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Ch 10 Antimicrobial Agents

Terms in this set (111)

Do you understand why there are more antibacterial drugs compared to antiviral? (include why so few antifungal, antiprotozoan, and antihelmintic drugs are available)
-because there are so many differences between the structure and metabolism of pathogenic bacteria and their eukaryotic hosts, antibacterial drugs constitute the greatest number and diversity of antimicrobial agent
-Fewer antifungal, antiprotozoan, and anthelminitic drugs are available because fungus, protozoa, and helminthis are eukaryotic and thus share many common features (but there are differences that drugs can target)
-The number of antiviral drugs is also limited, despite the major differences in structure, because viruses utilize their host cells' enzymes and ribosomes to metabolize and replicate. Therefore, drugs that are effective against viral replication are likely toxic to the host as well
Can you list the six (6) categories/mechanism of antimicrobials? (major ways to fight microbial infections)
-Drugs that inhibit cell wall synthesis. These drugs are selectively toxic to certain fungal and bacterial cells, which have cell walls, but not to animals, which lack cell walls
-Drugs that inhibit protein synthesis (translation) by targeting the differences between prokaryotic and eukaryotic ribosomes
-Drugs that disrupt unique components of the cytoplasmic membrane (different between humans and prokaryotes)
-Drugs that inhibit general metabolic pathways not used by humans
-Drugs that inhibit nucleic acid synthesis (DNA or RNA synthesis)
-Drugs that block a pathogen's recognition of or attachment to its host
Penicillin (who discovered it, who produces it, what it does, one of the first_)
-Discovered by Alexander Flemming
-Secreted by a mold Penicillium
-Inhibits the growth of bacteria
-One of the first microbiotics discovered
what was the first practical antimicrobial agent in efficacious in treating a wide array of bacterial infections?
Sulfanilamide
What category/mechanism does penicillin use?
Cell Wall Inhibitor
what is the major structural component of a bacterial cell wall?
peptidoglycan
Describe how cell walls are composed and made in bacteria
-a bacterial cell wall is composed of a macromolecule of peptidoglycan composed of NAG-NAM chains (layers) that are cross-linked (bonded) by peptide bridges between the NAM subunits
-New NAG and NAM subunits are inserted into the wall by enzymes, allowing the cell to grow. Normally, other enzymes link new NAM subunits to old NAM subunits with peptide cross-links
what antimicrobial agents inhibit cell wall synthesis? (6)
-Penicillin
-Isoniazid
-Vancomycin
-Bacitricin
-Cephalosporin
-Methicillin
Can you briefly describe how penicillin acts? (include the end result of bacteria)
*Penicillin effect on peptidoglycan in preventing NAM-NAM cross links
-Penicillin interferes with the linking enzymes, and NAM subunits remain unattached to their neighbors. However, the cell continues to grow as it adds more NAG and NAM subunits
-The cell bursts from osmotic pressure (movement of water into the cell) because the integrity of peptidoglycan is not maintained
What is meant by beta-lactam?
