Current treatment of sepsis and endotoxaemia

Bibliography

• VINCENT J-L: New therapies in sepsis. Chest (1997) 112:330S–338S.
   Google Scholar
• •None of the compounds investigated within new therapies for sepsis have consistently improved the outcome because Exp. Opin. Pharmacother. (2000) 1(6) the research approach has been too narrowly focused. Attempts to completely block the sepsis response deprive the host of an essential defence mechanism.
   Google Scholar
• NYSTROM P-0: The systemic inflammatory response syndrome: definitions and aetiology. J. Antimicrob. Chemother. (1998) 41 (Suppl. A) :1–7.
   Google Scholar
• GULLO A: Sepsis and organ dysfunction/failure. An overview. Minerva Anestiol. (1999) 65(7-8) :529–540.
   PubMedGoogle Scholar
• BONE RC, BALK RA, CERRA FB et al: American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest (1992) 101:1644–1655.
   PubMed Web of Science ®Google Scholar
• GLAUSER MP, HEUMANN D, BAUMGARTNER JD, COHEN J: Pathogenesis and potential strategies for prevention and treatment of septic shock: an update. Clin. Infect. Dis. (1994) 18 (Suppl. 2):S205–S216.
   Google Scholar
• NATANSON C, DANNER RL, ELIN RJ et al: Role of endotoxemia in cardiovascular dysfunction and mortality. Escherichia coli and Staphylococcus aureus challenges in a canine model of human septic shock. J. Clin. Invest. (1989) 83:243–251.
   Google Scholar
• CHABY R: Strategies for the control of LPS-mediated pathophysiological disorders. Drug Discov. Today (1999) 4(5):209–221.
   PubMed Web of Science ®Google Scholar
• FINCH RG: Design of clinical trials in sepsis: problems and pitfalls. J. Antimicrob. Chemother. (1998) 41 (Suppl. A):95–102.
   Google Scholar
• MICHIE HR: The value of animal models in the develop-ment of new drugs for the treatment of the sepsis syndrome. J. Antimicrob. Chemother. (1998) 41 (Suppl. A) :47–49.
   Google Scholar
• QUEZADO AMN, NATANSON C, ALLING DW et al: A controlled trial of HA-1A in a canine model of Gram-negative septic shock. j Am. Med. Assoc. (1993) 269:2221–2227.
   Web of Science ®Google Scholar
• PERITI P, MAZZEI T: Antibiotic-induced release of bacterial cell wall components in the pathogenesis of sepsis and septic shock: a review. J Chemother. (1998) 10 (6):427–448.
   PubMed Web of Science ®Google Scholar
• DINARELLO CA: Proinflammatory and anti-inflammatory cytokines as mediators in the pathogenesis of septic shock. Chest (1997) 112 (6):321S-329S.
   Google Scholar
• •Biological properties of IL-1 and TNF mimic host responses to infection, inflammation, injury or immunologic challenge. In animal models of systemic inflammation, such as septic shock, specific blockade of either IL-1 or TNF results in a reduction in the severity of the inflammatory response.
   Google Scholar
• PERITI P, MAZZEI T: New criteria for selecting the proper antimicrobial chemotherapy for severe sepsis and septic shock - Review article. Int. J Antimicrob. Chemother. (1999) 12:97–105.
   Google Scholar
• ••The risk of septic shock in a septic patient depends onwhether the patient is immunocompromised and on the dimension of the bacterial load, which can affect the efficacy (inoculum effect) of antimicrobial therapy administered. In the course of severe sepsis, it is very important to use antimi-crobial agents which induce rapidly and prevalently fragile aberrant cells or spheroplasts, and thus are rapidly bactericidal.
   Google Scholar
• PERITI P, MAZZEI T: Opinion - antimicrobial therapyfor sepsis and septic shock: time for a change. AntibioL Chemother. (1999) 3 (2) :15–16.
   Google Scholar
• NORIMATSU M, MORRISON DC: Correlation ofantibiotic-induced endotoxin release and cytokine production in Escherichia coli - inoculated mouse whole blood ex vivo. J. Infect. Dis. (1998) 17 7 :1302–1307.
   Google Scholar
• ENG RHK, CHERUBIN C, SMITH SM, BUCCINI F: Inoculumeffect of I3-lactam antibiotics on Enterobacteriaceae. Antimicrob. Agents Chemother. (1985) 2 8 (2):601–606.
   Google Scholar
• DAVEY PG, BARZA M: The inoculum effect withGram-negative bacteria in vitro and in vivo. J. Antimi-crob. Chemother. (1987) 20:639–644.
   PubMed Web of Science ®Google Scholar
• REILLY J, COMPAGNON A, TUORNIER P, BASTIN R,DUBUIT H: Izs accidents du traitment des fievres typhoides par la chloromycetine. Ann. Med. (Paris) (1950) 51:597–629.
