How much is LD50 of ampicillin, penicillin and streptomycin for E.coli and Staphylococcus aureus?
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It depends upon the strains that you use.
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INTRODUCTION — Shortly after the introduction of methicillin in 1959, outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) infections were reported in the early 1960s [1]. Methicillin resistance in S. aureus is defined as an oxacillin minimum inhibitory concentration (MIC) 4 µg/mL. Isolates resistant to oxacillin or methicillin are also resistant to all beta-lactam agents including cephalosporins.\n\nMethicillin resistance is mediated by the mecA gene, which encodes for an abnormal low-affinity binding protein, PBP-2a that permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics. (See "Mechanisms of antibiotic resistance in Staphylococcus aureus").\n\nThe evidence suggests that a single clone of MRSA accounted for most of the isolates recovered during the 1960s [2,3] and that five major MRSA clones had emerged worldwide by 2002 [4]. Dissemination of resistance was mediated by horizontal transfer of the mecA gene and related regulatory sequences [5]. Since that time, MRSA has increased in prevalence worldwide as both a nosocomial and, more recently, a community-associated pathogen.\n\nThe epidemiology and clinical manifestations of MRSA infection in adults will be reviewed here. The prevention and control and the treatment of MRSA infections in adults is discussed separately. (See "Prevention and control of methicillin-resistant Staphylococcus aureus" and see "Treatment of methicillin-resistant or vancomycin resistant Staphylococcus aureus infection in adults").\n\nEPIDEMIOLOGY — MRSA was at first primarily a healthcare-associated (nosocomial) infection, with only small numbers of community-associated cases [4]. However, it is now an increasingly prevalent community-associated pathogen. Such patients acquire MRSA infection in the outpatient setting, and are infected at the time of hospital admission.\n\nCommunity-associated (CA) MRSA isolates usually have different molecular and antimicrobial susceptibility characteristics from healthcare-associated (HA) MRSA. However, nosocomially acquired MRSA can spread to household and community contacts and be a source of community-associated infection [6]. In addition, CA-MRSA is emerging as a significant cause of nosocomial infection as illustrated by analysis of 132 cases of MRSA blood stream infection in patients collected at an urban public hospital in 2004 [7]. Molecular typing studies demonstrated that 39 of 116 isolates (34 percent) were MRSA USA300 genotype, the predominant cause of CA-MRSA infection in the area.\n\nGenetics of methicillin resistance — Molecular typing techniques have provided insights into the epidemiology of MRSA and to differences between HA-MRSA and CA-MRSA. The genetic determinants of antibiotic resistance in MRSA are discussed in detail separately, but will be reviewed briefly here. (See "Mechanisms of antibiotic resistance in Staphylococcus aureus").\n\nThe mecA gene responsible for methicillin resistance is located on a mobile genetic element called staphylococcal cassette chromosome (SCCmec). Sequencing SCCmec from many MRSA strains has revealed that there are five SCCmec types (I-V) that vary in genetic makeup and size. Transfer of SCCmec from MRSA into well-adapted strains of methicillin-susceptible S. aureus (MSSA) has occurred on a number of occasions, resulting in new MRSA strains that spread rapidly in healthcare institutions. A majority of HA-MRSA clones have type I, II, or III SCCmec and are multidrug resistant [8].\n\nIn contrast, a majority of CA-MRSA strains have type IV SCCmec [9-11]. Because type IV SCCmec does not carry the multiple antibiotic resistance genes common among types I to III [10,11], CA-MRSA are usually resistant only to methicillin, other beta-lactam antibiotics, and erythromycin, but are usually susceptible to other classes of antibiotics, particularly trimethoprim-sulfamethoxazole and clindamycin [10,12-16]. CA-MRSA in so
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Yes.  Fluoroquinolones like cipro, levaquin, avelox, and Tequin are not at all related to penicillin structurally, and can therefore be used in patients with a penicillin allergy.
