BackgroundMalaria is a serious infectious disease. According to the World Health Organization, it is responsible for nearly one million deaths each year. There are various techniques to diagnose malaria of which manual microscopy is considered to be the gold standard. However due to the number of steps required in manual assessment, this diagnostic method is time consuming (leading to late diagnosis) and prone to human error (leading to erroneous diagnosis), even in experienced hands. The focus of this study is to develop a robust, unsupervised and sensitive malaria screening technique with low material cost and one that has an advantage over other techniques in that it minimizes human reliance and is, therefore, more consistent in applying diagnostic criteria.MethodA method based on digital image processing of Giemsa-stained thin smear image is developed to facilitate the diagnostic process. The diagnosis procedure is divided into two parts; enumeration and identification. The image-based method presented here is designed to automate the process of enumeration and identification; with the main advantage being its ability to carry out the diagnosis in an unsupervised manner and yet have high sensitivity and thus reducing cases of false negatives.ResultsThe image based method is tested over more than 500 images from two independent laboratories. The aim is to distinguish between positive and negative cases of malaria using thin smear blood slide images. Due to the unsupervised nature of method it requires minimal human intervention thus speeding up the whole process of diagnosis. Overall sensitivity to capture cases of malaria is 100% and specificity ranges from 50-88% for all species of malaria parasites.ConclusionImage based screening method will speed up the whole process of diagnosis and is more advantageous over laboratory procedures that are prone to errors and where pathological expertise is minimal. Further this method provides a consistent and robust way of generating the parasite clearance curves.

Histiocytic disorders are an exceptionally rare group of diseases with diverse manifestations and a paucity of approved treatments, thereby leading to various challenges in their diagnosis and management. With the discovery of novel molecular targets and the incorporation of targeted agents in the management of various adult histiocytic disorders, their management has become increasingly complex. In an attempt to improve the understanding of the clinical features and management of common adult histiocytic disorders (Langerhans cell histiocytosis, Erdheim-Chester disease, Rosai-Dorfman disease, and hemophagocytic lymphohistiocytosis), we created this document based on existing literature and expert opinion.

is a rare disorder in children. It mostly occurs secondary to disorders such as malignancy, vitamin D deficiency, autoimmunity, and infections. 1,2 Primary MF has been reported in a limited number of children. [3][4][5] Germline mutations in genes such as MPL, VPS45, and RBSN are associated with primary MF. 6-8 A recent report described an Arab family with MF associated with a homozygous mutation in MPIG6B (also known as G6B or C6orf25). 9Another report described four unrelated Arab families with homozygous loss-of-function variants in MPIG6B associated with childhood MF. 10 MPIG6B is located in the class III region of the major histocompatibility complex and encodes G6B protein that interacts with protein tyrosine phosphatases Shp1 and Shp2. 11,12 G6B is primarily expressed in platelets. [13][14][15] G6B knockout mice had low platelet count, increased platelet volume, and platelet dysfunction. 10,16 We report two unrelated patients who presented during infancy with anemia, thrombocytopenia, and focal MF and had homozygous mutations in MPIG6B. The first case is a 10-year-old female who presented at 7 months of age with epistaxis and had thrombocytopenia and anemia. Her parents are first cousins. Physical examination was unremarkable. Blood smear showed some giant platelets and anisopoikilocytosis with teardrop cells, schistocytes, elliptocytes, and spherocytes. Bone marrow (BM) at age 1 year was hypercellular with megakaryocyte clusters, as shown in Figure S1. BM was infiltrated with large cells with vesicular nuclei and prominent nucleoli and was surrounded by a mixture of small lymphocytes and eosinophils.The large cells were positive for CD10, CD20, CD45, and CD79a and negative for CD3, CD7, CD15, CD30, CD34, CD56, CD57, pan CK, desmin, and synaptophysin. The background cells were positive for CD15, CD45, MPO and negative for other markers. There was a mild increase in reticulin fibers. Follow-up BM studies showed subsequent fading of lymphocytic infiltration, dysplastic megakaryocytes, a slight reduction in erythropoiesis, and a marked increase in MF with no myelodysplasia (Figure S1). Cytogenetic analysis was normal.Chromosomal fragility test, vitamin D, vitamin B12, and folate levels were normal. The patient required intermittent platelet transfusion.There was no major bleeding. The spleen progressively increased in size with an increase in platelet transfusion requirements. Splenectomy led to transient improvement in platelet counts. Whole exome sequencing (WES) revealed a homozygous loss-of-function mutation in MPIG6B: c.523C>T (p.Arg175Ter). Recently, the patient started to

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