Microbiology Flashcards

1
Q

Describe the pattern of micro-organism colony growth.

A
Lag phase - very little growth
Log/ exponential phase - doubling at a constant rate
Stationary phase - growth levels off
Death phase
Lecture 23/11/17.
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2
Q

Give 3 methods of gene transfer in bacteria.

A
  1. Transformation via plasmids
  2. Transduction via phages
  3. conjugation via sex pili.
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3
Q

Give 3 types of mutation.

A

Base substitution, deletion and insertion.

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4
Q

Give an example of a gram positive aerobic coccus.

A

Neisseria meningitides and gonorrheae,
staphylococcus,
streptococcus.

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5
Q

Give an example of a spirochaete.

A

Treponema Pallidum, which causes syphilis.

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6
Q

Give an example of a staphylococcus.

A

Staph. aureus,

staph. epidermis

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7
Q

Give an example of an a-haemolytic streptococcus.

A

S. pyogenes, s. agalactiae

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8
Q

Give an example of a b-haemolytic streptococcus.

A

S. pneumoniae, S. oralis

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9
Q

Give an example of a non-haemolytic streptococcus.

A

S. bovis.

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10
Q

Give an example of a gram positive anaerobic rod.

A

Clostridium - c. difficile, C. tetani, proprionibacterium acnes

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11
Q

Give an example of a gram negative anaerobic coliform.

A

Escherichia coli

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12
Q

What are the sterile areas?

A

Lungs, bladder, kidney, gallbladder.

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13
Q

What are the differences between gram positive and gram negative bacteria?

A

Gram negative have a second outer membrane containing LPS endotoxin while gram positives have a thicker peptidoglycan cell wall. Gram positive bacteria take up the purple gram stain so they appear purple. Both have a cytoplasmic membrane.
Lecture 23/11/17

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14
Q

What is the most common cause of osteomyelitis?

A

Staphylococcus aureus

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15
Q

What is the coagulase test?

A

Coagulase is an enzyme produced by bacteria that clots blood plasma. A fibrin clot forms around coagulase-positive bacteria which may protect against phagocytosis.

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16
Q

How is staph. aureus spread?

A

By aerosol (coughing and sneezing) and touch.

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17
Q

What is MRSA resistant to?

A

Beta-lactams, gentamycin, erythrocycin, tetracyclin.

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18
Q

Give an example of a virulence factor of staph aureus.

A
  1. Protease secretion eg exfoliatin which causes scalded-skin disease in infants;
  2. Toxic Shock Syndrome Toxin which causes lots of Il-1 and IFN-gamma to be released which triggers a harmful inflammatory response
  3. Protein A secretion
  4. Pore-forming toxins
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19
Q

What is the main virulence factor of staphylococcus epidermidis?

A

Forms persistent biofilms which antibiotics struggle to penetrate.

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20
Q

What is alpha-haemolysis?

A

H2O2 reacts with Hb to give a green area around the bacteria on blood agar due to partial haemolysis. S. intermedius shows alpha haemolysis.

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21
Q

Give an infection caused by strep. pyogenes

A

Wound infections such as cellulitis
otitis media
impetigo
scarlet fever

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22
Q

How is the risk of complications from strep pyogenes estimated?

A

Anti-SLO titre >200 IU/ml indicates risk of complications. if streptococcal antibodies are present, reaction occurs.

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23
Q

Give a virulence factor of s. pyogenes.

A

Hyaluronic acid capsule protects it from phagocytosis
M protein encourages complement degradation
Toxin release - streptolysins O and S bind cholesterol; erythrogenic toxin causes an excessive immune response, eg in scarlet fever.
Produces enzymes, such as streptokinase which lyses blood clots.

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24
Q

Give a virulence factor of s. pneumoniae.

A

The peptidoglycan wall is pro-inflammatory;
Its polysaccharide capsule is coated with antiphagocytic,
It produces pneumolysin cytotoxin which causes a pore to form in cell membranes causing leakage of cell contents.
Forms draughtsman colonies.

