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MicroBio > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

A single microbe causes

A

a particular disease

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2
Q

Symbiosis

A

an association of two or more different species of organisms
- organisms living together
- at least one benefits from relationship
- other may be injured, relatively unaffected, may also benefit

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3
Q

When microbe interacts with a larger organism:
- microbe =
- larger organism =

A

symbiont, host

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4
Q

T / F: the term symbiosis is restricted to mutually beneficial relationships

A

F

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5
Q

T / F: a disease can have multiple microbial causes

A

T

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6
Q

Ectosymbiont

A

organism located on surface of another organism

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7
Q

Example of ectosymbiosis

A

bacteria on skin

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8
Q

Endosymbiont

A

organism located within another organism

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9
Q

Endosymbiosis example

A

bacteria in gut

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10
Q

Consortium

A

hosts that have more than one associated symbiont

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11
Q

Types of microbial interactions (7)

A

mutualism, cooperation, commensalism, predation, parasitism, amensalism, competition

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12
Q

Microbial interactions/relationships can be

A

intermittent, cyclic or permanent

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13
Q

Mutualism

A
  • reciprocal benefit to both partners
  • relationship with some degree of obligation (typically cannot live separately)
  • mutualist and host are codependent on each other
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14
Q

An example of mutualism between organisms supports the idea of

A

coevolution

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15
Q

Ruminants

A

animals (like cattle, sheep) that have a stomach with four compartments

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16
Q

Rumen

A

upper part of the ruminant stomach

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17
Q

Cooperation

A

relationship that benefits both organisms
- not an obligatory relationship (organisms could live independently)

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18
Q

Cooperation typically involves

A
  • syntrophic relationships
  • linked carbon and nitrogen/sulfur cycles
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19
Q

Commensalism

A
  • similar to cooperation but it is unidirectional
  • one organism benefits, other is not affected
  • often syntrophic
  • commensal can live separated from host
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20
Q

Commensal lives off

A

metabolic byproducts of host

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21
Q

An organism changing an environment, making it more suitable for another is an example of

A

commensalism

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22
Q

Formation of multispecies biofilms is an example of

A

commensalism

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23
Q

Predation

A
  • one organism gains (predator) and the other is harmed (prey)
  • predator usually kills prey
  • predatory can attack from inside or outside
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24
Q

Parasitism

A
  • one organism gains (parasite) and the other is harmed (host)
  • typically, host is not killed (until parasite can reproduce)
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25
Q

T / F: parasitism is between commensalism and predation

A

T

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26
Q

There is always some degree of ____ in a parasitic relationship

A

co-existence

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27
Q

Successful parasites have evolved to

A

co-exist in equilibrium with their hosts

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28
Q

Hallmark of parasitic relationship

A
  • not beneficial for host
  • host grows better without parasite
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29
Q

Ammensalism

A

association between two organisms where one organism is inhibited (harmed) and other is unaffected

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30
Q

Antibiosis

A
  • specific type of ammensalism
  • based on release of a specific compound
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31
Q

Example of ammensalism

A

antibiotic production by fungi and bacteria (antibiosis)

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32
Q

Competition

A

occurs when two organisms try to acquire or use the same resource

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33
Q

Two possible outcomes of competition

A
  • one organism dominates
  • two organisms share the resource
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34
Q

What organism learned how to use antibiotics before humans?

A

ants

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35
Q

Microbiome/microbiota

A

all of the microbes living in/on the human body

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36
Q

___ : ___ ratio of bacteria to human cells

A

1 : 1

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37
Q

___ : ____ ratio of nucleated cells

A

10 : 1

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38
Q

Metagenome

A

all the genes of the host and microbiota

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39
Q

Human microbiome (numerical value)

A

1,000,000+ genes

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40
Q

Human genome (numerical value)

A

23,000 genes

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41
Q

Superorganisms

A
  • the gene-encoded metabolic processes of the host become integrated with those of the symbiont
  • a blend of host and microbial traits where host and microbial cells co-metabolize various substrates, resulting in unique products
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42
Q

Microbiota varies depending on

A
  • anatomical site
  • age
  • sex
  • diet
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43
Q

Human microbiota begins at

A

birth
- unborn baby is sterile, inoculated during birthing process

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44
Q

What can disrupt the human microbiota?

A

antibiotic treatment, returns to “normal” after antibiotics are removed

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45
Q

Consortium

A

when microbiome becomes reasonably stable

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46
Q

Normal microbiota interaction with humans

A

mutualism

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47
Q

Normal microbiota often prevent

A

colonization by pathogens

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48
Q

Opportunistic pathogens

A
  • under certain circumstances, the normal microbiota can become pathogenic
  • compromised host
  • debilitated host with lowered resistance to infection
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49
Q

T / F: microbiota can be considered part of the immune system

A

T

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50
Q

Pathogen

A

any disease-producing microorganism

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51
Q

Dysbiosis

A

a change in the microbiome, can result in health risks/illness

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52
Q

Pathogenicity

A

ability to produce pathological change or disease

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53
Q

In order to cause disease pathogens must

A
  • get inside the host
  • survive inside the host
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54
Q

Immunology

A

science concerned with immune responses

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55
Q

Immune system composition

A

composed of widely distributed molecules, cells, tissues, and organs

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56
Q

Immune system function

A

recognizes foreign substances (or microbes) and acts to neutralize or destroy them

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57
Q

Immunity

A

ability of host to resist a particular disease or infection

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58
Q

Innate immune system, specific or non specific?

A

non specific

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59
Q

Adaptive immune system, specific or non specific?

