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Year 5: Pathology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the potential targets for antibiotics?

A

Inhibit cell wall synthesis

Inhibit protein synthesis

Inhibit DNA synthesis

Inhibit RNA synthesis

Cell membrane toxin

Inhibit folate metabolism

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2
Q

Which classes of antibiotics inhibit cell wall synthesis

A

Beta lactams

Glycopeptides

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3
Q

What are the different types of beta-lactam?

A

Penicillins e.g. benzylpenicillin

Cephalosporins: ceftriaxone

Carbapenems e.g. meropenem

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4
Q

What are the indications for beta-lactams?

A

Gram positive

[Gram negative- 3rd generation cephalosporin)

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5
Q

What are some examples of glycopeptides?

A

Vancomycin, Teicoplanin

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6
Q

What are the indications for glycopeptides?

A

MRSA, C. Diff

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7
Q

Which classes of antibiotics inhibit protein synthesis?

A

Aminoglycosides

Tetracyclines

Macrolides

Chloramphenicol

Oxazolidines

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8
Q

Give an example of an aminoglycoside

A

Gentamicin

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9
Q

Give an example of a tetracycline

A

Doxcycline

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10
Q

Give an example of a macrolide

A

Erythromycin

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11
Q

Give an example of a chloramphenicol

A

Eye drops

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12
Q

Give an example of an Oxazolidinone

A

Linezolid

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13
Q

What are the indications for aminoglycosides

A

Gram -ve sepsis

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14
Q

Gram -ve sepsis

A

Gentamicin

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15
Q

What are the indications for tetracyclines

A

Intracellular- chlamydia

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16
Q

Rx for chlamydia

A

Doxycycline

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17
Q

What are the indications for macrolides

A

Gram +ve in context of Pen Allergic

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18
Q

Rx Gram +ve in context of pen allergic

A

Erythromycin (macrolide)

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19
Q

What are the indications for chloramphenicol

A

Bacterial conjunctivitis

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20
Q

Rx bacterial conjunctivitis

A

Chloramphenicol

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21
Q

What are the indications for oxazolidinones

A

Gram +ve, MRSA + VRE

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22
Q

Rx for Gram +ve, MRSA + VRE

A

Linezolid

or

Daptomycin

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23
Q

What classes of antibiotics inhibit DNA synthesis

A

Fluoroquinolones

Nitroimidazoles

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24
Q

Given an example of a fluoroquinolone

A

Ciprofloxacin

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25
Q

Given an exmple of a nitroimidazole

A

Metronidazole

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26
Q

Indications for fluoroquinolones

A

Gram -ve

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27
Q

Indications for nitroimidazoles

A

Anaerobes and protozoa

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28
Q

What class of antibiotics inhibits RNA synthesis?

A

Rifamycin

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29
Q

Given an example of a rifamycin

A

Rifampicin

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30
Q

Indications for rifamycins

A

MTB

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31
Q

Rx for anaerobes and protozoa

A

Metronidazole

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32
Q

What classes of antibiotics act as cell membrane toxins

A

Polymyxin

Cyclic lipopeptide

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33
Q

Give an example of a polymyxin

A

Colistin

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34
Q

Give an example of a cyclic lipopeptide

A

Daptomycin

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35
Q

What are the indications for polymyxins?

A

Gram -ve

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36
Q

What are the indications for cyclic lipopeptide

A

Gram +ve, MRSA +VRE

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37
Q

What classes of antibiotics inhibit folate metabolism?

A

Sulfonamides

Diaminopyrimidines

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38
Q

Give an example of a sulfonamide

A

Sulphamethoxazole

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39
Q

What are the indications for sulfonamides?

A

PCP (with trimethoprim: co-timoxazole)

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40
Q

What are the indications for diaminoprimidines?

A

UTI e.g. Trimethoprim

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41
Q

What are some broad spectrum antibitoics?

A

Co-amoxiclav

Tazocin

Ciprofloxacin

Meropenem

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42
Q

What is tazocin?

A

Combination antibotic containing penicllin (piperacillin) and a beta-lactamasae inhibitor tazobactam

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43
Q

What is co-amoxiclav?

A

Combination antibiotic containing penicllin amoxillin and beta-lactamase inhibitor clavulanic acid

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44
Q

What are some narrow spectrum antibiotics?

A

Flucloxacillin, metronidazole, gentamicin

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45
Q

Features of beta-lactams

Activity?

Ineffective against?

A
  • Inactivate the enzymes that are involved in the terminal stages of cell wall synthesis (transpeptidases also known as penicillin binding proteins) – β-lactam is a structural analogue of the enzyme substrate
  • Bactericidal
  • Active against rapidly-dividing bacteria
  • Ineffective against bacteria that lack peptidoglycan cell walls (e.g. Mycoplasma or Chlamydia)
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46
Q

Penicllin uses

Broken down by?

A

Gram +ve organisms e.g. strep, clostridia

Broken down by beta-lactamase, prod by S. aureus

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47
Q

Amoxicillin uses

Broken down by?

A

Broad spectrum, extends coverage to enterococci and Gram -ve organisms

Beta-lactamase produced by S. aureus and many gram negative organisms

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48
Q

flucloxacillin uses

NB

A

Similar to penicllin although less active

Stable to beta-lactamase produced by S. aureus

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49
Q

Uses of piperacillin

A

Similar to amoxicillin, extends coverage to pseudomonas and other non-enteric gram negatives

Broken down by beta-lactamase producing organisms e.g. S. aureus and gram negatives

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50
Q

Clavulanic acid and tazobactam

A

Beta-lactamase inhibitors extend coverage of penicllins to include S.aureus, Gram negatives and anaerobes

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51
Q

What changes with the generations of cephalosporins?

A

Increasing activity against gram negative bacilli

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52
Q

What is a 1st generation cephalosporin?

A

Cephalexin

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53
Q

What is a What is a 2nd generation cephalosporin?

A

Cefuroxime

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54
Q

What is a 3rd generation cephalosporin?

A

Cefotaxime

Ceftriaxone

Ceftazidime

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55
Q

What are ESBL organisms resistant to?

A

All cephalosporins regardless of in vitro results

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56
Q

Use of cefuroxime

A

•Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes

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57
Q

With what is ceftriaxone associated?

A

C diff

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58
Q

What is the use of ceftazidime?

A

anti-Pseudomonas

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59
Q

What are the uses of carbapenems?

What is an issue

A

Stable to ESBL enzymes

Carbapenemase enzymes becoming more widespread

There are multidrug resistant Acinetobacter and Klebsiella species

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60
Q

What are the key points for beta-lactams

A
  • Relatively non-toxic
  • Renally excreted (so ↓dose if renal impairment)
  • Short half life
  • Will not cross intact blood-brain barrier
  • Cross-allergenic (penicillins approx 10% cross-reactivity with cephalosporins or carbapenems)
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61
Q

Why are glycopeptides effective against Gram +ve?

A
  • Large molecules, unable to penetrate Gram –ve outer cell wall
  • Active against Gram +ve organisms
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62
Q

Rx for MRSA administration

A

IV only

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63
Q

What is used to treat serious C diff?

A

Oral vancomycin

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64
Q

What is an issue with glycopeptides?

As a consequence?

A

Nephrotoxic

Need to monitor drug levels to prevent accumulation

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65
Q

Rx vs P. aeruginosa?

A

Gentamicin and tobramycin

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66
Q

Features of aminoglycosides

What is significant

A
  • Bind to amino-acyl site of the 30S ribosomal subunit
  • Rapid, concentration-dependent bactericidal action
  • Require specific transport mechanisms to enter cells (accounts for some intrinsic R)

Ototoxic and nephrotoxic: monitor levels

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67
Q

Combination of beta-lactams and aminoglycosides?

A

Synergistic

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68
Q

What are the features of tetracyclines

What is significant

Side-effect?

A
  • Broad-spectrum agents with activity against intracellular pathogens (e.g. chlamydiae, rickettsiae & mycoplasmas) as well as most conventional bacteria
  • Bacteriostatic
  • Widespread resistance limits usefulness to certain defined situations

Do not give to children or pregnant women

Light-sensitive rash

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69
Q

Features of macrolides

A
  • Bacteriostatic
  • Minimal activity against Gram –ve bacteria
  • Useful agent for treating mild Staphylococcal or Streptococcal infections in penicillin-allergic patients
  • Also active against Campylobacter sp and Legionella. Pneumophila
  • Newer agents include clarithromycin & azithromycin with improved pharmacological properties
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70
Q

Rx for Campylobacter and L. pneumophila

A

Macrolide

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71
Q

MOA Macrolides

A

•Bind to the 50s subunit of the ribosome

1) Interfere with translocation 2)Stimulate dissociation of peptidyl-tRNA

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72
Q

MOA tetracyclines

A
  • Reversibly bind to the ribosomal 30S subunit
  • Prevent binding of aminoacyl-tRNA to the ribosomal acceptor site, so inhibiting protein synthesis.
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73
Q

MOA aminoglycosides

A

) Prevent elongation of the polypeptide chain

2) Cause misreading of the codons along the mRNA

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74
Q

What are the significant adverse effects of chloramphenicol

A

Aplastic anaemia

Grey baby syndrome in neonates: inability to metabolise drug

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75
Q

MOA chloramphenicol

A

•Chloramphenicol binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

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76
Q

MOA Nitroimidazoles

A
  • Include the antimicrobial agents metronidazole & tinidazole
  • Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage
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77
Q

What are nitrofurans?

A

Compounds related to nitroimidazoles e.g. nitrofurantoin used for UTIs

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78
Q

Considerations when Rxing rifampicin

A

Monitor LFTs

beware interactions with other drugs that are metabolised by the liver

Orange secretions

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79
Q

Why should you never use rifampicin as a single agent?

A
  • Except for short-term prophylaxis (vs. meningococcol infection) you should NEVER use as single agent because resistance develops rapidly
  • Resistance is due to chromosomal mutation.
  • This causes a single amino acid change in the ß subunit of RNA polymerase which then fails to bind Rifampicin.
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80
Q

Features of colistin

A

Colistin – a polymyxin antibiotic that is active against Gram negative organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella. pneumoniae. It is not absorbed by mouth. It is nephrotoxic and should be reserved for use against multi-resistant organisms

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81
Q

Why is sulphonamide and diaminopyrimidine combined Rx useful?

A
  • Act indirectly on DNA through interference with folic acid metabolism
  • Synergistic action between the two drug classes because they act on sequential stages in the same pathway
  • Sulphonamide resistance is common, but the combination of sulphamethoxazole+trimethoprim (Co-trimoxazole) is a valuable antimicrobial in certain situations (e.g. Treating Pneumocystis. jiroveci pneumonia)
  • Trimethoprim is used for Rx community-acquired UTIs
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82
Q

What are the mechanisms of antibiotic resistance?

A

Inactivation

Altered target

Reduced Accumulation

Bypass

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83
Q

How does resistance to beta-lactams occur?

NB

A

Beta lactamases

Not the mechanism of resistance in penicllin resistant pneumoccoci and MRSA

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84
Q

How does beta-lactam resistance develop in MRSA?

A

Altered target: mecA encodes novel PBP (2a) which has a low affinity for binding beta lactams, substitutes for teh essential functions of high affinity PBPs at otherwise lethal concentrations othe antibiotic

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85
Q

How does Strep pneumonia resist Beta lactams?

A

Altered target: Penicllin is the result of the acquisition of stepwise mutations in PBP genes, lowe rlevel resistance can be overcome by increasing the dose

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86
Q

What are ESBLs?

What can they do?

NB?

A

Extended spectrum beta lactamases

Able to break down cephalosporins, becoming more common

Resistant to cephalosporins regardless of in vitro finding

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87
Q

What leads to macrolide resistance?

A

Altered targets:

  • Adenine-N6 methyltransferase modifies 23S rRNA
  • Modification reduces the binding of MLS antibiotics and results in resistance
  • Encoded by erm (erythromycin ribosome methylation) genes.
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88
Q

IFV vaccines in use today

A

Triaelent or quadrivalent inactivated vaccine: split or subunit HA rich. Given to those at risk. Short term strain specifica immunity mediated by Ab to HA head.

Live attenuated vaccine also quadrivalent or trivalent: cold adapted virus limited to URT, given to children, broader more cross reactive immunity

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89
Q

Features of IFV

A

Orthomyxovrius

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90
Q

What are the three strains that tend to affect humans each year?

How is this combatted?

A

IFV: A (H1: peaks begnning of January)

IFV: A (H1N1: peaks end of December)

IFV B: Peaks march

Trivalent vaccine in targetted populations which consists of a purified fraction with HA + NA of inactivated virus

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91
Q

What is the natural resrvoiir of IFV A

Why is these limited human-human transmission

A

Ducks

Because the vrius doesn’t replicate in the colder URT

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92
Q

What is the structure of IFV

A

8 RNA segements of nucleocaspid protein very prone to mutation

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93
Q

Outline IFV viral entry

A

NA (sialidase): cleaves sialic acid residues exposing receptor son host cell disrupting mucin barrier

HA: binds sialic acid receptors-> virus entry. Endosomal-viral envelope fusion= release

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94
Q

How are IFVs named?

A

H1= HA1

N1= N1

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95
Q

What is antigenic drift?

A

Mutation of HA/NA to give new viral strains

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96
Q

What is antigenic shift?

A

Complete change of HA/NA

Reassortment of RNA segments between IFV strains

Can only occur in IFVA

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97
Q

What is the pathogenesis of IFV H5N1

A

Cleavage of HA by clara-tryptase in the lung leads to exteded tropism/grwoth for H5 + H7

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98
Q

What are the causes of severe outcome in flu?

A

Secondary bacterial pneumonia

Mutant virus

Co morbidity

Cytokine storm

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99
Q

What is amantadine

Indication

MOA

Issue

A

Antiviral for IFV

IFVA only

Targets M2 ion channel but single AA mutation in M2= resistance

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100
Q

Give some examples of neuraminidase inhibitors

A

Oseltamivir (tamiflu)

Zanamivir (relenza)

Sialic acid

Only effective if given <48hrs aftern infection

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101
Q

What are the various issues with the different ROA in vaccines?

A

Subcute: good, uptake, processing and presentation to Langherans cells

IM: OK

IV Ag: taken to spleen

Orally: good response and local response within GIT

Intranasal: OK but may get allergic response

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102
Q

What are some examples of APCs?

A

Macrophages

B-lymphocytes

Langerhans

DCs

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103
Q

What does clonal expansion of CD4 cells require?

A

Specific antigent in combination with a cytokine e.g. IL-2

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104
Q

What response does the TH1 subset mediate

What cytokines are involved?

A

Cell-mediated immune response

IL-2

IFN-G

TNF

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105
Q

What response does the TH2 mediate?

What cytokines are involved?

A

Humoral response

IL-4

IL-5

IL-6

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106
Q

Why is it called haemagglutinin?

A

Causes agglutination of RBCs/URT cells

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107
Q

What are the 2 subsets of memory cells?

A

Central memory T cells: CCR7+CD62Lhigh: migrate efficiently to peripheral LNs, produce IL-2 but no IFN or perforin

Effector memory T cells: found in other sites, produce high levels of IFN and perforin but no IL-2

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108
Q

What are the three phases of T cell immunological memory?

A

Expansion

Contraction

Memory

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109
Q

What does the choice of antibiotic depend on?

CHAOS

A

Choice

Host

Antimicrobial susceptibilites of the

Organism itself and also the

Site of the infection

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110
Q

Choice of drug best features

A

Narrow spectrum

Bactericidal

Based on local sensitivity

Patient characteristics

Cost

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111
Q

When is IV antibiotic use indicated

A

Serious infection or no PO absorption

If need to access deep site or CNS

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112
Q

What factors influence antibiotic dose?

A

Age

Renal/hepatic function

Drug monitoring

Allergy

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113
Q

Principles for empirical treatment with antibiotics:

A

Collect specimens

Use a broad-spectrum antibiotic

Empirical cover may then be changed to a more specific agent on the basis of culture results

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114
Q

What are thhe preliminary investiations for identification of a bacterial infection

A

Gram stain: CSF, joint aspirate, Pus

Rapid antigen detection: immunofluorescence, PCR

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115
Q

What are the important factors to consider about the site of the infection?

A

pH

Lipid-solubility

CNS penetration

Special considerations required for Rx of endocarditis or osteomyelitis

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116
Q

Administration of antibiotics route of choice

A

IV : serious or deep seated infection

PO: usually easy but differential absorption between different antibiotic classes

IM: not an option for long term use, avoid id bleeding tendency

Topical: limited application that may cause local sensitisation

Generally after a patient has been on IV antibiotc for 48hrs switch to oral if they have stabilised

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117
Q

What is a type 1 pattern of antibiotic activity?

What is the goal of therapy?

Which antibiotics?

A

Concentration-dependant killing and prolonged persistent effects

Maximise concentrations

Aminglycosides, daptomycin, fluoroquinolines, ketolides

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118
Q

What is a type 2 pattern of antibiotic activity?

Goal of therapy

Antibiotics?

A

Time-dependant killing and minimal persistent effects

Maximise duration of exposure

Carabapenems, cephalosporins, erythromycin, linezolid, penicllins

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119
Q

What is a type 3 pattern of antibiotic activity?

Goal of therapy

Antibiotics

A

Time-dependent killing and moderate-to prolonged persistent effects

Maximise amount of drug

Azithromycin, clindamycin, oxazolidinones, tetracyclines, vancomycin

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120
Q

Recommended Rx course for N. meningitides meningitis?

A

7d

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121
Q

Recommended Rx course for acute adult osteomyelitis?

A

6w

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122
Q

Recommended Rx course for bacterial endocarditis

A

4-6w

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123
Q

Recommended Rx course for GpA streoptococcal pharyngitis

A

10d

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124
Q

Recommended Rx course for simple cystitis

A

3d

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125
Q

Skin infections common types

Common organism

Rx?

A

Impetigo, cellulitis, wound infection

S.aureusm, beta-haemolytic streptoccoci

Fluclox unless penallergic or MRSA

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126
Q

Invasive group A strep treatment

A

Aggressive and early debridement

Antibiotics: adjunctive use of protein synthesis inhibitors esp. clindamycin

Use of IVIG

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127
Q

What is the Eagle effect?

Proposed mechanism?

A
  • Named after Harry Eagle who first described it, originally referred to the paradoxically reduced antibacterial effect of penicillin at high doses, though recent usage generally refers to the relative lack of efficacy of beta-lactam antibacterial drugs on infections having large numbers of bacteria.
  • Penicillin is a bactericidal antibiotic that works by inhibiting cell wall synthesis but this synthesis only occurs when bacteria are actively replicating (or in the log phase of growth).
  • In cases of extremely high bacterial burden (such as with Group A Strep), bacteria may be in the stationary phase of growth.
  • In this instance since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity.
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128
Q

Rx in pharyngitis?

A

Benzyl-pen 10d

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129
Q

CAP Rx (mild)

A

Amoxicllin

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130
Q

CAP Rx (severe)

A

Co-amoxiclav and clarithromycin

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131
Q

HAI

Rx

A

Second most common cause of HAI

Associated with highest mortality

Greatest risk associated with tracheal intubation and mechanical ventilation

Cephalosporin, ciprofloxacin, tazocin, if MRSA colonised ris consider addition of vancomycin

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132
Q

What are the main pathogens in bacterial meningitis?

Rx?

A

N meningitidis

S pneumonia

+/- Listeria in very young/elderly/immunocompromised

Ceftriaxone +/- amoxycilllin if Listeria likely

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133
Q

Meningitis in neonate Rx

A

Cefotaxime + amoxicillin

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134
Q

Why is cefotaxime used in neonates?

A

Used insteead of ceftriaxone as it displaces bilirubin from albumin and can cause biliary sludging

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135
Q

N menigitidis treatment

A

Benzylpen or ceftriaxone/cefotaxime

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136
Q

Rx simple cystitis in community

A

Trimethoprim

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137
Q

HA-UTI Rx

Infected urinary catheter?

A

Cephalexin or Augmentin

Change under gentamicin cover

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138
Q

Rx for C diff

A

Stop offending antibiotic: usually a cephalosporin

If severe, RX with PO metronidazole

If fails use PO vancomycin

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139
Q

Def: bacturia

Def: cystitis

A

Presence of bacteria in urine

Inflammation of the bladder, often caused by infection

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140
Q

Classification of UTIs?

A

Uncomplicated: infection in a structureally and neurologically normal urinary tract

Complicated: with functional or structural abnormalities including catheters/calculi

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141
Q

Which patients are generally affected by complicated UTIs?

A

Men

Pregnant Women

Children

Patients who are hospitalised or in healthcare settings

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142
Q

Prevalence of bacturia in young non-pregnant women?

Incidence of symptomatic UTIs in women?

A

1-3%

40-50%

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143
Q

What causes 95% of UTIs?

A

E. coli

•Urinary tract infections are caused by many species of microorganisms, however, only a few serogroups of E. coli, O1, O2, O4, O6, O7, O8, O75, O150, and O18ab, cause a high proportion of infections

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144
Q

What other orangisms cause UTIs?

A
  • Proteus mirabilis
  • Klebsiella aerogenes
  • Enterococcus faecalis
  • Staphylococcus saprophyticus
  • Staphylococcus epidermis
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145
Q

What is significant in recurrent UTIs, especially those with structural abnormalities?

A

The relative frequency of infections caused by atypical organisms (i.e. not E. Coli) increases greatly

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146
Q

What are the antibacterial host defences in the urinary tract?

A

Urine: osmolality, pH, organic acids

Urine flow and micturition

Urinary tract mucosa: bactericidal activity, cytokines

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147
Q

Causes of renal obstruction

A

Mecahnical:

Extrarenal: valves, stenosis or bands, cacluli, extrinsic ureteral compression and BPH

Intrarenal: nephrocalcinosis, uric acid nephropathy, analgesic nephropathy, PKD, hypokaelmic nephropathy and the renal lesions of sickle cell trait/disease

Neurogenic:

Polio

Tabes dorsalis

Diabetic neuropathy

SC injuries

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148
Q

What dose vesicoureteral reflux lead to?

A

Perpetuation of infection by maintaining a residual pool of infected urine in the bladder after voiding

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149
Q

What is significant about infection in the kidney?

A

Frequently a site of abscesses in patients with S aureus bacteremia or both

Infection by gram negative bacilli rarely occurs by the haematogenous

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150
Q

Symptoms of UTI in neonates/children <2y/o?

>2y/o?

A

Failure to thrive, Vomiting, Fever

Frequency, dysuria, abdo or flank pain

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151
Q

Lower UTI symptoms?

A
  • The lower tract symptoms result from bacteria producing irritation of urethral and vesical mucosa, causing frequent and painful urination of small amounts of turbid urine.
  • Patients sometimes complain of suprapubic heaviness or pain.
  • Occasionally, the urine is grossly bloody or shows a bloody tinge at the end of micturition.
  • Fever tends to be absent in infection limited to the lower tract.
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152
Q

Upper UTI symptoms

A
  • fever (sometimes with rigors)
  • flank pain
  • and frequently lower tract symptoms (e.g., frequency, urgency, and dysuria)
  • at times, the lower tract symptoms antedate the appearance of fever and upper tract symptoms by 1 or 2 days
  • the symptoms described, although classic, may vary greatly
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153
Q

Symptoms of UTI in older patients

A
  • The vast majority of older adult patients with urinary infection are asymptomatic
  • Symptoms, when present, are often not diagnostic, because noninfected older adults often experience frequency, dysuria, hesitancy, and incontinence
  • Symptoms of upper tract infection are often atypical e.g., abdominal pain, change in mental status
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154
Q

Ix of UTI (uncomplicated):

A

Urine Dip

MSU for MCS

Bloods: FBC, UE, CRP

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155
Q

Ix of complicated UTI

A

Renal US

IV urography

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156
Q

What indicates contamination of a urine sample on microscopy?

A

Squamous epithelial cells

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157
Q

Causes of sterile pyruia?

A

(pus in urine)

Prior treatment with antibiotics

Calculi

Catheterisation

Bladder neoplasm

TB

STI

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158
Q

What are the differentiating culture forming units/mL in urine sample

A

10^5 cf/mL in infection

Patients without infection: <10^4 cfu/mL

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159
Q

What is the most common cause of candida infection in UT?

A

Occurs with indwelling catheters

Can be cured by removal of catheter

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160
Q

Rx of fungal UTI

A

There is no demonstrated benefit in treatment of asymptomatic infection

Exceptions made for renal transplant patients and patients who are to undergo elective urinary tract Sx

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161
Q

Features of pyelonephritis

A

Commonly associated with sepsis and septicaemia

Requires more aggressive Rx

Broad spectrum bios

Co-amoxiclav +/- gent

Imaging: calculi, structural cause

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162
Q

Rx of pyelonephritis?

A

Co-amoxiclav +/- gent

Cefuorxime +/- gent

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163
Q

Cxs of pyelonephritis?

A

Perinephric abscess

Chronic pyelonephritis- scarring, chronic renal impairment

Septic shock

Acute papillary necrosis

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164
Q

What are the most common causes of UTI

A

E Coli

Proteus

Klebsiella

Staph saprophyticus

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165
Q

What is the dipstick finding in UTI?

A

Nitrites + leucocytes +ve

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166
Q

Rx of UTI?

A

Timeothprim or nitrofurantoin

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167
Q

What is tabes dorsalis?

A

abes dorsalis, also known assyphilitic myelopathy, is a slow degeneration (specifically,demyelination) of the nerves primarily in the dorsal columns(posterior columns) of the spinal cord (the portion closest to the back of the body). These nerves normally help maintain a person’s sense of position (proprioception), vibration, anddiscriminative touch.

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168
Q

What are the routes of entry for meningitis?

A

Haematogenous spread

Direct implantation (e.g. surgery, LP)

Local extension (secondary to established infection)

And PNS into CNS (viruses)

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169
Q

Meningitis def:

A

Infection of the meninges and CSF

Dura mater

Pia mater

Arachnoid mater

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170
Q

Symptoms of meningitis

A

Headache

Stiff neck

Soome disturbance of brain function

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171
Q

Organsisms causing meningitis

A

N meningitidis

Pneumococcus

H influenzae

L monocytogenes

GBS

E Coli

Staph aures

Treponema pallidum

TB

Virus

Cryptococcus neoformans

Candida

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172
Q

Grows on chocolate agar, gram negative cocci=

A

N meningitidies

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173
Q

Transmission of N meningitidis

A

Person-person from asymptomatic carriers

Pathogenic strain found in only 1% of carriers

Through nasopharyngeal mucosa in susceptible individuals

Causes infection in less than 10 days

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174
Q

Outcome of N meningtiides infection

A

Septicaemia in 7-10%

Meningitis in 50%

Both in 40%

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175
Q

NB re LP in septicaemia?

A

Coagulopathy…

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176
Q

Neuropathology of N. meningitis

A

Direct bacterial toxicity, indirect inflammatory process and cytokine release and oedema

Shock seizures and cerebral hypoperfusion

10% mortality with 5% of survivors having neurological sequelae (predominantly sensorineural deafness)

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177
Q

Clinical spectrum of septicaemia?

A

Produced by four processes

Capillary leak: albumin, and other plasma proteins leading to hypovolaemia

Coagulopathy: leads to bleeding and thrombosis

Metabolic derangement: acidosis

Myocardial failure and multi-organ failure

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178
Q

Acute meningitis

A

Usually bacterial

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179
Q

Chronic meningitis

A

Headaches for months

TB or cryptococcus or spirochetes

More common in immunosuppressed

Involves the meninges and basal cisterns of the brain and SC

Can result in tuberculous granulomas, abscesses or cerebritis

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180
Q

Aspetic meningitis

A

Usually acute biral, most common CNS infection

Presents with headache, fever, neck stiffness, photophobia

Non-specific rash

Most frequent in children younger than 1y

Self-limiting course that resolves in 1-2w

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181
Q

Most commo organisms causing aseptic meningitis

A

80-90% caused by coxsackie virus group B and echoviruses

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182
Q

Most common causes of bacterial meningitis in enonates

A

GI flora: GBS, L monocytogenes, E Coli

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183
Q

Most common cause of bacterial meningitis in elderly

A

GBS

Listeria

MTB (subacute)

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184
Q

What is another important cause of aseptic meningitis

A

HSV

Remember to ask re symptoms of HsV infection

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185
Q

Def: encephalitis

Symptoms

A

Infection of the brain parenchyma

(Meningoencephalitis- inflammation of the meninges and brain parenchyma)

Disturbances of brain function

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186
Q

Organisms causing encephalitis?

A

Rabies

Arboviruses

Trapanasome brucei gambiense

TB

Prions

Amoeba

West Nile

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187
Q

Features of Brain abscesss

A

SOL on imaging: looks like cancer, needs histopathology to say which

Spreads from otitis media, mastoiditis, paranasal sinuses, endocarditis, haematogenously

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188
Q

Organisms likely to cause brain abscesses

A

Streptococci

Staph

Gram negative (particulalry in neonates)

MTB

Fungi

Parasites

Actinomyces

Nocardia specias

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189
Q

Def: myelitis

A

Infection of the spinal cord

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190
Q

What is a common form vertebral infection?

Spread?

Px?

A

Pyogenic vertebral osteomyelitis

Direct pen trauma, infections in adjacent structures, from haematogenous spread

If left untreated can lead to permanent neurological deficit, significant spinal deformity or death

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191
Q

Symptoms of myelitis

Significant organism?

A

Disturbance of nerve transmission

Polio

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192
Q

What are the factors for myelitis

A

Advanced age

IVDU

LT-systemic steroids

DM

Organ transplantation

Malnutrition

Cancer

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193
Q

Neurotoxin causing rigid paralysis?

A

Tetanus from C tetani

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194
Q

Neurotoxin causing flaccid paralysis?

A

Botulism

C botulinum

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195
Q

Risk factors for N meningitis?

A

Complement deficiency

Hyposplenism

Hypogammaglobulinameia

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196
Q

Risk factors for Strep meningitis?

A

Complement deficiency

Hyposplenism

Immune defect (ETOH)

Infection (pneumonia)

Entry #

Previous head trauma with CSF leak

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197
Q

Gram -ve cause of meningitis?

A

Neisseria

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198
Q

Gram +ve cause of meningitis?

A

Strep pneumoniae

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199
Q

MRI in meningitis

A

Better than CT in detecting parenchymal abnormalities such as abscesses and infarctions

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200
Q

Meningitis Ix

A

Clinical and blood cultures

Throat swabs (neisseria)

Serum-Ag

EDTA-PCR

CSF: WCC, protein, glucose

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201
Q

Different types of CSF study

A

Colour/clarity

WCC/differentaition

Protein, glucsoe

Culture: blood agar, chocolate agar, sabourand’s agar

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202
Q

Limitations of the Ix in meningitis?

A

MRI oedema pattern and moderate mass effect cannot be differentiated from tumour or stroke or vasculitis

Abx given before culture samples

Amount of CSF

PCR

Methods to detect amoebic infections

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203
Q

CSF:

Clear

0-5 leukocytes

Negative gram stain or Ag test

Protein 0.15-0.4

Glucose 2.2-3.3

A

Normal

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204
Q

CSF normal WCC

A

0-5

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205
Q

Protein CSF normal?

