Summary
Synopsis
Teicoplanin is a glycopeptide antibiotic with a molecular structure which is related to that of vancomycin. Gram-positive bacteria such as staphylococci (including methicillinresistant strains), streptococci, enterococci and many anaerobic Gram-positive bacteria are susceptible to teicoplanin in vitro. Teicoplanin has an exceptionally long half-life, allowing once-daily intramuscular or intravenous administration.
Teicoplanin is clinically and bacteriologically effective against a wide variety of Grampositive infections such as septicaemia, endocarditis, skin and soft tissue infections and infections associated with venous catheters. The drug is equally efficacious against methicillinresistant and - susceptible staphylococci. Adverse effects with teicoplanin are generally limited to local effects or hypersensitivity reactions. While teicoplanin has the potential for ototoxicity and nephrotoxicity, the incidence appears to be quite low when recommended serum concentrations are maintained.
Teicoplanin is a valuable alternative to vancomycin, and providing controlled comparative studies prove equivalent safety and efficacy between the 2 glycopeptides the more easily administered teicoplanin should become the preferred antibacterial agent.
Antibacterial Activity
Gram-positive bacteria, including staphylococci (S. aureus, S. epidermidis, S. hominis, S. haemolyticus, S. saprophyticus), streptococci (S. pyogenes, S. pneumoniae, S. agalactiae, S. bovis, S. milled, S. mitis, S. sanguis, viridans Group streptococci, and Groups B, C, F and G streptococci), enterococci and many anaerobic Gram-positive bacteria (Clostridium difficile, Clostridium perfringens, Propionibacterium acnes, Listeria monocytogenes and Corynebacterium jeikeium) are susceptible to teicoplanin in vitro [minimum inhibitory concentration (MIC) < 4 mg/L]. β-Lactamase-producing and/or methicillin-resistant strains of staphylococci are generally equally susceptible to teicoplanin as are nonresistant strains. In general, MIC90 values for teicoplanin are the same or a 2-fold dilution lower than those of vancomycin against most susceptible species. However, teicoplanin is several times more potent an inhibitor of enterococci than is vancomycin, although vancomycin-resistant enterococci may be cross-resistant to teicoplanin. In some studies reduced susceptibility of coagulase-negative staphylococci to teicoplanin was observed, with 2 to 4 times more teicoplanin than vancomycin required for inhibition. Most such strains have proved to be S. haemolyticus when full identification has been performed.
Gram-negative bacteria are not susceptible to teicoplanin and vancomycin because these large polar molecules cannot penetrate the external lipid membranes of Gram-negative organisms to bind with the terminal acyl-D-alanyl-D-alanine of cell wall peptidoglycan building blocks. Inhibition of peptidoglycan polymerisation of susceptible species results in cell wall damage and eventually cell death, probably through the activities of cell wall hydrolytic enzymes. Surprisingly, several vancomycin-resistant strains of pigmented Bacteroides species (Gram-negative anaerobic bacteria) are highly susceptible to teicoplanin, and some strains of Neisseria gonorrhoeae are also susceptible.
The apparent in vitro activity of teicoplanin is more affected by changes in inocula, media and testing conditions than is that of vancomycin. Higher teicoplanin MICs are recorded for Gram-positive cocci in media containing serum, presumably because of differences in protein binding, and there is greater variation in apparent activity in agar than in broth/media. Coagulase-negative staphylococci are less susceptible when tested in Diagnostic Sensitivity Test agar than in Iso-Sensitest or Mueller-Hinton agar.
In general, teicoplanin is bactericidal against most species of Gram-positive cocci. However, results varied between studies depending on whether activity was assessed by minimum bactericidal activity or killing curves, with several reports suggesting that teicoplanin may be primarily bacteriostatic against coagulase-negative staphylococci.
As seen with vancomycin, synergy studies have shown that the combination of teicoplanin with rifampicin is generally additive or subadditive, and that teicoplanin antagonises ampicillin. However, aminoglycosides, imipenem, fosfomycjn and several other antibacterial drugs are synergistic with teicoplanin against some strains of Gram-positive cocci, the percentages of such strains so affected varying widely between studies.
