TRYPANOSOMIASIS

• Trypanosomes are flagellated protozoan parasites that live in the

blood and other body fluids of vertebrate hosts.
• Greek word
• Trypano -borer
• Soma –body

• With the help of the flagellum, they swim in body fluids, boring
their way between cells

• They generally possess a kinetoplast and undergo cyclical

development in an arthropod vector
DOMAIN Eukaryota

KINGDOM Protista

PHYLUM kinetoplasta

CLASS kinetoplastida

ORDER Trypanosomatida

FAMILY Trypanosomatidae

GENUS Trypanosoma
subgenus species

schizotrypanum T.cruzi

Duttonella T.vivax

Nannomonas T.congolense

Trypanozoon T.brucei
T.brucei brucei
T.b.rhodesiense
T.b.gambiense
T.equiperdum
T.evansi

pycnomonas T.suis
 HISTORY
• In 1841, Gabriel Valentin found flagellates that today are
included in Trypanoplasma in the blood of trout

• The genus (T. sanguinis) was named by Gruby in 1843, after

parasites in the blood of frogs

• 1880-Griffith Evans ,found trpanosomes horses,mules and

camels blood….suffering from a fatal wasting disease called
surra
• 1895-discovered T.brucei as the cause of cattle trpanosomiasis
• 1901-Robert Michael Forde first observed trypanosomes in
human bood in Gambia
• 1902-Joseph Everett Dutton proposed the species name
T.gambiense

• In 1903, David Bruce identified the protozoan parasite and the

tsetse fly vector of African trypanosomiasis
• 1905-T.vivax discovered by Hans Ziemann
• 1909-Carlos Justiniano Ribeiro Chagas first described chagas
disease
• A firm but elastic pellicle, supported by fine microtubules
covers the body and maintain its shape
• A long thread like flagellum project from the front end of the
body.

• All along its length over the body, the flagellum is connected by
a fin-like undulating membrane formed of cytoplasm and
folded pellicle
• There is a large oval nucleus and a long oval narrow band like
mitochondrion in the cytoplasm
• A conspicuous mass of DNA called Kinetoplast is embedded in
the mitochondrion near the gullet
• In between the reservoir and the nucleus, Golgi apparatus is found

• In trypanosomes large deeply-staining volutin granules are found

scattered in the cytoplasm

• These granules represent the stored glycogen or protein or nucleic

acids

• Endoplasmic reticulum with ribosome’s is also present

• As trypanosomes progress through their life cycle they undergo
a series of morphological changes as is typical of
trypanosomatids

• The life cycle often consists of the trypomastigote form in the

vertebrate host and the trypomastigote or promastigote form in
the gut of the invertebrate host

• Intracellular lifecycle stages are normally found in the

amastigote form

• The trypomastigote morphology is unique to species in the

genus Trypanosoma.
Promastigote(leptomonas stage)
• Elongated/fusiform with flagella extending
forward
• kinetoplastid located distally at the anterior end
• without undulating membrane
Epimastigote(crithidia stage)
• Elongated with anterior flagella and
undulating membrane
• Kinetoplastid located near the nucleus
Trypomastigote
• Seen in blood stream
• Flagellum runs entire length from
posterior
• Kinetoplastid is posterior to nucleolus
salivarian
• develop in the anterior gut of
insects, most importantly the
Tsetse fly
• infective organisms are
inoculated into the host by the
insect bite before it feeds.
• Trypanosoma evansi
• Trypanosoma brucei (including
the human infective subspecies T.
b. gambiense and T. b.
rhodesiense),
• Trypanosoma vivax
• Trypanosoma congolense
stercorarian
• developing in the posterior
gut followed by release into
the feces and subsequent
depositing on the skin of
the host
• The organism then
penetrates and can
disseminate throughout the
body
• Insects become infected
when taking a blood meal.
• T. brucei, T. congolense infections are limited to the sub-Saharan
tsetse belt.
• In contrast, as T. vivax and T. evansi can be mechanically
transmitted, these parasites have migrate beyond the tsetse belt,
out of Africa and into South America and Asia
• Cyclic transmission of salivarian trypanosomes mediated by tsetse
and other biting flies
• Most lifecycle data of African Trypanosomes is based on the T.
brucei cycle involving the tsetse
• short stumpy form parasite are taken up by the fly, progress
through the body of the insect vector passing via the midgut,
proventiculus and salivary gland, to be re-injected though the
proboscis as infective metacyclic trypomastigotes into a new target
• In the bloodstream, differentiation to long slender forms occurs
followed by binary fission proliferation
• Differentiation back to short stumpy forms will complete the cycle
• While T. congolense and T. vivax can follow a similar cyclic
transmission mode, the latter also is known to be spread through
mechanical transmission as is the case for T. evansi
• T. equiperdum spreads through sexual transmission
 NAGANA
SAMORE
AFRICAN TRYPANOSOMOSIS
TSETSE FLY DISEASE

Zulu word‘N’gana’
-powerless/useless
• Trypanosoma vivax, T congoiense, T. brucei brucei and T. simiae
are the four main species responsible for African
trypanosomoses affecting virtually all domestic mammals
• T. vivax and T. congoiense are the main pathogens of cattle.
• salivarian trypanosomes
• T. vivax is usually numerous
• The organisms that cause African animal trypanosomiasis have
been found in many species of mammals, including all
domesticated animals and some free-living or captive wildlife
• Wildlife known to be susceptible to infection include ruminants
such as South American white-tailed deer/ cariacou (Odocoileus
gymnotis)), duikers (Cephalophus spp.), antelope and African
buffalo (Syncerus caffer), as well as wild equids, felids, warthogs
(Phacochoerus spp.), capybaras (Hydrochoerus hydrochaeris),
elephants, nonhuman primates and various rodents.
• Cattle are reservoir hosts for T. congolense, T. vivax and T. b.
brucei, but other animals including small ruminants, pigs and
some wildlife (e.g., African buffalo) are also thought to
maintain these organisms.
• Clinical cases have been seen in a number of species
including cattle, sheep, goats, pigs, camels, horses, donkeys,
water buffalo, alpacas, llamas, dogs, cats and captive wild
ungulates
• T. godfreyi, T. simiae and T. suis are mainly known to affect
pigs.

