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BIO-360: Microbiology > Exam 3 (Ch. 10, 13, & 14) - Conner > Flashcards

Exam 3 (Ch. 10, 13, & 14) - Conner Flashcards

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1
Q

Who discovered the first anti-microbial drug, and what was it used for?

A

Paul Ehrlich and Sahachiro
-Salvarsan, an arsenic compound, was used as a chemical to inhibit Treponema pallidum

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2
Q

What is the Therapeutic Index?

A

compares the blood concentration at which a drug becomes toxic and the concentration at which the drug is effective

Lowest dose that is toxic to humans / Usual therapeutic dose of the drug

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3
Q

What is Selective Toxicity

A

The dosage that kills or inhibits a microbe while not damaging the host

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4
Q

Which is better: a HIGH or LOW Therapeutic Index?

A

HIGH - the higher the TI the safer it is because a patient would have to take a much higher dose of such a drug to reach the toxic threshold than the dose taken to elicit the therapeutic effect

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5
Q

SOLVE THE FOLLOWING TI QUESTION:

Which drug is better?

Drug A:
-Toxic at dose of 10 mg; therapeutic at 5 mg

Drug B:
-Toxic at dose of 100mg; therapeutic at 5 mg

A

DRUG B

Lowest dose that is toxic to humans / Usual therapeutic dose of the drug

Drug A: 10 toxic dose / 5 therapeutic dose
= TI of 2

Drug B: 100 toxic dose / 5 therapeutic dose
= TI of 20

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6
Q

Describe the discovery of Sulfa Drugs

A

In 1932 Germany, the red dye Prontosil was found to inhibit the growth of S. aureus in animals

However, this did not work on cultures

But, it was later determined that Sulfanilamide, a breakdown product, was the active form!

So, in 1935, Gehard Domagk gave the drug to his daughter who was gravely ill…and she survived!

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7
Q

What drug did Alexander Fleming discover when he closely examined a Staphylococcus culture contaminated with mold?

A

Penicillin!

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8
Q

Where was Sir Alexander Fleming entombed?

THIS IS A TRIVIA QUESTION ON THE SLIDES…SO POSSIBLE EXTRA CREDIT… MAYBE??

A

St. Paul’s Cathedral, London

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9
Q

Describe the discovery of Penicillin

A

In 1928, Alexander Fleming returned from a holiday to find mold growing on a Petri dish of Staphylococcus bacteria. 

He noticed the mold seemed to be preventing the bacteria around it from growing - a zone of inhibition! He soon identified that the mold produced a self-defense chemical that could kill bacteria (Penicillium notatum).

He named the substance Penicillin

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10
Q

What anti-bacterial enzyme did Alexander Fleming discover in tears and saliva?

THIS IS A TRIVIA QUESTION ON THE SLIDES…SO POSSIBLE EXTRA CREDIT… MAYBE??

A

lysozyme

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11
Q

Why did Alexander Fleming decide to become a microbiologist?

THIS IS A TRIVIA QUESTION ON THE SLIDES…SO POSSIBLE EXTRA CREDIT… MAYBE??

A

So he could be in the St. Mary’s rifle club. There were no surgery spots available at St. Mary’s

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12
Q

What Bacterial Cell structures would you target for Antibacterial Drug development?

A

-Cell Wall (inhibition of cell wall synthesis and cell membrane function)
-Ribosomes (inhibition of translation)
-DNA (inhibition of transcription and replication)
-Metabolism (inhibition of metabolism

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13
Q

What are some Mechanisms of Action of Microbial Drugs?

DEFINITELY AN EXAM QUESTION!

A
  1. Inhibition of pathogen’s ATTACHMENT or ENTRY into the host cell
    -e.g., Arildone
  2. Inhibition of CELL WALL SYNTHESIS
    -e.g., Penicillins
  3. Inhibition of DNA or RNA SYNTHESIS
    -e.g., Quinolones
  4. Inhibition of GENERAL METABOLIC PATHWAY
    -e.g., Dapsone
  5. Inhibition of PROTEIN SYNTHESIS
    -e.g., Tetracyclines
  6. Disruption of CYTOPLASMIC MEMBRANE
    -e.g., Polymyxins
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14
Q

Explain how Penicillin works as an antibacterial drug.

What is the active portion of a Penicillin molecule?

DEFINITELY AN EXAM QUESTION!

A

Penicillin is a Beta-Lactam Drug, meaning that it interferes with the FORMATION of the peptide side chains between adjacent strands of PEPTIDOGLYCAN by INHIBITING penicillin-binding proteins

Penicillin IRREVERSIBLELY binds to enzymes that crosslink NAM subunits.

Active Portion = BETA-LACTAM RING!

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15
Q

DISRUPTION OF BACTERIAL CELL WALL

What are drugs that affect the cell wall, and how?

