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GRACE Phase 2a Medicine > ICS - Microbiology > Flashcards

ICS - Microbiology Flashcards

1
Q

What is meant by gram positive bacteria?

A

They have a thick peptidoglycan layer and no outer lipid membrane. They retain the colour of the crystal violet stain in the gram stain

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2
Q

What is meant by gram negative bacteria?

A

They have a thin peptidoglycan layer and have an outer lipid membrane

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3
Q

What does a gram stain tell you?

A

If you have a bacterial infection - will either show gram positive or gram negative

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4
Q

Approach to identifying bacteria - 3

A
  1. Gram +’ve / -‘ve
  2. Morphology/ shape - cocci, bacilli, etc.
  3. In clusters or chains
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5
Q

Colour of gram stain positive ?

A

purple

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6
Q

Colour of gram stain negative ?

A

pink

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7
Q

How many membranes do gram stain negative bacteria have?

A

2

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8
Q

Bacteria shapes

A

Cocci, bacilli, spirochaete

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9
Q

Coccus bacteria shape

A

Oval/ spherical

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10
Q

Bacilli bacteria shape

A

Rod shaped

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11
Q

Staphylcocci bacteria

A

gram-positive cocci that grow in clusters

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12
Q

Strepococci bacteria

A

gram-positive cocci that grow in pairs or chains

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13
Q

Define pathogen

A

disease causing microorganism

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14
Q

Define commensal

A

organism which colonises the host but does not cause disease

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15
Q

Define opportunist pathogen

A

Microbe that only causes disease if the host defenses are compromised

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16
Q

Define virulence/ pathogenicity

A

degree to which an organism is pathogenic

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17
Q

Define asymptomatic carriage

A

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

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18
Q

Purpose of the catalase test?

A

to differentiate between staphylococci and streptococci

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19
Q

Explaining the results of the catalase test

A

Enzyme in bacteria which catalyses the decomposition of H2O2 –> H2O and O2. Therefore, when a bacterium possesses catalase, when H2O2 is added, oxygen bubbles are observed. particular types of bacteria (e.g. Staphylococci) are catalase-positive

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20
Q

Catalase test

A

Add H2O2 to bacteria and see for bubbles (oxygen) = positive result

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21
Q

Results of catalase test?

A

Bubbling = staph

No bubbling = non staph

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22
Q

Coagulase enzyme

A

produced by Staphylococcus. aureus that converts soluble fibrinogen –> insoluble fibrin

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23
Q

What does the coagulase test differentiate between?

A

Staphylococci. aureus and other Staphylococci

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24
Q

Results of the coagulase test?

A

Staphylococcus. aureus - coagulase positive - clumping

Other Staphylococci - coagulase negative - no clumping

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25
Q

Gram stain test procedure

A
  1. Apply primary stain such as crystal violet to bacteria
  2. Add iodide which binds to crystal violet and fixes it to the cell wall
  3. Decolourise with ethanol/ acetone
  4. Counterstain with safranin (pink)
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26
Q

Haemolysis is the ability of bacteria to

A

Break down RBC in blood agar, it requires the expression of haemolysin

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27
Q

Substance in bacteria that causes haemolysis

A

Haemolysin

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28
Q

Beta haemolysis

A

Clear colourless zone appears around the bacteria colonies

e.g. Staphylococci pyogenes, Staphylococci agalactiae, etc.

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29
Q

Alpha haemolysis

A

Indistinct zone of partial lysis of RBCs around the colonies of bacteria, often gives a green/brown discolourisation

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30
Q

Important bacteria that you need to distinguish that is alpha haemolytic

A

streptococcus pneumoniae - causes lobar pneumonia and meningitis

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31
Q

How to test for streptococcus pneumoniae?

A

Perform the optochin test

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32
Q

Result of optochin test?

A

streptococcus pneumoniae are optochin +’ve, whereas other alpha streptococci are resistant

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33
Q

alpha streptococci that cause infective endocarditis?

A

streptococci viridans

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34
Q

result of optochin test for streptococci viridans?

A

resistant, no clear ring

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35
Q

Positive result of optochin test?

