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Microbes > Module 7 - Epidemiology, Antibiotics and Antibiotic Resistance > Flashcards

Module 7 - Epidemiology, Antibiotics and Antibiotic Resistance Flashcards

1
Q

Distinguish between Endemic, Epidemic and Pandemic disease

A

Endemic = Constantly present, low level frequency of disease at regular intervals
Epidemic = Sudden increase above expected level, each individual infects more than 1 other susceptible host
Pandemic = simultaneous increase over wide/global area

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2
Q

Name the disease that is responsible for the amphibian decline, and what kind of outbreak/disease is this?

A

Chytridiomycosis (panzootic -> animal pandemic)

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3
Q

Name 6 pandemic plant diseases

A

Maize Lethal Necrosis
Rice tungro
Sweet potato virus
Banana bunchy top
Citrus Tristeza Virus
Plum Pox

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4
Q

Name the two parameters for measuring disease rate (and define these)

A

Morbidity rate -> number of individuals becoming ill
Mortality rate -> rate of death from disease

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5
Q

What number is sometimes used as the threshold to define epidemics?

A

400 cases per 100,000 population per week

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6
Q

What are the two types of epidemics? (And define them)

A

Common source epidemic -> sharp rise to a peak and rapid decline (e.g., food poisoning)
Propagated epidemic -> slow rise and gradual decline

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7
Q

Approximately what percentage of population immunity is required to prevent the spread of measles, flu and polio respectively?

A

Measles: 90-95%
Flu: 90%
Polio: 70%

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8
Q

What is the approximate susceptible population size required to sustain measles in a community?

A

250,000 - 300,000

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9
Q

What are the two main sources of change in organisms that can render immunity ineffective?

A

Antigenic drift and antigenic SHIFT

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10
Q

Define antigenic drift

A

Minor antigenic variation -> Haemagglutanin or Neuraminidase can change due to genetic mutations altering amino acid sequences

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11
Q

Define Antigenic Shift

A

More significant antigenic variation -> reassortment of segments of genome due to gene exchange between strains

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12
Q

What four main things do epidemiologists investigate to understand disease?

A

The pathogen
The source of the pathogen
Reservoirs and Carriers
Transmission of Pathogens (e.g., airborne/contact/vector)

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13
Q

What are the three main types of disease control measure?

A

Eliminate source
Break connection between source and host
Raise level of herd immunity (vaccinate)

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14
Q

What genus of virus causes Zika (also genome type)

A

Flavivirus (ssRNA)

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15
Q

How is Zika virus transmitted?

A

Mosquito, Sexually, Blood Transfusion, in utero

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16
Q

What are some of the main factors responsible for emergence of new pathogens and re-emergence of known pathogens?

A

Demographics (e.g., cities)
Transportation (^ speed of spread)
Economic development + Changes in Land Use
International Travel
Microbial Adaptation
Biological Warfare
Breakdown of Public Health Measures

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17
Q

Name the organism that causes the Black Death

A

Yersinia pestis

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18
Q

Who first proposed the idea of antibiotics (and approx when)?

A

Paul Ehrlich - 1900s

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19
Q

Summarise the ideas proposed by Paul Ehrlich

A

That antibiotics could kill the target pathogen but leave the host unharmed (selective toxicity), and target structures and processes which are unique to humans

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20
Q

What was the first dye with antibiotic activity discovered by Ehrlich, and which disease + microbe did it target?

A

Salvarsan (containing Arsenic) -> targeted Syphilis + Treponema pallidum

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21
Q

What was the first antibiotic species to be discovered?

A

Penicillium (penicillin)

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22
Q

What was the first sulphonamide/first commercially available antibiotic?

A

Prontosil

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23
Q

Name (and give examples for) the four main types of antibiotic

A
  1. Cell Wall Synthesis Inhibitors (e.g., penicillin)
  2. Protein Synthesis Inhibitors (e.g., aminoglycosides + macrolides)
  3. Nucleic Acid Synthesis inhibitors (e.g., quinolones)
  4. Folic Acid Biosynthesis (e.g., sulphonamides)
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24
Q

Name the two types of effects of antibiotics on bacterial growth

A

Bacteriostatic (prevents growth) and Bactericidal (kills bacteria)

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25
Q

What is the structure found in Cell Wall Synthesis Inhibitor antibiotics, and what molecule does it prevent from being synthesised?

A

ß-lactam -> inhibits Peptidoglycan biosynthesis

26
Q

What types of bacteria is Penicillin active against?

A

Gram-positives, e.g., pneumococci, streptococci (does not penetrate Gram-negative outer membrane)

27
Q

How must Penicillin be administered, and why?

A

Via injection - it is destroyed by gastric pH

28
Q

How does ß-lactam inhibit Peptidoglycan synthesis?

A

ß-lactam structure mimics D-Ala-D-Ala at end of peptide, so can bind to carboxypeptidase instead of D-Ala-D-Ala

29
Q

How can semi-synthetic Penicillins be made to target Gram-negative bacteria (and name two examples)?

A

Modification of R1 group by adding hydrophillic NH2 side group allows the antibiotic to pass through outer membrane pores of Gram-negatives (e.g., amoxycilin and ampicillin)

30
Q

What enzyme gives some bacteria penicillin resistance, and what are the two main solutions?

A

ß-lactamases hydrolyse the ß-lactam ring.
1. Combine with clavulanic acid, a ß-lactamase inhibitor
2. Synthesise ß-lactamase resistant penicillins, e.g., methicillin

31
Q

What are carbapenems and what do they do?

