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Flashcards

Antibiotic Resistance

Adrianna Bialecka Microbiology University English 100 cards

How do bacteria metabolize folate?

Cards in this deck (100)

  1. 1What mostly kills the western world?Tuberculosis 18%
    Pneumonia/Influenza 18%
    Gastrointestinal infections: 13%
    Diphtheria: 4%
    53% of all deaths dues to infectious diseases
  2. 2What were diseases blamed on in the old ages?blamed on bad air, wrath of god, devil, witchcraft, minority groups, astronomical events etc
  3. 3What were the cures for disease in the old days?Included prayer, magic potions, amulets, blood letting, burning people, secret rituals
  4. 4What are diseases blamed on in the 21st century?blamed on wrath of god, devil, minority groups, energy and other imbalances, broken aura
  5. 5What are the cures in the 21st century?Include homeopathy, faith healing, prayer, crystal healing, chiropractic, reiki magnet therapy, chakra clearing, aura healing, chromotherapy
  6. 6Where does disease come from?-Miasma theory was dominant
    -Diseases such as cholera, the plague and tuberculosis caused a poisonous mist contaminating the air
    -Arises from decaying organic matter
    -Not passed on between individuals, but affecting individuals in an area filled with bad air
    -Florence Nightingale was a proponent of the miasma theory
  7. 7What did Robert Koch do?Microbiologists in the 19th century linked disease commonly associated with water to the presence of pathogenic microorganisms
  8. 8What did John Snow do?Distribution of pathogenic microorganisms usually associated with poor quality of drinking water
  9. 9What did Louis Pasteur do?In western world: no water purification until early 20th century
  10. 10Why is waste water treatment essential?The Thames in London was an open sewer, leading to frequent cholera outbreaks
    -Linked to amongst other contaminated drinking water
    -Bazalgette builds the London sewerage system
  11. 11What is the importance of drinking water treatment?-Incidence of typhoid fever in Philadelphia
    -Filtration of water reduction in particles and associated microbes
    -Chlorination of water as effective disinfectant introduced in 1913
    -Provision of clean drinking water has had major impact on public health and thus life expectancy
  12. 12Why was 16% of all deaths in 19th century Britain due to consumption or pulmonary tuberculosis?-Until the early/mid-twentieth century infectious diseases were not curable
    -This is unthinkable for most of us now: Leprae, Syphilis, Gonorrhea, Tuberculosis- Pneumonia, Meningitis Plague were untreatable
  13. 13What is a chemotherapeutic agent?Antimicrobial agents that can be used internally
  14. 14What is the key to a successful chemotherapeutic agent is?Selective Toxicity
    -The Magic Bullet
    -Drugs that inhibit or kill the microorganism, but do not harm the host. This is based on difference in biochemistry and biology between pathogen and host
  15. 15What are some common targets?Cytoplasmic membrane: Bacteria do not have sterols, fungi have ergosterols, mammalian cells have cholesterol
    Cellular metabolism: Differences in biochemical pathways
    Chromosome function: Differences in DNA replication transcription between Bacteria and Eukarya
    Bacterial cell wall: Mammalian cells do no have a peptidoglycan layer
    Protein Synthesis: Bacteria and Eukarya have different ribosomes
  16. 16Why are bacteria the most available of magic bullets while fungi and viruses are less available?-Bacteria are the most different from the mammalian host in terms of metabolism, cell structure, DNA replication and protein synthesis
    -Viral pathogens make use of the hosts metabolic and replication machinery
  17. 17What are growth factors?Specific compounds that are required in the growth medium because the organism can not synthesize it itself
  18. 18What are growth factor analogs?Compounds that mimic growth factors, but can not be used by the microbes
  19. 19How do growth factor analogs kill or inhibit microorganisms?-Inactivation of enzymes
    -Incorporation in biosynthetic pathway leads to formation of dead-end products or toxic intermediates
    -Disruption of cellular regulation (e.g. quorum sensing inhibitors)
  20. 20What was the first discovered growth factor analog?Arsphenamine by Sahachiro Hata in the lab of Paul Ehrlich as a cure of syphilis in 1909
  21. 21How do bacteria metabolize folate?-Bacteria are unable to take up and utilize exogenous folate and synthesize it themselves
    -They need the enzyme Dihydropteroate synthase do metabolize it into Dihydrofolate.
