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70 Cards in this Set
- Front
- Back
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active immunity
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- body is exposed to antigens and actively mounts for a specific immune response
- e.g. by an infection |
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passive immunity
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transfer of another's antibodies (or immune cells) specific to an antigen into a nonimmune person
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passive immunity
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- can neutralize antigen
- the body does not mount immune response = no memory |
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natural active immunity
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- get infected and sick
- initiates a specific immune response |
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natural passive immunity
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a nonimmune persons acquisition of performed immune cells or antibodies from someone who is immune
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natural passive immunity
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e.g. transfer of antibodies from mother to infant (transplacental; IgA antibodies from breast milk, especially colostrum)
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artificial active immunity
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vaccines ➡antigens that can induce a specific immune response without illness are introduced into the body
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vaccination or immunization
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the purposeful induction of immunity to a particular infectious disease
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Attenuated
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alive but unable to cause disease
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vaccines
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- killed or attenuated microbes
- cell parts or inactivated toxins - e.g. DPT (D, T-inactivated toxins), influenza (inactivated virus) |
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artificial passive immunity
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- injection of antibodies into the body
- source: a person or animal already immune to the disease - e.g. snake or spider bite, post-exposure rabies |
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vaccinations
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- repetition are usually required to boost antibody titers and replenish memory cells
- very important to control disease in a population |
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vaccinations
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many viral pathogens cannot effectively be treated once contracted, so this can be the best or only way to combat
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herd immunity
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if a high proportion of individuals in a group are immune to a pathogen, then most of the population will be protected
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attenuated whole-agent
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- microbes have lost virulence due to mutations within virulence or metabolic genes
- may occur naturally - may occur after long-term lab culturing of organism = accumulation of mutations |
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attentuated whole-agent
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- most effective type, especially against viral disease
- polio, measles, mumps and rubella, intransal influenza - since alive, should not use in immunocompromised |
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inactivated whole-agent
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- microbes killed by heat, chemical
- not always as effective/robust immune response as live vaccines - rabies, influenza, pneumococcal pneumonia, pertussis, typhoid, cholera, etc. |
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toxoids
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- exotoxins inactivated chemically but still immunogenic
- usually need series of injections for full immunity - e.g. diphtheria and tetanus vaccines |
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subunit
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- use of specific antigen(s) that is highly immunogenic
- e.g. OM proteins, fimbriae, flagella, capsule - e.g. hepatitis B viral coat protein produced by genetically-modified yeast |
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subunit
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- relatively new type of constructed using molecular biology techniques = recombinant DNA technology
- can be encoded on DNA or synthetic peptide |
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conjugated
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- combination of subunit and toxoid vaccine
- some Ags are poor immunogens - when combined with immunogenic proteins they can be very effective vaccines - e.g. Haemophillus influenzae capsule combined with diphtheria toxoid |
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nucleic acid
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- DNA encoding for an antigen that elicits a strong immune response is cloned and isolated
- injected or coated on tiny gold beads introduced into the body with a "gene gun" - DNA enters host cell and is translated but not replicated |
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absolutely not !
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do vaccines cause autism?
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chemotherapy
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treatment of disease by using chemical substances
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antimicrobial drug
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any drug that kills or interferes with the growth of microorganisms
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synthetic drugs and antibiotics
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what are the two types of chemotherapy
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synthetic drugs
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prepared from chemicals in the laboratory
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antibiotics
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- products produced naturally by living organisms (bacteria and fungi) that act against other organisms
- usually in small amounts - can be modified in lab |
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Alexander Fleming
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who discovered antibiotics by accident?
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contaminated plate (penicillin)
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how did Fleming discover antibiotics
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narrow-spectrum
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- drug has a limited range of microbial types it affects
- e.g. Penicillin G: Gram + and a few Gram - |
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broad spectrum
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- affect a broad range of microbes
- Gram + and Gram - bacteria |
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minimal inhibitory concentration (MIC)
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lowest antibiotic concentration that prevents visible bacteria growth
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additive
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activity of two drugs same as separate added activities
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synergistic
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activity of two drugs is greater together than alone
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antagonistic
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less than effective together than separately
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bactericidal
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kill bacteria directly
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bacteriostatic
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prevent growth of bacteria
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harm the microbe and not the host
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what is the goal of the modes of action of antimicrobial drugs?
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main modes of action of antimicrobial drugs
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1. inhibit cell wall synthesis
2. inhibit protein synthesis 3. injure cell membrane 4. inhibit nucleic acid synthesis 5. inhibit synthesis of essential metabolites |
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inhibit cell wall synthesis
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- mode of action of antimicrobial drugs
- e.g. penicillin and vancomycin - prevents synthesis of intact peptidoglycan = weaken wall - specific: humans don't have cell walls/peptidoglycan - target synthesis = drug only works on actively growing cells |
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natural penicillin
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- penicillin G and V from cultures of Penicillium
- narrow but useful for Staph, Streptococci, spirochetes - susceptible to penicillinases ( bact enzymes that cleave it) |
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semisynthetic penicillin
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modify natural so penicillinase-resistant, extended-spectrum, etc.