A

0.15-0.4

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206
Q

CSF glucose?

A

2.2-3.3 (>50% serum)

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207
Q

CSF:

Turbid

100-200 polymorphs

Positive gram stain

0.5-3 on protein (raised)

Reduced glucose

A

Bacterial menintisi

?Meningococcus

?pneumococcus

?Listeria

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208
Q

CSF: clear or slightly turbid

15-500 lymphocytes

Negative gram stain

0.5-1 protein

Normal glucose

A

Aseptic meningitis

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209
Q

CSF:

Clear or slighlty turbid

300-500 mixed lymphocytes and polymorphs

Negative gram satin

Raised protein

Reduced glucose

A

MTB or cryptococcal meningitis

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210
Q

CSF:

Glucose normal

WCC high with polymorphs

A

Think partiall treated bacterial infection

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211
Q

What CNS infections may show a normal CSF?

A

Cerebral abscesses (Streptococci)

Viral encephalitis

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212
Q

Mx of bacterial meninigits

A

ABC

Corticosteroids before Abx

Ceftriaxone (2g IV BD) for pneumo and meningococcus

If elderly/immunocompromsied add amoxicillin or ampicillin to cover for Listeria)

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213
Q

Mx of Meningoencephalitis

A

Aciclovir

Ceftriaxone

If >50y or immunocompromised add amoxicillin for Listeria cover 2g IV 4 hourly

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214
Q

Mx of aseptic meningitis

A

Give ceftriaxone until you know it is herpes, no aciclovir

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215
Q

Doses of ceftriaxone?

A

2g IV BD

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216
Q

Dose of acicvlovir?

A

10mg/kg IV TDS

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217
Q

Dose of amoxicillin

A

2g IV 4 hourly

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218
Q

What are the features of the Glasog Meningococcal Septicaemia prognostic score?

A

Systolic BP

Skin-Rectal T difference

Modified coma scale

Deterioration

Neck stiffness

Extent of purpura

Base deficit

Used as a tool to identify those who may need transfer to a tertiary centre with a PICU

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219
Q

Kwashiorkor?

A

Acute form of childhood protein-energy malnutrition: oedema, anorexia, ulcerating dermatoses and heaptomegaly

Insufficient protein consumption but with sufficient calorie intake

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220
Q

Marasmus

A

Severe malnutrition, charactersied by energy deficiency. Emaciated

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221
Q

What are the Helminth diseases?

A

Schistosomiasis

Hookworm

Threadworm

Filiarisis

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222
Q

What are the protozoal dieases?

A

Leishmaniasis

Typanosomoiasis

Amoebiasis

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223
Q

Def: Sanitation

A

The state of being clean and conductive to health

The hygienic separation of human waste form contact. Safe containment, transporation, treatment and disposal of human excreta

Primary barrier to disease transmission

Fluids, fields, flies, fingers and food

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224
Q

Features of Hep A

A

Acute hepatitis, ofetn subclinical, short period 2-6w

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225
Q

Transmission of Hep A

A

Faecal-oral spread

Outbreaks associated with occupational risk e.g. sewage workers.

Soft fruit, sewage works, shellfish

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226
Q

anti-HAV IgM

A

Recent infection disappears after a few months or vaccine

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227
Q

anti-HAV IgG

A

Previous infection, lifelong or vaccine

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228
Q

Which of the hepatitis vrisuses are RNA?

A

A

C

D

E

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229
Q

What type of virus is Hep B?

A

dsDNA virus

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230
Q

What is a good screening test for Hep V and why?

A

Vrisu makes an excess of surface antigen

Therefore it is a good screening ttest

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231
Q

What is the timefrime for Hep B infection?

A

Acute <6m

Chronic

Latent virus can reactivate in immunocompromised

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232
Q

Transmission of Hep B

A

Sexual, vertical, horizontal

Blood products

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233
Q

Clinical picutre for Hep B

A

Causes and acute or chronic heaptitis

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234
Q

Pathophysiology in Hep B

A

Over decades leads to scarring and cirrhosis, eventually resulting in HCC. This is accelerated in males and drinkers

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235
Q

Mx of Hep A

A

Supportive

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236
Q

Mx of Hep B

A

Pegylated IFn alpha 2a

Lamivudine

Tenofovir

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237
Q

When is Hep B treatment initiated?

A

When liver damage occurs

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238
Q

Dx of Hep B?

A

ALT and AST

HbsAg

HBeAg (infectivity, changes form +ve to negative)

HBcAb (acute- IgM, chronic IgG)

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239
Q

Timeframe in Hep C infection

A

Acute,

80% progress to chronic

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240
Q

Transmission of Hep C

A

Blood products

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241
Q

How does the Hep C genotype inform treatment?

A

Genotpyes 1 and 4= 48w

2&3= 24w

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242
Q

Dx of Hep C

A

ALT

Anti-HCV

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243
Q

Mx of Hep C

A

Cure 54% treated with peg IFN alpha-2b and ribavirin combination therapy.

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244
Q

Considerations around Peginterferon alpha 2-b

A

Attacks bone marrow: low WCC, low platelets

Can lead to depression

Care in treating cirrhotic patients as will kill infected hepatocytes

Kidney trransplant is contraindication for IFN

Wariness about treating genotypes 1 and 4 and in elderly patients as there is less chance of a response and treatment is expensive

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245
Q

Hep D features

A

Only infect Hep B patients.

Transmitted through contaminated blood

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246
Q

Features of Hep B and D infection

A

Superinfection and likely to have a very acute hepatitis and develop cirrhosis in 2-3y

Treat with prolonged course of IFN

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247
Q

Hep E features

A

Faeco-oral spread

Mainly seen in tropical areas

Causes GI symptoms e.g. cramps, pain.

High mortality rate, esp in pregnant.

Usually just acute but can cause chronic if untreated

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248
Q

What are the different types of diarrhoea?

A

Secretory

Inflammatory

Enteric fever

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249
Q

What is the mechanism of secretory diarrhoea

A

Toxin production affecting the lumen

No fever or a low grade fever

No white cells on stool sample

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250
Q

What is the mechanism for inflammatory diarrhoea

A

Invasion of bacteria into the lamina propria causing exudative into the lumen or intiaiing an innate immune response mainly through LPS acting on TLR4,5

Fever, WBCs in stool samples, neutrophils +/- blood

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251
Q

What are two common causes of secretory diarrhoea?

A

Cholera toxin

Superantigens from E COli

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252
Q

What bacteria can cause an inflammatory diarrhoea?

A

C jejuni

Shigella

Atypical salmonella species

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253
Q

What is the mechanism for enteric fever?

A

Invasion, Peyer’s patches, interstitial inflamamtion, monocytes, innate immune response

Fever, WBC in stool, can be blood

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254
Q

Causes of enteric fever?

A

Typphoidal, salmoneall subtypes, enteropathic Yersinia spp. Brucella spp.

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255
Q

What differentiates between inflammatory diarrhoea and enteric fever

A

Depends on immune status of patient

Both have bacteraemia

If immunocompetenet there is interstitial inflammation aned enteric fever

If they are immunocompromised there is exudative inflamamtion and exudative diarrhoea. This leads to neutrophilia and spetic shock

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256
Q

What are the anaerobic causes of Gi infection

A

Clostriida:

botulinum

perfringens

difficile

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257
Q

What differentiates between GBS and botulism?

A

Botulism is a descending paralysis

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258
Q

Treatment of botulism

A

Antitoxin

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259
Q

C botulinum infeciton

A

Canned/vacuum packed foods: honey, beans

(ingestion of preformed toxin which would usually be inactivated by cooking0

Blocks Ach from peripheral nerves leading to paralysis

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260
Q

Features of C perfringens

A

Reheated meats, superantigen enterotoxin leads to massive cytokine production by CD4 leading to systemic toxicitiy

Acts on small bowel

Watery diarrhoe and cramps lasting 24hrs

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261
Q

What bacteria causes gas gangrene?

A

C perfringens

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262
Q

Features of C difficile

A

2 endotoxins (A and B)

Causes pseudomembranous colitis

Caused by Abx use, usually cephalosporins and fluorguinoloines

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263
Q

Mx of C diff

A

PO metronidazole

2nd line Vanco

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264
Q

Which antibiotics are associated with C diff infection

A

Cephalosporins/fluoroquinolones

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265
Q

What are the aerobic bacteria causing GI infection?

A

Bacillus cereus

S. aureus

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266
Q

Featuers of B cereus GI infection

A

Reheated rice, spores gerimnate. Sudden vomiting

Superantigen

Watery, non bloody diarrhoea

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267
Q

Mx of B cereus infection

A

Self-limiting

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268
Q

Features of S. aureus GI infection

A

Prominent vomiting and watery non bloody diarrhoea

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269
Q

Main virulence fctor i protein A.

Catalase, coagulase +ve

Appears in tetrads

Clusters on gram stain

Beta haemolytic on blood agar

A

S aureus

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270
Q

Mx of S. auerus GI infection

A

Don’t treat, self limited

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271
Q

Lactose fermenting cause of GI infection?

A

Gram -ve enterobacteriacae (faculative anaerobes, oxidase negative)

E. COli

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272
Q

What are the strains of E Coli causing GI infection?

A

ETEC

EIEC

EHEC

HUS

EPEC

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273
Q

ETEC

A

Toxigenic E coli, travellers diarrhoea.

Food/water contaminated with human faecaes

Enterotoxins: Heat labile: stimulates adenyl cyclase and cAMP

Heat stable: stimulates guanylate cyclase

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274
Q

EIEC

A

Invasive dysentry

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275
Q

EHEC

A

Haemorrhagic E Coli: caused by verotoxin

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276
Q

HUS

A

E Coli 01571:H7 toxin

Anaemia, thrombocytopenia, renal failure

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277
Q

EPEC

A

Infantile diarrhoea

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278
Q

Mx of E Coli

A

Self-limiting but can treat with ciprofloxacin if needed

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279
Q

Non lactose fermenters causing GI infection

A

Salmonella

Shigella

Yersinia

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280
Q

O, H, Vi Ag’s

H2S produces

TSI agar

XLD agar

Selenite F broth

A

Salmonella

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281
Q

What are the three species of Salmonella

A

Typhi (and paratyphi)

Enteritidis

Cholearsuis

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282
Q

Features of Salmonella Enteritidis

A

Transmitted from poultry, eggs, meat

Invades small and large bowel

Bacteraemia is infrequent

Self-limiting

Blood

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283
Q

Mx of S. enteritides

A

Ceftriaxone or ciprofloxacin (if required)

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284
Q

Features of S. Typhi

A

Human trtansmission

Multiplies in Peyer’s patches

Bactaeremia, 3% become carriers (gallbladder)

Slow onset fever + constipation

Splenomegaly and rose spots

Aneamia and leukopaenia

Haemorrrhage and perforation

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285
Q

Slow onset fever + constipation

Splenomegaly and rose spots

Aneamia and leukopaenia

Haemorrrhage and perforation

A

S. Typhi

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286
Q
A

Rose spots

Enteric (Typhoid) fever

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287
Q

Non-lactose fermenters, non H2S producers, non-motile

A

Shigella

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288
Q

Mx of Salmonella typhi

A

Ceftriaxone or ciprofloxacin

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289
Q

Features of Shigella

A

Mainly affects the distal ileum and colon.

Infalmmation, fever, pain, bloody diarrhoea

Dysentry

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290
Q

Mx of shigella

A

Avoid Abx, ciprofloxacin if required

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291
Q

Non-lactose fermenting preferring cold temperatures cause of GI infection

A

Yersinia enteroclitis

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292
Q

Features of Yersinia enterocolitis infection

A

Enterocolitis, mesenteric adenitis with necrotising granulomas

Associated reactive arthritis and erythema nodosum

Reye’s syndrome

Transmitted via food contaminated with domestic animal excreta

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293
Q

What are the different species of Vibrios

A

Cholear

Parahaemolyticus

Vulnificus

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294
Q

Curved, comma shaped, late lactose fermenters, oxidase positive

A

Vibrios

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295
Q

Features of Vibrio cholera

A

Rice water stool, human faecas

Increased cAMP causes massive diarrhoea without inflammation

O1 group: epidemic

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296
Q

Mx of cholera

A

Supportive

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297
Q

Features of vibrio parahaemolyticus

A

Ingestion of raw or undercooked seafoood

Major cause of diarrhoea in Japan or in the carribean

Self-limiting

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298
Q

Features of Vibrio Vulnificus

A

Cellulitis in shellfish handlers

Fatal septicaemia with D+V in HIV

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299
Q

Mx of vulnificus and parahaemolyticus

A

Doxy

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300
Q

Features of C jejuni

A

Drinking unpasteurised milk, food, egg

Prodrome of headache and fever with abdominal cramps

Bloody (foul smelling diarrhoea)

Associated with GBS, reactive arthritis

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301
Q

Mx of C jejnuni

A

Erythromycin or cipro if first 4-5/7

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302
Q

Curved, S sjaped, microaeriphilic, oxidase positive, motile, sensitive to nalidixic acid

A

Campylobacter

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303
Q

V or L shaped, beta haemolytic

Aesculin positive with tumbling motility

A

L monocytogenes

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304
Q

Features of Listeria GI infection

A

GI watery diarrhoea, cramps, headache, fever, little vomiting

Perinatal infection, immunocompromised patients

Refrigerated foods: unpasteurised dairy, vegetables

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305
Q

Mx of Listeria

A

Ampicillin

Ceftraixone

Cotrimoxazole

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306
Q

What are the protozoa causing GI infection

A

Entamoeba histolytica

Giardia lamlia

Cryptosporidium parvum

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307
Q

Protozoa

MSM, food, water, soil

A

Entamoeba histolytica

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308
Q

Protozoa

Travellers, hikers, MSM, mental hospitals

A

Giardia

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309
Q

Motile trophozoite in diarrhoea

Non-motle cyst in non-diarrhoeal illness

4 nuclei

A

Entamoeba histolytica

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310
Q

Flask shaped ulcer on histology

A

Entamoeaba

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311
Q

Features of Entamoeba infection

A

Dysentry

Wind

Tenesmus

Chronic weigtht loss and RUQ pain due to liver abscess

Stool microscopy

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312
Q

Mx of entamoeba histolytica

A

Metronidazole and paramomycin (if luminal disease)

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313
Q

Pear shaped 2 trophozoite with 2 nuclei and trophozoites and cysts in stooll

A

Giardia

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314
Q

Foul smelling, non-bloody diarrhoea

A

Giardia

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315
Q

Mx of Giardia

A

Metronidazole

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316
Q

Features of cryptosporidium

A

Infects jejunym

Severe diarrhoea in immunocompromised

Oocysts seen in stool by modified Kinyoun acid-fast stain

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317
Q

Mx cryptosporidum

A

Paromomycin

Nitazoxanide

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318
Q

What are the viruses causeing secretory diarrohea

A

Rotavirus

Adenovirus

Norovirus

Poliovirus

Enteroviruses (coxsackie, ECHO)

Hepatitis A

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319
Q

Features of rotavirus infection

A

Secretory diarrhoea with no inflammation

Watery diarrhoea through stimulation of the enteric nervous system

Very common in children <6.

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320
Q

Which types of adenovirus cause non bloody diarrhoea?

Which age group are affected?

A

Types 40, 41

<2y/o

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321
Q

Gram +ve

Aerobic

Acid alcohol fast

Thick waxy cell wall

A

Mycobacteria

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322
Q

Mycolic actids

A

Mycobacteria

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323
Q

Cough +/- haemoptysis

Fever with night sweats

Weight loss

Malaise

Ethnicity

A

Mycobacteria

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324
Q

Post primary TB occurs in?

A

Young adults

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325
Q

Features of post-primary TB

A

?Re-activation/re-infection

Upper lobes- may progress rapidly to cavitation

Caseating granuloma

Miliary spread rare

Healing by fibrosis and calcification

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326
Q

1st line treatment for TB

A

RIPE

Rifampicin and isoiazid for 6/12

Pyrazinamide and ethambutol for 2/12

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327
Q

Treatment of TB meningitis

A

Increase isoniazid and rifampicin to 8-10/12

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328
Q

Treatment of latent TB

A

6/12 isoniazid

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329
Q

Side effects of Rifampicin

A

Drug interactions (raised transaminases, cytochrome p450 induction)

Orange secretions

Hepatotoxicity

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330
Q

Drug interactions (raised transaminases, cytochrome p450 induction)

Orange secretions

Hepatotoxicity

A

Rifampicin

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331
Q

Side effects of isoniazid

A

Peripheral neuropathy (give B6/pyridoxine

Hepatotoxcityi

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332
Q

Peripheral neuropathy (give B6/pyridoxine

Hepatotoxcityi

A

Isoniazid

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333
Q

Side effects of pyrazinamide

A

Hyperuricaemia

Hepatotoxicity

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334
Q

Hyperuricaemia

Hepatotoxicity

A

Pyrazinamide

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335
Q

Side effects of ethambutol

A

Optic neuritis

Visual disturbance

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336
Q

Optic neuritis

Visual disturbance

A

Ethambutol

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337
Q

Additional considerations in treating TB

A

DOTS

Vit D therapy

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338
Q

Why is Vit D therapy important in treatment of TB

A

Accelerates clinical recovery

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339
Q

Mono resistant TB=

A

Resistance to one drug only

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340
Q

Prophylaxis of TB

A

Isoniazid

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341
Q

MDRTB=

A

Resistance to rifampicin and isoniazid

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342
Q

XDRTB=

A

Resistance to rifampicin, isoniazid and injectables (kanmycin/amikacin)/ quinolones

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343
Q

Injectables used as 2nd line in TB

A

Capreomycin

Kanamycin

Amikacin

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344
Q

What are the second line TB treatments

A

Injectables

Quinolones

Cycloserine

Ethionamide

PAS

Linelozid

Clofazamine

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345
Q

Subacute presentation

Weight loss, fever, neck stiffness

Personality change

Reduced GCS

Focal neurological signs

A

TB meningitis

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346
Q

Dx if TB meningitis

A

CT- tubercolmata

LP- lymphocytic

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347
Q

Lymphadenitis

Pericarditis

Peritonitis/ileitis

Genito-urinary, renal testicular

Skin liver etc

(maybe +HIV positive)

A

Extrapulmonary TB

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348
Q

What is a Ghon focus

A

A Ghon focus is a primary lesion usually subpleural, often in the mid to lower zones, caused by mycobacterium bacilli (tuberculosis) developed in the lung of a nonimmune host (usually a child).

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349
Q
A

Ghon focus

Primary TB

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350
Q

Which patient group gets primary TB?

A

Nonimmunocompetent=

Elderly

Children

HIV

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351
Q

What is progressive primary TB?

A

Focus or node ulcerates into bronchus-> pneumonia

Cavity formation, bronchiectasis, consolidation, collapse

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352
Q

What is primary complex TB

A

TB taken by macrophase to LN, generalised lympho-haematogenous spread

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353
Q

Rich foci seen in?

A

Miliary TB

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354
Q
A

Miliary TB

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355
Q

Ix in TB

A

Imaging: CXR (upper lobe cavitation), CT

Culutre: Sputum x3, BAL, urine (EMU), Lowenstein Jensen medium (gold standard)

Sputum microscopy- ZN, auramine staingin: gram +ve, acid fast, aerobic intracellular rods

Tuberculin skin test

IGRA

NAAT

Liquid culture mediums

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356
Q

gram +ve, acid fast, aerobic intracellular rods

A

TB

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357
Q

Risk factors for contracting TB

A

Recent migrant

HIV+

Homeless

Drug user

Prison

Close contacts

Young adults/elderly

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358
Q

Risk factors for reactivation of latent TB?

A

Immunosuppression

Malnutrition

Ageing

Chronic alcohol excess

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359
Q

Fever, sweats, weight loss, back pain

A

?Spinal TB

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360
Q

Ix of spinal TB

A

MRI/CT +/- biopsy/aspirate

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361
Q

Treatment of spinal TB

A

12/12 anti-TB

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362
Q

Pathophysiology of spinal TB

A

Haematogenous spread

Initial discitis

Vertebral destruciton and collapse +/- anterior extension causing iliopsoas abscess

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363
Q

Potts Disease

A

Pott disease or Pott’s disease is a form of tuberculosis that occurs outside the lungs whereby disease is seen in the vertebrae. Tuberculosis can affect several tissues outside of the lungs including the spine, a kind of tuberculous arthritis of the intervertebral joints.

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364
Q
A

Potts Disease

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365
Q

What is the BCG vaccination?

A

Attenuated strain of M. Bovis

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366
Q

Efficacy of BCG

A

0-80%

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367
Q

Use of BCG

A

Bad for pulmonary TB

Good for leprosy, TB meningitis, disseminated TB

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368
Q

Inidications for BCG

A

Babies born in or with parents/grand parents from areas with incidence ?40/100000

Previously unvaccinated new immigrants from high prevalence countries for TB

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369
Q

HIV and TB

A

HIV-ve latent TB -> active TB 5-10% lifetime risk

HIV+ve, yearly risk is 5-10%

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370
Q

Hansen’s disease

A

Leprosy

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371
Q

What are the organisms causing Hansen’s disease

A

M. Leprae

M. Lepromatosis

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372
Q

Skin: depigmentation, macules, plaques, nodules, trophic ulcers

Nerves: thickened nerves, sensory neuropathy

Keratitis, iridocyclitis

Periostitis aseptic necrosis

A

Leprosy

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373
Q

Rx in leprosy

A

Rifampicin, dapsone, clofazimine (if multibacillary)

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374
Q

What is the immunological spectrum of leprosy

A

Tuberculoid

BT

Borderline

Lepromatous

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375
Q

Tuberculoid leprosy

A

Paucibacillary

TH1 mediated

Depigmented lesions

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376
Q

BT leprosy

A

Nerve damageq

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377
Q

BB leprosy

A

Multiple plaques

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378
Q

Lepromatous leprosy

A

Multibacillary

Th2 mediated

Neuropathic ulcers

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379
Q

What are the indicators that an infection is being caused by NT Mycobacteria?

A

Environmental

No person-person transmission

Associated with impaired immunity, poor response to standard anti-TB regime

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380
Q

What is MAIC?

A

M. avium intracellulare complex

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381
Q

Presentation of MAC in children

A

Pharyngeal/cervical addenitis

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382
Q

Pulmonary MAC

A

Underlying lung disease, resembles TB

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383
Q

Disseminated MAC seen in?

A

Cytotoxics, lymphoma

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384
Q

Features of MAC infection in AIDS?

A

Disseminated multibacillary infection

Mycobacteraemia

Consider in HIV patients with longstanding diarrhoea

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385
Q

What is fish tank granuloma caused by?

A

M. Marinarum

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386
Q

Single or clusters of papules/plaques in swimming pool/aquarium owners?

A

M. Marinarum

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387
Q

What causes Buruli ulcer

A

M. Ulcerans

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388
Q

Transmission of M. uclerans

A

By insects, tropics/australia

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389
Q

Treatment of M. Ulcerans

A

Rifampicin

Streptomycin

Sx

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390
Q

Painless early nodule

Slowly progressive leading to ulceration, scarring and contractures

Seldom fatal but with hideous deformity

A

Buruli ulcer

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391
Q
A

Buruli Ulcer

M. Ulcerans

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392
Q

Def: pneumonia

A

Inflammation of lung alveoli

Can be lobar or bronchopneumonia

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393
Q

Def: bronchitis

A

Inflammation of medium sized airways, mainly in smokers.

Cough with sputum most days for 3m or 2 or more consecutive years

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394
Q

Organisms in bronchitis

A

Viruses

S. pneumoniae

H. influenzae

M. catarrhalis

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395
Q

CXR in bronchitis

A

Often normal

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396
Q

Rx in bronchitis

A

Bronchodilation, PT +/- Abx

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397
Q

CURB 65

A

Confusion of new onset (defined as an AMTS of 8 or less)

Blood Urea nitrogen greater than 7 mmol/l (19 mg/dL)

Respiratory rate of 30 breaths per minute or greater

Blood pressure less than 90 mmHg systolic or diastolic blood pressure 60 mmHg or less

Age 65 or older

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398
Q

CURB 0-1

A

Treat as an outpatient

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399
Q

CURB 2

A

Consider hospital

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400
Q

CURB 3-5

A

Hospitalise

?ITU

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401
Q

What are te classical causes of pneumonia

A

S. Pneumoniae

H. influenzae

M. catarrhalis

S. aureus

K. pneumonia

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402
Q

Pneumonia with:

Rust coloured sputum

Lobar on CXR

A

S. pneumonia

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403
Q

Pneumonia with:

Smoking/COPD

A

H. influenza

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404
Q

Pneumonia with:

Smoking

A

M. catarrhalis

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405
Q

Pneumonia with:

Recent viral infection (post-influenza) and cavitaiton on CXR

A

Staph aureus

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406
Q

Pneumonia with:

Alcoholic

Elderly

Haemoptysis

A

Klebsiella

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407
Q

Pneumonia with:

+ve diplococci

A

Strep pneumoniae

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408
Q

Pneumonia with:

-ve cocci-bacilli

A

H. infleunza

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409
Q

Pneumonia with:

-ve cocci

A

M. catarrhalis

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410
Q

Pneumonia with:

+ve cocci in grape bunch clusters

A

S. aureus

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411
Q

Pneumonia with:

-ve rod, enterobacter

A

Klebsiella

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412
Q

Atypical pneumonia clinically

A

No signs or chest XR or signs not in keeping with CXR

May be extrapulmonary signs e.g. hepatitis, hyponatraemia

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413
Q

Causes of atypical pneumonia

A

Legionella

Mycoplasma

Chalmydia pneumonia

Chlamydia psittaci

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414
Q

Other causes of pneumonia

A

Bordatella pertussis

TB

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415
Q

Pneumonia with:

Travel, air conditioning, water towers

HEPATITIS

HYPONATRAEMIA

A

Legionella

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416
Q

Pneumonia with:

Systmic symptoms

Joint pain

Cold agglutination test

Erythema multifrome

RIsk of SJS, AIHA

A

Mycoplasma

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417
Q

Pneumonia with:

TWAR agent

A

Chlamydia pneumonia

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418
Q

Pneumonia with:

Birds in hx

A

Chlamydia psittaci

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419
Q

Pneumonia with:

Whooping cough in unvaccinated

A

Bordatella pertussis

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420
Q

Pneumonia with:

Poor response to Abx

A

TB

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421
Q

Causes of pneumonia in patient with:

HIV

A

PCP

TB

Cryptococcans

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422
Q

Causes of pneumonia in patient with:

Neutropenia

A

Fungi- aspergillus

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423
Q

Causes of pneumonia in patient with:

BMT

A

Aspergillus

CMV

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424
Q

Causes of pneumonia in patient with:

Spleenctomy

A

Encapsulated organisms: H. influenzae, S. pneumonia, N. meningitides

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425
Q

Causes of pneumonia in patient with:

CF

A

Pseudomonas aeruginosa

Burkholderia cepacia (v. high mortality)

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426
Q
A

Lobar pneumonia

Strep

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427
Q
A

Cavitating pneumonia

Staph aureus

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428
Q
A
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429
Q

Ix in pneumonia

A

Non microbiological: FBC, U&E, CRP, ABG, CXR

Microbiology: sputum MC+S, blood cultures, effusion aspiration/BAL

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430
Q

Test in severe CAP for S. pneumoniae and Legionella?

A

Urine antigen tests

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431
Q

What is the use of antibody tests in pneumonia

A

Paired serum samples at presentation and 10-14/7

Rise in Ab level over time

Useful for difficult to culture (chalmydia, legionella)

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432
Q

Silver stain, boat shaped oragnisms

A

PCP

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433
Q

Def: HAP

A

>48 hours into hospital stay without previous infection

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434
Q

What is BAL used for?

A

To differentiate URT and LRT microbes

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435
Q

CAP

Classical

Mild-moderate

A

Amoxicillin or macrolide 5-7d

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436
Q

CAP

Classical

Moderate-Severe

A

Clarithromycin + co-amoxiclav/cefuroxime (2-3w)

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437
Q

CAP

Atypical

(Chlamydia, Mycoplasma)

A

Macrolide/tetracycline

Clarithromycin

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438
Q

What is consideration re durg interaction of clarithromycin

A

Increases anticoagulant effect of Warfarin

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439
Q

HAP 1st line

A

Ciprofloxacin +/- vancomycin

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440
Q

HAP second line/ITU

A

Piptazobactam + vancomycin

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441
Q

Abx in aspiration pneumonia

A

Cefuroxime

Metronidazole

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442
Q

Legionella abx

A

Macrolide + rifampicin

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443
Q

Staph aureus Abx

A

Fluclox

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444
Q

Pseudomonas Abx

A

Piperacillin + tazobactam (tazocin) or ciprofloxacin +/- gentamicin

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445
Q

Causative organism in HAP

A

Coliforms and pseudomonas more likely the longer the stay

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446
Q

Coliform bacteria

A

Escheria

Klebsiella

Citrobacter

Enterobacter

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447
Q

Causes of ventilator associated pneumonia

A

P. aeruginosa, acinetobacter, stenotrophomonas maltophilia

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448
Q

Alcoholic, acute SOB, fever, dirty brown sputum, pleuritic
chest pain, malaise, N&V
o Examiniation: tachypnoea, tachycardia, dullness to
percussion, crackles

A

Pneumococcal pneumonia

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449
Q

Army cadet, 2 week hx, headache, malaise, non-productive cough, examination unremarkable,
normal inflammatory markers

A

Mycoplasma pneumoniae

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450
Q

Confusion, fever, headache, myalgia, abdominal pain and diarrhoea.
o Low sodium and deranged LFTs

A

Legionella

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451
Q

MOA aciclovir

A

Guanosine analogue, blocks viral DNA extension through activation by thymidine kinase present in HSV

NB CMV doesn’t have this enzyme

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452
Q

Indication aciclovir

A

HSV

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453
Q

Indication ganciclovir

A

CMB, EBV, HHV-6

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454
Q

MOA ganciclovir

A

Nucleoside analgoue

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455
Q

SE of ganciclovir

A

BM suppression

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456
Q

RCHEP

A

CMV conseuqnecs

Retinitis

Colitis

Hepatitis

Encephalitis

Pneumonitis

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457
Q

Owl eye inclusions=

A

CMV infected cells

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458
Q
A

CMV infection

Owl eye inclusions

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459
Q

What is used as an alternative to ganciclovir if resistant/severe side effects

A

Foscarnet

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460
Q

MOA foscarnet

A

pyrophosphate analgoue. Inhiits nucleic acid synthesis without requring activation

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461
Q

Foscarnet indication

A

Used when CMV resistant to ganciclovir

Also used as prophylaxis post organ transplant

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462
Q

MOA Cidofovir

A

Nuceloside phosphonate

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463
Q

Indications Cidofovir

A

CMV retinitis

Often used in treatment of non-herpes viral infections in opportunistive post-transplant setting e.g. BK virus for BK nephropathy/BK cystitis/adenovirus/PML (JC virus)

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464
Q

What is a consideration re Foscarnet and cidofovir

A

Nephrotoxic

Maintain hydration and co=administer probenecid

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465
Q

HSV infection

Act Very Fast

A

Acyclovir

Valaciclovir

Famciclovir

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466
Q

Foscarnet/cidofovir in herpes infection

A

If it s resistant

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467
Q

When to treat VZV?