    -Sulfonamides inhibit the bacterial enzyme dihydropteroate synthase, preventing the formation of folate    How do bacteria metabolize folate?
  22. 22What causes the Elixir sulfanilamide disaster 1937?Toxic solvent: diethylene glycol killing over 100 people
    -caused the enactment of the 1938 Federal Food, Drug, and cosmetic Act, basis of current FDA regulations- toxicology testing
  23. 23What did Alexander Fleming do?he noticed that a contaminating fungus kills Staphylococcus aureus colonies on an agar plate
    -Penicillium produces a secreted antimicrobial compound: Penicillin
  24. 24What did Howard Florey and Ernst Boris Chain do?worked out how to mass produce and purify penicillin (1940)
  25. 25What is the strict definition of antibiotics?Chemical substances produced by microorganisms that inhibit or kill other microorganisms
  26. 26What is the modern definition of antibiotics?Substance produced by microorganisms, or similar substance produced wholly or partially by chemical synthesis, which in low concentrations inhibit the growth of other microorganisms
  27. 27Why do microbes produce antibiotics?to gain a competitive advantage while competing for nutrients in soil
  28. 28Example of how antibiotics and growth factor analogs can be broad or narrow spectrum?Isoniazid is effective against M. tuberculosis and some other Mycobacteria
    Tetracycline is effective against most bacteria
  29. 29What is the broad spectrum?comprehensive treatment when infectious agent is unknown
  30. 30What is the narrow spectrum?only targets a select group while leaving the normal bacteria flora intact
  31. 31What is an example of Antibiotic resistance?e.g. against Mycobacterium tuberculosis
    First line drugs: isoniazid, rifampin (treatment takes 6 months)
    -Multi Drug Resistant (MDR) M tuberculosis resistant to isoniazid and rifampin
    -Treatment with second line drugs 100x more expensive, takes 2 years
    -Extensive Drug Resistant (XDR) M tuberculosis resistant to at least three of the size second line drugs as well
  32. 32What are the two types of resistances?Inherent or acquired
  33. 33What are the mechanisms of resistance in bacteria?-Lack of the structure the antibiotic inhibits
    -Impermeable to the antibiotic
    -Antibiotic is pumped out
    -Alteration of the antibiotic to an inactive form
    -Modification of the target of the antibiotic
    -Modification of the metabolic pathways inhibited by the antibiotic    What are the mechanisms of resistance in bacteria?
  34. 34What is the mechanism of resistance bacteria use against tetracyclin?-Sub inhibitory concentration of tetracycline induce an effux system which counteracts the influx of tetracycline in the cell
    -The cell will survive as long as it can pump tetracycline out faster than it comes in    What is the mechanism of resistance bacteria use against tetracyclin?
  35. 35How do beta-lactamases do?hydrolyse the betalactam ring of betalactam antibiotics such as penicillinHow do beta-lactamases do?
  36. 36What are some other ways of altering an antibiotic to inactive form?Acetylation e.g. chlorampenicol, aminoglycoside antibiotics
    Adenylation e.g. amino glycoside antibiotics
    Phosphorylation e.g. amino glycoside antibiotics
  37. 37What are spontaneous mutations?-usually point mutations altering the genetic code: 1 amino acid change at a timeWhat are spontaneous mutations?
  38. 38How do these spontaneous mutations give bacteria resistance?Usually many mutations are required to achieve full resistance. The chances of this happening is very small
    BUT selection of pre-existing mutants or selection for antibiotics resistance markers on mobile genetic elements is a problem    How do these spontaneous mutations give bacteria resistance?