   PubMedGoogle Scholar
• SHENEP JL, FLYNN PM, BARRETT FF, STIDHAM GL, WESTENKIRCHNER DF: Serial quantitation of endotoxemia and bacteremia during therapy for Gram-negative bacterial sepsis - Concise communica-tions. J. Infect. Dis. (1988) 15 7 (3) :565–568.
   Google Scholar
• FRIELING JTM, MULDER JA, HENDRIKS T, CURFS JHAJ,VAN DER LINDEN CJ, SAUERWEIN RW: Differential induction of pro-and anti-inflammatory cytokines in whole blood by bacteria: effects of antibiotic treatment. Antimicrob. Agents Chemother. (1997) 41 (7):1439–1443.
   PubMed Web of Science ®Google Scholar
• SHENEP JL, BARTON RP, MOGAN KA: Role or antibioticclass in the rate of liberation of endotoxin during therapy for experimental Gram-negative bacterial sepsis. J Infect. Dis. (1985) 151:1012–1018.
   PubMed Web of Science ®Google Scholar
• GEMMEL C, LORIAN V: Effects of low concentrations ofantibiotics on bacterial ultrastructure, virulence and susceptibility to immunodefenses: clinical signifi-cance. In: Antibiotics in Laboratory Medicine (4th Edition). Lorian V (Ed.), Williams and Wilkins, Baltimore, USA (1996):397–452.
   Google Scholar
• KIRIKAE T, NAKANO M, MORRISON DC: Antibiotic-induced endotoxin release from bacteria and its clinical significance - Review. Microbiol. Immunol. (1997) 41 (0285–294.
   PubMed Web of Science ®Google Scholar
• ENG RHK, HSIEH A, SMITH SM: Antibiotic killing ofbacteria: comparison of bacteria on surfaces and in liquid, growing and non-growing. Chemotherapy (1995) 41:113–120.
   PubMed Web of Science ®Google Scholar
• PUCCI MJ, BOICE-SOWEK J, KESSLER RE, DOUGHERTY TJ:Comparison of cefepime, cefpirome and cefaclidine binding affinities for penicillin-binding proteins in Escherichia coli K-12 and Pseudomonas aeruginosa 5C83 2 9. Antimicrob. Agents Chemother. (1 9 9 1) 35(10:2312-2317. Exp. Opin. Pharmacother. (2000) 1(6)
   Google Scholar
• LORIAN V: Phagocytosis of staphylococci after exposure to antibiotics. J. Antimicrob. Chemother. (1985) 16:129–133.
   PubMed Web of Science ®Google Scholar
• SATTA G, CORNAGLIA G, MAZZARIOL A, GOLINI G, VALISENA S, FONTANA R: Target for bacteriostatic and bactericidal activities of 13-lactam antibiotics against Escherichia coli resides in different penicillin-binding proteins. Antimicrob. Agents Chemother (1995) 39 (4):812–818.
   PubMed Web of Science ®Google Scholar
• ••I3-lactam antibiotics cause bactericidal effects of verydifferent intensities, depending on the PBPs that are partially or fully saturated. The intensity of the bactericidal effect is lowest when the antibiotics bound and saturated only one of the essential PBPs, higher when two of them were bound and highest when all three essential PBPs were saturated.
   Google Scholar
• HOLZHEIMER RG: The significance of endotoxin release in experimental and clinical sepsis in surgical patients - Evidence for antibiotic-induced endotoxin release? Infection (1998) 2 6 (2) :77–84.
   Google Scholar
• STRATTON CW: Mechanisms of action for antimicro-bial agents: general principles and mechanisms for selected classes of antibiotics. In: Antibiotics in Labora-tory Medicine (4th Edition). Lorian V (Ed.), Williams and Wilkins, Baltimore, USA (1996) :579–603.
   Google Scholar
• GOULD IM: Pharmacodynamics and the relationship between in vitro and in vivo activity of antimicrobial agents. J. Chemother. (1997) 9 (Suppl. 1):74–83.
   Google Scholar
• ••Optimal cidal activity of I3-lactam antibiotics may beachieved only when all crucial heavy weight PBPs are saturated, which may be at concentrations approaching 100, or even 1000, times the MIC, depending on factors such as the inoculum and specific binding site preferences. At these concentrations, spheroplasts form and rapid bacterial cell lysis occurs. Depending on the antibiotic, these high concentration levels can be achieved in vivo for many organisms but only at higher doses than are normally administered.
   Google Scholar
• LI RC, ZHU ZY: In vitromodels for prediction of antimi-crobial activity: a pharmacokinetic and pharmacody-namic perspective. J. Chemother. (1997) 9 (Suppl. 1):55–63.