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Penicillin refers to a group of β-lactam antibiotics used in the treatment of bacterial infections caused by susceptible, usually Gram-positive, organisms. The name “penicillin” can also be used in reference to a specific member of the penicillin group. Penicillins have the molecular formula R-C9H11N2O4S, where R is a variable side chain.\n\nThe serendipitous discovery of penicillin is usually attributed to Scottish scientist Alexander Fleming in 1928, though others had earlier noted the antibacterial effects of Penicillium. He noticed a halo of inhibition of bacterial growth around a contaminant blue-green mould on a Staphylococcus plate culture. Fleming concluded that the mould was releasing a substance that was inhibiting bacterial growth. He grew a pure culture of the mould and discovered that it was Penicillium notatum (now known as Penicillium chrysogenum) – he later named the bacterial inhibiting substance “penicillin” after the Penicillium notatum that released it. Fleming was convinced after conducting some more experiments that penicillin could not last long enough in the human body to kill pathogenic bacteria and stopped studying penicillin after 1931, but restarted some clinical trials in 1934 and continued to try to get someone to purify it until 1940.\n\nIn 1939, Australian scientist Howard Walter Florey and a team of researchers (Ernst Boris Chain, A. D. Gardner, Norman Heatley, M. Jennings, J.Orr-Ewing and G.Sanders) at the Sir William Dunn School of Pathology, University of Oxford made significant progress in showing the in vivo bactericidal action of penicillin. Their attempts to treat humans failed due to insufficient volumes of penicillin, but they proved its harmlessness and effect in mice. On 1942-03-14 John Bumstead and Orvan Hess became the first in the world to successfully treat a patient using penicillin\n\nDuring World War II, penicillin made a major difference in the number of deaths and amputations caused by infected wounds amongst Allied forces. Availability was severely limited, however, by the difficulty of manufacturing large quantities of penicillin and by the rapid renal clearance of the drug necessitating frequent dosing. Penicillins are actively secreted and about 80% of a penicillin dose is cleared within three to four hours of administration. During those times it became common procedure to collect the urine from patients being treated so that the penicillin could be isolated and reused. (Silverthorn, 2004)\n\nThis was not a satisfactory solution, however, so researchers looked for a way to slow penicillin secretion. They hoped to find a molecule that could compete with penicillin for the organic acid transporter responsible for secretion such that the transporter would preferentially secrete the competitive inhibitor. The uricosuric agent probenecid proved to be suitable. When probenecid and penicillin are concomitantly administered, probenecid competitively inhibits the secretion of penicillin, increasing its concentration and prolonging its activity. The advent of mass-production techniques and semi-synthetic penicillins solved supply issues, and this use of probenecid declined. (Silverthorn, 2004) Probenecid is still clinically useful, however, for certain infections requiring particularly high concentrations of penicillins. (Rossi, 2004)\n\nThe chemical structure of penicillin was determined by Dorothy Crowfoot Hodgkin in the early 1940s, enabling synthetic production. A team of Oxford research scientists led by Australian Howard Walter Florey and including Ernst Boris Chain and Norman Heatley discovered a method of mass producing the drug. Florey and Chain shared the 1945 Nobel prize in medicine with Fleming for this work. Penicillin has since become the most widely used antibiotic to date and is still used for many Gram-positive bacterial infections.\n\nAntibiotic resistance to penicillin was first observed in 1947, shortly after its introduction. Resistance to penicill
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The penicillins are beta lectam antibiotics.  They work by preventing bacteria from producing cell walls by blocking the transpeptidation reaction. The reaction cross links glycan linked peptide chains, and without these, the cell wall is no longer stong enough. Also they stimulate the release of bacterial enzymes called autolysins which degrade the cell wall.\n\nPenicillins act on gram positive bacteria, and some modern synthetic penicillins are able to penetrate the capsule and act on gram negative.\n\nTaking this into account, i would say thats as a group they are broad spectrum because they act on most gram positive indescrimenantly and some gram negative. However, individually, some in the group may be considered narrow because they only act on a small group.\n\nI hope that helps
544788
I'm glad I live in Canada, because it is really cheap here. I would ask your doctor for samples. Many doctors will give them to patients who don't have insurance, or the means to pay for medication.
33539
the first answer is a very good one, but for someone who may not be in the medical profession, penicillin can be inactivated by drinking pop,orange juice, activated charcoal, alcoholic beverages...many things. if you are a medical student sorry, if you aren't ask dr and pharmacist
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hi my name is Geeth Prajwal from India i hope this will help you\n\n\n\nIn order to be useful in treating human infections, antibiotics must selectively target bacteria for eradication and not the cells of its human host. Indeed, modern antibiotics act either on processes that are unique to bacteria--such as the synthesis of cell walls or folic acid--or on bacterium-specific targets within processes that are common to both bacterium and human cells, including protein or DNA replication. Following are some examples. \n\nMost bacteria produce a cell wall that is composed partly of a macromolecule called peptidoglycan, itself made up of amino sugars and short peptides. Human cells do not make or need peptidoglycan. Penicillin, one of the first antibiotics to be used widely, prevents the final cross-linking step, or transpeptidation, in assembly of this macromolecule. The result is a very fragile cell wall that bursts, killing the bacterium. No harm comes to the human host because penicillin does not inhibit any biochemical process that goes on within us. \n\nBacteria can also be selectively eradicated by targeting their metabolic pathways. Sulfonamides, such as sulfamethoxazole, are similar in structure to para-aminobenzoic acid, a compound critical for synthesis of folic acid. All cells require folic acid and it can diffuse easily into human cells. But the vitamin cannot enter bacterial cells and thus bacteria must make their own. The sulfa drugs such as sulfonamides inhibit a critical enzyme--dihydropteroate synthase--in this process. Once the process is stopped, the bacteria can no longer grow. \n\nAnother kind of antibiotic--tetracycline--also inhibits bacterial growth by stopping protein synthesis. Both bacteria and humans carry out protein synthesis on structures called ribosomes. Tetracycline can cross the membranes of bacteria and accumulate in high concentrations in the cytoplasm. Tetracycline then binds to a single site on the ribosome--the 30S (smaller) ribosomal subunit--and blocks a key RNA interaction, which shuts off the lengthening protein chain. In human cells, however, tetracycline does not accumulate in sufficient concentrations to stop protein synthesis. \n\nSimilarly, DNA replication must occur in both bacteria and human cells. The process is sufficiently different in each that antibiotics such as ciprofloxacin--a fluoroquinolone notable for its activity against the anthrax bacillus--can specifically target an enzyme called DNA gyrase in bacteria. This enzyme relaxes tightly wound chromosomal DNA, thereby allowing DNA replication to proceed. But this antibiotic does not affect the DNA gyrases of humans and thus, again, bacteria die while the host remains unharmed. \n\nMany other compounds can kill both bacterial and human cells. It is the selective action of antibiotics against bacteria that make them useful in the treatment of infections while at the same time allowing the host to live another day.
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Originally classified in the 1930s as Group D Streptococci, Enterococci were officially given genus status in 1984 after hybridization studies showed a more distant relationship to Streptococci. Enterococci are gram-positive, spherical bacteria that colonize in groups or chains. They are naturally found as part of the digestive tract flora in many organisms, including humans. They are robust microbes able to tolerate relatively high salt and acid concentrations. They also seem to be able to withstand low levels of detergents, explaining why inadequate cleaning procedures can promote Enterococcus infections.\n\nWhat is now recognized as pathogenic Enterococcus was studied as early as the late 1900s. Currently, Enterococcus infections account for 12% of all nosocomial infections, second only to E. coli. An Enterococcus infection can cause complicated abdominal infections, skin and skin structure infections, urinary tract infections and infections of the blood stream. These infections can be difficult to treat, particularly in cases where the strain involved has developed resistance to several antibiotics. Infection can be life threatening in such instances, especially if the patient is already immunodeficient. \n\nThere are two species of Enterococci which cause the symptoms described above, E. faecalis, which accounts for the majority of infections (79%), and E. faecium. In a study conducted between 1995 and 1997, data were collected from over 15,000 Enterococcus isolates. Of those, less than 2% of E. faecalis were found to be resistant to ampicillin and vancomycin, whereas 83% of the E. faecium isolates were resistant to ampicillin and 52% were resistant to vancomycin. \n\nE. faecium is known to have a resistance to several types of antibiotics including quinolones and aminoglycosides. Resistance to penicillin was first observed in E. faecium in 1983, and in 1988 the first cases of resistance to the "antibiotic of last resort", vancomycin, were detected in Europe. Vancomycin-resistant strains of E. faecium were reported in the US in 1989. Resistance to several antibiotics and tolerance for adverse conditions makes E. faecium a major concern for the medical community, which has dubbed this microbe a "supergerm".