-Antimicrobial whose functional proportion is composed of beta-lactam rings, which inhibit peptidloglycan formation by irreversibly binding to the enzymes that cross-link NAM subunits
-lactam ring irreversibly bind to the enzymes that cross-link NAM subunits (peptidoglycan layers)
-Block linkages that actually bond one layer of peptidoglycan to the next
Can you List 4 benefits of a semi-synthetic derivative of penicillin over the original? (4)
-More stable in acidic environments (aka stomach)
-More readily absorbed in intestinal tract by the body
-Less susceptible to deactivation by bacterial enzymes
-More active against more types of bacteria (spectrum of action)
Simplest beta-lactams effective only against_
effective only against aerobic Gram-negative
Vancomycin (mechanism, what it does in which type of bacteria, end result)
-Inhibitor of cell wall synthesis
-interferes with alanine-alanine bridges that link NAM subunits in many Gram-positives
-Result in cell lysis due to effects of osmotic pressure
-Block linked bonds between peptidoglycan layers
Bacitracin (mechanism, what it does, end result)
-Inhibitor of cell wall synthesis
-blocks secretion (release from a cell) of NAG and NAM (peptidoglycan) from cytoplasm
-Result in cell lysis due to effects of osmotic pressure
Isoniazid (what it does, and what disease it treats caused by what pathogen? Include the diseases that the pathogen causes)
-Inhibition of cell wall synthesis
-disrupts formation of mycolic acid in mycobacterial species (mycobacterium causes tuberculosis and leprosy)
Can you summarize the action of cell wall inhibiting drugs? (prevent bacteria from_, effect on what?, type of cells that are affected?, no effect on which type of cells and reason)
-Prevent bacteria from increasing amount of peptidoglycan
-Have no effect on existing peptidoglycan layer (only new cell walls)
-Effective only for growing cells (dividing cells)
-No effect on plant or animal cells; no peptidoglycan
Which pathogen has becta-lactamase? (include the meaning of becta-lactamase)
-Staphyloccocus aureus
-Enzyme that destroys beta-lactam
-bacterial enzyme that breaks the beta-lactam rings of penicillin and similar molecules, rendering them inactive
what is a solution to the becta-lactamase?
use semisyntethic derivatives of penicillin that are less susceptible to deactivation by Beta-lactamase
what are the semi-syntethic derivative of penicillin?
-Methicillin
-Cephalosporin
-Monobactram
Why can we target protein synthesis of bacterial cells since our cells also make proteins? (include the name of the process that synthesis proteins)
-Drugs can selectively target translation
-Prokaryotic ribosomes differ from eukaryotic ribosomes in structure and size
-Many antimicrobial agents take advantage of the differences between ribosomes to selectively target bacterial protein translation without significantly affecting eukaryotes
How are prokaryotic ribosomes different from eukaryotic ribosomes?
Prokaryotic ribosomes are 70S (30S and 50S)
Eukaryotic ribosomes are 80S (40S and 60S)
Be able to give 2-3 examples of antimicrobials that are in this category: inhibition of protein synthesis (include what each affect)
Inhibit functions of the 30S ribosomal subunit:
aminoglycosides (streptomycin; gentamicin)
tetracyclines
Inhibit functions of the 50S ribosomal subunit:
chloramphenicol
Macrolides (erythromycin, azithromycin)
List the mechanism by which antimicrobials inhibit protein synthesis by targeitng prokaryotic ribosomes (6)
1. Aminoglycosides change the shape of the 30s subunit, causing incorrect pairing of tRNA anticodos with mRNA codons (unable read codons of mRNA correctly)
2.Tetracyclines block the tRNA docking site (A site) on the 30s subunit, preventing protein elongation (prevent additional amino acids into growing polypeptide)
3. Chloramphenicol blocks enzymatic activity of the 50s subunit, preventing the formation of peptide bonds between amino acids
4. Macrolides (erythromicin) bind to the 50s subunit, preventing movement of the ribosomes along the mRNA
What are the antimicrobials that disrupt the cytoplasmic integrity? (cell membrane)
Amphotericin B
Polymyxin
Briefly explain how amphotericin B functions as an anti-fungal drug (including effects on humans and the final outcome ) Include function of cytoplasmic membrane
-attaches to ergosterol found in fungal membranes
-In the process of attachment, it disrupts the membrane and causes lysis of the cell
-Amph-B has a structure that attaches to the ergesterol, and in doing so forms a large pore in the cell membrane
-The function of the cell membrane as a permeable barrier (regulate what gets in and what gets out) is disrupted because of the pore formed by amph-B. Thus cell will not function well
-Humans somewhat susceptible because cholesterol similar to ergosterol
-Disrupt fungal membranes primarily rather to our own because cholesterol does not bind amphotericin B as well as does ergesterol (selective toxicity)
Why is ampho B not used against bacteria?
Bacteria lack sterols in their cell membrane; not susceptible
What is mode of action of polymyxin? (effective to treat which pathogen?)