A
  1. Beta-Lactam Drugs
    -INTERFERE with the FORMATION of the PEPTIDE SIDE CHAINS between adjacent strands of PEPTIDOGLYCAN by INHIBITING penicillin-binding proteins…so prevents cross-linking!
  2. Vancomycin
    -BINDS to the AMINO ACID SIDE CHAIN of NAM molecules, INTERFERING with PEPTIDOGLYCAN SYNTHESIS (remember the inter bridge on that you had to draw before?)
  3. Bacitracin
    -INTERFERES with the transport of PEPTIDOGLYCAN PRECURSORS across the cytoplasmic membrane
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16
Q

DISRUPTION OF BACTERIAL CELL WALL

In broad terms, how exactly do drugs that affect the cell wall inhibit growth?

A

For bacteria to enlarge and divide, a cell synthesizes more peptidoglycan by adding new NAG and NAM subunits to existing NAG – NAM chains, the new NAM subunits then must be bonded to other new nearby NAM subunits.

This is being inhibited when drugs (like Beta-Lactams) prevent the cross-linking between the NAM subunits!

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17
Q

DISRUPTION OF BACTERIAL CELL WALL

In what way do Vancomycin-resistant bacteria form their resistance to the drug?

A

modifies the cross-bridge of the altered D-alanine adding a lactic acid side chain.

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18
Q

DISRUPTION OF BACTERIAL CELL WALL

After a bacterial cell is treated with a Beta-Lactam drug, what physical changes occur?

A

The cell loses its membrane integrity, inflating as it is unable to withstand changes in osmotic pressure

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19
Q

DISRUPTION OF PROTEIN SYNTHESIS

What are some of the types of antibiotics that affect ribosomes, and what do they do?

A
  1. Aminoglycosides
    -BLOCK the initiation of translation and causes the MISREADING of mRNA
  2. Tetracyclines
    -BLOCK the attachment of tRNA to the ribosome
  3. Chloramphenicol
    -PREVENTS peptide bonds from being formed
  4. Lincosamides
    -PREVENT the continuation of protein synthesis
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20
Q

DISRUPTION OF PROTEIN SYNTHESIS

List 3 ways antibiotics target translation

MUST KNOW 3 FOR THE EXAM!

A
  1. Aminoglycosides, like Streptomycin, cause a CHANGE IN THE SHAPE of the 30S subunit, causing the mRNA to be misread - leading to incorrect amino acids being added
  2. Tetracycline and some Aminoglycosides BLOCK the DOCKING SITE of tRNA, inhibiting translation
  3. Oxazolidinone PREVENTS the 50S subunit from BINDING to the mRNA
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21
Q

DISRUPTION OF BACTERIAL NUCLEIC ACID SYNTHESIS

How does Sulfonamide inhibit nucleic acid synthesis?

A

The structure of Sulfonamide is similar to PABA, except that the side chain differs.

  1. Normally, PABA sits in the active site of an enzyme to allow for the synthesis of FOLIC ACID…this across other steps forms the nucleic acids necessary for DNA and RNA
  2. Sulfonamide is able to bind into the active site of this enzyme instead due to its similar structure, inhibiting the formation of FOLIC ACID SYNTHESIS…stopping the ability for the necessary nucleic acids to be created for DNA and RNA
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22
Q

What considerations must be made when prescribing an antibiotic?

A
  1. Spectrum of Action (broad or narrow?)
  2. Effectiveness (how well does an antibiotic have on a specific bacteria?)
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23
Q

What is the difference between broad- and narrow-spectrum antibiotics? When would you use each?

A

Broad-spectrum = antibiotics that target many types of bacteria (gram + and -)
-used when a bacterial infection is suspected, but the group of bacteria is unknown

Narrow-spectrum = antibiotics that target only a few types of bacteria
- used when the causative organism of specific infection is known

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24
Q

What are the advantages/disadvantages of broad- and narrow-spectrum antibiotics?

A

BROAD:
(+) very powerful and flexible drugs
(+) can used to treat bacterial infections when the infecting bacterium has not yet been identified or remains unknown
(-) attacks normal bacterial flora of the host
(-) is a leading cause of more drug-resistant bacteria

NARROW:
(+) prevent the treatment from causing widespread collateral damage to the body’s good bacteria
(+) less likely to encourage superinfection or produce “superbugs”
(-) identity of the bacterium needs to be known in advance
(-) choosing the wrong drug can result in the patient’s condition worsening when multiple bacteria are in question

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25
Q

Are broad-spectrum antibiotics always better?

A

No - they can attack the body’s normal bacterial flora and have been shown to lead to more drug-resistant bacteria

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26
Q

REVIEW QUESTION

What chemical structure is responsible for the DISRUPTION of CELL WALL SYNTHESIS in many antibiotics?

A

Beta-Lactam Rings

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27
Q

List some of the Routes of Administration for antibiotics

A

-Topical
-Oral
-Intramuscular (IM)
-Intravenous (IV)

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28
Q

Describe the relative concentration of an antibiotic in the blood for the following methods:

  1. Oral
  2. Intramuscular (IM)
  3. Intravenous (IV)
A
  1. Oral: lower concentration, decreases over time
  2. Intramuscular: higher concentration at first, but greatly decreases shortly after
  3. Intravenous: HIGH concentration, remains constant and continuous until the IV is removed
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29
Q

What are some notable side effects that need to be considered when prescribing antibiotics?

