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My ESA 3 > Infection > Flashcards

Infection Flashcards

1
Q

What gram stain is Neisseria meningitidis?

A

Gram negative

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2
Q

What antibiotic would you use to treat meningitis in a middle aged person (~19)?

A

Ceftriaxone

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3
Q

Can you be a carrier of Neisseria meningitidis without having symptoms?

A

Yes, approximately 25% of the population are carriers

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4
Q

Define infection

A

An invasion of a hosts tissues by micro organisms

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5
Q

What 3 things may cause disease?

A

Microbial multiplication
Toxins
Host response

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6
Q

What is microbiotica?

A

The ecological community of commensal, symbiotic and pathogenic microorganism that literally share our body space. Are normally harmless, or even beneficial, but if transferred to other sites can be harmful.

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7
Q

Describe mechanisms of horizontal transmission

A

Contact
Inhalation
Ingestion

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8
Q

Describe mechanisms of vertical transmission

A

Mother –> child

Before or during birth

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9
Q

What are the processes involved in the initiation of infection?

A

Exposure, adherence, invasion, multiplication, dissemination

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10
Q

What are the patient factors that determine the effect of a disease on a person?

A

Site of infection

Co-morbidities e.g. Diabetes

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11
Q

What are the pathogen factors that determine the effect of a disease on a person?

A

Virulence factors (degree of damage caused to host)
Inoculum size
Antimicrobial resistance

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12
Q

What supportive investigations might you do for infections?

A

FBC - neutrophils, lymphocytes
C Reactive Protein CRP
Blood Chemistry - liver and kidney function tests
Imaging - X-ray, ultrasound, MRI
Histopathology
Bacteriology - swabs, fluids, tissues
MCS (Microscopy, Culture, antibiotic Susceptibility)
Antigen Detection
Nucleic Acid Detection
Virology - antigen, antibody, viral DNA/RNA Detection

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13
Q

What are the types of DNA viruses?

A

Single stranded non-enveloped
Double stranded non-enveloped
Double stranded enveloped

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14
Q

What are the types of RNA viruses?

A

Single stranded, positive strand, icosahedral, non-enveloped
Single stranded, negative strand, helical, enveloped
Single stranded, positive strand, icosahedral OR helical, enveloped
Double stranded, icosahedral, non-enveloped

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15
Q

What’s the difference between gram positive and negative bacteria?

A

Positive - thick peptidoglycan cell wall, retain crystal violet dye thus are purple
Negative - appear red, no thick peptidoglycan cell wall.

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16
Q

What’s the difference between mounds and yeasts?

A

Mounds are multicellular, whereas yeasts are single celled

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17
Q

What 2 main groups are parasites split into, and what defines them?

A

Protozoa - single celled

Helminths - multicellular (worms)

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18
Q

What are the classification categories for antibacterial agents?

A 
Bactericidal or bacteriostatic
Spectrum - 'broad' vs 'narrow' (but in reality there are lots in between)
Target site (mechanism of action)
Chemical structure (antimicrobial class)
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19
Q

What are the classification categories for antimicrobial agents?

A

Antibacterial
Antifungal
Antiviral
Antiprotozoal

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20
Q

What are the 6 ideal features of antimicrobial agents?

A 
Selectively toxic
Few adverse effects
Reach site of infection
Oral/IV formulation
Long half life (infrequent dosing)
No interference with other drugs
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21
Q

What are the classes of antibacterials?

A

Cell wall synthesis (beta-lactans, glycopeptides)
Protein synthesis (tetracyclines, aminoglycosides, macrolides)
Nucleic acid synthesis (quinolones)
Cell membrane function (polymixins)

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22
Q

What are the mechanisms of antibiotic resistance?

A 
Drug inactivating enzymes (produced by resistant organisms) e.g. Beta-lactamases, aminoglycoside enzymes
Altered target (target enzyme has lowered affinity for drug e.g. meticillin, macrolide resistance)
Altered uptake (decreased permeability e.g. Beta-lactams/increased efflux e.g. Tetracyclines)
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23
Q

What are the 2 mechanisms to measure antibiotic activity?

A

Disk testing

Minimum inhibitory concentration (gives numerical answer)

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24
Q

List 3 forms of bets-lactam drug

A

Penicillins
Cephalosporins
Carbapenems

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25
Q

List 2 types of penicillin (mainly active against streptococci) and what they’re notably active against

A

Amoxicillin- also has some activity against gram-negatives

Flucloxacillin - active against staphylococci and streptococci

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26
Q

What are penicillins mainly active against?

A

Streptococci

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27
Q

List 2 beta lactamase inhibitor combinations

A

Co-amoxiclav- active against gram negatives, staphylococci, streptococci and anaerobes.
Pipercillin/tazobactam - as above, only even better against gram negative, including pseudomonas

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28
Q

What are cephalosporins active against?

A

Generations with increased gram negative, or gram positives. Broad spectrum, but no anaerobic activity.

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29
Q

Give an example of a celhalosporin, and what it is used for

A

Ceftriaxone has good activity in the CNS, so if used for meningitis

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30
Q

Give an example of a meropenem

A

Meropenem

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31
Q

Give some features of meropenem

A

Very broad spectrum (including anaerobes). Active against most gram negatives, and generally safe in penicillin allergy

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32
Q

Give an example of a glycopeptide

A

Vancomycin

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33
Q

Give some features of vancomycin

A

Active against most gram positive. Not absorbed (oral for C. difficile only). Therapeutic drug monitoring required (narrow therapeutic window)
Some enterococci resistance, although resistance in staphs rare

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34
Q

Give an example of a tetracycline

A

Doxycycline

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35
Q

Give some features of doxycycline

A

Oral use only. Broad spectrum, but specific use in penicillin allergy, usually for gram positive. Active in atypical pathogens in pneumonia. Active against chlamydia and some protozoa. Shouldn’t be give to children <12yrs

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36
Q

Give an example of an aminoglycoside

A

Gentamicin

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37
Q

Give some features about gentamicin

A

Profound activity against gram negatives. Good activity in blood/urine. Potentially neohrotoxic/ototoxic. Therapeutic drug monitoring required. Generally reserved for severe gram negative sepsis

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38
Q

Give an example of a macrolide

A

Erythromycin

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39
Q

Give some features about erythromycin

A

Well distributed including intracellular penetration. Alternative to penicillin for mild gram positive infections. Also active against atypical respiratory pathogens

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40
Q

Give an example of a quinolone

A

Ciprofloxacin

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41
Q

Give some features of ciprofloxacin

A

Inhibits DNA gyrase. Very active against gram negatives. Also active against atypical pathogens. Increasing resistance and risk of c. Difficile

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42
Q

What is trimethoprim used for?

A

UTI

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43
Q

What is trimethoprim called when combined with sulphamethoxazole?

A

Co-trimoxazole

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44
Q

What is co-trimoxazole used for?

A

Used to treat PCP, and also has activity against MRSA

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45
Q

What are the 2 types of antifungal, and how do they work?

A

Azoles (inhibit cell membrane synthesis, active against yeast/moulds)
Polymers (inhibit cell membrane function)

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46
Q

Give an example of an azole antifungal drug, and what it’s used to treat

A

Fluconazole, used to treat candida

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47
Q

Give an example of an antiviral, how it works and what it’s used to treat

A

Aciclovir. Phosphorylation inhibits viral DNA polymerase, e.g. Herpes simplex

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48
Q

What is metronidazole active against?

A

Anaerobic bacteria and Protozoa.

