Microbiology

Question 1

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

Answer 1

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

Question 2

List the targets for antibiotics

Answer 2

• Cell wall peptidoglycans
• Metabolism
• DNA
• Ribosomes

Question 3

Describe the types of action of antibiotics

Answer 3

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

Question 4

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

Answer 4

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

Question 5

Compare broad and narrow spectrum antibiotics

Answer 5

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

Question 6

List and give examples of different types of bacteria

Answer 6

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

Question 7

How can antibiotics cause harm?

Answer 7

• 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

Question 8

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

Answer 8

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

Question 9

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

Answer 9

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

Question 10

What causes resistance to ß-lactam antibiotics?

Answer 10

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

Question 11

What are the types of ß-lactam antibiotics?

Answer 11

Penicillin

• Benzylpenicillin, Amoxicillin, Flucloxacillin

Cephalosporins

• Ceftriaxone

B-lactam/B-lactamase inhibitor combination

• Co-amoxiclav

Question 12

What are the adverse effects of B-lactams?

Answer 12

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

Question 13

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

Answer 13

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

Question 14

What is the class, indication and action of flucloxacillin?

Answer 14

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

Question 15

What is the class, indication and action of amoxicillin?

Answer 15

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

Question 16

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

Answer 16

• 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

Question 17

What is the class, indication and action of ceftriaxone?

Answer 17

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

Question 18

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

Answer 18

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

Question 19

List 3 side effects of Vancomycin

Answer 19

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

Question 20

List the different protein synthesis inhibitors used for antibiotic treatment

Answer 20

50s ribosomal subunit: macrolides

• Clarithromycin and erythromycin

30s ribosomal subunit: aminoglycosides

• Gentamicin

Question 21

What is the class, indication and action of clarithromycin?

Answer 21

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

Question 22

List 2 different penicillins

List a cephalosporin

List 2 macrolides

List a glycopeptide

List an aminoglycoside

Answer 22

Penicillin: flucloxicillin and amoxicillin

Cephalosporin: ceftriaxone

Macrolide: erythromycin and clarithromycin

Glycopeptide: vanocmycin

Aminoglycoside: gentamicin

Question 23

List the adverse effects and drug interactions of clarithromycin/erythromycin

Answer 23

Adverse effects:

• diarrhoea, vomiting, QT prolongation, ototoxicity

Drug interactions:

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

Question 24

What is the class, indication and action of erythromycin?

Answer 24

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

Question 25

How are Closridium Difficile infections caused by abx and what is the issue with these infections? How do you avoid C. Diff infection?

Answer 25

- 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

Question 26

List 4 antibiotics associated with clostridium difficile infection

Answer 26

- Clindamycin - Ceftriaxone/Cephalosporins - Co-amoxiclav - Ciprofloxacin

Question 27

What is the class, indication and action of Gentamicin?

Answer 27

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

Question 28

What are the side effects of Gentamicin? How is it adminstered?

Answer 28

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**

Question 29

What is the class, indication and action of ciprofloxacin?

Answer 29

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

Question 30

What are the side effects of ciprofloxacin?

Answer 30

- Quinolone Side effects: - GI toxicity, QT prolongation, C. Diff infection, tendonitis (rare)

Question 31

What is the class, indication and action of trimethoprim?

Answer 31

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

Question 32

What are the side effects of trimethoprim?

Answer 32

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

Question 33

What is cystitis?

Answer 33

- 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

Question 34

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

Answer 34

- Most are self-limiting, so recommend fluids and analgesia (NSAIDs) 1st line treatment: Trimethorpim - Avoid in 1st trimester of pregnancy (weak anti-folate activity)

Question 35

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

Answer 35

E. Coli and other coliforms

Question 36

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?

Answer 36

- 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

Question 37

What abx should be avoided during pregnancy?

Answer 37

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

Question 38

Define antimicrobial resistance (AMR)

Answer 38

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

Question 39

What is One Health? What are the main areas of concern? What is the One Health Approach?

Answer 39

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

Question 40

How is antibiotic resistance monitored? Define clinical resistance

Answer 40

- 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

Question 41

What mechanisms can bacteria adopt to cause antimicrobial resistance?

Answer 41

**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

Question 42

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

Answer 42

- 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)

Question 43

Compare/Define intrinsic and extrinsic resistance of bacteria

Answer 43

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

Question 44

What are the methods for intrinsic resistance of bacteria?

Answer 44

- 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

Question 45

What are the methods for extrinsic resistance to abx?

Answer 45

**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

Question 46

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

Answer 46

- 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

Question 47

Why are carbapenem-resistant bacteria worrying?

Answer 47

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

Question 48

What antibiotics target: - Cell wall - Protein synthesis (ribosomes) - DNA

Answer 48

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)

Question 49

What are antibiotics used for?

