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Phase 3 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the key difference between Gram +ve and -ve bacteria?

A

Peptidoglycan cell wall is much thicker in Gram +ve

  • Fxn of cell wall: help bacteria protect itself against external factors that could cause harm
  • Fixed cell wall allows the Gram +ve bacteria to hold its shape and acts as a means of defence, however bacteria can’t decide what comes into contact with the cell wall

Gram -ve: the outer membrane and periplasm allows the bacteria to decide what can gain access to the cell wall

  • These help Gram -ve become resistant to antibiotics
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2
Q

List the targets for antibiotics

A
  • Cell wall peptidoglycans
  • Metabolism
  • DNA
  • Ribosomes
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3
Q

Describe the types of action of antibiotics

A

Bacteriocidal:

  • Achieve direct sterilisation of the infected site by directly killing bacteria
  • Negative effect: lysis of bacteria can lead to release of toxins and inflammatory material (in meningitis, a steroid is also given to reduce inflammation)

Bacteriostatic:

  • Suppresses growth but doesn’t directly sterilise the infected site
  • Requires additional factors to clear bacteria ie. immune mediated killing
  • In immune compromised area (eg. heart valves) or immunosuppressed patient, when the Abx is stopped, there is nothing to celar the bacteria
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4
Q

With abx - what’s the difference between resistance and lack of activity?

A

Lack of activity: some abx don’t work on specific bacteria due to internal components of the bacteria

Resistance: the bacteria develops components within itself allowing resistance to develop and render the antibiotic ineffective eg. genetic mutations

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5
Q

Compare broad and narrow spectrum antibiotics

A

Broad Spectrum:

  • Antibiotics active against a wide range of bacteria
  • Treat most causes of infection but also have a substantional effect on colonising bacteria
  • Most prone to antibiotic related harm

Narrow Spectrum:

  • Antibiotics that are active against a limited range of bacteria
  • Useful only where the cause of infection is well defined
  • Much more limited effect on colonising bacteria and less likely to cause antibiotic associated harm
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6
Q

List and give examples of different types of bacteria

A

Gram +ve aerobic bacteria:

  • Streptococcus, enterococcus, staphylococcus

Gram -ve aerobic bacteria:

  • E. Coli, psuedomonas, haemophilus

Gram +ve anaerobic bacteria: clostridium

Gram -ve anaerobic bacteria: bacteriocides

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7
Q

How can antibiotics cause harm?

A
  • Disruption of bacterial flora leads to overgrowth of yeasts (thrush) and overgrowth of gut bacteria (diarrhoea)

Antibiotic use associated with

  • Development of infection eg. C Difficile colitis
  • Future colonisation and infection with resistant organisms
  • These are not isolated to the individual patient being treated, it can easily pass to other patients in the ward/hospital/world
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8
Q

What are the different ways in which antibiotics can be used?

A

Guided therapy: depends on identifying cause of infection and selecting abx based on sensitivity testing

Empirical therapy: best educated guess therapy based on clinical/epidemiological acumen. Used when therapy cannot wait for culture (common, not gold standard)

Prophylactic therapy: preventing infection before it beings eg. used for management of patients going to surgery

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9
Q

How do abx choice and administration differ between guided and empirical therapy?

A

Guided therapy

  • Use narrow spectrum antibiotic
  • If possible, limit penetration to site of infection
  • Achieve clinical cure with as little impact on colonisation and resistance as possible

Empirical therapy

  • Use broad spectrum antibiotic (with extensive action against any bacteria that might be causing infection)
  • Needs to penetrate broadly through the body
  • Accept the impact on colonisation and resistance may be great
  • Increased risk of resistance
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10
Q

What causes resistance to ß-lactam antibiotics?

A

Beta-lactamases

  • Enzymes produced by bacteria that lyse and inactivate beta-lactam drugs
  • Commonly secreted by Gram -ves and S. aureus
  • Confer high level resistance to antibiotics (total abx failure is likely to result)
  • If the bacteria secrete a substance that breaks down the abx, that abx will not work
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11
Q

What are the types of ß-lactam antibiotics?

A

Penicillin

  • Benzylpenicillin, Amoxicillin, Flucloxacillin

Cephalosporins

  • Ceftriaxone

B-lactam/B-lactamase inhibitor combination

  • Co-amoxiclav
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12
Q

What are the adverse effects of B-lactams?

A

GI toxicity

  • Nausea and vomiting; Diarrhoea; Cholestasis

Hypersensitivity

  • Type 1 (anaphylaxis); Type 4 (mild-severe dermatology)

Infection

  • Candidiasis; C. diff infection; resistant bacteria

Rarer

  • Seizures; Haemolysis; Leukopenia
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13
Q

What is the mechanism of action of Beta-lactam antibiotics?

A
  • All share the same structural feature: B-lactam motif analogue
  • Inhibits cross-linking of cell wall peptidoglycans
  • Causes lysis of bacteria (bacteriocidal)
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14
Q

What is the class, indication and action of flucloxacillin?

A

Class: B-lactam, Penicillin

Indication: soft tissue infections, staphylococcus endocarditis, otitis externa, S. aureus infections

  • Resistant against b-lactamase produced by staphylococci
  • No activity against gram -ve’s, good cover against gram +ve’s (covers against s. aureus which amoxicillin can’t)

Action:

  • Attaches to penicillin binding proteins on forming bacterial cell walls
  • This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall
  • Failure to cross-link induces bacterial cell autolysis
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15
Q

What is the class, indication and action of amoxicillin?

A

Class: B-lactam, penicillin

Indication: non-severe community acquired pneumonia

  • Inc. activity against Gram -ve as well as Gram +ve

Action:

  • Attaches to penicillin binding proteins on forming bacterial cell wall
  • This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall
  • Failure to cross-link induces bacterial cell autolysis
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16
Q

What is the role of beta lactamase inhibitors and give one example?

A
  • Effectively inhibit some beta-lactamases
  • Co-administered with penicillin abx to protect the abx, allowing it to work more effectively
  • Broadens spectrum of penicillins against Gram -ve and S. aureus

Example:

  • Clavulanic acid given with amoxillin: Co-amoxiclav
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17
Q

What is the class, indication and action of ceftriaxone?

A

Class: B-lactam, cephalosporin

Indication: severe infection (septicaemia, meningitis, pneumonia) and often CNS infections

  • Gram +ve and Gram -ve cover
  • Less susceptible to beta-lactamases

Action:

  • attaches to penicillin binding proteins on forming bacterial cell walls
  • this inhibits the transpeptidase enzyme that cross-links bacterial cell wall
  • Failure to cross-link induces bacterial cell autolysis
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18
Q

What is the class, indication, action and route of administration of Vancomycin?

A

Class: Glycopeptide

Indication: severe Gram +ve infection, MRSA, severe C. Diff infection

  • NO Gram -ve cover

Action:

  • Bactericidal
  • Inhibits cell wall synthesis in Gram +ve bacteria
  • Not dependent on penicillin binding proteins so effective against resistant organisms
  • Narrow therapeutic range

Administration: IV unless treating C. Diff infection (orally)

  • Long 1/2 life so loading dose always given
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19
Q

List 3 side effects of Vancomycin

A

Vancomycin - faily toxic

  • Nephrotoxicity
  • Fever
  • Rash
  • Red-man syndrome if injected too quickly (anaphylactoid reaction and patient develops rash over their bodies)
  • Ototoxicity
  • Blood disorders inc. neutropenia
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20
Q

List the different protein synthesis inhibitors used for antibiotic treatment

A

50s ribosomal subunit: macrolides

  • Clarithromycin and erythromycin

30s ribosomal subunit: aminoglycosides

  • Gentamicin
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21
Q

What is the class, indication and action of clarithromycin?

A

Class: Macrolide

Indication:

  • Good spec. against Gram +ve and respiratory Gram -ve
  • Atypical organisms causing pneumonia / severe community acquired pneumonia
  • Severe campylobacter infection, mild/moderate soft tissue infection, otitis media, H. pylori eradication
  • Active against atypicals eg. chlamydia, legionella, mycoplasma

Action:

  • Binds to the 50s ribosomal subunit
  • Inhibits bacterial protein synthesis
  • Bactericidal and bacteriostatic
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22
Q

List 2 different penicillins

List a cephalosporin

List 2 macrolides

List a glycopeptide

List an aminoglycoside

A

Penicillin: flucloxicillin and amoxicillin

Cephalosporin: ceftriaxone

Macrolide: erythromycin and clarithromycin

Glycopeptide: vanocmycin

Aminoglycoside: gentamicin

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23
Q

List the adverse effects and drug interactions of clarithromycin/erythromycin

A

Adverse effects:

  • diarrhoea, vomiting, QT prolongation, ototoxicity

Drug interactions:

  • Simvastatin (avoid co-prescription)
  • Warfarin
  • Atorvastatin
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24
Q

What is the class, indication and action of erythromycin?

A

Class: Macrolide

Indication:

  • Good spec. against Gram +ve and respiratory Gram -ve
  • Atypical organisms causing pneumonia / severe community acquired pneumonia
  • Severe campylobacter infection, mild/moderate soft tissue infection, otitis media, H. pylori eradication
  • Active against atypicals eg. chlamydia, legionella, mycoplasma

Action:

  • Binds to the 50s ribosomal subunit
  • Inhibits bacterial protein synthesis
  • Bactericidal and bacteriostatic
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25
Q

How are Closridium Difficile infections caused by abx and what is the issue with these infections?

How do you avoid C. Diff infection?

A
  • C. Diff commonly colonises the human colon
  • Abx alter the normal colonic flore, allowing C. Diff to grow and develop and therefore it will occupy a greater area
  • C. Diff then forms spores which can be difficult to eradicate from hospitals
  • Has developed resistance to common abx classes
  • All antibiotics can cause C. Diff
  • To avoid: keep abx as narrow spectrum as possible
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26
Q

List 4 antibiotics associated with clostridium difficile infection

A
  • Clindamycin
  • Ceftriaxone/Cephalosporins
  • Co-amoxiclav
  • Ciprofloxacin
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27
Q

What is the class, indication and action of Gentamicin?

A

Class: aminoglycoside

Indication: severe infection

  • Severe Gram -ve infections eg. biliary tract infection, pyelonephritis, hospital acquired pneumonia
  • Severe Gram +ve infections: soft tissue infection and endocarditis

Action:

  • Binds to the 30s subunit, inhibiting bacterial protein synthesis, inducing a prolonged post-antibiotic bacteriostatic effect
  • Bacteriocidal action on bacterial cell wall results in rapid killing early in dosing interval and is prominent at high doses
  • Provides a synergistic effect when when used alongside other abx eg. flucloxacillin or vancomycin
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28
Q

What are the side effects of Gentamicin?

How is it adminstered?

A

Adverse effects:

  • Nephrotixicity and ototoxicity (hearing loss and loss of balance)
  • Related to prolonged exposure to high-drug concentrations

Administration:

  • IV dosing
  • High initial dose to take advantage of rapid killing (bactericidal effect)
  • Long disoing intervals (24-48hrs) to minimise toxicity
  • Max. 3 days to minimise side effects
  • Used empirically and short term
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29
Q

What is the class, indication and action of ciprofloxacin?

A

Class: quinolone

Indication: Better against Gram -ves

  • Commonly used in UTI/abdominal infection
  • Gram -ve bacterial infections
  • Resp tract infection, upper UTI, periotneal infection, gonorrhoea, prostatits, E. Coli cover

Action:

  • Interfers with bacterial DNA replication and repair
  • Broad spectrum bactericidal antibiotics
  • Both gram +ve and -ve cover
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30
Q

What are the side effects of ciprofloxacin?

A
  • Quinolone

Side effects:

  • GI toxicity, QT prolongation, C. Diff infection, tendonitis (rare)
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31
Q

What is the class, indication and action of trimethoprim?

A

Class: inhibitor of folate synthesis

Indication:

  • 1st line therapy for uncomplicated UTI (good E. Coli cover - E. Coli is the most common cause of uncomp. UTI)
  • Acute/Chronic bronchitis
  • Pnuemocystis pneumonia (PCP)
  • Good Gram -ve and Gram +ve cover including MRSA

Action:

  • Inhibits folate metabolism pathway, leading to impaired nucleotide synthesis
  • Therefore interfers with bacterial DNA replication
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32
Q

What are the side effects of trimethoprim?

