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MMG 101 > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

epidemiology

A

studies the frequency and distribution of disease and health-related factors in human populations

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2
Q

two general goals of epidemiology

A
  1. describe the nature, cause, and extend of new or existing diseases in populations
  2. intervene to protect and improve health in populations
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3
Q

how does disease occur

A

the epidemiological triangle

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4
Q

factors of the epidemiological triangle

A

host
environment
etiological agent
-diagnosing, treating, and preventing disease requires understanding all relevant factors

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5
Q

environmental factors of the epidemiological triangle

A 
source
reservoir
transmission
vector
climate
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6
Q

sources of pathogens

A

endogenous: from the host’s own body; microbes or exogenous source: external to the host

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7
Q

sources of infectious disease

A

animate: other humans or animals
inanimate: water, food, soil fomites
reservoir: natural environmental location in which the pathogen normally resides
vector: organism that spreads disease from one host to another
EX: mosquitoes, ticks, fleas, mites, or biting flies

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8
Q

four main transmission routes

A 
airborne
contact
vehicle-inanimate
vector-borne
-also vertical transmission
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9
Q

healthcare-acquired infection (HAI)

A

an infection that a patient develops while receiving care in a healthcare setting
AKA nosocomial infections

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10
Q

public health strategies to target disease

A

education
increase herd immunity
quarantine
vector control

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11
Q

factors contributing to the increase of emerging diseases

A 
population crowding
poverty
tropical climates
deforestation
urbanization
vaccine hesitation
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12
Q

one health

A

goal of achieving optimal health outcomes recognizing the interconnection between people, animals, plants, and other shared environment

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13
Q

bioterrorism

A

intentional or threatened use of microbes (their products) to produce death of disease in humans, animals, and plants

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14
Q

pathogen

A

microbes that cause disease

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15
Q

true pathogen

A

does not require a weakened host to cause disease

never part of normal microbiota

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16
Q

opportunistic pathogens

A

agents of disease under certain circumstances
only cause disease when their host is weakened (weak immune system) or can be normal microbiota that enters a different body site

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17
Q

establishing normal microbiota

A

colonization during delivery and post-natally

adult microbiome established by ~3 years old

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18
Q

where do we find normal microbiota

A

skin
mouth/pharynx/upper respiratory tract
gastrointestinal tract (GI)
genitourinary tract (GU)

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19
Q

skin: normal microbiota and conditions

A

conditions: slightly acidic pH, high concentration of NaCl, dry areas; also moist areas (sometimes containing sebum)
common skin microbiota:
dry areas: staphylococcus species
oil glands: cutibacterium acnes

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20
Q

upper respiratory tract: normal microbiota

A

upper respiratory tract-nostrils, sinuses, pharynx, and oropharynx
-colonized by a diverse group of microbes including non-pathogenic viruses
closest to skin-resembles skin flora
nasal cavity-resembles mouth flora
oropharynx-resembles mouth flora

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21
Q

oral cavity/teeth: normal microbiota

A

anoxic environment (between teeth and gums)
-anaerobes predominate
teeth and buccal surface (gums)
-streptococcus species

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22
Q

small intestine normal microbiota: gastrointestinal tract

A

duodenum: contains a few organisms due to stomach acid
Jejunum: enterococcus, lactobacillus, corynebacterium, yeast
ileum: similar to that in colon

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23
Q

colon (large intestine): normal microbiota: gastrointestinal tract

A

colon
largest microbial population on body
anaerobes: bacteroides, clostridia, prevotella
facultative anaerobes: enterobacteriaceae

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24
Q

genitourinary tract: normal microbiota

A

kidneys, ureter, bladder: sterile
distal portions of urethra: colonized by skin/GI tract flora: S. epidermidis, enterococcus, and corynebacterium spp.
female genital tract: acid-tolerant lactobacillus predominate

