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Y5 Pathology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Give 5 examples of broad-spectrum antibiotics.

A

Broad

  • Co-amoxiclav
  • Ceftriaxone
  • Doxycycline
  • Tetracycline

Very-broad

  • Tazocin
  • Meropenem
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2
Q

What are the 4 different mechanisms of antibiotics.

A

Inhibit cell wall synthesis
Inhibit protein synthesis
DNA/nucleic acid synthesis inhibitors
Inhibit folate synthesis

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3
Q

What 2 subtypes of antibiotics are inhibitors of cell wall synthesis?

A
  • Beta-lactams
  • Glycopeptides
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4
Q

What 5 subtypes of antibiotics are inhibitors of protein synthesis?

A
  • Chloramphenicol
  • Aminoglycosides
  • Lincosamide
  • Macrolides
  • Tetracyclines
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5
Q

What 3 subtypes of antibiotics are DNA/nucleic acid synthesis inhibitors?

A
  • Quinolones
  • Nitroimidazoles
  • Miscellaneous - Rifampicin
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6
Q

What subtype of antibiotics is a inhibitor of folate synthesis?

A

Sulphonamides

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7
Q

Name some beta-lactams.

A

Penicillin
Cephalosporins
Carbapenems

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8
Q

Name some glycopeptides.

A

Vancomycin
Teicoplanin

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9
Q

Name some tetracyclines.

A

End in -cycline

  • Tetracycline
  • Doxycycline
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10
Q

Name some aminoglycosides.

A

End in -cin

  • Gentamycin
  • Amikacin
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11
Q

Name some macrolides.

A

End in -mycin

  • Erythromycin
  • Clarithromycin
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12
Q

Name some oxazolidinones.

A

End in - zolid
- Linezolid

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13
Q

Name some quinolones.

A

End in -xacin

  • Ciprofloxacin
  • Ofloxacin
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14
Q

Name some nitroimidazoles.

A
  • End in azole
    Metronidazole
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15
Q

Name some sulphonamides.

A

Trimethoprim
Septrin

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16
Q

What is the mechanisms of glycopeptides?

A

Cell wall synthesis inhibitors

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17
Q

What is the mechanisms of aminoglycosides?

A

Binds/blocks amino-acyl site of 30S ribosomal subunits

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18
Q

What is the mechanisms of tetracyclines?

A

Reversibly bind to ribosomal 30S subunit
- Bacteriostatic

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19
Q

What is the mechanisms of macrolides?

A

Binds/blocks 50S subunits of ribosomes

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20
Q

What is the mechanisms of oxazolidinones?

A

Protein synthesis inhibitor via 23S of 50S subunit inhibition

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21
Q

What is the mechanisms of nitroimidazole?

A

DNA synthesis inhibition

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22
Q

What is the mechanisms of the penicillins?

A

Transpeptidase inhibitor - weakens cell walls
- Bactericidal

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23
Q

How well do penicillin’s penetrate into the CNS?

A

Not well
- Can only do so in inflamed meningitis

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24
Q

What bacteria is penicillin active against?

A

Gram +ve

  • Strep
  • Clostridium
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25
Q

What bacteria is IV benzylpenicillin (Penicillin G) most and least effective against?

A

Very effective = strep - particularly strep A sore throat
Least effective = gut bacteria

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26
Q

How does flucloxacillin differ from penicillin?

A

Not broken down by beta lactamase produced by Staph aureus = BL resistant
- Develops resistance through alteration of target

Chemically similar to penicillin but less active

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27
Q

What are the clinical uses of flucloxacillin?

A

Staph aureus
Skin infections

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28
Q

How do amoxicillin and piperacillin differ to penicillin and what are the similarities?

A

Developed as a broad-spectrum penicillin - extended coverage compared to penicillin to cover enterococcus and some gram-neg organisms
Better absorbed

Similar as it is broken down by beta lactamase produce by Staph aureus and many gram neg organisms

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29
Q

What are the clinical uses of amoxicillin?

A

First line for pneumonia

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30
Q

What are the clinical uses of ampicillin?

A

Listeria
- Listeriosis - severe sepsis, meningitis, or encephalitis

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31
Q

What are the clinical uses of piperacillin?

A

Hospital acquired infections

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32
Q

Name 2 beta lactamase inhibitors.

A

Clavulanic acid
Tazobactam

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33
Q

What is co-amoxiclav?
What are the clinical uses of co-amoxiclav?

A

Amoxicillin + clavulanic acid

Covers haemophilus influenzae and staph

  • Severe CAP
  • Staph skin infections
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34
Q

What is tazocin?
What are the clinical uses of tazocin?

A

Piperacillin + tazobactam

Covers gram positive, negatives, anaerobes, pseudomonas and beta-lactamases but NOT MRSA

  • CF, bronchiectasis cover/prophylaxis
  • Neutropenic sepsis
  • Severe pseudomonas - administered with aminoglycoside for synergistic effect
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35
Q

What percentage of penicillin allergies cross-react with carbapenems or cephalosporins?

A

5-10%

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36
Q

What alternative antibiotics should be used in patients with penicillin allergies?

A

If just rash = cephalosporin

If anaphylaxis = alternative

  • Doxycycline for pneumonia
  • Erythromycin for impetigo
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37
Q

What is the mechanism of cephalosporins?

A

Beta-lactams

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38
Q

How well do cephalosporins penetrate into the CNS?

A

Good penetration - used for meningitis

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39
Q

What bacteria are cephalosporins active against?

A

Very broad spectrum

Gram positive, some cover over proteus, E.coli and Klebsiella (UTI)
- Higher generations are less gram positive and more negative

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40
Q

Name some 1st, 2nd and 3rd generation cephalosporins.

A

1st = Cefalexin
2nd = Cefuroxime
3rd = Ceftriaxone, Cefotaxime, Ceftazidime
- All have t in the name

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41
Q

What is the cover of 2nd generation cephalosporins/cefuroxime?

A

Stable to many beta lactamases produced by gram negative

Similar cover to co-amoxiclav but less active against anaerobes (abdominal/gut infections)

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42
Q

What is the cover of 3rd generation cephalosporins?

A

More activity against gram -ve and less against gram +ve - still very broad-spectrum

Really good CNS penetration - bacterial meningitis

Used in HAPs

Do not cover Listeria

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43
Q

What is the serious side effect of ceftriaxone?

A

C. diff

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44
Q

Name 2 carbapenems.

A

Meropenem
Imipenem

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45
Q

What bacteria are carbapenems active against?

A

Very broad spectrum
Used for severe infections when beta-lactams would not work - usually not first line

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46
Q

What are the indications for carbapenems?

A

Extended spectrum beta-lactamase (ESBL)
Pseudomonas
Anaerobes
Sepsis of unknown origin
Severe abdominal infections

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47
Q

Does carbapenems resistance exist?

A

Carbpenemase enzymes becoming more widespread - in multi-drug resistant acinetobacter and klebsiella species and now in more

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48
Q

What bacteria are glycopeptides active against?

A

Gram +ve
- Too larger molecule to pass through Gram -ve outer membrane

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49
Q

What are the side/adverse effects of glycopeptides?

A

Nephrotoxic

Ototoxic - Vancomycin more so than
Teicoplanin

Vancomycin has narrower therapeutic range so easier to overdose so need monitoring

Vancomycin can cause red man syndrome - sudden onset erythematous, pruritic rash on face, neck, upper torso

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50
Q

What bacteria are tetracyclines active against?

A

Intracellular bacteria - no cell wall
- e.g. Mycoplasma and chlamydia

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51
Q

What are the indications for tetracyclines?

A

Chlamydia (doxycycline)
TB
MRSA

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52
Q

What are the draw backs off tetracyclines?

A

Widespread resistance

Contraindicated in children and pregnant women (deposit in growing bones, discolouration in growing teeth)

Light-sensitive rash so be cautious in sun

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53
Q

What bacteria are aminoglycosides active against?

A

Gram -ve

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54
Q

What are the indications for aminoglycosides?

A

Blood and urinary sepsis

Pseudomonas (gentamicin or tobramycin)

Endocarditis - synergistic with beta-lactams for multi-drug resistance

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55
Q

What are the side/adverse effects of aminoglycosides?

A

Nephrotoxic and Ototoxic - requires therapeutic drug monitoring

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56
Q

What bacteria are macrolides active against?

A

Gram +ve

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57
Q

What are the indications for macrolides?

A

Mild staph or strep in penicillin-allergic patients or pregnant patients (safe in pregnancy)

Campylobacter or legionella

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58
Q

What bacteria are chloramphenicol active against?

A

Very broad-spectrum

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59
Q

What are the indications for chloramphenicol?

A

Meningitis or strep pneumoniae - in penicillin allergy

Eye infections

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60
Q

What are the side/adverse effects of chloramphenicol?

A

Aplastic anaemia

Grey baby syndrome in neonates due to reduced metabolic activity

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61
Q

What bacteria are oxazolidinones active against?

A

Only Gram +ve
- MRSA and VRE

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62
Q

What are the indications for oxazolidinones?

A

MRSA and VRE

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63
Q

What are the side/adverse effects of oxazolidinones?

A

Thrombocytopenia (relatively common)
Optic neuritis with prolonged use

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64
Q

What bacteria are quinolones active against?

A

Both Gram +ve and -ve
- especially -ve

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65
Q

What is an advantage of quinolones opposed to other antibiotic types?

A

Very well orally absorbed

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66
Q

What are the indications for quinolones?

A

UTI and pyelonephritis
Pneumonia
Atypical pneumonia
Bacterial gastroenteritis
Chlamydia

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67
Q

What are the side/adverse effects of quinolones?

A

Achilles tendonitis
C diff

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68
Q

What bacteria are nitroimidazoles active against?

A

Anaerobic bacteria
Protozoa

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69
Q

What are the indications for nitroimidazoles?

A

C diff
Parasites - entamoeba, giardia, trichomonas

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70
Q

What are the side/adverse effects of nitroimidazoles?

A

Avoid alcohol - severe reaction causing vomiting, SOB, flushing
- Metronidazole it is the 1 antibiotic were it must be avoided

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71
Q

Why is nitrofurantoin useful for UTIs?

A

Accumulates in the bladder - not systemically absorbed
- best to take just after the patient has gone to the toilet so it stays in the bladder longer

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72
Q

What is the empirical treatment of a lower UTI?

A

Nitrofurantoin

  • could consider co-amoxiclav
  • trimethoprim isn’t used much now due to resistance
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73
Q

What is the treatment for pyelonephritis?

A

Co-amoxiclav + gentamicin

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74
Q

What are the 4 resistance mechanisms??

A
  1. Inactivation/chemical modification of antibiotic
  2. Altered target
  3. Reduced antibiotic accumulation
  4. Bypass antibiotic-sensitive step in cell division
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75
Q

What percentage of resistance means empirical use is no longer advised?

A

>10%

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76
Q

What resistance mechanism is used by MRSA?

A
  • Beta-lactamase
  • mecA gene - encodes new PBP2a penicillin-binding protein
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77
Q

What resistance mechanism is used by strep pneumoniae?

A

PBP gene mutations
- low-level resistance can be overcome by increasing the dose

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78
Q

How do some bacteria become resistant to macrolides?

A

Methylation of ribosomal subunit - reduces binding of macrolides

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79
Q

Define minimum inhibitory concentration.

A

Minimum about of drug needed to limit the growth of an organism

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80
Q

Define break-point in terms of antibiotics.

A

Concentration of antibiotic that it becomes clinically useful

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81
Q

What are the routes of pathogen entry into the CNS?

A
  • Haematogenous (e.g. pneumococcus, meningococcus) - MOST COMMON
  • Direct implantation (e.g. penetrative trauma, surgery)
  • Local extension (e.g. from the ear)
  • PNS into CNS (e.g. rabies)
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82
Q

Define Meningitis.

A

Inflammation of the meninges and CSF

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83
Q

Define Meningoencephalitis.

A

Inflammation of the meninges and brain parenchyma.

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84
Q

What are the routes of neurological damage due to meningitis?

A
  • Direct bacterial toxicity
  • Indirect inflammatory process and cytokine release and oedema
  • Shock, seizures and cerebral hypoperfusion
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85
Q

What are the causes of acute meningitis?

A
  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Other
    • Listeria monocytogenes
    • Group B Streptococcus
    • Escherichia coli
  • Rare
    • TB, S. aureus, T. pallidum, Cryptococcus neoformans
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86
Q

What types of rash occur due to Neisseria meningitidis infection?

A
  • Non-blanching rash (80% of children)
  • Maculopapular rash (13% of children)
  • No rash (7% of children)
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87
Q

What percentage of patients infected with Neisseria meningitidis suffer from meningitis, septicaemia and both?

A
  • 50% have meningitis
  • 10% have septicaemia
  • 40% have meningitis AND septicaemia
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88
Q

What causes of acute meningitis have a bimodal (children/neonates and elderly) distribution?

A
  • Streptococcus pneumoniae
  • E coli
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89
Q

What cause of acute meningitis is found in blue cheese and mayonnaise?

A

Listeria monocytogenes

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90
Q

What are the 4 key features/processes of septicaemia?

A
  • Capillary leakage
  • Coagulopathy
  • Metabolic derangement
  • Myocardial failure
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91
Q

What are the signs and symptoms of meningitis?

A
  • Fever
  • Headache
  • Stiff neck
  • Some disturbance of brain function - not usually severe and/or to all brain functions
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92
Q

What are the signs and symptoms of encephalitis?

A
  • Widespread disturbance to brain function
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93
Q

What are the signs and symptoms of myelitis?

A
  • Disturbance to nerve transmission
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94
Q

What are the signs of neurotoxin - tetanus?

A

Rigid paralysis

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95
Q

What are the signs of neurotoxin - botulism?

A

Flaccid paralysis

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96
Q

What are the causes of chronic meningitis?

A
  • TB
  • Spirochetes
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97
Q

Define Chronic meningitis.

A

Meningitis that takes several days and up to weeks to develop

  • Similar presentation as acute
  • Far lower mortality (0.00005% compared to 10%)
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98
Q

What group of patients are more susceptible to chronic meningitis?

