Biomedical subjects

Reinaldo Salomao

Publications and source records attributed to Reinaldo Salomao.

10 recordsLinked to original sources

PubMed2006

Device-associated nosocomial infections in 55 intensive care units of 8 developing countries.

BACKGROUND: Health care-associated infections from invasive medical devices in the intensive care unit (ICU) are a major threat to patient safety. Most published studies of ICU-acquired infections have come from industrialized western countries. In a Centers for Disease Control and Prevention (CDC) National Nosocomial Infections Surveillance (NNIS) System report, the U.S. pooled mean rates of central venous catheter (CVC)-related bloodstream infections, ventilator-associated pneumonia, and catheter-associated urinary tract infections were 4.0 per 1000 CVC days, 5.4 per 1000 mechanical ventilator days, and 3.9 per Foley catheter days, respectively. OBJECTIVE: To ascertain the incidence of device-associated infections in the ICUs of developing countries. DESIGN: Multicenter, prospective cohort surveillance of device-associated infection by using the CDC NNIS System definitions. SETTING: 55 ICUs of 46 hospitals in Argentina, Brazil, Colombia, India, Mexico, Morocco, Peru, and Turkey that are members of the International Nosocomial Infection Control Consortium (INICC). MEASUREMENTS: Rates of device-associated infection per 100 patients and per 1000 device days. RESULTS: During 2002-2005, 21,069 patients who were hospitalized in ICUs for an aggregate 137,740 days acquired 3095 device-associated infections for an overall rate of 14.7% or 22.5 infections per 1000 ICU days. Ventilator-associated pneumonia posed the greatest risk (41% of all device-associated infections or 24.1 cases [range, 10.0 to 52.7 cases] per 1000 ventilator days), followed by CVC-related bloodstream infections (30% of all device-associated infections or 12.5 cases [range, 7.8 to 18.5 cases] per 1000 catheter days) and catheter-associated urinary tract infections (29% of all device-associated infections or 8.9 cases [range, 1.7 to 12.8 cases] per 1000 catheter days). Notably, 84% of Staphylococcus aureus infections were caused by methicillin-resistant strains, 51% of Enterobacteriaceae isolates were resistant to ceftriaxone, and 59% of Pseudomonas aeruginosa isolates were resistant to fluoroquinolones. The crude mortality rate for patients with device-associated infections ranged from 35.2% (for CVC-associated bloodstream infection) to 44.9% (for ventilator-associated pneumonia). LIMITATIONS: These initial data are not adequate to represent any entire country, and likely variations in the efficiency of surveillance and institutional resources may have affected the rates that were detected. CONCLUSIONS: Device-associated infections in the ICUs of these developing countries pose greater threats to patient safety than in U.S. ICUs. Active infection control programs that perform surveillance of infection and implement guidelines for prevention can improve patient safety and must become a priority in every country.

Catheterization, Central Venous↗

PubMed2006

TLR2, TLR4, CD14, CD11B, and CD11C expressions on monocytes surface and cytokine production in patients with sepsis, severe sepsis, and septic shock.

Bacterial recognition and induced cellular activation are fundamental for the host control of infection, yet the limit between protective and harmful response is still inexact. Forty-one patients were enrolled in this study: 14 with sepsis, 12 with severe sepsis, and 15 with septic shock. Seventeen healthy volunteers (HV) were included as control. The expression of TLR2, TLR4, CD14, CD11b, and CD11c was analyzed on monocytes surface in whole blood. sCD14 was measured in serum, and TNF-alpha, IL-6, and IL-10 cytokine levels were measured in PBMC supernatants after LPS, IL-1beta, and TNF-alpha stimuli by ELISA. An increase in sCD14 and a decreased mCD14 were found in patients as compared with HV (P < 0.001). However, no differences in the expression of TLR2, TLR4, and CD11c were found among the groups. A trend toward differential expression of CD11b was observed, with higher values found in patients with sepsis as compared with HV. A negative regulation of the inflammatory cytokine production was observed in patients with severe sepsis and shock septic in relation to sepsis and HV, regardless of the stimulus. No significant difference in IL-10 production was found among the groups. In this study, we show that the inflammatory response is associated with the continuum of clinical manifestations of sepsis, with a strong inflammatory response in the early phase (sepsis) and a refractory picture in the late phases (severe sepsis and septic shock). Correlation between cell surface receptors and cytokine production after IL-1beta and TNF-alpha stimuli and the observation of a single and same standard response with the different stimulus suggest a pattern of immunology response that is not dependent only on the expression of the evaluated receptors and that is likely to have a regulation in the intracellular signaling pathways.

Antigens, CD↗

PubMed2006

Bacterial recognition and induced cell activation in sepsis.

