microbiology- exam 2 red questions part2

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157 Terms

1
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What is the definition of selective toxicity of antibiotics?

Killing harmful microbe’s w/o damaging the hosts

2
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Who discovered the first antibiotic and what was it?

Alexander Fleming discovered penicillin. It is produced my fungus penicillium

3
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How did Alexander Fleming discover penicillin?

He accidentally left agar plate with bacterial culture uncleaned on workbench

4
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What do the clear zones indicate?

Surrounded with mold colonies no bacterial growth

5
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Why do bacteria and fungi produce antibiotics?

They compete with each other for nutrients and space.

6
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More than half our antibiotics are produced by a certain genus of bacteria. What is the genus of bacteria?

Bacillus (bacilli)

7
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Why are antibiotics with a very broad spectrum of activity not as useful as one might first think?

It’s useful to defeat the pathogen before it’s identified but it can’t distinguish harmful from the good, and lead to superinfection

8
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What is superinfection?

Killing off too much of the body’s normal microbiota

9
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Penicillin G

Effective against gram (+) but not gram (-) because it can’t penetrate the outer membrane

10
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Which antibiotic has a possibility to cause superinfection?

Chlamydia and Rickettsia

11
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Many antibiotics are bacteriostatic. How do the bacteriostatic antibiotics work against infection?

It inhibit the growth; bacteria can grow again when removed

12
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What are the major action modes of antimicrobial drugs and which one has the lowest selective toxicity?

Cell wall synthesis, nucleic acid synthesis, including DNA replication and RNA transcription, protein synthesis (translation), synthesis of essential metabolites, membrane integrity. Membrane disruption for lowest toxicity

13
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Bacterial cell walls are made with what materials and how are they assembled?

NAG and NAM (peptidoglycan), assembled by cross-linked by short peptides to create mesh like structure to maintain the cell wall

14
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Why don’t penicillins show toxicity to human cells and what is this property called?

It’s because if it’s w/o proper formality of the cell wall or even withstand internal pressure, it will rupture. As they called it lyse

15
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What properties are improved in semi-synthetic penicillins?

β-lactam ring or nucleus

16
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What is penicillinase?

Target and cleave the beta lactam ring, inactivating the antibiotic

17
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What is another name of penicillinase?

Beta lactamase

18
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Why isn‘t penicillin G taken orally?

Unstable in stomach acid

19
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What are some disadvantages of natural penicillins?

There are two types of natural penicillin that helps an individual, one does injection the other is taken orally

20
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Name two semisynthetic penicillins. 

Oxacillin and Ampicillin

21
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Which part is produced by the mold and which part is added chemically to make semisynthetic penicillins?

-

22
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What are the ways used to overcome the penicillinase problem?

Prescribe antibiotics, use inhibitors, modifying the structure of lactam core

23
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What are the ways used to overcome the penicillinase problem?

Carbapenems and Monobactams

24
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Can the same penicillinase that degrades penicillin destroy cephalosporins?

No

25
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What are advantages of using cephalosporins instead of using penicillins?

It had fewer allergic reactions and it’s resistant to most penicilinases

26
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What properties are upgraded in later generations of cephalosporins?

It’s more effective against gram (-), can be oral, fewer side effects

27
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Why do antibiotics affecting protein synthesis inhibit bacterial cell growth but not human cell growth?

It is because the host’s immune system can defeat the cells, the prokaryotic ribosome (translation) helps to affect protein synthesis

28
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What is the action of chloramphenicol?

Produced entirely through synthetic processes, synthesized through chemical processes, potent drug/toxic

29
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Which antibiotic is entirely synthesized?

Chloramphenicol

30
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What antibiotics are aminoglycosides and how do they inhibit protein synthesis?

Streptomycin, kanamycin, neomycin, and gentamicin. They inhibit by binding to 30S of prokaryotic ribosomes and altering the shape to be misread

31
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What cellular function is inhibited by tetracyclines?

tRNA attachment to ribosome-mRNA

32
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What are side effects of tetracyclines?

Staining of teeth and gastrointestinal trouble in changes of normal flora which can lead to superinfection

33
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How does erythromycin inhibit bacterial growth? 

It binds to 50S subunit and blocks the exit tunnel. Prevent translocation step in protein synthesis

34
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Why does erythromycin, a macrolide antibiotic, have activity limited largely to gram-positive bacteria?

The structure is large, and due to the chemical properties (along with the size), cannot penetrate the outer membrane of gram (-), so it’s effective to gram positive infections

35
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What is the action of rifampin and what infection is it mostly used against?

Inhibits RNA synthesis binding to RNA polymerase, blocking mRNA production and used for tuberculosis (TB)

36
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Which bacterial enzyme makes the chromosomal DNA a very compact form?

Gyrase

37
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What is the role of bacterial gyrase?