A

specific

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60
Q

Innate immune system: speed

A
  • very fast response
  • components always present
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61
Q

Innate immune system: specificity

A
  • not very specific
  • active against a wide variety of infectious agents
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62
Q

Innate immune system: memory

A
  • no memory
  • not enhanced upon repeated contact with pathogen
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63
Q

Adaptive immune system: speed

A
  • response is slow
  • components must be made
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64
Q

Adaptive immune system: specificity

A
  • very specific
  • active against a narrow range of infectious agents
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65
Q

Adaptive immune system: memory

A
  • retains memory of invading pathogen
  • response is enhanced upon repeated contact with pathogen
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66
Q

Innate immunity first line of defense

A
  • barriers (skin, mucus membranes)
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67
Q

Innate immunity second line of defense

A
  • antimicrobial peptides
  • complement
  • cytokines
  • inflammation
  • phagocytes
  • NK cells
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68
Q

Adaptive immunity specific defense mechanisms (third line of defense)

A
  • antibodies
  • lymphocytes
  • B cells
  • T cells
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69
Q

Examples of excretions that keep microbes out

A

mucous, tears, wax, skin oils

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70
Q

T / F: skin is a highly effective barrier

A

T

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71
Q

T / F: innate and adaptive are completely separate systems

A

F

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72
Q

First and second line of defense are specific or non specific?

A

non specific

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73
Q

Skin

A
  • strong mechanical barrier to microbial invasion
  • inhospitable environment for most microbes
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74
Q

What characteristics of skin make it inhospitable for most microbes?

A
  • dry, acidic environment
  • dead, keratinized cells
  • sloughing of surface cells
  • toxic lipids, lysozyme
  • normal microbiota
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75
Q

Common areas with mucous membranes/secretion

A
  • mouth
  • eyes
  • ears
  • nares (nose)
  • respiratory tract
  • gastrointestinal tract
  • urogenital tract
  • anus
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76
Q

Common antimicrobial substances in mucous

A
  • lysozyme
  • RNAse enzymes
  • lactoferrin
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77
Q

Lysozyme

A

hydrolyzes bond connecting sugars in peptidoglycan
^ disintegrates cell wall

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78
Q

RNAse enzymes

A

degrade RNA (found in tears!)

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79
Q

Lactoferrin

A

sequesters iron
^ most bacterial pathogens need iron, lactoferrins “hide it,” bacteria cannot get what they need

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80
Q

Two components of innate immune system

A
  • chemical (humoral)
  • cellular
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81
Q

Chemical (humoral) component of innate immune system

A
  • antimicrobial peptides
  • complement
  • cytokines
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82
Q

Cellular component of innate immune system

A
  • phagocytes
  • natural killer cells
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83
Q

Antimicrobial peptides

A

small peptides ( ~ 12-50 amino acids) that have antimicrobial activity

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84
Q

Amphipathic

A

have hydrophobic and hydrophilic regions

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85
Q

Most antimicrobial activities function by

A

inserting into membrane

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86
Q

Antimicrobial peptides (AMPs) are abundant in

A
  • external mucosa (eyes, genitourinary, skin, lung, trachea, mouth)
  • immune cells (neutrophils)
  • intestinal tract (duodenum)
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87
Q

The complement system

A
  • heat sensitive component of serum (human blood)
  • complement antibodies in the killing of bacteria
  • complex system of > 30 serum proteins
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88
Q

Major activities of the complement system

A
  • directly kill bacteria
  • opsonizing bacteria
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89
Q

Membrane attack complex (MAC)

A

5 different complement proteins combine to form this
- C5b, C6, C7, C8 and C9

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90
Q

Opsonization

A

a process in which the surface of a microbe is coated with a substance called opsonin

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91
Q

What is special about opsonized microbes?

A

they are much more easily recognized and destroyed by phagocytic cells

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92
Q

Two types of opsonins

A
  • complement protein C3b
  • antibodies
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93
Q

Opsonization by antibodies or complement _____ affinity of phagocytes for microbe

A

increases

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94
Q

Opsonization by antibodies and complement further ____ binding and phagocytosis

A

increases

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95
Q

Cytokines

A
  • soluble proteins or glycoproteins
  • signaling molecules released by one cells population that act as intercellular mediators
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96
Q

Opsonized with antibodies degree of binding

A

+

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97
Q

Opsonized with complement C3b degree of binding

A

++

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98
Q

Opsonized with antibody and complement C3b

A

+++

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99
Q

One primary function of cytokines is to

A

induce inflammation

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100
Q

The inflammatory response

A

response of host tissues to damage or infection

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101
Q

The inflammatory response purpose

A

to recruit components of the immune system to the site of damage/infection

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102
Q

Cytokine signaling makes the tissue

A
  • leaky to fluid (influx of plasma; containing antibodies, complement, etc.)
  • sticky for leukocytes, leading to influx of neutrophils (pus)
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103
Q

Phagocytosis

A

process by which phagocytic cells recognize, ingest, and kill extracellular microbes

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104
Q

Two mechanisms for recognition of microbe by phagocyte

A
  • opsonin-dependent recognition
  • opsonin-independent recognition
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105
Q

Phagocytosis is greatly increased by

A

opsonization

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106
Q

Opsonin-independent mechanism is based on

A

detection of conserved microbial molecular structures that occur in patterns

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107
Q

Pathogen-associated molecular patterns (PAMPs)

A
  • molecule/polymer found on surface of microbe but not host
  • LPS of Gram (-) bacteria
  • peptidoglycan / teichoic acids of Gram (+) bacteria
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108
Q

PAMPs are recognized by _______ on ____ cells

A

PRRs, phagocytic

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109
Q

One class of PRRs important in fighting infection are

A

toll-like receptors (TLRs)

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110
Q

TLRs

A

recognize and bind unique PAMPs of virus, bacteria, or fungi

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111
Q

Binding of TLRs and PAMPs

A

triggers a signal within the host cell which initiates the host response, resulting in phagocytosis

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112
Q

Once bound, microbes can be internalized into a

A

phaogsome

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113
Q

Phagosome fuses with a lysosome to become a

A

phagolysosome

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114
Q

Exocytosis

A

process used by neutrophils to expel microbial fragments after they have been digested

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115
Q

Phagolysosome fuses with ____, resulting in

A

cell membrane, extracellular release of microbial fragments

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116
Q

Macrophages and dendritic cells undergo process called

A

antigen presentation

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117
Q

Antigen presentation

A

links innate immunity with adaptive immunity

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118
Q

Cells of the immune system are collectively known as

A

leukocytes

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119
Q

Leukocytes

A

white blood cells

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120
Q

Phagocytic cells

A
  • monocytes
  • macrophages
  • dendritic cells
  • neutrophils
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121
Q

Natural killer cells (NK)

A

small population of lymphocytes

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122
Q

NK cells play an important role in

A

innate immunity

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123
Q

NK cells kill what type of cells?

