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Medicine Phase 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define Pathogen?

A

Organism that causes or is capable of causing disease

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2
Q

Define a Commensal?

A

Organism which colonises the host but causes no disease in normal circumstances

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3
Q

Define an opportunistic pathogen?

A

Microbe that only causes disease if hosts defenses are compromised

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4
Q

Define Virulence?

A

The degree to which an organism is pathogenic

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5
Q

Define Asymptomatic carriage?

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

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6
Q

What test can be done to distinguish between staphylococcus and streptococcus?

A

The catalase test; detects the presence of catalase enzyme using hydrogen peroxide.

Staph = catalase + ve

Strep = catalase - ve

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7
Q

How do staphylococcus appear under the microscope?

A

Clusters of cocci

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8
Q

How do streptococcus appear under the microscope?

A

Chains of cocci

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9
Q

What colour are Gram positive and Gram Negative bacteria under a microscope?

A

Gram positive - Purple/blue

Gram negative - pink/red

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10
Q

What kind of bacteria are gram positive mostly?

A

Cocci

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11
Q

What kind of bacteria are gram negative mostly?

A

Bacili

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12
Q

What stain would you use to detect acid fast organisms?

A

Ziehl-Neelsen stain
Used for Mycobacteria (eg. M.tuberculosis)
Appear pink

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13
Q

What stain would be used for Mycobacteria tuberculosis?

A

Ziehl Neelsen stain
Because it is an acid fast bacilli (AFB)

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14
Q

What is the cell wall structure of a gram positive bacteria?

A

Capsule
Large peptidoglycan layer
Phospholipid membrane

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15
Q

What is the cell wall structure of a gram negative bacteria?

A

Capsule
Outer membrane with endotoxin - such as LPS
Small peptidoglycan layer
Phospholipid inner membrane

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16
Q

Describe the characteristics of Gram positive bacteria?

A
  1. Single membrane
  2. Thick peptidoglycan layer

Often cocci

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17
Q

Describe the characteristics of Gram negative bacteria?

A
  1. Double membrane
  2. Small peptidoglycan area
  3. LPS (endotoxin area)

often bacilli

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18
Q

What temperature ranges and pH can bacteria grow in?

A

Between -80°C → +80°C

Between pH 4 → 9

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19
Q

What is an endotoxin?

A

component of the outer membrane of gram-negative bacteria e.g. LPS in Gram negative bacteria

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20
Q

What is an exotoxin?

A

secreted proteins of Gram positive and Gram negative bacteria

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21
Q

What are the features of Exotoxin?

A

Protein
Specific
Heat liable (changes in heat)
Strong antigenicity
Can be converted to toxoids

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22
Q

What are the features of Endotoxin?

A

Lipopolysaccharide (LPS)
Non-specific
Heat stable
Weak antigenicity
Not converted to toxoids

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23
Q

What are the 3 ways that bacteria can transfer genes?

A

Transformation - via plasmids
Transduction - via bacteriophages
Conjugation - via sex pilus

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24
Q

How does transformation bacterial gene transfer work?

A

Horizontal gene transfer where some bacteria take up foreign genetic material from the environment and release this as plasmids taken up by other bacteria

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25
Q

How does transduction bacteria gene transfer work?

A

Genetic recombination where genes from a host cell (bacterium) are incorporated into a bacterial virus genome (bacteriophage) and then transferred to another bacteria when the bacteriophage infects another cell.

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26
Q

What are obligate intracellular bacteria?

A

Bacteria that can only grow inside a host cell
Therefore we cannot grow them on agar plates

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27
Q

Give examples of obligate intracellular bacteria?

A

Chlamydia
Rickettsia
Coxiella

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28
Q

How would you carry out a gram stain?

A

ComeInAndStain

  1. Apply primary stain - crystal violet (purple) - to heat fixed bacteria
  2. Add iodine which binds to crystal violet and helps fix it to the cell wall
  3. Decolourise with ethanol or acetone
  4. Counterstain with safranin (pink)
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29
Q

What test is used to distinguish between different streptococcal bacteria?

A

Blood agar haemolysis

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30
Q

What are the different results of blood agar haemolysis and what do they mean?

A

alpha haemolysis - partial (appears green) = Streptococcus pneumonia or Viridans group streptococcus

Beta haemolysis - full = Group A,B,C,G strep - Requires further Lancefield serotype test to determine species

Gamma haemolysis - none = Enterococcus

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31
Q

What test is done for the alpha haemolytic streptococcus to distinguish the species?

A

Optochin Test
Optochin sensitive - Streptococcus pneumonia
Optochin Resistant - Viridans group Streptococcus

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32
Q

Give some examples of different Lancefield group streptococci?

A

Group A - Streptococcus pyogenes
Group B - Streptococcus agalactiae

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33
Q

What type of bacteria are grown on MacConkey Agar?

A

Gram negative Bacilli

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34
Q

What is MacConkey Agar?

A

Contains bile salts, lactose and a pH indicator
If an organism ferments lactose - lactic acid is produce and the agar will appear red/pink.

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35
Q

What are the main bacteria that give a positive result on MacConkey agar?

A

Escherichia Coli
Klebsiella pneumoniae
Enterobacter

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36
Q

What are the main bacteria that give a negative result on MacConkey agar?

A

Salmonella
Shigella
Proteus
Yersinia
Pseudomonas

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37
Q

Are streptococci mainly aerobic or anareobic?

A

Aerobic

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38
Q

What are the 3 methods to classify streptococcus?

A

Haemoloysis on blood agar

Lancefield typing (sero grouping based on surface carbohydrate antigens)

Biochemical properties

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39
Q

What does a facultatively anaerobic bacteria mean?

A

Means that the bacteria likes aerobic conditions mainly but can adapt if conditions tun anaerobic

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40
Q

Give an example of a bacteria that is facultatively anaerobic?

A

Streptococcus pyogenes

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41
Q

What haemolysis classification does Streptococcus pyogenes fall into?

A

beta haemolysis
Group A strep

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42
Q

What antibiotic would be used against streptococcus pyogenes?

A

Penicillin

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43
Q

What are some associated conditions caused by S.pyogenes?

A

Wound infections - cause cellulitis
Tonsilitis and Pharyngitis
Otitis media
Impetigo
Scarlet Fever

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44
Q

Wha are some complications caused by S.pyogenes infection?

A

Can cause rheumatic fever
Can cause glomerulonephritis

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45
Q

What are the virulence factors of S.pyogenes?

A

Streptokinase

Streptolysin O and S

Erythrogenic Toxin

M Toxin

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46
Q

Where is Streptococcus pneumoniae often found as a commensal organism?

A

In the oropharynx in roughly 30% of the population

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47
Q

What are the associated conditions caused by S.pneumoniae?

A

Pneumonia
Otitis media
Sinusitis
Meningitis

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48
Q

what predisposing features can increase your risk of S.pneumoniae infection?

A

Impaired mucus trapping (caused by viral infection)
Hypogammaglobulinaemia (low antibody count)
Asplenia - Absence of normal spleen function

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49
Q

What are the virulence factors of S.pneumoniae?

A

Capsule - polysaccharide
Inflammatory wall constituents - Teichoic acid and peptidoglycan
Cytotoxin - pneumolysin.

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50
Q

How does S.pneumoniae respond to the Optochin test?

A

They are sensitive to it so they die.

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51
Q

What is the name given to oral streptococci?

A

Viridans group streptococci

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52
Q

What is the most virulent group of the Viridans group streptococci?

A

S.milleri

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53
Q

What are the associated conditions caused by viridans group strep?

A

Dental caries and abscesses
Infective endocarditis
Deep organ abscesses

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54
Q

Are staphylococcus mainly aerobic or anaerobic?

A

Mainly aerobic

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55
Q

What is the most important stapyhlococcus?

A

Staphylococcus aureus

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56
Q

What is the habitat of staphylococcus aureus?
How is it spread?

A

Nose and skin

Spread via aerosol and touch

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57
Q

What result would S.aureus give in the coagulase test?

A

Positive result

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58
Q

What is the purpose of bacteria possessing the coagulase enzyme?

A

This means that they can clot the blood plasma around the bacteria to attempt to protect themselves from phagocytosis

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59
Q

How would S.aureus appear on blood agar?

A

yellow colonies

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60
Q

What is MRSA?

A

Methicillin (flucloxacillin) Resistant Staphylococcus aureus

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61
Q

What drugs are MRSA typically resistant too?

A
  • β-lactams
  • Gentamicin
  • Erythromycin
  • Tetracycline
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62
Q

What main drug would you give to treat MRSA infection?

A

Vancomycin

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63
Q

What are the 4 virulence factors of S.aureus?

A
  1. Toxins: pore-forming e.g. α-haemolysin and PVL = causes hemorrhagic pneumonia
  2. Proteases: exfoliatin = scalded skin syndrome
  3. Toxic shock syndrome toxin (TSST): stimulates cytokine release
  4. Protein A: a surface protein which binds Ig’s in wrong orientation so they can’t be recognised by the immune system.
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64
Q

What are the associated conditions caused by Staphylococcus aureus?

A

Wound infections
Abscesses
Impetigo
Septicaemia
Osteomyelitis
Pneumonia
Endocarditis

Toxins could also cause toxic shock syndrome and food poisoning

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65
Q

What result would Staphylococcus epidermidis give on the coagulase test?

A

Negative result

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66
Q

What does S.epidermidis look like on blood agar?

A

White/colourless colonies

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67
Q

What is the virulence factor of S.epidermidis?

A

Its ability to form persistent biofilms

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68
Q

Where are the likely sites of infection for S.epidermidis?

A

Prostheses
Catheters

Mainly affects immunocompromised individuals

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69
Q

What are the associated conditions caused by Staphylococcus saprophyticus?

A

Acute cystitis

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70
Q

What are the virulence factors of S.saprophyticus?

A

Haemagglutinin - adhesion to cell
Urease enzyme - cause kidney stones

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71
Q

What is the major Corynebacterium species that can cause disease?

A

C.diphtheriae

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72
Q

How does C.diphtheriae infection present?

A

child with severe sore throat and fever for 2 days
Lymphadenopathy in neck
rapid breathing
thick greyish membrane on tonsils
Swab - shows irregular gram positive rods
Stain shows metachromatic granules

All leads to C.diphtheriae

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73
Q

What can we use to treat C.diphtheriae?

A

Anti-toxin
Erythromycin

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74
Q

How do we grow C.diphtheriae in the lab from a throat swab?

A

Grow it in the presence of potassium tellurite
This will kill other types of bacteria except corynebacterium

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75
Q

How is C.diphtheriae spread?

A

Via droplets

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76
Q

How can we prevent C.diphtheriae spread?

A

Vaccination
Toxoid vaccine

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77
Q

What test could be done to further distinguish between staphylococci bacteria.

A

Coagulase test; looks at whether a fibrin clot is produced

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78
Q

What bacteria would be coagulase positive and negative?

A

Positive - S.aureus

Negative - S.epidermidis, S.saprophyticus

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79
Q

What are the 4 major phyla of Gram negative bacteria?

A

Proteobacteria
Bacteroidetes
Chlamydiae
Spirochaetes

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80
Q

What is the morphology of proteobacteria?

A

All gram negative bacilli
(except Neisseria (diplococci) and Campylobacter/helicobacter (spiral))

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81
Q

What bacteria fit in the phyla proteobacteria?

A

Enterobacteriaceae
Vibrio cholerae
Pseudomonas aeruginosa
Haemophilus influenzae
Legionella pneumophila
Bordetella pertussis
Neisseria
Campylobacter
Helicobacter pylori

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82
Q

What is the morphology, respiration and habitat of the Enterobacteriaceae

A

Rods - most have flagellum
Facultatively anaerobic
Some species will colonise the gut - both commensal and pathogenic

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83
Q

What bacteria fit in the phyla proteobacteria?

A

Enterobacteriaceae
Vibrio cholerae
Pseudomonas aeruginosa
Haemophilus influenzae
Legionella pneumophila
Bordetella pertussis
Neisseria
Campylobacter
Helicobacter pylori

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84
Q

What are the different species of the Enterobacteriaeceae?

A

Escherichia coli
Shigella
Salmonella
Proteus mirabilis
Klebsiella pneumonia

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85
Q

What is Escherichia coli?

A

A commensal bacterium that is abundant as a facultative anaerobe
They have a flagella

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86
Q

What antigens would be found on E.coli?

