Livestock Health, Management and Production › High Impact Diseases › Vector-borne Diseases ›
Trypanosomoses
Trypanosomoses
Author: Vincent Delespaux
Adapted from: R.J. CONNOR and P. VAN DEN BOSSCHE, 2004, African animal trypanosomoses, in
Infectious diseases of livestock, edited by J.A.W. Coetzer & R.C. Tustin. Oxford University Press, Cape
Town, 12: 251 – 295
Licensed under a Creative Commons Attribution license.
TABLE OF CONTENTS
Introduction ................................................................................................................... 2
Epidemiology................................................................................................................. 4
Pathogenesis ............................................................................................................... 12
Diagnosis and differential diagnosis ......................................................................... 15
Diagnosis and differential diagnosis .....................................................................................15
Clinical signs and pathology ........................................................................................15
Laboratory confirmation ...............................................................................................21
Differential diagnosis ............................................................................................................22
Control / Prevention .................................................................................................... 23
FAQs............................................................................................................................. 26
References ................................................................................................................... 27
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Trypanosomoses
INTRODUCTION
The trypanosomoses are diseases of humans and domestic animals that result from infection with
parasitic protozoa of the genus Trypanosoma. Trypanosomes parasitize all classes of vertebrates: fish,
amphibians, reptiles, birds and mammals. The parasites, with the exception of Trypanosoma equiperdum,
the cause of dourine, are transmitted from host to host by haematophagous vectors, and usually cause
little appreciable harm to either the vector or the vertebrate host. However, several species of
trypanosomes which parasitize mammals are less well adapted and commonly cause disease.
Trypanosomosis is generally characterized by the intermittent presence of parasites in the blood and
intermittent fever. Anaemia usually develops in affected animals, and this is followed by loss of body
condition, reduced productivity and, often, high mortality.
The first report that associated trypanosomes with disease was made from India in 1880. In 1895 a major
discovery was made in Zululand, South Africa that trypanosomes were the causal organisms of ‘nagana’,
or tsetse fly disease.
Two forms of human trypanosomosis exist: Chagas' disease occurs in Central and South America and is
transmitted by bloodsucking reduviid bugs, certain small wild animals and dogs harbouring the infection.
The second form is human sleeping sickness. This occurs in Africa and is transmitted by bloodsucking
flies of the genus Glossina, commonly known as ‘tsetse flies’ or simply as ‘tsetse’. The majority of animal
diseases caused by trypanosomes occur in the tropics. In Africa, several species of tsetse-transmitted
trypanosomes cause African trypanosomoses in domestic animals, which in southern Africa are
collectively known as ‘nagana’, a word derived from the Zulu word ‘nakane’ meaning tsetse fly disease.
‘Surra’ is transmitted by biting flies other than tsetse flies and, although it occurs in many parts of the
tropics, including northern Africa, it is not present in southern Africa.
The large populations of wild animals, which have thrived for millennia in the tsetse-infested tracts of
Africa have evolved with these flies and the trypanosomes they transmit. Hosts and parasites have
become mutually adapted and co-exist in a balanced relationship. Humans first brought domestic animals
into the tsetse belts of Africa relatively recently. Because of this recent introduction, the relationship
between tsetse-transmitted trypanosomes and domestic animals has not fully evolved and infection with
these parasites frequently produces disease.
The devastation which resulted from the rinderpest pandemic of the 1890s destroyed almost entire
populations of wild animals and millions of cattle. Without hosts on which to feed, tsetse disappeared from
large areas. However, a few decades later, tsetse were dispersing from residual pockets, and
trypanosomosis again became a problem for livestock owners. By 1931, tsetse were spreading at a rate
of 2500 square kilometres (1000 square miles) annually, and game elimination to control tsetse began in
1932. Since then strenuous efforts have been made to contain the tsetse fly. In many other parts of
southern Africa, livestock owners have also had to live with the tsetse fly and its consequences.
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Tsetse infest 10 million square kilometres and affect 37 countries, which makes African animal
trypanosomosis a problem of truly continental magnitude. They live in frost-free areas that have an
annual rainfall of 650 mm or more. In arid, marginal habitats, tsetse only exist in the better wooded and
better watered strips where the host species concentrate during critical times, such as in the late, hot, dry
season. Most of the settled areas of the tsetse fly belts of southern Africa are used for traditional mixed
farming, but the presence of tsetse seriously handicaps development.
Tsetse fly
Cattle
Trypanotolerant cattle
General distribution of tsetse flies and cattle in Africa
Concerted efforts to control tsetse over the past 50 years have resulted in significant changes in the
distribution of tsetse and tsetse-transmitted trypanosomosis. Unfortunately, few of these achievements
have been sustained. In many countries of southern Africa, the current distribution of tsetse and, hence,
tsetse-transmitted trypanosomosis is not much different from the ecological limits of the fly distribution.
Early work on trypanosomosis, much of it conducted in southern Africa, concentrated on describing the
trypanosomes and studying the natural history of the parasites, their vectors and their hosts. The greatest
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advances in knowledge of trypanosomosis over the past two decades have been made in the areas of
molecular biology and immunology.
EPIDEMIOLOGY
Trypanosomes are protozoan parasites of the genus Trypanosoma, order Kinetoplastida, and have, as
characteristic organelles, a kinetoplast and a flagellum. Typically, trypanosomes are digenetic parasites
and thus require two hosts to complete their life cycle: they multiply in the blood, tissues or body fluids of
a vertebrate host and, with the exception of T.equiperdum which is venereally transmitted, are ingested
by a haematophagous invertebrate vector. With a few notable exceptions, a cycle of development and
maturation occurs in the vector, after which the parasites are transmitted to another vertebrate host as the
vector feeds. Transmission is either by inoculation of trypanosomes with saliva or by contamination of
mucosa or broken skin with trypanosomes in the vector's faecal material, voided during the blood meal.
The type of development cycle within the vector determines whether or not infective, metacyclic parasites
are present in saliva or faeces. On this basis mammalian trypanosomes are classified into the two broad
sections of ‘salivaria’ and ‘stercoraria’.
In Africa, the pathogenic trypanosomes that cause sleeping sickness in humans and nagana in domestic
animals are salivarian, and cyclical development occurs in tsetse flies. Transmission of any trypanosome
species can take place mechanically without cyclical changes occurring in the vector. In nature, this is
effected by biting flies, such as Tabanus, Stomoxys and Lyperosia spp., which feed on more than one
animal before repletion.
