Vancomycin

Gefahreninformationscode (GHS)

• Bildanzeige (GHS)

  

• Alarmwort

  Achtung

• Gefahrenhinweise

  H334：Kann bei Einatmen Allergie, asthmaartige Symptome oder Atembeschwerden verursachen.

• Sicherheit

  P261：Einatmen von Staub vermeiden.

  P285：Bei unzureichender Belüftung Atemschutz tragen.

  P304+P341：BEI EINATMEN: Bei Atembeschwerden an die frische Luft bringen und in einer Position ruhigstellen, die das Atmen erleichtert

  P342+P311：Bei Symptomen der Atemwege: GIFTINFORMATIONSZENTRUM/Arzt/... (geeignete Stelle für medizinische Notfallversorgung vom Hersteller/Lieferanten anzugeben) anrufen.

  P501：Inhalt/Behälter ... (Entsorgungsvorschriften vom Hersteller anzugeben) zuführen.

Vancomycin Chemische Eigenschaften,Einsatz,Produktion Methoden

• Beschreibung

  Vancomycin is produced by fermentation of Amycol atopsis orientalis (formerly Nocardi a orientalis). It has been available for approximately 40 years, but its popularity has increased significantly with the emergence of MRSA in the early 1980s. Chemically, vancomycin has a glycosy lated hexapeptide chain that is rich in unusual amino acids, many of which contain aromatic rings cross-linked by aryl ether bonds into a rigid molecular framework.

• Originator

  Vancocin,Lilly,US,1958

• Verwenden

  Antibacterial.

• Verwenden

  Vancomycin is used for serious bacterial infections caused by microorganisms sensitive to this drug when penicillins and cephalosporins are ineffective for diseases such as sepsis, endocarditis, pneumonia, pulmonary abscess, osteomyelitis, meningitis, and enterocolitis, or when penicillins and cephalosporins cannot be tolerated by patients. Vancomycin is the drug of choice for infections caused by methicillin-resistant forms of S. aureus, S. epidermidus, and other coagulase-negative staphylococci, as well as for endocarditis, diphtherioid infections, and for patients very sick with colitis caused by C. difficile. A synonym of this drug is vancocin.

• Definition

  ChEBI: A complex glycopeptide from Streptomyces orientalis. It inhibits a specific step in the synthesis of the peptidoglycan layer in the Gram-positive bacteria Staphylococcus aureus and Clostridium difficile.

• Manufacturing Process

  An agar slant is prepared containing the following ingredients: 20 grams starch, 1 gram asparagine, 3 grams beef extract, 20 grams agar, and 1 liter water. The slant is inoculated with spores of S. orientalis, Strain M43-05865, and is incubated for about 10 days at 30°C. The medium is then covered with sterile distilled water and scraped to loosen the spores. The resulting suspension of spores is preserved for further use in the process.
  A liquid nutrient culture medium is prepared containing the following ingredients: 15 grams glucose, 15 grams soybean meal, 5 grams corn steep solids, 2 grams sodium chloride, 2 grams calcium carbonate, and 1 liter water. The medium is sterilized at 120°C for about 30 minutes in a suitable flask and cooled. 10 ml of a spore suspension prepared as set forth above are used to inoculate the medium. The inoculated medium is shaken for 48 hours at 26°C on a reciprocating shaker having a 2-inch stroke, at 110 rpm. The fermented culture medium which comprises a vegetative inoculum is used to inoculate a nutrient culture medium containing the following ingredients: 20 grams blackstrap molasses, 5 grams soybean peptone, 10 grams glucose, 20 grams sucrose, 2.5 grams calcium carbonate, and 1 liter water.
  The medium is placed in a container having a suitable excess capacity in order to insure the presence of sufficient oxygen and is sterilized by heating at 120°C for about 30 minutes. When cool, the medium is inoculated with about 25 ml of a vegetative inoculum as described above, and the culture is then shaken for about 80 hours at 26°C. The pH of the medium at the beginning of fermentation ranges from about 6.5 to about 7.0 and the final pH is about 7.0 to about 8.0. A fermentation broth thus obtained contained about 180 μg of vancomycin per ml.

• Trademarks

  Vancocin Hydrochloride (ViroPharma); Vancoled (Baxter Healthcare); Vancor (Pharmacia & Upjohn).

• Therapeutic Function

  Antibacterial

• Acquired resistance

  Only very recently, despite decades of intensive use, have some vancomycin-resistant bacteria emerged (vancomycin-resistant enterococcus [VRE] and vancomycin-resistant Staphylococcus aureus) [VRSA]. It is alleged that these resistant strains emerged as a consequence of the agricultural use of avoparcin, a structurally related antibiotic that has not found use for human infections in the United States but was used in Europe before its recent ban. The mechanism of resistance appears to be alteration of the target D-alanyl-D-alanine units on the peptidoglycan cell wall precursors to D-alanyl-D-lactate. This results in lowered affinity for vancomycin due to lack of a key hydrogen bonding interaction. It is greatly feared that this form of resistance will become common in the bacteria for which vancomycin is presently the last sure hope for successful chemotherapy. If so, such infection would become untreatable. These resistant strains are not yet common in clinically relevant strains, but most authorities believe that this is only a question of time. Vancomycin-intermediate S.aureus, also called glycoprotein-intermediate S.aureus (VISA), also has been reported. It appears to be resistant because of a thickened peptidoglycan layer.