A

Immunosuppressed

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99
Q

What are the complications of chronic meningits?

A
  • Tuberculous granulomas
  • Tuberculous abscesses
  • Cerebritis
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100
Q

What are the causes of Aseptic meningitis?

A
  • Viral
    • Coxsackie group B
    • Echoviruses
    • Herpes
    • Developing world – Mumps, Measles, Varicella zoster, EBV
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101
Q

What are the features of aseptic meningitis?

A
  • Presentation: headache, stiff neck, photophobia
    • Non-specific rash may accompany these symptoms
  • Usually occurs in children <1 year
  • Self-limiting disease that resolves in 1-2 weeks
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102
Q

Define Encephalitis.

A

Inflammation of the brain parenchyma.

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103
Q

What are the routes of transmission for causes of encephalitis?

A
  • Person-to-person
  • Vectors - mosquitoes, lice, ticks)
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104
Q

What are the causes of viral encephalitis?

A
  • Viruses = 80-90%
  • Most common
    • UK = HSV-2
    • Worldwide = Arboviruses but becoming West Nile Virus
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105
Q

What are non-viral causes of encephalitis?

A
  • Bacterial
    • Listeria monocytogenes
  • Amoeba
    • Naegleria fowleri
    • Acanthamoeba spp.
    • Balamuthia mandrillaris
  • Toxoplasmosis (obligate intracellular protozoal parasite – Toxoplasma gondii)
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106
Q

What are the features of toxoplasmosis encephalitis?

A
  • Spread via the faeco-oral, transplacental or organ transplant route
  • Causes severe infection in immunocompromised patients
  • Affected organs = grey & white matter of brain, retinas, alveolar lining of lungs, heart, skeletal muscle
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107
Q

What is the pathophysiology of brain abscesses?

A
  • Direct extension (e.g. otitis media, mastoiditis, para-nasal sinuses)
  • Occasionally spread haematogenously (e.g. endocarditis)
  • Cause death due to pressure-related issues
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108
Q

What are the causative organisms for brain abscesses?

A
  • Streptococci (anaerobic and aerobic)
  • Staphylococci
  • Gram-negative organisms (mainly in neonates)
  • TB, fungi, parasites, actinomyces and Nocardia species
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109
Q

What are the risk factors for spinal infections?

A
  • Age
  • IVDU
  • Long-term systemic steroids
  • Diabetes mellitus
  • Organ transplantation
  • Malnutrition
  • Cancer
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110
Q

What are the appropriate investigations for suspected CNS infections?

A
  • MRI > CT
    • In detecting parenchymal abnormalities such as abscesses and infarctions
  • Suspected meningitis
    • Blood culture
    • Throat swab
    • Blood PCR
  • CSF Studies:
    • Colour/clarity
    • Cell counts
    • Chemistry
    • Stains
    • Cultures
    • PCR
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111
Q

What are normal CSF results?

A
  • Clear
  • 0-5 leukocytes
  • 0.15-0.4 g/L of protein
  • 2.2-3.3 mmol/L of glucose - 60% of blood glucose
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112
Q

What are the CSF results for bacterial/purulent meningitis?

A
  • Turbid
  • 100-2000 polymorphs
  • Positive Gram stain/antigen test
  • 0.5-3.0 g/L of protein
  • 0-2.2 mmol/L of glucose
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113
Q

What are the CSF results for aseptic meningitis?

A
  • Clear or slightly turbid
  • 15-500 lymphocytes
  • Negative Gram stain/antigen test
  • 0.5-1.0 g/L of protein
  • 2.2-3.2 mmol/L of glucose - normal
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114
Q

What are the CSF results for Tuberculous meningitis?

A
  • Clear or slightly turbid
  • 30-500 lymphocytes or some polymorphs
  • Negative Gram stain/antigen test - Positive Acid fast bacilli
  • 1.0-6.0 g/L of protein
  • 0.2-2.2 mmol/L of glucose
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115
Q
A

Gram positive cocci

  • S. Pneumoniae
  • Alpha-haemolytic diplococcus
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116
Q
A

Gram negative cocci

  • Diplococcus
  • N meningitidis
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117
Q
A

Gram positive rod

  • L. monocytogenes
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118
Q
A

M. Tuberculosis

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119
Q
  • Hx: MSM, 3/7 history
  • High opening pressure on LP
  • HOP pathogenomic of C. neoformans
  • Occurs in immunocompromised people
A

Cryptococcus neoformans

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120
Q

What are the limitations of the diagnostic techniques used in CNS infections?

A
  • MRI oedema pattern and moderate mass effect cannot be differentiated from tumour or stroke or vasculitis
  • Serology may not be useful in early stages of infection
  • Difficulties obtaining sufficient CSF
  • PCR techniques are expensive
  • Methods to detect amoebic infections
  • Availability of good laboratory technique
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121
Q

What is the management of meningitis?

A
  • Aciclovir - 10mg/kg IV TDS
  • Ceftriaxone - 2g IV BD
    • If 50+ years or immunocompromised add Amoxicillin 2g IV 4 hourly - for L. monocytogene cover
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122
Q

What is the management of meningo-encephalitis?

A
  • Aciclovir - 10mg/kg IV TDS
  • Ceftriaxone - 2g IV BD
    • If 50+ years or immunocompromised add Amoxicillin 2g IV 4 hourly
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123
Q

What are the adjunctive therapies for CNS infections?

A
  • Corticosteroids - don’t give without speaking to a specialist, but it can be useful for cerebral oedema
  • Repeat LP
  • Public health
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124
Q

Define Fungi.

A

Eukaryotic organisms possessing chitinous cell walls, plasma membranes containing ergosterol and 80S RNA

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125
Q

What are the kinds of fungi?

A
  • Yeasts → single celled, reproduce by budding
    • Candida
    • Cryptococcus
    • Histoplasma (dimorphic)
  • Moulds → multicellular hyphae, grow by branching and extension
    • Dermatophytes
    • Aspergillus
    • Agents of mucormycoses
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126
Q

Which is the commonest cause of fungal infection in humans?

  1. Aspergillus spp
  2. Dermatophytes
  3. Candida spp
  4. Cryptococcus spp
  5. Pneumocystis jiroveci
A

Candida spp

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127
Q

You are an FY1 on the MFE ward. The nurse looking after F bay bleeps you

“Doctor, Mr A in F 4 is complaining of a painful mouth and his tongue looks strange..’

A

Oral candidiasis

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128
Q

‘Whilst you’re here doctor, Mrs B has a rash on her groin… Could you look at it please?’

A

Cutaneous candidiasis

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129
Q

What is the management of superfifcial candida infections?

A
  • Topical
    • Oral thrush = Nystati
    • Vulvovaginitis = Co-trimazole
    • Localised cutaneous = Co-trimazole
  • Oral
    • Vulvovaginitis = Fluconazole
    • Oesophagitis = Fluconazole
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130
Q
A

1

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131
Q

What are the risk factors for candidaemia?

A
  • Malignancies → esp haematological
  • Burns patients
  • Complicated post-op courses → eg Tx or GIT Sx
  • Long line
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132
Q

What are the appropriate investigations for suspected candidaemia?

A
  • Look for source and signs of dissemination
    • Imaging
    • Serology for beta-D-glucan
    • ECHO
    • Fundoscopy
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133
Q

What is the management of candidaemia?

A
  • Antifungals for at least 2/52 (from date of first –ve BC)
    • Echinocandin eg anidulafungin - whilst a/w identification and susceptibilities
  • BC every 48 hours
  • Remove any lines/prosthetic material
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134
Q

What are the causes and management of CNS candida infection?

A

Causes = dissemination, trauma, Sx

Treatment = ambisome/voriconazole

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135
Q

What are the causes and management of endocarditis candida?

A

Causes = abnormal valves/prosthetic valves, long lines, IVDU

Treatment = ambisome/voriconazole

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136
Q

What are the causes and management of urinary tract candida?

A

Causes = ascending vulvovaginits, catheters

Treatment = fluconazole

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137
Q

What are the causes and management of bone and joint candida?

A

Causes = dissemination, trauma

Treatment = ambisome/voriconazle

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138
Q

What are the causes and management of intra-abdominal candida?

A

Causes = peritoneal dialysis, perforation

Treatment =echinocandin/fluconazole

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139
Q

What group of patients get infected by cryptococcus?

A
  • Serotypes A&D = C neoformans = Immunodeficient
  • Serotypes B&C = C gattii = Immunocompetent
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140
Q

Which animal is Cryptococcus associated with?

  1. Bats
  2. Pigeons
  3. Dogs
  4. Rats
  5. Camel
A

Pigeons

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141
Q

What are the risk factors for cryptococcosis?

A
  • Impaired T-cell immunity → e.g patients with HIV, who have reduced CD4 helper T-cell numbers
  • Patients taking T-cell immunosuppressants for solid organ transplant - also have a 6% lifetime risk
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142
Q

You’re the FY1 on the medical take. A patient known to the HIV team and has refused ARVs has presented with fever, headache and confusion. Your SpR has asked you to go and review the patient and clerk them in.

Below is their MRI. What is the diagnosis?

A

Multiple cryptococcomas in the brain

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143
Q

What type of ink is used for a cryptococcal stain?

  1. India
  2. Congo
  3. Sudan
  4. Tibet
  5. Laos
A

India

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144
Q

What are the appropriate investigations for suspected cryptococcomas in the brain?

A
  • Typical clinical history/features - immunosuppressed host etc
  • Imaging
  • India ink staining of CSF
  • Serum/CSF cryptococcal Ag (CRAG)
  • Culture from blood/body fluids
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145
Q

What is the management of cryptococcomas in the brain/invasive cryptococcus?

A
  • Induction = Amphotericin B + Flucytosine (at least 2/52)
  • Consolidation = High dose fluconazole (at least 8/52)
  • Maintenance = Low dose fluconazole (at least 1 year)
  • Repeat LP for pressure management
  • Pulmonary disease → If mild = Fluconazole alone
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146
Q

What is the spectrum of diseases caused by aspergillus?

A
  • Mycotoxicosis → ingestion of contaminated foods
  • Allergy and sequelae → presence of conidia/transient growth of the organism in body orifices
  • Colonization → in preformed cavities and debilitated tissues
  • Invasive → invasive, inflammatory, granulomatous, necrotizing disease of lungs, and other organs
  • Systemic and fatal disseminated disease
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147
Q

You are the FY1 on a respiratory ward. Your consultant has referred a patient from clinic who is experiencing heamoptysis and weight loss. PMHx includes treated pulmonary TB. With the CXR what investigations should be ordered and what is the likely diagnosis?

A
  • Investigations
    • Imaging
    • Sputum/BAL – MC&S, Ag testing
    • Aspergillus Abs (precipitans)
    • Galactomannan
  • Diagnosis = Aspergillus granuloma in the right upper lobe
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148
Q

What is the management of invasive asperillosis?

A
  • Voriconazole
  • Ambisome
  • Duration based on host/radiological/mycological factors → at least 6/52
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149
Q

What is unique about pneumocystis jiroveci?

A

Lacks ergosterol in it’s cell wall

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150
Q

What infection does pneumocystis jiroveci cause?

A

Pneumonia (PCP) → extrapulmonary disease is very rare

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151
Q

What are the risk factors for pneumocystis jiroveci/PCP?

A
  • Immunodeficiency
  • Immunosuppressive drugs
  • Debilitated infants
  • Severe protein malnutrition
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152
Q

You are the FY1 on the renal team. You have been asked to go and review a patient in the renal assessment unit who has a cough and SOB. The nurse tells you that the patient is desaturating when she walks. The patient is also on high-dose immunosuppressants. What are the appropriate investigations and what is the diagnosis?

A
  • Investigations
    • CXR
    • Microscopy
    • PCR
    • Beta-D-glucan
  • Diagnosis = PCP
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153
Q

What is the management of PCP?

A
  • High dose cotrimoxazole 2-3/52
    • Alternatives: atovaquone, clindamycin + primaquine
  • Steroids if hypoxia present
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154
Q

Why might antifungals targeting the cell membrane not work in PCP?

  1. It lacks ergosterol in it’s cell wall
  2. It’s a prtozoa
  3. It lacks β-D-glucan
  4. They interact with ARVs
  5. Antifungals targeting the cell membrane to not penetrate the chest
A

It lacks ergosterol in it’s cell wall

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155
Q

What is mucormycosis?

A
  • Clinical syndrome caused by a number of fungal species belonging to the order
    • Mucorales eg Rhizopus, Rhizomucor, Mucor
  • Inoculation via inhalation of spores or primary cutaneous inoculation
  • Risk factors = immunosuppressed/diabetic patients
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156
Q

What are the clinical features of mucormycosis?

A
  • Rhinocerebral → CNS
    • Cellulitis of the orbit and face with discharge of black pus from the palate and nose
    • Retro-orbital extension produces proptosis, chemosis, ophthalmoplegias and blindness
    • As the brain is involved, there are decreasing levels of consciousness
  • Pulmonary
  • Cutaneous
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157
Q

What is the management of mucomycosis?

A
  • Ambisome/Posaconazole
  • Symptom control
  • Rx guided by response
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158
Q

What are dermatophytes?

A
  • A group of fungi capable of invading dead keratin of skin, hair and nails
  • Classified by site infected e.g tinea capitis
  • Spread via contact with desquamated skin scales
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159
Q

What are the risk factors for dermatophyte infection?

A
  • Moisture
  • Deficiencies in cell mediated immunity
  • Genetic predisposition
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160
Q
A
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161
Q

What are the appropriate investigations for suspected dermatophyte infection?

A

Skin scrapings, nail specimens and plucked hairs → MC&S

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162
Q

What is the management of dermatophyte infection?

A
  • Topical - eg clotrimazole, ketoconazole
  • Oral - eg griseofulvin, terbinafine, itraconazole
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163
Q
A
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164
Q

What are the targets for antifungal therapy?

A
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165
Q

What antifungals target the cell membrane?