Surra is a disease that affects a wide range of host animals, and it occurs in North Africa, the Near and
Far East, Central and South America, Philippines and Mauritius. It is caused by Trypanosoma evansi, a
dyskinetoplastic form of which — known as Trypanosoma equinum — also causes disease in equids in
Central and South America where it is known as ‘mal de Caderas’ or ‘Murrina’. These parasites have
adapted to an entirely mechanical, non-cyclical mode of transmission by blood-sucking flies other than
tsetse. Trypanosoma theileri is a stercorarian parasite of cattle which deserves greater mention. It was
first reported by Theiler in South Africa in 1903, and has since been found to occur in cattle throughout
the world. It is transmitted by tabanid flies and is widely regarded as being non-pathogenic, but in certain
circumstances it has been associated with disease.
Human sleeping sickness is caused by T. brucei gambiense and T. b. rhodesiense. Whilst these two
subspecies do infect some domestic and wild animals, there are other, more significant pathogens of
livestock.
The remarkable alternate adaptations of these extracellular parasites to mammalian and insect hosts are
reflected in morphological changes which are readily detectable by light microscopy. Bloodstream forms
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are trypomastigotes; from the posterior portion of an elongated body, some 8 – 35 µm long, arises a
flagellum which extends anteriorly, and which is connected to the body by an undulating membrane.
Beyond the anterior extremity of some species, the flagellum may extend free of attachment to the
undulating membrane. The beating of the flagellum pulls the trypanosome forwards, imparting
characteristic motility. Within the cell, in a posterior position and at the base of the flagellum, a kinetoplast
is found, and a single nucleus is located almost halfway along the body. In the tsetse fly, trypomastigotes
transform to epimastigotes in which the kinetoplast has migrated anteriorly, to a position adjacent to the
nucleus. Differences in the morphology of the trypomastigote stages of the various species form the basis
for differential diagnosis. The major characteristics are clearly seen in thin blood smears, stained with
Giemsa's, Leishman's or other Romanovsky stains.
a
b
c
d
Trypanosomes in thin blood smears, x1 000 stained with Diff-Quick. a = Trypanosoma congolense: note
absence of free flagellum; b = Trypanosoma vivax : note long free flagellum and large kinetoplast; c =
Trypanosoma brucei : note polymorphism, prominent undulating membrane and free flagellum; d =
Trypanosoma brucei dividing by longitudinal binary fission. (Unpublished photomicrographs by courtesy of
Dr L. Logan-Henfrey, International Laboratory for Research on Animal Diseases, PO Box 30709, Nairobi,
Kenya)
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Electron microphotograph of Trypanosoma congolense: cross-section showing flagellum (F), nucleus (N),
mitochondrion (M) and variable surface glycoprotein coat (VSG), x86 000. Bar represents 0,2 μm.
(Unpublished electron micrograph by courtesy of Dr P. Webster, Yale University School of Medicine,
Department of Cell Biology, New Haven, CT)
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Electron micrograph of Trypanosoma brucei : section through the flagellar pocket (FP) region of the cell.
Microtubules are longitudinally sectioned, x44 000. Bar represents 0,4 μm. (Unpublished electron micrograph
by courtesy of Dr P. Webster, Yale University School of Medicine, Department of Cell Biology, New Haven,
CT)
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Scanning electron micrograph of an intermediate (bloodstream) form of Trypanosoma brucei from the blood
of a mouse. Note the prominent undulating membrane, pointed posterior end and long, free flagellum. A
‘streamer’ or filopodium can also be seen. (By courtesy of Dr P. Gardiner and reprinted by kind permission of
Vinand Nantulya and Parasitology Today )
Trypanosomes show remarkable adaptation. They survive not only in the turbulent blood stream, where
they face vigorous immunological assault, but they also withstand the digestive enzymes of the tsetse
fly's alimentary tract.
Trypanosomes reproduce by longitudinal binary fission, both in the bloodstream and in the fly, although a
sexual process can apparently occur in the tsetse fly. Multiplication in each host culminates in the
presence of mature trypanosomes, which stop dividing and are pre-adapted to the conditions that they
will encounter in the next cyclical host. As a tsetse fly takes its blood meal from an infected host it ingests
trypanosomes. Pre-adapted parasites survive in the fly, but trypanosomes that are not metabolically
adapted to the new physiological conditions die. The transformation of bloodstream trypanosomes into
procyclic or midgut forms within the fly’s midgut is a crucial first step in the establishment of a
trypanosomal infection. The mechanism of maturation of a midgut infection is complex and, once
established does not always progress to maturation. Before the infection is mature, procyclic forms
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transform into epimastigote and then to metacyclic forms. From the midgut, trypanosomes migrate to the
mouthparts or salivary glands.
As the infective tsetse fly feeds, metacyclic trypanosomes and saliva pass through the hypopharynx and
are inoculated intradermally; it is here that infection is established. From the skin, the trypanosomes
reach the blood via the draining lymphatics within a few days. Trypanosomes multiply in the bloodstream,
and although initially their low numbers make detection difficult, the generation time of only a few hours
soon leads to high levels of parasitaemia. Trypanosomes may leave the bloodstream to reach various
extravascular sites.
The ability of trypanosomes to establish prolonged infections is attributable to the phenomenon of
antigenic variation. Each bloodstream trypanosome is completely clad in a dense surface glycoprotein
coat. Within a population of trypanosomes originating from a single infection, almost all bear the same
glycoprotein coat and are thus of the same antigen type. As parasitaemia rises, a swift antibody response
is elicited against the antigen type exposed on the surface of the bloodstream trypanosomes. These
specific antibodies attach to the surface glycoprotein and produce complement-mediated lysis of all
trypanosomes of that antigen type. However, before antibodies reach trypanolytic levels, some
trypanosomes — as few as one in 100 000 — switch off the gene that controls the production of the initial
surface glycoprotein and activate a gene that codes for a different protein. Trypanosomes which bear the
new surface glycoprotein are of a different antigen type and are not destroyed by antibody against the
first antigen type; they survive to produce another parasitaemic wave, which in turn is removed by
antibody specific for that antigen type. By this time a third variant has arisen, and, escaping the effect of
host antibody, it survives to produce the next parasitaemic peak. This antigenic variation is the result of
sequential expression of variable surface glycoproteins (VSGs) which constitute a repertoire of variable
antigen types (VATs). Infections arising from a single trypanosome may have a repertoire of more than
100 VATs. Thus shielded from total destruction, trypanosome infections usually run prolonged courses,
since each VAT is present for several days before being removed. Although within a parasitaemic peak
there is a mixture of a small number of VATs, the sequence of expression of VATs tends to be quite
stable in clonally-derived trypanosomes. This imparts immunologically distinct characteristics to a strain of
trypanosomes, the distinct strain being called a ‘serodeme’. In the course of successive parasitaemic
waves, some trypanosomes stop dividing and transform to the pre-adapted form able to survive in the
tsetse.
