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Phase 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogen

A

Organism that causes/is capable of causing disease

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2
Q

Define commensal

A

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

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3
Q

What is an opportunist pathogen?

A

Microbe that only causes disease if host defences are compromised

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4
Q

What is virulence/pathogenicity?

A

Degree to which a given organism is pathogenic

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5
Q

What is asymptomatic carriage?

A

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

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6
Q

How are bacteria named?

A

By genus (staphylococcus), then species (aureus)

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7
Q

What colour does gram positive stain?

A

Purple/blue

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8
Q

What colour does gram negative stain?

A

Red/pink

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9
Q

What shape is bacillus?

A

Rod-like

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10
Q

What shape is described by ‘coccus’?

A

Circular

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11
Q

What is a vibrio?

A

Curved rod

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12
Q

What is a spirochaete?

A

Spiral rod

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13
Q

Which bacteria is more complex, gram positive/negative?

A

Negative

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14
Q

Describe the structure of a gram positive bacteria

A

-Cytoplasmic membrane
-Lipoteichoic acid
-Peptidoglycan
-Capsule

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15
Q

Describe the structure of a gram negative bacteria

A

-Inner membrane
-Outer membrane
-Peptidoglycan
-Periplasmic space
-Lipoprotein
-Lipopolysaccharide (endotoxin)
-Capsule

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16
Q

Name the stain that turns gram +ve bacteria purple

A

Crystal violet

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17
Q

What is the temperature of the bacterial environment?

A

< -80 degrees - +80 degrees

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18
Q

What is the ideal temp for spores?

A

120 degrees

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19
Q

What is the pH of the bacterial environment?

A

<4-9

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20
Q

What light is ideal in the bacterial environment?

A

UV

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21
Q

How often do E.coli + S.aureus double?

A

20-30 min

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22
Q

What is an endotoxin?

A

Component of the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria

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23
Q

What is an exotoxin?

A

Secreted proteins of Gram positive and Gram negative bacteria

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24
Q

What are the 2 methods by which genetic variation is created in bacteria

A

-Mutations
-Gene transfer

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25
Q

Name 3 types of mutation by which bacteria have genetic variation

A

-Base substitution
-Deletion
-Insertion

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26
Q

Name 3 methods of gene transfer by which bacteria have genetic variation

A

-Transformation e.g. via plasmid
-Transduction e.g. via phage
-Conjugation e.g. via sex pilus

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27
Q

What are bacteriophages?

A

Viruses that infect bacteria

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28
Q

Describe transduction

A

DNA transferred between bacteria by donor bacterium DNA being packaged into a virus + transferred during infection

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29
Q

Describe bacterial transformation

A

Free DNA is taken up from environment + incorporated into chromosome

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30
Q

Describe bacterial conjugation

A

Small tube forms between 2 bacterial cells + plasmid is transferred

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31
Q

Name a key obligate intracellular bacteria

A

Chlamydia

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32
Q

Name a key bacteria that can be cultured on artificial media + has no cell wall

A

Mycoplasma pneumoniae

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33
Q

What type of bacteria are N. meningitidis + N. gonorrhoeae

A

Neisseria-aerobic, gram -ve, cocci, growing as single cells

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34
Q

What type of bacteria are S. aureus + S. epidermidis

A

Aerobic, gram +ve, cocci

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35
Q

Name the 2 categories of aerobic gram positive cocci

A

Staphylococcus + streptococcus

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36
Q

Name the 3 types of streptococcus, aerobic, gram +ve, cocci

A

Alpha-haemolytic, Beta-haemolytic + Non haemolytic

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37
Q

Name the 3 types of bacteria that grow as single cells

A

Rods, cocci + spirochaetes

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38
Q

Name the 3 types of bacteria that are rods

A

-Gram +ve
-Gram -ve
-ZIEHL-NEELSEN
STAIN POSITIVE

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39
Q

How are staphylococci classified?

A

Coagulase positive
Coagulase negative

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40
Q

What is coagulase?

A

Enzyme produced by bacteria that clots blood plasma

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41
Q

What is the most important staphylococcus?

A

S. aureus - coag +ve

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42
Q

What is the normal habitat of staphylococci?

A

Nose + skin

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43
Q

How can you visually differentiate between staphylococcus + streptococcus?

A

Strep=chains
Staph=clusters

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44
Q

How does staphylococcus aureus spread?