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25
Q

Which infections are caused by s. pneumoniae?

A

Pneumonia, otitis media, sinusitis, meningitis.

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26
Q

What test is used to confirm presence of s. pneumoniae?

A

Optochin - s. pneumoniae is optochin sensitive.

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27
Q

How might someone present with diptheria?

A

Severe sore throat, fever, malaise, ‘bull neck’ lymphadenopathy, thick pseuedomembrane in throat.

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28
Q

How is c. diptheriae spread?

A

Droplet spread, kissing

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29
Q

How is diptheria prevented?

A

Inactivated toxin (toxoid) vaccine.

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30
Q

What is a colonisation factor?

A

A type of virulence factor that helps the organism colonise, eg, adhesins, invasins, defence.
Lecture 24/11/17

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31
Q

What is a toxin?

A

A type of virulence factor which is normally a protein secreted by the organism which causes damage to the host.

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32
Q

What is needed to culture proteobacteria?

A

They are facultatively anaerobic and grow on macConkey agar, which contains bile salts, lactose and ph indicator.

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33
Q

Give 3 examples of enterobacteria.

A

Shigella flexneri, escheriscia coli, salmonella enterica, klebsiella pneumoniae.

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34
Q

How would you distinguish between E. coli and salmonella/ shigella?

A

E. coli ferments lactose, salmonella/ shigella do not.

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35
Q

How would you distinguish between salmonella and shigella?

A

Use serology. The O antigen is the serogroup, the H antigen (flagellum) is the serotype. Salmonella is motile, shigella is not, so salmonella has the H antigen (flagellum) while shigella does not.

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36
Q

What is the most common cause of UTIs in females?

A

E. Coli

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37
Q

What infections can be caused by E. Coli?

A

Surgical wound infections
Gastroenteritis, such as traveller’s diarrhoea
UTIs

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38
Q

What is a virotype? Give an example.

A

A pathogenic strain. Eg, a virotype of E. Coli is ETEC (enterotoxigenic E. Coli)

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39
Q

How does E. Coli cause diarrhoea?

A

Its pili adhere to the SI mucosa. It produces heat labile toxin which is taken up by epithelial cells and modifies G-proteins by adding ADP-ribose. This permanently activates the G protein which stimulates adenylate cyclase. This upregulates cAMP which activated CFTR channels, causing loss of Cl- and H2O in faeces.

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40
Q

Which virotypes of E. Coli occur in the small intestine?

A

Enteropathogenic (EPEC) and enterotoxigenic (ETEC). Others occur in the large intestine.

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41
Q

What is the main difference between E. coli and shigella?

A

Shigella has a virulence plasmid.

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42
Q

What is the reason for the low infective dose of shigella?

A

it is acid tolerant.

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43
Q

How does shigella cause disease?

A

Shiga toxin stops binding of EF-1 and EF-2, which stops protein synthesis.
Shigella invades colonic mucosa in macrophages, then induces macrophage apoptosis and escapes the macrophage. Inflammation is caused by cytokines produced when the macrophage dies.

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44
Q

What diseases does salmonella cause?

A

Gastroenteritis
Enteric fever, typhoid
bacteraemia

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45
Q

Which salmonella species causes salmonellosis?

A

s. enterica

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46
Q

What has a protective effect for salmonella?

A

Chocolate (perhaps because of milk. It reduces the infective dose.

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47
Q

How does salmonella cause diarrhoea?

A

They cause endocytosis, causing chemokine release and neutrophil migration, resulting in fluid loss.

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48
Q

Which has the higher infective dose - shigella or salmonella?

A

Salmonella has a high ID, shigella’s is low.

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49
Q

Which organisms are mainly responsible for GI infections?

A

Enterobacteria, mainly shigella, salmonella, E. coli

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50
Q

What opportunistic enterobacterium can cause UTIs?

A

Proteus mirabilis

51
Q

What opportunistic enterobacterium can cause hospital acquired infections?

A

klebsiella pneumoniae

52
Q

Are enterobacteria gram positive or gram negative?