A

clear demarcated ring around optochin disc

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36
Q

Optochin

A

Antibiotic that will inhibit the growth of sensitive bacteria e.g. pneumococci

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37
Q

Staphylococcus aureus is beta haemolytic, therefore what two tests can identify this strain?

A
  • Positive coagulase test (clumping)

- Positive beta haemolysis test - clear ring around colony

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38
Q

Gamma haemolysis

A

Implies no haemolysis

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39
Q

Bacteria sensitive to optochin

A

streptococci pneumoniae

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40
Q

Bacteria resistant to optochin

A

viridans streptococci and other alpha haemolytic streptococci

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41
Q

Oxidase test purpose?

A

Test if the bacteria contain cytochrome oxidase enzymes (in oxidative phosphorylation) - i.e. respires aerobically

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42
Q

All bacteria that are oxidase positive are –>

A

aerobic

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43
Q

bacteria that are oxidase negative are –>

A

either aerobic or anaerobic

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44
Q

Oxidase positive

A

blue result - bacteria is aerobic

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45
Q

Oxidase negative

A

no colour change

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46
Q

Macconkey agar only grows

A

gram-negative bacilli

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47
Q

Staphylococcus are gram

A

positive

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48
Q

Lancefield grouping

A

Method of grouping catalyse negative, coagulase negative bacteria based on bacterial carbohydrate surface antigens

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49
Q

Staphylococcus

A
  • > 40 species
  • Coagulase +’ve or -‘ve
  • Catalase positive
  • S. aureus - coagulase +’ve
  • Normal habitat - nose or skin
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50
Q

Staphylococcus aureus - common clinical presentation

A

pain in shoulder, elevated temperature, causes osteomyelitis (bone infectio)

treat with flucloacillin for 3 months

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51
Q

Staphlococcus aureus

A
  • Coagulase positive

- Spread by aerosol and touch

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52
Q

MRSA =

A

methicillin resistant Staphylococcus aureus

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53
Q

MRSA is resistant to

A

Beta-lactams antibiotics, gentamicin, erythromycin, tetracycline

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54
Q

Virulence factors of staphylococcus aureus

A
  • Pore-forming toxins
  • Proteases
  • Toxic shock syndrome
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55
Q

Associated conditions with staphylococcus aureus

A

Wound infections, osteomyelitis, toxic shock syndrome, food poisoning

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56
Q

Two examples of coagulase negative staphylococci?

A

staphylococcus epidermis, staphylococcus saprophyticus

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57
Q

Three ways of classifying streptococci?

A
  1. haemolysis
  2. Lancefield typing
  3. Biochemical properties
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58
Q

Lancefield typing of both catalase and coagulase negative bacteria based on carbohydrate cell surface antigens - important groupings

A

Group. A - S. pyogenes

Group B - S agalactiae

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59
Q

Infections caused by Streptococci pyogenes

A

Cellulitis, tonsilitis, scarlet fever

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60
Q

Streptococci pneumoniae - common presentation

A

heavy smoker with nasal congestion and fever, gets cough and chest pain, rust coloured sputum, chest x-ray shows fluid in lung

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61
Q

Viridans streptococci is the collective name for

A

oral streptococci

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62
Q

Where is the normal commensal of Streptococci pneumoniae?

A

oropharynx

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63
Q

Infections caused by Streptococci pneumoniae?

A

Pneumonia, meningitis, otitis media (middle ear infection), sinusitis

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64
Q

Virulence/pathogenic factors of Streptococci pneumoniae?

A
  • Polysaccharide capsule

- Cytotoxin

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65
Q

Types of bacterial toxins?

A

Endo and exotoxins

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66
Q

Endotoxin

A

Component of the outer membrane of bacteria - e.g. lipopolysaccharide in gram -‘ve bacteria

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67
Q

Exotoxin

A

secreted proteins of gram +’ve and gram -‘ve bacteria

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68
Q

Major difference betwen gram +’ve and gram -‘ve bacteria?

