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1st Year Medicine > Microbiology. > Flashcards

Microbiology. Flashcards

0
Q

Describe micro-organism nomenclature?

A

The first word is the genus and the second is the species. The first word has a capital and the second is lower case.

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1
Q

List the infectious agents we deal with in decreasing size order.

A

Parasites, fungi, bacteria, virus and prion proteins.

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2
Q

Describe prion proteins?

A

Infections with no DNA or RNA. Give prion diseases or transmissible spongiform encephalopathies. CJD - very rare but incurable brain infection.

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3
Q

Describe viruses.

A

Very small, RNA or single/double stranded DNA. Protein coat (capsomere) +/- lipid envelope. They are obligate intracellular parasites. Can be: cultured, detected by serology (antibody or antigen detection in blood), PCR (to detect DNA or RNA.

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4
Q

Describe bacteria.

A

Contain DNA or RNA. One double stranded chromosome but sometimes have extra bits of circular DNA in the cytoplasm (plasmids). They have a cell membrane and cell wall +/- capsule. Have flagellae (movement) and Pili (fimbrae for adhesion).

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5
Q

What are the three different bacteria shapes?

A

Coccus - round.
Bacillus - rod shaped.
Spirochaetes - spirals.

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6
Q

What does a gram stain do?

A

Stains the bacterial cell wall. Positive turns purple and negative turns pink.

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7
Q

What types of organism are klebsiella, E. coli and proteus?

A

Gram negative coliforms.

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8
Q

What type of organisms are staph aureus, steps and enterococci?

A

Gram positives.

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9
Q

What streps are beta haemolytic?

A

ABCG.

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10
Q

What kind of toxins do gram negative bacteria make?

A

Endotoxins. Part of cell wall.

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11
Q

What kind of toxins do gram positive bacteria make?

A

Exotoxins. Made inside and exported out.

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12
Q

Why is gram staining important?

A

Antibiotics tend to work on the cell wall so knowing what type of cell wall we have in important for treatment.

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13
Q

What colour do gram positive bacteria turn?

A

Purple.

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14
Q

What colour do gram negative bacteria turn?

A

Pink.

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15
Q

What do gram positive cell walls look like?

A

Inner membrane made of phospholipids and proteins and an outer wall of layers of peptidoglycans. (Look like positive signs).

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16
Q

What do gram negative cell walls look like?

A

Inner membrane of phospholipids and proteins.
Middle layer of peptidoglycans in the periplasmic space (look like negative signs).
Outer membrane of phospholipids, proteins, LPS and porins.

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17
Q

What two organisms don’t gram stain well?

A

Mycobacterium tuberculosis and treponema pallidum (causes syphillis).

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18
Q

What is contaminant?

A

An organism that has got into a sample by accident.

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19
Q

What is pathogenicity?

A

The ability of an organism to cause disease.

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20
Q

What is the virulence of an organism?

A

Degree of pathogenicity e.g. How easily an organism causes disease.

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21
Q

What are the three main types of atmosphere bacteria grow in?

A

Aerobic, microaerophilic and anaerobic.

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22
Q

Can aerobic organisms grow without oxygen?

A

Some will but less well.

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23
Q

What is a microaerophillic atmosphere?

A

Reduced O2 enriched with CO2.

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24
Q

What two important types of bacteria can make spores and therefore last for long times in adverse conditions?

A

Clostridium e.g. C diff

Bacillus e.g. Bacillus anthracis.

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25
Q

Where does anthrax usually come from?

A

Animals like cows and sheep.

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26
Q

What different methods can we use to identify bacteria?

A

Microscopy of a gram stained film.
Culture.
Detection of antigen.
Serology - detection of antibodies in blood.
Molecular methods e.g. PCR to see DNA or RNA.

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27
Q

What tests do we get back same day?

A

Microscopy, PCR and serology.

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28
Q

How long does a culture take?

A

48 hours to identify and get antibiotic sensitivity.

