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Jack 2a > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the definition of a pathogen?

A

Organism that causes or is capable of causing disease

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2
Q

What is the defintion of a commensal organism?

A

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

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3
Q

What is the defintion of an opportunistic pathogen?

A

Microbe that only causes disease if host defenses are compromised. Sometimes happens when commensal organisms get into the wrong places, or if we are immune compromised.

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4
Q

What is the defintion of virulence/pathogenicity?

A

The degree to which a given organism is pathogenic

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5
Q

How do we name bacteria? What is the first/second name denoting?

A

Staphylococcus aureus

First (staphylococcus) name is genus name. Often shortened to S.
Second (aureus) name is the species

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6
Q

Are gram positive bacteria purple or pink?

A

Gram positive = appear purple

Gram negative = appear pink

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7
Q

Name some features of bacterial ultrastructure

A
  1. Outer membrane (gram positive have 1, gram negative have 2)
  2. A singular circular double stranded chromosome
  3. Pili or fimbriae - help bacteria adhere to surface
  4. Flagella - help with motility
  5. Some have capsules made o polysaccharide
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8
Q

Describe the gram positive bacteria cell wall

A
  1. Inner cytoplasmic membrane
  2. A very large peptidogylcan layer

Some have a capsule

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9
Q

Describe the gram negative bacteria cell wall

A
  1. Inner cytplasmic membrane
  2. A thin peptidoglycan layer
  3. A second “outer” membrane
  4. Outside this they have endotoxin lipopolysaccharide

Some have a capsule

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10
Q

Why do gram positive bacteria stain purple?

A

The thick peptidogylcan layer retains crystal violet,.

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11
Q

What are bacterial spores?

A

Dormant forms of bacteria that can survive in environments which do not promote growth.

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12
Q

Describe bacterial endotoxins and exotoxins

A

Endotoxin - component of the outer membrane which is toxic, e.g. lipopolysaccharide in gram negative.

Exotoxin - secrete proteins of either gram positive or gram negative bacteria.

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13
Q

What is a toxoid?

A

A chemical from a microorganism that is not toxic, but its still antigenic (can be used as a vaccine)

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14
Q

What are the 2 methods of genetic variation in bacteria?

A

Mutation: changes in amino acid sequence of genome

Gene transfer: transformation, transduction, conjugation

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15
Q

In gene transfer, describe transformation

A

Transformation - genetic alteration of a bacterial cell via the uptake of an exogenous substance such as a plasmid.

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16
Q

What is endotoxic shock?

A

When the host immune system recognises an endotoxin and amounts a huge response.

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17
Q

In gene transfer, describe transduction

A

The process by which foreign DNA is introduced into a bacteria via vector or virus, e.g. bacteriophage (virus)

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18
Q

In gene transfer, describe conjugation

A

The transfer of genetic material between bacterial cells by direct cell-cell contact, e.g. via sex pilus

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19
Q

Name 3 genera of gram positive bacteria

A

Streptococcus - S.pyogenes
Staphylococcus - S.aureus
Corynebacterium - C.diphtheriae

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20
Q

What is coagulase?

What does it catalyse?

A

An enzyme produced by some bacteria that clots blood plasma. This is protective as it prevents immune cells migrating

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21
Q

For staphylococcus Aureus, which of the following are true:

  1. It is coagulase positive
  2. It is beta lactam resistant
  3. It produces toxins
A
  1. T
  2. T
  3. T
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22
Q

What are virulence factors?

A

Molecules produced by pathogens that add to their effectiveness and enable them to achieve colonisation, immunoevasion, immunosuppression, entry and exit into and out of cells or nutrition from the host.

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23
Q

What are pyogenic conditions?

A

Conditions relating to the production of pus

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24
Q

Is Staphyloccocus epidermidis coagulase positive or negative?

A

It is coagulase negative.

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25
Q

What are the 3 types of haemolysis of bacteria on blood agar?

A

Beta haemolysis - blood is completely broken down (e.g. S.pyogenes)
Alpha haemolysis - blood is partially broken down (e.g. S.pneumonaie)
Gamma haemolysis - there is no haemolysis (S.mutans)

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26
Q

What is sero-group?