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25
Q

holobionts

A

hosts and microbes live together and evolve together

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26
Q

disrupted microbiota

A

dysbiosis

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27
Q

metabolic syndrome of dysbiosis

A

associated with chronic low-level inflammation

linked to metabolic endotoxemia

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28
Q

cardiovascular disease of dysbiosis

A

risk factor: diet increased red meat and high fat foods
increased production of trimethylamine (TMA)
TMA is oxidized by liver to trimethylamine N-oxide–>associated with atherosclerosis

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29
Q

cancer of dysbiosis

A

infection may cause the host become cancerous (flavor proliferation)
or cancers may be linked to inflammatory state associated with dysbiosis

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30
Q

virulence

A

describes the degree of harm/disease that a pathogen causes

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31
Q

virulence factors

A

microbial products or characteristics that increase ability to cause disease

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32
Q

infections dose 50

A 
ID50
# of pathogens that will infect 50% of inoculated hosts
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33
Q

lethal dose 50

A

LD50

dose that kills 50% of experimental animals within a specified period

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34
Q

types of virulence factors

A

adhesion colonization factors; adhesions
invasion factors; invasins
surviving/overcoming host defenses: evade or suppress immune factors
direct damage to host tissues: exotoxins, endotoxins

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35
Q

adherence

A 
sticking to:
mediated by special molecules called adhesions
pili
fimbriae
membrane and capsular materials
viral spikes
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36
Q

colonization

A

establishing permanence
a site of microbial replication on or within host
dose no necessarily result in tissue invasion or damage

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37
Q

invasion

A

depends of pathogen
invasins
mechanism of action

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38
Q

overcoming host defenses

A

most microbes are eliminated before they can cause disease due to immune system

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39
Q

strategies to evade host immune response

A

antigenic masking
antigenic mimicry
antigenic variation

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40
Q

antigenic masking

A

pathogenic may conceal antigenic features

coats itself with host molecules

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41
Q

antigenic mimicry

A

emulating host molecules

capsules can resemble host carbohydrates

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42
Q

antigenic variation

A 
periodically altering the surface molecules
prevents a rapid immune response
causes include:
-mutations in the genome
-change in protein expression
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43
Q

strategies to suppress host immune response

A

interference of phagocytosis
pathogens suppress immune function by:
-directly targeting/invading immune system cells
-making proteases that break down host antibodies
-interfering with the molecular signaling that activities parts of the immune response
-form biofilms

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44
Q

endotoxins

A

endo=inside
part of gram negative cell wall
higher LD50=less toxic
outer membrane of gram negative bacteria only
Lipid A portion is embedded in outer membrane
lipid A triggers an excessive inflammatory response
-endotoxic shock or septic shock

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45
Q

exotoxins

A

secreted by pathogen
soluble proteins; heat-labile
secreted by live bacteria
hight toxicity; low LD50

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46
Q

toxigenic

A

microbes that make toxins

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47
Q

toxemia

A

toxins in the bloodstream

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48
Q

types of exotoxins

A

A-B toxins

super antigens

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49
Q

A-B toxins

A 
A subunit (responsible for toxic effects)
B subunit (binds to specific target cell)
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50
Q

superantigens

A

activate T helper cells non-specifically
increased pro-inflammatory cytokine
may lead to toxic shock and organ failure

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51
Q

first line defesnses

A

physical/mechanical barriers:

  • skin
  • epithelial cell layers: respiratory, GI tract, HU tract, eye
  • mucous membranes
  • fluids: mucus, tears, saliva, sweat, stomach acid
  • mechanical: cilia, peristalsis
  • normal microbiota
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52
Q

the physical/mechanical barriers of skin

A 
keratinocyte: keratin, dead cells
slightly acidic pH: sebum
dry
salt (perspiration)
lysozyme: protects follicle, gland
normal microbiota
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53
Q

second line defenses

A

chemical/molecular defenses

cellular defenses

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54
Q

second line chemical/molecular defenses

A 
lysozyme
lactoferrin
lactoperoxidase
complement
cytokines
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55
Q

second line cellular defenses

A

lymphatic system
leukocytes
phagocytosis
inflammation

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56
Q

lysozyme

A

a second line chemical/molecular defense
hydrolyzes peptidoglycan
cervical mucus, prostatic fluid, tears