A

Gram negative.

53
Q

Which pathogen is responsible for cholera?

A

Vibrio cholerae.

54
Q

How is vibrio cholerae transmitted?

A

Faeco-oral contamination. ID is high, because it is acid sensitive, and this means person-to-person spread is not possible.

55
Q

How does vibrio cholerae cause disease?

A

Like ETEC produces heat labile toxin, it produces a cholera toxin (more potent) which acts on CFTR channels to increase loss of water and chloride, causing watery diarrhoea.

56
Q

Why is pseudomonas aeruginosa difficult to treat?

A

It is intrinsically resistant to many antibiotics.

57
Q

Which free-living bacteria causes infections in immunocompromised patients?

A

P. aeruginosa.

58
Q

What acute infections can be caused by p. aeruginosa?

A

Burn infections, UTIs, and bacteraemia. (opportunistic)

59
Q

Why are patients with CF more likely to get and retain p. aeruginosa infections?

A

P. aeruginosa is opportunistic. CF patients produce lots of viscous mucus which increases their susceptibility to infection. Then they cannot get antibiotics into lungs in high enough concentrations to kill it.

60
Q

Who is more likely to be infected with haemophilus influenzae?

A

Young children and adult smokers.

61
Q

Which infections are caused by h. influenzae?

A

Meningitis, epiglottitis and bacteraemia (capsulate strains)
Bronchopneumonia, pneumonia in patients with CF/COPD/HIv (non-capsulate strains)
NOT FLU

62
Q

H. influenzae is fastidious. What does this mean?

A

It requires haemoglobin and NAD to grow - so it is cultured on chocolate agar

63
Q

What does legionella pneumophila cause and what is it associated with?

A

Legionnaire’s disease, which is a severe inflammatory pneumonia
Man made aquatic environments, eg showers and air conditioning

64
Q

What are virulence factors of legionella?

A

It can invade and reprogram alveolar macrophages to stop formation of a phagolysosome and then break out.
It up-regulates pro-inflammatory genes in alveolar macrophages, causing excessive influx of neutrophils into the lungs.

65
Q

Bordetella pertussis is an obligate human pathogen. What does this mean?

A

Its only known reservoir is humans.

66
Q

What diseases are caused by bortetella pertussis?

A

Whooping cough (pertussis), mild pharyngitis

67
Q

How is b. pertussis transmitted?

A

It is very contagious, transmitted by aerosol, low infective dose. Obligate human pathogen.

68
Q

How does b. pertussis cause disease?

A

Adheres to ciliated epithelia.
Secretes 2 toxins: eg pertussis toxin which locks G1 in the off state, which stops it from inhibiting adenylate cyclase. Therefore there is more adenylate cyclase and therefore cAMP.

69
Q

How is neisseria meningitides transmitted?

A

Obligate human pathogen. Person to person spread at unis, army barracks, pilgrimage.

70
Q

How does n. meningitides cause disease?

A

Spreads from nasopharynx to bloodstream causing either asymptomatic bacteraemia or sever septicaemia.
The capsule protects it against phagocyctosis. The LPS packages (blebs) pinch off and enter bloodstream, triggering a cytokine cascade.

71
Q

How is neisseria gonorrhoeae transmitted?

A

Sexually and MTCT. obligate human pathogen.

72
Q

What type of bacterium is campylobacter?

A

Proteobacteria, gram negative.

73
Q

What is the most common cause of food poisoning in the UK and US?

A

Campylobacter

74
Q

How does campylobacter present?

A

Mild-severe diarrhoea, often with blood, 1 week, usually self-limiting.

75
Q

What does microaerophilic mean? Give an example of a microaerophilic bacterium.

A

Needs CO2 - eg H. pylori.

76
Q

What spiral shaped bacterium is a common cause of ulcers and gastritis?

A

H. pylori.

77
Q

Are bacteroides aerobic or anaerobic?

A

Obligate anaerobes.

78
Q

Describe chlamydia growth.