A

They are ß-lactamase inhibitors, which acylate penicillin binding proteins. They are used to treat penicillin-resistant (i.e. ß-lactamase producing) bacteria

32
Q

How must carbapenems be administered and why?

A

Intravenously/intramuscularly - they cannot cross the gastrointestinal membrane

33
Q

What are the two main types of carbapenem resistance?

A
  1. Enzymes which hydrolyse the ß-lactam ring (3 classes)
  2. Mutations that reduce influx or increase efflux of the drug
34
Q

Which gene allows Methicillin Resistance in MRSA (and how)?

A

mecA - it encodes penicillin binding protein 2A (which has low affinity for ß-lactam antibiotics and does not bind to them)

35
Q

What does vancomycin do and what is its role as an antibiotic?

A

It inhibits cell wall synthesis in Gram-positives by binding to D-ALA-D-ALA INSTEAD OF CARBOXYPEPTIDASE;
it is used as a drug of last resort to treat MRSA

36
Q

Name the microbe that produces vancomycin

A

Amycolatopsis orientalis

37
Q

How do some bacteria develop resistance to vancomycin?

A

Modification of D-Ala-D-Ala target by exchanging terminal D-Ala for L-serine or D-lactate

38
Q

Name the three main types of Protein Synthesis Inhibitor antibiotics; and provide three examples of the first type

A

Aminoglycosides (e.g., kanamycin, gentamycin, streptomycin), Tetracyclines, Macrolides

39
Q

What do Aminoglycosides do and how must they be administered?

A

They bind to 30S in aerobic bacteria, preventing 50S from joining; they also create fissures in the outer membrane (enhanced antibiotic uptake).
They must be administered intramuscularly/intravenously as they cannot be absorbed through the gut

40
Q

What do tetracyclines do?

A

They are broad spectrum and they bind to the 30S -> notably, they can penetrate macrophages for intracellular infections

41
Q

What do macrolides do (and name one example)?

A

Macrolides (e.g., erythromycin) bind to the 50S in Gram-positives, and prevent incoming tRNAs + Amino Acids from binding to nascent polypeptide chain

42
Q

Name the major group of Nucleic Acid Synthesis inhibitors (and one example)

A

Fluoroquinolones (e.g., ciproflaxin)

43
Q

What do fluoroquinolones (e.g., ciproflaxin) do?

A

They bind to - and inhibit - DNA gyrase, preventing it from supercoiling DNA. Thus, they inhibit DNA replication

44
Q

What are the two main groups of antimetabolite antibiotics (and what process do they both target)?

A

Sulphonamides and Trimethoprim (usually used in combination) -> Folic Acid Synthesis!

45
Q

What do sulphonamides do?

A

They are antimetabolites: competitive inhibitors of dihydropeterate synthase (which is required for Folate Synthesis)

46
Q

What does Trimethoprim do?

A

Inhibits dihydrofolate reductase (which is required for Folate Synthesis)

47
Q

Name the antibiotic discovered in 2015 (mentioned), what does it essentially do, and what types of bacteria does it target?

A

Teixobactin:
- it inhibits peptidoglycan biosynthesis
-in Gram-positives

48
Q

What does Teixobactin do?

A

It binds to and forms ß-sheets, then fibrilliar oligomers, with Lipid II (a peptidoglycan precursor), thus obstructing peptidoglycan synthesis

49
Q

Name two recently discovered antibiotics besides Teixobactin

A

Malacidin (similar to Teixobactin) and retinoids (kills MRSA)

50
Q

Name the bacteria that causes serious food poisoning and has poultry as its reservoir (NOT salmonella)

A

Campylobacter jejuni (gram-negative motile spirillium) -> especially cipR strains

51
Q

Which type of antibiotic was commonly used PROPHYLACTICALLY in chickens for over 20 years?

A

Fluoroquinolones (e.g., ciprofloxacin)

52
Q

Name the (first?) multi-resistant strain of bacteria that emerged in 1998

A

Salmonella typhimurium DT104 (resistant to 6 antibiotics)

53
Q

Name the (mentioned) species of penicillin-resistant penumococci

A

Streptococcus pneumoniae

54
Q

Name the (mentioned) species of multidrug-resistant mycobacteria

A

Mycobacterium tuberculosis

55
Q

Name the (mentioned) species of methicillin-resistant bacteria that is only sensitive to vancomycin

A

Staphylococcus aureus

56
Q

Name the commensal that has become resistant to Vancomycin (species and “other” name)

A

Enterococcus faecalis: vancomycin-resistant enterococci (VRE)

57
Q

What two reasons can a bacterium have INNATE/NATURAL/INTRINSIC resistance? (And one key example)

A

Lack of target structure; or impermeable to antibiotic (e.g., mycoplasma pneumoniae lack peptidoglycan)

58
Q

What are the three main mechanisms for acquired antibiotic resistance?

A
  1. Enzymatic inactivation of antibiotic
  2. Modification of target
  3. Efflux of antibiotic
59
Q

Name the three mechanisms for transfer of resistance genes (and which ones are narrow/broad host range)

A
  1. Transduction via bacteriophage (narrow)
  2. Transformation via naked DNA (narrow)
  3. Conjugation (broad - between different genera)
60
Q

What is the mechanism for resistance to Aminoglycosides (e.g., streptomycin)?

A

Enzymes inactivate the antibiotic by adding groups (e.g., acetyl, adenyl), reducing transport into cell

61
Q

What is the mechanism for resistance to tetracycline?

A

Active efflux - cytoplasmic membrane proteins catalyse transport of Tet out of the cell

Microbes (7 decks)

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