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57
Q

lactoferrin

A

a second line chemical/molecular defense

sequesters iron in plasma

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58
Q

lactoperoxidase

A

a second line chemical/molecular defense
create superoxide radicals
mucous membranes

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59
Q

the complement system

A

composed of >30 heat-labile serum proteins
circulate in inactive form
three major activities:
-stimulates inflammation
-forms membrane attack complex
-promotes phagocytosis through opsonization

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60
Q

complement activation contributes to opsonizatoin

A

process in which microbes are coated by serum components (opsonins)
complement proteins are the first opsonins
prompts phagocytosis

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61
Q

cytokine

A

second line defenses

soluble protein/glycoprotein released by one cell that acts as a signaling molecules

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62
Q

cytokine functional groups

A

chemokines
interleukins
interferons

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63
Q

chemokines

A

stimulate cell migration

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64
Q

interleukins

A

regulate cell growth and differentiation

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65
Q

interferons

A

nonspecific antiviral activity

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66
Q

lymphatic system second line defense

A 
plasma-->interstitial fluid-->lymph
primary lymphoid tissues:
-lymphocyte maturation (B and T cells)
-thymus and bone marrow
secondary lymphoid tissues:
-encapsulated: spleen, lymph nodes
-diffuse:
--mucosa-associated lymphoid tissue (MALT)
---peyers patches and tonsils
---skin associated lymphoid tissue (SALT)
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67
Q

phagocytosis second line defenses

A

endocytic process encloses large particles in vacuole; digestion

  • opsonin-dependent: complement and/or antibody
  • opsonin-independent
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68
Q

phagocytosis: opsonin independent pathogen recognition

A

phagocytosis
microbe associated molecular patters (MAMPs)
-conserved molecules seen in microbes; not host
phagocytes have pattern recognition receptors (PRRs) which recognize MAMPs
toll-like receptors are one of the four types of PRRs

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69
Q

phagocytosis: toll like receptors (TLRs)

A

PRRs that function as signaling receptors
recognize and bind unique MAMPs
found on macrophages and dendritic cells
-antigen-presenting cells

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70
Q

phagocytosis: intracellular digestion

A

phagolysosome
exocytosis
antigen-presenting cells

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71
Q

phagolysosome

A

phagocytosis: intracellular digestion
acidic pH
degradative enzymes
reactive oxygen species (ROS)

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72
Q

exocytosis

A

phagocytosis: intracellular digestion
debris is expelled
neutrophils

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73
Q

antigen-presenting cells

A

phagocytosis: intracellular digestion
macrophages and dendritic cells (and B cells)
debris is packed with MHC2 molecules; sent to cell membrane

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74
Q

phagocytes: second line defenses

A

neutrophils contain mili-lobed segmented nucleus
macrophages are an antigen-presenting cell
dendritic cells are an antigen-presenting cell

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75
Q

inflammation: nonspecific response to tissue injury:

A

vascular changes
leukocyte recruitment
resolution/repair

76
Q

vascular changes

A

nonspecific inflammation response to tissue injury
vasodilation
increased permeability

77
Q

leukocyte recruitment

A

nonspecific inflammation response to tissue injury
margination
diapedesis
extravasation

78
Q

three goals of inflammation

A

recruit immune defenses to injured tissue
limit the spread of infectious agents
deliver O2, nutrients, and chemical factors essential for tissue recovery

79
Q

five cardinal signs of inflammation

A 
redness (rubor)
heat (calor)
swelling (tumor)
pain (dolor)
loss of function
80
Q

innate immunity

A

generalized responses
non-specific immunity
phagocytes: pattern recognition receptors (PRRs) recognize microbe-associated molecular patterns (MAMPs)