The pathogenesis of sepsis involves complex interaction between the host and the infecting microorganism. Recognition and processing of microorganism antigens are essential functions of the cells of innate immune systems, and will ultimately, through the antigen presentation to the cells of adaptive immunity and the synthesis and secretions of mediators, such as cytokines, drive a coordinated immune response. Neutrophils and monocytes will therefore function as sensing and effectors cells. Fundamental in this process is the ability to discriminate self from non-self molecules. Of major interest in sepsis is that the protective and damaging host responses are part of the same process, that is, the inflammatory response that controls the infection process also underscores many of the pathophysiological events of sepsis. Moreover, this is a dynamic process according to the continuum of sepsis and its complications; up and down regulation of cellular activities may be differently regulated in different tissues, different cells and even in different functions of the same cell. This review will focus on microorganism recognition and signalization in sepsis, with emphasis on the neutrophils and monocytes adaptation during the ongoing disease.

Animals↗

PubMed2006

Surviving sepsis campaign: a project to change sepsis trajectory.

Sepsis is an acute and severe disease associated with early and late high mortality, high and growing prevalence, and impressive costs. In October 2002, during the European Society of Intensive Care Medicine annual congress, the Surviving Sepsis Campaign was launched through a "Barcelona Declaration" -- a document calling critical care providers, governments, health agencies and lay people to join the fight against sepsis. The aim of the campaign was to reduce the sepsis mortality rate by 25% within 5 years (actually, this deadline has been ended from 2007 to 2009). In 2003, a group of international critical care and infectious disease experts in the diagnosis and management of infection and sepsis met to develop guidelines that the bedside clinician could use to improve the outcome of severe sepsis and septic shock. A comprehensive document created from the committee's deliberations was published in prestigious journals. Thus, the SSC is a global, multi-organizational initiative to fight sepsis and undoubtedly, this campaign is a historic step for critical care medicine. This paper highlights the recommendations and the strategies proposed by SSC to implement them in intensive care units.

Humans↗

PubMed2006

Pathogenesis-oriented targets for adjunctive therapy.

The outcome of patients with sepsis arises from multiple factors affecting both the host and the invading microorganisms. Even within the setting of adequate antimicrobial use, patients still die of sepsis. Thus, strategies focusing on further therapy targets are an important area of interest for basic and clinical research. Although such adjunctive sepsis therapy has failed to achieve consistent better survival rates so far, the progress in understanding of the pathophysiology of sepsis seen in recent years is so profound, that the possibility that a new and effective treatment may arise should be warmly considered. Indeed, it may be considered that efficacious interventions, such as early and vigorous fluid replacement, strict blood glucose control, low-dose corticosteroid reposition, protective mechanical ventilation and activated-protein C are pathogenic-oriented targets of therapy. In this paper we aim to review some aspects of the pathogenesis of sepsis, focusing on possible targets for adjunctive therapy. Published clinical trials and experimental data supporting such trials are commented on.

Animals↗

PubMed2003

Impaired production of interferon-gamma and tumor necrosis factor-alpha but not of interleukin 10 in whole blood of patients with sepsis.

It has been demonstrated that lipopolysaccharide (LPS)-induced cytokine response in patients with sepsis differ from the normal host, yet this has not been controlled for the presence of underlying disease. We studied the ability of LPS and killed gram-negative bacteria (GNB) to induce tumor necrosis factor (TNF)-alpha and interleukin (IL) 10, and of phytohemagglutinin (PHA) to induce interferon (IFN)-gamma, in whole blood from patients with sepsis (SP, n = 20), patients with matched underlying disease and without sepsis (control patients, n = 20), and healthy volunteers (HV, n = 20). LPS-induced TNF-alpha production was lower in SP (median = 638 pg/mL) compared with control patients (4060 pg/mL; P= 0.003), and control patients production was lower compared with HV (5329 pg/mL; P < 0.001). Pseudomonas aeruginosa-induced TNF-alpha production was lower in SP (1443 pg/mL) than in control patients (7319 pg/mL; P < 0.05), and was not different between control patients and HV (6612 pg/mL; P = 0.6). IFNy production was lower in SP (948 pg/mL) compared with control patients (5516 pg/mL; P < 0.001), and the control patients production was lower compared with HV (11,282 pg/mL; P < 0.001). IL-10 production was not different among the three groups. Down-regulation of TNF-alpha production in patients with sepsis, although not restricted to them, was more pronounced with LPS than with GNB. Although the presence of underlying disease may be involved in the regulatory mechanisms of host response, the use of controls with matched underlying diseases provides strong evidence for the septic condition in the down-regulation of inflammatory response in patients with sepsis.

Adult↗

PubMed2003

Distribution of naive and memory/effector CD4 + T lymphocytes and expression of CD38 on CD8 + T lymphocytes in AIDS patients with tuberculosis.

CD(4)(+) and CD(8)(+) T lymphocyte counts, naive and memory/effector CD(4)(+) T subpopulations, and the expression of CD(38) on CD(8)(+) T lymphocytes were evaluated in four groups: AIDS patients with tuberculosis (HIV/TB, n=14), HIV-1 infected patients (HIV, n=10), HIV-1 negative patients with tuberculosis (TB, n=20) and healthy controls (CTL, n=17). TB and HIV had fewer +CD(4)(+) T cells than CTL, with the lowest values observed in TB/HIV (p<0.001). No difference between groups was observed in the percentage of naive and memory/effector subpopulations in +CD(4)(+) T lymphocytes. TB (355 cells/ micro L) and HIV (517 cells/ micro L) had diverging effects on +CD(8)(+) T cell counts, with a marked depletion observed in HIV/TB (196 cells/ micro L). TB and HIV up-regulated CD(38) expression on CD(8)(+) T cells, a finding also present in TB/HIV. While the decrease of +CD(4)(+) T cell counts in HIV/TB may be attributed to HIV and tuberculosis, the decrease of +CD(8)(+) T cell counts is likely to be due to tuberculosis.

