Biomedical subjects

S Sapatnekar

Publications and source records attributed to S Sapatnekar.

7 recordsLinked to original sources

PubMed2001

Methicillin-resistant Staphylococcus aureus sepsis associated with the transfusion of contaminated platelets: a case report.

BACKGROUND: Platelet transfusion-associated sepsis is usually due to donor skin flora introduced into the unit during phlebotomy. An unusual case of a platelet component contaminated with methicillin-resistant Staphylococcus aureus (MRSA) is reported. CASE REPORT: A 54-year-old man, terminally ill with progressive non-Hodgkin's lymphoma, developed fever and hypotension during a platelet transfusion. He was receiving multiple antibiotics, including vancomycin. Blood cultures taken soon after transfusion were negative. An aliquot taken from the platelet pool grew MRSA at a count of 1.6 x 10(8) CFUs per mL. One of the individual bags constituting the pool showed MRSA at a count of 5.1 x 10(8) CFUs per mL. The patient died soon after the platelet transfusion. This case was reported to the FDA and submitted to the BaCon Study. The identity of the isolate and its methicillin resistance were confirmed by the CDC as part of the BaCon Study protocol. The source of contamination of the implicated unit could not be established with certainty. CONCLUSION: The emergence of antimicrobial-resistant organisms poses additional challenges for the diagnosis and treatment of transfusion-associated sepsis. Measures to prevent or intercept the transfusion of contaminated platelets should be developed.

Blood Platelets↗

PubMed1997

Leukocyte-biomaterial interactions in the presence of Staphylococcus epidermidis: flow cytometric evaluation of leukocyte activation.

The adhesion of bacteria on a biomaterial surface is believed to be the first step in the development of biomaterial-related infection. The goal of this study was to investigate the mechanisms that permit adherent bacteria to persist on the surface of an implanted cardiovascular biomaterial. We hypothesized that circulating leukocytes are unable to adhere to the biomaterial surface under physiologic shear stress conditions, and this prevents them from interacting with adherent bacteria. To address this hypothesis, we investigated the adhesion profiles of Staphylococcus epidermidis and polymorphonuclear leukocytes (PMN), incubated under controlled shear stress conditions with the test biomaterial. We found that bacteria could adhere on the biomaterial surface, even when their concentration in the test medium was as low as 10(3) cfu/mL. At this concentration, the bacteria did not induce significant complement activation. PMN adhesion on the biomaterial surface was sensitive to shear stress and minimal at shear stress > 10 dynes/cm2. Low concentrations of bacteria could induce a significant increase in the expression of PMN adhesion molecules CD11b and CD11c. We conclude that the presence of bacteria induces PMN activation but does not increase PMN adhesion on biomaterial surfaces under physiologic shear stress conditions. This could be a major mechanism that protects adherent bacteria from PMN antibacterial activity.

Bacterial Adhesion↗

PubMed1996

Complement-mediated leukocyte adhesion on poly(etherurethane ureas) under shear stress in vitro.

Blood-contacting biomaterials may activate the complement cascade, thus promoting leukocyte adhesion to the biomaterial surface. We hypothesize that the extent of complement activation is modulated by biomaterial formulation and the presence of fluid shear stress. To investigate this hypothesis, we tested base poly(etherurethane ureas) formulated with or without Santowhite antioxidant, a nucleophilic additive. We found that adherent leukocyte densities decreased with increasing shear stress. Moreover, leukocyte adhesion was decreased significantly further by Santowhite additive under shear stress but not under static conditions. Monocytes showed a higher propensity for adhesion than did neutrophils under shear and static conditions. Under static conditions, adherent cells on the Santowhite-containing polyurethane had a slightly more activated morphology than those on the base polyurethane. Cell adhesion under shear stress was significantly decreased when C3 or fibronectin was depleted from the suspension medium. Santowhite additive increased Factor B adsorption to the test surface while shear stress increased Factor H adsorption. The combination of Santowhite additive and shear stress increased the adsorption of both Factor B and Factor H and the serum protein S-terminal complement complex levels, but it did not further increase the state of activation of adherent cells. We conclude that leukocyte adhesion on poly(etherurethane urea) surfaces is sensitive to the levels of shear stress and that both C3 and fibronectin are required to maintain adhesion in the presence of shear stress. The low state of cellular activation and increased Factor H adsorption may explain the decreased adherent leukocyte density on the Santowhite-containing polyurethane.

Biocompatible Materials↗

PubMed1996

Surface-bound heparin fails to reduce thrombin formation during clinical cardiopulmonary bypass.

