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ESA3 > Infection And Immunity > Flashcards

Infection And Immunity Flashcards

1
Q

Name three modes of horizontal transmission.

A

Direct/indirect contact (incl. vectors)
Inhalation of droplets or aerosols
Ingestion (faecal-oral)

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2
Q

What is the difference between an exotoxin and an endotoxin?

A

Exotoxins- chemicals produced by microbes into the local environment.
Endotoxins- parts of micro organisms recognised by the body e.g. A
antigens.

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3
Q

Name some disease determinants.

A 
Virulence factors
Inoculum size 
Antimicrobial resistance 
Site of infection
Co-morbidities
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4
Q

Describe the main features of a virus.

A

Have nuclei can acid (RNA/DNA)
May have an envelope/capsule
Invade and multiply within host cells

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5
Q

What is a bacteriophage and what is its significance in antimicrobial resistance?

A

Viruses that can infect bacteria, thus permitting transfer of DNA between bacteria as a vector.

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6
Q

Name some virulence factors.

A

Host entry
Adherence
Invasiveness
Iron sequestration

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7
Q

Name some gram positive cocci.

A

Staphylococcus aureus
Streptococcus pneumoniae
Enterococcus faecalis

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8
Q

Name some gram positive bacilli.

A

Listeria monocytogenes

Bacillus anthracis

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9
Q

Name some gram negative cocci.

A

Neisseria meningitidis
Neisseria gonorrohoeae
Moraxella catarrhalis

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10
Q

Name some gram negative bacilli.

A 
E. Coli
Salmonella typhi
Pseudomonas aeruginosa
Haemophilus influenzae
Kleibsella pneumoniae
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11
Q

What investigations might you carry out for a suspected infection?

A 
Full blood count including neutrophils and lymphocytes 
C-reactive proteins
Liver and kidney function
Imaging e.g. CXR
History theology
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12
Q

How can we classify antimicrobials?

A

They can be classified as bactericidal or bacteriostatic, by spectrum, target site or chemical structure.

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13
Q

What are the ideal features of an antimicrobial?

A 
Selectively toxic
Reach site of infection
Have few adverse side effects
Long half life (infrequent dosing)
No cross-reactivity with other drugs
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14
Q

What is the action of beta-lactams?

A

Prevent cell wall synthesis by blocking bacterial cross-linking proteins.

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15
Q

Name four types of beta-lactams with examples of each.

A

Penicillins e.g. Amoxicillin
Cephalosporins e.g. Cefalexin, Ceftriaxone
Carbapenems e.g. Meropenem
Combination with a beta-lactamase inhibitor e.g. Co-amoxiclav

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16
Q

What is the action of glycopeptides?

A

Affect cell wall synthesis by preventing the binding of cross-linking proteins e.g. Vancomycin

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17
Q

Name the classes of antibiotics that affect protein synthesis.

A

Tetracyclines e.g. Doxycycline
Aminoglycosides e.g. Gentamicin
Macrolides e.g. Erythromycin

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18
Q

What is the mechanism of action of quinolones?

A

Bonds two nuclear enzymes thus inhibiting DNA replication and nucleic acid synthesis e.g. Ciprofloxacin

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19
Q

Name the two classes of antifungals and their action.

A

Azoles inhibit cell membrane synthesis e.g. Fluconazole

Polyenes inhibit cell membrane function e.g. Nystatin, Amphoteracin

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20
Q

What is the action of the antiviral Aciclovir?

A

Inhibits viral DNA polymerase when phosphorylated.

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21
Q

What is the mechanism of action of Oseltamivir (Tamiflu)?

A

Inhibits viral neuraminidase.

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22
Q

What classes of antibiotics may you use for a gram positive infection?

A

Beta-lactams
Glycopeptides
Macrolides
Tetracyclines

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23
Q

What classes of antibiotics might you use for a gram negative infection?

A

Beta-lactams
Aminoglycosides
Quinolones

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24
Q

What are the mechanisms of antimicrobial resistance?

A

Drug inactivation by enzymes
Altered target site
Altered drug uptake e.g. Decreased permeability or increased active reflux

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25
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome
Requires 2 or more of:
Temperature below 36 degrees or above 38
Heart rate greater than 90bpm
Respiratory rate greater than 20 breaths per minute
WBC count less than 4x109L or greater than 12

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26
Q

What is sepsis?

A

SIRS and a documented/presumed infection

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27
Q

What is severe sepsis?

A

SIRS + organ dysfunction/hypoperfusion

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28
Q

What is septic shock?