Answer 49

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

Question 50

Describe the spectrum of activity of different penicillins

Answer 50

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

Question 51

What is the correlation between antibiotic use and resistance?

Answer 51

- 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

Question 52

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

Answer 52

- 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

Question 53

How do we reduce antimicrobial resistance?

Answer 53

- Limit the use of abx ie. antibiotic stewardship

Question 54

What are the problems associated with unnecessary antibiotic use?

Answer 54

- 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

Question 55

What factors are driving antibiotic prescription?

Answer 55

- 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

Question 56

Define antimicrobial stewardship

Answer 56

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

Question 57

How is antimicrobial stewardship achieved?

Answer 57

- 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

Question 58

What is monitored to ensure antimicrobial stewardship?

Answer 58

- 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

Question 59

What are important factors to consider when prescribing antibiotics?

Answer 59

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)

Question 60

What situations would you not give antibiotics?

Answer 60

- 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)

Question 61

How are UTIs treated?

Answer 61

Asymptomatic bacteriuria: if no urinary symptoms, don't prescribe Abx Uncomplicated UTI (cystitis) - Majority are self-limiting - R**ecommend 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

Question 62

What signs/symptoms would point towards bacterial infection needing abx? Localising for urinary, resp and soft tissue

Answer 62

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

Question 63

What would be the choice of Abx for: Non-severe - LRTI (lower resp tract infection) - Lower UTI - Mild cellulitis Severe/Life threatening

Answer 63

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

Question 64

How is a COPD exacerbation treated? How long are community and hospital acquired pnuemonia treated for?

Answer 64

- COPD exacerbation: Amoxicillin for 5 days CAP and HAP: 5 days

Question 65

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

Answer 65

Restrictive: short-term benefits inc. reduction in resistance Persuasive: longer term benefits through behavioural changes Guideline adherence (empirical guidelines and de-escalation): reduced mortality

Question 66

Define sepsis

Answer 66

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

Question 67

How is sepsis quantified?

Answer 67

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

Question 68

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

Answer 68

- Hypotension: Systolic BP \<100 - Tachypnoea: RR \>22 - Altered mental state: GCS \<15 Interpretation: Score \>1 suggests sepsis

Question 69

Compare Systemic Inflammatory Response Syndrome (SIRS) and sepsis

Answer 69

SIRS: relates to inflammation Sepsis: result of infection overwhelming the body's defences

Question 70

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

Answer 70

2+ of: - Tachycardia: HR \>90 - Temp \<36 or \>38 - RR \>20 - WWC \<4 or \>12

Question 71

What should be undertaken within 1 hour of sepsis recognition?

Answer 71

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

Question 72

What are the indications for IV antibiotic therapy?

Answer 72

- 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

Question 73

What is the treatment for S. aureus bacteraemia?

Answer 73

- 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

Question 74

What are the links in the chain of infection

Answer 74

- Infectious agent - Reservoirs - Portal of exit - Means of transmission - Portal of entry - Susceptible host

Question 75

What are the main reservoirs used by infectious agents

Answer 75

Environment: need to control water quality in hospitals Animals: eg. flies Humans: symptomatic or asymptomatic (carriers)

Question 76

What are the 3 main ways of preventing infection

Answer 76

- Water control - Rodent control - Isolation

Question 77

Give 3 examples of infectious agent and their portal of exit

Answer 77

Tuberculosis: air borne infection Salmonella: faeco-oral Norovirus: vomit Hep B or HIV: bloodborne - Enterovirus: conjunctival secretions eg. watery eyes

Question 78

Compare the modes of transmission of infectious agents

Answer 78

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

Question 79

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

Answer 79

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

Question 80

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

Answer 80

Susceptible hosts: - New hosts - Immunocompromised Reduce risk - stop smoking, lose weight, control diabetes, vaccinations, prophylaxis, nutiriton, protective isolation

Question 81

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

Answer 81

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*

Question 82

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

Answer 82

Contact: - isolation, cleaning the environment, gloves, apron eg. salmonella Droplet: - Surgical mask and eye protection Airborne: - FFP3 masks eg. TB, pandemic flu

Question 83

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

Answer 83

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

Question 84

Give 5 principles involved in the aseptic technique

Answer 84

- 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

Question 85

Define pneumonia

Answer 85

Inflammation of one or both lungs, with dense areas of lung inflammation - Frequently but not always due to infection

Question 86

What are the bacterial causes of pneumonia?

Answer 86

Typical pneumonia - Strep. pneumoniae - Haemophilus influenza Atypical pnuemonia - Mycoplasma pneumoniae - Legionella pheumophila

Question 87

List 3 risk factors for acquiring strep. pneumonia infection?