Antibacterial and antiprotozoal agent

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49
Q

Define sepsis

A

A life threatening organ dysfunction due to a dysregulated hose response to infection. Mortality drastically changes for every hour it goes unnoticed

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50
Q

Define septic shock

A

Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation

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51
Q

What is bacteraemia?

A

The presence of bacteria in the blood (with or without clinical features )

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52
Q

What is a blanching rash?

A

It ‘disappears’ on pressure

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53
Q

What is septicaemia?

A

An outdated term for generalised sepsis

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54
Q

What are Early Warning Signs (EWS)?

A

Basic observations (RR, HR, BR, BP, Temp)

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55
Q

List some ‘red flags’

A

Unresponsive
Low BP
High RR

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56
Q

What is significant about ‘red flags’?

A

Immediate action is required - inform senior Dr, send urgent investigations, refer to ICU

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57
Q

What is the sepsis six?

A 
Oxygen
Blood cultures
IV antibiotics 
Fluid challenge
Lactate
Measure urine output
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58
Q

What investigations might you do for sepsis?

A 
FBC
Urea and electrolytes
Blood sugar
Liver function tests
CRP
Coagulation 
Blood gases
Other microbiology samples
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59
Q

What are the stages of the inflammatory cascade?

A

Local - endotoxins bind to macrophages. Cytokines and tissue necrosis factors and interleukins e.g. TNF-alpha, stimulates inflammatory response and recruits RE system
Systemic - Cytokines released into circulation, stimulates growth factors, macrophages and platelets
Sepsis - infection is not controlled. Cytokines lead to activation of humoral cascades and RE system. Circulatory insults, DIC and organ injury.

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60
Q

How does sepsis effect coagulation?

A

Cytokines initiate production of thrombin and thus promote coagulation
Cytokines inhibit fibrinolysis
Coagulations cascade leads to microvascular thrombosis, hence organ iscaemia, dysfunction and failure
Microvascular injury is the major cause of shock and multiorgan failure

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61
Q

What is the major cause of shock and multiorgan failure in sepsis?

A

Coagulations cascade activation, leads to microvascular thrombosis, hence organ iscaemia, dysfunction and failure.

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62
Q

What are the factors effecting the outcome of an infection?

A

Infectivity of pathogen, virulence/mechanism of infection, patients immune response, management

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63
Q

Define immune system

A

Cells and organs that contribute to immune defences against infectious and non-infectious conditions (Self Vs Non-Self)

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64
Q

Define infectious disease

A

When the pathogen succeeds in evading and/or overwhelming the hosts immune defences

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65
Q

What are the roles of the immune system?

A

Pathogen recognition
Containing/eliminating the infection
Regulating itself - minimum damage to hose, stop when done
Remembering pathogens - immunisation

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66
Q

Describe some basic futures of innate immunity

A

Fast, non specific, no memory, no change in intensity

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67
Q

Describe some basic futures of adaptive immunity

A

Slow (days), specific, immunologic memory, changes in intensity (differentiates between cell types)

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68
Q

What are the first immunological line of defences?

A 
Physical barriers (skin, mucous membranes, bronchial cilia)
Physiological barriers (diarrhoea, vomiting, coughing, sneezing)
Chemical barriers (low pH, antimicrobial molecules e.g. Lysozyme, IgA, gastric acid, pepsin, beta-defensins)
Biological barriers (normal flora - compete with pathogens, and produce antimicrobial chemicals and vitamins)
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69
Q

Describe what the immunological first line of defence is

A

Factors that prevent entry and limit growth of pathogens

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70
Q

What might happen if normal flora are depleted by antibiotics? Give examples

A

Succumb to disease as no pathogenic organisms no longer contained as normal flora are depleted
E.g. Sever colitis (clostridium difficile)
Thrush (Candida albicans)

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71
Q

What is the second immunological line of defence?

A

Phagocytes/chemicals. Inflammation (to contain and clear the infection)
Phagocyte - microbe interaction. The recognition process, then killing of infectious microbe.

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72
Q

What do dendritic cells do?

A

Present antigens to T cells. Part of acquired immune system

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73
Q

What are PAMPs? What are they used for?

A

Pathogen Associated Molecular Patterns
E.g. Carbohydrates, lipids, proteins, nucleic acids.
Used for recognition of pathogens by binding to Pathogen Recognition Receptors (PRRs) on phagocytes

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74
Q

What are PRRs

A

Pathogen Recognition Receptors

On phagocytes, enable recognition of pathogen when PAMPs bind

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75
Q

What is opsonisation?

A

Enhanced attachment of phagocytes and defence microbes (e.g. C3b, C4b. Antibodies IgG, IgM)

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76
Q

What do acute phase proteins do? Give 2 examples

A

They are essential in clearing encapsulated bacteria e.g. Neisseria meningitidis, streptococcus pneumoniae
E.g. C-reactive protein CRP
Mannose-binding lectin (MBL)

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77
Q

What are the stages of phagocytosis?

A

Recognition, Engulfment, Degradation,

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78
Q

What are phagocytes killing mechanisms?

A

Oxygen dependent pathway - toxic O2 products e.g. H2O2 produced (respiratory burst)
Oxygen independent pathway - lysozyme, lactoferrin/transferrin, cationic proteins, proteolytic and hydrolytic enzymes

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79
Q

How many serum proteins are there in the complement system? Which are the most important?

A

20 serum proteins

C1-C9 most important

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80
Q

What are the 2 activating pathways for the complement system?

A

MBL pathway - initiated when MBL binds to mannose containing residues of proteins, found on many microbes (e.g. Salmonella spp, Candida albicans)
Alternative pathway - initiated by cell surface microbial constituents (e.g. Endotoxins on E. Coli)

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81
Q

What do C3a and C5a of the complement system do?

A

Recruitment of phagocytes

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82
Q

What do C3b - C4b of the complement system do?

A

Opsonisation of pathogens

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83
Q

What do C5 - C9 of the complement system do?

A

Killing of pathogens (membrane attack complex)

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84
Q

What type of cell is reduced in number when small/no spleen is present?

A

Neutrophils

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85
Q

What does the 1 st line of deference against pathogens do?

A

Limits entry and growth of pathogens at portals of entry

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86
Q

What does the 2nd line of defence against pathogens do?

A

Contains and eliminates infection

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87
Q

What do macrophages do?

A

In all organs. Phagocytise microbes and parent antigens to T cells. Produce cytokines and chemokines.

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88
Q

What do monocytes do?

A

Circulate in blood. Recruited to infection site and differentiate into macrophages.

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89
Q

What do neutrophils do?

A

Increased during infection. 60% of blood leukocytes, recruited by chemokines. Ingest and destroy bacteria

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90
Q

What do basophils/mast cells do?

A

Early actors of inflammation (histamine!). Important in allergic responses.

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91
Q

What do eosinophils do?

A

Defence against multi-cellular parasites

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92
Q

What do natural killer cells do?

A

Kill abnormal host cells

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93
Q

What do dendritic cells do?

A

Present microbial agents to T cells (aquired immunity)

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94
Q

What is a ‘healthcare infection’?

A

Any infection which was acquired in association with healthcare - doesn’t have to be in a hospital. Includes workers and visitors.
Mustn’t have been present or incubating at time of admission (onset at least 48hrs after admission)

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95
Q

What are the 4 Ps of infection?

A

Patient
Pathogen
Practise
Place

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96
Q

Briefly explain ‘patient’ as one of the 4 Ps of infection.

