Exam 3 Flashcards
(185 cards)
1
Q
epidemiology
A
studies the frequency and distribution of disease and health-related factors in human populations
2
Q
two general goals of epidemiology
A
- describe the nature, cause, and extend of new or existing diseases in populations
- intervene to protect and improve health in populations
3
Q
how does disease occur
A
the epidemiological triangle
4
Q
factors of the epidemiological triangle
A
host
environment
etiological agent
-diagnosing, treating, and preventing disease requires understanding all relevant factors
5
Q
environmental factors of the epidemiological triangle
A
source reservoir transmission vector climate
6
Q
sources of pathogens
A
endogenous: from the host’s own body; microbes or exogenous source: external to the host
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
8
Q
four main transmission routes
A
airborne contact vehicle-inanimate vector-borne -also vertical transmission
9
Q
healthcare-acquired infection (HAI)
A
an infection that a patient develops while receiving care in a healthcare setting
AKA nosocomial infections
10
Q
public health strategies to target disease
A
education
increase herd immunity
quarantine
vector control
11
Q
factors contributing to the increase of emerging diseases
A
population crowding poverty tropical climates deforestation urbanization vaccine hesitation
12
Q
one health
A
goal of achieving optimal health outcomes recognizing the interconnection between people, animals, plants, and other shared environment
13
Q
bioterrorism
A
intentional or threatened use of microbes (their products) to produce death of disease in humans, animals, and plants
14
Q
pathogen
A
microbes that cause disease
15
Q
true pathogen
A
does not require a weakened host to cause disease
never part of normal microbiota
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
17
Q
establishing normal microbiota
A
colonization during delivery and post-natally
adult microbiome established by ~3 years old
18
Q
where do we find normal microbiota
A
skin
mouth/pharynx/upper respiratory tract
gastrointestinal tract (GI)
genitourinary tract (GU)
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
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
21
Q
oral cavity/teeth: normal microbiota
A
anoxic environment (between teeth and gums)
-anaerobes predominate
teeth and buccal surface (gums)
-streptococcus species
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
23
Q
colon (large intestine): normal microbiota: gastrointestinal tract
A
colon
largest microbial population on body
anaerobes: bacteroides, clostridia, prevotella
facultative anaerobes: enterobacteriaceae
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
25
holobionts
hosts and microbes live together and evolve together
26
disrupted microbiota
dysbiosis
27
metabolic syndrome of dysbiosis
associated with chronic low-level inflammation
| linked to metabolic endotoxemia
28
cardiovascular disease of dysbiosis
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
29
cancer of dysbiosis
infection may cause the host become cancerous (flavor proliferation)
or cancers may be linked to inflammatory state associated with dysbiosis
30
virulence
describes the degree of harm/disease that a pathogen causes
31
virulence factors
microbial products or characteristics that increase ability to cause disease
32
infections dose 50
```
ID50
# of pathogens that will infect 50% of inoculated hosts
```
33
lethal dose 50
LD50
| dose that kills 50% of experimental animals within a specified period
34
types of virulence factors
adhesion colonization factors; adhesions
invasion factors; invasins
surviving/overcoming host defenses: evade or suppress immune factors
direct damage to host tissues: exotoxins, endotoxins
35
adherence
```
sticking to:
mediated by special molecules called adhesions
pili
fimbriae
membrane and capsular materials
viral spikes
```
36
colonization
establishing permanence
a site of microbial replication on or within host
dose no necessarily result in tissue invasion or damage
37
invasion
depends of pathogen
invasins
mechanism of action
38
overcoming host defenses
most microbes are eliminated before they can cause disease due to immune system
39
strategies to evade host immune response
antigenic masking
antigenic mimicry
antigenic variation
40
antigenic masking
pathogenic may conceal antigenic features
| coats itself with host molecules
41
antigenic mimicry
emulating host molecules
| capsules can resemble host carbohydrates
42
antigenic variation
```
periodically altering the surface molecules
prevents a rapid immune response
causes include:
-mutations in the genome
-change in protein expression
```
43
strategies to suppress host immune response
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
44
endotoxins
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
45
exotoxins
secreted by pathogen
soluble proteins; heat-labile
secreted by live bacteria
hight toxicity; low LD50