A
  1. Toxicity
  2. Special Cases:
    -Tetracycline + Calcium can lead to stained teeth and a malformed skill in an infant
    -Pregnancy and breast-feeding
  3. Allergies
  4. Disruption of Normal Microbiota
    -overgrowth of yeast can lead to thrush
    -C. diff leads to inflamation in inner lining of large intestine
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30
Q

Essentially, antibiotic resistance is __________

A

NATURAL SELECTION!

-sensitive organisms are killed or inhibited by an antimicrobial drug

-resistant survivors can multiply without competition

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31
Q

More than 50 million unnecessary antibiotic prescriptions are written each year for patients outside of hospitals.

Why is this?

A

Many people go to the doctor wanting “something” to feel better, like a pill.
There are no laws on how a doctor can prescribe an antibiotic. However, for a viral infection, an antibiotic does nothing to the patient, its simply some “placebo”

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32
Q

If you were a bacterial cell, what tools would you use to protect yourself from antibiotics?

A

-Formation of endospores
-Pass resistance from one bacterial strain to another
-Changing the binding site of the antibiotics
-Alter ribosomes into a different shape

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33
Q

List the various Mechanisms of Antibiotic Resistance

BE ABLE TO THINK ABOUT WHAT MECHANISM OF RESISTANCE YOU WOULD USE IN THE PRESENCE OF AN ANTIBIOTIC…WILL BE AN ESSAY QUESTION!

A
  1. Production of an enzyme that INACTIVATES the drug (e.g., Beta-Lactamase)
  2. Altered porins (chromosomal mutation, prevent entry into cell)
  3. Altered target molecule (chromosomal, drug cannot bind target)
  4. Changing metabolic activity, which produces MORE of an enzyme or NOT using a pathway
  5. Efflux Pumps (ejects drug out of cell, R plasmids)
  6. Biofilms - slower MR and diffusion of the drug
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34
Q

How does Beta-Lactamase inactivate Penicillin?

(these used to be called “Pencillinases”)

BE ABLE TO THINK ABOUT WHAT MECHANISM OF RESISTANCE YOU WOULD USE IN THE PRESENCE OF AN ANTIBIOTIC…WILL BE AN ESSAY QUESTION!

A

This enzyme, secreted from the bacterial cell, CLEAVES and HYDROLYZES the cyclic amide bond in the beta-lactam ring of penicillin, rendering it INACTIVE

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35
Q

T/F: Mutations can alter the shape of a receptor that transports the drug so that it CANNOT enter the cell

BE ABLE TO THINK ABOUT WHAT MECHANISM OF RESISTANCE YOU WOULD USE IN THE PRESENCE OF AN ANTIBIOTIC…WILL BE AN ESSAY QUESTION!

A

TRUE

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36
Q

Explain how a bacterial cell may use an alternative metabolic pathway as a mechanism of resistance.

BE ABLE TO THINK ABOUT WHAT MECHANISM OF RESISTANCE YOU WOULD USE IN THE PRESENCE OF AN ANTIBIOTIC…WILL BE AN ESSAY QUESTION!

A

Some drugs BLOCK the usual metabolic pathway

So, organisms can CIRCUMVENT this by using an ALTERNATIVE, UNBLOCKED, pathway that produces the REQUIRED PRODUCT

This can also be done by producing MORE of an enzyme

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37
Q

Explain what the activation of “drug pumps” does as a mechanism of resistance

BE ABLE TO THINK ABOUT WHAT MECHANISM OF RESISTANCE YOU WOULD USE IN THE PRESENCE OF AN ANTIBIOTIC…WILL BE AN ESSAY QUESTION!

A

specialized membrane proteins are ACTIVATED and CONTINUALLY PUMP the drug OUT of the cell

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38
Q

Efflux pumps are particularly interesting as a mechanism of resistance but also concerning.

How so?

A

Some eject MANY DIFFERENT ANTIBIOTICS as well as DISINFECTANTS and ANTISEPTICS

-E. coli has over 35 genes that code for efflux pumps
-Pseudomonas contains 4 families of a 3-protein efflux system

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39
Q

Vertical Evolution is a mechanism for Acquiring Antibiotic Resistance.

Explain this

A
  1. A spontaneous mutation occurs in the genome of a bacterial cell (sometimes beneficial or not)
  2. This cell rapidly divides, and eventually there is a large population of bacteria that contain this mutation within their genomes
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40
Q

Horizontal Evolution is a mechanism for Acquiring Antibiotic Resistance.

Explain this

A
  1. A bacterial cell containing an R plasmid attaches to another cell with its F pilus
  2. The F pilus transfers the plasmid, resulting in these new cells to contain it and become resistant
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41
Q

How is antibiotic resistance transferred from one cell to another? Within a human? Within a community?