A

General and specific patient risk factors. Interactions with other patients, healthcare workers, visitors.

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97
Q

Briefly explain ‘pathogen’ as one of the 4 Ps of infection.

A

Virulence factors. Ecological interactions (other bacteria, antibiotics/disinfectants)

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98
Q

Briefly explain ‘practice’ as one of the 4 Ps of infection.

A

General and specific activities of healthcare workers. Policies and their implementation. Organisational structure and engagement. Regional and national political initiatives. Leadership at all levels from government to the ward.

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99
Q

Briefly explain ‘place’ as one of the 4 Ps of infection.

A

Healthcare environment. Fixed and variable features. Toilets, hand wash basins, furniture cleaning, medical devices (single use), Positive/negative pressure rooms, theatres….

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100
Q

What does I-Five for infectious patients stand for?

A 
Identify
Isolate
Investigate
Inform
Initiate
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101
Q

What is the ONLY way to activate T cells?

A

Via an antigen presenting cell

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102
Q

What are the features of an antigen presenting cell?

A 
In a strategic location - B and T cell interaction (skin, mucous membranes, lymphoid organs, blood circulation)
Pathogen capture (phagocytosis, macropinocytosis soluble particles)
Diversity in pathogen sensors (PRRs) (extracellular/bacteria and intracellular/viral pathogens)
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103
Q

Name 4 types of antigen presenting cell

A

Dendritic cell
Langerhans cells
Macrophages
B cells (BCR)

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104
Q

Where are dendritic cells found?

A

Lymph nodes, mucous membranes, blood

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105
Q

To which cells do dendritic cells present antigens to?

A

T cells and B cells

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106
Q

Where are langerhans cells found?

A

Skin

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107
Q

To which cells do langerhans cells present antigens to?

A

T cells

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108
Q

Where are B cells found?

A

Lymphoid tissue

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109
Q

To which cells do macrophages present antigens to?

A

T cells

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110
Q

To which cells do B cells present antigens to?

A

T cells

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111
Q

What does PAMP stand for?

A

Pathogen associated molecular pattern

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112
Q

What does MHC stand for with regards to immunity?

A

Major histocompatibility complex

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113
Q

What are the two classes MHC can found, and where are they located?

A

Class 1 molecules - found on all nucleated cells

Class 1 molecules - found on dendritic cells, macrophages, B cells.

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114
Q

What can MHC (major histocompatibility complex) also be called?

A

Human Leukocyte Antigen (HLA)

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115
Q

What are the key features of MHC (class 1 and 2) molecules?

A

Co-dominate expression - both parental genes are expressed (increases number of different MHC molecules)
Polymorphic genes - different alleles among different individuals (increases presentation of different antigens/microbes)

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116
Q

What is the main function of MHC class 1 molecules?

A

Present peptides from intracellular microbes

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117
Q

What is the main function of MHC class 2 molecules?

A

Present peptides from extracellular microbes

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118
Q

What cells are responsive to MHC class 1?

A

CD8+ T cells

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119
Q

What cells are responsive to MHC class 2?

A

CD4+ T cells

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120
Q

What structural feature gives MHC molecules broad specificity? (Many peptides presented by the same MHC molecule)

A

Peptide binding cleft has a variable region with highly polymorphic residues

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121
Q

What is an MHC?

A

The protein on an antigen presenting cell, which actually presents the antigen to the WBC

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122
Q

How do MHC molecules effect susceptibility to infections?

A

Susceptibility to infections depends on the types of MHC molecules - e.g. Elite controllers of HIV

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123
Q

Why are some people ‘elite controllers’, or ‘long term nonprogressors’ for HIV?

A

Their MHC molecules present key peptides for the survival of the (unmutated) virus, so have an effective T cell response
Generally have a high CD4+ T cell count

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124
Q

What are possible clinical problems with MHC molecules?

A

Major cause for organ transplant rejection (HLA molecules mismatch between donor and recipient - graft versus host reaction)

HLA association and autoimmune disease - insulin dependent diabetes mellitus, ankylosing spondylitis

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125
Q

What is an allograft? I

A

A tissue/organ transplant from donor of the same species as recipient, but not genetically identical

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126
Q

Describe the process by which humoral immunity is initiated

A

Extracellular microbes (e.g. Bacteria, helminth, fungi…) are presented via exogenous pathways by MHC class 2 molecules to CD4+ T cells

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127
Q

Describe the process by which cell-dependent immunity is initiated

A 
Intracellular microbes (viruses, bacteria, protozoa) are presented via the exogenous or endogenous pathway by 
MHC class 1 molecules to CD8+ T cells, producing cytotoxic T cells
or by MHC class 2 molecules to CD4+ T cells, activating macrophages, B cells and complement
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128
Q

What do MHC class 1 cells activate?

A

CD8+ T cells, which activates cytotoxic T cells

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129
Q

What do MHC class 2 cells activate?

A

CD4+ T cells, which activate complement, B cells (antibody) ect

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130
Q

What must be activated before CD8+ T cells can be activated, leading to cytotoxic T cells?

A

CD4+ cells (aiding humoral immunity)

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131
Q

Where do T lymphocytes mature?

A

In the thymus

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132
Q

What antigen receptor do T lymphocytes use?

A

T cell receptor TCR

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133
Q

What causes TCR diversity in T lymphocytes?

A

Gene rearrangement

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134
Q

Name some types of T cells

A

CD3+, CD4+ (TH1, TH2, TH17 cells)

CD3+, CD8+ (cytotoxic T cells, CTL)

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135
Q

Can T lymphocytes form memory cells?

A

Yes

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136
Q

What cytokines do CD4+ TH1 (T lymphocyte) cells produce?

A

TNFalpha

IFNgamma

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137
Q

What cytokines do CD4+ TH2 (T lymphocyte) cells produce?

A

IL-4
IL-5
IL-10

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138
Q

What cytokines do CD4+ -TH17 (T lymphocyte) cells produce?

A

IL-17

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139
Q

What does a TCR (T cell receptor) do?

A

Antigen recognition

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140
Q

What does a CD3 molecule do on the surface of a T lymphocyte?

A

Co-receptor molecules, involved in signal transduction

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141
Q

What is costimulation?

A

Activation of naïve CD4+ T cells requires 2 stimulations, one antigen specific via TCR, the other is antigen nonspecific on membrane of APC

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142
Q

If an APC presents MHC to TCR on T cell, what’s its response?

A

Apoptosis, anergy

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143
Q

If an APC presents MHC to TCR on T cell, AND CD80/86 to CD28, what’s the T cells response?

A

Proliferation
Differentiation
Effector function

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144
Q

If an APC presents MHC to TCR on T cell, AND CD80/86 to CTLA-4 on T cell, what’s the T cells response?

A

Cell cycle arrest

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145
Q

What T cells deal with intracellular microbes?

A

TH1

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146
Q

What T cells deal with extracellular microbes?

A

TH2

TH17

147
Q

What do TH1, CD4+ cells do?

A

Enhance macrophage phagocytic activities
Cause isotope switching of B cells (IgG antibody production)
Aid CD8 cells

148
Q

What do CD8 cells do?

A

Stimulate cytotoxic T lymphocytes which bind to MHC1 on infected cells leading to their apoptosis via perforins/granzymes

149
Q

What do TH17 CD4+ cells activate when stimulated?

A

Neutrophils - phagocytosis

150
Q

What do TH2 CD4+ cells activate when stimulated?