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29
Q

How long does a TB culture take?

A

4-12 weeks.

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30
Q

What is the commonest cause of mould infections in humans?

Does it stain?

A

Aspergillus.

Doesn’t gram stain.

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31
Q

What is the most common cause of yeast infection in humans?

Does it gram stain?

A

Candida.

Stains as large positive oval structures that replicate by budding.

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32
Q

What is sterilisation?

What does it not work on?

A

Destruction and removal of 99% of organisms and spores.

May not inactivate prions.

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33
Q

What is disinfection?

A

Removal and destruction of pathogenic micro organisms enough to make the item safe.

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34
Q

What are the 5 ways any infection can spread?

A 
5 Is.
Inhalation.
Mother to infant.
Inoculation.
Ingestion.
Intercourse.
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35
Q

What are the components of the chain of infection?

A 
Pathogenic organism
Reservoir
Means of escape.
Mode of transmission.
Means of entry.
Host susceptibility.
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36
Q

What are standard precautions?

A

Precautions in place for all patients at all times e.g. Droplet, contact and airborne precautions.

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37
Q

What are contact precautions?

A

Gloves, apron and single rooms/cohort bay.

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38
Q

What are droplet precautions?

A 
Single rooms
Ensuite.
Gloves
Apron
Mask
Eye protection
Vaccination.
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39
Q

What are airborne precautions?

A

Negative pressure room
PPE
FFP3 masks
Vaccination

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40
Q

What order to we take gloves and aprons on and off?

A

Apron gloves gloves apron.

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41
Q

How do viruses attach to cells?

A

By forming Ligands with it using one of its protein spikes.

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42
Q

Why do antibiotics not kill viruses?

A

Because they target specific structures in bacteria such as cell wall, ribosomes and enzymes etc. viruses don’t have these to cannot be killed with antibiotics.

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43
Q

How can viruses enter cells?

A

Either by membrane fusion or pinocytosis of the virus doesn’t have a membrane.

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44
Q

What are the steps in viral cell invasion?

A 
Attachment.
Viral entry.
Uncoating.
Nuclei acid and protein synthesis.
Assembly
Release.
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45
Q

How are viruses released from cells?

A

Budding and lysis.

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46
Q

What might we see under the microscope if viruses are assembling?

A

Crystals of assembling virus as inclusions.

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47
Q

How do viruses cause cell death?

A

Due to lysis or hijacking of machinery.

Cell death due to immune system response.

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48
Q

What kinds of viruses can cause cancer?

A

HPV - cervical.
Hepatitis B and C can cause primary hepatocellular carcinoma.
EBV - kaposis sarcoma.
Helicbactor pylori - gastric cancer.

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49
Q

How can we detect viruses?

A

Detect the virus itself e.g. By PCR. or the presence of antibodies against it.

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50
Q

What antibodies can neutralise viruses?

A

IgM and IgG.

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51
Q

What can happen to viruses after the enter the body?

A

They can become latent and possibly reactivate at a later date or remain continually active.

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52
Q

How can we differentiate a recent infection from a past one?

A

Detection of virus specific IgM.
Detection of rising titre of IgG.
Detection of very high titre of IgG.

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53
Q

How does the body respond after detecting a virus?

A

The hum oral response of IgM and then specific IgG.

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54
Q

Why are antibiotics selectively toxic?

A

They affect all parts of the body including the flora so they must be specific or they would cause great harm.

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55
Q

What does bacteriocidal mean?

A

Bacterial killing.

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56
Q

What does bacteriostatic mean?

A

Inhibition of bacterial growth.

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57
Q

When do PO antibiotics achieve peak serum levels?

A

In about an hour.

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58
Q

When do IV antibiotics achieve peak serum levels?

A

In about 15 mins.

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59
Q

When antibiotics are given orally are they 100% available systemically?

A

No a lot of it is endorsed and excreted u changed in the feces.

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60
Q

How are antibiotics excreted?

