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Tracing the nightmarish effects of the \"wonder drug\" Lomidine in preventing sleeping sickness in Africa. Winner of the George Rosen Prize by the American Association for the History of Medicine After the Second World War, French colonial health services, armed with a newly discovered drug, made the eradication of sleeping sickness their top priority. A single injection of Lomidine (known as Pentamidine in the United States) promised to protect against infection for six months or longer. Mass campaigns of \"preventive lomidinization\" were launched with immense enthusiasm across Africa. But the drug proved to be both inefficient and dangerous. Contaminated injections caused bacterial infections that progressed to gangrene, killing dozens of people. Shockingly, the French physicians who administered the shots seemed to know the drug's risk: while they obtained signed consent before giving Lomidine to French citizens, they administered it to Africans without their consent—sometimes by force. In The Lomidine Files, Guillaume Lachenal traces the medicine's trajectory from experimental trials during the Second World War, when it was introduced as a miracle cure for sleeping sickness, to its abandonment in the late 1950s, when a series of deadly incidents brought lomidinization campaigns to a grinding halt. He explores colonial doctors' dangerously hubristic obsession with an Africa freed from disease and describes the terrible reactions caused by the drug, the resulting panic of colonial authorities, and the decades-long cover-up that followed. A fascinating material history that touches on the drug's manufacture and distribution, as well as the tragedies that followed in its path, The Lomidine Files resurrects a nearly forgotten scandal. Ultimately, it illuminates public health not only as a showcase of colonial humanism and a tool of control but also as an arena of mediocrity, powerlessness, and stupidity.

Tsetse flies, the blood-sucking insects that transmit the potentially fatal sleeping sickness disease, are usually found in Sub-Saharan Africa. But a large colony can currently be found at the Institute of Tropical Medicine in the historic city of Antwerp. Professor Jan van den Abbeele is genetically modifying the flies to neutralise the disease-spreading parasites that live within them.

Sleeping Sickness is the deadliest disease in the world. The Democratic Republic of Congo suffers more cases than any other country. Without treatment, parasites called trypanosomes invade the victim's brain and ravage their sleep cycle, driving them mad before finally killing them. But dedicated doctors and medics are fighting back. In this television documentary produced for the BBC we tell the stories of those who have lost family to the disease and of the lucky ones who have survived this deadly disease. This is the heart-rending story of people who have to keep fighting to survive, despite this terrible disease taking lives in their villages every day. Last year, Reagan lost four brothers to disease. One of them died from sleeping sickness. Now, in spite of his mother's fears and efforts, Reagan himself has fallen victim to the parasites – Trypanasomes – that cause deadly sleeping sickness. The parasites enter the body through the bites of the Tsetse fly, common along the banks of the Congo and in the village of Nioki, where Reagan lives. Nioki has a population of 35,000 and patients here are treated for free, the cost of their treatment covered by foreign aid. Reagan's condition is not good. His mother Zozo noticed changes in his behaviour. He started sleeping in school. That's when she decided to bring him to the hospital, leaving his brothers and sisters to fend for themselves back home. The bites of the Tsetse flies are clearly visible on Reagan's body and it is likely that the parasites are now in his brain. Left untreated, his condition will be fatal. He is given an injection of Melarsoprol, an extremely dangerous treatment based on an arsenic compound. It kills the parasites, but can cause fatal inflammation of the brain, killing one patient in 20. It is so corrosive that it is kept in glass bottles, as it melts plastic containers. Half of all patients that have an adverse reaction to the treatment will die. Reagan reacts badly to the injection. It causes him to go into shock. He's given an anti-inflammatory drug to stabilize him and it works. He survives the Melarsoprol this time, but will need a full course of injections to kill all the parasites in his body. Without the injections, he will die. With them, there's a high risk of him having another bad and potentially life threatening reaction to the drug. Melarsoprol is the only treatment available to him in Nioki. Luckily, Reagan survived both the injections and his illness and made a full recovery. However, due to the lack of supplies and the dangers of Melarsoprol, many others like him are not so lucky.

Human African trypanosomiasis (HAT), or sleeping sickness, is caused by Trypanosoma brucei gambiense, which is a chronic form of the disease present in western and central Africa, and by Trypanosoma brucei rhodesiense, which is an acute disease located in eastern and southern Africa. The rhodesiense form is a zoonosis, with the occasional infection of humans, but in the gambiense form, the human being is regarded as the main reservoir that plays a key role in the transmission cycle of the disease. The gambiense form currently assumes that 98% of the cases are declared; the Democratic Republic of the Congo is the most affected country, with more than 75% of the gambiense cases declared. The epidemiology of the disease is mediated by the interaction of the parasite (trypanosome) with the vectors (tsetse flies), as well as with the human and animal hosts within a particular environment. Related to these interactions, the disease is confined in spatially limited areas called \"foci\", which are located in Sub-Saharan Africa, mainly in remote rural areas. The risk of contracting HAT is, therefore, determined by the possibility of contact of a human being with an infected tsetse fly. Epidemics of HAT were described at the beginning of the 20th century; intensive activities have been set up to confront the disease, and it was under control in the 1960s, with fewer than 5,000 cases reported in the whole continent. The disease resurged at the end of the 1990s, but renewed efforts from endemic countries, cooperation agencies, and nongovernmental organizations led by the World Health Organization succeeded to raise awareness and resources, while reinforcing national programs, reversing the trend of the cases reported, and bringing the disease under control again. In this context, sustainable elimination of the gambiense HAT, defined as the interruption of the transmission of the disease, was considered as a feasible target for 2030. Since rhodesiense HAT is a zoonosis, where the animal reservoir plays a key role, the interruption of the disease's transmission is not deemed feasible.