Responsible for introducing supercoils into bacterial DNA

38
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Which drug inhibits bacterial gyrase?

Fluoroquinolones

39
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Why is polymyxin B effective to only gram-negative bacteria?

It binds and disrupts the outer membrane, it is very toxic and topical

40
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How do competitive enzyme inhibitors work as antibiotics?

Targeting key enzymes in essential metabolic pathways, resemble natural substrate if enzyme and compete to bind

41
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What is MIC and what methods can be used to measure the MIC of an antibiotic against a microbe?

MIC stands for minimal inhibitory concentration. Methods to use are disk diffusion method, gradient diffusion method, and broth dilution method

42
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Explain how to interpret the result of the disk-diffusion method.

A small filter paper disk is soaked with a known concentration of an antibiotic and then placed on the surface of an agar plate that has been uniformly inoculated with the test organism. After incubation, if the antibiotic is effective, it will inhibit bacterial growth in the area surrounding the disk, creating a clear zone, larger the zone, more effective it is

43
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How do you read the MIC in the E test?

a plastic strip containing a predefined gradient of antibiotic concentrations is placed on the surface of an agar plate that has been inoculated with the test bacterium. As the antibiotic diffuses into the agar, it creates a gradient of concentrations. After incubation, a tear-shaped zone of inhibition appears around the strip, and the point at which the bacterial growth intersects the strip corresponds to the MIC, indicated in micrograms per milliliter (µg/mL) directly on the strip. This method provides a precise, quantitative measurement of antibiotic effectiveness.

44
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How do you read the MIC in the broth dilution test?

performing a serial dilution

45
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Describe four mechanisms how microorganisms become antibiotic resistant?

blocking entry, inactivation by enzymes, alteration of target molecules, and efflux of antibiotics

46
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What are the two routes for microorganisms to obtain antibiotic resistance?

Spontaneous mutations and acquisition of new genes

47
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slide 58

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48
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How does adding antibiotics to animal feed threaten the treatment of human infections?

It has no effect as the pathogen is already immune

49
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Why are viruses not sensitive to antibacterial drugs?

It’s because they cant reproduce on their own, they need a host to produce. Viruses are not true cells

50
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What is the typical structure of viruses?

Have DNA or RNA but never both, protein coat, some have an envelope, many have spikes

51
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Explain about viral host and tissue specificity?

Viruses only affect host specific cells, like human virus only affects humans, plants virus affects plants, etc. Tissue specificity is known for infecting only certain types of cells

52
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What determines these specificity?

It determine how viruses attach to host cells, if the receptor of the host cell is not there, then the virus can’t attach and infect the cell

53
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What is the general size of viruses?

Bigger than a protein

54
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What properties are used to classify viruses?

By their nucleic acid, shape, and host

55
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Based on its genetic composition, the Covid-19 virus is a/an _______ virus.

single stranded RNA

56
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Do all viruses have the same shape?

No, they do not

57
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What are capsomeres and capsids?

Capsomeres are the subunits of capsids. Capsids are a protein coat that is protecting material of a virus

58
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How are capsomeres arranged in helical viruses?

They are arranged in a spiral/helix forming long rod like shapes.

59
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How are capsomeres arranged in polyhedral viruses?

They are arranged to look like a ball made of 20 triangular faces and 12 corners, generally a icosahedron

60
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What are viral spikes and what are their roles?

Viral spikes are made out of protein or glycoprotein (protein and sugar), they help to attach the virus to specific host, determine which cells to infect, and identify different viruses

61
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What is the most common shape of polyhedral viruses?

The most common is Icosahedral

62
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Where is the envelope located in enveloped viruses ?

On the outer layer

63
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Where are viral spikes located in enveloped viruses?

On the surface of the enveloped virus

64
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What is a viral tegument (or viral matrix)?

A cluster of proteins located in the space between the envelop and nucleocapsid, that surrounds the viral genetic material

65
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Where does the envelope of enveloped viruses come from?

It comes from a mix of lipids, proteins, and carbohydrates

66
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Is the envelope essential for their life cycle?

No, since it is often made by the virus itself or with the host cells, or even together

67
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Why are bacteriophages considered complex viruses?

Have more complicated structures

68
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What is the role of each part of the T4 bacteriophage?

Capsid (head): shaped like a 20 sided polygon, have viral DNA to inject into bacterial cell. Tail Sheath: long tube like structure connect the head to the base, it push the DNA into the host. Tail Fibers: leg like sticking out of the base plate, attach to the surface of a bacterial cell. Baseplate and pins: the baseplate anchors the virus to the surface, the pins help pierce the cell wall during DNA injection

69
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How are viruses grown in a laboratory?

Labs use fertilized chicken eggs or cultured cells

70
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What is the definition of a plaque and a plaque forming unit (PFU)?