A

Presence of lipopolysaccharide on gram-negative bacteria

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69
Q

Lipopolysaccharides (LPOs)

A

Constituent of the outer membrane of gram-negative bacteria and are also referred to as endotoxins

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70
Q

Function of LPOs

A

Help protect bacterium from host defences and can contribute to illness in the host

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71
Q

Toxic portion of the LPO

A

Lipid A

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72
Q

Why do gram negative bacteria have more difficulty secreting toxins?

A

Needs to cross 2 membranes instead of one

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73
Q

4 major groups of gram-negative pathogens?

A

Proteobacteria, bacteroids, chlamydia, spirochaetes

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74
Q

Important gram +’ve bacilli

A

Listeria monocytogenes, propionibacterium acne (acne)

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75
Q

What does Macconkey agar indicate?

A

whether the bacteria can ferment lactose

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76
Q

Two key pathogenicity factors/ virulence factors of gram negative bacteria?

A

colonisation factors, toxins

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77
Q

colonisation factors of gram negative bacteria

A

adhesins and invasins

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78
Q

toxins released from gram negative bacteria?

A

secreted proteins

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79
Q

Enterobacteria (coliforms)

A
  • Bacilli
  • Most are motile due to flagella
  • Macconkey agar can differentiate between lactose and non-lactose fermenting
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80
Q

Infections caused by E.COli

A
  • wound infections
  • UTIs
  • Gastroenteritis
  • Traveller’s diarrhoea
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81
Q

Shigella

A

Family of gram negative bacteria which cause damage to the intestinal mucosa, causing acute infection of the large intestine and painful diarrhoea

82
Q

Infections caused by salmonella?

A

Gastroenteritis, enteric fever (typhoid), bacteraemia

83
Q

Example of a slow growing bacteria?

A

TB

84
Q

Example of a fast growing bacteria?

A

E.Coli, S. aureus

85
Q

What types of bacteria release endotoxin?

A

Gram -‘ve

86
Q

What types of bacteria release exotoxin?

A

Gram +’ve and -‘ve

87
Q

What are endotoxins?

A

Lipopolysaccharides, outer membrane component released when bacteria are damaged

88
Q

What are exotoxins?

A

Proteins secreted from gram positive and gram negative bacteria

89
Q

test to distinguish between staphylococcus and streptococcus?

A

catalase test

add H2O2, bubbles of oxygen identifies staphylococcus

90
Q

Flagella is the whole structure, whereas the slender threadlike portion of the flagella is called the?

A

H antigen

91
Q

Does shigella have an H antigen?

A

No, non-motile therefore no flagella and no H antigen

92
Q

Does Salmonella have an H antigen?

A

Yes, since it has a flagellum

93
Q

Does E.coli have an H antigen?

A

Yes, since it has a flagellum

94
Q

MacConkey agar result

A

Positive - pink - lactose fermenting

Negative - yellow/ colourless - non-lactose fermenting

95
Q

MacConkey agar result for shigella and salmonella?

A

Negative - yellow/ colourless

96
Q

MacConkey agar result for E.Coli?

A

Positive - pink

97
Q

Why are there different pathogenic strains of E.Coli?

A

Due to the acquisition of genes from other bacteria

98
Q

Strain of E.Coli associated with traveller’s diarrhoea?

A

Enterotoxigenic E.Coli (ETEC)

99
Q

How does ETEC cause traveller’s diarrhoea?

A

Pilli enable it to adhere to the tissue of the small intestine, binding leads to release of toxin that alters the function of a protein on the GI cell surfaces. Leads to the release of Cl- ions into the GI tract and thus water follows down an osmotic gradient - results in diarrhoea

100
Q

Symptoms of a shigella infection?

A

severe bloody diarrhoea and frequent passage

101
Q

Shigella is acid intolerant - how is this advantageous?

A

Can pass through the acidic stomach without being destroyed and move to the intestine

102
Q

Action of shigella in the small intestine?

A

Macrophage apoptosis, causing release of cytokines and neutrophils –> inflammation

103
Q

What is gastroenteritis?

A

Frequent cause of food poisoning

104
Q

Symptoms of v.cholerae? Why is it so dangerous?