A

cells infected with pathogens

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124
Q

NK cells release

A

cytotoxic enzymes (granzymes)

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125
Q

NK cells play an important role in

A

innate immunity

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126
Q

Normal cells express a membrane protein called

A

class 1 major histocompatibility complex (MHC class 1)

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127
Q

Two ways NK cells recognize infected cells

A
  1. NK cell encounters a host cell without MHC-1, releases granzymes and kills cells
  2. ADCC (antibody-dependent cell-mediated cytotoxicity): antibodies bind to antigens on surface of infected host cells, NK cells bind to antibodies, kill infected cell
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128
Q

Antigens

A

substances that elicit an immune response

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129
Q

T / F: antigens cannot be large or complex molecules

A

F

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130
Q

Epitopes

A

antigenic determinant sites

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131
Q

Antibody affinity

A

strength with which antibody binds to its antigen at a given antigen-binding site

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132
Q

Antibody or immunoglobulin

A

large glycoprotein made by B lymphocytes

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133
Q

Where are antibodies found in the body?

A

found free in the body

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134
Q

Antibodies function

A

recognize and bind specific antigen

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135
Q

Immunoglobulin structure

A

4 polypeptide chains
- 2 heavy chains
- 2 identical light chains
- chains connected by disulfide binds

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136
Q

2 different regions in immunoglobulin chains

A
  • constant regions
  • variable regions
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137
Q

5 main modes of transmission

A
  • airborne
  • contact (direct or indirect)
  • vehicle (food, water)
  • vector borne (arthropod [insects], zoonotic [animal])
  • vertical
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138
Q

Example of indirect contact transmission

A

needle/syringe, contaminated public surface

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139
Q

Dust particles are an important route of ______ transmission

A

airborne

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140
Q

Airborne transmission: pathogen suspended in air and travels less than or equal to ____

A

1 meter

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141
Q

Droplet nuclei

A
  • usually propelled from respiratory tract of source organisms by sneezing, coughing, or vocalization
  • can travel long distances
  • smaller droplets can remain suspended
  • small particles (1-4 micro m diameter)
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142
Q

COVID-19 is the ___ name

A

disease/syndrome

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143
Q

SARS-CoV-2 is the name of the ______

A

virus

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144
Q

SARS-CoV-2 genome is approximately _________ nt long

A

30,000

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145
Q

SARS-CoV-2 genome structure

A
  • 4 structural genes it encodes
  • 16 NSPs (non-structural proteins)
  • 9 accessory factors
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146
Q

Influenza (the flu)

A

disease

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147
Q

Influenza is caused by

A

influenza virus

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148
Q

Influenza virus

A
  • RNA virus; segmented genome
  • 3 groups (A, B, C)
  • family Orthomyxoviridae
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149
Q

Total genome size of influenza virus

A

12,000-15,000 nts

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150
Q

___ segments of RNA (-) in influenza virus

A

8

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151
Q

____ genes/proteins in influenza virus

A

11

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152
Q

Flu virus structure

A
  • enveloped virus
  • 2 viral proteins in the envelope (hemagglutinin [HA], neuraminidase [NA])
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153
Q

Influenza virus viral replication

A
  • HA attaches to host sialic acid receptors
  • receptor mediate endocytosis
  • HA undergoes conformational change
  • releases nucleocapsid into cytoplasm
  • viral replication, transcription and assembly of new virions
  • release by budding
  • NA protein cleaves receptors, releasing new virions
  • NA inhibitor, Tamiflu
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154
Q

Rarest flu type

A

C

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155
Q

____ different types of HA

A

16

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156
Q

____ different types of NA

A

9

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157
Q

Antigenic drift

A

accumulation of mutations in a strain within a geographic area
- nucleotide/amino acid changes

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158
Q

Antigenic shift

A

re-assortment of genomes (8 RNAs)
- two different strains of flu viruses infect the same cell and are incorporated into a single new capsid

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159
Q

Arboviruses

A

viruses transmitted by bloodsucking arthropods from one vertebrate host to another

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160
Q

An important feature of the influenza viruses is the

A

frequency with which changes in antigenicity occur

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161
Q

Arboviruses multiplication

A

multiply in tissues of vector without producing disease

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162
Q

T / F: arboviruses typically have vaccines

A

F

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163
Q

Contact transmission

A

coming together or touching of source/reservoir and host

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164
Q

Direct contact

A

physical interaction between source/reservoir and host

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165
Q

Indirect contact

A

involves an intermediate (usually inanimate)

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166
Q

AIDS is caused by

A

HIV

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167
Q

T / F: (technically) HIV does not kill

A

T

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168
Q

AIDS leads to

A

infection by opportunistic pathogens

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169
Q

HIV is a(n) RNA, protein or DNA virus?