The hypothesis that heparin-coated perfusion circuits reduce thrombin formation and activity; fibrinolysis; and platelet, complement, and neutrophil activation was tested in 20 consecutive, randomized adults who had cardiopulmonary bypass. Twenty identical perfusion systems were used; in 10, all blood-contacting surfaces were coated with partially degraded heparin (Carmeda process; Medtronic Cardiopulmonary, Anaheim, Calif.). All patients received a 300 U/kg dose of heparin. Activated clotting times were maintained longer than 400 seconds. Cardiopulmonary bypass lasted 36 to 244 minutes. Blood samples for platelet count, platelet response to adenosine diphosphate, plasma beta-thromboglobulin, inactivated complement 3b, neutrophil elastase, fibrinopeptide A, prothrombin fragment F1.2, thrombin-antithrombin complex, tissue plasminogen activator, plasminogen activator inhibitor-1, plasmin alpha 2-antiplasmin complex, and D-dimer were obtained at these times: after heparin was given, 5 and 30 minutes after cardiopulmonary bypass was started, within 5 minutes after bypass was stopped, and 15 minutes after protamine was given. After cardiopulmonary bypass, tubing segments were analyzed for surface-adsorbed anti-thrombin, fibrinogen, factor XII, and von Willebrand factor by radioimmunoassay. Heparin-coated circuits significantly (p < 0.001) reduced platelet adhesion and maintained platelet sensitivity to adenosine diphosphate (p = 0.015), but did not reduce release of beta-thromboglobulin. There were no significant differences between groups at any time for fibrinopeptide A, prothrombin fragment F1.2, or thrombin-antithrombin complex or in the markers for fibrinolysis: D-dimer, tissue plasminogen activator, plasminogen activator inhibitor-1, and alpha 2-antiplasmin complex. In both groups, concentrations of prothrombin fragment F1.2 and thrombin-antithrombin complex increased progressively and significantly during cardiopulmonary bypass and after protamine was given. Concentrations of D-dimer, alpha 2-antiplasmin complex, and plasminogen activator inhibitor-1 also increased significantly during bypass in both groups. Fibrinopeptide A levels did not increase during bypass but in both groups increased significantly after protamine was given. No significant differences were observed between groups for levels of inactivated complement 3b or neutrophil elastase. Radioimmunoassay showed a significant increase in surface-adsorbed antithrombin on coated circuits but no significant differences between groups for other proteins. We conclude that heparin-coated circuits used with standard doses of systemic heparin reduce platelet adhesion and improve platelet function but do not produce a meaningful anticoagulant effect during clinical cardiopulmonary bypass. The data do not support the practice of reducing systemic heparin doses during cardiac operations with heparin-coated extracorporeal perfusion circuitry.

Anticoagulants↗

PubMed1995

Blood-biomaterial interactions in a flow system in the presence of bacteria: effect of protein adsorption.

An in vitro continuous flow system with whole human blood was used to study blood-biomaterial interactions on a base polyurethane and three modified surfaces in the presence and absence of circulating Staphylococcus epidermidis. We hypothesized that the composition of the protein layer adsorbed on the surface of the biomaterial would influence the response of blood components and bacteria. We examined the test surfaces for adsorption of nine plasma proteins and adsorption profiles differed on the four surfaces. The positively charged surface, UC, adsorbed significantly higher amounts of fibronectin (P < .01), von Willebrand factor (P < .01), and fibrinogen (P < .05) than the other materials. As a consequence of increased adsorption of these adhesive proteins, the adhesion of platelets and bacteria was greater on UC than on any other surface. On the base polyurethane, BC, and the negatively charged surface, UA, protein adsorption was low, and these materials were largely free of adherent blood cells and bacteria. The heparinized surface, UH, adsorbed higher quantities (P < .01) of Hageman factor and high molecular weight kininogen relative to the other surfaces. Platelet adhesion, and surface coagulation were prominent on UC, and may have contributed to increased bacterial adhesion on this surface. In the presence of circulating bacteria, adsorption was generally lower than in the absence of bacteria. The pattern of protein adsorption was largely unaffected by the strain of circulating bacteria, but platelet responses (adhesion and activation) were greater in the presence of slime-producing S. epidermidis as compared to the non-slime-producing strain, suggesting that slime may have a direct activating effect on platelets.

Adsorption↗

PubMed1995

Bacteria/blood/material interactions. I. Injected and preseeded slime-forming Staphylococcus epidermidis in flowing blood with biomaterials.

Blood-material interactions were studied using in vitro recirculation with human blood, slime-forming Staphylococcus epidermidis, and cardiovascular materials. Staphylococcus epidermidis, under preseeded or injected conditions, adhered to nonsmooth materials and elevated plasma levels of fibrinopeptide A (FpA) and C3a in the presence of all materials. Increased white blood cell (WBC) and platelet adhesion and thrombospondin and platelet factor 4 (PF4) release were noted for respective materials in the presence of injected bacteria. Materials that adhered significant quantities of injected S. epidermidis exhibited low levels of adsorbed proteins. Materials with high levels of preseeded S. epidermidis showed high levels of adsorbed proteins. Adhesion of preseeded bacteria and blood plasma elevations of C3a and FpA were lowest on semicrystalline polymer substrates, intermediate on halogenated substrates, and highest on amorphous substrates. In the presence of injected bacteria, WBCs and platelets adhered at earlier recirculation times to amorphous substrates than to semicrystalline substrates.

Bacterial Adhesion↗

PubMedDate not supplied

Impact of prolonged saline solution prime exposure on integrity of extracorporeal membrane oxygenation circuits.

OBJECTIVE: Our purpose was to evaluate the safety of the common practice of preparing extracorporeal membrane oxygenation (ECMO) circuits in advance with saline solution priming by analysis of the surfaces of circuit components and analysis of the prime solution for toxic contaminations. STUDY DESIGN: In vitro analysis of eight ECMO circuits exposed to saline prime solution for 0, 2, or 4 weeks was performed with scanning electron microscopy. Prime solution analyzed for contamination with aluminum, silicone, and diethylhexylphthalate. RESULTS: The silicone membrane and heat exchanger demonstrated surface degradation in contact with saline solution. The prime solution showed increasing concentrations of both aluminum and silicone but not diethylhexylphthalate over time. CONCLUSIONS: Advance preparation of ECMO circuits by prepriming with normal saline solution leads to significant circuit degradation. Prepriming should be avoided.

Aluminum↗