Answer 87

alcohol, smoking, cancer

Question 88

List 3 clinical features and 3 examination findings for typical pneumonia

Answer 88

Clinical features: - Fever - pleuritic chest pain - cough (+/- sputum) - abrupt onset - non-resp symptoms Signs: - dull percussion - coarse crepitations - inc. vocal resonance

Question 89

what are 2 risk factors for haemophilus influenza?

Answer 89

- elderly - underlying lung disease

Question 90

What complications can arise due to infection with mycoplasma pneumoniae

Answer 90

- haemolysis - Guillain-Barre - erythema multiforme - cardiac problems - arthritis

Question 91

What clinical assessments are crucial for a patient with pneumonia? How is severe pneumonia determined

Answer 91

CURB65 **C**onfusion, **U**rea \>7, **R**esp rate \>30, **B**P 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

Question 92

What investigations are important for a patient with suspected pneumonia?

Answer 92

Bloods: - FBC, U&Es, ABG Micro: - blood cultures, sputum culture, throat swab, urine legionella antigen Investigations: - CXR and ECG

Question 93

What is the management for pneumonia?

Answer 93

ABC - airways, breathing, circulation Antibiotics: IV or oral Potential admission to hospital Depends on: - CURB65, qSOFA, hypoxia

Question 94

What is the treatment for strep pneumoniae?

Answer 94

Penicillin (resistance is rare in UK) If penicillin allergy: - macrolides (clarithromycin) - tetracyclines (doxycycline)

Question 95

What is the abx treament for haemophilus influenza?

Answer 95

co-amoxiclav If penicillin allergy: - macrolides (clarithromycin) - tetracycline (doxycycline)

Question 96

What is the abx treatment for legionella pneumophila?

Answer 96

- Macrolides (clarithromycin) - quinoline (ciprofloxacin) - tetracyclines (doxcycline)

Question 97

how do you treat typical pneumonia?

Answer 97

- penicllin if penicillin allergy: tetracyclines (doxycycline) or macrolides (clarithromycin)

Question 98

Give thee bacterial causes of traveller's diarrhoea

Answer 98

- enterotoxigenic e. coli - enteroaggregative e. coli - campylobacter - salmonella - c. diff

Question 99

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

Answer 99

Virus: - norovirus - rotavirus Parasite - Giardia - Cyclospora - Microsporidia

Question 100

What are the clinical features of traveller's diarrhoea

Answer 100

- often day 4-14 of travel - Self-limiting: lasts 1-5 days

Question 101

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

Answer 101

- 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

Question 102

What is the management for traveller's diarrhoea?

Answer 102

**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

Question 103

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

Answer 103

- many illnesses are mosquito borne Aedes: spread yellow fever and Dengue fever (day feeding) Anopheline: spreads Malaria (noctural feeding)

Question 104

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

Answer 104

- 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)

Question 105

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

Answer 105

malaria

Question 106

How is malaria acquired?

Answer 106

Anopheline mosquito bites

Question 107

List 3 clinical presentations of malaria

Answer 107

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

Question 108

Give 3 complications of severe malaria

Answer 108

- parasitaemia - cerebral malaria - severe anaemia - renal failure - septic shock - DIC (disseminated intravascular coagulation) - acidosis - pulmonary oedema

Question 109

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

Answer 109

Increased RBC breakdown - Anaemia - Jaundice (severe disease due to RBC lysis) - Renal impairment (poor microcirculation)

Question 110

How do you prevent infection with Malaria?

Answer 110

Bite avoidance Chemoprophylaxis in high prevalent areas (eg. sub-saharan africa) - Mefloquine: once weekly - Doxycycline: daily (SE: photosensitisation) - Malarone: daily (minimal SE)

Question 111

What are the causative agents of Typhoid? How is typhoid acquired?

Answer 111

- 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

Question 112

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

Answer 112

Incubation period: 5-21 days Dependent on: age, gastric acidity, immune status, infectious load

Question 113

Give 5 clinical manifestations of Typhoid What would happen if left untreated?

Answer 113

**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

Question 114

How do you prevent Typhoid fever? Where is typhoid prevalent?

Answer 114

- Prophylactic vaccinations - Only drink bottled or boiled water - avoid foods that may be contaminated with typhoid causative organisms Prevalent: India, Bangladesh

Question 115

How is typhoid treated?

