EXAM 4 Flashcards

1
Q

Explain why viruses are not considered to be alive

A

Acellular, uses host machinery to replicate, don’t make their own energy etc

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2
Q

Describe the events leading to the discovery of viruses

A

1886: Tobacco Mosaic Disease can spread from plant to plant
1892: the causative agent of TMD could be passed through a filter
1935: TMD is purified and its structure was able to be studied using electron microscopy

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3
Q

Explain how we distinguish viruses from other lifeforms

A

-contain a single type of nucleic acid (DNA or RNA)
- contain a protein coat
-multiply within a host’s cells using hos machinery
- responsible for synthesis of structures that transfer viral nucleic acids to other cells

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4
Q

Define host range/tropism

A

Host range is the spectrum of host cells that a virus can infect

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5
Q

Explain why viruses exhibit host/tissue/cell tropism

A

Host range is determined by the virus’s ability to attach to the host cells using viral proteins and a receptor. So, some host cells do not have the appropriate structures for the virus to attach and reproduce.

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6
Q

Describe how viruses vary in size and shape

A

Most viruses are substantially smaller with some being as big as a bacterium.

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7
Q

Define virion, capsid, and envelope

A

Virion: a completely developed, infectious viral particle, found outside a host cell
Capsid: protein coat that surrounds a virus’s genome
Envelope: lipid layer covering the capsid

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8
Q

Describe the basic structure of a virus

A

ALL viruses have a capsid, a nucleic acid genome. Some may have an envelope, segmented vs non-segmented genome, single/double-stranded genome, circular vs linear genome, and their general shape can vary.

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9
Q

Describe the ways in which viral genomes vary

A

circular vs linear, segmented vs nonsegmented, single vs double-stranded,

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10
Q

Describe the origin and purpose of the viral envelope

A

Formed from the plasma membrane when a virus exits a host cell. The envelope protects genetic information as the virus goes from host cell to host cell.

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11
Q

Explain how viruses are cultured

A

require a host cell to be cultured; cell culture

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12
Q

Describe cell/tissue cultures and their role in culturing viruses

A

cell cultures allow viruses to be grown and maintained in the lab. Cell lines can be continuous (derived from cancer cells) or primary (derived from tissue and survive for a few generations).

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13
Q

Describe the steps of the lytic cycle of a bacteriophage

A

A phage attaches to the bacterial cell using tail fibers. The phage injects its DNA into the bacterial cell. Phage DNA directs the synthesis of viral components by the host cell. The viral components get assembled into virions. The host cell lyses, releasing the new virions.

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14
Q

Explain the lysogenic cycle

A

Phage genome is integrated into the bacterial genome and passed down as the cell divides.

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15
Q

Define ‘prophage’ and ‘temperate phage’

A

Prophage: lysogenic life cycle; integrates into the bact. genome
Temperate phage: phages that can choose between and lytic and lysogenic life cycle

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16
Q

Describe the steps of the life cycle of an animal virus

A

The virus binds to a receptor on a host cell. The virus enters the host cell via injection, fusion, and receptor-mediated endocytosis. The capsid is lost and releases nucleic acids into the host cell. The virus will synthesize its chosen nucleic acid depending on the Baltimore classification system. The nucleic acids and capsid assemble and the virus is released from the cell via budding or rupture.

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17
Q

Explain the Baltimore classification system for viruses

A

The Baltimore classification system is a system used to determine the manner in which viruses synthesize mRNA.

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18
Q

Distinguish between acute, chronic/persistent, and latent infections

A

Acute: infection doesn’t last for very long before being killed off by the immune system
Chronic/persistent: long-lasting and gradually increase over time
Latent: viruses that can lay dormant for an extended period; virus is present without causing symptoms

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19
Q

Provide a description of a prion

A

proteins that cause host proteins to misfold

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20
Q

Explain how a prion converts the PrPC into PrPSc

A

The human genome encodes and human cells normally express PrpC. The secondary structure of the normal PrPC protein is primarily alpha helices. When PrPC encounters a prion, its secondary structure changes to beta sheets and is then referred to as PrPSc. The PrpSc continues to convert other PrPC proteins leading to the formation of amyloids that disrupt cellular functions.

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21
Q

Explain the relationship between the following terms: pathogen, infection, and
infectious disease

A

Pathogen: a disease-causing microbe
Infection: invasion/colonization by a pathogen
Infectious disease: infection leading to a change from a state of health

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22
Q

Explain why not all infections lead to disease

A

An individual can be a carrier or asymptomatic meaning they have an infection but it does not present itself or cause damage

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23
Q

Define ‘normal microbiota/flora’

A

microbes found in/on a healthy human; all microbial genes present in/on the body

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24
Q

Explain how humans acquire their microbiota and the factors that impact the
composition of a microbiota

A

Human microbiota development begins at birth and how you are born matters. The microbiota changes significantly over several years because of food, people, and pets. Nutrients, physical/chemical factors, host defense, and mechanical factors influence the composition of the microbiome as well.