A

Either in urine or via the liver and biliary tract into the feces.

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61
Q

What factors should we consider when choosing an antibiotic?

A

Infection site.
Likely infecting organism.
What route should it be given
Local prescribing policies.

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62
Q

What three reasons do we give antibiotics in combination?

A

To cover a broad range of organisms.
To prevent development of resistance.
For the synergistic effect.

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63
Q

What types of antibiotics work in the cell wall?

A

Penicillins
Cephalosporins
Glycoproteins.

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64
Q

What penicillins do we use for gram positive organisms?

A

Flucloxacillin IV or oral.

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65
Q

What penicillins do we use for gram positive and gram negative organisms?

A

Amoxicillin IV or oral.
Co-amoxiclav IV or oral.
Tazocin IV only.

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66
Q

What penicillins do we use for gram negative organisms?

A

Temocillin IV.

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67
Q

How do penicillins work?

A

Inhibit cell wall synthesis by preventing the cross linking of peptidoglycan subunits. It is a bactericidal.

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68
Q

How are the penicillins excreted?

A

Rapidly via the kidneys.

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69
Q

Are the penicillins safe in pregnancy?

A

Yes.

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70
Q

What drawback does penicillin excretion have?

A

It is rapid so requires frequent dosing.

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71
Q

If a patient is allergic to penicillin what also might they be allergic to?

A

Definitely all the rest of the penicillins and sometimes the cephalosporins.

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72
Q

What organisms are flucloaxacillin exclusively useful for?

A

Staphylococci and streptococci.

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73
Q

What ring do the penicillins have and what is a problem with this in terms of microbial resistance?

A

A beta lactam ring.

Some bacteria make beta lactamase, an enzyme that destroys it.

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74
Q

Whip at is Coamoxiclav a mixture of and why does it work?

A

Mixture of amoxicillin and clavulanic acid.

The acid stops beta lactamase breaking down the beta lactam ring in the amoxicillin.

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75
Q

What type of bacteria is temocillin exclusively active against?

A

Coliforms.

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76
Q

What kind of cephalosporin antibiotic do we use?

A

Ceftriaxone.

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77
Q

How do cephalosporins work?

A

They inhibit cell wall synthesis.

78
Q

How are cephalosporins excreted?

A

Kidneys and urine.

79
Q

Are cephalosporins safe in pregnancy?

A

Yes.

80
Q

What spectrum of antibiotics are cephalosporins and what does this result in?

A

Broad spectrum.

They kill of bowel flora leading to C diff infections.

81
Q

What two types of glycopeptides do we use?

A

Vancomycin and teicoplanin.

82
Q

How does vancomycin work?

A

Attaches to the cell wall during peptidoglycan synthesis stopping cross linking and weakening the cell wall.

83
Q

Are the glycopeptides bactericidal or bacteriostatic?

A

Bactericidal.

84
Q

How are glycopeptides excreted? What consequence does this have for vancomycin?

A

Via the kidneys and urine. Vancomycin can build up to a toxic level in patients with kidney failure causing further damage.

85
Q

What types of bacteria are glycopeptides active against?

A

Gram positive.

86
Q

What antibiotics inhibit bacterial protein synthesis?

A

The macrolides, tetracyclines, aminoglycosides and clindamycin and chloramphenicol.

87
Q

Do the cephalosporins have a beta lactam ring?

A

Yes.

88
Q

How do antibiotics stop bacterial protein synthesis?

A

Attach to bacterial ribosomes.

89
Q

What macrolides do we use?

A

Erythromycin, clarythromycin and azithromycin.

90
Q

Are macrolides bactericidal or bacteriostatic?

A

Bacteriostatic.

91
Q

Are tetracyclines bactericidal or bacteriostatic?

A

Bacteriostatic.

92
Q

Are ahminoglycosides bactericidal or bacteriostatic?

A

Bactericidal.

93
Q

How are the macrolides excreted?