  39. 39How does genetic transfer happen?Functional systems conferring antibiotic resistance are transferred by:
    -transformation
    -transudction
    -conjugation
  40. 40How do these resistant strains arise?due to
    -overusage in humans
    -Prophylactic use in humans and animals
    -Incomplete therapies
  41. 41What is lateral transduction?-discovered in 2018
    -Phage particles package hundreds of kilobases of bacterial DNA at very high frequency
    -Extremely high rates of lateral gene transfer, including virulence genes and antimicrobial resistance genes    What is lateral transduction?
  42. 42What is One health?human, animals and environmental health are interlinked
    -zoonoses
    -food safety
    -Antibiotic resistance
  43. 43Antibiotic use in agriculture selects for antimicrobial resistanceAntibiotic use in agriculture selects for antimicrobial resistance
  44. 44Antibiotic use in people selects for antimicrobial resistanceAntibiotic use in people selects for antimicrobial resistance
  45. 45How does antimicrobial resistant genes into the environment and in urban populations?How does antimicrobial resistant genes into the environment and in urban populations?
  46. 46Mentagenome water concentration how it works?Mentagenome water concentration how it works?
  47. 47How does agricultural and urban activities drive changes in the resistome of riverine systems?How does agricultural and urban activities drive changes in the resistome of riverine systems?
  48. 48How are UK coastal water users exposed to a colonisation by antibiotic-resistant E. coli?How are UK coastal water users exposed to a colonisation by antibiotic-resistant E. coli?
  49. 49What result do complete therapies have?-following uptake of the antibiotic the concentration in tissues exceeds that what is required to eliminate the pathogen
    -Regular use of antibiotic is required to keep high antibiotic levels    What result do complete therapies have?
  50. 50What result to incomplete therapies show?When the antibiotic drops below the threshold concentration bacterial numbers will increase
    -selection on resistant bacteria
    -spread of resistance markers    What result to incomplete therapies show?
  51. 51What is Directly Observed Therapy?a healthcare worker meets with a person who has TB to help him or her remember to take the medicines to treat TB
    -free TB medication
    -free tokens, food, and gift certificates to fast food restaurants
    -free social services
    -frequent medical checkups
    -help with transportation to and from clinics
    DOT is not just to help those who cant help themselves, either due to forgetfulness, homelessness, no health insurance
    -TB is highly contagious and without DOT the disease and multidrug resistant strains will spread
  52. 52What will happen if we don't start using antibiotics correctly?Only one new group of antibiotics discovered in 30 years
    -the way we are going now is that infectious diseases will again be largely untreatable
    -Urgent action/investment is required
  53. 53What did people think disease came from in the late 19th century?the Miasma (bad air) theory was dominant
  54. 54What was the first example of biological warfare?Siege of Caffa by the Mongols (1346)
    -Intolerable stench would kill everyone inside = MIASMA theory
  55. 55What is the origins of microbiology?-In 1665 Robert Hooke publishes his Micrographia
    -Study of insects, plants and molds
    -Cell was used for the first time to describe the composition of cork
    -First to describe a microorganism: fruiting bodies of moulds
  56. 56Who was the first person to observe bacteria?Antonie van Leeuwenhoek
  57. 57What was the downfall of Spontaneous generation and bad air (Miasma theory)What was the downfall of Spontaneous generation and bad air (Miasma theory)
  58. 58What did Robert Koch do?Development of techniques to grow bacteria on a solid surface
    -Koch noticed the growth of colonies each with their own characteristics
    -These could be grown in "pure cultures"
    -Analysis of the properties of individual bacterial species was now possible
  59. 59How bacteria survived in guts of insects?Isolation of living Bacillus sp from guts of insects trapped in amber 20-45 million years ago
    -Spores as survival pods
    -A staggering diversity in biochemistry, structure and genetic fluidity allow micro-organisms as a group to deal with almost any environment
    -A human body contains approximately 100 bacterial cells for every human cell