A
  • Azoles
    • Ketoconazole
    • Itraconazole
    • Fluconazole
    • Voriconazole
    • Miconazole
    • Clotrimazole (and other topicals)
  • Polyene antibiotics
    • Amphotericin B
    • Nystatin (topical)
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166
Q

What is the mechanism of action of azoles?

A
  • Azoles bind to lanosterol 14a-demethylase inhibiting the production of ergosterol
    • Some cross-reactivity is seen with mammalian cytochrome p450 enzymes
      • Drug Interactions
      • Impairment of steroidogenesis (ketoconazole, itraconazole)
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167
Q

What is the mechanism of action of polyene antibiotics?

A
  • Binds sterols in fungal cell membrane
  • Creates transmembrane channel and electrolyte leakage
  • Active against most fungi → EXCEPT Aspergillus terreus, Scedosporium spp
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168
Q

What antifungals target the cell wall?

A
  • Echinocandins
    • Caspofungin acetate (Cancidas)
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169
Q

What is the mechanism of action of echinocandins?

A
  • Cyclic lipopeptide antibiotics that interfere with fungal cell wall synthesis by inhibition of ß-(1,3) D-glucan synthase
  • Loss of cell wall glucan results in osmotic fragility
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170
Q

What antifungals target the fungal DNA/RNA synthesis?

A
  • Pyrimidine analogues
    • Flucytosine
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171
Q

How has flucytosine resistance developed and what is the mechanism of resistance?

A
  • Acquired Resistance
    • Result of monotherapy
    • Rapid onset
  • Mechanism
    • Decreased uptake (permease activity)
    • Altered 5-FC metabolism
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172
Q

Define R0.

A

Number of people that one sick person will infect on average → i.e. the basic reproductive rate

  • Must be in a totally susceptible population
  • If the R0 is reduced to <1 transmission of disease is halted; whereas if >1 tramission is accelerating
    • Measles R0 = 18
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173
Q

Define Herd Immunity.

A

Herd Immunity = a form of immunity that occurs when vaccination of a significant proportion of the population provides a measure of protection for individuals that are not immune

  • HIT = Herd Immunity Threshold
    • 𝐻𝑒𝑟𝑑 𝐼𝑚𝑚𝑢𝑛𝑖𝑡𝑦 𝑇ℎ𝑟𝑒𝑠ℎ𝑜𝑙𝑑 = 1 − 1/𝑅0
      • % of fully immune people required to stop the spread
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174
Q

What type of vaccines are there?

A
  • Inactivated → whole micro-organisms destroyed by heat/chemicals/radiation/antibiotics
  • Live Attenuated → modified live organism that is less virulent
  • Viral Vectored → modified virus to deliver genetic code for an antigen
  • Nucleic Acid vaccines → DNA/RNA from pathogen in lipid capsule
  • Toxoid → inactivated toxin
  • Subunit → protein components of the micro-organism
  • Conjugate → poorly immunogenic antigens are paired with a protein that is highly immunogenic
  • Heterotypic → pathogens that infect other animals but don’t cause severe disease in humans
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175
Q

Name some inactivated vaccines?

A
  • Influenza
  • Polio (IPV = inactivated)
  • Cholera
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176
Q

Name some live attenuated vaccines?

A
  • MMR
  • Yellow fever
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177
Q

Name some viral vectored vaccines?

A
  • Ebola
  • Janzzen and AZ Covid-19
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178
Q

Name some nucleic acid vaccines?

A
  • Pfizer and Moderna Covid-19
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179
Q

Name some toxoid vaccines?

A
  • Diphtheria
  • Tetanus
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180
Q

Name some subunit vaccines?

A
  • HBV
  • HPV
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181
Q

Name some conjugate vaccines?

A
  • NHS bacteria vaccines
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182
Q

Name some heterotypic vaccines?

A
  • BCG - uses bovine strain
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183
Q

What are the differences between monovalent and multivalent vaccines?

A
  • Monovalent = targeting one strain
  • Multivalent = targets several strains
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184
Q

What are the common components of vaccines

A
  • Active Component
  • Stabilisers - substances added to keep it chemically stable for transport from the site of production to the site of use
  • Adjuvants - AL(OH)3 is a commonly used adjuvant
  • Preservatives
  • Antibiotics - used to prevent contamination
  • Trace components - left over from vaccine manufacture
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185
Q

What are the determinants of primary vaccine antibody response?

A
  • Vaccine type (i.e. live attenuated > inactivated)
  • Antigen nature
  • Vaccine schedule
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186
Q

What determines duration of protection post-immunisation?

A
  • Vaccine type (live = longer lasting)
  • Vaccination schedule
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187
Q

What are the contraindications for a vaccine?

A
  • Confirmed anaphylaxis reaction to previous dose or component of vaccine
  • Live vaccines
    • Immunocompromising treatment or condition
    • Pregnancy
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188
Q

What are the precautions for a vaccine?

A
  • Acutely unwell
  • Pregnancy
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189
Q

What must be considered for vaccination programmes?

A
  • Administered before peak-age-incidence of the disease
  • Targeted to high risk groups or widely disseminated to everyone
  • Effective R0 needs to be <1
  • Catch up campaigns to pick up anyone that missed vaccinations should be considered
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190
Q

What are the factors for successful disease eradication?

A
  • No animal reservoir
  • Antigenically stable pathogen with only one/few strains
  • No latent reservoir of infection and no integration of pathogen genetic material into the host genome
  • Vaccine must induce a lasting immune response
  • High coverage required for very contagious pathogens
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191
Q

Describe the microbiology of mycobacterium.

A
  • Non-motile rod-shaped bacteria
  • Relatively slow-growing compared to other bacteria
  • Long-chain fatty (mycolic) acid, complex waxes and glycolipids in cells
  • Acid alcohol fast
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192
Q

Who level of disease is caused by mycobacterium avium complex?

A
  • Immunocompetent
    • May invade bronchial tree
    • Pre-existing bronchiectasis or cavities
  • Immunosuppressed
    • Disseminated infection
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193
Q

What is associated with mycobacterium chimera?

A

Cardiothoracic procedures

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194
Q

What are caused by M. ulcerans?

A
  • Skin lesions → e.g. Bairnsdale ulcer, Buruli ulcer
  • Chronic progressive painless ulcer
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195
Q

How can TB be prevented?

A
  • Detection and contact tracing
  • PPE
  • Negative pressure isolation
  • Vaccination
  • Address risk factors
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196
Q

What are the risk factors for TB re-activation?

A
  • Immunosuppression
  • Chronic alcohol excess
  • Malnutrition
  • Ageing
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197
Q

What are the presentation of TB?

A
  • Pulmonary
    • Lung parenchyma
    • Mediastinal LNs
  • Lymphadenitis
    • Cervical LNs most commonly
    • Abscesses and sinuses
  • Gastrointestinal
    • If TB is ingested
  • Peritoneal
  • Genitourinary
    • Slow progression of renal disease
  • Bone and Joints
    • Most commonly spinal - Pott’s disease
  • Miliary TB
    • Millet seeds on CXR
  • Tuberculous Meningitis or Tuberculoma
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198
Q

What are the risk factors for TB?

A
  • South Asian/Sub-saharan African Origin
  • HIV/Immunocompromised
  • Homeless
  • Drug User
  • Close Contact
  • Young Adults
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199
Q

What are the signs and symptoms of TB?

A
  • Fever
  • Weight loss
  • Night sweats
  • Cough
  • Haemoptysis
  • Malaise
  • Anorexia
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200
Q

What are the appropriate investigations for suspected TB?

A
  • CXR
  • Sputum
    • Stain for AAFBs
    • Culture
    • NAAT
    • Histology
  • Bronchoscopy
  • Biopsies
  • EMU
  • Tuberculin skin test
  • IGRAs
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201
Q

What is the management of TB?

A
  • Antibiotics
    • Rifampicin - 4 months
    • Isoniazid - 4 months
    • Pyrazinamide - 2 months
    • Ethambutol - 2 months
  • Vitamin D
  • Nutrition
  • Surgery if unresponsive
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202
Q

How does the management change for multi-drug resistant TB?

A
  • MDR = resistant to rifampicin and isoiazid
  • XDR = also fluoroquinolones
  • 4/5 drug regimen for a longer duration
    • Quinolones
    • Aminoglycosides
    • PAS
    • Cycloserine
    • Ethionamide
203
Q

What are the major causative pathogens for surgical site infections?

A
  • Staphylococcus aureus (MSSA and MRSA)
  • Escherichia coli
  • Pseudomonas aeruginosa
204
Q

What are the 3 levels of surgical site infection?

A
  • Superficial Incisional - skin and subcutaneous tissues
  • Deep Incisional - fascial and muscle layers
  • Organ/Space Infection - any part of the anatomy other than the incision
205
Q

What are the risk factors/considerations for pre-operative surgical site infections?

A
  • Consider age (an independent risk factor)
    • Direct linear trend of increasing risk until 65 years
  • Treat all remote infection (e.g. pneumonia, UTI)
  • Underlying illness risk factor:
    • ASA score >3
    • Diabetes (2-3x increased risk à control blood glucose, HbA1c <7)
    • Malnutrition
    • Low serum albumin
    • Radiotherapy and steroids
    • Rheumatoid arthritis (stoop DMARDs before operation)
    • Obesity (adipose poorly vascularised à poor access for immune system à risk of SSIs)
    • Smoking (nicotine delays)
  • Pre-operative Showering
  • Hair removal
    • Shaving increases risk of SSI (micro-abrasions from shaving can multiply bacteria) → electric clipper should be used instead on the day of surgery with a single-use head
  • Nasal Decontamination
  • Antibiotic Prophylaxis
    • Administer at time of induction of anaesthesia
206
Q

How can surgical site infection risk be reduced intra-op?

A
  • Limit number of people in theatre
  • Ventilation of theatre (positive pressure)
    • Laminar flow for orthopaedics
  • Sterilisation of Surgical Instruments
  • Skin Preparation
    • Povidine-iodine
    • Chlorhexidine (in 70% alcohol)
  • Surgical Technique
    • Remove all dead tissue
    • IV devices should follow aseptic procedures
  • Normothermia (if <36C, consider warming)
  • Oxygenation (SpO2>95%)
207
Q

What are the risk factors for septic arthritis?

A
  • Rheumatoid arthritis
  • Osteoarthritis
  • Crystal arthritis
  • Joint prosthesis
  • IVDU
  • Trauma - intra-articular injection, penetrating injury
  • Immunosuppression - e.g. steroids, diabetes, CKD, chronic liver disease etc
208
Q

What is the pathophysiology of septic arthritis?

A
  • Organisms adhere to synovium
  • Bacterial proliferation in synovial fluid → host inflammatory response → joint damage
  • Joint damage → exposure of host derived protein (e.g. fibronectin) to which bacteria can adhere
209
Q

What are the causative organisms of septic arthritis?

A
  • Staphylococcus aureus = 46%
  • Streptococci = 22%
    • Streptococcus pyogenes
    • Streptococcus pneumoniae
    • Streptococcus agalactiae
  • Gram-negative organisms = 28%
    • Escherichia coli
    • Haemophilus influenzae
    • Neisseria gonorrhoea
    • Salmonella
  • Coagulase-negative staphylococci = 4%
  • Lyme disease, Brucellosis, Mycobacteria, Fungi = Rare
210
Q

What are the signs and symptoms of septic arthritis?

A
  • 1-2-week history of:
    • Red
    • Painful
    • Swollen joint with restricted movement
  • Monoarticular in 90%
  • Knee is involved in 50%
211
Q

What are the appropriate investigations for suspected septic arthritis?

A
  • Blood cultures (before ABx)
  • Synovial fluid aspiration MC&S
    • Synovial count >50,000 WBC/mL = suggestive of septic arthritis
  • ESR and CRP
  • CT – check for erosive bone change, periarticular soft tissue extension
  • MRI – joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis
212
Q

What is the management of septic arthritis?

A
  • ABx
    • IV cephalosporin or flucloxacillin
    • Narrow once bacteria is known
    • 4-6 weeks (outpatient setting)
  • Drainage of the joint
213
Q

What are the causes of vertebral osteomyelitis?

A
  • Acute haematogenous spread (bacteraemia)
  • Exogenous (after disc surgery, implant associated)
214
Q

What are the causative organisms of vertebral osteomyelitis?

A
  • Staphylococcus aureus (48.3%)
  • Coagulase-negative staphylococcus
  • Gram-negative rods
  • Streptococcus
215
Q

What are the signs and symptoms of vertebral osteomyelitis?

A
  • Back pain
    • Lumbar
    • Cervical
    • Cervico-thoracic
  • Fever
  • Neurological impairment
216
Q

What are the appropriate investigations for suspected vertebral osteomyelitis?

A
  • MRI (90% sensitive)
  • Blood cultures
  • CT-guided/open biopsy
217
Q

What is the management of vertebral osteomyelitis?

A

ABx for 6 weeks

218
Q

What are the signs and symptoms of chronic osteomyelitits?

A
  • Pain
  • Brodies abscess
  • Sinus tract issues
219
Q

What are the appropriate investigations for suspected chronic osteomyelitis?

A
  • XR (often first line to screen; early changes take 10 days)
  • MRI (much more sensitive for changes)
  • Bone biopsy (culture and histology)
220
Q

What is the management of chronic osteomyelitis?

A
  • Radical debridement to living bone:
    • Modified Lautenbach technique
      • Every week 1L of Hartmann’s solution is infused through each drain and fluid is sent for culture
  • Oral ABx (up to 6 weeks after discharge)
  • Papineau Technique
    • Success rate of 89-93%
221
Q

What are the signs and symptoms of prosthetic joint infection?

A
  • Pain
  • Patient complain joint was ‘never right’ after the operation → early failure
  • Sinus tract issues
222
Q

What are the causative organisms of prosthetic joint infections?

A
  • Gram-positive cocci:
    • Coagulase-negative staphylococci > S. aureus
    • Streptococci
    • Enterococci
  • Aerobic Gram-negative bacilli:
    • Enterobacteriaceae
    • Pseudomonas aeruginosa
  • Anaerobes
  • Polymicrobials
  • Culture-negative
  • Fungi
223
Q

What are the appropriate investigations for suspected prosthetic joint infection?