A

Via the liver and biliary tract into the gut.

94
Q

Are the macrolides safe in pregnancy?

A

Erythromycin is.

95
Q

What tetracyclines do we use?

A

Doxycycline.

96
Q

How must gentamicin be given and why?

A

IV and occasionally IM as it cannot be absorbed from the gut.

97
Q

What aminoglycasides do we use?

A

Gentamicin.

98
Q

What is gentamicin mainly used for?

A

Gram negative aerobic organisms such as coliforms and pseudomonas aeruginosa and life threatening gram negative infections in hospital.

99
Q

How is gentamicin excreted?

A

In the urine.

100
Q

What serious side effect can come from aminoglycasides and what does it cause?

A

Toxicity - Damage to kidneys and 8th cranial nerve (deafness and dizziness).
Need to monitor blood levels.

101
Q

What antibiotics act on bacterial DNA?

A

Metronidazole.
Trimethoprim
Fluoroquinolones.

102
Q

What is metronidazole used to treat?

A

Aerobic and some protozoal infections.

103
Q

How does trimethoprim work?

A

Inhibits bacterial folic acid synthesis.

104
Q

How is trimethoprim given?

A

Orally.

105
Q

How is trimethoprim excreted?

A

Via the urine.

106
Q

What kind of cover does trimethoprim have?

A

Gram negative and positive.

107
Q

What fluoroquinolones do we use?

A

Ciprofloxacin IV oral and levoflaxacin IV.

108
Q

Are fluoroquinolones bactericidal or bacteriostatic?

A

Bactericidal.

109
Q

How are fluoroquinolones excreted?

A

Via the urine.

110
Q

Should fluoroquinolones be used readily?

A

No they are prohibited in Tayside due to c diff.

111
Q

What are the 4 C antibiotics we shouldn’t use?

A

Cephalosporins.
Co amoxiclav.
Ciprofloxacin
Clindamycin.

112
Q

What kind of environment do staphylococcus and enterococcus grow in?

A

Best aerobically but can grow anaerobically too.

Faculatively anaerobic.

113
Q

What kind of bacteria arestaphylococcus and enterococcus?

A

Gram positive cocci in chains.

114
Q

What types of bacteria are differentiated by haemolysis?

A

Streptococci.

115
Q

What different kind of haemolysis do we get and what culture medium do we need? What do they look like on the medium?

A

Alpha - partial - looks like a green ring.
Beta - complete - clears the agar completely round it.
Non haemolytic strains.
Grown on blood agar.

116
Q

What two groups of streptococcus are alpha haemolytic?

A

Streptococcus pneumonia and streptococcus Viridans.

117
Q

What is streptococcus pneumonia otherwise called?

A

Pneumococcus.

118
Q

What type of bacteria is streptococcus pneumonia?

A

Gram positive in short chains or pairs.

119
Q

What type of bacteria is streptococcus Viridans?

A

Gram positive cocci in chains.

120
Q

What are the main infections caused by streptococcus pneumonia?

A

Meningitis and pneumonia.

121
Q

What two types of beta haemolytic strep are there?

A

Group A e.g. Strep pyogenes.

122
Q

What are the most pathogenic streps?

A

The beta haemolytic.

123
Q

What is the most pathogenic of all the streptococci?

A

Strep pyogenes.

124
Q

How does strep pyogenes damage cells?

A

Produces a powerful exotoxin that damages cells.

125
Q

What can strep pyogenes cause?

A

Streptococcal sore throat (tonsillitis) if a rash is also present its scarlet fever.
Skin and soft tissue infection with necrotising fasciitis being the worst.
Pererpal sepsis.

126
Q

What are all strains of strep pyogenes sensitive to?

A

Penicillin and amoxicillin.

127
Q

What is the most important group of the non haemolytic streptococci?

A

The enterococci: enterococcus faecalis or enterococcus faecium.

128
Q

What are the most common cause of UTIs?

A

The enterococci.

