Exam 4 Flashcards

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1
Q

Virus Shape: Helical

A

Nucleic acid within a hollow, cylindrical capsid made of capsomeres

Spring-looking

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2
Q

Virus Shape: Polyhedral

A

Many-sided, often icosahedral (20 triangular faces)

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3
Q

Virus Shape: Complex

A

Lack symmetry

Ex. bacteriophage

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4
Q

Prions

A

Misfolded proteins that cause host proteins to also misfold

Short for proteinaceous infectious particles

Have no genome involved; just a protein –> simpler infectious agent than a virus

Responsible for Mad Cow Disease and other neurological diseases

Prion diseases are genetic or acquired from the outside

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5
Q

We’ve only known about viruses for ~____ years

A

100

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6
Q

Tissue tropism

A

Even within a single host, a virus can only infect certain tissues

The virus has viral proteins that recognize receptors that are displayed on certain cells

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7
Q

Cellular tropism

A

Ex. a virus can infect a macrophage that has receptors, neurons don’t express those receptors so HIV can’t infect them

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8
Q

Virion

A

A complete, fully developed, infectious viral particle, found outside a host cell

Composed of nucleic acid surrounded by a protein coat

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9
Q

Capsid

A

Protein coat that surrounds a virus’s genome

Present in all viruses

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10
Q

Viruses require a ___ ___ for replication

A

host cell

Can’t be cultured in media like bacteria

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11
Q

Latent Viruses

A

Viruses that lay dormant in a host for an extended period of time

Virus still present, but doesn’t cause symptoms

Examples: Herpes simplexvirus (cold sores), Varicella virus (chicken pox, shingles, latent in nerve cells)

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12
Q

Viral genomes also vary in these ways (aside from DNA/RNA, single/double stranded)

A

Circular vs linear

Segmented (little fragments) vs non-segmented (one continuous piece)

Genome size – 1000’s to 250,000 nucleotides (smaller virus → smaller genome)

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13
Q

Envelope

A

Lipid bilayer that covers the capsid

Only found in some viruses

Formed from plasma membrane when a virus exits a host cell

Not made by the virus, just a part of the host cell’s membrane

Many viruses lack an envelop → naked (or nonenveloped)

Enveloped viruses are more susceptible to alcohol
Hand sanitizer helps tamper spread of infection;
COVID virus has envelope → alcohol dissolves spike proteins + envelope → no longer able to bind to host cell receptor

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14
Q

Lytic Cycle: Steps

A
  1. Attachment – phage attaches by the tail fibers to a receptor of the bacterial cell
  2. Penetration – DNA (genome) is injected into the bacterial cell; only the genome gets injected, not the whole phage
  3. Biosynthesis – production of phage DNA and proteins
  4. Maturation – assembly of phage particles
  5. Release – phage lyse the bacterial cell and release into the environment
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15
Q

Some RNA viruses are retroviruses, meaning…

A

They have an RNA genome they convert into a DNA version so that it can integrate into the host cell genome (ex.HIV)

Opposite of central dogma

Requires an enzyme that reads RNA and synthesizes DNA - Host cells do not have such an enzyme – cells never have to synthesize DNA from an RNA template

Retrovirus encode their own RNA-dependent DNA polymerase → reverse transcriptase (RT)

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16
Q

Lysogenic Cycle

A

Phage genome integrates/recombines into the bacterial genome → Prophage

Passed down as the bacterial cell divides (vertical)

At any given time, for a cell that contains a prophage, the prophage can excise itself and transition back into the lytic cycle

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17
Q

Temperate phage

A

Can choose between lytic and lysogenic cycles

Temperate phage and prophage are the same phage; depends on decision it makes

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18
Q

Life Cycle of Animal Viruses: Steps

A
  1. Attachment
  2. Entry
  3. Uncoating
  4. Biosynthesis
  5. Maturation
  6. Release
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19
Q

Attachment step in Life Cycle of Animal Viruses

A

virus binds to receptor on host cell

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20
Q

Entry step in Life Cycle of Animal Viruses

A

Virus enters host cell

Can occur through injection, receptor-mediated endocytosis (engulfed by host cell), fusion (only occurs for enveloped viruses)