Answer 115

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)

Question 116

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

Answer 116

Incubation period: 5-14 days 'Breakbone fever' - headache - fever - retro-orbital rash, general rash - arthralgia/myalgia - cough, nausea, sore throat, diarrhoea

Question 117

List 3 labatory findings for Dengue fever

Answer 117

- leukopenia - thrombocytopenia - transaminitis (high levels of transaminases produced by the liver)

Question 118

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

Answer 118

Spread via aedes mosquitos Mosquito prevention strategies - Indoors, repellent, keep covered with clothing and impregnated nets when sleeping

Question 119

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

Answer 119

Malaria: parasite (Plasmodium parasite) Dengue fever: virus (flaviviridae family) Typhoid: bacteria (salmonella typhoid or paratyphoid)

Question 120

What is the management for Dengue fever?

Answer 120

- Symptomatic: rest, fluids, paracetamol

Question 121

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

Answer 121

Examples: ebola and yellow fever Non-specific febrile illness - haemorrhagic manifestations - septic shock - death

Question 122

Define gastroenteritis

Answer 122

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

Question 123

Define diarrhoea

Answer 123

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

Question 124

Define dysentery

Answer 124

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

Question 125

Define enterocolitis

Answer 125

Inflammation involving mucosa of both the small and large intestine

Question 126

Give 3 examples of barriers to infection in the GI tract

Answer 126

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

Question 127

What is the role of the microbiome in the gut and what does it consist of? What can occur if the contents are disrupted?

Answer 127

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

Question 128

What are the sources of GI infection?

Answer 128

- 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)

Question 129

What are the main routes of transmission of GI infections?

Answer 129

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

Question 130

How are GI infections managed?

Answer 130

- 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

Question 131

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

Answer 131

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

Question 132

What are the 3 biggest causes of GI infection?

Answer 132

- Salmonella - Campylobacter - E. Coli

Question 133

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

Answer 133

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

Question 134

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

Answer 134

Treatment: - fluid replacement - abx reserved for severe infections and bacteraemia: b-lactams, quinolones, aminoglycosides (gentamicin) Control: - immunisation of poultry flocks

Question 135

What is the microbiology and epidemiology for campylobacter

Answer 135

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

Question 136

What is the treatment and specific control points for campylobacter?

Answer 136

Treatment: - fluid replacement - persistent/severe: clarithromycin - quinolones and gentamicin if invasive Control: - reduction in contamination of raw, retail poultry meat - adequate cooking

Question 137

What is the microbiology of Escherichia Coli

Answer 137

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

Question 138

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

Answer 138

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

Question 139

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

Answer 139

Mode of transmission: foodborne (raw/undercooked land meat, raw milk and raw vegetables) Spread: faeco-oral and direct contact (hand to mouth)

Question 140

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

Answer 140

Management: - Adequate rehydration Control: - education of food prep eg. washing hands, adequate cooking, avoid cross-contamination

Question 141

What is the microbiology and epidemiology of Shigella

Answer 141

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

Question 142

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

Answer 142

Treatment: - usually self-limtiing - fluid replacement Control: - sanitation and personal hygiene

Question 143

What is the microbiology and epidemiology of Vibrio Cholera

Answer 143

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

Question 144

How is Vibrio Cholera treated and controlled?

Answer 144

Management: - prompt oral/IV rehydration CRUCIAL - tetracycline abx potential Control: - Clean drinking water supply and proper sanitation

Question 145

Give three examples of pathogens causing infective GI infection

Answer 145

- Salmonella - E. Coli - Camylobacter - Less common: vibrio cholera and shigella

Question 146

Give three examples of pathogens causing GI infection through intoxication

Answer 146

Staphylococcus aureus Bacillus cereus Clostridium difficile Helicobacter pylori Listeria monocytogenes

Question 147

Define intoxication

Answer 147

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

Question 148

Describe the microbiology and epidemiology of staphylococcus aureus

Answer 148

Microbiology: - Gram +ve Epidemiology: - head stable and acid-resistant protein toxins (enterotoxins produced) - Transmission: food contaminated by human carriers - Spread: direct contact / droplet spread

Question 149

What is are the management and control measures for Staphylococcus aureus

Answer 149

Management: self-limiting Control: hygienic food prep and refrigerated storage

Question 150

What is the microbiology and epidemiology of bacillus cereus

Answer 150

Microbiology: - aerobic, spore-forming Gram +ve bacilli Epidemiology: - Emetic disease: associated with fried rice - Diarrhoeal disease Both: foodborne transmission

Question 151

How do you treat bacillis cereus

Answer 151

Treatment: self-limiting

Question 152

What is the microbiology and epidemiology of closridium difficile

Answer 152

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)

Question 153

How is clostridium difficile treated and controlled?

Answer 153

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

Question 154

What is the microbiology and epidemiology of helicobacter pylori? How is it diagnosed?

Answer 154

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

Question 155

What is the treatment for H. Pylori?

Answer 155

Omeprazole (PPI) with clarithromycin, amoxicillin and metronidazole - eradicates carriage and facilitates ulcer healing

Question 156

What is the class, action and indication of omeprazole?