A
  • Elevated serum creatinine
  • Hyperkalaemia (need to note if patient is on ACEi)
  • Depressed haematopoiesis
  • Rash and GI disturbance
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33
Q

What is cystitis?

A
  • An uncomplicated UTI

Lower urinary tract symptoms and absence of sepsis or evidence of upper tract involvement (pyelonephritis)

  • Treatment only needs to sterilise urine
  • Low risk infection so can often wait for culture results
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34
Q

What is 1st line treatment for an uncomplicated UTI/cystitis?

A
  • Most are self-limiting, so recommend fluids and analgesia (NSAIDs)

1st line treatment: Trimethorpim

  • Avoid in 1st trimester of pregnancy (weak anti-folate activity)
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35
Q

What is the most common causative agent of urinary tract infections?

A

E. Coli and other coliforms

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36
Q

How might a complicated UTI case present and what would be the management plan?

What would the management plan be if the patient was severely unwell?

A
  • May present with back pain and fever but not depaerately unwell: starting to develop early kidney infection
  • Main concern: patient is at a higher risk of detioration
  • Choice: ciprofloxacin as resistance is less common as with trimethoprim

Severely unless: temp >40, looks unwell

  • Send to hospital
  • Gentamicin: IV abx not an issue bc already going to hospital and need good cover and resistance is unlikely
  • Amoxicillin co-administered: esp in older patients and querying pneumonia so need good strep cover
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37
Q

What abx should be avoided during pregnancy?

A
  • Trimethoprim: neural tube defects (1st trimester)
  • Aminoglocosides: otoxicity (2nd/3rd trimester)
  • Quinolines: bone/joint abnormalities
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38
Q

Define antimicrobial resistance (AMR)

A

Antimicrobial resistance occurs when microorganisms such as bacteria, viruses, fungi and parasites change in ways rendering the medications used to cure the infections they cause inefffective

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39
Q

What is One Health?

What are the main areas of concern?

What is the One Health Approach?

A

The approach to designing and implementing programmes, policies, legislation and research in which multiple sectors communicate and work together to achieve better pubilc health outcomes

Relevant areas:

  • Food safety
  • Control of zoonoses (diseases that can spread between animals and humans)
  • Combating antibiotic resistance

Approach: Human-Animal-Environment

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40
Q

How is antibiotic resistance monitored?

Define clinical resistance

A
  • In-vitro quantitative testing of bacterial suspensions to antibacterial agents
  • Minimum inhibitory concentration = the minimum concentration of an antibiotic required to inhibit the growth of bacteria

Clinical resistance - when infection is highly unlikely to respond even to maximum doses of abx

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41
Q

What mechanisms can bacteria adopt to cause antimicrobial resistance?

A

Efflux pumps: membrane protein complexes that transport molecules from inside to outside the cell, some of which can transport abx

Inactivating enzymes: enzymes that degrade/inactivate specific antibiotics eg. ß-lactamase enzyme breaking down penicillin

Target alterations (mainly cell wall): the target for penicillin is penicillin binding proteins (PBPs) which zip-up the cell wall. Penicillin resistant bacteria have altered the shape of their PBPs

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42
Q

In terms of the antibiotic, what are the reasons for resistance?

A
  • Highly specific cellular target
  • There’s an upper limit to the conc. that can be used without harming the patient, which is often close to the MIC (Minimum Inhibitory Conc)
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43
Q

Compare/Define intrinsic and extrinsic resistance of bacteria

A

Intrinsic resistance: the ability of a type of bacteria species to resist the action of an antibiotic due to a natural structual or functional characteristic of the bacteria (due to natural genetic makeup of the bacteria)

Extrinsic resistance: the result of the acquisition of new genetic information/mutation of the existing genome, for example when plasmids carrying the genes for abx resistance are acquired by a bacterium

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44
Q

What are the methods for intrinsic resistance of bacteria?

A
  • Bacterium has resistant genes in its genome
  • Lack of the target of the antibiotic
    eg. Gram -ve bacteria are intrinsically resistant to Vancomycin due to protective outer membrane and periplasm
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45
Q

What are the methods for extrinsic resistance to abx?

A

Transduction:

  • Phage mediated ie. acquiring genes from a bacterial virus
  • Information is encapsulated in a bacteriophage, which attaches to the bacterium and bacterial information is injected into the bacterium and incorporated into the chromosome

Transformation:

  • Incorporation of naked DNA ie. acquiring genes from the environment
  • Occurs when bacteria lyse, and segments of DNA are released into the environment. These are taken up naturally by transformable bacteria and incorporate the DNA into their chromosome

Conjugation:

  • Bacterial sex, involving cell-to-cell contact
  • Aquiring genes from another bacterium
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46
Q

How do extended spectrum beta-lactamases (ESBL) occur?

How are ESBL infections treated?

A
  • B-lactam (penicillin) produced
  • Bacteria become resistant
  • Chemists add amolecule to make antibiotic structurally different
  • Beta-lactamases then change to adapt to abx changes
  • Cycle continues, and the new beta-lactamases are called ESBL

Treat with carbapenem

- Broad specturm abx

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47
Q

Why are carbapenem-resistant bacteria worrying?

A

Carbapenems are views are the last therapeutic option to treat complex infections caused by MDR (multi-drug resistant) bacteria

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48
Q

What antibiotics target:

  • Cell wall
  • Protein synthesis (ribosomes)
  • DNA
A

Cell wall:

  • B-lactams: Penicillin, Co-amoxiclav and cephalosporin (ceftriaxone)
  • Glycopeptide: Vancomycin

Protein Synthesis/Ribosomes:

  • Macrolides: Clarithromycin and erythromycin
  • Aminoglycosides: Gentamicin

DNA

  • Inhibitor of folate synthesis: Trimethorpim (impaired replication)
  • Quinolones: ciprofloxacin (replication and repair)
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49
Q

What are antibiotics used for?

A
  • To treat infection
  • Used in a majority of surgical procedures: implant surgery, cancer surgery, cardiac
  • Cancer chemotherapy
  • Immunotherapy
  • Organ transplantation
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50
Q

Describe the spectrum of activity of different penicillins

A

Benzylpenicillin: narrow spectrum

  • Activity against strep

Flucloxacillin: broader spectrum

  • Activity against Gram +ves, including S. aureus and Strep

Amoxicillin: broader spectrum

  • Some activity against Gram -ves and anaerobes (C. diff) as well as Gram +ves
  • No effect on S. aureus

Co-amoxiclav: broad spectrum

  • Strengthens axomicillin’s activity against anaerobes and Gram -ves
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51
Q

What is the correlation between antibiotic use and resistance?

A
  • High correlation
  • the more antibiotics a patient is given, the more likely they are to develop AMR
  • ie. resistance can be due to inappropriate dosing of abx for wrong periods of time
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52
Q

What is the connection between animals and humans with antibiotic use?

A
  • many abx are used for both animals and humans
  • use of abx in animals is having an impact on resistance in humans
  • waste from animals goes into slurry and streams/water, which ends up being consumed by humans in some parts of the world
  • therefore AMR that develop in animals are directly transferred into humans
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53
Q

How do we reduce antimicrobial resistance?

A
  • Limit the use of abx ie. antibiotic stewardship
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54
Q

What are the problems associated with unnecessary antibiotic use?

A
  • Avoidable toxicity eg. renal, haem, GI
  • Vascular device complication with IV abx
  • Prolonged hospitalisation
  • ‘Opportunity cost’: IV abx divert nursing time from patient care
  • Unnecessary prolonged prescription: wasteful and expensive
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55
Q

What factors are driving antibiotic prescription?

A
  • Education/Experience/Behaviour
  • Misconceptions: ‘withholding abx is always harmful/wrong’
  • Experience and expectations drive abx seeking behaviour either with patients or our own behaviour: ‘I prescribed it last time’
  • Lack of evidence evolution knowledge: not keeping up to date. Eg. used to think we need to finish a course of abx, however this has been disproven
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56
Q

Define antimicrobial stewardship

A

The systematic approach to safe and effective use of abx - optimising outcome, minimising harm and preserving future therapies ie. taking care of abx

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57
Q

How is antimicrobial stewardship achieved?

A
  • Monitoring/Surveillance: monitor prescribing, AMR, adverse effects
  • Implementing guidelines/protocols
  • Specific restrictions on abx prescriptions
  • Specific interventions: how to control abx when problems with start to occur
  • Multidisciplinary working: nurses, pharmacists, doctors
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58
Q

What is monitored to ensure antimicrobial stewardship?

A
  • Volume of abx prescribing (pharmacy records, type of abx)
  • Quality of prescribing (is it the right abx for the right indication for right time at right dose?)
  • AMR
  • Clostridium Difficile (direct effect of over-prescribing Abx)
  • Other adverse events related to prescribing/interventions
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59
Q

What are important factors to consider when prescribing antibiotics?

A
  1. Is an abx required?
  2. Choice - which abx?
  3. Route of administration -IV or oral?
    - Life-threatening infections: IV
  4. Dose and interval
  5. Adjunctive measures - controlling the source eg. surgeru
  6. Duration and IVOST (IV-Oral Switch Therapy)
    - Short duration and earlier IVOST are good
    - For IVOST: clinical improvement + oral route available + uncomplicated infection
  7. Severity assessment and Therapeutic drug monitoring (TDM)
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60
Q

What situations would you not give antibiotics?

A
  • Viral or self-limiting bacterial respiratory tract infections
  • Asymptomatic bacteruria or uncomplicated UTI
  • In-growing toenails
  • Leg ulcer without cellulitis
  • Varicose ezcema (mistaken for cellulitis)
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61
Q

How are UTIs treated?

A

Asymptomatic bacteriuria: if no urinary symptoms, don’t prescribe Abx

Uncomplicated UTI (cystitis)

  • Majority are self-limiting
  • Recommend fluids and analgesia
  • Consider delayed abx: Trimethoprim or Nitrofuratonin for 3 days (women) or 7 days (man)

Catheter associated UTI

  • Remove catheter and treat if symptoms/sepsis
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62
Q

What signs/symptoms would point towards bacterial infection needing abx?

Localising for urinary, resp and soft tissue

A

Signs/symptoms of infection: fever, sweats, rigors, shivers and shakes

Localising signs/symptoms

  • Dysuria and frequency
  • Dyspnoea, cough and green/brown sputum
  • Sore throat with exudate and lymphadenopathy
  • Erythema, heat, swelling
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63
Q

What would be the choice of Abx for:

Non-severe

  • LRTI (lower resp tract infection)
  • Lower UTI
  • Mild cellulitis

Severe/Life threatening

A

Non-severe

  • LRTI: amoxicillin
  • Lower UTI: trimethoprim
  • Mild cellulitis: flucloxacillin

Severe/life-threatening

  • Initially IV combination therapy: B-lactam (amoxicillin) and gentamicin (no time to culture, need prompt administration)
  • Use of protected abx if multidrug resistance
  • Prompt (<1hr) administration
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64
Q

How is a COPD exacerbation treated?

How long are community and hospital acquired pnuemonia treated for?

A
  • COPD exacerbation: Amoxicillin for 5 days

CAP and HAP: 5 days

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65
Q

What Antimicrobial Stewardship intervention types are implemented and what have been their benefits?

A

Restrictive: short-term benefits inc. reduction in resistance

Persuasive: longer term benefits through behavioural changes

Guideline adherence (empirical guidelines and de-escalation): reduced mortality

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66
Q

Define sepsis

A

Life-threatening organ dysfunction which occurs as a result of a dysregulated host response to infection

Sepsis is systemic response to infection ie. presence of SIRS in addition to documented organ dysfunction

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67
Q

How is sepsis quantified?

A

An increased in the Sequential Organ Failure Assessment (SOFA): Score >2

OR

Quick SOFA (qSOFA): determines sepsis

Sepsis is systemic response to infection ie. presence of SIRS in addition to documented organ dysfunction

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68
Q

What are the components of the qSOFA score and what does it mean?

A
  • Hypotension: Systolic BP <100
  • Tachypnoea: RR >22
  • Altered mental state: GCS <15

Interpretation: Score >1 suggests sepsis

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69
Q

Compare Systemic Inflammatory Response Syndrome (SIRS) and sepsis

A

SIRS: relates to inflammation

Sepsis: result of infection overwhelming the body’s defences

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70
Q

What is the criteria in systemic inflammatory response syndrome (SIRS)

A

2+ of:

  • Tachycardia: HR >90
  • Temp <36 or >38
  • RR >20
  • WWC <4 or >12
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71
Q

What should be undertaken within 1 hour of sepsis recognition?

