Kenya Eliminates : A Landmark Public Health Victory

The World Health Organization (WHO) has officially certified Kenya as free from human African trypanosomiasis (HAT), commonly known as sleeping sickness, marking a major milestone in global health.

With this achievement, Kenya becomes the tenth country in the world to eliminate the disease as a public health problem. This marks Kenya’s second neglected tropical disease elimination, following WHO’s certification of the nation as Guinea worm disease-free in 2018.

Understanding Sleeping Sickness

Sleeping sickness is a parasitic disease caused by protozoa of the genus Trypanosoma. It is transmitted to humans through the bite of infected tsetse flies (Glossina species) and is endemic to sub-Saharan Africa.

If untreated, the disease is almost always fatal.

The Tsetse fly which spreads African sleeping sickness

Etiology

Two main subspecies of Trypanosoma brucei cause human infection:

1. Trypanosoma brucei rhodesiense (TBr) – Acute form, mainly in East & Southern Africa, progresses rapidly.

2. Trypanosoma brucei gambiense (TBg) – Chronic form, prevalent in West & Central Africa, may take years to develop severe symptoms.

Life Cycle of the Parasite

In the Tsetse Fly:

1. The fly ingests bloodstream trypomastigotes from an infected host.

2. Parasites transform into procyclic trypomastigotes in the gut, multiply, then migrate to salivary glands.

3. They develop into metacyclic trypomastigotes, the infective stage for humans.

In Humans:

1. Infection occurs when the tsetse fly injects metacyclic trypomastigotes into the bloodstream.

2. Parasites multiply as bloodstream trypomastigotes.

3. In later stages, they cross the blood-brain barrier, causing central nervous system (CNS) disease.

Transmission

• Primary: Bite from infected tsetse fly.

• Other routes:

  • Contaminated blood transfusion (rare)

  • Mother-to-child during pregnancy or childbirth

Hosts:

• T. b. gambiense: Pigs, dogs, antelopes, cows, sheep, goats, humans

• T. b. rhodesiense: Antelopes, pigs, humans (main reservoir)

Vectors:

• Glossina palpalis – Riverine tsetse, transmits T. b. gambiense

• Glossina morsitans – Woodland tsetse, transmits T. b. rhodesiense

Pathogenesis

• Initial stage: Parasite multiplies in blood & lymph.

• Later stage: Crosses into CNS, causing neurological damage.

• Toxins from parasites damage tissues, cause inflammation, interfere with serotonin regulation (leading to sleep disturbances).

• Hypersensitivity reactions can cause itching & skin rashes.

Clinical Stages & Symptoms

Stage 1 – Haematolymphatic Stage

(Parasite in blood & lymphatic system)

• Chancre at bite site

• Lymphadenopathy

• Fever, headache

• Skin rash, pruritus

• Hepatosplenomegaly

• Musculoskeletal pain

• Anemia, edema, ascites

• Cardiovascular & endocrine disorders

• Renal involvement (albuminuria)

• Intercurrent lung infections

Stage 2 – Meningoencephalitic Stage

(CNS involvement)

• Sleep disturbances (daytime sleepiness, nighttime insomnia)

• Altered mental state

• Abnormal reflexes & tone disorders

• Abnormal movements, sensory loss

• Coordination problems

• Neurological issues: convulsions, hemiplegia, archaic reflexes, loss of consciousness

• Cachexia, coma

Diagnosis

• Clinical exam – History of tsetse exposure, signs & symptoms

• Microscopy – Wet/thick blood smear, Giemsa/Wright stain

• Serology – Detect antibodies

• Lumbar puncture – Detect parasites in cerebrospinal fluid (CNS stage)

• Molecular – PCR for parasite DNA

Differential Diagnosis: Malaria, tuberculosis, meningitis, HIV/AIDS, encephalitis.

Treatment

Early Stage (No CNS involvement)

• T. b. rhodesiense: Suramin (test dose → 20 mg/kg IV every 5 days × 5 doses)

• T. b. gambiense: Pentamidine (4 mg/kg IM daily × 7 days)

Late Stage (CNS involvement)

• T. b. rhodesiense: Melarsoprol (2.2 mg/kg IV daily × 10 days)

• T. b. gambiense:

  • Children <35 kg: Eflornithine (150 mg/kg every 6h × 14 days)

  • Adults: NECT regimen (Nifurtimox + Eflornithine)

Precautions:

• Monitor for drug reactions (melarsoprol is toxic)

• Avoid suramin in onchocerciasis areas (can cause blindness)

Prevention & Control

• Vector control (tsetse traps, insecticides, habitat clearing)

• Active case finding & screening

• Public health education on avoiding bites

• Treatment of animal reservoirs

Prognosis

• Untreated: Nearly 100% fatal

• Treated early: Good recovery

• Late-stage: Higher risk of complications, relapse possible

Kenya’s Road to Elimination

Kenya’s success stems from decades of coordinated action:

• Nationwide tsetse fly control programs

• Community-based screening & treatment campaigns

• Cross-border disease surveillance with neighbors

• Integration of animal and human disease control (One Health approach)

By August 2025, WHO verified zero indigenous cases for several consecutive years, the key criterion for elimination as a public health problem.

Significance

• For Kenya: A healthier rural population, reduced economic loss from cattle infections, and improved agricultural productivity.

• Globally: A step toward WHO’s 2030 target of eliminating sleeping sickness as a public health problem worldwide.