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52-608: Kinetoplastida (or Kinetoplastea , as a class ) is a group of flagellated protists belonging to the phylum Euglenozoa , and characterised by the presence of a distinctive organelle called the kinetoplast (hence the name), a granule containing a large mass of DNA . The group includes a number of parasites responsible for serious diseases in humans and other animals, as well as various forms found in soil and aquatic environments. The organisms are commonly referred to as "kinetoplastids" or "kinetoplasts". The kinetoplastids were first defined by Bronislaw M. Honigberg in 1963 as

104-495: A top-level genus (genus summum) – was first introduced by French botanist Joseph Pitton de Tournefort in the classification of plants that appeared in his Eléments de botanique of 1694. Insofar as a general definition of a class is available, it has historically been conceived as embracing taxa that combine a distinct grade of organization—i.e. a 'level of complexity', measured in terms of how differentiated their organ systems are into distinct regions or sub-organs—with

156-541: A class. Use of Kinetoplastida as an order also creates confusion as there is already an older name Trypanosomatida Kent, 1880, under which the kinetoplastids are most often placed. Kinetoplastida is divided into two subclasses - Metakinetoplastina and Prokinetoplastina . Kinetoplastids are eukaryotic and possess normal eukaryotic organelles, for example the nucleus , mitochondrion, golgi apparatus and flagellum. Along with these universal structures, kinetoplastids have several distinguishing morphological features such as

208-434: A distinct type of construction, which is to say a particular layout of organ systems. This said, the composition of each class is ultimately determined by the subjective judgment of taxonomists . In the first edition of his Systema Naturae (1735), Carl Linnaeus divided all three of his kingdoms of nature ( minerals , plants , and animals ) into classes. Only in the animal kingdom are Linnaeus's classes similar to

260-558: A fixed (dried) smear can be stained using Giemsa 's or Field 's technique and examined under a microscope. Often, the parasite is in relatively low abundance in the sample, so techniques to concentrate the parasites can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat ; mini anion-exchange/centrifugation; and the quantitative buffy coat (QBC) technique. For other samples, such as spinal fluid, concentration techniques include centrifugation followed by examination of

312-595: A limb, abnormal muscle tone, gait disturbance, ataxia, speech disturbances, paraesthesia, hyperaesthesia, anaesthesia, visual disturbance, abnormal reflexes, seizures, and coma. Parkinson -like movements might arise due to non-specific movement disorders and speech disorders. Individuals may exhibit psychiatric symptoms which may sometimes dominate the clinical diagnosis and may include aggressiveness, apathy , irritability, psychotic reactions and hallucinations , anxiety , emotional lability , confusion , mania , attention deficit, and delirium . Without treatment,

364-466: A passive phase for months or years before symptoms emerge and the infection can last about three years before death occurs. T. b. rhodesiense is the acute form of the disease, and death can occur within months since the symptoms emerge within weeks and it is more virulent and faster developing than T. b. gambiense . Furthermore, trypanosomes are surrounded by a coat that is composed of variant surface glycoproteins (VSG). These proteins act to protect

416-428: Is 1–3 weeks for T. b. rhodesiense, and longer (but less precisely characterised) in T. b. gambiense infection. The first/initial stage, known as the hemolymphatic phase, is characterized by non-specific, generalised symptoms like: fever (intermittent) , headaches (severe), joint pains , itching , weakness, malaise, fatigue, weight loss, lymphadenopathy, and hepatosplenomegaly . Diagnosis may be delayed due to

468-430: Is a large, brown, biting fly that serves as both a host and vector for the trypanosome parasites. While taking blood from a mammalian host, an infected tsetse fly injects metacyclic trypomastigotes into skin tissue. From the bite, parasites first enter the lymphatic system and then pass into the bloodstream. Inside the mammalian host, they transform into bloodstream trypomastigotes, and are carried to other sites throughout