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It is an antibiotic in the class cephalasporins.  If you are allergic to penicillin antibiotics there is a small chance you could be allergic to this too.  Generally it is used to treat a variety of infections (broad spectrum).  Check out rxlist.com for many frug questions.
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Penicillin is most effective against Gram positive bacteria, so any diseases caused by these bacteria may be treated with penicillin.  Some examples include strep throat, staph infections, and food poisoning caused by Listeria.
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The niosh pocket guide is free and has a lot of info but not LD50\n\nyou can do a MSDS search for the compound and that will give you the ld50, just be sure that the compound is in a similar product.
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It will depend on a number of things.\n\nFirst:  you can plate them on media without antibiotics and they still might conjugate, there is nothing magical about antibiotics that tells the bacteria time to make a sex pilus and have at it.\n\nSecond:  what are the mechanisms of resistance.  If the streptomycin resistance is a mutation to a chromosomal ribosome subunit-encoding gene (normally how that works), then it wont initiate conjugation, unless it happens to also have a Hfr plasmid integrated into the chromosome at the same time (which could then initiate conjugation of the entire chromosome).\nIf ampicilin resistance is due to a plasmid-borne beta lactamase gene, and that plasmid happens to be a F plasmid, or other conjugatable system, then it can potentially initiate conjugation.\n\nIf both resistances are contained on conjugatable plasmids of the same origin then they will most likely be incompatable with each other, and no conjugation will take place.\n\nThird:  Are we talking about the same species of bacteria or different species of bacteria?  It shouldn't be assumed that two different species will readily conjugate.\n\nFourth:  (This is more a theoretical concern than one that I know to be truly an issue)\n\nHow does the antibiotic work?  Lets say in your example, you have 1 strep resistant strain of E. coli and 1 amp resistant strain of E. coli.  If you plated in the presence of streptomycin, the amp resistant strain wouldn't be able to synthesize new proteins, and if there weren't cells already producing conjugation proteins prior to plating, then there won't be any conjugation either, as the streptmycin inhibits protein synthesis.\n\n1, 2 and 3 are concerns I know to be valid, 4 maybe is maybe isn't but occured to me as I was typign the rest of it.
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It is a bacteria.\n\nThe antibiotics we use to fight E. coli depend a bit on where the infection is. Different antibiotics tend to have different penetrations into various body parts.\n\nUrinary infections: we will use trimethoprim, amoxycillin&clavulanic acid combination, cephalexin\nKidney infections: often intravenous antibiotics eg amoxycillin&gentamicin IV or cephalexin/cephazolin/ampicillin instead of amoxycillin\n\nIn some cases we use norfloxacin or ciprofloxacin.
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multi drug resistant bacteria.ex---psuedomonas staphylococcus
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They do not sell OTC penicillin...but you can try Musinex.\nIt is OTC and will get rid of the mucus. Kinda pricy, but no where near prescption prices. Any pharmacy or grocery has it.
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Try calling the fda. There are operators who might be able to help you.\n\nor visit their website: http://www.fda.gov\n\nYou are talking about Antibiotics......\nThere are other antibiotics that work slightly differently... like MAcrolides (aZithromycin, Erythromycin),