As we have mentioned, there are strains of two African trypanosome species that have adapted to mechanical transmission by biting flies in various animal species, or to life in tissue fluids and venereal transmission in horses and donkeys. Much of what has been written on AAT in other chapters also applies to these forms of trypanosomosis, and in this chapter we shall briefly mention some of the peculiarities of the parasites involved, their distribution and, where relevant, disease and control aspects.
T. evansi has almost certainly arisen from T. brucei brucei by adaptation to mechanical transmission by biting flies, and it remains very closely related to T. brucei. It has lost the capability of being cyclically transmitted by tsetse flies and in the process has become almost monomorphic, the great majority of the parasites being indistinguishable from the long slender forms of T. brucei. It has spread far outside the tsetse regions of sub-Saharan Africa and is at present known to occur throughout the Sahel region of Africa, in North Africa, most Near and Far East Asian countries (including southern Siberia, China and Indonesia) and many countries in Latin America, from Argentina in the south to at least Venezuela and Colombia in the north. The situation in central America is not well defined, but in the past the parasite has been reported from at least one country, Panama.
T. evansi is the cause of the most important parasitic disease of camels, and is also highly pathogenic for horses (and mules and donkeys) and for dogs. It is also of considerable economic importance in Asian (domestic) buffalo, and to a less extent in some countries in cattle as well. Many other host species, wild as well as domestic, have been found naturally infected. The most common name for this disease is surra, of Indian origin, now generally accepted, but in Africa and Latin American countries there are various other names (see below).
Apart from the name surra, which originates from India, the disease is known in many Arabic-speaking parts of Africa as el debab, and many other local names exist, e.g. gufar in the Sudan. It probably occurs wherever camels are reared.
Surra in camels is usually a chronic wasting disease, and the general description of the symptoms of African animal trypanosomosis in Chapter 2 applies.
Striking clinical symptoms develop a month or so after infection, with acute bouts of fever, associated with dullness, lack of appetite and lachrymation, coinciding with peaks of high parasitaemia. Gradually the animal loses condition, the hump shrinks and progressive weakness becomes noticeable. Oedemas may occur. Pregnant animals often abort. The disease is usually fatal, sometimes rather quickly, a few weeks or more often a few months after the onset of the disease; the evolution is much more often chronic, and may last as long as two or three years. In chronic cases it is usually very difficult to find parasites in the blood by direct means.
The most important mechanical vectors of surra in camels are probably tabanids; hippoboscids (Hippobosca camelind) are also suspected, but so far there is no formal proof of their vector role.
40 The word camel is used here in the orginal (Arabic) sense, and encompassess both the one-humped camel (or dromedary) and the two-humped bactrian camel.
Outbreaks of acute disease may occur in buffalo41 and cattle in areas where the disease is introduced for the first time.
Even in endemic areas T. evansi may cause anaemia and loss of condition in buffalo, and although the infection is usually not fatal, the disease may assume real economic significance. Draught animals are particularly prone to the effects of the infection.
Cattle are rarely seriously affected, but the parasite may have a negative influence on fertility and dairy breeds may not attain their production potential.
Although experimental infections of small ruminants may cause disease, in the field sheep and goats are rarely seriously affected.
41 Only domestic buffalo (Bubalus bubalis) are concerned, the wild African buffalo (Syncerus caffer) is not affected by T. evansi.
Horses are extremely susceptible to infection with T. evansi. It has even been possible to cause fatal infection by inoculating one single trypanosome. The disease often runs an acute course, lasting from a few weeks to one or two months; more chronic cases are also found and the animal may survive even a year or more. In long-lasting cases, cerebral symptoms often develop.
Mules are said to be as susceptible as horses, but donkeys are more resistant.
This species is readily transmitted mechanically, even in Africa, wherever sufficient biting flies occur, particularly (but not exclusively) tabanids and stable flies (Stomoxys). In the past T. vivax has also occurred on the island of Mauritius, in the absence of tsetse flies, but has apparently been eradicated there. T. vivax invaded the western hemisphere a long time ago, possibly with the introduction of West African cattle in the Caribbean region in the eighteenth and nineteenth centuries, and has since then established a firm foothold in the Americas. It has been found in the past as far south as Paraguay, and nowadays is known to occur at least from Bolivia in the south to El Salvador, in Central America, in the north, but the limits of its distribution are not well known. Cuba has also been reported to be infected.
The disease caused by the mechanically transmitted T. vivax does not appear to be essentially different from that caused by the tsetse-transmitted parasite.
The venereal disease dourine is confined to equines, members of the horse family. Horses are most susceptible, donkeys much less so. (Mules are not really concerned, because they are not normally used for breeding, so they do not become infected.)