Answer 156

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

Question 157

What is the microbiology and epidemiology of listeria monocytogenes?

Answer 157

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

Question 158

How is listeria monocytogenes treated and controlled

Answer 158

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

Question 159

Define viral gastroenteritis

Answer 159

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

Question 160

Who are most at risk of viral gastroenteritis?

Answer 160

Children under 5 elderly immunocompromised

Question 161

What ages are most affected by norovirus?

Answer 161

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

Question 162

What ages are most affected by rotavirus?

Answer 162

affects mainly children \<2, elderly and immunocompromised not often seen in adults

Question 163

List 3 important viruses that can cause gastroenteritis

Answer 163

- norovirus, rotavirus, adenovirus 40&41, astrovirus

Question 164

Describe the structure and transmission of norovirus

Answer 164

Structure: - family: calciviridae - non enveloped, single stranged RNA Transmission - highly contagious - Transmission: person-to-person, foodborne, water - Can affect all ages

Question 165

How is norovirus managed? Can you develop immunity to norovirus what measures are involved in infection control

Answer 165

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

Question 166

Describe the structure and transmission of rota virus

Answer 166

Structure: - family: reoviridae - non-enveloped, double stranded RNA virus Transmission - low infectious dose - person-to-person via faeco-oral or fomites

Question 167

How do you diagnose viral gastroenteritis infections? What type of sample is used?

Answer 167

PCR (Polymerase Chain Reaction) - This detects DNA samples and amplifies them, allowing them to be studied to make a diagnosis Sample: vomit or stool

Question 168

What is the structure and treatment for adenovirus Is there a vaccine

Answer 168

Structure: double stranded DNA virus - Adenovirus 40&41 cause gastroenteritis Treatment: supportive - No vaccine

Question 169

Can immunity be developed to rotavirus?

Answer 169

Yes - Vaccine: rotarix, part of the childhood immunisation schedule - Live attenuated vaccine

Question 170

What is the structure of astrovirus?

Answer 170

Single stranded, small, non-enveloped RNA virus

Question 171

List a viral cause for each of the following Common cold Pharyngitis Croup Acute Bronchitis Bronchiolitis Pneumonia

Answer 171

Common cold: rhinovirus and coronavirus Pharyngitis: adenovirus Croup: parainfluenza virus Acute Bronchitis: RSV (Respiratory Syncytical Virus) Bronchiolitis: RSV Pneumonia: (haemophilus) influenza and RSV

Question 172

Outline the modes of transmission of viral respiratory tract infections

Answer 172

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

Question 173

Outline the aetiology and clinical presentation of the common cold

Answer 173

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

Question 174

Outline the potential complications and management for the common cold

Answer 174

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

Question 175

Outline the aetiologies of pharyngitis

Answer 175

- 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

Question 176

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

Answer 176

**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

Question 177

Outline the aetiology and clinical presentation of Croup How is Croup managed?

Answer 177

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

Question 178

Outline the complication with Croup

Answer 178

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

Question 179

Outline the aetiology and clinical presentation of bronchiolitis

Answer 179

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

Question 180

What is the risk of respiratory syncytical virus?

Answer 180

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

Question 181

How bronchiolitis treated (if caused by RSV)?

Answer 181

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%

Question 182

Outline the aetiology of influenza

Answer 182

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

Question 183

Outline the clinical presentation of influenza

Answer 183

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

Question 184

List 3 complications of influenza

Answer 184

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

Question 185

List 3 risk factors for developing complicated influenza

Answer 185

- 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

Question 186

Outline the management for influenza

Answer 186

M2 inhibitors - amantadine, rimantadine Broad spectrum antivirals - ribavirin Neuraminidase inhibitors - neuraminidase is a surface protein on viruses and allows release of new virus progenies

Question 187

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?

Answer 187

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

Question 188

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

Answer 188

Rhinovirus: common cold Adenovirus: pharyngitis RSV: acute bronchitis, bronchiolitis, pneumonia Influenza virus: influenza, pneumonia Parainfluenza virus: Croup Coronavirus: common cold

Question 189

Define septic arthritis and outline the complications if left untreated

Answer 189

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

Question 190

List 3 common pathogens causing septic arthritis

Answer 190

Common: Staphylococcus: MSSA or MRSA Streptococci Less common: - H. influenza - N. meningitis - N. gonorrhoea - E. coli

Question 191

Outline the clinical presentation of septic arthritis

Answer 191

- fever - single 'hot' joint (knee, hit) - polyarticular involvement in 10-20% - loss of movement - pain

Question 192

Outline the key investigations to diagnose septic arthritis

Answer 192

Blood cultures Joint aspirate: microscopy for crystals and culture - Need to ensure aseptic technique (don't want to introduce micro-organisms) FBC CRP Imaging

Question 193

How is septic arthritis managed?