A

RNA

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170
Q

Zika virus is special because

A

it is an Arbovirus and a vertical transfer disease

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171
Q

Contact with body fluids or contact with an open wound is an example of

A

direct contact

172
Q

HIV life cycle

A
  • virion has several viral protein spikes
  • attachment to human cells is mediated by gp120 (attaches to CD4 receptor)
  • enters cell by receptor mediated endocytosis
  • carries reverse transcriptase into host cell
  • also carries integrase and protease enzymes
  • RNA genome is reverse transcribed into dsDNA, which integrates into human genome as provirus
  • can remain latent (asymptomatic)
  • can direct synthesis of viral RNA –> synthesis of new viral particles
173
Q

Virion core consists of ___ viral proteins

A

4

174
Q

4 viral proteins

A

P24, P17, P9, P7

175
Q

4 viral proteins are generated from one precursor polyprotein called

A

Gag

176
Q

Acute

A
  • 2-8 weeks after infection
  • acute retroviral syndrome
  • infection is brought under control
  • very non descript symptoms that go away quickly
177
Q

Asymptomatic (latent) (HIV)

A
  • may last from 6-10 months or years
  • levels of detectable HIV in blood decease, although viral replication continues
  • effects on immune functions may occur
178
Q

Chronic symptomatic (HIV)

A
  • can last months to years
  • viral replication continues
  • patient at risk of opportunistic pathogens and AIDS related cancers
179
Q

3 proteins that must be found in HIV for viral genome to work

A

RT (reverse transcriptase), protease, integrase

180
Q

Clinical definition of AIDS

A

HIV-infected individuals who have fewer than 200 CD4+ T cells/microliter of blood or a CD4+ cell percentage of lymphocytes of less than 14

181
Q

Food/water transmission

A

transmission of pathogens in water and food (food poisoning)

182
Q

T / F: food/water transmission may be the most common transmission type

A

T

183
Q

Gastroenteritis (viral) is caused by what four major groups of viruses?

A

rotavirus, adenovirus, astrovirus and norovirus

184
Q

Rotavirus, adenovirus and astrovirus deaths per year

A

~5-10 million deaths/year worldwide

185
Q

Rotavirus, adenovirus and astrovirus transmission

A

viral diarrhea transmitted by fecal oral route

186
Q

Norovirus cases per year

A

~23 million

187
Q

Zoonotic diseases

A

human viral infection in animal reservoirs before transmission to and between animals

188
Q

Zoonotic diseases genome type

A

RNA

189
Q

T / F: many zoonotic diseases are on Select Agents list as potential bioweapons

A

T

190
Q

Ebola hemorrhagic fever genome type

A

ssRNA (-)

191
Q

What animal is a natural reservoir for ebola?

A

bats

192
Q

T / F: there is a carrier state for ebola

A

F

193
Q

Fab binds

A

antigen

194
Q

T / F: Fab-antigen binding is highly specific

A

T

195
Q

Fc mediates binding to

A
  • cells of immune system
  • complement system
196
Q

Fc mediating binding of cells of immune system leads to

A

triggering of phagocytosis, opsonization

197
Q

Fc mediating binding to complement system leads to

A

activation of complement

198
Q

Primary antibody response is

A

slow

199
Q

Concentration of antibody in serum is known as

A

antibody titer

200
Q

Upon secondary exposure to same antigen, antibody production is

A

quicker

201
Q

Secondary exposure characteristics

A
  • shorter lag
  • more rapid log phase
  • longer persistence
  • higher titer
  • production of antibodies with a higher affinity for the antigen
202
Q

Consequence of antibody-antigen binding

A
  • opsonization
  • agglutination
  • complement
  • neutralization
  • precipitation
203
Q

Major populations of lymphocytes include

A

T cells and B cells

204
Q

B and T lymphocytes originate in _____ from ______

A

bone marrow, stem cells

205
Q

Lymphocytes are only activated by

A

binding or recognition of specific antigen

206
Q

Consequence of activation of lymphocytes is the production of

A

memory cells

207
Q

B cells are mature in

A

bone marrow

208
Q

B cells circulate in

A

blood

209
Q

One of the primary roles of B cells is to

A

produce antibodies

210
Q

T cells are mature in the

A

thymus

211
Q

T cells can remain in the thymus, circulate in ______, or reside in _______

A

blood, lymphoid tissue

212
Q

Activated T cells differentiate into

A
  • T helper cells
  • cytotoxic T lymphocytes (CTLs)
213
Q

T helper cells (TH)

A

assist in antibody production

214
Q

Cytotoxic T lymphocytes (CTLs)

A

ability to kill infected cells

215
Q

TH cells help

A

B cells

216
Q

CTLs are similar (in role) to

A

NK cells

217
Q

T / F: of all the known bacterial species, very many are pathogenic to humans

A

F

218
Q

Virulence factors are…

A

molecules produced by pathogens that contribute to the pathogenicity of the organism

219
Q

Virulence factors are typically what type of molecules?

A

proteins

220
Q

Common types of virulence factors

A
  • toxins
  • adhesions (pili/fimbriae)
  • flagella
  • immune evasion molecules
221
Q

T / F: pathogenic bacteria can have one, few, or many virulence factors

A

T

222
Q

Diphtheria is caused by what type of bacteria?

A

Gram (+), Corynebacterium diphtheriae

223
Q

Some bacterial strains (of Corynebacterium diphtheriae) harbor

A

lysogenized bacteriophage

224
Q

Bacteriophage genome contains

A

tox gene

225
Q

Strains containing bacteriophage produce a(n) ______, that inhibits protein synthesis and is responsible for pathogenesis

A

exotoxin

226
Q

Only virulence factor of C. diphtheriae

A

exotoxin

227
Q

Diphtheriae toxin

A

AB toxin

228
Q

AB toxin

A
  • A and B protein held together by disulfide bond
  • B portion binds to host cell receptors, triggers endocytosis
  • A portion is released, enters and is active in cytoplasm of host cell, inhibits protein synthesis, kills cell
229
Q

Diphtheria is a virus or a disease?

A

disease

230
Q

Mycobacteria characteristics

A
  • large group of bacteria
  • normally found in soil, water, and house dust
  • can cause a number of human infections that are difficult to treat
231
Q

What is unusual about mycobacteria?

