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Infection Flashcards

0
Q

In what ways can you get an infection?

A

Directly from a source
Indirectly from a source via an intermediary (vector) or the environment (water, air, food, surfaces)
Directly from animals
From the patient themselves (microbiota= commensals)

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1
Q

What is infection?

A

The invasion of a hosts tissues by micro organisms causing disease

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2
Q

What are microbiotae/ commensals?

A

Microorganisms carried on skin and mucosal surfaces that are normally harmless or even beneficial, but can be harmful and cause disease if and when they are transferred to other sites

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3
Q

What are some methods of horizontal transmission?

A

Contact- direct, indirect and vectors

Inhalation- droplets (influenza) and aerosols (TB, chickenpox - spreads vastly)

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4
Q

What are some methods of vertical transmission?

A

Mother to child

Before or at birth

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5
Q

What 5 stages are involved in how microorganisms cause disease?

A 
Exposure
Adherence 
Invasion
Multiplication
Dissemination
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6
Q

What are some virulence factors of infection?

A

Exotoxins - cytolytic, AB toxins, super antigens, enzymes

Endotoxins

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7
Q

What are virulence factors?

A

Molecules expressed and secreted by pathogens that enable them to achieve Exposure, Adherence, Invasion, Multiplication and Dissemination and cause host cellular damage

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8
Q

What are the 4 P determinants of disease?

A

Pathogen (virulence factors, inoculum size (dose), antimicrobial resistance (antibiotics))
Patient (site of infection, comorbidities)
Practice
Place

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9
Q

What precedent would you follow to find out whether a patient has an infection?

A

History
Examination
Investigation

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10
Q

What history would you take of a patient you’re suspecting of having an infection?

A

Symptoms
- focal (specific), systemic (not specific)
- severity
- duration
Potential exposures
- e.g. Travel- where? what? who with? animals involved?

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11
Q

What main examination would you do on a patient you’re suspecting of having an infection?

A

Check for organ dysfunctions

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12
Q

What investigations would you do on a patient you’re suspecting of having an infection?

A

Specific
- looking at microorganisms directly
Supportive
- full blood count - neutrophils and lymphocytes
- C Reactive Protein
- blood chemistry- liver and kidney function tests
- imaging - x ray, ultrasound, magnetic resonance imaging (MRI)
- histopathology
—-> virology - antigen detection, antibody detection, detecting viral nucleic acid (DNA/RNA)
—-> bacteriology - specimen types (swabs, fluids, tissues), MC&S microscopy (bacterial and patient cells), culture, antibiotic susceptibility

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13
Q

What’s a pathogen?

A

Disease causing microorganism

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14
Q

Briefly describe viruses

A

10^-8 - 10^-7 m
Spikes- for attaching to specific surfaces
Envelopes
Protein coats (protects and organises)
Can be antigens - immune response promoted, facilitates viral entry into cell

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15
Q

What is the Baltimore classification of viruses?

A 
I dsDNA 
II ssDNA 
III dsRNA 
IV (+)ssRNA , (-)ssRNA 
V (-)ssRNA 
VI ssRNA- RT DNA RNA dsDNA
VII ds-DNA-RT

–> mRNA

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16
Q

Briefly describe bacteria

A

10^-6 - 10^-5m
Pilii, cell wall, capsule, cytoplasm, plasma membrane, plasmid, nucleoid, ribosomes, flagellum

Coccus- (circular) Stapphy (clusters) Strepty (chains)
Spirillus- (spiral)
Bacillus- rods

Gram positive
Gram negative

Aerobes (obligate)
Anaerobes (obligate)
*exception of obligate anaerobe - require O2 free environment for survival –> spores - survive at high temperature, pressure etc, don’t cause disease as spores

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17
Q

What is the pathogenesis of bacteria?

A

Virulence factors
- host entry (polysaccharide capsule)
- adherence to host cells (Pilii, fimbriae)
- invasiveness (collagenases)
- iron sequestration
Toxins- exo (diphtheria) endo (lipopolysaccharide)

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18
Q

Briefly describe fungi

A 
Yeasts (single celled) 
- Candida albicans (thrush) 
- cryptococcosis neoformans (trees)
- pneumocystis jiroveci
Moulds (multicellular) 
- aspergillus species (bread) 
- dermatophytes (ringworm, athletes foot)
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19
Q

Briefly describe parasites

A 
Protozoa (single celled) 
- gardia lamblia (diarrhoea) 
- cryptosporidium parvum (diarrhoea) 
- plasmodium falciparum (malaria) 
- trypansosoma cruzi 
Helminths (worms, multicellular)
- roundworms (enterobius vermicularis)
- tapeworms (taenia saginata)
- flukes (schistosoma mansoni)
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20
Q

What does Coccus mean?

A

Round bacteria

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21
Q

What does stapphy- mean?

A

Clusters of cocci bacteria

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22
Q

What does strepto- mean?

A

Chains of cocci bacteria

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23
Q

What does spirillus mean?

A

Spiral bacteria

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24
Q

What does bacillus mean?

A

Rod shaped bacteria

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25
Q

What is an example of a single-stranded, non-enveloped DNA virus?

A

Parvovirus 19

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26
Q

What are some examples of double-stranded, non-enveloped DNA viruses?

A

Adenovirus
BK virus
Human papilloma virus
JC virus

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27
Q

What are some examples of double-stranded, enveloped DNA viruses?

A

Herpes virus
Hepatitis B
Molluscum contagiosum

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28
Q

What are some examples of single-stranded, positive, icosahedral, non-enveloped RNA viruses?

A 
Coxsackievirus
Echovirus
Enterovirus
Hepatitis A & E
Norovirus
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29
Q

What are some examples of single-stranded, positive, icosahedral or helical, enveloped RNA viruses?

A 
HIV 
Hepatitis C
Rubella virus
Encephalitis viruses
Yellow fever virus
West Nile virus
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30
Q

What are some examples of single-stranded, negative, helical, enveloped RNA viruses?

A

Ebola, Lassa, Marburg
Influenza, Parainfluenza
Respiratory syncytial virus (RSV)

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31
Q

What is an example of a double-stranded, icosahedral, non-enveloped RNA virus?

A

Rotavirus

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32
Q

Describe parvovirus

A 
Single stranded 
Non enveloped 
DNA virus
Child hood rash
Slap cheek syndrome
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33
Q

Describe adenovirus

A 
Double stranded
Non enveloped
DNA virus
Respiratory
Common cold
Pneumonia
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34
Q

Describe BK virus

A 
Double stranded
Non enveloped
DNA virus
Polyomavirus
Immunosuppressed
Asymptomatic
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35
Q

Describe human papilloma virus

A 
Double stranded
Non enveloped
DNA virus 
Keratinocytes, mucous membranes
Benign papillomas/cancers, warts
STDs
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36
Q

Describe JC Virus

A 
Double stranded
Non enveloped
DNA virus 
Polyoma virus 
Immunosuppression
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37
Q

Describe herpes virus

A 
Double stranded
Enveloped
DNA virus 
STD 
Hepstein Barr
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38
Q

Describe Hepatitis B

A 
Double stranded
Enveloped
DNA virus 
Liver
Flu like symptoms
Unprotected sex 
Sharing needles
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39
Q

Describe molluscum contagiosum

A 
Double stranded
Enveloped
DNA virus 
Small firm raised papules on skin
Not painful but itchy
Highly contagious- skin to skin
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40
Q

Describe coxsackievirus

A 
Single stranded
Positive
Icosahedral
Non enveloped 
Enterovirus
Digestive tract
Unwashed hands and contaminated surfacesFlu symptoms
Red blisters
Haemorrhagic conjunctivitis
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41
Q

Describe echovirus

A 
Single stranded
Positive
Icosahedral
Non enveloped 
GI tract
Liver failure 
Myocarditis
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42
Q

Describe Enterovirus

A 
Single stranded
Positive
Icosahedral
Non enveloped 
Genus
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43
Q

Describe Hepatitis A & E

A 
Single stranded
Positive
Icosahedral
Non enveloped 
Virus found in stool
Liver
E in particular - pets/eating meat
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44
Q

Describe norovirus

A 
Single stranded
Positive
Icosahedral
Non enveloped 
High temp, stomach cramps, headache, aching limbs, dehydration, vomiting, diarrhoea
Very contagious
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45
Q

Describe HIV

A 
Single stranded
Positive 
Icosahedral of helical
Enveloped
Lentivirus (AIDS) 
Affects helper T cells (CD4+)
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46
Q

Describe hepatitis C

A 
Single stranded
Positive 
Icosahedral of helical
Enveloped
Liver
Conc in blood
Blood to blood contact
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47
Q

Describe rubella virus

A 
Single stranded
Positive 
Icosahedral of helical
Enveloped
First week of pregnancy 
German/ 3 day measles
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48
Q

Describe encephalitis viruses

A

Single stranded
Positive
Icosahedral of helical
Enveloped
(Japanese, St. Louis, tick borne, Venezuelan, equine)
Inflammation of brain
Most commonly caused by herpes simplex virus

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49
Q

Describe Yellow fever virus

A 
Single stranded
Positive 
Icosahedral of helical
Enveloped
Fevers, chills, loss of appetitie  nausea, muscle pain, headache
Bite of female mosquito
Vaccine exists 
Flavivirus genus
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50
Q

Describe West Nile fever

A 
Single stranded
Positive 
Icosahedral of helical
Enveloped
Flavivirus genus
Mosquito
Africa--> NY --> USA 
No vaccine
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51
Q

Describe Ebola, Lassa, Marburg

A 
Single stranded 
Negative
Helical
Enveloped
Vomiting
Diarrhoea
Rash
Deceased liver and kidney function
Fruit bats
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52
Q

Describe influenza, parainfluenza viruses

A 
Single stranded 
Negative
Helical
Enveloped
Flu symptoms
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53
Q

Describe respiratory syncytial virus (RSV)

A 
Single stranded 
Negative
Helical
Enveloped
Lower respiratory tract infections
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54
Q

Describe rotavirus

A 
Double stranded 
Icosahedral
Non enveloped 
Severe diarrhoea among infants
Stools- virus passes out
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55
Q

What are some examples of gram positive cocci bacteria?

A 
Staph aureus
Coagulate -ve staph
Alpha haemolytic streptococci
Beta haemolytic streptococci (inc. strep pyogenes)
Streptococcus pneumoniae
Enterococcus faecalis
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56
Q

What are some examples of gram negative cocci bacteria?

A

Neisseria meningitidis
Neisseria gonorrhoea
Mortadella cattarhalis
Acinetobacter baumannii

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57
Q

What are some examples of gram positive bacilli bacteria?

A

Listeria monocytogenes
Bacillus anthracis
Bacillus cereus

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58
Q

What are some examples of gram negative bacilli bacteria?

A 
Escherichia coli
Klebsiella pneumoniae
Proteus species
Salmonella typhi
Pseudomonas aeruginosa
Haemophilus influenzae
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59
Q

What are the main constituents of the infection model?