As transmission of dourine does not require insect vectors that are influenced by climatic factors, the disease may, in principle, been found anywhere. It has indeed spread in the past as far north as Canada and Russia, and as far south as Chile and South Africa. The present distribution of dourine is discussed in Distribution, p. 38. The disease has been eradicated from many parts of the world, mainly by serological testing and slaughter of positive animals. The complement fixation test has been -used for this purpose in the past. Although it is still mandatory in some countries, modern, more sensitive tests are now preferable, e.g. the IFA test, or the ELISA. One great problem is the fact that none of these tests differentiates between T. equiperdum and T. evansi (or even T. brucei).
The symptoms of the disease are variable. Classically, there are three stages. During the first stage the genitalia become swollen and in mares there is a discharge from the vagina, and loss of pigment in the mucosa of the vulva or penis; this depigmentation occurs in patches. Slight fever and a loss of appetite may be noticeable. After a month or so the second stage starts with round urticarial eruptions, plaques (patches), on the neck, the chest, the flanks and the rump. A plaque looks “as if a coin has been inserted under the skin”. They are visible for a few days and then disappear, but may come back. In the third stage a paralysis sets in, involving various muscles, and spreading to the hind legs, causing incoordination. Complete paralysis of the four legs may finally occur.
This is the classical evolution of the disease but, often, particularly in long-standing endemic regions, the symptoms are rather mild and not all stages are always apparent. It has for example been reported that the typical cutaneous plaques are not normally observed in dourine cases in South Africa. There also appear to be differences in virulence between strains. Even in cases terminating fatally, the disease may last for a year or even two years.
The diagnosis of dourine is not always easy. Clinical symptoms, if typical, can be of great help in an area where the disease is known to occur. Trypanosomes are not normally found in the circulating blood, but can often be detected in fresh preparations or stained smears from the mucous discharge from the vagina or tissue fluid taken from the swollen genitalia or the urticarial plaques. In atypical cases it may be impossible to detect the parasite. Mice, rats, rabbits and dogs are susceptible to infection with T. equiperdum, once it is established in laboratory animals, but animal inoculation is of little use as a routine method of diagnosis because it is very difficult and often impossible to obtain a first passage.42 Serological tests have been decisive in eradication campaigns, with positive animals being slaughtered or at least prevented from breeding. However, it must be realized that these tests, while extremely valuable in areas where T. equiperdum is the only pathogenic trypanosome present, do not distinguish between this and other members of the subgenus Trypanozoon.
42 After adaptation to life in the circulating blood of laboratory animals, T. equiperdum becomes indistinguishable from T. evansi and from the long slender forms of T. brucei.
As stated at the beginning, we will not deal with the American trypanosome T. cruzi. Although it infects a large number of host species, including humans, it probably has little economic significance for livestock. As stated before, the economically important livestock trypanosomes have been introduced: T. evansi, T. vivax and T. equiperdum. T. vivax was probably introduced with cattle imported from West Africa, perhaps as early as the eighteenth century, while T. evansi and T. equiperdum may well have arrived much earlier with horses of the Spanish colonizers.
As no tsetse flies occur in the western hemisphere, it is generally accepted that the transmission of T. evansi and T. vivax is essentially mechanical, by biting flies as well as iatrogenic. Congenital transmission may sometimes also play a role. Special mention should be made of the transmission of T. evansi by vampire (blood-sucking) bats. The bats become infected when ingesting blood from a parasitaemic animal. The trypanosomes multiply in the bat, and the parasite is again transmitted, through the mucosa of its mouth, during subsequent bloodmeals. Thus, these bats are not only vectors but also reservoirs of infection. Apart from vampire bats, T. evansi is found in various other wild animals in Latin America, such as the capybara (giant rodent), wild carnivores, monkeys, and deer, which all may be reservoirs of infection for domestic livestock, including llamas and alpacas.
The disease caused by T. evansi in horses is known as mal de caderas in Brazil, as derrengadera in Venezuela and as murrina in several other Latin American countries. T. evansi infection in Latin America is probably in the first place an economic problem in horses (and donkeys).
T. vivax has also been found occasionally in some wild animals, such as deer, in the western hemisphere, and these may, in principle, act as reservoirs of infection for domestic livestock. Nevertheless, it is believed that domestic animals (cattle, buffalo, sheep and goats, and also llamas) are themselves the main reservoirs of infection. Some local names for the disease are secadera, huequera and cacho hueco. The economic importance in Latin America has not been properly assessed. T. vivax is mainly of economic importance for cattle, but losses have also occurred in domestic buffaloes in Brazil.
Dourine (T. equiperduni) has occurred in the Americas from Chile in the south to Canada in the north. It has since been eradicated in North America, but its present distribution in the western hemisphere is not well known. Since 1975 it has only been reported in Bolivia, but it is a disease which sometimes leads a secret existence.
Information on the economic impact, the epidemiology and the distribution of trypanosomoses of domestic animals of Latin America is still insufficient, although progress has been made in some countries, for example, Colombia, Brazil, Venezuela and French Guyana.