129
Q

What are most strains of enterococcus faecalis sensitive to?

A

Amoxicillin but not penicillin.

130
Q

What is VRE?

A

Vancomycin resistant enterococci. Commonly E.faecium.

131
Q

What environment do Staphylococci grow best in?

A

Best aerobically but can be anaerobic.

132
Q

What type of bacteria are Staphylococci?

A

Gram positive cocci in grape like structures.

133
Q

How do we distinguish staph aureus from the other types of staph?
What does it look like on culture?

A

Coagulase test.

Staph aureus is positive and so looks golden on culture.

134
Q

What do coagulase negative staph look like on culture?

A

White on blood agar.

135
Q

What infections are the coagulase negative staph a common cause of?

A

Prosthetic joint, heart valve and IV line infection that can be difficult to treat.

136
Q

Where does staph aureus commonly colonise?

A

The nose and upper respiratory tract.

137
Q

What can the exotoxins produced by Staphylococci cause?

A

Toxic shock syndrome toxin and Payton Valentine leukocidin which can damage white blood cells.

138
Q

What is MRSA resistant to?

A

Penicillins, cephalosporins and other antibiotics.

139
Q

What can the different strains of staph aureus cause?

A

Skin and soft tissue infections and food poisoning.

140
Q

What is the antibiotic choice for MSSA? (Sensitive).

A

Flucloxacillin.

141
Q

How does staph aureus spread within the body?

A

Arterial affection multiplies at the site of acquisition causing local infection and inflammation e.g. Abscess. Gets into blood stream and disseminates possibly causing abscesses in liver, spleen and kidneys etc.

142
Q

What is SAB?

A

Staph aureus bacteraemia.

143
Q

What is one of the most common causes of bacteraemia?

A

Staph aureus.

144
Q

What is another complication of SAB other than abscess formation at distant sites?

A

Sepsis.

145
Q

How are most SABS contracted?

A

Hospital acquired.

146
Q

What are a common cause of SAB?

A

Infected IV lines.

147
Q

What are local symptoms of infection?

A

Heat, redness, swelling, pain and loss of function.

148
Q

What are symptoms of systemic infection?

A

Fever, sweats and rigors.

149
Q

What non specific tests can we do for an infection?

A

A white cell count.

150
Q

What signs will we find on examination of an early infection?

A

Fever, tachycardia, and inflammatory signs.

151
Q

What signs will we find on examination of a very advanced infection?

A

Low BP, increased HR, blood clotting abnormalities and organ failure.

152
Q

What is fever defined as?

A

A temp of over 38 deg.

153
Q

Why does the temperature rise in infection?

A

Pathogens grow best at 37 deg and growth slows above this, so the body is attempting to slow the growth.

154
Q

What are the steps involved in fever production?

A

Antigen is detected by macrophages, which release cytokines into the blood stream. Cytokines travel to the anterior hypothalamus (also cause the adverse effects of sepsis). Prostaglandin is then released which increases the body’s thermal set point. Body thinks it’s cold and takes measures to heat up. Results in fever.

155
Q

What is sepsis?

A

The hosts response to severe infection.

156
Q

What happens during sepsis?

A

Small vessels become leaky and lose fluid.
Lower blood volume requires increased cardiac effort.
Poor tissue oxygen perfusion means non essential organs receive less blood.
Blood clotting system is activated causing clotting in tiny vessels. This uses up all the clotting factors increasing clotting risk.

157
Q

What are the two aerobic gram negative cocci we should remember and what do they look like?

A

Neisseria menningitis and neisseria gonorrhoea.

Appear in pairs

158
Q

What are coliforms?

A

Gram negative bacilli that look like e.coli.

159
Q

What environment do coliforms grow best in?

A

Best Aerobically but will also grow anaerobically.

160
Q

What is the first line antibiotic used for coliforms infection?

A

Gentamicin.

161
Q

What happens to people with sepsis from gram negative infection?