A
  1. One cell to another? -> horizontal evolution
  2. Within a human? -> improper use of antibiotics that allows for resistant bacteria to proliferate as part of natural selection
  3. Within a community? -> spread of germs from surfaces, directly (e.g., coughing), and indirectly (e.g., unclean hands); via animals who retain resistant bacteria that remain in their meat…when not handled/cooked properly it can spread to humans; contamination of water or fertilizer on crops, which make their way into food eaten by humans
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42
Q

How are multi-drug resistant strains created?

A

By accumulation, on-resistance (R) plasmids or transposons, genes, with each coding for resistance to a specific agent, and/or by the action of multidrug efflux pumps

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43
Q

Is antibiotic resistance inevitable?

A

Sadly, yes - it is a naturally occurring process.

Resistance can be VERY QUICK! (e.g., took only 3 years for resistance to penicillin)

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44
Q

What are ways to PREVENT the development of resistance?

A
  1. Maintain a HIGH enough concentration of the drug for sufficient time in a patient (DON’T STOP ANTIBIOTIC TREATMENT WHEN PRESCRIBED!)
  2. Drug cocktails - different targets or synergism (or both!)
  3. DON’T USE ANTIBIOTICS FOR NON-BACTERIAL INFECTIONS!
  4. Limit the use of certain antibiotics to “save” them for MRD strains

*MRD = multi-resistant drug

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45
Q

So…are we losing the race?

A

…Yes

-As microorganisms gain resistance to the current anti-microbial drugs, new ones need to be found

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46
Q

What are Virulence Factors?

A

molecular determinants of VIRULENCE

pathogen components that are NON-ESSENTIAL to in vitro growth in rich media, BUT cause INCREASED virulence during INFECTION OF A HOST

*Virulence Factors are the KEY target of anti-virulence drugs

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47
Q

Are virulence factors “evolution-proof?”

A

It depends on whether the virulence factors provide an ADVANTAGE to bacteria

i.e., the balance between COST of producing VF and the advantage to the bacterium

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48
Q

What are some examples of “targeting virulence factors?”

A
  1. Bicyclic 2-pyridones = inhibits pilus formation in E. coli; prevents interaction of chaperone-pilus complex
  2. Virstatin = inhibits the expression of cholera toxin and the toxin co-regulated pilus in V. cholerae
  3. 2-imino-5-arylidene thiazolidinedione = inhibits porins in a wide range of Gram- pathogens
  4. Urtoxazumab = antitoxin antibody that acts as an inhibitor of Shiga toxin function in enterohaemorrhagic E. coli (still in clinical trials)
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49
Q

READING RESPONSE

What is a zoonotic disease?

A

disease that is transferred from an animal host to a human

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50
Q

READING RESPONSE

How did human evolution impact viral disease spread?

A

By settling down and no longer being hunter-gathers, humans were in closer contact with each other.

This along with the domestication of animals served as a breeding ground for bacteria to thrive and infect - it essentially lead to zoonosis and the prevalence of diseases like measles

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51
Q

READING RESPONSE

What two diseases is the Measles virus related to?

A

Most closely related to 1) Rinderpest virus of cattle and (2) Distemper virus of canine

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52
Q

READING RESPONSE

What does R0 refer to in pathogens? What is the R0 for Measles?

A

The infectivity of a pathogen (<1 is less infective; >1 is very infective)

Measles R0 = around 18 today

*This means that 1 person can infect 18 people!

53
Q

READING RESPONSE

Which group is most affected by the Measles?

A

Malnourished children

54
Q

REVIEW QUESTION

A patient has a severe infection and you need to get antibiotics into their circulation very quickly.

What route of administration do you select, and why?

A

IV - this contains a high continuous concentration of the antibiotic in the blood. Other routes decrease in concentration over time and will be less convenient

55
Q

REVIEW QUESTION

You have a mixed population of antibiotic-resistant and antibiotic-sensitive cells.

What happens if:

You stop taking your antibiotics

A

Both populations continue to grow and expand, making it much harder for the immune system to fight off both populations

56
Q

REVIEW QUESTION

You have a mixed population of antibiotic-resistant and antibiotic-sensitive cells.

What happens if:

You continue taking your antibiotics

A

Sensitive bacteria die, leaving the most resistant ones. The immune system is able to target and clear these cells up more easily

57
Q

REVIEW QUESTION

You have a mixed population of antibiotic-resistant and antibiotic-sensitive cells.

What happens if:

You forget to take the second dose of antibiotics several days in a row

A

Antibiotic concentration will kill some of the sensitive bacteria, but not all. This leads to expansion and transformation of the sensitive bacteria to resistance

58
Q

REVIEW QUESTION

What are two mechanisms of antibiotic resistance?

NOTE: You should know how to explain one of these as it will likely be an essay question

A
  1. drug inactivation (beta-lactamase)
  2. change in the shape of the receptor
  3. use of alternative metabolic pathway
  4. activation of drug pumps
59
Q

T/F: C. diff infections are CAUSED by antibiotics.