A 
Pathogen
Patient
Mechanism of infection
Infection
Management 
Outcome
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60
Q

Expand on Pathogens in the infection model

A

Virus
Bacterium (prokaryotic)
Fungus - yeast, mould (eukaryotic)
Parasites - protozoa, helminthology (worm) (eukaryotic)

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61
Q

Expand on the patient in the infection model

A

Person - age, gender, physiological state, pathological state, social factors
Time - calander time, relative time
Place - current, recent

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62
Q

Expand on the mechanism of infection in the infection model

A 
Contiguous spread (direct)
Inoculation
Haematogenous
Ingestion
Inhalation
Vector
Vertical transmission
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63
Q

Expand on the infection in the infection model

A

Attachment –> toxin production –> host damage
Attachment –> interaction with host defences –> host damage
Attachment –> interaction with host defences –> inflammation –> host damage

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64
Q

Expand on management in the infection model

A

History
Examinations
Investigations
Treatment
- Supportive - symptom relief, physiological restoration
- Specific - antimicrobials, surgery- drainage, debridement, dead space removal
Infection prevention - hospital and community
- prevent infection transmission to - other patients, staff and contacts

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65
Q

Expand on the outcome of the infection model

A

Spectrum of Cured to Death with disability and chronic infection being intermediates

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66
Q

How are antimicrobials classified?

A

Antibacterial agents
Antifungal agents
Antiviral agents
Antiprotozoal agents

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67
Q

How are antibacterials classified?

A 
Bactericidal/ bacteriostatic
Spectrum- broad vs narrow
Target site (mechanism of action)
Chemical structure (antibacterial class)
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68
Q

What does bactericidal mean?

A

Antibiotic kills organism completely

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69
Q

What does bacteriostatic mean?

A

Antibiotic inhibits the organism but it can come back

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70
Q

What is the relevance of ‘classes of drugs’?

A

Groups together drugs with the same basic function and mechanism of action

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71
Q

What are the ideal features of antimicrobials?

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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72
Q

What are the 4 mechanisms of action of antibacterials?

A 
Those that affect:
Cell wall synthesis
Cell membrane function
Protein synthesis 
Nucleic acid synthesis
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73
Q

What antibacterials affect cell wall synthesis?

A

B-lactams (penicillin, cephalosporins)

Glycopeptides (vancomycin)

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74
Q

What antibacterials affect cell membrane function?

A

Polymixins (colistin)

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75
Q

What antibacterials affect protein synthesis?

A

Tetracyclines
Aminoglycosides (gentamicin)
Macrolides (erythromycins)

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76
Q

What antibacterials affect nucleic acid synthesis?

A

Quinolones (ciprofloxalin, trimethoprim, rifampcin)

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77
Q

How do B-lactams work to affect cell wall synthesis?

A

Cross linkage between peptidoglycan - gives cell wall rigidity
Achieved by penicillin binding protein
Penicillin gets in and blocks penicillin binding protein so protein can no longer bind to chains of amino acids- no cross linkage

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78
Q

How do Glycopeptides work to affect cell wall synthesis?

A

Sits on peptidoglycan chains and stops penicillin binding protein from binding (acts at an earlier stage than B- lactams)

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79
Q

What is the most common mechanism of action of antibacterials?

A

Interupting cell wall synthesis

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80
Q

What is the rarest mechanism of action of antibacterials?

A

Interrupting cell membrane function

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81
Q

In what three ways can organisms become resistant to antibacterials?

A

Drug inactivating enzymes- B-lactamases, aminoglycoside enzymes
Altered target- target enzyme has lowered affinity for antibacterials e.g. resistance to meticillin, macrolides and trimethoprim
Altered uptake- reduced ability of antibiotic to get close to bacteria; decreased permeability (e.g. B-lactams) or increased efflux (e.g. Tetracyclines)

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82
Q

What is the genetic basis of antibiotic resistance?

A

Chromosomal gene mutation- bacteria undergo spontaneous gene mutation conferring resistance; when exposed to antibiotics, bacterial cell with resistance survives and multiplies
Horizontal gene transfer- plasmid to plasmid or plasmid to chromosome; genetic material moves from one organism to another by conjugation, transduction and transformation

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83
Q

In what two ways can you measure antibiotic activity?

A

Disc testing- impregnate antibody into paper filter disc and observe bacterial growth- organism won’t grow where there is sufficient antibiotic to inhibit its growth
Minimum inhibitory concentration- more mathematical, lots of test tubes with a range of antibiotic concentrations and the same concentration of organism- organism growth is monitored

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84
Q

What are the 4 types of B-lactams?

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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85
Q

What is the mechanism of action of B-lactams?

A

Affect cell wall synthesis

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86
Q

Benzylpenicillin

A

B-lactam, penicillin
Affect cell wall synthesis
Mainly active against streptococci

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87
Q

Penicillin V

A

B-lactam, penicillin
Affect cell wall synthesis
Mainly active against streptococci

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88
Q

Amoxicillin

A

B-lactam, penicillin
Affect cell wall synthesis
Mainly active against streptococci
Also active against gram negatives

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89
Q

Flucoxacillin

A

B-lactam, penicillin
Affect cell wall synthesis
Active against staphylococci and streptococci

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90
Q

Coamoxiclav

A

B-lactam, penicillin
Affect cell wall synthesis
Active against staphylococci, streptococci, anaerobes and Gram negatives

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91
Q

Tazocin

A

B-lactam, penicillin
Affect cell wall synthesis
Active against staphylococci, streptococci, anaerobes, and High activity against gram negatives including pseudomonas

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92
Q

Describe cephalosporins

A

B-lactam,Cephalosporin
(Generations with high gram negative and low gram positive activity; broad spectrum but no anaerobe activity: concern over association with C. difficile)

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93
Q

Cefalexin

A

1st generation cephalosporin, B-lactam

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94
Q

Cefuroxime

A

2nd generation cephalosporin, B-lactam

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95
Q

Cefotaxime

A

3rd generation cephalosporin, B-lactam

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96
Q

Ceftriaxone

A

3rd generation cephalosporin, B-lactam
Blindness/ meningitis
Good activity in CSF

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97
Q

Ceftazidime

A

3rd generation cephalosporin, B-lactam

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98
Q

Meropenem/ imipenem

A

Carbapenem, B-lactam
Very broad spectrum (including anaerobes)
Active against most(not all) gram negatives
Generally safe in penicillin allergy, other than anaphylaxis

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99
Q

Aztreonam

A

Monobactam, B-lactam

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100
Q

What is the main mechanism of action of Glycopeptides?

A

Affect Cell wall synthesis

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101
Q

Vancomycin

A

Glycopeptides
Affects cell wall synthesis
Active against most Gram positive (not gram negative)
Some enterococci resistant (VRE)
Resistance in staphs is rare
Not absorbed (oral for C.difficile only)
Therapeutic drug monitoring (TDM) required as there is a narrow therapeutic window - give enough, not too much, toxicity

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102
Q

Teiccplanin

A

Similar activity to vancomycin, but much easier to administer
Glycopeptides
Affects cell wall synthesis
Active against most Gram positive (not gram negative)
Some enterococci resistant (VRE)
Resistance in staphs is rare
Not absorbed (oral for C.difficile only)
Therapeutic drug monitoring (TDM) required as there is a narrow therapeutic window - give enough, not too much, toxicity

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103
Q

What is the main mechanism of action of tetracyclines?

A

Affecting protein synthesis

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104
Q

Tetracycline and doxycycline

A

Similar, broad spectrum
Both oral only
Specific use in penicillin allergy usually from gram positive
Active in atypical pathogens in pneumonia
Active against chlamidya and some Protozoa
Shouldn’t be given to children younger than 12 years

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105
Q

What is the main mechanism of action of aminoglycosides?

A

Affecting protein synthesis

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106
Q

Gentamicin

A

Aminoglycosides
Most common agent
Profound activity against gram negative
Good activity in blood and urine
Potentially nephrotoxic/ototoxic
Therapeutic drug monitoring (TDM) required- toxicity to kidney
Generally reserved for sever gram negative sepsis

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107
Q

What is the main mechanism of action of macrolides?

A

Affecting protein synthesis

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108
Q

Erythromycin and clanthromycin

A

Macrolides
Affects protein synthesis
Well distributed including intracellular penetration
Alternative to penicillin for mild gram positive infections
Also active against atypical respiratory pathogens

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109
Q

What is the main mechanism of action of Quinolones?

A

Affects nucleic acid synthesis

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110
Q

Ciprofloxacin

A 
Quinolone
Affects nucleic acid synthesis 
Commonest example
Inhibits DNA gyrase (coiling of nucleic acid) 
Very active against gram negatives
Also active against atypical pathogens 
Increasing resistance and risk of CDI
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111
Q

Trimethoprim and sulphonamides

A

Inhibitors of frolic acid synthesis
Trimethoprim used alone in UK for UTIs
When combined with sulphamethoxazole- cotrimoxazole, used to treat PCP (pneumocystitis pneumonia) , has activity against MRSA

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112
Q

What are two types of antifungals?

A

Azoles

Polyenes

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113
Q

How do Azoles work?

A

Antifungal
Active against yeasts, and or moulds
Inhibit cell membrane synthesis

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114
Q

Fluconazole

A 
Antifungal
Inhibits cell membrane synthesis
Used to treat candida
Hra, vori, posaconazol
Also active against aspergillus
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115
Q

How do polyenes work?

A

Antifungals

Inhibit cell membrane function

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116
Q

Nystatin and amphotericin

A

Antifungals
Inhibit cell membrane function
Nystatin for topical treatment of candida
Amphotericin for IV treatment of systemic fungal infections (e.g. Aspergillus)

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117
Q

What are two common antivirals?

A

Aciclovir

Oseltamivir (tamiflu)

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118
Q

Aciclovir

A

Antiviral
When phosphorylates inhibits viral DNA polymerase
Herpes simplex - genital herpes, encephalitis
Varicella zoster - chicken pox and shingles

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119
Q

Oseltamivir (Tamiflu)

A

Antifungal
Inhibits viral neuraminidase
Influenza A & B

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120
Q

Metronidazole

A 
Antibacterial and antiprotozoal agent 
Active against anaerobic bacteria
Also active against Protozoa
- amoebae (dysentery and systemic) 
- giardia (diarrhoea) 
- trichomonas (vaginitis)
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121
Q

Look at infection model for acute sepsis in the emergency model

A

Neisseria Meningitidis

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122
Q

Define the immune system

A

Cells and organs that contribute to immune defences against infections and non infectious conditions (harmless substances)

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123
Q

Define infectious disease

A

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

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124
Q

What are the four broad stages of an immune response?

A

Pathogen recognition - cell surface and soluble receptors
Containing / eliminating the infection - killing and clearance mechanisms
Regulating itself - minimum damage to host (resolution)
Remembering pathogens - preventing disease from recurring

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125
Q

What are the two types of immunity?

A

Innate

Adaptive

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126
Q

What are the 4 first lines of defence in innate immunity?

A

Physical barriers
Physiological barriers
Chemical barriers
Biological barrier

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127
Q

What are the physical barriers of the first line of defence of innate immunity?

A

Skin (SA 1-2m^2)
Mucous membrane (mouth, resp tract, GI tract, urinary tract)
Bronchial cilia

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128
Q

What are the physiological barriers of the first line of defence of innate immunity?

A

Diarrhoea- food poisoning, allergies
Vomiting- food poisoning, hepatitis, meningitis
Coughing- pneumonia
Sneezing- sinusitis

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129
Q

What are the chemical barriers of the first line of defence of innate immunity?

