Hunt Africa, become a zombie?
African trypanosomiasis is a disease with many names--sleeping sickness, African lethargy--and is as iconic to the Dark Continent as Stanley and Livingstone. It has been present in Africa since at least the 14th century, but its origins could be thousands of years earlier. Prior to the arrival of Arab slave traders there was very little geographical movement of native tribes and so human trypanosomiasis was confined to isolated regions. But, along with the Arab invaders, it ultimately followed the Congo River, killing hundreds of thousands of people.
It wasn't until 1903 that the tsetse fly was identified as the parasite's vector by David Bruce, thereby offering new insights as to how the spread of the disease could be controlled. Similar in many respects to malaria--the result of a protozoan parasite spread by an insect which forms a crucial phase of its life cycle--Trypanosoma brucei is transmitted by the tsetse fly (Glossina sp) and is endemic in various parts of subSaharan Africa. It is believed to affect as many as 70,000 people in up to 37 countries in Africa. Some 48,000 people --mostly rural Africans--are believed to have died from the disease in 2008, though the problem epidemiologists face when trying to quantify trypanosomiasis is that the majority of cases occur in under-developed areas and go unreported.
A friend of mine, Dave Winall manager of the Rifa Education Camp run along the banks of the Zambezi by the Zimbabwe Hunters' Association -is currently recovering from a bout of trypanosomiasis which saw him hospitalised. Living proof that sleeping sickness is not some vestige of the age of African exploration, but a modern reality of life in the bush. As Dave recently said, the initial stages of the disease are very similar to those of malaria, so even an old Africa hand or a doctor can be forgiven for not recognizing the true culprit at the onset. A doctor in the United States or Europe treating a hunter recently returned from an African safari would be even less likely to make a right guess--it would be up to a laboratory technician knowing what to look for to confirm the presence of the disease. The catch? The common blood test for malaria picks up the trademark "signet-ring" appearance of erythrocytes--red blood cells--which are swollen and distorted with malarial parasites. The common tests for trypanosomiasis either look for living trypanosomes in a wet culture, or parasites stained with Giemsa dye in a fixed preparation. There are also various serological tests for trypanosomiasis, but they must be specifically performed, so the doctor has to be going in the right direction in the first place.
Like malaria, the first indication a person will have of trypanosome infection will be fever, headache, joint pains, and itching. Also, severe swelling of lymph nodes, sometimes including "Winterbottom's sign", the signature swollen lymph nodes along the back of the neck. This is the so-called haemolymphatic phase. And, like the malarial parasite, if not treated or incorrectly treated the parasite overcomes the body's defenses and can go on to cause anemia, endocrine, cardiac, and kidney dysfunctions. And, as the malarial parasite can and will eventually pass into the cerebro-spinal fluid, so will the trypanosome. This brings about the second phase of the disease, the neurological phase. The trypanosome produces a chemical known as tryptophol, a sleep-inducing drug in humans, and it is in the neurological phase that the classic symptoms of "sleeping sickness" occur--confusion, reduced coordination, disrupted sleep cycle, and alternating bouts of fatigue and manic periods eventually causing daytime donnancy and insomnia at night. If not correctly identified and treated, trypanosomiasis is invariably fatal as progressive mental deterioration leads to coma and death. Once the malady enters the neurological phase, and damage done is irreversible.
Trypanosomiasis occurs in two forms, each caused by a separate subspecies of Trypanosoma brucei T b gambiense or T b rhodesiense. Gambiense, found in central and western Africa occurs mainly in the human population and rhodesiense from southern and eastern Africa is found mostly in animals--in Zimbabwe, for instance, elephant, buffalo, kudu, bushbuck and warthog are the main animal host species, while less than 4% of impala in a contiguous area are infected. Animal populations acquire an immunity and co-exist with the parasite.
The tsetse fly of the genus Glossina is a large, brown biting fly that serves as a vector for the trypanosomes. Feeding on blood from a mammalian host, a tsetse fly injects trypomastigotes--the developmental form of the parasite into skin tissue. The parasites then enter the lymphatic system and progress into the bloodstream in which they are distributed throughout the body, continually reproducing by mitotic cell division. The tsetse fly is an integral part of the process, as parasites which are absorbed when feeding on an infected host develop into a new infectious generation in the mid-gut of the fly. Given the above, the disease of trypanosomiasis can theoretically be controlled by one of three approaches--immunisation of the population, treatment designed to eradicate the parasites in an infected host, and control of the fly.
The latter two control measures are to date the only ones which have shown any effectiveness. Large scale immunisation is unlikely to become a reality in the foreseeable future because the parasite's genome--its genetic makeup--contains over eight hundred genes that make proteins the parasite "mixes and matches" to confuse the body's immune system.
The first treatment brought out for the disease in an infected person was atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga in 1910. Blindness was a side effect which rendered the drug impractical. Pentamidine was introduced in 1939 to treat the haemolymphatic phase, and is still in use today. In the 1940s, melarsoprol was introduced to treat the neurological phase, but it produces serious side-effects such as convulsions, coma and psychotic episodes in as many as 10% of people treated with it. It is effective, however, and is also still in use today.
Because a trypanosome's generation is around three weeks, there is the potential for rapid genetic change and response--read resistance--to various drugs used. Difluoromethylornithine is the most modern treatment, and came out in the 1970s. Approved by the United States Food and Drug Administration in 1990, in 2001 the manufacturing firm of Aventis, together with association with Medecins Sans Frontieres and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.
But, as with malaria, the best "cure" is prevention, and there is a decided economic aspect to the depredations of the disease insofar as trypanosomiasis adversely affects not only people but also their domestic livestock. Therefore tsetse fly control measures are at the forefront --or used to be--of halting the spread of the disease. Zimbabwe is a good case in point as to how those measures have been compromised.
During the 1970s, an aggressive two-pronged campaign was waged to keep the fly out of commercial farming areas. Control measures consisted of erecting a cordon between wilderness and farmland, and then decimating the fly population within the "no-fly's land". This was achieved by culling the main tsetse host species of elephant, buffalo, kudu, bushbuck and warthog within the 6km wide corridor (which the relatively fragile tsetse fly could not cross without a blood meal), and selective application by handheld spraying apparatus of insecticide to the likely refuge sites of the fly. Because of sanctions against what was then Rhodesia, DDT was one of the only insecticides available and combined with the culling programme the control measures were seen as environmentally-unfriendly but economically necessary. And--a very important consideration local villagers living within the Zambezi valley were not permitted to own cattle. At the same time, a research programme was under way, aimed at placing a series of traps between the fly and the farmers which would capture wild tsetse, sterilize them in situ, and release them back into the wild. The latter approach was really the only one that would have stood the test of time and held any real chance of long-term success.
When Zimbabwe achieved its independence, restrictions on ownership of cattle in tsetse areas were lifted, aerial spraying of endosulfan was carried out, much of the research programme fell away, and the old tsetse control measures were gradually scaled back or abandoned. The result is that the fly has staged an amazing comeback, and trypanosomiasis is now as great a threat, if not greater, than it ever was. And, unlike mosquitoes, tsetse flied do not react badly to personal repellents--in fact, they seem to enjoy most of them!
Today, cases like Dave Winall's depend on timeous and correct diagnosis of the infection, and a vigorous treatment regimen. Trypanosomiasis was prevalent when the Zimbabwe ruins were built, was a disease of David Livingstone's day, and Ernest Hemingway's day and it's alive and well in the 21st century--so traveller beware!