A

unusual cell wall

232
Q

What is unusual about mycobacteria cell wall?

A
  • Gram (+) but does not stain Gram (+)
  • outer membrane made of mycolic acids
233
Q

Why do mycobacteria not stain Gram (+)?

A

do not retain the crystal violet stain because of mycolic lipid layer

234
Q

“Outer membrane” made of mycolic acids (characteristics)

A
  • protective waxy layer
  • acts like outer membrane
  • very hydrophobic
  • resistant to penetration of some antibiotics
235
Q

Staining process of mycobacteria (name and process)

A
  • Ziehl-Neelson stain
  • stain with carbol fuchsin
  • heat over bunsen burner
  • destain with HCl in isopropyl alcohol
  • stain is removed from cells that are unprotected by a mycolic lipid bilayer
  • cells are counter-stained with methylene blue
236
Q

Tuberculosis transmission

A
  • person to person spread of droplet nuclei in respiratory tract (cough)
  • also transmitted from infected animals and their products
  • reactivation of old, dormant infections
237
Q

Does TB develop slowly or quickly?

A

slowly

238
Q

Tuberculosis is caused by ______, and this was shown by ______

A

Mycobacterium tuberculosis (Mtb), Robert Koch

239
Q

How many people worldwide have been infected with TB?

A

2 billion

240
Q

Mtb virulence factors

A
  • cell envelope composed of toxic components
  • ability to survive phagocytosis
241
Q

Toxic components of Mtb cell envelope and what they do

A
  • mycolic acid, liparabinomannan, tregalose, dimycolate, phthiocerol dimycocerosate
  • kill eukaryotic cells and protect Mtb from lysozyme and osmotic lysis
242
Q

How Mtb is able to survive phagocytosis?

A
  • kill macrophages
  • resistant to oxidative killing
  • inhibit diffusion of lysosomal enzymes
243
Q

To prevent further spread of Mtb, what does the immune system do?

A

“walls off” the infection in hard nodules called Tubercle

244
Q

Over time, tubercle can develop into

A
  • caseous lesion
  • Ghon’s complex (calcified caseous lesion)
  • tuberculous cavities
245
Q

Tuberculous cavities

A
  • tubercle liquefies
  • forms air-filled cavity from which bacteria can spread
  • spreading is called miliary tuberculosis
  • also called reactivation tuberculosis because bacteria reactivated at initial infection site
246
Q

Lyme disease and plague are examples of what type of disease?

A

arthropod-borne disease

247
Q

T / F: arthropod-borne diseases are generally rare

A

T

248
Q

Lyme disease is caused by

A

spirochete Borrelia burgdorferi

249
Q

Three stages of lyme disease

A

initial, disseminated, late stage

250
Q

Initial (localized) stage of lyme disease

A
  • develops 1 week to 10 days after infection
  • expanding, ring shaped, skin lesion
  • flu like symptoms
  • may go undiagnosed
251
Q

Disseminated stage of lyme disease

A
  • occurs weeks or months after infection
  • neurological abnormalities
  • heart inflammation
  • arthritis
252
Q

Late stage of lyme disease

A
  • occurs years later
  • demyelination of neurons
  • behavioral changes
  • symptoms resembling Alzheimer’s disease and multiple sclerosis
253
Q

Plague (black death, Bubonic plague) was caused by what type of bacteria?

A

Gram (-) bacteria Yersinia pestis

254
Q

How many people did the plague kill?

A

75-200 million people (in Europe)

255
Q

Plague transmission

A
  • rodent to human, bite of infected flea
  • direct contact with infected person, animal or product
  • inhalation of contaminated airborne droplets
256
Q

Yersinia pestis in the body

A
  • multiply in blood and lymph
  • survive and proliferate in phagocytic cells
257
Q

Symptoms of plague

A
  • subcutaneous hemorrhages
  • fever
  • buboes (enlarged lymph nodes)
258
Q

If plague is acquired through ______, chances of death are extremely high

A

inhalation

259
Q

Most critical virulence factor of Yersinia pestis

A

type III secretion system

260
Q

Type III secretion system

A
  • molecular syringe
  • used to deliver yersinal proteins (YOPS) into host cells
  • shuts down defence mechanisms
261
Q

Clinical manifestations of Yersinia pestis

A
  1. bubonic plague
  2. pneumonic plague
262
Q

Bubonic plague

A
  • enlarged lymph nodes (buboes)
  • 50-70% lethal of untreated
263
Q

Pneumonic plague

A
  • arises from primary exposure to infectious respiratory droplets of infected persons or cats
  • 100% mortality if untreated
264
Q

T / F: Y. pestis is a select agent

A

T

265
Q

STDs worldwide cases per years

A

~300 million

266
Q

T / F: STDs can be transmitted by nonsexual means

A

T

267
Q

What is the most frequently reported sexually transmitted bacterial infection?

A

chlamydia

268
Q

What type of bacteria is chlamydia?

A

Gram (-)

269
Q

Chlamydial diseases in males

A
  • asymptomatic
  • urethral discharge, itching and inflammation of genital tract
270
Q

Chlamydial diseases in females

A
  • sometimes asymptomatic
  • may cause pelvic inflammatory disorder
  • if pregnant, can lead to miscarriage, stillbirth, and infant pneumonia
271
Q

Venereal syphilis

A
  • sexually transmitted
  • infection results from intimate contact with an infected lesion of a sexual partner
272
Q

Congenital syphilis

A
  • acquired in utero
  • passed from mother to baby
273
Q

Syphilis is what a(n) _______ disease

A

ulcerative

274
Q

____ stages of syphilis

A

3

275
Q

Primary stage of syphilis

A
  • appearance of chancre
  • small, painless, reddened ulcer
  • contains spirochetes
  • highly infectious
  • 33% of cases resolve at this stage
276
Q

Secondary stage of syphilis

A
  • bacteria spread throughout the body via lymph and blood
  • appearance of skin rash
  • rash is infectious
  • loss of hair, malaise, fever
277
Q

Second stage is followed by _____, which is

A

latent period, non-infectious

278
Q

Tertiary stage of syphilis

A
  • 40% of cases reach this stage
  • formation of gummas (masses of dead, fibrous tissue in skin, bone and nervous systems)
  • cognitive defects
  • blindness
  • madness
279
Q

Antibiotic intervention is most effective

A

in early stages

280
Q

Neisseria gonorrhoeae

A

causative agent of gonorrhea

281
Q

Second most prevalent bacterial STI

A

gonorrhea

282
Q

Neisseria gonorrhoeae can infect

A

the genitals, rectum, eyes and throat of men and women

283
Q

Transmission of gonorrhea

A

sexual and/or vertical

284
Q

Why is gonorrhea such a problem?

A
  • no vaccine
  • resistant to many, many antibiotics
285
Q

Why is gonorrhea so resistant?

A
  • extremely competent, highly efficient transformation system
  • type IV pili
  • retractable pili
  • bind extracellular DNA
  • bring it into the cell
286
Q

Pili has an even higher affinity for DNA if it contains

A

DNA uptake sequence

287
Q

Gastroenteritis

A

inflammation of stomach and intestinal lining

288
Q

Food poisoning

A

food is source of pathogen

289
Q

Food-borne infection

A

pathogen must colonize host

290
Q

Food intoxication

A

ingesting a toxin made my bacteria

291
Q

Botulism

A

caused by Clostridium botulinum

292
Q

Clostridium botulinum

A
  • obligate anaerobe
  • endospore-forming
  • Gram (+) rod
293
Q

Botulinum toxin

A
  • neurotoxin that binds to synapses of motor neurons
  • prevents signal being transmitted across synapse
  • causes flaccid paralysis (cannot contract muscles)
294
Q

T / F: botulinum toxin is the most powerful toxin known to humans

A

T

295
Q

Most common form of botulism

A

infant botulism

296
Q

Anthrax is what type of disease?

A

zoonotic

297
Q

T / F: anthrax is not a select agent

A

F

298
Q

What determines anthrax disease manifestation?

A

portal of entry

299
Q

3 forms of anthrax

A
  • cutaneous
  • inhalation
  • gastrointestinal
300
Q

Cutaneous anthrax

A
  • infection through cut or abrasion of skin
  • clinical manifestations ( 1-15 day incubation, skin papule that ulcerates, headache, fever, nausea)
  • treatable with antibiotics
301
Q

Inhalation/pulmonary anthrax

A
  • inhalation of endospores
  • resembles influenza
  • if bacteria reach the bloodstream, usually fatal
  • even with antimicrobial therapy (75% fatality)
302
Q

Gastrointestinal anthrax

A
  • ingestion of endospores
  • very uncommon
303
Q

Cryptococcosis

A

systemic fungal disease causes by a yeast Cryptococcus neoformans

304
Q

Cryptococcosis characteristics

A
  • acquired by inhalation of dried pigeon droppings
  • mild disease
  • pneumonia-like disease
  • serious disease including meningitis in immunocompromised patients (AIDS)
305
Q

Prevalence of Hepatitis B

A

2 billion people

306
Q

Prevalence of malaria

A
  • 200-300 million people annually
  • 500,000-1 million deaths
307
Q

Hep C prevalance

A

180 million people

308
Q

Dengue prevalance

A

50-100 million people

309
Q

Tuberculosis prevalance

A

2 billion people chronically infected

310
Q

Malaria is a(n) _____ borne disease

A

arthropod

311
Q

Malaria is endemic in ____ countries

A

106

312
Q

Malaria is caused by

A

species of parasitic protozoan called Plasmodium

313
Q

5 plasmodium species that commonly cause human infection

A
  • P. falciparum
  • P. vivax
  • P. malariae
  • P. ovale
  • P. knowlesi
314
Q

What is the most dangerous species of plasmodium?

A

P. falciparum

315
Q

What is the most common species of plasmodium?

A

P. falciparum

316
Q

Malaria involves ___ reproductive stages

A

3

317
Q

Malaria has ______ and ______ stages

A

haploid, diploid

318
Q

Plasmodium life cycle: Part 1

A
  • in liver
  • mosquito takes a blood meal and injects infective form of plasmodium known as sporozoites
  • haploid sporozoites migrate to the liver and enter hepatic cells
  • undergo asexual reproduction to form a schizont
  • schizont ruptures and releases merozoites into bloodstream (haploid)
319
Q

Only diploid section occurs

A

within the mosquito

320
Q

Part 2 of plasmodium life cycle

A
  • erythrocyte replication cycle
  • merozoite enters red blood cell
  • forms a ring structure called the trophozoite
  • the trophozoites matures into a schizont which produces more merozoites
  • erythrocyte lyses, releasing merozoites into blood stream
321
Q

Part 3 of plasmodium life cycle

A
  • some trophozoites mature into a gametocytes
  • gametocytes differentiate into male (microgametocytes) and female (macrogametocytes) forms
  • gametocytes are ingested by mosquito when it takes a blood meal from an infected person
322
Q

Mosquito stage of plasmodium life cycle

A
  • in the mosquito gut the microgametocyte (male) and macrogametocyte (female) fuse to form diploid zygote called ookinete (diploid)
  • ookinete migrates through the gut wall and forms the oocyst
  • oocyst undergoes meiosis to form haploid sporozoites
  • oocyst ruptures and sporozoites migrate to the mosquito salivary glands
323
Q

_________ can result from erythrocyte lysis

A

anemia

324
Q

T / F: diploid stage of plasmodium life cycle is large

A

F

325
Q

Why are periodic attacks of chills, fever and sweating experienced with malaria?