A

This is where different strains/species have the same cell surface antigens. We can recognise certain carbohydrate cell surface antigens by adding anti-sera (antibodies) to a sample of bacteria and see if they clumb.

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27
Q

What is lancefield grouping? (what does it distinguish)

A

Another way of categorising bacteria by looking at the bacterial carbohydrate cell surface antigens.

It can only be used to for catalse negative bacteria.

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28
Q

Name the genus of S.pyogenes and S.pnuemoniae

A

Streptococci pyogenes and streptococci pneumoniae

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29
Q

What are viridians streptococci?

A

A collective term for oral streptococci.

These often cause dental abscesses and endocarditis and deep organ abscesses.

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30
Q

What is the name of the most virulent streptococci?

A

The milleri group

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31
Q

Name the genera and species of some gram positive bacilli?

A 
Corynebacterium (diphtheriae)
and bacillus (anthrancis)

Others include Clostridia: tetani, Botulinum, Difficule

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32
Q

Describe the typical presentation of staphylococcus aureus

signs, symptoms, method of diagnosis, treatment, spread

A

Pain in shoulder, elevated temperature, osteomyelitis.
Diagnose by blood cultures, treat with glycopeptide (e.g. Vancomycin)
It is spread by aerosol and touch

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33
Q

Name the 2 most important groups of lancefield typing.

A

Group A - Strep.Pyogenes

Group B - Strep.Agalactiae

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34
Q

Is lipopolysaccharide on gram positive bacteria?

A

No - it is only on gram negative bacteria.

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35
Q

What are the three parts of lipopolysaccharide?

A

Lipid A - the toxic bit anchored to the outer membrane
Core (R) antigen - short chains of sugars
Somatic (O) antigen - highly antigenic repeating chain of oligosaccharides

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36
Q

Name 3 gram negative bacteria in the phylum proteobacteria and the family endobacteria

A

E.coli
Shigella
Salmonella

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37
Q

Describe the term Strain/Isolate

A

Bacteria of the same speciaes that have been isolated from its parent and have a slightly different genome.

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38
Q

Describe the term serovar/serotype

A

Strains that have different antigenic properties - have slightly different antigens but are largely the same otherwise

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39
Q

Describe the term pathovar/pathotype

A

Strains that are distinguished by the possession of particular pathogenic mechanisms.

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40
Q

Describe the term biovar/biotype

A

Strains that differ physiologically or biochemically from other strains in a particular species

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41
Q

Describe the term “pathogenicity island”

A

A section of a chromosome/a gene which is transferred horizontally between bacteria.

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42
Q

Describe 5 facts of proteobacteria

Classification etc.

A
  1. Gram negative
  2. Bacilli
  3. Motile
  4. Faculatively anaerobic
  5. Some colonies the GI tract
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43
Q

Describe the 2 outcomes of bacteria on a MacConkey plate and the reasons we see these.

A

MacConkey plate has lactose on it. If bacteria have lactase they metabolise this to make lactic acid causing pH change and agar to change red (red colonies)

If you have a non-lactose bacteria, they stay white/yellow)

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44
Q

Describe how we could distinguish the gram negative bacteria: shigella, E.coli and salmonella

A

Shigella - non-lactose and non-motile
E.Coli - lactose and motile.
Salmonella - non-lactose and motile

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45
Q

Name the following for E.Coli:

  1. Gram status
  2. Conditions caused
A
  1. Negative

2. Gastroenteritis, UTIs, diarrhoea

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46
Q

Name the following for Shigella:

  1. Gram status
  2. Conditions caused.
  3. Is it similar to E.coli?
  4. What toxin does it produce?
A
  1. Negative
  2. Bloody diarrhoea
  3. Yes
  4. Shiga toxin
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47
Q

Name the following for Salmonella:

1. 3 conditions caused

A
  1. Gastroenteritis
  2. enteric fever (fever),
  3. bacteraemia
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48
Q

Name 2 more gram negative bacteria not in the enterobacteria family that are still proteobacteria