After ingestion by the tsetse, pre-adapted trypanosomes shed the glycoprotein coat, transform, multiply
and finally mature. Infective tsetse then transmits metacyclic trypanosomes to another host. Irrespective
of the VAT of the bloodstream trypanosomes ingested by a fly, the metacyclic VATs of a serodeme are
relatively constant. The antigenic diversity within a species leads to the possibility of animals in a tsetseinfested area being exposed to a large number of antigenically distinct trypanosomes, but although
trypanosomes within a species may be antigenically dissimilar, they are morphologically indistinguishable.
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The characterization of trypanosomes relied for a long time on comparisons of their morphology, motility,
host specificity, tsetse transmissibility and their development within the fly, but more recent
characterization methods include isoenzyme typing, analysis of kinetoplast DNA by polyacrilamide gel
electrophoresis, pulsed field gradient electrophoresis of chromosomal digests and DNA hybridization.
The sequel to infection with salivarian trypanosomes is not always disease. The outcome is determined
by many factors, frequently related to the susceptibility of the host and the pathogenicity of the
trypanosome. In the case of wild animals, a natural cycle of trypanosome transmission occurs which is
not associated with disease. Similarly, in some breeds of domestic animals, infection with salivarian
trypanosomes is tolerated, and host and parasite reach an equilibrium. Disturbance of the equilibrium
may precipitate disease a long time after establishment of the infection. Thus, although the tsetsetransmitted trypanosomes are aetiological agents of African trypanosomosis, infection is not always
synonymous with disease. The occurrence of T. theileri in healthy cattle throughout the world exemplifies
a well-developed host-parasite relationship.
Similar events occur in many wild animals which harbour tsetse-transmitted trypanosomes. Infected
animals show no clinical signs, but when they are subjected to the stress of capture, for example, their
immunity is reduced, parasitaemia flares up and clinical disease may be precipitated.
The epidemiology of African trypanosomosis is almost entirely dependent on tsetse flies. African
trypanosomes are well-adapted parasites of many species of wild animals, and sylvatic cycles of
trypanosome transmission occur throughout the 10 million square kilometres infested by this unique
vector. The natural hosts of salivarian trypanosomes usually show no clinical signs of infection, host and
parasites being in equilibrium. The large numbers of naturally infected wild animal hosts constitute a huge
reservoir of trypanosomes. Once infected, tsetses remain so for life and thus they too form a reservoir of
infection. Consequently, when domestic animals are introduced into areas in which sylvatic cycles of
trypanosome transmission occur, trypanosomosis always emerges as a serious disease. Wild animals are
the natural hosts of T. brucei rhodesiense, the aetiological agent of human sleeping sickness in central,
eastern and southern Africa. Thus, people living and working in tsetse areas are at risk of contracting the
disease, but for animal trypanosomosis to occur it is not always necessary for livestock to enter tsetseinfested areas; tsetse also move.
Changes in land use may also alter the extent of tsetse infestation. The abandonment of cultivation, for
various reasons, permits the regrowth of vegetation, which may then provide suitable tsetse habitat.
Conversely, the intensive settlement and cultivation seen in some areas destroy tsetse habitat.
The trypanosomal infection rate in tsetse is of prime importance. The ease with which infections develop
in tsetse depends upon the fly’s vectorial capacity and specific factors related to the blood of host
animals. Generally speaking, the duration of the development of trypanosomes in tsetse increases with
increasing complexity of the developmental cycle.
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The prevalence of trypanosomal infections in tsetse is also affected by host preference. Two aspects are
important in this context: first, there is diversity of host preference among Glossina and, second, different
species of hosts vary in their susceptibility to infection with the different species of trypanosomes. Of
particular importance is the relationship between absolute tsetse density and biting rate. A good
understanding of this relationship is essential when predicting the impact of tsetse control interventions.
Usually the challenge increases with the tsetse population density but even at low densities tsetse can
still cause a substantial disease problem. This is partly attributed to the often observed, increased
frequency with which flies that have metacyclic infections in their mouthparts probe.
Management practices may also alter the challenge to which livestock are subjected, and in this sense
management is central to the epidemiology of trypanosomosis. The different management of calves and
adult cattle can reduce significantly the level of challenge to which young animals are subjected.
Observations on the grazing ranges of livestock in West Africa showed that while cattle foraged widely in
tsetse-infested habitat, sheep, goats and donkeys remained closer to the villages. As a result, small
ruminants and equids were less exposed to attack by tsetse than cattle.
A major influence on the epidemiology of trypanosomosis is the use of trypanocidal drugs. Whilst
permitting the use of tsetse-infested land, chemotherapy may alter the prevalence of trypanosome
species in the area. In Zimbabwe, it was reported that the use of diminazene increased the prevalence of
T. vivax in cattle. Furthermore, the repeated use of trypanocides may result in the emergence of drug
resistant strains of trypanosomes, and the epidemiological picture then changes.
Wild animal hosts of tsetse, such as kudu, warthog, bushbuck, bushpig, buffalo, elephant and rhinoceros,
are vital to sylvatic cycles of trypanosome transmission and they form a major reservoir of infection. The
increasing popularity of game ranching or farming frequently entails the translocation of these animals
from tsetse habitats to tsetse-free areas. As a result, clinical disease may occur in animals normally
regarded as ‘immune’, in the absence of the tsetse vector. There is also the possibility that trypanosomes
could be mechanically transmitted from these species to livestock.
Wild animal hosts of tsetse and certain West African taurine cattle are tolerant of tsetse-transmitted
trypanosomes. Carefully controlled experiments have shown that the trypanotolerance of N’Dama cattle
and of African buffalo (Syncerus caffer) is an innate characteristic. This trait also occurs in some breeds
of sheep and goats. Lower trypanosomal parasitaemias and less severe anaemia occur in trypanotolerant
livestock than in trypanosusceptible animals. The epidemiological significance of this trait lies in the lower
morbidity and mortality due to trypanosomosis in tolerant breeds. Although trypanosome-infected
animals may effect self-cure, the usual sequel to infection in tolerant animals is the establishment of a
balance between host and parasite. If the host is stressed, the equilibrium is disturbed and a clinical
episode of variable severity is precipitated. Stress takes many forms. Animals in late pregnancy or which
are lactating are more susceptible to trypanosomosis. Overwork also constitutes a stress, which in
infected trypanotolerant stock may precipitate disease. This has serious consequences for animal traction
and for hard-working bulls used in restricted breeding seasons in tsetse-infested areas. In a similar
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manner, intercurrent disease is stressful; trypanosome-infected animals with helminthosis or other
diseases are more severely affected than those with either disease alone. The combined effect of poor
nutrition and increased exercise is often associated with an increased incidence of trypanosomosis in the
dry season.
Age also has a significant effect on resistance to trypanosomosis. It is widely recognized that cattle born
in an infested area do not immediately succumb to disease, even though they acquire trypanosomal
infections when young, whereas cattle brought into the area readily succumb.
