Clinicopathological Analysis of Hematological Disorders in Tube-Fed Patients with Copper Deficiency

Object Anemia and leukopenia caused by copper deficiency are well-documented consequences of long-term total parenteral nutrition. We measured the serum copper levels of bed-ridden patients receiving enteral feeding, and evaluated optical and ultrastructural features of bone marrow before and after copper supplementation.Patients and Methods Serum samples were obtained from 15 bed-ridden elderly patients receiving tube feeding (TF) and 10 age-matched bed-ridden patients who took food orally (CO), and the copper ceruloplasmin concentration of each sample was measured. Bone marrow samples were obtained from patients who exhibited copper deficiency and leukopenia and/or anemia before and after the copper supplementation, for use in light and electron microscopic analysis.Results The tube-fed patients had significantly lower mean serum copper and ceruloplasmin concentrations than the control patients. Seven of the 15 tube-fed patients had reduced serum copper concentrations and leukopenia. Six of those 7 patients also had anemia. Copper sulfate was administered to those 7 patients by enteral tube;their copper concentration, anemia and leukopenia improved within 1 month after they were administered copper sulfate. In the bone marrow examination before copper supplementation, light microscopy showed cytoplasmic vacuolization in both myeloid and erythroid precursors, and electron microscopy showed electron-dense deposits in mitochondria and cytoplasm of erythroid and myeloid cells. After copper supplementation, these pathological changes disappeared.Conclusions Bicytopenia is likely to occur in tube-fed patients with copper deficiency. Copper deficiency appears to be associated with cytoplasmic vacuolization and electron-dense deposits in mitochondria in erythroid and myeloid cells

Climate change impacts on plant canopy architecture: implications for pest and pathogen management

Climate change influences on pests and pathogens are mainly plant-mediated. Rising carbon dioxide and temperature and altered precipitation modifies plant growth and development with concomitant changes in canopy architecture, size, density, microclimate and the quantity of susceptible tissue. The modified host physiology and canopy microclimate at elevated carbon dioxide influences production, dispersal and survival of pathogen inoculum and feeding behaviour of insect pests. Elevated temperature accelerates plant growth and developmental rates to modify canopy architecture and pest and pathogen development. Altered precipitation affects canopy architecture through either drought or flooding stress with corresponding effects on pests and pathogens. But canopy-level interactions are largely ignored in epidemiology models used to project climate change impacts. Nevertheless, models based on rules of plant morphogenesis have been used to explore pest and pathogen dynamics and their trophic interactions under elevated carbon dioxide. The prospect of modifying canopy architecture for pest and disease management has also been raised. We offer a conceptual framework incorporating canopy characteristics in the traditional disease triangle concept to advance understanding of host-pathogen-environment interactions and explore how climate change may influence these interactions. From a review of recent literature we summarize interrelationships between canopy architecture of cultivated crops, pest and pathogen biology and climate change under four areas of research: (a) relationships between canopy architecture, microclimate and host-pathogen interaction; (b) effect of climate change related variables on canopy architecture; (c) development of pests and pathogens in modified canopy under climate change; and (d) pests and pathogen management under climate change