81
Q

adaptive immunity

A

specific diverse responses
exhibits immunological memory
recognizes specific antigen (foreign molecules) along with MHC molecules (self)
creates specific tailored response

82
Q

adaptive immunity based on activity of lymphocytes

A 
lymphocyte: leukocyte frequently found in lymphatic system
T lymphocytes (T cells) mature in the thymus
B lymphocytes (B cells) mature in the bone marrow
83
Q

two branches of adaptive immunity (third line of defense)

A

cell mediated immunity: based on action cytotoxic T cell
humoral immunity: based on antibody activity (made by B cells)
-assisted by T helper cells

84
Q

antigen

A

antigen elicit immunity
epitope fragment of an antigen recognized by specific antibodies
hapten-incomplete antigen

85
Q

how does the immune system recognize itself

A

major histocompatibility complex (MHC) molecules= “self” proteins

  • unique to each person; close relatives have similar MHC molecules
  • also called HLA molecules (human leukocyte antigens)
86
Q

two main classes of MHCs

A

MHC1

NHC2

87
Q

MHC 1

A

on all human cells except red blood cells
binds antigens that originate in the cytoplasm
displays antigen epitopes to cytotoxic T cells

88
Q

MHC 2

A

only on antigen-presenting cells (APCs)
macrophages, dendritic cells, and B cells
binds antigens that originate outside the cell
displays antigen epitopes to T helper cells

89
Q

why 2 classes of MHC molecules

A

intracellular pathogens

extracellular pathogens

90
Q

intracellular pathogens

A

antigens will be displayed with MHC1
recognized by cytotoxic T cells
infected cells will be killed

91
Q

extracellular pathogens

A

antigens will be processed by antigen-presenting cells
antigens will be displayed with MHC2
recognized by T helper cells which can activate B cells
antibodies will be produced–>antigen will be eliminated

92
Q

epitopes are recognized by lymphocyte receptors

A

each lymphocyte has unique surface receptors that are specific for one epitope
-TCR-T cell receptor (has 1 epitope binding site)
-BCR-B cell receptor (has 2 epitope binding sites)
BCR and TCR are result of somatic gene rearrangement
-random process
-creates nearly unlimited diversity

93
Q

intracellular antigen

A

intracellular antigen associated with MHC1
epitope-MHC 1 complex displayed on surface of infected cell
cytotoxic T cell with specificity for that epitope will bind
binding requires co-receptor, CD8

94
Q

cytotoxic T cells (Tc)

A

also known as CD8+ T cells
activated by specific epitope-MHC1 complex
once activated:
-rlease cytokines to attract macrophages (and natural killer cells)
-release performs and granzymes
-target cell undergoes apoptosis; cell death

95
Q

T cell activation

A

leads to more cells with same specificity and memory cells
activation–>proliferation (cell division/same specificity)
differentiation–>effector cells and memory cells

96
Q

extracellular antigen

A

uptake by APCs (phagocytosis)
epitope-MHC2 displayed on cell surface
T helper cell with specificity for that epitope will bind
binding requires co-receptor, CD4

97
Q

T helper cells

A

Th
also known as CD4+ T cells
activated by specific epitope-MHC2 complex
regulate activities of macrophages, B cells, and Tc cells
Th0: naive T cells
Th1: active macrophages, Tc
Th2: activate B cells

98
Q

B lymphocytes (B cells)

A

BCR can bind to free antigen
act as APCs; present antigen-MHC2 complexes
differentiate into plasma cells–>antibodies
-antibodies=secreted form of BCR
-antibodies=immunoglobulins (Ig)
activation:
-by TH2 cells (common)
-by free antigen binding BCR (less common)