Despite the antigenic complexity of trypanosomes, infected animals do mount immune responses which,
especially when supported by chemotherapy, can confer specific protection against homologous
serodemes. Thus, within a defined area, animals may acquire protective immunity against locally
prevalent serodemes. However, the movement of these animals to another area may expose them to
different strains, or serodemes, to which they may succumb. This type of tolerance requires continuous
challenge and explains the low mortality of cattle in high challenge, endemic areas (such as the Eastern
Province of Zambia) where trypanocidal drugs are used to prevent animals from succumbing to nagana.
The introduction of tsetse control measures in such areas would result in a loss of immunity that would
render the population highly susceptible to infection and disease. If tsetse control measures breakdown
severe outbreaks of trypanosomosis would ensue, probably with high mortality.
The African continent is experiencing considerable environmental changes as a result of an
unprecedented demographic growth.The increasing human pressure and the demand for arable land is a
major driver of land-use change resulting in deforestation, erosion and loss of biodiversity and suitable
habitats for tsetse flies Like many other arthropods, tsetse flies rely for their survival on habitats with
suitable conditions.The destruction and fragmentation of habitats has had important repercussions for the
density and distribution of tsetse flies. Insome instances,the drastic changes have resulted in the
disappearance of certain species In many cases, however, tsetse flies persist at lower densities in what
might appear to be unsuitable environments probably occupying microclimatic niches. The effects of
anthropogenic environmental changes on the epidemiology and impact of livestock trypanosomosis are
largely driven by the degree with which the tsetse flies adapt to an environment where domestic animals
are becoming increasingly important for their survival.These changes have been demonstrated in
southern Africa where epidemiological studies have clearly revealed the effect of such anthropogenic
changes on the impact of the disease on livestock and the appropriatenesss of particular control
strategies.
PATHOGENESIS
The precise pathogenesis of the trypanosomoses remains far from clear. Three features — anaemia,
tissue damage and suppression of immune responses — dominate the pathology of trypanosomosis.
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Infection becomes established at the site of inoculation of metacyclic trypanosomes in the skin, where a
chancre may form. Multiplication of the parasites induces an inflammatory response, the severity of which
depends upon the size of the inoculum, the species of parasite and the breed and species of the host.
These may originate from either the host or the parasites. The chancre reaches a maximum diameter, of
some 100 mm, ten to 14 days after an infective tsetse fly feed, its development preceding invasion of the
bloodstream by trypanosomes, and is accompanied by enlargement of the draining lymph nodes.
Trypanosomes are detectable in the blood 13 to 16 days after an infective tsetse fly has fed. At this time
the chancre begins to regress, and the characteristic series of intermittent parasitaemias begins.
Bone marrow impression smear from a calf with an acute Trypanosoma vivax infection, showing a
macrophage which has phagocytosed several erythrocytes x1 200. Stained with Wrights-Leishman.
(Unpublished photomicrograph by courtesy of Dr L. Logan-Henfrey, International Laboratory for Research on
Animal Diseases, PO Box 30709, Nairobi, Kenya)
After an infection has become established, a protracted battle ensues as the parasite provokes an
immune response. Anti-VSG antibodies destroy large numbers of trypanosomes. The destruction of large
numbers of parasites releases lysosomal and other enzymes as well as structural proteins. Some of these
enzymes have been identified and are thought to be directly harmful to the host. Many biological
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mediators such as the vasoactive amines are released from activated or damaged host cells. Anaemia is
a cardinal sign of trypanosomosis in many domestic animals, and the aetiology is probably similar in all
species. There is no single cause of the anaemia in trypanosomosis; the pathogenesis is complex and
involves a variety of mechanisms. Accompanying anaemia is leukopenia, which possibly arises from
direct inhibition of stem cell differentiation.
There are several possible sequelae to the early phase of infection, which depend largely on the nature of
the parasite and the susceptibility of the animal. There may be spontaneous recovery or death, but very
often there is a chronic phase which is characterized by infrequent, low-grade parasitaemias. Animals
lose weight and condition and, as a result of dyshaemopoiesis, remain anaemic. Extensive
haemosiderosis occurs as a result of erythrophagocytosis, and the trapping of iron in phagocytes is
believed to contribute to the failure of erythropoiesis. Despite the apparent absence of parasites in the
circulation, red blood cell destruction continues, and insufficient erythropoietic compensation results in
persistent anaemia.
The pathogenesis of tissue lesions varies with the species of trypanosome. Trypanosoma congolense
and T. vivax are mainly intravascular parasites; they induce changes in the endothelium of capillaries,
and so indirectly cause damage to adjacent tissues. Trypanosoma brucei, on the other hand, has an
affinity for tissues. Its presence in the extravascular compartment is associated with marked lesions in
parasitized tissues.
The severity of endothelial injury also depends on the interaction of host and parasite.
Trypanosoma congolense often attaches to erythrocytes and capillary endothelium. Damage to
endothelial cells by parasite products, immune complexes, vasoactive amines and cytokines increases
vascular permeability. In T. congolense infections a generalized dilatation of capillary beds, which alters
the haemodynamics, is observed. The concomitant anaemia and more sluggish tissue perfusion affect
the exchange of metabolites and are associated with intracellular oedema of capillary endothelial cells.
Fibrinous microthrombi form in response to endothelial damage. These changes can be prominent in
T. vivax infections, with which disseminated intravascular coagulation is more commonly associated.
Alterations to the microcirculation produce secondary degenerative changes in tissues. As capillary
permeability increases, phagocytes and products of the parasite extravasate more readily and are
responsible, in part, for some of the tissue lesions. Cytokines and parasite-derived substances, such as
proteases, may directly injure host cells, an effect that is exacerbated by the formation of immune
complexes in tissues. In the case of T. brucei, parasites localized in tissues cause mechanical disruption
of host cells and probably also have some direct toxic effect on host cells, possibly mediated by their
enzymes. The cellular response provoked by parasites within the tissues causes further damage, and
auto-antibodies are also thought to play a role in inducing lesions. The influence of all of these changes
on the course of the disease depends upon their severity and upon the degree of impairment of the
affected organs.
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An important feature of the pathogenesis of trypanosomosis is the effect on lymphoid tissue. As the
disease progresses, the volume of tissue in the spleen, lymph nodes and bone marrow inreases
markedly. This hyperplasia of reticuloendothelial cells reduces lymphoid cell density, and eventual
lymphoid depletion can occur.
Chronic disease is associated with progressive emaciation and eventually cachexia. This is usually
accompanied by low levels of parasitaemia but the pathogenesis is poorly understood. The reduced lifespan of red blood cells, the increased catabolism of many proteins, and the associated negative nitrogen
balance of clinically affected animals would appear to be largely responsible for the pitifully thin condition
of animals suffering from chronic trypanosomosis.
DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS
Diagnosis and differential diagnosis
Clinical signs and pathology
Cattle
Recognition of the wide range of clinical signs associated with the disease is important, both
within and outside endemic areas. The course of disease due to infection with salivarian
trypanosomes is variable and there are no clinical signs specific to bovine trypanosomosis.
Trypanosomosis in cattle may be acute, subacute or chronic; acute disease may be fatal after
brief illness lasting two to six weeks, but chronic disease lasting many months or even years is
more common.
Chancres are rarely seen in cattle with naturally-acquired infections. The first signs of disease are
due to the fever which accompanies the onset of parasitaemia. As parasitaemia falls, so does
fever; the course of infection is therefore characterized by fluctuating parasitaemia and parallel
fluctuations in body temperature. Intermittent parasitaemia and malaise are followed by
increasingly severe clinical signs.
Acute trypanosomosis causes sudden reduction of milk yields and also abortion. Oxen, bulls and
young stock with acute infections are reported to be suddenly ‘off-colour’. They are generally in
good bodily condition but are dejected, their ears droop and they may walk stiffly. Pulse and
respiratory rates are raised in febrile animals and there may be piloerection. Conjunctival
mucosae may be congested early in the acute phase but later, as anaemia develops, pallor of the
mucous membranes is evident.
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Acutely affected animals quickly lose weight and body condition, although they continue to eat.
They become weak, dejected and lethargic, often standing alone, away from the rest of the herd,
not seeking shade. Excessive lachrymation is sometimes seen at this stage. After a short illness
some acutely affected cattle become recumbent for a few days before death occurs. A proportion
of acutely affected cattle gradually improve to enter the chronic phase of the disease.
Subacute trypanosomosis in an ox: the animal has lost weight and condition and it is dejected, with
drooping ears and flaccid tail. (Reprinted by kind permission of FGU Consulting and Engineering
GmbH, Königstein, Germany, and the Regional Coordinator, RTTCP, Harare, Zimbabwe)
In contrast to the acute disease, subacute trypanosomosis is more common and runs a more
prolonged course, with many animals apparently making a spontaneous recovery. In subacute
cases, animals are intermittently ‘off-colour’, becoming weak and dejected, with drooping ears
and flaccid tail. Within a few weeks they lose weight and condition, the coat becomes dull and a
marked jugular pulse develops. Superficial lymph nodes and haemal lymph nodes are frequently
enlarged and are readily visible. Gradually, the frequency and intensity of parasitaemia decrease
and fever subsides. Dependent oedema, particularly in the submandibular region, may develop.
Thin, rough-coated, anaemic, lethargic cattle with generalized lymph node enlargement are said
to have a ‘fly-struck’ appearance. Death may occur between 4 and 6 months after the onset of
disease, but many animals make a gradual recovery, which is assisted by a good plane of
nutrition.
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Chronic bovine trypanosomosis is by far the most common form of the disease in endemic areas.
Severely affected cattle may be extremely emaciated, having lost a large proportion of their
muscle mass; they are often just ‘skin and bone’. Their general condition is very poor — the hair
is sparse and the coat is rough, dull and staring. Mucous membranes are very pale, the pulse is
rapid, and breathing is laboured; in resisting restraint, the animal may collapse in respiratory
distress after brief exertion. The combined effect of anaemia, circulatory disturbance and
myocardial damage frequently produces acute cardiac decompensation which leads to sudden
death from congestive heart failure.
The gross pathology of affected animals varies with the duration and severity of the disease, and
many organs and tissues are affected. The overall appearance of the carcass is one of paleness
and petechial and ecchymotic haemorrhages are frequently present, especially on serosal
surfaces. Lymph nodes are enlarged and, when incised, are oedematous and often have a dark
pigmented medullary area. Typically, the spleen is greatly enlarged and dark red. Excessive
peritoneal fluid is present which is often blood-tinged.
The gross pathology of chronic trypanosomosis is characterized by cachexia and anaemia. The
coat is dry and dull, the skin is scaly and inelastic, the eyes sunken and skeletal muscles are
atrophied. There is hydrothorax, hydropericardium and ascites, and the carcass, in general,
appears oedematous. Residual fat around the heart and kidneys is gelatinous. Lymph nodes,
haemal nodes and spleen are generally enlarged and have an appearance similar to that seen in
acute trypanosomosis, but after prolonged disease there may be splenic atrophy. The heart is
enlarged and flabby, the liver swollen and pale. Whereas red marrow is present in the long bones
in acute trypanosomosis, all the bone marrow is yellow and gelatinous in the chronic disease.
Gross changes are not always obvious, but microscopic lesions are extensive. These are found
particularly in the cardiovascular system and lymphoid tissues, and there is widespread infiltration
of many organs by mononuclear inflammatory cells. Dilation of the microvasculature, and oedema
and structural changes in vessel walls are usually seen, and trypanosomes are commonly
present in the lumens of blood vessels. A constant feature of trypanosomosis is initial hyperplasia
of the lymphoid tissues and of the mononuclear phagocytic system. The heart is commonly
affected, and macrophages, lymphocytes and plasma cells infiltrate the myocardium.
Degenerative changes and focal necrosis of myocytes and, in long-standing infections, fibrosis
are evident in the heart. Infiltrations also occur frequently in other organs such as the pituitary,
thyroids, adrenals, kidneys and gonads. Congestion and interstitial oedema also occur, and,
when the substantia propria is affected, corneal opacity then develops.
Sheep and goats
The general clinical signs of trypanosomosis of goats and sheep are similar to those in cattle.
Acute disease is characterized by intermittent and increasing dullness. During bouts of fever, sick
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animals walk stiffly, or stand with head held low, ears drooping and tail flaccid. Early morning
rectal temperatures may exceed 41 C in the febrile periods, when the pulse is rapid and the
breathing shallow and fast. Anaemia develops rapidly and the PCV falls from 0,35 l/ – 0,18 l/ or
less in two to four weeks, when mucous membranes become pale. Affected animals rapidly lose
weight and condition, and may die within a month of the onset of detectable parasitaemia. The
signs of subacute trypanosomosis are less marked, and the course of the infection resembles
that in cattle. Chronic infections are very common and may develop without marked clinical signs.
Parasites are rarely found in the blood and animals are afebrile. Clinically, it is difficult to
distinguish such animals from those with helminthosis. Furthermore, the immunosuppression
induced by trypanosomosis in goats and in sheep permits the establishment of large helminth
burdens, which thus exacerbate the clinical signs in affected animals. The pathology of
trypanosomosis in goats and sheep does not differ greatly from that in cattle.