A

Severe sepsis and persistent low blood pressure despite IV fluid resuscitation

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29
Q

What is the mechanism that brings about septic shock?

A

Binding of endotoxins to macrophages activates cytokines that in turn activate the inflammatory response.
Failure to restore homeostasis and activation of humoral cascades leads to circulatory insult.

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30
Q

Why is there a risk of thrombosis in septic shock?

A

Cytokines also initiate production of thrombin and inhibit fibrinolysis, thus promoting coagulation

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31
Q

What are the sepsis six?

A

To be delivered in one hour:
High flow rate oxygen
Blood and other cultures to be taken
Empirical IV antibiotics e.g. Ceftriaxone
Measure serum lactate
IV fluid resuscitation
Urine output measurement (catheterisation)

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32
Q

What are complications of sepsis?

A 
Irreversible hypotension
Respiratory failure
Renal failure
Raised intercranial pressure 
Ischaemic necrosis
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33
Q

Define the immune system.

A

Cells and organs that contribute to immune defences against infectious and non-infectious conditions and organisms.

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34
Q

Roles of the immune system?

A

Pathogen recognition
Killing/clearance mechanisms
Regulating itself to minimise damage to host
Remembering pathogens to prevent recurrence

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35
Q

Give four examples of barriers that prevent entry and limit growth of pathogens?

A

Physical barriers e.g. Skin, mucus membranes
Physiological barriers e.g. Diarrhoea, vomiting
Chemical barriers e.g. Low pH, IgA
Biological e.g. Normal flora

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36
Q

What steps are involved in pathogen recognition?

A

Pathogen associated molecular patterns (PAMPs) detected by pathogen recognition receptors (PRRs) and opsonisation (enhanced attachment of phagocytes).

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37
Q

Give examples of opsonins.

A

Complement factors e.g. C3b
Antibodies e.g. IgG, IgM
Acute phase proteins e.g. CRP

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38
Q

Describe oxygen dependent and independent mechanisms of phagocytosis:

A

Oxygen dependent respiratory burst using hydrogen peroxide

Oxygen independent e.g. Lysozyme, lactoferrin and proteolytic enzymes

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39
Q

Define infection:

A

Invasion of host tissues by microbes and disease caused by multiplication, toxins or the host response.

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40
Q

Why do you get a fever with infection?

A

TNF-alpha, IL-1 and IL-6 act on the hypothalamus to increase body temperature

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41
Q

Why might an individual have reduced ability for phagocytosis?

A

Decreased splenic function
Decreased neutrophils
Decreased neutrophil function e.g. Chronic granulomatous disease (no resp burst) and Chediak-Higashi syndrome (no phagolysosomes)

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42
Q

Define a healthcare infection:

A

Neither present or incubating at time of admission, onset 48hrs post-admission e.g. Norovirus, MRSA, C. diff

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43
Q

How can we prevent healthcare related infections?

A

Activities of healthcare workers e.g. PPE
Virulence factors
Healthcare environment e.g. Sterile
General and specific risk factors
Interactions with healthcare workers and other patients e.g. Isolation

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44
Q

Name some APC in the adaptive immune system:

A

Dendritic cells, langerhans cells, macrophages, B cells

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45
Q

How are antigens presented to lymphocytes?

A

Presented by Major Histocompatibility Complex e.g. HLA

  • class I on all nucleated cells present intracellular antigens
  • class II on dendritic, macrophage and B cells present extracellular antigens
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46
Q

Describe the antigen processing pathways:

A

Endogenous: virus attaches to LMP2 with antigenic peptide which leads to presentation of MHC I

Exogenous: exogenous antigen undergoes phagocytosis and is then passed on to MHC II

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47
Q

Describe features of T lymphocytes:

A

T cell receptors have alpha and beta chains responsible for antigen recognition
Produced in bone marrow and mature in thymus
CD4+ activate helper cells and produce TNF-alpha/ILs
CD8+ activate cytotoxic T cells and T killer cells

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48
Q

Describe features of B lymphocytes:

A

Undergo isotope switching to produce IgG antibodies

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49
Q

Why are B cells crucial for the immune response?

A

IgGs produce a faster and longer response in future infections and produce a stronger and higher affinity response

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50
Q

Describe the function of each antibody type:

A

IgG- complement activation, opsonisation for phagocytosis, neonatal immunity, toxin neutralisation
IgE- mast cell degranulation, immunity against helminths
IgA- mucosal immunity
IgM- complement activation

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51
Q

What are the main features of malarial infection?

