what are the mechanism of action for erythromycin?
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"Erythromycin is a macrolide antibiotic produced by Streptomyces erythraeus and was the first of several macrolide antibiotics now on the market. Although erythromycin is active against many microbes, its clinical applications are relatively few"\n\n"Mechanism of Action: Erythromycin binds to the 50 S ribosomal subunit, inhibiting bacterial protein synthesis. It is effective against a wide range of microorganisms and, like other antibiotics that inhibit protein synthesis, erythromycin is mainly bacteriostatic. Activity of erythromycin against gram-positive organisms generally is greater than against gram-negative organisms due to its superior penetration into gram-positive organisms.\n\nGram-positive organisms susceptible to erythromycin include Staphylococcus aureus, Streptococcus agalactiae, S. pyogenes, S. pneumoniae, S. viridans group, and Corynebacterium diphtheriae. Gram-negative coverage is limited. In general, erythromycin should not be used against Haemophilus influenzae, although in some cases this organism may be susceptible. Other organisms that have shown susceptibility include Chlamydia trachomatis, Entamoeba histolytica, Listeria monocytogenes, Borrelia burgdorferi (causative agent of Lyme disease), Mycoplasma pneumoniae, Treponema pallidum, and Ureaplasma urealyticum. Clinicians are advised to consult susceptibility data at the institution in which they practice to determine erythromycin's activity.\n\nErythromycin has actions which make it useful outside of the infectious disease field. Erythromycin mimics the effect of the gastrointestinal polypeptide motilin on gastrointestinal motility. This action is probably due to agonism at the motilin receptors. Motilin receptors are found mainly in the gastric antrum and proximal duodenum. The physiologic action produced is an increased motility during the interdigestive (between-meal) period, without affecting postprandial motility. Erythromycin does not affect either dopamine receptors or increase acetylcholine concentrations in the gut."\n\n\nLet me know if this isn't quite it, or more assistance is needed!\n\nJanice (email available through my profile)
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well,here is a useful brief answer:\nA-Tetracycline:\n# mode of action:\n1.Bacteriostatic.\n2.Prevents bonding  of tRNA to mRNA on ribosome.\n# uses:\n1.Treats intestinal amebiasis.      \n2.Effective against Rickettsia and Chlamydia.     \n3.Against syphilis and gonorrhea.  \n\nB-Streptomycin:\n# mode of action:\n1.Bacteriostatic \n2.Inhibits peptide bond formation.  \n# uses:\n1.Tuberculosis.\n2.Used for tularemia,plague.  \n2.Urinary tract infections.  \n3.Enteric infections.  \n4.Nosocomial infections.  \n5.Against penicillin-resistant gonorrhea       \n\nC-Polymyxin B:\n# mode of action:\n1.Bacteriocidal  \n2.Causes disorientation of lipoprotein constituents resulting in a distortion.     \n# uses:\n1.Against Pseudomonal infection.      \n2.Against Gram -ve in wounds,abrasions,and burns.\n3.Against E.Coli infection.\n\nD-Pencillin:\n# mode of action:work by inhibiting the formation of peptidoglycan cross links in the bacterial cell wall.\n# uses:\n1.STD:like syphilis & gonorrhea.\n2.Cardiac infection:Bacterial Endocarditis.  \n3.Brain infectins:Meningitis,Encephalitis.\n4.Respiratory infections:Pneumonia,Lung abscess.\n5.Miscellanous:Tonsilitis,Pharyngitis.\n6.Skin infections.\n7.Prophylasis:Rheumatic Fever .\n8.Septicemia in children.\n\nE-Cephalosporins:\n# mode of action:work by inhibiting the formation of peptidoglycan cross links in the bacterial cell wall.\n# uses:\n1.Against Staphylococcal & Streptococcal infections.\n2.Against Escherichia coli,Klebsiella pneumoniae and Proteus mirabilis.\n3.Hospital-acquired infections.