A

huge volumes of watery stools, losing huge amounts of water which can result in hypovolemic shock and severe dehydration

105
Q

Pathogenesis of gastroenteritis

A
  1. Endocytosis
  2. Chemokine release
  3. Neutrophil recruitment
  4. Neutrophil induced tissue injury
  5. Fluid and electrolyte loss –> diarrhoea
106
Q

In which individuals do you normally get fungal infections?

A

Immunocompromised

107
Q

Fungal skin infections are usually caused by which type of fungi?

A

Dermatophytes

108
Q

Dermatophytes reside in the epidermis and require what for growth?

A

Keratin

109
Q

What is meant by dimorphic fungi?

A

Can exist as both yeast and mould - switch between the two forms

110
Q

Aim of antimicrobial drug therapy?

A

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

111
Q

Why are fungal infections rare?

A

Unable to grow at 37C and are often killed by body’s innate and adaptive immune responses

112
Q

3 common fungal infections

A

nappy rash, tinea pedis (athlete’s foot), onychomycosis (fungal nail infection)

113
Q

What might antifungal treatments target?

A

cell wall and the ergosterol containing plasma membrane

114
Q

What is ergosterol?

A

Steroid alcohol that serves the same purpose as cholesterol does in membranes for fungi. Crucial for fungi survival, therefore acts as a good target for drugs

115
Q

Antifungal treatments - how does amphtericin work?

A

targets ergosterol in the plasma membrane and causes pore formation, leading to cell death

116
Q

Antifungal treatments - how do azoles work?

A

they affect the ergosterol synthetic pathway

117
Q

What is candida?

A

a yeast, grows in warm moist areas e.g. vagina, penis

118
Q

Test to identify fungal antigens?

A

Beta-D-glucan test

119
Q

Pneumocystis pneumonia

A

fungal infection causing fluid build up and inflammation in the lungs, often in the immunocompromised people, presents as a symptom due to HIV infection

120
Q

What are moulds composed of?

A

branched filamentous filaments called hyphae

121
Q

Difference between bacteria and mycobacteria?

A

Mycobacteria have an outer membrane, no capsule. Their distinguishing feature is that their cell wall is thicker than in many other bacteria

122
Q

Characteristics of mycobacteria

A

Aerobic, non-motile, non-spore forming, bacilli, slow reproduction, slow response to treatment, slow growing

123
Q

Two examples of mycobacteria?

A

M. tuberculosis (TB)

M. leprae (leprosy)

124
Q

Why is it difficult to perform a gram stain on mycobacteria?

A

They have a very thick cell wall with a high lipid content

125
Q

Clinical relevance of slow growth of mycobacteria?

A

Difficult for antibiotics to target the division phase

126
Q

Clinical relevance of thick cell wall of mycobacteria?

A

Difficult for immune system to target/ damage

127
Q

Acid-fastness is a physical property of some bacteria, what does it mean?

A

Their resistance to decolourisation by acids during laboratory staining procedures

128
Q

How would you stain mycobacteria?

A

Using Ziehl-Neelsen stain for acid fast-bacili

129
Q

Positive result for Ziehl-Neelsen stain

A

Red/pink

130
Q

Nuclei acid detection

A

Amplification using PCR, produces a rapid result for mycobacterium tuberculosis

131
Q

Mycobacteria immunology

A
  • Acid fast bacilli which are phagocytosed by macrophages to form a phagolysosome
  • They have adapted to withstand this phagolysosomal killing and escape into the cytosol
132
Q

Why is antimicrobial treatment prolonged?

A

Bacteria are slowly replicating

133
Q

Characteristics of viruses?

A
  • Acellular - no membranes or cell organelles
  • Outer protein coat and strand of nucleic acid (DNA or RNA)
  • Do not carry out metabolic reactions of their own, require host organelles and enzymes
134
Q

Stages of viral replication

A
  1. Attachment - viral and cell receptors (e.g. HIV)
  2. Entry - only the viral contents enters host cell (viral nucleic acid and proteins)
  3. Interaction with host cell - uses cell materials for replication
  4. Replication
  5. Assembly - may occur in nucleus, cytoplasm or cell membrane
  6. Release - bursting open of a cell or leaking from the cell
135
Q

How do viruses cause disease? (5) COMED

A
  1. Cell proliferation and immortalisation
  2. Over-reactivity of the host in response to infection
  3. Modification of host cell structure
  4. Evasion of extracellular and intracellular host defences
  5. Destruction of host cell
136
Q

How might a virus evade host defences?