A

Sepsis 6

  • Take blood cultures
  • Give IV antibiotics
  • Give high flow oxygen to achieve target sats
  • Give IV fluids
  • Measure Hb and lactate
  • Measure hourly urine output
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72
Q

What are the indications for IV antibiotic therapy?

A
  • Sepsis syndrome, SIRS or rapidly progressive infection
  • Infective endocarditis
  • CNS infection
  • Bacteraemia (S. aureus)
  • Osteomyelitis (initially)
  • Moderate-severe skin/soft tissue infection
  • Infection with compromised oral route
  • No oral formulation of abx available
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73
Q

What is the treatment for S. aureus bacteraemia?

A
  • Flucloxacillin 2g 6-hourly
  • If true penicillin allergy or MRSA - Vancomycin
  • If persistent fever/ no improvement, do TOE (transoesophageal echocardiogram)
  • Treat with IV therapy for >2 weeks
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74
Q

What are the links in the chain of infection

A
  • Infectious agent
  • Reservoirs
  • Portal of exit
  • Means of transmission
  • Portal of entry
  • Susceptible host
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75
Q

What are the main reservoirs used by infectious agents

A

Environment: need to control water quality in hospitals

Animals: eg. flies

Humans: symptomatic or asymptomatic (carriers)

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76
Q

What are the 3 main ways of preventing infection

A
  • Water control
  • Rodent control
  • Isolation
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77
Q

Give 3 examples of infectious agent and their portal of exit

A

Tuberculosis: air borne infection

Salmonella: faeco-oral

Norovirus: vomit

Hep B or HIV: bloodborne

  • Enterovirus: conjunctival secretions eg. watery eyes
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78
Q

Compare the modes of transmission of infectious agents

A

Direct:

  • Direct contact eg. coughing on hands and shaking someone’s hand
  • Droplet spread: someone coughing on someone else (small particles travel <2m)

Indirect:

  • Airborne
  • Vehicle borne (food water fomites)
  • Vector borne (mechanical or biologic)
    eg. cough on a surface then someone comes and touches that surface
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79
Q

What portal’s of entry are available for infectious agents?

A
  • Respiratory tract
  • Mucous membranes
  • Non-intact skin eg. surgery cuts, IV lines
  • Mouth (faeco-oral)
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80
Q

Who is susceptible to infection and list 3 ways in which the risk of developing infection can be reduced?

A

Susceptible hosts:

  • New hosts
  • Immunocompromised

Reduce risk

  • stop smoking, lose weight, control diabetes, vaccinations, prophylaxis, nutiriton, protective isolation
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81
Q

What are the standard precautions that must be undertaken with every patient?

A
  1. Assess patients for infection risk and ensure they’re cared for in a safe place
  2. Practice good hand hygiene
    - Before touching a patient, before procedure, after procedure/body fluid exposure risk, after touching patient, after touching patient’s surroundings
  3. Cover nose and mouth when coughing/sneezing
    - Catch it, bin it, kill it
  4. Wear suitable PPE
  5. Keep all reusable care equipment clean and well maintained
  6. Keep the care environment clean and tidy
  7. Safely handle used linen
  8. Safely clean up all blood and body fluid spillages
  9. Safely dispose of all household and care activity waste
  10. Take corrective action if injured or exposed to blood and bodily fluids
    * every patient, every time, every interaction*
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82
Q

What transmission based precautions are also adopted in addition to standard precautions?

A

Contact:

  • isolation, cleaning the environment, gloves, apron
    eg. salmonella

Droplet:

  • Surgical mask and eye protection

Airborne:

  • FFP3 masks
    eg. TB, pandemic flu
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83
Q

List 5 strategies to prevent organisms causing hospital acquired infections (HAI)

A
  • isolation
  • screening
  • cohorting
  • standard and transmission-based precautions
  • surveillance: eg. how many specific infections there are per year
  • antimicrobial stewardship
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84
Q

Give 5 principles involved in the aseptic technique

A
  • reduce activity in the area
  • keep exposure of a susceptible site to a minimum
  • check sterile packs for evidence of damage or moisture
  • ensure all fluids and materials are in date
  • don’t reuse single use items
  • hand decomtamination prior to procedure
  • disposable apron
  • use sterile gloves
  • appropriate waste disposal
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85
Q

Define pneumonia

A

Inflammation of one or both lungs, with dense areas of lung inflammation

  • Frequently but not always due to infection
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86
Q

What are the bacterial causes of pneumonia?

A

Typical pneumonia

  • Strep. pneumoniae
  • Haemophilus influenza

Atypical pnuemonia

  • Mycoplasma pneumoniae
  • Legionella pheumophila
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87
Q

List 3 risk factors for acquiring strep. pneumonia infection?

A

alcohol, smoking, cancer

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88
Q

List 3 clinical features and 3 examination findings for typical pneumonia

A

Clinical features:

  • Fever
  • pleuritic chest pain
  • cough (+/- sputum)
  • abrupt onset
  • non-resp symptoms

Signs:

  • dull percussion
  • coarse crepitations
  • inc. vocal resonance
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89
Q

what are 2 risk factors for haemophilus influenza?

A
  • elderly
  • underlying lung disease
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90
Q

What complications can arise due to infection with mycoplasma pneumoniae

A
  • haemolysis
  • Guillain-Barre
  • erythema multiforme
  • cardiac problems
  • arthritis
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91
Q

What clinical assessments are crucial for a patient with pneumonia?

How is severe pneumonia determined

A

CURB65

Confusion, Urea >7, Resp rate >30, BP diastolic <60 or systolic <90, age >65

Multilocular consolidation on CXR or hypoxia on room air

severe pneumonia:

  • >2 in CURB65 or multilocular consolidation on CXR/hypoxia on room temp

Sepsis: qSOFA

  • GCS <13 (confusion), resp rate >22, sBP <100mmHg
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92
Q

What investigations are important for a patient with suspected pneumonia?

A

Bloods:

  • FBC, U&Es, ABG

Micro:

  • blood cultures, sputum culture, throat swab, urine legionella antigen

Investigations:

  • CXR and ECG
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93
Q

What is the management for pneumonia?

A

ABC

  • airways, breathing, circulation

Antibiotics: IV or oral

Potential admission to hospital

Depends on:

  • CURB65, qSOFA, hypoxia
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94
Q

What is the treatment for strep pneumoniae?

A

Penicillin (resistance is rare in UK)

If penicillin allergy:

  • macrolides (clarithromycin)
  • tetracyclines (doxycycline)
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95
Q

What is the abx treament for haemophilus influenza?

A

co-amoxiclav

If penicillin allergy:

  • macrolides (clarithromycin)
  • tetracycline (doxycycline)
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96
Q

What is the abx treatment for legionella pneumophila?

A
  • Macrolides (clarithromycin)
  • quinoline (ciprofloxacin)
  • tetracyclines (doxcycline)
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97
Q

how do you treat typical pneumonia?

A
  • penicllin

if penicillin allergy:

tetracyclines (doxycycline) or macrolides (clarithromycin)

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98
Q

Give thee bacterial causes of traveller’s diarrhoea

A
  • enterotoxigenic e. coli
  • enteroaggregative e. coli
  • campylobacter
  • salmonella
  • c. diff
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99
Q

Give 2 viral and 1 parasitic cause of traveller’s diarrhoea

A

Virus:

  • norovirus
  • rotavirus

Parasite

  • Giardia
  • Cyclospora
  • Microsporidia
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100
Q

What are the clinical features of traveller’s diarrhoea

A
  • often day 4-14 of travel
  • Self-limiting: lasts 1-5 days
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101
Q

What is the clinical presentation of enterotoxigenic e. coli (ETEC)?

A
  • Anorexia, malaise and abdominal cramps
  • Watery diarrhoea (no blood)
  • Fever, nausea, vomiting
  • Can cause ‘colitic symptoms’: having to rush to the toilet, blood in stool, pain when opening bowels
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102
Q

What is the management for traveller’s diarrhoea?

A

Fluid replacement

  • rarely give abx
  • antimotility agents (to get through a flight/long travel): caution as it slows the function of diarrhoea which is to remove the organism from the gut
  • if prolonged: need to investigation
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103
Q

What bugs can transmit illness when travelling and which one’s should you be worried about?

A
  • many illnesses are mosquito borne

Aedes: spread yellow fever and Dengue fever (day feeding)

Anopheline: spreads Malaria (noctural feeding)

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104
Q

List 3 physical measures can be put in place to avoid mosquito bites?

A
  • indoors: air conditioning, screens for windows
  • impregnated netting: permethrin, tucked in under the mattress
  • Clothing: cover up (arms, legs, ankles, feet), spray
  • repellent: deet (30% deet reapplied every 3-4hrs)
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105
Q

What is the most common cause of undifferentiated fever in travellers from sub-Saharan africa?

A

malaria

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106
Q

How is malaria acquired?

A

Anopheline mosquito bites

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107
Q

List 3 clinical presentations of malaria

A
  • undifferentiated fever
  • malaise, myalgia (muscle pain)
  • headache
  • GI: diarrhoea
  • resp: dry cough
  • anaemia
  • jaundice
  • renal impairment
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108
Q

Give 3 complications of severe malaria

A
  • parasitaemia
  • cerebral malaria
  • severe anaemia
  • renal failure
  • septic shock
  • DIC (disseminated intravascular coagulation)
  • acidosis
  • pulmonary oedema
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109
Q

What is the main resulting pathogenesis of malaria and how does it present

A

Increased RBC breakdown

  • Anaemia
  • Jaundice (severe disease due to RBC lysis)
  • Renal impairment (poor microcirculation)
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110
Q

How do you prevent infection with Malaria?

A

Bite avoidance

Chemoprophylaxis in high prevalent areas (eg. sub-saharan africa)

  • Mefloquine: once weekly
  • Doxycycline: daily (SE: photosensitisation)
  • Malarone: daily (minimal SE)
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111
Q

What are the causative agents of Typhoid?

How is typhoid acquired?

A
  • enteric fever causative organisms: salmonella typhi (s. typhi), s. paratyphi
  • s. paratyphi is similar to but more subtle than s. typhi

Only human reservoirs ie. need human carriers

  • acquired through contaminated food/water
  • faeco-oral transmission
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112
Q

What is the incubation period for Typhoid and what determines it?

A

Incubation period: 5-21 days

Dependent on: age, gastric acidity, immune status, infectious load

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113
Q

Give 5 clinical manifestations of Typhoid

What would happen if left untreated?

A

Undifferentiated fever

GI symptoms:

  • diarrhoea or constipation (50:50)
  • abdominal pain, rectal bleeding and bowel perforation

Other:

  • undifferentiated fever, myalgia, headache, cough
  • altered consciousness/confusion
  • bacteriaemia (metastatic infection)
  • bradycardia

If left untreated: can lead to septic shock and death

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114
Q

How do you prevent Typhoid fever?

Where is typhoid prevalent?

A
  • Prophylactic vaccinations
  • Only drink bottled or boiled water
  • avoid foods that may be contaminated with typhoid causative organisms

Prevalent: India, Bangladesh

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115
Q

How is typhoid treated?

A

Early infection: treated with abx at home

  • Cephalosporins (Cefriaxone): 1st line
  • Quinolones (Ciprofloxacin): if resistant organisms

Rest, keep hydrated, regularly wash hands and avoid handling/preparing food (faeco-oral route)

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116
Q

List 3 clinical features of Dengue fever and it’s incubation period

A

Incubation period: 5-14 days

‘Breakbone fever’

  • headache
  • fever
  • retro-orbital rash, general rash
  • arthralgia/myalgia
  • cough, nausea, sore throat, diarrhoea
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117
Q

List 3 labatory findings for Dengue fever

A
  • leukopenia
  • thrombocytopenia
  • transaminitis (high levels of transaminases produced by the liver)
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118
Q

How is Dengue fever acquired and how can it be prevented?

A

Spread via aedes mosquitos

Mosquito prevention strategies

  • Indoors, repellent, keep covered with clothing and impregnated nets when sleeping
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119
Q

What are the causative agents for Malaria, Dengue fever and Typhoid

A

Malaria: parasite (Plasmodium parasite)

Dengue fever: virus (flaviviridae family)

Typhoid: bacteria (salmonella typhoid or paratyphoid)

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120
Q

What is the management for Dengue fever?

