Guide to Parasites Common in Refugee Populations
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Section 8: Hematology CHAPTER 47: ANEMIA
Section 8: Hematology CHAPTER 47: ANEMIA Q.1. A 56-year-old man presents with symptoms of severe dyspnea on exertion and fatigue. His laboratory values are as follows: Hemoglobin 6.0 g/dL (normal: 12–15 g/dL) Hematocrit 18% (normal: 36%–46%) RBC count 2 million/L (normal: 4–5.2 million/L) Reticulocyte count 3% (normal: 0.5%–1.5%) Which of the following caused this man’s anemia? A. Decreased red cell production B. Increased red cell destruction C. Acute blood loss (hemorrhage) D. There is insufficient information to make a determination Answer: A. This man presents with anemia and an elevated reticulocyte count which seems to suggest a hemolytic process. His reticulocyte count, however, has not been corrected for the degree of anemia he displays. This can be done by calculating his corrected reticulocyte count ([3% × (18%/45%)] = 1.2%), which is less than 2 and thus suggestive of a hypoproliferative process (decreased red cell production). Q.2. A 25-year-old man with pancytopenia undergoes bone marrow aspiration and biopsy, which reveals profound hypocellularity and virtual absence of hematopoietic cells. Cytogenetic analysis of the bone marrow does not reveal any abnormalities. Despite red blood cell and platelet transfusions, his pancytopenia worsens. Histocompatibility testing of his only sister fails to reveal a match. What would be the most appropriate course of therapy? A. Antithymocyte globulin, cyclosporine, and prednisone B. Prednisone alone C. Supportive therapy with chronic blood and platelet transfusions only D. Methotrexate and prednisone E. Bone marrow transplant Answer: A. Although supportive care with transfusions is necessary for treating this patient with aplastic anemia, most cases are not self-limited. -
A Distant Gene Deletion Affects Beta-Globin Gene Function in an Atypical Gamma Delta Beta-Thalassemia
A distant gene deletion affects beta-globin gene function in an atypical gamma delta beta-thalassemia. P Curtin, … , A D Stephens, H Lehmann J Clin Invest. 1985;76(4):1554-1558. https://doi.org/10.1172/JCI112136. Research Article We describe an English family with an atypical gamma delta beta-thalassemia syndrome. Heterozygosity results in a beta-thalassemia phenotype with normal hemoglobin A2. However, unlike previously described cases, no history of neonatal hemolytic anemia requiring blood transfusion was obtained. Gene mapping showed a deletion that extended from the third exon of the G gamma-globin gene upstream for approximately 100 kilobases (kb). The A gamma-globin, psi beta-, delta-, and beta-globin genes in cis remained intact. The malfunction of the beta-globin gene on a chromosome in which the deletion is located 25 kb away suggests that chromatin structure and conformation are important for globin gene expression. Find the latest version: https://jci.me/112136/pdf A Distant Gene Deletion Affects ,8-Globin Gene Function in an Atypical '6y5-Thalassemia Peter Curtin, Mario Pirastu, and Yuet Wai Kan Howard Hughes Medical Institute and Department ofMedicine, University of California, San Francisco, California 94143 John Anderson Gobert-Jones Department ofPathology, West Suffolk County Hospital, Bury St. Edmunds IP33-2QZ, Suffolk, England Adrian David Stephens Department ofHaematology, St. Bartholomew's Hospital, London ECIA-7BE, England Herman Lehmann Department ofBiochemistry, University ofCambridge, Cambridge CB2-lQW, England Abstract tologic picture of f3-thalassemia minor in adult life. Globin syn- thetic studies reveal a ,3 to a ratio of -0.5, but unlike the usual We describe an English family with an atypical 'yS6-thalassemia fl-thalassemia heterozygote, the levels of HbA2 (and HbF) are syndrome. -
Anemia in Heart Failure - from Guidelines to Controversies and Challenges
