Interleukin-10 is a potent macrophage-deactivating cytokine that inhibits lipopolysaccharide-induced tumor necrosis factor production. We determined the plasma levels of immunoreactive interleukin-10 in 16 patients with septic shock and in 11 patients with circulatory shock of nonseptic origin. In septic shock, interleukin-10 levels peaked during the first 24 h (median: 48 pg/ml) and decreased progressively till Day 5. In nonseptic shock, interleukin-10 plasma levels also increased during the first 24 h but to a lesser extent (median: 17 pg/ml). In septic shock patients, interleukin-10 plasma levels were positively correlated with tumor necrosis factor (r = 0.8, p = 0.01) and with parameters of shock severity including lactate levels (r = 0.56, p < 0.05) and correlated negatively with blood platelet counts (r = -0.65, p < 0.05). The decreased production of tumor necrosis factor-alpha and interleukin-6 after in vitro incubation of whole blood from septic shock patients with lipopolysaccharide was not influenced by in vitro neutralization of interleukin-10. We conclude that interleukin-10 is produced in patients with circulatory shock of septic and nonseptic origin and that the production of this anti-inflammatory cytokine during septic shock correlates positively with the intensity of the inflammatory response.

Coagulase-negative staphylococci (CNS) form part of the skin flora and commonly cause nosocomial bloodstream and catheter-related infections [l]. The increasing use of intravascular catheters and the high number of immunocompromised patients contribute to the importance of CNS as a cause of catheter-related infection. It is commonly assumed that catheter-related bloodstream infection arises from multiplication of a single infecting clone of CNS, whereas blood-culture contamination by skin flora is polyclonal, reflecting the diversity of CNS clones colonizing the skin [2]. However, there are recent reports of polyclonal endocarditis with multiple species or strains of CNS [3,4]. Different strains of CNS may exhibit the same morphology and since identification tests are usually made from a single colony, the true extent of infection remains to be investigated by identification and typing of different isolates from the same samples. Molecular fingerprinting methods can be used to investigate whether blood-culture isolates of CNS represent bacteremia or contamination. We describe a case of catheter-related bacteremia with polyclonal infection by Staphylococcns epidermidis and Staphylococcus hominis documented by molecular identification based on tRNA gene spacer polymorphism [5] and genotyping based on IS256 spacer polymorphism 161.A 58-year-old women suffering from a common acute lymphocytic leukemia diagnosed 6 months previously was receiving chemotherapy treatment through a totally implanted central venous catheter. This patient had neutropenia (total leukocytes 700/p,L, with 89% neutrophils) and developed fever (39.5"C) complicated by septic shock and hypotension (blood pressure: 8 mmHg systolic and 4 mmHg diastolic), which led to her admittance to the intensive care unit. Blood tests showed a CRP level of 26 mg/mL, and a fibrinogen level of 902 mg/mL. On the same day, two quantitative comparative blood samples were taken by reflux from the catheter and from a peripheral vein. As described previously [7], 1.

A 26-year-old woman receiving intrathecal chemotherapy for acute leukemia developed Ommaya-catheter-associated cerebritis and bacteremia caused by two clones of Staphylococcus epidermidis. Genomic fingerprinting of 19 staphylococcal isolates from the cerebrospinal fluid, blood, catheter and skull biopsy was necessary to establish the etiologic diagnosis and to guide medical and surgical therapy.