A

Low pH - skin(5.5) stomach(1-3) vagina(4.4)
Antimicrobial molecules
-IgA (tears, saliva)- binds specifically to microorganisms and prevents it from attaching to mucous membrane
-Lysozyme (sebum, perspiration, urine)
-Mucous (mucous membrane)
-Beta defensins (epithelium)
-Gastric acid and Pepsin

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130
Q

What are the biological barriers of the first line of defence of innate immunity?

A

Normal flora
- non pathological microbes
- strategic locations- nasopharynx, mouth/throat, skin, GI tracts, vagina, (lactobacillus spp)
- absent in internal organs
Benefits - compete with pathogens for attachement sites and resources, produce antimicrobials chemicals, synthesise vitamins (K, B12 and others)

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131
Q

What are some normal flora found on skin?

A 
Staphylococcus aureus 
Staphylococcus epidermidis
Streptococcus pyogenes
Candida albicans
Clostridium perfringens
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132
Q

What are some normal flora found in the nasopharynx?

A

Streptococcus pneumoniae
Neisseria meningitidis
Haemophilius species

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133
Q

What are some clinical problems associated with normal flora?

A

–>Normal flora can be displaced from its normal location to a sterile location
-breaching skin integrity (skin loss, burns; surgery; injection drug users; IV lines)
-fecal oral route (food borne infection)
-fecal perineal urethral route (UTI)
-poor dental hygiene/ dental work (dental extraction, gingivitis, flossing) (common cause of harmless bacteraemia)
Serious infection in high risk patients
-asplenic/hyposplenic
-damaged prosthetic valves
-previous infective endocarditis
-antibiotic prophylaxis

  • -> Normal flora overgrows and becomes pathogenic when host becomes immunosuppressed
  • diabetes, AIDS, malignant diseases, chemotherapy (neutrophils)
  • -> When normal flora is depleted by antibiotics
  • intestine –> severe colitis (clostridium difficile)
  • vagina –> thrush (Candida albicans)
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134
Q

What are the second lines of defence of innate immunity?

A

Phagocytes

Chemicals

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135
Q

How are phagocytes involved in the second line of defence in innate immunity?

A

Phagocyte-microbe interaction

  • RECOGNITION
  • -microbial structures: Pathogen Associated Molecular Patterns (PAMPs) - carbohydrates, lipids, proteins, nucleic acid
  • -phagocytes: Pathogen Recognition Receptors - Toll like receptors
  • -opsonisation of microbes: coating proteins called opsonins that bind to the microbial surfaces leading to enhanced attachment of phagocytes and clearance of microbes
  • ENGULFMENT
  • DEGRADATION OF INFECTIOUS MICROBES
  • -phagocyte intracellular killing mechanisms
  • –O2 dependent - ROS via NADPH oxidase
  • –O2 independent - lysozyme, lactoferrin/transferrin, cationic proteins, proteolytic and hydrolytic enzymes
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136
Q

PAMP- lipopolysaccharide (LPS) G-

PRR?

A

PRR- TLR4

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137
Q

PAMP- lipoproteins and lipopeptides G-

PRR?

A

PRR- TLR2

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138
Q

PAMP- peptidoglycan G+

PRR?

A

PRR- TLR2

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139
Q

PAMP- lipoteichoic acid G+

PRR?

A

PRR- TLR4

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140
Q

PAMP- lipoarabinomannan and mannose rich glycans (Mycobacterium)
PRR?

A

PRR- TLR2

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141
Q

PAMP- flagellin (bacterial flagella)

PRR?

A

PRR- TLR5

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142
Q

Describe opsonins and when they are required

A

Complement proteins- C3b C4b
Antibodies- IgM, IgG
Acute phase proteins - CRP, mannose binding pectin (MBL)

Essential in clearing encapsulated bacteria

  • neisseria meningitidis
  • streptococcus pneumoniae
  • haemophiliis influenzae b
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143
Q

How are chemicals involved in the second line of defence in innate immunity?

A

Complement system- 20 serum proteins, most important C1-C9

  • 2 activating pathways (actually 3)
    • alternative pathway - initiated by cell surface microbial constituents
    • MBL pathway - initiated when MBL binds to mannose containing residues of proteins found on Salmonella spp Candida albicans

Cytokines

  • phagocytosis - chemo attraction, phagocyte activation, inflammation
  • antimicrobials actions of macrophage derived TNF alpha, IL-1, IL-6
    • liver (opsonins) CRP, MBL (complement activation)
    • bone marrow - neutrophil mobilisation
    • inflammatory actions - vasodilation, vascular permeability, adhesion molecules, attraction of neutrophils
  • -hypothalamus- increased body temp
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144
Q

What are some examples of major complement proteins and their action?

A

C3a and C5a - recruitment of phagocytes
C3b and C4b - opsonisation of pathogens and inflammation
C5 - C9 - killing of pathogens in the Membrane Attack Complex

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145
Q

What are some clinical problems associated with the second line of defence in innate immunity?

A

Infection –> microbial toxins (LPS) –> overreaction of TLR4 receptor –> overreaction of complement (neutrophils, endothelium and monocytes) –> excessive systemic inflammatory response –cytokines shower, coagulopathy, vasodilation, capillary leak (tissue organ perfusion)–> sepsis and multi organ failure

Clinical problems start when phagocytosis is reduced

  • deceased spleen function (asplenic, hyposplenic)
  • decreased neutrophil number (cancer chemo, certain drugs, leukaemia and lymphoma)
  • decreased neutrophil function (chronic granulomatous disease, no resp burst)
  • chediak higashi syndrome (no phagolysosomes formed)
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146
Q

What is a hospital acquired infection?

A

Infections arising as a consequence of providing healthcare
So in hospital patients- infection is not present nor incubating at the time of admission -e.g. Onset is at least 48 hours after admission
Can also include infections in hospital visitors and health workers

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147
Q

What are some common viruses which cause a hospital acquired infection?

A

Blood borne: Hepatitis B, C, HIV
Norovirus
Chicken pox
Influenza

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148
Q

What are some common bacteria which cause a hospital acquired infection?

A 
Staphylococcus aureus (inc. MRSA)
Clostridium Difficile
Escherichia Coli, Klebsiella
Pseudomonas pneumoniae, aeruginosa 
Mycobacterium TB
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149
Q

What are some common fungi which cause a hospital acquired infection?

A

Candida albicans

Aspergillus species

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150
Q

What is a common parasite which causes a hospital acquired infection?

A

Malaria plasmodium falciparum

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151
Q

What are some patient factors which increase the risk of getting a hospital acquired infection?

A 
Extremes of age
Obesity/ malnourished
Diabetes
Cancer
Immunosuppression
Smoker 
Surgical patient
Emergency admission
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152
Q

What are some general patient interventions, used to manage a HAIs?

A

Optimise patients condition- smoking, nutrition, diabetes
Antibiotic microbial prophylaxis
Skin preparation
Hand hygiene

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153
Q

What are some specific patient interventions, used to manage a HAIs?

A

MRSA screens
Mupirocin nasal ointment
Disinfectant body wash

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154
Q

How can you avoid patient to patient transmission of a HAI?

A

Physical barriers- isolation of infected patients, protection of susceptible patients

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155
Q

What are some health worker interventions, used to manage a HAIs?

A

Healthy- disease free and vaccinated

Good practice- good clinical techniques, hand hygiene, PPE, antimicrobial prescribing

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156
Q

What are some environmental interventions, used to manage a HAIs?

A

Built environment- space, layout, toilets, wash hand basins
Appropriate furniture and furnishings
Cleaning- disinfectants/ steam cleaning/ H2O2 vapour
Medical devices- single use equipment, sterilisation, decontamination
Appropriate kitchen and ward facilities, good food hygiene practice
Theatres- positive/ negative pressure rooms
Immune suppressed patients

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157
Q

What are the 4 Ps for infection prevention and control?

A

Patient - general and specific patient risk factors; interactions with other patients, healthcare workers and visitors
Pathogen - virulence factors; ecological interactions- other bacteria and antibiotics/ disinfectants
Practice - 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 world
Place - healthcare environment- fixed and variable features

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158
Q

What type of organism is clostridium difficile?

A

Gram positive anaerobic, bacillus, spore forming bacteria

Example of a hospital acquired infection

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159
Q

How does the carriage frequency of clostridium difficile change with length of hospital stay?

A

Carriage frequency increases with duration of hospital stay

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160
Q

Describe the mechanism of infection of clostridium difficile

A

When gut micro flora are disturbed by antibiotics (cephalosporins and amoxicillin) overgrowth can occur
Enterotoxin A and B and binary toxin production causes tissue damage and fluid diarrhoea
Some strains which are fluoroquinolone resistance and have evidence of enhanced toxin production are associated with more ever disease and extensive hospital outbreaks

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161
Q

What are some clinical features and symptoms of a patient infected with clostridium difficile?

A

History of previous antibiotic exposure
3/4 loose/ unformed stools per day
Possible development of abdominal pain
Pseudomembranes seen on sigmoidoscopy on mucosal surface of rectum and sigmoid colon
Possible complications of toxic mega colon, bowel perforation and systemic toxicity —> high mortality

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162
Q

What is the treatment pattern for clostridium difficile?

A

Stop the inciting agent (antibiotic)
Treat with metronidazole for 10 days
Oral vancomycin and IV metronidazole for severe cases and treatment failures
Rapid and strict isolation is essential

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163
Q

What investigations would you carry out for clostridium difficile detection?

A

Detection of toxin or glutamate dehydrogenase (GDH) by enzyme immunoassay (EIA)
Detection of toxin genes by nucleic acid amplification test (NAAT)
Typing- generally by ribotyping

Full blood count
U&Es
CRP
MC&S

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164
Q

How can you prevent clostridium difficile infection?

A 
Enhanced ward cleaning and attention to hand hygiene is essential 
Suspect
Isolate
Gloves and apron
Hand hygiene
Toxin test
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165
Q

What are some other clostridium bacteria? And what diseases do they cause?

A

Botulinum- botulism
Perfringens- gas gangrene, food poisoning
Tetanii- tetanus

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166
Q

What are some common travel infections?

A 
Malaria
Typhoid
Meningococcal septicaemia
Dengue
Yellow fever
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167
Q

What is the incubation period for malaria?

A

1-3 weeks or longer after bite

168
Q

What are the four main species that cause malaria?

A

Plasmodium falciparum, vivax, ovale and malariae

169
Q

What is the vector of malaria?

A

Female anopheles mosquito

170
Q

What areas of the world is malaria common in?

A

Africa, Asia, Middle East and South and Central America

171
Q

What is a typical history taken of someone with malaria?

A 
Headache 
Cough
Fatigue
Malaise
Asthsalgia
Myalgia
Fever chills and sweats which eventually cycle every 3rd/4th day
172
Q

What signs of malaria are there (ie. From examinations)?

A

Other than fever, often few signs (+/- splenomegaly)
Cerebral features - coma
Respiratory distress (metabolic acidosis, pulmonary oedema)

173
Q

What investigations should be carried out for malaria?

A

Should be managed by an ID physician
Blood smear to detect parasites
FBC, U&Es, LFTs, glucose
Head CT if CNS symptoms

174
Q

What treatment is available for malaria?

A

Depends on species causing malaria

  • plasmodium falciparum- (malignant) quinine, artemisinin
  • p, vivax, ovale, malaria- (benign) chloroquine +/- primaquine for exo erythrocytic phase)
175
Q

How can one prevent malaria?