The relative immunity of vancomycin to development of resistance in bacterial isolates encountered clinically, and the difficulty with which resistance to teicoplanin is induced in vitro, has suggested that resistance would not be a problem with these glycopeptide antibacterials. Unfortunately, more recent reports of teicoplanin and vancomycin resistance developing in vitro and in vivo to enterococci and coagulase-negative staphylococci have tempered this impression. More worrying still is the identification of a plasmid from Enterococcus faecium, which has the potential ability to self-transfer to E. faecalis, L. monocytogenes and several species of streptococci (S. sanguis, S. pyogenes, S. lactis), thus conferring glycopeptide resistance.
Pharmacokinetic Properties
Intravenous injection of teicoplanin 3 mg/kg and 6 mg/kg produced peak plasma concentrations of 53.5 and 111.8 mg/L, respectively, with similar dosage proportionality demonstrated in the areas under the concentration-time curves. Plasma concentrations decreased to approximately 4 mg/L at 24 hours and were still detectable (0.4 mg/L) at 10 days. Bioavailability following intramuscular injection of 3 mg/kg was 90%, with a peak plasma concentration of 7.1 mg/L at 2 hours and a trough of 2.3 mg/L at 24 hours. Teicoplanin was not significantly absorbed from the gastrointestinal tract.
A 3-compartment analysis has been most frequently utilised to describe teicoplanin pharmacokinetics, giving mean volumes of distribution at steady state ranging from 40 to 77L. Teicoplanin is approximately 90% protein bound. Following bolus administration of single 400mg intravenous doses, concentrations likely to be inhibitory to susceptible bacterial strains have been reported in blister fluid, gall bladder wall, bile, tonsils, cartilage, mucosa, liver, pancreas and bone; lower concentrations were achieved in fat, skin and cerebrospinal fluid. Urinary concentration was high (16 to 156 mg/L) during multiple-dose administration (200mg 12- or 24-hourly) and the drug was still detected (0.9 to 9 mg/L) the second week following discontinuation.
Teicoplanin is eliminated almost entirely by renal mechanisms and does not appear to undergo extensive metabolism. Total clearance and renal clearance are both consistently lower than that of creatinine, suggesting renal tubular reabsorption or a protein binding associated limitation of the fraction of free drug available for elimination. The elimination half-life varied widely depending on the pharmacokinetic model used and the duration of the sampling interval, but a value of 45 to 70 hours after single-dose administration is probably most accurate.
With decreasing renal function both total and renal clearances are reduced, and the elimination half-life is increased, but the volume of distribution is not affected. Teicoplanin is not removed by haemodialysis, and has a low clearance in continuous ambulatory peritoneal dialysis, failing to attain concentrations in peritoneal effluent which are likely to be inhibitory to bacteria implicated in peritonitis. However, intraperitoneal administration of teicoplanin 3 mg/kg into the dialysate resulted in approximately 70% absorption through noninflamed peritoneum during a 6-hour dwell time, with peak serum concentrations of 2.8 to 5.5 mg/L. Teicoplanin pharmacokinetics in elderly patients reflect the reduced renal function in this population, with reduced clearance of the drug and increased elimination half-life. Similarly, in neonates immaturity of renal and extra-renal excretory functions may result in decreased clearance and prolonged elimination half-life, although a recent study suggested an increased teicoplanin dosage may be required in this group. Pharmacokinetics in children aged 2 to 12 years are probably similar to those in normal adults, although an increased rate of total clearance (but not renal clearance) has been reported, with a correspondingly decreased elimination half-life.
Therapeutic Use
A large multicentre study assessing more than 1300 patients with Gram-positive infections reported teicoplanin clinical efficacy rates of 90% or more in infections of skin and soft tissue, urinary tract, upper and lower respiratory tract, gastrointestinal tract and in meningitis. Clinical efficacy was also achieved in 89% of patients with septicaemia, 87% with bone and joint infections and 83% with endocarditis. In this study, the overall clinical efficacy of teicoplanin, generally administered as a loading dose of 400mg on the first day followed by 200 to 400mg daily, was 92%. Efficacy was similar in adults, children and the elderly, and between those administered teicoplanin monotherapy and combination antibacterial therapy, but was lower in patients with diabetes mellitus, immuno-suppression, malignant diseases and in the presence of foreign bodies. A teicoplanin dosage of at least 400mg daily was more effective (p < 0.05) than a lower dosage in patients with endocarditis. Bacteriological cure was achieved in 79% of the 1333 patients.
