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Your body may get too much iron (iron overload), either from frequent blood transfusions or the disease itself. Too much iron can cause damage to your heart, liver, and endocrine system. Your endocrine system includes glands that produce hormones that regulate processes throughout your body.
You may get frequent severe infections, especially if you receive a lot of blood transfusions. The infections may be carried in the blood you receive during a transfusion. Healthcare providers carefully screen donor blood during transfusions to prevent this from happening.
Sickle cell disease is a group of disorders that affects hemoglobin, the molecule in red blood cells that delivers oxygen to cells throughout the body. People with this disease have atypical hemoglobin molecules called hemoglobin S, which can distort red blood cells into a sickle, or crescent, shape.
Signs and symptoms of sickle cell disease usually begin in early childhood. Characteristic features of this disorder include a low number of red blood cells (anemia), repeated infections, and periodic episodes of pain. The severity of symptoms varies from person to person. Some people have mild symptoms, while others are frequently hospitalized for more serious complications.
The signs and symptoms of sickle cell disease are caused by the sickling of red blood cells. When red blood cells sickle, they break down prematurely, which can lead to anemia. Anemia can cause shortness of breath, fatigue, and delayed growth and development in children. The rapid breakdown of red blood cells may also cause yellowing of the eyes and skin, which are signs of jaundice. Painful episodes can occur when sickled red blood cells, which are stiff and inflexible, get stuck in small blood vessels. These episodes deprive tissues and organs, such as the lungs, kidneys, spleen, and brain, of oxygen-rich blood and can lead to organ damage. A particularly serious complication of sickle cell disease is high blood pressure in the blood vessels that supply the lungs (pulmonary hypertension), which can lead to heart failure. Pulmonary hypertension occurs in about 10 percent of adults with sickle cell disease.
Sickle cell disease is the most common inherited blood disorder in the United States, affecting an estimated 100,000 Americans. The disease is estimated to occur in 1 in 500 African Americans and 1 in 1,000 to 1,400 Hispanic Americans.
Abnormal versions of beta-globin can distort red blood cells into a sickle shape. The sickle-shaped red blood cells die prematurely, which can lead to anemia. Sometimes the inflexible, sickle-shaped cells get stuck in small blood vessels and can cause serious medical complications.
A 17-year-old refugee from Eritrea presented with sudden fever (to 41C), myalgias, and headache. Three days before admission, he had arrived in Switzerland after a long journey through the Sudan and Libya and across the Mediterranean and Italy. Other than mild anemia, he had unremarkable blood values (hemoglobin, 122 g/L; white blood cells, 5.6 109/L; platelets, 187 109/L) and an increased C-reactive protein of 55 mg/L. No localizing infection was found by clinical examination, chest radiograph, or urine analysis. During a search for malaria, spirochetes were spotted in the blood film (Giemsa stained, original magnification 100). Given the travel history and clinical symptoms, louse-borne relapsing fever (LBRF) was diagnosed, caused by Borrelia recurrentis. A treatment with doxycycline for 7 days was effective.
B recurrentis is transmitted by human body lice and is endemic in the highlands of eastern Africa, southern Sudan, and the Andean foothills. The disease occurs typically in overcrowded areas and in situations with reduced hygiene like war and mass migration. In recent months, an increasing number of cases have been reported in migrants to Europe. Wright- or Giemsa-stained blood smear during fever showing spirochetemia is considered diagnostic. Mortality in LBRF can be up to 5% even if treated. Treatment-induced Jarisch-Herxheimer reaction can occur.
Malaria is caused by infection with protozoan parasites belonging to the genus Plasmodium transmitted by female Anopheles species mosquitoes. Our understanding of the malaria parasites begins in 1880 with the discovery of the parasites in the blood of malaria patients by Alphonse Laveran. The sexual stages in the blood were discovered by William MacCallum in birds infected with a related haematozoan, Haemoproteus columbae, in 1897 and the whole of the transmission cycle in culicine mosquitoes and birds infected with Plasmodium relictum was elucidated by Ronald Ross in 1897. In 1898 the Italian malariologists, Giovanni Battista Grassi, Amico Bignami, Giuseppe Bastianelli, Angelo Celli, Camillo Golgi and Ettore Marchiafava demonstrated conclusively that human malaria was also transmitted by mosquitoes, in this case anophelines. The discovery that malaria parasites developed in the liver before entering the blood stream was made by Henry Shortt and Cyril Garnham in 1948 and the final stage in the life cycle, the presence of dormant stages in the liver, was conclusively demonstrated in 1982 by Wojciech Krotoski. This article traces the main events and stresses the importance of comparative studies in that, apart from the initial discovery of parasites in the blood, every subsequent discovery has been based on studies on non-human malaria parasites and related organisms.