A

Plasmodium falciparum/vivax/ovale/malariae
Vector is the female anopheles mosquito
No case-to-case spread
Incubation period of 1-3 weeks

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52
Q

What are the symptoms of malaria?

A

Fever, chills, night sweats cycle, may have splenomegaly due to increased RBC lysis (malarial trophozoite infiltrates)
Sever malaria may cause CVS symptoms, ARDS, AKI, cerebral malaria etc.

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53
Q

What investigations should be carried out if you suspect malaria?

A 
3x blood smears
Full blood count
Urea and electrolyte analysis
LFTs
Glucose
Coagulation
CXR
54
Q

Treatment of malaria:

A

For plasmodium falciparum: quinine/artemisinin

Other: chloroquine/primiquine

55
Q

Features of typhoid:

A 
Salmonella enterica typhi/paratyphi
Faecal-oral contamination 
Produces endotoxin VI antigen 
Fimbriae allow bacteria to adhere to epithelium (Peyer's patches)
7-14 day incubation period
56
Q

Symptoms of typhoid:

A

Fever, headache, abdominal discomfort, constipation, dry cough, bradycardia, intestinal haemorrhage/perforation

57
Q

Typhoid treatment:

A

Ceftriaxone or azithromycin

58
Q

Dengue fever features:

A

Arbor virus from insects
4 serotypes
Lasts 1-5 days

59
Q

Symptoms of Dengue fever:

A

Macular rash with areas of confluence
Abrupt onset
Severe myalgia
Retro-orbital headache

60
Q

Features of Leigonnaire’s disease:

A 
Legionella pneumophilia 
Gram negative atypical pneumonia
Transmitted by aerosolised infected water
Invades and replicates in macrophages
Treat with fluoroquinolones/macrolides
61
Q

What is a retrovirus?

A

RNA virus that produces DNA in CD4 cells leading to new viral RNA cells

62
Q

What is the mechanism of HIV?

A

Binds and fuses with CD4 cells
Reverse transcriptase produces DNA from viral RNA
Integrase Enzyme incorporates viral DNA into cell DNA
Transcription produces new viral RNA
New RNA buds off and matures using cleavage with protease enzymes

63
Q

How does HIV progress in a host?

A

Initial infection causes period of seroconversion where body attempts to amount an immune response
This is followed by a period of latent infection that can last years
An individual will then become symptomatic as their CD4 count drops and virus is reactivated
When the CD4 count is below 200 it becomes AIDS

64
Q

Features of human immunodeficiency virus?

A

Associated with MSM, subsaharan africa, IVDU, poverty and social circumstances
Transmitted sexually, by sharing infected equipment and vertically

65
Q

Tests for HIV:

A 
HIV Antigen 
HIV antibody (may get false negative)
Rapid tests (may get false positives)
66
Q

Common HIV related infections:

A 
PCP pneumonia
Meningitis 
Kaposi's sarcoma
Candidiasis 
Shingles
Cancers e.g. Lymphoma
67
Q

Why are 3 drugs used at the same time to treat HIV?

A

The virus mutates very quickly and can become resistant to one drug

68
Q

Hepatitis B features:

A

Transmission by blood/sex/vertically
Incubation period of 6 weeks to 6 months
Infection cleared in 6mths giving lifelong immunity unless chronic

69
Q

Symptoms of hepatitis:

A

Jaundice, fatigue, abdominal pain, arthralgia, anorexia, nausea, vomiting

70
Q

Progression of hepatitis B infection:

A 
Surface antigen 
E antigen 
IgM
E antibody 
Surface antibody
IgG (indicates chronic infection)
71
Q

Features of hepatitis C:

A

Transmitted by blood/sexual partners, IVDU particularly at risk
Leads to chronic liver disease
Has vague symptoms- fatigue, anorexia, dark urine, RUQ abdominal pain

72
Q

Define microbiota:

A

Ecological community of commensal, symbiotic and pathogenic microorganisms that literally share our body space

73
Q

Common skin commensals:

A

Herpes simplex virus
Staph aureus
Enterobactericaeae

74
Q

Common mucosal flora:

A

Neisseria meningitidis
Streptococcus pneumoniae
Viridans streptococci
Lactobacillus

75
Q

Give examples of some external surface infections:

A

Cellulitis, pharyngitis, gastroenteritis, UTI, pneumonia

76
Q

Examples of internal surface infections:

A

Endocarditis, vasculitis, septic arthritis, osteomyelitis, empyema

77
Q

How do you develop prosthetic valve endocarditis?

A

Endothelium peeled off due to turbulent flow over abnormal heart valves
Bacteria settle on sub-endothelial tissues e.g. Viridans strep, staph aureus
Vegetative embolism can lead to local abscesses if broken off into circulation

78
Q

Pathogenesis at surfaces?

A

Adherence using pili
Biofilm formation- active secretion of mucopolysaccharides
Invasion and multiplication
Host response may be pyogenic, granulomatous

79
Q

Prevention of surface infections:

A

Maintain barrier integrity, prevent surface colonisation and remove colonising bacteria.
Prevent contamination of prosthetics, inhibit surface colonisation and remove colonising bacteria

80
Q

What is hypersensitivity?

A

Antigen-specific immune responses that are either inappropriate or excessive and result in harm to host.
Have sensitisation phase and an effector phase.

81
Q

Types of hypersensitivity response:

A

I: immediate reaction, allergy, IgE mediated
II: antibody mediated IgG, IgM
III: immune complex mediated, IgG and IgM
IV: cell mediated, T cells and macrophages

82
Q

Mechanism of mast cell activation:

A

Mast cells located near blood vessels and on mucosal surfaces
Plasma cells produce allergen-specific IgE
Binds to complementary receptor on mast cells
IgE cross linking activates mediator release (histamine, leukotrienes, prostaglandins)

83
Q

Define anaphylaxis:

A

The systemic activation of mast cells leading to hypotension, cardiovascular collapse, generalised urticaria, angioedema and breathing problems.

84
Q

Management of hypersensitivity allergies:

A 
Allergen avoidance 
Education
Medic alert identification 
Drugs e.g. Antihistamines, corticosteroids 
Allergen desensitisation
85
Q

What is meant by endemic disease?

A

The usual background rate of cases of a disease

86
Q

What quantifies an outbreak?

A

Two or more cases linked in time and place

87
Q

What is meant by epidemic?

A

Rate of infection greater than the usual background rate

88
Q

What is a pandemic?

A

Very high rate of infection spreading across many regions, countries and continents

89
Q

What is the basic reproduction number?

A

Average number of cases that one case generates over the course of its infectious period in an otherwise unaffected non-immune population

90
Q

Reasons for outbreaks:

A

New pathogen (antigenic drift/shift)
New hosts
New practice

91
Q

What is a potential consequence of poorly controlled infection prevention?

A

Decreased exposure leads to a decreased immune stimulus in individuals who then have an increased susceptibility to the disease and a later age of exposure e.g. Congenital rubella syndrome

92
Q

Define MDR:

A

Non-susceptibility to at least one agent in three or more antimicrobial categories

93
Q

Define XDR:

A

Non-susceptibility to at least one agent in all but two or fewer antimicrobial categories

94
Q

Define PDR:

A

Non-susceptibility to all agents in all categories

95
Q

Objectives of antimicrobial stewardship:

A

Appropriate use of antibiotics
Optimal clinical outcomes
Minimise toxicity and adverse effects
Reduce costs of healthcare for infections
Limit selection for antimicrobial resistant strains

96
Q

Examples of persuasive intervention:

A

Education, consensus, opinion leaders, audit and feedback

97
Q

Examples of restrictive intervention:

A

Restricted susceptibility reporting, formulary restriction, prior authorisation, automatic stop orders

98
Q

Examples of structural intervention:

A

Computerised records, rapid lab tests, expert systems, quality monitoring

99
Q

How are chronic diseases related to infection risk?

A

Chronic diseases cause a change on structure/function of affected tissues and organs that may change the interaction between patient and microbes

100
Q

Common infections in cystic fibrosis patients:

A

H. Influenzae, Staph. Aureus, pseudomonas aeruginosa, aspergillus fumigatus

101
Q

Why is pseudomonas aeruginosa difficult to treat?

A

It is mucoid and can produce vast amounts of mucopolysaccharide

102
Q

Why are patients with COPD at increased susceptibility to respiratory infection?

A

Increased mucus production and damage to mucociliary escalator prevents removal of pathogens from lower respiratory tract

103
Q

Why are diabetic patients at increased risk of infection?

A

Hyperglycaemia and acidaemia impair humoral immunity and lymphocyte functions
Poor tissue perfusion and neuropathy results in unnoticed skin

104
Q

What is malignant otitis externa?