46
toxigenic
microbes that make toxins
47
toxemia
toxins in the bloodstream
48
types of exotoxins
A-B toxins
| super antigens
49
A-B toxins
```
A subunit (responsible for toxic effects)
B subunit (binds to specific target cell)
```
50
superantigens
activate T helper cells non-specifically
increased pro-inflammatory cytokine
may lead to toxic shock and organ failure
51
first line defesnses
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
52
the physical/mechanical barriers of skin
```
keratinocyte: keratin, dead cells
slightly acidic pH: sebum
dry
salt (perspiration)
lysozyme: protects follicle, gland
normal microbiota
```
53
second line defenses
chemical/molecular defenses
| cellular defenses
54
second line chemical/molecular defenses
```
lysozyme
lactoferrin
lactoperoxidase
complement
cytokines
```
55
second line cellular defenses
lymphatic system
leukocytes
phagocytosis
inflammation
56
lysozyme
a second line chemical/molecular defense
hydrolyzes peptidoglycan
cervical mucus, prostatic fluid, tears
57
lactoferrin
a second line chemical/molecular defense
| sequesters iron in plasma
58
lactoperoxidase
a second line chemical/molecular defense
create superoxide radicals
mucous membranes
59
the complement system
composed of >30 heat-labile serum proteins
circulate in inactive form
three major activities:
-stimulates inflammation
-forms membrane attack complex
-promotes phagocytosis through opsonization
60
complement activation contributes to opsonizatoin
process in which microbes are coated by serum components (opsonins)
complement proteins are the first opsonins
prompts phagocytosis
61
cytokine
second line defenses
| soluble protein/glycoprotein released by one cell that acts as a signaling molecules
62
cytokine functional groups
chemokines
interleukins
interferons
63
chemokines
stimulate cell migration
64
interleukins
regulate cell growth and differentiation
65
interferons
nonspecific antiviral activity
66
lymphatic system second line defense
```
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)
```
67
phagocytosis second line defenses
endocytic process encloses large particles in vacuole; digestion
- opsonin-dependent: complement and/or antibody
- opsonin-independent
68
phagocytosis: opsonin independent pathogen recognition
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
69
phagocytosis: toll like receptors (TLRs)
PRRs that function as signaling receptors
recognize and bind unique MAMPs
found on macrophages and dendritic cells
-antigen-presenting cells
70
phagocytosis: intracellular digestion
phagolysosome
exocytosis
antigen-presenting cells
71
phagolysosome
phagocytosis: intracellular digestion
acidic pH
degradative enzymes
reactive oxygen species (ROS)
72
exocytosis
phagocytosis: intracellular digestion
debris is expelled
neutrophils
73
antigen-presenting cells
phagocytosis: intracellular digestion
macrophages and dendritic cells (and B cells)
debris is packed with MHC2 molecules; sent to cell membrane
74
phagocytes: second line defenses
neutrophils contain mili-lobed segmented nucleus
macrophages are an antigen-presenting cell
dendritic cells are an antigen-presenting cell
75
inflammation: nonspecific response to tissue injury:
vascular changes
leukocyte recruitment
resolution/repair
76
vascular changes
nonspecific inflammation response to tissue injury
vasodilation
increased permeability
77
leukocyte recruitment
nonspecific inflammation response to tissue injury
margination
diapedesis
extravasation
78
three goals of inflammation
recruit immune defenses to injured tissue
limit the spread of infectious agents
deliver O2, nutrients, and chemical factors essential for tissue recovery
79
five cardinal signs of inflammation
```
redness (rubor)
heat (calor)
swelling (tumor)
pain (dolor)
loss of function
```
80
innate immunity
generalized responses
non-specific immunity
phagocytes: pattern recognition receptors (PRRs) recognize microbe-associated molecular patterns (MAMPs)
81
adaptive immunity
specific diverse responses
exhibits immunological memory
recognizes specific antigen (foreign molecules) along with MHC molecules (self)
creates specific tailored response
82
adaptive immunity based on activity of lymphocytes
```
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
two branches of adaptive immunity (third line of defense)
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
antigen
antigen elicit immunity
epitope fragment of an antigen recognized by specific antibodies
hapten-incomplete antigen
85
how does the immune system recognize itself
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
two main classes of MHCs
MHC1
| NHC2
87
MHC 1
on all human cells except red blood cells
binds antigens that originate in the cytoplasm
displays antigen epitopes to cytotoxic T cells
88
MHC 2
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
why 2 classes of MHC molecules
intracellular pathogens
| extracellular pathogens
90
intracellular pathogens