Infection begins when (1) sporozoites, the infective stages, are injected by a mosquito and are carried around the body until they invade liver hepatocytes where (2) they undergo a phase of asexual multiplication (exoerythrocytic schizogony) resulting in the production of many uninucleate merozoites. These merozoites flood out into the blood and invade red blood cells where (3) they initiate a second phase of asexual multiplication (erythrocytic schizogony) resulting in the production of about 8-16 merozoites which invade new red blood cells. This process is repeated almost indefinitely and is responsible for the disease, malaria. As the infection progresses, some young merozoites develop into male and female gametocytes that circulate in the peripheral blood until they are (4) taken up by a female anopheline mosquito when it feeds. Within the mosquito (5) the gametocytes mature into male and female gametes, fertilization occurs and a motile zygote (ookinete) is formed within the lumen of the mosquito gut, the beginning of a process known as sporogony. The ookinete penetrates the gut wall and becomes a conspicuous oocyst within which another phase of multiplication occurs resulting in the formation of sporozoites that migrate to the salivary glands of a mosquito and are injected when the mosquito feeds on a new host.
Our understanding of the life cycle of the malaria parasites did not proceed in the logical order just outlined but more like a jigsaw in which the various pieces were painstakingly put into place and, like a jigsaw, often involved mistakes and false starts. The story begins with the discovery of the stages in the blood. Many textbooks merely state that 'in 1880 Laveran discovered the malaria parasite' words that do not give this discovery the credit it deserves. In order to understand the background of this discovery it is necessary to go back to the 1870s. The discoveries of Pasteur and Koch had precipitated a search for a bacterial cause for many diseases including malaria. By 1879 the miasma theory was going out of favour and the two theories vying for contention were whether the microorganisms responsible were transmitted (1) by air and inhalation or (2) by water and ingestion. The leading theory was that proposed by the Italian Corrado Tommasi-Crudeli and the German, Theodor Albrecht Edwin Klebs, an eminent microbiologist who had been the first person to see the bacteria responsible for typhoid and diphtheria. Tommasi-Crudeli and Klebs claimed that they had isolated from the waters of the Pontine Marshes, where malaria was prevalent, a bacterium, Bacillus malariae, which when isolated in culture and injected into rabbits caused febrile infections accompanied by enlarged spleens reminiscent of malaria [14]. It was against this background that Charles Louis Alphonse Laveran, an unknown French army officer working in Algeria, challenged the perceived wisdom and began in his own words 'to follow the pigment'. Beginning with the known fact that the spleens of malaria patients contained pigment he began to look for pigment in the fresh unstained blood of patients and observed it first in leucocytes and then in or on red blood cells. Looking more carefully, he observed several different forms of erythrocytic organism including crescents, spherical motionless bodies with pigment, spherical moving bodies with pigment and bodies that extruded flagella-like structures all of which he thought were on the outside of the red cells. These observations are particularly interesting because Laveran not only used fresh blood but also a dry objective with a maximum magnification of 400 diameters. He also suggested a course of events that began with clear spots that grew, acquired pigment and filled the corpuscle which then burst coinciding with the fevers associated with malaria. Laveran meticulously examined the blood of 200 patients and in 148 observed the crescentic bodies in all cases of malaria but never in those without malaria. He also noted that quinine removed these stages from the blood. Laveran quickly realised that he had found a parasitic protozoan which he called Oscillaria malariae. He presented his findings to the French Academy of Medical Sciences in December 1880 [15] but failed to persuade any of the eminent microbiologists, zoologists or malariologists of the day that he was seeing anything other than disintegrating red blood cells. Nevertheless he persevered and by 1884 had convinced the leading Italian malariologists including Bignami, Golgi and Marchiafava that malaria was caused by a protozoan and not a bacterium [16]. His biggest triumph came in the same year when he also convinced the more cynical microbiologists Louis Pasteur, Charles Edouard Chamberland and Pierre Paul Émile Roux. Robert Koch, one of the most influential microbiologists of his time, however, remained sceptical until 1887. Nevertheless in some quarters the miasma theory persisted and as late as 1895 the American R. C. Newton, a supporter of Tommasi-Crudeli, wrote that 'Aerial and aquatic transportation of malaria has been proved' [17]. (This paper is worth reading in full because, although based on what we now know to be false premises, it contains a mass of interesting information about the prevention of malaria such as the use of screens or mosquito nets to exclude insects, closing doors at night and lighting fires out of doors). Laveran was awarded the Nobel Prize for Medicine in 1907 and his discoveries are described in some detail by the Sergent brothers [18] and Bruce-Chwatt [19] as well as in the various histories of malaria listed above. 153554b96e
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