A

Assess risk - knowledge of at risk areas
Bite prevention- repellant, adequate clothing, nets, chemo prophylaxis before travel (must include regular returning travellers)
Chemoprophylaxis - specific to region, start before and continue after return -doxycycline

176
Q

What is the most common species that causes typhoid (enteric fever)?

A

Salmonella enterica serorar Typhi/ Paratyphi A, B or C

177
Q

What type of bacteria is Salmonella enterica serorar Typhi/ Paratyphi A, B or C?

A

Enterobacteriaceae

Aerobic gram negative rods

178
Q

What is the mechanism of infection of Salmonella enterica serorar Typhi/ Paratyphi A, B or C?

A

Gram negative endotoxin VI antigen
Invasion which allows IC growth
Fimbriae adhere to epithelium over ideal lymphoid tissue (Peyers patches)–> RE system

179
Q

What are some symptoms and signs of typhoid and paratyphoid?

A 
Fever, headache
Incubation period- 7-14 days
Abdominal discomfort, constipation, dry cough, hepatosplenomegaly, occasionally rash 
Relative bradycardia 
Intestinal haemorrhage and perforation
Paratyphoid generally milder
180
Q

What is usually found upon investigation in someone with typhoid?

A

Moderate anaemia
Relative lymphopenia
Raised LFTs (transaminase and bilirubin)
Culture- faeces, blood
Serology (antibody detection)- no longer used

181
Q

What is the pattern of treatment of typhoid?

A

Usually treated with ceftriaxone or azithromycin 7-14 days

Resistance may be present against chloramphenicol, ampicillin. Cotrimoxazole, ciprofloxalin

182
Q

How can typhoid be prevented?

A

Food and water hygiene precautions
Typhoid vaccine- high risk travel, lab personnel
Vicapsular polysaccharide antigen or live attenuated vaccine
Modest protective effect (50-75%)

183
Q

What are some examples of non typhoid all salmonella infections?

A

Food poisoning salmonellas- salmonella typhimurium, S.enteritidis
Symptoms- diarrhoea, fever, vomiting, abdominal pain
Generally self limiting but bacteraemia and deep seated infections may occur- excreting organism in diarrhoea

184
Q

What causes brucellosis?

A

Primary animal pathogen
- brucella abortus (cows)
- brucella melitensis (goats and sheep)
Gram negative cocobacillus - short rounded rods

185
Q

Where is brucellosis most common?

A

South Europe, Africa, Asia, central and South America

186
Q

What is the mechanism of transmission of brucellosis?

A

Transmission through skin breaks / GI tract (milk)

187
Q

What are some symptoms/ clinical signs of brucellosis?

A

Non specific febrile illness (undulant fever)
Bone, joint involvement
Epididymitis - inflammation/ swollen testes

188
Q

How is brucellosis generally diagnosed?

A

From blood cultures

189
Q

How is brucellosis commonly treated?

A

With doxycycline and rifampicin

190
Q

In adaptive immunity, what type of pathogens are considered intracellular microbes? And what MHC class do they correspond to?

A

Bacteria, viruses, Protozoa
Class I MHC (found on all nucleated cells)
HLA: A, B, C

191
Q

In adaptive immunity, what type of pathogens are considered extracellular microbes? And what MHC class do they correspond to?

A

Bacteria, parasites, worms, fungi
Class II MHC (found on all dendritic cells. Macrophages, B cells)
HLA: DR, DQ, DP

192
Q

In adaptive immunity relating to MHC class I what is the endogenous pathway?

A

Virus (protein) is taken up and presented on cell surfaces

193
Q

In adaptive immunity relating to MHC class II what is the exogenous pathway?

A

Bacteria taken up and presents in endocytic vesicle which fuses with lysosomes and destroys bacteria

194
Q

What does the endogenous pathway of adaptive immunity stimulate?

A

CD8+ T cells
- cytotoxic T lymphocytes - process and kill the virus
CD4+ T cells (stimulates CD8+ T cells and..)
- B cells- antibodies- opsonisation, neutralisaiton, complement activation
- macrophages- kill opsonised microbes

195
Q

What does the exogenous pathway of adaptive immunity stimulate?

A

CD4+ T cells

  • eosinophils- killing of parasites
  • B cells- Antibody: IgG4 (opsonisation), IgA (mucosal protection), IgG&IgE (antibody dependent cell toxicity) and IgE (allergies)
  • mast cells- local inflammation allergies (IgE)
  • neutrophils- phagocytosis
196
Q

What type of pathogen is streptococcus pneumonia?

A 
Gram positive, diplococcus (seen in pairs)
Alpha haemolytic (can be variable)
197
Q

Describe how streptococcus pneumoniae causes infection

A

Streptococcus pneumoniae has a polysaccharide capsule that protects it’s from phagocytosis
There are over 90 highly antigenic capsule sero types and antibodies to specific types are protective
Pathogenicity-
- pro inflamm cell wall components (e.g. c-polysaccharide) F-antigen
- IgA2 protease
- pneumolysin, a cytotoxin that stimulates immune responses
- adhesins that bind to cell surface carbohydrates (e.g. Choline binding protein A, pneumococcal surface protein A)
- tissue damaging enzymes

198
Q

Describe how non invasive pneumococcal infections present

A
  • these occur outside the major organs or the blood and tend to be less serious
  • bronchitis- infection of bronchi
  • Otis media - ear infections
  • sinusitis - infection of sinuses
199
Q

Describe how invasive pneumococcal infections presents

A

These occur inside the major organs or the blood and tend to be more serious than non invasive ones

  • Bacteraemia
  • Septicaemia
  • Osteomyelitis
  • Septic arthritis
  • Pneumonia
  • Meningitis
200
Q

What investigations should be carried out when suspecting streptococcus pneumoniae infection and what results are expected?

A 
Distinctive crackles on chest
Blood test
Radiography- x ray fluid on lungs
Ct scan, MRI scan
Blood pressure (low) 
Lumbar puncture test - sample of CSF
Urinary antigen test- urine sample, immunochromatographic assay
201
Q

What treatment can be given to someone with a streptococcal pneumonia infection?

A

Non invasive infection
- treating bronchitis, middle ear infection, sinusitis

Invasive infection
- confusion, resp rate >30, low BP, 65 years old ***

202
Q

How can you prevent streptococcal pneumonia infections?

A

Conjugate vaccine incorporating 13 capsular stereotypes

Highly immunogenicity in small children

203
Q

What are 11 different causes of (travellers) diarrhoea?

A 
Enterotoxigenic escherichia coli
Enteroinvasive escherichia coli 
Campylobacter 
Salmonella typhi
Shigella
Vibrio cholera
Giardia lamblia
Entamoeba histolytica
Cryptosporidium parvum
Rotavirus
Norovirus
204
Q

What type of diarrhoea do you get with Enterotoxigenic escherichia coli?

A

Profuse and watery

205
Q

What type of diarrhoea do you get with Enteroinvasive escherichia coli?

A

Mild with abdominal cramp

206
Q

What type of diarrhoea do you get with campylobacter?

A

Bloody

207
Q

What type of diarrhoea do you get with salmonella typhi?

A

Bloody

208
Q

What type of diarrhoea do you get with shigella?

A

Bloody

209
Q

What type of diarrhoea do you get with vibrio cholera?

A

Profuse and secretory

210
Q

What type of diarrhoea do you get with giardia lamblia?

A

Explosive

211
Q

What type of diarrhoea do you get with entamoeba histolytica?

A

Bloody

212
Q

What type of diarrhoea do you get with cryptosporidium parvum?

A

Watery

213
Q

What type of diarrhoea do you get with rotavirus?

A

Watery mild-severe

214
Q

What type of diarrhoea do you get with Norovirus?

A

Watery

215
Q

Describe the structure of influenza virus and how this affects it function

A 
Enveloped orthomyoxovirus (100nm) 
Contains a negative single stranded RNA genome divided into 8 segments
Structure allows genetic reassortment- so that virus can change its surface antigens
216
Q

What fluenza strains can influenza virus take up genetic material from?

A

Avian and pig

217
Q

How many proteins does influenza virus express? Describe their arrangement.

A

7 proteins - 3 of which are responsible for RNA transcription
Nucleoprotein has 3 antigenic types that designate 3 main virus groups- A , B and c
Matrix protein forms a shell under the lipid envelope with haemagglutin and neuraminidase proteins - expressed as 10 nm spikes on the envelope which interact with host cells - virus immunity directed against H and N

218
Q

What are some clinical features of influenza virus?

A

Incubation period- 1 to 4 days
Patients infectious for 3 days - starting from one day before symptoms emerge
Headache, myalgia, fever, cough lasts for 3 - 4 days
Complications which are more common in elderly people and patients with cardiopulmonary disease, include primary viral and secondary bacterial pneumonia

219
Q

How is influenza diagnosed?

A

Immunofluorescence inf A, B and C
Nucleic acid amplification test (NAAT)
- more sensitive and can identify specific stereotype which can indicate whether a patient is infected with a pandemic strain

220
Q

Describe the treatment of influenza

A

Amantadine

Neuraminidase inhibitors- zanamivir, oseltamivir (tamiflu), vaccination

221
Q

Where is legionella pneumophilia often found?

A

Found in rivers, lakes, warm springs, domestic water supplies, fountains, air conditioning systems, swimming pools and jacuzzis

222
Q

Between what temperatures does multiplication of legionella pneumophilia occur?

A

Multiplication occurs at temps between 20 and 40 degree Celsius inside acanthamoeba

223
Q

How is legionella pneumophilia transmitted from person to person?

A

Transmission via aerosols generated from showers, and air conditioning systems

224
Q

What are some risk factors for legionella pneumophilia infections?

A

Infection associated with previous lung disease, smoking, high alcohol intake, but previously healthy patients can be infected.
Immunocompromised patients in hospitals are vulnerable to infection if the hospital air conditioning is not adequately maintained

225
Q

What is the pathogenesis of legionella pneumophilia?

A

Major outer membrane protein that inhibits acidification of phagolysosomes
Macrophage infectivity is required for optimal internalisation
Legionella pneumophilia expresses a potent exoprotease

226
Q

What are some clinical features of legionella pneumophilia?

A

Mild influenza like illness (pontiac)
Severe pneumonia (legionnaires disease) which can lead to respiratory failure and high mortality
Patients may complain of nausea, vomiting, malaise before lung symptoms become prominent
Cough which is unproductive and dyspnoea which is progressive
Confusion is common
Inappropriate natiuretic hormone production associated with low serum sodium

227
Q

How is legionella pneumophilia infection diagnosed in the lab?

A

Culture of sputum, bronchoalveolar, lavage fluid
Rapid diagnosis by antigen detection in urine
Direct Immunofluorescence or nucleic acid amplification test (NAAT) of respiratory specimens
Serum antibodies can provide retrospective diagnosis for epidemiological purposes

228
Q

How is infection by legionella pneumophilia treated and prevented?

A

Effective regimens usually consist of a macrolide antibiotic together with rifampicin
Legionellosis- prevented by adequate maintenance of air con systems and by ensuring that hot water supplies are above 45 degrees Celsius to prevent multiplication

229
Q

What type of bacteria is neisseria meningitidis?

A

Gram negative diplococcus bacteria

230
Q

Describe the structure of neisseria meningitidis and relate this to the function of the structure

A

Number of sero groups (ABC, W-135) based on polysaccharide capsular antigen (acts as endotoxin) - promotes adherence, prevents phagocytosis, and triggers inflammation by cytokines
Evades immune system by preventing phagocytosis
Outer membrane acts as an endotoxin

231
Q

How does neisseria meningitidis cause disease?