A goat with a naturally acquired Trypanosoma vivax infection: prescapular lymph nodes are
greatly enlarged
Pigs
Trypanosoma brucei and T. congolense infections in pigs generally produce only mild disease.
Occasionally, anaemia occurs, which is accompanied by loss of condition and progressive
weakness leading to incoordination. Trypanosoma suis infections are of minor clinical importance
and have only rarely been recorded; infections run a chronic course, but may kill young pigs in
less than two months.
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Trypanosoma simiae infections in pigs eclipse in importance all other trypanosomal infections in
this host. This parasite may kill pigs after an incubation period of only four to six days, and
infected pigs may collapse and die within 24 hours of the first signs of disease. Affected pigs are
dull and inappetant or completely anorexic. They have a stiff, unsteady gait and eventually
become prostrate. Dyspnoea is evident and cyanosis may be seen. Some pigs froth at the mouth
and there may be diarrhoea. Rectal temperatures reach 41 C but the extremities are usually
cold.
The necropsy findings vary considerably, and there are no pathognomonic changes. The blood is
usually cyanotic, clots slowly, and chicken fat clots may be found in the heart. Haemorrhages
affect the epi- and endocardium, kidneys and serosal surfaces. The spleen is usually enlarged
and the pulp soft with a ‘strawberry jam’ appearance; there is excessive serous or serosanguinous fluid in the pericardial sac and pleural and peritoneal cavities; the trachea may be
filled with froth when there is also pulmonary oedema. Thoracic and abdominal lymph nodes are
usually enlarged and oedematous, and may be haemorrhagic.
Horses and donkeys
The general clinical signs resemble those seen in ruminants. Horses with acute trypanosomosis
are very dejected. Intermittent parasitaemia occurs and is accompanied by fever; rectal
temperatures may reach 40,5 C and there is tachycardia. Oedema of the lower limbs occurs
early in the course of disease, as affected horses are less active than normal. Subcutaneous
oedema then affects the ventral thorax and abdomen. Oedematous plaques may form on the
flanks, but dependent oedema is more pronounced. Weakness sets in rapidly. Initially, mucous
membranes may be congested and icteric but they become pale as the disease progresses. The
condition of the animal deteriorates rapidly and weakness may progress to paraplegia. Oedema
becomes increasingly severe. Animals die within two to four weeks from the onset of clinical
signs.
Chronic trypanosomosis commonly occurs in horses and donkeys. Animals lose condition and
weight and the coat becomes harsh and dry. Animals become extremely weak and show signs of
ataxia, but usually continue to eat. Subcutaneous oedema, initially affecting the limbs and ventral
abdomen, may extend to the sheath, scrotum, perineum and occasionally the head.
The general pathology of equine trypanosomosis resembles that occurring in cattle.
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A horse with a chronic Trypanosoma congolense infection showing emaciation and ventral oedema
Dogs
The general clinical signs of trypanosomosis in dogs resemble those in livestock, but the course
and severity of the disease are modified by the virulence of the parasite and the susceptibility of
the host. In acute disease the dog suddenly becomes dejected and inappetant. Pulse rate,
respiratory rate and rectal temperature are raised. Anaemia develops rapidly; mucous
membranes become pale and the dog shows signs of weakness and depression. There is
progressive weight loss; as the condition deteriorates, the coat becomes dry and subcutaneous
oedema, particularly of the head and limbs, may develop.
Ocular lesions characterize both T. brucei and T. congolense infections but are more severe in
the former case. Trypanosoma brucei invades all tissues of the eye, producing blepharitis,
conjunctivitis, keratitis and uveitis. Additionally, T. brucei invades many other tissues, and by
entering the cerebrospinal fluid causes ataxia and partial paralysis. Death ensues within four to
10 weeks of the onset of signs.
Infections with T. congolense generally follow a more protracted course. In chronic cases, dogs
become severely emaciated, and ulceration of the oral and gastrointestinal mucosa may develop,
leading to haemorrhage and melaena. Inappetance may only be intermittent, with animals being
periodically ‘off colour’.
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Lesions of trypanosomosis in dogs are broadly similar to those found in livestock. Anaemia is the
most readily detectable change early in the course of infection, and the PCV drops markedly.
Whilst T. congolense infections produce extensive interstitial oedema and ulceration of
gastrointestinal mucosa, tissue lesions induced by T. brucei are much more severe. There is
marked cellular infiltration and cellular degeneration and necrosis. The heart, choroid plexus and
eyes are consistently and severely affected.
Laboratory confirmation
The specific diagnosis of trypanosomosis is notoriously difficult. Not only are there no specific
clinical signs, but the intermittent and frequently low parasitaemias make detection of the
parasites difficult. Furthermore, infection is not synonymous with disease; many subclinically
infected animals live in delicate balance with potentially pathogenic trypanosomes. An element of
clinical judgment is, therefore, necessary when making a diagnosis of trypanosomosis. The
detection of infection in a few clinically affected cattle warrants careful examination of the entire
herd.
The only way to confirm diagnosis in clinically infected animals is to demonstrate and identify the
parasites in body fluids. The parasite detection methods are highly specific but their diagnostic
sensitivity is relatively low. This is especially the case when results are considered for an
individual animal rather than in a herd. As a result, the apparent prevalence of trypanosomosis
determined by parasitological diagnostic tests is an underestimate of the true parasitological
prevalence. This is a problem in areas where the disease is present at low prevalence or is
seasonal, or when attempting to confirm the absence of the disease in a particular area.
The body fluid most commonly examined is blood, either capillary blood from the tip of the tail or
venous blood from an ear vein or from the jugular vein. Lymph, aspirated from a punctured
superficial lymph node (usually the prescapular), provides useful supplementary diagnostic
material.
Wet blood smears are prepared by placing a drop of blood (about 2 µl), taken directly from a
punctured ear vein or the tip of the tail, onto a clean, dry, grease-free slide. This is immediately
covered with a cover slip and examined microscopically as a fresh, wet preparation with a x25 or
x40 objective lens. Approximately 50 to 100 fields are examined. Live, motile trypanosomes may
be seen as they bore their way between blood cells (the name “trypanosome” is derived from the
Greek “trypanon” a borer and “soma”, meaning body).
More commonly, for routine diagnosis in veterinary practice, thick and thin smears of blood are
prepared. A drop of blood taken directly from a punctured blood vessel in the ear or tail tip is
placed on a glass slide; a thick and a thin blood smear can then be made on a single slide.
Lymph smears are prepared in a similar manner. The unfixed de-haemoglobinized thick smear
allows approximately 120 times more blood to be scanned than a thin smear and, thus, has
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higher diagnostic sensitivity than the thin smears. Trypanosomes are easily recognized by their
general morphology but may be damaged during the staining process. This makes it difficult to
make a species-specific identification on thick smears. The thin smear, on the other hand, permits
accurate speciation of the parasites. However, due to the staining process, results are delayed.
