Trypanosomiasis in Dogs: The Tsetse-Borne Blood Parasite

What these microscopic swimmers are, how they reach your dog, why they are so hard to catch, how we diagnose and treat them, and what the risk is to your family.

Trypanosomiasis is a group of diseases caused by trypanosomes, tiny parasites made of a single cell that swim using a whip-like tail called a flagellum. They belong to the protozoa, the same broad group that includes the parasites behind babesiosis and malaria. In Africa, the important species are spread mainly by insects, and they infect a wide range of wild and domestic mammals (Desquesnes, Gonzatti, et al., 2022). In cattle, the disease is known across East Africa as nagana. In people, a related parasite causes sleeping sickness (WHO, 2023).

Dogs are often forgotten in this story, but they should not be. Recent surveys across the region keep finding trypanosomes in dogs. A long-term study of village dogs in eastern Zambia found parasite DNA in about 71% of the dogs followed (Lisulo et al., 2024). A review of Ugandan data found that Trypanosoma brucei was the most common species detected in dogs (Rascón-García et al., 2023), and a Nigerian survey found 11.3% of 450 dogs infected (Obi et al., 2022). Here in Kenya, canine cases have been described both in western Kenya and in a dog seen at a Nairobi small-animal clinic (Kimeli et al., 2014; Matete, 2003).

Under the microscope, a trypanosome looks like a tiny, twisting ribbon moving between the red blood cells. Its body is built around a few parts that matter for understanding the disease and its treatment. The nucleus holds most of its genes. Near the tail end sits the kinetoplast, a dense knot of DNA inside the parasite's single large mitochondrion, its energy centre. The flagellum starts beside the kinetoplast and runs along the body, attached by a thin, rippling fold called the undulating membrane, which pulls the parasite through the blood (Desquesnes, Gonzatti, et al., 2022). The whole parasite is wrapped in a dense coat of one protein, the variant surface glycoprotein (VSG). This coat is the parasite's disguise. Each trypanosome carries a large library of different VSG genes and can switch from one coat to another, so the dog's immune system is always chasing a target that keeps changing (Silva Pereira et al., 2022).

Several species can infect dogs in East Africa, and they behave differently. Laboratories tell them apart partly by size and movement in a fresh blood sample and more reliably by DNA testing (Lisulo et al., 2024; Ochieng et al., 2022). How each species develops in the fly also differs, which affects who spreads it (Silva Pereira et al., 2022).

The classic route runs through the tsetse fly (Glossina). When an infected fly bites, it injects infective parasites into the skin. These move into the lymph and blood, where they multiply rapidly by dividing in two. When another tsetse feeds on the dog, it swallows parasites with the blood. Inside the fly's gut, the parasites change form, multiply, and then travel forward to the mouthparts or salivary glands, depending on the species. There they mature into a new infective stage, ready for the fly's next meal (Silva Pereira et al., 2022).

Tsetse is not the only way in. Stable flies (Stomoxys) and horse flies (Tabanus) can carry trypanosomes mechanically, simply on blood left on their mouthparts when a feed is interrupted (Ochieng et al., 2022). This is how T. evansi spreads among camels in northern Kenya, well away from tsetse belts (Mdachi et al., 2023). Dogs can also be infected by mouth. In the Zambian study, dogs that ate fresh raw game meat and bones were at extra risk, because the parasites can enter through small cuts in the mouth (Lisulo et al., 2024). Farm, ranch, and hunting dogs that scavenge carcasses are therefore exposed even when few tsetse are seen.

As parasites multiply, the dog's immune system makes antibodies against their current VSG coat and clears most of them. A few, however, have already switched to a new coat. These survivors multiply into a fresh wave, and the cycle repeats (Silva Pereira et al., 2022). This explains two things owners notice: fever that comes and goes and blood tests that can look clear one week and positive the next. In chronically infected dogs, the number of parasites in the blood is often very low (Lisulo et al., 2024).

The illness follows the parasite as it moves from the bite site, through the blood, and into deeper tissues. Infection with T. congolense can be severe in dogs, and some dogs die within weeks (Kimeli et al., 2014; Matete, 2003). Others, particularly local dogs living with constant exposure, carry the parasite quietly with few outward signs (Ochieng et al., 2022).

No single test catches every case. Current expert guidance recommends combining three approaches: finding the parasite itself, finding its DNA, and finding the dog's antibodies against it, all interpreted alongside the dog's history and signs (Desquesnes, Sazmand, et al., 2022).

• Seeing the parasite. A fresh blood film, or blood spun in a fine glass tube so that parasites concentrate just above the white-cell layer (the buffy coat), lets us watch trypanosomes swimming. It is fast and cheap (Ochieng et al., 2022).

• Finding DNA (PCR). PCR detects tiny amounts of parasite genetic material and identifies the species, including the human-infective subspecies (Lisulo et al., 2024).

• Detecting antibodies (ELISA). Shows exposure, though a positive result does not always mean an active infection (Lisulo et al., 2024).

• Supporting tests. A complete blood count, biochemistry profile, and eye examination show how badly organs are affected and guide supportive care (Jayanthy et al., 2023).

Treatment combines a trypanocidal drug with supportive care. The drug most often used in dogs is diminazene aceturate, given by deep intramuscular injection at a dose calculated from an accurate body weight. A dog treated at the University of Nairobi small-animal clinic with diminazene and supportive care recovered within about a week (Kimeli et al., 2014). Supportive care may include fluids, nutrition, treatment of anaemia, anti-inflammatory medicine and eye care (Jayanthy et al., 2023).

Pharmacokinetics describes what the body does to a drug: how it is absorbed, where it travels and how it is removed. Diminazene belongs to a family of drugs called diamidines. It enters the parasite through a nutrient "doorway" in the parasite's membrane, known as the P2 transporter, and then binds to the parasite's kinetoplast DNA, shutting the parasite down. When a parasite's P2 doorway changes through mutation, less drug gets in, and this is one of the main routes to resistance (Kasozi et al., 2022).

After injection, the drug reaches high levels in the bloodstream quickly, then the level falls as the body clears it. Much less of it crosses the blood–brain barrier. Parasites hiding in the brain can therefore survive a treatment that clears the blood and later cause a relapse with nervous signs, as happened in a dog that first improved fully (Jayanthy et al., 2023; Kasozi et al., 2022).

Because relapses occur, we recommend repeat blood checks after treatment, ideally including PCR, and an immediate recheck if fever, a cloudy eye or any unusual behaviour returns (Desquesnes, Sazmand, et al., 2022; Jayanthy et al., 2023).

There is no vaccine against animal trypanosomiasis (Rascón-García et al., 2023), so prevention rests on reducing contact with flies and infected meat, and on early testing. Integrated control of the disease and its vectors is recommended over relying on drugs alone (Mdachi et al., 2023).

Most trypanosomes that infect dogs, such as T. congolense, T. vivax, and T. evansi, are animal parasites. One subspecies, T. brucei rhodesiense, causes acute sleeping sickness in people in eastern and southern Africa, and domestic and wild animals are its main reservoir (WHO, 2023). In parts of eastern Zambia, dogs have been found carrying this human-infective parasite, which is why researchers argue that dogs should be included in control programmes (Lisulo et al., 2024).

The good news for Kenya is significant. In August 2025, the World Health Organization validated Kenya as having eliminated human African trypanosomiasis as a public health problem, although surveillance continues because elimination does not mean the parasite has vanished (WHO, 2025). People catch sleeping sickness mostly through tsetse bites. Rare routes include mother-to-child infection and accidental needle-stick injuries in laboratories; ordinary contact with an infected animal is not a recognised route (WHO, 2023).