A 
Eosinophils (killing of parasites)
B cells (antibody - phagocytosis, complement)
Mast cells (local inflammation, allergies IgE)
151
Q

What antibody forms the primary response?

A

IgM

152
Q

What antibody forms the secondary response?

A

IgG

153
Q

What are the functions of the antibody IgG?

A

Fc-dependent phagocytosis
Complement activation
Neonatal immunity
Toxin/virus neutralisation

154
Q

What are the functions of the antibody IgE?

A

Immunity against helminths

Mast cell degranulation (allergies)

155
Q

What are the functions of the antibody IgA?

A

Mucosal immunity

156
Q

What are the functions of the antibody IgM?

A

Complement activation

157
Q

What cells are involved with dealing with extracellular microbes/humoral immunity?

A

CD4+ TH2-TH17 cells

158
Q

What type of immunity deals with extracellular microbes?

A

Humoral immunity

159
Q

What type of immunity deals with intracellular microbes?

A

Cell-dependent immunity

160
Q

What cells are involved in cell-dependent immunity?

A

CD4+ TH1 cells

CD8+ T cells

161
Q

Define surface

A

An interface between a solid and either a liquid or gas

162
Q

What could body surfaces be?

A

Skin - epithelium, hair, nails

Mucosal surfaces - conjunctival, GI, respiratory, genitourinary

163
Q

What viruses may be commensals on the skin?

A

Papilloma, heroes simplex

164
Q

What gram positive bacteria may be commensals on the skin?

A

Gram positive Staph. Aureues (coagulase positive)
Gram positive Coagulase negative staphylococci
Gram negative enterobacteriaceae

165
Q

If a bacterium is coagulase positive, what does this mean?

A

Can initiate coagulation cascade. Used for identification. Useful to bacterium as walls it off from bloodstream/immune system

166
Q

What fungi may be commensals on the skin?

A

Yeasts e.g. Candida albicans

Dermatophytes (mounds, cause dematophytoses e.g. Ringworm, athletes foot)

167
Q

Give some mucosal flora examples for the eye

A

Coagulase negative staphylococci, Neisseria species, viridans group streptococci

168
Q

Give some mucosal flora examples for the nares (nostril)

A

Staph aureus

169
Q

Give some mucosal flora examples for the nasopharynx

A

Neisseria meningitidis, haemophilus influenzae, streptococcus pneumoniae

170
Q

Give some mucosal flora examples for the mouth

A

Viridans streptococci, Neisseria, bacteroides, clostridia, candida,

171
Q

Give some mucosal flora examples for the stomach

A

Helicobacter, streptococci, staphylococci, lactobacilli

172
Q

Give some mucosal flora examples for the intestine

A

Bacteroides, coliforms, aerobic and anaerobic streptococci, clostridium, yeasts, lactobacillus

173
Q

Give some mucosal flora examples for the urethra

A

Enterococci, lactobacilli, diptheroids, enterobacteriaceae

174
Q

Give some mucosal flora examples for the vagina

A

Lactobacilli, diptheroids, coagulase negative staphylococci, ureaplasmas, yeasts

175
Q

What are the possible mechanisms of microbiotica infection?

A

Invasion
Migration
Innoculation
Haematogenous

176
Q

Prosthetic valve endocarditis presenting less than a year after surgeries is usually caused by what type of organism?

A

Coagulase negative staphylococci

177
Q

Prosthetic valve endocarditis presenting more than a year after surgeries is usually caused by what types of organism?

A

Viridans strep, enterococcus faecalis, staph aureus, HACEK group, candida

178
Q

What sort of organism usually causes prosthetic joint infections?

A

Coagulase negative staphylococci

Staphylococcus aureus

179
Q

What sort of organism usually causes cardiac pacing wire endocarditis?

A

Coagulase negative stahpylococci

Staphylococcus aureus

180
Q

What are the major processes in the pathogenesis of infection at surfaces?

A

Adherence to host cells or prosthetic surface
Biofilm formation
Invasion and multiplication
Host response (pyogenic - neutrophils - pus, or granulomatous - fibroblasts, lymphocytes, macrophages - nodular inflammatory lesions)

181
Q

When are bio films produced?

A

When bacteria sense that other bacteria are nearby (by quorum sensing)
Otherwise too energy expensive to build

182
Q

Why is a biofilm beneficial to bacteria?

A

Provides a physical barrier to antibiotics/the immune system

183
Q

What does quorum sensing control?

A

Sporulation
Biofilm formation
Virulence factor secretion

184
Q

What are the principles of quorum sensing?

A

Signaling molecules - autoinducers
Cell surface or cytoplasmic receptors
Gene expression - cooperative behaviours and more autoinducer production

185
Q

Why is travel history so important with regards to infection?

A 
Recognising imported diseases (rare/unknown in the U.K.)
Infection prevention (on the ward and in the lab)
Different strains of pathogens (antigenically different, impacts on protection/detection, antibiotic resistance)
186
Q

What are some key aspects to a patients travel history?

A

Any unwell travel companions/contacts?
Pre-travel vaccinations/preventative measures?
Recreational activities?
Healthcare exposure?

187
Q

What are the 4 main species of plasmodium (which cause malaria)

A

Falciparum
Vivax
Ovale
Malariae

188
Q

Which species of malaria causes the most deaths?

A

Plasmodium falciparum

189
Q

What species of plasmodium are mostly found in Africa?

A

Falciparum (90% of African cases)

Malariae

190
Q

What type of plasmodium is commonest in west Africa?

A

Ovale

191
Q

What type of plasmodium is common in Asia and South America?

A

Vivax

192
Q

What is the vector used for malarial transmission?

A

Female anopheles mosquito

193
Q

Is there case to case spread in malaria?

A

No

Requires female anopheles mosquito as a vector

194
Q

What is the minimum incubation period for malaria?

A

6 days

Can be much longer (1yr+ for plasmodium vivax/ovale)

195
Q

What are some possible symptoms of malaria?

A

Fever, chills and sweats cycle (every 3rd or 4th day)
Cardiovascular - tachycardia hypotension, arrhythmias
Respiratory - ARDS (acute respiratory distress syndrome)
GIT - diarrhoea, deranged LFTs, bilirubin (haemolysis)
Renal - acute kidney injury
CNS - confusion, fits, (cerebral malaria)
Blood - low/normal WBC, thrombocytopenia, disseminated intravascular coagulation
Metabolic - metabolic acidosis, hypoglycaemia
Secondary infection

196
Q

What is ARDS?

A

Acute respiratory distress syndrome

Widespread inflammation of the lungs, occurring in critically ill patients

197
Q

What is thrombocytopenia?

A

A disorder in which there is a relative decrease of thrombocytes (also known as platelets) present in the blood.

198
Q

What investigations should be carried out for suspected malaria?

A 
Blood smear x 3
FBC
U&amp;Es
LFTs
Glucose
Coagulation
Head CT if CNS symptoms
CXR
199
Q

What treatment would you give a patient with malaria caused by plasmodium falciparum?

A

Artesunate,

Quinine and doxycycline

200
Q

What treatment would you give a patient with malaria caused by plasmodium vivax/ovale/malariae?

A

Chloroquine and primaquine
Hypnozoites
Be aware that it can recur months or years later

201
Q

What does the ABC for prevention of malaria stand for?

A

A - assess risk (knowledge of risk areas)
B - bite prevention (repellant, adequate clothing, nets. Chemoprophylaxis before travel, must include regular/returning travellers)
C - specific to region, start before and continue after return (generally for 4 wks)

202
Q

What other diseases may present similarly to malaria?