A

TRUE - a 2019 CDC report showed that 223,900 people were hospitalized and 12,800 died

60
Q

What are some examples of “superbugs”, more accurately known as multi-drug resistant strains?

TOP 5 BIGGEST ANTIBIOTIC RESISTANCE THREATS!

A
  1. Carbapenem-resistant Acinetobacter: naturally competent; we used this in the tranformation lab
  2. Candida auris: fungal, yeast infection, causes thrush in mouth…can become more severe
  3. Carbapenem-resistant Enterobacteriaceae (CRE): gut bacteria that causes GI disease
  4. C. diff
  5. Drug-resistant Neisseria gonorrhea
61
Q

What are a few strategies that the CDC is promoting for combating the problem of antibiotic resistance.

A
  1. PREVENT infection and PREVENT the spread of resistance
  2. TRACKING resistant bacteria
  3. IMPROVING the use of today’s antibiotics
  4. INVEST in development of vaccines, therapeutics, and diagnostics
  5. IMPROVE sanitation and access to safe water (keep antibiotics out of environment)
62
Q

What was the impact of the COVID-19 pandemic on the spread of antibiotic-resistant bacteria?

A

an increase in antimicrobial resistance as a focus on research was placed on treating the COVID virus, allowing for greater resistance and spread once quarantine controls were stopped

63
Q

What are the characteristics of virus families?

A

CLASSIFIED BY: Nucleic Acid (DNA or RNA)

SYMMETRY OF CAPSID: icosahedral; helical; complex

NAKED or ENVELOPED?

TYPES OF NUCLEIC ACID: double-stranded; single-standed

GETS TO FAMILY NAME! - e.g., corona, pox, jerpes, baculo, toga

64
Q

The first step in the infectious process is ATTACHMENT.

How does a virus attach to a host cell?

A

proteins on the surface of the virus (capsid or spikes on envelope) BIND to receptors on host cells

However, some viruses like HIV require a co-receptor

Or, there are smart viruses, like adenovirus, that has an ICAM-1 receptor that is an adhesion molecule important in inflammation..upregulated when infection occurs

65
Q

REVIEW QUESTION

Why are we seeing an increase in Measles spread?

A

There has been a rise in fear of vaccinations after false claims of a link to autism with the MMR vaccine

This has lead to under-vaccinations, causing an easier spread of the virus

66
Q

REVIEW QUESTION

Can all animal viruses jump directly to humans, or do they need an intermediate host?

A

Some can, but a certain spread (e.g., from bird, then to pig, and then human) will lead to a GREATER viral spread than in different spread patterns.

So, an intermediate host can lead to a greater spread

67
Q

What is an enveloped virus versus a naked virus?

A

Naked = only the capsid, no envelope

Enveloped = contain an extra lipid bilayer membrane around capsid

68
Q

Where does the envelope of an enveloped virus come from? And how does it differ from the host cell

A

comes from the infected host cell in a process called “budding off.”

During the budding process, newly formed virus particles become “enveloped” or wrapped in an outer coat that is made from a small piece of the cell’s plasma membrane.

DIFFERS: modify the envelope by inserting its own proteins, which were left in the plasma membrane during penetration

69
Q

What are the THREE ways in which animal viruses can enter cells?

A
  1. Direct Penetration (naked)
    -capsid binds to receptors on the cytoplasmic membrane of the host and viral genome is transferred in
  2. Membrane Fusion (enveloped)
    -virus binds to receptors on cytoplasmic membrane of host, fusing
    -the capsid is released into the cell, and the viral glycoproteins that held it remain in the cytoplasmic membrane
    -the capsid is then uncoating, releasing the viral genome
  3. Endocytosis (enveloped)
    -virus binds to receptors on cytoplasmic membrane of host
    -the cytoplasmic membrane of the host ENGULFS the virus (endocytosis)
    -the virus released the capsid
    -the capsid is uncoated, releasing the viral genome
70
Q

What are the two ways in which enveloped viruses enter a host cell?

A
  1. Membrane Fusion
  2. Endocytosis
71
Q

How is a virus able to uncoat the envelope to release the capsid?

A

through Receptor-Mediated Endocytosis

this allows for a fusion with a lysosome with degradative enzymes for uncoating

-may occur at the plasma membrane, within endosomes, and at the nuclear membrane

72
Q

DNA viruses and retroviruses NEED to get their genome to the nucleus of the host.

When does this happen?

A

During mitosis when the host DNA replicates and the nuclear membrane dissolves

-reverse transcriptase makes a DNA copy of the viral RNA and uses the newly made DNA as a template to make a complementary DNA strand

-this copy strand is integrated into the host chromosome using an integrase enzyme

73
Q

Does a host cell have RNA-dependent RNA Polymerase?

