Microbiology Block 3

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Last updated 1:01 AM on 4/17/26
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99 Terms

1
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Where are the major microbial habitats in/on humans?

Ear, Nose, Hair, Skin, Gut and Mouth

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How is the human microbiome originally inoculated?

Vaginal birth vs c section

Breast feed vs formula

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What is the primary factor that drives community composition in the human microbiome?

Nutrients consumed, habitat and community.

4
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Two locations of high microbial diversity in humans

Skin and nostrils are exposed to external environment

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Two locations of low microbial diversity in humans

Mouth and gut because they are only exposed to what it given to them

6
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Why might microbe diversity be different between different body parts?

Different areas of skin interact with different surfaces

7
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Why is transplanting microbes between body parts mostly unsuccessful?

Habitats are the main driver of diversity so being moved to unfamiliar places doesn’t usually work

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What bacteria is involved with tooth decay?

Gram-negative bacteria and spirochetes

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What bacterium commonly is the source of ulcers?

Helicobacter pylori

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How does H. pylori live in the stomach?

It burrows into the stomach lining and the ulcer is created by immune response

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Why is microbial activity in small intestines minimal?

Rapid flow of contents washes bacteria away and human body takes many nutrients

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Why is microbial activity in the colon greater than small intestine?

Flow is very slow and humans don’t absorb as many nutrients

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What critical metabolic benefit to bacteria provide for the colon?

Polysaccharides are hard to be broken down so bacteria assist with this process

14
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What is the relationship between C. diff and antibiotics?

Antibiotics disrupt normal microbiota, allowing hard to kill C. difficile to overgrow.

15
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What benefits are provided by natural vaginal microbiota?

Some protect from fungal infection while some lower pH to protect from STIs

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Probiotics

Contain living microbes such as Bifidobacterium and Lactobacillus

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Prebiotics

Contain nutrients to feed beneficial bacteria

18
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What is a fecal transplant and when is it used?

Transfer of healthy microbiota to restore gut balance, often for C. difficile infections.

19
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What is an advantage of fecal transplants over antibiotics?

They restore microbial diversity instead of killing microbes broadly.

20
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How can gut microbes affect other parts of the body?

They influence metabolism, immune function, and even brain activity.

21
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What is the gut-brain axis?

The connection between gut microbiota and the brain/CNS.

22
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How can microbiome knowledge shape future medicine?

Personalized medicine to boost beneficial microbial communities and prevent pathogen invasion

23
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Main difference between beneficial and pathogenic bacteria

Pathogens have virulence factors that allow them to cause disease; most bacteria don’t have this

24
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Why is adherence required but not sufficient for disease?

Bacteria must attach to a host but also need to colonize, invade, and produce damage for nutrients.

25
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What are adhesins? Give 2 examples

Surface molecules that help bacteria attach to host cells;

Capsules and fimbriae

26
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What is the difference between colonization and invasion?

Colonization is growth on surfaces where invasion is penetration and spread into tissue

27
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Is septicemia due to colonization, invasion, or both?

Invasion since bacteria enters the bloodstream

28
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What is a virulence factor?

A trait that enables a pathogen to cause disease

29
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Why does virulence vary among pathogens?

Difference in virulence factors and genetic makeup

30
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What is LD₅₀ and how does it relate to virulence?

The number of cells needed to kill 50% of hosts; lower value means higher virulence

31
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How can virulence be attenuated/reduced?

By losing or mutating virulence genes

32
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What is a pathogenicity island?

A cluster of virulence genes on a chromosome

33
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What is the role of horizontal gene transfer in virulence?

It spreads virulence genes between bacteria

34
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What is an example of an enzyme virulence factor?

Hyaluronidase breaks down host tissues to aid spread

35
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What is the difference between exotoxins and endotoxins?

Exotoxins are secreted proteins where endotoxins are LPS components of gram-negative cell walls

36
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What are three types of exotoxins and examples?

AB toxins: diphtheria toxin

Cytolytic toxins: hemolysins

Superantigens: toxic shock toxin

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What is an example of an endotoxin and which bacteria use it?

Lipopolysaccharide (LPS) in gram-negative bacteria

38
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In what context are antibiotics naturally produced?

Microbes produce antibiotics to compete with and inhibit other microorganisms

39
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What is selective toxicity and why is it important?

It allows antibiotics to target bacteria without harming human cells, making them safe for treatment

40
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Who discovered antibiotics and how?

Alexander Fleming discovered penicillin from mold inhibiting bacteria

41
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What is the difference between bactericidal and bacteriostatic antibiotics?

Bactericidal kill bacteria where bacteriostatic stop growth so immune system can clear infection

42
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Why use broad-spectrum antibiotics and what is a consequence?

Used when pathogen is unknown but can disrupt normal microbiota and cause infections

43
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Why can’t antiseptics and disinfectants be ingested?

They lack selective toxicity and damage human tissues

44
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How to β-lactam antibiotics work?

They inhibit peptidoglycan cross-linking in cell walls, causing cell lysis

45
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Which bacteria are β-lactams most effective against and why?

Gram-positive bacteria because of their thick and exposed peptidoglycan layer

46
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How do polypeptide antibiotics like vancomycin differ from β-lactams?

They bind directly to cell walls precursors instead of targeting enzymes

47
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How do quinolones work and why are they selectively toxic?

They inhibit DNA gyrase in prokaryotes which differed from eukaryotic enzymes

48
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How do tetracyclines work and why are they selectively toxic?

