host
  • Contributes to the complexisity of infection and influence course of disease
45
Q

TB treatment

A
  • Priority of treatment (active/latent)
  • active->non infectious within 2 weeks of treatment
  • > Isoniazid,rifampin, ethambutol: Directly observed treatment shortcourse (DOTS)

MM Revision (15 decks)

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