Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 - Clinical Science and Professionalism > Bacterial infections in the immunocompromised > Flashcards

Bacterial infections in the immunocompromised Flashcards

1
Q

When should you think “could this patient have an immune deficiency”

A
  • every patient who has an infection

- every infection can be viewed as a failure of the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

for the majority of infections…

A

there is a reasonable explanation why the infection occurred e.g.

  • Cellulitis - dry skin, infection as portal of energy
  • UTI - urinary stasis
  • LRTI - architectural or cilia issues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When do you investigate further for immune deficiency

A
  • Consider an immune defect in all patients with infections but particularly in those with infections that are
  • recurrent
  • severe
  • unusual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

one aspect of the immune system will…

A

affect susceptibility to some but not all micro-organisms thus if you have one defect of the immune system you might only be defect to some infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

multiple …

A

immune defects can and often do co-exist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a pathogen

A

a micro-organism that causes disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a commensal organism

A
  • A microorganism that derives benefit from another organism without causing damage
  • e..g Staphylococcus epidermises, pneumocystis jiroveci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a primary pathogen

A

An organism that can cause disease in a healthy host

e. g.
- staphylococcus aureus , Streptococcus pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is an opportunistic pathogen

A
  • Pathogen that is generally only able to cause disease in the setting of a weakened immune system and which rarely cause disease in healthy individuals
    E.g.
  • Staphylococcus Epidermidis, Pneumocystis Jiroveci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is primary immunodeficiency

A
  • Immune defect that the patient is born with
  • often due to genetic mutation
  • often but not always manifest in childhood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is secondary immunodeficiency

A

Immune defect that is associated with or related to another condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the types of secondary immunodeficiency

A
  • Iatrogenic

- Non-iatrogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is an Iatrogenic immunodeficiency

A
  • Immune suppression due to treatment for another condition e.g. steroids, chemotherapy, biologics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a non-iatrogenic immunodeficiency

A

Immune suppression related to a disease process

  • cancer
  • diabetes
  • malnutrition
  • infections e.g. HIV, sepsis, post measles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the basics of the immune system

A
  • Physical barriers - Skin and mucous membranes
  • Innate immune system - phagocytes and complement cascade
  • Humeral immunity - B cells and antibodies
  • Cell mediated immunity - T cells and cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main function of physical barriers

A

Prevent the invasion of micro-organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name the main physical barriers

A

Skin

  • low pH
  • low free water
  • antimicrobial peptides
  • cell sloughing

Gut Mucosa

  • low pH
  • antimicrobial peptides
  • cell sloughing
  • commensal flora
  • tight junctions

Respiratory tract

  • ciliated epithelium
  • antimicrobial peptides
  • cell sloughing
  • resident commensals

Urinary tract

  • urethral sphincter
  • one way flow
  • antimicrobial peptides
  • cell sloughing

Vagina

  • Commensal flora
  • pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What can damage the skin and cause entrance to bacteria

A
  • Surgery, cannula, burns, trauma

Which organisms

  • Skin flora
  • perineal flora
  • environmental usually by inoculation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can damage the gut mucosa and what organisms infect it

A
  • Chemotherapy, broad spectrum antibiotics (alter the normal flora of the GI tract)
  • translocation of normal commensal flora ( gram negative, candida, anaerobes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What can damage the respiratory tract and which organisms can infect it

A
  • Intubation
  • commensals from the respiratory tract and upper GI
  • e.g. S.aureus, gram negative, candida
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What can damage the urinary tract and which organisms can infect it

A
  • urinary catheter

- perineal flora (gram-negative, candida)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What can damage the vaginal mucosa and which organisms can infect it

A
  • Broad spectrum antibiotics

- candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can you prevent damage to physical barriers

A
  • prevent surgical site infection
  • prevent line infection = preparation, inspection, care
  • catheter associated infection - insertion, secure, need
  • ventilator associated pneumonia - PPI, position, cuff
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you recognise a pathogen

A
  • Pathogen recondition receptors such as TLRs and C-type Lectins recognise PAMPs which are present on pathogens therefore recognise the pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Phagocytes express..

A

receptors for and can be activated by complement and antibodies - tis links together different aspects of the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the main role of phagocytes

A
  • defect against extracellular pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does a phagocyte kill pathogens

A

Phagocytosis and intracellular killing
- Phago-lysosmoe fusion and reactive oxygen specific

Release of extraceullar substances
- antimicrobial peptides, NETs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the problems associated with phagocyte

A

defects in numbers or function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are primary problems associated with phagocytes

A
  • Chronic granulomatous disease

- defects in neutrophil migration and granule release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are secondary problems associated with phagocytes

A
  • Disease related e.g. AML, Aplastic anaemia, diabetes
  • Chemotherapy-associated neutropenia
  • impaired neutrophil function e.g. corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the impact of phagocyte issues

A
  • Increased susceptibility to range of infections

Bacterial
- often associated with breaches in cutaneous and mucosal integrity - gut commensals, line infections, wound infection

