Lecture 1: Acute & Chronic Infections Flashcards

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1
Q

What role do N-formylated peptides have in Neutrophil Signalling?

A

They play a major role as potent chemoattractants

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2
Q

What are N-formylated peptides recognised by?

A

Recognised by the macrophage

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3
Q

Where do N-formylated peptides originate from?

A

Degraded bacterial proteins

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4
Q

What changes occur in macrophages to allow for engulfing?

A

Changes in actin filaments

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5
Q

How do antigen presenting cells act?

A

Presenting antigenic determinants to T cells via MHC II proteins

(communication between T-helper and macrophage)

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6
Q

How do antigen presenting cells become effective ‘killers’?

A

They become up-regulated

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7
Q

What is involved in the acute response to infection?

A

Hypothalamus - fever, re-setting body temperature
Brain - somnulence

Vascular permeability changes - hypotension & shock
(tight junctions between blood capillaries opening up)

Mobilisation of WBC - neutrophilia
(from the bone marrow)

Enhancement of neutrophil killing mechanism

Release of acute phase proteins from liver

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8
Q

What are the characteristics of the chronic response to infection?

A

Muscle and fat mobilisation - weight loss
(chronic bacterial infections are a catabolic process)

Fibroblasts stimulated - healing and repair

(continued release of acute phase proteins)

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9
Q

What are the components of acute phase proteins and what is the role of each?

A

C-reactive protein, mannose binding lectin and fibrinogen

Mannose binding lectin: binds non-specifically to the surface of bacteria - aids phagocytic process

C-reactive protein: marker of the response to infection

Fibrinogen: increases erythrocyte sedimentation rate

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10
Q

What is the cause of the increased erythrocyte sedimentation rate in the acute response to infection?

A

Fibrinogen binds to red blood cells and causes them to sediment faster

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11
Q

What are the differences between the 3 complement activation pathways?

A

Classical pathway: antigen-antibody complexes (pathogen surfaces)

MB-lectin pathway: mannose-binding lectin binds mannose on pathogen surfaces

Alternative pathway: pathogen surfaces

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12
Q

What marker drives a pathogen for phagocytosis?

A

C3b

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13
Q

What do C3a and C5a do in the complement activation pathway?

A

Peptide mediators of inflammation

Phagocyte recruitment

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14
Q

What does C3b do in the complement activation pathway?

A

Binds to complement receptors on phagocytes

Opsonization of pathogens

Removal of immune complexes

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15
Q

What do the terminal complement components do?

A

Membrane-attack complex

Lysis of certain pathogen and cells

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16
Q

What do Mannose binding lectin binding sites recognise?

A

D-mannose
L-fucose
N-acetylglucosamine

17
Q

What does Mannose binding lectin bind with?

A

MBL binds with high affinity to mannose and fucose residues with correct spacing

18
Q

How much do C-reactive protein levels increase within hours of inflammation? And what it the increase induced by?

A

Increase up to 10,000 fold

Indue by infection or injury

19
Q

What are the rough baseline levels of C-reactive protein naturally circulating?

A

Low levels

20
Q

What is bacteraemia?

A

The presence of bacteria in the blood

21
Q

What are the 3 types of bacteraemia?

A

Transient: lasts less than 20 mins

Intermittent: implying an extravascular source

Continuous: implying intravascular source (growing within circulatory system)

22
Q

What is the normal range of bacteria in a bacteraemic patient?

A

20-50/ mL

23
Q

How are blood cultures taken?

A
  1. Inform patient of procedure
  2. Apply tourniquet and select vein for puncture
  3. Wash hands using alcohol hand rub and clean puncture site with alcohol wipe
  4. Enter being within palpating site again
24
Q

What are the different types of growth media for blood cultures?

A

Blood in 5% CO2
Blood agar anaerobic
Chocolate agar in 5% CO2
Enteric agar for coliforms
Sensitivity agar (antimicrobial sensitivity)

25
Q

What is the process of gaining a positive blood culture sample?

A

Sample is inoculated into bottle and incubated.

Signal received of a positive test (changes in pH, CO2 production, absorbance)

Sample removed from positive bottle

Sample gram stained

26
Q

What would be an indication of a gram-positive cocci?

A

Dark blue/ violet in colour

27
Q

What type of bacteria is gram positive?

A

Streptococcal

28
Q

What type of bacteria is gram negative?

A

Meningococcus

29
Q

What would be an indication of a gram-negative bacteria?

A

Pink in colour

30
Q

What is bacterial endocarditis?

A

Physical damage to the value endothelium

31
Q

What is bacterial endocarditis caused by?

A

Occurs by blood turbulence or the impact of micro-particles

32
Q

What is deposited in the blood as a result of bacterial endocarditis? What can occur as a result of the deposits?

A

Fibrin and platelets

Bacteria passing by in the blood can attach to and colonise the deposits

33
Q

What do bacteria in a valve give rise to?

A

Local pathology (local tissue damage)

Distant pathology due to septic emboli

Immune response (continued bacteraemia)

Untreated can cause death

34
Q

What is prosthetic valve endocarditis?

A

Bacteria can be introduced at the time of operation

The infection may manifest weeks or months after the opeation

35
Q

What can prosthetic valve endocarditis be divided into?

A

Early: < 1 year

Late: > 1 year

36
Q

What is the process of blood culturing for endocarditis?

A

3-4 blood sets are collected from different sites

37
Q

How is a positive test identified with continuous bacteraemia?

A

When 7/8 bottles are positive within 2 days

Antibiotic sensitivity tests are then conducted

38
Q

What antibiotics are commonly used in endocarditis?

A

Bacteria commonly sensitive to penicillin

Benzylpenicillin (4-hourly) AND Gentamicin (2-4 weeks)

Vancomycin and teicoplanin (glycopeptides): streptococcal and staphylococcal endocarditis (penicillin allergy)

39
Q

What ae the signs bacterial endocarditis is being overcome?

A

Patient’s temperature returns to normal

Return of C-reactive protein and erythrocyte sedimentation rate