A
  • Antigenic variability (ability to change antigens in order to evade the host’s immune system
  • Prevention of host cell apoptosis
  • Down regulation of interferon and other intracellular host defence proteins
137
Q

Function of interferons

A

Modulate the response of the immune system to viruses

138
Q

3 classes of worms?

A

Nematodes (roundworms)
Trematodes (flatworms)
Cestodes (tapeworms)

139
Q

Nematodes (roundworms)

A
  • Intestinal e.g ascarius lumbricoides
  • Skin e.g. larva migrans
  • Tissue e.g. filaria
140
Q

Trematodes (flatworms)

A
  • Blood
  • Liver
  • Lungs
  • Intestinal
141
Q

Cestodes (tapeworms)

A
  • Non-invasive

- Invasive

142
Q

What is the pre-patent period?

A

Period between infection and appearance of eggs in stools

143
Q

How are intestinal nematodes (roundworms) normally diagnosed?

A

Stool microscopy looking for eggs

144
Q

How to roundworms get into the host’s body?

A

When the host eats food or drinks water containing the worms, the worm penetrates the hosts skin, an insect such as a mosquito

145
Q

When might humans be infected with cestodes (tapeworms)?

A

By eating raw contaminated pork, beef or fish, or by consuming food contaminated by faeces from infected animals

146
Q

How are intestinal nematodes spread?

A

Human to human transmission via eggs or larvae

147
Q

Signs and symptoms of an ascarius lumbricoides infection

A

Loeffler’s syndrome - larval migration to lungs results in a cough, fever and wheeze (infection however is often asymptomatic)

148
Q

Wucheria bancroftii

A

Filariasis causing lymphoedema

149
Q

Enterobius vermicularis

A

common in UK, itchy bum, spreads in households

150
Q

Schistosomiasis

A

Causes squamous cell bladder cancer

151
Q

Hookworm

A

worldwide cause of iron-deficiency anaemia

152
Q

What are protozoa?

A

single-celled eukaryotic organisms

153
Q

Main biological role of protozoa?

A

Consumers of bacteria, algae and microfungi

154
Q

5 major groups of protozoa?

A

Flagellates, amoebae, sporozoans, ciliates, microsporida

155
Q

How is malaria transmitted?

A

via the bite of a female mosquito from dusk till dawn

156
Q

Why are there different clinical manifestations of malaria?

A

Due to the variation in the plasmodia life cycle - has stages in the human and the mosquito

157
Q

Stages of the plasmodia lifestyle in humans?

A

Exo- and endo-erythrocytic stages

158
Q

Malaria is a protozoan infection caused by ?

A

Plasmodia sporozoan

159
Q

4 species of malaria causing protozoae?

A

P. falciparum
P. ovale
P. vivax
P. malariae

160
Q

Why do you get anaemia as a result of malaria?

A
  • Haemolysis of infected RBC
  • Haemolysis of non-infected RBC
  • Splenomegaly
  • Folate depletion
161
Q

Clinical features of malaria

A
  • Fever
  • Chills and sweats
  • Headache
  • Myalgia
  • Fatigue
162
Q

Exo-erythrocytic stage of plasmodia life cycle in humans

A

Hepatocytes become infected by sporozoites, the cells mature and develop, released as tropozoites

163
Q

Endo-erythrocytic stage of plasmodia life cycle in humans

A

Tropozoites invade teh RBCs, parasite numbers expand rapidly with a sustained cycling of the parasite population

164
Q

Which two specides of the plasmodia genus lie dormant and cause late relapse of malaria?

A

P. ovale and P. vivax

165
Q

Genetic condition that may give you immunity to malaria?

A

Sickle cell anaemia

166
Q

Clinical features of haemolysis?

A

Anaemia, jaundice (dark urine due to increased Hb)

167
Q

Pathogenesis of P.falciparum?