A

Aerosol + touch

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45
Q

Name 4 virulence factors of staphylococcus aureus

A

-Pore-forming toxins
-Proteases
-Toxic shock syndrome toxin
-Protein A

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46
Q

Name some examples of a s. aureus infection

A

-Scalded skin syndrome
-Toxic shock syndrome
-Food poisoning
-Abscesses
-Impetigo
-Pneumonia
-Endocarditis

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47
Q

Give 2 examples of coagulase-negative Staphylococci

A

S,epidermis + S.saprophyticus

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48
Q

Give an example of beta haemolysis

A

S.pyogenes

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49
Q

What are the most important Lancefield groups?

A

A + B

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50
Q

Which Lancefield group is S,pyogenes?

A

A

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51
Q

Which Lancefield group is S.galactiae?

A

B

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52
Q

Name 3 S.pyogenes enzyme virulence factors + what they do

A

-Hyaluronidase - spreading
-Streptokinase - breaks down clots
-C5a peptidase - reduces chemotaxis

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53
Q

Name 2 S.pyogenes toxin virulence factors + what they do

A

-Streptolysins O&S - binds cholesterol
-Erythrogenic toxin - SPeA – exaggerated response

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54
Q

Name 5 infections caused by S.pyogenes

A

-Wound infection e.g. cellulitis, puerperal fever
-Tonsillitis + pharyngitis-most common
-Otitis media
-Scarlet fever
-Impetigo

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55
Q

Name 4 conditions caused by S.pneumoniae

A

-Pneumonia
-Otitis media
-Sinusitis
-Meningitis

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56
Q

Name 3 predisposing factors for S.pneumoniae infection

A

-impaired mucus trapping (e.g. viral infection)
-Hypogammaglobulinaemia
-Asplenia

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57
Q

Name 3 S.pneumoniae virulence factors

A

Capsule-antiphagocytic
-Inflammatory wall constituents
-Cytotoxins

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58
Q

What group are Viridans streptococci in?

A

Alpha/non-haemolytic

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59
Q

What do Viridans group streptococci do?

A

-Cause dental caries abscesses
-Important with infective endocarditis
Cause deep organ abscesses

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60
Q

Name 4 gram +ve bacilli

A

-Listeria monocytogenes
-Bacillus anthracis
-Corynebacterium diphtheriae
-Clostridia

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61
Q

Name 3 signs/symptoms of Clostridia infection

A

-Neck stiffness
-Sore throat
-Difficulty opening mouth (due to masseter spasm)

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62
Q

What stain is used for gram -ve bacteria?

A

Fuchsin/safranin counterstain

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63
Q

What is the toxic part of LPS + what can it cause?

A

Lipid A-can cause sepsis when broken down + released into blood

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64
Q

What are virulence factors?

A

Any product/strategy that contributes to pathogenicity/virulence

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65
Q

Name 4 colonisation factors

A

-Adhesins
-Invasin
-Nutrient acquisition
-Defence against the host

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66
Q

What are coliforms?

A

Rod-shaped, motile, anaerobic bacteria that colonise the intestinal tract

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67
Q

What is another name for coliforms?

A

Enterobacteria

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68
Q

Name a process that helps differentiate between different enterobacteria

A

Lactose fermentation-produces acids

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69
Q

How does lactose fermentation bacterial differentiation work?

A

Fermentation product (acid) changes colour of different test substances

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70
Q

How does MacConkey agar work?

A

Acid produced by fermentation turns neutral dye red

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71
Q

What is XLD + how does it help differentiate bacteria?

A

-XLD=xylose lysine deoxycholate
-Lactose fermentation by some bacteria turns phenol red -> yellow
-Salmonella can’t ferment lactose but reduces thiosulphate to make hydrogen sulphide (black)

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72
Q

What kind of bacteria are mycobacteria?

A

Gram positive, aerobic, slightly curved, beaded, bacilli-but don’t take up Gram stain

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73
Q

What stain is used on myobacteria?

A

Ziehl-Neelsen/acid fast positive

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74
Q

What bacteria causes TB?

A

Mycobacterium tuberculosis

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75
Q

What does M. kansasil cause?

A

Chronic lung infection

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76
Q

What does M. leprae cause?

A

Leprosy

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77
Q

What property of mycobacteria make them resistant to Gram stain?

A

High lipid content with mycolic acids in cell wall

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78
Q

What are the components of Ziehl-Neelsen stain?

A

-Carbol fuchsin
-Acid alcohol
-Methylene blue

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79
Q

What are 2 key lipid components of myobacteria?

A

-Mycolic acids
-Lipoarabinomannan

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80
Q

Is M.tuberculosis fast/slow growing?

A

Slow growing

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81
Q

What are the ramifications of TB being slow growing?

A

-Gradual disease onset
-Much longer to diagnose
-Longer to treat

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82
Q

What is primary TB?