  60. 60What is the innate immune system?-skin
    -epithelial cells
    -mucin
    -phagocytic cells
    -complement
  61. 61What is the acquired immune system?-antibodies
    -cytotoxic T cells
  62. 62How do the innate and acquired immune system interact with each other?-Signaling by cytokines
    -Antibodies produced by the specific defence system affect the non-specific defense
    ->AB activate complement
    ->AB help phagocytes to ingest and kill bacteria
  63. 63What are pathogens?pathogens are microbes that are able to overcome or circumvent our immune system
    -required specialization by the microbe: co-evolution of host and pathogen
  64. 64What are primary pathogens?cause disease in healthy humans (few species, e.g. Mycobacterium leprea)
  65. 65What are opportunistic pathogens?cause disease in immuno-compromised humans (many species e.g. Bifidobacterium and Lactococcus species
  66. 66What are Harmless bacteria?many are beneficial for humans
    e.g. Bifidobacterium and Lactococcus species
  67. 67Where do pathogens come from?-Soil contains 4000 prokaryotic and eukaryotic species per gram
    -Fungi
    -Bacteria
    -Protozoa
    -Nematodes
    -10^9 organisms/gram of rhizosphere
  68. 68What results in the development of traits allowing proliferation of bacteria in mammalian hosts?Combination of Selective Pressures in soil and Genome Instability
  69. 69What is an example of selective pressure from abiotic factors?Iron limitations
    -In soils iron exists as ferric iron (Fe3+): ubiquitous yet insoluble
    -In hosts iron is sequestered by iron binding protein and cofactors
    For example:
    -lactogerrin
    -transferrin
    -ferritin
    -hemoglobin
    -heme
    >In both environments the free iron concentration is too low to support growth
  70. 70What iron acquisition systems do bacteria use?Production of siderophores: structurally diverse group of compounds with extremely high affinity for ironWhat iron acquisition systems do bacteria use?
  71. 71What is Pseudomonas Aeruginosa?-It is an opportunistic pathogen infecting people with underlying conditions e.g.
    >cystic fibrosis
    >burn wounds
    >piercing of skin
    >cancer treatment
    -Fluorescent siderophore Pyoverdin is required for virulence
  72. 72What is an example of selective pressure from biotic factors?Predation by protozoa and nematodes
    -Nematodes are voracious predators of bacteria
    -Pseudomonas aeruginosa produces a diffusible toxin pyocyanine to kill the nematode Caenorhabditis elegans
    -The same toxin is an important virulence determinant in burn sepsis and lung infections to kill mammalian cells
    -Predatory protozoa eat bacteria
    -Macrophages of our immune system kill invading bacteria
    -There is a large evolutionary divide between protozoa and human macrophages however the mechanisms used by these cells to kill bacteria are remarkably similar
  73. 73What does the bacterial genome consist of?Core gene pool: -homogenous G+C content
    -located in stable section of genome
    -encode essential functions (e.g, DNA replication)
    Flexible gene pool: -Often located on mobile genetic elements
    -variable in G+C content
    -encode functions required under certain circumstances
    e.g. virulence
  74. 74What are pathogenicity islands?-Comparison of virulent and avirulent strains of E. coli identified virulence determinants located in genomic clusters not present in avirulent strainsWhat are pathogenicity islands?
  75. 75What do pathogenicity islands look like in a bacterial genome?-Different G+C content than the rest of the genome, arrived via lateral gene transfer (conjugation, lateral transduction)
    -Frequently unstable, often mobilisable to other bacteria
  76. 76What is Tuberculosis?-Highly infectious airborne disease
    -16% of all deaths in 19th century Britain due to pulmonary tuberculosis aka consumption
    -No cure until mid 20th century
  77. 77What is the genus Mycobacterium?-characterised by a high G+C content of the genome
    -Gram positive bacteria
    -Unique cell envelope characterised by the presence of mycolic acids
  78. 78What are the two main groups of mycobacterium?Saprophytic species, usually fast growing
    e.g. Mycobacterium smegmatis
    Pathogenic species, usually slow growing
    e.g. Mycobacterium bovis
    Mycobacterium tuberculosis
    Mycobacterium leprae
  79. 79What is the M. tuberculosis complex?a group of very closely related pathogenic speciesWhat is the M. tuberculosis complex?