Fungal

  • candida from GI tract
  • Aspergillus from the air
32
Q

How do you manage phagocytes

A
  • lower index of suspicion for infection
33
Q

What are the pathways in the complement system

A
  • Classical pathway
  • mannose binding lectin pathway
  • alternative pathway
34
Q

What is the classical pathway

A

C1q binds to antibody-antigen complex

35
Q

What is the mannose binding lectin pathway

A
  • Binds to repeating sugars
36
Q

What is the alternative pathway

A

failure to inactivate the intrinsic activation

37
Q

What is the role of the complement system in immunity

A
  • trigger other aspects of the immune system - mainly against bacteria
  • kill pathogens
38
Q

What are the three ways the complement system responds

A
  • Opsonisation - complement receptors on phagocytes
  • chemotaxis - complement receptors on phagocytes
  • Direct killing - C5-9 membrane attack complex
39
Q

What are primary complement problems

A
  • defect in amount and or function of complement components
40
Q

What are secondary complement problems

A

Eculizumab

  • monoclonal antibody vs C5
  • used for PNH and acute rejection

Autoantibodies e.g. in myeloma

41
Q

What happens if the complement pathway doesn’t work

A
  • There is a high degree of redundancy in immune pathways around initial immune recognition and immune activation
  • the overall impact of complement defects is limited
  • defective membrane attack complex is associated with significantly increased risk of Neisseria meningitides infection
42
Q

How does the humeral immunity system responds to pathogens

A
  • Activated B cells produce antibodies

Binding of antibodies to the antigen leads to

  • neutralisation - block binding of pathogens to cels
  • complement activation - antigen-Antibody complexes bind to C1q which triggers the classical complement cascade
  • opsonisation - Fc portion of the antibody recognised by receptors on phagocytes which leads to increased phagocytosis
  • Antibody dependent cytotoxicity: Fc portion of antibody is recognised by NK cells which leads to release of pre-formed granules leading to death of the target cell
43
Q

What are the types of antibody binding

A
  • blocking
  • CDC
  • ADCC
  • opsonisation and phagocytosis
44
Q

What is the main roles of humoral immunity

A

Enhanced killing of extracellular pathogens

  • Bacteria and fungi
  • parasites (IgE vs multi-cellular helminths)
  • +/- virally infected cells
45
Q

What causes primary humoral immune defects

A
  • Range of primary immunodeficiencies associated with impaired humoral immune response
  • SCID, CVID, IgA deficiency
46
Q

What are the causes of secondary humoral immune defects

A
  • Disease related: CLL
  • treatment related: corticosteroids, rituximab
  • transplantation: Solid and stem cell
  • splenectomy
47
Q

What organisms tend to evade phagocytosis and complement

A
  • Streptococcus pneumonia
  • haemophilus influenza
  • Neisseria meningitis

these are encapsulate organisms meaning that they have a thick capsule which helps them avoid phagocytosis and complement

48
Q

What does IgA deficiency predispose to

A
  • Prediposes to GI infection such as Protozoa (Giardia and cryptosporidium), Bacteria (e.g. Campylobacter) and viruses (e.g. Norovirus)
49
Q

How do some cells evade the immune system

A

Cover themselves in carbohydrate capsule

  • so no peptide is available
  • these are encapsulated bacteria
  • essentially invisible to T cells as they only recognise peptides
50
Q

T cells can only recognise..

A

Peptides - so T cells can only help B cells when the antigen is a peptide

51
Q

How have B cells evolved to recognise carbohydrate capsule pathogens

A
  • subset of B cells have evolved to recognise the repeating carbohydrate motifs that make up the capsule of these bacteria
  • they are able to be activated without T cell help
  • T cell independent
52
Q

Where do the subset of B cells live that can recognise carbohydrate covered pathogens

A
  • They live in the marginal zone of the spleen and are called splenic marginal zone B-cells
53
Q

What happens to individuals with no spleen

A
  • individuals with no spleen or with a spleen that doesn’t work will not have any splenic marginal zone B cells
  • so therefore they are at increased risk of infection due to encapsulated organisms (S.pneumo, HiB, N.men)
  • they are also at risk of more severe infection due to a number of other pathogens e.g. Capnocytophaga, babesiosis and malaria
54
Q

What are the two types of T cells

A
  • T helper cells - CD4+

- Cytotoxic T cells - CD8+

55
Q

What are the difference between the two types of T cells

A

T helper cells

  • recognise antigen presented by APC using MHC II antinges from pathogens that have been phagocytksed
  • e.g. antigens from pathogens that have been phagocytosed

Cytotoxic T cells
- recognise antigens presented by any cell type using MHC I molecules e.g. antigens from within cell cytsole and are designed to detect intracellular pathogens such as viruses

56
Q

How do T cells recognise pathogens

A
  • Naive T cells become activated when they recognise there antigen that matches their specific T cell receptor
  • T cells require a 2nd single which includes other receptors expressed on the surface of the APC, or cytokines within the localenvironemtn
  • the balance of factors at the time the the naive T cel encounters its antigen will either promote or inhibit activation of naive T cells
57
Q