A
  • Symptomatic: rest, fluids, paracetamol
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121
Q

Give two examples of viral haemorrhagic fever and the progression of the disease

A

Examples: ebola and yellow fever

Non-specific febrile illness - haemorrhagic manifestations - septic shock - death

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122
Q

Define gastroenteritis

A

Inflammation of the stomach and intestinal epithelium, typically resulting from bacterial toxins or viral infection

A syndrome characterised by GI symptoms including nausea, vomiting, diarrhoea, abdominal discomfort

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123
Q

Define diarrhoea

A

Frequent and/or fluid stool, at least 3 episodes a day

  • Disease of the small intestine and involves increased fluid and electrolyte loss, severity can vary
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124
Q

Define dysentery

A

Inflammation disorder of the large intesting resulting in severe diarrhoea with blood and pus in stools, usually with abdominal pain and fever

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125
Q

Define enterocolitis

A

Inflammation involving mucosa of both the small and large intestine

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126
Q

Give 3 examples of barriers to infection in the GI tract

A

Mouth: lysozymes

Stomach: acidic pH

Small Intestine: mucous, bile, secretory IgA, lymphoid tissue (Peyer’s patches), epithelial turnover, normal flora

Large Intestine: epithelial turnover and normal flora

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127
Q

What is the role of the microbiome in the gut and what does it consist of?

What can occur if the contents are disrupted?

A

Function: protection and metabolic function

Contents:

  • Good and bad bacteria: balance is important
  • Loss of balance: leads to overgrowth of some normal gut flora that can cause harm eg. C. difficile
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128
Q

What are the sources of GI infection?

A
  • Zoonotic: b/v/p that spread between animals and humans
  • Human carriers: eg. typhoid
  • environmental sources eg. contamination of sioul and produce (e.coli and listeria)
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129
Q

What are the main routes of transmission of GI infections?

A

3 F’s

  • Food: contamination (farm to fork) or cross-contamination (domestic kitchen)
  • Fluids: water or contaminated juices
  • Fingers: importance of hand-washing (after using bathroom and before/after preparing or consuming food)

Ie.

Faeco-oral: any means by which infectious organism from faeces can gain access to GIT of another susceptible host

Person-to-person

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130
Q

How are GI infections managed?

A
  • Most mild infections resolve spontaneously
  • Main: maintenance hydration

Abx: reserved for severe/prolonged symptoms

Abx use may:

  • prolong symptom duration, exacerbate symptoms, promote abx resistance, may be harmful
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131
Q

Give 3 ways in which general control of GI infections can be achieved

A

Need to break chain of infection

Adequate public health measures:

  • provision of safe, clean drinking water
  • porper sewage disposal

Education in hygienic food prep

  • hand hygiene
  • avoid cross contamination
  • cook food properly

Pasteurisation of milk and dairy products

Sensible travel food practices

132
Q

What are the 3 biggest causes of GI infection?

A
  • Salmonella
  • Campylobacter
  • E. Coli
133
Q

What is the microbiology and epidemiology of Salmonella (including reservoirs and transmission)

A

Microbiology:

  • Gram -ve bacilli
  • Enterobacteriales group

Epidemiology:

  • found in a wide range of animals
  • S. typhi and s. paratyphi are the only causal organisms of enteric fever (Typhoid/Paratyphoid) and don’t have animal reservoir

Modes of transmission

  • Contaminated food (meat, dairy products) ie. foodborne
  • Secondary spread: person-to-person transmission (need to isolate infected pateints)

Spread: faeco-oral

134
Q

What is the treatment for salmonella infection and what specific control points are there?

A

Treatment:

  • fluid replacement
  • abx reserved for severe infections and bacteraemia: b-lactams, quinolones, aminoglycosides (gentamicin)

Control:

  • immunisation of poultry flocks
135
Q

What is the microbiology and epidemiology for campylobacter

A

Microbiology:

  • Gram -ve bacilli
  • thermophilic (thrives at high temp)

Epidemiology:

  • commonest bacterial foodborne infection in UK
  • large animal reservoir (cattle, poultry etc.)

Mode of transmission: foodborne via uncooked food esp. poultry

Spread: faeco-oral

136
Q

What is the treatment and specific control points for campylobacter?

A

Treatment:

  • fluid replacement
  • persistent/severe: clarithromycin
  • quinolones and gentamicin if invasive

Control:

  • reduction in contamination of raw, retail poultry meat
  • adequate cooking
137
Q

What is the microbiology of Escherichia Coli

A
  • Gram -ve bacilli
  • Important component of gut flora of humans and animals
  • 6 different diarrhoea-causing groups including eneteropathogenic (EPEC), enterotoxigenic (ETEC), enterohaemorrhagic (EHEC)
138
Q

Compare the epidemiological features of E. Colic groups EPEC, ETEC, EHEC

A

Entero-pathogenic E. Coli:

  • sporadic cases and outbreaks of diarrhoea in infants and children
  • can cause some cases of traveller’s diarrhoea

Entero-toxigenic E. Coli:

  • maj. cause of traveller’s diarrhoea
  • maj. diarrhoeal cause in infants and children in developing world

Entero-haemorrhagic E. Coli

  • large animal reservoirs and persistent in the environment
139
Q

What is the mode of transmission and spread of E. Coli?

A

Mode of transmission: foodborne (raw/undercooked land meat, raw milk and raw vegetables)

Spread: faeco-oral and direct contact (hand to mouth)

140
Q

How is E. Coli treated and what control measures can be implemented?

A

Management:

  • Adequate rehydration

Control:

  • education of food prep eg. washing hands, adequate cooking, avoid cross-contamination
141
Q

What is the microbiology and epidemiology of Shigella

A

Microbiology:

  • Gram -ve bacilli
  • Member of enterbacteriales

Epidemiology:

  • Mainly associated with diarrhoeal disease in children
  • Reservoir: only humans
  • Spread: person-to-person via faeco-oral and contaminated food and water
142
Q

How is shigella infection treated and how can it be controlled?

A

Treatment:

  • usually self-limtiing
  • fluid replacement

Control:

  • sanitation and personal hygiene
143
Q

What is the microbiology and epidemiology of Vibrio Cholera

A

Microbiology:

  • Gram -ve

Epidemiology

  • cause of pandemic and epidemic cholera
  • Transmission: contaminated fresh water
  • Reservoir: only affects humans with asymptomatic human reservoir
  • Spread: contaminated food
144
Q

How is Vibrio Cholera treated and controlled?

A

Management:

  • prompt oral/IV rehydration CRUCIAL
  • tetracycline abx potential

Control:

  • Clean drinking water supply and proper sanitation
145
Q

Give three examples of pathogens causing infective GI infection

A
  • Salmonella
  • E. Coli
  • Camylobacter
  • Less common: vibrio cholera and shigella
146
Q

Give three examples of pathogens causing GI infection through intoxication

A

Staphylococcus aureus

Bacillus cereus

Clostridium difficile

Helicobacter pylori

Listeria monocytogenes

147
Q

Define intoxication

A
  • food poisoning
  • bacterial pathogens grow in foods and produce toxins
  • short incubation time as toxins alread preformed: couple of hours
148
Q

Describe the microbiology and epidemiology of staphylococcus aureus

A

Microbiology:

  • Gram +ve

Epidemiology:

  • head stable and acid-resistant protein toxins (enterotoxins produced)
  • Transmission: food contaminated by human carriers
  • Spread: direct contact / droplet spread
149
Q

What is are the management and control measures for Staphylococcus aureus

A

Management: self-limiting

Control: hygienic food prep and refrigerated storage

150
Q

What is the microbiology and epidemiology of bacillus cereus

A

Microbiology:

  • aerobic, spore-forming Gram +ve bacilli

Epidemiology:

  • Emetic disease: associated with fried rice
  • Diarrhoeal disease

Both: foodborne transmission

151
Q

How do you treat bacillis cereus

A

Treatment: self-limiting

152
Q

What is the microbiology and epidemiology of closridium difficile

A

Microbiology:

  • Anaerobic, spore-forming gram +ve
  • heat resistant spores

Epidemiology:

  • infection requires disruption of the normal gut flora
  • most commonly due to antibiotic therapy (4C’s)
  • predominant in the elderly
  • maj. cause of hospital associated infection (HAI)
153
Q

How is clostridium difficile treated and controlled?

A

Treatment:

  • stop precipitating abx
  • oral metronidazol
  • oral vancomycin

Control:

  • antimicrobial stewardship: avoid unnecessary antimicrobial treatment and develop restrictive abx formulaes
  • source isolation, hand hygiene, PPE
154
Q

What is the microbiology and epidemiology of helicobacter pylori?

How is it diagnosed?

A

Microbiology:

  • Gram -ve
  • Diagnosis: urea breath test or faecal antigen

Epidemiology:

  • Transmission: faeco-oral or oral-oral
  • Reservoir: humans
  • infection acquired in childhood and persists throughout life unless treated
155
Q

What is the treatment for H. Pylori?

A

Omeprazole (PPI) with clarithromycin, amoxicillin and metronidazole

  • eradicates carriage and facilitates ulcer healing
156
Q

What is the class, action and indication of omeprazole?

A

Class: proton pump inhibitor (PPI)

Indication:

  • peptic ulcers, gastro-oesophageal reflux disease, H. pylori infection and prophylaxis for patients on long term NSAIDs use

Action:

  • Binds to the H/K ATPase pump on gastric parietal cells
  • Reduces HCl production therefore reduces gastric acidity
157
Q

What is the microbiology and epidemiology of listeria monocytogenes?

A

Micro:

  • Gram +ve coccobacilli

Epidemiology:

  • reservoir: animals and environment
  • affects mostly pregnant women, elderly and immunosuppressed
  • transmission: foodborne (contaminated food) esp unpasturised milk, soft cheese, pate, smoked fish
158
Q

How is listeria monocytogenes treated and controlled

A

Management:
- IV antibiotics: ampicillin and synergistic gentamicin

Control:

  • suspectible groups should avoid high risk foods
  • observe use-by dates
  • wash raw fruit and vegetables and avoid cross contamination
159
Q

Define viral gastroenteritis

A

Inflammation of the stomach and intestines caused by a virus and characterised by diarrhoea and vomiting

160
Q

Who are most at risk of viral gastroenteritis?

A

Children under 5

elderly

immunocompromised

161
Q

What ages are most affected by norovirus?

A

can affect all ages and healthy individuals but often more serious in the young and elderly

162
Q

What ages are most affected by rotavirus?

A

affects mainly children <2, elderly and immunocompromised

not often seen in adults

163
Q

List 3 important viruses that can cause gastroenteritis

A
  • norovirus, rotavirus, adenovirus 40&41, astrovirus
164
Q

Describe the structure and transmission of norovirus

A

Structure:

  • family: calciviridae
  • non enveloped, single stranged RNA

Transmission

  • highly contagious
  • Transmission: person-to-person, foodborne, water
  • Can affect all ages
165
Q

How is norovirus managed?

Can you develop immunity to norovirus

what measures are involved in infection control

A

Management:

  • symptomatic therapy: analgesics, oral/IV fluids, antipyretics

Immunity:

  • only lasts 6-14 weeks hence why norovirus can be a recurrent infection

Infection Control:

  • isolation, exclude symptomatic staff, don’t move patients, thorough cleaning of area
  • hand hygiene: contaminated hands are the single most common vector for norovirus spread
166
Q

Describe the structure and transmission of rota virus

A

Structure:

  • family: reoviridae
  • non-enveloped, double stranded RNA virus

Transmission

  • low infectious dose
  • person-to-person via faeco-oral or fomites
167
Q

How do you diagnose viral gastroenteritis infections?

What type of sample is used?

A

PCR (Polymerase Chain Reaction)

  • This detects DNA samples and amplifies them, allowing them to be studied to make a diagnosis

Sample: vomit or stool

168
Q

What is the structure and treatment for adenovirus

Is there a vaccine

A

Structure: double stranded DNA virus

  • Adenovirus 40&41 cause gastroenteritis

Treatment: supportive

  • No vaccine
169
Q

Can immunity be developed to rotavirus?

A

Yes

  • Vaccine: rotarix, part of the childhood immunisation schedule
  • Live attenuated vaccine
170
Q

What is the structure of astrovirus?