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Certain antibiotics can interact with birth control pills, making the birth control pills less effective and pregnancy more likely. Spotting - or ‘mid-cycle’ bleeding - may be the first sign that an antibiotic is interfering with the effectiveness of your birth control pills. \nAntibiotics that have been shown to interact with birth control pills include rifampin (brand name Rifadin), penicillin (Veetids), amoxicillin (Amoxil), ampicillin (Omnipen), cotrimoxazole (Septra or Bactrim), tetracycline (Sumycin), minocycline (Minocin), metronidazole (Flagyl), and nitrofurantoin (Macrobid or Macrodantin). \n\nTo help women avoid pregnancy while taking an antibiotic - and for at least one week afterward - doctors generally recommend they use a condom or spermicide as a back-up method of birth control. If you are taking both antibiotics and birth control pills, be sure to check with your doctor about how long you should continue to use a back-up method. Also, discuss any other questions you may have about this information. \n\nSources:\nDickey, R.P. Managing Contraceptive Pill Patients. EMIS Inc.,1998. \nHansten, P.D, J.R. Horn. Drug Interactions Analysis and Management, Applied Therapeutics, 2000.\nDipiro, J,T, Pharmacotherapy A Pathophysiologic Approach. Fourth Edition. Appleton &Lange. 1999
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Antibiotics work on the protein in a cell's membrane, usually denaturing the proteins and causing the cell to rupture.\n\nVirus do not have a cell membrane. They are not actually living, but instead take over the operations within a host cell. In order for an antibiotic to work on a virus, it would have to rupture the cell membrane of the host cell. In that case, the antibiotic would be toxic, and probably more deadly than the viral infection.
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There are five main ways that enzyme activity is controlled in the cell.\n\nEnzyme production (transcription and translation of enzyme genes) can be enhanced or diminished by a cell in response to changes in the cell's environment. This form of gene regulation is called enzyme induction and inhibition. For example, bacteria may become resistant to antibiotics such as penicillin because enzymes called beta-lactamases are induced that hydrolyse the crucial beta-lactam ring within the penicillin molecule. Another example are enzymes in the liver called cytochrome P450 oxidases, which are important in drug metabolism. Induction or inhibition of these enzymes can cause drug interactions. \n\nEnzymes can be compartmentalized, with different metabolic pathways occurring in different cellular compartments. For example, fatty acids are synthesized by one set of enzymes in the cytosol, endoplasmic reticulum and the Golgi apparatus and used by a different set of enzymes as a source of energy in the mitochondrion, through β-oxidation.\n\nEnzymes can be regulated by inhibitors and activators. For example, the end product(s) of a metabolic pathway are often inhibitors for one of the first enzymes of the pathway (usually the first irreversible step, called committed step), thus regulating the amount of end product made by the pathways. Such a regulatory mechanism is called a negative feedback mechanism, because the amount of the end product produced is regulated by its own concentration. Negative feedback mechanism can effectively adjust the rate of synthesis of intermediate metabolites according to the demands of the cells. This helps allocate materials and energy economically, and prevents the manufacture of excess end products. Like other homeostatic devices, the control of enzymatic action helps to maintain a stable internal environment in living organisms. \n\nEnzymes can be regulated through post-translational modification. This can include phosphorylation, myristoylation and glycosylation. For example, in the response to insulin, the phosphorylation of multiple enzymes, including glycogen synthase, helps control the synthesis or degradation of glycogen and allows the cell to respond to changes in blood sugar. Another example of post-translational modification is the cleavage of the polypeptide chain. Chymotrypsin, a digestive protease, is produced in inactive form as chymotrypsinogen in the pancreas and transported in this form to the stomach where it is activated. This stops the enzyme from digesting the pancreas or other tissues before it enters the gut. This type of inactive precursor to an enzyme is known as a zymogen. \n\nSome enzymes may become activated when localized to a different environment (eg. from a reducing (cytoplasm) to an oxidising (periplasm) environment, high pH to low pH etc). For example, hemagglutinin of the influenza virus undergoes a conformational change once it encounters the acidic environment of the host cell vesicle causing its activation.
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it's generally used with sulfamethoxizole(together, that's bactrim)\ntrimethoprim kills only bacterial cells because of the enzyme it inhibits...humans i think don't have it...something to do with dihydrofolate reductase i think.