A

Immunocompromised

Pregnants

Adults with pneumonitis

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468
Q

Treatment of CMV in BMT

A

Pre-emptive therapy: monitor CMV viral load during high rrisk period

Acute therapy: reduce immunosuppression

1st line: ganciclovir (BM toxicity)

2nd line: foscarnet (+GCV) (nephrotoxic)

3rd line: cidofovir (nephrotoxic)

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469
Q

What determines when to treat HBV

A

Serum HBV DNA levels (>2000IU)

Serum transaminitis (above normal limit)

Liver biopsy histological grade and stage: moderate-severe active necroinflammation and or fibrosis

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470
Q

Treatment goals in HBV Rx?

A

Prevent progression to cirrhosis and HCC

Maintain serum HBV DNA as low as possible

Attain histological improvement

ALT normalisation

Loss of HBVeAg and seroconversion to HBVeAb

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471
Q

What are the drugs used in HBV Rx?

A

Pegylated INF alpha 2a

Nucelos(t)ide analogues

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472
Q

What is the MOA of INFa2a

A

Direct antiviral effect and upregulates expression of MHC on cell surfaces

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473
Q

(HBV) MOA:

Lamivudine

A

Inhibitor of viral polymerase

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474
Q

(HBV) MOA:

Adefovir dipivoxil

A

Inhibitor of viral polymerase

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475
Q

(HBV) MOA:

Entecavir

A

Inhibitor of viral polymerase (no resistance)

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476
Q

(HBV) MOA:

Telbivudine

A

Inhibitor of viral polymerase

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477
Q

(HBV) MOA:

Tenofovir

A

Inhibitor of reverse transcriptase

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478
Q

What is the preferred first line treatment in HBV infection?

A

Entecavir

PegINF a2a

Tenofovir

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479
Q

What is the treatment goal in HCV?

A

Sustained virologic response: persistent absence of HCV RNA in serum >6/12 after completing antiviral treatment

Prevent progression to cirrhosis, HCC or decompensated liver disease requiring treatment

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480
Q

MOA Ribavirin

A

RNA nucleoside analgoue

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481
Q

Major SE of ribavirin

A

Haemolytic anaemia

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482
Q

Treatment of HCV

A

PegINF a2a

Ribavirin

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483
Q

Which HCV genotypes have a worse treatment prognosis?

A

1,4,5,6

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484
Q

Which HCV genotypes have a better treatment outcome

A

2 and 3

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485
Q

What is the MOA and indication of:

Zanamivir (INH)

A

IFVA

NA inhibitor

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486
Q

What is the MOA and indication of:

Oseltamavir

A

IFVA

NA inhibitor

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487
Q

M” cWhat is the MOA and indication of:

Amantidine

A

M2 Channel

IFVA

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488
Q

What is the MOA and indication of:

Ribavirin

A

RSV/ parainfluenza

Guanosine analgoue

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489
Q

Live atttenuated vaccines=

A

MMR

Yellow fever

BCG

OPV

Varicella

Typhoid

Flu

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490
Q

Inactivated vaccines=

A

Rabies, pertussis, IPV, Hep A, typhoid

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491
Q

Recombinant protein vaccine=

A

HBV

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492
Q

Subunit vaccines=

A

Hib

Men C

PCV

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493
Q

Toxoid vaccines=

A

Tetanus

Diptheria

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494
Q

What causes SSPE?

A

Subacute sclerosing pancencephalitis

Measles

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495
Q

Special risk groups for vaccines

A

Pts on CTx, pts <6/12 after BMT, children on high dose steroids +/- cytotoxics

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496
Q

Can HIV patients be given MMR?

A

Yes if susceptible

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497
Q

What does DTP cause (side effect)

A

Anaphylaxis

Protracted crying

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498
Q

What does OPV/IPV vaccine cause (side effect)

A

Poliomyelitis (OPV)

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499
Q

What does measles vaccine cause (side effect)

A

Thrombocytopenia

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500
Q

What does rubella vaccine cause (side effect)

A

Acute arthritis

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501
Q

Should HIV patients be given BCG and yellow fever vaccines?

A

No

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502
Q

Sx: SOB, green sputum, fever. Hypoxic, heavy smoker.
o X ray: shadowing, ground glass changes and hypoxia exacerbated by exercise.
o Immunosuppression – HIV

A

PCP

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503
Q

Widespread lung fibrosis with ground glass shadowing on histology with a cough

A

PCP

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504
Q

India ink with halo=

A

Encapsulated yeast i.e. cryptococcus

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505
Q

Mx of CPC

A

Co-trimoxazole and oral prednisolone

2nd line= clindamycin and primiquine. IV methylprednisolone

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506
Q

Aerobic gram positive rod with branches

Seen in relatively immunocompromised patients, produces copious amounts of pus in abscess

Commo in alcohlics

Associated with lung abscess or pelvic asbscess

Slow growing and hard to treat

A

Actinomyces

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507
Q

How does rifampicin help in septic arthritis?

A

Affects biofilm formation

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508
Q

What are the STIs causing discharge?

A

Gonorrhoea

Chlamydia

Trichomonas

Candida

BV

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509
Q

What are the STIs causing ulceration?

A

Syphillis

HSV

LGV

Chancroid

Donovanosis

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510
Q

What are the STIs causing rashes/lumps/growths

A

Genital warts- HPV

Molluscum contagiosum

Scabies

Pubic lice

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511
Q

Painful genital ulcers=

A

Herpes

Chancroid

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512
Q

Painless genital ulcers=

A

Syphillis

Lymphogranuloma venereum

Granuloma inguinale

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513
Q

Obligate intracellular Gram -ve diploccocus causing STI

A

N. gonorrhoea

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514
Q

Opthalmia neonatorum=

A

Conjunctivitis that develops if gonorrhoea left untreated when child transfers to birth canal

515
Q

What happens in N. gonorrhoea infection in patients with complement deficiencies?

A

Get disseminated gonococcal infection- septicaemia, rash and or arthritis

516
Q

Dx of Gonorrhoea

A

Urethral/rectal smears

Culture from these is gold standard

517
Q

Treatment of gonorrhoea

A

Ceftriazone IM-250mg one dose

or cefixime PO 400mg single dose

518
Q

Treatment of resistant gonorrhoea?

A

Spectinomycin IM 2g single dose

519
Q

What is the most most common STI in Europe

A

Non-gonoccocal urethritis

520
Q

Features of NGU

A

Mucoid/mucopurulent discharge

521
Q

What is PGU

A

Post gonococcal urethritis

Follows gonorrhoea Rx

Can be prevented by concomittant Rx with tetraceline

522
Q

Rectal prostatitis in gonorrhoeal infection seen in

523
Q

Complicated gonorrhoea infectio in men=

A

Prostatitis

524
Q

Common manifestation of gonorrhoeal infection in women=

A

Mucopurulent cervicitis

Erythema and oedema

Urethra from vaginal leakage

525
Q

What is the most common cause of increased infertility in Europe?

526
Q

Gram negative obligate intracellular pathogen involved in STIs that cannot be cultured on agar?

A

Chlamydia trachomatis

527
Q

Symptoms of C. trachomatis infection

A

Often assymptomatic (50% men, 80% women)

528
Q

What is the growth cycle of C. trachomatis?

A

Exists ion 2 forms

Elementary bodies: stable, extracellular

Reticulate particles: intracellular, metabolically active

529
Q

What are the A,B.C chlamydia serovars associated with?

A

Trachoma which can cause blindness

530
Q

What are the D-K Chlamydia serovars associated with?

A

Genital chlamydia, opthalmia neonatorum

531
Q

What are the Cx of chlamydia infection?

A

PID

Tubal factor infertility

Increased risk of ectopics

Increased risk of endometriosis

Chronic pelvic pain

Epididymitis

Reiters

Adult conjunctivitis

Opthalmia neonatorum

532
Q

Dx of chlamyydia

A

NAAT= gold standard

533
Q

Rx of chlamydia

A

Azithromycin 1g (4 capsules) STAT

Doxycycline 100mg BD 7/7

Erythromycine 500mg QDS 7/7 or 500mg BD 2/52

534
Q

SE of doxycycline

A

N+V

Photosensitivity

C/I in pregnancy

535
Q

SE of erythromycin

536
Q

What is LGV

A

Lympho-granuloma venereum

Lymphatic infection with chlamydia trachomatis serovars L1, L2, L3

537
Q

What is associated with chlamydia infection with serovars L1, 2 and 3

A

Lymphogranuloma venereum

539
Q

What are the stages of LGV?

A

Early LGV Primary

Early LGV Secondary

Late LGV

Current LGV outbreak

540
Q

What are the features of primary early LGV

A

3-12/7

Genital ulcer, painless, non-indurated, balantitis, proctitis, cervicitis

541
Q

Features of secondary early LGV

A

2-25/52

Inguinal buboes: painful, 2/3rd unilateral

May rupture

Fever, malaise

Rarely (hepatitis, meningo-encephalitis, pneumonitis)

Proctocolitis

Hyperplasia of lymphoid tissue

542
Q

Features of late LGV

A

Inguinal lymphadenopathy

Abscess formation

Genital elephantiasis

Genital ulcers

Frozen pelvis

Rectal strictures

Peri-rectal abscesses + fistulae

Lymphorroids

543
Q

Features of current LGV outbreak

A

Rectal symptoms- pain, tenesmus, bleeding, mucus discharge

O/E: proctitis

544
Q

Dx of LGV

A

NAAT (currently unlicensed)

If positive will be sent to HPA

Confirmation of C trachomatis by RT-PCR on 2 platforms

And identification of L1-3 serovars

545
Q

Rx LGV

A

Doxycycline 100mg BD for 21/7

Erythromycin 500mg QDS for 21/7

Azithromycin 3/52 1g weekly

546
Q

Obligate gram-negatve spriocahete causing STI=

A

Treponema pallidum (Syphillis)

547
Q

Epidemiology of syphillis

A

Majority of cases are in those who are HIV +ve

Patients often co-infected with HCV or another STI

548
Q

Detection of treponemas

A

Seen in primary lesions by dark-ground micrscopy

Can be detected with RT-PCR

549
Q

What are the diagnostic methods for syphillis

A
  1. Non-treponemal tests:

Detect nonspecific antigens

VDRL: detects lipoidal antiboddy (can get biological false +ves)

RPR is modified VDRL test, positive is indicative of treponemal infection.

Used in primary syphillis.

Can be used to monitor treatment response.

  1. Treponemal tests:

Detect Ab against specific Ags from T .pallidum

e.g. EIA, FTA, TPHA, TP-PA

More specfic than non-treponemal test but remains positive after infection treated

550
Q

What are the phases of syphillis infection

A

Primary

Secondary

Latent

Tertiary

551
Q

What are the features of primary syphillis

A

Macule-> papule-> induracted painless genital ulcer appearing 1-12w following transmission.

Often solitary

May persist for 4-6w= CHANCRE

Clean base with serous exudate

Regional LNadeopathy

552
Q
A

Chancre

Syphillis

553
Q

What are the features of secondary syphillis

A

Systemic bacteraemia with low grade fever, mailaise

Symmetrical, non-pruritic, maculopapular rash on back, trunk, arms, legs, soles face 1-6/12 following infection

Mucosal lesions, uveitis, choroidoretinitis, elopecia

Snail track oral uclers

Condyloma cuminate

Neurological involvements (aseptic meningitis, cranial nerve palsies, optic neuritis, acute nerve deafness)

554
Q

What are features of latent syphillis infection

A

No clinical

Serological infection

555
Q

What are the features of tertiary syphillis

A

Gumma (granuloma)- rare. Skin, bonem mucosa, scanty spirochaetes

CV: uncomplicated and complicated aortitis +++ spirochaetes, +++ inflammation

Neurosyphillis: seen in HIV patients. General paresis of the insane, tabes dorsalis, gumma, spirochaetes in CSF, small vessel vasculitis

Argyll Robertson pupil

556
Q

Argyll Robertson pupil

A

Prostitute’s pupil

Accomodates but doesn’t react

Syphillis

557
Q

Rx in Syphillis

A

Single dose IM benpen (doxy if pen allergic)

Monitor RPR, need to see a 4x reduction to consider tx succesful

558
Q

What is the Jarisch-Heimer reaction

A

Fever, headache, myalgia, sometimes and exacerbation of syphillitic symptoms commonly developing within hours of abx administration

559
Q

Features of congenital syphillis

A

May occur during pregnancy or birth

Often develops features over the first couple of years including hepatosplenomegaly, rash, fever, neurosyphillis and pneumonitis

560
Q

Gram negative coccobacillus causing STI

561
Q

Causative organism in Chacnroid

A

Haemophilus ducreyi

562
Q

Features of chancroid

A

Tropical ulcer disease mainly seen in africa

Often multiple ulcers, frequently painful

563
Q

Chocolate agar

STI

564
Q

Dx of chancroid

A

Culture on chocolate agar

PCR

565
Q
A

Chancroid

Haemophilus ducreyi

566
Q

Gram negative bacillus, klebsiella cuasing STI

A

Donvoanosis: Ganuloma inguinale

567
Q

Causative organism donovanosis

A

Klebsiella granulomatis

568
Q

Features of donovanosis

A

Africa, India, PNG, Autralian

Large, expanding ulcers starting as a papule or nodule that breaks down with a beefy red appearnce

569
Q
A

Donovanosis

570
Q

Dx of donovanosis

A

Giemsa stain of biopsy or tissue crush showing Donovan bodies

571
Q

Rx in donvoanosis

A

Azithromycin

572
Q

Enteric pathogens causing STI

A

(oro-anal contact)

Shigella

Salmonella

Giardia

Occasionally others e.g. Strongyloides

573
Q

Flagellated protozoan causing STI

A

Trichomonas

574
Q

Dx of Trichomonas vaginalis

A

Wet prep micrscopy, PCR

575
Q

Symptoms of T. vaginalis infection

A

Asymptomatic/ urethritis in men

Discharge in women

576
Q

TV and HIV

A

Associated with increased risk of HIV acquisition

577
Q

Rx trichomoniasis

A

Metronidazole

578
Q

Features of BV

A

Abnormal vaginal flora, polymicrobial, discharge, odour

Sexually associated but not transmitted

May be associated with hygiene practices

579
Q

Dx of BV

A

Microscopy of gram stain

raised pH

Whiff test

Clue cells

580
Q

frothy, often unpleasant-smelling discharge

blood spotting in the discharge

itching in and around the vagina

swelling in the groin

the urge to urinate frequently —

  • See more at: https://www.plannedparenthood.org/learn/stds-hiv-safer-sex/trichomoniasis#sthash.TuBPPa9G.dpuf
A

Trichomoniasis

581
Q

Implications of BV

A

Associated with preterm delivery

582
Q

Features of candidasis

A

Usually candida albicans

If symptomatic: white thick discharge, itching, soreness, redness

Common presentation in women as vulvovaginitis, men as balanitis

Not an STI

583
Q

Rx candidal genital infection

A

Clotrimazole or fluconazole (i.e. oral antifungals)

584
Q

Cause of molluscum contagiousm

Features

A

Pox virus

Caused by skin to skin contact

In adults causes genital lesions and is spread via sexual contact

585
Q

Facial molluscum in adult=

A

HIV until proven otherwise

There are giant lesions in the immunocompromised

586
Q

Treatment of molluscum contagiosum

A

If required= destructive cryotherapy

587
Q

Cause of genital warts?

A

Human papillmoavirus

588
Q

Causes of visible genital warts=

A

HPV6 or 11 (not associated with increased risk of cervical dysplasia)

589
Q

Incubation time for warts?

590
Q

Dx of genital warts

A

Exmaintion: papular, planar, pedunculated, carpet, keratinised, pigmented

591
Q

Home treatment of genital warts

A

Podophyllotoxin solution or cream

Can’t be used in pregnant women

592
Q

Treatment of genital warts in clinic

A

1st line: cryotherapy

2nd line: Imiquimod

593
Q

Viral STIs

A

HAV, HBV, HCV (mainly HIV +ve MSM)

Herpes

HIV

594
Q

Def: HAI

A

Infeciton acquired >48h after admission

595
Q

What is the common HAI of the GIT

596
Q

Transmission of C diff

A

Spore ingestion

597
Q

3Cs in C. diff infection

A

Clindamycin

Cephalosporins

Cprofloxacin

598
Q

Common HAI UTI

599
Q

Resistance in E COli

A

ESBeta lactamases

600
Q

What are the HAIs associated with bacteraemia?

A

MRSA

Coag negative staph

E Coli

601
Q

Most prevalent coag negative staph

A

Staph epidermis

602
Q

Organisms commonly causing surgical site infection

A

MRSA

Coag negative Staph

603
Q

Organisms causing environmental hygiene outbreaks in hospitals

A

C diff

Norovirus

Acinetobacter

604
Q

Environmental source:

Cooling towers

A

Legionella

605
Q

Environmental source:

Building works

A

Aspergillus

606
Q

What infections require negative pressure isolation?

A

TB, chicken pox, RSV

607
Q

What is the most common HAI?

A

UTI> surgical site infection> HA pneumonias

608
Q

How can HAIs be characterised?

A

By organism or by syndrome

609
Q

What are the HAI syndromes

A

Catheter associated blood stream infection

Urinary catheter associated UTI

Surgical site infeciton

Ventilator associated penumonia

Antibiotic associated diarrhoea

610
Q

Degree of resistance accumulation in gram negatives

A

Enterobacter> Klebseilla> E. Coli

ESBLs

611
Q

Features of superficial incisional SSI

A

Skin and subcutaenous tissue, red hot and tender

612
Q

Deep incisional SSI

A

Down to deep soft tissue, fascia, muscle

Wound may reopen

613
Q

Organ/space SSI

A

Organ/space

Reoperation and drainage

614
Q

Gram positive spore forming anaerobe

615
Q

C diff virulence factors

A

Toxin A and B: diarrhoea, colitis

Tonxiotype: III/BI/NAP1/027: proinflammatory, cytotoxic, enterotoxic

616
Q

Pathogenesis of C diff infectoin

A

Mild colitis-> severe colitis-> pseudomembranous colitis and perforation

617
Q

Features of severe C Diff infection

A

Physiologically unstable: PR/ BP/ T/ RR
 High WCC >15
 Rising or high creatinine > 20
 Clinical- peritonism, ileus, obstruction
 Radiological: colitis.
 Others: age, albumin etc.

618
Q

Abx vs:

G+ve, narrow

619
Q

Abx vs:

Gram +ve, community

G-ve anaerobes

Broad

A

Co-amoxiclav

620
Q

Abx vs:

Anaerobes

Narrow

A

Metronidazole

621
Q

Abx vs:

Hosp G-vem some, G+Ve

Pseudomonas

Broad and antipseudomonal

A

Tazocin (piperacillin-tazobactam)

622
Q

Abx vs:

Gram +ve, G-ve, anaerobes (<co-amox>
</co-amox>

A

Amoxicillin

623
Q

Abx vs:

Mainly G-ve

Pseudomonal

Broad

A

Ciprofloxacin

624
Q

Abx vs:

G-ve

Narrow

A

Gentamicin

625
Q

Abx vs:

Hosp G-ve

G+ve

Aeroe

Pseudomonas

Broad

626
Q

Features of parvovirus B19 infection

A

Resp/blood-borne infection 6-8d incubation

Fever, malaise, erythema infectiosum, transient aplastic crisis (especially those with sickel cell, spherocytosis)

627
Q

Implications of parvovirus infection for foetus

A

Infection <20w assocaited with 30% risk of hydrops foetalis

>20w= no risk

628
Q

Flu-like symptoms followed by pinpoint-macular papular rash and lymphadenopathy in adults

Diagnosed via serology of saliva swabs

629
Q

Transmission of Rubella

A

Respiratory

630
Q

Rubella infection before 10/40

A

90% develop congeital rubella syndrome

631
Q

Rubella infection 13-18w

A

Hearing defects, retinopathy

632
Q

Rubella infection >20w

A

No documented rsik

633
Q

Features of CRS

A

Cataracts, congenital glaucoma

Deafness

Congeital heart defects

Purpura

Splenogemgaly

mIcroencephaly

Mental retardation

Meningoencephalitis

634
Q

Implications of influenza infection in pregnancy?

A

Risk of stillbirth x5

Preterm delivery x3

No congenital malformations

635
Q

Recommendations for IFV in pregnant women

A

Vaccination and treatment of pregnant women with antivirals (oseltamivir, zanamivir)

636
Q

Measles in pregnancy

A

Can cause IUD/miscarraige, preterm devliery and increased maternal morbidity

637
Q

Cxs of measles infection

A

Opportunistic bacterial infections: otitis media, pneumonia, bronchitis

Encepahlits and subacute sclerosing pancencephalitis

638
Q

Implications of coxsackie infection during pregnancy

A

Associated with early onset neonatal hepatitis, congenital myocarditis, early onset childhood IDM and abortion of intrauterine death

639
Q

Gram positive cocci in clusters

640
Q

Gram positive cocci in clusters

Coagulase +ve

A

Staph auerus

641
Q

Gram positive cocci in clusters

Coagulase negative

A

Staph epidermis

642
Q

Gram positive cocci:

Diplocci

643
Q

Gram positive cocci in chains

A

Enterococcus

644
Q

Gram positive Rods

ABCDL

A

Actinomyces

Bacillus

Clostridium

Diptheria

Listeria

645
Q

With what are actinomyces assocaited?

A

Dental/oral infections

646
Q

Clostridium=

A

Difficile, perfringens, botulinum, tetani

647
Q

Gram positive rods, obligate anaerobes?

A

Actinomyces

Clostridium

Bacteroides (gram -ve)

648
Q

Treatment of obligate anaerobes

A

Metrondiazole, cephamycins

649
Q

Aminoglycosides vs obligate anaerobes found in GIT

650
Q

Gram negative cocci

A

Neisseria: meningtidis, gonorrhoea

Moraxella catarrhalis

651
Q

Gram negative rods

A

E. Coli

Salmonella

Shigella

Klebseilla

Yersinia

Enterobacteriaceae

652
Q

Gram negative coccobacilli

A

H. infleunza/ducreyi

Bordatella pertussis

Pseudomonas aeruginosa

Chlamydia trachmoatis

653
Q

Gram negative spirochaetes

A

Trep pallidum

Leptospoirosis

Borrelia e.g. Lyme disease

654
Q

What are the boligate intracellular bacteria

A

Chalmydia trachomatis

Rickettsia

Coxiella (Q fever)

M leprae

655
Q

What are the obligate intracellular protozoa?

A

Toxoplasma

Cryptosporidium

Leishmania spp

656
Q

PCP intracellular or extracellular microbe?

A

Obligate intracellular

657
Q

Congenital infections TORCH

A

Toxoplasmosis

Other (HIV/HBV)

Rubella

CMV

HSV

658
Q

Infections screened for in the UK in pregnant women

A

Rubella

Syphillis

HBV

HIV

659
Q

Thrombocytopenia

Eyes/ears affected

Cataracts

Choroidoretinitis

Rash

Cerebral abnromality

Hepatosplenomegaly

A

Classical symptoms of congenital infection

660
Q

Classical symptoms of congenital infection

TORCH

A

Thrombocytopenia

Optic, otitic

Rash

Cerebral abnromality

Hepatosplenomegaly

661
Q

Toxoplasmosis as a congenital infection

A

60% asymptoamtic at birth but go on to develop LT sequelae: deafness, low IQ, microencephaly

40%: symptomatic at birth: choroidoretinitis, microcephaly, hydrocephalus, intracranial calcificaiton, seizures, jaundice, hepatosplenomeagaly

662
Q

Why is there a higher incidence in preterm infants

A

Less maternal Ig

NICU care

Exposure to organisms

663
Q

Early onset sepsis=

A

<48h after birth

664
Q

Causes of early onset sepsis

A

GBS!!

E. Coli

Listeria

665
Q

Fever, unwell in neonate <48h

A

Early onset sepsis

666
Q

Associations of early onset sepsis

A

Maternal:

PROM

Fever

Foetal distress

Foetal:

Respiratory distress

Acidosis

Asphyxia

667
Q

Dx of neonatal sepsis

A

Septic screen: FBC, CRP, blood cultuie, deep ear swab, CSF, surface swab, CXR

668
Q

Mx of early onset sepsis

A

Supprtoive: admission to NICE, ventiulation, circulation, nutrition (TPN)

Benpen and gentamicin (E Coli cover)

Listeria: ampicillin or amoxicillin

669
Q

Rx for Listeria causing neonatal sepsis

A

Ampicillin or amoxicillin

670
Q

Late onset sepsis=

671
Q

Causes of late onset sepsis

A

Coag negative staph

GBS

E COli

Listeria

S. aureus

Enterococci

Gram negatives kleb, enterobacter, pseudomonas

Candida

672
Q

Clinical presentation of late onset sepsis

A

Bradycardia

Apnoea

Poor feeding

Irritability

Billious aspirate

Convulsions

Jaundice

Respiratory distress

673
Q

Ix in late onset sepsis

A

Septic screen and urine

674
Q

1st line Abx in late onset sepsi

A

Fluclox and gentamicin

675
Q

2nd line abx in late onset sepsis

A

Tazocin and vancomycin: consider ability to cross BBB if meningitis

676
Q

2nd line Abx in community acquired late onset sepsis

A

Cefotazime and amoxicllin +/- getamicin

677
Q

Causes of bacterial meningitis in children

A

Neisseria
meningitides

Strep pneumoniae

Hib

678
Q

Sensitive to optochin

Grown on blood agar

A

Strep pneumoniae

679
Q

Causes of meningitis <3/12

A

N meningitides

S pneumonia

(Hib)

GBS

E Coli

Listeria

680
Q

Causes of meningitis 3/12- 5y

A

N meningitidis

S pneumonia

Hib if unvaccinated

681
Q

Causes of meningitis >6y

A

N meningitis

S pneumoniae

682
Q

Organisms causing respiratory infection in children?

A

Viruses

S pneumoniae

atypica Myocplasma if >4y

Bordatella

MTB

683
Q

Def UTI

A

Culture >10^5cfu/ml

Pyuria

Clincal symptoms

684
Q

Broad spectrum Abx

A

Co-amoxiclav

Tazoin

Ciprofloxacin

Meropenem

685
Q

Narrow spectrum Abx

A

Fluclox

Metronidazole

Gentamicin

686
Q

BEAT Drug action

A

Bypass antibiotic sensitive step

Enzyme-mediated drug inactivation

Impairment of drug accumulation

Modification of drug target

687
Q

Genetics involved in prion disease

A

Codon 129 polymorphism: MM massively increases the susceptiblity

Specific PRNP mutation

688
Q

Symptomatic treatment of prion disease

A

Clonazepam

Myoclonas (valproate, levetiracetam, priacetam

689
Q

What Rx may be used to delay prion conversion

A

Quinacrine

Pentosan

Tetracycline

690
Q

EEG in:

sCJD

A

Serial EEG shows periodic triphasic changes

691
Q

EEG in:

vCJD

A

Non-specifc slow waves

692
Q

EEG in:

Inherited prion disease

A

Non-specific changes

693
Q

MRI in:

sCJD

A

Normal/highlighting basal ganglia

694
Q

MRI in:

vCJD

A

Posterior thalamus highlighted on MRI- T2: pulvinar sign

695
Q

Pulvinar sign

A

The pulvinar sign refers to bilateral FLAIR hyperintensities involving the pulvinar thalamic nuclei. It is classically described in variant Creutzfeldt-Jakob disease (vCJD). It is also described in other neurological conditions:

Fabry disease (although the hyperintense signal is seen on T1WI)

bilateral thalamic infarcts

acute disseminated encephalomyelitis

696
Q

MRI in

Inherited prion disease

A

Sometimes high signal in BG

697
Q

CSF analysis in:

sCJD

A

14-3-3 +ve

698
Q

CSF analysis in:

vCJD

A

14-3-3 can be normal

699
Q

PNRP analysis in:

sCJD

A

No mutations

700
Q

PNRP analysis in:

vCJD

A

No mutations

701
Q

PNRP analysis in:

iatrogenic CJD

A

No mutations

702
Q

PNRP analysis in:

Inherited prion disease

A

Mutations present and diagnostic

703
Q

Codon 129 in:

sCJD

A

Most are MM

704
Q

Codon 129 in:

vCJD

705
Q

Codon 129 in:

iatrogenic CJD

A

Most homozygous MM and VV

706
Q

Codon 129 in:

Inherited prion disease

A

129 codon homozygosity may confer earlier onset

707
Q

Western blot PrPsc in:

sCJD

708
Q

Western blot PrPsc in:

vCJD

A

Type 4t from tonsillar biopsy (100% sensitive and specific)

709
Q

Western blot PrPsc in:

Iatrgoneic CJD

710
Q

Spongiform vacuolation

PrP amyloid plaques

711
Q

PrPsc 4t detectable in CNS
and lymphoreticular tissue

Florid plaques

712
Q

What is the most common form of prion disease?