  80. 80What is the correlation between geography and strains?Resembles human migration patterns
    (european strains found in Andean pre-hispanic period mummies: two waves of infection?)
    -Africa has most diversity in strains
  81. 81What are the first line drugs for tuberculosis?isoniazid, rifampin (treatment takes 6 months)
  82. 82What TB is resistant to first line drugs?Multi Drug Resistant (MDR) TB- need second line drugs
    Extensive Drug Resistant (XDR) TB resistant to at least three of the six second line drugs as well
  83. 83How did Robert Koch identify Mycobacterium tuberculosis as the cause of consumption in 1882?How did Robert Koch identify Mycobacterium tuberculosis as the cause of consumption in 1882?
  84. 84How do macrophages kill bacteria (innate immune system)?1. Phagocytosis by macrophages
    2. Bacteria in the phagosome
    3. Destruction of bacteria in the phagolysosome    How do macrophages kill bacteria (innate immune system)?
  85. 85What are M tuberculosis survival strategies?-Prevents phagosomal lysosomal function
    -Prevents activation of the macrophage
    -Reduce signaling to immune system
    -Prevents apoptosis
    -Prevents acidification of phagosome
    -Multiplication in phagosome
  86. 86What are the steps in the development of tuberculosis?What are the steps in the development of tuberculosis?
  87. 87Active vs latent tuberculosisActive vs latent tuberculosis
  88. 88What are zoonoses (intermezzo)?Infectious diseases that are transmitted from animals to humans
    -60% of human pathogens are zoonotic
  89. 89How are zoonoses transmitted?contact with:
    -Infected animals
    -Faeces or urine of infected animals (in for example drinking water
    -Contaminated food products (dairy/meat)
  90. 90What are some examples of Dog zoonoses?-Hookworm
    -Tapeworm
    -Cryptosporidium
  91. 91What are some other well known zoonoses?What are some other well known zoonoses?
  92. 92What is the mycobacterium bovis?pathogen with broad host range
    -predominantly cattle but also humans = Zoonosis
  93. 93What is Mycobacterium tuberculosis?pathogen with narrow host range
    i.e. humans
  94. 94What does comparative genomics do?it aims to answer questions such as
    -What are the evolutionary origins of pathogens?
    -Which genes are involved in pathogenesis?
    -Why is there a preference for a host? (tropism)
  95. 95How is comparative genomics done?Comparison of three genomes indicating the position of insertion/deletion and homologous genes
  96. 96How does comparative genomics hint at the evolution of bacterial species?How does comparative genomics hint at the evolution of bacterial species?
  97. 97What are the differences in the genomes of the M. tuberculosis complex?-Single Nucleotide Polymorphisms (SNP e.g. CTG->CGG
    -Insertions (phage) and deletions
  98. 98What did genomic comparison of M. bovis and M. tuberculosis H37Rv show?14 regions of differences (RD1-14 are absent in M. bovis BCG)
  99. 99What caused RD9 in M tuberculosis?-Absent in other members of the M. tuberculosis complex
    -Sequence surrounding RD9 is exactly the same in all species
    -Shows that RD9 is due to deletion from MTb and not an insertion into the other genomes
  100. 100Is M. tuberculosis derived from M. bovis?-M tuberculosis is not derived from M. bovis
    -Instead M bovis branched off a common human ancestral line prior to M tuberculosis
    -The ancestral strain of M tuberculosis and M. bovis was most likely a human pathogen, not an animal pathogen
    -Ancestor M. tuberculosis was not a zoonosis but perhaps M. bovis is the result of a reverse zoonosis (human to animal)    Is M. tuberculosis derived from M. bovis?

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University Microbiology Flashcards on Antibiotic Resistance, created by Adrianna Bialecka on 14/02/2025.
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