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Molecules, Cells and Diseases (MCD) and Epidemiology in Practice (EiP) > Microbiology > Flashcards

Microbiology Flashcards

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Organic Chemistry 101 flashcards
1
Q

What are the small spherical bacteria called?

What are the rod shaped ones called?

A

Cocci

Bacilli

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2
Q

What is present sticking out of the outer membrane of gram negative bacteria’s cell walls?

A

LPS; lipopolysaccharide.

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3
Q

What is function of a) the flagellum and b) the injectisome

A

Flagellum = locomotion. Injectisome = transfer of virulence proteins into the host cell.

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4
Q

How does salmonella invade a cell?

A

Injects proteins into the host cell by injectisome. The proteins induce actin polymerisation, driving membrane ruffling and allowing bacterial invasion.

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5
Q

What is transformation

A

Uptake of free DNA and integration into circular DNA.

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6
Q

Describe conjugation.

A

A mating bridge is established between 2 bacteria. A plasmid joins: each cell has a plasmid with one original strand and one newly synthesised strand.

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7
Q

Describe phage transduction

A

Phage replicates its DNA and cuts up bacteria DNA. Some bacterial DNA may be packaged in phage heads. Phage injects bacterial DNA into another bacterial cell.

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8
Q

Which two factors affect pathogenicity?

A

Virulence and infectivity.

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9
Q

Name some gram negative bacteria.

A

Neisseria (meningitidis and gonorrhoeae), haemophilus influenza, vibrio cholerae.

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10
Q

Name some gram positive bacteria.

A

Staphylococcus aureus, streptococcus, Listeria.

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11
Q

How are viruses classified?

A

How their genome is stored (RNA, DNA, negative sense RNA etc).

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12
Q

What is iatrogenic transmission?

A

HCW infects patient e.g. contaminated needles

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13
Q

What is nosocomial transmission?

A

Infections acquired in hospital

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14
Q

What is vertical transmission?

A

Infection passed from mother to baby in period before and after birth.

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15
Q

Give three concepts which define tropism.

A

Receptor interactions - SUSCEPTIBILITY
Ability to use host cell to complete replication - PERMISSIVITY
Whether the virus can reach the tissue - ACCESSIBILITY.

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16
Q

Define prophylaxis.

A

Preventing disease before the aetiological agent is acquired (vaccination or drugs given before infection).

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17
Q

What is therapy?

A

Treating the disease after the host became infected.

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18
Q

How are viruses attenuated?

A

Isolated and grown in human cultured cells. Cultured virus used to infect monkeys. Acquires mutations allowing replication in monkey cells. Virus no longer replicates well in human cells.

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19
Q

Evaluate live vaccinations.

A

Rapid, broad, long-lived immunity. Dose sparing. Cellular immunity.
Requires attenuation: the pathogen may revert.

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20
Q

Evaluate inactivated vaccines.

A

Safe

Frequent boosting required and high doses needed.

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21
Q

What is passive immunisation?

A

A type of therapy involving giving an infected patient antibodies against the pathogen.

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22
Q

Give an example of an enzyme expressed by resistant bacteria which degrades or alters an antibiotic to render it ineffective.

A

Beta-lactamase.

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23
Q

How can antibiotic resistance arise?

A

1 – altered target site
2 – inactivation of antibiotic
3 – altered metabolism
4 – decreased drug accumulation

24
Q

How can drug accumulation be decreased by bacteria?

A

Reduced penetrance of AB into cell or increased efflux.

25
Q

Name 3 sources of AB resistance genes.

A 
Plasmids
Transposons (integrate into chromosomal DNA)
Naked DNA (DNA from dead bacteria released into environment).
26
Q

Why is there a strong selective pressure for AB resistance in hospitals?

A

Large numbers of infected people receiving high doses of ABs.

27
Q

How can we address AB resistance?

A

Tighter prescription control, temporary removal of certain classes.
Use only for serious cases.
Combination therapy.

28
Q

What makes an ideal vaccine?

A

Stimulates an effective immune response.
Safe
Inexpensive to manufacture and distribute.
Stable (e.g. in heat).
Easy to administer
Simple for both manufacturer and regulatory authorities to control.

29
Q

What is the equation for vaccine efficacy?

A

1 - (Attack rate in vaccinated group)/(attack rate in unvaccinated group).
((Usually expressed as a percentage)).

30
Q

What is the equation for herd effect?

A

1 - (Attack rate in unvaccinated post introduction)/(attack rate in unvaccinated pre introduction).

31
Q

What do adjuvants do?

A

Enhance and modulate the immune response (they may deliver the antigen).

32
Q

What is the role of excipients in a vaccine?