A

Chlamydia is an obligate intracellular parasite. It has a unique growth cycle with 2 stages/forms -
1. Elementary body - dormant, non-metabolic
2. Differentiates into reticulate body - larger, generates vacuole full of chlamydia
(then de-differentiates back to EB)

79
Q

What is the most common STD in the UK?

A

Chlamydia trachomatis.

80
Q

How does chlamydia present in women?

A

Usually asymptomatic, can spread to uterus and ovaries causing pelvic inflammatory disease.

81
Q

How are c. trachomatis A-C transmitted?

A

Eye to eye, eg sharing towels or mascara

82
Q

What does chlamydophila pneumoniae cause?

A

Respiratory tract infections, ‘walking’ pneumonia.

83
Q

How does the structure of a spirochaete enable it to move in viscous fluids?

A

Spirochaetes have an endoflagellum between peptidoglycan layer and outer membrane, fixed at each end of the bacterium. It also has an axial filament, which rotates in the opposite direction to the endoflagellum, allowing the spirochaete to move in viscous fluids such as the extracellular matrix.

84
Q

What are the 3 major spirochaetes?

A

Borrelia burgdorferi - lyme disease
Leptospira interrogans - leptospirosis, Weil’s disease
Treponema pallidum - syphilis

85
Q

Describe the course of infection by treponema pallidum.

A

Primary stage: ulcer (chancre), localised symptoms, highly transmissible.
Secondary stage: systemic, 1-3 months post-infections, highly transmissible
Tertiary stage: Several years post-infection, eg cardiovascular syphilis, neurosyphilis, non-infectious.

86
Q

Describe the structure of fungi.

A

They are eukaryotic (have a nucleus), and have a cell wall containing chitin.
Lecture 24/11/17

87
Q

Fungi are heterotrophic. What does this mean?

A

It ingests CO2 to produce energy.

88
Q

How do fungi move?

A

They release spores.

Fun fact - the smell before a storm comes from spores released by fungi.

89
Q

What is a yeast?

A

Small single-celled organisms which divide by budding.

90
Q

What is a mould?

A

A fungus which grows in multicellular filaments called hyphae.

91
Q

Most species of fungi do not cause infection. Why is this?

A

They can’t survive at 37 degrees, and are susceptible to human host defences.

92
Q

Give examples of common fungal infections

A
Nappy rash and vulvovaginal candidasis
Tinea pedis (athlete's foot)
Onychomycosis (Fungal nail infections)
Otitis externa
Fungal asthma
93
Q

Which patients are more likely to get candida and aspergillosis?

A

Immunocompromised patients.

94
Q

How are fungal infections diagnosed?

A

Various methods - Microscopy, histology, culture, serology. Lateral flow assay (like a pregnancy test). Increased B-D glucan levels.
Easy to detect but often not looked for.

95
Q

What fungi can cause dystrophic nail?

A

Trichophyton rubrum. Diagnosed using microscopy.

96
Q

What is selective toxicity? Why is it more difficult to achieve in fungi than bacteria?

A

Selective toxicity aims to achieve inhibitory levels of the agent at the site of infection without host cell toxicity. It relies on differences between the fungi and the host cells, and is more difficult for fungi because they are eukaryotic and therefore more similar to human cells.

97
Q

What are the differences between human and fungal cells targeted by echinocandin drugs?

A

Fungal cell walls contain mannoproteins, glucans and chitin

98
Q

What difference between human and fungal cells does amphoterecin target?

A

Human cell membrane contains cholesterol, fungal contains ergosterol.

99
Q

What are polyenes?

A

Amphoteric molecules which kill fungi by forming pores in ergosterol-containing membranes. They still cause toxicity in humans which causes side-effects.

100
Q

What are allylamines? Give an example

A

Allylamines such as terbinafine are anti-fungal drugs which work by inhibiting squaline epoxidase. They can reach poorly perfused sites and are used to treat dematophytes.

101
Q

What are azoles? Give an example.