Answer 193

3 weeks IV Abx followed by 3 weeks oral abx - monitor response by CRP and clinical signs

Question 194

# Define: arthroplasty arthrodesis arthrosis pseudo-arthrosis resection arthroplasty revision arthroplasty

Answer 194

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)

Question 195

List 3 risk factors for needing a primary arthroplasty

Answer 195

- rheumatoid arthritis - diabetes mellitus - poor nutritional status - obesity - concurrent UTI

Question 196

List 3 risk factors for needing a revision arthroplasty

Answer 196

prior joint surgery prolonged operating room time pre-op infection (skin, teeth, UTI)

Question 197

Outline the pathogenesis of prosthetic joint infections

Answer 197

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

Question 198

Outline the clinical presentation of a prosthetic joint infection

Answer 198

- 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

Question 199

How do you avoid a prosthetic joint infection?

Answer 199

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

Question 200

Outline the investigations needed to diagnose a prosthetic joint infection

Answer 200

Diagnosis based on macroscopic appearance, histopathology and microbiology Sample: tissue/**pus**/fluid

Question 201

Outline the management for a PJI

Answer 201

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

Question 202

Outline the surgical management for prosthetic joint infections

Answer 202

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

Question 203

Define osteomyelitis

Answer 203

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

Question 204

Outline the pathology of osteomyelitis

Answer 204

- 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

Question 205

Outline the treatment for osteomyelitis

Answer 205

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

Question 206

# Define vertebral discitis Outline the clinical presentation List 3 complications

Answer 206

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

Question 207

Define tuberculosis

Answer 207

- an infectious bacterial disease characterised b growth of granulomas in the tissues, especially the lungs

Question 208

What is the causative agent for tuberculosis? Outline the characteristics of the substance

Answer 208

mycobacterium tuberculosis (M. tuberculosis) - Weak Gram +ve - Slow-growing - Stain: Ziehl-Neelsen (ZN) stain (pink-purple beaded gram +ve rods)

Question 209

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

Answer 209

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)

Question 210

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

Answer 210

- 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

Question 211

Outline the immunology of tuberculosis

Answer 211

- 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

Question 212

Outline the progression of tuberculosis

Answer 212

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

Question 213

What is the histological hallmark feature of tuberculosis?

Answer 213

**Granulomas** - Macrophages turn into multinucleated giant cells and foam cells and create tight intracellular junctions

Question 214

Outline the clinical presentation of mycobacterium tuberculosis

Answer 214

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

Question 215

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

Answer 215

**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

Question 216

What tests are available to determine TB exposure?

Answer 216

**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

Question 217

How is TB diagnosed?

Answer 217

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

Question 218

Outline the treatment for latent TB What is the risk with tuberculosis treatment?

Answer 218

- Isoniazid monotherapy for 6 months OR - Rifapmicin plus isoniazid daily for 3 months Risk: liver dysfunction

Question 219

Outline the treatment for active tuberculosis What are the complications of this treatment?

Answer 219

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

Question 220

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

Answer 220

Risk of generating drug resistance

Question 221

Define meningitis and meningo-encephalitis

Answer 221

Meningitis: inflammation of the meninges Meningo-encephalitis: inflammation of the meninges and cerebral inflammation

Question 222

Outline the clinical presentation of meningitis

Answer 222

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

Question 223

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

Answer 223

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

Question 224

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

Answer 224

Neurology: - focal signs: fever, headache, malaise, neck stiffness, photophobia - seizures - VII (facial) palsy More severe infection: - community acquired pneumonia - ENT problems - Endocarditis

Question 225

What clinical presentations would indicate meningitis caused by meningococcal species?

Answer 225

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

Question 226

List 3 poor prognosis indicators in bacterial meningitis

Answer 226

- 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

Question 227

How do you investigate a suspected meningitis case?

Answer 227

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

Question 228

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

Answer 228

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

Question 229

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

Answer 229

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

Question 230

Outline the treatment for _suspected_ bacterial meningitis

Answer 230

- 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

Question 231

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

Answer 231

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

Question 232

Outline secondary prevention of meningococcal meningitis

Answer 232

- 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

Question 233

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

Answer 233

- Pneumococcal - Meningococcal - Haemophilus Influenza Type B

Question 234

When would a diagnosis of viral meningitis be made? How does it present?

Answer 234

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

Question 235

List 3 causes of viral meningitis

Answer 235

- enterovirus (most common) - HSV 2 - VZV (Varicella Zoster Virus) - HSV 1 - HIV

Question 236

How is viral meningitis treated?