A

Typhoid, dengue, rickettsial, non-travel related e.g. Meningococcal septicaemia

203
Q

How is typhoid fever caught?

A

Fecal-oral route (via contaminated food and water)

204
Q

What type of organism is salmonella enterica (causing typhoid)?

A

Aerobic, gram negative, rod

205
Q

What is the incubation period for typhoid fever?

A

7-14 days

206
Q

What are the symptoms for typhoid fever?

A

Fever, headache, abdominal discomfort, constipation, dry cough, relative bradycardia

207
Q

Is typhoid, or parathyroid fever more severe generally?

A

Typhoid

208
Q

What investigations might suggest typhoid?

A

Raised LFTs (transaminase and bilirubin)
Moderate anaemia
Relative lymphopenia (decreased lymphocyte levels in blood)
Culture blood and faecea (serology)

209
Q

What is common treatment for typhoid?

A

Ceftriaxone of azithromycin 7-14days

210
Q

What prevention is available for typhoid fever?

A

Food and water hygiene!

Typhoid vaccine

211
Q

What possible dangerous complications may occur with typhoid?

A

Intestinal haemorrhage and perforation

212
Q

What could cause fever and a rash?

A

‘Childhood’ viruses - measles, rubella, parvovirus
Infectious mononucleosis (EVB/CMV)
Acute HIV infection
Rickettsia (spotted fever)

213
Q

What type of virus is Zika virus?

A

Arbovirus (flavivirus)

214
Q

How is Zika virus transmitted?

A

By the Andes mosquitoes

Sexually

215
Q

Is there any treatment/vaccine currently available for Zika virus?

A

No

216
Q

What effect can Zika virus have on a foetus?

A

Can cause congenital microcephaly, and foetal loss

217
Q

What is antigenic drift?

A

A mechanism for variation in viruses that involves the accumulation of mutations within the genes that code for antibody binding sites
(Influenza A, B and C)

218
Q

What is antigenic shift?

A

The process by which 2 or more different strains of a virus combine to form a new subtype having a mixture of the surface antigens of the 2 or more original strains
(Influenza A only, as it effects more than just humans)

219
Q

What type of DNA has a retrovirus got?

A

RNA

Converts this to DNA, and back again during replication process

220
Q

Outline the process of HIV replication (10 steps)

A

1 - Free virus
2- Binding and fusion - virus binds to CD4 molecule and 1 of two coreceptors (CCR5 or CXCR4), common on cell surface
3 - Infection - virus penetrates cell and empties contents into cell
4 - Reverse transcriptase - single strands of viral RNA are converted to double-stranded DNA by reverse transcriptase enzyme
5 - Integration - Viral DNA combined with cells own DNA by integrate enzyme
6 - Transcription - when infected cell divides, viral DNA is read, and long chains of proteins are produced
7 - Assembly - sets of viral protein chains come together
8 - Budding - Immature virus pushes out of cell, taking some cell membrane with it
9 - Immature virus breaks free of infected cell
10 - Maturation - protein chains in the new viral particle are cut by the protease enzyme into individual proteins that combine to make a working virus

221
Q

What are the stages of HIV infection?

A

Primary HIV infection - Asymptomatic or seroconversion (flu like symptoms). Normal CD4 count or temporary drop
Stage 1 - Asymptomatic, CD4 count >500
Stage 2 - Mild symptoms, CD4 count <500
Stage 3 - Advanced symptoms, CD4 count <350
Stage 4, or AIDS - Severe, or AIDS defining symptoms, CD4 count <200

222
Q

What are the possible symptoms of HIV infection?

A

Fever, weight loss, malaise, headache, sores, thrush/sores of mouth, rash, nausea, vomiting, HIV wasting syndrome…

223
Q

How is HIV transmitted?

A

Sex (of any kind)
Sharing of injecting equipment
Medical procedures - blood-blood products
Vertical transmission (birth, breastfeeding)

224
Q

What factors effect transmission of HIV/likelihood of infection?

A

Type of exposure
Viral level
Other STIs
Breaks in skin or mucosa

225
Q

What is the life expectancy of a person with HIV?

A

The same as the general population (77yrs) with appropriate medication

226
Q

How is HIV tested for?

A

HIV antigen and antibody detected
Test must be done 4-6wks post exposure (else may get false negative result)
Result given on same day as test. If negative, very accurate, but may give false positive so further testing needed to confirm.

227
Q

What should a patient do once they have been diagnosed with HIV?

A

Start HAART (antiretroviral treatment), regardless of CD4 count

228
Q

What are the aims of HIV treatment?

A 
Undetectable HIV load
Reconstituted immune system
Good quality of life
Normalised lifespan
Reduced risk of transmission
229
Q

What are the 3 targets in the HIV lifecycle targeted by drugs?

A

HIV attaching itself to CD4 cell and entering
HIV copies itself to make more viruses (in nucleus)
HIV grows mature (outside host cell) and goes off to invade more CD4 cells

230
Q

Why are 3 drugs taken for HIV?

A

Millions of virus made each day, so mutates very quickly. Can become resistant to drugs, so having 3 makes resistance harder to develop.

231
Q

What can you do if you have been exposed to HIV to reduce your risk of getting the disease?

A

PEP

Post exposure prophylaxis

232
Q

How may Hep B be transmitted?

A 
IVDU
Sexual contact
Vertical (mother - child/perinatal)
Long term household contacts
HCW via needlestick injuries (1:3 risk)
233
Q

What are the symptoms of Hep B?

A

Jaundice, fatigue, abdominal pain, anorexia, nausea, vomiting, arthralgia (joint pain)
Up to 50% with no/vague symptoms

234
Q

What is the incubation period for Hep B?

A

6wks - 6mths

235
Q

What is the usual outcome of Hep B?

A

Usually self heal within 6mths

236
Q

In what percentage of cases does Hep B become chronic?

A

6-10% of infected adults (more in infancy)

237
Q

What is the main mechanism of transmission for Hep A?

A

Fecal-oral

238
Q

What is the main mechanism of transmission for Hep E?

A

Fecal-oral

239
Q

What drugs would you prescribe to a HIV infected patient?

A 
2 X NRTI (e.g. Tenofovir, abacavir, lamivudine)
And 
NNRTI (e.g. efavirenz, nevirapine)
OR
Protease inhibitor (e.g. Darunavir, atazanavir)
OR
Integrase inhibitor (e.g. Raltegravir)
CCR5 (entry) inhibitor (e.g. Maraviroc)
240
Q

Can Hep A become chronic?

A

No

241
Q

Can Hep E become chronic?

A

No

242
Q

What will a patient with Hep Bs AST/ALT levels be?

A

In the 1000s (inflammatory response)

243
Q

Describe the serology of Hep B (order of which antigens/antibodies appear)

A 
1 - Surface antigen
2 - Followed by e-antigen
3 - Core antibody (IgM)
4 - Followed by e-antibody
5 - Surface antibody
6 - Core antibody (IgG)
244
Q

What is chronic Hep B infection?

A

Persistence of HBsAg after 6 months

245
Q

Is there a cure for Hep B?

A

Nope

246
Q

What treatment is used for chronic Hep B?

A

Lifelong antiretrovirals

Not required for everyone

247
Q

How is Hep C transmitted?

A 
IVDU
Crack or heroin smokers
Vertical transmission
Sexual contact
Needlestick injury
(Blood transfusion prior to 1991)
248
Q

What proportion of people infected with Hep C become chronically infected?