A
  • Radiology – loosening (bone loss along the cement-bone interface)
  • Raised CRP:
    • CRP >13.5 for prosthetic knee joint infection
    • CRP >5 for prosthetic hip joint infection
  • Joint Aspiration:
    • If >1,700 WCC/mL → knee PJI
    • If >4,200 WCC/mL → hip PJI
  • Intraoperative Microbiological Sampling:
    • Tissue specimens taken from at least 5 sites around the implant
    • Histopathology
224
Q

What infections are currently screened for during pregnancy?

A
  • Hep B
  • HIV
  • Syphilis
225
Q

What infections are not screened for during pregnancy but can be tested?

A
  • CMV - most common cause of congenital deafness in the UK
  • Toxoplasmosis
  • Hep C
  • Group B Streptococcus - only if mother has asymptomatic bacteriuria
  • Rubella status
226
Q

What is the lifecycle of Toxoplasmosis?

A
  1. Acute infection will start off in a cat
  2. Faeces containing oocysts
  3. Mice and birds eat the faeces
  4. Cats eat birds and mice
  5. This ends up becoming a cycle
227
Q

What are the consequences of congenital toxoplasmosis?

A
  • May be asymptomatic (60%) at birth but may still go on to have long-term sequelae such as
    • Deafness
    • Low IQ
    • Microcephaly
  • 40% of babies are symptomatic at birth (4 C’s)
    • Choroidoretinitis
    • Microcephaly/hydrocephalus
    • Intracranial calcifications
    • Convulsions/Seizure
    • Hepatosplenomegaly/jaundice
228
Q

What is the mechanism of pathology of congenital rubella syndrome?

A
  • Mechanism
    • Mitotic arrest of cells
    • Angiopathy
    • Growth inhibitor effect
229
Q

What are the signs and symptoms of congenital rubella syndrome?

A
  • Classical Triad
    • Cataracts
    • Congenital heart disease (PDA; ASD/VSD)
    • Deafness/SNHL
  • Other features:
    • Microphthalmia
    • Glaucoma
    • Retinopathy
    • ASD/VSD
    • Microcephaly
    • Meningoencephalopathy
    • Developmental delay
    • Growth retardation
    • Bone disease
    • Hepatosplenomegaly
    • Thrombocytopaenia
    • Rash
230
Q

What are the signs and symptoms of congenital HSV?

A
  • Disseminated infection
  • Liver dysfunction
  • Meningoencephalitis
231
Q

What are the consequences of congenital chlamydia trachomatis?

A
  • Infection transmitted during delivery
  • Mother may be asymptomatic
  • Causes neonatal conjunctivitis or pneumonia (RARE)
232
Q

What is the treatment of congenital chlamydia trachomatis?

A

Erythromycin

233
Q

What are the causes of early onset neonatal infections?

A
  • With 48 hours from birth
  • GBS
  • E. coli
  • Listeria monocytogenes
234
Q

What are the features of GBS?

A
  • Gram +ve coccus → Beta haemolytic
  • Catalase -ve - Lancefield Group B
  • 33% of women have GBS commensal
235
Q

What are the consequences of GBS in the neonate?

A
  • Bacteraemia
  • Meningitis
  • Disseminated infection (i.e. joint infection)
236
Q

What are the features of E. coli?

A
  • Gram -ve rod
    • K1 antigen is particularly problematic
237
Q

What are the consequences of E. coli in the neonate?

A
  • Bacteraemia
  • Meningitis
  • UTI
238
Q

What are the features of Listeria monocytogenes?

A

Gram +ve rod

239
Q

What are the consequences of Listeria monocytogenes?

A

Sepsis - also in the mother

240
Q

What are the risk factors for early-onset sepsis in a neonate?

A
  • Baby
    • Birth asphyxia
    • Resp. distress
    • Low BP
    • Foetal distress
    • Acidosis
    • Meconium staining
    • Hypoglycaemia
    • Neutropenia
    • Rash
    • Hepatosplenomegaly
    • Jaundice
  • Mother
    • PROM/PPROM
    • Fever
    • Previous history GBS
241
Q

What are the appropriate investigations for suspected early onset neonatal sepsis investigations?

A
  • FBC
  • CRP
  • Blood culture
  • Deep ear swab
  • LP
  • Surface swabs
  • CXR (full body)
242
Q

What is the treatment of early onset neonatal sepsis?

A
  • Supportive
    • Ventilation
    • Circulation
    • Nutrition
  • Antibiotics - e.g. benzylpenicillin & gentamicin → used in combination because…
    • GBS is treated by benzylpenicillin
    • E. coli is treated by gentamicin
    • Amoxicillin added if there is meningitis
243
Q

What are the causes of late onset neonatal sepsis?

A
  • 48-72hrs after birth
  • Coagulase-negative Staphylococci
  • GBS
  • E. coli
  • Listeria monocytogenes
  • Staphylococcus aureus
  • Enterococcus sp.
  • Candida species
  • Gram-negatives
    • Klebsiella
    • Enterobacter
    • Pseudomonas aeruginosa
    • Citrobacter koseri
244
Q

What are the signs and symptoms of late onset neonatal sepsis?

A
  • Bradycardia
  • Apnoea
  • Poor feeding/abdominal distension
  • Irritability
  • Convulsions
  • Jaundice
  • Respiratory distress
  • Increased CRP
  • Sudden changes in WCC & platelets
  • Focal inflammation (e.g. umbilicus/drip sites)
245
Q

What are the appropriate investigations for suspected late onset neonatal sepsis?

A
  • FBC
  • CRP
  • Blood cultures
  • Urine analysis
  • ET secretions if ventilated
  • Swabs from any infected site
  • LP
246
Q

What is the management of late onset neonatal sepsis?

A
  • Treat early → low threshold for starting therapy
    • Review and stop antibiotics if cultures are negative and clinically stable
  • Antibiotics
    • 1st line = cefotaxime + vancomycin
    • 2nd line = meropenem
    • Community-acquired = cefotaxime, amoxicillin ± gentamicin
247
Q

What is the most common cause of paediatric morbidity and mortality?

A

Meningitis

248
Q

What are the appropriate investigations for suspected childhood meningitis?

A
  • Clinical features
  • Blood cultures
  • Throat swab
  • LP if possible (may be dangerous)
  • Rapid antigen test
  • EDTA blood for PCR
  • Clotted serum for serology
249
Q

What are the LP pressures for normal, bacterial and viral meningitis?

A
  • Normal = 5-20 cmH2O
  • Bacterial = >30 cm H2O
  • Viral = Normal or mildly increased
250
Q

What is the CSF appearance for normal, bacterial, viral and fungal/TB meningitis?

A
  • Normal = Normal
  • Bacterial = Turbid
  • Viral = Clear
  • Fungal/TB = Fibrin web
251
Q

What is the CSF appearance for normal, bacterial, viral and fungal/TB meningitis?

A
  • Normal = Normal
  • Bacterial = Turbid
  • Viral = Clear
  • Fungal/TB = Fibrin web
252
Q

What is the CSF protein (g/L) for normal, bacterial, viral and fungal/TB meningitis?

A
  • Normal = Normal
  • Bacterial = Turbid
  • Viral = Clear
  • Fungal/TB = Fibrin web
253
Q

What is the CSF glucose (mmol/L) for normal, bacterial, viral and fungal/TB meningitis?

A
  • Normal = 2.5-3.5
  • Bacterial = <2.2
  • Viral = 2.5-3.5
  • Fungal/TB = 1.6-2.5
254
Q

What is the CSF WCC for normal, bacterial, viral and fungal/TB meningitis?

A
  • Normal = <3
  • Bacterial = >500
  • Viral = <1000
  • Fungal/TB = 100-500
255
Q

Describe streptococcus pneumoniae.

A
  • Gram-positive diplococcus, Alpha-haemolytic, Optochin-sensitive
  • 90 capsular serotypes
  • Increasing penicilin resistance
  • Can lead to:
    • Meningitis
    • Bacteraemia
    • Pneumonia
256
Q

Describe the pneumococcal conjugate vaccine.

A
  • Previously there was a polysaccharide vaccine with 23 capsular types of pneumococcus
  • Children <2 showed a poor response to this vaccine à antibody response was improved by conjugating the polysaccharide with proteins such as CRM
    • The conjugate vaccine is immunogenic in children from 2 months
    • This conjugate vaccine was called Prevenar 7 which targeted 7 serotypes
    • These serotypes were almost eradicated à however, we are still seeing a lot of cases of invasive pneumococcal disease (may be due to serotype replacement)
      • This could lead to a change in phenotype
        • More serotypes were added to create Prevenar 13
257
Q

What are the common causes of meningitis <3 months?

A
  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • GBS
  • E. coli
  • Listeria monocytogenes
258
Q

What are the common causes of meningitis from 3 months to 5 year olds?

A
  • Neisseria meningitis
  • Streptococcus pneumoniae
  • Haemophilus influenzae
259
Q

What are the common causes of meningitis from 6+ year olds?

A
  • Neisseria meningitis
  • Streptococcus pneumoniae
260
Q

Describe haemophilus influenzae.

A
  • Gram-negative rod
  • Grows glossy colonies on blood agar
261
Q

What are the most common causes of death in children <5 years old?

A
  • Neonatal (0-27 days)
    • Prematurity
    • Intrapartum-related complications
  • Post-neonatal (1-59 months)
    • Pneumonia
    • Congenital anomalies
262
Q

What is the most important bacterial cause of respiratory tract infections?

A

Sensitive to amoxicillin or penicillin

263
Q

What are the features of mycoplasma pneumoniae?

A
  • Tends to affect older children (> 4 years)
  • Person-to-person droplet transmission
  • Incubation period 2-3 weeks
  • Epidemics evert 3-4 years
  • Occurs in school children / young adults
  • Mainly asymptomatic
264
Q

What are the signs and symptoms of mycoplasma pneumoniae?

A
  • Fever
  • Headache
  • Myalgia
  • Pharyngitis
  • Dry cough
  • Extrapulmonary Manifestations
    • Haemolysis
    • Neurological
      • Encephalitis
      • Aseptic meningitis
      • Peripheral neuropathy
      • Transverse myelitis
      • Cerebellar ataxia
    • Cardiac
    • Joints
      • Polyarthralgia
      • Myalgia
      • Arthritis
    • Otitis media
    • Bullous myringitis
265
Q

What is the treatment of mycoplasma pneumoniae respiratory tract infections?

A

Macrolide - Azithromycin

266
Q

What should be considered if a childhood respiratory tract infection that fails to respond to antibiotics?

A
  • Whooping cough - Bordatella pertussis
  • TB
267
Q

What are the common causes of childhood UTI’s?

A
  • Escherichia coli– MAIN ORGANISM
  • Other coliforms - Proteus, Klebsiella, Enterococcus sp.
  • Coagulase-negative Staphylococcus - Staphylococcus saprophyticus
268
Q

What is important for childhood UTI?

A
  • Early diagnosis and antibiotic treatment is important
  • Obtain sample before starting treatment
  • Renal tract imaging may be required to check for congenital anomalies
  • Antibiotic prophylaxis may be given after treatment of the infection
269
Q

If a child gets recurrent or persistent infections what should be considered?

A
  • May be a feature of immunodeficiency – either congenital (e.g. SCID) or acquired (e.g. HIV)
  • Warrants investigation by paediatric infectious diseases specialist
270
Q

What does squamous epithelial cells in a MSU mean?

A

The sample has not been taken properly

271
Q

Define Bacteriuria.

A

Presence of bacteria in the urine.

272
Q

What is the significance of bacteriuria?

A
  • Asymptomatic bacteriuria is not usually relevant
  • However, asymptomatic bacteriuria with coliform is significant in pregnancy
273
Q

Define Cystitis.

A

Inflammation of the bladder, often caused by infection.

274
Q

What is the difference between uncomplicated and complicated cystitis?

A
  • Uncomplicated = infection is in a structurally and neurologically normal urinary tract
  • Complicated = infection with functional or structural abnormalities (including indwelling catheters and calculi)
275
Q

In what patients is cystitis regarded as a complicated UTI?

A
  • Men
  • Pregnant women
  • Children (not young girls)
  • Patients in a healthcare or HC-associated settings
276
Q

What organism cause UTI’s?

A
  • Escherichia coli - most common
    • O1, O2, O4, O6, O7, O8, O75, O150, O18ab - have adherence factors preventing them being flushed out by the passage of urine
  • Proteus mirabilis – associated with kidney stones
  • Klebsiella aerogenes – associated with catheters
  • Enterococcus faecalis – associated with catheters
  • Staphylococcus saprophyticus
    • 2nd most common cause of UTI in younger women
    • P-fimbriae allows adherence to the epithelium
  • Staph epidermidis - UTI in the presence of prosthesis
277
Q

Define Recurrent UTI.

A

Relative frequency of infection caused by non-E. coli organisms increases greatly.

  • Especially in presence of structural abnormalities
278
Q

What are the host defences of the urinary tract from bacterial infection?

A
  • Urine
    • Osmolality
    • pH
    • Organic acids
  • Urine flow and micturition
  • Urinary tract mucosa
    • Bactericidal activity
    • Cytokines
279
Q

What is an ascending UTI?

A
  • Urethra is normally colonised by bacteria
  • Female urethra is short and in proximity to the vulvar and perianal areas, making contamination likely
  • Massage of the urethra and sexual intercourse can force bacterial into the female bladder
  • Once in the bladder, bacteria multiply and pass up the ureters to the renal pelvis and parenchyma → pyelonephritis
280
Q

What are the causes of obstruction to the urinary tract?

A
  • Mechanical
  • Extrarenal
    • Valves, stenosis or bands
    • Calculi
    • BPH
  • Intrarenal
    • Nephrocalcinosis
    • Uric acid nephropathy
    • Analgesic nephropathy
    • PKD
    • Hypokalaemic nephropathy
    • Renal lesions of SCD
  • Neurogenic malfunction
    • Poliomyelitis
    • Tabes dorsalis
    • Diabetic neuropathy
    • Spinal cord injuries
281
Q

What is Vesicoureteric reflux (VUR)?