52 Education Anemia in heart failure - from guidelines to controversies and challenges Oana Sîrbu1,*, Mariana Floria1,*, Petru Dascalita*, Alexandra Stoica1,*, Paula Adascalitei, Victorita Sorodoc1,*, Laurentiu Sorodoc1,* *Grigore T. Popa University of Medicine and Pharmacy; Iasi-Romania 1Sf. Spiridon Emergency Hospital; Iasi-Romania ABSTRACT Anemia associated with heart failure is a frequent condition, which may lead to heart function deterioration by the activation of neuro-hormonal mechanisms. Therefore, a vicious circle is present in the relationship of heart failure and anemia. The consequence is reflected upon the pa- tients’ survival, quality of life, and hospital readmissions. Anemia and iron deficiency should be correctly diagnosed and treated in patients with heart failure. The etiology is multifactorial but certainly not fully understood. There is data suggesting that the following factors can cause ane- mia alone or in combination: iron deficiency, inflammation, erythropoietin levels, prescribed medication, hemodilution, and medullar dysfunc- tion. There is data suggesting the association among iron deficiency, inflammation, erythropoietin levels, prescribed medication, hemodilution, and medullar dysfunction. The main pathophysiologic mechanisms, with the strongest evidence-based medicine data, are iron deficiency and inflammation. In clinical practice, the etiology of anemia needs thorough evaluation for determining the best possible therapeutic course. In this context, we must correctly treat the patients’ diseases; according with the current guidelines we have now only one intravenous iron drug. This paper is focused on data about anemia in heart failure, from prevalence to optimal treatment, controversies, and challenges. (Anatol J Cardiol 2018; 20: 52-9) Keywords: anemia, heart failure, intravenous iron, ferric carboxymaltose, quality of life Introduction g/dL in men) (2). -
Pathophysiology and Gastrointestinal Impacts of Parasitic Helminths in Human Being
Research and Reviews on Healthcare: Open Access Journal DOI: 10.32474/RRHOAJ.2020.06.000226 ISSN: 2637-6679 Research Article Pathophysiology and Gastrointestinal Impacts of Parasitic Helminths in Human Being Firew Admasu Hailu1*, Geremew Tafesse1 and Tsion Admasu Hailu2 1Dilla University, College of Natural and Computational Sciences, Department of Biology, Dilla, Ethiopia 2Addis Ababa Medical and Business College, Addis Ababa, Ethiopia *Corresponding author: Firew Admasu Hailu, Dilla University, College of Natural and Computational Sciences, Department of Biology, Dilla, Ethiopia Received: November 05, 2020 Published: November 20, 2020 Abstract Introduction: This study mainly focus on the major pathologic manifestations of human gastrointestinal impacts of parasitic worms. Background: Helminthes and protozoan are human parasites that can infect gastrointestinal tract of humans beings and reside in intestinal wall. Protozoans are one celled microscopic, able to multiply in humans, contributes to their survival, permits serious infections, use one of the four main modes of transmission (direct, fecal-oral, vector-borne, and predator-prey) and also helminthes are necked multicellular organisms, referred as intestinal worms even though not all helminthes reside in intestines. However, in their adult form, helminthes cannot multiply in humans and able to survive in mammalian host for many years due to their ability to manipulate immune response. Objectives: The objectives of this study is to assess the main pathophysiology and gastrointestinal impacts of parasitic worms in human being. Methods: Both primary and secondary data were collected using direct observation, books and articles, and also analyzed quantitativelyResults and and conclusion: qualitatively Parasites following are standard organisms scientific living temporarily methods. in or on other organisms called host like human and other animals. -
Eosinophilic Gastroenteritis Presenting with Severe Anemia and Near Syncope
J Am Board Fam Med: first published as 10.3122/jabfm.2012.06.110269 on 7 November 2012. Downloaded from BRIEF REPORT Eosinophilic Gastroenteritis Presenting with Severe Anemia and Near Syncope Nneka Ekunno, DO, MPH, Kirk Munsayac, DO, Allen Pelletier, MD, and Thad Wilkins, MD Eosinophilic gastrointestinal disorders or eosinophilic digestive disorders encompass a spectrum of rare gastrointestinal disorders that includes eosinophilic esophagitis, eosinophilic gastroenteritis, and eosinophilic colitis. Eosinophilic gastroenteritis is a rare inflammatory disease characterized by eosino- philic infiltration of the gastrointestinal tract. The clinical manifestations include anemia, dyspepsia, and diarrhea. Endoscopy with biopsy showing histologic evidence of eosinophilic infiltration is consid- ered definitive for diagnosis. Corticosteroid therapy, food allergen testing, elimination diets, and ele- mental diets are considered effective treatments