antigens will be displayed with MHC1
recognized by cytotoxic T cells
infected cells will be killed
91
extracellular pathogens
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
epitopes are recognized by lymphocyte receptors
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
intracellular antigen
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
cytotoxic T cells (Tc)
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
T cell activation
leads to more cells with same specificity and memory cells
activation-->proliferation (cell division/same specificity)
differentiation-->effector cells and memory cells
96
extracellular antigen
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
T helper cells
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
B lymphocytes (B cells)
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
antibody structure
```
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
antibody functions
```
neutralization
agglutination
precipitation
opsoninization
activation of complement
```
101
antibody classes/immunoglobulin classes
can undergo isotope switching
102
B cell activation
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
primary immune response
slow: 4-7 days
104
secondary immune response
```
rapid, efficient, prevents illness
activity of memory lymphocytes
quickly respond:
-higher # of specific lymphocyte
-higher titers of specific antibody
```
105
vaccine
injection of microbial antigen as a prevention for a disease
106
herd immunity
communal immunity that protects unvaccinated individuals if majority of population is vaccinated
immunization programs aim to create her immunity
107
vaccine formulations
```
live attenuated vaccines
whole-agent killed/inactivated vaccines
purified subunit vaccines
DNA/RNA vaccines
recombinant vector vaccines
```
108
eradication of smallpox
1980
109
live attenuated vaccines
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
whole agent vaccines
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
subunit vaccines
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
adjuvants
additives that enhance immunogenicity
- aluminum salts
- monophosphoryl lipid A
113
subunit vaccine types
purified subunit vaccines
toxoid vaccines
conjugate (or polysaccharide) vaccines
114
purified subunit vaccines
purified antigenic components of pathogen
115
toxoid vaccines
purified and inactivated toxins
116
conjugate (or polysaccharide) vaccines
polysaccharide antigens conjugated to a more immunogenic protein antigen
117
DNA/RNA vaccine formulation
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
recombinant vector vaccine formulation
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
laboratory diagnostics: immunologic methods
```
serology
immunologic methods:
-maboratory techniques involving immunologic reactions (antibody-antigen)
common immunological methods:
-agglutination directions
-ELISA
-immunochromatography assay (ICA)
```
120
agglutination reactions are commonly used for
blood typing
identify infections
diagnose noninfectious immune disorders
121
serology
the study of what is in a patient's serum
| detect antigens/antibodies in patient blood sample
122
elisa requires
```
microtiter plate
patient sample
specific antibody
enzyme
plate reader
```
123
microtiter plate
plastic dish with many wells
124
patient sample
may or may not contain antibody or antigen of interest
125
specific antibody
will bind antigen of interest
126
enzyme
will cause a color change when substrate is added
127
plate reader
can detect/quantify the color change in each well
128
immunochromatography assay
ICA
| combination of chromatography and immunologic reactions
129
immunodeficiency
the lack of a properly functioning immune system
130
types of immunodeficiency
primary and secondary
131
primary immunodeficiency
congenital immunity
affects >1 immune factors and leads to deficient immune response
relatively rare
therapies include: bone marrow transplants, IV Ig, cytokine therapies
132
secondary immunodeficiency
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
autoimmunity
lack of self tolerance
| an immune system attack against healthy self-tissues
134
autoimmune disorders
chronic conditions due to damaging self-tissue attacks
135
self-tolerance
body's screening mechanisms
136
T and B cells are screened for self-tolerance
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
molecular mimicry
microbial antigen that is similar to self-antigen
| rheumatic fever-antibodies against Streptococcus progenies (GAS) attach heart valves
138
superantigens
microbial antigen that can activate T cells non-specifically
| may cause anti-self reactions
139
cytopathic effects
infection--> host APCs process/present self-antigens to T cells
140
genetic predispositions
+/- infections and other environmental factors
141
what leads to autoimmune disorders
theories:
- molecular mimicry
- superantigens
- cytopathic effects
- genetic predispositions
