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Infection > Session 7 > Flashcards

Session 7 Flashcards

(48 cards)

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1
Q

What is a surface?

A

Interface between a solid and either liquid/gas.

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2
Q

What surfaces can be found on the patient?

A
  • Skin (epithelium/hair/nails)

- Mucosal surfaces (GI/conjunctival/genitourinary/resp)

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3
Q

What causes most infections?

A

Patient’s own resident flora that migrated to different places

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4
Q

What microorganisms can be found on the skin?

A
  • HSV & papilloma (V)
  • Staph aureus, coagulase-negative strep (+), enterobacteriaceae (-) B
  • Yeasts and dermatophytes (F)
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5
Q

What is the normal flora in the eye?

A
  • Coagulase negative staph

- Saprophytic Neisseria species

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6
Q

What is the normal flora in the nasopharynx?

A
  • Neisseria meningitidis
  • Strep pneumoniae
  • Haemophilus influenzae
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7
Q

What is the normal flora in the mouth?

A
  • Viridans streptococci
  • Lactobacillus
  • Clostridia
  • Candida
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8
Q

What is the normal flora in the stomach?

A
  • Helicobacter
  • Strep
  • Staph
  • Lactobacilli
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9
Q

What is the normal intestinal flora?

A
  • Eubacterium
  • Aerobic/anaerobic strep
  • Bifidobacterium
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10
Q

What is the normal vaginal flora?

A
  • Lactobacilli
  • Coagulase-negative staph
  • Enterococcus faecalis
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11
Q

What is the normal urethral flora?

A
  • Enterobacteriaceae

- Enterococci

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12
Q

How do people get infections?

A

Normally harmless/beneficial microbiota transferred to other sites

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13
Q

Through which mechanisms can patients get infection?

A
  • Invasion (acquired, eg. strep pyrogenes)
  • Migration (from different site, eg. escherichia coli)
  • Inoculation (introduction to other site via surgery, eg. coagulase-negative staphylococcus)
  • Haematogenous spread (bacteria sticking, eg. viridans and endocarditis)
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14
Q

What are some examples of external natural surface infections?

A
  • Cellulitis
  • Pharyngitis
  • Conjunctivitis
  • Gastroenteritis
  • UTI
  • Pneumonia
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15
Q

What are some examples of internal natural surface infections?

A
  • Endocarditis and vasculitis
  • Septic arthritis
  • Osteomyelitis
  • Empyema (pus in pleural cavity)
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16
Q

What are some examples of prosthetic surface infections?

A
  • IV lines
  • Peritoneal dialysis catheters
  • Prosthetic joints
  • Cardiac valves
  • Pacing wires
  • Grafts
  • Ventriculoperitoneal shunts
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17
Q

What can cause naive valve endocarditis or prosthetic valve endocarditis over a year post-op?

A
  • Viridans
  • Streptococci
  • Enterococcus faecalis
  • Staph aureus
  • Candida
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18
Q

What can cause prosthetic valve endocarditis under a year post-op and why?

A
  • Coagulase-negative staphylococci

Skin bacteria are introduced at the time of surgery

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19
Q

What can cause prosthetic joint infections?*

A
  • Staph aureus

- Coagulase negative staphylococci

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20
Q

What is the treatment for prosthetic joint infections?

Study These Flashcards
A
  • Joint may have to be removed and antibiotics may have to be administered without the joint present in the limb
  • A new joint may then have to be put in
  • Alternatively, open patient up and place antibiotics in wound.
21
Q

What can cause cardiac pacing wire endocarditis?

Study These Flashcards
A
  • Staph aureus

- Coagulase negative staphylococci

22
Q

How can pathogens spread and multiply on the surfaces?

Study These Flashcards
A
  • Can adhere to host cells/prosthetic surfaces
  • Biofilm formation
  • Invasion and then multiplication
23
Q

What are the host responses to infections on surfaces?