LIKELY AN EXAM QUESTION…SHE SAID THIS IN CLASS

A

No - host cells do not have this, so a virus must bring its own

74
Q

Regarding replication and transcription of RNA viruses, what is the + strand? The - stand?

A

+ strand = used as mRNA

(-) strand = the complement (template) of the mRNA

75
Q

How do viruses with dsDNA genomes replicate

A

OCCURS IN NUCLEUS OF HOST

Unwinding and transcription of dsDNA allows for the formation of an mRNA strand

the mRNA strand codes for a capsomere protein

dsDNA is placed into the capsid produced from the capsomere protein (naked)

76
Q

Where does Transcription of a +ssDNA virus occur?

What about Replication?

A

Transcription occurs in the NUCLEUS

Replication occurs in the CYTOPLASM

77
Q

How do viruses with ssDNA genomes replicate

A

+ssRNA is used as mRNA, and a - strand is formed to complement this (now we have a dsDNA)

+ strand is used to code for capsomere protein

(-) strand is used to form a complement + strand, which is placed into a capsid made by the capsomere protein

78
Q

How do viruses with dsRNA genomes replicate?

A

the dsRNA is first unwound

the + strand (mRNA) codes for a capsomere protein

the - strand is used to make a complementary + strand, which forms back to a double-strand (both + and - stand)

this new dsRNA is placed within the capsid formed by the capsomere protein (enveloped)

79
Q

How do viruses with +ssRNA genomes replicate?

A

the + strand is used as mRNA, which codes for the formation of a capsomere protein

a - strand is made that complements the + strand (or mRNA). This is used to further make an additional +RNA strand (via viral RNA Polymerase) that is placed within the capsid formed by the capsomere protein (naked)

80
Q

How do viruses with -ssRNA genomes replicate?

A

the - strand is used with RNA-dependent RNA Polymerase to form a + strand and an mRNA strand.

the mRNA strand goes to code for a capsomere protein

the + strand is used to form a complementary - strand, which is placed within the capsid that is formed by the capsomere protein (in an envelope)

81
Q

What is a Retrovirus?

A

A type of virus that has RNA instead of DNA as its genetic material

Using Reverse Transcriptase, an RNA-dependent DNA Polymerase, to incorporate its dsDNA into the host genome

82
Q

What is a Latent Virus, and an example?

A

When a virus is present in the body but exists in a resting (latent) state without producing more virus

e.g., Epstein Barr virus (EBV): incorporates its genome into the host, so NOT gearing up to make lots of copies of its genome or lots of coat protein

83
Q

Capsid proteins and genome are brought into a particular location for ASSEMBLY

Where is this for Enveloped viruses?

What about Non-Enveloped viruses?

A

Enveloped = assembly near the membrane where budding will take place

Non-Enveloped = assembles in the nucleus

84
Q

How does “budding” of an enveloped virus work?

A
  1. Viral proteins made by the viral genome are brought in with the capsid, becoming “spikes” of virus that attach to the host plasma membrane
  2. The viral matrix protein COATS inside of plasma membrane
  3. The nucleocapsid becomes ENCLOSED by the viral envelope, which is composed of the host cell’s plasma membrane
  4. Budding is completed, and the virus is enveloped with viral spikes surrounding it. The host membrane stays intact.
85
Q

What are some of the effects of animal viruses on cells?

A

-Normal cells are transformed into TUMOR cells

-Latent infection

-Acute infection (host cell dies and virus is released when cells lyse)

-Persistent infection (virus is released by budding and cell usually survives)

86
Q

T/F: Viruses do not need to be grown in cells

A

FALSE - viruses MUST be grown in cells, like a tissue culture

87
Q

T/F: Some viruses, such as influenza, are grown in fertilized chicken eggs

A

TRUE

88
Q

Give an example of a how a virus can be grown in the lab

A

TISSUE CULTURE

  1. Tissue is minced into small fragments
  2. This is incubated with a protease to disperse the cells
  3. Tissue fragments are placed into a flask with growth media to allow for cells to grow
  4. Cells settle on the surface of the glass and grow in a confluent single layer (monolayer)
89
Q

REVIEW QUESTION

What are the 3 ways viruses enter cells?

A
  1. Direct Penetration
  2. Membrane Fusion
  3. Endocytosis
90
Q

REVIEW QUESTION

Where does transcription of a +ssDNA virus occur

What about DNA replication?

A

Transcription occurs in NUCLEUS

Replication occurs in CYTOPLASM

91
Q

What are the differences between the following infections, and an example of each:

Acute
Chronic
Latent

A

Acute = virus disappears after disease ends (e.g., influenza, measles)

Chronic = After initial infection with or without disease symptoms, virus is released from host with no symptoms (e.g., Hep. B, AIDS)

Latent = virus that is maintained in neurons in a non-infectious state after initial infection, but activated to produce new disease symptoms at a later time (e.g., Chickenpox, Herpes Simplex)

92
Q

What is Hemagglutination?