A 
Vibrio cholerae
Pseudomonas 
Haemophilus influenzae 
Legionella
Neisseria Gonorrhoeae
Helicobacter pylori
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49
Q

Name some other gram negative bacteria that are not proteobacteria

A

Chlamydia

Spirochaetae

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50
Q

Name the morphology of the four major groups (phyla) of gram negative pathogens

A

Proteobacteria - all rod shaped (bacilli)
Bacteriodes - rod shaped
Chlamydia - round (cocci)
Spirochaetes - spiral/helical

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51
Q

Why are gut pathogens (the gram negative bacteria we have covered) facultative or obligate anaerobes

A

Since gut pathogens need to survive in low oxygen environments

As such bacteriodes, endobacteria, V.cholerae and helicobacteria are anaerobic.

Most of the other pathogenic species are aerobic.

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52
Q

Name two differences between yeast and moulds

A

Yeasts are single celled - reproduced asexually

Moulds are multicelled and reproduced either sexual or asexually

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53
Q

What are the 3 forms of fungal infection

A

Skin infections - ringworm, usually mild
Mucosal infection - usually mild but a bit worse
Invasive infection - life threatening

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54
Q

Where do most fungi come from?

A

Environment, some are commensal.

There are very few known animal vectors

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55
Q

what is the determining factor to why fungi can live in humans?

A

The temperature they can survive in, since generally humans are much hotter than their natural environment

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56
Q

What is the difference between dermatophytes and saprophytes (hint skin infection).

A

Dermatophytes are fungal cells that eat keratin, whilst most fungi are saprophytes (meaning they live off dead stuff)

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57
Q

Are different genera of skin infecting fungi location specific?

A

No - they can grow anywhere.

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58
Q

Name 2 common fungal skin infections

A

Ringworm

Athletes foot

59
Q

What are the 4 major fungal pathogens causing invasive disease (in the immunocompromised)?

A
  1. Candidiasis (thrush)
  2. Aspergillosis - usually cause pulmonary problems
  3. Pneumocystis pneumonia (PCP) also caused pulmonary problems
  4. Cryptococcus - environmental, has a capsule and can cause meningitis
60
Q

In which individuals do fungal infections usually cause serious complications?

A

The immunocompromised

61
Q

Why is selectively killing fungi often more difficult than bacteria?

A

Fungi are eukaryotic, so share a lot more human features such as DNA and protein synthesis

62
Q

Name an antifungal drug that inhibits cell wall synthesis

A

Echinocandins - they have a poor bioavailability (large molecules)

63
Q

What are the 3 fungal drug targets - indicate if humans also have these

A
  1. DNA/RNA synthetis (fungi and humans)
  2. Cell wall - doesnt exist in humans
  3. The plasma membrane contains lots of ergosterol (as opposed to cholesterol in humans)
64
Q

Name 2 types of drugs that act on the cell membrane of fungal cells

A

Polyenes - e.g. amphotericin

Ergosterol synthetic pathway inhibitors - e.g. azoles, allylamines, morpholines

65
Q

What kind of drugs are fluconazole, itracanazole, voriconazole?

A

Azoles - ergosterol synthetic pathway inhibitors

66
Q

What is onchymycosis?

What is its treatment?

A

A fungal infection of the nail, caused by dermatophytes

Treatment is local amorolfine and systemic itraconazole (azole)

67
Q

Describe 5 features of mycobacteria

A

Mycobacteria are:

  1. Immobile
  2. Slow-growing
  3. Rod-shaped (bacilli)
  4. Gram poisitive bacteria
  5. They have an outer membrane and no capsules but a thick cell wall.
68
Q

Is TB a modern disease?

A

No - it is ancient. Mycobacteria are well adapted to the host.

69
Q

Name 2 problems of treating TB

A

4-9months long treatment

There are emerging antimicrobial strains (we use a combination of drugs for these)

70
Q

How is TB spread and what are the 4 stages in its cycle?

A 
TB is transmitted by aerosols (gets into lungs)
1st Primary TB
2st Latent TB 
3rd Pulmonary TB
4th TB spread beyond
71
Q

Describe the first stage of TB pathogenesis

A

Primary TB.