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25
Q

Describe the importance/role of the human microbiota

A

Protects the host from pathogens via microbial antagonism (competitive exclusion). They outcompete the pathogens for resources, effectively killing them off.

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26
Q

Explain the relationship between the microbiota and opportunistic pathogens

A

If a microbe found in/on one part of the body reaches another body site it can become pathogenic. As well as for immunocompromised people, the natural microbiome can be harmful.

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27
Q

list Koch’s postulates

A

1) Microbe is present in an infected individual and not in a healthy individual
2) Microbe can be isolated from the diseased host in a pure culture
3) The isolated microbe causes disease when inoculated into a healthy host
4) The pathogen can be isolated from the inoculated host

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28
Q

Provide some exceptions to Koch’s postulates

A

Some microbes are unculturable, some require host cells, some diseases can be caused by multiple infectious agents, some cause multiple diseases

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29
Q

Explain the difference between signs and symptoms

A

Signs: objective changes that can be measured or observed (fever, swelling, paralysis)
Symptoms: subjective changes that aren’t apparent to the naked eye (pain, nausea, malaise)

30
Q

Explain the relationship between infectious diseases and communicable diseases

A

Infectious diseases are caused by pathogens and spread when the pathogen infects a new host. Communicable diseases are diseases that spread from person to person.

31
Q

Define ‘prevalence’ and ‘incidence’ and explain how the terms are related

A

Prevalence: total number of individuals w/ a disease at a given time
Incidence: new cases over time
These terms are related because prevalence is affected by incidence.

32
Q

Explain the difference between endemic, epidemic, and pandemic

A

Endemic: constantly present w/in a population, predictable (common cold for example)
Epidemic: increase above endemic levels in a region
Pandemic: epidemic across multiple continents or worldwide

33
Q

List and describe various disease reservoirs

A

Humans as carriers, animals via zoonosis (a disease that spreads from animal to human), Nonliving things such as microbes in water or soil

34
Q

List and describe various transmission routes

A

Contact (direct, indirect, congenital, droplet), vehicle (air, water, food), vector (arthropods like mosquitoes, ticks, and fleas)

35
Q

Explain the origin of emerging diseases

A

often zoonotic or jumped the species barrier; pathogens ‘learn’ how to infect new hosts or a vector’s geographical range expands

36
Q

Define epidemiology

A

the study of how and why diseases spread in a population

37
Q

Explain John Snow’s role in controlling London’s cholera outbreak in the 19th century

A

Traced the origin of cholera to a contaminated well in London

38
Q

Describe the methods used by epidemiologists to control the spread of disease

A

treatment (antibiotics), prevention (vaccines, reservoir control, water treatment, hygiene/sanitation), public health organizations

39
Q

Explain WHY pathogens cause disease

A

to survive and reproduce, cause symptoms that aid in transmission

40
Q

List ways for pathogens to enter into and exit from hosts

A

mucous membranes (urinary tract, gastro tract etc), skin, parenteral (puncture, bite, injection, etc.). Pathogens tend to exit hosts in the same ways

41
Q

Explain how ID50 is used to describe how many cells are required for a pathogen to
produce an infection

A

ID50 is used to describe how many cells are required to cause disease in 50% of a population.

42
Q

Explain the difference between pathogenicity and virulence

A

Pathogenicity: the ability of a pathogen to cause disease
Virulence: the severity of a disease (degree of pathogenicity); highly virulent = deadly

43
Q

Define ‘virulence factor’ and provide examples

A

Virulence factor: component of a bacterial pathogen that contributes to its pathogenicity
EX: adhesins, toxins, extracellular enzymes

44
Q

explain the significance of adherence and the role of adhesins

A

Often the first step in bacterial pathogenesis; pili/fimbriae mediate long-range attachment, other adhesins mediate short term attachment

45
Q

Explain how and why coagulase and hyaluronidase/collagenase modify the host
environment

A

coagulase causes blood clots; bacteria secrete coagulase to protect themselves from phagocytosis and other defenses
hyaluronidase breaks down connective tissue; used to disseminate from the original site of infection and invade the body further

46
Q

Explain how antigenic variation allows pathogens to outrun the host immune response

A

They constantly change the proteins expressed on their surface to avoid the immune system recognizing them and killing them

47
Q

Describe the structure of a biofilm and the steps involved in making a biofilm

A

biofilms are made up of a collection of bacteria held together by an extracellular matrix called exopolysaccharide.
1) attachment to a mono layer via flagella
2) micro-colonies form
3) EPS production
4) maturation of biofilm
5) dissolution and dispersal

48
Q

Describe the purpose of quorum sensing and explain (at a molecular level) how quorum sensing is performed

A

Quorum sensing is used to complete complicated tasks that a bacterium wouldn’t be able to do on its own. Bacteria have a quorum-sensing signal that is always expressed so when a bacterium senses a lot of other signals it will express certain genes that allow it to perform group behaviors such as the formation of a biofilm.

