Terms in this set (71)
minimal or no effect on host cells but maximum effect against the infecting microorganism
all inclusive term for any antimicrobial drug regardless of its origin
substance produced by the natural metabolic processes of some microorganisms that can inhibit or destroy other microorganisms
the use of chemical interactions to synthesize antimicrobial compounds in the laboratory
use of a drug to prevent imminent infection of a person at risk
any chemical used in the treatment, relief, prophylaxis of a disease
the use of chemotherapeutic drugs to control infection
drugs that are chemically altered in a laboratory after being isolated from natural sources
What is a superinfection & what can cause one?
An overgrowth of bacteria or fungal microorganisms not affected by the antibiotic being used for treatment; can happen when using a broad spectrum antibiotic that destroys normal microbiota that normally keep pathogenic microbes in check
Characteristics of Ideal antimicrobial drug.
1) selective toxicity 2) microbicidal, not microbistatic 3) Soluble 4) Remains potent long enough to act 5) Doesn't lead to antimicrobial resistance 6) Complement's hosts defenses 7) Remains active in tissues/body fluids 8) Easily delivered to site of infection 9) Reasonably priced 10) Doesn't cause other health problems like allergies or predispose to other infections
Capable of destroying or inhibiting the growth of disease-causing microorganisms
What is the main goal of antimicrobial therapy?
To destroy the infective agent and to be nontoxic to the host and produce no side-effects
Differentiate between narrow-spectrum & broad spectrum antibiotics. How does the mode of action effect the spectrum of a drug?
Narrow spectrum affect only a few types of microbes and broad spectrum affect a broad range of G+ or G- organisms. Antimicrobial drugs target certain essential function of the microbe - what they target affects whether they are narrow or broad spectrum.
What is the major source of antibiotics?
Bacteria and fungi
What is the natural function of antibiotics?
Increase their resources by reducing competition for nutrients and space
Why is it better for a drug to be microbicidal than microbiostatic?
A microbicidal antibiotic is advantageous because it destroys the pathogen with no likelihood for future reproduction. In contrast, microbistatic antibiotics only inhibit growth as long as they are present, but when therapy is stopped, remaining microbes can resume reproductive activities.
Who is credited with discovering antibiotics and how did they make their discovery?
Alexander Fleming discovered antibiotics by accident when culture plates became contaminated with a mold. He noticed that bacterial growth was inhibited around the areas of mold growth, leading to the discovery of penicillin
spectrum of microbial activity
range of distinctly different types of microorganisms affected by an antimicrobial drug; can be broad or narrow
Action of Antimicrobial Drugs: Inhibiting Cell Wall Synthesis
prevent the cross-linking of NAM subunits in the peptidoglycan which weakens te cell walls leading to lysis. Beta -lactam rings bind to the enzymes that cross link the subunits (Penicillins,Cephalosporin, Carbapenems, Bacitracin, Vancomycin)
an enzyme that cleaves the b-lactam ring in penicillin molecule; a type of b-lactamase
enzymes that cleave the beta-lactam ring, and thereby render penicillins and other beta-lactam antibiotics inactive
Concentration of the drug that causes harm to the host
The concentration of the drug that effectively destroys or eliminates the pathogen from the host
Highest level of the drug tolerated by the host divided by the lowest level of the drug that will eliminate the infection or pathogen; Higher Therapeutic Index is better
Action of Antimicrobial Drugs:Inhibiting Protein Synthesis - Tetracyclines
Tetracycline interferes with the attachment of tRNA to mRNA ribosome complex
Action of Antimicrobial Drugs: Injure Plasma Membrane
Cause loss of selective permeability;
Action of Antimicrobial Drugs: Inhibit Synthesis of Folic Acid
Sulfonamides compete with the substrate PABA for the active site on the enzyme. PABA is the substrate for the enzymatic reaction leading to sythesis of folic acid, a vitamin that functions as a coenzyme for synthesis of nucleic acid bases & many amino acids
Drugs that are Cell Wall Inhibitors
Polypeptide Antibiotics (Bacitracin, Vancomycin)
Antimycobacterial Antibiotics (Isoniazid, Ethambutol)
Drugs that are Protein Synthesis Inhibitors
Aminoglycosides (Streptomycin, Neomycin)
Tetracylines (Tetracycline, oxytetracycline)
Action of Antimicrobial Drugs: Inhibit DNA/RNA Synthesis
Inhibits replication and transcription
Determine the selective toxicity for each class of drug discussed in class based on their mode of action.
Penicillins - High Selective Toxicity - High Therapeutic Index
Vancomycin - Low therapeutic index (unsafe)
Penicillin plus B-lactamase inhibitor - High Therapeutic Index
Carbapenems - High Selective Toxicity
Cephalosporins - High Therepeutic Index
Bacitracin - Safe if topical; Low therapeutic index taken orally
Antimycobacterial Antibiotics - High Selective Toxicity
Polyenes (Antifungals) - Intermediate Toxicity
Aminoglycosides - Low therapeutic index (unsafe)
Tetracyclines - High Selective Toxicity
Macrolides - High Selective Toxicity
Chloramphenicol - Very Low therapeutic index (unsafe)
Sulfa Drugs - High Selective Toxicity
Antiviral - High Selective Toxicity - difficult to maintain
Explain the significance of beta-lactamases and how they interact with antibiotics.