Answer 236

Supportive management - Only consider antivirals in **immunosuppressed** ie. acyclovir

Question 237

How would viral encephalitis present? What is the most common causative agent?

Answer 237

Presentation: - confusion, fever +/- seizures - dangerous infection Common cause: HSV encephalitis - HSV 1 usually but can be HSV 2

Question 238

How would you investigate for suspected viral encephalitis?

Answer 238

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

Question 239

Patient presents with headache, fever and confusion What must they be treated for and what treatment would they be given?

Answer 239

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

Question 240

What is the management for viral encephalitis?

Answer 240

IV acyclovir for 2-3 weeks

Question 241

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

Answer 241

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

Question 242

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

Answer 242

Secondary = caused by environmental factors - can be due to underlying disease state eg. HIV, malnutrition - treatment for disease

Question 243

Identify 3 factors contributing to increasing population of immunocompromised patients

Answer 243

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

Question 244

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

Answer 244

Infection

Question 245

Define neutropenia

Answer 245

Low levels of neutrophils (low neutrophil count) - Defined as \<0.5 x10⁹/L or \<1.ox10⁹/l and falling

Question 246

Identify 2 causes of neutropenia and how they lead to neutropenia

Answer 246

- Cytotoxic chemotherapy - Therapeutic irradiation (TB) These lead to: - reduced proliferation of haematopoietic progenitor cells and depletion of marrow reserves - result in neutropenia

Question 247

How to cytotoxic drugs and steroids affect neutrophils

Answer 247

They affect neutrophil count and **functionality of neutrophils** - Reduce chemotaxis - Reduce phagocytic killing - Reduce intracellular killing

Question 248

Identify 3 pathogens that affect neutrophil function

Answer 248

Gram +ve cocci: - Staph aureus - Enterococci Gram -ve cocci: - E. Coli

Question 249

How is Chronic Granulomatous disease inherited? What is it?

Answer 249

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

Question 250

Outline the humoral and cell-mediated immunity

Answer 250

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

Question 251

Identify 3 ways in which cellular immunity can be suppressed

Answer 251

- 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

Question 252

Idenity 2 causes of humoral immunodeficiency

Answer 252

- Bruton agammaglobulinemia - Antibody production is reduced in lymphproliferative disorders: Chronic lymphoid leukaemia (CLL), multiple myeloma (Preserved in acute leukaemia)

Question 253

Outline the function of the spleen

Answer 253

Splenic macrophages eliminate non-opsonised microbes eg. encapsulated bacteria Site of the primary immunoglobulin response: specific opsonising antibody required for phagocytosis of encapsulated bacteria

Question 254

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

Answer 254

- Strep. pneumoniae - Haemophilus influenzae type B - Neisseria meningitis

Question 255

Identify 3 physical barriers against microbial invasion

Answer 255

- skin - conjunctiva - mucous membranes: gut, respiratory tract, GU tract

Question 256

How does skin act as a barrier to microbial invasion?

Answer 256

it creates an environment that's difficult for organisms to get a hold of: - desquamates - dry - pH 5-6 - Secreotry IgA in sweat

Question 257

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

Answer 257

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

Question 258

Identify 3 ways in which the microbiome can be altered

Answer 258

- H2 antagonists - PPIs - Abx - diarrhoea

Question 259

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

Answer 259

**Focus on prevention** ie. prophylaxis - patients who will be neutropenic for \>1 week need prophylaxis

Question 260

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

Answer 260

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

Question 261

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

Answer 261

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

Question 262

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

Answer 262

- bloodstream

Question 263

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

Answer 263

Sepsis 6: - Take: blood culture, measure urine output, measure lactate and Hb - Give: high flow oxygen, IV fluids, abx

Question 264

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

Answer 264

- warfare - poor sanitation - poverty - poor nutrition - poorly developed healthcare system - poorly developed women's rights

Question 265

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

Answer 265

- diarrhoea - pneumonia (and other respiratory tract infections) - malaria

Question 266

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

Answer 266

- naive immune system - not yet immunised - immune system functionally immunodeficient at birth

Question 267

Why are pregnant women naturally immunosuppressed?

Answer 267

- 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

Question 268

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

Answer 268

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

Question 269

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)

Answer 269

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

Question 270

Outline 2 methods of acquiring immunity

Answer 270

**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

Question 271

Compare antibody-mediated and cell mediated immunity

Answer 271

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

Question 272

Outline the role of vaccines - What is the prime and secondary response to vaccines

Answer 272

- 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

Question 273

Outline how live attenuated vaccines work Who should not receive live attenuated vaccines Give an example of an attenuated vaccine

Answer 273

- 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

Question 274

What is meant by herd immunity

Answer 274

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**

Question 275

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

Answer 275

Streo. pneumonia

Question 276

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

Answer 276

Meningitis - Frequently accompanied by: bacteraemia, pneumonia, cellulitis

Question 277

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

Answer 277

Neisseria Meningitis

Question 278

what is involved in the standard sexual health screen?