The development of anti-trypanosomal antibody detection techniques has been a major
improvement in the serodiagnosis of trypanosomosis. The indirect immunofluorescent antibody
test (IFAT) has been and still is used widely to diagnose trypanosomosis. The test has undergone
several modifications so that it can differentiate, to a limited extent, between trypanosome
species in ruminants. The serodiagnosis of trypanosomosis has greatly benefited from the
introduction of enzyme immunoassays. The ELISA compares favourably with the IFAT and has
been found to give results that correlate with the local history of trypanocide usage. However,
even if a trypanosomal infection has been cured, anti-trypanosomal antibodies persist for several
months and antibody detection tests do not distinguish between current and past infections. They
can only provide a presumptive diagnosis.
A polymerase chain reaction (PCR) method has been developed for the diagnosis of infections
with African trypanosomes in humans, animals and tsetse flies. Specific repetitive nuclear DNA
sequences can be amplified for T. vivax and each of the three T. congolense subgroups. A
common primer set is available for detection of the three T. brucei subspecies. Despite the
development of more sensitive, more sophisticated and expensive diagnostic methods the
clinician will, for the foreseeable future, have to rely upon examination of blood smears, buffy coat
preparations and findings at necropsy to confirm diagnoses of trypanosomosis.
The diagnosis of trypanosomosis in small ruminants is no different from that already discussed for
cattle, but it is much more difficult because of the larger proportion of subclinical infections. In
these cases very low parasitaemias occur in the absence of obvious clinical signs. It is
undoubtedly these factors which are responsible for the serious underestimation of
trypanosomosis in small ruminants.
Differential diagnosis
In its various stages bovine trypanosomosis resembles a number of other disease conditions, and it
frequently occurs at the same time as other infections. In the acute febrile stage, bovine trypanosomosis
must be differentiated from redwater (babesiosis), anaplasmosis and East Coast fever. The haemorrhagic
syndrome in acute T. vivax infection can be distinguished from anthrax and haemorrhagic septicaemia
(Pasteurella multocida infection) by examination of Giemsa-stained blood smears, when large numbers of
trypanosomes are found.
The main disease entity which resembles trypanosomosis in goats and sheep is helminthosis, especially
haemonchosis. Anaemia, illthrift, weight loss, submandibular oedema and high mortality rates are
common to the two disease complexes, although diarrhoea sometimes accompanies helminthosis.
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A history of sudden death in a number of pigs, combined with clinical signs as described, is suggestive of
T. simiae in areas adjacent to tsetse infestations. Other causes of sudden death that should be
differentiated include African and European swine fevers and anthrax.
Chronic trypanosomosis in pigs should be differentiated from helminthosis and malnutrition.
Acute disease in horses and donkeys must be distinguished from African horsesickness, anthrax and
babesiosis. In chronic trypanosomosis the oedema has to be differentiated from that occurring in African
horse-sickness and the anaemia from that of equine infectious anaemia. Chronic babesiosis may also
produce signs similar to chronic trypanosomosis.
The signs of weight loss, emaciation and oedema caused by dourine (T. equiperdum infection),
strongylosis, malnutrition and dental disorders should be differentiated from those caused by salivarian
trypanosomes.
The anaemia in dogs caused by trypanosomosis must be differentiated from that arising from infection
with Ancylostoma caninum, Babesia canis or Ehrlichia canis. Hookworm infection may be concurrent with
trypanosomosis. Bilateral corneal opacity produced by trypanosomosis must be distinguished from that
seen in canine hepatitis (adenovirus-2 infection).
CONTROL / PREVENTION
For more than 60 years, Governments in southern Africa have made concerted efforts to control tsetse in
their battle against trypanosomosis. The ultimate goal, and the basis of many control strategies, was the
eradication of the tsetse fly. Despite considerable gains in some countries, few achievements have been
sustained because of the prohibitive cost of preventing tsetse from re-invading previously cleared areas in
the absence of natural barriers. Nagana, therefore, remains a serious constraint to development
throughout much of Africa and new approaches towards its control have been devised.
The new control strategy aims at intervening in areas where achievements are likely to be sustained by
the beneficiaries. Consequently, in most cases, trypanosomosis will be controlled on a smaller, localized
scale in areas that have to be selected carefully.
Several methods are available to control trypanosomosis. They may be directed against the vector or the
parasite, or towards the livestock and modified management. In choosing a method, technical and
economic aspects have to be considered and the most viable option selected.
Some of the tsetse control techniques, which have been developed with large-scale eradication in mind,
are not well suited for use in localized, small-scale control operations. Currently, tsetse control utilizes
odour-baited, insecticide-treated cloth targets and insecticide-treatments of cattle. Odour-baited,
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insecticide-treated targets have been very effective in Zimbabwe and have been employed in other
African countries to control various species of tsetse under different ecological conditions. Despite the
proven effectiveness of insecticide-treated cattle and odour-baited targets, the success of a tsetse control
operation will depend largely on its planning and implementation.
Trypanocidal drugs will continue to play an important role in the integrated control of trypanosomosis.
They appeal to communal cattle owners because they provide a means of protecting private goods and
may achieve impressive results at low costs. Although the low-level usage of these drugs may reduce
mortality rates, such usage generally has low impact on animal production. This will be the case
particularly in high challenge areas and when farmers use trypanocides therapeutically rather than
prophylactically. The development of resistance in trypanosomes to trypanocides is a continuous threat to
their sustainable use in the control of nagana. Even in areas where resistance to trypanocides has not yet
been demonstrated, the probability of its development should influence the selection of an appropriate
control strategy.
Millions of domestic animals are kept in tsetse-infested areas, but the degree to which they are exposed
to tsetse is frequently determined by management practices. The avoidance of heavily infested watering
points or grazing reserves reduces challenge, and thus controls trypanosomosis to some extent, but the
availability of alternative water sources and supplies of feed are then necessary. Prevention of livestock
movement into tsetse habitats also limits the disease, but the enforcement of livestock movement control
in Africa is not easy, because of communal grazing practices, seasonal migrations and local political
pressures usurping the law.
Under light tsetse challenge a therapeutic approach to control can be successful and economical. There
are numerous well-documented examples of susceptible breeds of livestock being successfully reared in
many tsetse-infested areas of Africa as a result of chemotherapy or chemoprophylaxis. To control
trypanosomosis successfully by chemoprophylaxis, it is necessary to treat a high proportion of cattle at
risk at regular intervals. This is not always possible, especially if owners have to pay for treatment, and
consequently, a therapeutic approach to control is widely used. There is considerable evidence that such
therapeutic control assists the acquisition of protective immunity to locally prevalent trypanosome
serodemes, whereas with chemoprophylaxis immunity to trypanosomes does not seem to develop.