Beta-lactamases cleave the beta-lactam ring in the penicillin molecule, making the antibiotic ineffective
Identify which cell wall antibiotics are affected by beta-lactamases and which are not in the beta lactam category.
Affected by beta-lactamases: Penicillin, Cephalosporins, Carbapenems
Not Affected by beta-lactamases: Polypeptide Antibiotics that interfere with cell wall synthesis & Antimycobacterial Antibiotics
What is competitive inhibition?
compete for active site on the enzyme
How can a metabolic analog molecule inhibit metabolism?
a enzymatic activity of a microbe can be competitively inhibited by a substance that closely resembles the normal substrate for the enzyme - stopping synthesis of essential metabolites
Why does the penicillin group of drugs have milder toxicity than many other antibiotics?
because penicillins affect cell wall synthesis and eukaryotic cells do not have cell walls therefore lower toxicity
It is harder to treat a patient with a fungal, protozoan, or helminth parasite than a bacterial infection. Give 2 reasons why that is true.
1) since they are eukaryotes they use the same mechanisms to synthesize proteins & nucleic acids so it hard to find a point of selective toxicity 2) fungal infections are becoming more frequent as opportunistic infections in immunosuppressed individuals
Polyenes are commonly used to treat fungal infections. Name 1 common polyene used & how it works to destroy the fungal organism. Is selective toxicity high or low? Why?
Amphotericin B most commonly used. It target the sterol, ergosterol in the plasma membrane by interrupting biosynthesis causing the membrane to become excessively permeable & killing the cell. Humans somewhat susceptible because cholesterol if similar to egosterol.It has a high toxicity to the kidneys which limits its use. Nystatin is a topical form used to treat candidiasis.
What 3 antibiotics are in Neosporin? What are their modes of action? Why should they only be applied after a scab has formed & not taken orally?
Bacitracin (polypeptide antibiotic that interferes with linear stands in peptidoglycan, Polymyxin (affects permeability of plasma membrane), & Neomycin (interferes with protein synthesis). Polymyxins are nuerotoxic so it can't be taken orally. Polypeptide antibiotics are highly toxic if taken orally.
developed to overcome disadvantages of natural penicillin. Keeps the antibiotic nucleus & adds functional groups in the lab
Penicillin plus B-Lactamase Inhibitor
combines penicillin with clavulanic acid which is a noncompetitive inhibitor of penicillinase (no antimicrobial activity of its own). Ex: Augmentin
class of B-lactam antibiotics; substitutes a C atom for a S atom & adds a double bond to the penicillin nucleus; broad activity; effective against 98% of bacteria in hospital patients
Cephalosporium mold; widely used; over 70 forms; later generations are broad spectrum; some useful on MRSA; resistant to penicillinases, susceptible to other B-lactamases; inhibits cell wall synthesis (NAM/NAG bond)
very specific; used against Mycobacterium tuberculosis (isoniazid inhibit synthesis of mycolic acids / ethambutol inhibits the incorporation of mycolic acid into cell wall
Aminoglycosides (Streptomycin & Neomycin (topical))
inhibit protein synthesis by changing the shape of the 30S portion of the ribosome; derived from Streptomyces & Micromonospora; broad spectrum; used to treat bubonic plague & STDs; toxic side effects include auditory nerve damage & kidney damage
interferes with the attachment of tRNA to mRNA ribosome complex; broad spectrum & low cost; penetrates tissues well, intracellular rickettsias & chlamydias, UTIs, STDs
Synthetic tetracycline; longer retention in body; used to be added to animal feed
similar structure to tetracyclines; best known Tygacil; effective against certain antibiotic resistant bacteria (MRSA)
structure - macrolide ring; inhibits protein synthesis by binding to ribosome, preventing ribosome from moving along mRNA to read message; most common prophylactic drug used; broad spectrum
synthetic antimicrobial used only in dire situations - very toxic to humans. Inhibits protein synthesis by blocking peptide bonds in both prokaryotic & eukaryotic cells; suppresses bone marrow activity & causes irreversible damage;
Antiviral drugs are typically more difficult to develop & maintain selective toxiciity. Give 2 reasons why.
1) because the virus replicates in the hosts cells using host cells genetic & metabolic mechanisms its hard to target the virus without damaging the host cell machinery 2) Most drugs are unable to affect latent or extracellular viruses
Explain the mechanism of Acyclovir
its a synthetic nucleotide analog (structurally similar) that targets DNA replication, blocking DNA synthesis
What type of infections is Acyclovir used for? How is it able to maintain selective toxicity?
herpes virus infections; it maintains selective toxicity because it blocks viral DNA synthesis
Your pregnant neighbor has been prescribed a daily dose of oral tetracycline for acne. Do you think this therapy is advisable for her? Why or why not?