A
  • Perpetuate infection by maintaining a residual pool of infected urine in the bladder after voiding
  • The reflux can result in scarring of the kidneys
282
Q

What is the haematogenous route of infection of the urinary tract?

A
  • Kidney infection/abscess in patients with S. aureus bacteraemia or endocarditis
    • S. aureus doesn’t have appropriate virulence factors to cause ascending infection
    • Infection of the kidney with Gram-negative bacilli rarely occurs by the haematogenous route → more likely to be from a bacteraemia
283
Q

What are the symptoms of an UTI in a child <2 years old?

A
  • Symptoms are non-specific
    • Failure to thrive
    • Vomiting
    • Fever
284
Q

What are the symptoms of an UTI in a child >2 years old?

A
  • Localised symptoms
    • Frequency
    • Dysuria
    • Abdominal or flank pain
285
Q

What are the symptoms of a lower UTI?

A
  • Bacteria → irritation of urethral & vesical mucosa → frequent/painful urination of small amounts of turbid urine
    • Suprapubic heaviness or pain
    • Gross haematuria
    • No fever - if infections confined to lower UT
286
Q

What are the symptoms of an upper UTI?

A
  • Lower UT symptoms = frequency, urgency, nocturia, dysuria / FUND HIPS
    • May precede UUTS by 1-2 days
    • Symptoms may vary greatly
    • Fever - sometimes with rigors
    • Flank pain
287
Q

What are the symptoms of an UTI in older patients?

A
  • Vast majority will be ASYMPTOMATIC
  • Diagnosis difficult as non-infected older patients often experience frequency, dysuria, hesitancy & incontinence
  • Symptoms of upper urinary tract infections are often atypical - abdominal pain, confusion etc
288
Q

What are the appropriate investigations for a suspected UTI?

A
  • Urine dipstick
  • MSU for urine MC&S
  • Bloods – FBC, U&E, CRP
  • For complicated UTI
    • Renal USS
    • IV urography
289
Q

What is the outcome for the following investigation results?

290
Q

In what patient groups should laboratory testing for MC&S be done?

A
  • Pregnancy - asymptomatic bacteriuria is an issue
  • Suspected UTI in children
  • Suspected UTI in men
  • Suspected pyelonephritis
  • Catheterised patients
  • Failed antibiotic treatment / Resistance
  • Abnormalities of the genitourinary tract
  • Renal impairment
291
Q

What are the results of urine culture for:

  • Culture of single organisms >105 CFUs/mL + urinary symptoms
  • Culture of E. coli or S. saprophyticus >103 CFUs/mL + urinary symptoms
A

Diagnostic of UTI

  • If symptomatic can treat below these thresholds
292
Q

What is the definition of pyuria?

A
  • White cells >104/mL (or 107/L) = Inflammation
  • Pyuria is usually absent in children
293
Q

What shows that a MSU is contaminated?

A
  • Mixed growth reduces the significance of culture
  • Epithelial cells present in high numbers - poor technique
294
Q

What are the differential diagnoses for sterile pyuria?

A

Raised WCC but no growth on culture:

  • Prior treatment with antibiotics = most common
  • Calculi
  • Catheterisation
  • Bladder neoplasm
  • TB
  • STI - Chlamydia trachomatis is the most common
295
Q

What are the appropriate investigations for suspected UTI?

A
  • Microscopy
  • Culture
    • Pink → E. coli
    • Blue → other coliforms
    • Light blue → gram +ve
  • Sensitivities
296
Q

What is the management of UTI?

A
  • Send an MSU before starting Abx
  • Empirical therapy – based on the presence of classical symptoms of UTI - COMPLICATED
    • Guided by local policies - normally Trimethoprim, Nitrofurantoin or Cephalexin
  • 3 days of standard dose - UNCOMPLICATED
297
Q

In what situations do fungal UTIs occur?

A
  • Most Candida UTIs occur in patients with indwelling catheters
    • Most cases of candiduria die to vaginal thrush rather than infection of urinary tract
298
Q

What is the management of fungal UTIs?

A
  • Removal of the catheter → antifungals no more effective than no therapy
  • No benefit in treating asymptomatic infection - except:
    • Renal transplant patients
    • Patients who are waiting to undergo elective urinary tract surgery
299
Q

How many organisms are required to infect the kidneys?

A
  • Renal medulla = Few organisms
  • Cortex = Many organisms
300
Q

What is the management of pyelonephritis?

A
  • Requires aggressive treatment):
    • Prior to culture results = amoxicillin or ciprofloxacin
    • Culture results = co-amoxiclav ± gentamicin (broad spectrums)
301
Q

What are the complications of pyelonephritis?

A
  • Perinephric abscess
  • Chronic pyelonephritis → scarring, chronic renal impairment
  • Septic shock
  • Acute papillary necrosis
302
Q

What is the classification of immunocompromise?

A
  • Primary:
    • SCID
    • UNC93B deficiency and TLR3 deficiency → herpes simplex encephalitis
    • EVER1 or EVER2 → HPV → Epidermodysplasia verruciformis
    • Perforin deficiency → EBV → Haemophagocytic lymphohistiocytosis
    • STIM1 mutation → HHV8
  • Acquired - more common
    • Solid organ transplantation
    • Bone marrow transplantation
    • Immunosuppressive drugs
    • Advanced HIV or measles infection
303
Q

What is the hierarchy in the relative risk for opportunistic viral infection in acquired causes?

A
  1. Allogenic stem cell transplant
  2. Advanced HIV / AIDS
  3. Solid organ transplant
  4. Various monoclonal antibody therapies
  5. Cytotoxic chemo
  6. DMARDS and Steroids
304
Q

At what CD4 count do opportunistic infection begin in HIV?

A

<200 → defined at AIDS

305
Q

Which opportunistic infections are commonly seen in HIV / AIDS (CD4 <200)

A
  • Candidiasis
  • Cryptosporidiosis
  • Histoplasmosis
  • Mycobacterium - avium complex, tuberculosis, etc
306
Q

What immunosuppressants are given to transplant patients?

A
  • Glucocorticoids or steroids
  • Calcineurin inhibitors
    • Cyclosporine
    • Tacrolimus
  • Antiproliferative agents
    • Azathioprine
    • Mycophenolate mofetil
    • Sirolimus
  • Antibodies
    • Depleting
    • Non-depleting (anti-CD25r ABs, costimulation blockers)
307
Q

What is the timeline of virus infections in transplant recipients?

A
  • <1m = Virus acquired from grafts (i.e. HBV) – risk has decreased with donor serostatus and risk assessments
  • 1-12m = Viral reactivation (i.e. HSV) – risk has decreased with serostatus, monitoring, prophylaxis, pre-emptive therapy
  • >12m = Novel infection (i.e. VZV) – risk has decreased with barrier nursing, advice, PEP, vaccinating contacts, diet control
  • Remember: = BM transplantation follows a different path due to intensive immunosuppression:
    • Some viral infections tend to occur EARLY (within 1 month) – HSV, HHv6, HHv7
    • Others occur past 30 days = CMV, EBV and VZV
308
Q

What diagnostic protocol is in place for opportunistic infections in transplant recipients?

A
  • Pre-transplant serology - HIV Ag/Ab, HBV sAg/cTAb, HCV Ab, etc.
  • CMV monitoring or prophylaxis
  • EBV monitoring
  • Adenovirus monitoring (paediatrics)
  • HSV prophylaxis if indicated
  • If someone gets an infection, screening is done for common causes → image
309
Q

What are the symptoms of herpes simplex virus?

A
  • Cold sores
  • Stomatitis
  • Mouth ulcers
  • Recurrent genital disease (HIV and adult transplant)
310
Q

What are the complications of herpes simplex virus?

A
  • Cutaneous dissemination
  • Oesophagitis - most likely occurance after liver transplant → pain on swallowing
  • Hepatitis
  • Viraemia
311
Q

What is the management of herpes simplex virus?

A
  • Aciclovir or Valaciclovir
  • Foscarnet
312
Q

What are the complications of primary VZV infection?

A
  • Pneumonitis
  • Encephalitis
  • Hepatitis
  • Purpura fulminans in the neonate → DIC + coagulation in small vessels → skin necrosis
  • Immunocompromised
    • Acute retinal necrosis
    • Progressive outer retinal necrosis
    • VZV-associated vasculopathy
313
Q

How is Shingles / multi-dermatomal / disseminated zoster prevented in immunocompromised?

A
  • Aciclovir prophylaxis
  • VZV IVIG post-exposure prophylaxis
  • Late manifestation post transplant
  • Early manifestation of HIV
314
Q

What are the manifestations of cytomegalovirus?

A
  • Retinitis
  • Encephalitis
  • Pneumonia
  • Gastroenteritis
315
Q

What is the pathognomonic histological feature of CMV?

A

Owl’s eye lung pneumocytes = Inclusion bodies

316
Q

Which patients within both solid and HSCT transplants are at the greatest risk of CMV reactivation?

A
  • Solid organ transplantation
    • Donor +ve for past CMV
    • Recipient -ve
  • HSCT / BM transplant
    • Donor -ve for past CMV
    • Recipient +ve
  • Develops within 6m of transplantation
317
Q

What prevention strategies aim to prevent CMV reactivation post-transplant?

A
  • Haematological transplant
    • CMV viral load twice weekly → treat only if virus reactivates
  • Solid organ transplant
    • Valganciclovir prophylaxis for 100 days regardless of state
318
Q

What is the management of CMV?

A
  • Solid organ = Ganciclovir (IV) (bone marrow suppression) → never give to post-HSCT patient
  • HSCT = Foscarnet (IV)
  • Valganciclovir
  • Cidofovir
  • IVIG (with another drug for pneumonitis)
319
Q

What is the biggest concern with EBV post-transplantation?

A
  • Post-Transplant Lymphoproliferative Disease (PTLD)
    • Latent infected B cells have polyclonal activation → predispose to lymphoma
    • Suspicion on rising EBV viral load (>105c/mL) and CT scan → confirm on biopsy of LN
320
Q

What is the management of Post-Transplant Lymphoproliferative Disease?

A
  • Reduce immunosuppression
  • Rituximab (anti-CD20 monoclonal ABs) → removes B cells
321
Q

What malignancies are associated with HHV-8?

A
  • Kaposi’s sarcoma
  • Primary effusion lymphoma (PEL)
  • Multicentric Castleman disease
322
Q

Describe Kaposi sarcoma.

A
  • Presents with brownish/purplish vascular lesions that can be cutaneous or visceral
  • Diagnosis from biopsy → characteristic histological findings
    • Spindle cell proliferation
    • Neo-angiogenesis
    • Inflammation and oedema
  • Treatment:
    • Chemotherapy
    • Antiretroviral therapy
323
Q

Name at least 2 polyomaviruses.

A
  • JC virus
  • BK virus (dsDNA)
324
Q

What is JC virus associated with?

A
  • Progressive multifocal leukoencephalopathy
    • Destruction of myelin leading to a dementing process characterised by loss of higher functions
      • Personality change
      • Motor deficits
      • Focal neurological signs
325
Q

What is associated with JC viruses?

A
  • Progressive multifocal leukoencephalopathy:
    • A dementing process characterised by loss of higher functions
      • Personality change
      • Motor deficits
      • Focal neurological signs
326
Q

How is JC virus infection diagnosed?

A
  • MRI and PCR of CSF
    • Demyelination of white matter → corresponds to area of brain affected
327
Q

What increases a person chance of becoming infected with JC virus?

A
  • Immunocompromise
    • Before HAART → PML occurred about 5% of AIDS → high mortality
  • Natalizumab (monoclonal antibody used in MS)
  • Rituximab
  • Mycophenolate mofetil (post solid organ transplant)
328
Q

What is associated with BK virus?

A
  • BK cystitis (post-HSCT)
    • Treatment = intravesical cidofovir (direct into bladder to avoid nephrotoxicity)
  • BK nephropathy (post-renal solid organ transplant)
    • Treatment = IVIG
  • Both also helped by reducing immunosuppression
329
Q

What are the manifestations of adenovirus?

A
  • Fever → septic appearance
    • High mortality in disseminated infection
  • Encephalitis
  • Pneumonitis
  • Colitis
330
Q

In which group of patients is adenovirus most notably an issue and how is it avoided?

A
  • BM transplant / HSCT
    • Regular screening of:
      • Urine
      • Respiratory secretions
      • Blood
      • Stool
331
Q

Which respiratory viruses have an increased risk of complications / pneumonitis in immunocompromised?

A
  • Influenza A and B
    • Treatment = Oseltamivir, OD, 5 days
  • Parainfluenza 1, 2, 3, 4
  • RSV
  • Adenovirus
  • SARS-2 (COVID)
  • MERS coronavirus
  • Diagnosed by taking NPA, BAL, nose and throat swabs
  • Multiplex PCR is the investigation of choice
332
Q

How is human parvovirus B19 diagnosed?

A
  • PCR of blood
  • Serology (IgM) → not useful in the immunocompromised
333
Q

What is the management of human parvovirus B19 diagnosed?

A
  • IVIG
    • May require blood transfusion → B19 causes aplastic / chronic anaemia
334
Q

If a patient is currently positive for HBV, what antibody results would be expected?

A
  • Positive
    • HBV sAG
    • HBV core Ab
  • Negative
    • HBV surface Ab
335
Q

If a patient is currently negative for HBV but has had a previous infection, what antibody results would be expected?

A
  • Positive
    • HBV core Ab
    • HBV surface Ab
  • Negative
    • HBV sAg
336
Q

If a patient has been vaccinated against HBV, what antibody results would be expected?

A
  • Positive
    • HBV surface Ab
  • Negative
    • HBV sAg
    • HBV core Ab
337
Q

What are the consequences of HBV in immunocompromised patients?