A
  1. O antigen: part of LPS
  2. K antigen: capsule
  3. H antigen: flagellin
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87
Q

What are the associated infections caused by E.coli?

A
  1. Wound infections (surgical)
  2. UTIs (cystitis; ~80% of female UTIs - faecal source or sexual activity; catheterisation - most common nosocomial infection)
  3. Gastroenteritis
  4. Traveller’s diarrhoea
  5. Bacteriemia
  6. Meningitis (infants) - rare in the UK
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88
Q

What are the major pathogenic types of E.coli?

A

ETEC - Enterotoxigenic Escherichia coli
EHEC - Enterohaemorrhagic Escherichia coli
EPEC - Enteropathogenic Escherichia coli
STEC - Shiga toxin producing Escherichia coli

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89
Q

What is ETEC?

A

Enterotoxigenic Escherichia coli
An E.coli that produces special toxins that stimulates the lining of the intestines causing them to secrete excessive fluid.
This results in watery diarrhoea - Travellers Diarrhoea

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90
Q

What are the toxins produced by ETEC?

A

LT and ST enterotoxin

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91
Q

How does ETEC cause travellers diarrhoea?

A

Heat labile ETEC toxin modifies Gs protein to a ‘locked on’ state.
Adenylate cyclase is activated - increased cAMP.
increased secretion of Cl- into the intestinal lumen,
H2O follows this down an osmotic gradient
results in traveller’s diarrhoea.

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92
Q

What does EHEC cause?

A

Enterohaemorrhagic Escherichia coli
Causes bloody diarrhoea

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93
Q

What is EPEC?

A

Enteropathogenic Escherichia coli
They lack ST and LT toxins
Use adhesin called intimin to bind to host cells
cause watery diarrhoea

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94
Q

What are the 4 medically important species of shigella?

A

S.dysenteriae
S.flexneri
S.boydii
S.sonnei

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95
Q

What is special about shigella?

A

It is acid tolerant and so it will not be destroyed by gastric acid

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96
Q

How is shigella spread?

A

Via person to person contact
Via contaminated food and water

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97
Q

What are the symptoms of shigella infection?

A

Severe bloody diarrhoea
Frequent passage of stools > 30/day
small volume
pus and blood in stool
prostrating cramps
fever

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98
Q

What is the toxin produced by shigella?

A

Shiga toxin

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99
Q

Describe the pathogenesis of shigella infection?

A

Enters through colonic M cells:
In the intestine it induces self-uptake
leads to macrophage apoptosis.
Cytokines are released and neutrophils are attracted
Causes inflammation.
Shigella spread to adjacent cells.

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100
Q

What is an important complication of shigella infection?

A

Systemic absorption of shiga toxin will target the kidney
Causes Haemolytic Uremic Syndrome (HUS)
Can lead to kidney failure

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101
Q

What is the main medically important Salmonella species?

A

Salmonella enterica
Has over 2500 serovars

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102
Q

How is salmonella spread?

A

Through the ingestion of contaminated food and water

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103
Q

What are the associated infections caused by salmonella infection and name the serovars responsible for them?

A

Gastroenteritis - Serovar Enteritidis and Typhimurium
Enteric Fever -Serovar Typhimurium and Paratyphi
Bacteraeima - Serovar Cholerasuis and Dublin

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104
Q

What is the pathogenesis of Salmonella infection?

A
  1. Invasion of gut epithelium (SI)
  2. Intestinal secretory and inflammatory response: serovars Enteritidis and Typhimurium - (Does NOT produce toxins)
  3. Transcytosed to basolateral membrane
  4. Enters submucosal Macrophages; survive and replicate within the macrophage.
  5. Systemic infection due to dissemination within macrophages: serovar Typhi
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105
Q

What are the associated infections of Proteus mirabilis?

A

UTI - 30% of cases
Opportunistic infection
Can lead to pyelonephritis and sepsis

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106
Q

What is the virulence factor of Proteus mirabilis?

A

Urease
Causes and increase in urine pH
leads to calcium and magnesium phosphate precipitation
forms kidney stones

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107
Q

What kind of bacteria is Klebsiella pneumonia?

A

Environmental - not gut
It is an opportunistic pathogen and so will infect immunocompromised subjects

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108
Q

What kind of patients get infected with Klebsiella?

A

It is an opportunistic pathogen so will infect immunocompromised patients
Including:
Neonates
Elderly
Immunocompromised

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109
Q

What are the associated infections caused by Klebsiella pneumonia?

A

UTIs
Pneumonia
Surgical wound infection
Sepsis

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110
Q

What is significant about Klebsiella?

A

It is MDR (multi-drug resistant)
it is resistant to carbapenems - the most broad spectrum drugs

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111
Q

What is Vibrio cholerae?

A

The bacteria responsible for causing cholera
A facultative anaerobe
notorious for causing pandemics

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112
Q

How is V.cholerae spread?

A

Ingestion of shellfish
Contamination of drinking water - due to flooding of costal areas or poor sanitation

Faecal-oral route

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113
Q

Is V.cholerae spread from person to person

A

Not very transmissible like this as it is highly susceptible to acid and therefore cannot survive in the stomach for long periods

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114
Q

What are the symptoms of V.cholerae infection?

A

Voluminous watery stools (secretory diarrhoea) - rice water stools
Can lose 20L of fluid/day

Dehydration leads to hypovolaemic shock which causes death
No blood or pus or fever - no invasion or damage to mucosa

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115
Q

What is the treatment for cholera?

A

Oral rehydration therapy (ORT)

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116
Q

What is the pathogenesis of cholera?

A

TCP pili - required for colonisation
Cholera toxin - causes Gs subunit to be locked on
uncontrolled cAMP production
increase PKA
Increased activity of CFTR channel
Loss of Cl- and Na+
Water follows and massive H2O loss

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117
Q

What is Pseudomonas aeruginosa?

A

Ubiquitous free-living aerobe
Motile - has a flagellum
opportunistic
Difficult to treat - MDR

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118
Q

What are the associated infections caused by P.aeruginosa?

A

Acute:
burns/surgical wounds
UTI
keratitis

Systemic:
Sepsis

ICU:
Pneumonia - leading cause of pneumonia in ICU

Chronic:
Patients with CF

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119
Q

What is Haemophilus influenzae?

A

Exclusively human parasite
opportunistic infection
Fastidious - requires chocolate agar to culture
non-motile

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120
Q

Where is Haemophilus influenzae often found on the body?

A

Nasopharyngeal carriage in 25-80% of the population

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121
Q

What are the associated infections caused by H.influenzae?

A

Meningitis - 5-10% of cases at <5yrs
bronchopneumonia
Epiglotitis, Sinusitis, Otitis media
Bacteraemia
Pneumonia in patients with CF, COPD, HIV

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122
Q

What are the virulence factors of H.influenzae?

A

Capsule
LPS

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123
Q

What are some facts about Legionella?

A

causes severe disease - 15-20% mortality
Fastidious - cultured on charcoal agar

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124
Q

How is Legionella spread?

A

air conditioning
shower heads
nebulisers
humidifiers

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125
Q

What are the associated infections caused by Legionella?

A

Legionnaires disease - severe inflammatory pneumonia

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126
Q

How is Bordetella pertussis spread?

A

Aerosol transmission
high contagious

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127
Q

What is the major associated condition caused by Bordetella pertussis?

A

Whooping Cough (pertussis)
Caused by the Pertussis toxin

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128
Q

What are some facts about Neisseria?

A

Non-flagellated gram negative diplococci
Fastidious
Obligate human pathogen

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129
Q

What are the 2 medically important species of Neisseria?

A

Neisseria meningitidis
Neisseria gonorrhoea

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130
Q

How is N.meningitidis spead?

A

Via aerosol transmission

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131
Q

Where is N.meningitidis infections common?

A

In universities
In barracks

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132
Q

What are the virulence factors of N.meningitidis?

A

Capuse
LPS

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133
Q

What is the pathogenesis of N.meningitidis infections?

A

Exists in the nasopharynx
Crosses nasopharyngeal epithelium and enters the blood stream
Can cause low level bacteraemia (asymptomatic)
or full sepsis (high mortality if not treated)
Can cross BBB and enter CSF or subarachnoid space
Lead to invasion of the meninges (meningitis)

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134
Q

What is gonorrhoea?

A

The second most common STD worldwide

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135
Q

How is N.gonorrhoea spread?

A

Person to person contact only
Sexually transmitted

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136
Q

What are the associated infections caused by N.gonorrhoea?

A

Infections can be asymptomatic
Gonorrhoea
Urethritis - In women can lead to PID (pelvic inflammatory disease)
Proctitis, gingivitis, pharyngitis
Conjunctivitis

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137
Q

What are the virulence factors of N.gonorrhoea?

A

LPS
Twitching motility pili

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138
Q

Give some facts about Campylobacter?

A

spiral rods
Microaerophilic - need low O2 levels and requires CO2

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139
Q

What are the 2 medically important Campylobacter species?

A

C.jejuni
C.coli

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140
Q

What are the associated infections caused by Campylobacter?

A

Most common cause of food poisoning
-undercooked poultry, cattle, unpasteurised milk

Causes mild to severe diarrhoea - often with blood
infection is mild but can be severe in immunocompromised Px

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141
Q

What are some facts about Helicobacter pylori?

A

Proteobacteria
Microaerophilic - low O2
Spiral shaped

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142
Q

Is helicobacter spread?

A

YES
Present in 50% of global population
But only a small Fraction of this will develop disease

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143
Q

What are the associated infections caused by Helicobacter pylori?

A

Gastritis
Peptic ulcer disease - causes 80-90% of ulcers
Implicated in 10% of gastric adenocarcinomas and MALT lymphoma

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144
Q

What is the morphology of the bacteroidetes?

A

Rod shaped bacili

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145
Q

What is the most common Bacteroides infection?

A

Bacteroides fragilis
Most common cause of anaerobic infections

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146
Q

Give some facts about Bacteroides?

A

Non motile rods
obligate anaerobes
Make up commensal flora of large bowel
Most abundant flora - 30-40% of total flora

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147
Q

What are the associated infections caused by bacteroides?

A

opportunistic
Only occur with tissue injury - surgery, perforated appendix or ulcer

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148
Q

What is the morphology of Chalmydiae

A

Round - elementary bodies
Pleiomorphic - reticulate bodes
Small non motile

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149
Q

What kind of bacteria is Chlamydiae?

A

Gram neg
Obligate intracellular parasite

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150
Q

What is the pathogenesis of Chlamydiae?

A

Unique growth cycle - 2 developmental stages
1. Elementary bodies - infectious and will enter cells via endocytosis
2. Reticulate bodies - Replicative (non-infectious), will acquire nutrients from host

Reticulate bodies are converted back to elementary bodies to be release and infect other cells

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151
Q

What are the 2 medically important genus and species within of chlamydiae?

A

Chlamydia:
C.trachomatis

Chlamydophila:
C.pneumonia
C.psittaci

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152
Q

What are the associated infections caused by Chlamydia trachomatis?

A

Trachoma - blindness

Genital tract STD - Most common STD
Usually, asymptomatic

Lympho-granuloma venereum (LGV)

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153
Q

What are the associated infections caused by C.pneumonia?

A

Respiratory tract infection - mild pneumonia

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154
Q

What proportion of N.gonorrhoea infections are asymptomatic?

A

Men - 10%
Women - 50%

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155
Q

What is the morphology of Spirochaetes?

A

Spiral/helical

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156
Q

What are the medically important Spirochaetes?

A

Borrelia burgdorferi - Lime diesase
Treponema pallidum - Syphilis

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157
Q

What is the associated infection caused by Borrelia burgdorferi and how is it spread?

A

Lyme disease (300 cases in UK)
Spread via tick bites

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158
Q

What is the pathogenesis of Borrelia burgdorferi?

A
  1. Bacteria infects small mammals i.e. rodents
  2. Tick larvae acquire from the rodents; transmitted to humans by nymphs.

→ bull’s eye rash and flu-like symptoms.

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159
Q

What is the associated infection caused by Treponema pallidum?

A

Syphilis (STD)
(2800 cases in UK)

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160
Q

What is the culture medium to grow Borrelia burgdorferi?

A

In a medium containing rabbit serum

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161
Q

What is the pathogenesis of Treponema pallidum?