What does a TH1 cell do

A

Stimulate APC to kill intra-cellar pathogens by enhancing phagolysosome fusion, production of ROS etc
e.g. TB, salmonella, histoplasmosis, leishmania, toxoplasma

58
Q

What does a TH2 cell do

A

Stimulate B cells to make antibodies to act against extracellular pathogens

59
Q

What does a TH17 cell do

A

Stimulate epithelial cells to produce antimicrobial peptides to counter pathogens encountered at epithelial and mucosal surfaces
e.g. the skin and respiratory tract

60
Q

What do CD8 cells do

A

Kill human cells that are expressing non self antigens including

  • antigens derived from pathogens that are infecting and replicating inside the human cell e.g. viruses
  • antigens derived from aberrant host cell pathways e.g. malignancy
61
Q

What are the mechanisms of CD8 cells killing pathogens

A
  • Perforin - makes spores in the cell membrane

- Fas ligand - induces apoptosis

62
Q

What are the primary cell mediated immune defects

A
  • Most are combined immune deficiencies as T cells are important for B cell development e.g. SCID, IgM, Di-Geroge
63
Q

What are the secondary cell mediated immune defects

A
  • Disease related: Infection (HIV), malignancy
  • treatment related - anti-rejection mediation, steroids, Anti-TNF, stem cell transplant, radiotherapy
  • malnutrition
64
Q

what is the main driver of rejection in a solid organ transplant initially

A

cell mediated immunity

- mainly via presentation of non self MHC to CD4+ T helper cells by APC and B cells

65
Q

Describe the order of rejection from the immune system in a solid organ transplant

A

Initially cell mediated immunity
- mainly via presentation of non self MHC to CD4+ T helper cells by APC and B cells

T cell activation is followed by secretion of cytokines, chemokine and adhesion molecules to promote local inflammation
- this leads to immune mediated damage of the graft

66
Q

What is the main target of anti-rejection therapies

A

Main target is the removal or inhibition of T cell activation

  • Anti-thymocyte globulin (ATG) and anti-lymphocyte globulin (ALG)
  • anti- CD52 - alemtuzumab
67
Q

name the anti rejection therapies that are used in solid organ transplantation

A

Inhibition of T cell activation

  • anitmetabolites - azathioprine and mycphenolate
  • these interfere with DNA synthesis in lymphocytes

Calcineurin inhibitors

  • tacrolimus and cyclosporine
  • these interference with cell signalling in T cells

mTOR inhibitors

  • Limus and everolimus
  • interfere with cell signalling in T cells

Inhibition of co stimulation (IL-2 signalling)
- belatacept

Corticosteroids

68
Q

Why does immune suppression occur with haemipoietic stem cell transplant (HSCT)

A
  • the underlying condition being treated e.g. aplastic anaemia or AML
  • chemotherapy to treat the underlying condition prior to HSCT
  • chemotherapy to get risk of the current immune cells int he recipient so that the incoming donor stem cells are not rejected
  • prevention and treatment of the graft v host
69
Q

what are the three main time periods in HSCT

A
  • Pre engraftment - transplantation to approximately day 30 - immune system suppressed enough to have the transplantation occur
  • Early post-engraftment - from engraftment to day 100 - this is when the transplanted cell begin to make cells
  • Late post-engraftment - after day 100
70
Q

What are the infection risks in an allogenic stem cell transplant

A
  • transplanted cells come rom someone else

- vulnerable to infection from all three time periods

71
Q

What are the infection risk sin the autologous stem cell transplant

A
  • Transplanted cells come from the patient
  • no risk of graft versus host disease
  • risk of infection due pre engraftment and early post-engraftment
72
Q

what are the main issues in pre-engraftment in HSCT

A
  • mucositis
  • lines
  • neutropenia
  • and lymphopenia which arises in day 30
73
Q

What are the main issues in early post-engraftment in HSCT

A
  • ongoing lymphopenia

- development of graft versus host disease

74
Q

What are the main issues in late post-engraftment in HSCT

A
  • Slow recover of T and B cells

- graft versus host disease and requirement of immunosuppression

75
Q

What do you take in a history of someone who has an immunodeficiency

A

History of pressing complaint

  • details of current and past immuno suppression
  • details and timing are important - when was the transplant, what immunosuppression drugs are Theon
  • prior infection and microbiology results
  • vaccines and prophylaxis and are they taking the prophylaxis
  • co-mordbities and current medication
76
Q

How do you investigate immunodeficiency

A
  • routine - FBC, U+E, LFT, CRP

Microbiology and virology
- blood cultures - ideally 2 sets, ideally from the lumen of any line and peripheral

  • urine
  • resp viral PCR

others directed by symptoms and signs
- stool sample
fungal biomarkers

Imaging
- as directed by signs and symptoms

77
Q

How can you prevent an person with immunosuppression from becoming ill

A
  • treat the immunodeficiency or try to reduce it
  • replacement what is missing - e.g. immunoglobulin replacement
  • try to generate a protective response to pathogens the patient may be at risk of acquiring - immunise the patient ideally before the immunosuppression occurs

Year 3 - Clinical Science and Professionalism (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions