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 sub-Saharan 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 someone recently returned from Africa would be even less likely to make the 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 defences and can go on to cause anaemia, endocrine, cardiac, and kidney dysfunctions. And, as the malarial parasite can and will eventually pass into the cerebra-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 dormancy 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, 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 midgut 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 forseeable 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 in1939 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 the1970s. Approved by the United States Food and Drug Administration in 1990, in 2001 the manufacturing firm of Aventis, together with association with Médecins Sans Frontières and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.
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Sleeping Sickness Alive & Well?
An Excerpt from the African Hunter's Guide to Bush Medicine
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.
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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. Unfortunately, Zimbabwe’s war on the tsetse has been compromised and 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 flies do not react badly to personal repellants - 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!
An Editorial Taken from African Fisherman Volume 23 #3
By Ant Williams
Africa can be a particularly nasty place to live, especially if you love the outdoors and get to interact with the abundant creatures that inhabit our Dark Continent. Elephant, lion, hippos and crocodiles... while thrilling to look at, all seem to be waiting for that one careless mistake, or can be triggered by a thoughtless invasion of their safety zone. Sometimes though, it is not the big and hairy creatures that might pose a danger to us as fishermen, and I am left pondering their effect on our psyche.
My love of wild animals is garnered with healthy respect. This is because I have been “tracked” by elephant following my scent in the bush, ambushed by sneaky buffalo watching my approach, and determinedly stalked by hippo as I have dragged stuck boats across shallow sand bars. Experience and knowledge of animal behaviour helps, but at best I consider myself a novice at this, and prefer instead to avoid situations where lack of good judgement could get me stomped on.
I get particularly twitchy around hippo though. While I have never been capsized by one, or truly threatened to the point where I doubted my survival, I have been the target of several charges - on land as well as water - and have gained what many consider an unnatural fear of them. I know the fishing can be good around a pod of lazily basking hippo, and have also learned that for the most part, they will endeavour to get out of my way. But, it is those times when they do not behave as they should, that have given me cause for the irrational behaviour I exhibit when in close proximity to the beasts. Over the years, I have tried to master the art of staring into their eyes to judge their intent, and on occasion have adopted an air of bravado to demonstrate my lack of fear. It works with dogs, so why not hippo? In truth, I have never really mastered the art of reading their minds, or even specific behaviour with any great confidence, and seem unable to intimidate them with my presence.
But one of God’s creatures which has had a profound effect on my psyche, is the tsetse fly. I am both afraid and amused by this little stinging insect, and the effect it has on behaviour... mine and that of others. I call it the “Tsetse Jive”. Experience has taught me, that a mature fly is capable of landing on your skin - usually some soft area such as your neck - ingesting a body-full of blood, and escaping undetected. This can happen many times over a relatively short period, and the first inkling one has of a bite, is at the onset of the first itch. For some reason, scratching one bite tends to activate all the others, and within seconds you do not have enough hands or long enough nails to satisfy your itching body as you contort into a convulsive flurry of scratching and slapping. This marks the onset of the Tsetse Jive.
Perhaps the most terrifying thing about these little flies, is their tenacity for life. Simply swatting them seems to goad them, and they go into super-stealth mode, flying faster and quieter so you never really know where they are. The only sure way to kill them, is to catch the culprit and crush him between your fingers till an audible crunch is heard, or simply bite its head off. I have, on occasion, done this out of sheer spite, though I suspect the act of malice was lost on the fly!
On my recent visit to the Mana area, we drove through several belts of flies, and as would be expected, ended up with some unwanted guests in the cab. My passenger had little experience of tsetse flies, and while extolling the many virtues of this super insect, I sat back and watched as one lone fly in the vehicle turned her into a blithering idiot.
In almost choreographed sequence, the “jive” started, and as is inevitable, with the casual “swat” at the passing fly. At this, the fly knew the game was on, and disappeared from sight. A few seconds ticked past, and I watched Renee grab the back of her neck, and run her fingers through her hair while suspiciously looking over both shoulders. This was the fly’s cue, and it lazily flew past her and dived at her feet, to once again disappear. As a little shudder rippled up her spine, she once again slapped her neck, then went into hyper-speed slapping her legs and ankles in some rendition of the Gum-Boot Dance. By this time the fly had manoeuvred under the seat, up the back and landed on her head. Now jumping up to fold both her legs under her on the seat, she began slapping herself in earnest, a growing look of terror turning her eyes wide. The shudder which rippled her spine minutes before, had become a series of twitches as she begun uttering sounds of panic while scratching at imagery bites. She in fact, had not been bitten at all.
Then, as if appearing by magic, the fly landed on the dashboard. Armed with a map book, she swatted it with a loud clap, and smeared it on the dashboard, a vindictive smile crossing her face. Knowing as I did, that neither the swat nor the smear were sufficient to dispatch the fly, I watched as she lifted the book, and stared in horror as the fly began wiggling its legs, and took flight before she could launch another attack. At this, the whole dance started again, but this time with more fervour, and while I laughed uncontrollably at her antics, I too was engaged in my own little Tsetse Jive, but without the ability to fold my legs on the seat, had sustained several bites.
We did eventually manage to kill the fly... it is still smeared on my list of notes taken during the trip. But, for the rest of the drive home, any time I looked left or right sharply, or slapped or scratched at my body (which I did just to tease her), she began a new Tsetse Jive. Talk about conditioning! What fun. Even as I write this, I have run my fingers through my hair more than once, and scratched at my ankles. If you have ever been bitten by a Tsetse fly, I’ll bet you have done the same as you read this.
As funny as this all is, the proliferation of the tsetse fly in many parts of Zimbabwe again, brings with it a real danger of contracting sleeping sickness, and care should be taken in assessing symptoms of possible malaria after visiting the bush.
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