A

~80%

249
Q

What are some complications of chronic Hep C infection?

A

Chronic liver disease/cirrhosis, resulting in decompensated liver disease, hepatoma, transplant or death

250
Q

What are the symptoms of Hep C?

A

80% - no symptoms

20% - vague symptoms, fatigue, anorexia, dark urine, nausea, abdominal pain

251
Q

Is a cure available for Hep C?

A 
Yes!
£50,000 - £80,000 per course
8-12 weeks
Directly acting antiviral drug combo
No immunity, can be re-infected
252
Q

Is there a vaccine for Hep C?

A

No

253
Q

What is an outbreak?

A

2 or more cases of a disease linked in time and place

254
Q

What is an endemic disease?

A

The usual background rate of disease

255
Q

What is an epidemic?

A

A rate of infection greater than the usual background rate

256
Q

What is a pandemic?

A

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

257
Q

What is Ro?

A

The basic reproduction number (of a disease)

258
Q

What is the basic reproduction number of a disease?

A

The average number of cases one case generates over the course of its infectious period, in an otherwise uninflected non-immune population

259
Q

What happens if Ro > 1?

A

Increase in the number of cases of the disease

260
Q

What happens if Ro = 1?

A

Stables number of cases of disease

261
Q

What happens if Ro < 1?

A

Decrease in the number of cases

262
Q

What might be 3 reasons for outbreaks/epidemics/pandemics…?

A 
New pathogen (antigens, virulence factors, antibacterial resistance)
New hosts (non-immune, healthcare effects)
New practise (social, healthcare)
263
Q

What factors determine transmissibility of a disease?

A 
Infectious dose (number of microorganisms required to cause infection)
Epidemic curves (number of people infected at each time interval - susceptible, infected, recovered)
264
Q

What interventions can be made to reduce the transmission of disease?

A

Pathogen (+vector) - reduction or eradication
Patient - improved health/immunity
Practise - behavioural, change, protective, equipment
Place - environmental, engineering

265
Q

How might one reduce/eradicate a pathogen?

A

Antibacterials, including disinfectants. Decontamination, sterilisation

266
Q

How might one reduce/eradicate a vector?

A

Eliminate vector breeding sites

267
Q

How might one reduce a patients susceptibility to infection?

A 
Improve health (Nutrition, medical treatment)
Immunity (passive e.g. IV Ig, maternal antibody, or active e.g. Vaccine)
268
Q

How might one implement avoidance of a pathogen or vector?

A

Geographic - don’t go to areas with them
Protective clothing/equipment - e.g. long sleeves against mosquito bites. PPE in hospitals e.g. Gloves/mask
Behavioural - safe sex, disposal of sharps, food/drink prep

269
Q

How might environmental engineering help avoid transmission of disease?

A

Safe water, safe air, good quality housing, well designed healthcare facilities

270
Q

What are the possible good consequences of good infection control?

A

Decrease incidence or elimination of disease/organisms, e.g. Polio, smallpox, dracunculiasis

271
Q

What are the possible BAD consequences of good infection control?

A

Decreased exposure to pathogen, decreased immune stimulus, decreased antibody, increased susceptibles, outbreak.
Later average age of exposure, so increased severity of disease

272
Q

What are the consequences of antimicrobial resistance?

A

Treatment failure
Prophylaxis failure
Economic costs

273
Q

What is multi drug resistance (MDR)?

A

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

274
Q

What is extensive drug resistance (XDR)?

A

Non-susceptibility to at least one agent in all but 2 or fewer antimicrobial categories

275
Q

What is pan-drug resistance (PDR)?

A

Non-susceptibility to all agents in all antimicrobial categories

276
Q

What are the elements of an antimicrobial stewardship programme?

A

Multidisciplinary team and relationships to other quality/safety teams
Surveillance - process measures - outcome measures
Interventions - persuasive, restrictive, structural

277
Q

What is the ISDA definition for outcomes of antimicrobial stewardship?

A

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

278
Q

Who might feature in a multi-disciplinary team relevant to microbial resistance?

A 
Medical microbiologist/infectious diseases physician
Antimicrobial pharmacist
Infection control nurse
Hospital epidemiologist
Information system specialist
279
Q

What are the 3 antibiotic stewardship intervention types?

A

Persuasive - education, consensus, opinion leaders, reminders, audit
Restrictive - restricted susceptibility reporting, formulary restriction, prior authorisation, automatic stop orders
Structural - computerised records, rapid lab tests, expert systems, quality monitoring

280
Q

What are the requirements for successful antimicrobial stewardship?

A

Long term confirmed and appropriate resources
Hospital leadership support and delegated authority to challenge/change inappropriate antimicrobial therapy
Integration into organised patient safety and quality of care structure and processes

281
Q

What are the different types of acquired disease? VITAMIN NDEI

A 
Vascular 
Infective
Traumatic
Autoimmune 
Metabolic
Inflammatory 
Neurological 
Neoplastic 
Degenerative
Environmental 
Idiopathic
282
Q

What are the different types of congenital disease?

A

Genetic

Developmental

283
Q

What inheritance pattern does cystic fibrosis show?

A

Autosomal recessive

284
Q

What genetic defect is present in cystic fibrosis?

A

Defect in cystic fibrosis transmembrane conductance regulator gene (CFTR) in exocrine glands

285
Q

What is the most common version of cystic fibrosis?

A

AF50 (deletion of phenylalanine at position 508)

286
Q

Why does cystic fibrosis have an increased incidence of infection?

A

Defects in CFTR leads to defects in Cl- transmembrane transport
Mucus becomes dehydrated and thick, causing blockages of small ducts
Lung colonisation and infection with procession of different organisms
Lung damage - antibacterial and steroidal treatment

287
Q

What infections might a person with cystic fibrosis typically get?

A 
H. Influenzae
Staph aureus
Pseudomonas aeruginosa
Burkholderia cepcacia
Atypical mycobiotica
Cadida albicans
Aspergillus fumigatus
288
Q

Why is cystic fibrosis so common?

A

It is thought heterozygosity provides resistance to cholera, typhoid, TB….

289
Q

What is chronic obstructive pulmonary disease?

A

Chronic inflammatory response to inhaled irritants, primarily mediated by neutrophils and macrophages.
Breakdown of lung tissue (emphysema) and small airways disease (bronchitis)
Increases mucus production

290
Q

What bacterial organisms frequently cause acute exacerbation of COPD?

A

S. Pneumoniae, H influenzae, ps aeruginosa, moraxella catarrhalis, E. coli

291
Q

What viral organisms frequently cause acute exacerbation of COPD?

A

Respiratory syncytial virus, rhino virus, parainfluenza virus, coronavirus, adenovirus, influenza virus

292
Q

How does diabetes mellitus increase susceptibility to infection?

A

Hyperglycaemia and acidaemia impair humoral immunity and polymorphonuclear leukocyte and lymphatic functions.
Diabetic microvascular and macrovascular disease results in poor tissue perfusion and increased risk of infection.
Poor resistance to infection as poor neutrophil infiltration.
Diabetic nephropathy causes diminished sensation resulting in unnoticed skin

293
Q

What ENT infections are associated with diabetes?

A

Malignant or necrotising otitis externa. Pseudomonas aeruginosa.
Infection starts in the external auditory canal and spreads to adjacent soft tissue, cartilage and bone. Patients typically present with severe ear pain and otorrhoea

294
Q

What pathogen causes malignant or necrotising otitis externa?

