Lecture Exam 2 Flashcards
(189 cards)
1
Q
Operon
A
Set of genes transcribed as a single mRNA, under the control of one promoter. Transcription/translation simultaneous.
2
Q
Promoter
A
rRNA polymerase binding site, to do transcription. Produces mRNA.
3
Q
Genes that code for proteins
A
Structural genes
4
Q
Genes that regulate structural genes
A
Regulatory genes, make regulatory proteins
5
Q
Genes that are always expressed (~75%)
A
Constitutive genes
6
Q
Genes that are turned on/off as a cell’s needs change
A
Facultative genes. Inducible/repressible operons.
7
Q
Inducible operons
A
Off by default. Activated by inducers. Lactose operon
8
Q
Lactose operon
A
In absence of lactose operon is OFF. Repressor protein binds to operator, blocking RNA polymerase. In presence of lactose operon gets turned ON, RNA polymerase can work. Genes get turned back off when lactose levels go down
9
Q
Repressible operon
A
ON by default. Must be turned off by co-repressors. Tryptophan operon.
10
Q
Tryptophan operon
A
When tryp levels are low operon is ON, RNA polymerase is transcribing DNA. As long as levels are low operon will stay on. When tryp levels are high operon is turned off by allosteric activation.
11
Q
Transfer of DNA between cells of the same generation
A
Horizontal gene transfer
12
Q
3 Mechanisms of horizontal gene transfer
A
- Transformation
- Transduction
- Conjucation
13
Q
Bacterial cell takes up naked DNA from environment
A
Transformation
14
Q
Viral mistake, virus brings in new DNA
A
Transduction
15
Q
DNA sharing via pilus, plasma DNA is shared
A
Conjugation
16
Q
Property of cells that can naturally be transformed
A
Competency.
17
Q
Manipulation of cells so they can be transformed
A
Artificial competency
18
Q
Gene transfer via bacteriophage
A
Transduction
19
Q
Generalized transduction
A
Lytic phage! Mistake made during the packaging of a random DNA fragment from the host bacterial chromosome into the bacteriophage.
20
Q
Specialized transduction
A
Lysogenic phage! Mistake in the excision of a prophage from a host chromosome results in some bacterial DNA becoming attached to viral DNA.
21
Q
Conjugation
A
Requires contact via sex pilus. F+ pilus holds to F-, each cell gets a copy of the other, allowing for exponential sharing of this plasmid. These plasmids often contain abs resistance genes.
22
Q
Mutation
A
Change in the nucleotide (DNA) sequence of a gene. Can be repaired, sometimes.
23
Q
Causes of mutation
A
- Spontaneous: unrepaired mistakes by replication enzymes. Cells 1 in 250, Viruses 1 in 250,000 bases replicated. Viruses mutate more rapidly.
- Induced: external forces increase the mutation rate, up to 1000x greater. Chemical or physical agents.
24
Q
Mutagen
A
UV light = physical mutagen. Causes thymine dimers.
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UV mutation repair (2)
Excision repair
| Light repair - photo reactivation.
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HA in influenza
Attachment to host cell. Primary target of vaccines.
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Antigenic drift
Spontaneous mutations during RNA copying lead to minor changes in HAs. Increase in # of cases every 2 years.
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Antigenic shift
Mistake during assembly with new combo of two segments. Very rare. ~10 years. 2009 H1N1 = pig, bird, human strains
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Biotechnology
Use of biological system to make a product, does not require genetically engineered organisms.
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Genetic engineering
Requires the use of biotechnology. Intentional modification of genomes for practical purposes. Change the genotype deliberately to change the phenotype. First example = insulin
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DNA made from combining DNA from one or more sources into novel DNA molecules.
Recombinant DNA
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Applications of biotechnology
- Drugs/hormones
- Vaccines
- Genetic sequencing
- Infection diagnosis
- Industrial microbiology
- Genomics
- Microbiomes
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Innate immunity
Not dependent on antigens. Immediate response upon exposure. No memory. First/second line of defense.
Use physical/chemical/mechanical barriers. Inflammation, fever. No specific target.
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Acquired immunity
Dependent on antigens. Lag between exposure/response. Immunologic memory. Third line of defense
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Normal microbiota
Beneficial bacteria/microorganisms found in/on the body. Promote overall health by providing vitamins to host, help stimulate immune system. Microbial antagonism. Produce conditions that do not promote growth of harmful bacteria.