-Antibacterial agent
-disrupts outer membranes of Gram-negatives; -toxic to human kidneys (so use in skin creams or on external diseases)
-Binds to Lipid A (LPS, endotoxin), and disrupts outer membrane
-Effective against Pseudomonas external infections
Amphotericin B
-polyene
-Disrupts the cytoplasmic membrane of a targeted cell
-antifungal drug
-It attaches to ergesterol in the process disrupting the membrane and causing lysis of cell
-treats systemic fungal infections
Ergesterol
-lipid constituent of fungal membranes
-the antifungal group of drugs called polyenes, including amphoterecin B, attach to it to disrupt the membrane and cause lyse of the cell
Fungicide
-Includes amphoterecing B and plymyxin
-drug that kills fungi
What is mode of action of sulfonamides? (include the normal mechanism of the organisms using whatever sulfonamide affect) and the name given (starts with M and A)
--Metabolic antagonist
--Structurally similar to PABA (para-aminobenzoic acid) which is necessary for nucleic acid synthesis.
-Inhibits folic acid synthesis in bacterial cells by binding to the active site of the enzyme, instead of PABA, and blockig the enzyme's action of manufacturing of dihydrofolic acid
-Sulfonamide acts as a competitive inhibitor
-Structual analogs of (chemically very similar) para-aminobenzoic acid (PABA), which (PABA) is crucial in the synthesis of nucleotides required for DNA and RNA synthesis
-Many organisms (including pathogens) enzymatically convert PABA into dihydrofolic acid, and then dihydrofolic acid into tetrahydrofolic acid (THF), a form of folic acid that is used as a coenzyme in the synthesis of purine and pyrimide nucleotides
-As analogs of PABA, sulfonamides compete with PABA molecules for the active site of the enzyme involved in the production of dyhydrofolic acid. This competition leads to a decrease in the production of THF, and this of DNA and RNA
-The end result of sulfonamide competition with PABA is the cessation of cell metabolism, which leads to cell death
How are PABA, Folic Acid, sulfonamides, and nucleotides involved in this process?
-PABA is crucial in synthesis of nucleotides required for DNA and RNA synthesis by being converted to dyhydrofolic acid->tetrahydrofolic acid (THF), which is a form of folic acid that is used as a coenzyme in the synthesis of purine and pyrimide nucleotides of RNA and DNA
-Sulfonamides (as analog of PABA) compete with PABA molecules for the active site of the enzyme involved in the production of dihydrofolic acid-> competition lead to decrease in production of THF->decrease in production of DNA and RNA->decrease and cessation of metabolism->cell death
-Important only for bacteria because obtain folic acid from alimentation
Why are humans not negatively affected by sulfonamides even if we too require folic acid to make nucleotides?
-Humans do not synthesize THF from PABA; instead, humans take folic acids found in their diets and convert them into THF
-as a result, human metabolism unaffected by sulfonamides
examples of 3 that work in inhibition of metabolic pathway (antimetabolic agents)?
-sulfanilamide
-Heavy metals
-Antiviral agents
write the Bacterial Enzymatic Pathway of DNA and RNA (including PABA)
PABA--(enzymes)-->Dyhydrofolic acid--(enzyme)-->tetrahydrofolic acid (THF)-->purine and pyramide-->DNA and RNA
sulfanomides
Antimetabolic drugs that is a structural analog of para-aminobenzoic acid (PABA)
what are the mechanisms of action of microbial drugs within inhibition of nucleic acid synthesis? (2 examples)
-Nucleotide analogs
Quinolones
Rifampin
Explain the basis of inhibition of nucleic acid synthesis
Several drugs function by blocking DNA replication or mRNA transcription
What does rifampin target? (prefers what type of whatever it affects? and especifically give an example of an organism that is affected by it)
-inhibit action of RNA polymerase during transcription (RNA->DNA)
-Prefers prokaryotic RNA polymerase.
-Affects bacterial transcription
-Used primarily against M. tuberculosis (metabolize slowly thus are less susceptible to antimicrobials targeting active metabolic processes)
DNA gyrase (who affects it and what it does?)