A
  • Carriers may have a flare of the disease
  • Reactivation in though with past disease
    • Particularly important in patients on B-cell depleting therapies such as Rituximab
338
Q

How can HBV be prevented (particularly flares or reactivation) in immunocompromised patients?

A
  • Nucleoside/nucleotide analogue prophylaxis - e.g. lamivudine, tenofovir
339
Q

What is the major cause of enterically transmitted viral hepatitis?

340
Q

Which genotypes are the dominant HEV genotypes?

A
  • In developed countries = a zoonosis caused by genotype 3
  • In developing countries = mainly caused by genotype 1
    • Endemic in UK
341
Q

When is HEV pparticularly dangerous?

A

Pregnancy → high mortality rate (20-25%)

342
Q

Define Gastroenteritis.

A

Rapid onset diarrhoeal illness, lasting <2 weeks with diarrhoea (loose or unformed stool) ≥3/day or ≥200g of stool which is due to a pathogen.

343
Q

Define diarrhoea.

A

Loose or watery stool, ≥3 times in 24 hours.

344
Q

In what 2 ways can diarrhoea be categorised?

A
  • Time
    • Acute = <14 days (may be viral or bacterial)
    • Persistent = 14-29 days
    • Chronic = >30 days (may be due to parasites and non-infectious aetiology)
  • Anatomy
    • Small bowel diarrhoea = watery, crampy abdominal pain, bloating and gas; inflammatory cells rare
    • Large bowel diarrhoea = small volume, painful, occur with blood/mucous; inflammatory cells common
345
Q

What are the risk factors for gastroenteritis?

A
  • Food borne
  • Exposure-related
    • Outbreak situation (>2 cases of common food source or exposure)
    • Travel history (exposure to poor settings and water facilities)
    • Occupational exposure / Health-care related exposure (recent ABx = C. diff)
    • Animal contacts → reptiles are importnat to ask about
    • Institution / childcare facility
  • Host-related
    • Young children and elderly
    • Immunosuppressed patients
    • MSM
    • Anal-genital, oral-anal, or digital-anal contact
    • Haemochromatosis or haemoglobinopathy
346
Q

Is bacterial or viral gastroenteritis more common?

A

Viral (i.e. norovirus) >>> bacterial

347
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for S. aureus?

A
  • 1-6 hrs
  • 24-48 hrs
  • Under-refrigerated food - pre-formed toxin
  • Watery diarrhoea with fever
348
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for norovirus?

A
  • 24-48 hrs
  • 48-72 hrs
  • Molluscs / shellfish, leafy veg, fruit (melon / raspberries), seasonal
  • Watery diarrhoea
349
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Clostridium perfingens?

A
  • 8-16 hrs
  • 24-48 hrs
  • Meat, poultry, canned foods
  • Watery diarrhoea with fever
350
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for enteric viruses?

A
  • 10-16 hrs
  • 2-9 days
  • Faecal contaminated food / water
  • Watery diarrhoea
351
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for listeria monocytogenes?

A
  • 24 hrs
  • Variable
  • Processed / delicatessen meat, hot dogs, soft cheese, pates, fruits
  • Watery diarrhoea with fever
352
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for enterotoxigenic E. coli?

A
  • 24-72 hrs
  • 48-72 hrs
  • Faecal contaminated food / water
  • Watery diarrhoea
353
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for salmonella?

A
  • 24-72 hrs
  • 1-7 days
  • Poultry, eggs, meat, fish, unpasteurized milk
  • Inflammatory diarrhoea with fever, mucus or blood stools
354
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Campylobacter?

A
  • 24-72 hrs
  • 5-14 days
  • Poultry, meat, unpasteurized milk
  • Inflammatory diarrhoea with fever, mucus or bloody stools
355
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Shigella?

A
  • 24-72 hrs
  • 48-72 hrs
  • Raw veg, MSM
  • Inflammatory diarrhoea with fever, mucus or bloody stools
356
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Vibrio parahemolyticus?

A
  • 24-72 hrs
  • 72 hrs
  • Raw seafood / shellfish, deep sea diving
  • Inflammatory diarrhoea with fever, mucus or bloody stoolsWatery diarrhoea
357
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Enterohaemorrhagic E. coli?

A
  • 1-8 days
  • 7 days
  • Ground beef / meat, unpasteurized milk
  • Inflammatory diarrhoea with fever, mucus or bloody stools
358
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Yersinia?

A
  • 4-6 days
  • 1-3 weeks
  • Pork, untreated water
  • Inflammatory diarrhoea with fever, mucus or bloody stools
359
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Giardia lamblia?

A
  • 7-14 days
  • Days to weeks
  • Faecal contamination of water / food
  • Watery diarrhoea
360
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Cyclospora cayetanensis?

A
  • 1-11 days
  • Remit and relapse over several weeks
  • Herbs, berries
  • Watery diarrhoea
361
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Cryptosporidium parvum?

A
  • 2-28 days
  • Remit and relapse over weeks
  • Veg, fruit, unpasteurized milk
  • Watery diarrhoea
362
Q

What are the:

  • Incubation period
  • Duration of illness
  • Risk factors
  • Diarrhoea character

for Campylobacter?

A
  • N/A
  • Varies → 10-14 days but can be longer
  • Antibiotics, PPI
  • Inflammatory diarrhoea with fever, mucus or bloody stools
363
Q

What are the mechanisms of diarrhoea?

A
  • Secretory diarrhoea (from toxin production):
    • Cholera toxin → subunit production → cAMP opens Cl- channels at the apical membrane of the enterocytes
    • Superantigens → bind directly to TCRs and MHC molecule → massive cytokine production by CD4 cells
  • Inflammatory diarrhoea
  • Enteric fever – host responses in bacteraemia are:
    • Inflammatory (exudative) diarrhoea
    • Enteric fever = interstitial inflammation
364
Q

What are the clinical features of secretory diarrhoea?

A
  • No / Low grade fever
  • No WC in stool
365
Q

What are the clinical features of inflammatory diarrhoea?

A
  • Fever
  • WC in stool - neutrophils
366
Q

What are the clinical features of enteric fever?

A
  • Fever
  • WC in stool - mononuclear cells
367
Q

What investigations are appropriate for suspected GI infections

A
  • Stools testing – cultures or independent methods (i.e. multiplex molecular PCR)
  • Enteric fever – blood and stool tested by culturing and independent testing methods (BM, duodenal fluid and urine)
  • Parasites – stools for microscopy and culture (inc. ova cysts and parasites)
368
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of aortitis, osteomyelitis, deep tissue infection?

A
  • Salmonella
  • Yersinia
369
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of haemolytic anaemia?

A
  • Campylobacter
  • Yersinia
370
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of glomerulonephritis?

A
  • Shigella
  • Campylobacter
  • Yersinia
371
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of HUS?

A
  • STEC
  • Shigella
372
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of erythema nodosum?

A
  • Yersinia
  • Campylobacter
  • Salmonella
  • Shigella
373
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of reactive arthritis?

A
  • Salmonella
  • Shigella
  • Campylobacter
  • Yersinia
374
Q

What gastroenteritis causing pathogen has the extra-intestinal manifestations of meningitis?

A
  • Listeria
  • Salmonella (<3m)
375
Q

Describe S aureus gastroenteritis?

A
  • Food poisoning – catalase, coagulase +ve, gram +ve coccus
    • 1/3 population chronic carriers, 1/3 transient
    • Spread by skin lesions on food handlers
    • Appears in tetrads, clusters on gram stain à yellow colonies on blood agar
    • Superantigen: produces enterotoxin → release IL1 and IL2 causing prominent vomiting and watery, non-bloody diarrhoea
    • Mx: self-limiting
376
Q

Describe Bacillus cereus gastroenteritis?

A
  • Food poisoning - gram +ve rod-spores
    • Spores germinate in reheated fried rice (heat-stable emetic toxin / not destroyed by reheating)
    • Watery non-bloody diarrhoea; self-limiting
    • Rare cause of bacteraemia in vulnerable population
    • Can cause cerebral abscesses
377
Q

Describe Clostridium botulinum gastroenteritis?

A
  • Botulism - gram +ve anaerobe
    • Source: canned or vacuum-packed food (honey in infants)
    • Ingestion of preformed toxin (inactivated by cooking)
    • Blocks ACh release from peripheral nerve synapses: paralysis
    • Treatment with antitoxin
378
Q

Describe Clostridium pefringens gastroenteritis?

A
  • Food poisoning - gram +ve anaerobe
    • Source: reheated food (meat)
    • Normal flora of colon but not small bowel, where the enterotoxin acts (superantigen)
    • Incubation is 8-16hrs
    • Watery diarrhoea, cramps, vomiting lasting 24hrs
379
Q

Describe Clostridium difficile gastroenteritis?

A
  • Pseudomembranous colitis - gram +ve anaerobe
    • Produces 2 toxins – Toxin A and Toxin B
      • Toxin A = enterotoxin = inflammation
      • Toxin B = cytotoxin = virulence factor (more dangerous than A)
    • 3% of community, 30% of hospitalised patients
    • Antibiotic related colitis - mainly cephalosporins, cipro and clindamycin
    • Infection control – isolate and hand-washing
    • Treatment: PO vancomycin and stop other antibiotics where possible
380
Q

Describe Listeria gastroenteritis?

A
  • Gram +ve, spore forming
    • Bad for pregnant women
    • Outbreaks of febrile gastroenteritis
    • ß-haemolytic, aesculin positive with tumbling-weed motility
    • Source: refrigerated food (“cold-enhancement”), unpasteurized dairy, vegetables (grows at 4ºC)
    • Symptoms: Watery diarrhoea, cramps, headache, fever, little vomiting
    • At risk: perinatal infection, immunocompromised patients, elderly (confused)
    • Treatment: amoxicillin
381
Q

What Enterobacteriaceae cause gastroenteritis?

A
  • E. coli
  • Salmonella
  • Shigella
382
Q

Describe E. coli gastroenteritis?

A
  • Escherichia coli (Traveler’s diarrhoea) - gram -ve rod
    • Source: food/water contaminated with human faeces.
    • Enterotoxins:
      • Heat labile stimulates adenyl cyclase and cAMP
      • Heat stable stimulates guanylate cyclase
      • Act on the jejunum/ileum not on colon
    • Avoid antibiotics
  • ETEC; toxigenic → main cause of traveller’s diarrhoea
  • EPEC; pathogenic → infantile diarrhoea
  • EIEC; invasive → dysentery
  • EHEC; haemorrhagic → O157:H7 EHEC: shiga-like verocytotoxin causes HUS
383
Q

How does salmonella show up on an agar plate?

A

Black colonies in TSI agar → H2S is produced

384
Q

Describe Salmonella enteritidis gastroenteritis.

A
  • Enterocolitis - gram -ve rod
    • Transmitted from poultry, eggs, meat
    • Invasion of epi- and sub-epithelial, tissue of small and large bowel
    • Bacteraemia infrequent, no fever
    • Self-limited non-bloody diarrhoea with abdominal pain (4-7 days), usually no treatment
    • Stool +ve
385
Q

Describe Salmonella typhi gastroenteritis.

A
  • Typhoid (enteric) fever - gram -ve rod
    • Transmitted only by humans
    • Multiplies in Peyer’s patches, spreads ERS
    • Bacteraemia, 3% carriers
    • Slow onset, fever and constipation, splenomegaly, rose spots, anaemia, leucopaenia, bradycardia, haemorrhage
    • Blood cultures are positive
    • Treatment: ceftriaxone
386
Q

Describe Shigella gastroenteritis.

A
  • Gram -ve rod
  • Antigens:
    • Cell wall O antigens
    • Polysaccharide (groups A-D): S. sonnei, S. dysenteriae, S. flexneri (MSM)
  • The most effective enteric pathogen (low infectious dose 50)
  • No animal reservoir → higher rates in MSM
  • No carrier states
  • Dysentery
    • Invading cells of mucosa of distal ileum and colon
    • Producing enterotoxin (Shiga toxin)
  • Avoid antibiotics → ciprofloxacin if required
387
Q

Describe Yersinia gastroenteritis.

A
  • Non-lactose fermenter - gram -ve rod
  • Prefers 4ºC “cold enrichment”
  • Transmitted via food contaminated with domestic animal’s excretions
  • Enterocolitis, mesenteric adenitis and associated reactive arthritis, Reiter’s
388
Q

Describe Vibrio cholerae gastroenteritis?

A
  • Curved, comma shaped, late lactose fermenters, oxidase positive - gram -ve rods
    • Faeco-oral transmission inc. shellfish, oysters, shrimp
    • Colonisation of small bowel and secretion of enterotoxin with A and B subunit, causing persistent stimulation of adenylate cyclase
    • Causes massive diarrhoea (rice water stool) without inflammatory cells
    • Treat the losses / Electrolyte replacement and fluids
389
Q

Describe Vibrio parahaemolyticus gastroenteritis?

A
  • Curved, comma shaped, late lactose fermenters, oxidase positive - gram -ve rods
    • Ingestion of raw or undercooked seafood (i.e. oysters)
    • Major cause of diarrhoea in Japan or when cruising in the Caribbean
    • Self-limited for 3 days
    • Cholerae: grows in salty 8.5% NaCl
    • Treat with doxycycline
390
Q

Describe Vibrio vulnificus gastroenteritis.

A
  • Curved, comma shaped, late lactose fermenters, oxidase positive - gram -ve rods
    • Cellulitis in shellfish handlers and fatal septicaemia with D+V in HIV patients
    • Treat with doxycycline
391
Q

Describe campylobacter gastroenteritis.

A
  • Curved, comma or S shaped; Microaerophilic - gram -ve rod
    • Transmitted via contaminated food and water with animal faeces (poultry, meat, unpasteurised milk)
    • Enterotoxin (watery diarrhoea) with invasion (+/- blood)
    • Symptoms: Watery, foul smelling diarrhoea, bloody stool, fever and severe abdominal pain à treat with erythromycin or cipro if in the first 4-5days
    • Self-limiting but symptoms can last for weeks (20 days)
      • Only tx if immunocompromised (macrolide)
    • Extra outcomes: GBS, ReA, Reiter’s
392
Q

Describe Entamoeba histolytica gastroenteritis.