A

Endotoxin binds to macrophages
Local- Cytokines (tissue necrosis factors and interleukins TNF alpha and IL1) stimulate inflammatory response to promote wound repair and recruit RE system
Systemic- Cytokines released into circulation stimulate oath factor macrophages and platelets, goal is for homeostasis to be restored
SIRS- homeostasis not restored
Also - cytokines promote coagulation and inhibit fibrinolysis causing microvascular thrombosis and organ ischaemia and failure

232
Q

What is SIRS?

A

Systemic inflammatory response syndrome

Response to non specific insult (trauma, Ischaemia and infection)

233
Q

What is bacteraemia?

A

Presence of bacteria in blood with or without clinical features

234
Q

What is septicaemia?

A

Generalised clinical term related to generalised sepsis

235
Q

What is sepsis?

A

Systemic response to infection- SIRS + documented/ presumed infection

236
Q

What is severe sepsis?

A

SIRS + organ dysfunction / hypoperfusion –> hypotension/ decreased urine output

237
Q

What is septic shock?

A

Severe sepsis + persistently low BP despite administration of IV fluids

238
Q

How can SIRS be diagnosed?

A 
2 or more of :
Temp- 38 degrees Celsius 
H/R > 90/min
R/R >20/ min
WBC 12x10^9/L.
239
Q

What are some common symptoms of an infection caused by neisseria meningitidis?

A

Abdominal pain, fever, nausea, weakness, muscle aches, eye pain on exposure to light, pale, cool extremities, widespread purpuric rash

240
Q

What investigations are required for diagnosis of neisseria meningitidis?

A 
FBC
U&Es 
EDTA bottle for PCR
Blood sugar
Liver function test
C Reactive Protein
Clotting studies
Blood gases
241
Q

What 3 investigations would confirm the diagnosis with neisseria meningitidis?

A

Blood culture
PCR of blood
Lumbar puncture- culture of CSF (only after checking contraindications- glucose and protein elimination in biochem M&C) PCR of CSF (appearance- turbidity and colour, microscopy - WBCs and RBCs, gram stain- PCR referral)

242
Q

How would you treat neisseria meningitidis?

A

Sepsis 6 within 1 hour

1) give high flow O2
2) take blood cultures and other cultures
3) administer empirical antibiotics (IV)
4) measure serum lactate
5) start IV fluid resuscitation
6) commence accurate urine output measurement

Antibiotics : ceftriaxone

243
Q

How would you prevent infection by neisseria meningitidis?

A

Vaccination- meningococcal vaccines conjugate, achy vaccine- immunocompromised patients and travel protection, serogroup B vaccine,
Antibiotic prophylaxis- close contact to infected individuals

244
Q

What are some life threatening complications cause by infection with neisseria meningitidis?

A 
Irreversible hypotension
Respiratory failure 
Acute kidney injury (renal failure) 
Raised IC pressure
Ischaemic necrosis of digits, hands and feet
245
Q

What type of bacteria is escherichia coli?

A

Gram negative, anaerobic, rod shaped bacterium
Commonly found in lower intestine of warm blooded organisms (commensal)

Strains vary in fimbriae - giving the consequential disease and mechanism of infection differences

246
Q

Describe the 5 main strains of E. coli.

A

Enterotoxigenic E. coli - produce LT and ST toxins that act on the enteric yet to stimulate fluid secretion- diarrhoea
Enteroaggregative E. coli - secrete plasma encoded toxin, a serine protease that binds alpha ford in and causes disruption of actin cytoskeleton - strains express ST toxins and haemolysin like toxins - chronic diarrhoea
Enteropathogenic E. coli- colonise epithelial cell lining of small intestin and inject effector proteins that causes efface net of microvilli and intimate adherence
Enterohaemorrhagic E. coli- strains produce a veto toxin (in vitro) - Haemorrhagic diarrhoea, complicated by haemolysis and acute renal failure (commensal in cattle - transmitted via hygiene failure)
E. coli in ureter- express mannose binding fimbriae - associated with lower UTIs and cystitis

247
Q

How is E. coli transmitted?

A

Eatubg/ drinking food contaminated with faeces
Meat (infected during processing) - if not heated above 71 degrees celsius
Milk and dairy products and raw fruit and veg (which could have come in contact with faeces)

248
Q

What are some symptoms of E. coli infections?

A

Bloody diarrhoea, stomach cramps, nausea and vomiting, dehydration, some are Asymptomatic, blood, kidney problems
Fever, weakness, bruising, passing only small amounts of urine

249
Q

What investigations are used to diagnose a E. coli infection?

A

Stool sample, M,C&S, microbiological investigation (blood, and or mucus in stool or immunocompromised patient)
FBC
Renal function
Urea and electrolytes

250
Q

How is E. coli treated?

A

Most cases- home care and plenty of fluids
IV fluids if hospitalised
Antibiotics

251
Q

How is E. coli prevented?

A

Washing hands
Washing fruit and veg properly
Avoiding cross contamination
Using a meat thermometer and cooking meat at proper temp

252
Q

What type of virus is Norovirus?

A

Single stranded, positive, icosahedral, non enveloped, RNACalcivirus- can cause outbreaks of acute diarrhoea and vomiting in hospitals, care homes, cruise ships and other confined communities
Divided into 5 genogroups

253
Q

How is Norovirus transmitted?

A

Faecal oral route

Aerosols

254
Q

How long is the incubation period for Norovirus?

A

Symptoms develop after a short incubation period of 24-48 hours

255
Q

Where does Norovirus replication occur? What is the consequence of this?

A

Virus replication occurs in the mucosal epithelium of the small intestine which results in broadening and flattening of villi and hyperplasia of crypt cells

256
Q

What are the main symptoms of Norovirus infections?

A

Self limiting acute diarrhoeal illness

Can be present with sudden onset projective vomiting and explosive diarrhoea

257
Q

How can Norovirus be diagnosed?

A

NAAT

Sequencing is required for epidemiological purposes and to monitor design of future NAAT detection assays

258
Q

How is Norovirus transmission prevented?

A

Isolation
Ward closure
Good hand washing techniques

259
Q

What type of bacteria is staphylococcus aureus?

A

Gram positive clusters of cocci

260
Q

Where is staphylococcus aureus found commensally?

A

A symptomatic carriage found on 40% of healthy people
In nose, skin, axilla or perineum- important in. Healthcare workers especially if they carry an invasive or resistant strain (MRSA)

261
Q

What are the 5 main potential pathogenicity determinants of staphylococcus aureus?

A 
Coagulase
Adhesion molecules
Lytic enzymes
Protein toxins
Biofilm formation
262
Q

What is the activity and effect of coagulase in the pathogenicity of staphylococcus aureus?

A

Coagulase converts fibrinogen to fibrin and may be involved in forming a protective Barrier

263
Q

What is the activity and effect of adhesion molecules in the pathogenicity of staphylococcus aureus?

A

Adhesion molecules bing fibronectin and assist with adherence

264
Q

What is the activity and effect of lytic enzymes in the pathogenicity of staphylococcus aureus?

A

Lytic enzymes such as lipase breakdown the host tissue

265
Q

What is the activity and effect of protein toxins in the pathogenicity of staphylococcus aureus?

A

Protein toxins such as panton valentine leucocidin (pvl), the toxic shock syndrome toxin (tsst), enterotoxins cause shock and toxicity

266
Q

What is the activity and effect of biofilm formation in the pathogenicity of staphylococcus aureus?

A

Biofilm formation causes slower growth in extracellular matrix and is difficult to treat with antibiotics- adheres to plastics

267
Q

What is the clinical importance of staphylococcus aureus infection?

A

Primary skin infections- impetigo- person to person
Secondary skin infections- associated with eczema, surgical wounds, intravenous devices, burns
Pneumonia- rare but may follow influenza and progress rapidly with cavity formation
Endocarditis- rapid and destructive, associated with intravenous drug misuse or colonisation of IV devices
Osteomyelitis
Septic arthritis

268
Q

Describe the antibiotic resistance of staphylococcus aureus

A

It was initially susceptible to penicillin but strains that produce B lactamases soon predominated so methicillin and related (flucoxacillin) agents were introduced and replaced penicillin
Methicillin resistant S.Aureas (MRSA) emerged- resistance caused by presence of mecA gene - codes for a penicillin binding protein that binds the drug less well. Glycopeptides such as vancomycin or teicoplanin started to be required for these strains
Intermediate or hetero resistance to Glycopeptides emerged as an increasing issue and fully Glycopeptide resistant strains (GRSA) have now emerged, resistance being mediated from vanA and vanB genes acquired from enterococci

269
Q

How is staphylococcus aureus treated?

A

Penicillin if susceptible
Flucoxacillin if penicillin resistant
Vancomycin or teicoplanin if MR
Contril measures are needed in hospitals

270
Q

How is staphylococcus aureus infection prevented and controlled?

A

Isolation of MRSA and GRSA

Topical mupirocin and chlorhexidune to eradicate carriage

271
Q

How is staph Aureas spread from individual to individual?

A

Spreads by airborne transmission and hands of healthcare workers

272
Q

How is staph aureus infection investigated and diagnosed?

A

Blood, U&Es
Grows readily on most lab media- selective medium contents high salt to which staph aureus is relatively tolerant
Phenotypic identification depends on demonstrating coagulase, catalase enzymes and typical cluster of grapes morphology on gram stain
Typing by molecular means can support interventions to control outbreaks

273
Q

What genus is HIV from?

A

Lentivirus

274
Q

Describe the structural composition of HIV

A 
Spherical 
Enveloped
Diploid ss +RNA virus
80-100nm in diameter
Non segmented 
Linear
275
Q

How does HIV cause disease?

A

Retrovirus- uses reverse transcriptase to produce a DNA copy from viral RNA that is incorporated into the host nucleus to become the template for further viral RNA
3 genes are required for viral replication- gag, pol and env
2 types of HIV that are pathogenic to humans- HIV1 (most common around world) and HIV2 (largely confined to W Africa, appears less virulent)

276
Q

How is HIV transmitted from person to person?

A

Sexually
By blood and body fluids
From mother to child

277
Q

What is the pathogenesis of HIV?

A

Viral RNA is transcribed to ssDNA and integrates into host genome
Antigenic variation is rapid
Virus principally infects cells with a CD4+ receptors- (T Cells and macrophages)
Viral replication results in progressive T cell depletion and diminished cell mediated immunity
Lacking T cells means that B cell function is also reduced
Damage to neural cells stimulates cytokines release - neurological damage
Clinical signs mostly caused by secondary infections which occur because CD4+ is decreased and cell mediated immunity is non functional

278
Q

What are the clinical features of HIV?

A

50-70% of patients have an acute syndrome occurring 2-6weeks after acquisition of HIV –> rash, fever and lymphadenopathy
Only about 25% of these patients have symptoms severe enough to have to seek medical attention
CD4+ count declines and if untreated reaches a point ( AIDS
Non specific symptoms- fever, malaise, arthralgias, headache, sore throat, with lymphadenopathy
Early invasion of nervous system - meningitis, encephalitis, peripheral neuropathy, myclopathy

279
Q

In HIV infection, what secondary infections commonly occur?