A

-Initial contact made by alveolar macrophages
-Bacilli taken in lymphatics to hilar lymph nodes

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83
Q

What is latent TB?

A

-Cell mediated immune response from T-cells
-No clinical disease, but detectable response on tuberculin skin test

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84
Q

What is pulmonary TB?

A

-Can happen straight after primary infection or months later after reactivation
-Granulomas form around bacilli that have settled in apex
-TB can spread in lung-more lesions

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85
Q

How does TB spread?

A

Aerosol transmission

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86
Q

How does the body’s immune system react to TB?

A

-Macrophages phagocytose mycobacteria
-BUT, mycobacteria adapted to intracellular environment + can withstand

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87
Q

How is intracellular killing of mycobacteria activated?

A

-CD-4 T cells generate interferon gamma-activates killing

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88
Q

What happens if granulomas fail to contain myobacteria?

A

Cavity full of live mycobacteria forms-causes TB

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89
Q

What does the body form to contain mycobacteria?

A

Granulomas-cause metabolic shutdown in mycobacteria

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90
Q

What is a granuloma made of?

A

-Macrophages
-Type 1 helper T cells
-These make IFN-y + other cytokines

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91
Q

What can cause granumlomas to become unstable?

A

-CD4 delpetion
-TNF-alpha depletion

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92
Q

How does nucleic acid detection work?

A

-Purifies + concentrates M.TB
-Sonicates to release genomic material
-Perform PCR

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93
Q

What is a positive about nucleic acid detection?

A

-Rapid diagnosis

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94
Q

How does the Tuberculin skin test work?

A

-Intradermal injection of purified protein derivative
-Stimulates T cell response-measured
-Diagnostic test

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95
Q

Name 4 drugs that are standard therapy for TB

A

-Isoniazid
-Rifampicin
-Pyrazinamide
-Ethambutol

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96
Q

What are second-line Tx for TB?

A

-Injectable agents e.g. streptomycin, cycloserine

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97
Q

Do TB Tx’s have side effects?

A

Many wide-ranging + severe side effects-include liver damage

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98
Q

What are some challenges with TB Tx?

A

-Long Tx
-Expensive
-Lots of antibiotic resistance

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99
Q

What is a virus?

A

-Infectious, obligate intracellular parasite comprising genetic material surrounded by a protein coat and/or a membrane

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100
Q

What does obligate mean?

A

Totally dependent on living cells for replication + existence

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101
Q

What are the main differences between viruses + bacteria?

A

-Bacteria have cell walls, organelles, DNA + RNA, and are alive
-Viruses have none of these and aren’t alive

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102
Q

Name 3 viral shapes

A

-Helical
-Icosahedral
-Complex

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103
Q

What are virions?

A

Viruses outside of an infected cell-can survive for some time but can’t replicate

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104
Q

What is a viral envelope?

A

Lipid coat derived from plasma membrane of host cell

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105
Q

How do viruses replicate?

A

-Using machinery of host cell

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106
Q

What are the 5 steps of viral replication?

A

-Virus attachment to specific receptor on host cell
-Central viral core carrying nucleic acid + proteins enters cell
-Virus uses host materials to replicate-transcription to mRNA
-Assembly of virion
-Release of new virus particles

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107
Q

What are the 2 ways in which new viral particles are released + examples?

A

-Bursting out of cell-causes cell death e.g. rhinovirus
-Budding/exocytosis e.g. HIV, influenza

108
Q

Name 5 ways in which viruses cause disease

A

-Direct destruction of host cells
-Modification of host cell
-Over-reactivity of immune system
-Damage through proliferation
-Evasion of host defences

109
Q

Give an example of how viruses can cause disease by modifying host cells

A

Rota virus atrophies villi + flattens epithelial cells-decreases small intestine s.a.-nutrients not absorbed, hyperosmotic state, profuse diarrhoea

110
Q

Give an example of how viruses can cause disease by causing over-reactivity of the immune system

A

Hepatitis B

111
Q

Give an example of how viruses can cause disease by causing cell proliferation

A

HPV->cervical cancer
-partial viral replication + expression of some HPV proteins
-continuous expression of oncoproteins, causing cellular DNA mutations
-dysplasia + neoplasia

112
Q

Give 5 examples of how viruses can cause disease by evading host defences

A

-Latency-virus not detectable but viral DNA lies latent + can reactivate, especially when immune system weakened e.g. herpes viridae, chickenpox->shingles
-Cell-cell spread e.g. with measles + HIV
-Antigenic variability-can change antigens e.g. influenza, HIV
-Prevention of host cell apoptosis e.g. herpesviridae
-Downregulation of interferon + other host defence proteins

113
Q

What are the main infections caused by E.coli?

