Daniel Smith

Detection of bacterial contamination in prestorage culture-negative apheresis platelets on day of issue with the Pan Genera Detection test.

BACKGROUND: Bacterial contamination is currently the most important infectious risk associated with transfusion of platelet (PLT) products. Prestorage culture has reduced but not eliminated this problem.

Fatal transfusion‐transmitted Babesia microti in the Midwest

Fatal transfusion-transmitted Babesia microti is rare. Because it is not uniformly reported, its incidence can only be estimated at less than 1:1,000,000 per red blood cell (RBC)-containing product. Transfusion transmission usually occurs in northeastern United States with more than 50 cases now reported. The disease is usually asymptomatic; however, in asplenic, elderly, or immunosuppressed individuals, it may be fatal. This fatal case is unique because it was contracted in Indiana from an Indiana donor. A 61-year-old woman with end-stage renal disease and congestive heart failure received 4 RBC units for lower gastrointestinal bleeding. Subsequently, she complained of nausea and fever to 39.4°C. Approximately 15 percent of her RBCs contained trophozoites, which were reduced to 1 to 2 percent by RBC exchange. Her treatment included intravenous quinidine and clindamycin and then converted to quinine. Unfortunately, disseminated intravascular coagulation and septic shock developed, and she expired within 1 week. No autopsy was performed. One of the transfused units showed evidence of B. microti infestation by immunofluorescence antibody, immunoglobulin M 1:20, and immunoglobulin G of more than 1:256. Her only risk factor was transfusion, and B. microti was confirmed by the Centers for Disease Control and Prevention morphologically, serologically, and by polymerase chain reaction. The implicated asymptomatic donor recalled exposure to wooded areas but not a tick bite and was permanently deferred.The photomicrograph illustrates polyparasitism with tetrad or Maltese cross formation and polymorphism, all characteristic of Babesia infection.

Ethanol effects on local cerebral glucose utilization in high-alcohol-drinking and low-alcohol-drinking rats

Divergent ethanol-drinking behavior in rats selectively bred for high- or low-ethanol-drinking behavior could be related to differences in the sensitivity of the CNS to ethanol. In the current study, we examined the effects of acute (i.e., single injection) ethanol administration on local cerebral glucose utilization (LCGU) within selected brain regions of high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats. Adult, male, HAD and LAD rats from replicate line 2 were injected intraperitoneally with saline, or ethanol, at doses of 0.25 g/kg or 1.0 g/kg, during their dark cycle; 10 min later, [14C]-2-deoxyglucose ([14C]-2-DG; 125 microCi/kg) was injected into the femoral vein. Timed arterial blood samples were collected over 45 min and assayed for plasma glucose, ethanol, and [14C]-2-DG levels. Rats were then decapitated, and their brains were quickly extracted and frozen in isopentane at -50 degrees C. Coronal brain sections were prepared and apposed to x-ray film for 2 days, and image densities were determined by using quantitative autoradiography. Data were collected from several key limbic (nucleus accumbens, ventral tegmental area, olfactory tubercle, amygdala, hippocampus, ventral pallidum, and septum), basal ganglia, cortical (medial prefrontal, frontal, parietal, temporal, occipital, entorhinal, piriform, and cingulate), and subcortical (thalamus, habenula, and superior colliculus) structures. After administration of both low (0.25 g/kg) and moderate (1.0 g/kg) doses of ethanol, LCGU values were lower, relative to those for saline controls, in several CNS regions (lateral septum; posterior cingulate, frontal, parietal, and temporal cortices; dorsomedial striatum; and dorsomedial thalamus) of LAD but not HAD rats. These findings may indicate that certain CNS regions of LAD-2 rats are more sensitive than regions of HAD-2 rats to the effects of low-to-intermediate doses of ethanol.

Arsine toxicity treated with red blood cell and plasma exchanges

BACKGROUND:  Acute toxicity due to inhalation of arsine gas (AsH3) has no known antidote. Exchange transfusion may be beneficial, and dialysis is often required because arsine may cause acute intravascular hemolysis and renal failure. A patient with arsine toxicity has recently been treated by both red blood cell exchange (RBC‐E) and plasma exchange (PE) therapy and our experience is reported.

Local cerebral glucose utilization after relapse in ethanol drinking in alcohol-preferring (P) rats.

The [(14)C]-2-deoxyglucose ([(14)C]-2-DG) quantitative autoradiographic technique was used to determine rates of local cerebral glucose utilization (LCGU) in discrete brain regions of adult, male alcohol-preferring (P) rats after 2 weeks of ethanol deprivation (E-D), 3 and 14 days of ethanol-relapse drinking (E-R3; E-R14), and in P rats, which were chronically drinking ethanol (E-C) for 8 weeks during daily 3-h scheduled-access sessions to 15% (vol./vol.) ethanol and water, or were ethanol-naive (E-N). The hypothesis to be tested was that ethanol-relapse drinking is initiated to restore changes in functional activity back to their chronic ethanol-exposed state. The LCGU rates were measured 1 h before the scheduled-access session. Mean ethanol intake did not differ among the groups. The LCGU rates were decreased in 41 of 57 regions or subregions examined in E-C rats compared with findings for E-N rats, including subregions of the cerebral cortex, hippocampus, and structures in the mesocorticolimbic and nigrostriatal systems. After 2 weeks of deprivation, LCGU values tended to return toward control values (E-N) in most CNS regions and did not differ significantly from control values in 12 regions or subregions (e.g., parts of the limbic system, cerebral cortex). Compared with LCGU values that recovered toward control levels in the E-D group, ethanol-relapse drinking was associated with decreased LCGU values in (1) 4 of 10 limbic structures, (2) all 6 cerebral cortical regions, (3) 1 of 4 basal ganglia regions, (4) 2 of 7 hippocampus subregions, and (5) 1 of 6 thalamic nuclei. The present results indicate that ethanol-relapse drinking was associated with reduced LCGU rates in most CNS regions that recovered toward control values and suggested to us that ethanol-relapse drinking may be initiated to restore neuronal function to its prior chronic ethanol-exposure state.