   Google Scholar
• CRAIG WA: Interrelationship between pharmacoki-netics and pharmacodynamics in determining dosage regiments for broad-spectrum cephalosporins. Diagn. Microbiol. Infect. Dis. (1995) 22:89–96.
   PubMed Web of Science ®Google Scholar
• SCHENTAG J: Pharmacokinetic issues and implica-tions. 2nd European Congress of Chemotherapy and 7th Biennal Conference on Anti-infective Agents and Chemotherapy, May 10–13, 1998 Hamburg, Final Programme. Futuramed, Germany (1998)94.
   Google Scholar
• NITSCHE D, SCHULZE C, OESSER S, DALHOFF A, SACK M: Impact of different classes of antimicrobial agents on plasma endotoxin activity. Arch. Surg. (1996) 1 31 :192–199.
   Google Scholar
• CRAIG WA: Antimicrobial resistance issues of thefuture. Diagn. Microbiol. Infect. Dis. (1996) 25:213–217.
   PubMed Web of Science ®Google Scholar
• VOGELMAN B, GUDMUNDSSON S, LEGGETT J, TURNIDGE J, EBERT S, CRAIG WA: Correlation of antimi-crobial pharmacokinetic parameters with therapeutic efficacy in an animal model. J. Infect. Dis. (1988) 158:831–847.
   PubMed Web of Science ®Google Scholar
• HYATT JM, MCKINNON PS, ZIMMER GS, SCHENTAG JJ: The importance of pharmacokinetic/pharmacody-namic surrogate markers to outcome. Clin. Pharma-cokinel (1995) 28:143–160.
   PubMed Web of Science ®Google Scholar
• FORREST A, NIX DE, BALLOW CH, GOSS TF, BIRMINGHAM MC, SCHENTAG B: Pharmacodynamics of intravenous ciprofloxacin in seriously ill patients. Antimicrob. Agents Chemother. (1993) 37:1073–1081.
   PubMed Web of Science ®Google Scholar
• GOSS TF, FORREST A, NIX DE et al.: Mathematicalexamination of dual individual principles. II. The rate of bacterial eradication at the same area under the inhibitory curve is more rapid for ciprofloxacin than for cefmenoxime. Ann. Pharmacother. (1 99 4) 28:863–868.
   Google Scholar
• THOMAS JK, FORREST A, BHAVNANI SM et al.: Pharmaco-dynamic evaluation of factors associated with the development of bacterial resistance in acutely ill patients during therapy. Antimicrob. Agents Chemother. (1998) 42(3):521–527.
   PubMed Web of Science ®Google Scholar
• •The probability of developing bacterial resistance during therapy increases significantly when the antimicrobial exposure corresponds to an AUC0 24/MIC ratio of 100. Dosing regimens which provide a ratio of at least 100 appear to reduce the rate of the development of bacterial resistance intratherapy in acutely ill patients.
   Google Scholar
• TRAUTMANN M, ZICK R, RUKAVINA T, CROSS AS, MARRE R: Antibiotic-induced release of endotoxin: in vitro comparison of meropenem and other antibiotics. J Antimicrob. Chemother. (1998) 41:163–169.
   PubMed Web of Science ®Google Scholar
• YOURASSOWSKY E, VAN DER LINDEN MP, LISMONT MJ, CROKAERT F: Turbidimetric and microscopic analysis of Bacteroides fragilis exposed to tazobactam and pip eracillin alone and in combination. Chemotherapy (1990) 36:215–221.
   PubMed Web of Science ®Google Scholar
• QADRI SM, UENO Y, CUNHA BA: Susceptibility of clinical isolates to expanded-spectrum beta-lactams alone and in the presence of beta-lactamase inhibitors. Chemotherapy (1996) 42(5) :334–342.
   PubMed Web of Science ®Google Scholar
• BOHME A, SHAH PM, STILLE W, HOELZER D: Piper acillin /tazobactam versus cefepime as initial empirical antimicrobial therapy in febrile neutro-p enic patients: a prospective randomized pilot study. Eur. J. Med. Res. (1998) 3(7):324–330.
   PubMedGoogle Scholar
• FONTANA R, VALISENA S, CORNAGLIA G: Comparative affinities for penicillin-binding proteins of multipolar ionic amphoteric cephalosporins in Gram-negative bacteria. J Chemother. (1996) 8 (Suppl. 2):23–30.
   Google Scholar
• PERITI P, NICOLETTI P: Classification of beta-lactam antibiotics according to their pharmacodynamics. Chemother. (1999) 11(5) :323–330.