A

-Wound infections
-UTIs
-Gastroenteritis
-Traveller’s diarrhoea
-Meningitis
-Bacteraemia

114
Q

What is shigellosis + what causes it?

A

-Caused by shigella bacteria
-Severe bloody diarrhoea

115
Q

What other bacteria shigella similar to? But how is it different?

A

-Similar to E.coli but has extra virulence plasmid

116
Q

What are the two types of salmonella?

A

-S. enterica-salmonellosis
-S. bongori (rare)

117
Q

What are the 3 forms of salmonellosis caused by S.enterica?

A

-Gastroenteritis-frequent cause of food poisoning
-Enteric/typhoid fever-bad drinking water/sanitation
-Bacteraemia-uncommon

118
Q

How is shigella transmitted?

A

Person-to-person/contaminated water + food

119
Q

How is salmonellosis transmitted?

A

Ingestion contaminated food/water

120
Q

Describe the pathogenesis of salmonellosis

A

-Invasion of gut epithelium
-Transcytosed to basolateral membrane
-Enters submucosal macrophages
-Intracellular survival/replication

121
Q

What is the most problematic bacterial infection for CF patients?

A

Pseudomonas aeruginosa

122
Q

How does Vibrio cholerae spread?

A

-Shellfish ingestion
-Contaminated drinking water
-Faecal-oral route

123
Q

Describe the structure of campylobacter

A

Spiral rod, uni/bipolar flagella

124
Q

Describe the shape of helicobacter pylori

A

Spiral shaped + tuft of polar flagella

125
Q

What conditions does H.pylori play a major role in?

A

-Gastritis
-Peptic ulcer disease

126
Q

Name the 4 categories of aerobic gram negative rods + key examples

A

-Coliforms-escheria, salmonella, shigella
-Pseudomonads
-Vibrio-cholerae, campylobacter, helicobacter
-Parvobacteria-influenza

127
Q

What are bacteroides?

A

Non-motile anaerobic rods

128
Q

What are neisseria?

A

Gram negative aerobic cocci

129
Q

Name the 2 clinically important species of neisseria

A

-N.meningitidis
-N.gonarrhoeae

130
Q

What are spirochates?

A

Bacteria with a cell wall growing as single cells-not rods or cocci

131
Q

Describe the structure of spirochates

A

Long, slender, helical, highly flexible, modified outer membrane, endoflagella

132
Q

What bacterial infection causes Lyme disease + how?

A

-Borrelia burgdorferi infects small mammals
-Tick larvae feeds on infected animal
-Tick bites human - characteristic bull’s eye rash

133
Q

What bacteria causes symphilis?

A

Treponema pallidum

134
Q

What are the 3 groups of obligate intracellular bacteria?

A

-Rickettsia
-Chlamydia
-Coxiella

135
Q

What is unique about the growth cycle of chlamydia?

A

-2 developmental stages:
-Elementary bodies-infectious
-Reticulate bodies-replicative

136
Q

What is a biovar?

A

A variant prokaryotic strain that differs physiologically or biochemically from other strains in a particular species

137
Q

Name the 3 medically important members of Chlamydia

A

-C.trachomatis-3 biovars
-C.pneumoniae
C.psittaci

138
Q

What are the 3 serovars of C.trachomatis + what do they cause?

A

-Trachoma biovar->blindness
-Genital tract biovar->most common STD, can cause infertility
-LGV biovar->causes LGV STD, mostly in tropics

139
Q

What are fungi?

A

-Eukaryotic cells with chitin cell walls
-Heterotrophic (get food from other plants + animals)
-Move by growth or generation of spores

140
Q

What is the difference between yeast + mould?

A

-Yeast = small single cell that divides by budding
-Mould = multicellular spores

141
Q

What does dimorphic mean for fungi?

A

They can switch between being yeast + being mould when conditions suit-dangerous, can cause severe infection in healthy hosts

142
Q

What is the main challenge with developing anti-fungals?

A

Fungi are eukaryotic-limited options for selective toxicity

143
Q

What are the risk factors for mucosal candidiasis?

A

-Suppressed immune system (normally exists in humans with no harm to health)
-Diabetes
-Antibacterial therapy
-Mucosal disruption

144
Q

How is mucosal candidiasis treated?

A

With topical or oral azoles (anti-fungals)

145
Q

What is the worry with recurrent infections of mucosal candidiasis?

A

Recurrent infections can cause acquired resistance-sig. morbidity

146
Q

What are dermatophytes?

A

Fungal organisms that require keratin for growth

147
Q

What causes dermatophyte infections?