They bind to the 30S ribosomal subunit which difference from eukaryotic ribosomes

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How do sulfa drugs work and why are they selectively toxic?

They inhibit folic acid synthesis which bacteria must produce but humans obtain from diet

50
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How do bacteria resist penicillins?

By producing β-lactamase enzymes that degrade the antibiotic.

51
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How do bacteria resist vancomycin?

By modifying the D-Ala-D-Ala target (3 enzymes) so the drug cannot bind

52
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How do bacteria resist ciproflaxin?

By modifying DNA gyrase, reducing drug entry, or using EFFLUX PUMPS.

53
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How do bacteria resist tetracycline?

By using efflux pumps to remove antibiotics

54
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How do bacteria resist sulfonamides?

By modifying enzymes involved in folic acid synthesis

55
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Why are efflux pumps a major concern?

They can remove multiple antibiotics which causes multidrug resistance

56
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Where are antibiotic resistance genes found?

On chromosomes and plasmids

57
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What is clavulanic acid?

A β-lactamase inhibitor that protects antibiotics like penicillin.

58
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Why does resistance evolve at different rates for different antibiotics?

Some resistance mechanisms are more complex and harder to evolve

59
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What is the concern with Neisseria gonorrhoeae?

It rapidly develops resistance to antibiotics

60
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What factors spread antibiotic resistance?

Overuse of antibiotics, agriculture use, and horizontal gene transfer

61
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Is there hope for antibiotics in the future?

Yes, through new drugs, better practices, and alternative therapies like phage therapy.

62
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How are viruses different from bacteria in structure and metabolism?

Viruses lack cells, ribosomes, and metabolism structures and must replicate inside a host

63
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What are viral capsids and envelopes?

Capsids are protein shells around the genome; envelopes are host-derived membranes some viruses acquire

64
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What does the Baltimore classification system use?

Genome type and how viruses generate mRNA

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Why can’t viruses be classified using rRNA?

They lack ribosomes and rRNA genes

66
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What must all viruses ultimately produce?

mRNA (+ strand) for protein synthesis

67
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What are the 5 stages of the viral replication cycle?

Attachment, penetration, synthesis, assembly, and release.

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What happens during (virus) attachment?

Viral proteins bind specific receptor cells on host

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What happens during (virus) penetration?

Viral genome enters the host (or entire virion in eukaryotes)

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What happens during (virus) synthesis?

Viral genomes and proteins are made using host machinery

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What happens during (virus) assembly?

New viral particles are constructed from genomes and capsid proteins

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What happens during (virus) release?

Viruses exit via lysis (prokaryotes) or budding (eukaryotes)

73
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How do bacteriophage T4 attach to E. coli?

Tail fibers bind to specific receptors on the bacterial surface

74
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What role do endosomes and lysosomes play in viral infection?

They help engulf and uncoat viruses in eukaryotic cells

75
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Where does viral genome replication and protein synthesis occur?

Replication occurs in cytoplasm in nucleus; translation occurs in cytoplasm

76
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Why is ATP needed for phage genome packaging?

It powers the packaging motor that inserts DNA into capsids

77
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What is the difference between lysis and budding?

Lysis destroys the host cell; budding releases the virus without killing the cell

78
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What is the difference between lyric and lysogenic cells?

Lyric kills host immediately; lysogenic integrates into host genome and remains dormant

79
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What viruses undergo lysogeny?

Temperature bacteriophages

80
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How is a virus involved in diphtheria?

A phage carries the toxin gene that makes the bacterium pathogenic

81
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How are retroviruses similar to temperate phages?

Both integrate their genome into the host DNA

82
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What is a latent viral infection?

A virus remains dormant in the host and can reactive later (ex: herpes)

83
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What is the main difference between influenza types A, B, C, and D?

They differ in severity and host range, with Influenza A causing pandemics and infecting multiple species.

84
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What is the antigenic drift vs antigenic shift?

Drift is small mutations; shift is a major changes from recombination, leading to new strains

85
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What is viral recombination and why is it important?

Exchange of genetic material between viruses during co-infection, creating new strains that can infect new host

86
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Why was the 1918 influenza pandemic so deadly?

The virus had novel antigens the immune system couldn’t recognize, causing severe immune responses.

87
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How did SARS-CoV-2 likely evolve to infect humans?

Through recombination of animal viruses (bats and pangolins), allowing binding to human receptors

88
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Which part of SARS-CoV-2 mutates to increase infectivity and why?

Spike protein; it controls attachment to host cells

89
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What stage of viral replication is affected by spike protein mutations?

Attachment

90
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What are common targets for antiviral defenses?

Steps in viral replication like attachment, genome entry, replication, and assembly

91
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How do microbes prevent viral adsorption?

By altering or masking receptors or producing decoys

92
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How do viruses overcome adsorption prevention?

By mutating to recognize new receptors or degrading barriers

93
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How does restriction-modification provide innate immunity?

Bacteria cut unmethylated viral DNA while protecting their own methylated DNA

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How do viruses evade restriction-modification?

By methylating their DNA or altering recognition sites

95
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How does CRISPR-Cas provide adaptive immunity?

stores viral DNA sequences and uses them to recognize and cut future infection

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How is CRISPR used in gene editing?

It targets specific DNA sequences for precise cutting and modification

97
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What is abortive infection?

Infected cells self-destruct to stop virus spread and protect the population

98
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Why do microbes need multiple defense strategies?

Viruses evolve quickly, so multiple defenses increase survival chances

99
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Why are defense genes often on mobile genetic elements?

They can spread quickly between microbes via horizontal gene transfer