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Mechanical barriers for immunity
Peristalsis, urination, blinking, coughing, sneezing, vomiting
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Physical barriers for immunity
Skin, mucus
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Chemical barriers for immunity
pH, lysozyme (enzyme that breaks down peptidoglycan), lactoferrin, antimicrobial peptides, complement
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Lysozyme
Enzyme that breaks down peptidoglycan, v effective agains G-pos bacteria. In tears, saliva, milk, mucus
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Lactoferrin
Binds to iron, making it unavailable to microbes. Binds to LPS, leads to lysis.
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Antimicrobial peptides
Small proteins, many are cations, attracted to negative charge of cells. Bind to cells and disrupt cell function.
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Cathelicidins, Defensins
Macrophages, neutrophils
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Dermicidins
Sweat glands
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Complement
Set of >30 serum proteins.
- Membrane attack complex: complement proteins form a ring in the membrane of a target cell, leading to lysis. Only for pathogens with a membrane.
- Opsonization: increases likelihood of phagocytosis. Cell "tagged" for recognition.
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Cellular barriers
Neutrophils
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Neutrophil Extracellular Trap (NETs)
Type of programmed cell death. Neutrophil dies, spills out its DNA to trap cells, pathogens no longer can cause infection. Major component of pus
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Phagocyte pathogen recognition
- PAMPS (Pathogen-associated molecular patterns)
- TLRs (toll-like receptors)
- PRRs (pattern recognition receptors)
- Flagellin, LPS, peptidoglycan, lipoteichoic acid
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Inflammation
Nonspecific response to tissue damage. Dilation, increased permeability of blood vessels, triggered by mast cells, which release histamine. Red, swelling, heat, pain
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Fever
Elevated body temp, increased overall metabolic rate
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Antigens
Generate antibodies. Large, complex molecules
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Exogenous antigen
Product/part of microbe in body
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Endogenous antigen
Antigen from intracellular pathogen presented on surface of host cell. What our cells do when infected with a virus, telling others "come kill me!"
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Epitope
The portion of an antigen structure that interacts with antibodies. Very specific. One molecule can have multiple epitopes.
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Antibodies
Protein with 4 polypeptide chains, 2 heavy, 2 light. Human body can produce 10^23. Our cells interact with the constant region, variable region binds with epitopes.
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Functions of antibodies
1. Neutralization - before infection
2. Opsonization
3. Agglutination - clump together several cells to make phagocytosis more efficient
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Helper T cells
activate other components of immunity
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Cytotoxic T cells
Kill infected host cells
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B cells
Strongest immune response is with B and T cells.
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Plasma B cells
Produce large amounts of antibodies, only for a few days
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Memory B cells
Point of vaccination! Can live as long as you do, immunologic memory.
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Passive immunity
Receiving antibodies, no memory
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Natural passive immunity
Immunoglobulins from placenta
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Artificial passive immunity
Tetanus shot if infected with tetanus. Antivenin.
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Natural active immunity
Have the disease, then you make the antibodies
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Artificial active immunity
Vaccines
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Vaccination
Intentional introduction of antigens to elicit an immune response. Development of memory cells.
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Variolation
First form of vaccination. Scab infection -> mild case
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4 types of vaccines
1. Attenuated
2. Inactivated
3. Toxoid
4. Subunit
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Attenuated vaccine
Viable, but weakened pathogen. Can't cause disease but can cause infection. Strong immune response, but must be refrigerated, remote possibility of disease causation.
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Inactivated vaccine
Organism is dead. More stable and safer than attenuated, but immune response not as strong, requires boosters.
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Toxoid vaccine
Produce antibodies to toxins. No exposure to pathogen, only to toxin, but does require boosters.
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Subunit/conjugate vaccine
Purified antigens that elicit an immune response. Never exposed to pathogen, only its antigens (HPV), so can be given to people with weakened immune systems. Very expensive, immune response is less strong, can require multiple doses
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When enough members of a population are immunized to protect those who lack immunity
Herd immunity
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Immune disorders
1. Hypersensitivities: allergies
2. Autoimmune diseases: lupus, MS, rheumatoid arth
3. Immunodeficiencies: AIDS, SCID
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Disease
Altered or impaired body function
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Infection
When an organism evades the body's external defenses, multiplies, becomes established in the body
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Signs
Objective manifestations that can be observed by others
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Syptoms
Subjective characteristics of disease felt by the pt
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Infectious disease
Illness due to a microbial pathogen
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Communicable disease
Infectious disease that is transmitted from person to person
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Contagious disease
Highly communicable disease
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Non-communicable disease
Infectious disease that is not typically transmitted person to person. (diabetes, heart disease)
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Zoonotic disease
Infectious disease acquired from an animal.