A

-Human-human or animal-human transmission
-Caused by Trichophyton spp., Microsporum spp. Or Epidermophyton floccosum

148
Q

How are dermatophyte infections treated?

A

Topical/oral azoles or terbinafine

149
Q

Give 3 examples of dermatophyte infections

A

-Tinea capitis-infection of scalp hair
-Tinea corporis-aka ringworm (not a worm)
-Tinea cruris-affects genitals + inner thigh

150
Q

At what temperatures are dimorphic fungi mould + yeasts?

A

-Mould at 25-30 degrees
-Convert to yeast at 37 degrees

151
Q

Give 3 examples of dimorphic fungi

A

-Histoplasma capsulatum
-Blastomyces dermatitidis
-Sporothrix schenkii

152
Q

What condition does coccidioides cause, where is it found?

A

Coccidioidomycosis aka Valley fever, found in warmer, arid regions of America

153
Q

What are the symptoms of coccidioidomycosis?

A

-2/3 cases asymptomatic
-Most of rest=pneumonia 1-3wks post-exposure
-Can get fine papular rash, myalgia, headache, chest pain
-Severe disease can lead to resp failure or septic shock

154
Q

Name 5 late manifestations of coccidioides

A

-Cavitatory lung disease
-Vertebral osteomyelitis/chronic arthritis
-Ulcers + abscesses
-Cervical lymphadenopathy
-Chronic meningitis

155
Q

What are the main causes of invasive candidiasis?

A

-Infection of prosthetics
-Intra-abdominal disease

156
Q
A
157
Q

Name 6 infective differential diagnoses of meningitis

A

-TB
-Cryptococcus
-Dimorphic fungi
-Lyme
-Brucella
-Syphilis

158
Q

Name 5 non-infective differential diagnoses of acute/chronic meningitis

A

-Sarcoidosis
-Behcet’s
-SLE
-Malignant meningitis
-Drug induced meningitis

159
Q

Name the 2 species of Cryptococcus that cause most disease in humans

A

-C.neoformans
-C.gatti

160
Q

What is Cryptococcus infection associated with + why?

A

Rotting wood + bird guano - Cryptococci grow at 40 degrees-birds have higher body temp

161
Q

How would you treat a Cryptococcal infection?

A

-Liposomal amphotericin B
-Flucytosine
-Maintenance fluconazole

162
Q

What fungi cause Mucormycosis? is it a serious infection?

A

Mucoraceous moulds aka zygomyctes cause rare but severe + rapidly progressing disease

163
Q

Name 5 key anti-fungals

A

-Amphotericin B
-Echinocandins
-The azoles e.g. fluconazole, Isavuconazole

164
Q

What are protozoa?

A

Single-celled animals

165
Q

What are the 5 major groups of protozoa?

A

-Flagellates
-Amoebae
-Microsporidia
-Sporozoa
-Cilliates

166
Q

Give 3 examples of flagellates + how they spread

A

-Trypanosoma-insect bites, African + American species
-Leishmania-sandfly bite
-Trichomonas vaginalis-sexually transmitted
-Giardia lamblia-faeco-oral spread

167
Q

Give an example of a amoebae + how it spreads

A

Entaemoeba histolytica, spread by faeco-oral route

168
Q

Give 3 examples of sporozoa + how they spread

A

-Toxoplasma gondii-ingestion of contamintaed food + water/feline faeces
-Cryptosporoidium-waterborne
-Plasmodium

169
Q

How is malaria transmitted?

A

Female anopheles mosquito

170
Q

How many species of malaria are there? Name them

A

5:
-Plasmodium falciparum
-Plasmodium ovale
-Plasmodium vivax
-Plasmodium malariae
-Plasmodium knowlesi

171
Q

How is malaria diagnosed?

A

Blood film-light microscopy

172
Q

What are the symptoms of malaria?

A

FEVER
Chills
Headache
Myalgia
Fatigue
Diarrhoea
Vomiting
Abdo pain

173
Q

What are the signs of malaria?

A

-Anaemia
-Jaundice
-‘Black water fever’
-Hepatosplenomegaly

174
Q

How is black water ever caused in malaria patients?

A

Haemoglobin passes into urine from haemolysis

175
Q

What is the lifecycle of a mosquito?

