| Blackwater fever | |
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| Specialty | Infectious disease |
Blackwater fever is a complication of malaria infection in which red blood cells burst in the bloodstream (hemolysis), releasing hemoglobin directly into the blood vessels and into the urine, frequently leading to kidney failure. The disease was first linked to malaria by the Sierra Leone Creole physician John Farrell Easmon in his 1884 pamphlet entitled The Nature and Treatment of Blackwater Fever. Easmon coined the name "blackwater fever" and was the first to successfully treat such cases following the publication of his pamphlet.
Within a few days of onset there are chills, with rigor, high fever, jaundice, vomiting, rapidly progressive anemia, and dark red or black urine.
The cause of hemolytic crises in this disease is unknown (mainly due to intravascular haemolysis). There is rapid and massive destruction of red blood cells resulting in hemoglobinemia (hemoglobin in the blood, but outside the red blood cells), hemoglobinuria (hemoglobin in urine), intense jaundice, anuria (passing less than 50 milliliters of urine in a day), and finally death in the majority of cases.[ citation needed ]
The most probable explanation for blackwater fever is an autoimmune reaction apparently caused by the interaction of the malaria parasite and the use of quinine. Blackwater fever is caused by heavy parasitization of red blood cells with Plasmodium falciparum . However, there have been other cases attributed to Plasmodium vivax, [1] Plasmodium malariae , [2] Plasmodium knowlesi . [3]
Blackwater fever is a serious complication of malaria, but cerebral malaria has a higher mortality rate. Blackwater fever is much less common today than it was before 1950. [4] It may be that quinine plays a role in triggering the condition, [5] and this drug is no longer commonly used for malaria prophylaxis. Quinine remains important for treatment of malaria. [6]
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Blackwater fever should be suspected in a malaria patient who is intermittently passing dark-red to black urine, and is diagnosed using a urine dipstick test, which will be positive for hemoglobin. Microscopy of urine will be negative for erythrocytes. [7]
The treatment is antimalarial chemotherapy, intravenous fluid and sometimes supportive care such as intensive care and dialysis.[ citation needed ]
Malaria is a mosquito-borne infectious disease that affects vertebrates and Anopheles mosquitoes. Human malaria causes symptoms that typically include fever, fatigue, vomiting, and headaches. In severe cases, it can cause jaundice, seizures, coma, or death. Symptoms usually begin 10 to 15 days after being bitten by an infected Anopheles mosquito. If not properly treated, people may have recurrences of the disease months later. In those who have recently survived an infection, reinfection usually causes milder symptoms. This partial resistance disappears over months to years if the person has no continuing exposure to malaria. The mosquito vector is itself harmed by Plasmodium infections, causing reduced lifespan.
Quinine is a medication used to treat malaria and babesiosis. This includes the treatment of malaria due to Plasmodium falciparum that is resistant to chloroquine when artesunate is not available. While sometimes used for nocturnal leg cramps, quinine is not recommended for this purpose due to the risk of serious side effects. It can be taken by mouth or intravenously. Malaria resistance to quinine occurs in certain areas of the world. Quinine is also used as an ingredient in tonic water and other beverages to impart a bitter taste.
Antimalarial medications or simply antimalarials are a type of antiparasitic chemical agent, often naturally derived, that can be used to treat or to prevent malaria, in the latter case, most often aiming at two susceptible target groups, young children and pregnant women. As of 2018, modern treatments, including for severe malaria, continued to depend on therapies deriving historically from quinine and artesunate, both parenteral (injectable) drugs, expanding from there into the many classes of available modern drugs. Incidence and distribution of the disease is expected to remain high, globally, for many years to come; moreover, known antimalarial drugs have repeatedly been observed to elicit resistance in the malaria parasite—including for combination therapies featuring artemisinin, a drug of last resort, where resistance has now been observed in Southeast Asia. As such, the needs for new antimalarial agents and new strategies of treatment remain important priorities in tropical medicine. As well, despite very positive outcomes from many modern treatments, serious side effects can impact some individuals taking standard doses.