A

Primary stage:
Localised infection: ulcer (chancre) that occurs days-weeks post infection; highly transmissible

Secondary stage:
~50% cases: systemic - skin, lymph nodes, joins, muscles occurs 1-3months post infection; highly transmissible

Tertiary stage:
~30% cases: granuloma (gummas) in bone and soft tissue:
Cardiovascular syphilis: aorta
Neurosyphilis: brain and spinal cord
Occurs several years post infection; non-infectious stage

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162
Q

What is the culture medium used to grow Treponema pallidum?

A

Cannot grow on cultures
Detected using serology

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163
Q

What is a dermatophyte?

A

A fungi that requires keratin for growth

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164
Q

What are the forms of fungal infection?

A
  • Skin infection
    • Good prognosis - tends to be mild but occasionally debilitating
  • Mucosal infection
    • Good prognosis - tend to be mild but occasionally debilitating
  • Invasive infection (including wound infection)
    • Poor prognosis - can be life threatening even with ideal medical care
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165
Q

Are fungal infections primary pathogenic or opportunistic normally?

A

Normally opportunistic

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166
Q

What causes fungal skin infections?

A

Dermatophytes

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167
Q

Where do dermatophytes get nutrients from?

A

Keratin in the skin.
they are associated with the epidermis as the can feed off the dead skin tissue for keratin

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168
Q

When might a fungus become invasive?

A

in immunocompromised patients

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169
Q

What part of the immune system is required to clear fungal infections?

A

Innate - macrophages

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170
Q

What is eye karatitis?

A

Ulcerative corneal infection
(also called mycotic keratitis or keratomycosis)

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171
Q

What agents cause eye keratitis?

A

Fungus
Bacteria

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172
Q

What can eye keratitis lead to if left untreated?

A

Reduced vision or blindless
(second most common cause of blindness behind cataracts)

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173
Q

Why is candidiasis a cause for concern?

A

It is treatment resistant

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174
Q

What are the main species of Candidiasis?

A

Candida albicans
Candida glabrata
Candida tropicalis

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175
Q

Where is aspergillosis found?

A

An environmental organism

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176
Q

How does aspergillus infection occur?

A

From spores - these are inhaled and infection occurs through the lungs
(it is a conidial fungas)

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177
Q

What are the 2 main asperigllus species?

A

Aspergillus fumigatus
Aspergillus nidulans

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178
Q

What is allergic aspergillus a complication of?

A

Asthma
Cystic fibrosis
Sinusitis

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179
Q

When is Aspergillus invasive?

A

In immunocompromised patients

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180
Q

What is chronic pulmonary aspergillosis?

A

A difficult to treat ongoing infection.
If there is a significant underlying lung disease then this can lead to a reduced lung function making this infection difficult to clear leading to it becoming chronic.

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181
Q

What disease does a pneumocystis infection cause?

A

Pneumocystis pneumonia

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182
Q

What species of Pneumocystis causes Pneumocystis pneumonia?

A

Pneumocystis jirovecii
An obligate human parasite of the lung

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183
Q

What kind of people get infected with Pneumocystis?

A

Immunocompromised

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184
Q

Where is cryptococcus found?

A

In the environment

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185
Q

What are the 2 main species of cryptococcus?

A

Cryptococcus neoformans
Cryptococcus gattii
Tends to only infect immunocompromised patients

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186
Q

What is the aim of antimicrobial drug therapy?

A

To achieve inhibitory levels of agent at the site of infection without host cell toxicity

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187
Q

What does antimicrobial drug therapy rely on?

A

Identifying molecules with selective toxicity for organism targets

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188
Q

List the factors required for antifungal drug selective toxicity?

A
  • Target does not exist in humans
  • Target is significantly different to human analogue
  • Drug is concentrated in organism cell with respect to humans
  • Increased permeability to compound
  • Modification of compound in organism or human cellular environment
  • Human cells are “rescued” from toxicity by an alternative metabolic pathways
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189
Q

What are the main structural differences between human and fungal cells?

A

Fungi have cell walls
These cell walls are comprised of ergosterol

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190
Q

What are the 2 classes of fungal cell membrane active agents?

A

Polyenes
Ergosterol Synthetic pathway inhibitors

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191
Q

Give 2 examples of polyenes?

A

Amphotericin - broad spectrum
Nystain - Topic treatment

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192
Q

What is the mechanism of action of polyenes?

A

Form a pore in the ergosterol membrane
10x less affinity for cholesterol in mammalian membranes

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193
Q

What are some unwanted effects of using polyenes on mammalian cells?

A

Salt shifts

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194
Q

What is the mechanism of action of Ergosterol synthetic pathway inhibitors?

A

Dose dependent inhibitors of 14alpha-sterol demethylase
Secondary targets in the synthetic pathway inhibited by triazoles

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195
Q

Give 5 examples of Azoles and the fungi they act on

A

Fluconazole - Candida and Cryptococcus

Itraconazole - Aspergillus

Voriconazole - Invasive Aspergillus

Posaconazole and Isavuconazole - Zygomycetes

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196
Q

What are some side effects of Azoles?

A

liver dysfunction
GI symptoms: 10% of patients may discontinue drugs because of it
Nausea
vomiting
pain
Diarrhoea

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197
Q

What class of drugs are fungal cell wall acting agents?

A

Echinocandins

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198
Q

What is the mechanism of action of Echinocandins?

A

Inhibit 1,3-beta-glucan synthase

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199
Q

Give 3 examples of Echinocandins

A

Caspofungin
Micafungin
Anidulafungin

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200
Q

What fungi do Echinocandins tend to work on?

A

Susceptible yeasts
Mould

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201
Q

How are Echinocandins administered and why?

A

Via intravenous
Poor oral bioavailability

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202
Q

What are the main Mycobacteria of medical importance?

A

Mycobacteria tuberculosis
Mycobacteria leprae

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203
Q

How are mycobacteria classified in Gram staining?

A

They sit with the Gram-Positive bacteria family
They however do not stain on Gram stain
Require Ziehl-Neelsen stain

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204
Q

Why do Mycobacteria not stain on Gram stain?

A

The composition of their cell wall makes it impervious to staining
They have a high lipid content with Mycolic acids
Acid-Fast Bacteria

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205
Q

What stain is used to stain Mycobacteria?

A

Ziehl-Neelsen

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206
Q

Are Mycobacteria:
Spore forming
Aeorobic/Anaerobic
Motile?

A

Mycobacteria are
Non spore forming
Aerobic
Non motile

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207
Q

What is the significance of the Waxy cell wall on Mycobacteria?

A

Difficult to target with antibacterial agents
It allows them to survive inside macrophages at low pH environments

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208
Q

What is the growth rate of Mycobacteria?

A

Very slow
Weeks

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209
Q

What about the biology of Mycobacteria makes Mycobacteria difficult to treat?

A

Slow reproduction time
Slow growth in humans - gradual onset of disease
Slow growth in culture - increased time to make diagnosis
Slow response to treatment - cannot target fast reproduction times like other bacteria

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210
Q

What happens after a macrophage phagocytoses a Mycobacterium?

A

Bacterium is adapted to the intracellular environment
It can withstand phagolysosomal killing and will escape into the cytosol.

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211
Q

How can macrophages kill mycobacteria?

A

Release microbicidal molecules to kill the bacteria
They then present the antigen on MHC II molecules
This is detected by CD4 T cells
CD4 cells secrete IFNy andTNFa to activate intracellular macrophage killing

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212
Q

What composes a granuloma?

A

Infected macrophage in the centre
Other recruited Macrophages aggregated together (aggregates of epithelioid histocytes)
Surrounded by Lymphocytes (T and B cells)

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213
Q

What is the function of a granuloma?
What is a problem with this?

A

It will wall off the bacteria
However this can create a niche for the bacteria to enter latency and survive

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214
Q

What cell type is responsible for walling off the granuloma?

A

Fibroblasts

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215
Q

What conditions can make granulomas unstable and at risk of rupture?

A

CD4 depletion caused by HIV

TNFa depletion caused by therapies against RA or organ transplant

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216
Q

What are the 2 ways to diagnose Mycobacteria with culture?

A

Solid culture:
Microscopy positive 2-4 weeks
Microscopy negative 4-8 weeks

Liquid culture:
1-3 weeks

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217
Q

What other way can be used to diagnose Mycobacteria without culture?
What are the benefits of this?

A

Nucleic Acid Detection:
Uses PCR based testing
Faster results
Can detect for resistance
Sensitive and very specific

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218
Q

How can TB be diagnosed using a skin prick test?

A

The Mantoux test:
Intradermal injection of purified TB protein derivatives
Induced swelling and redness is a positive result

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219
Q

What is the treatment for tuberculosis?

A

4 Drugs: (RIPE)
Rifampin - 6 months
Isoniazid - 6 months
Pyrazinamide - 2 months
Ethambutol - 2 months

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220
Q

What is the length of time for treatment of TB?

A

4-9 months of combination therapy

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221
Q

Why are second line drugs sometimes used in TB?

A

Antibiotic resistant strains

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222
Q

What is the issue with the long length of time of TB treatment?

A

Side effects
Hepatotoxicity
Peripheral Neuropathy
Optic Neuritis

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223
Q

What are the different types of resistance TB strains?

A

MDR TB - resistant to multiple first line drugs

EDR (extensively drug resistant) - resistant to second line drugs

Totally drug resistant - TB resistant to treatment

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224
Q

What are the routes of infection of TB?

A

Aerosol
Patient to Patient Transfer

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225
Q

What is primary TB?

A
  • Initial contact made by alveolar macrophages
  • Tuberculosis evades killing by macrophage
  • Use macrophage to get transported through the lymphatics to the hilar lymph node
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226
Q

What is latent TB?

A
  • Primary infection contained but cell mediated immunity persists
  • Therefore in latent TB there is no clinical disease
  • But the response to TB can be measured in tuberculin skin test
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227
Q

What is Pulmonary TB?

A
  • Failure of immune system leads to the clinical presentation of disease:
  • Granulomas form around bacilli that have settled in the apex of the lung
    • In the apex there is more air and less blood
      • More air for bacteria
      • Less blood access for white blood cells to clear infection
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228
Q

What happens as a result of a latent TB granuloma rupturing?

A

Abscess formation
Necrosis occurs in the centre of the granuloma (caseous)
Caseous (cheesy) material gets coughed up

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229
Q

When does pulmonary TB occur?

A

Immediately after primary infection
After latent activation

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230
Q

Following TB activation, where can it spread to?

A

Other areas of the lung to create other TB lesions
Other body tissues:
TB meningitis
Miliary TB
Pleural TB
Bone and joint TB
Genitourinary TB

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231
Q

What are the risk factors for the reactivation of dormant TB?

A

Age - infants, young adults, elderly
Malnutrition
Intensity of initial exposure
Immunosuppression

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232
Q

Define a virus?

A

An infectious obligate intracellular parasite
Comprised of genetic material (DNA OR RNA) Surrounded by a protein coat or membrane

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233
Q

What viruses prevalent in the UK can cause miscarriages or birth defects?

A

Cytomegalovirus (CMV)
Varicella Zoster Virus (VZV)
Herpes Simplex Virus (HSV)
Rubella

234
Q

What viruses in the UK can cause outbreaks?

A

Influenza
Measles
Mumps
Norovirus

235
Q

What viruses in the UK can cause Cancer?

A

Epstein Barr Virus (EBV) - Lymphoma
Hepatitis B/C - Hepatocellular Carcinoma
Human Papilloma Virus (HPV) - Cervical/anal cancer
HIV - Increase risk of contracting other cancer causing viruses

236
Q

What are some characteristics of a virus?

A

Grow inside living cells - replicate inside host machinery
Possess only one type of nucleic acid - DNA OR RNA (not both)
No cell wall - Have a protein coat (capsid) or membrane lipid evenlope
Inert outside of host cell
Protein receptors on virus surface to allow for attachment to susceptible host cells

237
Q

What are the different clinical presentations of viruses and give examples for each?

A

Acute:
Symptomatic - Chicken pox caused by VZV
Asymptomatic - Herpes and CMV

Chronic:
Hepatitis B and C
HIV

Latent:
Reactivation of VZV causes shingles in adulthood

238
Q

What diagnostic tests are used to identify viruses?

A

PCR - identifies viral genetic material
Serology - detection of immunological memory of a virus
Histopathology - features of viral infection
Viral culture
Electron Microscopy

239
Q

What are the stages of Viral Replication?