A

Single stranded, small, non-enveloped RNA virus

171
Q

List a viral cause for each of the following

Common cold

Pharyngitis

Croup

Acute Bronchitis

Bronchiolitis

Pneumonia

A

Common cold: rhinovirus and coronavirus

Pharyngitis: adenovirus

Croup: parainfluenza virus

Acute Bronchitis: RSV (Respiratory Syncytical Virus)

Bronchiolitis: RSV

Pneumonia: (haemophilus) influenza and RSV

172
Q

Outline the modes of transmission of viral respiratory tract infections

A

Complex dependent on different variables

  • eg. environment (humid, temp), crowded spaces, host factors (eg. receptor distribution in resp tract)

Contact

  • direct or indirect

Droplet spread

  • cough, sneeze, talking
  • can spread for about 1m

Aerosol spread

  • can spread up to 3m
  • occurs when people are being incubated or suction
173
Q

Outline the aetiology and clinical presentation of the common cold

A

Aetiology:

  • Rhinovirus: ssRNA, there’s 3 species and >100 types for each species therefore don’t develop immunity
  • Coronavirus: ssRNA, enveloped

Clinical Presentation:

  • sore, scratchy throat
  • rhinorrhoea (nasal cavity filled with mucous fluid)
  • nasal obstruction
  • onset in 1-3 days post inoculation, persists for a week
174
Q

Outline the potential complications and management for the common cold

A

Complications:

  • sinusitis
  • otitis media (infection of the middle ear)

Management:

  • self-limiting
  • can cause severe infection in: elderly, immunocompromised, chronic lung conditions eg. asthma, COPD, CF
175
Q

Outline the aetiologies of pharyngitis

A
  • Bacterial
  • Viral: adenovirus

Can be due to systemic infection

  • infectious mononucleosis (glandular fever) which is caused by the epstein-Barr virus (EBV)
  • HIV seroconversion illness
  • Herpes simplex virus
176
Q

Outline the clinical presentation of pharyngitis and how to identify if the causative agent is viral or bacterial

A

Sore throat, pharyngeal inflammation and fever

  • swollen red tonsils and throat redness

Viral: nasal symptoms

Bacterial: swollen uvula, whitish spots, furry grey tongue, no nasal symptoms

177
Q

Outline the aetiology and clinical presentation of Croup

How is Croup managed?

A

Aetiology:

  • influenza virus types 1-4 (usually parainfluenza virus type 1)

Clinical presentation:

  • brassy cough (distinctive)
  • difficulty breathing
  • increased respiratory rate
  • affects children 6 months - 3 years

Management: supportive

178
Q

Outline the complication with Croup

A

Croup is mostly mild but responsible for sig. number of emergency visits due to rapid onset and difficulty breathing

  • inflamed trachea and larynx, narrowing the airway causing difficulty breathing
  • inc. RR, can be so severe that the child fatigues and dont’ have enough energy to support breathing
179
Q

Outline the aetiology and clinical presentation of bronchiolitis

A

Respiratory Syncytical Virus (RSV)

  • Commonly seen in children under 2
  • Associated with development of asthma if infected under 6 months

Clinical presentation:

  • rhinorrhoea, fever
  • rasping or dry cough
  • wheeze
  • feeding less and vomiting after feeding
180
Q

What is the risk of respiratory syncytical virus?

A

A major nosocomial hazard to at risk patients (hospital / care home breakout)

therefore:

  • isolation, use PPE and handwashing

high-risk of respiratory failure:

  • immunocompromised, adults with chronic lung disease, elderly
181
Q

How bronchiolitis treated (if caused by RSV)?

A

Supportive treatment

Ribavirin (benefit unclear)

IV immunoglobulin (only benefits some patients)

Prophylactic monoclonal antibody: Palivizumab

  • IM given over 5 month RSV season (from Oct) and reduces hospitalisation of high-risk infants by 45%
182
Q

Outline the aetiology of influenza

A

influenza virus

  • 4 types (A-D)
  • A & B: cause serious problems (B found in humans whereas A is found more in aquatic birds)
  • C: mild infection, mainly in children
  • D: only affects cattle
183
Q

Outline the clinical presentation of influenza

A

Has varying severity and affects all age groups

  • Causes annual epidemics and occasional pandemic
  • can cause wide range of presentation from asymptomatic to acute respiratory distress

Symptoms:

  • Neurological: fever, headache, confusion
  • Respiratory: dry cough, sore throat, nasal congestion
  • GI: nausea, vomiting, diarrhoea

MSK: myalgia, fatigue

184
Q

List 3 complications of influenza

A

Complication influenza = an infection that requires hospital admission

Neurological:

  • febrile convulsions, Reyes syndrome
  • meningitis, encephalitis, transverse myelitis, Guillian-Barre syndrome

Cardiac:

  • Pericarditis, myocarditis, exacerbation of CV disease

Respiratory:

  • sinusitis, bronchitis, pharyngitis, exacerbation of chronic lung disease
  • pneumonia (viral or secondary bacterial)

Pregnancy:

  • inc. maternal complications, lower birth weight

MSK:

  • myositis, rhabdomyolitis
185
Q

List 3 risk factors for developing complicated influenza

A
  • pulmonary eg. asthma, COPD, CF
  • chronic cardiac eg. HF
  • diabetes mellitus
  • severe immunosuppression
  • pregnancy
  • extremes of afe <6 months or >65 years
  • those with underlying conditions in neurological, hepatic, renal
186
Q

Outline the management for influenza

A

M2 inhibitors

  • amantadine, rimantadine

Broad spectrum antivirals

  • ribavirin

Neuraminidase inhibitors

  • neuraminidase is a surface protein on viruses and allows release of new virus progenies
187
Q

What investigation is useful for detecting upper and lower respiratory tract infections?

What samples are taken from the patient?

What are the benefits of this test?

A

Real-time Polymerase Chain Reaction (PCR)

  • amplification of a target gene
  • good for influenza, adenovirus and RSV

Samples:

  • nasal pharyngeal swab, throat swab, gargle, sputum

Benefits of molecular testing:

  • improves the diagnosis
  • rapid detection: reduces unnecessary abx treatment and can isolate/cohort groups according to result
188
Q

give an example of a respiratory tract infection that each of the following cause

Rhinovirus

Adenovirus

Respiratory Syncytical Virus (RSV)

Influenza Virus

Parainfluenza Virus

Coronavirus

A

Rhinovirus: common cold

Adenovirus: pharyngitis

RSV: acute bronchitis, bronchiolitis, pneumonia

Influenza virus: influenza, pneumonia

Parainfluenza virus: Croup

Coronavirus: common cold

189
Q

Define septic arthritis and outline the complications if left untreated

A

Definition: joint inflammation caused by infection either from sepsis (infection travelling from another body part) or when a penetrating injury delivers the micro-organisms directly to the joint

  • Treat as a medical emergency

If left untreated:

  • cartilage destruction leading to osteoarthritis
  • severe sepsis leading to septic shock
190
Q

List 3 common pathogens causing septic arthritis

A

Common:

Staphylococcus: MSSA or MRSA

Streptococci

Less common:

  • H. influenza
  • N. meningitis
  • N. gonorrhoea
  • E. coli
191
Q

Outline the clinical presentation of septic arthritis

A
  • fever
  • single ‘hot’ joint (knee, hit)
  • polyarticular involvement in 10-20%
  • loss of movement
  • pain
192
Q

Outline the key investigations to diagnose septic arthritis

A

Blood cultures

Joint aspirate: microscopy for crystals and culture

  • Need to ensure aseptic technique (don’t want to introduce micro-organisms)

FBC

CRP

Imaging

193
Q

How is septic arthritis managed?

A

3 weeks IV Abx followed by 3 weeks oral abx

  • monitor response by CRP and clinical signs
194
Q

Define:

arthroplasty

arthrodesis

arthrosis

pseudo-arthrosis

resection arthroplasty

revision arthroplasty

A

Arthroplasty: putting in an artificial joint

Arthrodesis: fusing two bones together

Arthrosis: a joint

pseudo-arhtosis: allowing two bones to articulate against one another but without a joint (in end-stage or no rehabilitation) eg. girglestone

Resection arthroplasty: taking the diseased joint out and putting in an artifical one

Revision arthroplasty: re-operating on an artificial joint (eg. tightening screws and taking out dead tissue)

195
Q

List 3 risk factors for needing a primary arthroplasty

A
  • rheumatoid arthritis
  • diabetes mellitus
  • poor nutritional status
  • obesity
  • concurrent UTI
196
Q

List 3 risk factors for needing a revision arthroplasty

A

prior joint surgery

prolonged operating room time

pre-op infection (skin, teeth, UTI)

197
Q

Outline the pathogenesis of prosthetic joint infections

A

After surgery, there is a continuous space for organisms to travel down to the deep layers of the skin into the joint

Prosthesis requires fewer bacteria to establish sepsis than soft tissue

  • Avascular surface allow survival of bacteria as it protects from circulating immunological defences and most abx
  • cement can inhibit phagocytosis and lymphocyte/complement function

Local spread (60-80% PJI)

  • mostly organisms from skin surface
  • direct communications between skin surface and prosthesis while fascial planes heal
  • usually manifests in immediate post-up period: acute <4 weeks and delayed >4 weeks

Haematogenous Spread

  • presents later
  • intact surrounding connective tissue often limits infection to bone/cement surface
  • looking for a secondary cause - must have come from somewhere
198
Q

Outline the clinical presentation of a prosthetic joint infection

A
  • classical inflammatory signs (swelling, pain, loss of function, heat, redness)
  • pain (life-changing)
  • effusion
  • warm joint
  • fever and systemic symptoms
  • loosening of prosthesis on X-ray
  • discharging sinus
  • mechanical dysfunction
199
Q

How do you avoid a prosthetic joint infection?

A

Prophylactic antibiotics 24hrs before surgery and one dose post-surgery

  • evidence supports use of cephalosporin

Further reduce risk

  • stop smoking before surgery
  • treat UTI an do dental work before surgery
200
Q

Outline the investigations needed to diagnose a prosthetic joint infection

A

Diagnosis based on macroscopic appearance, histopathology and microbiology

Sample: tissue/pus/fluid

201
Q

Outline the management for a PJI

A

Surgical options

  • DAIR (debridement, abx and implant retention) to keep joint in
  • remove joint and replace: girdlestone procedure, one stage revision or two-stage revision
  • if recurrent joint infection, may need amputation

Abx Treatment

  • the abx chosen needs to penetrate bone
  • cephalosporins, carbapenems, trimethoprim, clindamycin, ciprofloxacin
  • give IV followed by oral
  • combo therapy including rifapmicin have greater success in chronic staphylococcus osteomylitis
202
Q

Outline the surgical management for prosthetic joint infections

A

Surgical options

  1. DAIR (Debridement, Abx and Implant Retention) to leave infected joint in
    - If infection is acute (<30days) then it’s still mechanically functional and can be kept in, but infected tissues should be debrided (removed) and the joint washed out to reduce burden of infection
    - Followed by abx for 4-6 weeks (cephalosporin)
  2. Take out the infected joint
    - if delayed infection (>30days) since surgery, joint may not be fully functional therefore may neeed removed
    - removal: take out prosthesis and all cement
    - options: girdlestone procedure, one stage revision (remove infected and add new joint during same procedure, inc. risk of re-infection as joint not cleared out) or two stage revision (treat infection for 4-6 weeks before new joint put in)
  3. Patients with recurrent PJIs
    - each time a revision is performed, the chances of success reduce dramatically
    - amputation may be a possibility
203
Q

Define osteomyelitis

A

Progressive infection of bone characterised by death of bone and the formation of sequestra

204
Q

Outline the pathology of osteomyelitis

A
  • bone tissue is full of cells (osteoblasts, osteoclasts etc) in a constant state of action to maintain bone marrow
  • very dynamic tissie
  • sequestrum = a piece of dead bone tissue formed within a diseased or injured bone, typically seen in chronic myelitis

Spread:

haematogeneous

contiguous spread ie. adjacent tissue

  • overlying infection (eg. cellulitic ulcer)
  • trauma (compound fracture)
  • surgical inoculation
205
Q

Outline the treatment for osteomyelitis

A
  • surgery to debulk infection and manage the dead space that remains
  • stabilise infected fractures (usually external fixation)
  • antibiotic treatment (4-6 weeks IV)
206
Q

Define vertebral discitis

Outline the clinical presentation

List 3 complications

A

Def: infection of a disc space and adjacent vertebral end plates

  • often missed as it’s forgotten

Clinical presentation:

  • back pain with fever

At risk of:

  • deformity
  • spinal instability, cord compression
  • paraplegia
  • disability
207
Q

Define tuberculosis

A
  • an infectious bacterial disease characterised b growth of granulomas in the tissues, especially the lungs
208
Q

What is the causative agent for tuberculosis?