713
Q

Aetiology of sCJD

A

Either somatic PRNP mutation or spontaenous conversion of PRPc to PrPSc

714
Q

45-75 y/o

Rapid, progressive dementia with myoclonus, cortical blindness, akinetic mutism and LMN signs

715
Q

30y/o

Psychiatric symptoms (anxiety, paranoia, hallucinations)

Followd by development of neurological symptoms (peripheral sensory symptoms, ataxia, myoclonus)

Later symptoms include chorea, ataxia, dementia

716
Q

Causes of acquired CJD

A

vCJD

Iatrogenic

Kuru

717
Q

Progressive ataxia initially

Dementia and myoclonus at later stages

Speed of progression depends on route of innoculation

718
Q

Progressive cerebellar syndorme following 45y incubation

Dementia late or absent

719
Q

Causes of inherited CJD

A

fCJD

GSS

FFI

Various atypical dementias

720
Q

Insomnia and paranoia progressing to hallucinations and weight loss

Mute period

Death 1-18/12 after start of symptoms

721
Q

Inheritance of FFI

722
Q

Develps between 2-60y

Dysarthria progressing to cerebellar ataxia, ending in dementia

A

Gesrtmann-Straussler-Scheinker syndrome

723
Q

Inheritance of GSS

724
Q

Tonsillar bx in sCJD

A

Not useful

725
Q

What to exclude following triphasic EEG in ?CJD

A

Exclude nonspecific e.g. hepatic encepahlopathy

Lithium toxicity

NB only 2/3rds will have abnormal EEG

726
Q

Dx of sCJD

727
Q

Most common pathogen causing surgical site infection

A

Staph aureus

728
Q

Pathogens causing surgical site infection

A

Staph aureus

E Coli

Pseudomonas

Haemolytic strep

729
Q

Rx in surgical site infection

730
Q

What are the patient related factors contributing to surgical site infection

A

DM

Peri-operative hyperglycaemia

Current smoker

Remote infection at time of sx

Obesity

Malnutrition

Low preoperative albumin

Concurrent steroid use

731
Q

Clean wound=

A

Sterile site e.g. THR

732
Q

Common pathogen in clean wounds

733
Q

Clean-contaminated wound=

A

Post-appendectomy

734
Q

Contaminated wounds

A

Perforated bowel

735
Q

Dirty infected wounds=

736
Q

Risk factors for septic arthritis

A

Abnormal joint (RA/OA/gout/prosthesis)

Immunosuppressed (CLD, steroids)

Bacteraemia (e.g. DM, IVDU)

Trauma/penetrating injury

737
Q

Causes of septic arthriits

A

Staph aureus most common

Streptococci 22%

Gram -ve less commonly e.g. E. Coli

738
Q

Unwell febrile patient with red hot swolllen joint

Unable to weight bear

50% knee

A

Septic arthritis

739
Q

Dx of septic arthritis

A

Blood culturebefore Abx

Joint aspirate (>50,000 cells/ml)

Inflammatory markers

Imaging shows effusion

740
Q

Mx septic arthritis

A

IV antibiotics (cephalosporin or fluclox)

MRSA: Vancomycin

Drain joint

741
Q

Lack of IL-10=

A

Increased severity of staph infection

742
Q

Lack of macrophage derived cytokines reduces host protection in

A

Staph aureus sepsis

743
Q

Organisms causing septic arthritis

Staph

Strep

Gram negative

Rarely

A

Staph aureus

Staph epidermis (4%)

Strep pyogenes

Strep pneumonias

Strep agalactiae

E Coli

Hib

Neisseira gonorrhoea

Salmonella

Brucellosis

MTB

Fungi

744
Q

Brodie abscess

A

Subacute osteomyleitis which may pesrist for years before converting to frank OM

745
Q

Pain, fever, local swelling of joint

746
Q

Pathogens causing OM

A

Staph aureus

747
Q

Dx of OM

A

MRI

Bone biopsy for culture/histology

748
Q

Rx in OM

A

Debride
and remove infected bone and soft tissue

749
Q

Lautenbach technique

A

Debridement

After devridement double lumen suction irrigation system is introduced

Abx instilled through central lumen followed by streptokinase

Remains in situ until finishing giving Abx

3w then PO Abx for 6/52

750
Q

Papineau technique

A

Complete excision of infected tissue and necrotic bone

Open cancellous grafting of the osseous defect

Skin grafting for wound closure

751
Q

Risk factors for prostthetic joint infection

A

Local wound infection

Previous revision

Bilateral athrtoplasty

Wound healing complications

752
Q

Pain, joint never right, early failure, sinus tract formation

A

Prosthetic joint infection

753
Q

Most common organism causing prosthetic joint infection

A

Coag negative staph

754
Q

Organisms causing prosthetic joint infection

A

Staph

Aureus

Strep

Enterococci

Gram negative: enterobacteria, pseudomonas

Anaerobes, fungi etc

755
Q

Loosening on XR

A

Prosthetic joint infection

756
Q

Dx of prosthetic joint infection

A

XR

Inflammatory markers

Aspirate

757
Q

CRP in prosthetic knee infection

758
Q

CRP in prosthetic hip infection

759
Q

WCC in aspirate prosthetic knee infection

760
Q

WCC in aspirate prosthetic any joint except knee

761
Q

Rx of prosthetic joint infection

A

Single or two stage revision

Use Abx-impregnated cement

762
Q

Single stage revision of infected prosthesis

A

remove all foreign material and dead bone,  change gloves and drapes etc  re implant
the new prosthesis w/ ABx impregnated cement and give IV antibiotics.

763
Q

Two stage revision of infected prosthesis

A

remove prosthesis, take samples for microbiology and histology. Spacer put in place. Period
of IV antibiotics (6 weeks), stop ABx for 2 weeks. Re-debride and sample at second stage. Re-implantation w/
antibiotic impregnated cement. No further ABxs if samples are clear.

764
Q

Rx in prosthetic joint infection:

Strep, staph, propioni

A

Clindamycin + Gentamicin

765
Q

Rx in prosthetic joint infection:

MRSA

A

Vancomycin, ofloxacin & gentamicin

766
Q

Rx in prosthetic joint infection:

Enterococci

A

Vanc

Ampicillin

Gent

767
Q

Rx in prosthetic joint infection:

Enterobacter and E Coli

A

Cefotaxime

Ofloxacin

Gent

768
Q

Rx in prosthetic joint infection:

Pseudomonas

A

Clindamyinc, gentamicin, cefoperazone

769
Q

Rx in prosthetic joint infection:

MTB

A

Amikacin

Streptomycin

770
Q

Rx in prosthetic joint infection:

Unknown pathogen

A

Vanc

Clindamycin

Gent

771
Q

Def: complicateed UTI

A

Funcitonally or structurally abnormal tract

772
Q

Rx pyelonephritis

A

Broad spec IV Abx e.g. co-amoxiclav and gent

or

cefuroxime and gent

773
Q

Treatment of uncomplicated vs complicated UTI

774
Q

Draw classifciation of abnromalities of the renal tract

Signifcance

A

One of the main defences is bacterial flushing

775
Q

Staph aureus renal infection aetiology

A

Likely to be due to haematogenous spread i.e. staph sepsis

776
Q

Typical symptoms of UTI

A

Dysuria

Urgency

Frequency

Polyuria

Suprapubic tenderness

Haematuria

777
Q

Empirical UTI treatment of uncomplicated female

A

Trimethoprim

or cephalexin for 3d

NFT for 7d

NB 7d of treatment recommended for women who have had previous UTI

778
Q

Empirical UTI treatment of breast feeding/pregnant woman

A

Cephalexin BD for 7d

2nd line: coamoxiclav QDS for 7d

779
Q

Treatment of fungal UTI

A

May occur in patients with indwelling catheters

Catheter removal may result in cure

ORal fluconazole is no more effective than therapy, therefore not recommended in asymptomatic infections

780
Q

What are the stages of PCR

.

.

A

Denature

Primer annealing

Chain elongation with Taq polymerase

781
Q

CMV causes what in AIDs?

782
Q

CMV causes what in BMT?

A

Pneumonitis

783
Q

What are the 3 sources of viral infections post-transplant

A

Reactivation of latent infection e.g. Herpes

Graft brought infection with it e.g. HBV

Exogenous opportunistic infection post-transplant

784
Q

Dx of viral infection in immunocompromised

A

Due to immune systems inability to mount a full response serology of limited diagnostic value

Viral detection preferable e.g. PCR

785
Q

What are he human herpes viruses?

A

HSV1+2, VZV, CMV, HHV6, 7, 8 EBV

786
Q

Where are HSV and VZV latent?

A

Sensory nerve ganglia

787
Q

Where are CMV and EBV latent?

A

Leucocytes

788
Q

Significance of VZV in immunocompromised

A

As a higher rate of Cx e.g. pneuonitis and hepatitis

789
Q

Rx in VZV infection

790
Q

Prevention of VZV infection

791
Q

When is there are a risk of CMV in solid organ transplant?

A

Seropositive donor and seronegative recipient due to recipient viral exposure

792
Q

When is there a risk of CMV reactivation in BMT

A

Serongetive donor but seropositive recipient due to loss of protective Abs

793
Q

What causes post-transplant lymphoproliferative disease?

794
Q

Rx of CMV in BMT

A

Pre-emptive treatment with ganciclovir

795
Q

Mx of PTLD

A

Reduce immunosuppression

Rixumiab

CTx once it becomes lymphoma

796
Q

Spindle cells and KSHV proteins when biopsied

797
Q

Castleman’s disease

A

Castleman disease, also known as giant or angiofollicular lymph node hyperplasia, lymphoid hamartoma, angiofollicular lymph node hyperplasia, is a group of uncommon lymphoproliferative disorders that share common lymph node histological features that may be localized to a single lymph node (unicentric) or occur systemically (multicentric)

Can be associated with HHV8

798
Q

HHV6 in transplant

A

Can cause graft rejection

799
Q

Rx in HHV infection

A

Ganciclovir

Foscarnet/cidofovir

800
Q

Implications of adenoviruspost-transplant

A

Affects paediatric patients

High mortality with disseminated infection

Weekly PCR surveillance

Treated with reduction of immunosuppression and ribavirin

801
Q

Treatment of measles in immunocompromised

A

Consider HNIG

802
Q

BK virus associated with what in BMT

A

Haemorrhagic cystitis

803
Q

BK virus associated with what in renal transplant

A

Ureteric stenosis

804
Q

Def: endocarditis

A

Infection of the innermost layer of the heart, usually the valves

805
Q

PUO

Anorexia, weight loss, amalise, fatigue, rigors, night sweats and weakness

Acutely: SOB, chest tightness, embolic complications

Dental history

PMH: RhF, CHD, cardiac surgery, valve replacemen, LT lines, bcateraemia, GI/bowel

IVDU Hx

A

Infective endocarditis

806
Q

Heart murmurs that often change

A

?Infective endocarditis

807
Q

Signs of infective endocarditis

A

Subactue:

Clubbing, splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth spots, splenomegaly, haematuria

808
Q

Ix in infective endocarditis

A

FBC (anaemia), U&E, CRP

ESR

3x blood cultures without Abx

Serology if culture negative

CXR

Echo

809
Q

Dukes criteria: fulfilling endocarditis

A

2 major

or

1 major + 3 minor

or

5 minor

810
Q

Duke’s criteria: Major

A

Persistent bacteraemia (>2 +ve blood cultures)

Echo findings: vegetations

+ve serology for bartonella, coxiella, brucella

811
Q

Duke’s criteria: Minor

A

Predisposing risk factor e.g. murmur, IVDU

Fever >38 or raised CRP

Evidnce of immune complex fromation: splinter haemorrhages, haematuria

Vascular phenomena: major arterial emboli

Positive echo that does not meet major criteria

Positive blood culture that does not meet major criteria

812
Q

Pathogen in subacute endocarditis

A

Low virulence strep: Strep viridans

813
Q

Clinical course of subacute endocarditis?

A

Mild-moderate illness progressing over weeks to months

Decrease propensity haematogenously to seed extracardiac sites

814
Q

What is the most common cause of prosthetic vavle endocarditis

A

Coag negative staph

815
Q

Common cause of acute bacterial endocarditis

816
Q

Clinical course of acute bacterial endocarditis

A

Fulminant illness d-w

817
Q

Most common cause of culture -ve infective endocarditis

A

Cultures taken after abx

818
Q

Causative organisms in infective endocarditis (culture negative)

HACEK

A

Haemophilus

Aggregatibacter/Actinobacillus

Cardiobacterium hominis

Eikenella corrodens

Kingella Kingae

Aspergillus, brucella, coxiella, chlamydia, mycoplasma

819
Q

Empirical treatment of infective endocarditis: prosthetc vavle

A

Vanc + Gent + Rifampicin

820
Q

Empirical treatment of infective endocarditis: native valve, acute

821
Q

Empirical treatment of infective endocarditis: native valve, indolent

A

Pen and Gent

822
Q

Treatment of strep viridans causing infective endocarditis

A

Pen + Gent

823
Q

Treatment of MSSA endocarditis

A

Fluclox for 4/52

824
Q

Treatment of MRSA endocarditis

A

Vanc + gent/rifamp/fucidin

825
Q

Treatment of enterococcal endocarditis

A

Ampiciliin + Gent

826
Q

What are the indications for surgical intervention in infective endocarditis?

A

>1 serios sytemic emoblus/high risk

Uncontrolled infection

Significant valve dysfunction

Lack of Abx response

Local suppurative cx e.g. perivavlular abscess

CHF

Prosthetic valve endocarditis

827
Q

What are the different types of PUO

A

Classical

Healthcare associated PUO

Neutropaenic PUO

HIV associated PUO

828
Q

Def: PUO

A

>38C on several occassions for >3w in spite of at least 1 week of investiagations

829
Q

Classical PUO

A

As for PUO oncluding 3/7 in hospital or >3O/P with ambulatory Ix

830
Q

Causes of classical PUO

A

Infections

Neoplasms

CTD

Misc conditions: abscesses, endocarditis, TB, complicated UTIs

Undiagnosed conditions

831
Q

Healthcare associated PUO

A

Develoops in hospital following >38h in hospital

832
Q

Causes of PUO in children

A

Kawasaki’s

JIA

833
Q

Causes of PUO in elderly

A

CTD predominant: temporal arteritis, PMR

Infections

834
Q

Causes of healthcare associated PUO

A

Sx

Drugs

Medical devices

LRTI

C diff colitis

Immobilisation

835
Q

Drugs causing PUO

A

Vancomyin

Penicllins

Serotonergics

836
Q

Neutropaenic PUO

A

Fever concomittant with neotrpaenia and subsequent lack of cellular response =

MEDICAL EMERGENCY

837
Q

Causes of Neutropaenic PUO

A

Infections

CTx

Haematological malignancies

Look for conditiosn that require neutrophils e.g. fungal infection, bacterial, MTB

GVHD

Drug fever

838
Q

HIV-associated PUo

A

HIV +ve patients frequently have PUO

Cause related to CD4 count

839
Q

Causes of HIV PUO

A

Seroconversion

TB

Kaposi’s

Bacterial

Disseminated MAI

PCP

CMV

Cryptococcus

Toxoplasmosis

Lymphoma

Histoplasmosis

Drug fever

840
Q

Ix in PUO

A

Observe fever, if possible withold therapy until Dx

In febrile neutropaenia, therapy should be witheld until samples have been taklen unless patient is unstable

Vasculitis screen

Bence Jones protein

Dip urine

Familial diseases

Fever in returning traveller

841
Q

Causes of fever in a returning traveller

A

Malaria (21%)

Dengue

Typhoid

Rickettsia

Bacterial diarrhoea

UTI

Pneumonia

HIV seroconversion

Viral haemorrhagic fevers

Timing is key

842
Q

What is the key in fever in a returning traveller?

843
Q

Anaerobic gram negative bacillus causing enteric fever

A

S. typi and paratyphi

844
Q

Def: tyohiud

A

Enteric fever infecting Peyers patches, transmitted by food and water

845
Q

Fever, headache, abdominal pain, diarrhoea or constipation

Rose spots

Relative bradycardia

Hepatosplenomegaly

846
Q

Consequences of chronic typhoid carriage

A

Gallstones

Immunosuppression

847
Q

Dx of typhoid

A

Hx

Blood cultures

Stool

848
Q

Mx of typhoid

A

IV fluids

Oral or IV Abx

HPA notification

849
Q

Transmission of typhoid

A

Food or water

850
Q

What is the most common species of malaria?

A

Falciparum

851
Q

What are the organims causing malaria

A

P. falciparum

P. vivax

P. ovale

P. malariae

852
Q

Which plasmodium species have a tertian rhythmn?

A

Falciparum

Vivax

Ovale

(48hr)

853
Q

Which plasdoium species have a quartan rhythm?

A

P malariae

854
Q

Severity and liver stage:

falciparum

A

V severe

Parasitaemia

855
Q

Severity and liver stage:

vivax

A

Chronic liver stage (hypnozoites)

856
Q

Severity and liver stage:

Ovale

A

Chronic liver stage

Hypnozoites

857
Q

Severity and liver stage:

Malariae

858
Q

Young trophozoites in the absence of mature trohpozoites and schizonts

Crescent shaped gaemtocytes

A

P falciparum

859
Q

Schuffner’s dots

>20 merozoites?schizont

860
Q

Schuffner’s dots

A

P Ovale

(vivax with merozites)

861
Q

Ix in malaria

A

Thick film: parasitaemia

Thin film: species

Various antigen tests

Bloods:

WCC rarely raised

70% have a reduced platelet count

50% have deranged LFTs

30% anaemic

862
Q

Commonly: Fever. splenomegaly, no signs

Uncommonly:

Focal neurology, reduced GCS/ coma/ shock/hepatomegaly

A

P falciparum malaria

863
Q

Fevers and rigors

Flu-like illness

Headache

Back pain

Myalgia

N + V

Uncommonly:

Diarrhoea

Abdominal cramps

Cough

Dark urine

A

P. falciparum malaria

864
Q

Treatment of no falciparum malaria

A

Chloroquine

then

Primaquine if resistant or minimal response

865
Q

Treatment of mild falciparum malaria

A

Quinine + doxycylcine/clindamycin

OR malaronie (atovoquone/proguanil)

or RIamet (artemether and lumefantrine)

866
Q

Treatment of severe falciparum malaria

A

Artemisinin combination therapy (ACT)

or

IV quinine + doxycycline/clindamycin

867
Q

What should always be considered in terms of fever in a returning traveller?

A

HIV

Malaria

TB

Typhoid

Rabies

868
Q

Fever in returning traveller, incubation:

<10d

A

ARboviruses: denghue, yellow fever, japanese encephalitis

SARS

Haemorrhagic fevers: lassa, ebola

Meningococcoaemia

Rarely: rabies

869
Q

Fever in returning traveller, incubation:

10-21d

A

Flavivirus: tickborune and japanese encephalitis

Typhoid

Toxoplasma

Haemorrhagic fevers

Measles

Rarely: Hep A

870
Q

Fever in returning traveller, incubation:

>21d

A

Schistosomiasis

TB

Viral hepatits

Filiarisis

Rarely: EBola/ Lassa

871
Q

What are the major features of severe or complicated falciparum malaria

A

Altered consciousness/ seizures

Renal impairment

Acidosis (<7.3)

Hypoglycaemia (<2.2mmol)

Pulmonary oedema/ARDS

Anaemia

Spontaneous bleeding/DIC

Shock

Haemoglobinuria

Parasitaemia >2%

Pregnancy

Vomiting

872
Q

Algid malaria

A

Definition: a form of falciparum malaria chiefly involving the gut and other abdominal viscera; gastric algid malaria is characterized by persistent vomiting; dysenteric algid malaria is characterized by bloody diarrheic stools in which enormous numbers of infected red blood cells are found.

873
Q

What should be used as an alternative to doxy in the treatment of malaria in pregnancy?

A

Clindmaycin

874
Q

Dosing structure for complicated malaria

A

Quinine 20mg/kg loading doese IV over 4h

then 10mg/kg/IV over 4h every 8 hours

+ oral doxy 200mg/clindamycin for 7d.

875
Q

Taenia solium cysticercosis

A

infection of the tissues with pork tapeworm larvae

common in all non-Muslim developing countries

commonest cause of adult-onset epilepsy in many countries

e.g. causes 20-30% of adult onset epilepsy in Peru

876
Q

What are the herpes viruses

A

HSV

VZV

CMV

EBV

HHV6

HHV8

877
Q

What are the neurotropic herpes virses?

A

HSV 1+ 2

VZV

878
Q

dsDNA

No anoimal reservoir

Persistent latent hpase in DRG

lytic infection of fibroblasts and epithelial cells

Transmitted via mucocutaenous contact

A

HSV1 and HSV2

879
Q

dsDNA

Droplet spread

Viral replication in LNs then in liver + spleen

Develops rash 48h post infection

880
Q

Oral: Incubation 2-12/7

Severe painful ulceration

Tendency to coalesce

Erythematous base and submandibular lymphadenopathy

Ddx Coxscakie A

A

HSV infection

881
Q

Which HSV is predominantly associated with oral herpes

882
Q
883
Q

Gential:

Incubation 4-2/7

Fever, dysruia, inguinal lymphadenopathy

+++Pain

Vesicular rash

Meningitis 1-2/52 later in 4-8% with primary

A

HSV infection

884
Q

What is a potential consequence of genital herpes

A

Sacral radiculomyelitis leading to urinary retention (self-limiting)

885
Q

Coxsackie A infection

A

Herpangina, also called mouth blisters, is the name of a painful mouth infection caused by coxsackieviruses. Usually, herpangina is produced by one particular strain of coxsackie virus A (and the term “herpangina virus” refers to coxsackievirus A)[1] but it can also be caused by coxsackievirus B or echoviruses.[2] Most cases of herpangina occur in the summer,[3] affecting mostly children. However, it occasionally occurs in adolescents and adults. It was first characterized in 1920.

886
Q

Eyes:

Unilateral/bilateral conjunctivitis and pre-auricular LNs

A

Ocular herpes infection HSV

887
Q

What is a consideration in ocular herpes infection

A

Acute retinal necrosis if immunocompetent

888
Q

What is seen in herpetic eye infeciton in the immunocompromsied

A

Progressive Outer Retinal Necrosis (also caused by VZV, EBV, CMV)

889
Q

Which strain of HSV causes most herpetic encephalitis

890
Q

Flu-like prodrome 2/52

Focal neurology, fever, confusion, behavioural change, cahgnge in consciousness, seizures, N+V, coma, death

A

Herpetic encephalitis

891
Q

Mollaret’s meningitis

A

Recurrent benign lymphocytic meningitis

892
Q

What commonly casues Mollaret’s meningitis

893
Q

CSF: lymphocytic pleiocytosis

Cytology may be normal

N glucose

Raised protein

A

Herpes encephalitis

894
Q

Treatment of herpes encephalitis

A

IV aciclovir STAT

Don’t wait for results

10mg/kg TDS then oral ACV for total of 2-3/52

895
Q

Scrum pox
Painful blisters, + inguinal lymphadenopathy in rugby players

A

Herpes gladiatorum

896
Q

Herpetc whistlow

A

Painful red finger

897
Q
A

Herpetic whitlow

898
Q

What are the potential skin manifestations of herpes

A

Gladiatorum

Whitlow

Erythema multiforme

HS dermatitis

Eczema herpeticum

Zosteriform HS (painless)

899
Q

Fever, malaise, headache followed by dew on rose petal rash

Lesions scab and no longer contagious after 1/52

900
Q

Cx of VZV

A

Scarring

Pneuominitis

Haemorrhage

Eye involvement

Reyes’s syndrome

Neurological

901
Q

What are the potential neurological manifestations of VZV infection

A

Acute cerebellar ataxia

GBS

Ramsay hunt syndrome

Encephalitis

Post-herpetic neuralgia

902
Q

Ramsay Hunt Syndrome

A

Ramsay Hunt syndrome (RHS) type 2 also known as herpes zoster oticus is a disorder that is caused by the reactivation of pre-existing Varicella zoster virus in the geniculate ganglion, a nerve cell bundle, of the facial nerve.[1]

Ramsay Hunt syndrome type 2 typically presents with inability to move many facial muscles, pain in the ear, taste loss on the front of the tongue, dry eyes and mouth, and the eruption of an erythematous rash.

903
Q

Dx of VZV

A

Exam- vesicles

Cytology: Tzanck cells

Immunofluorescnece cytology

PCR: if rash is old, in CNS/ocular disease

904
Q

Tzanck cells

A

Multinucleated giant cells found in VZV and HSV infections

905
Q

VZV vaccien in pregnancy?

A

CIed as a live vaccine

906
Q

Shingles

A

VZV reactivation (DRG) in times of stress/ reduced immunity

Painful, dermatomal rash

907
Q

When to treat shingles

A

Symptomatic children

or healthy adult smokes, chronic lung disease

908
Q

Treatment of shingles

A

Aciclovir 800mg PO or famciclovir or valaciclovir

Topical eye drops

PEP for immunocompromised

909
Q

What are the epitheliotropic herpes viruses?

A

CMV and Roseola virus

910
Q

What are the lymphotropic herpes viruses?

911
Q

Possible manifestations of CMV infection

A

Asymptomatic

Congenital

CMV mononcucleosis

Immunocompromised

912
Q

What are the consequences of congenital CMV infection

A

IUGR/Jaundice/hepatosplenomegaly

Chorioretintis

Encephalitis

Microcephaly

Death

Late progressive sensorineural deafness

LD

Cyotmegalic inclusion disese

913
Q

Manifestations of CMV infection in the immunocompromised?

A

Fever, heapatitis

Colitis

Retinitis

Pneuopnitis

BM suppression

Addison’s disease

Radiculopathy

914
Q

Which cells does CMV infect

A

Macrophages, endothelial cells, B and T lymphocytes

BM cells

915
Q

What is the cytological test used to diagnose CMV

A

Paul Bunnel/Monospot

916
Q

What are the possible manifestations of EBV infection

A

Infectious mononucleosis

Burkitt’s

Nasopharyngeal Ca

Post-transplant lymphoproliferative disease

917
Q

Fever, pharyngitis, lymphadenopathy

+ maculopapular rash

A

Infectious mononucleosis

918
Q

Rx of HHV8

A

Gancilcoivr and Foscarnet

919
Q

When does IFV A peak?

A

H1` peaks beginning of January each year

920
Q

When does H1N1 peak?

A

End of december

921
Q

When does IFV B peak?

922
Q

H5N1=

923
Q

H1N1=

924
Q

SARs caused by

A

Coronavirus

925
Q

Effectiveness of antiflu drugs

A

Only effective if administered within 48h of infection

926
Q

Zoonoses:

Mice borne

A

Hantan viruses

Lyme borrelliosis

Erhlichia

Bartonella

Lymphocytic choriomeningtiis

927
Q

Zoonoses:

Rats

A

Rabies

Leptospirosis

Lassa fever

Hantan viruses

Plague

Pasterullosis

Haverhill fever

928
Q

Zoonoses:

Cats

A

Bartonellosis (cat scratch)

Leptospirosis

Q fever

Toxoplasmosis

Rabies

Ringworm

Toxocariasis

929
Q

Zoonoses:

Dogs

A

Hydatid

Leptospirosis

Q fever

Rabies

MRSA

Ringworm

Toxocariasis

930
Q

Zoonoses:

Small ruminants

A

Anthrax

Brucellosis

Q fever

Cryptosporidiosis

Enzootic abortion

Louping ill

Orff virus

Rift valley fever

Toxoplasmosis

931
Q

Zoonoses:

Cattle

A

Anthrax

Leptopspirosis

Brucella

Bovine TB

Anaplasmosis

Toxoplasmosis

E Coli 0157

Rift valley fever

Ringworm

932
Q

Zoonoses:

Swine

A

Brucellosis

Leptospirosis

Erysipeloid

Cysticerosis

Trichinella

HEV

IAV

Streptococcal sepsis

933
Q

Zoonoses:

Birds

A

Psitticosis

IFV

Cryptococcus

IAV

Poultry: salmonella

WNV

934
Q

Zoonoses:

Water sports associated

A

Leptospirosis

HAV

Giardia

Toxoplasmosis

Mycobacterium marinum/ulcerans

Brukholderia

Pseudomallei

E Coli

935
Q

Zoonoses:

Water borne

A

Campylobacter

Salmonella

VTEC 0157

Cryptosporidium

936
Q

Zoonoses:

Food associated

A

Listeria

Taenia

Cysticerosis

Toxoplasmosis

Trichinellosis

Yersiniosis

Giardia

937
Q

Def: zoonosis

A

Diseases and infections which are transmitted naturally between vertebrate animals and man

938
Q

Gram negative bacilus (faculative intracellular) zoonosis

A

Brucellosis

939
Q

Mode of transport

Brucellosis

A

Inhalation

Skin or mucus membrane contact

940
Q

Consumption of contaminated food, (untreated milk/dairy products)

Animal contact or environmental contamination

Also includes labarotory acquired

A

Brucellosis

941
Q

Classically undulant fever (peaks in eve, normal by monring)

Malaise

Rigors

Sweating

Myalgia/arthralgia

Tiredness

3-4/52 incubation

A

Brucellosis

942
Q

Arthritis

spinal tenderness

Lymphadenopathy

Splenomegaly

Hepatomegaly

Epididymo-orchitis

Rarely:

Jaundice, CNS abnromalities, cardiac murmur, pneumonia

A

Brucellosis

943
Q

Ix in Brucellosis

A

Serology: anti-O-polysaccharide Ab

WCC usually normal

Leucocytosis rare

Signficant number of patients may become neutropaenic

944
Q

Rx Brucellosis

A

4-6/52: tetracycline or doxycline combined with streptomycin or PO doxy and rifampicin 8/52

945
Q

Rhabdovirus affecting warm-blooded animals

Dogs and bats most common vectors

Bullet shaped

946
Q

Negri bodies

A

Pathognomic for rabies

947
Q

Prodrome: fever, headache, sore throat

Acute encephalitis (fatal): hyperactive state

948
Q

Ix in Rabies

A

IFA for rabies antigens in animals brain

Neutralisaiton/ELISA for rabies IgM

949
Q

Treatment of rabies

A

Rabies specific Ig post exposure

950
Q

Gram negative lactose fermenter found in rats

A

Yersinia pestis

951
Q

What are the potential manifestations of yersinia infection

A

Bubonic plague: swollen LNs- dry gangrene

Pulmonary: usually seen during epidemics due to person-person spread

952
Q

Rx of Yersinia

A

Streptomycin

Doxy

Gent

Chloramphenicol in meningitis

953
Q

Gram negative obligate aerobic motile spirochaates

A

Leptospirosis

954
Q

Organism in leptospirosis

A

L. interrogans

955
Q

Excreted in dog/rat urine

Penetrates broken skin or as a conseuqnce of swimming in contaminated water

A

Leptospirosis

956
Q

High siking fever

Headache

Conjuncitval haemorrhages

Jaundice

Malaise

Myalgia

Meningism

Carditis

Renal failure

HA

10-14/7

A

Leptospirosis

957
Q

Rx of leptospirosis

A

Amoxicllin

Erythromycin

Doxy or ampicillin

958
Q

Rx of anthrax

A

Ciprofloxacin or doxy

959
Q

Woolsorters disease

A

Pulmonary anthrax

960
Q

Painless round black lesions + rim of oedema

A

Cutaneous anthrax

961
Q

Massive lymphadenopathy and mediastinal haemorrhage

Pleural effusion

Respiratory failure

A

Woodsorter’s disease

962
Q

Arthropod borne (ixodes tick) spirochaete

A

Lyme disease (Borrelia burgdorferi)

963
Q

What are the stages of Lyme disease

A

Early localised

Early disseminated

Late persistent

964
Q

Cyclical fevers

Non-specific flu like symptoms

Erythema chronicum migrans (Bullseye rash)

A

Lyme disease

965
Q

Malaise, lymphadenopathy, hepatitis, carditis, arthritis

A

Early disseminated Lyme disease

966
Q

Arthritis

Focal neurology

Neuropsychiatric disturbance

Acrodermatitis chronic atrophicans

A

Late persistent lyme disease

967
Q

Dx of lyme disease

A

Bx edge of ECM + ELISA for lyme Abs

968
Q

Treatment of lyme disease

A

Doxy 2-3/52 (also amoxicillin, cephalosporins)

NB post infection some patients get ME type symptoms

969
Q

Treatment of Lyme disease with CNS involvement

A

IV ceftriazone

970
Q

Causative organism in Q fever

A

Coxiella burnetii

971
Q

Fever, dry cough

Fatigue

Pleural effusion

Diarahoea

Looks like atypical pneumonia

NO RASH

Cattle/sheep exposure

972
Q

Rx Q fever

973
Q

What are the manifestations of Leishmania?