A
  1. Attachment to specific receptor
  2. Cell entry
  3. Host cell interaction
  4. Replication of viral DNA into host cell
  5. Assembly of virion - Translation of viral mRNA to produce Viral genome, structural proteins and non-structural proteins
  6. Release of new viral particles - viral bursting (cell death) or budding/exocytosis
240
Q

How do viruses cause disease?

A

Direct destruction of host cells
Modification of host cells
Over reactivity of the immune system
Damage through cell proliferation
Evasion of Host defenses

241
Q

Give an example of a virus that causes disease by destroying host cells?

A

Poliovirus:

  • Infects and replicates within nerves, over 4 hours
  • Host neuron lysis and death
  • Causing paralysis
242
Q

Give an example of a virus that causes disease by modifying host cells?

A

Rotavirus:

  • Atrophies villi and flattens epithelial cells of the gut
    • Decreases small intestine surface area
    • Nutrients (including sugar) are not absorbed
    • Hyperosmotic state - sugar remains in lumen so draws in water
    • Profuse diarrhoea

**Rotavirus is resistant to acidic pH*

243
Q

Give an example of a virus that causes disease by over activating the immune system?

A

Hepatitis B:

  1. Virus infects hepatocyctes, and cause the presentation of the viral antigen on outside the hepatocyte.
  2. Cytotoxic T lymphocytes recognise the antigen as foreign and kill the hepatocyte infected with virus, leading to a reduced number of hepatocytes
244
Q

What symptoms are caused by a reduced number of hepatocytes as found in Hepatitis B/C infections?

A
  • Jaundice (increased bilirubin)
    • Pale stool (increased bilirubin)
    • Dark urine (increased bilirubin)
    • Right Upper Quadrant (RUQ) pain
    • Fever and malaise
    • Itching (bile salts released into body)

**Hepatitis B tends to become chronic. Sustained viral replication and liver cell destruction occurs but at a lower level, presenting fewer clinical symptoms*

245
Q

Give an example of a virus that causes disease by damage through cell proliferation

A

Human Papillomavirus (HPV):

  1. Acquired through direct contact
  2. Partial viral replication and expression of HPV proteins - these are oncoproteins
  3. Viral DNA integration into host chromosomes
  4. Continous expression of oncoproteins (cancer causing proteins) causing cellular DNA mutations → dysplasia and neoplasia
246
Q

What are the different methods of host defence evasion that viruses use?

A
  1. Virus persistence or latency.
  2. Down regulation of interferons.
  3. Virus variability due to gene reassortment or mutation.
  4. Prevention of host cell apoptosis.
  5. Viral modulation of host defences.
247
Q

What are the different clinical presentations of Herpes Simplex Virus (HSV)?

A
  • Skin
    Orofacial herpes - cold sores
    Genital herpes - warts
    Herpetic whitelow - sores on the fingers
    Erythema multiforme - systemic rash across the body
    Herpes gladiatorum - rash affecting the chest
  • Visceral
    Oesophagitis - inflammation of the oesophagus
    Pneumonitis - inflammation of the lungs
    Hepatitis - inflammation of the liver
  • CNS
    Meningitis - inflammation of the meninges surrounding the brain
    Encephalitis - inflammation of the brain
    Transverse myelitis - inflammation across the spinal cord (can cause paralysis, sensation changes)
  • Eye
    • Conjunctivitis
    • Keratitis
248
Q

What is the ONLY clinical presentation of JC virus (Human polyomavirus 2)

A

CNS - progressive multifocal leukoencephalopathy

249
Q

What are Protozoa?

A

Single cell eukaryotic organisms
Unicellular
Can be free living or parasitic

250
Q

How are Protozoa classified?
What are their classifications

A

Based on locomotion:
Amoebaoids
Sporozoa
Flagellates
Cilliates
Microsporidia

251
Q

Give an example of an Amoeboid?

A

Entamoeba histolytica

252
Q

How is Entamoeba Histolytica spread?

A

Faeco-oral route

253
Q

How are Entamoeba Histolytica infections treated?

A

With Metronidazole

254
Q

Give examples of diseases caused by flagellates?

A

Human African Trypanosomiasis (sleeping sickness)
American Trypanosomiasis (Chagas disease)
Leishmaniasis
Trichomoniassis
Giardiasis

255
Q

Give examples of diseases caused by flagellates?

A

Human African Trypanosomiasis (sleeping sickness)
American Trypanosomiasis (Chagas disease)
Leishmaniasis
Trichomoniasis
Giardiasis

256
Q

What are the symptoms of Human African Trypanosomiasis infection?

A
  • Chancre
  • Fever
  • Headaches
  • Extreme fatigue
  • Lymphoadenopathy
  • Spenomegaly
  • CNS involvement (e.g. personality changes)
257
Q

How is Human African Trypanosomiasis spread?

A

Vector - infected via Tsetse fly

258
Q

How is Human African Trypanosomiasis diagnosed?

A

Blood film or CNS

259
Q

What are the symptoms associated with American Trypanosomiasis?

A
  • Slower illness manifestations
    • Headache
    • Fever
    • Lymphadenopathy
    • Chagoma - swelling at site of innoculation
    • Romana’s sign - swelling around the eyes, eyelids and conjunctiva
  • Late disease manifestations
    • Dilated cardiomyopathy
    • Megaoesophagus
    • Megacolon
260
Q

What specific flagellate cause American Trypanosomiasis?

A

Trypanosoma cruzi

261
Q

How is American Trypanosomiasis spread?

A

Vector - transmitted through faeces of triatomine bug
Through blood, vertical transmission and contaminated food

262
Q

How is American Trypanosomiasis diagnosed?

A

Visualisation of tropmastigotes on blood film
Amastigoes on biopsy in chronic illness

263
Q

What symptoms are associated with Leishmaniasis?

A
  • Cutaneous
    • Incubation; weeks to months
    • Ulcers on exposed parts of body; these heal and leaving permenant scars
    • Usually benign
  • Mucocutaneous
    • Partial or total destruction of mucous membranes of nose, mouth and throat cavities
  • Visceral
    • Known as Kala-Azar (black fever)
    • Incubation period; days to years
    • Associated with multi-organ failure
    • Associated with bone marrow suppression, lymphodenopathy, weight loss.
    • High mortality rat
264
Q

How is Leishmaniasis spread?

A

Via saliva of the female sand fly

265
Q

What symptomas are associated with Giardiasis?

A

Diarrhoea
Cramps
Bloating

266
Q

How is Giardiasis spread?

A

Faeco-oral route

267
Q

How is Giardiasis diagnosed?

A

Stool microscopy - presence of trophozoites

268
Q

How is Giardiasis treated?

A

Metronidazole and tinidazole

269
Q

What symptoms are associated with Trichomoniasis in women?

A
  • Purulent discharge
  • Abdominal pain
  • Vulvar/ cervical lesions
  • Dysuria
  • Dyspareunia
270
Q

What symptoms are associated with Trichomoniasis in men?

A
  • Urethritis
  • Epididymitis
  • Prostatitis

Often asymptomatic

271
Q

What specific flagellate causes Trichomoniasis?

A

Trichomonas vaginalis

272
Q

How is Trichomoniasis spread?

A

Sexually Transmitted Infection (STI)

273
Q

How is Trichomoniasis treated?

A

Metronidazole

274
Q

Give some examples of diseases caused by sporozoids?

A

Cryptosporidiosis
Toxoplasmosis

275
Q

What symptoms are associated with Cryptosporidiosis?

A
  • Watery diarrhoea (no blood)
  • Vomiting
  • Fever
  • Weight loss
276
Q

What specific sporozoid causes Cryptosporidiosis?

A

Cryptosporidium spp

277
Q

How is Cryptosporidiosis spread?

A

Water/ food bourne infection - occurs through the ingestion of mature cysts

278
Q

How is Cryptosporidiosis diagnosed?

A

Acid fast staining - oocysts seen in stool sample

279
Q

How is Cryptosporidiosis treated?

A
  • Hydration and replacement of electrolytes
  • Self-limiting disese - usually lasting no more than 2-3 weeks
280
Q

What symptoms are associated with Toxoplasmosis?

A
  • Usually asymptomatic - severe consequences in pregnancy and immunodeficiency
  • Disseminated disease (particualarly affecting the eyes!)
    • Chorioretinitis
    • Retinochoroiditis
    • Toxoplasma encephalitis
281
Q

What specific sporozoid causes Toxoplasmosis?

A

Toxoplasma gondii

282
Q

How is Toxoplasmosis spread?

A

Acquired through ingestion of oocytes!

  • Contaminated food
  • Undercooked meat and shellfish
  • Vertical transmission
  • Trasmission via water/ feline species
283
Q

How is Malaria spread?

A

Vector; spread of Plasmodium via the bite of a female Anopheles mosquito

284
Q

What are the five species of Malaria-causing Plasmodium?

A
  • Plasmodium falciparum (important!)
  • Plasmodium ovale
  • Plasmodium vivax
  • Plasmodium malariae
  • Plasmodium knowlesi
285
Q

What species of plasmodium is responsible for the most number of malaria cases and what percentage is this?

A

P. falciparum
Responsible for 75% of malaria cases in the UK

286
Q

What non-specific symptoms and signs are associated with Malaria?

A

Non-specific symptoms:
- Fever, night sweats and rigors
- Chills
- Myalgia
- headache
- Vomiting

Signs:
Pallor - due to anaemia
Hepatosplenomegaly
Jaundice - bilirubin released due to RBC haemolysis

287
Q

What haemolysis specific symptoms are associated with Malaria?

A

Haemolysis due to infected cell lysis and immune-mediated killing!

  • Anaemia
  • Jaundice
  • Hepatosplenomegaly
  • Black water fever - Hb passes into urine
  • Monocytosis and lymphopenia - loss of WBC response
  • Thrombocytopenia - reduced platelets
288
Q

How does the malarial Plasmodium cause haemolysis?

A

1️⃣ Parasite develops in the RBC, producing waste products and toxic factors
2️⃣ Infected cells releasing merozoites surface proteins and hemozoin into the blood
3️⃣ Stimulates macrophages to release pro-inflammatory cytokines and inflammatory mediators (TNF, IFN-y)

289
Q

How is Malaria diagnosed?

A

Blood film - visualisation of Trophozoite seen under light microscopy

  • Thick film - to detect whether person has malaria
  • Thin film - identify species and calculate parasitaemia percentage
290
Q

How is Malaria treated? How does this vary depending on severity of disease?

A
  • Uncomplicated malaria
    Oral:
    1. Artemether with lumefantrine (Riamet)
    2. Proguanil and atovaquone (Malarone)
    3. Quinine sulphate
    4. Doxycycline
  • Complicated or severe malaria
    IV:
    1. Artesunate: this is the most effective treatment but is not licensed.
    2. Quinine dihydrochloride
291
Q

Explain how malaria causes disease?

A
  • Human Liver Stage (exo-erythrocytic):
    • 1️⃣ Mosquito takes a blood meal, injecting the indiviual with sporozoites (infected for of the Plamsodium)
    • 2️⃣ Sporozoites travel in the blood and infect liver cells (hepatocytes)
    • 3️⃣ Sporozoites can mature into Shizoints or lay dormant as hypnozoites (in P. vivax/ P. ovale)
    • 4️⃣ Shizoints mature into merozoites which enter the blood and infect RBCs
  • ⭕ Human Blood Stage (Endo-erythrocytic):
    • 5️⃣ Merozoites infect RBCs - The merozoites reproduce every 48 hours.
    • 6️⃣ Merozoite develop into immature trophozoite. This can then go down two maturation routes:
    • 7️⃣ 🅰️ Trophozoite develop into Schizonts and then merozoites, which ruptures the RBC which releases more merozoites to infect other RBCs
      This cycle repeats every 48 hours.
    • ✳️ At this stage, as RBCs rupture, the individual develops cyclical fever and haemolytic clinical manifestations, such as anaemia, jaundice (bilirubinaemia), haemoglobinuria
    • 7️⃣ 🅱️ Some Trophozoites differentiate into sexual stage gametocytes
292
Q

Why do patients with malaria experience high fever spikes every 48 hours?