520-522: Is found at the base of a cell's flagella and is associated to the flagellum basal body by a cytoskeletal structure. The cytoskeleton of kinetoplastids is primarily made up of microtubules . These make a highly regular array, the sub-pellicular array, which runs parallel just under the cell surface along the long axis of the cell. Other microtubules with more specialised roles, such as the rootlet microtubules , are also present. Kinetoplastids are capable of forming actin microfilaments but their role in

572-561: Is to target its nucleotide metabolism. The nucleotide metabolism studies have both led to the development of adenosine analogues looking promising in animal studies, and to the finding that downregulation of the P2 adenosine transporter is a common way to acquire partial drug resistance against the melaminophenyl arsenical and diamidine drug families (containing melarsoprol and pentamidine, respectively). Drug uptake and degradation are two major issues to consider to avoid drug resistance development. In

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624-482: The Congo Basin , and two in 1920 and 1970, in several African countries. It is classified as a neglected tropical disease . Other animals, such as cows, may carry the disease and become infected in which case it is known as Nagana or animal trypanosomiasis . African trypanosomiasis symptoms occur in two stages: the hemolymphatic stage and the neurological stage (the latter being characterised by parasitic invasion of

676-585: The blood-brain barrier . The treatment for first-stage disease is fexinidazole by mouth or pentamidine by injection for T. b. gambiense . Suramin by injection is used for T. b. rhodesiense . Fexinidazole may be used for the second stage of TbG, if the disease is not severe. Otherwise a regimen involving the combination of nifurtimox and eflornithine , nifurtimox-eflornithine combination treatment (NECT), or eflornithine alone appear to be more effective and result in fewer side effects. These treatments may replace melarsoprol when available. NECT has

728-655: The actual stage of the disease is achieved by examining the cerebrospinal fluid for the presence of the parasite. Sleep-wake disturbances are a leading feature of the neurological stage and give the disease its common name of "sleeping sickness". Infected individuals experience a disorganized and fragmented sleep-wake cycle. Those affected experience sleep inversion resulting in daytime sleep and somnolence, and nighttime periods of wakefulness and insomnia. Additionally, those affected also experience episodes of sudden sleepiness. Neurological symptoms include: tremor , general muscle weakness, hemiparesis , paralysis of

780-560: The backbone of the strategy used to control sleeping sickness. Systematic screening of at-risk communities is the best approach, because case-by-case screening is not practical in endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to areas of high infection rates. Such screening efforts are important because early symptoms are not evident or serious enough to warrant people with gambiense disease to seek medical attention, particularly in very remote areas. Also, diagnosis of

832-460: The benefit of requiring fewer injections of eflornithine. Intravenous melarsoprol was previously the standard treatment for second-stage (neurological phase) disease and is effective for both types. Melarsoprol is the only treatment for second stage T. b. rhodesiense ; however, it causes death in 5% of people who take it. Resistance to melarsoprol can occur. Drug development projects . A major challenge has been to find drugs that readily pass

884-408: The bite of an infected tsetse fly and are most common in rural areas. Initially, the first stage of the disease is characterized by fevers, headaches, itchiness, and joint pains, beginning one to three weeks after the bite. Weeks to months later, the second stage begins with confusion, poor coordination, numbness, and trouble sleeping. Diagnosis is by finding the parasite in a blood smear or in

936-456: The blood-brain barrier. The latest drug that has come into clinical use is fexinidazol, but promising results have also been obtained with the benzoxaborole drug acoziborole (SCYX-7158). This drug is currently under evaluation as a single-dose oral treatment, which is a great advantage compared to currently used drugs. Another research field that has been extensively studied in Trypanosoma brucei

988-429: The body, reach other body fluids (e.g., lymph, spinal fluid), and continue to replicate by binary fission . The entire life cycle of African trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host. In the fly's midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave

1040-459: The case of nucleoside analogues, they need to be taken up by the P1 nucleoside transporter (instead of P2), and they also need to be resistant against cleavage in the parasite. If untreated, T. b. gambiense almost always results in death, with only a few individuals shown in a long-term 15 year follow-up to have survived after refusing treatment. T. b. rhodesiense , being a more acute and severe form of