Outline the characteristics of the substance

A

mycobacterium tuberculosis (M. tuberculosis)

  • Weak Gram +ve
  • Slow-growing
  • Stain: Ziehl-Neelsen (ZN) stain (pink-purple beaded gram +ve rods)
209
Q

What populations of mycobacterium tuberculosis can be identified within a patient with TB and what drug targets each population

A

Four populations as cells are not all growing at the same rate:

  • actively growing organisms (killed by isoniazid)
  • semi-dormant organisms inhibited by an acid environment (killed by pyrazinamide)
  • semi-dormant organisms with spurts of active metabolism (killed by rifampicin)
  • completely dormant organisms (not killed by standard drugs)
210
Q

What is the role of whole-genome sequencing of mycobacterium tuberculosis?

A
  • Identifies the organism, the likely genotypic resistance of the organism and whether the TB is being passed between populations (can tell if two people have the same strain of TB ie. has it been transmitted)
  • important for trying to prevent TB
211
Q

Outline the immunology of tuberculosis

A
  • unlike other infections, TB co-exists with humans (rather than one killing the other)

Complex immunological process:

  • cell-mediated immunity is crucial
  • macrophages are the key controlling cells: when Tb enters the lung, bacteria is taken up by macrophages
  • usually the macrophages would phagocytose and kill the bacteria but TB prevents this allowing it to persist and grow within the macrophage
  • the macrophages grow into multinucleated giant cells / foam cells and form granulomas
  • These eventually bursts and TB will spread which will activate more macrophages and allow TB to spread further
212
Q

Outline the progression of tuberculosis

A

Spread: close contact

Transmission: droplet spread (coughing, sneezing, talking)

Progression:

  • enters lung and taken up by macrophages
  • 5% of patients (inc. immunosuppressed) develop primary TB at this point
  • 95% of people in which TB has entered, will never develop TB due to macrophage walling mechanism (95% of those infected have haematogenous spread then TB held as the macrophages develop, they develop a mechanism to wall the TB)

In those that develop TB, it’s usually a post-primary infection rather than a primary infection

  • Cavitary TB (involves upper lobes of lungs, bacteria damage lungs and form cavities)
  • Period of latency followed by re-activation of TB
  • more common with immunosuppression

Development of active TB

  • develop cavitation in lungs and eventually will erode into the bronchi as they grow
  • infectious (can transmit to others via droplet spread)
  • may also cough up blood
213
Q

What is the histological hallmark feature of tuberculosis?

A

Granulomas

  • Macrophages turn into multinucleated giant cells and foam cells and create tight intracellular junctions
214
Q

Outline the clinical presentation of mycobacterium tuberculosis

A

Pulmonary TB = 90% of presentation

  • cough +/- haemopytsis
  • SOB

Constitutional Symptoms

  • fever/chills, night sweats, fatigue, loss of appetite and weight loss, lymphadenopathy

Progressive decline, symptoms of phthisis and constitutional symptoms, wasted patient followed by deterioration

215
Q

What is the biggest risk factor for developing active tuberculosis after being infected?

A

Immunosuppression

High risk:

  • transplantation (related to immunosuppression therapy), chronic renal failure, recent TB infection, HIV

Medium risk:

  • Steroid treatment, diabetes mellitus, infected at a young age (0-4years)

Slightly increased risk:

  • underweight (BMI <20), cigarette smoker, abnormal CXR
216
Q

What tests are available to determine TB exposure?

A

Mantoux reaction:

  • skin test in which dead TB antigens are injected under the skin to check for memory T-cells for TB
  • will become inflamed if positive
  • Problem: can’t determine if active or latent TB

Interferon Gamma Release Assays (IGRA)

  • blood test testing if T cells in blood released interferon gamma when exposed to TB specific reagents
217
Q

How is TB diagnosed?

A

Presence of TB:

  • Mantoux test (checking for memory T-cells for TB)
  • IGRA (looking for release of interferon gamma)

Diagnosis:

Acid-fast bacilli in respiratory or another sample

  • Microbiology (ZN stain) or histopathology (tissue from lung/LN)

M. tuberculosis growth in cultures

Clinical and/or radiological diagnosis

218
Q

Outline the treatment for latent TB

What is the risk with tuberculosis treatment?

A
  • Isoniazid monotherapy for 6 months

OR

  • Rifapmicin plus isoniazid daily for 3 months

Risk: liver dysfunction

219
Q

Outline the treatment for active tuberculosis

What are the complications of this treatment?

A

4-drug regimen

  • Isoniazid 6 months
  • Rifampicin 6 months
  • Ethambutol 2 months
  • Pyrazinamide 2 months

Complications: drug and adverse reactions

Rifampicin: bodily secretions turn orange, interferes with warfarin and OCP

Isoniazid: liver injury

Ethambutol: toxic optic neuropathy (visual disturbances)

Pyrazinamide: liver injury, raised lactate

220
Q

What is the main risk of non-adherence to tuberculosis medication?

A

Risk of generating drug resistance

221
Q

Define meningitis and meningo-encephalitis

A

Meningitis: inflammation of the meninges

Meningo-encephalitis: inflammation of the meninges and cerebral inflammation

222
Q

Outline the clinical presentation of meningitis

A

2 of:

  • headache
  • neck stiffness: if neck stiffness without swollen lymph nodes it’s meningitis until proven otherwise
  • reduced GCS
  • fever

Confusion: indicative of brain involvement ie. encephalitis

Rash: purpuric +/- petechial but macular ealry on

  • Seen mostly with meningococcal or enterovirus infections
223
Q

List 3 causes of bacterial meningitis and a risk factor for developing each

A
  • Meningococcal: pilgrimage
  • Pneumococcal: alcoholics, immunocompromised, head injury, otitis media, cochlear implants
  • Haemophilus influenza Type B
  • E. Coli
  • Listeria: immunosuppression, pregnancy, elderly
  • -* Tuberculous meninigitis: TB
224
Q

What specific clinical presentations may indicate meningitis caused by pneumococcal species?

A

Neurology:

  • focal signs: fever, headache, malaise, neck stiffness, photophobia
  • seizures
  • VII (facial) palsy

More severe infection:

  • community acquired pneumonia
  • ENT problems
  • Endocarditis
225
Q

What clinical presentations would indicate meningitis caused by meningococcal species?

A
  • Typical meningitis clinical manifestation
  • Bacteraemia (meningococcus sepsis)
  • Purpuric +/- petechial rash specific to meninigococcal meningitis
226
Q

List 3 poor prognosis indicators in bacterial meningitis

A
  • pneumococcal species: more likely to die with pneumococcal meningitis but meningococcal meningitis is more common
  • reduced GCS
  • CNS signs
  • older age (>60)
  • CN palsy (pneumococcal)
  • Bleeding (meningococcal): pectechiae
227
Q

How do you investigate a suspected meningitis case?

A

History and exam

  • examine throat: if pus on tonsils it’s group A Strep not meningitis

Blood cultures

  • Blood PCR for pneumo/meningococcal

Throat culture, viral gargle

  • Culture: meningo/pneumococcus is carried in the throat
  • viral gargle: looking for viral cause of symptoms

FBC, U&E, LFTs, CRP

Lumbar Puncture

  • major test for meningitis diagnosis
  • cell count, Gram stain, culture and PCR
  • protein and glucose
  • Viral PCR

CT

  • only to exclude mass lesion / mass effect / gross cerebral oedema
228
Q

List 3 scenarios in which a CT would be carried out before a LP in suspected meningitis

A

When a LP is contraindicated

  • GCS <12
  • CNS signs
  • Papilloedema (and any other signs of raised ICP)
  • immunocompromised
  • Seizure
  • resp/cardiac failure
  • infection at LP site
  • severe sepsis
  • rapidly evolving rash
229
Q

What are the basic principles when looking at the results from a LP for suspected meningitis?

A

WCC:

  • High lymphocytes: usually viral cause of meningitis
  • High neutrophils: bacterial

Protein:

  • High in all causes of meningitis

Glucose:

  • Low (less than half of that in the blood): bacterial
230
Q

Outline the treatment for suspected bacterial meningitis

A
  • do not delay IV antibiotics
  • treat everyone for meningo/pneumococcal
  • if likelihood of pneunococcal (seizures, reduced consciousness): add steroids

Treament: ceftriaxone or benzyl penicillin

  • If >60, immunosuppressed, pregnancy, alcoholic, liver disease or suspected Listeria meningitis: add IV amoxicillin
  • If bacterial meningitis is strongly suspected: add IV dexamethosone
231
Q

Once a causative agent for bacterial meningitis is identified, how are the following treated

Meningococcal

Pneumococcal

Listeria

A

Meningococcal
- IV ceftriaxone or benzylpenicillin

  • 5 days

Pneumococcal

  • IV ceftriazone or benzyl penicillin
  • 10 to 14 days
  • corticosteroids added if high likelihood of pneumococcal

Listeria

  • IV amoxicillin (stop ceftriaxone)
  • 21 days
232
Q

Outline secondary prevention of meningococcal meningitis

A
  • Chemoprophylaxis of ciprofloxacin or rifampicin
  • Given to close contacts to the infected patient
  • if you have septic BM, it must have been acquired from a close contact
  • Aim: identify the carrier who infected the patient to stop them infecting other people
233
Q

What causes of bacterial meningitis are involved in childhood immunisation scheme?

A
  • Pneumococcal
  • Meningococcal
  • Haemophilus Influenza Type B
234
Q

When would a diagnosis of viral meningitis be made?

How does it present?

A

only diagnosed after the exclusion of bacterial meningitis

  • never diagnose just viral meningitis, always empirically treat suspected bacterial meningitis because BM can kill whereas viral meningitis cannot

Presentation:

  • indistinguishable from bacterial meningitis until full results from CSF (from the LP)
  • no presentation of confusion
235
Q

List 3 causes of viral meningitis

A
  • enterovirus (most common)
  • HSV 2
  • VZV (Varicella Zoster Virus)
  • HSV 1
  • HIV
236
Q

How is viral meningitis treated?

A

Supportive management

  • Only consider antivirals in immunosuppressed ie. acyclovir
237
Q

How would viral encephalitis present?

What is the most common causative agent?

A

Presentation:

  • confusion, fever +/- seizures
  • dangerous infection

Common cause: HSV encephalitis

  • HSV 1 usually but can be HSV 2
238
Q

How would you investigate for suspected viral encephalitis?

A
  • CT: diffuse what matter changes
  • LP: lymphocytic CSF with normal glucose
  • PCR: nearly always positive for HSV encephalitis
  • EEG of temporal lobes
  • MRI
239
Q

Patient presents with headache, fever and confusion

What must they be treated for and what treatment would they be given?

A

Treated for suspected viral encephalitis and bacterial meningitis

Bacterial meningitis:

  • IV ceftriaxone or benzyl penicillin
  • IV amoxicillin if co-morbidities or suspected Listeria
  • IV dexamethasone if highly suspected BM

Viral encephalitis:

  • IV acyclovir
240
Q

What is the management for viral encephalitis?

A

IV acyclovir for 2-3 weeks

241
Q

Outline the primary causes of defects in the innate and adaptive immune responses

A

Primary = inherited ie. result of genetic defects

  • usually an unknown genetic susceptibility combined with environmental factors

Examples:

  • B-cell immunodeficiencies: adaptive, patients at risk of severe recurrent bacterial infections
  • T-cell immunodeficiencies: adaptive, can lead to combined inmmunodeficiencies (T-cells also activate B-cells)
  • Phagocyte disorders: innate, involves many WBCs, patients have a largely functional immune system but can be susceptible to certain bacterial and fungal infections
242
Q

Outline what is meant be secondary causes of defects in the innate and adaptive immune responses

A

Secondary = caused by environmental factors

  • can be due to underlying disease state eg. HIV, malnutrition
  • treatment for disease
243
Q

Identify 3 factors contributing to increasing population of immunocompromised patients

A
  • Improved survival at extremes of life
  • Improved cancer treatment
  • developments in transplant techniques
  • developments in intensive care
  • management of chronic inflammatory conditions
  • steroids development
244
Q

what is the principal cause of morbidity and mortality in the immunocompromised host?