A

Due to the replication of the merozoites in the RBCs taking 48 hours at which point the RBC ruptures leading to an inflammatory response

293
Q

Explain how malaria is spread

A
  • 8️⃣ Another mosquito takes a blood meal from this infected individual will ingest gametocytes
  • 9️⃣ Gametocytes mature into an oocyst
  • 🔟 Oocysts ruptures and release sporozoites
  • 🔟+ 1️⃣ Sporozoites are injected into the blood of a different individual - cycle.
294
Q

What is the most important Plasmodium species that causes malaria and why?

A

P. Falciparum
Causes complicated malaria - P. Falciparum replicates rapidly and causes microcirculatory obstruction.

295
Q

What is the difference between uncomplicated and complicated malaria?

A

Uncomplicated:
Most plasmodium-infected red blood cells get screened and destroyed by the spleen.

Complicated: P.falciparum:
Plasmodium falciparum avoids this fate by generating a sticky protein that coats the surface of the infected red blood cells.

The protein causes the red blood cells to clump together and occlude tiny blood vessels - a process called cytoadherence.

This blocks the flow of blood so that infected cells aren’t able to flow into the spleen, and it also blocks blood flow from reaching other vital organs which can cause ischaemia. This can eventually lead to organ failure (refer to complications).

296
Q

What is the pathogenesis for the obstructed microcirculation caused by P. Falciparum.

A
  • 1️⃣ Cytoadherence
    Infected RBCs present membrane proteins that bind to microvascular endothelial cells in vessels
  • 2️⃣ Rosetting
    Infected RBCs also adhere to non-infected RBCs, causing small vessels to become obstructed by clumbs of RBCs - this causes hypoxia.
  • 3️⃣ Sequestration
    Microinfarcts form in major organs (brain, heart, lungs, liver, kidney) where they are able to mature and evade the immune system.
297
Q

What are the different complications of malaria infection?
What is the treatment for each complication?

A

Cerebral malaria - Anti-epileptic drugs
Renal Failure - Fluids and dialysis
Acute Respiratory Distress Syndrome (ARDS) - Oxygen, Diuretics and ventilation
Bleeding - Blood products/Blood transfusion
Shock - Sepsis treatment via Broad Spectrum antibiotics

298
Q

What 2 species of the plasmodia genus lie dormant and cause late relapse of malaria?

A

P.ovale and p.vivax.

299
Q

What is the treatment for malaria infection

A

Chloroquine

300
Q

What are the 3 classifications of worms (helminths)

A

Nematodes
Trematodes
Cestodes

301
Q

Does HIV affect more women or men globally?

A

Women more than men

302
Q

What age group accounts for 50% of all new HIV infections worldwide?

A

19-24 year olds

303
Q

What has led to the high rates of AIDs drastically dropping?

A

HAART
(Highly Active Anti-retroviral Therapy)

304
Q

What is the 90/90/90 target?

A
  • Global target
  • 90% of people living with HIV should be diagnosed
  • 90% of people diagnosed with HIV started on anti-retroviral therapy
  • 90% of those on anti-retroviral therapy be viral suppressed
305
Q

What is the relationship between late HIV diagnosis and prognosis?

A

10-fold increase in risk of death within first year of diagnosis

306
Q

What are the HIV transmission routes?

A
  • Blood
    Less common due to blood screening before blood transufsions
  • Sexual
    Most often through Heterosexual transmission despite stigma of homosexual transmission
  • Vertical
    Called this now instead of “Mother to child transmission” as it had connotations of blaming the mother
307
Q

What does U=U mean?

A
  • Undetectable=Untransmissible
  • If the viral load is undetectable in the patient’s blood, they are not able to transmit the virus, even in unprotected sex
  • Therefore, if you take your medication properly and keep the viral load at 0 then it is not possible to pass HIV on regardless of condom use
308
Q

What is PrEP?

A
  • Pre-Exposure Prophylaxis - usually take tenofovir and entricitabine in one combined tablet
  • Take anti-retroviral therapy despite not having HIV to prevent infection
  • highly effective - much more effective than PEP
309
Q

What is PEP?

A
  • Post-Exposure Prophylaxis
  • Emergency medication taken after potential exposure to the virus
  • Must be started within 72 hours of exposure
310
Q

What are the benefits to HIV testing?

A
  • Cost-effective, testing is very cheap
    • Reduction in cost of social care, lost working days, benefits claimed, cost associated with further onward transmission
  • Gives patient access to appropriate treatment and care
  • Reduction of transmission
311
Q

What are the scenarios where you would carry out an HIV test?

A
  • Clinician indicate diagnoses - clinical indications of immunosuppressive disease
  • Routine screening in high prevalence locations
  • Antenatal screening
  • Screening in high risk groups
  • Patient initiated request for testing
312
Q

What conditions would indicate that an HIV test may be needed?

A
  • Unexplained lymphadenopathy
  • Unexplained weight loss or diarrhoea, night sweats of PUO
  • Oral or esophageal candidiasis or hairy leukoplakia
  • Flu like illness, rash, meningitis
  • Unexplained blood dyscrasias
313
Q

What are some recognised risk factors for HIV?

A

Heterosexual and homosexual sex (men to women and men to men)
IVDU
Multiple sexual parteners
Rape
Vertical transmission

314
Q

What must be done when offering HIV testing?

A
  • Document verbal consent given
  • Determine how results will be given
  • Do not need written consent
  • Do not need pre-test HIV counselling
315
Q

What HIV screening test is preferred?

A
  • Venous blood sample
  • 4th gen HIV tests detect vast majority of infections at 4 weeks
    • If there is a high degree of risk/suspicion of HIV infection repeat at 8 weeks if a negative result
316
Q

What is a HIV POCT?

A
  • Point of Care Test
  • Finger prick of blood
  • Lower sensitivity and specificity
  • This test is used in the community to increase access to the test, increases patient choice and case detection
  • Lower risk of complications and transmissions associated
317
Q

What type of virus is HIV?

A

Retrovirus

318
Q

What proteins/genetic material is found within a retrovirus?

A

RNA genetic material
Contain a reverse transcriptase enzyme

319
Q

What virus and species is HIV-1 derived from?

A

Chimpanzee derived Simian Immunodeficiency virus
(SIVcpz)

320
Q

What virus and species is HIV-2 derived from?

A

Sooty Mangabey-derived simian Immunodeficiency virus (SIVmp)

321
Q

what is the normal role of T cells in the immune response?

A

T-helper cells coordinates acquired immune response - responsible for organising, recruiting and facilitating maturation of B-antibody producing cells and CD8 (T-killer) cells.

322
Q

What is the role of Th-1 T cells?

A
  • CTLs produce perforin and granulysin enzyme that directly kills cells with antigen on.
  • NK cells kills any cell seen to be infected with specific foreign agent.
323
Q

What is the role of Th-2 T cells?

A

Produces specific interleukins (IL-4, 5, 10 and 13) whihc causes the maturation of B lymphocytes into plasma cells
- Plasma cells produce specific antibodies IgG against specific antigen
- Produces a rolonged and effective antibody response

324
Q

What is the structure of the HIV virus?

A

Icosahedral

protein capsid containing
2 RNA strands
2 enzymes: integrase and reverse transcriptase

Lipid envelope with spike projections of glycoproteins GP41 and GP120 to lock onto CD4 receptors on T cells

325
Q

What are the main cells that are infected via HIV?
What other cells also can be infected?

A

CD4 T cells

Dendritic cells, macrophages, astrocytes

326
Q

Explain the life cycle of the HIV virus?

A
  • 1️⃣ Glycoproteins on HIV molecule (gp160; formed of gp120 and gp41) allow it to adhere to;
    • CD4 receptors (gp120 and gp41 receptors)
    • CCR5 receptors on Macrophages
      -CXCR4 Receptors on CD4 T cells
  • 2️⃣ Once viral capsid enters cell, viral enzymes and nucleic acid are uncoated and released.
  • 3️⃣ Using reverse transcriptase, single stranded RNA is converted into double-stranded DNA.
  • 4️⃣ Viral DNA then is integrated into cell own DNA through the action of integrase enzyme.
  • 5️⃣ When infected cell divides the viral DNA is transcribed, producing long chains of viral proteinsWhilst infected cell is replicated, the viral DNA also replicates alongside.
  • 6️⃣ Viral RNA is spliced and the protein chains are cleaved and reassembled by protease enzyme into individual proteins - these combine to form a functioning virus.
  • 7️⃣ The immature virus exocytosed, taking some cell membrane with it to form a new lipid envelope
  • 8️⃣ Once outside of the cell, the virus undergoes further maturation.
327
Q

What is the journey (Natural History) of HIV through the body?

A

HIV infects CD4 T cells

HIV is detectable in the bloodstream around a week after initial infection

7️⃣ Production of the HIV virus increases exponentially as more and more T-cells become infected and die as the virus replicates

8️⃣ After around three weeks after infection, the viral load and p24 antigen are detectable.

the immune system responds with a full adaptive immune response to try and control the new pathogen. HIV antibody is detectable 2-4 weeks in. This is seroconversion (causing acute non-specific symptoms)

9️⃣ Immune system recovery establishes control of the virus;
This starts the viral latency (asymptomatic phase) as the viral load is kept at a plateau.
on average, this clinical latency period last for around seven years

🔟 Progressive immunological impairment (slow decrease in CD4 T-cells) and ongoing replication of HIV in virus reservoirs eventually leads to the clinical manifestation of immunodeficiency; HIV associated opportunistic malignancy/ infection

328
Q

What are the main events in the first few weeks after HIV infection?

A

Increase viral load
HIV p24 antigen detected
Antibodies against HIV
CD8 T cell activation
Seroconversion illness

329
Q

What are some methods by which HIV transmission can be reduced/prevented?

A
  • Consistent condom use (80-90% effective)
  • Male circumcision (60% reduction in infection; no benefit to female partners)
  • Treating STI’s e.g. genital ulcers and HSV infection which increase transmission risk
  • Microbicide gel for women (30-40% reduction in transmission risk)
  • Needle and syringe exchange for IVDUs
  • Post-exposure prophylaxis (PeP)
  • Treatment as prevention (TasP) (96% reduction)
  • Pre-exposure prophylaxis (PreP)
330
Q

How can paediatric HIV infection occur?

A
  1. In utero: transplacental; mostly during the third trimester
  2. Intra partum: exposure to maternal blood and genital secretions during delivery
  3. Breast milk: ingestion of large amounts of contaminated milk
331
Q

How many adults and children are estimated to be living with HIV globally?

A

38 million

332
Q

What markers are used for monitoring HIV infection?

A

CD4+ T cell count/ul

HIV Viral load (RNA copies/ml)

333
Q

When a patient presents with a fever, rash and non-specific symptoms, what 3 steps should you do?

A
  • Take a sexual history
  • Think of HIV seroconversion illness
  • Tell lab to check for antigen as well
334
Q

Which infections would a HIV test be indicated?

A
  • Recurrent shingles
  • Candidiasis
  • (Essentially infections associated with immunocompromised patients)
335
Q

What are the 3 main respiratory diseases associated with HIV infection?

A
  • Bacterial (often pneumococcal) pneumonia
  • Tuberculosis
    significantly higher mortaility when you have HIV and TB
  • Pneumocystis jirovecii pneumonia (PCP) (most common opportunistic infection in AIDs)
336
Q

What are the symptoms of PCP?

A

Fever
SOB
Dry cough
Pleuritic chest pain
Exertional drop in O2 saturations

337
Q

How is PCP treated?

A

Via Co-trimoxazole

338
Q

What are the HIV associated CNS diseases?

A
  • CNS Mass Lesions:
    • Cerebral taxoplasmosis
    • Primary CNS Lymphoma
    • Tuberculoma
  • Meningitis:
    • Cryptococcal
    • Tuberculous (Would have CSF with raised lymphocytes, raised protein and reduced glucose. They may also have an insidious onset CNVI palsy)
    • Pneumococcal
  • Ophthalmic Lesions:
    • CMV
    • Toxoplasmosis
    • Choroidal Tuberculosis
339
Q

What are the HIV associated neoplasms?

A
  • Lymphoma
    • Caused by EBV
  • Cervical neoplasia
    • Caused by HPV
  • Kaposi’s sarcoma
    • Caused by human Herpesvirus 8
  • Hepatocellular Carcinoma
    • Caused by Hepatitis B/C
340
Q

Describe the time course of HIV infection
(natural history)

A

Acute primary infection - Acute seroconversion illness:
Transient immunosuppression
Fall and then rise of CD4 count.
Rise of viral load

Asymptomatic phase:
Progressive loss of CD4
Clinical latency - may have generalised lymphadenopathy

Early symptomatic HIV

AIDS:
Symptoms of immune deficiency

341
Q

What is the marker for AIDS?