1092-589: The cell. The flagella are used for locomotion and attachment to surfaces. The bases of the flagella are found in a specialised pocket structure which is also the location of the cytostome . Kinetoplastids may be free-living or parasitic. The order trypanosomatida is notable as it includes many genera which are exclusively parasitic. Trypanosomatids may have simple life cycles in a single host or more complex ones which progress through multiple differentiation stages in two hosts. Dramatic morphological changes are possible between lifecycle stages. Diseases caused by members of

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1144-456: The central nervous system). Neurological symptoms occur in addition to the initial features, and the two stages may be difficult to distinguish based on clinical features alone. The disease has been reported to present with atypical symptoms in infected individuals who originate from non-endemic areas (e.g. travelers). The reasons for this are unclear and may be genetic. The low number of such cases may also have skewed findings. In such persons,

1196-447: The classes used today; his classes and orders of plants were never intended to represent natural groups, but rather to provide a convenient "artificial key" according to his Systema Sexuale , largely based on the arrangement of flowers. In botany, classes are now rarely discussed. Since the first publication of the APG system in 1998, which proposed a taxonomy of the flowering plants up to

1248-399: The cytoskeleton is not clear. Other cytoskeletal structures include the specialised attachment between the flagellum and the kinetoplast. All kinetoplastids possess at least one flagellum; species in the order trypanosomatida have one and bodonida have two. In kinetoplastids with two flagella most forms have a leading and trailing flagellum, the latter of which may be attached to the side of

1300-407: The disease in humans. Trypanosoma brucei gambiense causes the diseases in west and central Africa , whereas Trypanosoma brucei rhodesiense has a limited geographical range and is responsible for causing the disease in east and southern Africa. In addition, a third subspecies of the parasite known as Trypanosoma brucei brucei is responsible for affecting animals but not humans. Humans are

1352-561: The disease is difficult and health workers may not associate such general symptoms with trypanosomiasis. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir. A single case of sexual transmission of West African sleeping sickness has been reported. In July 2000, a resolution was passed to form the Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC). The campaign works to eradicate

1404-403: The disease is invariably fatal, with progressive mental deterioration leading to coma, systemic organ failure, and death. An untreated infection with T. b. rhodesiense will cause death within months whereas an untreated infection with T. b. gambiense will cause death after several years. Damage caused in the neurological phase is irreversible. Trypanosoma brucei gambiense accounts for

1456-520: The disease, is consistently fatal if not treated. Disease progression greatly varies depending on disease form. For individuals which are infected by T. b. gambiense , which accounts for 92% of all of the reported cases, a person can be infected for months or even years without signs or symptoms until the advanced disease stage, where it is too late to be treated successfully. For individuals affected by T. b. rhodesiense , which accounts for 2% of all reported cases, symptoms appear within weeks or months of

1508-485: The disease, the neurological phase (also called the meningoencephalic stage ), begins when the parasite invades the central nervous system by passing through the blood–brain barrier . Progression to the neurological phase occurs after an estimated 21–60 days in case of T. b. rhodesiens e infection, and 300–500 days in case of T. b. gambiense infection. In actuality, the two phases overlap and are difficult to distinguish based on clinical features alone; determining

1560-514: The early nineteenth century. African trypanosomiasis African trypanosomiasis is an insect-borne parasitic infection of humans and other animals. Human African trypanosomiasis (HAT), also known as African sleeping sickness or simply sleeping sickness , is caused by the species Trypanosoma brucei . Humans are infected by two types, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR). TbG causes over 92% of reported cases. Both are usually transmitted by

1612-460: The endemic countries afflicted with African trypanosomiasis. A pilot program in Senegal has reduced the tsetse fly population by as much as 99% by introducing male flies which have been sterilized by exposure to gamma rays . The treatment is dependent on if the disease is discovered in the first or second stage of the disease. A requirement for treatment of the second stage is that the drug passes

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1664-428: The fluid of a lymph node. A lumbar puncture is often needed to tell the difference between first- and second-stage disease. If the disease is not treated quickly, it can lead to death. Prevention of severe disease involves screening the at-risk population with blood tests for TbG. Treatment is easier when the disease is detected early and before neurological symptoms occur. Treatment of the first stage has been with