A

Cutaaneous

Diffuse cutaenous

Muco-cutaenous

Visceral: Kala Azar

974
Q

Which species cause cutaneous leishmaniasis

A

L. major

L. tropica

975
Q

Sandfly bite

Skin ulcer at site of bite

Heals after 1yleaving depigmeneted scar

May be single or multiple painless nodules which grow and ulcerate

T4HS

A

Cutaenous leishmaniasis

976
Q

Immunodefieicnt

Nodular skin lesions that do not ulcerate

Especially lots of nodules

A

Diffuse leishmaniasis

977
Q

Which speices cause muco-cutaenous leishmaniasis

A

L braziliensis

978
Q

Dermal ulcer

Months to yearslater ulcers in mucus membrane of mouth

A

L. brazilienis (muco-cutaneous)

979
Q

Which species cause visceral Leishmaniasis?

A

L donovani

L infantum

L chagasi

980
Q

Young malnourished child

Abdo discomfort + distension/anorexia/weight loss

981
Q

Clinical course of L donovani

A

Invasion of RES-> hepatosplenomegaly-> BM invasion

Later disfiguring dermal disease PKDL

982
Q
A

Acrodermatitis chronic atrophicans

Lym disease

Late persistent

983
Q

Flu like illness

Lymphadenopathy

Myalgia

Encephalitis

Necrotising retinochoroidits *Trainspotting)

A

Toxoplasmosis

984
Q

Causes cysts commonly in the liver

A

Hydatid disease

985
Q

Jaundice, conjunctival haemorrhage, canoeing in the US, felt run down

A

Leptospirosis

986
Q

Maltese man, headache, fever, slight splenomegaly, small gram negative coccobacilli seen on Castaneda’s medium

A

Brucellosis

987
Q

Biology field trip, leg lesion 5cm flat red edge with a dim centre, tired, headaches, fever, irregular heart beat

A

Lyme disease

988
Q

India, ulcerating papule on hand, centre is black and necrotic, gram positive rods on blood agar culture, responded to large doses of
penicillin

989
Q

Arm pain, hypersalivation, twitching, renal failure, death, confusion

990
Q

How can fungal infections be classified?

A

Yeasts

Dermatophytes

Moulds

991
Q

What are the yeasts

A

candida, Cryptococcus, pichia, rhodotorulla, saccharomyces, trichosporon etc

992
Q

What are hte dermatophytes

A

epidermophyton, microsporum, trichophyton

993
Q

What are the moulds

A

aspergillus, fusarium, mucor, penicillium, rhizopus etc.

994
Q

How to diagnose superficial fungal infections

A

Wood lamps

995
Q

The Tineas

A

ermatophytes

996
Q

Pityriasis versicolour

A

malassezia

997
Q

Otomycosis

A

yeasts & moulds. Fungal ear infection

998
Q

Black piedra

A

piedraia hortae

999
Q

White piedra

A

trichosporon beigelii

1000
Q

What are the different types of tineas?

A

Capitis: scalp and hair

Corporis: trunk, legs and arms

Cruris: groin and pubic region

Pedis

Manum

Ungium

1001
Q

Pityriasis

A

Malassezia globosa/furfur

Seborrhoic dermatitis

T. versicolor: depigmentation in those with darker skin

1002
Q
A

Tinea versicolour

1003
Q

Dx of deep seated candida

A

Culutre

Mannan

Abs

1004
Q

Pneumonia in immunocompromised

High mortality

A

Aspergilluis

1005
Q

Meningitis in immunocompromised

Insidious onset in HIV

A

Cryptoccous

1006
Q

Dx of aspergillus

A

ELISA

PCR

Beta-blucan test

1007
Q

Dx of crytpococcal meningitis

A

Cryptococcal antigen in CSF

1008
Q

Halo sign on CT

Ground glass attenuation surrounding a pulmonary nodule

A

Invasive pulmonary asperigllosis

1009
Q

Hyalohyphomycosis

A

o Oppourtunistic mycotic infection caused by non-dematiaceous moulds
 Dematiaceous moulds: dark coloured, produce melanin
 Fusarium, penicillium, paecilomyses, acremonium, scopulariopsis, beauvaria.
o Harmless saprophytic colonisation to acute invasive disease
 Saprophytic: organism that lives on dead organic matter.
o Predisposing factors: haematological malignancies, prolonged neutropenia, corticosteroid
therapy and IS supp.
o Only culture and microscopy

1010
Q

Caused by dematiaceous moulds (black/pigmented)
o Localised superficial infections of the stratum corneum, subcutaneous or invasive including brain
infections.
o Organisms: cladophialophora (bantiana), curvularia, exophiala, bipolaris, phialophora,
excerohium, wangiella.
o Detection: culture, microscopy: masson Fontana

A

Phaeohyphomycosis

1011
Q

Chronic granulomatous, pulmonary and disseminated disease due to blastomyces dermatitidis
o Blastomyces dermatitidis: dimorphic fungi
o Endemic to the Americas and Africa
o Detection: culture and microscopy, serological test, antibody

A

Blastomycosis

1012
Q

Initially a respiratory infection due to coccidioides immitis, in some patients e.g. HIV, chronic and systemic disease involving
the meninges, bone, joints and other tissues.
o Endemic to south-western USA, north Mexico and part of South America.
o Detection: culture, microscopy, serological test, antibody.

A

Coccidioidomycosis

1013
Q

Dimorphic
o Intracellular infection of the reticuloendothelial system caused by histoplasma capsulatum
o Can mimic TB
o Endemic to the Americas and Africa - Found in soil enriched with excreta from chickens and bats.

A

Histoplasmosis

1014
Q

Dimorphic
o Chronic granulomatous disease due to paracoccidioides brasiliensis
o Primary pulmonary, disseminates to form an ulcerative granuloma of the buccal, nasal or GI mucosa.
o Endemic to south and central America.

A

Paracoccidioidomycosis

1015
Q

Systemic disease in immunocompromised patients, particularly HIV
o Endemic to south east Asia
o Easy to culture in both the yeast and filamentous forms.

A

Penicillium marneffei

1016
Q

Dimorphic, Sporothrix schenckii
o A chronic infection of the Cutaneous or subcutaneous tissue and the adjacent lymphatics, nodular lesions which may
suppurate and ulcerate
o Spread to articular surfaces, bone and muscle.

A

Sporotrichosis

1017
Q

Cutaneous or subcutaneous infection resulting in necrotic patches
o Acute rapidly developing, often fatal infection in debilitated or diabetic
patients
o Due to; absidia, cunninghamella, mortierella, mucor, rhizomucor,
rhizopus, and saksenaea.
o Most devastating fungal disease

A

Mucormycosis

1018
Q

Conidiobolus coronatus
 Chronic granulomatous disease of the nasal submucosa,
polyps or palpable masses
 Rare: systemic and pulmonary
 Seen mainly in the tropics.
o Basidiobolus ranarum
 Chronic granulomatous disease limited to limbs, chest, back and buttocks
 Seen mainly in the tropics.

A

Entomophthoromycosis

1019
Q

o Infection due to fungi (eumycetoms) and actinomycetes resulting from traumatic
implantation.
o Cutaneous or subcutaneous tissues and bone of the foot & hand.
o Sinuses discharge serosanguinous fluid containing grains
o Organisms: madurella, acremonium, scedosporium, curvularis, exophiala, leptosphaeria,
fusarium, aspergillus.

1020
Q

o A slowly progressing cutaneous and subcutaneous infection due to dematiaceous planatedividing
sclerotic bodies resulting from traumatic implantation.
o Associated with wood
o Organisms: cladophialophora, phialophora, fonsecaea etc.

A

Chromoblastomycosis

1021
Q

Infection of humans and dolphins by unisolated and unclassified yeast like
fungus Loboa loboi- Not grown in the lab yet
o Chronic subepidermal infection - No systemic spread
o Keloidal, verrucoid nodular lesions or vegetating crusty plaques and tumours
o Restricted to the Amazon valley in Brazil.
o Improving culture - dimorphic = extended incubation

A

Lobomycosis

1022
Q

What are the different classes of antifungals

A

Polyene

Azole

Terbinafine

Flucytosine

Echinocandin

1023
Q

MOA:

Polyenes

A

Cell membrane integrity

1024
Q

MOA:

Azoles

A

Cell membrane synthesis

1025
Q

MOA:

Terbinafine

A

Cell membrane synthesis

1026
Q

MOA:

Flucytosine

A

DNA synthesis

1027
Q

MOA:

Echinodcandin

1028
Q

What is used to treat cryptococcal meningitis and invasive fungal infection?

A

Amphotericin B

1029
Q

What drugs are used to treat yeast infection

A

Polyenes

Azoles

Echinocandin

1030
Q

E.g. polyene

A

Amphotericin

1031
Q

E.g. azole

A

Fluconazole

1032
Q

Eg. echinocandin

A

Caspofungin

1033
Q

What is used to treat mould infection/dermatophytes

A

Terbinafine

1034
Q

SE: amphotericin

A

Permanent renal impairment

1035
Q

Flucytosine used to treat

1036
Q

Se of flucytosine

A

Bone marrow suppression

1037
Q

What is the treatment for candidaemia

A

Fluconazole

1038
Q

Clinical features of HIV infection in children

A

Systemic symptoms

Skin rashes: extensive follicular rash, disseminated scabies

Oesophageal candidiasis

Kaposi’s sarcoma

Primary zoster

Multidermal zoster infection

Molluscum contagiosum

HIV encephalopathy

Severe

FTT
CMV retinitis

1039
Q

Dramatic lymphadenopathy usuallly accompanied by hepatosplenomegaly and lymphoid intersitital pneumonitits

A

Sign of immune activation following HIV infection

1040
Q

caused by a threadlike nematode (roundworm) belonging to the superfamily of filarioidea. Transmitted by
clack flies and mosquitoes. Effect the lymph nodes

A

Filariasis

1041
Q

filariasis, river blindness,

1042
Q

Classically acquired on a beach holiday because of
hookworm in dog faeces. The conditions in a ropical
holiday are sufficiently sandy, warm and wet to sustain
the life cycle.
o Once acquired the cutaneous larva migrans on the bits of
skin which came into contact with the soil.
o Though the course of the worm can keep wandering, and
cause bullae to form. Very itchy.

A

Cutaenous larva migrans (ancylostoma braziliense)

1043
Q

Treatment of cutaenous larva migrans

A

Can do nothingh- may resolve spontaenously

Topical: thiabendazole

Oral: albendazole or ivermectin

1044
Q

Infestation by a fly larvae that feeds on the tissue
o Endemic to tropical
regions of Africe and south of Sahara desert. Eggs are laid on
damp clothing hanging out to dry, when the larvae hatch and
can penetrate a new host. This causes a swelling and takes 8-
12 days to develop through three larval stages. It then leaves
the host, drops to the floor, buries and pupates to emerge as
a fly.

A

Tumbu fly: cordylobia anthropophagi.

1045
Q

Uses humans as the
host for its larvae. But other vectors such as mosquitoes are
used to deposit larvae in humans. After about 8 weeks they drop out to pupate in the soil after developing in the
subcutaneous tissue. Rare for pts to experience infection unless they kill the larvae without removing it completely. Larvae
can produce antibiotic secretions to help prevent infections while it is feeding. They do not kill the host animal and thus are
true parasites. The fly larvae can only survive the entire 8 weeks if the wound does not become infected.

A

Human Bot Fly: Dermatobia hominis.

1046
Q

Parasitic arthropod found in tropical climates.
o Is 1mm long, and the smallest know flea
o Burrows head first into the hosts skin, often leaving the caudal top of its
abdomen visible through an orifice in a skin lesion. This orifice allows for the
jigger to breathe and defecate while feeding on blood.
o In the next 2 weeks is abdomen swells up with dozens of eggs which it releases
through the caudal orifice to fall to the ground when ready to hatch.
o The flea then dies and is sloughed off with the hosts skin. Within the next 3-4
days the eggs hatch and mature into adult fleas within 3-4 weeks.
o Infections almost always on the foot, feel like itching or irritation to begin with,
which then passes as the area around the flea calluses and become insensitive.
As the abdomen swells this may cause local pressures.
o Complications- bacterial superinfection, ulceration, nail destruction,
lymphoedema and tetanus.

A

Tungiasis: Tunga Penetrans / Jigger / Chigoe Flea

1047
Q

The antiviral which is given to untreated pregnant women with HIV to prevent vertical transmission of the virus during childbirth.

.

Zidovudine

B.

Aciclovir

C.

Oseltamivir

D.

Neuraminidase inhibitor

E.

Foscarnet

F.

Nevirapine

G.

Cidofovir

H.

Ganciclovir

I.

Entecevir

J.

Interferon-α (alpha)

K.

Aciclovir triphosphate

L.

Ribavirin

M.

Interferon-b (beta)

N.

Aciclovir monophosphate

O.

Interferon-g (gamma)

A

ZDV was the first drug for which efficacy was shown. NVP alone has been shown to be more effective than ZDV alone in certain groups (see below). ZDV + 3TC has also been shown to more effective than ZDV alone but efficacy with this regimen falters out by 18 months. Abbreviations ZDV zidovudine, NVP nevirapine, 3TC lamivudine, PLCS prelabour caesarean section PEP post exposure prophylaxis

1048
Q

The drug mechanisms which acts by stopping post-translational cleaving of polyproteins by inhibiting proteases

A.

Nevirapine

B.

Amantadine

C.

Zanamivir

D.

Ganciclovir

E.

Aciclovir

F.

Ribavarin

G.

Interferon

H.

Enfuvirtide

I.

Indinavir

J.

Human normal immunoglobulin

K.

Zidovudine

L.

Human specific immunoglobulin

M.

Efavirenz

1049
Q

The drug which can be delivered by inhalation to treat both influenza A and B.

A.

Nevirapine

B.

Amantadine

C.

Zanamivir

D.

Ganciclovir

E.

Aciclovir

F.

Ribavarin

G.

Interferon

H.

Enfuvirtide

I.

Indinavir

J.

Human normal immunoglobulin

K.

Zidovudine

L.

Human specific immunoglobulin

M.

Efavirenz

1050
Q

A nucleoside analogue which inhibits reverse transcriptase

A.

Nevirapine

B.

Amantadine

C.

Zanamivir

D.

Ganciclovir

E.

Aciclovir

F.

Ribavarin

G.

Interferon

H.

Enfuvirtide

I.

Indinavir

J.

Human normal immunoglobulin

K.

Zidovudine

L.

Human specific immunoglobulin

M.

Efavirenz

A

Zidovudine

1051
Q

Common side effects of NRITs?

A

Lactic acidosis

1052
Q

Main side effects of NNRTIs

A

Rash

SJS

TEN

Fatal fulminant hepatitis

1053
Q

Main side effects of protease inhibitors

A

Insulin resistance

Dyslipidaemia

Lipodystrophy

Bleeding in haemophilia

1054
Q

What are the 5 most important p450 substrates?

A

Warfarin

AEDs

OCP and prednisolone

Ciclosporin A, Tacrolimus

NNRTIs and PIs

Giving rifampicin or chronic alcohol use (or any enzyme inducer) will cause drug levels to fall, with DISASTROUS consequences for the patient and for your career (negligence). The renal transplant patient who catches TB will reject her kidney, the HIV patient will suffer fatal opportunistic infection, the young woman with TB becomes pregnant, the epileptic starts fitting and loses her driving licence for a year and maybe her pregnancy (during the fit), and the patient with a metallic aortic valve strokes out.

1055
Q

An 18 year old trainee clown is being seen in the cystic fibrosis clinic and is found to be colonised with a particularly persistent organism.

A.

Chlamydia psittaci

B.

S. pneumoniae

C.

Anaerobic infection

D.

Burkholderia cepacia

E.

PCP/ P jiroveci

F.

MRSA

G.

MSSA

H.

Legionella pneumophila

I.

M. Catarrhalis

J.

Chlamydia pneumoniae

K.

H. influenzae

L.

MSSA or MRSA

M.

M tuberculosis

A

Burkholderia

1056
Q

What are the side effects of the macrolides

A

they are motilin Receptor agonists so increase GI motility: diarrhoea, nausea, vomiting - acute cholestatic hepatitis esp erythromycin estolate (idiosyncratic reaction) - ENZYME INHIBITORS except azithromycin - increase QT interval CONTRA-INDICATED in pregnanc

1057
Q

Rx in VISA or VRSA?

1058
Q

What are VISA

VRSA

VRE

A

VISA: Staph aureus with intermediate level resistance to vancomycin VRSA: Vancomycin resistant Staph aureus VRE: Vancomycin resistant Enterococcus faecium or Enterococcus faecalis

1059
Q

On your elective in central Africa a 7 year old child comes to your clinic with a large mass on his jaw. You take a biopsy of the lump, which shows EBV positive large cell lymphoma B cells. Histology shows a starry sky appearance (isolated histiocytes on a background of abnormal lymphoblasts). Genetic testing shows the presence of a 14q/8q translocation. The consultant suggests treating with cyclophosphamide and a single dose leads to a spectacular remission.

A.

Chicken Pox

B.

Cytomegaloviruses

C.

Burkitt’s lymphoma

D.

Primary Genital Herpes

E.

Keratitis

F.

Herpes Labialis (Cold sores)

G.

Roseola infantum

H.

Shingles

I.

Glandular fever

J.

HHV 6

K.

HHV 7

A

Burkitt’s

1060
Q

Which of the above is a naturally occurring cytokine that is able to inhibit HIV fusion to CD4+ T-lymphocytes?

A.

Integrase

B.

CCR5/CXCR4

C.

CD8

D.

Kaposi’s sarcoma

E.

Candidiasis

F.

Viral load (PCR)

G.

Anti-HIV antibody (Western blot)

H.

CD4

I.

CD25

J.

gp120

K.

Reverse transcriptase

L.

Hairy leukoplakia

M.

MIP-1alpha

A

MIP-1alpha

1061
Q

56 year old male with endocarditis caused by VRE.

A.

Vancomycin

B.

Linezolid

C.

Ciprofloxacin

D.

Erthyromycin

E.

Ceftriaxone

F.

Gentamicin

G.

Metronidazole

H.

Flucloxacillin

I.

Benzyl Penicillin

A

Ceftriaxone

1062
Q

An 82 yr old gentleman, living at home, develops severe dyspnoea with a productive cough and fever. His PaO2 has fallen below 8kPa, and he is becoming confused.

.

isoniazid

B.

trimethoprim

C.

rifampicin

D.

vancomycin

E.

Ceftriaxone

F.

Amoxicillin

G.

Chloramphenicol

H.

cefuroxime & clarithromycin

I.

no antibiotics required

J.

linezolid

K.

Flucloxacillin

L.

Cefalexin

M.

Erythromycin

A

cefuroxime & clarithromycin

1063
Q

A 6 month old child whose father has just been diagnosed with tuberculosis.

A.

isoniazid

B.

trimethoprim

C.

rifampicin

D.

vancomycin

E.

Ceftriaxone

F.

Amoxicillin

G.

Chloramphenicol

H.

cefuroxime & clarithromycin

I.

no antibiotics required

J.

linezolid

K.

Flucloxacillin

L.

Cefalexin

M.

Erythromycin

1064
Q

Treatment of known N menginitides meningitis

1065
Q

First choice in bacterial meningitis of unknown aetiology

A

3rd gen cephalosporins

Ceftriaxone

1066
Q

This microbe is spread by faecal-oral route, and often occurs in epidemics. Shellfish from seawater contained by sewage can harbour this microbe.

A.

Entamoeba histolytica

B.

Escherichia Coli

C.

Salmonella

D.

Shigella

E.

Vibrio cholera

F.

Clostridium difficile

G.

Aeromonas

H.

Hepatitis A

I.

Yersinia

1067
Q

This microbes affects mainly the distal colon, producing acute mucosal inflammation and erosion. It is spread by person-to-person contact, and its clinical features include fever, pain, diarrhoea and dysentery.

A.

Entamoeba histolytica

B.

Escherichia Coli

C.

Salmonella

D.

Shigella

E.

Vibrio cholera

F.

Clostridium difficile

G.

Aeromonas

H.

Hepatitis A

I.

Yersinia

1068
Q

This microbe affects the ileum, appendix and colon. Its peyer patch invasion leads to mesenteric lymph node enlargement with necrotising granulomas. Complication can include peritonitis, pharyngitis and pericarditis.

A.

Entamoeba histolytica

B.

Escherichia Coli

C.

Salmonella

D.

Shigella

E.

Vibrio cholera

F.

Clostridium difficile

G.

Aeromonas

H.

Hepatitis A

I.

Yersinia

A

Yersinia enterocolitica undergoes multiplication in Peyer’s patches following invasion of human epithelial cells and penetration of the mucosa which occurs in the ileum. Complications include diarrhoea, mesenteric adenitis, mesenteric ileitis, or acute pseudoappendicitis, reactive arthritis and erythema nodosum. Ingestion of Entamoeba histiolytica cysts is followed by excystation in the small bowel and trophozite colonisation of the small colon. The trophozyte may then encyst and be excreted in faeces or it may invade the intestinal mucosal barrier, thereby gaining access to the circulation. Complications include amoebic colitis, liver abscesses, pleuropulmonary amoebiasis and cerebral amoebiasis

1069
Q

A 30 year old male is brought into hospital. He is very dehydrated and is feeling very weak. He has had unrelenting diarrhoea, which came on suddenly. He describes the stools as looking like rice water. He has no abdominal pain.

A.

Rotavirus

B.

Tuberculosis of the gut

C.

Clostridium difficile

D.

Bacillus cereus

E.

Verotoxin-producing E.coli

F.

Cholera

G.

Bacterial Dysentry

H.

Stress

I.

Salmonella

J.

Ulcerative colitis

K.

Giardiasis

1070
Q

Following a trip to Brazil, a patient develops bloody diarrhoea, with a high fever, sweating and on examination the patient is found to have RUQ pain.

A.

Giardia Lamblia

B.

Entamoeba Histolytica

C.

Camplyobacter Jejuni

D.

Typhoid

E.

Vibrio Cholera

F.

Taenia Saginata

G.

E. coli

H.

Taenia Solium

I.

Shigella

J.

Salmonella

K.

Clostridium Difficile

L.

Laxative abuse

M.

Yersinia Enterocolitica

A

Entamoeaba histolytica

1071
Q

Following a barbeque, a 41 year old develops watery diarrhoea and vomiting. On retrospect, he wondered whether he should have had that dodgy looking shish kebab.

A.

Giardia Lamblia

B.

Entamoeba Histolytica

C.

Camplyobacter Jejuni

D.

Typhoid

E.

Vibrio Cholera

F.

Taenia Saginata

G.

E. coli

H.

Taenia Solium

I.

Shigella

J.

Salmonella

K.

Clostridium Difficile

L.

Laxative abuse

M.

Yersinia Enterocolitica

A

Salmonella

1072
Q

A 40 year old homosexual man develops severe flatulence, accompanied by bloating and explosive diarrhoea.

A.

Giardia Lamblia

B.

Entamoeba Histolytica

C.

Camplyobacter Jejuni

D.

Typhoid

E.

Vibrio Cholera

F.

Taenia Saginata

G.

E. coli

H.

Taenia Solium

I.

Shigella

J.

Salmonella

K.

Clostridium Difficile

L.

Laxative abuse

M.

Yersinia Enterocolitica

1073
Q

Mr S became ill with nausea, vomiting and watery diarrhoea about 4 hours after eating some ham at a conference buffet lunch. Mr B’s illness was attributed to a heat stable, preformed toxin in the ham. His symptoms resolved within 24hours.

A.

Campylobacter

B.

Salmonella

C.

Rotavirus

D.

Shigella

E.

Escherichia coli

F.

Clostridium botulinum

G.

Entamoeba histolytica

H.

Staphylococcus

I.

Bacillus cereus

1074
Q

Mr C complained of fever and severe (>10 bowel movements/day) diarrhoea after looking after his neighbours dogs for a few days. Laboratory analysis of Mr C’s stools found the causative organism to be a S-shaped microaerophillic bacteria.

A.

Campylobacter

B.

Salmonella

C.

Rotavirus

D.

Shigella

E.

Escherichia coli

F.

Clostridium botulinum

G.

Entamoeba histolytica

H.

Staphylococcus

I.

Bacillus cereus

A

Campylobacter

1075
Q

A toxin-mediated organism that does not damage or invade the gastrointestinal epithelium

A.

Giardia lamblia

B.

Shigella

C.

E. coli

D.

Bacillus cereus

E.

Cholera

F.

Staphylococcus aureus

G.

C. difficile

H.

Salmonella

I.

Clostridium botulinum

1076
Q

Laryngeal spasm seen in?

A

Rabies encepalomyelitis

1077
Q

What differentiates between GBS and botulism

A

GBS is ascending

1078
Q

Inactivated preparations of the bacteria

A.

pneumococcal vaccine

B.

Hepatitis B virus vaccine

C.

tetanus vaccine

D.

BCG vaccine

E.

oral poliomyelitis vaccine

F.

Whole cell typhoid vaccine

G.

Hepatitis A virus vaccine

H.

Hib vaccine

A

Whole cell typhoid vaccine

1079
Q

A sub-unit / conjugate vaccine

A.

pneumococcal vaccine

B.

Hepatitis B virus vaccine

C.

tetanus vaccine

D.

BCG vaccine

E.

oral poliomyelitis vaccine

F.

Whole cell typhoid vaccine

G.

Hepatitis A virus vaccine

H.

Hib vaccine

A

A.

pneumococcal vaccine

1080
Q

Vaccine that is made using recombinant DNA technology.

A.

pneumococcal vaccine

B.

Hepatitis B virus vaccine

C.

tetanus vaccine

D.

BCG vaccine

E.

oral poliomyelitis vaccine

F.

Whole cell typhoid vaccine

G.

Hepatitis A virus vaccine

H.

Hib vaccine

A

Hepatitis B virus vaccine

1081
Q

An antigen assembled in a multimeric form and saponin that provokes a strong serum antibody response.

A.

IFN gamma

B.

Rubella vaccine

C.

Effector memory

D.

Yellow fever vaccine

E.

Immunostimulatory complexes (ISCOMS)

F.

Perforin

G.

Typhoid vaccine

H.

CpG sites

I.

Bacillus Calmette-Guerin

J.

Adjuvant

K.

Rabies vaccine

L.

IL2

M.

MMR vaccine

A

Immunostimulatory complexes (ISCOMS)

1082
Q

A feature of immunological central memory

A.

IFN gamma

B.

Rubella vaccine

C.

Effector memory

D.

Yellow fever vaccine

E.

Immunostimulatory complexes (ISCOMS)

F.

Perforin

G.

Typhoid vaccine

H.

CpG sites

I.

Bacillus Calmette-Guerin

J.

Adjuvant

K.

Rabies vaccine

L.

IL2

M.

MMR vaccine

A

IL2Central memory (CM) T cells migrate efficienctly to peripheral LNs and produce IL-2, no IFN-gamma and no perforin. In contrast, effector memory (EF) T cells do not migrate efficiently but are found in other sites such as the liver and lungs. EF T cells produce little IL-2, but high amounts of IFN-gamma and perforin.

1083
Q

Which vaccine is usually given to children at 12-15 months?

A.

Tetanus vaccine

B.

Influenza vaccine

C.

Mycobacterium bovis

D.

Diptheria vaccine

E.

Inactivated

F.

Poliomyelitis vaccine

G.

Mycobacterium tuberculosis

H.

MMR vaccine

I.

Haemophilus influenzae type b vaccine

J.

Varicella-zoster vaccine

K.

Smallpox vaccine

L.

Live attenuated

M.

Typhoid vaccine

1084
Q

Which vaccine is normally given to infants under the age of 13 months in the form of three doses at monthly intervals to protect against an infection that has symptoms similar to meningitis and predominantly occurs in children < 5 years?

A.

Tetanus vaccine

B.

Influenza vaccine

C.

Mycobacterium bovis

D.

Diptheria vaccine

E.

Inactivated

F.

Poliomyelitis vaccine

G.

Mycobacterium tuberculosis

H.

MMR vaccine

I.

Haemophilus influenzae type b vaccine

J.

Varicella-zoster vaccine

K.

Smallpox vaccine

L.

Live attenuated

M.

Typhoid vaccine

1085
Q

Conjugate vaccine routinely given to neonates in the UK.

A.

Varicella zoster

B.

HBV

C.

CpG

D.

BCG

E.

Typhoid

F.

IL-2

G.

H. influenzae B

H.

Meningococcal A

I.

Tetanus

J.

Polio (Sabin)

K.

Freund’s

L.

Influenza

M.

Alum

N.

MMR

O.

Rabies

P.

Polio (Salk)

1086
Q

Agent used in humans that promotes a predominantly antibody response through the release of Il-4 that primes naïve B-cells.

A.

Varicella zoster

B.

HBV

C.

CpG

D.

BCG

E.

Typhoid

F.

IL-2

G.

H. influenzae B

H.

Meningococcal A

I.

Tetanus

J.

Polio (Sabin)

K.

Freund’s

L.

Influenza

M.

Alum

N.

MMR

O.

Rabies

P.

Polio (Salk)

1087
Q

Live attenuated vaccine that is no longer given as standard in the UK since the rates of reverse mutation are higher than those of active disease

A.

Varicella zoster

B.

HBV

C.

CpG

D.

BCG

E.

Typhoid

F.

IL-2

G.

H. influenzae B

H.

Meningococcal A

I.

Tetanus

J.

Polio (Sabin)

K.

Freund’s

L.

Influenza

M.

Alum

N.

MMR

O.

Rabies

P.

Polio (Salk)

A

Polio (Sabin)

1088
Q

Subunit vaccine given to the elderly and immunocompromised

A.

Varicella zoster

B.

HBV

C.

CpG

D.

BCG

E.

Typhoid

F.

IL-2

G.

H. influenzae B

H.

Meningococcal A

I.

Tetanus

J.

Polio (Sabin)

K.

Freund’s

L.

Influenza

M.

Alum

N.

MMR

O.

Rabies

P.

Polio (Salk)

1089
Q

Vaccination with which of the above prevents a gram negative rod meningitis typically affecting children below 4 years of age?

A.

Rabies vaccine

B.

Influenza vaccine

C.

Polio vaccine

D.

Mumps vaccine

E.

Tetanus vaccine

F.

Hepatitis A vaccine

G.

Hepatitis B vaccine

H.

Rubella vaccine

I.

Diptheria vaccine

J.

BCG

K.

HIB vaccine

A

HIB vaccine

1090
Q

Which is recommended in all individuals over 65 years of age?

A.

Rabies vaccine

B.

Influenza vaccine

C.

Polio vaccine

D.

Mumps vaccine

E.

Tetanus vaccine

F.

Hepatitis A vaccine

G.

Hepatitis B vaccine

H.

Rubella vaccine

I.

Diptheria vaccine

J.

BCG

K.

HIB vaccine

A

Pneumococcal and influenza vaccinations are recommended routinely for those over 65 and also for both children and adults in special risk categories.

1) Pneumovax administration:

Routinely given as a one-time dose; administer if previous vaccination history is unknown. However..one-time revaccination is recommended 5yrs later for people at highest risk of fatal pneumococcal infection or rapid antibody loss (e.g., renal disease) and for people >65yrs of age if the 1st dose was given prior to age 65 and >5yrs have elapsed since previous dose

1091
Q

A conjugate vaccine

A.

BCG vaccine

B.

Meningococcal A vaccine

C.

Tetanus vaccine

D.

Hepatitis A virus vaccine

E.

Oral poliomyelitis vaccine

F.

Haemophilus influenzae type B vaccine

G.