A

CD4 count less than 200/ul

342
Q

What can influence the time from HIV infection to AIDS?

A

Host and viral genetic factors
Rapid onset - elderly/children, high viral load

343
Q

What are the NON-AIDS defining conditions that HIV can cause?

A

Oral candidiasis- Treated with Nilstat
Oral hairy leucoplakia
Generalised Lymphadenopathy
Shingles - Treated with Acyclovir
Chronic Diarrhoea

344
Q

What are the AIDS defining conditions caused by HIV

A

CD4 <500 ul
Mycobacteria Tuberculosis
Kaposi Sarcoma - HHV8
Coccidiodomycosis
Cervical Cancer

CD4 <200 ul (the 3 Ps)
Pneumocystis pneumonia
Progressive multifocal Leukoencephalopathy
Histoplasmosis

CD4 < 100ul: (4 Cs)
Candidiasis - eosophageal
Cerebral Toxoplasmosis
Cryptococcus
Cryptosporidiosis

CD4 < 50ul:
CNS lymphoma
CMV
MAC infection

345
Q

What are the symptoms associated with HIV seroconversion illness?

A

Abrupt onset of non-specific symptoms
Significant weight loss
Lethargy/depression

346
Q

What is an important differential diagnosis of HIV seroconversion illness?

A

Secondary Syphilis

347
Q

What could late HIV diagnosis lead to?

A

Increased transmission
Increased morbidity
Increased mortality

348
Q

What are the symptoms associated with acute HIV?

A
  • Fever, rash and non-specific symptoms
  • Similar to glandular fever
  • Diffuse symmetrical maculopapular rash
349
Q

What are the symptoms associated with early symptomatic HIV?

A
  • Oral/vaginal candidiasis/oral thrush
  • Oral Hairy Leukoplakia (associated with EBV)
  • VZV (shingles) with 2 or more episodes OR multiple dermatomes
  • Cervical dysplasia
  • Cervical carcinoma-in-situ
  • Peripheral neuropathy
  • Bacillary angiomatosis
  • Immune-mediated Thrombocytopaenic Purpura
  • Pelvic Inflammatory Disease
  • Listeriosis
  • Constitutional symptoms (i.e. fever or diarrhoea for more than 1 month)
  • persistent lymphadenopathy
350
Q

What are the 3 classes of HIV drugs?

A

Reverse transcriptase inhibitors - nucleoside/non-nucleoside
Protease inhibitors
Fusion inhibitors

351
Q

What drugs make up HAART?

A

2 Nucleoside reverse transcriptase inhibitors +
1 non-nucleoside reverse transcriptase inhibitor
OR
2 Nucleoside reverse transcriptase inhibitors +
1 Protease inhibitor

352
Q

Why in HAART are there 2 different types of drug used?

A

These act at different points on the HIV replication cycle

353
Q

How does HIV develop drug resistance?

A

Non adherence - not taking meds
Drug-drug interactions

354
Q

What determines the class grouping of antibiotics?

A

Where they work:
Cell wall synthesis
Nucleic acid synthesis
Protein synthesis
Folate synthesis

355
Q

What are bacteriostatic and bacteriocidal antibiotics?

A

Bacteriostatic - Prevent the growth of bacteria; defined as a ratio of Minimum Bactericidal Concentration (MBC) : Minimum Inhibitory Concentration (MIC) of > 4

Bacteriocidal - Will kill the bacteria; kills 99.9% in 18-24 hours

356
Q

What classes of antibiotics are bacteriostatic?

A
  • Inhibit protein synthesis
  • Inhibit DNA replication
  • Inhibit metabolism

Useful in disease where its the bacteria exotoxin that’s causing the symptoms as they reduce toxin production.

357
Q

What classes of antibiotics are bacteriocidal

A
  • Inhibit cell wall synthesis

Useful in cases of poor drug penetration due to poor blood supply (endocarditis); difficult to treat infections or when we need to eradicate infections quickly (meningitis).

358
Q

What does the MBC:MIC ratio tell us?

A

The Minimum Bactericidal Concentration (MBC) is the lowest concentration of an antibacterial agent required to kill a bacterium over a fixed time (18 hours or 24 hours), under a specific set of conditions.

The Minimum Inhibitory Concentration (MIC) is defined as the lowest concentration of an antimicrobial ingredient or agent that is bacteriostatic (prevents the visible growth of bacteria)

359
Q

When are antibacterial agents regarded as bactericidal?

A

If the MBC is no more than 4x the MIC

360
Q

What are the 2 major determinants of antibacterial effects of antibiotics?

A

Concentration - How high the conc is above the MIC
Time - Time that serum concentrations remain above MIC during the dose interval (t > MIC)

361
Q

Give examples of antibiotics that are governed by concentration?

A

Aminoglycosides
Quinolones

362
Q

Give examples of antibiotics that are governed by time?

A
  • β-lactams (penicillins; cephalosporins; carbapenems; monobactams)
  • Clindamycin
  • Macrolides
  • Oxazolidinones
363
Q

Give 4 methods by which a bacteria can resist an antibiotic?

A

Change the antibiotic target - MRSA cannot bind to PBP of staphylococci
Destroy the antibiotic - Staphylococci produce beta-lactamase
Prevent access of antibiotic - modify membrane channel no. size. selectivity
Remove antibiotic from bacteria - Export or efflux pumps

364
Q

What are the methods by which bacteria can develop resistance?

A

Intrinsic - naturally resistant

Acquired:
Spontaneous gene mutations
Horizontal gene transfer - Conjugation, Transduction, Transformation

365
Q

Name 2 Gram-Positive resistant strains of clinical importance

A

MRSA - Methicillin (Flucloxacillin) resistant Staphylococcus Aureus
VRE - Vancomycin resistant enterococci

366
Q

How does MRSA have antibiotic resistance?

A

Staphylococcus cassette chromosome mec (SCCmec) contains the resistant gene mecA which encodes penicillin-binding protein 2a (PDP2a).

Confers resistance to all β-lactams and methicillin

367
Q

How does VRE have antibiotic resistance?

A

Plasmid mediated acquisition of gene encoding altered AA on peptide chain preventing vancomycin binding - promoted by cephalosporin use.

368
Q

What mechanism do Gram Negative bacterial strains confer resistance?

A

Produce Beta-lactamase enzymes which hydrolise the beta-lactam ring of penicillins

369
Q

How can we combat drugs that have beta lactamases?

A

Design drugs that utilise agents that inhibit beta lactamase
Co-amoxiclav - Amoxicillin and Clavulanate
Clavulanate inhibits the beta lactamase

370
Q

What is ESBL?

A

A beta lactamase enzyme - extended spectrum beta lactamase
Produced by some bacterial that allows them to hydrolise third gen cephalosporins and aztreonam

371
Q

What is AmpC beta lactamase?

A

A cephalosporinase enzyme encoded by enterobacteriaceae

372
Q

What does AmpC beta lactamase provide antibiotic resistance against?

A

Cephalosporins,
most penicillins
Beta lactamase inhibitor combinations

373
Q

What are the 2 main classes of antibiotics that inhibit bacterial cell walls?

A

Beta Lactams
Glycopeptides

374
Q

What compound do beta lactam antibiotics target?

A

Peptidoglycan

375
Q

Give classes of antibiotics are beta lactams?

A

Possess a Beta lactam ring

  • Penicillins
  • Cephalosporins
  • Carbapenems
  • Monobactams
376
Q

What bacteria do beta lactams work on?

A

Better on Gram positive - have bigger peptidoglycan area
Can work on both Gram positive and Gram negative

377
Q

What is the mechanism of action of beta lactam antibiotics?

A

Disrupt peptidoglycan production by:

  1. Binding covalently and irreversibly to the penicillin-binding proteins (PBPs) particularly transpeptidase
  2. Cell wall synthesis is disrupted and cell lysis occurs as peptidoglycan crosslinking can not occur

→ Active only against rapidly multiplying organisms.

378
Q

Why do different classes of beta lactams differ in effectiveness?

A

Difference in the spectrum and activity of β-lactam antibiotics are due to their relative affinity for different PBPs

379
Q

When should cephalosporins be used?

A
  • Patients with penicillin allergy
  • Patients with meningitis as they can penetrate the head.
380
Q

What are carbapenems?

A

Antibiotics designed to overcome the actions of beta lactamases and cephalosporinases
Therefore these are the most broad specturm antibiotics and used as a last resort

381
Q

Name some Carbapenems

A

Ertapenem
Imipenem
Meropenem

382
Q

What is the problem with carbapenems?

A

They were the most broad spec antibiotic that could be used against anything however now there are carbapenem resistant bacteria

383
Q

What are CREs?

A

Carbapenem resistant enterobacteriaceae:
Pseudomonas aeruginosa
Escherichia coli
Klebsiella pneumoniae

384
Q

What antibiotics would be used to treat:
Cellulitis
Strep throat
Pneumonia

A

Gram positive bacteria so beta lactams:
Cellulitis (S.aureus, Group A, C, G strep) - Flucloxacillin
Strep throat (Group A,C, G strep) - PO penicillin V + IV Benzylpenicillin
S.pneumonia - PO Amoxicillin + IV Benzylpenicillin

385
Q

Give examples of some Glycopeptides

A

Vancomycin
Teicoplanin

386
Q

What is the route of administration for glycopeptides?

A

IV only

387
Q

When do we use glycopeptides?

A

Only work on Gram positive bacteria:
Used in MRSA
Those with penicillin allergy

388
Q

What types of antibiotics inhibit nucleic acid synthesis?

A

Rifampicin
Metronidazole
Fluoroquinolones

389
Q

What does Rifampicin target?

A

RNA polymerase

390
Q

What do fluoroquinolones target?

A

DNA gyrase and DNA topoisomerase IV

391
Q

Give an example of a fluoroquinolone?

A

Ciprofloxacin (restricted antibiotic)

392
Q

When do we use fluoroquinolones?

A

Gram negative > Gram positive:
Penicillin allergy
UTIs
Intra-abdominal infections

393
Q

What types of antibiotics will inhibit protein synthesis?
Give an example for each

A

Aminoglycosides - Gentamicin (30s)
Tetracyclines - Doxycycline (30s)
Lincosamides - Clindamycin (50S)
Macrolides - Clarithromycin/ Erythromycin (50s)
Chloramphenicol

394
Q

What is the route of administration of Aminoglycosides?

A

IV only

395
Q

When do we use aminoglycosides?

A

Gram negative and Staph
UTIs
Infective Endocarditis

396
Q

What is the route of administration of Tetracyclines?

A

PO only

397
Q

When do we use tetracyclines?

A

Broad specturm but mainly gram positive (S.aureus and Streps)
Cellulitis (if penicillin allergy)
Pneumonia

398
Q

What is the route of administration for lincosamides?

A

IV and PO

399
Q

When do we use Lincosamides?

A

Gram Positive (S.aureus, Beta haemolytic strep and anaerobes)
Cellulitis
Necrotising Fasciitis

400
Q

What is the route of administration of Macrolides?

A

IV and PO

401
Q

When do we use Macrolides?

A

Gram positive (S.aureus, Beta haemolytic strep, atypical pneumonia)
Severe pneumonia
Penicillin allergy

402
Q

What types of antibiotics inhibit folate synthesis?

A

Sulphonamides
Trimethoprim

403
Q

When do we use Trimethoprim?

A

Broad spectrum but mainly used for Gram negative
UTIs

404
Q

What questions should be asked before prescribing antibiotics?

A
  1. How does it work?
  2. What kind of bacteria will it cover?
  3. Does it need to be IV or PO?
  4. Does my patient have an infection caused by those bacteria?
  5. Could there be resistance?
  6. Are there any reasons why the patient couldn’t have antibiotics?
405
Q

What antibiotics do we commonly use to treat UTIs?

A

Nitrofurantoin
First line for UTI and it only works in the lower respiratory tract

Trimethoprim

406
Q

What can be done to prevent patient to patient transmission of infection?

A
  • Isolation
  • Antimicrobial stewardship - promoting and monitoring judicious use of antimicrobials to preserve their future effectiveness
407
Q

What can be done to prevent environment to patient transmission of infection?