for eosinophilic gastroenteritis. The treatment and prognosis of eosinophilic gastroenteritis is determined by the severity of the clinical manifestations. We describe a 24-year-old woman with eosinophilic gastroenteritis presenting as epigastric pain with a history of severe iron deficiency anemia, asthma, eczema, and allergic rhinitis, and we review the litera- ture regarding presentation, diagnostic testing, pathophysiology, predisposing factors, and treatment recommendations. (J Am Board Fam Med 2012;25:913–918.) Keywords: Case Reports, Eosinophilic Gastroenteritis, Gastrointestinal Disorders copyright. A 24-year-old nulliparous African-American woman During examination, her height was 62 inches, was admitted after an episode of near syncope asso- weight 117 lb, and body mass index 21.44 kg/m2. Her ciated with 2 days of fatigue and dizziness. She re- heart rate was 111 beats per minute, blood pressure ported gradual onset of dyspepsia over 2 to 3 121/57 mm Hg, respiratory rate 20 breaths per minute, months. -
Foodborne Anisakiasis and Allergy
Foodborne anisakiasis and allergy Author Baird, Fiona J, Gasser, Robin B, Jabbar, Abdul, Lopata, Andreas L Published 2014 Journal Title Molecular and Cellular Probes Version Accepted Manuscript (AM) DOI https://doi.org/10.1016/j.mcp.2014.02.003 Copyright Statement © 2014 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial- NoDerivatives 4.0 International (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited. Downloaded from http://hdl.handle.net/10072/342860 Griffith Research Online https://research-repository.griffith.edu.au Foodborne anisakiasis and allergy Fiona J. Baird1, 2, 4, Robin B. Gasser2, Abdul Jabbar2 and Andreas L. Lopata1, 2, 4 * 1 School of Pharmacy and Molecular Sciences, James Cook University, Townsville, Queensland, Australia 4811 2 Centre of Biosecurity and Tropical Infectious Diseases, James Cook University, Townsville, Queensland, Australia 4811 3 Department of Veterinary Science, The University of Melbourne, Victoria, Australia 4 Centre for Biodiscovery and Molecular Development of Therapeutics, James Cook University, Townsville, Queensland, Australia 4811 * Correspondence. Tel. +61 7 4781 14563; Fax: +61 7 4781 6078 E-mail address: [email protected] 1 ABSTRACT Parasitic infections are not often associated with first world countries due to developed infrastructure, high hygiene standards and education. Hence when a patient presents with atypical gastroenteritis, bacterial and viral infection is often the presumptive diagnosis. Anisakid nematodes are important accidental pathogens to humans and are acquired from the consumption of live worms in undercooked or raw fish. Anisakiasis, the disease caused by Anisakis spp. -
Alpha Thalassemia Trait
Alpha Thalassemia Trait Alpha Thalassemia Trait Produced by St. Jude Children’s Research Hospital, Departments of Hematology, Patient Education, 1 and Biomedical Communications. Funds were provided by St. Jude Children’s Research Hospital, ALSAC, and a grant from the Plough Foundation. This document is not intended to replace counseling by a trained health care professional or genetic counselor. Our aim is to promote active participation in your care and treatment by providing information and education. Questions about individual health concerns or specific treatment options should be discussed with your doctor. For general information on sickle cell disease and other blood disorders, please visit our Web site at www.stjude.org/sicklecell. Copyright © 2009 St. Jude Children’s Research Hospital Alpha thalassemia trait All red blood cells contain hemoglobin (HEE muh glow bin), which carries oxygen from your lungs to all parts of your body. Alpha thalassemia (thal uh SEE mee uh) trait is a condition that affects the amount of hemo- globin in the red blood cells. • Adult hemoglobin (hemoglobin A) is made of alpha and beta globins. • Normally, people have 4 genes for alpha globin with 2 genes on each chromosome (aa/aa). People with alpha thalassemia trait only have 2 genes for alpha globin, so their bodies make slightly less hemoglobin than normal. This trait was passed on from their parents, like hair color or eye color. A trait is different from a disease 2 Alpha thalassemia trait is not a disease. Normally, a trait will not make you sick. Parents who have alpha thalassemia trait can pass it on to their children. -
Hematology Unit Lab 1 Review Material