Hepatitis B virus vaccine

A

Haemophilus influenzae type B vaccine

1092
Q

Inactivated vaccine.

A.

BCG vaccine

B.

Meningococcal A vaccine

C.

Tetanus vaccine

D.

Hepatitis A virus vaccine

E.

Oral poliomyelitis vaccine

F.

Haemophilus influenzae type B vaccine

G.

Hepatitis B virus vaccine

A

Hepatitis A virus vaccine

1093
Q

Excreted in the stools of immunised individuals.

A.

BCG vaccine

B.

Meningococcal A vaccine

C.

Tetanus vaccine

D.

Hepatitis A virus vaccine

E.

Oral poliomyelitis vaccine

F.

Haemophilus influenzae type B vaccine

G.

Hepatitis B virus vaccine

A

Oral poliomyelitis vaccine

1094
Q

What do these have in common:

Measles, mumps, rubella (German measles), polio (Sabin vaccine), chicken pox, yellow fever, BCG

A

All live attenuated vaccines

1095
Q

What do these have in common:

Cholera, IFV, HAV, rabies, polio

A

All inactivated (killed) vaccines)

1096
Q

What type of vaccine is the HBV vaccine?

A

Subunit vaccine

1097
Q

What type of vaccines are the Hib and pneumococcal vaccine?

1098
Q

This is a vaccine made of recombinant protein.

A.

Freund’s adjuvant

B.

MMR

C.

Mantoux

D.

Live attenuated

E.

Polio

F.

Active immunity

G.

IL-12

H.

HAV

I.

HBV

J.

Conjugate

K.

Passive immunity

L.

Typhoid

M.

Menigococcal

N.

Alum

O.

Inactivated

1099
Q

A water-in-oil emulsion containing mycobacterial cell wall components that could be used to increase the immune response of a vaccine.

A.

Freund’s adjuvant

B.

MMR

C.

Mantoux

D.

Live attenuated

E.

Polio

F.

Active immunity

G.

IL-12

H.

HAV

I.

HBV

J.

Conjugate

K.

Passive immunity

L.

Typhoid

M.

Menigococcal

N.

Alum

O.

Inactivated

A

Freund’s adjuvan

1100
Q

A student who presented with two day history of bloody diarrhoea, vomiting, fever, headache and myalgia. He has just returned from camping in the country side near a farm where he had fresh cow’s milk for breakfast everyday.

A.

Brucella abortus

B.

Yersinia pestis

C.

Francisella tularensis

D.

Cryptosporidium parvum

E.

Campylobacter jejuni

F.

Borrelia burgdorferi

G.

Trypanosoma cruzi

H.

Rickettsia prowazekii

I.

Bartonella henselae

J.

Spirillum minus

A

Campylobacter jejuni

1101
Q

A 2 year old boy living in the slums who has a one day history of profuse watery diarrhoea, fever and abdominal cramps. His family’s main source of water is the river near their squatters.

A.

Brucella abortus

B.

Yersinia pestis

C.

Francisella tularensis

D.

Cryptosporidium parvum

E.

Campylobacter jejuni

F.

Borrelia burgdorferi

G.

Trypanosoma cruzi

H.

Rickettsia prowazekii

I.

Bartonella henselae

J.

Spirillum minus

A

Cryptosporidium parvum

1102
Q

Cat-scratch disease

A

Bartonella henselae

1103
Q

A man was bitten by a rat in Asia. Ten days later he complains of fever, malaise, headache and myalgia.

A.

Brucella abortus

B.

Yersinia pestis

C.

Francisella tularensis

D.

Cryptosporidium parvum

E.

Campylobacter jejuni

F.

Borrelia burgdorferi

G.

Trypanosoma cruzi

H.

Rickettsia prowazekii

I.

Bartonella henselae

J.

Spirillum minus

A

Spirillum minus

1104
Q

A zoonosis associated with hepatitis, jaundice, conjunctival injection and renal impairment. Transmission normally occurs by direct contact with either the urine or tissues of an infected animal.

A.

Rheumatic fever

B.

Leptospirosis

C.

Brucellosis

D.

Tularaemia

E.

Lyme disease

F.

Listeriosis

G.

Meningococcal Septicaemia

A

Leptospirosis

1105
Q

A 22 year old student, who returned from a holiday in the Mediterranean 3 weeks ago, presents with an undulant fever, malaise, weakness and generalized bone pain. Upon examination lymphadenopathy and hepatosplenomegaly are also noted.

A.

Rheumatic fever

B.

Leptospirosis

C.

Brucellosis

D.

Tularaemia

E.

Lyme disease

F.

Listeriosis

G.

Meningococcal Septicaemia

A

Brucellosis

1106
Q

A 25 year old Maltese man presented to his GP with lethargy for a month and headaches and fever. On examination, he had a temperature of 39°C and one fingerbreadth splenomegaly. Small Gram-negative coccobacilli were seen on culture in Casteneda’s medium.

A.

Brucella abortus

B.

Rickettsia typhi

C.

Leishmania major.

D.

Yersina pestis

E.

Leptospira interrogans

F.

Rabies

G.

Bacillus anthracis

H.

Borrelia burgdorferi

I.

Brucella melitensis

A

Brucella melitensis

1107
Q

A tanner on holiday from India presented to hospital with an ulcerating papule on his hand. On inspection of the ulcer, the centre was black and necrotic. Gram-positive rods grew on blood agar culture and responded to treatment with large doses of penicillin.

A.

Brucella abortus

B.

Rickettsia typhi

C.

Leishmania major.

D.

Yersina pestis

E.

Leptospira interrogans

F.

Rabies

G.

Bacillus anthracis

H.

Borrelia burgdorferi

I.

Brucella melitensis

A

Bacillus anthracis

1108
Q

A 21 year old man presents at his GP complaining of an itchy, scaly rash on the soles of his feet. Skin scrapings are taken and sent away for microscopic examination. Which fungi might be identified?

A.

Corynebacterium minutissimum

B.

Candida albicans

C.

Aspergillus flavus

D.

Epidermophyton floccosum

E.

Cryptococcus neoforms

F.

Pityrosporum orbiculare

G.

Histoplasmosis capsulatum

H.

Pneumocystis carinii

I.

Trichophytum rubrum

A

richophyton rubrum as it is the commonest fungus from feet. If there was laceration and lots of blisters then it will be Trichophyton interdigitale.

1109
Q

A 55 year old farmer is seen in the Oncology clinic with a diagnosis of hepatocellular carcinoma. He is a lifelong teetotal and his virology has all been negative. Which fungus may have indirectly been a cause of his cancer?

A.

Corynebacterium minutissimum

B.

Candida albicans

C.

Aspergillus flavus

D.

Epidermophyton floccosum

E.

Cryptococcus neoforms

F.

Pityrosporum orbiculare

G.

Histoplasmosis capsulatum

H.

Pneumocystis carinii

I.

Trichophytum rubrum

A

Aspergillus flavus

1110
Q

A 17 year old Nigerian girl presents at her GP with patches of hypopigmentation on her trunk. After an initial trial of steroid cream, the girl returns complaining that the rash is spreading. Woods lamp examination of the rash produces a yellow fluorescence. What is the causative fungus?

A.

Corynebacterium minutissimum

B.

Candida albicans

C.

Aspergillus flavus

D.

Epidermophyton floccosum

E.

Cryptococcus neoforms

F.

Pityrosporum orbiculare

G.

Histoplasmosis capsulatum

H.

Pneumocystis carinii

I.

Trichophytum rubrum

A

Pityrosporum orbiculare

1111
Q

Which fungi is normally associated groin infection?

A

E floccusum is normally associated with GROIN infections, the old joke with Rugby players’ groins

1112
Q

A 23 year old female on a camping holiday used the local rowing club showers nearby. A few days later she noticed an itchy sensation between some her toes. What is the most likely diagnosis?

A.

Pediculosis capitis

B.

Blastomyosis

C.

Zygomycosis

D.

Chromomycosis

E.

Mycetoma (Madura foot)

F.

Tinea cruris

G.

Tinea corporis

H.

Tinea pedis

I.

Candidiasis

J.

Aspergillosis

K.

Cryptococcis

L.

Sporotrichosis

M.

Coccidiodomyosis

A

Tinea pedis

1113
Q

A 45 year old female whose main hobby was pigeon racing was noted by her GP to an enlarged lymph node in her neck. What is the most likely diagnosis?

A.

Pediculosis capitis

B.

Blastomyosis

C.

Zygomycosis

D.

Chromomycosis

E.

Mycetoma (Madura foot)

F.

Tinea cruris

G.

Tinea corporis

H.

Tinea pedis

I.

Candidiasis

J.

Aspergillosis

K.

Cryptococcis

L.

Sporotrichosis

M.

Coccidiodomyosis

A

Cryptococcus neoformans, is a pathogenic fungus commonly found in pigeon droppings and pigeon nests (and also soil). The predominant clinical process usually in immunocompromised pts, is a variably subacute meningitis with occasional patients showing features of brain abscess or inflammatory cerebral vasculitis, so the clinical feats are usually - headache, fever, nausea, neck stiffness, feats of raised ICP. Histoplasmosis, is also spread from bird droppings -but apparently not so specific to pigeons. Disseminated histoplasmosis, as you correctly state can cause lymphadenopathy (resembles disseminated TB - fever, weight loss, lymph nodes). PS. Remember India Ink staining for cryptococcus, which is often a clue in questions.

1114
Q

What are the identifiers for the different strains of brucella?

A

Abortus comes from cattle

Melitensis comes from goats, seen in the Mediterranean region

1115
Q

A 19 year-old student presents to her GP with a macular rash and suboccipital lymphadenopathy. She also complains of pain on moving her hands and wrists.

A.

Tuberculous arthritis

B.

Staphylococcal osteomyelitis

C.

Infectious mononucleosis

D.

Staphylococcal arthritis

E.

Candidiasis

F.

Rubella

G.

Viral hepatitis

H.

Gonococcal arthritis

I.

Lyme disease

J.

Tuberculous osteomyelitis

K.

Brodie’s abscess

1116
Q

Mr PD, a 26 year old musician, arrives in A&E with a warm, painful abscess on his inner upper forearm surrounded by puncture marks, he has a low grade fever. He reports no problem in playing his guitar, but does forget lyrics on stage.

A.

Clutton’s joints

B.

Pott’s disease

C.

Osteoporosis

D.

Septic arthritis

E.

Staphylococcus osteomyelitis

F.

Tuberculous osteomyelitis

G.

Painful crisis

H.

Brodie’s abscess

I.

Leukaemia

J.

Paget’s disease

K.

Salmonella osteomyelitis

L.

Lateral epicondylitis

A

Salmonella osteomyelitis

Salmonella is a very rare cause of osteomyelitis, except in sickle cell disease. If you look up salmonella osteomyelitis, this is striking. It is suggested that the peculiar susceptibility of patients with sickle cell anaemia to salmonella osteomyelitis is due to spread of salmonella from the intestine facilitated by devitalisation of gut caused by intravascular sickling, and that infarcts in bone became infected either by transient bacteraemia or by activation of dormant foci of salmonella in bone marrow when tissues are devitalised. It is further suggested that immunological defects in sicklers may impair host response to infection, while haemolysis and hepatic dysfunction, both of which occur in sickle cell anaemia, favour propagation of salmonellae.

1117
Q

A 10 year old boy presents with moderate pain in his lower leg, little redness and swelling, remitting for 6 months. His mother gives you the X-ray report from the previous episode, which showed “a well defined ovoid shape with a surrounding sclerotic margin but little involucrum in his tibia”.

A.

Clutton’s joints

B.

Pott’s disease

C.

Osteoporosis

D.

Septic arthritis

E.

Staphylococcus osteomyelitis

F.

Tuberculous osteomyelitis

G.

Painful crisis

H.

Brodie’s abscess

I.

Leukaemia

J.

Paget’s disease

K.

Salmonella osteomyelitis

L.

Lateral epicondylitis

A

Brodie’s abscess

1118
Q

A 30 year old builder develops abdominal pain and diarrhoea 48 hours after having Texa Fried Chicken. Faecal culture shows motile, oxidase-positive colonies and gram stain shows gram-negative rods.

A.

Salmonella typhi

B.

Staphylococcus aureus

C.

Neisseria meningitides

D.

Streptococcus pneumoniae

E.

Haemophilus influenzae

F.

Campylobacter jejuni

G.

Clostridium difficile

H.

Escherichia coli

1119
Q

A 55 year old man comes into A&E complaining of a increasing difficulty in opening is mouth and that the muscles on his face occasionally spasm. On examination you observe that his eyes are partially closed and that the angles of his mouth are stretched outwards and slightly downwards. You also note that he has a very rigid abdomen. Which treatment option should be carried out first for this patient?

A.

Airborne contamination

B.

Heart valve replacement

C.

Escherichia coli

D.

Oral administration of ampicillin

E.

Staphylococcal aureus

F.

Oral administration with penicillin G

G.

Drainage and evacuation of pus

H.

Implantation of a prosthetic hip

I.

Streptococcus pneumoniae

J.

Haemophilus influenzae

K.

I. V. injection of tetanus antitoxin

L.

Oral administration of flucloxacillin

A

I. V. injection of tetanus antitoxin

1120
Q

Which of the above is an example where prophylactic systemic antibiotic therapy should not be used.

A.

Airborne contamination

B.

Heart valve replacement

C.

Escherichia coli

D.

Oral administration of ampicillin

E.

Staphylococcal aureus

F.

Oral administration with penicillin G

G.

Drainage and evacuation of pus

H.

Implantation of a prosthetic hip

I.

Streptococcus pneumoniae

J.

Haemophilus influenzae

K.

I. V. injection of tetanus antitoxin

L.

Oral administration of flucloxacillin

M.

Removal of a breast carcinoma

A

Removal of a breast carcinoma

1121
Q

A man is recovering from surgery and inspection of the wound reveals that it has become infected. A swab is taken and the laboratory results show Staphylococcal aureus infection. What is appropriate treatment for this man?

A.

Airborne contamination

B.

Heart valve replacement

C.

Escherichia coli

D.

Oral administration of ampicillin

E.

Staphylococcal aureus

F.

Oral administration with penicillin G

G.

Drainage and evacuation of pus

H.

Implantation of a prosthetic hip

I.

Streptococcus pneumoniae

J.

Haemophilus influenzae

K.

I. V. injection of tetanus antitoxin

L.

Oral administration of flucloxacillin

M.

Removal of a breast carcinoma

A

Oral administration of flucloxacillin

1122
Q

An 80 year old man returns to his GP two weeks after being prescribed co-trimoxazole for a UTI. His urinary symptoms have now eased, but he is still experiencing a fever. His blood count shows eosinophilia.

A.

Hodgkin’s lymphoma

B.

Hepatitis B

C.

Mycobacterium tuberculosis

D.

Hepatitis C

E.

Escherichia coli

F.

Brucellosis

G.

SLE

H.

Mycobacterium avium complex

I.

Sarcoidosis

J.

Plasmodium malariae

K.

Epstein-Barr virus

L.

Drug induced fever

M.

Hepatitis A

A

Drug induced fever

1123
Q

A 19 year-old student presents to her GP with a macular rash and suboccipital lymphadenopathy. She also complains of pain on moving her hands and wrists. Why is this Rubella? I thought this is a typical descrption of Infectious Mononucleosis.

A

The patient is female. Rubella is followed by a reactive polyarthritis in a RA-like distribution (PIP, MCP, wrist) in 50% of women and 6% of men. If she hasn’t had MMR, do a pregnancy test!

1124
Q

Viral causes of reactive arthritis

A

Rubella

Hep B

Parvovirus B19

1125
Q

Bacterial causes of reactive arthritis

A

INcludes Reiter’s which can be post-dysentry or post-urethritis

Dysentry: shigella, salmonella, yesrisina, campylobacter (which can also be a precedent of GBS)

Urethritis: CHlamydia, Ureaplasma

Other: GAS, N. gonorrhoea, brucella, TB

1126
Q

Peri-infectious causes of reactive arthritis

A

Borrelia burdorferia

Rheumatic fever

1127
Q

Poncet’s disease

A

Reactive arthritis as a consequence of TB infection

Aseptic form of arthritis observed in patients with TB

1128
Q

Brodie’s abscess

A

A Brodie abscess is a subacute osteomyelitis, which may persist for years before converting to a frank osteomyelitis. Classically, this may present after conversion as a draining abscess extending from the tibia out through the shin.Occasionally acute osteomyelitis may be contained to a localized area and walled off by fibrous and granulation tissue.This is termed as Brodie’s abscess.

Most frequent causative organism is Staphylococcus aureus.

1129
Q

Clutton’s joints

A

Clutton’s joints is a term describing the finding of symmetrical joint swelling seen in patients with congenital syphilis. It most commonly affects the knees, presenting with synovitis and joint effusions (collections of fluid within the joint capsules) lasting up to a year. It has also been reported affecting the ankles, elbows, wrists and fingers. It is usually painless, although pain in the absence of trauma can occur in a few cases. There is usually no disability associated with the joint swelling, and recovery is usually complete. It occurs between 5 and 20 years of age in both sexes.

1130
Q

These infections are almost invariably associated with functional or anatomical abnormalities of the renal tract. Tip: also causes cavitating pneumonia.

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Klebsiella

1131
Q

The 2nd commonest cause of uncomplicated UTI in young women

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Staph Saprophyticus

1132
Q

an be used as monotherapy for acute pyelonephritis and should always be prescribed orally because its bioavailability is near 100% and iv dosing is 30 times more expensive.

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Ciprofloxacin

1133
Q

Causes haemorrhagic cystitis in children.

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Adenovirus

1134
Q

A cephalosporin used for treating pseudomonal infections in cystic fibrosis

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Ceftazidime

1135
Q

In combination with iv ampicillin, this drug is used iv for very sick patients with obstructed infected upper UTIs and gram negative septicaemia.

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Gentamicin

1136
Q

Given IM as a single shot for gonococcal urethritis

A.

Ceftriaxone

B.

Gentamicin

C.

Staph epidermidis

D.

Ceftazidime

E.

Staph saprophyticus

F.

Trimethoprim

G.

Ciprofloxacin

H.

Escherichia coli

I.

Tuberculosis

J.

Nitrofurantoin

K.

Adenovirus

L.

Candida

M.

Klebsiella

N.

Piperacillin

O.

Ampicillin

P.

Pseudomonas

A

Ceftriaxone

1137
Q

A 40-year-old Indian male presents to A&E with dysuria and back pain. He has recently noticed blood in his urine and his past medical history reveals that he has had hypertension for 5 years. After some initial reluctance, he admits to having HIV, which was diagnosed on his arrival in the UK 7 years previously.

A.

Inadequately treated UTI

B.

Cystitis

C.

Calculi

D.

Acute Prostatitis

E.

Acute Pyelonephritis

F.

Papillary Necrosis from Analgaesic Overdose

G.

Bladder Tumour

H.

Interstitial Nephritis

I.

Urethral Syndrome

J.

Polycystic Kidney

K.

Intrarenal Abscess

L.

Renal Tuberculosis

M.

Perinephric Abscess

A

Renal Tuberculosis

1138
Q

A 23-year-old Caucasian women presents to her GP with urinary frequency, urgency and burning. She also complained of slow stream as well as suprapubic pain. She has had several UTIs in the past and analysis of her urine showed no significant bacteruria.

A.

Inadequately treated UTI

B.

Cystitis

C.

Calculi

D.

Acute Prostatitis

E.

Acute Pyelonephritis

F.

Papillary Necrosis from Analgaesic Overdose

G.

Bladder Tumour

H.

Interstitial Nephritis

I.

Urethral Syndrome

J.

Polycystic Kidney

K.

Intrarenal Abscess

L.

Renal Tuberculosis

M.

Perinephric Abscess

A

Urethral Syndrome

1139
Q

A 42-year-old African American male presents to A&E with severe loin pain that radiates to the groin. He complains of painful urination, interrupted flow and increased urinary frequency. Urine dipstick reveals the presence of leucocytes, nitrites, haematuria and proteinuria. Intravenous uretogram shows a filling defect of the right kidney.

A.

Inadequately treated UTI

B.

Cystitis

C.

Calculi

D.

Acute Prostatitis

E.

Acute Pyelonephritis

F.

Papillary Necrosis from Analgaesic Overdose

G.

Bladder Tumour

H.

Interstitial Nephritis

I.

Urethral Syndrome

J.

Polycystic Kidney

K.

Intrarenal Abscess

L.

Renal Tuberculosis

M.

Perinephric Abscess

1140
Q

A 63 year old gentleman has a two day history of fever and rigors with lower back pain and discomfort on passing urine. Urine microscopy and culture revealed 2 x 104 Escherichia Coli per ml urine.

A

Bacterial prostatitis

1141
Q

A 40 year old lady was previously diagnosed with acute UTI and treated with trimethoprim. Ten days later she returns to her GP with the same symptoms of dysuria and frequency, and urine microscopy reveals a positive culture of the same bacteria.

A

A relapse of a UTI implies re-infection with the SAME organism. Recurrent UTIs imply infection with DIFFERENT organisms. A sterile pyuria occurs in renal tuberculosis. A urine culture must show >/= 1 x 10^5 colony-forming units (CFU) / mL of mixed bacterial growth with one predominant organism to be diagnostic of a UTI. (OR (for interested persons) 1 x 10^4 if just one organism, or 1 x 10^3 if E.coli or S.saprophiticus).

1142
Q

A 74 year old male is soon to undergo colorectal surgery and hospital procedures of antibiotic prophylaxis is followed.

A

Cef. & Met. 0-2hrs before incision & no longer than 24 hrs post-surgery

1143
Q

An 18 year old boy with cystic fibrosis recently underwent a knee operation. After a couple of days recovering in the ward he starts to wheeze, becomes breathless and coughs up sputum. He has a fever and blood cultures indicate the presence of gram-negative bacteria.

A.

Hepatitis C

B.

MRSA

C.

Salmonella

D.

Amphotericin B

E.

Clostridium difficile

F.

Urinary Tract Infection

G.

Endocarditis

H.

Aspergillus Fumigatis

I.

Staph. aureus

J.

Toxoplasma gondi

K.

Legionella

L.

Burkholderia cepacia

M.

Pneumocystis pneumonia

A

Burkholderia cepacia

1144
Q

A 50-year-old man was admitted with acute pancreatitis and underwent emergency pancreatectomy. He was in ITU for four weeks for respiratory support where he remained febrile and septic. Blood cultures and wound swabs grew gram-positive cocci in chains, which grew on MacConkey plate and was aesculin-positive. This isolate was also resistant to the conventional anti-streptococcal antibiotics.

A.

Pseudomonas aeruginosa

B.

Rotavirus

C.

Salmonella enteridis

D.

Vancomycin-resistant enterococcus(VRE)

E.

Respiratory syncytial virus

F.

Herpes Simplex, Type 1

G.

Methicillin-resistant S. aureus (MRSA)

H.

Streptococcus Group A

I.

Klebsiella pneumoniae

J.

Streptococcus viridans

K.

Bacillus subtilis

A

Vancomycin-resistant enterococcus(VRE)

1145
Q

A patient with 20% burns with open wounds is awaiting skin grafting. The wound swab grew gram-negative bacilli that produced a green pigment and was oxidase-positive. A similar organism was isolated from other patients on the same unit. Bacteriological typing subsequently proved all the isolates were of the same type

A.

Pseudomonas aeruginosa

B.

Rotavirus

C.

Salmonella enteridis

D.

Vancomycin-resistant enterococcus(VRE)

E.

Respiratory syncytial virus

F.

Herpes Simplex, Type 1

G.

Methicillin-resistant S. aureus (MRSA)

H.

Streptococcus Group A

I.

Klebsiella pneumoniae

J.

Streptococcus viridans

K.

Bacillus subtilis

A

Pseudomonas aeruginosa

1146
Q

Sitting in on your consultant’s GUM clinic, you see a shy 30-year-old woman who admits to losing her virginity a week ago and now is worried about the appearance of insect bite-like marks in her genital region and a concurrent fever. On intense questioning, she reveals that her partner seemed to have a painful sore on his penis.

A.

Chlamidiae Pneumoniae

B.

Chlamydiae Trachomatis

C.

Syphilis

D.

HIV

E.

Non-gonococcal urethritis

F.

HSV type 2

G.

Lymphogranuloma venereum

H.

Gonorrhoea-associated salpingitis

I.

Chlamidiae Psittacosis

J.

Gonococcal conjunctivitis

K.

Disseminated gonococcal infection

L.

Chancroid

1147
Q

On Tuesday, a confident African friend comes to you for advice. He has noticed a painful ulcer on his penis, from which he has helpfully collected exudate. Sneaking into the labs at Chelsea & Westminster late one evening, you culture this. Later, you note the presence of Haemophilus ducreyi.

A.

Chlamidiae Pneumoniae

B.

Chlamydiae Trachomatis

C.

Syphilis

D.

HIV

E.

Non-gonococcal urethritis

F.

HSV type 2

G.

Lymphogranuloma venereum

H.

Gonorrhoea-associated salpingitis

I.

Chlamidiae Psittacosis

J.

Gonococcal conjunctivitis

K.

Disseminated gonococcal infection

L.

Chancroid

1148
Q

NB re Trimethoprim in pregnancy

A

Trimethoprim is one of the commonly used antibiotics to treat UTIs. However it is contraindicated in early pregnancy because of teratogenic risks (as it is a folate antagonist). Recommendations for the treatment of UTI in pregnancy vary between hospitals. Nitrofurantoin, amoxicillin or cephalexin may be used. Nitrofurantoin should be avoided at term as it may produce neonatal haemolysis.

1149
Q

How do quinacrine and tetracycline delay prion conversion

A

Both quinacrine and tetracycline have been shown in vitro to directly bind to and prevent polymerisation of prion protein. Therefore these are not acting in the way they work against parasites and bacteria respecitvely, but instead interact directly with the abnormal prion protein.

1150
Q

Mx of meningitis

A

If you know it is Neisseria- ben pen

If you do not know the answer, broader spectrum therefore ceftriaxone

1151
Q

DDx for ring enhancing lesion

A

cerebral abscess, tuberculoma, toxoplasmosis and sometimes CNS lymphoma. The ring usually represents vasogenic oedema.

1152
Q

What differentiates between S. haematobium and S. Mansone

A

The initial histories are liable to be similar - travel, contact with fresh water and associated swimmer’s itch then a period of 3-4 weeks symptom free then fever, rash, myalgia and possible pneumonitis (these more often in travellers than the local population) The only possible difference so far is that you are apparently able to pick up Mansoni infection from trips to the carribean and south america as well as Africa/Middle East unlike Haematobium (Africa/Middle east only) The difference then comes in that Haematobium infection typically migrates to the bladder (strictly, the vesical VEINS) and presents with painless haematuria which then progresses into LUTS and ascending urinary problems and rarely lung and neuro involvement. According to Underwood you can get right sided colon involvement from haematobium but this is less likely. Mansoni however prefers the bowel (strictly, the mesenteric VEINS which are part of the portal circulation) and so presents with bloody diarrhoea, progressive ulceration potentially up to strictures. Involvement is normally left sided but right sided infection does happen. Eggs end up in the liver via the portal circulation and present with a hepatitis and portal hypertension. - So in brief Mansoni - bowel and liver, Haematobium - bladder

1153
Q

A 45 year old female presents with fever. O/E she is pyrexial, has hepatosplenomegaly, lymphadenopathy and a severely swollen eyelid. She returned from Guatemala 2 days ago.

A.

Giardia lamblia

B.

Chagas Disease

C.

Tuberculosis

D.

Schistosomiasis

E.

Plasmodium malariae

F.

Plasmodium vivax

G.

Dengue fever

H.

Mucocutaneous Leishmaniasis

I.

Amoebiasis

J.

Tropical sprue

K.

Plasmodium falciparum

A

Chagas Disease

1154
Q

A 35 year old male complains of a persistent ulcer in the mucosa of the mouth. When questioned further admits to remembering a small ulcer on his upper arm which healed without treatment when holidaying in Brazil one year ago.

A.

Giardia lamblia

B.

Chagas Disease

C.

Tuberculosis

D.

Schistosomiasis

E.

Plasmodium malariae

F.

Plasmodium vivax

G.

Dengue fever

H.

Mucocutaneous Leishmaniasis

I.

Amoebiasis

J.

Tropical sprue

K.

Plasmodium falciparum

A

Mucocutaneous Leishmaniasis

1155
Q

A 45 year-old Egyptian male complains of haematuria. On further investigation, cystoscopy reveals a squamous cell carcinomatous lesion.

A.

Mycobacterium leprae

B.

Hepatitis B virus

C.

Trypanosoma brucei rhodesiense

D.

Schistosoma haematobium

E.

Wuchereria bancrofti

F.

Plasmodium falciparum

G.

Salmonella typhi

H.

Schistosoma mansoni

I.

Leishmania donovani

J.

Pneumocystis carinii

K.

Trypanosoma brucei gambiense

A

Schistosoma haematobium

1156
Q

A 23 year-old female presents with headache and fever 6 weeks after returning from her gap year.

A.

Mycobacterium leprae

B.

Hepatitis B virus

C.

Trypanosoma brucei rhodesiense

D.

Schistosoma haematobium

E.

Wuchereria bancrofti

F.

Plasmodium falciparum

G.

Salmonella typhi

H.

Schistosoma mansoni

I.

Leishmania donovani

J.

Pneumocystis carinii

K.

Trypanosoma brucei gambiense

A

Plasmodium falciparum

1157
Q

An African woman and her 33 year-old husband come to their doctor because she is worried that he is not as alert as he used to be. On examination, he has non-tender lymphadenopathy, hepatomegaly and marked CNS abnormalities. He is noted to be quite lethargic.

A.

Mycobacterium leprae

B.

Hepatitis B virus

C.

Trypanosoma brucei rhodesiense

D.

Schistosoma haematobium

E.

Wuchereria bancrofti

F.

Plasmodium falciparum

G.

Salmonella typhi

H.

Schistosoma mansoni

I.

Leishmania donovani

J.

Pneumocystis carinii

K.

Trypanosoma brucei gambiense

A

Trypanosoma brucei gambiense

1158
Q

A thin peripheral blood film from a 59 year-old female demonstrates eosinophilia and microfilariae. On examination, the skin overlying her superficial lymph nodes is streaky red and tender.

A.

Mycobacterium leprae

B.

Hepatitis B virus

C.

Trypanosoma brucei rhodesiense

D.

Schistosoma haematobium

E.

Wuchereria bancrofti

F.

Plasmodium falciparum

G.

Salmonella typhi

H.

Schistosoma mansoni

I.

Leishmania donovani

J.

Pneumocystis carinii

K.

Trypanosoma brucei gambiense

A

Wuchereria bancrofti

1159
Q

A 43 year-old Asian male with AIDS presents with a prolonged fever, dizziness and a persistent cough. On examination, he is found to have marked splenomegaly and rough, dry skin. Blood results reveal pancytopenia.

A.

Mycobacterium leprae

B.

Hepatitis B virus

C.

Trypanosoma brucei rhodesiense

D.

Schistosoma haematobium

E.

Wuchereria bancrofti

F.