A

Infection

245
Q

Define neutropenia

A

Low levels of neutrophils (low neutrophil count)

  • Defined as <0.5 x109/L or <1.ox109/l and falling
246
Q

Identify 2 causes of neutropenia and how they lead to neutropenia

A
  • Cytotoxic chemotherapy
  • Therapeutic irradiation (TB)

These lead to:

  • reduced proliferation of haematopoietic progenitor cells and depletion of marrow reserves
  • result in neutropenia
247
Q

How to cytotoxic drugs and steroids affect neutrophils

A

They affect neutrophil count and functionality of neutrophils

  • Reduce chemotaxis
  • Reduce phagocytic killing
  • Reduce intracellular killing
248
Q

Identify 3 pathogens that affect neutrophil function

A

Gram +ve cocci:

  • Staph aureus
  • Enterococci

Gram -ve cocci:

  • E. Coli
249
Q

How is Chronic Granulomatous disease inherited?

What is it?

A

Inherited disorder - X-linked recessive

Primary immunodeficiency disease

  • Increased body susceptibility to infections caused by bacteria and fungi
  • Defect in the gene coding for NADPH therefore causing defective intracellular killing
  • Inflammatory responses with widespread granuloma formation
250
Q

Outline the humoral and cell-mediated immunity

A

Part of the adaptive immune system

Humoral: the pathway by which antibodies are produced by B-cells which have differentiated into plasma cells to produce antibodies to target exogenous antibodies

Cell-mediated: the pathway occuring in the cell that targets endogenous antigens and is mediated by T-lymphocytes

251
Q

Identify 3 ways in which cellular immunity can be suppressed

A
  • DiGeorge syndrome (primary deficiency): inability of neutrophils to proliferate
  • Malignany lymphoma
  • Cytotoxic chemotherapy
  • Extensive irradiation
  • Immunosuppressive drugs eg. corticosteroids, cyclosporin
  • Allogenic stem cells transplantations esp. GvHD (which is treated with steroids)
  • Infection eg. HIV, mycobacterial infections, measles
252
Q

Idenity 2 causes of humoral immunodeficiency

A
  • Bruton agammaglobulinemia
  • Antibody production is reduced in lymphproliferative disorders: Chronic lymphoid leukaemia (CLL), multiple myeloma

(Preserved in acute leukaemia)

253
Q

Outline the function of the spleen

A

Splenic macrophages eliminate non-opsonised microbes eg. encapsulated bacteria

Site of the primary immunoglobulin response: specific opsonising antibody required for phagocytosis of encapsulated bacteria

254
Q

Identify 3 pathogens which a patient with humoral deficiency/splenectomy would be more susceptible to

A
  • Strep. pneumoniae
  • Haemophilus influenzae type B
  • Neisseria meningitis
255
Q

Identify 3 physical barriers against microbial invasion

A
  • skin
  • conjunctiva
  • mucous membranes: gut, respiratory tract, GU tract
256
Q

How does skin act as a barrier to microbial invasion?

A

it creates an environment that’s difficult for organisms to get a hold of:

  • desquamates
  • dry
  • pH 5-6
  • Secreotry IgA in sweat
257
Q

Identify 3 ways in which the integrity of the skin in impaired?

A
  • chemo/radiotherapy
  • insect bites / trauma wounds
  • burns
  • surgical site infections (HIA)
  • lines used in hospital (used to provide fluids, abx, nutrition, chemotherapy)
  • ventilation
258
Q

Identify 3 ways in which the microbiome can be altered

A
  • H2 antagonists
  • PPIs
  • Abx
  • diarrhoea
259
Q

What is the main aim in the management of infections in solid organ transplants

A

Focus on prevention ie. prophylaxis

  • patients who will be neutropenic for >1 week need prophylaxis
260
Q

Outline the cateogories of infections following a solid organ transplantation and the infections that cause each

A

Infection developing:

  • within 1 month: donor derived infections, endogenous ie. surgically acquired
  • 1-6 months: when patient is home still on immunosuppression, expousre to community-acquired pathogens ie. opportunistic infections
  • >6 months after SOT: opportunistic infection
261
Q

Identify 3 infections that patients with a SOT are more prone to

A

Exposure to community-acquired pathogens

  • pneumococcus, listeria, salmonella
  • virus: influenza, parainfluenza

Nosocomial infections

  • esp. early post transplant

Donor-derived infections

  • latent TB, syphilis
  • Active blood stream infections eg. Staphylococci, pneumococci, salmonella

Reactivation of infection

  • M. tuberculosis, HSV, VZV

Opportunistic infections

262
Q

what is the most common site of infection in the febrile patient

A
  • bloodstream
263
Q

Outline the initial management of sepsis in the neurtopenic/immunocompromised patient

A

Sepsis 6:

  • Take: blood culture, measure urine output, measure lactate and Hb
  • Give: high flow oxygen, IV fluids, abx
264
Q

Identify 3 risk factors worldwild for death in the under 5s

A
  • warfare
  • poor sanitation
  • poverty
  • poor nutrition
  • poorly developed healthcare system
  • poorly developed women’s rights
265
Q

Outline the 3 major causes of death in the under 5s worldwide

A
  • diarrhoea
  • pneumonia (and other respiratory tract infections)
  • malaria
266
Q

identify 2 reasons as to why under-5s are more likely to die from infection than adults

A
  • naive immune system
  • not yet immunised
  • immune system functionally immunodeficient at birth
267
Q

Why are pregnant women naturally immunosuppressed?

A
  • Mum needs to ignore foetal alloantigens (half of which are parental ie. foreign origin) to avoid rejection of the foetus
  • mum’s immune system has adapted for the baby therefore mum is more susceptible to infection
  • ‘immunosuppressive’ environment of the womb allows dampened responsiveness to avoid inflammatory responses to baby
268
Q

Describe one method in which immune protection is transferred from mum to baby

A

Immunoglobulin IgG: predominant in 3rd trimester

  • specific antibodies that cross the placenta
  • premature babies born before 3rd trimester will not receive these antibodies therefore will be immunodeficient

Breastfeeding: milk contains

  • innate immune agents
  • cytokines, chemokines
  • anti-inflammatory factors
  • prebiotics
269
Q

Identify a pathogen most likely to cause LRTI and meningitis in:

Neonates

Young infants (1-3 months)

Infants and young children (3m-5yr)

Older children (>6years)

A

Neonates:

  • LRTI: Group B Strep, E. Coli, resp virus, enterovirus
  • Meningitis: group B strep, E. Coli, haemophilus type B (hib), meningococcal strep

1-3months:

  • LRTI: resp. viruses, enterovirus, chlamydia
  • Meningitis: meningococcus, strep. pneumonia, Hib, listeria

3months -5years:

  • LRTI: strep. pneumonia, resp. viruses
  • Meningitis: meningococcus, strep. pneumonia, Hib

>6 years:

  • LRTI: mycoplasma pnuemonia, strep. pnuemonia, resp. viruses
  • Meningitis: Meningococcus, strep. pneumonia
270
Q

Outline 2 methods of acquiring immunity

A

Acquiring active immunity

  • involves cellular responses and serum antibodies acting against 1+ antigens on the infecting organism

Acquired by natural disease / vaccination

  • antibody mediated or cell mediated components
271
Q

Compare antibody-mediated and cell mediated immunity

A

Antibody-mediated immunity

  • B-cell encounters antigen it recognises and is stimulated to proliferate and differentiate into plasma cells (produce antibodies)
  • regulated by contact with antigen and interaction with T-cells

Cell-mediated immunity

  • T-cells mediate three principle fxn: help, suppression, cytotoxicity
  • T-helper: stimulate immune response of other cells ie. stimulate B cells to produce antibodies
  • T-suppressor: inhibitory role and control level and quality of the immune response
  • cytotoxic T-cells: recognise and destroy infected cells and activate phagocytes to destroy pathogens they have taken up
272
Q

Outline the role of vaccines

  • What is the prime and secondary response to vaccines
A
  • induce active immunity and immunological memory
  • can be made from inactivated or attenuated live organisms, secreted products or cell wall constituents

Primary response: IgM mediated followed by IgG

Secondary response: further injections lead to accelerated response led by IgG

  • Some inactivated vaccines contain adjuvants: substances that enhance the antibody response
273
Q

Outline how live attenuated vaccines work

Who should not receive live attenuated vaccines

Give an example of an attenuated vaccine

A
  • to produce an immune response, the live organism must replicate and grow in the vaccinated individual for a period of time (days-weeks)
  • usually promote a full, long-lasting immune response after 1-2 doses
  • vaccine virus is weakened ie. attenuated, but a mild form of the disease may occur
  • Do not give to immunocompromised individuals

Examples: MMR, VZV, intranasal influenza

274
Q

What is meant by herd immunity

A

A form of indirect protection from infectious disease that occurs when a large proportion of a population has become immune to an infection (either by vaccination or previous infection), thereby providing a measure of protection against those who are not immune

  • vaccinated individuals are less likely to get a disease and also less likely to be a source of infection to others
  • interrupts cycle of infection
275
Q

What is the most common cause of community acquired bacteraemia and meningitis

A

Streo. pneumonia

276
Q

What is the most common presentation of haemophilus influenza B (Hib)

A

Meningitis

  • Frequently accompanied by: bacteraemia, pneumonia, cellulitis
277
Q

What is a common cause of community acquired bacteraemia in the under 5s

A

Neisseria Meningitis

278
Q

what is involved in the standard sexual health screen?

A

Chlamydia and gonorrhoea

  • NAAT test - PCR

Syphilis and HIV

  • Blood test - big EDTA bottle
279
Q

Alongside the standard sexual health screen, what other tests may be carried out

A

Women: self-taken vulvovaginal swab

Male: first-pass urine sample

MSM: take a urine, throat and self-taken rectal swab

(Heterosexuals: if you have chlamydia/gonorrhoea in throat or rectum, it’ll be found in vagina/urine whereas it remains localised in MSM)

280
Q

Identify 2 presenting features for both males and females in which you would consider taken a sexual health history and screen?

A

Males:

  • urethritis: penile discharge, dysuria, meatal discomfort
  • epididymo-orchitis: swollen, painful testicle
  • proctitis: rectal discharge / pain / bleeding

Females:

  • vaginitis: change in discharge, dysuria, change in menstrual bleeding
  • pelvic inflammatory disease: pelvic pain, fever, change in discharge, dyspareunia

Both:

  • ulcer/lump on genitals
  • possible syphilis
  • possible HIV seroconversation
281
Q

Identify 2 high-risk groups of gonorrhoea

A
  • MSM
  • afro-caribbean
  • urban areas with deprivation
  • anyone having sex
282
Q

Name the causative organism of gonorrhoea

Outline the transmission

A

Causative organism: Gram -ve diplococcus Neisseria gonorrohoea

Transmission:

  • infects mucous membranes of urethra, endocervix, rectum, pharynx and conjunctiva
  • inoculation through secretions form one mucous membrane to another
283
Q

Outline the clinical presentation of gonorrhoea in both males and females, the pharynx and rectum

A

Male Urethra:

  • >90% symptomatic
  • yellow/green discharge and dysuria occuring 2-5 days post exposure

Females Endocervix/Urethra:

  • 50% asymptomatic
  • change in discharge, abdominal/pelvic pain, dysuria, altered bleeding (rare)

Pharynx: usually asymptomatic

Rectum: usually asymptomatic, can get anal discharge, pain and discomfort

284
Q

How is gonorrhoea diagnosed?

A

NAAT testing

  • Male: urine
  • Female: self-taken vaginal swab

Urethral sample microscopy

  • Gram -ve diplococci commonly seen in males and symptomatic

Culture

  • As 50% of gonorrhoea is resistant to at least 1 antibiotic used for treatment
285
Q

Identify 2 groups of individuals who would be treated with gonorrhoea and outline the treatment

A

Groups:

  • anyone with a positive test result
  • clinical suspicion in certain situations eg. outreach setting
  • recent or ongoing sexual contact with gonorrhoes eg. recently had sex without someone who has gonorrhoea within the last 2 weeks (testing may not be positive test)

Treatment:

- Ceftriaxone 1g IM stat in buttock

Repeat NAAT in 2 weeks to ensure treatment was effective

286
Q

Name a complication for men and women of gonorrhoea

A

Men:

  • epidimyo-orchitis
  • prostatitis

Women:

  • PID
287
Q

What is the most common bacterial STI in the UK and why?