A
  • Protozoa - 4 nuclei, motile trophozoite in diarrhoea; Non-motile cyst in non-diarrhoeal illness
    • Killed by boiling, removed by water filters
    • No animal reservoir
    • Ingestion of cysts → trophos in ileum which colonize cecum and colon causing a “flask shaped” ulcer
    • Symptoms: dysentery, flatulence, tenesmus or in chronic form: weight loss +/- diarrhoea, liver abscess
    • Treat = metronidazole and paromomycin in luminal disease
393
Q

Describe Giardia lamblia gastroenteritis.

A
  • Protozoa - trophozoite “pear shaped”, 2 nuclei, 4 flagella and a suction disk
    • Ingestion of cyst from faecal-contaminated water and food → excystation at duodenum, tropho attaches, no invasion but malabsorption of protein and fat
    • Travellers (cruise), hikers, day care, psychiatric hospitals, MSM
    • Symptoms: Foul smelling non-bloody diarrhoea, cramps, flatulence, no fever
    • Treatment = metronidazole
394
Q

Describe Crytposporidium parvum gastroenteritis.

A
  • Infects the jejunum
  • Severe diarrhoea in the immunocompromised (can cause outbreaks)
  • Oocysts seen in stool by modified Kinyoun acid fast stain
  • Treatment = treat immunocompromising issue
395
Q

What prevention and control measures are in place to prevent gastroenteritis?

A
  • Targets for promotion
    • Breastfeeding, improved weaning practice
    • Clean water for drinking
    • Safe disposal of stools of young children
    • Precautions when travelling
    • Food handling
    • Public health notification
    • Good handwashing
  • Vaccines
    • Cholera
    • Campylobacter
    • ETEC
    • Salmonella typhi
    • Rotavirus
  • Public health
    • Notifiable diseases = Campylobacter, Clostridium species, Listeria monocytogenes, Vibrio, Yersinia
396
Q

What changes occurs in influenza a that allows avian variants to adapt to mamalian hosts?

A
  • A single amino acid change in PB2 E627K
  • Antigenic shift - incorporation of appropriate genes due to reassortment
397
Q

What is the natural reservoir of influenza A?

A
  • Ducks / Other wild/migratory birds
  • Pigs
  • Horses
  • Dogs
  • Seals
  • Chickens
  • Bats
398
Q

What is the life cycle of influenza?

A
  • Influenza has 2 proteins on its surface
    • Haemagglutinin (HA) and Neuraminidase (NA)
  • HA binds to Sialic Acid receptors (SA-R) on human URT cells and human tryptase cleaves the HA to allow entry
  • The acidity of the endosome triggers a fusion event by which it releases its genome into the cell
  • The genome then travels to the nucleus and takes over host factors to drive transcription and translation
  • New viral products produced (proteins and genome) à assemble at surface of cell and bud off
399
Q

What are the routes of transmission of HAV?

A

Faecal-oral route (remember, faecal-oral)

  • More common in countries in which access to clean water is poor
  • Occasional outbreaks in schools and amongst MSM and IVDU
  • Occupational risks (sewage workers, plumbers, chefs)
400
Q

What are the virology features of HAV?

A
  • Single-stranded +ve sense RNA genome
  • Quasi-enveloped virus
401
Q

What are the clinical features of HAV?

A
  • 2-6 week incubation period
  • Wide disease spectrum from asymptomatic to fulminant hepatitis
    • Strong correlation with age: <10% symptomatic among children <6 years old versus 70% in adults
  • Typical symptoms = fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice ± extra-hepatic
  • Acute presentation; 99% resolution → not chronic
402
Q

What is the management of HAV?

A
  • Supportive + Notifiable disease
  • Pre/post-exposure prophylaxis in vulnerable / exposed
403
Q

What is the serology of HAV?

A

Diagnostic test = anti-HAV IgM + high ALT

  • Vaccine
    • High IgM; and
    • High IgG without high ALT
404
Q

What are the routes of transmission of HBV?

A
  • Sexually transmitted
  • Blood products
  • Mother-to-Baby (vertical)
405
Q

What are the virology features of HBV?

A
  • Enveloped DNA Virus with reverse transcriptase to replicate
  • 10 genotypes (A-J) with distinct geographical distribution
406
Q

What are the clinical features of HBV?

A
  • Causes acute and chronic (>6 months) infection
    • Adults = 5-10% chance of developing chronic infection
    • Babies = 95% chance of developing chronic infection
    • Incubation period: 2-6 months
  • 2-6 month incubation period
  • Acute = fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice ± extra-hepatic
  • Chronic = hepatic fibrosis
407
Q

What are the stages of chronic HBV?

A
  1. Immune tolerant
  2. Immune reactive
  3. Inactive HBV carrier state
  4. HBeAg -ve chronic HBV
  5. HBsAg -ve phase
408
Q

What the consequences of chronic HBV?

A
  • Hepatic fibrosis → cirrhosis → HCC
    • Resection of the tumour alone is unlikely to be a feasible option → rest of the liver is likely to be damaged and not functioning very well
409
Q

What is the management of acute HBV?

A
  • Supportive + Notifiable disease
  • Pre/post-exposure prophylaxis in vulnerable / exposed
410
Q

What is the management of chronic HBV?

A
  • Interferon Alpha (used in a subset of patients who look like they are clearing the virus by themselves)
    • Do not use in patients who may require a liver transplant
  • Lamivudine
  • Tenofovir
  • Entecavir
  • Emtricitabine
  • Liver Transplantation – requires hepatitis B Ig
  • Liver Failure
    • Antivirals are very effective in treating the viral hepatitis
    • HBV vaccine may also be used (there are some non-responders who need novel vaccines)
411
Q

What is the serology of HBV?

A
  • Immune due to past infection = HBsAb + HBcAb
  • Immune due to vaccination = HbsAB
  • Acute HBV = HBsAg ± HBc IgM
  • Chronic HBV = HBsAg + HBcAb
412
Q

What are the routes of transmission of HCV?

A
  • Mainly spread by blood products
    • Major groups affected: MSM and IVDU
413
Q

What are the virology features of HCV?

A
  • Part of the flaviviridae family
  • Consists of components for the Core (C), Envelope (E) and Non-Structural (NS) components
  • Single-stranded, positive sense RNA genome
  • 6 genotypes of HCV (1, 2 and 3 are most common)
    • Genotype 1 is the hardest to treat
414
Q

What are the clinical features of HCV?

A
  • 6-8 week incubation
  • Outcomes of acute infection:
    • Clear = 20-40%
    • Chronic infection = 60-80% (higher than others)
    • Complications = hepatic (cirrhosis and HCC) and extra-hepatic
  • Typical symptoms = fever, malaise, anorexia/nausea, abdominal discomfort, diarrhoea, jaundice ± extra-hepatic
415
Q

What is the management of HCV?

A
  • Interferon and Ribavarin treatment (>90% can be cured)
    • Measure SVR12 at 8 to12 weeks
  • Direct Acting Antivirals (DAAs) = used clinically (cures 94%)
    • NS3/4 serine protease = ‘-revir’
      • Genotype 1 + Low barrier to resistance
      • Many interactions
    • NS5a RNA (unknown action) = ‘-asvir’
      • All genotypes + Low barrier to resistance
    • NS5b RNA dependent RNA polymerase = ‘-buvir’
      • Sofosbuvir = All genotypes + High barrier to resistance
      • Other NS5b RNA dependent RNA polymerases = Genotype 1 + Low barrierto resistance
  • Prevention + Public health
    • Acute HCV = notifiable
    • No vaccine or post-exposure prophylaxis
416
Q

What is the serology of HCV?

A
  • Cannot check anti-HCV during acute hepatitis – check the viral load (HCV RNA) instead
    • Anti-HCV antibodies develop after acute infection (i.e. rise in ALT) has disappeared
  • Test = HCV RNA
417
Q

What are the routes of transmission of HDV?

A
  • Requires co-hepatitis B infection
  • Blood-borne
418
Q

What are the virology features of HDV?

A
  • Single-stranded, circular RNA genome
419
Q

What are the clinical features of HDV?

A
  • 3-6 week incubation
  • Hepatitis B and D co-infection
    • Similar to acute HBV – most self-limiting (<5% chronic)
  • HBV superinfection (someone with chronic hepatitis B is then inoculated by HDV) = more serious / severe
    • Further increased risk of cirrhosis and HCC
    • If anyone has HBV, we should routinely check them for HDV
420
Q

What is the management of HDV?

A
  • Hepatitis B and D co-infection = supportive
  • HBV superinfection = peg-IFNa
    • Medications used in HBV are not effective
421
Q

What are the routes of transmission of HEV?

A
  • Faecal-oral route
  • Zoonosis – mainly pigs
422
Q

What are the virology features of HEV?

A
  • Hepeviridae family
  • Genotypes
    • 1 + 2 = human, epidemic – mostly self-limiting
    • 3 + 4 = swine and other - very little person-to-person spread
423
Q

What are the clinical features of HEV?

A
  • 3-8 week incubation
  • Usually self-limiting
  • Rare complications
    • CNS Disease (Bell’s palsy, Guillain-Barre)
    • Chronic infection
    • Very dangerous to pregnant women (esp. in the third trimester) – particularly genotype 1
424
Q

What is the management of HEV?

A
  • Supportive + advice against alcohol during infection
  • Ribavirin if needed
  • Vaccine = effective but not necessary or licensed in the UK
425
Q

What is the serology of HAV?

A

Left = normal

Right = rare case with persistently high HEV RNA

426
Q

What factors limit antiviral therapy?

A
  • The natural host immune response is critical
  • Adherence to treatment
  • Antiviral drug resistance
  • Drug toxicity and interactions
427
Q

What is caused by HHV infection?

A
  • Primary = Chickenpox:
    • Uncomplicated in children
    • Susceptible to complications in adults (e.g. pneumonitis)
    • Severe disease in immunocompromised
  • Secondary / Reactivation (from dorsal root ganglia) = Shingles
    • Immunocompetent = Dermatomal distribution
      • Complications = post-herpetic neuralgia
    • Immunocompromised = Disseminated disease
428
Q

Define pro-drug.

A

Inactive precursor of a drug which is metabolised into the active form within the body.

429
Q

What is the management of HHV (if needed)?

A
  • Aciclovir (PO or IV) or Valaciclovir (aciclovir pro-drug, PO)
  • Famciclovir
  • 2nd line = Foscarnet or Cidofovir for aciclovir-resistant strains
    • High toxicity
430
Q

What is the mechanism of action of aciclovir?

A

Nucleoside (guanosine) analogue

  • Incorporated into the growing chain of viral DNA → blocks
431
Q

How is aciclovir specific to virus opposed to animal cells?

A
  • Requires activation by viral thymidine kinase (only found in infected host cells)
  • Higher affinity for viral DNA polymerase than host DNA polymerase
432
Q

What is the management of HSV encephalitis?

A
  • Immediate empirical treatment = IV Aciclovir 10mg/kg TDS (high dose) - treat without waiting for test results
  • If confirmed = treat for 14-21 days
433
Q

What is the management of HSV meningitis?

A
  • Immunocompetent = self-limiting - PO valaciclovir can be prescirbed and taken at home
  • Immunocompromised or require hospital admission
    • IV aciclovir 2-3 days → PO for 10 days
434
Q

What are the indication for VZV treatment?

A
  • Chickenpox in adults (risk of pneumonitis)
  • Shingles in adults >50 years (risk of post-herpetic neuralgia)
  • Immunocompromised patient
  • Neonatal chickenpox
  • If increased risk of complications (e.g. underlying lung disease, eye involvement)
435
Q

What is caused by CMV infection?

A
  • Opportunistic virus that can cause severe disease in immunocompromised
  • Primary infection = latent in blood monocytes and dendritic cells → reactivated following immunosuppression
  • Shed in asymptomatic patients via saliva, urine, semen and cervical secretions
436
Q

What are the consequences of CMV infection in an immunocompromised patient?

A
  • Bone marrow suppression
  • Retinitis
  • Pneumonitis
  • Hepatitis
  • Colitis
  • Encephalitis
437
Q

What is the histology of CMV?

A

Owl eyes inclusions

438
Q

What is the management of CMV in an immunocompromised individual?

A
  • 1st = Ganciclovir (IV) or Valganciclovir (PO)
  • 2nd = Foscarnet (IV or intravitreal)
  • 3rd = Cidofovir (IV)
439
Q

What is the mechanism of action of ganciclovir / valganciclovir?

A

Guanosine analogue

  • Needs activation by viral UL97 kinase
440
Q

What are the indications for ganciclovir / valganciclovir?

A
  • CMV in immunosompromised / neonates
  • Solid organ transplant (not HSCT)
441
Q

What are the side effects of ganciclovir / valganciclovir?

A
  • Bone marrow toxicity (hence not used in HSCT)
  • Renal toxicity
  • Hepatic toxicity
442
Q

What is the mechanism of action of foscarnet?

A

Non-competitive viral DNA polymerase inhibitor

443
Q

What are the indications for foscarnet?

A
  • CMV
  • HSV
  • HSCT CMV prophylaxis / pre-emptive
  • VZV
  • EBV
  • HHV-6
444
Q

What are the side effects of foscarnet?

A

Nephrotoxic

445
Q

What is the mechanism of action of cidofovir?

A

Nucleotide analogue → competitive inhibitor of viral DNA synthesis

446
Q

What are the indications for cidofovir?

A
  • CMV
  • HSV
  • Adenovirus
  • BK virus
447
Q

What are the indication for aciclovir / valaciclovir?

A
  • HSV1
  • HSV2
  • VZV
448
Q

What are the side effects of cidofovir?

A

Nephrotoxic

449
Q

What strategies are used for treatment of CMV in transplant patients?

A
  • Wait then Treat established disease – high mortality in HSCT
  • Prophylaxis with GCV/vGCV
    • Indication: solid organ transplant (not HSCT)
  • Pre-emptive with Foscarnet > GCV/vGCV
    • Indication: HSCT
  • Letermovir (PO and IV) - new / recently licensed
    • CMV DNA terminase inhibitor – specific to CMV
    • Indication: CMV prophylaxis in CMV +ve HSCT
    • Well tolerated and safe (low toxicity)
    • SEs: mainly GI side-effects
450
Q

What are the complications of EBV?