-affected by Quinolones
-DNA replication enzyme
-an prokaryotic enzyme necessary for correct coiling and uncoiling of replicating bacterial DNA
How nucleotide analogs interfere with DNA replication and RNA transcription?
Because of the distortions they cause in nucleic acids, nucleotide analogs do not form proper base pairs with normal nucleotides. This increases the number of mismatches in the transcription of RNA and replication of DNA
"ribosomes lose their function" is associated with which action of microbial drugs?
inhibition of protein synthesis
"the sterols in the cell membrane become nonfunctional" with which action of microbial drugs?
disruption of cytoplasmic membrane
PABA is
a. a substrate used in the production of penicillin
b. a type of B-lactamase
c. molecularly similar to cephalosporins
d. a substrate used to synthesize folic acid
D
What is one important negative consequence of using an antibacterial drug that has a broad spectrum of action?
-Broad-spectrum antimicrobials may allow for secondary or superinfections to develop
-Killing of normal flora reduces microbial antagonism (competition between the normal microbes and pathogens for nutrients and space->reinforces body's defense by limiting the ability of pathogens to colonize the skin and mucous membranes)
Is polymyxin a broad or narrow spectrum drug in contrast with other antimicrobials? include what group affects and how?
-Narrow spectrum drug
-Gram-negative bacteria
-Binds to lipid A (which is only found in the outer membrane of gram negative bacteria)
Is isoniazid a broad or narrow spectrum drug in contrast with other antimicrobials? include what group affects and how?
-narrow
-mycobacterium (tuberculosis and leprae)
-by targeting mycolic acid synthesis
Is penicillium a broad or narrow spectrum drug in contrast with other antimicrobials? include what group affects and how? why is better with this group?
-depends to which antimicrobial you are comparing
-gram positive (better for this group because has a thick layer of peptidoglycan)
-cell wall inhibiting
3 examples of broad spectrum antimicrobials within prokaryotic diseases?
-Erythromycin
-Tetracycline
-Sulfonamides
What is drug efficacy?
-Effectiveness of the drug to kill the bacteria
-Dose necessary to actually achieve what we want: kill the bacteria
List explain four tests used to determine drug efficacy?
1. broth diffusion test
2. Etest
3. Diffusion susceptibility tests (Kirby-Bauer test)
4.Minimum Bactericidal Concentration (MBC) Test
test that determine the minimum inhibitory concentration
-broth dilution test
-Etest
Broth dilution test (also called?, steps how to do it and results/ what question it answers?)
-Minimum inhibitory concentration tests (MIC)
-Wide range of concentrations of a single antibiotic within different broth tubes
1. It goes from the low concentration of antibiotic in a broth to a highest concentration tube
2. These tubes have a single bacteria at the same concentration
3. After being incubated, the tube with the least concentration that did not presented cloudiness or turbidity would be the Minimum inhibitory concentration
-Lack of turbidity indicates no growth.
-what is the lowest dose necessary to inhibit the growth of the microbe?
minimum inhibitory concentration (MIC)
The smallest amount of drug that will inhibit a pathogen
broth dilution test (official definition)
-Test for determining the minimum inhibitory concentration in which a standardized amount of bacteria is added to serial dilutions of antimicrobial agents in tubes or wells containing broth
Interpret results of broth dilution test
-After incubation
-Turbidity (cloudiness) indicates bacterial growth; lack of turbidity indicates that the bacteria were either inhibited or killed by the antimicrobial agent
Etest (what aspects combines, definition, steps, how get result)
-combines aspects of MIC test and a diffusion susceptibility test
-test for determining minimum inhibitory concentration; a plastic strip containing a gradient of the antimicrobial agent being tested is placed on a plate inoculated with the pathogen of interest
1. after incubation, an elliptical zone of inhibition indicates antimicrobial activity, and the minimum inhibitory concentration can be noted where the zone of inhibition intersects a scale printed on the strip
To get the results of Etest, which greately depends on_, look for_. Answers the question:_
-Plastic strip with concentration gradient.
-Look for intersection of ellipse.