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Pathogen
Organism that causes infectious disease
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Primary (true) pathogen
Organism that causes disease in an otherwise healthy individual
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Opportunistic pathogen
Organism that causes disease in an immunocompromised host. Often resident microbiota
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Iatrogenic disease
Infection duet o a medical procedure/action fo a health care provider
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Nosocomial
Infection acquired in a hospital setting
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HAI
Healthcare associated infection
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Periods of disease
1. Incubation (exposed, no signs/symptoms)
2. Prodromal (effects slightly noticeable)
3. Illness period
4. Decline period
5. Convalescence period
*Contagious times are pathogen specific!
91
Koch's postulates
Robert Koch 1850s. (Germ theory of disease)
1. Organism must be found in all sick individuals and not in healthy indivs
2. Microbe must be isolated and grown
3. Microbe should cause disease when inoculate into healthy indivs
4. Microbe must be re-isolated from newly diseased host, re-identified
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Pathogenicity
Ability of an organism to cause disease
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Virulence
Degree to which an organism can cause disease
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Infectious Dose (ID50)
of organisms necessary to cause disease
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Stages of pathogenesis
1. Exposure (portal of entry)
2. Attachment to host
3. Invasion of host/Evasion of host defenses
4. Infection of host
5. Transmission (portal of exit)
96
Virulence factors of pathogens
Adhesion via fimbriae (gonorrhea, shigella, E coli), pili, suckers, hooks (giardiasis, taeniasis), barbs, spikes (influenza)
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Virulence factors of invasion
Mucinase, collagenase, keratinase, staphylokinase
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Mucinase
Exoenzyme that digests mucus. Invasion.
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Collagenase
Exoenzyme that breaks down connective tissue. Invasion
100
Keratinase
Exoenzyme that breaks down keratin of skin. Invasion
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Staphylokinase
Exoenzyme that breaks down blood clots. Invasion
102
Virulence factors of evasion
Leukocidins, capsules, coagulase/kinase, DNAse, listeriolysin O, phospholipase
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Capsules
Prevent adherence of phagocytes/opsonization. Evasion
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Coagulase/kinase
Exoenzymes that form blood clots around cells to hid from phagocytes. S. Aureus. Evasion.
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DNAse
Exoenzyme that dissolves NETs. Evasion
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Listeriolysin O, Phospholipase
Escape phagosome before digestion. Evasion
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Virulence factors of toxins
Molecules that harm tissues or trigger host immune responses.
108
Endotoxin
LPS of a G-neg bacteria. Causes an intense and overwhelming immune response, leading to endotoxic shock.
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Exotoxins (4 types)
Secreted by G-neg, G-pos, fungi.
1. Neurotoxins
2. Cytotoxins
3. Enterotoxins
4. Mycotoxins
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Neurotoxins
- Botulism toxin: excitatory signal blocked, flaccid paralysis.
- Tetanus toxin: inhibitory signal blocked, spasmodic paralysis.
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Cytotoxins
- Alpha toxin: phospholipase
- Diptheria toxin: blocks protein synthesis, leading to cell death
- Hemolysins: lysis of RBCs to release iron/other nutrients.
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Enterotoxins - infections
- Cholera toxin: disrupts osmolarity, leads to severe diarrhea
- Shiga toxin: kills epithelial cells of intestines, leading to dystenary
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Enterotoxins - intoxication
Staphylococcal enterotoxin: heat stable, common cause of food poisoning. Vomiting. S aureus.
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Mycotoxins
- Aflatoxin: highly mutagenic and carcinogenic. Acute hepatic necrosis.
- Ergot alkaloids: hallucinatory. Burning, itching skin. Claviceps purpurea.
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Antimicrobial resistance
Decreased susceptibility of an organism to a drug. Acquired through new mutations of chromosomal genes, or through acquisition of plasmids/other DNA that harbors resistance genes.