49
Q

Explain the purpose of siderophores

A

All organisms require iron. Pathogens must acquire iron through the host but can’t due to the iron being bound to iron-transport proteins secreted by the host. Some pathogenic bacteria secrete siderophores that steal iron from the host’s iron-transport proteins.

50
Q

Distinguish between an exotoxin and an endotoxin

A

Most pathogenic bacteria secrete exotoxins that damage the host ( A-B toxins, membrane-disrupting toxins, superantigens). Endotoxins are another name for Lipid A, which is a part of the LPS that covers the outer membrane of Gram neg. bacteria. Lipid A gets released when Gram neg. cells die. Endotoxins cause the immune system to overheat causing symptoms such as fever.

51
Q

Describe the structure of an A-B toxin and explain the role of each component

A

A-B toxins involve enzymes that change their substrate. A- active (enzyme), B- (binding)

52
Q

Describe the effect of an endotoxin on the host

A

causes the immune system to heat up causing symptoms such as fever

53
Q

Define and distinguish between antimicrobial drugs and antibiotics

A

Antimicrobial drugs: chemical substances that kill or suppress the growth of microbes
Antibiotics: a TYPE of antimicrobial drug w/ specificity for bacteria

54
Q

Describe how the first antibiotic (Penicillin) was discovered

A

The first antibiotic was discovered in 1928 by Alexander Fleming while studying S. aureus. He noticed the growth of S. aureus on an agar was inhibited by a mold that contaminated the plate.

55
Q

Describe the origin of natural antibiotics

A

Natural antibiotics are produced by microbes

56
Q

Explain why microbes naturally produce antibiotics

A

To outcompete other microbes

57
Q

Distinguish between natural, semi-synthetic, and synthetic antibiotics

A

Natural: produced by microbes; can be improved on
Semi-synthetic: biologically produced then chemically modified
Synthetic: completely synthesized chemically

58
Q

Explain the concept of selective toxicity

A

Selective toxicity is the drug’s ability to affect the microbe w/o harming the host. They do this by targeting certain components/processes present in the microbe but not the host (peptidoglycan walls).

59
Q

Describe HOW and WHY the therapeutic index is calculated

A

The TI is calculated to measure the safety of antimicrobial drugs. TI is calculated as the ratio of tolerable dose to effective dose.

60
Q

Explain how antibiotics achieve selective toxicity

A

Achieved by targeting certain components that are present in the microbe but not the host

61
Q

Classify antibiotics based on spectrum and explain how spectrum should be taken into account when prescribing an antibiotic to treat an infection

A

Broad: effective against different sets of bacteria
Narrow: effective against certain species
This should be taken into account when prescribing if you don’t know which species is causing infection

62
Q

Explain why both bactericidal and bacteriostatic antibiotics are effective at treating infections

A

Even though bacteriostatic antibiotics don’t kill bacteria directly, they slow growth enough for the immune system to clear the infection.

63
Q

List some bacterial processes that are targeted by antibiotics

A

peptidoglycan walls, cell wall synthesis

64
Q

Describe how the bacterial cell wall is constructed including the enzymes involved

A

1) Precursors are synthesized in cytoplasm
2) Precursors are transported across cell membrane
3) Sugars are linked together by TRANSGLYCOSYLASES
4) Peptides are linked together by TRANSPEPTIDASES

65
Q

Describe the structure of beta-lactam antibiotics and explain how beta-lactam antibiotics inhibit cell wall synthesis

A

Beta-lactam antibiotics possess a beta-lactam ring that covalently bonds to the active site of the transpeptidase, preventing peptides from being cross linking peptidoglycan

66
Q

Explain how and why the MIC test is performed

A

HOW: Antibiotic is serially diluted in broth, then bacteria is added to each tube and incubated
WHY: to measure the effectiveness of antibiotics

67
Q

Explain how and why the Kirby-Bauer method is performed

A

HOW: a dilute culture is spread across an agar plate, disks with antibiotics are placed on top of the agar and the plate is incubated. During incubation, the antibiotic diffuses away from the disk into the agar and potentially inhibits growth of bacteria at that location,
WHY: to measure a bacterium’s susceptibility/resistance to many antibiotics simultaneously

68
Q

Describe antibiotic resistance/susceptibility based on the appearance of plates from a
Kirby Bauer Test

A

the smaller the ZOI the more resistant the bacteria is to the antibiotic

69
Q

List and explain 3 forms of antibiotic resistance

A

Intrinsic: the bacteria lack the components targeted by the antibiotic
Acquired: resistance acquired from another bacteria via HGT
Evolved: mutations render the bacteria resistant

70
Q

Explain how antibiotic resistance evolves during an infection

A

survival of the fittest; any sensitive bacteria die, only resistant bacteria survive, all resources will now go to resistant bacteria