The satisfactory treatment of trypanosomosis requires more than a correctly administered trypanocidal
drug, and the speed of recovery is largely determined by the plane of nutrition, the amount of exercise
during convalescence and the duration of the disease. Well-rested and well-fed animals recover more
rapidly after trypanocidal therapy than do undernourished animals which have to trek long distances to
pasture and water. However, chronic trypanosomosis often fails to respond to therapy.
Diminazene and homidium are therapeutic trypanocides, although homidium does provide prophylaxis for
several weeks. Isometamidium, whilst having a curative effect, is widely regarded as being the only
trypanocide worthy of being used for prophylactic purposes. Trypanocides are toxic compounds and have
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narrow therapeutic indices, so therefore the dosage rates cannot be greatly increased to obtain greater
trypanocidal efficacy. Furthermore, they are not equally effective in the treatment of all species of
trypanosomes. A single injection of diminazene cures T. congolense and T. vivax infections at a dosage
rate of 3, 5 mg/kg but a dosage rate of 7, 0 mg/kg is necessary to treat T. brucei infections. The efficacy
of the phenanthridine compounds, homidium and isometamidium against T. congolense and T. vivax is
more marked than against T. brucei at recommended dosage rates. Dosage rates of isometamidium in
excess of 2, 0 mg/kg are toxic to cattle, and even below this level, the drug is irritant and has marked
local effects.
The prophylactic effect of isometamidium depends upon the slow release of the drug from the depot
created at the intramuscular injection site. Isometamidium is irritant and at the site of injection, it induces
an intense inflammatory response and causes necrosis of muscle fibres. This lesion becomes
encapsulated and is later organized by fibrous connective tissue. From this depot, the drug is slowly
released. Attempts to overcome this irritant side effect by reformulation of the drug have been
unsuccessful to date. The repeated inoculation of cattle kept under tsetse challenge induces extensive
muscular scarring, and to reduce carcass damage and subsequent losses from condemnation, the drug is
usually administered into the less economically valuable neck muscles, often with untoward side effects.
The use of trypanocides at subtherapeutic levels is believed to promote drug resistance in trypanosomes.
Since diminazene is rapidly excreted, the risk of trypanosomes being exposed to sublethal levels of the
drug is less than is the case with isometamidium. Prophylactic levels of isometamidium wane over much
longer periods. Even when cattle receive isometamidium at the correct dosage rate, it may be
administered at the wrong time. Tsetse challenge may increase at a time when drug levels have declined
and are not protective.
True resistance to trypanocides is a spectre which looms large. The development of resistance has led to
the withdrawal of many trypanocides in the past, and resistance to the few remaining currently-used
trypanocides is well documented. The degree of resistance in trypanosomes is not clear cut; a spectrum
of drug sensitivity occurs, and resistance to low levels of a drug may be overcome by increasing the
dosage rate.
The antigenic complexity of trypanosomes has thwarted attempts to develop a vaccine. Although potential
immunological targets within the parasite have been identified, no vaccine will be commercially available
in the near future, and the greatest hope for the immunological control of animal trypanosomosis lies in
the exploitation of trypanotolerant breeds of livestock. It is intended, through a process of selective
breeding of trypanotolerant animals, to reduce the problem of trypanosomosis and to improve livestock
productivity. However, this approach offers little hope for southern Africa today: inheritance is complex
and the number of trypanotolerant animals is relatively small. On the other hand, the fact that some Zebu
cattle survive in tsetse-infested areas provides a basis for attempting to select the more tolerant of these
animals for breeding purposes.
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FAQS
1. Why is trypanosomiasis called “sleeping sickness”?
The infection by trypanosomes when reaching the brain causes nocturnal sleeping disorders.
Patients are then so tired that they are sleeping during the day.
2. In the literature the disease is called trypanosomiasis or trypanosomosis. What is the
correct term?
In the past, trypanosomiasis was the sole term that was used. The OIE (Office International des
Epizooties) proposed to use trypanosomosis which was accepted by the World Assembly of
Delegates of the OIE. Some authors now are using trypanosomiasis for the human forms of the
disease and trypanosomosis for the diseases affecting animals.
3. Why are tsetse flies called tsetse?
Tsetse (tsé-tsé in French) means in a local language of West Africa “fly that kills cattle”. Saying
thus tsetse fly is incorrect as it is repeating the term “fly”.
4. Are tsetse always involved in the transmission of trypanosomes?
No, T. equiperdum is transmitted sexually. T. vivax can also be transmitted mechanically by blood
sucking flies and evidences are accumulating that T. congolense might also be transmitted
mechanically.
5. It seems that sleeping sickness might be different from country to country. Is that indeed
the case?
Human sleeping sickness can be caused by two different trypanosomes: T. brucei gambiense or
T. brucei rhodesiense in West and East Africa respectively. In West Africa, the disease is longer
and more chronic than in East Africa where the disease is far more acute.
6. The disease is known for more than a century now. Why is there no vaccination available?
Trypanosomes developed a very clever strategy to escape the immune system of the host. The
proteins that are covering the trypanosomes and that are recognized by the immune system of
the host change regularly in composition. The host has to adapt his response at every change.
During this adaptation period, trypanosomes can multiply. This phenomenon is called “antigenic
variation”.
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REFERENCES
1. Bourn, D., Reid, R., Rogers, B., Snow, B., Wint, W., 2001. Environmental Changes and the
Autonomous Control of Tsetse and Trypanosomosis in Sub Saharan Africa Case Histories From
Ethiopia the Gambia Kenya and Zimbabwe. Information Press, Oxford UK.
2. Courtin, F., Rayaisse, J.B., Tamboura, I., Serdebeogo, O., Koudougou, Z., Solano, P., Sidibe, I.,
2010. Updating the Northern tsetse limit in Burkina Faso (1949-2009): Impact of global change.
International Journal of Environmental Research and Public Health 7, 1708-1719.
3. Ducheyne, E., Mweempwa, C., De Pus, C., Vernieuwe, H., De Deken, R., Hendrickx, G., Van den
Bossche, P., 2009. Assessing the impact of habitat fragmentation on tsetse abundance on the
plateau of eastern Zambia. Prev. Vet. Med. 91, 11-18.
4. Van den Bossche, P., 2001. Some general aspects of the distribution and epidemiology of bovine
trypanosomosis in southern Africa. Int. J. Parasitol. 31, 592-598.
5. Van den Bossche, P., de la Rocque, S., Hendrickx, G., Bouyer, J., 2010. A changing environment
and the epidemiology of tsetse-transmitted livestock trypanosomiasis. Trends Parasitol 26, 236243.
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