AIDS-Related Opportunistic Infections↗

PubMed2002

Influence of EDTA and heparin on lipopolysaccharide binding and cell activation, evaluated at single-cell level in whole blood.

BACKGROUND: The use of whole blood (WB) in studying lipopolysaccharide (LPS)-induced cellular activation preserves the milieu in which LPS-cell interaction occurs in vivo. However, little information is available on using such a system at a single-cell level. We evaluated LPS binding and cell activation in WB by using flow cytometry. The influence of heparin or EDTA as anticoagulants was also addressed. METHODS: Blood was obtained from healthy donors in EDTA and/or heparin tubes. Biotinylated LPS (LPSb) was used to evaluate cell binding of LPS in WB. Cells were surface stained with appropriate antibodies and LPSb was detected by adding streptavidin-allophycocyanin (APC). LPS-induced activation was evaluated by the expression of surface activation markers and by the detection of intracellular tumor necrosis factor-alpha (TNF-alpha). RESULTS: LPSb bound promptly to monocytes in EDTA- and heparin-treated blood. In EDTA-treated blood, membrane-bound LPSb decreased after 60 min of incubation, whereas it remained detectable in heparinized blood during the 6 h of incubation. LPS induced TNF-alpha and enhanced the expression of HLA-DR in monocytes, as well as the expression of CD69 in T and B lymphocytes. Induction of both TNF-alpha in monocytes and CD69 in lymphocytes was more efficient in heparinized blood. CONCLUSION: Detection of membrane-bound LPSb on monocytes differed in EDTA or heparin-treated blood, and cell activation was better obtained in heparinized blood.

Anticoagulants↗

PubMed2002

Peripheral blood mononuclear cell activation induced by Leptospira interrogans glycolipoprotein.

Leptospira interrogans glycolipoprotein (GLP) has been implicated in pathological and functional derangement seen in leptospirosis. The goal of this study was to evaluate GLP's ability to induce cellular activation, as assessed by cytokine production and expression of surface activation markers. GLP extracted from either pathogenic L. interrogans serovar Copenhageni or nonpathogenic Leptospira biflexa serovar Patoc (GLPp) was used to stimulate peripheral blood mononuclear cell cultures from healthy donors. Supernatant cytokine levels were measured by enzyme-linked immunosorbent assay. Expression of CD69 and HLA-DR on lymphocytes and monocytes, as well as lipopolysaccharide (LPS) binding, were measured by flow cytometry. At 6 h of incubation, GLP induced a significant rise in tumor necrosis factor alpha levels, which dropped progressively until 72 h of incubation. Interleukin-10 peak levels were obtained at between 24 and 48 h, with sustained levels until 72 h of incubation. The response magnitude was proportional to the GLP dose. CD69 expression on T lymphocytes and monocytes increased significantly, as did HLA-DR expression on monocytes. GLPp induced no CD69 or HLA-DR expression. GLP did not block biotinylated LPS binding to monocytes, suggesting that different pathways are used to induce cell activation. In conclusion, GLP induces cellular activation and may play a major role in the pathogenesis of leptospirosis.

Antigens, CD↗

PubMed2002

Lipopolysaccharide-cell interaction and induced cellular activation in whole blood of septic patients.

We used biotinylated LPS (LPSb) and flow cytometry to study LPS-monocyte interaction and LPS-induced cellular activation in whole blood from septic patients (SP). Expression of surface activation markers was evaluated on monocytes (HLA-DR) and T lymphocytes (CD69 and CD95), and intracellular TNF-alpha on monocytes. Saturating curve and kinetics of LPSb detection on monocytes were similar in SP and healthy volunteers (HV). LPSb bound to monocytes was detected after 5 min of incubation in both groups, with a more pronounced decay in SP. Monocytes from SP had a lower expression of HLA-DR as compared to HV, both constitutive and upon LPS stimulation. The proportion of monocytes producing TNF-alpha after LPS stimulus was higher in HV than SP (mean +/- SD = 25.2 +/- 14.2% and 2.2 +/- 2.6%, respectively, P < 0.001). LPS-induced CD69 on T CD8+ and CD8- lymphocytes was similar for patients and controls. Expression of CD95 on T lymphocytes was higher in SP as compared to HV on T CD8+ cells (GMFI, mean +/- SD = 22.3 +/- 14.6 and 8.6 +/- 5.0, respectively, P = 0.01) and CD8- cells (GMFI, mean +/- SD = 28.3 +/- 7.7 and 14 +/- 4.3 respectively, P < 0.001). Thus, monocytes and lymphocytes seem to respond differently to LPS in septic patients. Monocyte hyporesponsiveness appears not to be related to a decreased binding capacity of LPS, but rather to an impaired signal transduction.

Adolescent↗