Transfusion-related acute lung injury: A thrombotic thrombocytopenic purpura treatment-associated case report and concise review

Blood products are frequently required immediately prior to, during, or just after an apheresis procedure. Transfusion‐related acute lung injury (TRALI) is now the leading cause of transfusion‐related mortality, surpassing ABO‐incompatible hemolytic reactions. The reported incidence of TRALI varies but is estimated at 1 in 5,000 transfusions. The true incidence could be higher because of under‐reporting and under‐diagnosis. Plasma is the most frequently implicated blood product. While the pathogenesis of TRALI appears multifactorial, one contributing factor seems to be donor antibodies to cognate recipient neutrophil antigens. Biologically active neutrophil‐priming substances may also play a role. New diagnostic criteria have recently been proposed to aid in the diagnosis of TRALI. We report a thrombotic thrombocytopenic purpura (TTP) treatment‐associated case of TRALI and review the history, pathogenesis, diagnosis and management of this syndrome. Current risk reduction strategies are also discussed. J. Clin. Apheresis, 2008.

A radioassay for angiotensin converting enzyme

Current methods for measuring angiotensin converting enzyme activity (EC 3.4.15.1, ACE) are somewhat cumbersome and have limited the general availability of the test. We describe here a simple four-step radioassay for ACE which uses the substrate 14C-Hippurate-L-Histidyl-L-Leucine and measures the product, 14C-Hippurate. We found that incubation at pH 7.0 (Hepes buffer) increased the sensitivity of the test by 50 percent when compared to results obtained with the pH 8.0 buffer normally used for ACE assays. A split sample comparison study between the radioassay and the spectrophotometric method showed good correlation (n = 47; mean, spectrophotometric, 26.0 U/mL; mean, radioassay, 26.1 U/mL; m = 0.86; b = 3.9; r = 0.868). We found that there was no significant difference between the spectrophotometric, kinetic and radioassay (Newman-Keuls multiple range test), but the liquid chromatographic method gave results significantly different from the other methods. The assay for ACE described here combines enhanced technical ease with the sensitivity of a radioassay.

Mantle cell leukemia as a cause of leukostasis

A 72-year-old man was admitted with hypoxemic respiratory distress. Given a white blood cell count of 600 × 10 9 /L and symptoms of leukostasis, emergency leukapheresis was initiated. The white blood cell count immediately after the first leukapheresis was paradoxically increased to over 700 × 10 9 /L. Peripheral blood smear findings showed morphologically immature mononuclear cells and numerous circulating mitotic figures. Initial flow cytometry results showed a lambda light chain-restricted B lymphoid population positive for CD20, CD19, CD5, and FMC-7, and negative for TdT, CD10, CD23, CD34, CD117, and myeloid markers, suggesting classification as a blastoid variant of mantle cell lymphoma in a leukemic phase. Subsequent testing using DNA fluorescence in situ hybridization was positive for t(11;14), confirming the diagnosis of mantle cell leukemia. Although mantle cell lymphoma occasionally transforms or can even present as leukemia (leukocytes .40 × 109/L), it is rare for it to present with such profound leukocytosis and an overwhelming number of pleomorphic/blastoid forms. Although morphology suggested acute lymphoblastic leukemia, a more specific diagnosis of blastoid variant mantle cell lymphoma was obtained in 12 hours by applying complementary techniques of flow cytometry and rapid cytogenetics.

Retrograde transmission of Enterobacter cloacae during blood transfusion confirmed by pulsed-field gel electrophoresis: TRANSFUSION MEDICINE ILLUSTRATED

The transfusion service was consulted to evaluate an adverse reaction to a cellular transfusion product after transfusion of 128 mL of red blood cells (RBCs) characterized by a temperature change from 36.6 to 39.8°C, chills, nausea, and back pain in a septic patient. A hemolytic transfusion reaction was excluded. The RBC unit was sent to microbiology where a pansusceptible Enterobacter cloacae, which is rarely recovered from blood products, was recovered from the unit. Blood cultures from the patient drawn 26 hours before transfusion also grew an E. cloacae (see Fig. A, patient isolate [left] and blood unit isolate [right] on 5% sheep blood agar. Both isolates exhibit identical colony morphology with large, gray, entire colonies at 24 hours incubation at 35°C.) with an identical biotype (75101376; MicroScan NBC41 panel) and strain type by pulsed-field gel electrophoresis (PFGE) to the unit. Both organisms typed as XB-ETCA-009 (01) (see Fig. B, PFGE of the patient’s blood culture isolate [left lane] and the blood unit isolate [right lane] showing identical bands [arrows]. Gels imaged and compared to database at Texas Department of State Health Services, and both strains typed identically.). We concluded that the temperature spike was likely related to the patient’s sepsis and not to the transfusion. The patient was treated with piperacillin/tazobactam and ciprofloxacin and was discharged after negative blood cultures 48 hours later. Because E. cloacae are motile organisms, it is reasonable to speculate that the