Study These Flashcards
A
  • Pyogenic response (i.e. pus and neutrophils)

- Granulomatous (fibroblasts/lymphocytes/macrophages)

24
Q

How do bacterial cells adhere to host cells?*

Study These Flashcards
A

Have pili or fimbriae - thin strands that bind to surface receptors on the host cell membrane

25
What are biofilms?*
Extracellular material designed to protect bacteria from the normal host defences (antibody and complement attack and phagocytosis) Slimy structure of the biofilm allows nutrient to pass in.
26
What are the features of bacteria that can usually produce biofilms?
- Free living - Planktonic - Smaller division - Smaller cell size
27
What is the process of biofilm formation?*
1. Starvation causes bacteria to shrink and become spore-like until conditions become suitable for growth 2. Active bacteria can change from swimmers to stickers within minutes due to gene expression change 3. Attached bacteria multiply and encase colonies with slimy matrix 4. Nutrients diffuse into matrix - close cell proximity facilitates exchange of molecular signals that regulate behaviour 5. Chemical gradients create microenvironmens for different species 6. Resistant even though antibiotics can damage outer cell layers 7. Aggregated cells can detach by shear forces and still remain protected by biofilms
28
What is quorum sensing?** SLIDE 23!
Communication based on regulation in gene expression in response to cell population and density
29
What are cell control methods?
- Sporulation (formation of nearly-dormant growth to protect genetic material in lethal conditions) - Biofilm formation (protection) - Virulence factor secretion (assist colonisation)
30
What are the three principles of quorum sensing/control?
- Autoinducers: signalling molecules that can trigger biochemical processes and gene expression by picking up other bacteria - Cell surface/cytoplasmic receptors - Gene expression to produce more/co-operate
31
How to manage infections at the surface?
Identify organisms and its susceptibilities (antibiotic sensitivity testing) - Blood culture - Tissue/prosthetic material culture and sonication (sound energy for agitation)
32
What are the challenges in managing infections at cell surfaces?
- Organisms are adherent | - Low metabolic state and small colony variants
33
What are the aims of antibacterial treatments?
Sterilise tissue and reduce bioburden
34
What treatments are used for antibacterial surface infections?
- Antibacterials - Removing infected prosthetic material - Surgery to resect
35
What are the challenges in treating cell surface infections?
- Poor antibacterial penetration to the biofilm due to increased diffusion distance - Low metabolic activity of biofilm cells and antibiotics mainly attack actively multiplying bacteria - Dangers of surgeries
36
How to prevent infections at natural surfaces?
- Maintain surface integrity (eg. cover up any cuts etc) - Prevent colonisation - Remove colonising bacteria
37
How to prevent infections at prosthetic surfaces?
- Prevent contamination - Inhibit surface colonisation - Remove colonising bacteria
38
When do antigen presenting cells mature?
When they have captured microbe, as this allows full T cell activation
39
What happens if the pathogen gets into the lymphatics or the blood stream?*
- Detected by antigen presenting cells (dendritic cells, naive B cells) - Dendritic cell maturation then activates naive CD4 T cells and CD8 T cells - CD4 T cells become T helper cells and CD8 T cells become cytotoxic T cells - T helper cells help with antibody response and CTLs help with the effector cell response when released into peripheral tissue
40
Where are B and T lymphocytes produced?
Bone marrow
41
Where do B and T lymphocytes mature?
T cells = thymus (70% in blood) | B cells = in tissues following contact with an antigen (20% in blood)
42
Where do the B and T lymphocytes accumulate?
- Mucosa-associated lymphoid tissue (MALT) - Lymph nodes - Spleen
43
What is lymphadenopathy?*
Lymph node swelling that occurs when B and T cells are activated by the antigen
44
What is DiGeorge syndrome?
A condition in which the person does not have a thymus and experiences viable immunodeficiency due to the lack of T cells, and T and B cell function will be affected
45
How are antigens recognised by T lymphocytes?*
Antigen recognition receptor: - T cell receptor - CD3 main complex, which can accommodate different peptides - Accessory molecules (CD4 or CD8)
46
What forms of the antigen are recognised?
Peptides that are displayed by MHC molecules (MHC-associated peptide)
47
What subtypes of cells recognise which peptides?
- CD4+ helper T cells recognise peptide presented by MHC class II molecules - CD8+ cytotoxic T cells recognise peptide presented by MHC class II molecules
48
What is co-stimulation?*
- Once an antigen presenting cell captures microbe, expresses costimulatory protein

Infection (10 decks)

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