A

4 WEEKS

176
Q

Describe the steps before initial human infection for malaria

A

-Mosquito bites infected human
-It ingests plasmodium gametocytes
-Mosquito now infected for life
-Gametocytes develop in mosquito, end up as sporozoites in salivary glands

177
Q

Describe how malaria is transmitted to humans from mosquitos

A

-Mosquito takes next blood meal + injects sporozoites into human

178
Q

Describe what happens in humans after initial malaria infection

A

-Sporozoites infect hepatocytes in liver
-This develops into a schizont, which bursts + infects erythrocytes

179
Q

Describe the blood stage of malaria infection

A

-Trophozoite matures
-Develops into a schizont
-Schizont ruptures + re-infects another RBC

180
Q

How long does the blood stage of malaria last + what symptoms does it cause?

A

48hrs
-Causes cyclical fever when RBC’s rupture, haemolysis, anaemia + jaundice from bilirubinaemia

181
Q

What are the 3 stages of the malaria cycle?

A

-Mosquito stages
-Human liver stages
-Human blood stages

181
Q

What are the 3 cycles in malaria?

A

-Sporogonic cycle (in mosquito)
-Exo-erythrocytic cycle (in human liver)
-Erythrocytic cycle (in human blood)

182
Q

Which species of malaria can be more serious + why?

A

P.falciparum causes infected RBC’s to have knobs on surface that adhere to endothelial cells-causes more severe malaria as small vessels become blocked by clumps of RBC’s

183
Q

What are the cerebral symptoms of malaria?

A

-Drowsiness
-Increased ICP
-Seizures
-Coma

184
Q

What are the respiratory symptoms of malaria?

A

-Anaemia + lactic acidosis increase resp rate
-Increased vascular permeability causes fluid to leak into lungs = pulmonary oedema
-ARDS (acute resp disease syndrome)

185
Q

What are the symptoms of malaria related to the kidneys?

A

-Vascular occlusion->dehydration->hypotension
-Haemolysis->haemoglobinuria
-Fatigue
-Haematuria
-Renal failure

186
Q

How does malaria cause DIC?

A

DIC = disseminated intravascular coagulation caused as lots of micro clots in blood but lack of clotting factors causes bleeding

187
Q

How do you treat complicated malaria?

A

IV quinine + doxycycline

188
Q

How do you treat uncomplicated malaria?

A

-ACTs e.g. riamet
-Quinine
-Doxycycline
-PO Chloroquine

189
Q

What is primiquine used to treat?

A

Relapses of malaria-from dormant hypnozoites

190
Q

Define antibiotic

A

An agent produced by micro-organisms that kill/inhibit the growth of other micro-organisms in high dilution

191
Q

How do antibiotics work?

A

They bind to a crucial binding point on the bacteria-binding point varies by antibiotic class

192
Q

What 4 areas do antibiotics target?

A

-Cell wall synthesis
-Nucleic acid synthesis
-Protein synthesis
-Folate synthesis

193
Q

What kind of antibiotics target cell wall synthesis? Give an example

A

Beta lactams e.g. penicillins

194
Q

Name the 4 classes of beta lactams

A

-Penicillins
-Cephalosporins
-Carbapenems
-Monobactams

195
Q

How do beta lactams target the cell wall?

A

They attack the peptidoglycan by binding to penicillin binding protein sites covalently + irreversibly

196
Q

Which kind of bacteria are beta lactams best at targeting + why?

A

Gram positive (peptidoglycan protected in gram -ve by lipopolysaccharide layer)

197
Q

What types of antibiotic target nucleic acid synthesis + what do they target?

A

-Quinolones-DNA gyrase
-Rifampin-RNA polymerase

198
Q

What types of antibiotic target protein synthesis?

A

-Aminoglycosides e.g. Gentamicin
-Tetracyclines e.g. Doxycycline
-Lincosamides
Macrolides

199
Q

What kinds of antibiotic target folate synthesis?

A

-Sulfonamides
-Trimethoprim

200
Q

What do bactericidal antibiotics do?

A

Kill the bacteria by inhibiting cell wall synthesis

201
Q

What are bactericidal antibiotics used for + why?

A

Used for hard to treat infections/need to eradicate it quickly (meningitis), or if poor penetration (endocarditis)(kill >99% 8-24hrs)

202
Q

What do bacteriostatic antibiotics do?

A

Prevent bacterial growth by inhibiting protein synthesis/DNA replication/metabolism (still kill >90% bacteria in 18-24hrs)

203
Q

What is MIC?

A

Minimum inhibitory concentration

204
Q

What is MBC?

A

Minimum bactericidal concentration

205
Q

What are the 2 major determinants of anti bacterial effects?

A

-Antibiotic concentration (occupies enough binding sites)
-Antibiotic time (remains on binding sites long enough to inhibit metabolic processes of bacteria)

206
Q

What 4 ways can bacteria resist antibiotics?