Answer 278

Chlamydia and gonorrhoea - NAAT test - PCR Syphilis and HIV - Blood test - big EDTA bottle

Question 279

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

Answer 279

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)

Question 280

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

Answer 280

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

Question 281

Identify 2 high-risk groups of gonorrhoea

Answer 281

- MSM - afro-caribbean - urban areas with deprivation - anyone having sex

Question 282

Name the causative organism of gonorrhoea Outline the transmission

Answer 282

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

Question 283

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

Answer 283

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

Question 284

How is gonorrhoea diagnosed?

Answer 284

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

Question 285

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

Answer 285

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

Question 286

Name a complication for men and women of gonorrhoea

Answer 286

Men: - epidimyo-orchitis - prostatitis Women: - PID

Question 287

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

Answer 287

Chlamydia - Easily transmissible: if one partner in the relationship has it, likely the other does (couple concordance) - It's usually asymptomatic

Question 288

Identify 2 risk factors for acquiring chlamydia

Answer 288

- \<25yrs - new sexual partner or \>1 partner in last month - inconsistent condom use

Question 289

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

Answer 289

*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

Question 290

Outline the diagnosis and treatment for chlamydia

Answer 290

Diagnosis: - NAAT testing: male (urine), female (self-taken vaginal swab) - Too small for microscopy - Not resistant therefore no culture Treatment: **doxycycline 100mg BD weekly**

Question 291

Outline the main complication of chlamydia in men and women

Answer 291

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

Question 292

Name the causative agent of syphilis How is syphilis transmitted? Identify two populations most at risk of syphilis

Answer 292

Causative agent: treponema pallidum Transmission: - oral sex - vertical transmission from mother to child At risk: - MSM, anyone

Question 293

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

Answer 293

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

Question 294

Outline the diagnosis for syphilis

Answer 294

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

Question 295

What is the treatment for syphilis

Answer 295

Benzathine penicillin

Question 296

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

Answer 296

Anogenital warts Causative agent: human papilloma virus (HPV) - main types causing warts: HPV6 and HPV11

Question 297

what is the diagnosis and management for anogenital warts?

Answer 297

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

Question 298

which of the following STIs require partner notification: - gonorrhoea - chlamydia - syphilis - anogenital warts

Answer 298

Gonorrhoea, chlamydia and syphilis

Question 299

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

Answer 299

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**

Question 300

How is herpes simplex diagnosed and managed?

Answer 300

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

Question 301

Identify two complications of HSV

Answer 301

- CNS infection - balanitis (inflammation of the glans penis) - proctitis - urinary retention

Question 302

What is trichomonas vaginalis and outline the clinical presentation

Answer 302

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

Question 303

What is the treatment for trichomonas vaginalis?

Answer 303

- treat even if asymptomatic - metronadazole

Question 304

Identify 3 populations most at risk of HIV

Answer 304

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

Question 305

Define seroconversion

Answer 305

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

Question 306

Outline the clinical presentation of the seroconversion of HIV

Answer 306

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

Question 307

Identify 2 routes of HIV transmission?

Answer 307

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

Question 308

Identify 2 activities allowing HIV transmission

Answer 308

- 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

Question 309

Describe the pathophysiology of HIV

Answer 309

- 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

Question 310

What is the structure of HIV?

Answer 310

- 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

Question 311

Outline the natural history of HIV infection

Answer 311

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

Question 312

When is HIV testing needed? How is HIV diagnosed?

Answer 312

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

Question 313

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

Answer 313

- infectious mononucleosis - secondary syphilis - drug reaction rash - other viral infections eg. influenza

Question 314

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

Answer 314

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

Question 315

What is the aim of HIV treatment?

Answer 315

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**

Question 316

What is the management of HIV?

Answer 316

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

Question 317

Identify 2 challenges with antiretroviral therapy with HIV

Answer 317

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

Question 318

Identify 3 short-term side effects of HIV therapy

Answer 318

- Rash - Hypersensitivity reactions - CNS side effects - GI and hepatic side effects

Question 319

Identify the prevention strategies for HIV transmission

Answer 319

- 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

Question 320

Outline how PEP is used in HIV

Answer 320

- 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

Question 321

Who are eligable to receive pre-exposure prophylaxis?

Answer 321

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

Question 322

Identify a social implication of a HIV diagnosis

Answer 322

- 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

Question 323

Define 'viral latency' in terms of HIV

Answer 323

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

Question 324

Outline the challenges seen with HIV resistance

Answer 324

- 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