99
Q

antibody structure

A 
four polypeptide chains
-2 identical heavy chains
-2 identical light chains
--connected by disulfide bonds
stalk of y:
-crystallizable fragment (Fc)
-complement binding
-phagocyte receptor binding
top of Y
-2 antigen-binding fragments (Fab)
100
Q

antibody functions

A 
neutralization
agglutination
precipitation
opsoninization
activation of complement
101
Q

antibody classes/immunoglobulin classes

A

can undergo isotope switching

102
Q

B cell activation

A

leads to more cells with the same specificity and memory cells
activation–> proliferation (cell division/same specificity)
differentiation–> effector cells and memory cells
note: effector cell for B cells=plasma cell

103
Q

primary immune response

A

slow: 4-7 days

104
Q

secondary immune response

A 
rapid, efficient, prevents illness
activity of memory lymphocytes
quickly respond:
-higher # of specific lymphocyte
-higher titers of specific antibody
105
Q

vaccine

A

injection of microbial antigen as a prevention for a disease

106
Q

herd immunity

A

communal immunity that protects unvaccinated individuals if majority of population is vaccinated
immunization programs aim to create her immunity

107
Q

vaccine formulations

A 
live attenuated vaccines
whole-agent killed/inactivated vaccines
purified subunit vaccines
DNA/RNA vaccines
recombinant vector vaccines
108
Q

eradication of smallpox

A

1980

109
Q

live attenuated vaccines

A

live attenuated vaccines: contain microbes that can multiply but are too weak to cause disease

benefits: best immune response and most closely mimics natural infection
drawbacks: often need refrigeration, can cause disease in immune-compromised hosts, and possible mutation to an infectious form

110
Q

whole agent vaccines

A

inactivated vaccines: consists of whole dead/inactivated pathogens

benefits: good immune response, safe for immunocompromised patients, stable at room temperature
drawbacks: boosters required to achieve full immunity

111
Q

subunit vaccines

A

subunit vaccines: consist of purified antigens; immunogenic portion of the pathogen and harvested from growing pathogen or genetically engineered system

benefits: good immune response; safe for immunocompromised patients and exposure to most important microbial antigen; often VF
drawbacks: may require boosters and require adjuvants

112
Q

adjuvants

A

additives that enhance immunogenicity

  • aluminum salts
  • monophosphoryl lipid A
113
Q

subunit vaccine types

A

purified subunit vaccines
toxoid vaccines
conjugate (or polysaccharide) vaccines

114
Q

purified subunit vaccines

A

purified antigenic components of pathogen

115
Q

toxoid vaccines

A

purified and inactivated toxins

116
Q

conjugate (or polysaccharide) vaccines

A

polysaccharide antigens conjugated to a more immunogenic protein antigen

117
Q

DNA/RNA vaccine formulation

A

DNA vaccines or RNA vaccines

  • genes encoding highly immunogenic antigens are identified
  • plasmid is injected into a human host
  • human cells become the antigen producers
  • results in a humoral and a cellular immune response
118
Q

recombinant vector vaccine formulation

A

genes encoding highly immunogenic antigens are identified
genes from the pathogen are packed inside a harmless virus
new “recombinant” virus is injected into the body
harmless virus acts as vector for pathogen genes

119
Q

laboratory diagnostics: immunologic methods

A 
serology
immunologic methods:
-maboratory techniques involving immunologic reactions (antibody-antigen)
common immunological methods:
-agglutination directions
-ELISA
-immunochromatography assay (ICA)
120
Q

agglutination reactions are commonly used for

A

blood typing
identify infections
diagnose noninfectious immune disorders

121
Q

serology

A

the study of what is in a patient’s serum

detect antigens/antibodies in patient blood sample

122
Q

elisa requires

A 
microtiter plate
patient sample
specific antibody
enzyme
plate reader
123
Q

microtiter plate

A

plastic dish with many wells

124
Q

patient sample

A

may or may not contain antibody or antigen of interest

125
Q

specific antibody

A

will bind antigen of interest

126
Q

enzyme

A

will cause a color change when substrate is added

127
Q

plate reader

A

can detect/quantify the color change in each well

128
Q

immunochromatography assay

A

ICA

combination of chromatography and immunologic reactions

129
Q

immunodeficiency

A

the lack of a properly functioning immune system

130
Q

types of immunodeficiency

A

primary and secondary

131
Q

primary immunodeficiency

A

congenital immunity
affects >1 immune factors and leads to deficient immune response
relatively rare
therapies include: bone marrow transplants, IV Ig, cytokine therapies