Only uses one of these 3 routes

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21
Q

Fusion mode of entry in animal virus life cycle

A

Envelope (lipid bilayer) and membrane of host cell fuse

Only occurs for enveloped viruses

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22
Q

Uncoating step in Life Cycle of Animal Viruses

A

loss of capsid, releases nucleic acid into host cell

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23
Q

Biosynthesis step in Life Cycle of Animal Viruses

A

Production of nucleic acid and proteins

Process depends on Baltimore classification; If virus has DNA genome vs RNA genome

Important: 1. Viral genome must be replicated and 2. Viral proteins must be made

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24
Q

Maturation step in Life Cycle of Animal Viruses

A

nucleic acid and capsid proteins assemble

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25
Q

Release step in Life Cycle of Animal Viruses

A

New viral particles leaves the host cell

Can occur by rupture or budding (enveloped viruses)

Rupture/lysis: so many viruses are made that the cell bursts

Budding: new viruses made push against membrane, create bulge, keep pushing until membrane gives way and virus pops off, surrounded by the membrane.
The membrane parts now on it is the virus’ [new] envelope

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26
Q

Host range (tropism)

A

The spectrum of host cells a virus can infect

Certain viruses can infect only certain hosts, not everything out there

All organisms are susceptible to viruses [including bacteria]

Some viruses infect plants, others infect animals, others infect bacteria, etc; If they infect plants, for example, they don’t also infect animals → specificity

Within host, viruses typically only infect certain tissues/cells; Ex. COVID infects respiratory tract cells, not the liver or elsewhere

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27
Q

Host range is primarily determined by…

A

The ability of the virus to attach to the host cell and reproduce; does host produce the needed receptors or not

Attachment involves viral proteins and a receptor on the host cell

Tropism boils down to if the host cell is expressing a receptor on its surface that the virus can bind to so that it can get inside and cause an infection

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28
Q

Different viruses vary considerably in size

A

In general 20-1000 nm in length (very small)

Most are substantially smaller than bacteria

Some are roughly the same size as bacteria; these giant viruses are susceptible to smaller viruses (virophages)

Giant viruses can get infected by virophages

A prion is NOT a virus

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29
Q

All viruses have a nucleic acid genome

A

Some viruses have a DNA genome, other viruses have an RNA genome

Some viruses have a single-stranded genome, others have a double-stranded genome

These differences help us classify viruses → Baltimore classification system

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30
Q

Spike proteins

A

Project from the envelope of a virus

Spikes often bind receptors on the host cell

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31
Q

Bacteriophage (phage)

A

Virus that infects bacteria

Grown on media containing bacterial cells

Form plaques

Have been studied extensively as a model of virus replication; undergo lytic or lysogenic cycle

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32
Q

Lytic Life Cycle

A

When a bacteriophage docks on a cells surface, injects its genome, and converts the bacterial cell into a phage-producing factory

Results in lysis of the bacterial cell

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33
Q

Some viruses can cause persistent (or chronic) infections

A

number of virions gradually increases over time

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34
Q

Acute virus

A

A short-lived infection that resolves quickly

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35
Q

Viruses were initially distinguished from other infectious agents because they’re….

A

Small and obligate intracellular microbes

Obligates intracellular → viruses cannot reproduce on their own, need host cell to get into - however, some bacteria fit this description as well (e.g. Rickettsia)

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36
Q

We now distinguish viruses from cellular life forms based on their structure

A

Contain a single type of nucleic acid (DNA or RNA); cells have both, viruses have one or the other

Contain a protein coat (capsid)

Multiply within host cells using host machinery

Responsible for synthesis of structures that transfer viral nucleic acid to other cells; must exist host cell and infect new cells

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37
Q

Viruses can be grown in cell cultures

A

Plant/animals cells grown/maintained in media in the lab

Cell lines can be primary or continuous

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38
Q

Primary cell line

A

Derived from tissue, survive only a few generations

Aren’t able to receive survival signals from nearly cells

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39
Q

Continuous cell line

A

Derived from cancerous cells (immortal)

Ex. HeLa cells – isolated from cervical cancer from Henrietta Lacks

Cancer cells no longer rely on survival signals to survive

Much more useful; continue to grow

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40
Q

Virus Discovery

A

The study of viruses wasn’t possible until the 20th century

1886: Tobacco Mosaic Disease could be transferred from plant to plant

1892: the causative agent of Tobacco Mosaic Disease could pass through the pores of a filter. In contrast, bacteria get trapped in the filter. Infective agent was small enough to pass → tells us the agent wasn’t bacteria

1935: Tobacco Mosaic Virus was purified, enabling the study of its structure using electron microscopy

First time scientists ever saw viruses [within e. microscope]

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41
Q

[Bacterial] plaques

A

Zones of bacterial cell lysis

Formed by phages

Phage infects a bacterial cell, replicates to high numbers, lyses the cell, infects neighboring cells, etc.

