Human African Trypanosomiasis (HAT), commonly known as Sleeping Disease, is a parasitic infection found in specific regions of sub-Saharan Africa. It affects both humans and animals. The condition is caused by a microscopic organism transmitted through the bite of an insect vector, leading to a progressive illness that is nearly always fatal without medical intervention. The disease’s common name originates from the severe disruption it causes to the sleep-wake cycle in its advanced stages.
The Parasite and Tsetse Fly Transmission
Sleeping Disease is caused by the protozoan parasite Trypanosoma brucei. This single-celled organism is transmitted to humans through the bite of the tsetse fly (Glossina), a large, biting fly native to Africa. The tsetse fly acts as a biological vector, acquiring the parasite from an infected host and injecting the infectious form into a new host during a blood meal.
The disease manifests in two distinct forms, determined by the parasite subspecies. Trypanosoma brucei gambiense causes a chronic, slowly progressing illness found primarily in West and Central Africa, accounting for over 92% of reported cases. Trypanosoma brucei rhodesiense is found in East and Southern Africa, causing an acute, rapidly progressive infection. Humans are the primary reservoir for T. b. gambiense, while T. b. rhodesiense is primarily zoonotic, with wild game and domestic cattle serving as the main reservoirs.
The Two Distinct Stages of Illness
The progression of Sleeping Disease is characterized by two phases, reflecting the parasite’s movement through the body. The first is the hemolymphatic stage, where trypanosomes multiply in the blood, lymph, and subcutaneous tissues. Initial symptoms are often non-specific, typically appearing one to three weeks after infection.
These symptoms can include intermittent fever, headaches, joint pain, muscle aches, and generalized itching. A distinctive sign of the T. b. gambiense form is lymphadenopathy, or the swelling of lymph nodes, particularly in the posterior cervical triangle (Winterbottom’s sign). Because these symptoms resemble those of other endemic infections like malaria, the disease is often overlooked. The chronic T. b. gambiense form can persist for months or years before symptoms become severe.
The second stage is the meningoencephalitic stage, which begins when parasites cross the blood-brain barrier and invade the Central Nervous System (CNS). This invasion causes meningoencephalitis, triggering significant neurological and mental disturbances.
The disease earns its common name during this stage, as patients experience profound circadian rhythm disruption, leading to insomnia at night and overwhelming sleepiness during the day. Progressive neurological symptoms include behavioral changes, confusion, poor coordination, tremors, and sensory disturbances.
In the acute T. b. rhodesiense form, CNS progression is rapid, sometimes occurring within weeks. Patients may die from systemic complications like myocarditis before severe neurological symptoms fully develop. Once the CNS is invaded, the condition is fatal without treatment, often leading to coma and death.
Current Diagnostic Methods and Therapies
Diagnosis relies on a multi-step process: screening at-risk populations followed by confirmation of the parasite. For the chronic T. b. gambiense form, screening often uses serological tests, such as the Card Agglutination Test for Trypanosomiasis (CATT), to detect antibodies in the blood. Confirmation requires microscopic identification of the Trypanosoma parasite in a body fluid sample, such as blood, lymph node aspirate, or cerebrospinal fluid (CSF).
Determining the disease stage is necessary because it dictates the choice of treatment. A lumbar puncture (spinal tap) is often performed to analyze the CSF. Invasion of the CNS is indicated by the direct presence of trypanosomes or by an elevated white blood cell count (more than five per cubic millimeter) in the fluid.
The treatment regimen differs significantly between the two stages, requiring drugs that can cross the blood-brain barrier for the late stage. Fexinidazole, an oral drug, is a significant advancement as it treats both the first stage and non-severe second stage of T. b. gambiense HAT. This oral treatment simplifies the process, potentially reducing the need for hospitalization and systematic lumbar punctures.
For severe second-stage T. b. gambiense and all stages of acute T. b. rhodesiense infection, more complex treatments are required. The Nifurtimox-Eflornithine Combination Therapy (NECT), involving oral and intravenous drugs, is the current first-line treatment for advanced T. b. gambiense.
Surveillance and Prevention Strategies
Control of Sleeping Disease relies heavily on case detection and treatment, which reduces the human reservoir of the parasite, especially for the T. b. gambiense form. Surveillance is conducted in two ways. Active surveillance uses mobile medical teams to screen entire populations in at-risk communities using serological tests. Passive surveillance relies on patients presenting themselves at fixed health facilities, often when the disease is already advanced.
In low-risk areas, targeted door-to-door surveys near former patients are used as an efficient alternative to mass screening. Vector control efforts also aim to reduce the tsetse fly population through insecticide-treated traps and targets. These public health measures have been highly successful, and the number of reported cases has fallen dramatically in the past two decades.
The World Health Organization (WHO) aims for the elimination of the disease as a public health problem. Continued success depends on reinforcing surveillance systems within healthcare structures and ensuring access to newer, safer oral treatments.