Plasmodium falciparum

G.

Salmonella typhi

H.

Schistosoma mansoni

I.

Leishmania donovani

J.

Pneumocystis carinii

K.

Trypanosoma brucei gambiense

A

Leishmania donovani

1160
Q

A 5 year-old girl presents unconscious and unrousable. Neck rigidity is not present and kernig’s sign is negative. She dies 3 hours after presentation.

A.

Visceral leishmaniasis (kala-azar)

B.

Giadiasis

C.

Trypanosomiasis

D.

Miliary tuberculosis

E.

Amoebic dysentery

F.

Severe malaria

G.

Cutaneous leishmaniasis

H.

Trichuris trichiura

I.

Chagas disease

J.

Brain worm

K.

Pulmonary tuberculosis

A

Severe malaria

1161
Q

A 20 year-old man presents with a persisting intermittent fever which began whilst he was travelling in South America the previous week. He has a dry cough and a massively enlarged spleen. Sandfly parasites are detected in a spleen aspirate.

A.

Visceral leishmaniasis (kala-azar)

B.

Giadiasis

C.

Trypanosomiasis

D.

Miliary tuberculosis

E.

Amoebic dysentery

F.

Severe malaria

G.

Cutaneous leishmaniasis

H.

Trichuris trichiura

I.

Chagas disease

J.

Brain worm

K.

Pulmonary tuberculosis

A

Visceral leishmaniasis (kala-azar)

1162
Q

A 16 yr old boy complains of a one week history of fever, muscle aches, nausea/vomiting/diarrhoea with general malaise following a trip to Zimbabwe visiting relatives. On further questioning he remembers developing an itchy rash on his right thigh following wading in Lake Kariba whilst on holiday. O/E He has generalised lymphadenopathy with hepatosplenomegaly. Initial blood tests reveal raised WCC with eosinophillia.

A.

Loa-Loa

B.

Plasmodium falciparum

C.

Toxoplasma gondii

D.

Entamoeba histolytica

E.

Enchinococcus granulosus

F.

Giardia lamblia

G.

Leishmania donovani

H.

Wucheria bancrofti

I.

Clonorchis sinensis

J.

Trichinella spiralis

K.

Ancylostoma duodenale

L.

Taenia saginata

M.

Schistosoma mansoni

A

Schistosoma mansoni

1163
Q

A 25 yr old female humanitarian volunteer complaining of swinging fever, profound abdominal pain with severe malaise. On further questioning she reveals a history of self limiting diarrhoeal illness 3/52 ago during which she passed mucus and some blood. You are also informed she recently returned from a humanitarian mission to Ghana 6/52 ago. O/E she is unwell with exquisitely tender hepatomegaly. You also find increased breath sounds and a dull percussion note in the lower region of the right lung.

A.

Loa-Loa

B.

Plasmodium falciparum

C.

Toxoplasma gondii

D.

Entamoeba histolytica

E.

Enchinococcus granulosus

F.

Giardia lamblia

G.

Leishmania donovani

H.

Wucheria bancrofti

I.

Clonorchis sinensis

J.

Trichinella spiralis

K.

Ancylostoma duodenale

L.

Taenia saginata

M.

Schistosoma mansoni

A

Entamoeba histolytica

1164
Q

A 24 yr old male complaining of 3/52 history of fever/chills with muscular aches and spasms. On further questioning he reveals the he also an episode of diarrhoea/vomiting with a headache lasting 48hrs. This followed his participation in an amateur eating competition 1/12 ago, during which he may have eaten some improperly cooked pork. O/E he has marked periorbital oedema with conjunctivitis. Blood tests reveal a marked eosinophillia, while gastrocnemius biopsy demonstrates the presence of encysted larvae.

A.

Loa-Loa

B.

Plasmodium falciparum

C.

Toxoplasma gondii

D.

Entamoeba histolytica

E.

Enchinococcus granulosus

F.

Giardia lamblia

G.

Leishmania donovani

H.

Wucheria bancrofti

I.

Clonorchis sinensis

J.

Trichinella spiralis

K.

Ancylostoma duodenale

L.

Taenia saginata

M.

Schistosoma mansoni

A

Trichinella spiralis

1165
Q

An acutely unwell 42 yr old male presents to A&E with high fever accompanied by chills, sweats and vomiting with a 24 hour history. O/E he is clinically jaundiced with cool clammy skin. He is tachypnoeic and tachycardic. You note hepatosplenomegaly and that he is producing small amounts of dark brown urine in his catheter bag. His wife tells you that they recently returned from safari in Tanzania 10 days ago.

A.

Loa-Loa

B.

Plasmodium falciparum

C.

Toxoplasma gondii

D.

Entamoeba histolytica

E.

Enchinococcus granulosus

F.

Giardia lamblia

G.

Leishmania donovani

H.

Wucheria bancrofti

I.

Clonorchis sinensis

J.

Trichinella spiralis

K.

Ancylostoma duodenale

L.

Taenia saginata

M.

Schistosoma mansoni

A

Plasmodium falciparum

1166
Q

A 32 yr old female complaining of the presence of small pale bodies in her stools on a number of occasions. On further questioning she admits some occasional mild epigastric pain over the past 4/12. O/E she appears clinically well. There is no significant travel history.

A.

Loa-Loa

B.

Plasmodium falciparum

C.

Toxoplasma gondii

D.

Entamoeba histolytica

E.

Enchinococcus granulosus

F.

Giardia lamblia

G.

Leishmania donovani

H.

Wucheria bancrofti

I.

Clonorchis sinensis

J.

Trichinella spiralis

K.

Ancylostoma duodenale

L.

Taenia saginata

M.

Schistosoma mansoni

A

Taenia saginata

1167
Q

A 25yr old man who had recently returned from travel in Afrcia presented with fever, diarrhoea and hepatoslenomegaly. He also noted skin changes which had developed over the past month.

A.

African trypanosomiasis

B.

Babesiosis

C.

Toxoplasmosis

D.

American trypanosomiasis

E.

Ameobiasis

F.

Giardiasis

G.

Vivax malaria

H.

Visceral Leishmania

I.

Cryptosporidiosis

J.

Trichomoniasis

K.

Falciparum malaria

A

Visceral Leishmania

1168
Q

A 40 yr old Indian lady who was vacationing in the UK presented with fever which followed no particular pattern, vomiting and the production of brown-black urine.

A.

African trypanosomiasis

B.

Babesiosis

C.

Toxoplasmosis

D.

American trypanosomiasis

E.

Ameobiasis

F.

Giardiasis

G.

Vivax malaria

H.

Visceral Leishmania

I.

Cryptosporidiosis

J.

Trichomoniasis

K.

Falciparum malaria

A

Falciparum malaria

1169
Q

A 25 year old man presents with weight loss and diarrhoea. He has recently been on holiday in India. On examination of his stool cysts and “tear-drop” shaped trophozoites are present.

A.

Naegleria fowleri

B.

Cryptosporidium parvum

C.

Entamoeba histolytica

D.

Trypanosoma gambiense

E.

Plasmodium falciparum

F.

Leishmania donovani

G.

Trichomonas vaginalis

H.

Trypanosoma cruzi

I.

Giardia lamblia

J.

Toxoplasma gondii

K.

Trypanosoma rhodesiense

A

Giardia lamblia

1170
Q

A 10 year old girl presents with fever, hepatomegaly, splenomegaly and anaemia. She recently emigrated from the Sudan. Her mother tells you that 6 months ago the girl developed dark patches on her hands and forehead.

A.

Naegleria fowleri

B.

Cryptosporidium parvum

C.

Entamoeba histolytica

D.

Trypanosoma gambiense

E.

Plasmodium falciparum

F.

Leishmania donovani

G.

Trichomonas vaginalis

H.

Trypanosoma cruzi

I.

Giardia lamblia

J.

Toxoplasma gondii

K.

Trypanosoma rhodesiense

A

Leishmania donovani

1171
Q

An 18 month old girl from Brazil sees you whilst on a short holiday in Britain. Her parents are worried because she appears to have had fever for the last few weeks, seems more tired and out of spirits than usual, has loss of appetite, vomiting and diarrhoea and complains of pains in her legs. On examination she has general lymphadenitis and non-pitting oedema in her legs and feet. Her Machado-Guerreiro test is positive.

A.

Naegleria fowleri

B.

Cryptosporidium parvum

C.

Entamoeba histolytica

D.

Trypanosoma gambiense

E.

Plasmodium falciparum

F.

Leishmania donovani

G.

Trichomonas vaginalis

H.

Trypanosoma cruzi

I.

Giardia lamblia

J.

Toxoplasma gondii

K.

Trypanosoma rhodesiense

A

Trypanosoma cruzi

1172
Q

An infant is diagnosed with pneumonia in her 5th day of life. Vaginal swabs from the mother as well as umbilical and oral swabs from the neonate showed a Gram positive coccus. The infant is given antibiotics and is monitored in hospital for a period of time until respiration and appetite improve.

A.

Group B Streptococci Syndrome

B.

Chlamydial conjunctivitis in the newborn

C.

Neonatal Herpes Simplex Infection

D.

E.Coli infection

E.

EBV-related infectious mononucleosis

F.

Neonatal Respiratory Tract Infection

G.

Conjunctivitis caused by a blocked tear duct

H.

Neonatal Meningitis

I.

Congenital Rubella Syndrome

J.

Congenital Toxoplasmosis

K.

Neonatal HIV infection

A

Group B Streptococci Syndrome

1173
Q

A French mother brings her 2 month old daughter with fever to hospital. The infant is shown to have elevated hepatic enzymes and is treated with pyrimethamine, sulphadiazine and folic acid for a year after appropriate investigations are performed.

A.

Group B Streptococci Syndrome

B.

Chlamydial conjunctivitis in the newborn

C.

Neonatal Herpes Simplex Infection

D.

E.Coli infection

E.

EBV-related infectious mononucleosis

F.

Neonatal Respiratory Tract Infection

G.

Conjunctivitis caused by a blocked tear duct

H.

Neonatal Meningitis

I.

Congenital Rubella Syndrome

J.

Congenital Toxoplasmosis

K.

Neonatal HIV infection

A

Congenital Toxoplasmosis

1174
Q

An infant is born prematurely and subsequently has low birth weight. In addition, he has encephalitis and vesicular skin lesions. Despite being recommended to have a caesarean due to active viral lesions, the mother refuses and the neonate was delivered vaginally. Emperic Acyclovir is given to the neonate.

A.

Group B Streptococci Syndrome

B.

Chlamydial conjunctivitis in the newborn

C.

Neonatal Herpes Simplex Infection

D.

E.Coli infection

E.

EBV-related infectious mononucleosis

F.

Neonatal Respiratory Tract Infection

G.

Conjunctivitis caused by a blocked tear duct

H.

Neonatal Meningitis

I.

Congenital Rubella Syndrome

J.

Congenital Toxoplasmosis

K.

Neonatal HIV infection

A

Neonatal Herpes Simplex Infection

1175
Q

A 2 week old female had an enlarged liver and spleen and her skin was tinged yellow. She was not eating much nor was she vomiting. She also suffered from regular seizures. Investigation revealed intra-cranial calcification.

A.

Viral meningitis

B.

Congenital toxoplasmosis

C.

Neonatal HSV infection

D.

Congenital rubella syndrome

E.

Listeria

F.

E. coli

G.

Group B streptococci

H.

Hepatitis B

I.

Chlamydial ophthalmia

J.

Bacterial meningitis

K.

Bordetella pertussis

L.

Chickenpoc (VZV)

A

Congenital toxoplasmosis

1176
Q

A newly born male presented with microphthalmia, deafness and hepatosplenomegaly. His platelet count was 50 x 10^9/L. In addition, rashes were noticed on his body. He suffers from SOB and is unable to finish feeding.

A.

Viral meningitis

B.

Congenital toxoplasmosis

C.

Neonatal HSV infection

D.

Congenital rubella syndrome

E.

Listeria

F.

E. coli

G.

Group B streptococci

H.

Hepatitis B

I.

Chlamydial ophthalmia

J.

Bacterial meningitis

K.

Bordetella pertussis

L.

Chickenpoc (VZV)

A

Congenital rubella syndrome

1177
Q

The CSF in a neonate showed a raised WCC, consisting mainly of polymorphs. Culture showed pneumococcus.

A.

Viral meningitis

B.

Congenital toxoplasmosis

C.

Neonatal HSV infection

D.

Congenital rubella syndrome

E.

Listeria

F.

E. coli

G.

Group B streptococci

H.

Hepatitis B

I.

Chlamydial ophthalmia

J.

Bacterial meningitis

K.

Bordetella pertussis

L.

Chickenpoc (VZV)

A

Bacterial meningitis

1178
Q

A prematurely born 1 week old infant presented with microcephaly, chorioretinitis and vesicular skin lesions. He also had non-specific features of fever, irritability and failure to feed.

A.

Viral meningitis

B.

Congenital toxoplasmosis

C.

Neonatal HSV infection

D.

Congenital rubella syndrome

E.

Listeria

F.

E. coli

G.

Group B streptococci

H.

Hepatitis B

I.

Chlamydial ophthalmia

J.

Bacterial meningitis

K.

Bordetella pertussis

L.

Chickenpoc (VZV)

A

Neonatal HSV infection

1179
Q

Treponemes in dark-ground microscopy is diagnostic

1180
Q

What is a consideration re chancroid?

A

Patients with a chancroid ulcer are more susceptible to contracting HIV

1181
Q

What treatment should be prescribed for a 25-year old lady complaining of pruritus and a creamy vaginal discharge?

A

Oral fluconazole

1182
Q

A neonate is referred and presents with skin lesions, lymphadenopathy and failure to thrive.

1183
Q

S. haematobium associated with

A

SCC of the bladder (5% of all baldder Ca)

If outside the setting of chronic schistosomiasis- TCC

1184
Q

Gram positive cocci

A

Staph: aureus, epidermis

Strep: pneumoniae, pyogenes

1185
Q

Gram positive bacilli

A

Bacillus

Clostridium

Cornyebacterium

Listeria

1186
Q

Gram negative bacilli

A

E Coli

Kleb

Proteus

Salmonella

Shigella

Yersinia

Pseudomonas

Bordatella

Haemophilus

Legionella

1187
Q

Gram negative comma shaped

A

Vibiro

Campylobacter

Helicobacter

1188
Q

Spiral shaped bacteria

A

Treponema

Borrelia

1189
Q

Cell-wall defiicient bacteria

A

Mycoplasma

1190
Q

Quelling reaction

A

pneumococci
are mixed with anti-serum and methylene blue causes the capsule
to swell can be visualized under the microscope. Optochin-sensitivity
also differentiates pneumococcus from Streptococcus viridans (also
α-haemolytic), which is optochin-insensitve.

1191
Q

What differntiates between strep pneumonia and strep viridans

A

Strep viridans are optochin insensitivie

1192
Q

What differntaties between staph and strep

A

Strep are catalse negative

1193
Q

Pontiac fever=

A

Milder Legionella infection

1194
Q

are aerobic Gram-negative diploccoci. This bacterium
is particularly problematic in patients with chronic lung disease and
causes exacerbations of chronic obstructive pulmonary disorder (COPD).
Other targets of infection include ears, eyes and central nervous system.

A

Moraxella catarrhalis

1195
Q

are obligate intracellular bacteria which
cause an atypical pneumonia or a mild bronchitis. A cold-agglutinin
test can be used for the diagnosis. In rare cases, infection may lead to
Stevenson–Johnson syndrome.

A

Mycoplasma pneumoniae

1196
Q

are Gram-negative bacilli that cause influenza
(flu) outbreaks annually. Chocolate agar is used as a culture medium.
Further oxidase and catalase tests are positive.

A

Haemophilus influenzae

1197
Q

Chlamydia pneumoniae

A

are obligate intracellular bacteria which
cause an atypical pneumonia. Less commonly, this infection can cause
meningoencephalitis, arthritis, myocarditis and/or Guillain–Barré
syndrome.

1198
Q

is a β-haemolytic anaerobic Gram-positive
rod that may cause outbreaks of non-invasive gastroenteritis. Sources
include refrigerated food and unpasteurized dairy products.

A

Listeria monocytogenes

1199
Q

are comma-shaped oxidase positive bacteria, causing
profuse watery diarrhoea containing no inflammatory cells on microscopy.
Transmission occurs via the faecal-oral route.

A

Vibrio cholerae

1200
Q

How does vibrio cholera cause profuse watery diarrhoea

A

No inflammation

Vibrio cholerae
colonizes the small intestinal section of the gut and secretes enterotoxin
containing subunits A (active) and B (binding). B subunit binds to GM1
ganglioside on the intestinal epithelial cells. Intracellularly, there is activation
of cAMP by A subunit, which causes active secretion of sodium
and chloride ions; as a consequence water is lost due to the osmotic
pull of NaCl.

1201
Q

A 35-year-old woman presents to accident and emergency with fever, diarrhoea
and signs of shock. Her husband mentions that she had attended a work colleague’s
barbeque the previous day. The consultant believes superantigens are
responsible for the patient’s condition.

A Vibrio cholerae
B Staphylococcus aureus
C Enterobacteriaecae
D Listeria monocytogenes
E Salmonella enteritidis
F Shigellae
G Campylobacter jejuni
H Giardia lamblia
I Entamoeba histolytica

A

Staphylococcus aureus (B) are β-haemolytic Gram-positive cocci
arranged in grape-like clusters. In the gastrointestinal tract, S. aureus
produces the exotoxin TSST-1, which acts as a superantigen causing
non-specific activation of T cells and subsequent release of IL-1, IL-2
and TNF-α. A massive non-specific immune response follows causing
shock and multiple organ failure. Enterotoxin produced by bacteria
causes vomiting and diarrhoea 12–24 hours after the culprit food has
been consumed.

1202
Q

multiplies in
the Peyer’s patches of the small intestine. Clinical features include slow
onset fever, constipation and splenomegaly. Rose spots are pathognomonic.

A

Salmonella typhi

1203
Q

are oxidase positive, non-motile bacteria.
Transmission occurs via the faecal–oral route, generally due to contamination
by dog faecal matter, causing a watery, foul smelling diarrhoea.
Complications include Guillain–Barré syndrome and Reiter’s syndrome.

A

Campylobacter jejuni

1204
Q

is a motile trophozite. Ingestion of the cysts
leads to colonization of caecum and colon, which may cause a ‘flaskshaped’
ulcer to develop. Clinical features involve dysentery, chronic
weight loss and liver abscess formation.

A

Entamoeba histolytica

1205
Q

A tuberculous granuloma that occurs in the cortex of the brain,
subsequently rupturing into the subarachnoid space, is termed a

A

Rich
focus.

1206
Q

Transmission occurs via contact with animals. xx
are thin aerobic spirochaetes that are tightly coiled. The first stage of
infection is known as the xx phase, during which the patient
suffers non-specific symptoms such as fever, headache, malaise and
photophobia. In the second immune phase, IgM antibodies have formed
and meningitis, liver damage (causing jaundice) and renal failure may
develop. CSF examination will reveal a raised white cell count. The
microscopic agglutination test is considered the gold standard for diagnosing
xx

A

Leptospirosis

1207
Q

is a Gram-negative diplococcus.
Infants aged 6 months to 2 years are most at risk as well as large
numbers of adults living in close quarters. Virulence factors include its
capsule (antiphagocytic), endotoxin (lipopolysaccharide causes haemorrhage
from blood vessels resulting in characteristic petechiae in meningococcaemia)
and IgA1 protease (destroys IgA).

A

Neisseria meningitides (meningococcus

1208
Q

Diagnosis is made by examination of CSF; India ink staining reveals
yeast cells with a surrounding halo.

A

Cryptococcal meningitis

1209
Q

A 35-year-old man presents to an infectious disease specialist with a painful
penile ulcer and associated unilateral lymphadenopathy of the inguinal nodes. A
swab of the ulcer is cultured on chocolate agar

Treponema pallidum
B Klebsiella granulomatis
C Neiserria gonorrhoeae
D Trichomonas vaginalis
E Candidia albicans
F Chlamydia trachomatis
G Bacterial vaginosis
H Haemophilus ducreyi
I Herpes simplex virus 2

A

Haemophilus ducreyi (H) is a Gram-negative coccobacillus that causes a
tropical ulcer disease (chancroid) and is contracted by sexual transmission.
Chancroid is characterized by a painful genital ulcer that leads to
unilateral painful swollen inguinal lymph nodes. Infected lymph nodes
may rupture releasing pus. The differential diagnosis for genital ulcers
includes syphilis (painless ulcer with bilateral painless lymphadenopathy),
herpes simplex virus 1 and 2 (vesicles that eventually break down)
and lymphogranuloma venereum (slowly developing painless inguinal
lymph nodes). Haemophilus ducreyi can be cultured on chocolate agar.

1210
Q

is a Gram-positive rod that causes the ulcerating
sexually transmitted infection donovanosis. It is diagnosed using
giemsa stain of biopsy, which reveals Donovan bodies

A

Klebsiella granulomatis

1211
Q

is a flagellated protozoan that causes vaginal
discharge and urethritis in humans. It is otherwise asymptomatic and
can be diagnosed by wet preparation microscopy, culture or PCR.

A

Trichomonas vaginalis

1212
Q

Superficially, infection causes redness, itching and discharge
from the vagina. In immunocompromised patients, infection can involve
the oesophagus as well as causing xx

A

Candida albicans

1213
Q

rare side effect of xxx is cholestatic jaundice which
may develop weeks after treatment is stopped.

1214
Q

Side effects of xx include thrombocytopenia, megaloblastic
anaemia and hyperkalaemia (via antagonism of sodium channels
in the distal convoluted tubule of nephrons).

A

Trimethoprim

1215
Q

acts on 50S ribosomes to inhibit protein synthesis.
It is used in cases of Rocky Mountain spotted fever. Side effects include
aplastic anaemia.

A

Chloramphenicol

1216
Q

a broad-spectrum carbapenem antibiotic which is
used in the management of severely sick patients, usually in intensive
care. It is resistant to β-lactamase, including extended spectrum
β-lactamase producing bacteria

1217
Q

is a tetracycline antibiotic that interferes with protein
synthesis by binding to the 30S ribosomal subunit. It is used in COPD
exacerbations, sexually transmitted infections (gonorrhoea and chlamydia)
and acne.

A

Doxycycline

1218
Q

A 38-year-old man presents to his GP with vomiting, mild fever and loss of
appetite. He admits to travelling to sub-Saharan Africa 2 months previously. On
examination the patient is evidently jaundiced.

A Human immunodeficiency virus
(HIV)
B Epstein–Barr virus (EBV)
C Hepatitis B virus
D Cytomegalovirus (CMV)
E Hepatitis D virus
F Varicella zoster virus
G Hepatitis C virus
H Human herpes virus 8
I Influenza virus

A

Hepatitis B virus (HBV; C) is a double-stranded DNA virus that is prevalent
in sub-Saharan Africa. It is transmitted via sexual contact, contaminated
blood products, intravenous drug use as well as vertical transfer
from mother to child during child birth. The virus has an incubation
period of 2–6 months with 80 per cent of infections remaining acute
and 20 per cent becoming chronic with risk of cirrhosis and hepatocellular
carcinoma. HBV antigens include HBsAg (surface antigen), HBcAg
(core antigen) and HBeAg (soluble antigen).

1219
Q

A 40-year-old man presents to an infectious disease specialist with a 4-month
history of weight loss, fever and malaise. On examination the patient has
lymphadenopathy. His CD4 count is found to be 289 copies/μL. The patient is
started on lamivudine, ritonavir and one other drug.

A Acyclovir
B Oseltamivir
C Interferon-α
D Zidovudine
E Gancylcovir
F Lamivudine
G Efivarenz
H Ritonavir
I Adamantadine

A

Zidovudine (D) is a nucleoside reverse transcriptase inhibitor (NRTI)
used in the treatment of HIV/AIDS (as well as prevention of vertical
transmission from infected mothers). Treatment is commenced once the
CD4 count falls below 350 copies/μL. Zidovudine works by inhibiting
the action of the enzyme reverse transcriptase, preventing the conversion
of HIV RNA to DNA, which consequently cannot be incorporated
into the host DNA. Side effects include anaemia, neutropenia, hepatic
and cardiac dysfunction as well as myopathy. The standard treatment
regimen involves the use of two nucleoside reverse transcriptase
inhibitors (NRTIs) and a non-nucleoside reverse transcriptase inhibitor
(NNRTI; Efivarenz) or a protease inhibitor (PI; Ritonavir).

1220
Q

A 25-year-old man presents to his GP with a 3-day history of fever, cough,
body aches and severe headaches. The patient is told to rest and drink plenty of
fluids. However, he returns the following week stating his symptoms have not
improved and is started on a drug that acts on viral neuraminidase.

A Acyclovir
B Oseltamivir
C Interferon-α
D Zidovudine
E Gancylcovir
F Lamivudine
G Efivarenz
H Ritonavir
I Adamantadine

A

Oseltamivir (B) is a viral neuraminidase inhibitor used in the treatment
of influenza. Osteltamivir is in fact a pro-drug; once metabolized in the
liver the active form GS4071 is produced. Once a newly formed influenza
virion is produced, the surface viral protein haemagglutinin is bound
to sialic acid receptors along the upper respiratory tract. Neuraminidase
is normally responsible for cleaving the haemagglutinin–sialic acid
receptor bond, hence facilitating the release of newly formed virions.
Therefore, inhibiting neuraminidase activity prevents further viral
replication.

1221
Q

can cause bone marrow toxicity; it may
therefore be prescribed together with granulocyte-colony stimulating
factor (G-CSF)

A

Gancyclovir

1222
Q

Mechanism for acyclovir

A

It is converted to acyclo-guanosine monophosphate by viral thymidine kinase

Acyclo-GMP is further phosphorylated to acyclo-guanosine triphosphate which is then incorportaed into the viral DNA strand

1223
Q

is an M2 ion channel inhibitor preventing the uncoating
of influenza virions and therefore inhibiting entry into susceptible cells.

A

Amantadine

1224
Q

can lead to severe flu-like
symptoms and can be diagnosed by testing for blood β-D-glucan

A

Candidaemia

1225
Q

is a chronic fungal infection caused by
Malassezia furfur, characterized by hypopigmentation (in patients with
dark skin tones) and hyperpigmentation (in patients with pale skin tones). Spots affect the back, underarm, arms, legs, chest, neck and rarely
the face. Microscopic investigation of the M. furfur with potassium
hydroxide reveals a ‘spaghetti with meatballs’ appearance. Wood’s light
may also reveal an orange fluorescence in some cases.

A

Pityriasis versicolor (B)

1226
Q

Infection in pre-formed lung cavities
(for example in TB patients) may lead to a fungal ball visible on
chest X-ray

A

aspergilloma

1227
Q

is a fungus found in
soil and plants that causes sporotrichosis. A prick by thorns causes nodular
lesions to appear on the surface of the skin. Initially the lesions will
be small and painless; left untreated they become ulcerated. Infection
may also spread to joints, bone and muscle by this route. Inhalation of
spores may lead to pulmonary disease and systemic infection may lead
to central nervous system involvement. Treatment options include itraconazole,
fluconazole and oral potassium iodide.

A

Sporothrix schenckii

1228
Q

is a fungus transmitted by inhaled spores;
it is highly prevalent in the Mississippi River region. Although mostly
subclinical, a minority of infections will proceed to a chronic progressive
lung disease.

A

Histoplasma capsulatum

1229
Q

is a copper coloured soil saprophyte found on
rotting wood that causes chromoblastomycosis. Infection is characterized
by a warty lesion resembling a cauliflower

A

Phialophora verrucosa

1230
Q

is a cutaneous dermatophyte fungal infection of the
scalp leading to scaly red lesions with loss of hair. It primarily affects
children. Infection is characterized by an expanding ring on the scalp.

A

Tinea capitis (F)

1231
Q

is also known as ringworm. It is a cutaneous dermatophyte
fungal infection affecting the trunk, arms and legs. It is identified
by raised red rings.

A

Tinea corporis

1232
Q

A 45-year-old man has returned to the UK from a holiday to France. A week
later he presents with flu-like symptoms, drenching sweats, a recurring fever
and is beginning to complain of a lower back pain. He admits to have brought
back some local cheeses on visits to regional farms.

A

Brucellosis (C) is a Gram-negative rod-shaped bacterium that is harboured
by cattle (Brucella abortus), goats (B. melitensis), pigs (B. suis) and dogs
(B. canis). Brucella spp. are transmitted by inhalation, unpasteurized dairy produce and direct contact with animals. Symptoms include fever,
myalgia, arthralgia, tiredness and in chronic cases may be associated with
depression. Diagnosis is made by blood culture on Castaneda medium.
Complications include granulomatous hepatitis (histology of liver
biopsy demonstrates granulomata), endocarditis, oseteomyelitis and
thrombocytopenia.

1233
Q

A 48-year-old man presents to his GP with flu-like symptoms. On examination
the patient has a maculopapular rash on his trunk. The patient also shows an
area where a vague bite mark is visible.

A Psittacosis
B Rabies
C Brucellosis
D Q fever
E Leptospirosis
F Mycobacterium marinium
G Lyme disease
H Cat scratch disease
I Rocky mountain spotted fever

A

Rocky Mountain spotted fever (I) is caused by Rickettsia spp. infection,
a Gram-negative genus of bacteria, most prevalent in North and South
America. It is harboured in small wild rodents and domestic animals
(transmitted to humans by ticks). Rickettsia bacteria invade the endothelial
lining of capillaries causing a vasculitis. Clinical features include
headache, fever, myalgia, vomiting and confusion. Late signs include
a rash that is maculopapular and/or petechial on the distal parts of the
limbs which then spreads to the trunk and face. Rocky Mountain spotted
fever may lead to thrombocytopenia, hyponatraemia and/or elevated
liver enzymes.

1234
Q

Human symptoms mainly involve a
severe pneumonia (with or without hepatitis). Although the patient may
report mild symptoms, the X-ray will generally appear to show severe
pathology. Diagnosis is made by visualizing cytoplasmic inclusions on
Giemsa or fluorescent antibody stained sputum or biopsy sample.

A

Psittacosis

1235
Q

Cerebral Negri bodies (inclusion bodies) are pathognomonic.

1236
Q

Transmission occurs by
inhalation of aerosols of urine, faeces or amniotic fluid from infected
livestock.

1237
Q

Classically, infection results in tender and swollen
lymph nodes with headache and backache. Atypically, infection may
result in Parinaud’s oculoglandular syndrome

A

Cat scratch disease (H) is caused by Bartonella

1238
Q

viral respiratory system infection caused by the genus
Morbillivirus. Infection presents with cough, coryza, conjunctivitis and/
or a discrete maculopapular rash

1239
Q

Long-term complications include saddle-nose
deformity, Higoumenakis’ sign (unilateral enlargement of the clavicle)
and Clutton’s joints (symmetrical joint swelling).