132
Q

secondary immunodeficiency

A

acquired immunodeficiency
normal immune system–>decline in immune system rigor
more common
causes: age, medication, systemic disorders, certain infectious agents (HIV, epstein barr virus, measles)

133
Q

autoimmunity

A

lack of self tolerance

an immune system attack against healthy self-tissues

134
Q

autoimmune disorders

A

chronic conditions due to damaging self-tissue attacks

135
Q

self-tolerance

A

body’s screening mechanisms

136
Q

T and B cells are screened for self-tolerance

A

T and B cells recognize a wide variety of antigens due to gene rearrangement mechanisms
T and B cells that DONT exhibit self-tolerance=apoptosis
T cells: must recognize the “self” MHC and cannot attack “self cells
B cells: antibody won’t cross-react with self-antigens and damage host tissues

137
Q

molecular mimicry

A

microbial antigen that is similar to self-antigen

rheumatic fever-antibodies against Streptococcus progenies (GAS) attach heart valves

138
Q

superantigens

A

microbial antigen that can activate T cells non-specifically

may cause anti-self reactions

139
Q

cytopathic effects

A

infection–> host APCs process/present self-antigens to T cells

140
Q

genetic predispositions

A

+/- infections and other environmental factors

141
Q

what leads to autoimmune disorders

A

theories:

  • molecular mimicry
  • superantigens
  • cytopathic effects
  • genetic predispositions
142
Q

type 1 diabetes

A

immune system attacks insulin-producing cells of the pancreas
implicated infectious agents:
coxsackievirus B
-viral infection myocarditis or endocarditis

143
Q

guillain-barre syndrome

A

peripheral nerves are attacked and muscle weakness develops
implicated infectious agents:
campylobacter jejune
-bacterial diarrheal disease

144
Q

rheumatic heart disease

A

heart inflammation and scarring
implicated infectious agents:
streptococcus pyogens
-streptococcal pharyngitis (“strep throat”)

145
Q

multiple sclerosis (MS)

A

loss of myelin sheath on nerves leading to delayed nerve impulse transmission and pain
implicated infectious agents:
>20 possible viral agents
-possibly human herpesvirus 6 and epstein-barr virus

146
Q

hypersensitivities

A

inappropriate immune responses
can be localized or systemic
can be delayed or immediate
four classes

147
Q

type 1 hypersensitivity reaction

A

allergen: any antigen that triggers IgE production
allergy: scenario where the immune system fights off a perceived threat that would otherwise be harmless
mediated by IgE and Mast cells
testing: IgE titers in blood (RAST)
-atopic asthma-allergy-based asthma
-atopic dermatitis-inflamed, itchy skin condition; aka atopic eczema
granules contain histamine
antihistamines can block activity and relieve allergy symptoms

148
Q

type 1 hypersensitivity anaphylaxis

A 
localized anaphylaxis:
-isolated symptoms
-vasodilation, increased vascular permeability, increased mucus secretion
-hay fever-urticaria (hives)
systemic anaphylaxis:
-massive release of mast cell mediators
-system-wide response; potentially life threatening
--anaphylactic shock
149
Q

type 2 hypersensitivity

A 
cytolytic or cytotoxic reaction
involves IgG and IgM antibodies
stimulate complement pathway
-blood transfusion reactions
-hemolytic disease of the newborn
150
Q

type 2 hypersensitivity blood transfusion reactions

A

complement-mediated destruction of RBCs

151
Q

type 2 hypersensitivity hemolytic disease of the newborn (HDN)

