Amebiasis is a protozoan parasitic infection caused by the ameba Entamoeba histolytica, which lives in the large intestine of humans as part of the residentflora. Humans contract the infection is acquired by ingesting food or water contaminated with faeces. It occurs most often in poor countries where the standards of public hygiene and sanitation are low. Once ingested, the incubation period varies from a few days to several months. In rare cases, the symptoms may not appear for years. Entamoeba histolytica competes with the host for food in the large intestine. It multiples by simple division. Protective cysts develop and the organism is passed out with faeces. The cysts can survive long periods before the next host acquires them. Some strains of the ameba are harmless and the people carrying them show no symptoms. Other strains invade the intestinal wall causing bleeding and mucus secretion and diarrhoea. Ulcers are formed in the intestinal wall where the ameba gain access to the bloodstream and move to the liver and/or brain. Symptoms of severe amebiasis include persistent moderate to severe diarrhoea, jaundice, abdominal discomfort and in severe cases the development of an abscess in the liver or in the brain. Research Amebiasis
Blackwater fever is a rare and serious complication of chronic malaria caused by Plasmodium falciparum following quinine treatment and characterised by massive destruction of the red blood cells, producing dark red or blackish urine. The patient has fever, rigors, jaundice, vomitting, pain in the loins and thirst. Recovery may follow, or death may occur from exhaustion, high fever or suppression of urine. Research Blackwater Fever
Normal red blood cells are of four main groups in relation to their behaviour when mixed with bloodplasma (or serum) of another individual. Similarly the plasma (and serum) of each individual belongs to one of four groups. If cells of one group meet plasma of an 'incompatible' group, the cells stick together in blocks. These clumps obstruct blood vessels and may cause death. The interaction of the incompatible cells and plasma is called 'agglutination'. The provocative substance in the cells is called the agglutlnogen, while the defensive substance in the plasma is the agglutinin. A similar mechanism develops in relation to our immunity to infections by certain bacteria and viruses. In blood transfusion, the amount of plasma administered is small in relation to the large amount of plasma in the recipient's circulation. On the other hand, even a small quantity of cells given to a patient whose plasma will not tolerate that particular type of cell, will lead to clumping of the donor's cells in the recipient's blood vessels. The importance therefore lies in the cells of the donor and the plasma of the recipient.l Plasma and serum for this purpose are identical and the serum obtained when a small quantity of blood is allowed to clot is used for testing against the donor's red cells. In order to determine a patient's blood group, a small quantity of blood is obtained from a finger or ear prick and immediately mixed with citrate to prevent clotting; the cells are then tested against special serum of known groups. To obtain the patient's serum for cross-matching, 5 ml of blood is taken, by vein puncture, and allowed to clot.
The four common groups have been numbered variously. The Moss classification I, II, III, and IV was used extensively until the adoption of the International A, B, O classification, which describes the groups according to the presence or absence of the specific cell factors, which are of two types, A and B. Thus we have four blood groups in the international system. In the first of these, both cell factors are present but no serum factors. The serum factors are called anti-A and anti-B, and obviously the cellfactor A and the serum factor anti-A could not exist in the same person. The second group contains cellfactor A and serum factor anti-B. The third group contains cellfactor B with serum factor anti-A, and the fourth group contains neither cellfactor but both serum factors. The fourth group could therefore be given to any of the other groups and the cells, having no clumping factors, would be tolerated in any recipient. On the other hand, the first group with both cell factors could not be given to any other group. The terms universal donor, Group O (MossIV), and universal recipient, Group AB (MossI), were used to amplify the earlier grouping system. Transfusion with the wrong group of blood is usually fatal so that very great care has to be taken in the determination of the blood group, both of donor and recipient.
Since the 1950s hitherto unexplained incompatability was found to be due to the presence of other factors than the A, B, O, agglutinogens. The most important of these is the rhesus cellfactor. Certain monkeys (Rhesus species) have this factor naturally, but it is present in only 85 per cent of white people in England and America. The other 15 per cent - Rh negative - may become sensitized to Rh positive cells by repeated transfusion of Rh positive blood. A rhesus negative mother whose husband is ph positive may produce an Rh positive baby. A battle occurs between the unborn baby's cells and the mother's plasma. The baby may die before birth (miscarriage) or be born with very severe anaemia and jaundice. If born alive, the baby is treated by complete replacement of its blood to get rid of the mother' s sensitized Rh negative plasma. This is 'exsanguination-transfusion'. During the 1950s blood grouping in preparation for transfusion became a complex and very responsible task. In most hospitals it is undertaken by specialists - perhaps a pathologist or transfusion officer. During the 1980s as HIV paranoia spread, even more testing started to be done. Research Blood Groups
Glandular fever (infectiousmononucleosis) is a mild infectious disease most commonly caused by the Epstein-Barr (EB) virus, one of the herpes viruses. As with any harmful infection, the body's immune system fights the EB virus infection by activating large numbers of lymphocytes.
Glandular fever occurs most often in young adults but also strikes children and older people. Direct contact between people-kissing, for example - can spread the disease. The chief symptoms include chills, fever, sore throat, and fatigue. The disease is called glandular fever because swelling occurs in the lymphatic glands, especially those in the neck. Symptoms may also include an enlarged spleen, inflamed mouth and gums, skin rash, jaundice, and an enlarged liver. Depending on the seriousness of the case, most doctors recommend mild to complete bed rest for a glandular fever patient. The disease is not fatal, and most patients recover within three to six weeks. Blood tests are used to diagnose glandular fever. In a test used widely for many years, a sample of the patient' s blood is mixed with sheep's blood. If the patient has the disease, the sheep's blood cells stick together. Newer, more sophisticated tests identify glandular fever by detecting specific antibodies believed to be formed in the blood to fight the EB virus. Research Glandular Fever
Jaundice is a yellowing of the skin, conjunctivae, and mucous membranes caused by excessive amounts of bile pigments in the blood tissues. These pigments, normally present in blood as a result of the breakdown of haemoglobin in red blood cells, are filtered through the liver and excreted. Excessive amounts of these pigments produce four types of jaundice. In haemolytic jaundice there is increased production of bile pigment because of red blood-cell damage. This damage can be caused by antibodies created by a mismatched blood transfusion. In infants the antibodies can be caused by prenatal mismatch between the Rhfactor in the infant' s blood and that of the mother. Newborns can also be jaundiced as a consequence of the condition known as hyperbilirubinemia. In these cases, there is a temporary defect in synthesis of the enzyme that breaks down bile to an excretable form. Hepatocellular jaundice occurs when liver cells are damaged either by viruses or by excessive intake of alcohol and lose the ability to filter pigment. Obstructive jaundice
follows physical obstruction of the ducts that transport pigment from the liver to the intestine. Blockage can be due to gallstones, tumour, or inflammation. Research Jaundice
Abbreviations
Research Gallsickness