A

Pseudomonas aeruginosa.

295
Q

Who is particularly susceptible to rhinocerebral mucormycosis?

A

Patients with poorly controlled diabetes, especially those with diabetic ketoacidosis

296
Q

What is rhinocerebral mucormyocosis?

A

Mould fungi organisms colonise the nose and paranasal sinuses, spreading to adjacent tissues by invading blood vessels and causing soft tissue necrosis by bony erosion.

297
Q

Why are patients with diabetes mellitus more susceptible to UTIs?

A

Neurogenic bladder due to diabetic neuropathy leads to defects in bladder emptying
Increased risk of asymptomatic bacteriuria and pyuria, cystitis and upper UTI
Enterobacteriaceae (e.g. E. coli), Ps aeruginosa

298
Q

What are common causative organisms for skin and soft tissue infections in patients with diabetes mellitus?

A 
Staph aureus (cellulitis, folliculitis)
Group A beta-haemolytic streptococcus (cellulitis)
Polymicrobial including the above, enterobacteriaceae, and various anaerobes (diabetic foot ulcers and necrotising fasciitis)
299
Q

What forms of infection is more common in patients with Down’s syndrome?

A

Respiratory tract infections (bacterial and viral)

Due to true immune deficiency or other factors unknown

300
Q

Describe how humoral immunity is effected in patients with Down’s syndrome

A

Decreased neutrophil and monocyte function (chemotaxis, phagocytosis, and the oxidative burst)
Normal numbers of neutrophils and monocytes
Lowered (in infants) or raised (in adults) immunoglobulin levels, in spite of normal B lymphocyte numbers
Normal or raised levels of serum IgA and secretory IgA in older Down’s syndrome patients
Lowered specific antibody responses upon immunisation
Normal or raised levels of C3, C4 and C5

301
Q

Describe how cellular immunity is effected in patients with Down’s syndrome

A

Alt red distribution of T cell populations (e.g. Lower CD4/CD8 ratio), but normal T cell numbers
Lowered T cell function including the response to specific antigens and some mitogens
Altered T cell intracellular signalling
Abnormal cytokine production
Lowering of some, but not all NK cell functions but increased numbers of NK cells

302
Q

Define hypersensitivity

A

The antigen-specific immune responses that are either inappropriate or excessive and result in harm to the host

303
Q

What are the common phases of a hypersensitivity reaction?

A 
Sensitisation phase (1st encounter with antigen)
Effector phase (clinical pathology upon re-exposure to the same antigen)
304
Q

What are the types of hypersensitivity reaction?

A

Type 1 or immediate (<30 min): Allergies. Environmental non infectious antigens (allergens)
Type 2 or antibody mediated (5-12hr): Tissue antigen
Type 3 or immune complexes mediated (3-8hr): Soluble antigen
Type 4 or cell mediated (24-48hr): Autoimmune. Environmental infectious agents and self antigens

305
Q

What phenotype is more prevalent in the westernised world (where children are not as exposed to ‘dirt’)?

A 
TH2 phenotype (IgE production)
Atrophy of immune components
306
Q

What phenotype is more prevalent in less developed countries (where children are as exposed to ‘dirt’)?

A

TH1 phenotype

307
Q

Describe what happens after the 1st exposure to an allergen

A

IgE mediated triggering of mast cell - direct activation of mast cell
Plasma cell - antigen specific IgE

308
Q

Describe what happens after the 2nd exposure to an allergen

A

Triggering release of granule contents - histamine, chemokines. Synthesis of new mediators (leukotrienes, prostaglandins)
Increases vascular permeability, vasodilators, bronchial constriction

309
Q

What may aid diagnosis of an allergy?

A

Blood/serum levels of - serum allergen IgE, serum mast cell products tryptase, histamine
Clinical history - atopy, allergens, seasonality, route of exposure
Skin prick tests (range of allergens) - Wheal and flare reaction (>3mm), no antihistamines
Challenge tests - food and drug allergy (slight risk of anaphylaxis)

310
Q

Describe the effect of enzyme mast cell mediators

A

Remodel connective tissue matrix

E.g. Tryptase, Chymase

311
Q

Describe the effect of toxic mast cell mediators

A

Toxic to parasites. Increase vascular permeability. Cause smooth muscle contraction
E.g. Histamine, heparin

312
Q

Describe the effect of cytokine Il-4/Il-3 mast cell mediators

A

Stimulate and amplify

TH2 cell response

313
Q

Describe the effect of cytokine Il-3/Il-5/GM-CSFmast cell mediators

A

Promote eosinophil production and activation

314
Q

Describe the effect of cytokine TNF-alpha mast cell mediators

A

Promotes inflammation, stimulates cytokine production by many cell types, activates endothelium

315
Q

Describe the effect of chemokine (e.g. CCL3) mast cell mediators

A

Attracts monocytes, macrophages and neutrophils

316
Q

Describe the effect of cytokine leukotrienes C4, D4, E4 mast cell mediators

A

Cause smooth muscle contraction. Increase vascular permeability. Stimulate mucus secretion

317
Q

Describe the effect of cytokine platelet activating factor mast cell mediators

A

Attracts leukocytes. Amplifies production of lipid mediators. Activates neutrophils, eosinophils and platelets

318
Q

How might allergic reactions manifest on the skin?

A

Urticaria, ‘Hives’ - itchy, raised rash

Mast cells in epidermis

319
Q

How might allergic reactions manifest in the face?

A

Angioedema in lips, eyes, tongue, and upper respiratory airways. Mast cells in deep dermis

320
Q

Describe some possible systemic manifestations of allergic reactions (anaphylaxis)

A 
Hypotension
Cardiovascular collapse
Generalised collapse
Generalised urticaria
Angioedema
Breathing problems
321
Q

What are the 3 rules of anaphylaxis?

A

Sudden onset
Progresses rapidly
Involves 2 or more organ systems

322
Q

Describe some possible symptoms of an allergic reaction

A

Swelling of conjunctiva
Runny nose
Swelling of lips, tongue and/or throat
Heart and vasculature - fast or slow HR, low BP
Skin - hives, itchiness, flushing
Pelvic pain
CNS - lightheadedness, loss of consciousness, confusion, anxiety, headache
Respiratory - shortness of breath, wheezes or stride, hoarseness, pain with swallowing, cough
GI - crampy, abdominal pain, diarrhoea, vomiting
Loss of bladder control

323
Q

How does adrenaline help with anaphylactic shock?

A

Reduces peripheral vasoconstriction, reduces oedema and hypotension
Reverses airway obstruction/bronchospasm
Increases the force of myocardial contraction
Inhibits mast cell activation

324
Q

What are some important points about giving adrenaline for anaphylactic shock?

A

Given intramuscularly IM
Timesaver - still need to get patient to ED
Multiple doses may be required

325
Q

How might allergy be managed?

A

Allergen avoidance/elimination - read food labels, avoid high risk situations
Education - recognise symptoms, use EPIPEN, schools/social activities
Medic alert identification
Drugs - antihistamines, corticosteroids, Anti-IgE, EPIPEN
Allergen desensitisation - specialist hospital based unit

326
Q

What is allergen desensitisation?

A

Involves the administration of increasing doses of allergen extracts over a period of years, given to patients by injection or drops/tablet under the tongue.
90% effective in patients with bee and wasp venom anaphylaxis

327
Q

What are possible mechanisms explaining how allergen desensitisation works?