A

-Change antibiotic target
-Destroy antibiotic
-Prevent antibiotic access
-Remove antibiotic from bacteria

207
Q

Give 3 examples of bacteria changing the shape of antibiotic binding sites

A

-MRSA (methicilin resistant S.aureus)
-VRE-vancomycin binding to enterococci reduced
-MDR-TB-Rifampicin activity reduced by changes to RNA polymerase in MTB

208
Q

Give an example where antibiotic is destroyed/inactivated by bacteria

A

-Penicillins + cephalosporins hydrolysed-can’t bind to PBP

209
Q

Give an example of intrinsic antibiotic resistance

A

-Vancomycin can’t penetrate outer membrane of gram -ve bacteria

210
Q

Define acquired resistance

A

A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic

211
Q

How can bacteria acquire resistance?

A

-Spontaneous gene mutation
-Horizontal gene transfer

212
Q

Name 2 important gram +ve resistant bacteria

A

-MRSA-Methicillin resistant Staphylococcus aureus

-VRE-vancomycin-resistant enterococci

213
Q

Name an important gram -ve resistant bacteria

A

Extended spectrum beta lactamase (ESBL)

214
Q

Name a key, relatively new bacteria resistant to gram negative bacteria

A

Carbapenem resistant enterobacteriae

215
Q

What is the biggest challenge with MRSA

A

It confers resistance to all beta-lactam antibiotics, not just methicillin

216
Q

What antibiotics can be used to treat MRSA?

A

Glycopeptides e.g.
-Vancomycin-but can’t cross BBB
-Teicoplanin
also can be used for those with penicillin allergies

217
Q

What antibiotics are used to treat severe pneumonia

A

Macrolides e.g.
-Clarithromycin
-Erythromycin

218
Q

What can Clindamycin be used to treat?

A

-Cellulitis
-Necrosing fasciitis

219
Q

What is Doxycyline used to treat?

A

Broad spec, but mainly gram +ve, can be used to treat cellulitis if penicillin allergy, pneumonia

220
Q

What type of antibiotic is Gentamicin + what is it used to treat?

A

Aminoglycoside, used to treat gram -ve + streps e.g. UTIs + infective endocarditis

221
Q

Give an example of a folate antagonist antibiotic

A

Trimethoprim

222
Q

Name an antibiotic that is only used for the sickest patients, the immunocompromised, resistant gram -ves, whose use at STH is restricted

A

Meropenem-broad activity, works against ESBLs + AmpCs

223
Q

What are ESBLs?

A

Extended Spectrum Beta-Lactamase-resistant bacteria

224
Q

What are AmpCs?

A

Ampicillin Class C beta-lactamases-resistant to beta-lactams

225
Q

What antibiotic is used to treat S.aureus?

A

Flucloxacillin

226
Q

What are the UN AIDS 90/90/90 goals?

A

-90% of people living with HIV being diagnosed
-90% diagnosed on ART (antiretroviral therapy)
-90% viral suppression for those on ART by 2020

227
Q

How can HIV transmission be prevented?

A

-STI Tx
-Male + female condoms
-HIV counselling + testing
-Behavioural change
-Tx as prevention
-Pre + post exposure prophylaxis
-Male circumcision

228
Q

What is the U=U statement on HIV?

A

Undetectable = untransmittable
Those who receive effective antiretroviral therpay + have maintained an undetectable viral load cannot transmit the virus to a sexual partner

229
Q

How can HIV be transmitted?

A

-Sexual
-Vertical (mother to baby)
-Blood

230
Q

What is PreP?

A

Pre-exposure prophylaxis, can have a tablet/injection for HIV

231
Q

How effective is post-exposure prophylaxis? When can it be taken?

A

Not as effective as PreP, should be taken within 72hrs after sex

232
Q

What are the benefits of knowing HIV status?

A

-Access to appropriate treatment and care
-Reduction in morbidity and mortality
-Reduction of vertical transmission
-Reduction of sexual transmission
-Public health / partner notification
-Cost-effective

233
Q

When would you test for HIV?

A

-Clinician suspected-clinical indicators
-Routine in screening in high prevalence locations
-Antenatal routine screening
-Screening is high risk groups
-Patient initiated requests

234
Q

What are some symptoms of HIV?

A

-Flu-like-illness, rash
-Blood dyscrasias
-Multi-dermatomal shingles
-Lymphadenopathy
-Weight loss/diarrhoea/night sweats
-Oral/oesophageal candidiasis/hairy leukoplakia

235
Q

How do you screen for HIV?

A

-Venous blood sample is best-can detect most infections at 4 wks (can repeat at 7wks if suspicion). Test has high sensitivity + specificity
-HIV point of care test-immediate result, lower sensitivity + specificity

236
Q

What kind of virus is HIV?