A

Azoles are fungistatic drugs. Clotrimazole is sued to treat candida. Triazoles offer a greater range of treatments eg fluconazole. They are relatively safe.

102
Q

What are echinocandins? Give an example.

A

A class of anti-fungal drugs which work by inhibiting 1,3-beta-glucans. Large molecules so can’t enter brain and can only be given IV, but very few side-effects. Used for more resistant fungi.

103
Q

What diseases are caused by mycobacteria?

A

Tuberculosis - M. tuberculosis

Leprosy - m. leprae

104
Q

Are mycobacteria aerobic or anaerobic?

A

Mycobacteria are aerobic.

105
Q

What are the consequences of slow growth of mycobacteria?

A

Disease onset is gradual
Diagnosis takes longer because they take a long time to culture.
Treatment takes longer - at least 6 months.

106
Q

Describe the staining for mycobacteria.

A

Mycobacteria are acid-fast. Ziehl-Neelsen stain is when carbol fuchsin is used and then washed off using acid alcohol - the mycobacteria are resistant (‘fast’) to the acid wash due to their lipid coat.
Fluorochrome (fluorescence) can also be used.

107
Q

What is needed to culture mycobacteria on solid medium?

A

Decontamination to remove other bacteria. (lipid coat protects AFB)
Lowestein Jensen agar on a slope, containing egg yolk and minerals, because mycobacteria are fastidious.
(lecture 24/11/17)

108
Q

How can mycobacteria be detected? (4 ways)

A

Sputum microscopy
Grown on solid medium (agar)
Grown on liquid medium (more commonly used as facter; MGIT= mycobacterial growth indicator tube)
Nucleic acid detection using PCR

109
Q

How do mycobacteria infection lead to an immune response?

A
  1. Are phagocytosed and survive and replicate inside phagolysosome.
  2. The phagocyte activates the adaptive immune response by activating T cells
  3. CD4 T cells generate IFN-gamma which helps activate intracellular killing by macrophages
110
Q

What is a granuloma?

A

Lesion that arises in response to try to contain mycobacteria which have evaded phagocytosis.

111
Q

Why are people with HIV more susceptible to TB?

A

They have depleted CD4 T cell count, and these are important cells in the response against TB.

112
Q

Why are people on treatment for autoimmune diseases more susceptible to TB?

A

TNF-alpha neutralising drugs reduce TNF-a which is an important part of the response against TB.

113
Q

What is erythema nodosum?

A

Hypersensitivity response to mycobacterial antigens.

114
Q

What is the mantoux test? How is it performed today compared to previously?

A

Inject small amount of TB in skin, looks for T cell responses causing fairly immediate cardinal signs of inflammation. Will be positive if someone has had TB or the BCG vaccine. It used to be done on skin but now is done in a test tube with the patient’s blood.

115
Q

How is TB prevented?

A

BCG vaccine.

116
Q

What is leprosy?

A

Contagious disease affecting skin and nerves. Can be lepromatous or tuberculoid.

117
Q

What happens in primary TB?

A

Bacilli settle in the apex of the lung because there is less blood supply and therefore fewer white blood cells. A granuloma forms.

118
Q

What is miliary TB?

A

Widespread dissemination of TB.

119
Q

If someone comes back from a hot country and has a fever, what is the most important thing to exclude?

A

Malaria.

120
Q

Give an example of a flagellate protozoa and what disease it causes.

A

Giardia causes giardiasis. GI infections; can be caught in the UK; treated with metronidazole.

Trypanozoma cruziae causes African sleeping sickness

121
Q

Give an example of an amoeba protozoa and what it causes.

A

Amoebiasis - causes amoebic dysentery in travellers.
Amoebic liver abscess - more common in areas with poor sanitation, not UK. Curable with metronidazole, unlike most asbscesses.

122
Q

Give an example of a sporozoan protozoa and what it causes.

A

Plasmodium sp. , causes malaria.

123
Q

Give 3 properties of a virus

A
Only visible on an electron microscope
Only replicate inside living cells
Only possess RNA or DNA, never both
No cell wall
Outer protein coat