Plaque is the forming of clear spots between each bacteria. Plaque forming unit is the number of virus in the culture (maybe)

71
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What kind of viruses usually grow in embryonated eggs?

Animal viruses

72
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What can be advantages and disadvantages if a viral vaccine is produced using embryonated eggs instead of cell culture?

The advantages are a common method for isolating/growing cells, it inexpensive to use in the lab. The disadvantage is that people who are allergic to eggs could have a reaction

73
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Why are continuous cell lines of more practical use than primary cell lines for culturing viruses?

Continuous cells are usually cancerous and keep growing for unlimited number of generations, usually called immortal cells lines

74
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What is the cytopathic effect and give five examples?

Any visible damage/deterioration of host cells caused by viral infection. Disruption of host cell macromolecule synthesis, release of lysosomal enzymes, inclusion bodies in the cytoplasm or nucleus of some infected cells (can be viral or host materials), formation of a syncytium (a very large multinucleate cell), and changes in host cell function

75
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What is the inclusion body?

Clumps of viral material/altered cells parts inside the cells

76
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What is the syncytium?

Giant cell created when several infected cells fuse together

77
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Do all viruses show the same cytopathic effect?

No, some would swell, abnormal clumps, or fuse together

78
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Where does viral multiplication occur and what is its result?

It occurs when they hijack the host’s cell and multiply by the second (hundreds→thousands)

79
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Explain the two bacteriophage life cycles, lytic and lysogenic cycles. What are differences?

Lytic cycle is the phage infects a bacterial cells and making copies of itself inside the cells, bursts/lyses and release new ones into the environment. Lysogenic is inserting their DNA into the host’s DNA.

80
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What is the final outcome of the lytic cycle?

Death

81
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What can be found in the host cell during biosynthesis or maturation step in the lytic cycle?

New phage particles assembling

82
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What happens to bacteriophage DNA in the lysogenic cycle?

The DNA stay as it is for while after they insert their DNA to the host’s

83
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What is the bacteriophage genome incorporated into the host chromosome called?

84
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What is the benefit of the lysogenic cycle?

85
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Does lysogeny occur in an animal virus life cycle?

Some do

86
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Can the viruses in the lysogenic cycle spread diseases? e.g. HIV?

In the end, yes. Like you can have it and not have symptoms for sometime and can remain dormant

87
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Describe the principal events of attachment, entry, uncoating, biosynthesis, maturation, and release of an enveloped DNA-containing virus.

Attachment-viruses attach to the cell membrane attaching with the spike to the host receptor. Entry-entering through the membrane to the DNA. Uncoating-removing the capsid/host enzymes. Biosynthesis- production of viral nucleic acid/proteins. Maturation-the virus assemble. Release-releasing by budding (enveloped) or rupture (non-enveloped)

88
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What is used for viruses to attach on the host cell surface?

Spikes or capsid proteins to attach 

89
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What is the fate of the host after infection with non-enveloped animal viruses?

Burst open or rupture releasing all new virus at once

90
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What is a viral envelope composed of?

The spike proteins insert into the host cells plasma membrane. Newly formed viral particles move inside of the membrane. The host membrane wraps the virus and the virus buds off, taking a portion of the host’s membrane

91
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Does viral budding kill the host cell right away?

The host cell isn’t killed immediately

92
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Describe the similarities and differences between the life cycles of bacteriophages and animal viruses.

Similarities- both attach to the wall, enter, does biosynthesis, both also release. Differences-uncoating is not required in bacteriophages, bacteriophages is lysogeny, animal virus is latency, at the end bacteriophages the host cell is lysed, in animal virus it’s either enveloped or non-enveloped

93
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How do viruses cause cancers?

Anything change the genetic material inside a eukaryotic cell to change from normal to cancerous 

94
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What are characteristics of transformed cells?

Increased growth, loss of contact inhabitation, chromosomal abnormalities, virus specific antigen 

95
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Which DNA viruses cause cancer?

Hepatitis B (liver cancer)

96
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Which RNA viruses cause cancer?

Human T cell leukemia virus

97
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Describe the life cycle of retroviruses.

First the virus fuses with and enter the host cell, inside sheds outer coat (uncoating), releasing RNA genetic material with viral enzyme, reversing transcriptase, integrase, and protease. 

98
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What are the role of the reverse-transcriptase and integrase?

Converting the virus single RNA to double stranded DNA, this new viral travels to the cell’s nucleus. the viral integrase enzyme cuts the host cells DNA and insert DNA right into it, now its provirus 

99
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Give some examples of latent viral infections.

Cold sores, shingles, HIV

100
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How do latent and persistent infections differ?

Latent-virus enters into the body, goes into hiding, then years later it may reactivate and persistent- virus level builds slowly but steadily over time, so sudden peak