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polypeptides
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- bacitracin (tropical OTCs) and vancomycin (last line of defense; some enterococci et. al. now resistant)
- carbapenems (super broad) - monobactams (only E. coli and pseudomonads) |
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inhibit protein synthesis
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- specificity; structural difference b/w ribosomes of prokaryotes and eukaryotes
- different drugs target different aspects of synthesis - e.g. 50s: erythromycin (macrolides), chloramphenicol - e.g. 30s: tetracyclines, streptomycin (aminoglycosides) etc. |
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chloraphenical
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- cheap to synthesize chemically
- broad - inhibits ribosome formation of peptide bonds |
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aminoglycosides
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- e.g. streptomycin, gentamicin, neomycin-tropical OTCs, Gram -, but easily develop resistance
- can affect hearing and kidneys - charges 30s subunit shape; misread MRNA |
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tetracyclines
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- Gram + and -
- good at penetrating into body cells and tissues - interfere with attachment of tRNA to ribosome |
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chloramphenicol
aminoglycoside tetracyclines |
what are the three main inhibitors of protein synthesis?
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glycylcyclines, macrolides, etc.
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what are other examples of inhibitors of protein synthesis?
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injure cell membrane
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-polypeptides like polymyxin B, lipopeptides like daptomycin
- antifungals - after membrane permeability - not always specific - to avoid targeting host, usually target synthesis of membrane lipids |
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inhibit nucleic acid synthesis
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- interfere with DNA replication or RNA synthesis
- e.g. quinolones inhibit DNA gyrase - actinomycin inhibits RNA elongation |
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inhibit nucleic acid synthesis
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- rifamycin inhibit mRNA synthesis (mostly mycobacteria)
- good at penetrating tissues - sometimes limited usefulness b/c can also interfere with host/eukaryotic DNA and RNA synthesis |
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inhibit synthesis of essential metabolites
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- often competitive inhibition of a particular enzyme's activity
- e.g. sulfa drugs like sulfonilamide competes with para-aminobenzoic acid (PABA) for enzymes binding site - synergism with trimethoprim and sulfanethoxazole |
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nucleoside/nucleotide analogs
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- target viral genome synthesis
- look like RNA/DNA building blocks, but do not make functional viral genome = virus is dead in the water - e.g. acyclovir for herpes virus - renofovir and ziaoyudine for HIV |
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inhibit enzymes specific to virus
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reverse transcriptase and integrate to retoviruses like HIV
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inhibit attachment and uncoating
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e.g. inhibit neuraminidase, uncoating of jnfluenzavirus
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protease inhibitors
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often host cell needs to chop up large proteins with a protease enzyme in order to make new virus particles
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interferon
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- immune cytokine that inhibits cell-to-cellspread of virus
- e.g. viral hepatitis |
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combos
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- e.g. HIV mutates so quickly that "cocktails" of reversal drugs are used to reduce chances of resistant mutants
- e.g. analogs and protease inhibitors |
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antifungals
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target cell membrane sterols, cell walls, nucleic acids
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antiprotozoan
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- (chlora)quinine (malaria)
- often host side effects, but metromidazole interfere with anaerobic metabolism of protozoa and obligate anaerobe bacteria |
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antihelminthic
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- nidosamide for tapeworm
- mebendazole and abendazole (broad spectrum, good for jntestinal; interfere with nutrient absorption) |
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block entry
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- mechanisms of antibiotic resistance
- gram - cell wall - modify porins so can't get in |
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enzymes that destroy or inactivate the drug
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- usually against natural antibiotics
- B-lactamase of MRSA et al. - a mechanism of antibiotic resistance |
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alter drug target site
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- small nutrition can slightly alter ribosome structure so drugs can't recognize/bind
- same with MRSA and penicillin binding protein on cell membrane |
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rapid efflux (pumping out) of antibiotic
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- can have multiple pumps designed to eject numerous toxic things
- mechanism of antibiotic resistance |
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other variations on resistance
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- mechanism of antibiotic resistance
- increase gene expression and make a lot of enzymes targeted (not enough drug to shut down all) - make smaller amounts of sterol in membrane that drug targets |
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antibiotic resistance
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- overuse of antibiotics has led to strain of bacteria
- e.g. M. tuberculosis - e.g. methicillin-resistant staphylococcus aureus |
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antibiotics in animal feed
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major source of antibiotic resistance in bacteria
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