A

Unique cerebral malaria, fatal infection, parasites mature in RBCs and these collect in the small vessels and cause blockage of cerebro-microvasculature - hypoxia

168
Q

Diagnosis of malaria?

A

Thick and thin films

169
Q

Diagnosis of malaria - thick films

A

Tells you if malaria is present, sensitive but low resolution

170
Q

Diagnosis of malaria - thin films

A

Tells you species and parasite count

171
Q

Can immunity to malaria be acquired?

A

recurrent infections lead to some immunity, but the immunity is lost if not reinfected after a couple of years

172
Q

Humoral response to viral infections?

A

Antibodies (IgA - blocks binding of host cell and virus), opsonisation, complement cascade

173
Q

Cell-mediated response to viral infections?

A

Kill infected cells, macrophages

174
Q

How does virus’ evade the host defences?

A

Interfere with defence, influenza changes coat antigen

175
Q

Which type of antibody blocks the binding of the host cell and the virus?

A

IgA

176
Q

Bacterial infections - entry to host via?

A

Respiratory tract, GI tract, GU tract, skin breakage

177
Q

Evasion of host defences - mycobacteria?

A

Escape from the phagolysosome, live in cytoplasm

178
Q

What does the immune response to a protozoan infection depend on?

A

Location of parasite within the host (blood, tissue, etc.)

179
Q

immune response to a protozoan infection in the blood?

A

humoral immunity

180
Q

immune response to a protozoan infection in the tissue?

A

cell mediated immunity

181
Q

Immune response to worm infections

A

They do not multiply in humans and they are not intracellular. The immune response is poor and not sufficient enough to kill the worms

182
Q

Infection control - the health act 2006

A

Infection control is every health worker’s responsibility, no longer just the responsibility of the infection control team, possible to be prosecuted

183
Q

Key components of infection prevention and control

A

Infection prevention and control team, ward teams, microbiology/ virology laboratories, domestic services, pharmacy

184
Q

Diseases in hospital with important infection control policies?

A

MRSA, TB

185
Q

Hand hygiene - infection control

A

Single most effective method of preventing cross infection

186
Q

When to wash hands?

A

Before/ after handling patients, after using toilet, handling any soiled item, after an aseptic procedure

187
Q

When to use alcohol gel?

A

Following hand washing prior to an invasive procedure or caring for a patient with barrier precautions

188
Q

Endogenous infections

A

Infection of a patient by their own flora, important in hospitalised patients (especially those with invasive devices or surgical patients

189
Q

How to prevent healthcare endogenous infections?

A

Good nutrition and hydration, antisepsis, control the underlying disease (drain pus, remove lines and cathethers as soon as appropriate)

190
Q

Disposal of sharps - key points

A
  • Disposal bin is the responsibility of the person using the equipment
  • Sharps bin must be correctly assembled
  • Never re-sheath or bend needles
  • Never overfill a sharps bin
191
Q

Antibiotics

A

Agents produces by micro-organisms that kill or inhibit the growth of other micro-organisms in high dilution

192
Q

Where on bacteria would penicillin bind?

A

Bacterial cell wall

193
Q

Define bacteriostatic?

A

Antibiotics that prevent bacterial growth by inhibiting DNA synthesis

194
Q

Define bactericidal?

A

Antibiotics that kill bacteria by inhibiting cell wall synthesis

195
Q

What is MIC?

A

Minimum inhibitory concentration - lowest concentration of a chemical that prevents growth of a bacterium

196
Q

What is concentration dependent killing?

A

Antibiotics that eradicated pathogenic bacteria by achieving high concentrations at the site of binding

197
Q

What is time dependent killing?

A

The time that serum concentrations remain above the minimum inhibitory concentration

198
Q

4 diseases that haemophilus influenzae can cause?

A

Meningitis, otitis media, pharyngitis, exacerbations of COPD

199
Q

What does the HIV envelope contain?

A

RNA, capsid, reverse transcriptase

200
Q

What is ringworm?

A

fungal infection

201
Q

Can mycobacteria withstand phagolysosomal killing?

A

yes, they have adapted to escape into the cytosol

GRACE Phase 2a Medicine (20 decks)

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