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There are several medications that are known to be "ototoxic". The most famous is a class of antibiotics called aminoglycosides. These are very strong antibiotics given through an IV, they usually end in "-mycin" such as erythromycin, tobramycin and vancomycin.\n\nOther drugs include certain chemotherapy agents like bleomycin, cisplatin, and vincristine.\n\nMany other products can cause hearing loss but these are the big ones...p
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I believe that the vitamin niacin acts as a coenzyme in the electron transport system of cellular respiration in aerobes. This system is a major producer of ATP . A niacin defficiency would therefore cause an individual to experience early fatigue during exertion.
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You first have to realize that anitbiotics usually work by targeting some necessary life process that goes on within a cell. It could protein production (aka Translation), it could target gene expression (aka Transcription) or other processes like membrane and cell wall production. These are by far the most common targets for antibiotics (with protein production and cell wall production making up the biggest bulk of the targets.)\n\nAs far as viruses go, you have to realize that viruses don't do these things on their own. So you can't target something that doesn't exist in the agent you want to fight off.\n\nYou see viruses are obligate intracellular pathogens. Which means that have to invade a living cell in order to reproduce. Because viruses don't have the machinery to make their own proteins or transcribe their own genes they have to hijack the machinery of the cell they infect to do it for them.\n\nThis should make it easy to understand why we can't developer antiviral medications that work the same way antibiotics work to help rid our bodies of viral infections. If we develop a drug that stops viral protein production, because it is using the same machinery we normally use, we would in effect be killing all our cells, not just the ones that have viruses in them. These types of drugs would be way to toxic to our healthy cells.\n\nYou might ask yourself, well then why do antibiotics work on bacteria if they are targeting processes inside of bacteria that we need to do also (ie. protein production or cell membrane production)? The answer to that is evolution. Enough evolutionary time has passed that the processes we use to do these things aren't similar enough to cause cross reactivity. As time passes, things change. That's the basis for evolution. The longer two organisms have time to diverge from one another the more able researchers are able to use those differences to treat if one chooses to.\n\nIn the case of bacteria. We can take advantage of the differences between them and us to get rid of them if they infect us.
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If you read your package properly you can find out the proper spelling. With the proper spelling you will be able to find information on it on the internet: http://en.wikipedia.org/wiki/Erythromycin\nErythromycin prevents bacteria from growing by interfering with their protein synthesis. Erythromycin binds to the 23s rRNA molecule in the 50S of the bacterial ribosome, blocking the exit of the growing peptide chain thus inhibiting the translocation of peptides.\n\nBacterial ribosomes are similar to those of eukaryotes, but are smaller and have a slightly different composition and molecular structure. There are sufficient differences between bacterial ribosomes and eukaryotic ribosomes that some antibiotics will inhibit the functioning of bacterial ribosomes, but not a eukaryote's, thus killing bacteria but not the eukaryotic organisms they are infecting.
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Doxycycline is a tetracyline antibiotic that kills certain bacteria that cause infection or stops their growth. It’s used to treat many kinds of infections of the skin, bone, stomach, respiratory tract, sinuses, ear and urinary tract. Doxycycline also treats Lyme disease, all forms of Anthrax and certain sexually transmitted diseases. For those who travel to certain parts of the world where malaria is prevalent, doxycyline can be given to suppress the disease. Doxycycline is the preferred medication for elderly patients exposed to all forms of Anthrax. \nCommon Side Effects\nIf you experience any of the following serious side effects, stop taking Doxycycline and consult your health care provider immediately. Dark yellow or brown urine; difficulty breathing; increased sensitivity to the sun or ultraviolet light; headaches; itching in the rectal or genital area; stomach pain or cramps; skin rash or itching; tingling or numbness of the hands or feet; unusual bleeding or bruising; unusual tireness or weakness; yellowing or eyes or skin. \n\nIf you experience any of the following less serious side effects, talk to your doctor:\n\ndiarrhea; discolored tongue; loss of appetite; nausea, vomiting or sore mouth. \n\nContraindicators (drugs that should only be taken with a doctor’s permission while taking Doxycycline)\n\nDo not take antacids that contain magnesium or aluminum (such as Tums or Rolaids); barbituate medicines for inducing sleep or treating seizures (convulsions); calcium salts; carbamazepine; cholestyramine; colestipol; digoxin; female hormones including contraceptive or birth control pills; ferrous sulfate; magnesium salts; other antibiotics; phenytoin; or sodium bicarbonate\n\n Before taking Doxycycline, tell your doctor if you are taking any prescriptive medicines or over the counter medicines such as nutritional supplements, or herbal products. Also tell your doctor if you frequently drink caffeine or alcohol, if you smoke or if you use illegal drugs.