A
  • Design (e.g. ventilation)
  • Cleaning
  • Patient isolation
408
Q

What can be done to prevent staff to patient transmission of infection?

A
  • Handwashing
  • Barrier precaution (e.g. gloves, gowns, etc.)
  • Isolation
409
Q

Is handwashing or alcohol gel more effective at preventing Norovirus and C.diff?

A

Handwashing

410
Q

What are endogenous infections?

A

Infections caused by the patients own flora

411
Q

What common procedures often cause endogenous infections?

A

Surgery
Catheterisation
Cannulisation

412
Q

When is someone who has chicken pox most infectious?

A

1-2 days before the onset of symptoms until all blisters have crusted over

413
Q

What is the incubation period for chicken pox?

A

1-3 weeks

414
Q

When can chickenpox infection be serious?

A
  • Immunocompromised patients
  • Patients who have had transplants
  • Adults
  • Pregnant people
  • Smokers
  • Infants
415
Q

What does the chicken pox rash look like?

A
  • Erythematous macule which becomes an erythematous papule
  • Ends in a crust
416
Q

What is the distribution of the chicken pox rash?

A
  • Grows in warm areas of the body
  • Around neck and axillae
417
Q

How should you collect a sample for diagnosis of chicken pox?

A
  • Do not wipe the skin with alcohol swab
  • Pop lesion with a sterile needle
  • Absorb vesicle contents onto swab
  • Replace swab in casette and send for VZV/HSV PCR
418
Q

What are some complications associated with VZV infection?

A

Dehydration
Haemorrhagic change
cerebellar ataxia
Encephalitis
Varicella pneumonia
Skin and soft tissue infections

419
Q

Describe the process of dormancy for the VZV virus?

A
  • The virus travels along the sensory neurone axon until it reaches the dorsal root or cerebral ganglion
  • Here it lies dormant until reactivation
  • Shingles appear across single dermatomes for this reason - only 1 neurone is activated
420
Q

What can cause reactivation of VZV?

A

Age
Loss of immune response

421
Q

What is post herpetic neuralgia and where is the most common body part for this to occur following reactivation of VZV?

A

After the shingles infection, the nerve endings are inflamed and causes painful stimulus

The thorax

422
Q

What are some red flags for shingles?

A
  • ‘Weird’ dermatomes (where you wouldn’t expect to find shingles rash)
  • Dissemination of the rash
  • Haemorrhagic changes
  • All suggest immunocompromised
423
Q

What is the treatment for VZV infection?

A

Acyclovir

424
Q

What is the distribution of an enterovirus rash?

A

Hand
Foot
Mouth

425
Q

What care should be given to pregnant people with Hand, Foot and Mouth infection?

A

Not a danger to the foetus
Supportive care - hydration and manage fever

426
Q

What are some complications associated with Hand foot and Mouth infetion?

A

Cardiomyopathy
Encephalitis
Join inflammation (sternomastoid joint)

427
Q

What is the hallmark of a parovirus infection?

A

Slapped cheeks
Flushed cheeks with a reticular pattern

428
Q

What are the complications of a parovirus infection?

A

Joint aches and pains - may last weeks
Prevent RBC maturation - anaemia

429
Q

Why is parovirus infection a problem in pregnancy?

A

Lack of ability to produce mature RBCs can make the foetus non-viable
Foetus has to receive blood via the umbilicus

430
Q

What is the distribution of HSV I and II?

A

HSV I - Mouth (Vermillion border, border of mucosa of lips and epithelium of skin)

HSV II - Genitals

431
Q

What has caused the distribution of HSV I and HSV II to become less defined?

A

Oral sex

432
Q

Why is HSV infection a concern in pregnancy?

A

Can cause HSV encephalitis in the foetus

433
Q

What is used to treat HSV?

A

Acyclovir

434
Q

Describe a measles rash

A

Confluent morbidiform
Sparing on pressure points

435
Q

What are the symptoms of measles?

A
  • Cough
  • Coryza
  • Diarrhoea
  • Conjunctivitis
436
Q

Where does Macrolides, Cloramphenicol and Clindamycin act?

A

ACts on the 50S subunit of the ribosome to inhibt protein synthesis

437
Q

Where do Tertracyclines and aminoglycosides act?

A

Act on the 30S subunit of bacterial ribosomes to inhibit protein synthesis

438
Q

Where does Metronidazole and Nitrofurantoin act?

A

Damages DNA

439
Q

Where do Quinolones act?

A

DNA topoisomers

440
Q

Where does Rifampicin act?

A

RNA polymerase

441
Q

Where do Penicillins, Cephalosporins and Carbapenems act?

A

Inhibit peptidoglycan cross linking

442
Q

Where do Glycopeptides (vancomycin) act?

A

Inhibit peptidoglycan Synthesis

443
Q

Where do Trimethoprim and Sulfonamides act?

A

Folic acid synthesis

444
Q

What are some symptoms of Schistosomiasis?

A

Haematuria
Bladder calcifications

445
Q

What are the gram positive cocci?

A

Staphylococcus
Streptococcus
Enterococcus

446
Q

What are the Gram positive rods and how do you remember them?

A

Corney Mikes Lister of Basic Cars:

Corneybacteria
Mycobacteria
Listeria
Bacillus
Nocardia

447
Q

What are the Gram positive anaerobes and how do you remember them?

A

CLAP:
Clostridium
Lactobacillus
Actinomyces
Propionbacterium

448
Q

What are the major gram negative bacteria?

A

Neisseria meningitidis
Neisseria gonorrhoea
Haemophilia influenza
E.coli
Klebsiella
Pseudomonas aeruginosa
Morazella catarrhalis

449
Q

What is an atypical bacteria?

A

A bacteria that cannot be cultured in the normal way or detected using a gram stain.

450
Q

What are the atypical bacteria often implicated in?

A

Pneumonia

451
Q

How do you remember the atypical penumonia

A

Legions of Psittaci MCQs

Legionella pneumophilia a
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Q fever (coxiella)

452
Q

What antibiotics can be used to treat MRSA?

A

Doxycycline
Clindamycin
Vancomycin
Teicoplanin
Linezolid

453
Q

What are ESBLs usually susceptible to?

A

Carbapenems:
meropenem
imipenem

454
Q

What species of bacteria are ESBLs usually?

A

E.coli
Klebsiella
often cause UTIs

455
Q

When treating with antibiotics, what is the escalating process?

A

Start with Amoxicillin - covers streptococcus, listeria and enterococcus

Swtich to co-amoxiclav - additionally covers staphylococcus, haemophilus and e.coli

Switch to Tazocin to cover pseudomonas

Switch to meropenem to cover ESBLs

Add teicoplanin/vancomycin to cover MRSA

Add clarithromycin or doxycycline to cover atypical bacteria

456
Q

What is the most common cause of UTIs?

A

Escherichia coli

457
Q

What is the most common cause of cellulitis?

A

Staphylococcus aureus

458
Q

What is the most common cause of tonsilitis?

A

Streptococcus pyogenes

459
Q

What is the most common cause of otitis media?

A

Streptococcus pneumoniae

460
Q

What bacteria can amoxicillin be used against?

A

Gram positive

461
Q

What bacteria can co-amoxiclav be used against?

A

Gram positive
Gram negative
Anaerobic

462
Q

What type of bacteria is clarithromycin effective against?

A

Gram positive
Atypical

463
Q

What type of bacteria is gentamycin effective against?

A

Gram negative

464
Q

What type of bacteria is ciprofloxacin effective against?

A

Gram negative
atypical

465
Q

What type of bacteria is metronidazole effective against?

A

Anaerobic bacteria

466
Q

What type of bateria is doxycycline effective against?

A

Gram positive
Gram negative
Anaerobic
Atypical

467
Q

What type of bacteria is vancomycin effective against?

A

Gram positive

468
Q

What is the first line option for treating cellulitis?

A

Flucloxacillin

469
Q

What is the first lie option for treating UTIs?

A

Nitrofurantoin
Trimethoprim

470
Q

What is the first line treatment for treating chest infections?

A

Amoxicillin

471
Q

What is the first line treatment for treating tonsilitis?

A

Phenoxymethylpenicillin

472
Q

What is the primary function of the polysaccharide capsule?

A

Protection; prevents MAC or opsonisation molecules attacking.

473
Q

What is the name for a hospital acquired disease

A

Nosocomial infection

474
Q

What is a nosocomial infection?

A

An infection that originates within a hospital

475
Q

Name the 3 conditions caused by salmonellosis.

A
  1. Gastroenteritis.
  2. Enteric fever.
  3. Bacteraemia.
476
Q

Why is v.cholerae so dangerous?

A

You’re losing huge amounts of water which can result in hypovolemic shock and severe dehydration, this can lead to death.

477
Q

Why is v.cholerae not killed if you have a fever?

A

It grows at 18 - 42°C.

478
Q

Name 3 common fungal infections.

A
  1. Nappy rash.
  2. Tinea pedis.
  3. Onychomycosis (fungal nail infection).
479
Q

Name a drug that is good for treating onychomycosis.

A

Terbinafine - it reaches poorly perfused sites e.g. nails.

480
Q

Antifungal treatments: how do azoles work?

A

They affect the ergosterol synthetic pathway.

481
Q

Give 4 disadvantages of azoles.

A
  1. High first pass metabolism, bioavailability = 45%.
  2. ADR’s, can cause hepatitis.
  3. Drug interactions due to CYP450.
  4. Resistance can develop e.g. in candida.
482
Q

What is candida?

A

A yeast. It grows in warm, moist areas and has high levels of β-D-Glucan.

483
Q

Where in the body would you find normal flora (commensals)?

A
  1. Mouth.
  2. Skin.
  3. Vagina.
  4. Urethra.
  5. Large intestine.
484
Q

Which Lancefield groups are associated with tonsilitis and skin infection?
Give an example of a bacteria in the groups

A

A , C and G.

A - S.pyogenes

485
Q

Which Lancefield groups are associated with neonatal sepsis and meningitis?
Give an example of a bacteria in the groups

A

B - S.agalactiae

486
Q

Which group of streptococci can cause infective endocarditis?

A

Alpha haemolytic streptococci.
Streptococci viridans - S.sanguinis, S.oralis

487
Q

Why are there different clinical manifestations of malaria?

A

The difference in clinical manifestation can be due to variation in the plasmodia life cycle. The plasmodia life cycle has stages in the human and the mosquito.

488
Q

What are the stages of the plasmodia life cycle in the human called?

A

Exo-erythrocytic and endo-erythrocytic stages.

489
Q

What genetic conditions can give immunity to malaria?

A

Someone with sickle cell anaemia or thalassaemias.

490
Q

Which HPV viral gene product controls viral gene expression?

A

E2.

491
Q

Which HPV viral gene products inhibit p53 and Rb?

A

E6 and E7.

492
Q

How does HIV attach onto a host cell?

A

GP160 binds to CD4 receptors and also CCR5 co-receptors.

493
Q

Name 4 enzymes involved in HIV replication.

A
  1. Reverse transcriptase.
  2. Integrase.
  3. RNA polymerase.
  4. Proteases.
494
Q

How many genes are encoded in the HIV genome?

A

9

495
Q

What does Pol encode in the HIV genome?

A

Enzymes e.g. reverse transcriptase, integrase etc.

496
Q

Why might macrophages also be infected by HIV?

A

Macrophages also have CD4 and CCR5 receptors.

497
Q

Name 4 ‘sanctuary sites’ for HIV.

A
  1. Genital tract.
  2. GI tract.
  3. CNS.
  4. Bone marrow.
498
Q

What antibiotic might be used for the treatment of bacterial pharyngitis: ‘strep throat’?

A

Phenoxymethylpenicillin. (Penicillin V)

499
Q

What is the management/treatment of glandular fever?

A

Supportive therapy and advise the patient to avoid contact sport for 6 weeks in order to avoid splenic rupture.

500
Q

Give some signs and symptoms of infective mononucleosis (glandular fever).

A
  1. Reddening, swelling and white patches on the tonsils. 2. Swollen lymph nodes.
  2. Spleen enlargement.
  3. Chills, fever.
  4. Cough.
  5. Sore throat.
  6. Fatigue, malaise, loss of appetite, headache.
501
Q

Name 5 groups of people who are at high risk of HIV infection.