1716-533: The formation of new VSGs. Thus, the antibodies produced by the immune system will no longer recognize the parasite leading to proliferation until new antibodies are created to combat the novel VSGs. Eventually, the immune system will no longer be able to fight off the parasite due to the constant changes in VSGs and infection will arise. G. tachinoides G. fuscipes G. morsitans G. swynnertoni G. pallidipes G. fuscipes The tsetse fly (genus Glossina )

1768-502: The human disease form. Tryptophol is a chemical compound produced by the trypanosomal parasite in sleeping sickness which induces sleep in humans. The gold standard for diagnosis is identification of trypanosomes in a sample by microscopic examination. Samples that can be used for diagnosis include ulcer fluid, lymph node aspirates, blood, bone marrow , and, during the neurological stage, cerebrospinal fluid . Detection of trypanosome-specific antibodies can be used for diagnosis, but

1820-531: The infection is said to present mainly as fever with gastrointestinal symptoms (e.g. diarrhoea and jaundice) with lymphadenopathy developing only rarely. Systemic disease is sometimes presaged by a trypanosomal ulcer developing at the site of the infectious fly bite within 2 days of infection. The ulcer is most commonly observed in T. b. rhodesiense infection, and only rarely in T. b. gambiense (however, in T. b. gambiense infection, ulcers are more common in persons from non-endemic areas). Incubation period

1872-422: The kinetoplast, sub-pellicular microtubule array and paraflagellar rod. The kinetoplast, after which the class is named, is a dense DNA-containing granule within the cell's single mitochondrion, containing many copies of the mitochondrial genome . The structure is made up of a network of concatenated circular DNA molecules and their related structural proteins along with DNA and RNA polymerases . The kinetoplast

1924-503: The level of orders, many sources have preferred to treat ranks higher than orders as informal clades . Where formal ranks have been assigned, the ranks have been reduced to a very much lower level, e.g. class Equisitopsida for the land plants, with the major divisions within the class assigned to subclasses and superorders. The class was considered the highest level of the taxonomic hierarchy until George Cuvier 's embranchements , first called Phyla by Ernst Haeckel , were introduced in

1976-436: The main reservoir for T. b. gambiense but this species can also be found in pigs and other animals. Wild game animals and cattle are the main reservoir of T. b. rhodesiense . These parasites primarily infect individuals in sub-Saharan Africa because that is where the vector (tsetse fly) is located. The two human forms of the disease also vary greatly in intensity. T. b. gambiense causes a chronic condition that can remain in

2028-435: The majority of African trypanosomiasis cases, with humans as the main reservoir needed for the transmission, while Trypanosoma brucei rhodesiense is mainly zoonotic, with accidental human infections. The epidemiology of African trypanosomiasis is dependent on the interactions between the parasite (trypanosome), the vector ( tsetse fly ), and the host. There are two subspecies of the parasite that are responsible for starting

2080-508: The medications pentamidine or suramin . Treatment of the second stage has involved eflornithine or a combination of nifurtimox and eflornithine for TbG. Fexinidazole is a more recent treatment that can be taken by mouth, for either stage of TbG. While melarsoprol works for both types, it is typically only used for TbR, due to serious side effects. Without treatment, sleeping sickness typically results in death. The disease occurs regularly in some regions of sub-Saharan Africa with

2132-491: The members of the flagellated protozoans. They are traditionally divided into the biflagellate Bodonidae and uniflagellate Trypanosomatidae ; the former appears to be paraphyletic to the latter. One family of kinetoplastids, the trypanosomatids, is notable as it includes several genera which are exclusively parasitic. Bodo is a typical genus within kinetoplastida, which also includes various common free-living species which feed on bacteria . Others include Cryptobia and