A

Maintain pH, osmolarity and stability of vaccine, for example may use buffers, salts or proteins.

33
Q

Why do we use acellular pertussis in the DTaP-Hib-IPV vaccine?

A

While the whole cell version is effective (efficacy > 90%), it is associated with adverse effects.

34
Q

Why are polysaccharides bad antigens?

A

They are not readily degraded and have poor memory effect. They are low avidity (functional affinity).

35
Q

What is a conjugate vaccine?

A

One where the antigenic carbohydrate is linked to an immunogenic protein. The vaccine is expensive to produce but leads to long-lived, boostable immunity.

36
Q

What is mycotoxicosis?

A

A toxic reaction due to ingestion or inhalation of a mycotoxin, which are secondary metabolites of moulds which exert toxic effects on animals and humans.

37
Q

What is a superficial mycosis?

A

Where the fungus infects the skin or hair shaft, hence no living tissue is invaded so there is no immune response from the host.

38
Q

What are cutaneous mycoses?

A

The fungi produce extracellular enzymes (keratinases) which hydrolyse keratin. Inflammation is caused by the host response to metabolic by-products.

39
Q

What is the difference between primary and opportunistic fungi?

A

Primary fungi are able to establish infection in a normal, healthy host: opportunistic fungi require a compromised host in order to establish infection.

40
Q

What are the four targets of antifungals?

A

1) Membrane Function
2) Nucleic Acid Synthesis
3) Cell Wall Synthesis
4) Membrane ergosterol biosynthesis

41
Q

What is the optimum pH for lysozyme?

A

5: Asp 52 is ionised and Glu 35 is unionised, allowing lysis of bacterial cell walls.

42
Q

How does acyclovir work?

A

It is a substrate for viral thymidine kinase - which converts it to acyclo-GMP. This is converted to acyclo-GTP. This is an excellent substrate for viral DNA polymerase. Once incorporated, it blocks polymerisation of viral DNA as it has no 3’ OH group available for the next phosphate bond.

43
Q

Give the names and MOAs of major antifungals

A

Azoles: target cell membrane
Pyridine analogues: target DNA synthesis
Echinocandins: target cell wall

44
Q

Summarise the technique of gram staining

A

Violet dye + iodine
Alcohol rinse
Red dye

45
Q

Describe the course of an acute viral infection.

A

Infection, followed by response of the organism and quick and complete resolution of the infection.
FLU, ROTAVIRUS

46
Q

Describe how HSV causes a latent reactivating infection.

A

HSV hides in ganglions and re-emerges when there is reduced immune response and is able to re-establish itself.

47
Q

Give some extracellular bacteria

A

Staphylococcus
Streptococcus
Yersinia
Neisseria

48
Q

What are the 3 ways bacteria survive in a host cell, and give examples of each?

A

Escape - listeria, shigella.
Prevent fusion with lysosomes - Salmonella, mycobacteria
Survive in phagolysosome - coxiella

49
Q

What is the breakpoint?

A

The concentration of antibiotic that can be achieved in a clinical setting.
If a bacteria can divide at a concentration at or higher than the breakpoint it is deemed resistant.

50
Q

What are the 2 main phyla of fungi?

A

Ascomycota, Basidiomycota.

51
Q

What is the purpose of neuraminidase production by influenza?

A

Neuraminidase destroys sialic acid on the surface of host cells, so it doesn’t infect the same cell twice.

52
Q

What do adamantes (rimantadine and amantadine) do?

A

They block the M2 channel, prevent H+ influx. This means influenza is locked in its protein shell, as the purpose of acidosis is to break the bonds of the protein capsid of influenza.

53
Q

Define the tropism of HIV in terms of susceptibility.

A

Needs CD4 and CCR5 or CXCR4 receptor and gp120 viral attachment protein. As such, binds to T-helper cells.

54
Q

What is zanamivir?

A

A drug which is a neuraminidase inhibitor, preventing the spread of influenza as the assembled viruses can’t exit the cell.

55
Q

What are acid-fast bacteria?

A

Bacteria resistant to the Gram staining method and are thus stained using the acid-fast staining method.

56
Q

Give an example of each of the different types of vaccines.

A

Live attenuated: Sabin polio, smallpox, rubella
Inactivated: Salk polio, influenza
Cloned subunit: HPV, Hep B, acellular pertussis
Toxoid: diphtheria and tetanus
Conjugate: Hib (haemophilus influenza b)

57
Q

What is HAART?

A

Highly-active anti-retroviral therapy.
A combination of drugs are used, so even if HIV develops resistance against one, another drug is still able to prevent replication / protein synthesis.

Molecules, Cells and Diseases (MCD) and Epidemiology in Practice (EiP) (9 decks)

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