A
  1. Homosexual men.
  2. Heterosexual women.
  3. Sex workers.
  4. IV drug users.
  5. Truck drivers.
502
Q

Name 4 diseases that haemophilus influenzae can cause.

A
  1. Meningitis.
  2. Otitis media.
  3. Pharyngitis.
  4. Exacerbations of COPD.
503
Q

Name 5 diseases that are notifiable.

A
  1. Anthrax.
  2. Cholera.
  3. Rabies.
  4. Smallpox.
  5. Yellow fever.
  6. Acute encephalitis.
  7. Botulism.
  8. Enteric fever.
  9. Leprosy.
  10. Malaria.
504
Q

Name 6 vaccine preventable diseases that are notifiable.

A
  1. Diptheria.
  2. Measles.
  3. Mumps.
  4. Rubella.
  5. Tetanus.
  6. Whooping cough.
505
Q

A patient has profuse vomiting after eating contaminated rice. What bacteria is responsible?

A

Bacillus cereus.

506
Q

Name a bacteria that can cause ascending cholangitis.

A

Klebsiella pneumoniae.

507
Q

What is the first line antibiotic for s.pyogenes?

A

IV benzylpenicillin.

508
Q

What is the first line treatment for meningitis?

A

Cephalosporins - IV Cefotaxime.

509
Q

What is the treatment for malaria?

A

Chloroquine.

510
Q

What growth medium can be used to culture mycobacteria?

A

Lowenstein Jensen medium.

511
Q

What organism can cause neonatal sepsis?

A

Group B streptococci.

512
Q

Give examples of penicillin Antibiotics

A

Amoxicillin
Flucloxacillin
Benzylpenicillin
Phenoxymethylpenicillin (Penicillin V)

513
Q

Give examples of Cephalosporins Antibiotics

A

Cephalexin
Cefotaxime
Ceftriaxone

514
Q

What type of bacteria would cell wall synthesis inhibitors be good against and why?

A

Gram positive bacteria because they have thicker cells walls for protection.
Inability to synthesise their cell wall would make them vulnerable.

515
Q

Give examples of macrolide antibiotics?

A

Clarithromycin
Erythromycin

516
Q

Give examples of tetracycline antibiotics

A

Doxycycline

517
Q

Give examples of aminoglycoside antibiotics?

A

Gentamicin
Streptomycin

518
Q

What are the different classes of nucleic acid synthesis inhibitor antibiotics?

A

Folate synthesis inhibitors
DNA Gyrase inhibitors
RNA polymerase inhibitors
DNA Strand breakers

519
Q

What drugs inhibit folate acid synthesis?

A

Trimethoprim
Sulphonamides
Sulphamethoxazole

520
Q

Why should you not give a pregnant women trimethoprim?

A

Because it will inhibit folate acid synthesis which is required for neural tube closure and therefore could cause the child to have spina bifida or anencephaly

521
Q

What is Co-trimoxazole?

A

Combination therapy of:
Trimethoprim + Sulphamethoxazole

522
Q

What condition should you think of with fever and recent travel?

A

MALARIA
Specifically in Africa, south America, south east Asia

523
Q

What is Empirical Therapy?

A

Treating for a condition without knowing the specifics?

524
Q

How do chest infections often present?

A

Cough
Sputum production
SOB
Fever
Lethargy
Crackles on the chest

525
Q

What are the common causes of chest infections?

A

Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)

Pseudomonas - in patients with CF or bronchiectasis
Staph aureus - in patients with CF

526
Q

What are the causes of Atypical pneumonia?

A

Atypical bacteria

Legionella
Chlamydia Psittaci
Mycoplasma pneumoniae
Chlamydydophila pneumoniae
Q fever (coxiella)

527
Q

What is the antibiotic of choice to treat chest infections?

What are some alternatives that can be used?

A

Amoxicillin

Erythromycin/Clarithromycin
Doxycycline

528
Q

What antibiotics would be used to treat atypical bacterial pneumonia?

A

Macrolides - clarithromycin
Quinolones - Levofloxacin
Tetracyclines - Doxycycline

529
Q

Who are more affected by UTIs?

A

Women due to their urethra being much shorter and therefore it is easier for the bacteria to get into the bladder

530
Q

What is a UTI?

A

Infection involving the bladder causing cystitis and this can also spread up to the kidneys causing pyelonephritis.

531
Q

What is the main source of bacteria to cause a UTI?

A

Normal intestinal bacteria contaminate the urethral opening via faeces
Usually E.coli

532
Q

How may a UTI Present?

A

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Confusion is commonly the only symptom in older more frail patients

533
Q

How may pyelonephritis present?

A

Fever is a more prominent feature than lower urinary tract infections.
Loin, suprapubic or back pain. This may be bilateral or unilateral.
Looking and feeling generally unwell
Vomiting
Loss of appetite
Haematuria
Renal angle tenderness on examination

534
Q

What are the main causes of UTIs?

A

E.coli (most common)

Klebsiella
Enterococcus
Pseudomonas
S. saprophyticus
Candida albicans

535
Q

What are the antibiotics of choice for UTIs?

A

Trimethoprim

Nitrofurantoin

536
Q

When would Nitrofurantoin be avoided?

A

Third trimester as it is linked with haemolytic anaemia of the newborn

537
Q

When would Trimethoprim be avoided?

A

Generally safe in pregnancy but avoided in the first trimester as it can affect folic acid metabolism and synthesis.

538
Q

What is Cellulitis?

A

An infection of the skin and soft tissues underneath.

539
Q

What is the presentation of cellulitis?

A

Erythema
Warm/hot to touch
Tense
Thickened
Oedematous
Bullae (fluid filled blisters)
Golden yellow crust - indicative of S. aureus infection

540
Q

What are the most common causes of cellulitis?

A

Staphylococcus aureus

Group A strep - S. pyogenes

Group C strep - S. dysgalactiae

541
Q

What is the antibiotic of choice to treat cellulitis?

What are some alternatives that could be used?

A

Choice treatment: Flucloxacillin.

Clarithromycin
Clindamycin
Co-amoxiclav

542
Q

What is the most common cause of ENT infections?

A

Viral infections
Tend to resolve without treatment over 1-3 weeks

543
Q

What is the most common cause of bacterial tonsillitis?

A

Group A strep - S. pyogenes

544
Q

What is the likely cause of otitis media, sinusitis and tonsilitis if they are not caused by Group A strep?

A

Streptococcus pneumoniae

545
Q

How do you determine if tonsilitis is caused by a bacterial infection?

A

Via Centor Criteria

A score of 3 or more gives a 40-60% probability of bacterial tonsilitis?

546
Q

What is the Centor Criteria?

A

Bacterial tonsilitis indicated in a score of >3:

Fever > 38 degree Celsius
Tonsillar exudates
Absence of cough
Tender anterior cervical lymph nodes (lymphadenopathy)

547
Q

What is the first line treatment for bacterial tonsilitis?

What are some alternatives for broader spectrum?

A

Phenoxymethylpenicillin (Penicillin V)

Co-amoxiclav
Clarithromycin
Doxycycline

548
Q

What is otitis media?

A

It is difficult to distinguish between bacterial and viral otitis media.
It presents with ear pain.
Examination will reveal a bulging red tympanic membrane.
If the ear drum perforates there can be discharge from the ear.

549
Q

What is the first line treatment for Otitis media?

What are some alternatives?

A

Amoxicillin

Clarithromycin
Erythromycin

550
Q

What is the second line treatment for Otitis media if the patient is not responding to amoxicillin within 2 days?

A

Co-amoxiclav

551
Q

What is the first line treatment for Sinusitis?

What are the alternatives

What is the second line treatment?

A

Penicillin V

Alternatives are :
Clarithromycin
Erythromycin
Doxycycline

Second line is co-amoxiclav

552
Q

What are some common causes of Intra-abdominal infections?

A

Anaerobes - Bacteriodes and clostridium
E.coli
Klebsiella
Enterococcus
Streptococcus

553
Q

What are some common treatment regimes for intra abdominal infections?

A

Co-amoxiclav alone
Amoxicillin plus gentamicin plus metronidazole
Ciprofloxacin plus metronidazole (penicillin allergy)
Vancomycin plus gentamicin plus metronidazole (penicillin allergy)

554
Q

What is influenza?

A

The influenza virus is an RNA virus. There are three types: A, B and C, of which A and B are the most common.

Type A has different H and N subtypes

555
Q

Give some examples of Type A influenza subtypes?

A

H1N1 - Swine flu
H5N1 - Avian flu

556
Q

Who can receive the flu vaccine free on the NHS?

A

Aged 65
Young children
Pregnant women
Chronic health conditions such as asthma, COPD, heart failure and diabetes
Healthcare workers and carers

557
Q

What is the Presentation of viral influenza?

A

Fever
Coryzal symptoms
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache
Dry cough
Sore throat

558
Q

How is viral influenza diagnosed?

A

Viral nasal and throat swabs
PCR

559
Q

What are the treatment options of influenza in a patient at risk of flu complications?

A

Oseltamivir
Zanamivir

560
Q

What are some complications of influenza?

A

Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening of chronic health conditions such as COPD and heart failure
Febrile convulsions (young children)
Encephalitis

561
Q

What is the difference between:
Acute gastritis
Enteritis
Gastroenteritis?

A

Acute gastritis is inflammation of the stomach and presents with nausea and vomiting.

Enteritis is inflammation of the intestines and presents with diarrhoea.

Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

562
Q

What is the most common cause of gastroenteritis?

A

Viral infection

563
Q

What viruses commonly cause gastroenteritis?

A

Rotavirus
Norovirus
Adenovirus is a less common cause and presents with a more subacute diarrhoea

564
Q

What should be avoided if E.coli caused gastroenteritis is present?

A

Treatment with antibiotics as this may cause HUS

565
Q

What is the most common cause of bacterial gastroenteritis?

A

Campylobacter jejuni

566
Q

What are some symptoms of gastroenteritis?

A

Abdominal cramps
Diarrhoea often with blood
Nausea and Vomiting
Fever

567
Q

What are some bacterial causes of gastroenteritis?

A

E.coli
Campylobacter jejuni
Shigella
Salmonella
Bacillus Cereus - From reheated rice
Yersinia
Staphylococcus aureus
Giardiasis

568
Q

What are some potential complications of gastroenteritis?

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

569
Q

What are the different methods of HIV Testing?

A

Antibody blood test
Test for P24 antigen presence
PCR testing for HIV RNA

570
Q

What is used to monitor HIV?

A

CD4 T cell count

(500-1200 cells/mm3 is normal range)

571
Q

What type of bacteria is Group D streptococcus?

A

Enterococcus

572
Q

What bacteria is it likely to be if you have a Gram positive bacteria in chains that gives a positive result on MacConkney Agar?

A

Enterococcus:
Gram positive cocci
Commonly found in the GI tract and will lactose ferment.

573
Q

Give an example of an anti-pseudomonas penicillin?

A

Piperacillin + Tazobactam
= Tazocin

574
Q

Give an example of a monobactam

A

Aztreonam

575
Q

What classes of antibiotics are bacteriocidal?

A

Glycopeptides
Beta Lactams
Fluoroquinolones
Aminoglycosides

576
Q

What classes of antibiotics are bacteriostatic?

A

Folate acid inhibitors (trimethoprim, sulphathiazole)
Macrolides
Lincosamides
Chloramphenicol
Linezolid
Tetracyclines

577
Q

What classes of antibiotics are bacteriostatic?

A

Folate acid inhibitors (trimethoprim, sulphathiazole)
Macrolides
Lincosamides
Chloramphenicol
Linezolid
Tetracyclines

578
Q

What Antibiotics would be useful against Gram positive bacteria?

A

Amoxicillin
Co-Amoxiclav
Clarithromycin
Clindamycin
Doxycycline
Vancomycin

579
Q

What Antibiotics would be useful against Gram Negative Bacteria?

A

Co-Amoxiclav
Gentamycin
Ciprofloxacin
Doxycline

580
Q

What Antibiotics would be useful against Anaerobic Bacteria?

A

Co-amoxiclav
Clindamycin
Metronidazole
Doxycycline

581
Q

What Antibiotics would be useful against Atypical Bacteria?

A

Clarithromycin
Ciprofloxacin
Doxycycline

582
Q

How would you treat Clostridium Difficile?

A

Metronidazole
PO Vancomycin

Medicine Phase 2a (20 decks)

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