TB enters the lungs and bacilli settle in the apex. Granulomas form by macrophages and these migrate to the lymph nodes

72
Q

Describe the second stage of TB pathogenesis

A

Latent TB.
The cell mediated response controls the primary infection, but the CMI persists.
TB is not visual clinically but detectable on skin test.

The latent TB can cause a systemic infection when there is a failure in immunity

73
Q

Describe the third stage of TB pathogenesis

A

Pulmonary TB
This can occur immediately following primary infection or after latent reactivation.

The cell mediated immune response continues causing necrosis and caseous material coughed up.

74
Q

In the fourth TB stage, where can TB spread to?

A

Meningitis, Pleural TB, miliary TB, bone and joint TB, genitourinary TB

75
Q

Is TB technically gram positive or negative?

A

Gram positive, however we usually classify it slightly differently

76
Q

What stain do we use to stain TB (or other mycobacteria)?

A

Ziehl Neelson stain

TB are acid fast positive bacilli

77
Q

Why is TB resistant to gram stain?

A

There is a high content of lipid with myocolic acids in the cell walls.

78
Q 
Which of the following are true?
Mycobacteria are:
1. Aerobic 
2. Spore forming
3. Motile
A
  1. T
  2. F
  3. F
79
Q

What are the 2 key components in mycobacteria cell walls?

A

Mycolic acids

Lipoarabinomannan

80
Q

What are the four challenges to treating mycobacteria?

A

Slow reproduction (poor drug target)
Slow growth in humans - no symptoms
Slow growth in culture - long to diagnose
Slow response to treatment

81
Q

Can mycobacteria survive phagocytosis?

A

Yes, Mycobacteria escape the phagosome and live in the macrophage, to shelter and replicate.

To remove requires a strong CD4 response, hence HIV and TB do not go well/

82
Q

Which type of bacteria do granulomas characteristically form against?

A

Mycobacteria

83
Q

Give 2 reasons why granulomas can become unstable

A

CD4 depeletion as in HIV

Anti-TNFa therapies

84
Q

What type of bacterium is leprosy (M.leprae)

A

Mycobacterium, as such it behaves similar to TB.

85
Q

How do we detect TB (dormant)?

A

Slow growth in culture

Nucleic acid detection (PCR) - preferred

86
Q

What are the main components to a virus?

A

Can have envelop covered in glycoprotein (docks)

Capsid containing: RNA/genetic material and enzymes)

87
Q

From what is a viruses envelop derived?

A

Host plasma membrane

88
Q

What part of a virus enters the host cells?

A

Just the genome and viral enzymes (not the envelop etc.).

89
Q

Name stages to virus lifecycle

A 
Attachment to receptor
Cell entry
Host cell interaction
Assembly of virion in host cells
Release
90
Q

Name 5 different mechanisms by which viruses cause disease

A
  1. Destruction of host cells
  2. Modification of host cell
  3. Over-reactivity of the immune system
  4. Damage through proliferation
  5. Evasion of host defences
91
Q

Name some viruses which show latency?

A

Herpes viruses:

Herpes simplex 1 and 2, Epstein-Barr virus, Varicella Zoster virus.

92
Q

Describe 4 ways a virus can evade host defences at a molecular level

A
  1. Antigenic variability
  2. Prevention of host cell apoptosis
  3. Downregulation of interferon release
  4. Interferring with host cell antigen proessing pathways
93
Q

What is the difference between an antibiotic and an antimicrobial?

A

They generally mean the same thing.
Antibiotics generally refer to antibacterial (but technically mean everything) while antimicrobials can be antifungal, antiprotozoal etc.

94
Q

What is catalase in gram-positive bacteria?

A

It is an enzyme produced by bacteria that respire using oxygen, and protects them from the toxic by-products of oxygen metabolism.

95
Q

Define infectivity

A

The ability of a microorganism to become established in a host (can involve adherence and immune escape)

96
Q

Define virulence

A

A microganisms ability to cuase disease once established

97
Q

Define invasiveness

A

The capacity to penetrate mucosal surfaces to reach normally sterile sites

98
Q

What are the four stages of pathogenesis of pathogens?

