HUMAN AFRICAN TRYPANOSOMIASIS / SLEEPING SICKNESS

"He was weak, he slept all day – even during meals. I knew that when people sleep all the time, they could have sleeping sickness so we went to the hospital."

Placide’s mother

Placide, sleeping sickness patient, Democratic Republic of Congo

In 2011, Placide suffered a severe bout of sleeping sickness that came close to killing him. He was diagnosed with stage-2 HAT - when the parasites attack the brain - and was treated with NECT, which required more than two weeks in hospital. He was cured, but his family and doctors believe he has long-term neurological effects from the illness.

“There is still something not ‘right’ with him. He is very anxious and can’t continue at school, I’ve had to pull him out. He doesn’t have any friends,” said his mother.

Asked if he remembers his treatment, Placide nods and points to his lower back, where he received a lumbar puncture.

Today Placide is 11 years old and sits in his family’s courtyard, endlessly chipping away at a piece of wood, not far from the site of DNDi’s Phase III clinical trial for fexinidazole, a new oral therapy that will treat both stages of the disease, doing away with the need for lumbar puncture prior to treatment.

In 2009, DNDi and its partners delivered the combination therapy nifurtimoxeflornithine (NECT) which replaced earlier toxic treatments for HAT. NECT is now used to treat 100% of stage-2 g-HAT patients and has contributed to a dramatic reduction in HAT cases. However, the treatment is difficult to ship and administer, patients must undergo a lumbar puncture to confirm the disease stage, and must remain hospitalized for the full duration of treatment.

The development of new all-oral treatments would enable patients to be treated immediately, potentially at home, and would provide the tools needed to reach and sustain HAT elimination. If successful, this would represent a fundamental shift in disease management.

Caused by two subspecies: Trypanosoma brucei gambiense (g-HAT, comprising 98% of reported cases) and T. b. rhodesiense (r-HAT)
Humans are a reservoir for g-HAT; animals are a reservoir for r-HAT
Transmitted by the bite of a tsetse fly
Occurs in two stages: stage-1, often un- or misdiagnosed due to non-specific symptoms (headaches, chills), and stage-2, the late stage where the parasite crosses the blood-brain barrier, causing serious neurological disorders including sleep cycle disruptions, neurological manifestations, and progressive mental deterioration
Fatal without effective treatment
WHO Roadmap objective: to eliminate HAT as a public health issue by 2020

13MILLION

estimated to live in areas at moderate to very high risk

61MILLION

people at risk

1,447CASES

of g-HAT reported in 2017

24COUNTRIES

g-HAT endemic in West & Central Africa

53CASES

of r-HAT reported in 2016

13COUNTRIES

r-HAT endemic in Eastern and Southern Africa