A

AKA erythroblastosis fetalis
Rh- mother with Rh+ fetus; later pregnancies (not 1st)
maternal IgG (anti-Rh) antibodies destroy fetal RBCs
Prevention: RH(D) immunoglobulin (RhoGAM) is given

152
Q

type 3 hypersensitivity

A 
IgG or IgM bind soluble targets
excessive antibody-antigen complexes
complexes are deposited in tissues
causes complement activation and inflammation
acute glomerulonephritis (AGN)
-sequelae of GAS pharyngitis
153
Q

type 4 hypersensitivity

A 
T cell mediated
delayed hypersensitivity reaction
EX:
-contact dermatitis; latex sensitivity
-tuberculin skin test (PPD test)
-graft-versus-host disease
154
Q

contact dermatitis

A 
first exposure: 
-t cells sensitized (activated)
-creation of memory T cells
secondary exposure:
-memory T cell respond
-inflammation
155
Q

PPD test

A

tuberculin skin test (PPD test)

  • detects exposure to mycobacterium tuberculosis (TB)
  • tuberculin purified protein derivative (PPD) is injected into the skin of the forearm
  • injection site is observed within 48-72 hours
  • positive result recorded if area of induration develops
156
Q

graft-versus-host disease (GVHD)

A

transplant rejection: if T cytotoxic cells from host detect that the tissue is foreign
-donor and receipt must have similar MHCs
GVHD
-T cells from donor marrow (graft_ attack host tissues

157
Q

chemotherapeutic agents

A

chemical agents used to treat disease
destroy pathogenic microbes: -cidal
inhibit microbe growth: -static

158
Q

antibacterial drugs (antibiotics)

A

treat bacterial infections

159
Q

antiviral drugs

A

target viral infections

160
Q

anti fungal drugs

A

target fungal infections

161
Q

anti parasitic drugs

A

treat protozoan and helminthic (worm) infections

162
Q

prophylaxsis

A

process that prevents infection or disease or disease in person at risk

163
Q

how do clinicians chose an appropriate drug

A

empiric vs definitive antimicrobial therapy
considerations:
-administration rout: oral vs parenteral (IV)
-drug stability and elimination
-drug safety (toxicity; side effects)
–broad spectrum drugs: broad range
–narrow-spectrum drugs: limited range of bacteria

164
Q

antibacterial drugs may be grouped by their cellular targets

A 
ideal drug targets structures and processes that bacteria rely on, but human cells do not:
cell wall synthesis
plasma membrane
nucleic acids
protein synthesis
folic acid synthesis
165
Q

antibacterial drugs targeting cell wall synthesis

A

beta lactam: prevent cross-linking of peptidoglycan
-penicillins (end in “cillin”)
-cephalosporins (start with “cef” or “ceph”)
-carbapenems (end in “penem”)
-monobactams: aztreonam
non-beta lactam: glycopeptides
-vancomycin

166
Q

vancomycin

A
  • -for gram positive only; incl. MRSA
  • -preferred treatment for C. difficile
  • -“drug of last resort”
167
Q

antibacterial drugs targeting plasma membrane

A

daptomycin:

  • lipopeptide; bactericidal; calcium-dependent
  • uses: effective against Gram positive bacteria only, MDR strains; MRSA
168
Q

antibacterial drugs targeting nucleic acids

A

quinolone:
-synthetic antimicrobials; broad spectrum
-target DNA gyros and topoisomerase
-EX: ciprofloxacin, levofloxican
rifamycins:
-binds to RNA polymerase and inhibits production of mRNA
-EX: rifampicin
-uses: used for mycobacterium infections; esp. Tuberculosis