Avisible clear area within a dense layer of bacteria (“lawn”) grown on an agar plate, where bacteria have been killed by a virus (bacteriophage), creating a zone of clearing that appears as a plaque; it’s an indicator of the presence and activity of a bacteriophage on the plate.

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42
Q

Which of the following years is closest to when viruses (such as the Tobacco Mosaic Virus) were first discovered?

A

1900

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43
Q

The interaction between viral surface proteins and host cell receptors is often responsible for:

A

host tropism

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44
Q

Which of the following components is common to ALL viruses?

A

capsid

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45
Q

Where is a prophage found?

A

Integrated into the bacterial genome

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46
Q

Which of the following enzymes is used by an RNA virus?

A

Viral RNA-dependent RNA polymerase

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47
Q

How are prions unique compared to other infectious agents (like bacteria and viruses)?

A

Prions lack nucleic acids

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48
Q

E. coli is part of the human gut microbiota. Instead of causing disease, E. coli often outcompete pathogens for resources, thereby reducing infection. This is an example of

A

Microbial antagonism

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49
Q

Which of the following statements are TRUE? Select all that apply.

A

All infections are caused by pathogens, All infectious diseases are caused by pathogens, All infectious diseases are caused by pathogens

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50
Q

Why did Typhoid Mary doubt that she was responsible for spreading typhoid fever?

A

She did not exhibit signs or symptoms of disease.

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51
Q

Which of the following are exceptions to Koch’s postulates? Select all that apply.

A

In addition to causing urinary tract infections, Escherichia coli is a member normal flora of the gastrointestinal tract

Pneumonia is a disease caused by multiple infectious agents

Treponema pallidum causes syphilis but is unculturable.

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52
Q

Which of the following is considered a communicable disease?

A

Flu

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53
Q

The work performed by an epidemiologist is most likely to include:

A

Determining the frequency and distribution of a disease in a population

54
Q

The ability of some microbes to alter their surface molecules and evade destruction by the host’s antibodies is called:

A

Antigenic variation

55
Q

Quorum sensing enables bacteria to make decisions based on:

A

Population density

56
Q

Diseases caused by eukaryotic pathogens are difficult to treat because

A

Their cells are structurally and functionally similar to human cells

57
Q

All beta lactam antibiotics:

A

Contain a beta lactam ring

58
Q

In lab, you identify a bacterial isolate that is antibiotic resistant. Which of the following serve as an appropriate explanation for why/how the bacterial isolate is antibiotic resistant?

A

Bacteria can acquire resistance genes through horizontal gene transfer

Bacteria randomly accumulate mutations while growing, and some mutations render the bacteria resistant

Some bacteria lack the components targeted by the antibiotic

59
Q

Antibiotic resistance

A

The ability of bacteria to subvert the harmful effects of an antibiotic

3 types of resistance: Intrinsic, Acquired, Evolved

60
Q

Intrinsic resistance

A

The bacteria lack the components targeted by the antibiotic

Cells that naturally lack a cell wall (e.g. Mycoplasma) are not affected by beta-lactam antibiotics

61
Q

Acquired resistance

A

Resistance is acquired from other bacteria through HGT

Is inevitable (”life will find a way”)

E.g. Resistance plasmids (R plasmids) contain several antibiotic resistance genes

62
Q

Evolved resistance

A

Mutations render the bacteria resistant

Survival of the fittest (here, the ones that can still grow in the presence of antibiotic)

63
Q

Prevalence

A

Total number of individuals with the disease, at a given point in time

Ex. How many people were affected with COVID at WCU last Thursday

64
Q

Incidence

A

Number of new cases of disease, over a period of time

Ex. How many people came down with the flu over the past month

65
Q

Pathogen

A

disease-causing organism (microbial)

66
Q

Infection

A

invasion or colonization of a host by a pathogen

Not all infections lead to disease; can be a carrier (or asymptomatic)

Typhoid Mary unknowingly transmitted typhoid fever to hundreds as a carrier of Salmonella typhi

67
Q

Infectious Disease

A

infection leading to change from a state of health

68
Q

Signs

A

Objective changes that can be observed and measured

Swelling, fever, paralysis

69
Q

Symptoms

A

Subjective changes that aren’t apparent to an observer

Pain, malaise, nausea

70
Q

Endemic

A

constantly present within a region, predictable (ex. seasonal flu, malaria)