A

Bacteria- MTB, mycobacterium intracellulare, Salmonella, streptococcus pneumoniae
Protozoa- toxoplasma Gondi, cryptosporidium parvum
Fungi- candida sp, cryptococcus neoformans
Virus- varicella zoster

280
Q

What’s the lab diagnosis for HIV?

A

Virus can be cultured from circulating mononuclear cells
Genome detected by PCR and p24 antigen detected prior to seroconversion (where body makes and antibody to a virus)
ELISA is used for antibody screening tests
Confirmation either by western blot or line immunoassay

281
Q

What is the treatment for HIV infection?

A

Several classes of antiretrovirals
HAART- night a ruche anti retroviral therapy
-Nucleoside reverse transcriptase inhibitors (NRTI’s)
-Non NRTI’s
-Protease inhibitors
-Fusion inhibitors
-Integrase inhibitors
-Co receptor/ entry inhibitors
-Zinc finger inhibitors
(Prevent transmission, maintain virus at less than 50 copies, prevent emergence of resistance, restore immunological function)

282
Q

How is HIV infection prevented?

A

Avoidance of partners who have a high risk factor and unprotected intercourse
Screening of blood products
Health education and free needle exchange programme for IV drug users
Antigenic diversity has frustrated vaccine development
Antiretroviral prophylaxis for infected needle stick injury
Mother to child- c section

283
Q

Describe hepatitis b

A

Hepednavirus
Enveloped
Contains partially double stranded DNA encoding surface antigen (HBcAg) pre core protein (HBeAg) a large active polymerase protein and a transactivator protein

284
Q

How does hepatitis b virus replicate? Using what enzyme?

A

Replicates through reverse transcriptase

285
Q

How is hepatitis b transmitted?

A

Parenteral, congenital/ vertical and sexual routes

286
Q

What is the incubation period for hep b?

A

2-6months

287
Q

What are some clinical features of hep b?

A

Congenital infection carries high risk of
10% patients develop chronic hepatitis complicated by cirrhosis or hcc
Fulminant diseases carries a 1-2% mortality
Acute hepatitis of variable severity developes insidiously
Fever malaise jaundice
Liver failure, liver cirrhosis, hcc

288
Q

How is hepatitis b diagnosed?

A

Immunoassay so for HBsAg HBeAg and HBcAg (and associated antibodies) enable diagnosis of acute infection and previous exposure
Viral load measured by NAAT and sequencing for resistance mutations allows monitoring for therapy and directs drug choice

289
Q

What treatment is available for hep b infections?

A

Pegylated alpha interferon
Lamitudine, adefovir, entecavir, tenofovir, telbinudine and clerudine - antiviral efficacy
Emtricitabine and valtorcitabine are nearing clinical introduction
Therapy should be considered in chronic infection as responders have reduced risk of liver damage and liver cancer in the long term
HBeAg seroconversion often seen as a success of treatment

290
Q

How can hepatitis b be prevented?

A

Those at high risk should be immunised with recombinant HBV vaccine- HBsAg based, 3 doses at 0,1,6 months or 0,12,12 months, 95% effective
Vaccine and specific immunoglobulin should be administered to neonates of infected mother to reduce transmission
Post exposure prophylaxis- (HBsAg) positive source, newborns from HBsAg positive mothers, needle stick injury for HCW’s without protection
Blood donations must be effectively screened
Needle exchange programmes for drug misusers and sexual health education schemes can help to reduce transmission

291
Q

What two surfaces are commensal bacteria found on?

A

Skin- epithelia, hair, nails

Mucosal surfaces- conjunctival, gastrointestinal, respiratory, genitourinary

292
Q

What viruses are normally found on the skin?

A

Papilloma

Herpes simplex

293
Q

What bacteria are normally found on the skin?

A

G+ve staphylococcus aureus, coagulative negative staphylococci, corynebacterium
G -ve enterobacteriaceae

294
Q

What fungi are normally found on the skin?

A

Yeasts

Dermatophytes

295
Q

What parasites are normally found on the skin?

A

Mites

296
Q

What pathogens are normally found in the vagina?

A

Lactobacilli

Yeasts

297
Q

What pathogens are normally found in the urethra?

A

Enterobacteriaceae
Lactobacilli
Streptococci
Enterococci

298
Q

What pathogens are normally found in the intestine?

A

Eubacterium
Lactobacillus
Coliform
Clostridium

299
Q

What pathogens are normally found in the stomach?

A

Helicobacter
Streptococci
Staphylococci

300
Q

What pathogens are normally found in the mouth?

A

Viridans streptococci

301
Q

What pathogens are normally found in the nasopharynx?

A

Neisseria meningitidis
Streptococci pneumoniae
Haemophilius influenzae

302
Q

What pathogens are normally found in the nares?

A

Staphylococcus aureus

303
Q

What pathogens are normally found in the eye?

A

Coagulase negative staphylococci
Saprophytic neisseria
Viridans group streptococci

304
Q

How do people get infections?

A

Microbiota- commensals; microorganisms carried on skin and mucosal surfaces; normally harmless or even beneficial, transfer to other sites can be harmful
Invasion- e.g. Streptococcus pyogenes pharyngitis
Migration- e.g. E. coli urinary tract
Innoculation- e.g. Coagulase negative staphylococcus prosthetic joint infection
Haematogenous- e.g. Viridans streptococcus endocarditis

305
Q

What are some external natural surface infections?

A 
Cellulitis
Pharyngitis
Conjunctivitis
Gastroenteritis
UTI
Pneumonia
306
Q

What are some internal natural surface infections?

A

Endovascular- endocarditis, vasculitis
Septic arthritis
Osteomyelitis
Empyema

307
Q

What can prosthetic surface infections develop on?

A 
Intravascular lines
Peritoneal dialysis catheters
Prosthetic joints
Cardiac valves
Pacing wires
Endovascular grafts 
Ventriculooeritoneal shunts
308
Q

What bacteria can cause prosthetic valve endocarditis less than a year after operation?

A

Coagulase negative staphylococci

309
Q

What bacteriae (5) can cause prosthetic valve endocarditis more than a year after operation?

A 
Viridans streptococci
Enterococcus faecalis
Staphylococcus aureus
HACEK group
Candida
310
Q

What are the two main organisms that cause prosthetic joint infection and cardiac pacing wire endocarditis?

A

Coagulase negative staphylococci

Staphylococcus aureus

311
Q

What are the four broad stages in pathogenesis of an infection at a surface?

A

Adherence to host cell or prosthetic surfaces (pili, fimbriae)
Biofilm formation
Invasion and multiplication
Host response- pyogenic (neutrophils –> pus) or granulomatous (fibroblasts, lymphocytes, macrophages –> nodular inflammatory lesions)

312
Q

How does a biofilm form in infections at surfaces?

A

Starvation can induce bacteria to shrink and adopt a spore like state known as ultra-micro bacteria which wait in water soil rock or tissue until conditions are suitable for active growth
Active bacteria can attach to almost any surface – changes in gene expression transform swimmers to stickers within minutes
Attached bacteria multiply and encase colonies with a slimy matrix
Nutrients defuse into the matrix
Close proximity of cells in the matrix facilitates exchange of molecular signals that regulate behaviour
Although antimicrobials damage outer cell layers – biofilm community is
Propelled by shear forces aggregated cells can become detached or roll or ripple along the surface in sheets and remain in their protected biofilm state

313
Q

What is quorum sensing?

A

Controls- sporulation, biofilm formation, virulence factor secretion
3 principles- signalling molecules (auto inducers), cell surface cytoplasmic receptors, gene expression–> cooperative behaviour and more AI production

314
Q

How are surface infections managed?

A

Diagnosis- aim is to identify infecting organism and it’s antimicrobial susceptibilities (sterilise tissue and reduce bio burden); challenges- adherent organisms and low metabolic state/small colony variants; blood cultures; tissue/prosthetic material senication and culture; antibacterials; remove prosthetic material; surgery (resect infected material)
Challenges- low metabolic activity of biofilm microorganisms; poor antibacterial penetration into biofilm

315
Q

How do you prevent infection on natural surfaces?

A

Maintain surface integrity
Prevent bacterial surface contamination
Remove colonising bacteria

316
Q

How do you prevent infection on prosthetic surfaces?

A

Prevent contamination
Inhibit surface colonisation
Remove colonising bacteria

317
Q

What does hypersensitivity mean?

A

Antigen specific immune responses that are either inappropriate or excessive and result in harm to host

318
Q

Describe the sensitisation and effector phase of a hypersensitive reaction

A

Sensitisation phase - first encounter with the antigen

Effector phase - clinical pathology upon reexposure to the same antigen

319
Q

What are the 4 types of hypersensitivity reactions?

A

Type I - immediate, allergy, (<30min); environmental non infectious allergens (antigens)
Type II - antibody mediated (5-12 hours)- antibodies directed against an antigen on the surface of pathogen
Type III - immune complex mediated (3-8 hours)- antibodies directed against soluble antigens on immune complex
Type IV - cell mediated (24-48 hours)- T cells and B cells - environmental infectious agents and self antigens

320
Q

What is an anaphylaxis?

A

Most forms of hypersensitivity are non-life threatening. Anaphylaxis however is a severe form of Type I hypersensitivity reaction, triggered by the exposure of a pre-sensitised individual to an allergen, causing systemic mast cell degranulation. This leads to:
o Vasodilation
o Tissue oedema
o Airways obstruction
o Fall in blood pressure
o Shock
Acute anaphylaxis should be treated with intramuscular adrenaline, which promptly reverses the symptoms and signs with an increase in blood pressure and reversal of airways obstruction.

321
Q

What is the allergen hypothesis?

A

Explains why people have allergies

322
Q

List some common allergens

A

House dust mite, cockroaches
Animals especially domestic pets- cats and dogs
Tree and grass pollens
Insect venom such as that contained in wasp and bee stings
Medicines - e.g. Penicillin
Chemicals such as latex
Foods- peanuts, milk, nuts etc.

323
Q

What are the main cells involved in hypersensitivity reactions?

A

Mast cells

324
Q

What are the 5 broad mast cell mediators?

A 
Enzymes-  
Toxic mediators-  
Cytokines
Chemokines
Lipid mediator
325
Q

How do enzymes mediate mast cell action?

A

tryptase, chymase- remodel connective tissue matrix

326
Q

How do toxic mediators mediate mast cell action?

A

histamine, heparin- toxic to parasites, increase vascular permeability cause smooth muscle contraction

327
Q

How do cytokines mediate mast cell action?

A

IL4, IL13 - stimulate and amplify TH2 cell response
IL3-IL5 - promote eosinophil production and activation
TNF-alpha - promotes inflammation, stimulation of cytokines production by many cell types activates endothelium

328
Q

How do chemokines mediate mast cell action?

A

CCL3 (MIP-1alpha) - attracts monocytes, macrophage and neutrophils

329
Q

How do lipid mediators mediate mast cell action?

A

Leukotrienes- C4, D4, E4
Cause smooth muscle contraction increase vascular permeability, stimulate mucus secretion

Platelet activating factors- attracts leukocytes, amplifies production of lipid mediators , activates neutrophils, eosinophils and platelets

330
Q

Describe the immune mechanism of a type I hypersensitivity (allergic) reaction

A

Cross-Linking of Antigen-Specific IgE molecules on surface of mast cells or basophils.