• Mechanism of action

  Vancomycin is a bacterial cell wall biosynthesis inhibitor. Evidence suggests that the active species is a homodimer of two vancomycin units. The binding site for its target is a peptide-lined cleft having high affinity for acetyl-D-alanyl-D-alanine and related peptides through five hydrogen bonds. It inhibits both transglycosylases (inhibiting the linking between muramic acid and acetyl glucosamine units) and transpeptidase (inhibiting peptide cross-linking) activities in cell wall biosynthesis. Thus, vancomycin functions like a peptide receptor and interrupts bacterial cell wall biosynthesis at the same step as the β-lactams do, but by a different mechanism. By covering the substrate for cell wall transamidase, it prevents cross-linking resulting in osmotically defective cell walls.

• Clinical Use

  Vancomycin was discovered, developed, and approved by the US Food and Drug Administration in the 1950s. In 1956, it was introduced in the USA as a possible treatment for infections due to penicillinresistant S. aureus, but it was not used widely because of toxicity and the nearly simultaneous development of semisynthetic antibiotics and cephalosporins. Thus, its main indication was the treatment of serious Gram-positive infections in penicillin-allergic patients. In clinical practice, however, nafcillin remained the treatment of choice for staphylococcal bacteremia, largely because it had failure rates of only 4%. With the appearance of methicillin-resistant S. aureus and coagulase-negative staphylococci, vancomycin became the drug of choice for these infections. With the recognition and/or emergence of S. aureus strains (generally MRSA isolates) with reduced susceptibility to vancomycin 586 Glycopeptides and Lipopeptides, vancomycin efficacy may be less in some clinical situations than previously reported – especially in serious deep-seated infections, such as endocarditis and prosthetic device infections. This is demonstrated by increased mortality seen in patients with MRSA infection and markedly attenuated vancomycin efficacy caused by vancomycin heteroresistance in S. aureus. Resistance of S. aureus to vancomycin can be a continuous phenomenon, rather than a categorical one. Thus, this has resulted in some clinical microbiology laboratories having difficulty identifying S. aureus strains that have reduced vancomycin susceptibility based on standard laboratory susceptibility testing methodology. A better understanding is still needed of the pharmacodynamic relationship between vancomycin and MRSA as relates to optimal dosing strategies, including consideration of loading doses.

• Clinical Use

  Although a number of adverse effects can result from IV infusion, vancomycin has negligible oral activity. It can be used orally for action in the GI tract, especially in cases of Cl ostri di um difficile overgrowth. The useful spectrum is restricted to Gram-positive pathogens, with particular utility against multiply-resistant, coagulase-negative staphylococci and MRSA, which causes septicemias, endocarditis, skin and soft-tissue infections, and infections associated with venous catheters.

• Nebenwirkungen

  Vancomycin is highly associated with adverse infusion-related events. These are especially prevalent with higher doses and a rapid infusion rate. A rapid infusion rate has been shown to cause anaphylactoid reactions, including hypotension, wheezing, dyspnea, urticaria, and pruritus. A significant drug rash (the so-called red man syndrome) also can occur. These events are much less frequent with a slower infusion rate. In addition to the danger of infusion-related events, higher doses of vancomycin can cause nephrotoxicity and auditory nerve damage. The risk of these effects is increased with elevated, prolonged concentrations, so vancomycin use should be monitored, especially in patients with decreased renal function. The ototoxicity may be transient or permanent and more commonly occurs in patients receiving high doses, patients with underlying hearing loss, and patients being treated concomitantly with other ototoxic agents (i.e., aminoglycosides).

• Arzneimittelwechselwirkung

  Potentially hazardous interactions with other drugs
  Antibacterials: increased risk of nephrotoxicity and ototoxicity with aminoglycosides, capreomycin or colismethate sodium; increased risk of nephrotoxicity with polymyxins.
  Ciclosporin: variable response; increased risk of nephrotoxicity.
  Diuretics: increased risk of ototoxicity with loop diuretics.
  Muscle relaxants: enhanced effects of suxamethonium.
  Tacrolimus: possible increased risk of nephrotoxicity

• Stoffwechsel

  Little or no metabolism of vancomycin is thought to take place. It is excreted unchanged by the kidneys, mostly by glomerular filtration. There is a small amount of nonrenal clearance, although the mechanism for this has not been determined.

Vancomycin Upstream-Materialien And Downstream Produkte

Vancomycin Anbieter Lieferant Produzent Hersteller Vertrieb Händler.

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