A

Congenital syphillis

1240
Q

It is an obligate intracellular Gram-negative bacterium
found in farm animals and pets, and is transmitted by aerosol
or contact with animal products like milk or faeces. It manifests as
flu-like symptoms, but can progress to an atypical pneumonia or less
often a granulomatous hepatitis. Typical chest x-ray features include
a ground glass appearance. It does not grow on Lowenstein–Jensen
medium

A

Coxellia burnetti (Q fever)

1241
Q

A 24-year-old HIV-positive Asian man presents with a cough. A Mantoux test
is performed. After 72 hours, the wheal diameter is measured at 5.8 mm. This
indicates:
A He has never been exposed to TB
B He has been exposed to TB
C He has had a BCG vaccination in the past
D He has latent TB which is now reactivated
E It is not possible to say

A

1 An induration of 5 mm or more is considered positive in:
• Patients with HIV
• A recent contact of a person with TB disease
• People with fibrotic changes on chest radiograph consistent
with prior TB
• Patients with organ transplants
• People who are immunosuppressed for other reasons (for example
taking the equivalent of >15 mg/day of prednisone for 1
month or longer)
2 An induration of 10 mm or more is considered positive in:
• Recent immigrants (<5 years) from high-prevalence countries
• Intravenous drug users
• Residents and employees of high-risk congregate settings
• Mycobacteriology laboratory personnel
• Persons with clinical conditions that place them at high risk
• Children <4 years of age
• Infants, children, and adolescents exposed to adults in high-risk
categories
3 An induration of 15 mm or more is considered positive in any person,
including those with no known risk factors for TB

1242
Q

Organisation of strep

A

Can be divided into alpha haemolytic, beta haemolytic and non-haemolytic groups

Alpha= Strep pnuemonia and strep viridans (optochin insensitivie)
Beta= Lancefield groups A, B, C, F and G

Non haemolytic strep= enteroccoci

1243
Q

OVeR PS

A

Optochin- viridans resistance

Pneumonia- sensitive

1244
Q

If you get an HIV patient whose saturations
drop on exertion in a question, think about

A

Pneumocystis jirovecii

1245
Q

Signs of endocarditis: rules of 2

A

2 signs in the hands: clubbing and splinter haemorrhages

Two signs in the abdomen: splenomegaly and microscopic haematuria

Two signs elsewhere: New or changing heart murmurs and embolic phenomena

1246
Q

Acute vs subacute infective endocarditis

A

Acute: tricuspid, staph aureus IVDU

Subacute: mitral and aortic, damaged valves, strep viridans

1247
Q

Culture negative endocarditis

1248
Q

Maconkey agar and lactose fermenters

A

Lactose fermenters turn Maconkey agar pink

1249
Q

Staph saprophytics vs staph aureus

A

Staph saprophyticus is second most common cause of UTI in young sexually active woman, coagulase positive like other staph but catalase negative unlike Staph aureus

1250
Q

four runners ‘ent-ering’ a race, and the winner
gets a silver flask!

bloody diarrhoea

A

Entamoeba histolytica

1251
Q

Gram-negative bacterium that is also oxidase positive, but has a corkscrew
rather than a comma appearance

A

Campylobacter

1252
Q

Oxifase positive organism

PuNCH Me Very Lightly

A

Pseudomonas

Neisseria

Campylobacter

Helicobacter

Morazella

Vivrio

Legionella

1253
Q

A 35-year-old HIV-positive man presents to his GP complaining of a general
feeling of tiredness, weight loss and night sweats. On examination there is hepatosplenomegaly
and hyperpigmentation of the skin. The most likely diagnosis is:
A Visceral leishmaniasis
B Cutaneous leishmaniasis
C Mucocutaneous leishmaniasis
D Malaria
E Schistosomiasis

A

Leishmaniasis is transmitted by phlebotomine sandflies and occurs in
Africa, America and the Middle East. Visceral leishmaniasis (A) is also
known as ‘Kala-azar’, and the most common clinical features include
fever and splenomegaly. Hepatomegaly, skin hyperpigmentation and dry
warty skin occur less frequently, and bone marrow invasion can result

in pancytopenia. It can be mistaken for malaria, which is dangerous as
it can be fatal if left untreated. L. donovani and L. infantum are thought
to cause the disease in Africa, Asia and Europe, whilst L. chagasi is
implicated in South America

1254
Q

is transmitted by blood
flukes. An itchy rash, known as ‘swimmer’s itch’, may develop at the
site where the vectors penetrate the skin. They may then migrate to the
liver, causing ‘Katayama fever’ with clinical features such as fever, rash,
myalgia and sometimes hepatosplenomegaly. Following maturation in
the liver, the flukes migrate to either mesenteric veins causing intestinal
xx, or to the urinary tract leading to xx schistosomiasis.
Hepatosplenomegaly can occur, but again the dry warty skin lesions
described are not usually a feature.

A

Schistosomiasis

1255
Q

A 22-year-old student presents to accident and emergency with a raised, erythematous,
scaly ulcer on his forearm which has not been healing. On examination
he is also found to have lymphadenopathy. He gives a history of recently returning
from a 2-month trek in the rainforests of South America. Tissue is aspirated
from the margin of the ulcer, and the organism is cultured in Novy–MacNeal–
Nicolle medium. The organism implicated is:
A Toxoplasma gondii
B Treponema pallidum
C Leishmania dovani
D Leishmania major
E Leishmania braziliensis

A

The picture described is consistent with cutaneous leishmaniasis, the
most common form of leishmaniasis. An itchy, scaly papule develops
at the bite site and develops into a crusty ulcer with raised edges. Local
lymphadenopathy can also occur, but the lesion usually heals within
8 months leaving a depigmented scar called an oriental sore. The organisms
implicated are Leishmania major (D) and L. tropica. You can
remember this if you picture lots of skin lesions cropping up in travellers
from the ‘major tropics’! It is found in many countries, ranging
from South America to the Middle East. Diagnosis can be by Giemsa
staining of slit skin smears, or from tissue aspirated from the ulcer.The organism can be cultured on Novy–Macneal–Nicolle medium as
described in the question.

1256
Q

Mucocutaneous leishmaniasis can produce
destructive and disfiguring facial lesions, and so is the most
feared form of cutaneous leishmaniasis. It may begin in the same
way as the cutaneous form, but years later ulceration can appear in
mucous membranes leading to mutilation of those areas. It is most
often caused by

A

L. braziliensis

1257
Q

Visceral leishmaniasis is also known as ‘Kala-azar’, and the
most common clinical features include fever and splenomegaly.
Hepatomegaly, skin hyperpigmentation and dry warty skin occur less
frequently xx are thought
to cause the disease in Africa, Asia and Europe, whilst xx is impicated in South America

A

L donovani

L infantum

L chagas

1258
Q

Characteristically a CT scan may show ring enhancing lesions with surrounding
oedema.

A

Toxoplasmosis

1259
Q

Typhoid (E) is caused by Salmonella typhi, and again can present with
non-specific features like brucellosis. However, there are a few unusual
clinical features of typhoid that are worth remembering using the
mnemonic A.B.C.C.D.E:

A

Abdominal distension, Bradycardia, Cough,
Constipation, Diarrhoea and Erythematous rose spots. Antibiotics of
choice in the treatment of typhoid are the quinolones such as ciprofloxacin
for 2 weeks.

1260
Q

The two forms
of disseminated xxl infection are the septic arthritis form (as
described in this case), and the bacteraemic form. Other clinical features
of the bacteraemic form might include a migratory polyarthralgia and a
vesicular or papular rash.

A

Gonocchal infection

1261
Q

A 26-year-old squash player is admitted with a red, swollen left knee. He reports
no history of trauma. On examination he has a temperature of 38°C. A joint
aspirate is taken which grows Gram-negative diplococci. What is the antibiotic
treatment regimen of choice for this patient?
A Oral flucloxacillin for 4–6 weeks
B IV flucloxacillin for 4–6 weeks
C IV flucloxacillin for 2–4 weeks
D IV flucloxacillin and vancomycin for 6–8 weeks
E IV cefotaxime for 4–6 weeks

A

The patient in this question is presenting with septic arthritis, and the
most likely cause given the joint aspiration findings of Gram-negative
diplococci is Neisseria gonorrhoeae. The British National Formulary
(BNF) advises the use of intravenous cefotaxime for 4–6 weeks (E) if
gonococcal arthritis or a Gram-negative infection is suspected. The BNF
is a good source of information for looking up the latest guidelines
regarding antibiotic treatment regimens for common types of infection.
Cefotaxime is a third generation cephalosporin. Cephalosporins are part
of the beta-lactam group of antibiotics which work by inhibiting cell
wall synthesis. The penicillins are also part of this group. There are different
generations of cephalosporins, with those of later generations
having increasing Gram-negative but decreasing Gram-positive cover.
Cefotaxime is also used to treat meningitis and gonorrhoea. Some of the
other commonly used third generation cephalosporins are ceftizoxime
and ceftriaxone – you can remember these because they all have a ‘t’ in
their names, just like in ‘third’ generation.

1262
Q

Hep B

It is the first detectable antigen to appear after
someone has been infected, and can be positive in acute or chronic
disease. Patients who still carry this antigen after 6 months are
termed hepatitis carriers. It is this antigen that is used to make the
hepatitis B vaccine

1263
Q

This is an IgG antibody that appears after the host has
cleared the infection, and indicates recovery. It is also found in a
person who has been vaccinated against hepatitis B

1264
Q

HBV

is often used as a marker of infectivity, as
it is only found in the blood when the virus is actively replicating

1265
Q

this indicates that the patient has recently been
infected with hepatitis B, and is a marker of acute infection

A

Anti-HBc IgM

1266
Q

this is produced in response to the core antigen,
and often persists for life. You can remember this as the ‘c’ standing
for ‘chronicity’, as it is the difference between IgM and IgG antibodies
which can tell you whether the infection is acute or chronic

A

anti-HBc-Ig

1267
Q

A 79-year old woman is admitted to the hospital for treatment of pneumonia
and is commenced on intravenous antibiotic therapy. Her respiratory symptoms
begin to improve, but 5 days later she develops profuse diarrhoea. The most
appropriate treatment is:
A Oral metronidazole for 7 days
B Oral metronidazole for 14 days
C Isolation and treatment with intravenous fluids
D IV metronidazole for 7 days
E Oral co-amoxiclav for 7 days

A

First line treatment for infection with C. difficile is oral metronidazole,
with a suggested duration of treatment of 10–14 days (B). Metronidazole
is classified as a nitroimidazole antibiotic, and is particularly useful for
the treatment of anaerobic organisms and protozoa. You can remember
three of the key organisms it is used to treat by remembering that ‘Met
is out to G.E.T you difficult bugs!’ (Giardia, Entamoeba, Trichomonas
and C. difficile). Patients are usually advised to avoid consuming alcohol
whilst taking this antibiotic because of the potential reaction that
can occur characterized by nausea, shortness of breath, flushing and
vomiting.

1268
Q

A 79-year old woman is admitted to hospital for treatment of pneumonia and is
commenced on intravenous antibiotic therapy. Her respiratory symptoms begin
to improve, but 5 days later she develops profuse diarrhoea. After treatment with
oral metronidazole she shows gradual improvement, but the profuse diarrhoea
returns 2 weeks later. The same organism is found to be responsible. The most
appropriate course of action is:

A Oral metronidazole for 7 days
B Oral metronidazole for 14 days
C Isolation and treatment with intravenous fluids
D IV metronidazole for 7 days
E Oral vancomycin for 14 days

A

As explained previously, a 7-day course of metronidazole (A) is not
considered a sufficient duration of treatment to eradicate the bacterium.
Again, isolation and IV fluid resuscitation (C) is necessary but
not adequate as a single measure in the management of this woman.
Intravenous metronidazole (D) is only needed if a patient is not
responding to vancomycin, the infection is life-threatening, or for
patients with ileus.
Oral vancomycin for 10–14 days (E) is given for:
• Third or subsequent episodes
• Severe infection
• Infection not responding to metronidazole
• patients who cannot tolerate metronidazole

1269
Q

is ‘red man
syndrome’, a reaction to the drug which consists of a sudden onset erythematous,
pruritic rash over the face, neck and upper torso.

A

Vancomycina rare ADR

1270
Q

A 65-year old retired mechanic is brought by his family to his GP due to their
concern over his recent increase in confusion. This has occurred rapidly over the
past 4 months, and he now struggles to recognize members of his family. His
daughter also reports occasionally seeing intermittent, jerky movements of both
his arms. The GP organizes a CT scan and dementia screen, which are both found
to be normal. Which is the next most useful diagnostic test for the GP to order?
A MRI brain
B Electroencephalogram
C Electrocardiogram
D Ultrasound scan of both carotids
E Tonsillar biopsy

A

The diagnostic test of choice here is the electroencephalogram (B),
which is abnormal in two-thirds of patients and would classically demonstrate
generalized triphasic sharp wave complexes. Do not confuse
this with an electrocardiogram (ECG) (C), which would not be diagnostic
in this case. An MRI brain (A) may show increased signal in the basal
ganglia, but would not be the best investigation here. An ultrasound
scan of both carotids (D) is a useful test if investigating a transient
ischaemic attack (TIA) to look for carotid stenosis, but this is not
relevant with this patient. Finally, a tonsillar biopsy (E), is a useful
diagnostic test for variant CJD (for which it has 100 per cent sensitivity
and specificity), but not for sporadic CJD.

1271
Q

A 61-year-old patient has recently been diagnosed with sporadic CJD. His GP is
keen to do a lumbar puncture. Which of the following statements is true regarding
this investigation in this situation?
A The lumbar puncture is used to look for the levels of protein, glucose and
polymorphs
B The lumbar puncture is used to look for the levels of a protein called 14-3-3
C A lumbar puncture is the most specific test for variant CJD
D The lumbar puncture is not useful in sporadic CJD, but is an important test
in variant CJD
E A tonsillar biopsy would be a more useful test than a lumbar puncture for
sporadic CJD

A

The lumbar puncture in CJD is used to analyze the CSF for a protein
named ‘14-3-3’ (B). Note that routine analysis of the cerebrospinal fluid
(CSF) is normal in CJD, therefore looking at levels of protein, glucose
and polymorphs (A) would not be useful to distinguish between possible
causative agents of the clinical features as it is in meningitis

‘14-3-3’ is a term for a large group of proteins which have different
functions in eukaryotic cells, such as in cell signalling. However,
its measurement in CJD is a time consuming process, and as it is a
normal neuronal protein it can be released into the CSF as a result
of many other normal neuronal insults. It is therefore not a specific
finding (C), and the test can be positive in other conditions such as a
recent stroke, viral encephalitis or a subarachnoid haemorrhage. The
14-3-3 protein is present in both variant and sporadic CJD, therefore
(D) is incorrect.
Variant CJD has several important differences from sporadic CJD:
1 It typically occurs in younger patients (median age of onset 26 years)
than sporadic CJD
2 The median survival time is approximately 14 months, compared to
4
months for sporadic CJD
3 Psychiatric features may dominate in the initial stages, before
neurological features such as ataxia, myoclonus, chorea, dementia and
peripheral sensory symptoms appear
4 The MRI in variant CJD shows the ‘positive pulvinar sign’ (enhanced
signal of nuclei in the thalamus)
5 The classical EEG findings are often absent in the variant form
6 A tonsillar biopsy is sensitive and specific in the variant form, but is
not a useful test in the sporadic form (

1272
Q

A 42-year-old alcoholic is admitted with abdominal distension. The shifting
dullness test is positive and he is found to have diffuse abdominal tenderness.
His observations are as follows: pulse 115, blood pressure 116/83, temperature
37.9°C. The next best course of action is:
A Begin therapeutic paracentesis
B Observe, administer analgesia and closely monitor his vital signs
C Commence intravenous spironolactone
D Commence intravenous amoxicillin
E Commence intravenous cefotaxime

A

The pyrexia and tachycardia, in conjunction with the clinical features of
abdominal tenderness and ascites, make this the most likely diagnosis in
this patient. Other typical clinical features might include nausea, vomiting,
confusion, general malaise or features of hepatic encephalopathy.
In approximately 15 per cent of patients SPB can be asymptomatic.
A prompt diagnostic paracentesis is needed to make the diagnosis, and
SPB is confirmed by the presence of:
1 Ascitic fluid WCC of 500 cells/mm3
2 or Neutrophil count of >250 cells/mm3

Do not confuse a diagnostic paracentesis with a therapeutic paracentesis
(A): in the latter the purpose is to remove the fluid, for example
to relieve abdominal pressure or in the case of respiratory compromise.
This may be appropriate later, but only once SBP has been excluded
from the results of a diagnostic paracentesis or treated.
The most common organisms isolated in patients with SBP include
E. coli, Gram-positive cocci and enterococci. Although local antibiotic
guidelines may differ, of the options listed cefotaxime (E) is one of the
most extensively studied and has been proven to be effective. It is usually
given for at least 5 days. Other third generation cephalosporins
such as ceftriaxone can also be used. Amoxicillin (D) would not provide
sufficient cover against Gram-negative organisms.
Whilst analgesia and close observation are also important measures (B),
the high risk of mortality in SBP necessitates prompt antibiotic treatment.
Spironolactone (C) is used for the treatment of uncomplicated ascites, but
initial antibiotic treatment would take precedence in the case of SBP

1273
Q

A 63-year-old asymptomatic housewife is referred to a gastroenterologist after her
GP found that she had abnormal liver function tests on a routine blood test. A thorough
history reveals that she received a blood transfusion during her pregnancy in
1979. The best test to confirm whether the patient has hepatitis C would be:
A Liver biopsy
B Anti-hepatitis C antibodies
C Alanine aminotransferase levels
D Hepatitis C RNA PCR
E Viral genotyping

A

There are several different tests which are helpful in investigating the
disease:
1 Hepatitis C RNA PCR (D) – This can be used to differentiate between a
current and past infection. A quantitative test to detect the number of
hepatitis C RNA particles (called the ‘viral load’) can also be performed.
This can be very useful to detect a patient’s response to the anti-viral
treatment. Therefore, this is the best diagnostic test for hepatitis C
2 Anti-hepatitis C antibodies (B) – a positive test would indicate
exposure to the disease, but results should be interpreted with caution
because it cannot distinguish between current or past infection. In
addition, it can take up to 3 months for these antibodies to appear
after exposure, so an initial negative test can be misleading. It has
also been suggested that a weakly positive test might actually be a
false positive, so this is not the best diagnostic test. However, it may
be performed initially, and if the patient has two positive results a
hepatitis C RNA PCR is used to confirm the diagnosis
3 Viral genotyping (E) – this is used to determine the genotype of virus
present. The most common, genotype 1, is less likely to respond to
treatment than genotypes 2 or 3 and requires longer therapy
4 Liver biopsy (A) – this would be the most accurate means of
determining the stage and severity of liver damage caused by the
virus, and may be useful to assess the patient’s likelihood to respond
to treatment. However, it would be performed after the suspected
diagnosis has been confirmed
5 Alanine aminotransferase levels (ALT) (C) – this is not a diagnostic test,
but can be useful aid in the initial stages of confirming the diagnosis.
The ALT to AST (aspartate aminotransferase) ratio is typically <1 in

liver damage caused by hepatitis, whereas if it is >2 this is more
suggestive of alcoholic liver disease. You can remember this because
AST is indicative of Smirnoff drinking, whereas ALT is indicative of
viraL aetiology!

1274
Q

A 33-year-old backpacker visits his GP complaining of feeling weak, lethargic
and feverish since he returned from his trip to South Africa 3 months previously.
He is accompanied by his wife, who reports a change in his behaviour and disturbed
sleeping pattern since his return. On examination, his GP discovers that he
has enlarged cervical lymph nodes, and there is a small chancre on his forearm
that is approximately 2 cm in diameter. The most likely causative organism is:
A Plasmodium falciparum
B Trypanosoma brucei gambiense
C Trypanosoma brucei rhodesiense
D Trypanosoma cruzi
E Leishmania infantum

A

Human African trypanosomiasis is also known as sleeping sickness, and
is an infection transmitted by the tsetse fly in sub-Saharan Africa. There
are two main types:
1 Trypanosoma brucei gambiense (B) is found in west and central Africa,
is responsible for over 95 per cent of cases, and causes a chronic
infection. It can take months or even years for symptoms to appear.
You can remember this as gambiense causes a gradual infection
2 Trypanosoma brucei rhodesiense (C) is found in south and eastern
Africa, accounts for under 5 per cent of cases, and causes an acute
infection with symptoms appearing over a few weeks or months.
You can remember this as rhodesiense causes a rapid infection. As
this patient’s symptoms appeared 3 months after returning from his
travels, this is more likely to be the causative agent here
A subcutaneous chancre can develop at the site where the tsetse fly
bites, and symptoms such as fevers, weakness, arthralgia and headache
can then appear. Posterior cervical lymphadenopathy can also occur,
especially with T. brucei gambiense. This is known as Winterbottom’s
sign. Later the parasite can cross the blood–brain barrier resulting in
neurological features such as disturbance of the sleep cycle, ataxia,
behavioural changes and psychiatric disturbance. Treatment is with
drugs such as pentamidine and suramin in the early stages.
Plasmodium falciparum (A) is an organism responsible for causing
malaria. Whilst it should be considered in all patients with a fever
returning from an endemic area, the changes in behaviour and sleep
disturbance described in this patient make this a less likely cause.
Trypanosoma cruzi (D) causes Chagas disease which is carried by the
reduviid bug. Chronic infection can appear weeks to years after the
initial infection, affecting the cardiac and gastrointestinal systems.
Leishmania infantum (E) is responsible for leishmaniasis, features of
which can include fever, hepatosplenomegaly and lymphadenopathy.
Again, it is less likely to cause behavioural changes and sleep is unlikely
to be affected.

1275
Q

A 20-year-old student seeks medical attention due to recent difficulty in swallowing,
and severe weight loss. A thorough travel history reveals that he
returned several months ago from a gap year in Brazil. During his trip he
remembers becoming unwell at one point with a fever, diarrhoea, vomiting and
swollen eyelids, but this resolved in approximately 3 weeks with no treatment. A
chest x-ray is ordered as one of his investigations, and this reveals marked dilatation
of his oesophagus. The vector responsible for transmitting this disease is:
A Tsetse fly
B Reduviid bug
C Sandfly
D Aedes mosquito
E Ixodes tick

A

Trypanosoma cruzi is responsible for causing Chagas disease, a potentially
life-threatening disease which is spread by reduviid bugs (B) in Brazil. These are also known as ‘kissing bugs’. A red nodule, called a
chagoma, can appear at the site of the bite.
There are two forms of the disease: acute and chronic. In the acute phase,
patients may experience non-specific symptoms such as fever, lethargy,
diarrhoea, and vomiting. A characteristic feature, but one which occurs
in less than 50 per cent of cases, is a purplish swelling of the eyelids
(called Romana’s sign). To put this all together, picture Tom Cruise
(Trypanosoma cruzi) starring in a gladiator film as a Roman (Romana’s
sign) wearing purple sunglasses (swollen eyelids) and being kissed
(
kissing bugs) by lots of fans ‘ready with their video cameras’ (reduviid!)
The chronic phase can occur even years after the initial bite, and typically
affects the heart and gastrointestinal tract. You can remember
its effects by thinking of it causing both dilatation and dysfunction in
three organs: in the heart (dilatation = dilated cardiomyopathy, dysfunction
= arrhythmias), in the colon (dilatation = megacolon,
dysfunction = constipation) and in the oesophagus (dilatation = mega
oesophagus, dysfunction = dysphagia). Bennzimidazole or nifurtimox
are effective medications used to treat this disease.
The tsetse fly (A) is responsible for causing human African trypanosomiasis,
also known as sleeping sickness, in sub-Saharan Africa. The
clinical features of this disease can include changes to the sleep–wake
cycle and psychiatric disturbance. The sandfly (C) transmits Leishmania
species in Africa, America and the Middle East. The Aedes mosquito (D)
is a type of mosquito that causes Dengue fever. The Ixodes tick (E), also
known as the ‘deer tick’, transmits the organism responsible for causing
Lyme disease. None of these vectors would cause the spectrum of clinical
features described in this patien

1276
Q

The paralytic phase would
not typically have an ascending pattern of weakness, and fasciculations
prior to paralysis are an important feature.

1277
Q

A 46-year-old Somalian woman presents to her GP with a dry cough and weight
loss of 5 kg over 3 weeks. She is sent to the hospital, and a chest x-ray reveals
cavitating lung lesions. She is started on a course of anti-tuberculous medication.
Which of the following statements about this regimen is true?
A Liver function tests only need to be checked in those with pre-existing liver
disease
B Ethambutol can cause a peripheral neuropathy
C Pyridoxine should always be given with isoniazid treatment
D Rifampicin can cause optic neuritis
E Ethambutol should be avoided in renal failure

A

Remember that treatment for pulmonary TB usually consists of two
phases – an initial phase with rifampicin, isoniazid, pyrazinamide and
ethambutol for 2 months, and then a continuation phase with rifampicin
and isoniazid only for 4 months.
Streptomycin and ethambutol are two anti-tuberculous drugs which
should preferably be avoided in patients with renal impairment (
E).
If they have to be used the dosage should be reduced and the plasma
drug concentration closely monitored. A patient’s renal function
should be checked routinely before anti-tuberculous medication is
started.

The side effect that is particularly worrying with the use of ethambutol
is its ocular toxicity, and this is more likely in renal impairment as it is
renally excreted. This can present with changes in visual acuity, colour
blindness and restriction of visual fields. Therefore a patient’s visual
acuity should be assessed with a Snellen chart prior to starting treatment,
and they should be strongly advised to stop the medication and
seek advice if they become aware of any change in their vision. This
side effect does not occur with rifampicin (D).
Liver function should be tested in everyone before starting
antituberculous
therapy, as isoniazid, rifampicin and pyrazinamide are
all hepatotoxic (A). Further checks are not needed unless the patient has
pre-existing liver disease, is alcohol dependent or develops symptoms
of liver disease. Rifampicin can commonly cause a transient disturbance
to liver function tests in the first 2 months, but this does not usually
necessitate any changes to the treatment regimen.

The only common side effect of isoniazid is a peripheral neuropathy.
This can be remembered by ‘isoniazid causes a sensory neuropathy’.
Pyridoxine (vitamin B6) is not given routinely as a prophylactic measure
in patients using isoniazid, but may be given in those with preexisting
risk factors such as diabetes, alcohol dependence and HIV (C).
Ethambutol does not cause a peripheral neuropathy (B).

1278
Q

Quotidian fever malaria

A

Plasmadoium knowlesi

1279
Q

A young girl returns from visiting her relatives in India, feeling feverish and
with flu-like symptoms. A diagnosis of malaria is suspected. The form of the
malaria parasite which invades erythrocytes is known as a:

A Sporozite
B Schizont
C Merozite
D Hypnozoite
E Gametocyte

A

1 An infected mosquito injects sporozites (A) from its saliva into a
person’s blood stream when it bites
2 These enter the blood stream and are taken to the liver where they
infect hepatocytes
3 Here they multiply for a varying period of time, and then differentiate
to form haploid merozites (C). These have a ‘signet ring’ appearance.
Schizonts (B) are oval-shaped inclusions that contain the merozoites.
Note that P. vivax and P. ovale sporozoites may not develop into
merozites immediately, but can form hypnozoites (D) that remain
dormant in the liver
4 The merozites escape from the liver into the blood stream and infect
red blood cells – the erythrocytic phase
5 They multiply further in the erythrocytes, and will be released
from them at intervals. The waves of fever the patient experiences
correspond to when the merozites are released from the erythrocytes
6 Some of the merozoites develop into sexual forms of the parasite,
called male and female gametocytes (E). When a mosquito bites an
infected human, it ingests the gametocytes which form gametes inside
the mosquito
7 These then fuse to form oocytes and then sporozites – ready to inject
into a person.

1280
Q

A 55-year-old housewife returns from visiting her relatives in India, with a high
fever and with flu-like symptoms. A diagnosis of uncomplicated falciparum
malaria is confirmed. The most appropriate management plan is:
A Discharge with oral quinine and doxycycline
B Discharge with oral mefloquine and chloroquine
C Admit, give IV paracetemol and observe
D Admit and give IV quinine
E Admit and give oral quinine and doxycycline

A

All patients with falciparum malaria should be admitted to hospital
initially, so answers (A) and (B) are automatically excluded. Children
should be kept in for at least 24 hours, and infants, pregnant women
and the elderly need to be closely monitored because they can deteriorate
rapidly. The treatment options then depend on whether the malaria
is uncomplicated or complicated.
Uncomplicated malaria can be treated with one of the following:
1 Oral quinine plus doxycycline for 5–7 days (E)
2 Co-artem (artemetherelumefantrine) for 3 days
3 Atovaquone–proguanil (Malarone) for 3 days

Therefore the correct answer here is (E). Giving paracetamol without
anti-malarials would not be adequate, so clearly (C) is not suitable.
Chloroquine and mefloquine (B) are not recommended for the treatment
of falciparum malaria in the UK.
Oral treatment would suffice in an uncomplicated case of falciparum
malaria such as this, but in a severe case the first line anti-malarial
used in the UK is IV quinine (D). IV artesunate may also be considered
in the case of very severe disease instead of or in addition to quinine,
but this is not always widely available.
The treatment for non-falciparum malaria is quite different. In uncomplicated
infection, chloroquine is used initially followed by a 2-week
course of primaquine. The choloroquine treats the parasites in the erythrocytes
only, thus primaquine is still needed to kill the hypnozoites that
remain latent in the liver.
Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive
hereditary disease, and anti-malarial drugs can cause acute haemolysis
in these patients. The drugs thought to be particularly troublesome are
primaquine and choloroquine, but others may be dangerous at high
doses. For this reason glucose-6-phosphate dehydrogenase levels are
checked in patients before starting anti-malarial treatment.

1281
Q

A 55-year-old housewife returns from visiting her relatives in India, with a
high fever and with flu-like symptoms. thick and thin films are requested, and
Maurer’s clefts are seen under the microscope. The diagnosis is:
A Plasmodium falciparum
B Plasmodium vivax
C Plasmodium ovale
D Plasmodium malariae
E Plasmodium knowlesi

A

The most reliable way to diagnose malaria is via a blood film, and
traditionally a thick and thin blood film are requested. Most people
remember this fact, but not the reason behind it! Thick films are better
than thin films at picking up lower levels of infection, but thin films
allow the specific species to be identified. Both types of films are used
together to make the diagnosis.
In the erythrocytic life cycle of the malarial parasite, disc-like granulations
can be seen at the edge of the cell using an electron microscope.
These are known as Maurer’s clefts, and are found in falciparum malaria
(A). They are thought to be used by the parasite for protein sorting
and export. They are larger and coarser than the Schuffner’s dots seen
with P. vivax (B) and P. ovale (C). These are punctuate granulations
again seen under the microscope in erythrocytes invaded by the tertian
malaria parasite. These two structures are worth remembering for exam
questions!
P. malariae (D) causes ‘quartan’ malaria, meaning the fever occurs
every fourth day (i.e. days 1, 4, 7 and so on). P. knowleski (E) is much
less common, and mainly occurs in southeast Asia (such as in Borneo).
Maurer’s clefts and Schuffner’s dots would not typically be found in
infection with these species.

1282
Q

Maurer’s clefts

A

P falciparum

1283
Q

Schuffner’s dots

A

P vivax

P ovale

Year 5: Pathology (6 decks)

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