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About TAZOCIN®

Indications1

  • Piperacillin/tazobactam is indicated for the treatment of the following systemic and/or local bacterial infections in which susceptible organisms have been detected or are suspected.
 
  • Lower respiratory tract infections; urinary tract infections (complicated and uncomplicated); intra-abdominal infections; skin and skin structure infections; bacterial septicemia.
 
  • Polymicrobic infections: piperacillin/tazobactam is indicated for polymicrobic infections including those where aerobic and anaerobic organisms are suspected (intra-abdominal, skin and skin structure, lower respiratory tract).
​​​​​​​
  • Piperacillin/tazobactam, in combination with an aminoglycoside, is indicated for bacterial infections in neutropenic adults or children.

Mechanism of action1

Piperacillin/tazobactam is an injectable antibacterial combination consisting of the semisynthetic antibiotic piperacillin sodium and the β-lactamase inhibitor tazobactam sodium for intravenous administration.

Piperacillin sodium exerts bactericidal activity by inhibiting septum formation and cell wall synthesis.

Tazobactam is a potent inhibitor of many class A β-lactamase (penicillinases, cephalosporinases and extended spectrum enzymes). It has variable activity against class A carbapenemases and class D β-lactamases. It is not active against most class C cephalosporinases and inactive against Class B metallo-β-lactamases.

Mechanism of resistance

There are three major mechanisms of resistance to β-lactam antibiotics:

  • Changes in the target PBPs resulting in reduced affinity for the antibiotics
  • Destruction of the antibiotics by bacterial β-lactamases
  • Low intracellular antibiotic levels due to reduced update or active efflux of the antibiotics

Risk factors

For multidrug-resistant (MDR) pathogens in ventilator-associated pneumonia (VAP) and hospital-acquired pneumonia (HAP)2

Risk factors for MDR VAP
  • Prior intravenous antibiotic use within 90 days
  • Septic shock at time of VAP
  • Acute respiratory distress syndrome (ARDS) preceding VAP
  • Five or more days of hospitalisation prior to the occurrence of VAP
  • Acute renal replacement therapy prior to VAP onset
Risk factors for MDR pseudomonas VAP/HAP
  • Prior intravenous antibiotic use within 90 days

The importance of adequate antimicrobial therapy in intensive care unit (ICU)

 Crude or infection-related mortality associated with initial inadequate therapy in critically ill ICU patients with sepsis3–6

Adapted from Retamar P, et al. Antimicrob Agents Chemother. 2012, Lueangarun S, et al. lnterdiscip Perspect on Infect Dis. 2012, Vazquez-Guillamet C, et al. Crit Care Med. 2014, Kumar A, et al. Chest. 2009.

Mortality rates from severe sepsis are high. Sepsis is one of the leading causes of death in the ICU.5

Gram negative microorganisms are the major cause of sepsis:5

  • Escherichia coli
  • Pseudomonas aeruginosa
  • Klebsiella spp.
References:Pfizer Malaysia Tazocin® EF Prescribing Information. Available at: https://labeling.pfizer.com/ShowLabeling.aspx?id=17746. Accessed on 15 July 2024.Kalil AC, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016;63(5):e61–e111;Retamar P, et al. Impact of inadequate empirical therapy on the mortality of patients with bloodstream infections: a propensity score-based analysis. Antimicrob Agents Chemother. 2012;56(1):472–78;Lueangarun S, et al. Impact of inappropriate empiric antimicrobial therapy on mortality of septic patients with bacteremia: a retrospective study. lnterdiscip Perspect on Infect Dis. 2012;2012:765205;Vazquez-Guillamet C, et al. Using the number needed to treat to assess appropriate antimicrobial therapy as a determinant of outcome in severe sepsis and septic shock. Crit Care Med. 2014;42(11):2342–2349;Kumar A, et al. Initiation of inappropriate antimicrobial therapy results in a fivefold reduction of survival in human septic shock. Chest. 2009;136(5):1237–48.
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