A

Pseudomonas aeruginosa infection of external auditory canal that spreads to adjacent soft tissue cartilage and bone causing severe ear pain and otorrhoea

105
Q

What is rhinocerebral mucormyosis?

A

Caused by colonisation of the nose and paranasal sinuses with moulds spreading to adjacent tissues via invading blood vessels causing soft tissue damage, necrosis and bony erosion

106
Q

What is meant by immunodeficiency?

A

State in which the immune system is unable to respond appropriately and effectively to infectious microorganisms

107
Q

Features of immunodeficiency-related infections:

A

SPUR

severe, persistent, unusual, recurrent

108
Q

What is the difference between primary and secondary immunodeficiency?

A

Primary means there is an intrinsic defect, secondary means there is an underlying disease or condition affecting immune components

109
Q

What is common variable immunodeficiency?

A

Inability of B cells to mature into plasma cells so very little IgG can be produced

110
Q

What is X-linked agammaglobulinaemia?

A

X-linked genetic condition in which there is impaired B cell development

111
Q

What causes IgA deficiency?

A

Inability of B excels to switch to IgA production

112
Q

What is hyper IgM syndrome?

A

Defective CD40 ligand on at cells so B cells cannot switch to IgG, only IgM can be produced

113
Q

How may immunodeficiency conditions present?

A

Recurrent URT/LRT infection, GI complications, arthropathies, hides, increased incidence of autoimmune disease, lymphoma

114
Q

How are B cell deficiencies managed?

A

Prophylactic antibiotics
Immunoglobulin replacement therapy
Avoidance of radiation

115
Q

What is Leukocyte adhesion deficiency?

A

Lack of CD18 protein so phagocytes cannot adhere to endothelium and therefore cannot migrate

116
Q

What is chronic granulomatous disease?

A

Lack of respiratory burst

117
Q

How to phagocyte deficiencies present?

A

Prolonged and recurrent infections

118
Q

How would you manage a patient with a phagocyte deficiency?

A

Prophylactic antibiotics, antifungals agents, immunisation, interferon-G, steroids, stem cell transplantation

119
Q

What is Di George syndrome?

A

Defect in thymus embryogenesis leading to incomplete development affecting T cells.

120
Q

Severe combined immunodeficiency includes what two conditions?

A

Stem cell defects and Omenn’s Syndrome

121
Q

What causes severe combined immunodeficiency?

A

Defect in gamma chain used by receptors leads to inactive T cells.
Defect in ADA/PNP leads to death of developing thermocytes.
Defect in genes critical for TCR rearrangement and maturation.

122
Q

What is the presentation of SCID?

A

Failure to thrive, deep skin and organ abscesses, low lymphocyte count and infectious susceptibility

123
Q

How are T cell deficiencies managed?

A

Aggressive treatment and prevention of infection, no live vaccines, irradiated CMV-blood, bone marrow/stem cell transplant

124
Q

What condition is caused by a complement C1 inhibitor deficiency?

A

Hereditary angioedema

125
Q

What are the roles of the spleen?

A

Antibody production IgM and IgG
Splenic macrophages phagocytose opsonised microbes
Clearance of blood-borne pathogens esp. encapsulated bacteria

126
Q

How are asplenic patients managed?

A

Penicillin prophylaxis, immunisation against encapsulated bacteria and medic alert bracelet

127
Q

Why might patients with a haematological malignancy be at greater risk of infection?

A

Chemotherapy-induced neutropenia
Chemotherapy-induced damage to mucosal barrier
Vascular catheters e.g. Hickman line

128
Q

What are the features of Neisseria Meningitidis?

A

Gram negative diplococcus
Spread by aerosols and nasopharyngeal secretions
Causes non-blanching purpura, neck-stiffness, fever and headache

129
Q

Escherichia Coli features?

A

Gram negative bacillus
Faecal-oral transmission
Causes gastroenteritis/severe food poisoning
Treated with fluoroquinolones/azithromycin

130
Q

What are the features of Streptococcus pneumoniae?

A

Gram positive
Biggest cause of community-acquired pneumonia
Can cause meningitis in children and the elderly
Transmitted as aerosols or droplets
Treated with amoxicillin

131
Q

What are the features of clostridium difficile?

A

Gram positive bacillus
Associated with treatment with beta-lactams
Produces glycosyltransferases that inactivate GTPases
Faecal-oral transmission
Treated with metronidazole/vancomycin

132
Q

What are the features of staphylococcus aureus?

A

Gram positive
Positive for catalase and coagulase
MRSA strains
Standard treatment is penicillin

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