71
Q

Epidemic

A

Significant increase above endemic levels within a region, “outbreak”

Ex. COVID in the early months; was only in China and had huge spike

72
Q

Pandemic

A

Epidemic across multiple continents, usually worldwide

Ex. COVID after being an epidemic + spread to other countries/continents

73
Q

Reservoir

A

Source of a pathogen, where a pathogen resides

3 kinds: humans, animals, nonliving

74
Q

Human reservoir

A

Include carriers (ex. Typhoid Mary)

Ex. HIV

75
Q

Animals reservoir

A

Zoonosis – disease that spreads from animals to humans

Ex. rabies, Lyme disease

76
Q

Nonliving reservoir

A

Soil – tetanus (C. tetani)

Water – cholera (V. cholerae)

77
Q

Epidemiology

A

The study of how and why diseases spread in populations

Epidemiologists consider approaches for controlling a disease

78
Q

John Snow

A

The Father of Epidemiology (~1850)

Traced the origin of a cholera outbreak back to a contaminated well in the center of London

Slowed transmission by removing the handle of the well pump, preventing access to contaminated water

79
Q

Approaches for controlling a disease: Treatment

A

(e.g. antibiotics)
Public health organizations
Centers for Disease Control and Prevention (CDC), in the US
World Health Organization (WHO), global

80
Q

Approaches for controlling a disease: Prevention

A

Vaccines
Reservoir, vector control
Water treatment
Food inspection
Hygiene, sanitation

81
Q

Approaches for controlling a disease: Public health organizations

A

Centers for Disease Control and Prevention (CDC), in the US

World Health Organization (WHO), global

82
Q

Pathogenicity

A

The ability to cause disease

Yes (pathogenic) or no (non-pathogenic)

No gray area; either yes or no

83
Q

Virulence

A

The severity of disease (degree of pathogenicity)

E.g. highly virulent (deadly) like ebola or rabies

84
Q

Virulence factor

A

Component of a bacterial pathogen that contributes to its ability to cause disease

Includes adhesins, toxins, extracellular enzymes, etc.

Bacterial pathogens are pathogens because they exhibit virulence traits

85
Q

Quorum sensing

A

Bacteria’s ability to sense and respond to population density

Alter their behavior depending on how many other bacterial cells are around

If enough cells are nearby, they can work together to accomplish a complex task (e.g. biofilm)

86
Q

Exotoxins (toxins)

A

Secreted by pathogenic bacteria to damage host tissue

3 categories (SAM): Superantigens, A-B toxins, Membrane-disrupting toxins

87
Q

Membrane-disrupting toxins

A

Forms pores in or dissolves the cell membrane → cell dies

87
Q

Superantigens

A

Provokes the immune system to overreact leading to host damage

87
Q

Antimicrobial drugs

A

Chemical substances that kill or suppress the growth of microbes

A type of chemotherapy

87
Q

Endotoxin

A

Another term for lipid A, which is part of the lipopolysaccharide (LPS) that covers the outer membrane Gram negative bacteria

88
Q

Antibiotics

A

Antimicrobial drugs with specificity for bacteria

Doctor won’t subscribe antibiotics for a viral infection

89
Q

Natural antibiotics

A

Those naturally produced by microbes

Can be improved upon (ex. Penicillin G)

90
Q

Kirby Bauer Method

A

Measure a bacterium’s susceptibility/resistance to many antibiotics simultaneously

91
Q

Beta-lactam antibiotics

A

possess a beta-lactam ring that covalently bind the active site of the transpeptidase, preventing peptides from crosslinking the peptidoglycan

92
Q

Biofilms

A

A collection of bacteria that attach to a surface

Produced by bacterial pathogens

Held together by a matrix consisting of exopolysaccharide (EPS)

Serves as physical barrier from immune system (and antibiotics)

93
Q

Steps to biofilm process

A
  1. Planktonic cells attach to surface via flagella
  2. Cells reproduce and form microcolonies
  3. Produce EPS (“glue”)
  4. Continues until large group made, “mature”
  5. Leave either because its so big that a part breaks off or the cells choose to leave to go back to planktonic state
94
Q

A-B Toxins

A

2 components: A – active (enzyme) and B – binding (to receptor)

