Importance of Cell Wall Components of Gram-Positive Bacteria in Gram-Positive Septic Shock

Abstract

Over the past few years, there has been an increase in the incidence of bacteremia, sepsis and septic shock caused by Gram-positive organisms including Staphylococcus epidermis, Staphylococcus aureus and Streptococcus pyogenes [1, 2]. The bacteria most commonly implicated to be the cause of Gram-positive sepsis are (in descending order of frequency) Staphylococcus aureus, Streptococcus pneumonae, coagulasenegative Staphylococci, β-haemolytic Streptococci and Enterococci [1]. In patients with life-threatening Gram-positive shock, the events leading to septic shock may be triggered by cell wall components of these bacteria and/or by exotoxins released by these bacteria [3]. The fact that endotoxin (a component of Gram-negative bacteria) is not a prerequisite for causing septic shock is highlighted by the fact that in a canine model — in the absence of endotoxemia — Staphylococcus aureus causes cardiovascular abnormalities comparable to that caused by Escherichia coli [4]. Similarly, two other studies have concluded that there are no clinically important differences in the hemodynamic responses in patients with Gram-positive and Gram-negative sepsis [5, 6]. In contrast, however, Stewart et al. [7] have demonstrated differences in the alterations in pH, glucose, arterial oxygen pressure (PaO₂), heart rate, systemic vascular resistance and cardiac output in conscious rats receiving either Staphylococcus aureus or Escherichia coli.