A

due to the synchronized lysis of erythrocytes and release of merozoites

326
Q

Chloroquine

A

interferes with replication of plasmodium in erythrocytes

327
Q

Why would a malaria vaccine be challenging to develop?

A
  • eukaryotic cells
  • vaccine would have to work against all stages of the plasmodium life cycle
328
Q

RTS vaccine is based upon

A

recombinant protein

329
Q

Fungal infections are known as

A

mycoses

330
Q

Superficial mycoses

A
  • outermost layers of skin and hair
331
Q

Cutaneous mycoses

A
  • extend deeper into epidermis
  • invasive hair and nail diseases
  • different diseases distinguished according to causative agent and area of body affected
332
Q

Subcutaneous mycoses

A
  • involve dermis, subcutaneous tissue and fascia
  • caused by saprophytic inhabitants of soil
  • introduced in soil-contaminated puncture wounds
  • develops slowly over a period of years
  • nodules form and ulcerate
  • organisms spread along lymphatic channels, producing more nodules
333
Q

Most common fungal disease type

A

cutaneous

334
Q

Cutaneous mycoses are transmitted by

A

direct contact

335
Q

Why is it difficult to treat fungal infections?

A

fungi are eukaryotes

336
Q

Azoles (role and examples)

A
  • inhibit the synthesis of ergosterol (the main fungal sterol - equivalent of cholesterol in humans)
  • Fluconazole, Clotrimazole
337
Q

Polyenes (role and examples)

A
  • bind/interact with ergosterol in fungal membrane, alters membrane fluidity
  • Amphotericin B, Nystatin
338
Q

Echinocandins

A

inhibit cell wall synthesis (beta-glucans)

339
Q

What could/would cause an increase in fungal infections?

A

climate change

340
Q

Excystation is essentially the same as

A

germination

341
Q

Excystation leads to formation of

A

metacyst

342
Q

Toxoplasmosis

A
  • fecal-oral transmission from infected animals
  • ingestion of undercooked meat, congenital transfer, blood transfusion, or tissue transplant
343
Q

Toxoplasma gondii is a

A

protist

344
Q

Malaria diagnosis

A

demonstration of parasites within Wright or Giemsa-stained red blood cells and serological tests

345
Q

Amebiasis is caused by

A

protozoan Entamoeba histolytica

346
Q

Amebic dysentery (amebiasis) infection

A

ingestion of mature cysts from fecally contaminated water, foods or plants

347
Q

In the lower intestine, the ingested mature cyst undergoes ________

A

excystation

348
Q

The metacyst rapidly divides to produce

A

8 trophozoites

349
Q

Trophozoites move to the ______ where they can _______ and _______

A

large intestine, live asymptomatically, invade intestinal epithelium

350
Q

Trophozoites release a toxin that destroys ____, causing _____

A

epithelial cells, diarrhea

351
Q

T / F: trophozoites may spread to additional sites in the body and cause secondary infection

A

T

352
Q

Amebiasis diagnosis

A

observation of trophozoites in fresh, warm stools or cysts in ordinary stools, and serological tests

353
Q

Toxoplasma gondii reservoir(s)

A

wild rodents, birds, small mammals, cats (kittens)

354
Q

In toxoplasmosis, _____ are shed in animal feces

A

oocysts

355
Q

In toxoplasmosis, when oocysts are ingested, they transform into _____

A

tachyzoites

356
Q

T / F: tachyzoites cannot cross placenta and infect fetus

A

F

357
Q

Toxoplasmosis diagnosis

A

serological tests

358
Q

Toxoplasmosis clinical manifestations

A
  • usually asymptomatic or mild symptoms
  • encephalitis can be fatal in immunocompromised hosts
359
Q

Antimicrobial chemotherapy

A

compounds that destroy pathogenic microbes or inhibit their growth within host

360
Q

Most chemotherapeutic agents are

A

antibiotics

361
Q

Antibiotics

A

microbial products or their derivatives that kill susceptible microbes or inhibit their growth

362
Q

Who developed the concept of selective toxicity?

A

Paul Ehrlich

363
Q

Prontosil red

A

dye with antibacterial properties only in vivo

364
Q

T / F: prontosil red has effects in vitro

A

F

365
Q

Ernest Duchesne observed that

A

certain molds kill bacteria

366
Q

Who made the connection between Penicillium and the chemical penicillin?

A

Alexander Fleming

367
Q

One of the products of prontosil red once broken down

A

sulfanilamide

368
Q

Selman Waksman did what?

A
  • isolated Streptomycin from Streptomyces bacteria
  • discovered the antibiotic
369
Q

Prodrug

A

drug is only active once metabolically processed and product of this is active in the body

370
Q

Selective toxicity

A

ability of drug to kill or inhibit pathogen while not damaging host (or doing very little damage)

371
Q

Therapeutic dose

A

drug level in the body required for clinical treatment

372
Q

Toxic dose

A

drug level at which drug becomes too toxic for patient (produces side effects)

373
Q

Therapeutic index

A

ratio of toxic dose to therapeutic dose

374
Q

Side effects

A

undesirable effects of drugs on host cells

375
Q

Narrow-spectrum drugs

A

attack only a few different pathogens

376
Q

Broad spectrum drugs

A

attack many different pathogens

377
Q

Bacteriocidal drug

A

kills microbes

378
Q

Bacteriostatic drug

A

inhibits growth of microbes

379
Q

Three ways to clinically determine the level of antimicrobial activity

A
  1. dilution susceptibility tests
  2. disk diffusion tests
  3. the E-test (MIC and diffusion)
380
Q

Minimal inhibitory concentration (MIC)

A

lowest concentration of drug that completely inhibits growth of pathogen

381
Q

Disk diffusion tests

A
  • agar plate is inoculated with bacteria being tested for
  • antibiotic treated disks are placed on agar
  • drug diffuses into agar, establishing concentration gradient
  • zones of clearing can be observed
  • larger zone of clearing = drug is efficient against bacteria
382
Q

Kirby-Bauer method

A
  • standardized method for disk diffusion test
  • sensitivity/resistance determined from tables relating diameter of zone of clearing to efficacy
383
Q

The E-test

A
  • combination of disk diffusion method and MIC
  • uses strip containing a gradient of an antibiotic
  • intersection of elliptical zone of inhibition with strip indicates MIC
384
Q

When would it not be helpful to prescribe a bacteriostatic drug?

