click below
click below
Normal Size Small Size show me how
Ch 7
controlling microbial growth in the body
| Drugs | chemicals that affect the physiology of an organism in any manner, can be good or bad |
| chemotherapeutic agents | chemicals that act against diseases |
| antimicrobial drugs | drugs that treat infections and have high level of selective toxicity, includes antibiotics, synthetic chemicals, and semisynthetic chemicals. |
| synthetic chemicals | antimicrobials that are completely synthesized |
| antibiotics | substances that are secreted by another organism that cause the inhibition or death of another microbe and are 100% natural |
| semisynthetic chemicals | chemically altered antibiotics that are more effective, longer lasting and easier to administer than naturally occurring ones |
| Who is Alexander Fleming and what did he do? | discovered that mold penicillium notatum produced molecules that inhibit the growth of Staphylococcus aureus bacteria |
| what was the molecule discovered by Alexander Fleming called? | penicillin |
| When did Fleming discover penicillin | 1928 |
| Who is Selman Waksman? | discovered that bacterium streptomyces produced substance that inhibit the growth of other types of bacteria. coined the term antibiotics |
| What did Gerhard Domagk discover | A red dye, prontosil, was chemically altered in the body into sulfanilamide |
| Sulfanilamides | Compound that targets and inhibits the growth of bacteria by targeting pathway needed for DNA and RNA, It became the first antimicrobial drug used to treat many bacterial infections |
| Are sulfonamide considered antibiotics? | they are synthetic |
| What were antibiotics that had their molecular structure tweaked called? | semisynthetic antibiotics |
| what are the advantages of semisynthetic antimicrobials | they are more stable, last longer, more effective, and are easier to administer |
| What do antimicrobial drugs depend on? | selective toxicity, and take advantage of the structural and biochemical differences btw pathogens and human cells |
| selective toxicity | the ability of an antimicrobial drug to cause damage or destroy the pathogens in the body while leaving human cells unharmed or relatively unharmed |
| WWhat are some differences between bacterial cells and human cells? | peptidoglycan cell wall, different ribosomes, different RNA and DNA polymerase, DNA gyrus, different cell membrane |
| What are some differences between fungal cells and human cells? | cell wall made of chitin |
| What are the differences between viruses and human cells? | Viruses are nonliving and therefore require the use of host to replicate. viruses use the enzymes of the host so it is difficult to only target viral microbes. |
| Why is there for antibacterial drugs than drugs against eukaryotic pathogens | there are many differences between bacterial and human in biochemical processes and structure |
| What are the 6 common antimicrobial mechanisms of action? | Inhibition of cell wall, protein synthesis, disruption of cytoplasmic membrane, inhibition of general metabolic pathways, inhibition of nucleic acid synthesis, and inhibition of attachment or entry into host cell. |
| Antibacterial cell wall synthesis inhibitors | prevent bacteria from increasing amount of peptidoglycan and only effective against growing cells. |
| What do antibacterial do to acid fast bacteria | prevent the formation of mycolic acid |
| What are the main classes of antibacterial | Beta-lams which are the broadest group, vancomycin, bacitracin, isoniazid, ethambutol |
| What are some subtypes of beta-lactams | penicillin, Cephalosporins *semisynthetic), Carbapenems |
| Beta Lactams | three C and 1 N with double bonded O or beta=lactam rings, are the most prominent group of cell wall inhibitors |
| What do bacteria with compromised cell walls result in | weakened cell walls and lyse of cell |
| How do beta lactams target the cell wall | The functional groups of beta-lactam rings bind to active site of transpeptidase enzymes that cross-link NAM subunits during peptidoglycan synthesis. act as a competitive inhibitor |
| Penicillin | A naturally occurring beta lactam made by mold and are marrow spectrum. Are mainly effective against gram positive bacteria |
| Semisynthetic derivatives of beta lactam | Carbapenems, cephalosporins, and semisynthetic Penicillin (amoxicillin) |
| what are semisynthetic derivatives of beta lactam good | broader spectrum of activity, more stable in acidic environments, readily absorbed, less susceptible to deactivation |
| What are the three general mechanisms of protein synthesis | interference with bacterial ribosomes, bacterial mRNA, charging of transfer RNA molecules |
| Vancomycin | binds to uncrossed linked units of peptidoglycan monomers (nam and nag) and prevents crosslinking from occurring (gram positi |
| Bacitracin | Blocks transport process of NAM and NAG from the cytoplasm to its destination |
| Isoniazid and Ethambutol | disrupts mycolic acid formation by blocking transport of mycilic acid synthesis |
| Echinocandins | antifungal that inhibits the enzyme active site needed for glucan synthesis which is used in synthesis of chitin and other cell wall polysaccharides. |
| Chloramphenicol | targets protein synthesis by attaching to ribosome and preventing peptidyl transferase attachment |
| What differences in ribsomoes allows selectivity between bacterial and eukaryotic cells | prokaryotic ribosomes are 70S and eukarya are 80S, eukarya mitochondria is 70S similar to prokaryotes. |
| Examples of antibacterial that targets protein synthesis | Aminoglycosides, tetracycline, chloramphenicol, licosamides, streptogramins, macrolides |
| What interferes with bacterial mRNA | antisense nucleic acids, which are complementary sequences to mRNA and prevent translation and binding to ribosome |