A

They become very unwell very quickly as endotoxin is released from the bacterial cell walls when they die. These are taken up by macrophages, which in return release cytokines, leading to further sepsis.

162
Q

What are some common gut commensals?

A

Lots of e.coli strains, klebsiella, enterobacter and proteus.

163
Q

What are some common gut pathogens?

A

Salmonella, shigella, e.coli 0157 and 0104.

164
Q

What are the gram negative strict aerobes?

A

Pseudomonas aeruginosa.

Legionella pneumophilia.

165
Q

What three gram negative bacilli are curved or spiral?

A

Vibrio cholera, campylobacter and helicobacter pylori.

166
Q

What is the commonest cause of food poisoning/bacterial diarrhoea in the UK?

A

Campylobacter.

167
Q

What two bacteria are strict anaerobes?

A

Clostridium and bacteriodes.

168
Q

What is cholera?

A

A severe diarrhoeal illness.

169
Q

What kind of bacteria is clostridium?

A

Gram positive anaerobic bacilli.

170
Q

What does clostridium perfringens cause?

A

Gas gangrene.

171
Q

What does clostridium tetani cause?

A

Tetanus.

172
Q

What is the first line antibiotic treatment for anaerobes?

A

Metronidazole.

173
Q

What stains do we use for mycobacteria?

A

Acid fast bacilli or acid alcohol fast bacilli AAFB

174
Q

What does treponema pallidum cause?

A

Syphillis.

175
Q

What does borrelia burgdoferi cause?

A

Lyme disease.

176
Q

What factors allow bacteria to become resistant to antibiotics?

A

There is genetic variation amongst them.
Rapid multiplication increases the chance of mutation.
Gene transfer:
where genetic material from dead bacteria can be taken up by living bacteria.
Conjugation also happens where a plasmid DNA can be transferred between bacteria and
transduction by viruses infecting bacteria transferring DNA from one to another.

177
Q

What human factors allow antibiotic resistance to evolve?

A

Giving sub therapeutic doses.
Over prescribing e.g. Over the counter.
Using antibiotics in food production.

178
Q

How do cells change in order to resist antibiotics?

A

Produce antibiotic destroying enzymes.
Altered antibiotic binding sites.
Alteration of cell wall porins.
Up regulation of efflux pumps.

179
Q

What is the definition of diarrhoea?

A

3 or more loose stool in 3 hours.

180
Q

What bacteria do we tend to find in rice?

E.g. Food poisoning from takeaways.

A

Bacillus sereus.

181
Q

What bacteria can we get from contact with amphibians or reptiles e.g. Terrapins?

A

Salmonella.

182
Q

What pathogens do we commonly test for in 3 year olds with diarrhoea?

A

Salmonella, shigella, campylobacter, e.coli 0157 and cryptosporidium.

183
Q

Can children get C diff?

A

They are thought not to have C diff receptors in the gut, so no.

184
Q

What children’s trips can be a big source of e.coli 0157 infection?

A

Farm visits, as they can catch it from the animals.

185
Q

What tests do we do for e.coli 0157?

A

FBC, U and Es, lactate, CRP, LFTs.

186
Q

What can E. coli 0157 infection commonly cause in children?

A

HUS, haemolytic uraemia syndrome.

187
Q

How does E. coli cause HUS?

A

Toxins cause microangiopathic haemolytic anaemia which causes thrombosis to go to the kidney.

188
Q

How can we catch E. coli at places like festivals?

A

It is in cow dung so can catch it from camping in fields etc.

189
Q

What is the infecting dose for salmonella?

A

10^6 organisms.

190
Q

What is the infecting dose for shigella?

A

10^3 organisms.

191
Q

Why are older people usually more at risk of food poisoning?

A

A lot of them are on PPIs so have lost the natural gastric acid defence.

192
Q

What should we do if someone is symptomatic for E. coli but are culture negative?

A

PCR for verotoxin.

1st Year Medicine (64 decks)

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