   Web of Science ®Google Scholar
• ••Different affinities of I3-lactam antibiotics for PBPs mayexplain the differences in grown bacterial patterns, suggesting three main responses to this kind of antimicro-bial agents. Three classes of agents are delineated by the extent of PBP pattern saturation, bacterial biomass increase, PAE length and initial killing power. Some antibiotics do not have the propensity to provoke septic shock because their Exp. Opin. Pharmacother. (2000) 1(6) mechanism of action is rapidly bactericidal, such as the carbapenems, the cephems ceftriaxone and cefepime, the glycopeptides, some aminoglycosides and fluoroquinolones.
   Google Scholar
• ARTENSTEIN AW, CROSS AS: Inhibition of endotoxin reactivity by aminoglycosides. J. Antimicrob. Chemother. (1989) 24(5):826–828.
   PubMed Web of Science ®Google Scholar
• FOCA A, MATERA G, IANNELLO D, BERLINGHIERI MC, LIBERTO MC: Aminoglycosides modify the in vitro metachromatic reaction and murine generalized Schwartzman phenomenon induced by Salmonella minnesota R595 lip opolysaccharide. Antimicrob. Agents Chemother. (1991) 35:2161–2164.
   PubMed Web of Science ®Google Scholar
• FOCA A, MATER G, BERLINGHIERI MC, LIBERTO MC, DE SARRO GB: Teicoplanin reduces in vitro reactivity and murine lethality of Salmonella minnesota R595 lipopolysaccharide. j Antimicrob. Chemother. (1992) 29:443–446.
   PubMed Web of Science ®Google Scholar
• FOCA A, MATERA G, BERLINGHIERI MC: Inhibition ofen do toxin-induced in terleukin 8 release by teicoplanin in human whole blood. Eur. J. Clin. Microbic)]. Infect. Dis. (1993) 12:940–944.
   PubMed Web of Science ®Google Scholar
• SIEDLAR M, SZCZEPANIK A, WIECKIEWICZ J, PITUCH-NOWOROLSKA A, ZEMBALA M: Vancomycin down-regulates lipopolysaccharide-induced tumour necrosis factor alpha (TNF-a) production and TNF-a-mRNA accumulation in human blood monocytes - Short communication. Immunopharma-cology (1997) 35:265–271.
   PubMed Web of Science ®Google Scholar
• HACK CE, HART M, STRACK VAN SCHIJNDEL RJM et al:Interleukin-8 in sepsis: relation to shock and inflam-matory mediators. Infect. Immun. (1992) 60:2835–2842.
   PubMed Web of Science ®Google Scholar
• KIRIKAE T, KIRIKAE F, SAITO S et al.: Biological charac-terization of endotoxins released from antibiotic-treated Pseudomonas aeruginosa and Escherichia coli. Antimicrob. Agents Chemother. (1998) 42 (5):1015–1021.
   PubMed Web of Science ®Google Scholar
• MOCK CN, JURKOVICH GJ, DRIES DJ, MATER RV: Clinical significance of antibiotic endotoxin-releasing proper-ties in trauma patients. Arch. Surg. (1995) 130:1234–1241.
   PubMedGoogle Scholar
• PRINS JM, VAN AGTMAEL MA, KUIJPER EJ, VAN DEVENTER SJF, SPEELMAN P: Antibiotic-induced endotoxin release in patients with Gram-negative urosepsis: a double-blind study comparing imipenem and ceftazidime. J Infect. Dis. (1995) 172:886–891.
   PubMed Web of Science ®Google Scholar
• PERITI P, MAZZEI T, DE GAUDIO AR, TONELLI F: Attuali orientamenti nella scelta e modalità di somministra-zione degli agenti antimicrobici per una razionale chemioterapia della sepsi grave. Farm. Ter. (1998) XV(1/2):3–23.
   Google Scholar
• STUERTZ K, SCHMIDT H, EIFFERT H, SCHWARTZ P, MADER M, NAU R: Differential release of lipoteichoic and teichoic acids from Streptococcus pneumoniae as a result of exposure to 13-lactam an rifamycins, trovafloxacin, quinupristin-dalfopristin. Antimicrob. Agents Chemother. (1998) 42 (2):277–281.
   PubMed Web of Science ®Google Scholar
• VAN DER BERG C, DE NEELING AJ, SCHOT CS, HUSTINX WNM, WEMER J, DE WILDT DJ: Delayed antibiotic-induced lysis of Escherichia coli in vitro is correlated with enhancement of LPS release. Scand. J Infect. Dis. (1992) 24:619–627.
   PubMedGoogle Scholar
• HORII T, KOBAYASHI M, SATO K, ICHIYANA S, OHTA M: An in vitro study of carbapenem-induced morpho-logical changes and endotoxin release in clinical isolates of Gram-negative bacilli. J. Antimicrob. Chemother. (1998) 41:435-442. Piero Periti
   Google Scholar