142
type 1 diabetes
immune system attacks insulin-producing cells of the pancreas
implicated infectious agents:
coxsackievirus B
-viral infection myocarditis or endocarditis
143
guillain-barre syndrome
peripheral nerves are attacked and muscle weakness develops
implicated infectious agents:
campylobacter jejune
-bacterial diarrheal disease
144
rheumatic heart disease
heart inflammation and scarring
implicated infectious agents:
streptococcus pyogens
-streptococcal pharyngitis ("strep throat")
145
multiple sclerosis (MS)
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
hypersensitivities
inappropriate immune responses
can be localized or systemic
can be delayed or immediate
four classes
147
type 1 hypersensitivity reaction
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
type 1 hypersensitivity anaphylaxis
```
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
type 2 hypersensitivity
```
cytolytic or cytotoxic reaction
involves IgG and IgM antibodies
stimulate complement pathway
-blood transfusion reactions
-hemolytic disease of the newborn
```
150
type 2 hypersensitivity blood transfusion reactions
complement-mediated destruction of RBCs
151
type 2 hypersensitivity hemolytic disease of the newborn (HDN)
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
type 3 hypersensitivity
```
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
type 4 hypersensitivity
```
T cell mediated
delayed hypersensitivity reaction
EX:
-contact dermatitis; latex sensitivity
-tuberculin skin test (PPD test)
-graft-versus-host disease
```
154
contact dermatitis
```
first exposure:
-t cells sensitized (activated)
-creation of memory T cells
secondary exposure:
-memory T cell respond
-inflammation
```
155
PPD test
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
graft-versus-host disease (GVHD)
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
chemotherapeutic agents
chemical agents used to treat disease
destroy pathogenic microbes: -cidal
inhibit microbe growth: -static
158
antibacterial drugs (antibiotics)
treat bacterial infections
159
antiviral drugs
target viral infections
160
anti fungal drugs
target fungal infections
161
anti parasitic drugs
treat protozoan and helminthic (worm) infections
162
prophylaxsis
process that prevents infection or disease or disease in person at risk
163
how do clinicians chose an appropriate drug
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
antibacterial drugs may be grouped by their cellular targets
```
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
antibacterial drugs targeting cell wall synthesis
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
vancomycin
- -for gram positive only; incl. MRSA
- -preferred treatment for C. difficile
- -"drug of last resort"
167
antibacterial drugs targeting plasma membrane
daptomycin:
- lipopeptide; bactericidal; calcium-dependent
- uses: effective against Gram positive bacteria only, MDR strains; MRSA
168
antibacterial drugs targeting nucleic acids
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
antibacterial drugs targeting protein synthesis
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
antibacterial drugs targeting folic acid synthesis
```
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
antiviral agents
act to inhibit virus-specific enzymes and life cycle processes
- mainly effective when viruses are actively replicating
- oseltamivir (tamiflu)
- remdesiver
- acyclovir
- AZT
172
antifungal agents
common target: ergosterol
| -griseofulvin
173
antiparasitic agents
```
quinine/chloroquine/primaquine
praziquantel (biltricide)
antibacterial drugs that also target parasite:
-metronidazole (flagyl)
-bactrim
```
174
antibiotic resistance
occurs naturally, but misuse of antibiotics in humans and animals is accelerating the process
175
types of drug resistance
intrinsic
acquired
drug-tolerant bacteria (persisters)
176
intrinsic drug resistance
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
acquired drug resistance
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
drug-tolerant bacteria (persisters) drug resistance
growth patterns; lack the mechanisms for antibiotic resistance
179
mechanisms of drug resistance
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
the spread of antimicrobial resistance
HGT
- transformation
- transduction
- conjugation
181
detecting drug resistance
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
monitoring/surveillance of drug resistance
antibiotic stewardship
infection prevention teams in clinical settings
reporting of resistance lab isolates
183
antibiotic stewardship
promotes the appropriate use of antibiotics, decrease microbial resistance and spread MDR microbes
184
urgent threats
clostridium difficile
carbapenem-resistant Enterobacteriaceae (CRE)
drug-resistant Neisseria gonorrhoeae
candida auris
185
how do we respond to the rise in antibiotic resistance
```
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
```