A

Exposure (contact)
Adhesion
Invasion
Infection

99
Q

What are commensal microorganisms?

A

Resident flora and usually non-pathogenic but can cause disease in certain contexts

100
Q

What is a primary pathogen?

A

Always causes disease, irrespective of immunological status

101
Q

What is an opportunistic infection?

A

Only arises if host immune status is altered

102
Q

Describe the humoral and cell mediated responses to viruses

A

Humoral - IgM opsonises and agglutinates toxins, activates complement and ADCC
CMI - main response, mainly mediated through cytotoxic T cells and IFN

103
Q

How can viruses evade the immune system?

A

Change coat antigens/show antigenic variation
Can cause immune suppression
Can inhibit complement pathway

104
Q

Describe the difference between antigenic drift and antigenic shift?

A

Antigenic drift is sponatenous but there is only a slight change in antigens, antigenic drift is a sudden emergence of a new subtype.

105
Q

What is a zoonotic disease?

A

Spreads between animals and people

106
Q

What is the general/main immune response for intracellular and extracellular bacteria?

A

Extracellular bacteria - antibody response

Intracellular bacteria - cellular response

107
Q

What are bactieral adhesins?

A

Structures/proteins on bacterial cells which help them bind to mucosal surfaces.

108
Q

Name 3 types of adhesins

A

Fimbriae or pili
Lipid
Glycosaminoglycans

109
Q

What is a bacterial biofilm?

A

Where bacteria transition from planktonic into biofilm phase, working together to secrete an extracellular polymeric substance protein.
This protects against antimicrobials

110
Q

Name some ways bacteria can evade the host

A 
Secrete proteases that lyse IgA
Antigenic variation
Polysaccharide capsule
Express coagulase - makes clots
Mycobacteria can escape phagolysosome
111
Q

How do worms evade the host?

A

Stimulate Tregs
Decreased antigen expression (shielding)
Glycolipid/glycoprotein coat is host derived.

112
Q

Can chronic inflammation cause cancer?

A

Yes

113
Q

What are protozoa?

A

Unicellular eukaryotes, free living or parasitic.

114
Q

What are the 5 types of protozoa?

A 
Flagellates
Amoebae
Microsporidia
Sporozoa
Ciliates
115
Q

Do protozoa often colonise the gut in humans?

A

Yes

116
Q

Describe Trypanosoma

what microbe, what it causes

A

A flagellate protozoa, either causing african (sleeping sickness) or american trypanosomiasis (chagas disease)

Symptoms for both include fever, lethary, lymphadenopathy

117
Q

What type of protozoa is malaria?

A

Sporozoa, it is a plasmodium

118
Q

Describe the liver stage (exo-erythrocytic cycle) of malaria

A
  1. Infected mosquito injects sporozoites into human
  2. These travel to and infect the liver as Shizonts.
  3. They replicate in hepatocytes and eventually are released into the blood.

Some types of malaria can remain dormant in the live cause a relapse weeks to years later

119
Q

Describe the blood stage (erythrocytic cycle) of malaria

A
  1. Merozoites are released into the blood where they infect RBCs
  2. These then mature into “ring stage” trophozoiotes.
  3. These mature to Schizonts which rupture from the cell releasing more merozoites
120
Q

Describe the third (vector) stage of malaria

A
  1. A mosquito takes a blood meal of an infected persons blood, ingesting gametocytes
  2. These fuse into an oocyst which ruptures releasing sporozoites (takes around 9 days)
  3. Mosquito is now infected and can infect someone else.
121
Q

What are the symptoms of malaria and why do we get them?

A

Fever, flu-like, headache, muscle aches, headache, fatigue, spleno/hepatomegaly.

This is because infected cells lyse releasing merosites and other toxins which stimulates the immune system to cause inflammation

122
Q

With regard to malaria, what is cytoadherance, Rosetting and sequestration

A

Cytoadherence - infected RBCs display different membrane proteins which adhere to vascular endothelium
Rosetting - RBCs doing cytoadherence also stick to other blood cells
Sequestration - protozoa can get into major organs and hide from the immune system

123
Q

Name some of the complications of malaria

A
  1. Haematological changes - anaemia, Jaundice
  2. Cerebral malaria - vascular occlusion and hypoglycaemia
  3. Renail failure - due to vascular occulsion and hypotension
  4. ARDS - increased vascular permeability
  5. Bleeding - due to thrombocytopaenia
124
Q

How do you diagnose malaria?