The cross-linking leads to the degranulation of the cells and the release of vasoactive substances. Reactions typically occur in minutes and form the basis of most common types of allergies, and represent a component of childhood asthma (HDM etc.).

331
Q

Describe the immune mechanism of a type II hypersensitivity reaction

A

Type II – Antibody Mediated Hypersensitivity
IgG antibodies reacting with antigen present on tissues or on the surface of cells.

Once the antibodies have bound with the antigen, they interact with complement or the Fc receptor on phagocytic cells, activating these innate mechanisms leading to the induction of a localised inflammatory response and tissue damage.
These reactions may occur very quickly, but may also lead to prolonged activation.
Examples include:
o Goodpasture’s syndrome
• Autoantibodies to basement membrane in the lung and kidney
o Haemolytic anaemias / Rhesus disease
o Stimulating Ab’s
• TSH in Grave’s disease
o Blocking Ab’s
• Ach R in Myasthenia Gravis
• Insulin receptor in diabetes

332
Q

Describe the immune mechanism of a type III hypersensitivity reaction

A

Type III – Immune Complex Mediated Hypersensitivity
Deposition of immune complexes, usually IgG antibodies.

The immune complexes are deposited in various tissues, where they set up inflammatory reactions similar to Type II reactions (Complement activation, phagocyte Fc receptor).
The commonest sites of Type III reactions are the skin, joints and kidney, and so present with rash, arthritis and/or nephritis.
Examples include:
o Systemic Lupus Erythematosus
o Farmer’s lung

333
Q

Describe the immune mechanism of a type IV hypersensitivity reaction

A

Type IV – Delayed Hypersensitivity
T helper cells activate macrophages or cytotoxic T cells.

Activated macrophages/cytotoxic T cells cause tissue damage. Typically delayed hypersensitivity reactions occur two to three days after exposure to the antigen.
Examples include:
o External antigens
• Tuberculoid Leprosy
• Contact dermatitis
o Autoimmune
• Coeliac disease
• Multiple sclerosis
334
Q

What are three effects of the degranulation?

A

Increased vascular permeability
Vasodilatation
Bronchial constriction

335
Q

How can an allergy be diagnosed?

A

Blood, serum levels of mast cell products

336
Q

What is the skin prick test for allergies?

A

Inner arm usually
Mast cells in epidermis activated
Due to increased vascular permeability and vasodilation - wheal and flare reaction- urticaria

Needs a trained personell, risk of anaphylaxis in highly sensitive subjects

337
Q

What changes occur in the face during an allergic reaction?

A

Mast cells in deep dermis are activated

Angio oedema- lips, eyes, tongue, upper respiratory airways (fatal)

338
Q

What are some systemic changes in the body as a result of an allergic reaction?

A

Bloodstream-
Anaphylaxis
Systemic activation of mast cells
Hypoventilation, cardiovascular collapse, generalised urticaria, angio oedema - face and resp tract, wheezing

339
Q

What treatment is available for anaphylactic shock?

A

Epinephrine/ adrenaline (IM)-acts on alpha1, beta 1 and beta 2 receptors
Reverses peripheral vasodilation and reduces oedema
Reverses airway obstruction/ bronchospasm
Increases force of myocardial contraction
Inhibits mast cell activation
Do not delay treatment- 30 minute window
Monitor pulse, BP, EG and oximetry

340
Q

How would you diagnose the allergy?

A

Clinical history- atopy, allergens, seasonality and route of exposure
Blood test- serum allergen specific IgE
Serum mast cell tryptase, histamine (systemic degranulation)
Skin prick tests- range of allergens - wheal and flare reaction (>3mm), no antihistamines
Challenge tests: food and drug allergies - slight risk of anaphylaxis in highly sensitive patients

341
Q

How would you manage an allergy?

A

Allergen avoidance / elimination
Education- parents recognise symptoms, EPIPEN use and call emergency services
Medic alert identification tags
Drugs- antihistamines (alternate sedating/ non sedating), corticosteroids (topic/systemic), anti IgE igG (omalizulab), anaphylaxis- give injectable adrenaline 0.5mg
Allergen desensitisation - involves administration of increasing doses of allergen extracts over a period of years given to patient by injection/ drops/ tablet under tongue (sublingual) ; 90% effective in patients with bee and wasp venom anaphylaxis; given to patients with increased risk of systemic attacks; specialist hospital based unit with resuscitation equipment

342
Q

What is endocarditis?

A

Heart valves may become infected during transient bacteraemia
Congenitally abnormal or damaged valves are at greater risk
Bacteria may originate from mouth, urinary tract, intravenous drug misuse or colonised intravascular lines

343
Q

What are some causes of native valve and late prosthetic valve endocarditis?

A 
Viridans group streptococci
Enterococci
Other streptococci
Staphylococcus aureus 
Coagulase negative staphylococci
Fastidious gram negatives
344
Q

What are some causes of early prosthetic valve endocarditis?

A 
Coagulase negative staphylococci
Staphylococcus aureus 
Viridans group streptococci 
Enterococci and other streptococci 
Fungi
345
Q

What are some causes of culture negative endocarditis?

A 
NB. Serological diagnosis
Previous antibiotic therapy
Chlamydophila pneumoniae/chlamydia psittaci
Coxiella brunetti- Q fever 
Mycoplasma
346
Q

What are some causes of right sided endocarditis?

A

Nutritionally deficient strains
Staphylococcus aureus
Mixed infections
Fungi

347
Q

What’s the pathogenesis of endocarditis?

A

Damage and roughening of endothelium –> fibrin and platelet deposition –> colonisation of deposit –> bacterial multiplication, further fibrin and platelet deposition, immune activation –> systemic signs of infection! development of vegetation, toxic, embolic and immune complex phenomena

348
Q

What are some clinical features of endocarditis?

A

Malaise, fever, variable heart murmurs, arthralgia
Classical stigmata - splinter haemorrhages, oilers nodes, microhaematuria, retinal infarcts, finger clubbing, janeway lesions (only in long standing infection)
Later stages- septic emboli may cause a stroke
With aggressive organisms staphylococcus aureu, disease progresses rapidly and valves may rupture

349
Q

How would you diagnose endocarditis?

A

Diagnosis is made if there are two major Dulce criteria present, or 1 major and 3 minor

Major- blood culture with characteristic organisms; persistently positive blood cultures with any organism; evidence of endocardial involvement demonstrated by echocardiogram; new valvular regurgitation
Minor- predisposition, fever (>8C), immunological signs

350
Q

What are some complications of endocarditis?

A

Local progression may lead to aortic root abscess
Valve destruction may lead to cardiac decompensation
Cerebral / limb infarction ya follow septic embolus
Nephritis secondary to immune complex deposition can progress rapidly if sepsis is uncontrolled or if antibiotics with renal toxicity are given without care

351
Q

What investigations are involved in the diagnosis of endocarditis?

A

Echocardiography
Transthoracic or grand oesophageal demonstrate vegetations in valves
Plain chest x ray - evidence of cardiac failure
At least 3 sets of blood cultures an hour apart while fever is present
Antibiotic therapy should await blood culture - serum tested for antibodies to Coxiella, bartonella, and chlamidya psittaci

352
Q

How would you manage a patient with endocarditis?

A

Antibiotics - on,y when causative organism is known
Based on MIC and MBC of antibiotics
If gentamicin is used, concentrations must be monitored closely
2-6 weeks
Surgical management

353
Q

Describe the communicable nature of infection

A

Many (all) infections are transmissible:

  • From a non human source to a human ( food- E. coli, water- cholera, environment- legionella, animals- rabies)
  • From person to person directly (influenza, reovirus, neisserria gonorrhoea) or indirectly (mosquitoes- dengue, malaria, cats- cat scratch/ toxoplasmosis, ticks- Lyme disease, spotted fever)
354
Q

What are the four global consequences of transmission of an infection?

A

Endemic disease
Outbreak
Epidemic
Pandemic

355
Q

What is an endemic?

A

The usual background rate

356
Q

What is an outbreak?

A

Two or more places linked in time and place

357
Q

What is an epidemic?

A

A rate of infection greater than the usual background rate

358
Q

What is a pandemic?

A

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

359
Q

What is the basic reproduction number and how does it relate to infection?

A

R0 the average number of cases one case generates over the course of its infectious period in an otherwise uninfected, non immune population

If R0 > 1 => increase in cases
If R0 = 1 => stable number of cases
If R0 < 1 => decrease in cases

360
Q

What are the important concepts of antimicrobial stewardship?

A

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

361
Q

What are the main elements of an antimicrobial stewardship programme?

A

Multidisciplinary team and relationships to other quality/ safety teams
Surveillance- process measures (measuring what you do) and outcome measures (measuring results you get as a result of what you do)
Interventions- persuasive, restrictive, structural

362
Q

What is the infectious dose?

A

Number of microorganisms required to cause infection

Determines transmissibility

363
Q

How does infectious dose vary?

A

By organism
By presentation of microorganism
By immunity of potential host

364
Q

What interventions can help eradicate a pathogen?

A

Antibacterials including disinfectants
Decontamination
Sterilisation

365
Q

What interventions can help eradicate a vector?

A

Eliminate vector breeding sites

366
Q

What interventions help to improve the health of the patient?

A

Nutrition

Medical treatment

367
Q

What interventions help the immunity of the patient?

A

Passive- e.g. Maternal antibody, intravenous immunoglobulin

Active- i.e. Vaccination - herd immunity

368
Q

Define herd immunity

A

Herd immunity is a form of immunity that occurs when the vaccination of a significant portion of a population (or herd) provides a measure of protection for individuals who have not developed immunity or been vaccinated

369
Q

What interventions help to avoid the pathogen or vector in practice?

A

Geographic- don’t go there
Protective clothing/ equipment- long sleeves, trousers against mosquito bites; personal protective equipment in hospitals (PPE) (gowns, gloves, masks)
Behavioural- safe sex, safe disposal of sharps, food and drink prep

370
Q

What interventions or environmental engineering help with prevention of infection transmission in a place?

A

Safe water
Safe air
Good quality housing
Well designed healthcare facilities

371
Q

What are some good consequences of control of infection?

A

• Decreased incidence or elimination of disease/organism
– Smallpox
– Polio
– Dracunculiasis

372
Q

What are some bad consequences of control of infection?

A

• Decreased exposure to pathogen –> decreased immune stimulus –> decreased antibody –> increased susceptibles –> outbreak
• Later average age of exposure –> increased severity
– e.g. polio, hepatitis A, chicken pox, congenital rubella syndrome

373
Q

How do chronic diseases affect a patient?

A

Chronic diseases cause a change in the structure or function of affected tissues/ organs which may have the potential for changing the interaction between the patient and microorganisms
This may be subsequently and further affected by changes caused by the altered presence of microorganisms and the consequences of treatment e.g. with antibiotics and steroids

374
Q

Describe the basic pathogenesis of Cystic fibrosis

A

AR, defect in CF transmembrane conductance regulator gene in exocrine glands
Range of different mutations
Most frequent

375
Q

What are some clinical consequences of cystic fibrosis?

A

Defect in CFTR- defect in Cl- transmembrane transport
Mucus becomes dehydrated and thick causing blockage in small ducts / characteristic salty sweat
Long colonisation and infection with a procession of different organisms
Lung damage, antibacterial and steroid treatment

376
Q

What are some pathogens which are likely to cause infection in CF patients?

