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Session 2 Flashcards

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1
Q

What is needed for an infection to spread?

A

Both patient AND pathogen

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2
Q

How are most infections treated?

A

Small infections can resolve by themselves (e.g. UTI, small skin infection) but otherwise management involves looking at the patient and pathogen and seeing what can be done

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3
Q

What is the role of age in infection?

A

People of certain age groups are more immunocompromised and are more susceptible to infection (eg. children and elderly)

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4
Q

What is the role of gender in infection?

A

e.g. Women have a higher chance of having UTIs snd cystitis as bacteria from the rectum can easily be transmitted into the urinary tract

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5
Q

What is the physiological state in infection?

A

e.g. puberty, pre-puberty, menopause, pregnancy

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6
Q

What is the role of pathological state in infection?

A

Certain co-morbidities make people more susceptible to diseases and infection (e.g. diabetic neuropathy - cuts on feet - not realising as can’t feel - skin infection)

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7
Q

What is the role of social factors in infection?

A

How we behave, our contact with other people and animals can influence disease spread (eg. HIV via sexual contact)

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8
Q

What is the role of calendar time in infection?

A

Some diseases more common at certain time of year (eg. flu in winter)

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9
Q

What is the role of relative time in infection?

A

Refers to the incubation period and exposure. Incubation period = after how long symptoms will start appearing. Can be linked to exposure

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10
Q

What is the role of recent travel in infection?

A

People can contract diseases abroad that are not routinely tested for in the UK as they are uncommon so must know

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11
Q

What are the mechanisms of infection?

A 
Contiguous spread
Inoculation (sticking)
Haematogenous
Ingestion
Inhalation
Vector
Vertical transmission (mother/child)
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12
Q

How are infections diagnosed?

A

Taking history, examination, investigations

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13
Q

What is the mechanism of infection?

A

Attachment (specific binding to host cells), then causing toxin production and interacting with host cells (neutrophils and respiratory burst), which cause inflammation and host cell damage

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14
Q

What is supportive treatment?

A

Treatment that is not directly aimed at killing the pathogen but rather at relieving symptoms or physiological restoration (ventilators, inotropes, dialysis)

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15
Q

What is specific treatment?

A

Treatment aimed directly at killing the pathogen causing infection

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16
Q

What are examples of specific treatment?

A

Antimicrobial drugs

Surgery: drainage (abscess), debridement (removing dead tissue)

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17
Q

Why is infection prevention important?

A

To prevent transmission to patients, staff and other contacts

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18
Q

What is the outcome of treatments?

A

Infections can be cured but can also cause death if treatments not known/infection too severe (often systemic). May or may not cause disability.

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19
Q

What factors determine host-pathogen relationship?

A

Infectivity - ability to establish itself on host
Virulence - capacity to cause damage
Host immune response

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20
Q

Define immune system

A

Cells and organs that contribute to immune defences against infectious & non infectious diseases.

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21
Q

Define infectious disease

A

When a pathogen succeeds in evading immune defences

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22
Q

What are the roles of the immune system?

A

Pathogen recognition (PAMPs recognised by PRR)
Containing and eliminating infection (preventing systemic spread)
Regulating itself for minimum damage to host (if too much = autoimmune disease)
Remembering pathogens to prevent reinfection

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23
Q

What are the features of immediate protection?

A

Fast (seconds)
Non-specific
No memory

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24
Q

What are the features of long-lasting protection?

A

Slow (days) - some viruses may have shorter incubation period so may not be sufficient
Highly specific
Creates immunologic memory