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Every drug reacts differently and there are many chemical reactions.\n\nThe most common method a drug uses though is to inhibit an enzyme that is causing the anomaly.  It does this by binding to a "pocket" in the enzyme, most typically by ionic interactions.  These are either in the form of hydrogen bonding, pi-pi stacking etc.  These drugs are VERY specific and out of the thousands of different enzymes in your body they will target the right one.  Most commonly due to the new ionic interactions it causes the enzyme to change shape and deform very slightly, which means it cannot combine with another enzyme to promote the disease, or bind specifically to another molecule in your body which would otherwise promote the disease.\n\nThe reasons for drugs are several fold:\n\n1.  They are there to help initiate an enzyme-enzyme interaction that should occur naturally, but isn't;\n2.  They are used to bind to a rogue enzyme which is causing problems, deform the shape and de-activate it, letting your body carry on as normal;\n3.  They take over part of the bodies process and actually are a synthetic replacement for something that does occur naturally, but isn't functioning properly.\n\nHow individual drugs work is very specific usually to the ailment, so it is difficult to provide general chemical reactions.\n\nI hope this brief explanation marginally helps.
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That would be a two semester course in med or pharmacy school. I don't think the Yahoo managers would permit such a long answer to be posted.\n\nThere are different actions/mechanisms for each class of antibiotics.  They are given for bacterial infections of all sorts. Can you narrow the scope of the question any?  By the way, malaria is a protozoa, not bacterial, which is what antibiotics are directed against.
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I'll try to use a simple talk.\nAntibiotics work to kill bacteria. Bacteria are single-cell organisms. If bacteria make it past our immune systems and start reproducing inside our bodies, they cause disease. We want to kill the bacteria to eliminate the disease. \nAn antibiotic is a selective poison. It has been chosen so that it will kill the desired bacteria, but not the cells in your body. Each different type of antibiotic affects different bacteria in different ways. For example, an antibiotic might inhibit a bacterium's ability to turn glucose into energy, or its ability to construct its cell wall. When this happens, the bacterium dies instead of reproducing. At the same time, the antibiotic acts only on the bacterium's cell-wall-building mechanism, not on a normal cell's. Ok?
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Sorry, as much as we'd all like it, the only way to kick this icky "pink eye" is to use the ointment or drops. ERYTHROMYCIN OPHTH OINT 3.5 GM is the stuff we had to get the last bout at our house.  We asked our Dr. and checked out other sources and found that you gotta have the medicine!!  Good luck!
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There are two ways that antibiotics potentially can reduce the action of birth control pills. Birth control pills contain estrogens. Some antibiotics, e.g., rifampin, griseofulvin, cause the enzymes in the liver to increase the break-down of estrogens and thereby can decrease the levels of estrogens in the body and the effectiveness of the pills. This can result in unwanted pregnancy. Therefore, individuals taking birth control pills should use a second method of birth control when taking these antibiotics or other drugs that can increase the break-down of estrogens.\n\nThe other way that antibiotics could interfere with the effectiveness of birth control pills is by reducing the re-circulation of estrogens within the body. Estrogens, e.g., ethinyl estradiol, in birth control pills are broken-down by conversion in the liver to other chemicals which are then secreted into the intestines in the bile that is produced by the liver. Bacteria in the intestine are able to convert these chemicals back into the active estrogen which is then reabsorbed into the body.. This re-circulation is called entero-hepatic cycling. Theoretically, antibiotics can kill the bacteria that convert the inactive chemicals to the active estrogen, and, therefore, may interfere with the effectiveness of birth control pills. Unwanted pregnancies could occur. Although it has not been proven that unwanted pregnancies can occur by this means, drug manufacturers caution that antibiotics could decrease the effectiveness of birth control pills. Since it is better to be safe than sorry, individuals taking birth control pills are advised to use a second reliable method of birth control when taking antibiotics.
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Streptomycin is a broad spectrum drug. Unlike the other two drugs, mentioned, it does not block the A site aminoacyl - tRNA for peptidyl transfer reaction  in translation. This is the main step in protein formation.