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Problem of resistance
CDC estimates in 2013 2 million illnesses, 2-3 deaths due to antimicrobial resistance.
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Mechanisms of antimicrobial resistance
- Production of enzymes that destroy drugs
- Alteration of drug target
- After metabolic pathway: resistance to sulfa drugs
- Pump antimicrobial drug out of the cell. Active transport.
- Formation of biofilm that drugs cannot penetrate
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Multiple resistance
Pathogen carries multiple genes that confer resistance to multiple drugs. Super-bugs
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Cross resistance
Single mechanism that provides resistance to multiple drugs. Efflux pumps
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Efficacy
Effectiveness of an antimicrobial against its intended target organism.
- Disk diffusion assay
- MIC serial dilution (rapid, expensive, machine. Tells concentrations)
- E tests
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Antibiogram
Table that outlines susceptibility of tested isolates. Used in clinical setting to aid in decision on what drugs to prescribe.
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Preventing resistance
Use antimicrobials only when necessary. Use drugs for entire time prescribed. Reduce use in agricultural settings. Combination therapy. Development of new vaccines/new antimicrobials.
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Options for new antimicrobials
- Alter existing drugs
- Find drugs that inactivate the resistance mechanism
- Research new targets in pathogens
- Antimicrobial peptides
- Use of bacteriophage
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Bacteriophage therapy
- Specific to bacteria, will not infect humans
- Multiple strains for a given bacterium already isolated
- Mutate on their own, resistance circumvented
- Oral application, eye treatment, wound dressings
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John Snow
1854 London cholera outbreak. Tracked incidence of disease vs water sources.
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Florence Nightingale
1858. Crimean war. Kept records on morbidity/mortality of soldiers.
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Epidemiology
Study of disease transmission
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Etiology
Study of causes of disease
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Morbidity
Presence of disease
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Mortality
Death due to disease
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Prevalence
Total # of cases of disease in a population in a given time period
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Incidence
Total # of new cases of disease in a population in a given time period
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Patterns of incident (4)
1. Sporadic
2. Endemic
3. Epidemic
4. Pandemic
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Sporadic disease
Very small #s, occurs occasionally and unexpectedly. Prevalence and incidence usually zero. Tetanus, plague, rabies
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Endemic disease
Constant low #s of disease. Prevalence/incidence never zero. Salmonella.
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Epidemic disease
Greater than expected #s in a geographical region. Increased incidence and prevalence. Influenza, salmonella.
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Pandemic disease
Widespread/worldwide epidemic. Yellow fever, cholera, TB
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Spread of epidemics (2)
1. Common source: single, shared source. Foodborne. Shorter.
| 2. Propagated: spread person-person. Harder to stop. Longer duration.
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Reservoirs and carriers
Where pathogens are maintained in nature. Nonliving reservoirs = soil, water. Living reservoirs= humans (carriers), animals.
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Carriers
Humans who unknowingly shelter pathogens and spread them to others.
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Asymptomatic carrier
Person who is infected but has no symptoms
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Passive carrier
Person who is contaminated, but no infection. Often health care worker.
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Contact transmission (4)
Direct/horizontal contact: person to person
Vertical: birth canal
Droplet: respiratory liquids
Indirect: via inanimate object called fomite.
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Vehicle transmission
Pathogen enters body by consumption/intake of it in water, milk, food etc. Sometimes air.
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Biological vectors
Arthropod harbors pathogen within its body. Ticks, mosquitoes, please. Lyme, rickets, plague, malaria
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Mechanical vectors
Pathogen is found on surface of arthropod. Flies, cockroaches. Dysentery, salmonella, cholera.
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endogenous HAI
Infectious agent from microbiota of a pt
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exogenous HAI
Infection introduced in medical setting
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Emerging infectious disease
Diseases new to humans or increasing in prevalence and geographic range. Reemerging diseases reappear after a decline.
150
Louis Pasteur
1863. Noted that heat treatment prevented microbial contamination in wine
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Joseph Lister
1865. Used carbolic acid (phenol) to treat dressings, antiseptics prior to surgery
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-static
Inhibition of growth of target organisms
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Disinfection
A process to destroy vegetative pathogens on inanimate objects. Reduces # of bacteria
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Sanitization
Disinfection to meet public health standards.