Human African trypanosomiasis (HAT), also known as sleeping sickness, is one of the Africa's 'neglected diseases' and is caused by infection with protozoan parasites of the Trypanosoma genus. Transmitted by the bite of the tsetse fly, it puts 70 million people at risk throughout sub-Saharan Africa and is usually fatal if untreated or inadequately treated. In this brief overview, some important recent developments in this disease are outlined. These cover various aspects including a reduction in disease incidence, newly recognised parasite reservoir sites in humans, disease outcome, novel diagnostic methods, new and improved treatment, and disease neuropathogenesis.

Human African trypanosomiasis is a neglected tropical disease caused by the extracellular protozoan parasite Trypanosoma brucei, and targeted for eradication by 2030. The COVID-19 pandemic contributed to the lengthening of the proposed time frame for eliminating human African trypanosomiasis as control programs were interrupted. Armed with extensive antigenic variation and the depletion of the B cell population during an infectious cycle, attempts to develop a vaccine have remained unachievable. With the absence of a vaccine, control of the disease has relied heavily on intensive screening measures and the use of drugs. The chemotherapeutics previously available for disease management were plagued by issues such as toxicity, resistance, and difficulty in administration. The approval of the latest and first oral drug, fexinidazole, is a major chemotherapeutic achievement for the treatment of human African trypanosomiasis in the past few decades. Timely and accurate diagnosis is essential for effective treatment, while poor compliance and resistance remain outstanding challenges. Drug discovery is on-going, and herein we review the recent advances in anti-trypanosomal drug discovery, including novel potential drug targets. The numerous challenges associated with disease eradication will also be addressed.

Trypanosomiasis has been recognized as a scourge in sub-Saharan Africa for centuries. The disease, caused by protozoan parasites of the genus, is a major cause of mortality and morbidity in animals and man. Human African trypanosomiasis (HAT), or sleeping sickness, results from infections with or with accounting for over 95% of infections. Historically there have been major epidemics of the infection, followed by periods of relative disease control. As a result of concerted disease surveillance and treatment programmes, implemented over the last two decades, there has been a significant reduction in the number of cases of human disease reported. However, the recent identification of asymptomatic disease carriers gives cause for some concern. The parasites evade the host immune system by switching their surface coat, comprised of variable surface glycoprotein (VSG). In addition, they have evolved a variety of strategies, including the production of serum resistance associated protein (SRA) and -specific glycoprotein (TgsGP) to counter host defense molecules. Infection with either disease variant results in an early haemolymphatic-stage followed by a late encephalitic-stage when the parasites migrate into the CNS. The clinical features of HAT are diverse and non-specific with early-stage symptoms common to several infections endemic within sub-Saharan Africa which may result in a delayed or mistaken diagnosis. Migration of the parasites into the CNS marks the onset of late-stage disease. Diverse neurological manifestations can develop accompanied by a neuroinflammatory response, comprised of astrocyte activation, and inflammatory cell infiltration. However, the transition between the early and late-stage is insidious and accurate disease staging, although crucial to optimize chemotherapy, remains problematic with neurological symptoms and neuroinflammatory changes recorded in early-stage infections. Further research is required to develop better diagnostic and staging techniques as well as safer more efficacious drug regimens. Clearer information is also required concerning disease pathogenesis, specifically regarding asymptomatic carriers and the mechanisms employed by the trypanosomes to facilitate progression to the CNS and precipitate late-stage disease. Without progress in these areas it may prove difficult to maintain current control over this historically episodic disease.

The functions of human Apolipoproteins L (APOLs) are poorly understood, but involve diverse activities like lysis of bloodstream trypanosomes and intracellular bacteria, modulation of viral infection and induction of apoptosis, autophagy, and chronic kidney disease. Based on recent work, I propose that the basic function of APOLs is the control of membrane dynamics, at least in the Golgi and mitochondrion. Together with neuronal calcium sensor-1 (NCS1) and calneuron-1 (CALN1), APOL3 controls the activity of phosphatidylinositol-4-kinase-IIIB (PI4KB), involved in both Golgi and mitochondrion membrane fission. Whereas secreted APOL1 induces African trypanosome lysis through membrane permeabilization of the parasite mitochondrion, intracellular APOL1 conditions non-muscular myosin-2A (NM2A)-mediated transfer of PI4KB and APOL3 from the Golgi to the mitochondrion under conditions interfering with PI4KB-APOL3 interaction, such as APOL1 C-terminal variant expression or virus-induced inflammatory signalling. APOL3 controls mitophagy through complementary interactions with the membrane fission factor PI4KB and the membrane fusion factor vesicle-associated membrane protein-8 (VAMP8). In mice, the basic APOL1 and APOL3 activities could be exerted by mAPOL9 and mAPOL8, respectively. Perspectives regarding the mechanism and treatment of APOL1-related kidney disease are discussed, as well as speculations on additional APOLs functions, such as APOL6 involvement in adipocyte membrane dynamics through interaction with myosin-10 (MYH10).

African trypanosomes cause sleeping sickness in humans and nagana in cattle. These unicellular parasites are transmitted by the bloodsucking tsetse fly. In the mammalian host’s circulation, proliferating slender stage cells differentiate into cell cycle-arrested stumpy stage cells when they reach high population densities. This stage transition is thought to fulfil two main functions: first, it auto-regulates the parasite load in the host; second, the stumpy stage is regarded as the only stage capable of successful vector transmission. Here, we show that proliferating slender stage trypanosomes express the mRNA and protein of a known stumpy stage marker, complete the complex life cycle in the fly as successfully as the stumpy stage, and require only a single parasite for productive infection. These findings suggest a reassessment of the traditional view of the trypanosome life cycle. They may also provide a solution to a long-lasting paradox, namely the successful transmission of parasites in chronic infections, despite low parasitemia.