Kroppenstedtia pulmonis sp. nov. and Kroppenstedtia sanguinis sp. nov., isolated from human patients

Three human clinical strains (W9323T, X0209T and X0394) isolated from lung biopsy, blood and cerebral spinal fluid, respectively, were characterized using a polyphasic taxonomic approach. Comparative analysis of the 16S rRNA gene sequences showed the three strains belonged to two novel branches within the genus Kroppenstedtia: 16S rRNA gene sequence analysis of W9323T showed closest sequence similarity to Kroppenstedtia eburnea JFMB-ATE T (95.3 %), Kroppenstedtia guangzhouensis GD02T (94.7 %) and strain X0209T (94.6 %); sequence analysis of strain X0209T showed closest sequence similarity to K. eburnea JFMB-ATE T (96.4 %) and K. guangzhouensis GD02T (96.0 %). Strains X0209T and X0394 were 99.9 % similar to each other by 16S rRNA gene sequence analysis. The DNA-DNA relatedness was 94.6 %, confirming that X0209T and X0394 belong to the same species. Chemotaxonomic data for strains W9323T and X0209T were consistent with those described for the genus Kroppenstedtia: whole-cell peptidoglycan contained LLdiaminopimelic acid; the major cellular fatty acids were iso-C15 and anteiso-C15; and the major menaquinone was MK-7. Different endospore morphology and carbon utilization profiles of strains W9323T and X0209T supported by phylogenetic analysis enabled us to conclude that the strains represent two new species within the genus Kroppenstedtia, for which the names Kroppenstedtia pulmonis sp. nov. (type strain W9323T =DSM 45752 T) and Kroppenstedtia sanguinis sp. nov. (type strain X0209T =DSM 45749T=CCUG 38657 T) are proposed

Increasing hematocrit above 28% during early resuscitative phase is not associated with decreased mortality following severe traumatic brain injury

BACKGROUND: To prevent iatrogenic damage, transfusions of red blood cells should be avoided. For this, specific and reliable transfusion triggers must be defined. To date, the optimal hematocrit during the initial operating room (OR) phase is still unclear in patients with severe traumatic brain injury (TBI). We hypothesized that hematocrit values exceeding 28%, the local hematocrit target reached by the end of the initial OR phase, resulted in more complications, increased mortality, and impaired recovery compared to patients in whom hematocrit levels did not exceed 28%. METHODS: Impact of hematocrit (independent variable) reached by the end of the OR phase on mortality and morbidity determined by the extended Glasgow outcome scale (eGOS; dependent variables) was investigated retrospectively in 139 TBI patients. In addition, multiple logistic regression analysis was performed to identify additional important variables. FINDINGS: Following severe TBI, mortality and morbidity were neither aggravated by hematocrit above 28% reached by the end of the OR phase nor worsened by the required transfusions. Upon multiple logistic regression analysis, eGOS was significantly influenced by the highest intracranial pressure and the lowest cerebral perfusion pressure values during the initial OR phase. CONCLUSIONS: Based on this retrospective observational analysis, increasing hematocrit above 28% during the initial OR phase following severe TBI was not associated with improved or worsened outcome. This questions the need for aggressive transfusion management. Prospective analysis is required to determine the lowest acceptable hematocrit value during the OR phase which neither increases mortality nor impairs recovery. For this, a larger caseload and early monitoring of cerebral metabolism and oxygenation are indispensable