A

Thick and thin blood films

125
Q

How do you treat malaria?

A

IV Artesunate (or quinine)

Treat complications depending on patient and system invovled

126
Q

With malaria, what types of immune response do the blood stage and the tissue stage elicit?

A

Blood stage - humoral immunity

Tissue stage - cell mediated immunity

127
Q

How do protozoa evade the host immune system?

A

Surface antigen variation (VSG switching)
Intracellular phase
Outer coat sloughing

128
Q

Describe the 3 stages of HIV from first infection to AIDS

A
  1. Acute primary infection (acute seroconversion illness). The immune response struggles so CD4 count drops and viral load peaks
  2. Asymptomatic phase - immune system take hold, but declines (latency) over years as CD4 decreases and viral load increases
  3. AIDS - CD4<200
129
Q

What is normal CD4 count?

A

500-1500

130
Q

When do we classify CD4 count as low (we have picked up the virus “late”)?

A

<350

131
Q

What is AIDS?

A

Essentially just a list of conditions that a patient will only get if they have AIDS, including infections and neoplasms.

132
Q

What is the differential diagnosis to acute primary HIV infection?

A

Secondary syphilis

133
Q

What are some symptoms of acute HIV infection?

How long do they last?

A

Symptoms are largely non-specific: Fever, sweats, rash, lethargy, myalgia, diarrhoea, sore throat with no tonsilar enlargement

Symptoms usually last 2 weeks

134
Q

What laboratory test can confirm acute HIV diagnosis?

When are antibodies established?

A

P24 test (P24 is an HIV antigen and we can detect antibodies)

Around 4-10weeks

135
Q

What is the only symptom you usually get while HIV is in teh clinical latent phase?

A

PGL - persistent generalised lymphadenopathy

136
Q

Name the most common infection seen in AIDS

A

PCP - pneumocystis pneumonia

An infection caused by the fungus Pneumocystis jirovecii.

137
Q

What is HAART?

A

High activate anti-retroviral therapy - where drugs inhibit reverse transcriptase enzymes and proteases

138
Q

Does HIV have RNA or DNA?

A

RNA, as such to infect they need reverse transcriptase to turn it into DNA

139
Q

Describe in steps, the lifecycle of HIV

A
  1. HIV recognises CD4 receptor using glycoproteins and fuses
  2. In the cell, the capsid releases viral RNA and enzymes
  3. Reverse transcriptase turns the viral RNA into DNA and integrase splices this into the host cells genome
  4. When host replicates or translates it does the same to the virus, make new virus
  5. Viral proteases help chop up the amino acid sequences to make the capsid for the virus
  6. Virus matures and buds of, taking host cell membrane to make an envelop
140
Q

What are the 2 receptors on a Th cell needed to bind to the HIV glycoprotein (gp120)?

A

CD4
A coreceptor called CCR5

A genetic mutation can lead to no CCR5 making some people immune to HIV

141
Q

Why does HIV show genomic variability?

A

Reverse transcriptase is error prone

142
Q

Is the immune response good against HIV?

A

It is very large, but there is no demonstratable protective immunity

143
Q

What bacteria are in the mnemonic “Sexy Students Can Look Bad Come morning”?

A 
Gram positives
S - staphylococci 
S - streptococci 
C - corynebacterium
L - listeria 
B - bacilli 
C - clostridium
144
Q

What bacteria are in the mnemonic “Huge vaginas Can Not Provide Sexy Sex SHLCK”?

A 
Gram negatives
H - Helicobacteria
V - vibrio (cholerae)
C - coliforms
N - Neisseria 
P - Pseudomonas 
S - shigella 
S - salmonella 
S - Spirochaetes 
H - Haemophilus 
L - Legionella
C - Chlamydia 
K - Klebsiella

Jack 2a (8 decks)

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