Bacterial cell secretes A-B toxin outside of cell
B component of A-B toxin binds to host cell → B-component binds to its receptor → induces endocytosis → host cell engulfs A-B toxin

A component cuts up intracellular signals → causes host cell to not function normally

Examples: Tetanus toxin, Anthrax toxin, Diphtheria toxin
Each interfere with different signaling systems inside host cell but use same mechanism

Toxin causes signs/symptoms

95
Q

Semi-synthetic antibiotics

A

biologically-produced then chemically modified

96
Q

Synthetic antibiotics

A

completely synthesized chemically

97
Q

Broad spectrum

A

antibiotic is effective against a wide range of bacteria

98
Q

Narrow spectrum

A

antibiotic is only effective against certain species

99
Q

bactericidal antibiotics

A

kill bacteria

Compromised immune system → doctor should prescribe a bactericidal antibiotic

100
Q

bacteriostatic antibiotic

A

inhibit the growth of bacteria

101
Q

Transmission: Contact

A

Direct contact: person-to-person (ex. STDs)

Congenital: from mother to fetus/newborn

Indirect contact: via fomites (inanimate objects that harbor pathogens, ex. pen)

Droplet: produced by sneezing, coughing, etc. and travel less than 1 meter

102
Q

Transmission: Vehicle

A

Air: aerosols, travel more than 1 meter (ex. tuberculosis)

Water: often fecal contamination (fecal-oral route)

Food: undercooked, improper storage, unsanitary conditions

103
Q

Transmission: Vector

A

Spread by arthropods (mosquitoes, ticks, fleas)

Mechanical (passive transport, fly landing on food) or biological (part of pathogen lifecycle, malaria parasite goes through changes inside mosquito)

104
Q

Emerging diseases

A

New diseases that are becoming more common

Often zoonotic and recently jumped the species barrier (ex. COVID affected bats then humans)

105
Q

4 common mechanisms of resistance

A
  1. Alter the target: mutation prevents the antibiotic from binding its target
  2. Degrade the antibiotic: cleave beta lactam ring
  3. Modify the antibiotic: inactivate it
  4. Remove the antibiotic from the cell: drug efflux pumps pushes antibiotic out, can be multi-drug → resistant to multiple antibiotics
106
Q

Opportunistic pathogen

A

A microorganism that is normally harmless to healthy people but can cause disease in certain circumstances

Under the right circumstance, some members of the normal flora can become pathogenic

May occur if the host is immunocompromised → individuals with AIDS are susceptible to infection by microbes of the normal microbiota

If the microbe gains access to another body sites → E. coli reaches the urinary tract leading to a urinary tract infection

107
Q

Communicable infectious diseases

A

Spread from person-to-person

Chickenpox, flu, AIDS

108
Q

Noncommunicable infectious diseases

A

Malaria (requires mosquito intermediate), tetanus, botulism (via food), anthrax

109
Q

Pathogen Portals of Entry

A

Many pathogens have a preferred portal of entry into the host

  1. Mucous membranes, most common (respiratory, gastrointestinal, genitourinary)
  2. Skin
  3. Parenteral (puncture, injection, bite, cut, ex. tetanus)

Pathogens also exit the body through many of the same portals

Respiratory and gastrointestinal tract are most common

110
Q

Coagulase

A

Enzyme that causes blood clots

Secreted by Staph. aureus to protect the bacteria from phagocytosis and other defenses

Bacteria can express kinases to dissolve clots

Bacteria produce coagulase → clot forms → bacteria produce kinase, dissolving clot and releasing bacteria

111
Q

Hyaluronidase

A

Enzyme that breaks down connective tissue that holds epithelial cells together

Collagenase breaks down collagen → allows bacteria to enter + evade

Used to disseminate from the initial site of infection and invade further into the body

112
Q

Fleming’s Discovery of Penicillin

A

The first antibiotic was discovered in 1928 by Alexander Fleming

Fleming was studying the bacterium S.aureus and noticed that the growth of S. aureus on an agar was inhibited by a mold that had contaminated the plate

The mold Penicillin notatum produces a compound called penicillin

Penicillin was shown to possess antibacterial activity against streptococci, meningococci, and Corynebacterium diphtheriae

113
Q

Adherence

A

Attachment/adherence is often the first step in bacterial pathogenesis

Adherence is a virulence trait, adhesins/pili/fimbriae are the virulence factors

Bacterial pathogens express adhesins of their surface that binds to a receptor on the surface of a host cell

Pili/fimbriae mediate long-range attachment
Other adhesins mediate short-range attachment

114
Q

Ehrlich’s Magic Bullet

A

In the early 1900s, the German physician and scientist Paul Ehrlich set out to identify a “magic bullet” to treat infections by targeting infectious microbes without harming the patient.