Hematology Unit Lab 1 Review Material Objectives Laboratory instructors: 1. Facilitate lab discussion and answer questions Students: 1. Review the introductory material below 2. Study and review the assigned cases and questions in small groups before the Lab. This includes the pathological material using Virtual Microscopy 3. Be prepared to present your cases, questions and answers to the rest of your Lab class during the Lab Erythropoiesis: The process of red blood cell (RBC) production • Characterized by: − Increasing hemoglobin synthesis Erythroid maturation stages (Below): − Decreasing cell size - Average of 4 cell divisions during maturation − Decreasing cytoplasmic basophilia [One pronormoblast gives rise to 16 red cells] (increasing pink color) - pronormoblast → reticulocyte = 7 days − Progressive chromatin condensation of the - reticulocytes → mature RBC =1-2 days nuclei − Extrusion of nucleus (orthochromatic stage) − Extruded nuclei are subsequently phagocytized − Loss of mitotic capability after the early stage of polychromatophilic normoblast • Picture below: Erythroid progenitors (normoblasts) cluster around macrophages (arrows) in the bone marrow and spleen • Macrophages store iron • Iron is transferred from macrophages to erythroid precursor cells • Iron is used by normoblasts for hemoglobin synthesis aka nucleated rbc aka reticulocyte 1 Mature Red Blood Cell 7-8 microns; round / ovoid biconcave disc with orange-red cytoplasm, no RNA, no nucleus; survives ~120 days in circulation Classification of Anemia by Morphology 1. -
Molecular Epidemiology and Hematologic Characterization of Δβ
Jiang et al. BMC Medical Genetics (2020) 21:43 https://doi.org/10.1186/s12881-020-0981-x RESEARCH ARTICLE Open Access Molecular epidemiology and hematologic characterization of δβ-thalassemia and hereditary persistence of fetal hemoglobin in 125,661 families of greater Guangzhou area, the metropolis of southern China Fan Jiang1,2, Liandong Zuo2, Dongzhi Li2, Jian Li2, Xuewei Tang2, Guilan Chen2, Jianying Zhou2, Hang Lu2 and Can Liao1,2* Abstract Background: Individuals with δβ-thalassemia/HPFH and β-thalassemia usually present with intermedia or thalassemia major. No large-scale survey on HPFH/δβ-thalassemia in southern China has been reported to date. The purpose of this study was to examine the molecular epidemiology and hematologic characteristics of these disorders in Guangzhou, the largest city in Southern China, to offer advice for thalassemia screening programs and genetic counseling. Methods: A total of 125,661 couples participated in pregestational thalassemia screening. 654 subjects with fetal hemoglobin (HbF) level ≥ 5% were selected for further investigation. Gap-PCR combined with Multiplex ligation dependent probe amplification (MLPA) was used to screen for β-globin gene cluster deletions. Gene sequencing for the promoter region of HBG1 /HBG2 gene was performed for all those subjects. Results: A total of 654 individuals had hemoglobin (HbF) levels≥5, and 0.12% of the couples were found to be heterozygous for HPFH/δβ-thalassemia, including Chinese Gγ (Aγδβ)0-thal, Southeast Asia HPFH (SEA-HPFH), Taiwanese deletion and Hb Lepore–Boston–Washington. The highest prevalence was observed in the Huadu district and the lowest in the Nansha district. Three cases were identified as carrying β-globin gene cluster deletions, which had not been previously reported. -
Sickle Cell: It's Your Choice
Sickle Cell: It’s Your Choice What Does “Sickle Cell” Mean? Sickle is a type of hemoglobin. Hemoglobin is the substance that carries oxygen in the blood and gives blood its red color. A person’s hemoglobin type is not the same thing as blood type. The type of hemoglobin we have is determined by genes that we inherit from our parents. The majority of individuals have only the “normal” type of hemoglobin (A). However, there are a variety of other hemoglobin types. Sickle hemoglobin (S) is one of these types. There Are Two Forms of Sickle Cell. Sickle cell occurs in two forms. Sickle cell trait is not a disease; Sickle cell anemia (or sickle cell disease) is a disease. Sickle Cell Trait (or Sickle Trait) Sickle cell trait is found primarily in African Americans, people from areas around the Mediterranean Sea, and from islands in the Caribbean. Sickle cell trait occurs when a person inherits one sickle cell gene from one parent and one normal hemoglobin gene from the other parent. A person with sickle cell trait is healthy and usually is not aware that he or she has the sickle cell gene. A person who has sickle trait can pass it on to their children. If one parent has sickle cell trait and the other parent has the normal type of hemoglobin, there is a 50% (1 in 2) chance with EACH pregnancy that the baby will be born with sickle cell trait. When ONE parent has sickle cell trait, the child may inherit: • 50% chance for two normal hemoglobin genes (normal hemoglobin- AA), OR • 50% chance for one normal hemoglobin gene and one sickle cell gene (sickle cell trait- AS). -