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Sterilization
A process that destroys all viable microbes, including endospores
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Antisepsis
Destroy vegetative pathogens on living tissue. Reduces # of bacteria
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Degerming
Mechanical removal of microbes from skin. (Hand washing)
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Physical methods of control (4)
Temperature
Radiation
Filtration
Desiccation
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Temperature (5)
1. Incineration: dry heat. Long time, high heat
2. Autoclave: wet heat. More efficient
3. Pasteurization: kills vegetative pathogens, reduces spoilage organisms. Milder than autoclaving.
4. Refrigeration: slows growth except in psychrophilic microbes
5. Freezing: decreases microbial metabolism, limits amount of available water
160
Radiation (2)
Nonionizing: UV light, does not kill endospores. Disinfection.
Ionizing: gamma rays and x rays, break covalent bonds in DNA. Good penetrating power, useful for packaged, heat sensitive items. Sterilization.
161
Filtration
Physical barrier to trap microbes. Used for heat-sensitive materials and high volumes. Can be used to sterilize if pores are small enough
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Desiccation
Lowers water activity
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Disinfect...
...inanimate objects
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Antiseptics used on...
...animate objects
165
Phenolics
Based on phenol. Hand soap, cleaners
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Alcohols
70% most effective. Antiseptic and disinfectant.
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Halogens
React w/non-target molecules, inactivated by sunlight. Iodine/betadine, chlorine/bleach, fluoride
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Heavy Metals
Metal ions bind of proteins and other molecules, disrupting function. Topical!
169
Quats
Quaternary ammonium compounds. Antiseptics and disinfectants, easily inactivated by soaps
170
Bisbiguanides
Surgical prep, hand washing. Chlorhexidine, alexidine, hibiclens
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Soaps/detergents
Disrupt binding of bacteria to surfaces. Degerming. Handwashing.
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Paul Ehrlich and Sahachiro Hata
1909. "Magic bullet" chemical to target microorganisms but not us
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Alexander Flemming
1928. Penicillin.
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Antibiotic
Naturally occurring antibacterial
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Spectrum of activity
Types of #s of organisms that a drug is active on
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Superinfection
Consequence of broad-spectrum drugs. Secondary infection of opportunistic pathogen due to disruption of normal microbiota. C. Dificile.
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Selective toxicity
Drug is more toxic to target organisms than humans (host) due to differences in cellular physiology and metabolism. The greater the cellular difference the better the selective toxicity. # antibacterials > #antifungals > # antivirals
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Therapeutic index
Ratio of the amount of drug that is toxic to humans to the amount that is toxic to target cell.
TI= Amt of drug toxic to human/amt toxic to target
Want large number over small number
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Drug toxicity
Property of drugs that causes damage to human cells and tissues. Usually to kidneys, liver, nerves.
180
Mode of action (6)
How an antimicrobial works against a target organism.
1. Cell wall synthesis
2. Protein synthesis
3. Cell membrane structure
4. Metabolic pathways
5. Nucleic acid synthesis
6. Host attachment/entry/exit
181
Cell wall - antibacterials (5)
```
Beta-lactams: penicillin, ampicillin
Glycopeptides: Vancomycin
Antibacterial peptide: Bacitracin
Carbapenems: Imipenem
Echinocandins
```
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Protein synthesis - antibacterials (4)
Chloramphenicol
Aminoglycosides: streptomycin, neomycin
Tetracyclines: doxy
Macrolides: azithromycin, erythromycin
183
Cytoplasmic membrane disruption - antibacterials (1)
Polymixin B, Polymixin E
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Inhibition of metabolic pathways - antibacterials (3)
Folic acid:
- sulfonamides: sulfamethoxazole
- trimethoprim
Mycolic acid:
- isoniazid
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Inhibition of nucleic acid synthesis
Fluoroquionolones: cipro, levofloxacin
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Antifungal mode of action
Disruption of cytoplasmic membranes.
- Azoles: fluconazole target ergosterol synthesis
- Polyenes: amphotericin B target ergosterol binding. Only used in severe cases.
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Block attachment/entry/exit - Antivirals
Tamiflu, zanamivir, oseltamavir
188
Inhibition of nucleic acid synthesis - Antivirals
Acyclovir, ribavirin
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Anti retroviral therapy
- Protease inhibitors: Ritonavir
- Reverse transcriptase inhibitors: Etravirine, tenofovir
- Integrase inhibitors - Raltegravir. Blocks insertion of viral DNA into chromosome