A few studies have assessed the efficacy of teicoplanin in comparison with other anti-bacterials. An early study comparing teicoplanin 400mg initially, then 200mg daily, with flucloxacillin 2g 6-hourly in severe staphylococcal infections (most with concomitant septicaemia) was terminated after 0 of 9 patients who received teicoplanin, responded clinically (vs 8 of 9 flucloxacillin patients). In contrast, clinical efficacy rates of 92% and 100%, respectively, occurred with a higher dosage of teicoplanin (400mg daily) or vancomycin 1g twice daily in patients with severe methicillin-resistant 51. aureus infections, most of whom had concomitant septicaemia.
This apparent correlation of teicoplanin dosage with efficacy is further illustrated by the results of a noncomparative study in severely debilitated septicaemic patients, mostly with concomitant infective endocarditis or with an infected Hickman catheter; all 7 patients with streptococcal septicaemia were cured with a dosage of 400mg followed by 200mg daily, including 2 due to E. faecalis, but only 11 of 18 S. epidermidis and 2 of 6 S. aureus infections were cured. In a noncomparative study in endocarditis, teicoplanin 200mg daily was successful in the treatment of streptococcal but not staphylococcal infections, while teicoplanin 200 to 400mg daily and vancomycin lg twice daily were both 100% effective in patients with septicaemia associated with indwelling venous catheters.
Similarly, all 19 immunocompromised patients with staphylococcal Hickman catheter infections, 9 of which were associated with concomitant septicaemia, were cured with a teicoplanin dosage of 400mg initially, then 200mg daily; only 2 catheters had to be removed because of persistence of infection. Teicoplanin (400 or 800mg loading dose followed by 200 or 400mg daily) was of similar clinical efficacy to vancomycin 1g twice daily, alone or in combination with gentamicin plus piperacillin in the treatment of Gram-positive (mostly coagulase-negative staphylococci) Hickman catheter-associated infections in neutropenic patients with haematological malignancy. All septicaemias and most exit site infections were cured, but 60% of tunnel infections responded to teicoplanin and none to vancomycin.
Teicoplanin has also proven advantageous as part of an antibacterial regimen for empirical treatment of fever and suspected infection in immunologically compromised patients. Patients obtaining the greatest advantage from the addition of ‘antistaphylococca’ coverage are those with,profound and persistent neutropenia. Furthermore, in several case reports teicoplanin administered intraperitoneally in CAPD peritonitis, and intraventricularly in ventriculitis associated with neuroshunts, has demonstrated clinical efficacy.
Perioperative prophylaxis with teicoplanin alone (400mg at induction followed by 200mg at 24 hours or two 400mg doses within 24 hours) in cardiac surgery was not associated with the emergence of Gram-negative skin flora, but the lower dosage regimen was less effective than flucloxacillin plus tobramycin in preventing Gram-positive wound infections, despite being active against all of the organisms isolated, and was associated with a higher incidence of Gram-negative chest and urinary tract infections. The higher dosage teicoplanin regimen was associated with a similar incidence of wound and respiratory tract infections compared with flucloxacillin plus tobramycin, but even greater teicoplanin dosages may be justified in this indication. In prophylaxis of infection in orthopaedic implant surgery, preliminary results of a comparative study did not reveal statistically significant differences between a single preoperative dose of teicoplanin 400mg intravenously and 3 perioperative injections of cefuroxime 750mg.
In prophylaxis of septicaemia in dental patients, rates of bacterial isolation from blood cultures were greater in patients administered teicoplanin 200mg intramuscularly than in those administered amoxicillin 3g orally, but in a second study prophylaxis with teicoplanin 400mg intravenously was superior to amoxicillin 1g intramuscularly. Differences in achievable antibacterial serum concentrations related to dosage and to route and timing of administration probably explain the differing results.
Although findings in only small numbers of patients have been reported, teicoplanin 200mg orally 2 to 4 times daily for 3 to 12 days has been highly successful in the treatment of antibiotic-associated colitis and C. difficileassociated diarrhoea.