Diagnosis and Recommended Treatment of Helminth Infections
DRUG REVIEW n Diagnosis and recommended treatment of helminth infections Allifia Abbas BSc, MRCP, Paul Wade MSc, BPharm and William Newsholme MSc, FRCP, DTM&H L P A number of worm infections are seen in the S UK, often in migrants from tropical coun - tries, and it is essential to take a travel his - tory. Our Drug review discusses the features of the most common infections and details currently recommended treatments. elminth infections (see Table 1) are major causes of mor - Hbidity in all age groups in the developing world. Around a quarter of the world population is infected with soil-transmit - ted helminths like hookworm and Ascaris , and nearly 250 mil - lion with schistosomiasis. In the developed world, due to improvements in hygiene and food safety, local transmission of infection is infrequent, though infections such as Enterobius remain common. However, with the increase in international travel, migration and more adventurous behav - iour, unusual helminth infections may be encountered any - where. Worldwide it is nematodes, or roundworms, that cause the bulk of infection. The soil-transmitted intestinal helminths Ascaris , hookworm, Trichuris and Strongyloides are good pop - ulation-level markers of poor hygiene and general deprivation, and cause growth and educational impairment in children and anaemia in pregnancy. Filaria are endemic in over 70 countries and infect about 120 million worldwide but are rare in travellers. Tissue helminths, such as Trichinella , may Figure 1. Adult hookworms can live in the small gut for years and can cause an become more frequent with increasing travel and dietary iron-deficiency anaemia in patient groups such as pregnant women adventure – the same is true for the lung and intestinal trema - todes, or flukes. -
Parasites 1: Trematodes and Cestodes
Learning Objectives • Be familiar with general prevalence of nematodes and life stages • Know most important soil-borne transmitted nematodes • Know basic attributes of intestinal nematodes and be able to distinguish these nematodes from each other and also from other Lecture 4: Emerging Parasitic types of nematodes • Understand life cycles of nematodes, noting similarities and significant differences Helminths part 2: Intestinal • Know infective stages, various hosts involved in a particular cycle • Be familiar with diagnostic criteria, epidemiology, pathogenicity, Nematodes &treatment • Identify locations in world where certain parasites exist Presented by Matt Tucker, M.S, MSPH • Note common drugs that are used to treat parasites • Describe factors of intestinal nematodes that can make them emerging [email protected] infectious diseases HSC4933 Emerging Infectious Diseases HSC4933. Emerging Infectious Diseases 2 Readings-Nematodes Monsters Inside Me • Ch. 11 (pp. 288-289, 289-90, 295 • Just for fun: • Baylisascariasis (Baylisascaris procyonis, raccoon zoonosis): Background: http://animal.discovery.com/invertebrates/monsters-inside-me/baylisascaris- [box 11.1], 298-99, 299-301, 304 raccoon-roundworm/ Video: http://animal.discovery.com/videos/monsters-inside-me-the-baylisascaris- [box 11.2]) parasite.html Strongyloidiasis (Strongyloides stercoralis, the threadworm): Background: http://animal.discovery.com/invertebrates/monsters-inside-me/strongyloides- • Ch. 14 (p. 365, 367 [table 14.1]) stercoralis-threadworm/ Videos: http://animal.discovery.com/videos/monsters-inside-me-the-threadworm.html http://animal.discovery.com/videos/monsters-inside-me-strongyloides-threadworm.html Angiostrongyliasis (Angiostrongylus cantonensis, the rat lungworm): Background: http://animal.discovery.com/invertebrates/monsters-inside- me/angiostrongyliasis-rat-lungworm/ Video: http://animal.discovery.com/videos/monsters-inside-me-the-rat-lungworm.html HSC4933.