-what is the lowest dose necessary to inhibit the growth of the microbe?
Diffusion susceptibility test (other name and definition/ what question answer?/ benefit/ what discovers(what determine about the results))
-Kirby-Bauer test
-Simple, inexpensive test widely used to reveal which drug is most effective against a particular pathogen. Procedure involves inoculating a petri plate uniformly with a standardized amount of the pathogen in question and arranging on the plate disks soaked in the drugs to be tested
-How the bacteria grow in the presence of antibiotics?
-test variety of antibiotics at the same time
-See how bacteria grow in presence of antibiotics and determine if bacteria is susceptible, resistant, or intermediate to a drug
steps of diffusion susceptibility test
1. uniformly inoculating petri plate with a standardized amount of pathogen in question
2. Then small disks of paper (antibiotic disks) containing standard concentrations of the drugs to be tested are firmly arranged on the surface of the plate
3. Plate is incubated
4. the bacteria grow and reproduce to form a lawn everywhere but the areas where effective antimicrobial drugs diffuse throughout the agar
5. After incubation, the plates are examined for the presence of zone of inhibition
*zone of inhibition measured as the diameter of the clear region (mm)
zone of inhibition
In a diffuse susceptible test, a clear area surrounding the drug-soaked disk where the microbe does not grow
diagnose results of diffusion susceptibility test
-If all drugs were equal, then the larger zone of inhibition, the more effective that drug is
-However, the size of the zone depends on the rate of diffusion of antimicrobial (low molecular weights generally move quickly than those with higher molecular weights)
-The size of inhibition must be compared to a standard table for that particular drug before accurate comparisons can be made
-large zone of inhibition=sensitivity
classification of pathogens by diffusion susceptibility test?
-susceptible
-intermediate
-resistant
to each drug
Minimum bactericidal concentration (MBC) test (definition and what it determines/ what question answers?)
-An extension of the MIC test in which samples taken from clear MIC tubes are transferred to plates containing a drug-free growth medium and monitored for bacterial replication
-Determines the amount of drug required to kill the microbe rather than just the amount of inhibit it, as MIC does
-what is the minimum concentration that actually kills the bacteria?
steps and diagnosis of results of Minimum bactericidal concentration (MBC) test
-Samples taken from clear MIC tubes (from broth dilution test) (or, alternatively, from zones of inhibition form a series of diffusion susceptibility tests) are transferred to plates containing a drug-free growth medium
-The appearance of bacterial growth in these subcultures after appropriate incubation indicates that at least some bacterial cells survived that concentration of the antimicrobial drug and were able to grow and multiply once placed in a drug-free medium
If bacteria colonies grow, you can conclude there were still living bacteria-> concentration was not enough to kill the bacteria
-Look for tube with lowest concentration that does not yield colonies on free drug medium-> enough concentration of antibiotic to kill the bacteria->would be the minimal bactericidal concentration
Any drug concentration at which growth occurs in subculture is_, not_for the bacterium
-bacteriostatic
-bactericidal
minimum bactericidal concentration (MBC)
The lowest concentration of drug for which no growth occurs in the subcultures
bacterocidial
killing concentration of bacteria
normal microbiota
-Microorganisms that colonize the surfaces of the human body without normally causing disease
-they may be resident or transient
what a drug must do to be able to be effective?
An adequate amount of an antimicrobial agent must reach a site of infection
4 types of routes of administration?
-Tropical or local administration
-orally
-intramuscularly (IM)
-intravenously (IV)
which type(s) of routes of administration are used for external infections?
Tropical or local administration
which type(s) of routes of administration are used for systemic infections?