A

used for the diagnosis of some enveloped viruses such as influenza viruses

no hemagglutination indicates that there is a presence of antibodies, whereas clumping indicates that the virus is attaching to the RBCs

93
Q

Explain how Herpes Simplex is a latent infection.

A

Initial infection occurs at 3 - 5 years old, causing cold sores. This moves up to trigeminal nerve where it remains latent

The latent virus is activated and cold sores recur

94
Q

What does it mean if a virus is lytic or temperate?

A

Lytic = only one phase; phage reproduces within the bacterial cell, then lyse the cell

Temperate = two phases - lytic and lysogenic - where the latter is when a phage can incorporate their DNA into the host cell’s genome

95
Q

In what way can lytic viruses be quantified?

A

By counting the “plaques” they produce through lysing a bacterial host on an agar plate and calculating the titer

96
Q

Explain the process of how a Retrovirus (e.g., HIV) gets replicated?

A
  1. Virus attaches and enters into the host cell, uncoating the viral RNA from capsid
  2. Reverse transcriptase is used to make a DNA template from the viral RNA strand. This DNA strand is used to form the other complimentary strand - forming a double helix
  3. The dsDNA copy is integrated into the host chromosome
  4. Transcription occurs of the viral genes, and many RNA copies are formed that code for many proteins
  5. When translated, the viral RNA is able to produce capsid proteins, envelope proteins (spikes), and reverse transcriptase
  6. All of these parts go to assemble many new virus particles, each containing reverse transcriptase to do this process over again
97
Q

In host DNA, describe the process of how cancer may result from a virus

WILL BE ON THE EXAM, KNOW THE PROCESS!

A
  1. Normal State
    -the mRNA from a “repressor gene” allows for the formation of a repressor to repress the proto-oncogene, the gene that allows for more cell division
    -RESULT: no cancer
  2. FIRST HIT BY VIRUS
    -A virus inserts a promoter region before the proto-oncogene
    -the repressor still is able to repress the proto-oncogene
    -RESULT: no cancer
  3. SECOND HIT BY VIRUS
    -A virus then inserts a protein within the “repressor gene” due to its segmentation
    -This prevents a repressor from repressing the proto-oncogene, so the promoter is able to “run” this gene
    -mRNA from the proto-oncogene forms proteins that allow for cell division to occur
    -RESULT: rapid cell division and CANCER
98
Q

What are the targets of anti-viral drugs?

A
  1. Viral Uncoating (e.g., influenza)
  2. Nucleic Acid Synthesis (e.g., HIV)
  3. Assembly and Release of Viral Particles
99
Q

LIKELY SHORT ANSWER QUESTION ON EXAM

Describe 1 anti-viral drug and how it works.

A

Armantadine - an anti-viral drug that targets viral uncoating in Influenza A virus)

-neutralizes the acid environment within phagolysosomes that is necessary for viral uncoating

ADMINISTRATION: oral

ADVERSE EFFECTS: toxic to CNS; nervousness, insomnia, blurred vision

VIRAL RESISTANCE: mutation resulting in a single amino acid change in a membrane ion channel

100
Q

What are some ways viruses are transmitted?

A

-Fecal-oral
-Sexual
-Respiratory droplets
-Fomites
-Vectors
-Skin
-Placenta or breast milk
-Iatrogenic

101
Q

Some viruses infect humans only; others called ________ also infect animals

A

Zoonotic

102
Q

What is an example of a zoonotic virus?

A

-measles
-influenza

103
Q

How do viruses disseminate within the body?

A
  1. Begins at the site of entry
  2. Enters either lymph node or blood
  3. Replicates in muscles, liver, spleen, or blood vessels
  4. Enters blood again
  5. Replicates in skin, mucous membranes, lungs, kidneys, GI tract, or brain
104
Q

Influenza is an example of an antigenic variation.

What is Antigenic Drift and Antigenic Shift?

A

Antigenic Drift = point mutations

Antigenic Shift = genetic reassortment - “gene swapping”

105
Q

In segmented viruses, describe genetic reassortment.

A

-Replication of nucleic acid and synthesis of protein coats occurs in a cell with two different viruses

-Assembly occurs with the formation of protein coats, and the two viruses may now have different chromosomal structures (as a nucleic acid from the opposite virus enters in)

-Lysis of these protein coats leaves genetic reassortment of RNA segments

106
Q

Describe the following features of Influenza:

Symptoms
Incubation Period
Pathogenesis
Prevention/Treatment

A

SYMPTOMS:
-fever, muscle aches, lack of energy, headache, sore throat, nasal congestion

INCUBATION PERIOD: 1-2 days

PATHOGENESIS:
-infection of respiratory epithelium; cells destroyed and virus released to infect other cells

PREVENTION/TREATMENT:
-vaccines are 80-90% effective; Amantadine effective for Type A only; vaccine is best bet

107
Q

T/F: the Influenza pandemic of 2009 (H1N1) was more deadly than the pandemic on 1918, resulting in more total deaths

A

False - that pandemic led to the deaths of 50 million people. Only 12,700 died in 2009 (very low considering 300,000 children died of malaria that year, and 600,000 others died from diarrheal diseases)

108
Q

There are three different relationships between a human host and a microorganism

What are they?