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25
What are the first lines of defence?
Factors that prevent entry or growth of pathogens (e.g physiological, physical, chemical and biological barriers)
26
What are the physical barriers?
Skin - prevents entry Mucous membranes - can produce an immune response Bronchial cilia - mucocilliary escalator
27
What are physiological barriers?
Methods of expelling the microbes out (can also cause spread) - diarrhoea, vomiting, coughing, sneezing
28
What are the chemical barriers?
Low pH in the stomach, skin and vagina Antimicrobial molecules: Gastric acid + pepsin, beta-defensins, IgA (prevents attachment to host), lysozyme, mucus
29
What are the biological barriers?
Normal flora (not harmful if not migrating) - prevents pathogens from attaching to the sites in the nasopharynx, mouth, skin, GI tract and vagina and therefore prevents invasion. Produce antimicrobial chemicals Vitamin K + B12 synthesis Immune maturation
30
What are the normal flora on skin and what can they cause if pathogenic?
Staphylococcus aureus - cellulitis Staphylococcus epidermis - very resistant to treatment Streptococcus pyogenes - necrotising fascitis Candida albicans - thrush
31
When might normal flora be displaced to a sterile location?
- Skin integrity lost (eg. burns, IV, surgery, skin disease) - Faecal-oral route - Faecal-perineal-urethral route (eg. UTI) - Poor dental hygiene or work - will cause harmless bacteriaemia as spleen defends against bloodborne pathogens
32
In which patients can harmless bacteria be serious?
- Asplenic/hyposplenic patients - Patients with damaged/prosthetic valves - Patients who had infective endocarditis
33
When can normal flora overgrow?
Immunocompromised host. - Diabetes - HIV - Malignant diseases - Chemotherapy (mucositis allows flora to enter tissues)
34
What is inflammation?
A factor that will clear and contain the infection; interaction between phagocytes and microbes through recognition and killing
35
What are macrophages?
- Antigen presenting cells - Produce cytokines/chemokines - Phagocytosis
36
What are monocytes?
Cells recruited at infection site that develop into macrophages
37
What are neutrophils?
(Increase during infection) - Get recruited by chemokines to the site of infection - Destroy pyogenic bacteria - Short lived
38
What are basophils/mast cells?
Act in inflammation/allergic responses
39
What are eosinophils?
Defence against parasitic worms
40
What are natural killer cells?
Kill cells that are virus infected or malignant
41
What are dendritic cells?
Antigen presenting cells - acquired immunity
42
How are pathogens recognised?
Pathogens have PAMPs (pathogen-associated molecular patterns) that are lipids, carbs, etc. and that can be recognised. They are recognised by pathogen recognition receptors (PRRs) on phagocytes.
43
What are toll like receptors?
They're the most common PRRs.
44
What are opsonins?
Coating proteins that will bind to the microbial surfaces and then lead to enhanced attachment of phagocytes and therefore more effective clearance of microbes. They signal the phagocyte to kill the microbe.
45
Why is the spleen essential in clearing encapsulated bacteria?
Spleen reduces the risk of sepsis by getting rid of polysaccharide-encapsulated bacteria. There is a deficiency in t-lymphocytes. Lacks ability to clear opsonised bacteria from blood.
46
What are complement proteins?
Enhance ability to clear pathogens and damaged cells from the organism - C3b
47
What do PAMPs and PRRs activate?
Cytokine/chemokine production
48
What are acute phase proteins?
e.g. C reactive protein. Levels rise in response to inflammation and tissue injury.
49
What encapsulated bacteria can potentially cause sepsis?
- Neisseria meningitidis - Streptococcus pneumoniae - Haemophilus influenzae b
50
What is phagocytosis and how does it happen?
- Adherence of microbe to phagocyte - Ingestion of microbe - phagosome formation - Phagosome fuses with lysosome = phagolysosome - Microbe ingested by digestive enzymes - Residual body with indigestible material is formed - discharged out of the cell via exocytosis.
51
What are the 2 phagocyte intracellular killing mechanisms?
- Oxygen-dependent pathway (respiratory burst) - ROS | - Oxygen-independent pathway (eg. hydrolytic enzymes)
52
What is inflammation?
Factors that will contain and clear the infection
53
What are the roles of C3a and C5a complements?
Recruitment of phagocytes
54
What are the roles of C3b - C4b complements?
Opsonisation of pathogens
55
What are the roles of C5-C9 complements?
Killing of pathogens, membrane attack complex
56
What are complement systems?
A part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes, promotes inflammation, attacks pathogen membrane.
57
What do cytokines/chemokines do?
- Chemoattraction - Phagocyte activation - Inflammation
58
What are systemic antimicrobial actions of cytokines?
Neutrophil mobilisation, complement activation, CRP, elevated body temp
59
What are local antimicrobial actions of cytokines?
Vascular permeability, vasodilation, neutrophil attraction
60
What are some macrophage-derived cytokines?
IL-1, IL-6 (interleukin), TNF-alpha (tumour necrosis factor)
61
Summarise the innate immune response
- Breaching innate barriers and pathogens entering - Complement, mast cell + macrophage activation - opsonins, cyto + chemokines - Vascular changes - dilation + higher permeability - Chemoattraction - neutrophils, monocytes - Hypothalamus (fever) + acute phase response - LOCAL INFLAMMATION - redness, pain and swelling
62
Why does inflammation occur?
It's the best environment to contain an infection
63
What is an issue in asplenic/hyposplenic patients?
They have reduced phagocytosis - opsonised bacteria cannot get removed. Higher risk for serious infection.
64
What causes reduced phagocytosis?
- Low spleen functions - Low neutrophil count (leukaemia, lymphoma, chemotherapy) - Reduced neutrophil function (eg. chronic granulomatous disease, Chediak-Higashi syndrome)

Infection (10 decks)

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