A

if the patient has a weakened immune system

385
Q

4 different targets of antimicrobial drugs

A
  1. cell wall synthesis
  2. protein synthesis
  3. nucleic acid synthesis
  4. metabolic antagonists (folic acid biosynthesis)
386
Q

Penicillin mode of action (inhibition target)

A
  • blocks the enzyme that catalyzes transpeptidation (formation of cross-links in peptidoglycan)
  • inhibits cell wall formation
  • leads to lysis of cell
387
Q

T / F: penicillin only acts on growing bacteria

A

T

388
Q

Most crucial feature of penicillin molecule is the

A

beta lactam ring

389
Q

Penicillin’s are often called

A

beta lactam antibiotics

390
Q

Basic structure of penicillin

A

6-aminopenicillanic acid

391
Q

Cephalosporins are structurally and funcitonally similar to

A

penicillin’s

392
Q

T / F: cephalosporins are not considered beta lactam antibiotics

A

F

393
Q

No zone of inhibition in a disk diffusion indicates that the bacteria is _____ to the drug

A

resistant

394
Q

A large zone of inhibition in a disk diffusion indicates that the bacteria is ____ to the drug

A

sensitive to

395
Q

T / F: E-test is more quantitative than disk diffusion

A

T

396
Q

In protein inhibition, many antibiotics bind specifically to the _____, or they

A

bacterial ribosome, inhibit a step in protein synthesis

397
Q

Steps in protein synthesis that antibiotics might inhibit

A
  • aminoacyl-tRNA binding
  • peptide bond formation
  • mRNA reading
  • translocation
398
Q

Tetracyclines are bacteriostatic or bacteriocidal?

A

bacteriostatic

399
Q

Tetracyclines combine with _______, inhibiting

A

30S ribosomal subunit, binding of aminoacyl-tRNA molecules to the A site of the ribosome

400
Q

Two main mechanisms of nucleic acid synthesis inhibition

A
  • block DNA replication
  • block transcription
401
Q

Blocking of DNA replication

A
  • inhibition of DNA polymerase
  • inhibition of DNA helicase
402
Q

Blocking of transcription

A
  • inhibition of RNA polymerase
403
Q

T / F: drugs that inhibit nucleic acid synthesis are highly selectively toxic

A

F

404
Q

Quinolones act by inhibiting what?

A

bacterial DNA gyrase and topoisomerase II

405
Q

Are quinolones:
- broad or narrow spectrum?
- bacteriostatic or bacteriocidal?

A

broad, bacteriocidal

406
Q

Metabolic antagonists

A

molecules that are structurally similar to naturally occurring metabolic intermediates

407
Q

How do metabolic antagonists work?

A

block functioning of metabolic pathways by competitively inhibiting the use of metabolites by key enzymes

408
Q

Folic acid biosynthesis inhibitors are useful because

A
  • bacteria must synthesize their own folic acid
  • humans need to take up folic acid in their diet
  • humans do not have the mechanisms bacteria have for synthesizing folic acid, so folic acid biosynthesis inhibitors don’t effect human cells at all, but kill bacteria efficiently
409
Q

Virus-specific enzymes and life cycle processes

A
  • reverse transcriptase
  • protease
  • helicase
410
Q

Tamiflu is a ________ inhibitor

A

neuraminidase

411
Q

Anti-HIV drugs

A
  • reverse-transcriptase inhibitors
  • protease inhibitors
  • fusion inhibitors
412
Q

Reverse transcriptase inhibitors

A
  • nucleotide/nucleoside analogs
  • non-nucleoside RT inhibitors
413
Q

Protease inhibitors (HIV)

A

mimic peptide bond that is normally attacked by the protease

414
Q

Fusion inhibitors (HIV)

A

prevent HIV entry into cells

415
Q

Why are antifungal and antiprotozoal drugs less available and less effective?

A

because it is difficult to target the cells causing the disease/infection without targeting human cells

416
Q

Antifungal and antiprotozoal drugs often have _____ therapeutic index and are _____

A

low, toxic

417
Q

Some antibiotics that inhibit ________ synthesis are used against protozoa

A

bacterial protein

418
Q

Vaccine

A

preparation of microbial antigens used to induce protective immunity

419
Q

Immunization

A
  • result obtained when vaccine stimulates immunity
  • body produces antibodies and activated T cells to protect host from future infection
420
Q

Adjuvant

A
  • substance mixed with antigens in vaccines to enhance the rate and degree of immunization
  • can be any nontoxic material that prolongs antigen interaction with immune cells and stimulates the immune response to the antigen
421
Q

A vaccine may consist of

A
  • killed cells
  • living, weakened (attenuated) microbes
  • inactivated toxins (protein produced and secreted by microbe)
  • purified microbial material or antigen
  • mRNA
422
Q

If a microbe is attenuated, it is

A

live but avirulent

423
Q

If a microbe is inactivated it is

A

killed

424
Q

Possible problems from whole cell vaccines

A
  • immunosuppressed at risk of getting disease
  • attenuated strains may revert to being virulent
  • multiple boosters may be required
425
Q

Typical forms of subunit vaccines include

A
  • capsular polysaccharides
  • surface antigens
  • inactivated exotoxins (toxoids)

MicroBio (4 decks)

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