-orally
-intramuscularly (IM)
-intravenously (IV)
tropical or local administration
-Topical application of drug if infection is external
-For external infections
-can be applied directly
Oral (route of administration) (advantage and disadvantage)
-Pro: simplest (it requires no needles and is self-administered)
-CON: lower drug concentrations achieved in the body (comparing with other routes)
-no reliance on health care provider
-patients do not always follow prescribing information (CON)
Intramuscular (route of administration)
-requires needle for administration
-concentration never as high as IV administration (CON)
-PRO: allow drug to diffuse slowly into the many blood vessels within muscle tissue
Intravenous (route of administration) (pros, cons, and solution to cons)
-requires needle or catheter
-delivers the drug directly into the bloodstream
-achieves high concentration of drug in the blood (pro). Amount of concentration of drug initially is very high (pro)
-drug concentration diminishes as liver and kidneys remove drug from circulation (con)
-Solution: administer drug continuously
how determine which route of administration will be better for an infection? (besides considering the route of administration)
Must know how antimicrobial agent will be distributed to infected tissues
List the three main categories of drug side effects.
toxicity
allergies
disruption of normal microbiota
toxicity (category of drug side effect)
-Though antimicrobial drugs are ideally selectively toxic against microbes and harmless to humans, many infact have toxic side effects
-Exact cause of many adverse reactions poorly understood
-Drugs may be toxic to kidneys, liver, or nerves
-Considerations needed when prescribing drugs to pregnant women (effects on developing fetus)
Allergies (category of drug side effect)
-Some drugs may trigger allergic immune responses in sensitive patients
-Although allergic reactions are rare, they may be life threatening
-Anaphylactic shock: (immediate, violent reaction) may cause deaths
-People with mild allergies frequently lose their sensitivity to the drug over time
Disruption of normal microbiota (category of drug side effect) (result in_,what happens?,great concern about_)
-May result in secondary infections
-Overgrowth of normal flora (Candida; C. difficile) that are not affected by a drug, which cause superinfection
-Of greatest concern for hospitalized patients
what is a side effect of Antiprotozoan drug Flagyl? what type of side effect is this? (include when it results)
-Black, Hairy Tongue (results when the breakdown products of hemoglobin accumulate in the papillae of the tongue)
-toxic side effect
what is the side effect of tetracycline? what type of side effect is this? (include when it results/reason)
-Discoloration, Damage to tooth enamel (drug form complexes with calcium that can be incorporated into bones and developing teeth, causing malformation of skulls and stained, weakened tooth enamel)
-Toxic side effect
who should avoid taking tetracycline?
pregnant women and children should not use tetracycline
What is clinical resistance?
- the MIC (minimum inhibitory concentration) of the drug for a particular strain of bacteria exceeds that which is capable of being achieved with safety in vivo.
-When the concentration of the drug needed to inhibit growth of the bacteria is too high to be safe in humans. So not effective drug anymore
What are the two ways that an organism can acquire drug resistance (How genetically can they acquire resistance)?
-New mutations of chromosomal genes
-Acquisition of R-plasmids via transformation, transduction, and conjugation (horizontal gene transfer)
List the four mechanisms of resistance
-Inactivation of the antimicrobial agent
-Altered permeability of the antimicrobial agent
-Altered target site
-Replacement of a sensitive pathway
Inactivation of the antimicrobial agent (what specifically is doing to avoid action of drug?) (often where can be obtained?)
-enzyme inactivates the antimicrobial agent (b-lactamase)
-Often on R-plasmids
Altered permeability of the antimicrobial agent (what specifically is doing to avoid action of drug?)
inability to enter the bacterial cell
-This mechanism typically involves changes in the structure or electrical charge of the cytoplasmic membrane proteins that constitute channels or pores (called poring in gram negative) Altered pore proteins result from mutation in chromosomal genes
active export (pump) of the agent from the cell (out of the cell) So called resistance pumps
Altered target site (what specifically is doing to avoid action of drug?)
-Alteration of the target site for the antimicrobial agent.
-Alter the target of the drug so that the drug either cannot attach to it or binds it less effectively
Replacement of a sensitive pathway (what specifically is doing to avoid action of drug?)
Resistance can result from the acquisition of a new enzyme to replace the sensitive one
Some pathogens are _ or _ (deals with resistance)
-naturally partially
-completely resistant
What is multi-drug resistance? (how commonly called?, how obtain this?, problem and how arose this problem)
-resistance to more than one drug at a time
-superbugs (commonly called)
-Common when R-plasmids exchanged
-Develop in hospitals and nursing homes; constant use of drugs eliminates sensitive cells and encourages the development of resistant strains
What is cross resistance?