| Mupirocin | inhibits protein synthesis by selectively binding to isoleucyl-tRNA synthetases which prevents the loading of isoleucine, but only in gram positive bacteria. prevents charging of tRNA |
| Polymyxin | an antibacterial that disrupts the LPS and cytosolic membrane of gram negative bacteria. |
| Nystatin | attach to egosterol in fungal membrane and target specific steroids found in membrane. |
| Ergosterol | provides stucture integrity to phospholipid bilayer |
| Amphotericin B | Binds to ergosterol in fungal membranes and target specific steroid found in membrane |
| Antifungal that target cytoplasmic membrane do what? | create pores in cells leadisng to rupture due to osmotic pressure |
| What level of selective toxicity do antifungal that disrupt the cytoplasmic membrane have | low level because cholesterol have similar structure to ergosterol and are somewhat susceptible. |
| Azoles | inhibit ergosterol synthesis in cytosol and prevents transfer to cell membrane and lead to destabilized cell membrane and ruptured cell membrane |
| Allylamine | inhibit ergosterol synthesis in cytosol and prevents transfer to cell membrane and lead to destabilized cell membrane and ruptured cell membrane |
| When are metabolic pathways effective to target | when pathogen an host metabolic processes differ |
| Sulfonamides | block folic acid synthesis which is required for bacterial DNA and RNA synthesis and is a metabolic antagonist. Target specific enzyme and is often taken on conjunction with another metabolic antagonist |
| Trimethoprim | block folic acid synthesis which is required for bacterial DNA and RNA synthesis and is a metabolic antagonist. Target specific enzyme and is often taken on conjunction with another metabolic antagonist |
| Where is folic acid found | prokaryote and some protozoa have to synthesize folic acid while humans get it from their diet, folic acid is necessary for DNA and RNA synthesis |
| Synergistic | treatments that are taken in conjunction to improve treatment outcome. |
| Quinolones | an antibacterial gyrus inhibitor that inhibits nucleic acid synthesis, acts against bacterial DNA gyrus |
| fluoroquinolones | an antibacterial gyrus inhibitor that inhibits nucleic acid synthesis, acts against bacterial DNA gyrus |
| How do antivirals target nucleic acid synthesis? | By using nucleotide or nucleoside analogs, which are similar in structure to nt. |
| what do nucleotides and nucleoside analogs do? | distort shape of nucleic acid molecules and prevent further replication, transcription, or translation. used against viruses and effective against rapidly dividing cancer cells. |
| Reverse transcriptase inhibitors | an antiviral that inhibits DNA replication by turning RNA into DNA. Act against an enzyme HIV uses in its replication cycle. does not harm people bc they lack reverse transcriptase |
| Nuceloside and nucleotide analogs | inhibit transcription along with replication, transcription, or translation |
| Rifampin | an antibacterial that inhibits transcription by targeting RNA polymerase |
| Why are antimicrobials being develop that inhibit attachment and entry | viral infections depend on their coat to enter cell and uncoating to attach to host cell. if any stage is blocked, replication cycles is prevented. |
| Therapeutic index | ratio of the dose of a drug that can be tolerated to the drug's effective dose. the higher the therapeutic index the safer the drug |
| Spectrum of action | spectrum of activity effective against microbes. can be large or small. sulfonamides have a large spectrum of action |
| effectiveness tests | Diffusion susceptibility test, minimum inhibitory concentraruin |
| Diffusion susceptibility test | determines which antibiotics are effective against specific species of bacteria |
| minimum inhibitory concentration test | tests that determine the lowest concentration of an antimicrobial drugt that can inhibit the growth of an organism or MIC value |
| minimum bactericidal concentration test | Tests that determine the lowest concentration of an antimicrobial drug that can kill an organism or MBC value |
| Topical | application of drug for external infections |
| Oral route | requires no needles and is self-administered |
| Intramuscular | administration delivers drug via needle into muscle |
| Intravenous | administration delivers drug directly to bloodstream |
| why is it important that drugs be nonallergenic | Allergic reactions are rare but may be life threatening Anaphylactic shock |
| mechanisms of resistance 7 | produce enzyme that destroys or deactivates drug, slow or prevent entry of drug into the cell, alter target of drug so it binds less effectively, alter their own metabolic chemistry, pump antimicrobial drug out of the cell before it can act, |
| Mycobacterium tuberculosis | produces Mfp A protein that binds to DNA gyrus and prevents the binding of fluoroquinolone drugs |
| bacteria in biofilms and pump drugs out of cell are what | mechanisms of resistance |
| enzymes produced that destroy or deactivates drug | beta lactam ring |
| multiple resistance | pathogens resistant to more than one drug and is common when R plasmids are exchanged and are often developed in hospitals and nursing homes |
| what is the least amount of antimicrobial agents that multiple drugs resitant pathogens are resistant to? | three |
| what does the CDC do | define threat levels for microbial resistance |
| urgent | potential for widespread life-threatening disease |
| serious | alternative antimicrobials are available ore disease incidence is low or declining |
| concerning | low threat or numerous antimicrobials are available for treatment |
| maintaining a what for what is a way of preventing resistance | high enough concentration for sufficient time |
| using what in combination helps prevent resistance | antimicrobial agents enhance the effect of a second drug and antagonism occyrs when drugs interfere with each other |
| using what when can prevent resistance | antimicrobials only when necessary |