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2184-437: The midgut, and transform into epimastigotes. The epimastigotes reach the fly's salivary glands and continue multiplication by binary fission. The entire life cycle of the fly takes about three weeks. In addition to the bite of the tsetse fly , the disease can be transmitted by: Horse-flies ( Tabanidae ) and stable flies ( Muscidae ) possibly play a role in transmission of nagana (the animal form of sleeping sickness) and

2236-492: The order trypanosomatida include sleeping sickness and Chagas disease , caused by species of Trypanosoma , and leishmaniasis , caused by species of Leishmania . Trypanosoma brucei can undergo meiosis as a likely part of a sexual cycle. Leishmania major is also capable of a meiotic process that is likely part of a sexual cycle. Class (biology) The class as a distinct rank of biological classification having its own distinctive name – and not just called

2288-460: The parasite from any lytic factors that are present in human plasma. The host's immune system recognizes the glycoproteins present on the coat of the parasite leading to the production of different antibodies (IgM and IgG). These antibodies will then act to destroy the parasites that circulate around the blood. However, from the several parasites present in the plasma, a small number of them will experience changes in their surface coats resulting in

2340-433: The parasitic Leishmania . Honigberg created the taxonomic names Kinetoplastida and Kinetoplastea in 1963. Since then there is no consensus on the use of either of the two as a definite taxon . Kinetoplastea is more widely used as the class, while Kinetoplastida is mostly used to designate the order , but is also used as a class. Lynn Margulis , who initially accepted Kinetoplastida as an order in 1974, later placed it as

2392-589: The population at risk being about 70 million in 36 countries. An estimated 11,000 people are currently infected with 2,800 new infections in 2015. In 2018 there were 977 new cases. In 2015 it caused around 3,500 deaths, down from 34,000 in 1990. More than 80% of these cases are in the Democratic Republic of the Congo . Three major outbreaks have occurred in recent history: one from 1896 to 1906 primarily in Uganda and

2444-452: The risk of infection from a tsetse fly bite is minor (estimated at less than 0.1%), the use of insect repellants, wearing long-sleeved clothing, avoiding tsetse-dense areas, implementing bush clearance methods and wild game culling are the best options to avoid infection available for local residents of affected areas. Regular active and passive surveillance, involving detection and prompt treatment of new infections, and tsetse fly control are

2496-549: The sediment. Three serological tests are also available for detection of the parasite: the micro-CATT (card agglutination test for trypanosomiasis), wb-CATT, and wb-LATEX. The first uses dried blood, while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required. Currently there are few medically related prevention options for African trypanosomiasis (i.e. no vaccine exists for immunity). Although

2548-410: The sensitivity and specificity of these methods are too variable to be used alone for clinical diagnosis. Further, seroconversion occurs after the onset of clinical symptoms during a T. b. rhodesiense infection, so is of limited diagnostic use. Trypanosomes can be detected from samples using two different preparations. A wet preparation can be used to look for the motile trypanosomes. Alternatively,

2600-418: The tell-tale swollen lymph nodes along the back of the neck, may appear. Winterbottom's sign is common in T. b. gambiense infection. Those affected may additionally present with: skin rash, haemolytic anaemia, hepatomegaly and abnormal liver function, splenomegaly, endocrine disturbance, cardiac involvement (e.g. pericarditis, and congestive heart failure), and ophthalmic involvement. The second phase of

2652-482: The tsetse vector population levels and subsequently the protozoan disease, by use of insecticide-impregnated targets, fly traps, insecticide-treated cattle, ultra-low dose aerial/ground spraying (SAT) of tsetse resting sites and the sterile insect technique (SIT). The use of SIT in Zanzibar proved effective in eliminating the entire population of tsetse flies but was expensive and is relatively impractical to use in many of

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2704-645: The vagueness of initial symptoms. The disease may also be mistaken for malaria (which may in fact occur as a co-infection). Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Episodes of fever become less frequent over the course of the disease. Invasion of the circulatory and lymphatic systems by the parasite is associated with severe swelling of lymph nodes , often to tremendous sizes. Posterior cervical lymph nodes are most commonly affected, however, axillary, inguinal, and epitrochlear lymph node involvement may also occur. Winterbottom's sign ,

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