-Resistance to one antimicrobial agent may confer resistance to similar drugs.
-Typically occurs when drugs have similar structures
-EX: Resistant to streptomycin; resistant to similar aminoglycoside drugs?
R-plasmid
Extrachromosomal piece of DNA containing genes for resistance to antimicrobial drugs
transformation
-Method of horizontal gene transfer in which a recipient cell takes up DNA from the environment
Transduction
Method of horizontal gene transfer in which DNA is transferred from one cell to another via a replicating virus
conjugation
method of horizontal gene transfer in which a bacterium containing a fertility plasmid forms a conjugation pilus that attaches and transfers plasmid genes to a recipient; in reproduction of ciliates: coupling of mating cells
B-lactamase
-bacterial enzyme that breaks the beta-lactam rings of penicillin and similar molecules, rendering them inactive
-breaks down penicillin
Describe the development of a resistant strain of bacteria
1. A bacterial population contains both drug-sensitive and drug-resistant cells, although sensitive cells constitute the vast majority of the population because resistant cells are less efficient than the normal bacteria, in a free-drug environment, because they must expand extra energy to maintain resistance genes and proteins (resistant cells remain minority because they reproduce more slowly)
2. Exposure to an antimicrobial drug inhibits the sensitive cells; so long as the drug is present, reduced competition from sensitive cells facilitates the multiplication of resistant cells
3. Eventually resistant cells constitute the majority of the population
why do resistant strains of bacteria most often develop in hospitals and nursing homes than in college dorms?
Resistant strains are more likely to develop in hospitals and other heath care facilitates because the extensive use of antimicrobial agents in those places inhibits the growth of sensitive stains and selects for the growth of resistant strains
why is important to not over prescribe antibiotics?
because the resistant strain of bacteria will grow in large amounts or become the majority of the population since the sensitive-drug bacteria will not give competition to the resistant strain by decreasing in number due to the antimicrobials
the ability of Staph. aureus to be penicillin resistant is what kind of mechanism of resistance?
Inactivation of the antimicrobial agent by using B-lactamase
the ability of a microbe to contrast the effect of sulfonamides will be what kind of mechanism of resistance?
Altered target site
if a cell obtains the ability to absorb folic acid from the environment or synthesis folic acid in other way different of using PABA, which affects the ability of sulfonamide, what type of mechanism of resistance is?
Replacement of a sensitive pathway
what are important factors to avoid resistance? (6)
-Right dose and right duration of antibiotics
-Limit use of antimicrobials to necessary cases
-Development of new variations of existing drugs (novel side chains added to original molecule): Second-generation drugs; Third-generation drugs
-Use antimicrobial agents in combination so that pathogens resistant to one drug will be killed by other drug, and vice versa (use combos)
-use synergistic combination of drugs
-Not use antagonistic combination of drugs
What is synergism?
-Interplay between drugs that results in efficacy that exceeds the efficacy of either drug alone
-One drug sometimes enhances the effect of a second drug
-can also result from the combination of an antimicrobial and a chemical
What is antagonism?
-opposite to synergism
-Drugs interfere with each other
-The effect of one drug contrasts or almost eliminates the effect of the other drug
-they both might fight the disease well alone but together they cannot do it efficiently
Second generation drugs (how obtain them, what type of drugs?, and what is developed when the bacteria develop resistance to them?)
-Developing new variations of existing drugs can be done by adding novel side chains to the original molecule
-They are considered to be semisynthetic drugs
-If resistance develops to these drugs, third generation drugs may be developed to replace them
Cross-resistance is due to
a. the deactivation of an antimicrobial agent by a bacterial enzyme
b. the alteration of cells so an antimicrobial agent cannot attach
c. cell membrane changes that prevent entry of antimicrobial agents
d. the similarly of one antimicrobial agent to another
d
Sets with similar terms