No it is not advisable. It is a broad spectrum antibiotic which can suppress the normal gastrointestinal microbiota causing diarrhea & leading to superinfections, mainly from Candida albicans (yeast infection). It can also cause liver damage in pregnant women.
Why do drugs that act on bacterial & fungal membranes generally have high toxicity?
Bacterial and Fungal cell membranes are made up of phospholipids just like the human cell membranes. And this is why antibiotics that act on cell membranes are not that specific in their toxicity.
Drugs are often given to surgical patients, to dental patients with heart disease or to healthy family members exposed to contagious infections. What word would you use to describe this use of drugs? What the purpose of this treatment? Explain some undesirable effects of this therapy.
Known as antibiotic prophylaxis. It is given to prevent infection in people at risk. Undesirable effects include disruption of normal flora, allergies, toxicity
Do sulfonamide drugs have a high or low selective toxicity for humans? Why?
They have a low selective toxicity for humans because they inhibit the synthesis of folic acid. Humans don't synthesize folic acid, its ingested in their diet.
Give the basis for combined therapy. Give one reason why it could be helpful to use combined therapy in treating HIV infection.
Combined therapy is used to minimize the development of resistant strains. The HIV retrovirus lacks the proofreading ability of regular DNA replication resulting in frequent mutations. These mutations can make the virus resistant to a particular drug which is why a combination of drugs is used. Multiple drugs can work synergistically so you are much less likely to get drug resistance.
How does the misuse & abuse of antibiotics encourage the emergence of resistant forms?
Not completing the full course of antibiotics results in survival of the few resistant microbes which then multiply encouraging the survival of resistant bacteria. Taking the wrong antibiotic. Continous exposure to antibiotics in the environment allow the normal flora to acquire resistance plasmids which are constantly selected for & amplified which then "jump" to humans & share the plasmids that carry the resistance gene.
Explain a simple test one could do to determine if drug resistance was developing in a culture.
The Kirby Bauer test (disk diffusion) is used to determine if an organism is susceptible or resistant to a selection of antimicrobial agents. Lawn of bacteria is made on agar plate. Disks with. known concentrations of antimicrobial agents are added to agar. A "zone of inhibition" forms around the disk which can then be measured & compared against a standard table to determine if the organism is sensitive, intermediate, or resistant
Antiviral - Protease Inhibitors
When a new virus is made it begins by cutting up large proteins with protease enzymes. The fragments are then used to assemble new viruses. Analogs of amino acid sequences (structurally similar) can serve as inhibitors by interfering with their activity (protease inhibitors). Saquinavir is a brand of protease inhibitor.
a nucleotide analog reverse transcriptase inhibitor. It stops the action of reverse transcriptase in HIV, blocking viral DNA production
Blocks entry of the influenza virus by interfering with fusion of the virus with the cell membrane. Needs to be given within 1st 72hrs before virus replicates and spreads
Effective antiviral drugs do what?
Target viral replication by preventing entry, inhibiting nucleic acid synthesis, inhibiting viral protein function, & targeting viral assembly & release. They protect uninfected cells.
List then explain the five cellular or structural mechanisms that microbes use to resist antimicrobials.
Enzymatic destruction of the drug: microbe can enzymatically split apart the antibiotic ex: penicillinase
Prevention of penetration of the drug: surface receptors or channels are altered blocking drug
Alteration of drug's target site: change in the microbial ribosome so antimicrobic can't bind
Rapid ejection of the drug: Microbe creates a new pump with a high affinity for the drug which pumps the drug right back out
Changes in metabolic patterns: the drug blocks the ususal pathway so the microbe uses an alternate pathway by slightly changing its enzymes but still getting the same metabolic outcome
What is penicillinase? What effect does penicillinase have on beta-lactam antibiotics? How do bacteria acquire penicillinase? What effect does penicillinase have on eukaryotic cells?
Penicillinase is an enzyme secreted by many bacteria that cleave the b-lactam ring in b-lactam antibiotics. Bacteria can acquire penicillinase through conjugation, transformation, or transduction. It has not effect on eukaryotic cells because penicillin targets the peptidoglycan in cell walls (and penicillinase cleaves penicillin).
uses live microorganisms to replace or augment the normal flora
nutrients that encourage the growth of beneficial microbes in the intestine
- to predict the success or failure of antibiotic therapy (in vivo) in the body
- tests are performed (in vitro) outside the bdy that measure the growth response of the organism to particular drug(s)
-results should guide antibiotic choice
- results of susceptibility testing should be combined with clinical info & experience when selecting appropriate antibiotic
zone of inhibition
bacteria free circles of varying sizes around some disks in the Kirby Bauer test - indicate the organism is suseptible to antimicrobial; measure the diameter in MM can compare to the chart
Rise of Drug Resistance
microbes are gaining resistance faster than new drugs can be developed; 60% of hospital strains are resistant (MRSA & community acquired); drugs in animal feed to promote growth are increasing resistance
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