December 16, 2017 by
Omoro- Omoro District leaders, Acholi Region of Northern Uganda, have asked government to take over the Nodding Syndrome Care Facility in Odek Sub-county, citing financial constraints. The care centre has since 2012 been supported by Hope for Humans, a non-governmental organisation. Hope for Humans was providing medical and personal care, special schooling, and nutritious meals to children with nodding syndrome. The leaders say the facility currently lacks funds to adequately take care of children and carry out outreach programmes in homes of those recovering from nodding syndrome. A total of 29 are currently at the centre while 237, who were rehabilitated, have been reintegrated within communities. The district chairperson, Mr Douglas Peter Okello, told Daily Monitor in an interview recently that managing the care centre has been complex since Hope for Humans cut their support. The decision The organisation’s chief executive officer, Ms Suzanne Gazda, in a July email seen by Daily Monitor, noted that board of directors had made a ‘difficult decision’ to dissolve the organisation and transition the children into the care of Ugandan government. According to Mr Okello, the lives of the children are at a risk since they are not receiving adequate food ration and special care. “We have many children who had shown signs of recovery but they are now relapsing because of lack specialised care and treatment,” Mr Okello said. He revealed that many parents of the affected children are poor peasant farmers. However, Mr Okello also suggested that government should expand the centre into a special needs school to cater for special needs children. The district health officer, Mr Ben Ongom, said although the government through Office of the Prime Minister [OPM] recently gave some food donations, the high operational cost of the facility still remain a big challenge. He said the district health department cannot afford to support the budget and activities of the facility since they too are cash strapped. “Our proposal to government is that they should extend more support to the centre so that it operates normally. We are unsure of how the centre will operate next year without adequate funding,” Mr Ongom said. Mr Caesar Okot, the programme manager Hope for Humans, acknowledged the financial cut. “Our donor had initially intended to stop funding the centre by August but after a series of engagements, the donor accepted to extend support to December 31. What we are receiving currently is a minimum support,” Mr Okot said. He noted that they have made proposals in consultation with the district leaders seeking government’s intervention before they completely run out of funding. Ms Grace Kwiyocwiny, the State Minister for Northern Uganda, however, said government through the Ministry of Health has been supporting the centre for the past years. “Every quarter, the government has been giving financial support to the centre. The problem could be arising from how the district leadership are drawing their budget to use the money; government is supporting the centre…..” Ms Kwiyocwiny said in a telephone interview on Monday. She, however, did not specify how much the centre has been receiving quarterly from the government. But information this newspaper obtained contradicts the minister’s statement that government has been supporting the care centre. According to a source at the district, government only released Shs10 million in the last financial year when Omoro had just gained a district status to enhance outreach programmes. An estimated 3,000 children mainly in Kitgum, Gulu, Pader and Lamwo districts in Acholi Sub-region were affected by the strange since 2009 when its outbreak was first reported. By JULIUS OCUNGI

July 29, 2017 by
Between 1990 and 2013, thousands of children in war-torn South Sudan and northern Uganda suddenly developed a severe and puzzling form of epilepsy. When exposed to food or cold temperatures, affected children nodded their heads uncontrollably. Over time the seizures often worsened, leaving the children severely disabled. Many died of malnutrition, accidents, or secondary infections. A boy receives ivermectin to prevent river blindness. Some think the drug may also prevent nodding syndrome. In some communities, roughly half of families had at least one child with the condition, called nodding syndrome; by 2013, an estimated 1600 children in Uganda were affected. But the cause of the devastation was a mystery. Now, a study finds that a parasitic worm often found in the children might trigger the body’s own defenses to attack neurons. The study doesn’t prove the worm is the culprit, but it “is the first to show that a cause-effect relationship is plausible,” says Hermann Feldmeier, a parasitologist at the Charité University Hospital in Berlin, who was not involved in the study. The rash of cases in Uganda and South Sudan triggered an intense hunt for the cause, but searches for viruses, bacteria, environmental toxins, genetic factors, and nutritional deficits all came up empty. One key clue: Areas with nodding syndrome also had high rates of onchocerciasis, an infection with the parasitic worm Onchocerca volvulus. Spread through the bites of black flies, which breed in swift-flowing streams, the worms can invade the eye, and the infection is commonly known as river blindness. The World Health Organization estimates that at least 18 million people, most in sub-Saharan Africa, are infected. Researchers had suggested as early as the 1960s that high rates of epilepsy in Tanzania, with similar nodding symptoms, might be related to onchocerciasis. Others have noted that children with nodding syndrome are more likely to be infected than their healthy peers. But there’s no evidence that the worm invades the brain or directly causes seizures. Some researchers suggested that the worm instead causes an autoimmune reaction that damages the nervous system. Searches for antibodies that might play an autoimmune role had come up empty. But neuroimmunologists Avindra Nath and Tory Johnson of the National Institutes of Health in Bethesda, Maryland, decided to use an improved protein chip to screen for antibodies to thousands of proteins at once. The new tool proved its worth. Blood from nodding syndrome patients reacted strongly to four proteins; in the case of one protein, called leiomodin-1, patient sera reacted 33,000 times more strongly than did sera from unaffected controls. The researchers then looked for the antibodies causing the reaction. As they report this week in Science Translational Medicine, antibodies to leiomodin-1 turned up in 29 of 55 nodding syndrome patients but only 17 of 55 controls. Patients also carried much higher antibody levels than controls. Leiomodin-1, which likely plays a role in cell shape, is found in smooth muscle and thyroid cells. Johnson’s team showed that it is expressed in the nervous system and brain, too. They also found a clue to what might trigger an autoimmune reaction to the protein: Several O. volvulus proteins resemble it. After the immune system gears up to fight the worm, similarities between an O. volvulus protein and leiomodin-1 may cause the antibodies to mistakenly attack neurons. The study gives little hope to children already affected, Nath says. Although antiseizure drugs can help, if the immune system has attacked neurons, the damage is likely permanent. However, the work could suggest a straightforward way to eliminate the disease, says infectious disease specialist Robert Colebunders of the University of Antwerp in Belgium, because the drug ivermectin kills the worm. Existing campaigns to eliminate river blindness by giving the drug could have a collateral benefit: After the Ugandan government stepped up ivermectin treatment, new cases of nodding syndrome plunged to nearly zero, Colebunders says. “If you eliminate the onchocerciasis, the epilepsy really disappears.” Yet the link between the worm and nodding syndrome doesn’t explain why the illness suddenly appeared in a region where onchocerciasis has likely been common for centuries, or why nodding syndrome only affects children and youth. Johnson, now at Johns Hopkins University in Baltimore, Maryland, says malnutrition, exposure to other diseases, or genetic variation in how the body makes antibodies may also play a role. Other researchers have suggested that measles infection followed by malnutrition could trigger the disease. Neurologist Erich Schmutzhard of the Medical University of Innsbruck in Austria has other doubts. He says that the leiomodin-1 antibodies could be a result of epilepsy, not its cause. The protein seems to be on the inside of neurons, not the outside, he notes. Seizures kill neurons, and he speculates that dying neurons could spill the protein into the blood stream, triggering the antibodies. The onchocerciasis connection is intriguing but far from definitive, says neurologist Andrea Winkler of the Technical University of Munich in Germany. She, too, thinks the syndrome is likely caused by multiple factors, such as malnutrition, parasites, and viruses like measles. “There are still lots of links missing.” Original Article written by Gretchen Vogel from