A
  • Common childhood infection
  • Minimally symptomatic → infectious mononucleosis → life-long infection
    • Continuous low-grade viral replication in B lymphocytes kept in check by the cellular immune system
  • Lymphoproliferative disease in the immunocompromised
  • Post-Transplant Lymphoproliferative Disease (PTLD)
    • Polyclonal expansion of B cells associated with the immunosuppression used in organ transplants
    • Due to a breakdown of immunosurveillance keeping the B cells and EBV in check
    • Predisposes to lymphoma
451
Q

What is the management of post-transplant lymphoproliferative disease?

A
  • Reduce immunosuppression
  • Rituximab – anti-CD20 monoclonal antibody
452
Q

A 42-year-old lady is admitted with a 2 day history of fever and confusion and presents with new onset seizures. What antiviral medication should she receive as soon as possible? Choose the best answer.

  • Oral aciclovir
  • IV foscarnet
  • Oral valaciclovir
  • IV ganciclovir
  • IV aciclovir
A

IV aciclovir - HSV encephalitis

453
Q

What are the main surface protein on influenza?

A
  • Haemagglutinin (HA) and Neuraminidase (NA)
    • HA = binding and entry into the target cell
    • NA = release of progeny virus particles from the host cell
454
Q

What are the pharmaceutical options in the management of influenza?

A
  • Neuraminidase Inhibitors (NA is the main target of the current generation of anti-influenza drugs):
    • Oseltamivir (Tamiflu) – ORAL
    • Zanamivir (Relenza) – Dry Powder Inhaler
    • Peramivir (not licensed in UK + only for Influenza A)
  • Effective against influenza A and B
  • Baloxavir marboxil tablets / Xoflusa (PO)
    • Inhibits endonuclease activity of RNA polymerase complex (required for viral gene transcription)
455
Q

What are the indications for neuraminidase inhibitors?

A
  • Those unwell enough to be admitted to hospital
  • In the community if they have all 3 of:
    • National surveillance indicates influenza is circulating
    • Within 48 hours of symptom onset (36 hours for zanamivir)
    • Patient is in a ‘risk-group’
      • Age >65yo, immunosuppressed, chronic resp. disease, CHD, CLD, etc
456
Q

What are the antiviral management options for bronchiolitis?

A
  • Ribavirin (PO) – no evidence
  • IVIG – anecdotal evidence only
  • Palivizumab - monoclonal Ab against RSV
    • Prophylactically in the winter months for the prevention of serious lower respiratory tract disease caused by RSV in high risk infants (e.g. preterm, heart or lung disease, SCID)
457
Q

What is the mechanism of action of ribavirin?

A

Nucleoside/Guanosine analogue

458
Q

What are the indications for ribavirin?

A
  • Lassa fever
  • HEV
  • HCV
  • RSV - not sure if effective
459
Q

What is the management of SARS CoV-2?

A
  • Antiviral drugs
    • Remdesevir - nucleotide analogue
    • Molnupiravir - viral RNA mutagenic
    • Paxlovid - protease inhibitor
  • Neutralising monoclonal Abs - need early administration
    • Ronapreve
    • Sotrovimab
  • Immunomodulators
    • Steroids - dexamethasone
    • Cytokine release syndrome
      • Tocilizumab (IL-6 antagonsit)
      • Sarilumab (IL-6 antagonsit)
      • Anakinra (IL-1 antagonsit)
460
Q

The following statements concern the antiviral drugs oseltamivir and zanamivir. Choose the best answer.

  • Oseltamivir directly inhibits the influenza neuraminidase
  • Zanamivir blocks binding of viral haemagglutinin to host cell sialic acid
  • Oseltamivir inhibits influenza virus uncoating
  • Zanamivir is usually given intravenously
  • Zanamivir is usually given by nebuliser
A

Oseltamivir directly inhibits the influenza neuraminidase

461
Q

What is caused by BK virus infection?

A
  • Primary BK infection in childhood → minimal symptoms but lifelong carriage in the kidneys and urinary tract
  • Causes problems in the immunocompromised
    • HSCT = BK cystitis, nephritis
    • Renal transplants = BK nephropathy, ureteric stenosis
462
Q

What is the management of BK haemorrhagic cystitis?

A
  • Bladder washouts
  • Reduce immunosuppression
  • If significant morbidity = Cidofovir (IV)
  • If nephrotoxicity = Cidofovir (intravesical) - avoids nephrotoxicity if direct into bladder
463
Q

What is the management of BK nephropathy?

A
  • Reduce immunosuppression
  • IVIG
  • NO cidofovir as it is nephrotoxic
464
Q

What is the treatment of adenovirus?

A
  • Cidofovir (IV) or Brincidofovir (PO)
    • Less toxic on the GI tract
  • IVIG
465
Q

How is antiviral drug resistance thought to occur?

A
  • Selection = selection of pre-existing resistant strains due to inadequate drug levels
  • Diversity = quasispecies (population of virus that are genetically heterogenous rather than clonal)
466
Q

What are the implications of antiviral drug resistance?

A
  • Treatment failure
  • Need to use second-line drugs – less effective and often more toxic
  • Cross-resistance with other antivirals
467
Q

How can antiviral drug resistance be prevented?

A
  • Potent combination drug regimens
  • Increase adherence to treatment (i.e. lower pill burden)
468
Q

How is antiviral drug resistance identified?

A
  • Genotypic assays – sequencing genome to identify known drug resistance mutations
  • Phenotypic assays – culturing in cell monolayers in presence of increasing concentrations of antiviral drugs
    • AKA: Plaque Reduction Assay
469
Q

Describe HSV resistance.

A

Resistance to Aciclovir by HSV

  • Causes of resistance
    • 95% due to mutation in viral thymidine kinase
    • 5% of cases are due to mutations in viral DNA polymerase
  • Most of these will show cross-resistance with ganciclovir
  • Nearly always occur in immunocompromised patients
  • Treatment = foscarnet or cidofovir (not dependent on viral thymidine kinase activation)
470
Q

Describe CMV resistance.

A
  • Causes of resistance:
    • Common = mutations in protein kinase gene (UL97)
    • Rare = mutations in DNA polymerase gene (UL54)
  • More likely to occur in the context of prolonged therapy in immunocompromised patients
  • Treatment = foscarnet or cidofovir
471
Q

Describe influenza resistance.

A
  • Oseltamivir (NA inhibitor) resistance through H275Y mutation → commonly seen in H1N1
472
Q

Describe the uses of immunoglobulin.

A
  • Prophylactic: palivizumab (RSV)
  • Post-exposure prophylaxis:
    • VZV IVIG - immunocompromised / pregnant / neonates
    • HBV IVIG - unvaccinated recipient exposed to hepatitis B-positive source, non-responder to vaccine exposed to source of positive or unknown status
    • Human Rabies Immunoglobulin (HRIG)
  • Therapeutic:
    • Human normal immunoglobulin (IVIG) as adjunctive treatment for viral pneumonitis (e.g. CMV)
    • Rituximab (anti-CD20) for EBV-driven PTLD
473
Q

The following statements concern resistance to antiviral drugs. Choose the best answer.

  • Resistance of HSV to aciclovir is common in the immunocompetent
  • Phenotypic resistance testing is routinely used to detect resistance of CMV to ganciclovir
  • Aciclovir resistance in HSV is most commonly mediated by mutations in the viral thymidine kinase
  • Aciclovir resistance in HSV is most commonly mediated by mutations in the viral DNA polymerase
  • Antiviral drug resistance is most commonly associated with good adherence to treatment
A

Aciclovir resistance in HSV is most commonly mediated by mutations in the viral thymidine kinase

474
Q

What is the presentation of pneumonia?

A
  • Symptoms:
    • SoB
    • Productive cough
    • Fever and rigors
    • Pleuritic chest pain
    • Malaise
  • Examination:
    • Pyrexia
    • Tachycardia
    • Tachypnoea
    • Cyanosis
    • Bronchial breathing
    • Crackles
    • Dullness to percussion/tactile vocal fremitus
475
Q

What are the main causes of CAP?

A
  • Typical (85%)
    • Streptococcus pneumoniae
    • Haemophilus influenzae
  • Atypical (15%)
    • Legionella
    • Mycoplasma
    • Coxiella burnetii (Q fever) - exposure to farm animals
    • Chlamydia psittaci (Psittacosis) - exposure to birds
476
Q

What are the culture results of streptococcus pneumoniae?

A
  • Gram +ve strepto/diplo- cocci
  • Alpha-haemolytic and optochin sensitive
477
Q

What are the features of streptococcus pneumoniae infection?

A
  • 30-50% of CAP
  • Acute onset
    • Severe pneumonia
    • Fever and rigors
    • Lobar consolidation
  • Almost always penicillin-sensitive
    • Penicillin-resistance strains (Southern Europe)
478
Q

What are the appropriate investigations for suspected pneumonia?

A
  • Bloods
    • FBC
    • U&E
    • CRP
    • Blood cultures
  • ABGs
  • Sputum culture
  • MC&S
  • CXR
479
Q

What is CURB-65?

A

Screening / management tool for CAP

  • Confusion
  • Urea > 7 mmol/L
  • RR > 30
  • BP < 90 systolic or < 60 diastolic
  • 65+ years
  • 2 = consider admitting
  • 3 = manage as severe / consider ITU
480
Q

What is the presentation of bronchitis?

A
  • Cough
  • Fever
  • Increased sputum production
  • Increased shortness of breath
  • Smoker
  • Normal CXR
481
Q

What organisms cause bronchitis?

A
  • Viruses
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
482
Q

What is the management of bronchitis?

A
  • Bronchodilation / salbutamol
  • Physiotherapy
  • Antibiotics
  • Smoking cessation
483
Q

What are the causes of cavitating lung lesions?

A
  • Staphylococcus aureus
  • Klebsiella pneumoniae
  • Haemophilus influenzae
  • TB
484
Q

What are the features of H. inflenzae?

A
  • Gram-negative cocco-bacilli (stain on chocolate agar)
  • 15-35% of CAP
  • More common with pre-existing lung disease
  • May produce beta-lactamase
485
Q

Which pathogen that causes atypical pneumonia also causes hyponatraemia?

A

Legionella pneumophilia

486
Q

What pathogens causes atypical pneumonia?

A
  • Mycoplasma
  • Legionella
  • Chlamydia
  • Coxiella
487
Q

What are the features of of atypical pneumonia?

A
  • Usually pneumonia symptoms
  • Extra-pulmonary features - hepatitis, hyponatraemia
  • Flu-like prodrome
488
Q

What are the features of Legionella pneumophilia?

A
  • Aerosol spread and associated with environmental outbreaks
  • It is grown on a buffered charcoal yeast extract
  • Can cause multi-organ failure
  • Associated with:
    • Confusion
    • Abdominal pain
    • Diarrhoea
    • Lymphopaenia
    • Hyponatraemia
489
Q

What are the appropriate investigations for suspected atypical pneumonia?

A
  • Sputum = mycoplasma
  • Urinary antigens = Legionella
  • Serology = Coxiella and Chlamydia
490
Q

What are the S/S and investigative signs of empyema?

A
  • S/S
    • SOB
    • Fever
    • Pleuritic chest pain
    • Reduced percussion note
    • Decreased air entry right base
  • CXR
    • Homogenous shadowing with meniscus level
  • CT
    • Empyema with collapsed lung underneath
491
Q

What are the features of Coxiella burnetii?

A
  • Common in domesticated farm animals
  • Transmitted by aerosol or milk
492
Q

What are the causes of failing to improve despite treatment for suspected pneumonia?

A
  • Empyema/abscess
  • Proximal obstruction (tumour)
  • Resistant organisms (travel hx)
  • Not receiving/absorbing antibiotics
  • Immunosuppression
  • Other diagnosis
    • Lung cancer
    • Cryptogenic organising pneumonia
493
Q

Define HAP.

A

A pneumonia onset >48 hours post hospital admission

494
Q

What are the causes of HAP?

A
  • Enterobacteriaciae (e.g. E. coli, K. pneumoniae) – 31%
  • Staphylococcus aureus – 19%
  • Pseudomonas spp – 17%
  • Haemophilus influenzae – 5%
  • Acinetobacter baumanii – 4%
  • Fungi (Candida spp) – 7%
495
Q

What are the signs and symptoms of PCP?

A
  • Immunocompromised
  • Insidious onset
    • Dry cough
    • Weight loss
    • SOB
    • Malaise
496
Q

What are the appropriate investigations for suspected PCP?

A
  • CXR = bilateral ground-glass shadowing (“bat’s wing”)
  • Immunofluorescence from bronchoalveolar lavage
497
Q

What is the management of PCP?

A

Co-trimoxazole

498
Q

What aspergillus fumigatus disease affect the lungs?

A
  • Allergic bronchopulmonary aspergillosis
    • Chronic wheeze
    • Eosinophilia
    • Bronchiectasis
  • Aspergilloma
    • Fungal ball, often in pre-existing cavity
    • May cause haemoptysis
  • Invasive aspergillosis
    • Immunocompromised
    • Treatment: amphotericin B
499
Q

What respiratory pathogens are patients with HIV vulnerable against?

A
  • PCP
  • TB
  • Atypical mycobacteria
500
Q

What respiratory pathogens are patients with neutropaenia vulnerable against?

A

Fungi - Aspergillus

501
Q

What respiratory pathogens are bone marrow transplant patients vulnerable against?

502
Q

What respiratory pathogens are splenectomy patients vulnerable against?

A

Encapsulated organisms - S pneumoniae, H influenzae, malaria

503
Q

How can pneumonia be prevented?

A
  • Smoking cessation
  • Vaccination:
    • Childhood immunisation schedule
    • Adults
      • Annually = influenza and COVID
      • 5 yearly = pnemovax

Y5 Pathology (5 decks)

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