Adverse Effects
Adverse effects most frequently associated with teicoplanin are injection site intolerance and hypersensitivity, the latter usually limited to skin reactions but in some instances progressing to bronchospasm and anaphylactoid reaction. However, unlike vancomycin, teicoplanin may be administered rapidly without severe anaphylactoid effects; cross-reactivity between teicoplanin and vancomycin remains controversial. Teicoplanin also has the potential to cause ototoxicity and nephrotoxicity, although to date the incidence in teicoplanin patients not receiving concomitant oto- and/or nephrotoxic drugs is quite low and less than that associated with vancomycin. Similarly infrequent are reports of nonspecific adverse events such as tremor, tachycardia, headache, fatigue and diarrhoea. Transient elevation of liver enzymes may also occur.
Dosage and Administration
Teicoplanin is administered intramuscularly or intravenously (either rapid injection over 1 minute or more slowly by infusion) at a dosage sufficient to maintain trough serum concentrations of greater than 10 mg/L in severe infections. In adults with normal renal function a loading dose of 400mg (approximately 6 mg/kg) is administered on the first day, followed by once daily doses of 200 or 400mg on subsequent days; in life-threatening infections 6 to 12 mg/kg should be administered 12-hourly for the first day, followed by 6 mg/kg daily on subsequent days.
In children under 12 years, 3 doses of 10 mg/kg should be administered 12-hourly, followed by 6 mg/kg or 10 mg/kg daily according to the severity of infection. Doses of up to 12 mg/kg are recommended in granulocytopenic patients. Recent results have suggested teicoplanin 15 mg/kg on day 1 then 8 mg/kg/day may be required to maintain trough serum concentrations above 10 mg/L in neonates but this remains to be confirmed.
In acute or chronic renal impairment the normal recommended dosage of teicoplanin should be administered for the first few days, after which the dosage interval is modified to maintain trough serum concentrations of greater than 10 mg/L; 200 or 400mg daily or every 2 days in mild to moderate renal insufficiency, and 200 to 400mg every 2 to 3 days in severe renal insufficiency, should be adequate.
Peritonitis in patients undergoing CAPD is treated with teicoplanin 50mg in each 2L bag for the first 48 hours, then 25mg per 2L bag thereafter.
For prophylaxis of surgical infections, teicoplanin 400mg is administered intravenously at the induction of anaesthesia. In cardiac surgery additional 400mg doses are administered at the end of surgery and 24 hours later, although recent evidence suggests a higher dose regimen may be required for prophylactic efficacy in this indication.
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Various sections of the manuscript reviewed by: A.L. Barry, The Clinical Microbiology Institute Inc., Tualatin, Oregon, USA; J.E. Degener, Medische Microbiologie, Laboratorium voor de Volksgenzondheid in Friesland, Leeuwarden, The Netherlands; R. Fujii, Institute of Chemotherapy for Mother and Child, Tokyo, Japan; R.L. Greenman, Department of Medicine, Division of Infectious Diseases, University of Miami School of Medicine, Miami, Florida, USA; R.L. Greenwood, Department of Microbiology, University Hospital, Queen’s Medical Centre, Nottingham, England; H.C. Neu, Division of Infectious Diseases, Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, New York, USA; D. Pastel, Cedars-Sinai Medical Center, Los Angeles, California, USA; S.R. Smith, Magnetic Resonance Research Centre, Liverpool, England; Y. Van Laethem, Division of Infectious Diseases, St Pierre University Hospital, Brussels, Belgium; L. Verbist, Diagnostic Microbiology Laboratory, University Hospital S. Rafael, University of Leuven, Leuven, Belgium; A.P.R. Wilson, University College Hospital, Clinical Microbiology, London, England; D.J. Winston, Los Angeles, California, USA; R. Wise, Department of Medical Microbiology, Dudley Road Hospital, Birmingham, England.
An erratum to this article is available at http://dx.doi.org/10.1007/BF03259137.
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Campoli-Richards, D.M., Brogden, R.N. & Faulds, D. Teicoplanin. Drugs 40, 449–486 (1990). https://doi.org/10.2165/00003495-199040030-00007
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DOI: https://doi.org/10.2165/00003495-199040030-00007