A

CD4+ CD25 regulatory T cells
Shift from TH2 to TH1
Inhibitory anti-inflammatory cytokines
Allergen specific blocking IgG

328
Q

Define ‘immunocompromised host’

A

A state in which the immune system is unable to respond appropriately and effectively to infectious microorganisms, due to a defect in one of more components of the immune system.

329
Q

What causes a primary immunodeficiency?

A

Due to intrinsic gene defect, congenital. E.g. Missing protein, missing cell, non-functional components

330
Q

What causes secondary immunodeficiency?

A

Due to an underlying disease/treatment, acquired. E.g. Decreased production/function of immune components; increased loss or catabolism of immune components

331
Q

Who should you suspect of an immune deficiency? ‘SPUR’

A

Severe (death without treatment for illness)
Persistent
Unusual (site/location of infection or causative organism)
Recurrent

332
Q

What are the warning signs for recognition and diagnosis of PIDs?

A

4 or more new ear infections within a year
2 or more serious sinus infections within a year (absence of allergy)
2 or more months on antibiotics with little effect
2 or more pneumonias within a year, or pneumonia yr on yr
Failure of an infant to gain weight or grow normally
Failure to thrive (weight loss, chronic diarrhoea)
Recurrent thrush in mouth, or fungal infection of skin
Need for IV antibiotics to clear infections
2 or more deep-seated infections including septicaemia
Infection with normally harmless tuberculosis-like bacteria
Recurrent, deep skin of organ abscesses
Recurrent viral infections
Family history of PID

333
Q

What are the 3 most useful warning signs for PID?

A

Family history
Failure to thrive
Diagnosis of sepsis treated with IV antibiotics

334
Q

List some clinically significant predominantly antibody deficiencies

A 
X-linked agammaglobinanaemia - Brutons disease (BTK defect)
Autosomal recessive agammaglobinaemia 
Common variable immunodeficiency CVID
Selective IgA deficiency (majority asymptomatic)
IgG subclass deficiency (majority asymptomatic)
335
Q

List some clinically significant combined T and B cell deficiencies

A 
Severe combined immunodeficiency SCID (T cell deficiency)
Omenn syndrome (rare)
336
Q

List some clinically significant phagocytic defects

A

Chronic granulomatous disease
Severe congenital neutropenia
Cyclic neutropenia

337
Q

List some other clinically significant immunodeficiencies

A

Wiskott-Aldrich syndrome
DiGeorge syndrome
Hyper IgE syndrome
Ataxia-telangiectasia

338
Q

What immunodeficiency is the most prevelent?

A

CVID

339
Q

If symptom onset is under 6 months, what sort of immunodeficiency is likely?

A

Highly suggestive of a T cell or phagocyte defect

340
Q

If onset of symptoms is between 6months and 5yrs, what immunodeficiency is likely?

A

Suggestive of a B-cell/antibody or phagocyte defect

341
Q

What would a patient with a complement deficiency be susceptible to?

A

Bacteria - Neisseria sop, streptococci, haemophilus influenzae, other encapsulated bacteria

342
Q

What would a patient with a phagocyte deficiency be susceptible to?

A

Bacteria - staphylococcus aureus, pseudomonas aeruginosa, non-tuberculous mycobacteria
Fungi - candida spp, aspergillus spp

343
Q

What would a patient with a antibody deficiency be susceptible to?

A

Bacteria - streptococci, staphylocci, haemophilus influenzae, moraxella, catarrhalis, pseudomonas aeruginosa, mycoplasma, pneumoniae
Virus - enteroviruses
Protozoa - giardia lamblia

344
Q

What would a patient with a T cell defects be susceptible to?

A

Everything!
Bacteria - streptococci, staphylococci, haemophilus influenzae, moraxella, catarrhalis, pseudomonas aeruginosa, mycoplasma pneumoniae
Virus - all
Fungi - candida spp, aspergillus spp, cryptococcus neoformans, histoplasma capsulatum

345
Q

What sort of diseases might a patient with complement deficiency be more likely to present with frequently?

A

Pyogenic infections (C3), meningitis/sepsis/arthritis (C5-C9), angioedema (C1 inhibitor)

346
Q

What sort of diseases might a patient with phagocytic defects be more likely to present with frequently?

A

Skin/mucous infections, deep seated infections, invasive fungal infections (aspergillosis)

347
Q

What sort of diseases might a patient with antibody deficiency be more likely to present with frequently?

A

Bacteria, virus, protozoa. Sinorespiratory infections, arthropathies, GI infections, malignancies, autoimmunity

348
Q

What sort of diseases might a patient with T-cell defects be more likely to present with frequently?

A

Everything!

Death if not treated, failure to thrive, deep skin and tissue abscesses, opportunistic infections

349
Q

What supportive treatment might you give a patient with a primary immunodeficiency?

A 
Infection prevention (prophylactic antimicrobials)
Treat infections promptly and aggressively (passive immunisation)
Nutritional support (vitamins A and D)
Use UV-irradiated blood products only
Avoid live attenuated vaccines in patients with severe PIDs
350
Q

What specific treatment options might be available for patients with primary immune deficiencies?

A

Regular immunoglobulin therapy (IVOG or SCIG)

SCID - haematopoietic stem cell therapy (HSCT 90% success)

351
Q

What comobidities might be present alongside primary immune deficiencies?

A 
Autoimmunity and malignancies
Organ damage (lung function assessment)
Avoid non essential exposure to radiation
352
Q

What is the goal level of IgG in the blood during immunoglobulin replacement therapy?

A

Serum IgG more than 8g/l

353
Q

What is immunoglobulin replacement therapy?

A

Life long treatment given approximately every 3wks with the goal of maintaining serum IgG over 8g/l

354
Q

With what conditions might you give immunoglobulin replacement therapy?

A

CVID
XLA (Bruton’s disease)
Hyper-IgM syndrome

355
Q

What might result in decreased production of immune components, causing secondary immune deficiency?

A 
Malnutrition
Infection (HIV)
Liver disease
Lymphoproliferative disease
Splenectomy
356
Q

What do splenic macrophages do?

A

Removal of opsonised microbes, removal of immune complexes

357
Q

What might a spleenless patient be more suseptible to?

A

Blood borne pathogens - encapsulated bacteria (e.g. haemophilis influenzae, streptococcus pneumoniae, Neisseria meningitidis)

358
Q

What is OPSI?

A

Overwhelming post-splenectomy infection.

Sepsis and meningitis

359
Q

How do you manage a spleenless patient?

A

Penicillin prophylaxis (life long)
Immunisation against encapsulated bacteria
Medic alert bracelet

360
Q

Why do patients with haematological malignancy have increased susceptibility to infections?

A

Chemotherapy induced neutropenia
Chemotherapy induced damage to mucosal barriers
Vascular catheters

361
Q

What tests are there for cell mediated immunity?

A 
Lymphocyte count (FBC)
Lymphocyte subset analysis (CD4+, CD8+, T, NK, B, extended marker panels)
In vitro tests of T cell function
362
Q

What tests are there available for phagocytic cells?

A 
Neutrophil count (FBC)
Neutrophil function tests (e.g. Oxidative burst for CGD)
Adhesion molecule expression (for LAD)
363
Q

What tests are there for complement?

A

Individual components

Tests of complement function (CH50/AP50)

364
Q

What tests are there available for humoral (antibody) immunity?

A

IgG, IgM, IgA, (+-IgE)
IgG 1-4 subclasses
IgG levels to specific previous vaccines
Measure antibody in response to ‘test’ immunisation

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