A

Chlamydia

  • Easily transmissible: if one partner in the relationship has it, likely the other does (couple concordance)
  • It’s usually asymptomatic
288
Q

Identify 2 risk factors for acquiring chlamydia

A
  • <25yrs
  • new sexual partner or >1 partner in last month
  • inconsistent condom use
289
Q

Outline the clinical presentation of chlamydia in men and women in the urethra, pharynx and rectum

A

Most are asymptomatic

Male urethra:

  • clear discharge, dysuria, meatal discomfort

Female urethra/cervix:

  • post-coital/intermenstrual bleeding (also a RF for cancer)
  • cervicitis or contact bleeding
  • change in discharge
  • pelvic pain

Pharynx:

  • usually asymptomatic

Rectum:

  • can present with proctitis (inflammation of rectum and anus)
  • rectal pain, PR discharge, rectal bleeding, constipation
  • lymphogranuloma venereum (LGV): chlamydia subtype
290
Q

Outline the diagnosis and treatment for chlamydia

A

Diagnosis:

  • NAAT testing: male (urine), female (self-taken vaginal swab)
  • Too small for microscopy
  • Not resistant therefore no culture

Treatment: doxycycline 100mg BD weekly

291
Q

Outline the main complication of chlamydia in men and women

A

Women: pelvic inflammatory disease (PID)

  • Triad: pelvic pain, fever and dyspareunia
  • Infertility with chlamydia actually associated with PID

Men: epidiymo-orchitis

  • probably associated with male infertility
292
Q

Name the causative agent of syphilis

How is syphilis transmitted?

Identify two populations most at risk of syphilis

A

Causative agent: treponema pallidum

Transmission:

  • oral sex
  • vertical transmission from mother to child

At risk:

  • MSM, anyone
293
Q

Oultine the clinical presentation of syphilis and how this relates to the pathology

A

Pathology:

  • Syphilis has several stages and between these are periods of latency during which it replicates very slowly

Primary syphilis (9-90 days):

  • occurs quickly post contact
  • chancre: single painless ulcer in the genitals, can be dificult to spot (eg. if in vagina), spontaneously resolves
  • clear fluid

Latency:

  • asymptomatic

Secondary syphilis (3 months - 2yrs):

  • generalised macular papular rash affecting palms and soles
  • scaling often seen around the rash (diagostic)
  • muco-cutaneous lesions, condylomata lata, lymphadenopathy, fever

Tertiary Syphilis:

  • 8-15yrs
  • Neurosyphilis: neurological symtpoms inc. cognitive disturbances
  • CV syphilis: aortic regurgitation, aortic valve disease
294
Q

Outline the diagnosis for syphilis

A

If chancre present: dark ground microscopy / viral PCR swab

Blood test

  • looking for syphilis antibodies
  • 3-month window/incubation period before antibody will definitely be positive
  • want to know if individual has had syphilis before because this could give a positive result with no current syphilis

If antibody test is positive: rapid plasma reagin

  • quantatitive marker
  • useful if someone’s had syphilis previously and want to determine if they’ve got it again
295
Q

What is the treatment for syphilis

A

Benzathine penicillin

296
Q

What is the most common sexually transmitted infection and what is it’s causative agent?

A

Anogenital warts

Causative agent: human papilloma virus (HPV)

  • main types causing warts: HPV6 and HPV11
297
Q

what is the diagnosis and management for anogenital warts?

A

Diagosis: clincial

Management: advice

  • lifetime risk in unvaccinated population is 75%
  • reassure of high prevalence and benign
  • no requirements for partner notification as it is so prevalent
  • condoms reduce onward transmission

Treatment:

  • cyrotherapy
  • topical treatment
298
Q

which of the following STIs require partner notification:

  • gonorrhoea
  • chlamydia
  • syphilis
  • anogenital warts
A

Gonorrhoea, chlamydia and syphilis

299
Q

Outline the pathology of herpes simplex virus (HSV) and clinical presentation

A

Type 1: oral herpes

Type 2: genital herpes

First presentation: often a prodrome

  • viral, back pain, fever

Further episodes: less severe, less frequent and less bothersome

Causes the most emotional distress and feelings of isolation

Pain

300
Q

How is herpes simplex diagnosed and managed?

A

Diagnosis:

  • swab from ulcer and put in viral PCR

Management:

  • can treat acute episode but then will go into latent HSV
  • can’t cure HSV but can control symptoms

Advice:

  • condoms reduce transmission, don’t have sex while having symptoms

Treatment for acute symptoms: Acyclovir

301
Q

Identify two complications of HSV

A
  • CNS infection
  • balanitis (inflammation of the glans penis)
  • proctitis
  • urinary retention
302
Q

What is trichomonas vaginalis and outline the clinical presentation

A

What is it? Protozoon

  • Found in the vagina, urethral or para-urtheral glands

Clinical presentation:

  • 50% cases: asymptomatic
  • females: frothy, yellow vaginal discharge, vulval itch, dysuria, offensive odour
  • males: urethritis
303
Q

What is the treatment for trichomonas vaginalis?

A
  • treat even if asymptomatic
  • metronadazole
304
Q

Identify 3 populations most at risk of HIV

A
  • Sub-saharan Africa
  • MSM
  • children of people living with HIV
  • IV drug users
  • People having transactional sex
305
Q

Define seroconversion

A

The time period during which a specific antibody develops and becomes detectable in the blood

306
Q

Outline the clinical presentation of the seroconversion of HIV

A

ie the acute illness within 1-2 months after coming into contact with the virus

Systemic: weight loss, fever, flu-like symptoms

Pharyngitis

Mouth: sores, trush

Oesophagus: sores

Muscles: myalgia, aches and pains

Liver and spleen: enlargement

Central: malaise, headache

Lymphadenopathy

Skin: maculopapular rash

Gastric: nausea, vomiting

307
Q

Identify 2 routes of HIV transmission?

A
  • Open cuts, sores or breaks in the skin
  • Mucous membranes eg. inside anus/vagina
  • through direct injection
308
Q

Identify 2 activities allowing HIV transmission

A
  • anal or vaginal intercourse (oral sex not efficient route)
  • injecting drugs and sharing needles
  • mother-to-child transmission (before/during birth or through breast milk)
  • transmission in healthcare settings
  • transmission via donated blood or blood clotting factors
309
Q

Describe the pathophysiology of HIV

A
  • Infected with HIV, the virus gain entry to cells carrying CD4 receptors ie. T-helper cells, macrophages and dendritic cells
  • The HIV uses it’s own enzymes to convert RNA to DNA (reverse transcriptse)
  • DNA then moves into nucleus of the cells and integrates into our own DNA (HIV integrase)
  • After over the next several hours, the first infected cells carry HIV to the lymph nodes
  • Over the nect days/weeks, HIV continues to multiply in lymph nodes which are packed with CD4 cells (which HIV use to replicated)
  • HIV infection causes depletion of CD4 T helper cells by: direct killing of cells, apoptosis of uninfected bystander cells and CD8 cytotocic cell killing of infected CD4 cells
  • Eventually, the lymph node bursts as HIV continues to replicate, releasing HIV into the blood and it’s at this point that HIV levels become detectable
  • When CD4 cells fall below a critical number (<200), the person is at risk of opportunistic infections and some cancers
310
Q

What is the structure of HIV?

A
  • 2 RNA strands
  • HIV comes with 3 of it’s own enzymes (needed for reproduction): reverse transcriptase, HIV integrase, HIV protease
  • these enzymes are important targets for treatment
311
Q

Outline the natural history of HIV infection

A

Viral Load (RNA copies/ml)

  • undetectable until 3 weeks post infection
  • initially, exponential rise in viral load with symptoms of seroconversion expected
  • this is followed by a plateau (corresponds to clinical latency)
  • if left untreated: viral load will continually risk with opportunistic infection and eventual death

CD4 count

  • Starts at normal levels, then dips at seroconversion
  • high CD4 counts: oral thrust, oral hairy leucoplakia
  • declines over time
  • When CD4 count drops below 200, get opportunistic infections
312
Q

When is HIV testing needed?

How is HIV diagnosed?

A

Testing essential for:

  • someone presenting with HIV symptoms: primary HIV (acute infection) or HIV indicator conditions
  • HIV indicator conditions: trush, oral hairy leukiplakia, TB, bacterial pneumonia, aseptic meningitis, Hep B
  • people in the higher risk group

Diagnosis: Blood test

  • 4th generation testing
  • Test for p24 antigen or HIV antibody
  • NB window of 3-4 weeks
313
Q

What are 2 differentials for the maculopapular risk seen with HIV?

A
  • infectious mononucleosis
  • secondary syphilis
  • drug reaction rash
  • other viral infections eg. influenza
314
Q

What blood tests are routinely done in those with confirmed HIV?

A

HIV viral load

  • Can be >10mil
  • Aim is to maintain an undetectable viral load ie. below 200 copies/ml
  • In Scotland: aim for <40 copies/ml

CD4 count

  • calculated from total lymphocyte count and related to CD4 receptors on certain cells
  • HIV negative: 400-1600/mm3
  • risk of opportunistic infection increases sharply below 200
315
Q

What is the aim of HIV treatment?

A

Reduce morbidity and mortality

  • reduces risk of opportunistic infections, CV disease and cancer

Reduces risk of onward transmission

  • if viral load <200 consistently for >6 months and there is good adherence to treatment, there is no risk of onward transmission ie. undetectable
  • good motivator for good adherence
    ie. viral load suppression and CD4 recovery
316
Q

What is the management of HIV?

A

HAART - Highly Active Antiretroviral Therapy

  • Two nucleotide reverse transcriptase inhibitors and one drug from another class (1st try integrase inhibitors as fewer side effects)
  • combination pills are available
  • guided by patient choice, co-morbidities, drug-drug interactions, drug resistance
317
Q

Identify 2 challenges with antiretroviral therapy with HIV

A

Good adherence is essential: intermittent adherence increases the risk of resistance

Psychological impact: medication therapy is a daily reminder of thei HIV diagnosis

Short-term side effects

Longer-term toxicities

Drug-drug interactions

318
Q

Identify 3 short-term side effects of HIV therapy

A
  • Rash
  • Hypersensitivity reactions
  • CNS side effects
  • GI and hepatic side effects
319
Q

Identify the prevention strategies for HIV transmission

A
  • Condoms
  • Treatment as prevention (TasP)
  • Pre-exposure prophylaxis (PrEP)
  • Post-exposure prophylaxis (PEP)
  • Prevention of mother to child transmission (PMTCT)
  • harm reduction measures eg. needle exchange
320
Q

Outline how PEP is used in HIV

A
  • taken within 72 hours of potential exposure
  • 28-day course
  • available from sexual health or A&E
  • based on exposure type and risk of contact eg. condom
321
Q

Who are eligable to receive pre-exposure prophylaxis?

A
  • For those at higher risk of HIV through sexual transmission
  • Those in a high risk group or a partner of someone with undetectable HIV
322
Q

Identify a social implication of a HIV diagnosis

A
  • Often affects people from marginalised populations who are at risk of further marginalisation
  • High rates of psychological ill-health in those living with HIV
  • Stigma and isolation (don’t make assumptions)
  • There is currently an inappropriate focus on how the virus was acquired
323
Q

Define ‘viral latency’ in terms of HIV

A

Generally used to describe the long asymptomatic period between initial infection and advanced HV (AIDS)

  • At this point, the levels of the virus are high and continually replicating
  • With PCR, it’s becmoe clear that HIV replicates actively throughout the course of the infection even during the asymptomatic period
324
Q

Outline the challenges seen with HIV resistance

A
  • Variations of HIV that develop while an individual is taking HIV medication can lead to drug resistant strains of HIV
  • A person can be initially infected with drug-resistant HIV or develop drug-resistant HIV after starting HIV medication
  • Poor adherence can lead to resistance
  • Will render HIV medications ineffective
325
Q
A

Phase 3 (12 decks)

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