A

Retrovirus-uses reverse transcriptase to make DNA copy that is integrated into DNA of infected cell

237
Q

Describe the HIV genome structure

A

Small RNA virus-expresses just 10 genes

238
Q

What characterises HIV as a lentivirus?

A

Long incubation period

239
Q

How does HIV replicate?

A

-HIV glycoproteins dock + fuse to CD4 + CCR5 receptors
-Viral capsid enters cell + releases enzymes + n.a.
-Reverse transcriptase is used to convert RNA into DNA-viral DNA then integrated into host cells
-Viral DNA read + viral proteins made
-Buds out of cell, matures more + working virus created

240
Q

What is the primary receptor for HIV?

A

CD4

241
Q

Describe genetic resistance to HIV

A

1% Caucasians homozygous for depletion in CCR5 gene so can’t get HIV, ppl with 1 copy can catch disease but progression is much slower

242
Q

Why can HIV mutate so rapidly?

A

-Error-prone replication
-Rapid replication
-Large population sizes of new virus being produced

243
Q

Why is early initiation of ART for HIV benficial?

A

-Reduced transmission risk
-Smaller reservoir, delayed progression

244
Q

What are the signs + symptoms of acute HIV infection?

A

-V high viral load in blood
-Symptoms of acute retroviral syndrome:
-Glandular fever-like symptoms
-Fever
-Sore throat, oral ulcers
-Upper trunk skin rash

245
Q

Why is HIV relatively inaccessible to antibodies in the blood?

A

-HIV can pass directly from cell to cell
-HIV also has many genes that help virus evade immune system responses e.g. envelope spike is highly glycosylated-hard for antibodies to bind

246
Q

Why is life-expectancy of HIV patients on ART still reduced?

A

-Adherence, side effects, drug resistance issues
-Increase in NADIs (non-AIDS-defining illnesses), related to persistent immune activation + viral reservoir persisting

247
Q

What are the key populations for HIV?

A

-Sex workers + clients
-Gay men + men who have sex with men
-People who inject drugs
-Transgender ppl
-Prisoners

248
Q

What are the socio-economic impacts of HIV/AIDS in Africa?

A

-Reduced life expectancy
-Loss of economically-productive adults
-Increased spending on healthcare
-Change in social structure-orphans cared for by elderly grandparents
-Stigma persists

249
Q

Why does the transmission of HIV vary by sex?

A

-M->F transmission 2-3x more likely
-Young women + teenagers more vulnerable to infection
-Risk increases during pregnancy
-STIs cause inflammation/ulceration of female genital tract
-Sexual violence against women

250
Q

What are the 3 methods of paediatric transmission of HIV?

A

-In utero-particularly 3rd trimester-transplacental
-Intra partum-exposure to maternal blood + secretions during delivery
-Breast milk-ingestion of contaminated milk

251
Q

What 2 markers are used to monitor HIV infection?

A

-CD4 cell count
-HIV viral load

252
Q

What would CD4 levels be like in an AIDS patient?

A

<200

253
Q

What is the most common opportunistic infection in AIDS

A

PCP-pneumocystis pneumonia, symptoms = fevers, SOB, dry cough, pleuritic chest pain, exertional drop in O2 sats

254
Q

What is the Tx for HIV?

A

HAART (highly active anti-retroviral therapy)

255
Q

Name the 3 organisms most commonly found in blood cultures in infective endocarditis (from most common)

A

-Coagulase -ve staph (50%)
-Coliforms
-Staph. aureus

256
Q

What is the most common source of coagulase -ve staph in I.E.?

A

IV line contamination

257
Q

What is the most common source of coliforms in I.E.?

A

UTI bowel sepsis

258
Q

What is the most common source of staph. aureus in I.E.?

A

Skin, soft tissue, IV sites, pneumonia

259
Q

What is the most common source of pseudomonas spp. in I.E.?

A

UTI IV catheters

260
Q

What is the most common source of strep pneumoniae in I.E.?

A

Pneumonia

261
Q

What is the most common source of alpha-haemolytic streptococci in I.E.?

A

Oral cavity

262
Q

What criteria is used to diagnose infective endocarditis?

A

Modified Duke criteria

263
Q

What criteria must be met to diagnose ‘definite’ infective endocarditis?

A

-2 major OR
-1 major + 3 minor OR
-5 minor

264
Q

What are the major criteria for infective endocarditis?

A

-Positive blood culture with typical IE microorganism
-New partial dehiscence of prosthetic valve/ new valvular regurgitation

265
Q
A

Phase 2a (8 decks)

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