A

H. Influenzae
Staph Aureus
Pseudomonas Aeruginosa, Burkholderia Cepacia
Atypical Mycobacteria, Candida albicans, Aspergillus fumigatus

377
Q

Why is CF so common?

A

Heterozygosity provides resistance to cholera, typhoid, TB
In vitro interactions between CFTR protein and cholerol toxin, salmonella typhi, IC entry but no in vivo demonstration of benefit

378
Q

In COPD what cells primarily cause the chronic inflammatory response to inhaled irritants?

A

Neutrophils and macrophages

379
Q

What bacterial microorganisms can cause infection in a COPD patient?

A 
S.Pneumoniae
H.influenzae
Moraxella catarrhalis
Ps. Aeruginosa 
E.Coli
380
Q

What viral microorganisms can cause infection in a COPD patient?

A 
Respiratory syncytial virus
Rhinovirus
Parainfluenza virus
Human metapneumovirus
Coronavirus
Adenovirus
Influenza A virus
381
Q

How does having diabetes affect your immunity and consequently cause infections?

A

Hyperglycaemia and acidaemia impair- humoral immunity, polymorphonucleanuclear leukocytes and lymphocyte functions
Diabetic microvascular and macrovascular disease result in poor tissue perfusion and increased risk of infection
Diabetic neuropathy- diminished sensation resulting in areas of skin which become unnoticed

382
Q

What ENT infections are common in diabetic patients?

A

Malignant or necrotising otitis externa

  • pseudomonas aeruginosa
  • infection starts in external auditory canal and spreads to adjacent soft tissue, cartilage and bone
  • patients typically present with severe ear pain and otorrhoea

Rhino cerebral mucormycosis

  • in patients with poorly controlled diabetes - especially diabetic ketoacidosis
  • mould fungi
  • organisms colonise nose and paranasal sinuses, spreading to adjacent tissues by invading blood vessels and causing soft tissue necrosis and bony erosion
383
Q

What UTIs are common in diabetic patients?

A

Neurogenic bladder due to diabetic neuropathy leads to defects in bladder emptying
Increased risk of a symptomatic bacteriuria and pyuria, cystitis and upper UTIs
Enterobacteriaceae (e.g. E.Coli), Ps Aeuroginosa

384
Q

What neurological disorders affecting bladder control are common in diabetics?

A

CNS diseases- Alzheimers, MS, Parkinson’s, Encephalitis, Stroke
PNS diseases- nerve damage, due to long term heavy alcohol abuse, long term diabetes, neuropathy, syphilis, herniated disk, spinal canal stenosis, pelvic surgery; vitamin B12 deficiency

385
Q

Sensory neuropathy, atherosclerotic valvular disease and hyperglycaemia all predispose patients to an increased risk of infection of what? By what causative microorganisms?

A

Skin and soft tissue
S.Aureus (folliculitis, cellulitis)
Group A B haemolytic streptococcus (cellulitis)
Poly microbial- including 2 of above- enterobacteriaceae, various anaerobes - diabetic foot ulcers and necrotising fascitis

386
Q

What infections are common in patients with Down’s syndrome?

A

Respiratory tract infections (viral and bacterial)
More common in young people with DS
Due to true immunodeficiency or to other factors- altered mucus secretion/ structure of mouth and airways
Otherwise healthy person with DS will probably not suffer more serious infections than siblings and will respond to vaccinations

387
Q

How is humoral immunity affected in a patient with Down’s syndrome?

A

Decreased neutrophil and monocyte function (chemotaxis, phagocytosis, oxidative burst)
Normal number of neutrophils and monocytes
Lower (children) or raised (adults) Ig levels despite normal B cell number
Normal or high levels of serum IgA and secretory IgA
Lowered specific antibody responses upon immunisation
Normal/ raised levels of C3/C4/C5

388
Q

How is cellular immunity affected in a patient with Down’s syndrome?

A

Altered distribution of T cell populations (e.g. Low CD4+:CD8+) but normal T cell number
Decreased T cell function including response to specific antigens and some mitogens
Altered T cell intracellular signalling
Abnormal cytokines production
Lowering of some/ not all NK functions - increased number of NK cells

389
Q

What can pseudomonas aeruginosa infection generally cause?

A 
Endocarditis
Pneumonia
Bacteraemia
Meningitis
ENT- external otitis 
Eye infections
UTIs
GI tract infection
Skin and soft tissue infection
390
Q

What is an immunocompromised host?

A

State in which the immune system is unable to respond appropriately and effectively to infectious microorganisms
Qualitative and quantitative defect of one or more components of the immune system

391
Q

How is SPUR used to diagnose immunodeficiencies?

A 
Infections suggesting underlying immune deficiency are defined as SPUR and so will be:
Severe
Persistent
Unusual
Recurrent
392
Q

What are immunodeficiencies associated with?

A

An increase in frequency and severity of infections

Autoimmune deficiencies and malignancy

393
Q

What is a primary immunodeficiency?

A

Single gene disorder (or polygenic) which affects the immune system directly
HLA polymorphisms

394
Q

What is a secondary immunodeficiency?

A

Underlying disease or condition affecting immune components

Causing decreased components produced and increased loss and catabolism of immune components

395
Q

What are 4 examples of B cell deficiencies?

A

CVID- inability of B cells to mature into plasma cells
IgA deficiency- B cell unable to switch to IgA
Bruton’s disease- impaired B cell development
Hyper IgM syndrome- CD40 ligand on activated T cells

396
Q

How would someone with a B cell deficiency present?

A

Reduced production of IgA –> recurrent upper and lower respiratory tract infections (bronchiectasis); GI complications including infections (Giardia)
Arthropathies (including mycoplasma and urea plasma)
Increased incidence of AI disease and lymphoma & gastric carcinoma
Low IgM and IgG because vaccines don’t amount in antibody production

397
Q

How would you manage someone with a B cell deficiency?

A

Prophylactic antibiotics
Immunoglobulin replacement therapy ( serum IgG > 8)
Management of other infections and respiratory function
Avoid unnecessary exposure to radiation

398
Q

What are 4 examples of T cell deficiencies?

A

Di George syndrome- defect in embryogenesis and incomplete development of thymus gland
STEM CELL DEFECT- Severe combined immunodeficiency (SCID - decreased B and T cells)- defect in gamma chain used by many receptors- IL2,4,7,9
DEATH OF DEVELOPING THYMOCYTES - Severe combined immunodeficiency (SCID) - defect in adenosine deaminase (ADA) purine nucleoside phosphorylase (PNP)
DEFECTIVE T CELL DEVELOPMENT- Severe combined immunodeficiency (SCID) and Omenns syndrome- defect in genes critical for TCR rearrangement and maturation

399
Q

How would someone with DiGeorges syndrome present?

A 
Cardiac abnormalities 
Abnormal facies
Thymic hypoplasia 
Cleft palate
Hypocalcaemia
22- chromosomal abnormality
400
Q

How would you manage someone with Di George’s syndrome?

A

Neonatal cardiac surgery
Supplement to correct hypocalcaemia
Immune defect variable (low T cell number)
- if lower than 0.4x10^9/L- PCP prophylaxis with antibiotics
- bone marrow transplantation (severe forms)
Use only X irradiated and CMV (-) blood
No live vaccines (BCG, MMR, oral polio)

401
Q

How would someone with SCID present?

A 
Failure to thrive 
Long term Antibiotic therapy
Deep skin and abscesses of organs
Low lymphocyte count (<4-10 cells /ul)
Hugh susceptibility to fungal and viral infections - PCP, VZV, CMV, EBV
402
Q

How would you manage someone with SCID?

A

Short term- no live vaccines, only irradiated, CMV- blood products; aggressive treatment of infections, prevention of new infections
Long term- bone marrow/ stem cell transplant, gene therapy

403
Q

What are 4 examples of phagocyte deficiencies?

A

Periodicity- Cyclic neutropenia
Leukocyte adhesion deficiency (LAD)- adhesion to endothelium affected, lack of CD18 protein on phagocytes
Chronic granulomatous disease- intracellular killing affected, lack of respiratory burst- NADPH oxidase deficiency
Chediak Higashi syndrome- failure of phagolysosome formation

404
Q

How would someone with phagocyte deficiencies present?

A

Prolonged and recurrent infections

  • skin and mucous membranes
  • osteomyelitis
  • deep abscesses (staph A)
  • commonly staphylococcal (cat +ve)
  • invasive aspergillosis
  • inflammatory problems- (GRANULOMA)
405
Q

How would you manage a patient with phagocyte deficiencies?

A 
Prophylactic antibiotics/ Antifungal agent/ immunisation 
Surgical management 
Interferon gamma - CGD
Steroids- CHD 
Stem cell transplantation
406
Q

What is an example of a complement deficiency?

A

Hereditary angio oedema
C1 inhibitor deficiency
C1 inhibitor usually inhibits C1 and bradykinin preventing the complement cascade
But in deficiency in HAO there is little/no control over the complement cascaded
So you get vasodilation and increased vascular permeability as well as increased phagocytosis etc.

407
Q

How is hereditary angio oedema treated?

A

C1 inhibitor infusion

Fresh frozen plasma

408
Q

What conditions cause secondary immune deficiencies by decreasing the production of immune components?

A 
Malnutrition
Infection (HIV) 
Liver diseases
Lymphoproliferative diseases
Drug induced neutropenia 
Splenectomy
409
Q

What factors cause drug induced neutropenia?

A

Drugs- e,g, phenytoin, chloramphenicol, alcohol (abuse)
Autoimmune
Infections- hep B/C, HIV, CMV, Typhoid
Bone marrow infiltration with malignancy
Aplastic anaemia
Vitamin B12/ Folate/ Iron deficiency
Chemotherapy- cytotoxic and immunosuppressants
Exposure to chemical agents- benzene, organophosphate
Radiotherapy

410
Q

How would you manage drug induced neutropenia?

A

Neutrophils (< 1 x 10 ^ 9)
Treat suspected neutropenic sepsis as an acute medical emergency and offer empiric antibiotic therapy immediately
Assess patients risk of septic complications

411
Q

What may cause someone to have to have their spleen removed?

A 
Infarction (sickle cell anaemia) 
Trauma
Autoimmune haemolytic disease
Infiltration (tumour) 
Coeliac disease 
Congenital
412
Q

How would someone present post-splenectomy?

A

Increased susceptibility to encapsulated bacteria- haemophiliis influenzae, streptococcus pneumoniae, neisseria meningitidis
OPSI- (overwhelming post splenectomy infection) - sepsis and meningitis

413
Q

How would you manage someone having had a splenectomy?

A

Penicillin prophylaxis (life long)
Immunisation against encapsulated bacteria (at least 2 weeks before splenectomy if possible)
Patient info- medic alert bracelet

414
Q

What are the normal functions of the spleen?

A

Immune

  • blood borne pathogens- encapsulated bacteria
  • antibody production- acute response: IgM production; long term production: IgG production
  • splenic macrophages - removal of opsonised microbes, removal of immune complexes
415
Q

Which three bacteria are encapsulated and thus dealt with by the spleen?

A

haemophiliis influenzae, streptococcus pneumoniae, neisseria meningitidis

416
Q

What conditions cause secondary immune deficiencies by increasing the loss/ catabolism of immune components?

A

Protein losing conditions
- nephropathy and enteropathy
Burns

417
Q

Which infections are pyogenic? What immune cells deal with them?

A

Staph aureus and strep pyogenes

Neutrophils

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