A
  1. Mutualism (e.g., normal gut bacteria)
  2. Commensalism (e.g., skin flora, doesn’t harm the host)
  3. Parasitism: one organism benefits while the other is harmed (e.g., Chlamydia)
109
Q

What are some “reservoirs” of infectious disease?

A

Humans: (HIV, Polio)

Other Animals:
-Bat (SARS, Ebola)
-Mouse (Lyme Disease, Hantavirus)
-Cat (Toxoplasma)

Non-Living:
-Soil (Botulism)
-Water (cholera
-Food

110
Q

T/F: Rabies has several animal reservoirs

A

True - especially in Idaho with bats!

111
Q

In Lyme disease, which is the reservoir - a deer or a tick?

A

Deer - the tick is the vector that transmits the disease

112
Q

List the 3 Mechanisms of Transmission

A
  1. Contact Transmission
    -direct contact (e.g., rabies)
    -indirect contact by fomites (e.g, common cold)
    -droplets (e.g., influenza, common cold)
  2. Vehicle Transmission
    -waterborne
    -foodborne
    -airborne
  3. Vector Transmission
    -mechanical (on insect body parts, Salmonella)
    -biological (tick, flea)
113
Q

List some of the Portals of Exit

A

-Ear (earwax)
-Broken skin (blood)
-Skin (flakes)
-Anus (feces)
-Eyes (tears)
-Nose (secretions)
-Mouth (saliva, sputum)
-Mammary Glands (milk, secretions)
-Vagina (secretions, blood)
-Urethra (urine)
-Seminal Vesicles (semen, lubricating secretions)

114
Q

Define Epidemiology

A

The study of the mechanisms involved in the frequency and spread of disease

-not just infectious disease, but also cancer, heart disease, etc.

115
Q

Why is it important to study the Epidemiology of a disease?

A

It can aid in designing strategies to prevent disease

116
Q

What is the Mechanism of Action for the following exotoxins:

Botulism toxin
Tetanus toxin
Cholera toxin

A

Botulism = block presynaptic release of Acetylcholine; found in peripheral areas

Tetanus = block of neurotransmitters in CNS, causing larger-scale paralysis

Cholera = elevates cAMP levels in GI tract that leads to a disruption in function

117
Q

Define Incidence

A

number of NEW cases within a population in a specific period of time

118
Q

Define Prevalence

A

TOTAL number of people INFECTED within a population at a given time

119
Q

What is the Morbitity Rate?

A

Diseased Individuals / Total Population

120
Q

What is the Mortality Rate?

A

Deaths from Disease over Specified Time / Total Population

121
Q

What is a Sporadic Disease?

A

disease that occurs in RANDOM, UNPREDICTABLE pattern

122
Q

Differentiate Endemic, Epidemic, and Pandemic

A

Endemic = constantly in population in low numbers (e.g., Influenza)

Epidemic = incidence of disease suddenly becomes higher than normal (e.g., measles)

Pandemic = worldwide epidemic (e.g., COVID-19, Spanish Flu)

123
Q

What happens to normal flora when a pathogen is prominent?

A

Normal flora live in harmony with the host during healthy times, but it can become PATHOGENIC when host defenses are lowered

124
Q

How do you determine the Causative Agent

A

Koch’s Postulates!

  1. The microorganisms must be present in every case of the disease
  2. The organisms must be isolated from the diseased host and grown in culture
  3. The pure culture must cause the same disease when introduced to a new host
  4. The microorganism must be recovered from the experimentally infected host
125
Q

What are the Molecular Postulates?

A
  1. The virulence factor gene or its product should be found in pathogenic strains but not in non-pathogenic strains
  2. Introduction of a virulence gene should change a non-pathogenic to a pathogenic strain; disruption of the virulence gene should reduce virulence
  3. Virulence genes must be expressed during disease process
  4. Antibodies of immune cells specific for the virulence gene products should be protective
126
Q

How does a microbes “break through” the body’s defenses?

A

Adhesions allow binding to certain cell types (e.g., E. coli strains contain a special pili that binds to cells lining the bladder)

127
Q

DISEASE PRESENTATION

What is the pathogenesis of Hepatitis B? How can it be treated?

A

Transmitted through the genital tract or direct inoculation of the virus into the bloodstream (blood, semen)

SYMPTOMS: abdominal pain, dark urine, jaundice, nausea/vomiting, fever, cirrhosis

DIAGNOSIS: blood tests, liver ultrasound, liver biopsy

TREATMENT: there is a vaccine available for all age groups, this is the only preventative measure as there is no cure

128
Q

How can bacteriophages contribute to human diseases even though they do not infect human cells? Give an example

A

phages can introduce a gene that is harmful to humans (e.g., an antibiotic resistance gene or a toxin) from one bacterium to another.

BIO-360: Microbiology (6 decks)

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