After screening over 600 arsenic-containing compounds, he found one that targeted the bacterium Treponema pallidum, the causative agent of syphilis.

The compound was found to successfully cure syphilis in rabbits and soon after was marketed under the name Salvarsan as a remedy for the disease in humans

Ehrlich’s approach of systematically screening a wide variety of compounds remains a common strategy for the discovery of new antimicrobial agents today

115
Q

autoinducer

A

Quorum sensing signal, binds to receptor protein(s)

Constitutively expressed

If many bacteria are nearby, a lot of quorum sensing signal will be present in the local environment

If enough quorum sensing signal enters into the cell, expression of certain genes will be induced leading to group behaviors (e.g. biofilms)

Can occur between alike and different bacteria

116
Q

therapeutic index (TI)

A

Measure of the safety of an antimicrobial drug

Calculated as the ratio of Tolerable Dose: Effective Dose

Tolerable dose: how much host can tolerate without getting harmed

Effective dose: dose required to kill bacteria

We want tolerable dose to be high and effective dose to be low

Higher TI = safer the drug (read: a wide range of doses are tolerable yet effective)

117
Q

Minimal Inhibitory Concentration (MIC)

A

The smallest concentration necessary to kill/inhibit bacteria

Determines effectiveness of an antibiotic

Antibiotic is serially diluted in broth, then bacteria is added to each tube and incubated

MIC corresponds to the tube with the lowest concentration of antibiotic without growth

118
Q

Why do pathogens cause disease?

A

They are trying to survive and reproduce

Humans just happen to be harmed in the process

Many pathogens cause symptoms that aid in their transmission

119
Q

How many pathogens are required for infection?

A

Depends on the pathogen (and portal of entry)

120
Q

ID50

A

The number of cells required to produce an infection in 50% of a population

ID = infectious dose

121
Q

LD50

A

The number of cells required to cause death in 50% of a population

LD = lethal dose

Often done in animals not humans for ethical reasons → results in less precise data for human infections

122
Q

Siderophores

A

Secreted by some pathogenic bacteria

‘Steal’ the iron from the host’s iron-transport proteins

Bacterial cells express a siderophore receptor on their surface to mediate uptake of the siderophore-iron complex; binds to siderophore to bring it back

Siderophore binds to iron inside the body, bacteria import siderophore back into itself to use the iron

123
Q

Antigens

A

Bacterial pathogens change the identity of the proteins expressed on their surface (antigens) that could be recognized by our immune system

Allow the bacteria to outrun the immune response (takes ~1 week to produce antibodies)

The new ones made evade detection by the antibodies produced; gives 1 week head start

Immune responses (antibodies) are specific to the proteins of the bacteria (antigens)

Host recognizes infection occurring → immune system produces antibodies that match the antigens present (takes ~1 week) → means pathogen can increase in number → antibodies produced + bind to antigen + kill antigen → number of bacterial cells drops

124
Q

Prions convert what to what

A

Convert a normal host protein (PrPC) into a misfolded version (PrPSc)

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

Properly folded → misfolded (PrPSc)

The PrPSc then converts more PrPC to PrPSc leading to the formation of amyloids that interfere with cellular functions

125
Q

Antimicrobial drugs must exhibit ______ _________ to have clinical relevance

A

selective toxicity; targets components/process that are present in the microbe but absent in the host

Ex. bacteria have cell walls composed of peptidoglycan, humans do not

Selective toxicity is relatively easy to achieve for antibiotics because there are many cellular differences between prokaryotes and eukaryotes
E.g. ribosome structure

Selective toxicity is much harder to achieve for viruses (use host machinery to replicate) and fungi (eukaryotes like humans)

Many antivirals and antifungals harm the human host

126
Q

Selective toxicity

A

affect the microbe without harming the host

127
Q

Baltimore classification system

A

Differs between viruses with:

A DNA vs RNA genome

A double-stranded (ds) vs single-stranded (ss) genome

A positive (+) sense vs negative (-) sense genome
+ : genes are on that strand
- : genes on other strand

128
Q

dysbiosis

A

Altering of the microbiota

Can lead to infection

Caused by a number of factors including use of antibiotics

129
Q
A