169
Q

antibacterial drugs targeting protein synthesis

A

exploits differences between prokaryotic and eukaryotic ribosomes
50S subunit
-macrolide drugs: used for penicillin-allergic patients
–EX: erythromycin, azithromycin (“Z-Pak”)
-lincosamides: clindamycin; effective against MRSA-used sparingly
-phenicols: chloramphenicol; reserved for mDR bacteria
-oxazolidinones: linezolid; used for MRSA, VRE
30S subunit:
-tetracyclines: tetracycline and doxycycline
-aminoglycosides: tend to end in “-mycin” or “-micin”
–vancomycin and daptomycin NOT included
–EX: amikacin, tobramycin, gentamicin

170
Q

antibacterial drugs targeting folic acid synthesis

A 
sulfa drugs (or sulfonamides)
-resemble para-aminobenzoic acid (PABA)
-EX: sulfamethoxazole-->interrupt the pathway for folic acid metabolism
trimethoprim--> interrupt the pathway for folic acid metabolism
bactrim--sulfamethoxazole and trimethoprim=interrupt the pathway greater in combined version than alone because they work synergistically
171
Q

antiviral agents

A

act to inhibit virus-specific enzymes and life cycle processes

  • mainly effective when viruses are actively replicating
  • oseltamivir (tamiflu)
  • remdesiver
  • acyclovir
  • AZT
172
Q

antifungal agents

A

common target: ergosterol

-griseofulvin

173
Q

antiparasitic agents

A 
quinine/chloroquine/primaquine
praziquantel (biltricide)
antibacterial drugs that also target parasite:
-metronidazole (flagyl)
-bactrim
174
Q

antibiotic resistance

A

occurs naturally, but misuse of antibiotics in humans and animals is accelerating the process

175
Q

types of drug resistance

A

intrinsic
acquired
drug-tolerant bacteria (persisters)

176
Q

intrinsic drug resistance

A

naturally occurring resistance based on biological structures

  • microbe lacks structural target or are impermeable to drug
  • EX: mycoplasma pneumoniae, clostridium difficile, gram negative bacteria
  • -gem negative bacteria are intrinsically resistant to vancomycin
177
Q

acquired drug resistance

A

a change in the genome of a microbe that converts it from one that is sensitive to an antibiotic to one that is resistant

178
Q

drug-tolerant bacteria (persisters) drug resistance

A

growth patterns; lack the mechanisms for antibiotic resistance

179
Q

mechanisms of drug resistance

A
  1. Modify the target of the antibiotic
    - MRSA
    - Resistant to all beta-lactams
    - PBP2a instead of PBP; encoded by mea A gene
  2. Antibiotic degradation (inactivation):
    - hydrolysis of beta-lactam ring by beta-lactamases/penicillinases
  3. antibiotic alterations (inactivation)
    - acetylation of aminoglycosides
  4. minimize drug concentration in the cell
    - limiting drug entry
    - pumping drugs out of cells: Efflux pumps
180
Q

the spread of antimicrobial resistance

A

HGT

  • transformation
  • transduction
  • conjugation
181
Q

detecting drug resistance

A

identify resistance patterns in laboratory isolate: micro broth dilution
detection of specific resistance factors: alert PBP2a (ICA)
detection of specific resistance genes: verigene system (DNA microarray)

182
Q

monitoring/surveillance of drug resistance

A

antibiotic stewardship
infection prevention teams in clinical settings
reporting of resistance lab isolates

183
Q

antibiotic stewardship

A

promotes the appropriate use of antibiotics, decrease microbial resistance and spread MDR microbes

184
Q

urgent threats

A

clostridium difficile
carbapenem-resistant Enterobacteriaceae (CRE)
drug-resistant Neisseria gonorrhoeae
candida auris

185
Q

how do we respond to the rise in antibiotic resistance

A 
personal:
-infection prevention
-prescription compliance
healthcare
-infection prevention
-monitoring resistant infections
-appropriate antibiotic use
agriculture
-responsible antibiotic use
-responsible waste management
science/research
-support basic research
-support drug development and drug trials

MMG 101 (10 decks)

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