Plasmodium is a genus of unicellular eukaryotes that are obligate parasites of vertebrates and insects. The life cycles of Plasmodium species involve development in a blood-feeding insect host which then injects parasites into a vertebrate host during a blood meal. Parasites grow within a vertebrate body tissue before entering the bloodstream to infect red blood cells. The ensuing destruction of host red blood cells can result in malaria. During this infection, some parasites are picked up by a blood-feeding insect, continuing the life cycle.
Glucose-6-phosphate dehydrogenase deficiency (G6PDD), also known as favism, is the most common enzyme deficiency anemia worldwide. It is an inborn error of metabolism that predisposes to red blood cell breakdown. Most of the time, those who are affected have no symptoms. Following a specific trigger, symptoms such as yellowish skin, dark urine, shortness of breath, and feeling tired may develop. Complications can include anemia and newborn jaundice. Some people never have symptoms.
Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of Plasmodium that causes malaria in humans. The parasite is transmitted through the bite of a female Anopheles mosquito and causes the disease's most dangerous form, falciparum malaria. P. falciparum is therefore regarded as the deadliest parasite in humans. It is also associated with the development of blood cancer and is classified as a Group 2A (probable) carcinogen.
The Bight of Benin, or Bay of Benin, is a bight in the Gulf of Guinea area on the western African coast that derives its name from the historical Kingdom of Benin.
Artesunate (AS) is a medication used to treat malaria. The intravenous form is preferred to quinine for severe malaria. Often it is used as part of combination therapy, such as artesunate plus mefloquine. It is not used for the prevention of malaria. Artesunate can be given by injection into a vein, injection into a muscle, by mouth, and by rectum.
Plasmodium malariae is a parasitic protozoan that causes malaria in humans. It is one of several species of Plasmodium parasites that infect other organisms as pathogens, also including Plasmodium falciparum and Plasmodium vivax, responsible for most malarial infection. Found worldwide, it causes a so-called "benign malaria", not nearly as dangerous as that produced by P. falciparum or P. vivax. The signs include fevers that recur at approximately three-day intervals – a quartan fever or quartan malaria – longer than the two-day (tertian) intervals of the other malarial parasite.
Plasmodium knowlesi is a parasite that causes malaria in humans and other primates. It is found throughout Southeast Asia, and is the most common cause of human malaria in Malaysia. Like other Plasmodium species, P. knowlesi has a life cycle that requires infection of both a mosquito and a warm-blooded host. While the natural warm-blooded hosts of P. knowlesi are likely various Old World monkeys, humans can be infected by P. knowlesi if they are fed upon by infected mosquitoes. P. knowlesi is a eukaryote in the phylum Apicomplexa, genus Plasmodium, and subgenus Plasmodium. It is most closely related to the human parasite Plasmodium vivax as well as other Plasmodium species that infect non-human primates.
Hemoglobin C is an abnormal hemoglobin in which glutamic acid residue at the 6th position of the β-globin chain is replaced with a lysine residue due to a point mutation in the HBB gene. People with one copy of the gene for hemoglobin C do not experience symptoms, but can pass the abnormal gene on to their children. Those with two copies of the gene are said to have hemoglobin C disease and can experience mild anemia. It is possible for a person to have both the gene for hemoglobin S and the gene for hemoglobin C; this state is called hemoglobin SC disease, and is generally more severe than hemoglobin C disease, but milder than sickle cell anemia.
Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene, but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele. Those who are heterozygous for the sickle cell allele produce both normal and abnormal hemoglobin.
John Farrell Easmon, MRCS, LM, LKQCP, MD, CMO, was a prominent Sierra Leonean Creole medical doctor in the British Gold Coast who served as Chief Medical Officer during the 1890s. Easmon was the only West African to be promoted to Chief Medical Officer and he served in this role with distinction during the last decade of the 19th century. Easmon was a botanist and a noted expert on the study and treatment of tropical diseases. In 1884, he wrote a pamphlet entitled The Nature and Treatment of Blackwater Fever, which noted for the first time the relationship between blackwater fever and malaria. Easmon coined the term "blackwater fever" in his pamphlet on the malarial disease.
The history of malaria extends from its prehistoric origin as a zoonotic disease in the primates of Africa through to the 21st century. A widespread and potentially lethal human infectious disease, at its peak malaria infested every continent except Antarctica. Its prevention and treatment have been targeted in science and medicine for hundreds of years. Since the discovery of the Plasmodium parasites which cause it, research attention has focused on their biology as well as that of the mosquitoes which transmit the parasites.
Human genetic resistance to malaria refers to inherited changes in the DNA of humans which increase resistance to malaria and result in increased survival of individuals with those genetic changes. The existence of these genotypes is likely due to evolutionary pressure exerted by parasites of the genus Plasmodium which cause malaria. Since malaria infects red blood cells, these genetic changes are most common alterations to molecules essential for red blood cell function, such as hemoglobin or other cellular proteins or enzymes of red blood cells. These alterations generally protect red blood cells from invasion by Plasmodium parasites or replication of parasites within the red blood cell.
The mainstay of malaria diagnosis has been the microscopic examination of blood, utilizing blood films. Although blood is the sample most frequently used to make a diagnosis, both saliva and urine have been investigated as alternative, less invasive specimens. More recently, modern techniques utilizing antigen tests or polymerase chain reaction have been discovered, though these are not widely implemented in malaria endemic regions. Areas that cannot afford laboratory diagnostic tests often use only a history of subjective fever as the indication to treat for malaria.
Plasmodium coatneyi is a parasitic species that is an agent of malaria in nonhuman primates. P. coatneyi occurs in Southeast Asia. The natural host of this species is the rhesus macaque and crab-eating macaque, but there has been no evidence that zoonosis of P. coatneyi can occur through its vector, the female Anopheles mosquito.
Congenital malaria was first reported in 1876, it is an extremely rare condition which occurs due to transplacental transmission of maternal infection. Maternal prophylactic treatments of malaria can be important when talking about the risk of congenital malaria, as the absences of these treatments can increase the chance for a fetus to contract the disease. A positive cord or peripheral blood smear for malaria in a 24 hour to 7 day old newborn defines congenital malaria. This disease can persist past 7 days old, but after this mark it is then regarded as neonatal malaria rather than congenital.
Plasmodium cynomolgi is an apicomplexan parasite that infects mosquitoes and Asian Old World monkeys. In recent years, a number of natural infections of humans have also been documented. This species has been used as a model for human Plasmodium vivax because Plasmodium cynomolgi shares the same life cycle and some important biological features with P. vivax.
The Easmon family or the Easmon Medical Dynasty is a Sierra Leone Creole medical dynasty of African-American descent originally based in Freetown, Sierra Leone. The Easmon family has ancestral roots in the United States, and in particular Savannah, Georgia and other states in the American South. There are several descendants of the Sierra Leonean family in the United Kingdom and the United States, as well as in the Ghanaian cities of Accra and Kumasi. The family produced several medical doctors beginning with John Farrell Easmon, the medical doctor who coined the term Blackwater fever and wrote the first clinical diagnosis of the disease linking it to malaria and Albert Whiggs Easmon, who was a leading gynaecologist in Freetown, Sierra Leone. Several members of the family were active in business, academia, politics, the arts including music, cultural dance, playwriting and literature, history, anthropology, cultural studies, and anti-colonial activism against racism.
Don Adams, who played Maxwell Smart in the 1960s sitcom "Get Smart", combining clipped, decisive diction with appalling, hilarious ineptitude, died on Sunday at a Los Angeles hospital. He was 82.