• T. simiae has also been detected in sheep, goats, cattle,

camels, horses and wildlife
 EPIDEMIOLOGY
The epidemiology of African trypanosomosis is determined mainly
by the ecology of the tsetse fly which is found only in tropical Africa
T vivax is also transmitted mechanically by biting flies and occurs
also in Central and South America
Affected countries include Bolivia, Brazil, Colombia, French Guiana,
Guyana, Peru, Suriname, and Venezuela where it affects mainly
cattle and sheep
T congolense and T vivax are responsible for severe disease in
cattle, sheep and goats
T brucei brucei usually causes a subclinical infection in cattle, but a
severe disease in sheep, goats, horses and, occasionally, pigs
T simiae causes a very acute and highly fatal disease in exotic pigs
It is not pathogenic to cattle, sheep, or goats
• Morbidity rates during outbreaks are variable and may reach
70% in cattle infected with T vivax and up to 100% in pigs
infected with T. simiae
• It is usually much lower in sheep, goats, and horses since these
are not often the preferred hosts for tsetse or are less exposed
to tsetse challenges
• Sheep and goats are more vigorous than cattle in defending
themselves against successful feeding by tsetse flies
• Case fatality also depends on parasite species, host, and its
level of resistance. T. simiae is invariably fatal in exotic pigs
• African trypanosomes can be transmitted by 23 species of
tsetse (Glossina) found only in sub-Saharan Africa between
latitudes 14°N and 29°S, excluding areas of high altitude,
extreme drought or cold temperatures where tsetse cannot
survive
• Tsetse species can be grouped according to their preferred
habitats as savannah species, riverine species, and forest
species
• The savannah species (including G. morsitans, G. austeni, G.
pallidipes, G. swynnertoni, and G. longipalpis) pose the
greatest threat to livestock because they inhabit grasslands
where cattle are traditionally reared, they can easily adapt to
other ecological niches, they feed primarily on cattle and pigs,
and they are efficient vectors of trypanosomes.
• 13 or so forest species (including G. fusca, G. brevipalpis, and
G. longipennis) are not frequently incriminated vectors of
trypanosomes even though their preferred food hosts are
ruminants and suids.
• The life cycle of trypanosomes in tsetse involves cyclical
development for a varying length of time, depending on species
and ambient temperatures.
• T. vivax completes its developmental cycle in the proboscis and
pharynx and can be transmitted (as metacyclic trypanosomes)
within a week of the initial infective feed.
• The cycle of T. congolense involves the midgut and proboscis
and is completed in about 2 weeks.
• T. brucei takes 3 or more weeks and involves the midgut and
salivary glands
• Once infected, flies remain so for life (1-2 months).
• for any fly, its vectorial capacity and efficiency are highest for T.
vivax and least for T. brucei
• Non-cyclical
• After trypanosomes have been introduced into a herd,
transmission is possible even in the absence of Glossina.
• Biting flies such as Tabanidae, Stomoxyinae, and
Hippoboscidae are capable of mechanically transmitting
trypanosomes in their mouth parts if they feed on more
than one host within a short interval.
• This is how T. vivax is spread in areas outside the tsetse belt
in Africa, as well as in Central and South America
• Mechanical transmission can also occur through the needle
during inoculations and in carnivores feeding on infected
carcasses
 The carrier state
• Reservoirs of infection are found in many wild animals, in
trypanotolerant animals, and in chronically infected animals.
• Tsetse caught in and around game reserves tend to have
relatively high infection rates and the relative abundance of
wildlife in East Africa as compared to West Africa may
explain, at least in part, why the prevalence of the disease
appears to be declining more rapidly in the west
• The effect of infection varies with the host in that most wild
animals, and some domestic ones, establish a balance with
the parasite and remain as clinically normal carriers for long
periods.
• some breeds of cattle indigenous to Africa can tolerate light
to moderate challenge with tsetse flies by limiting the
multiplication of trypanosomes in their blood and by
apparently warding off the infection, especially T. vivax
• The phenomenon is called trypanotolerance
• Indigenous taurine breeds, such as the N'Dama, Baoule and
Muturu, are more tolerant than the West African zebuand
amongst East African zebu cattle, the Orma Boran and Maasai
zebu have superior tolerance when compared with Galana
Boran and Friesian breeds
• Crossbreeds of indigenous taurine and zebu animals are also
more tolerant than purebred zebu

• Trypanotolerance also occurs in some indigenous breeds of

small ruminants, notably the West African Dwarf sheep and
goats and the East African goats, whereas the Toggenburg,
British Alpine, Saanen, and Anglo-Nubian breeds of goats are
fully susceptible
• In cattle, T. vivax generally produces a higher level of
parasitemia than other species.
• since its life cycle in the tsetse is also shorter, T. vivax is more
readily transmitted than the others when animals are newly
introduced into a tsetse infested area
• Higher parasitemias also facilitate mechanical transmission.
• T. brucei is rarely detectable by direct examination of cattle
blood, even though infection can be confirmed through
other diagnostic methods
• Animals recovering from infection with one strain/serodeme
or species of trypanosome are not immune to infection with
another strain/serodeme or species.
• This is due to the ability of trypanosomes to readily change
their surface coat antigens through a process called antigenic
variation.
• The glycoprotein surface coat is continuously shed and
replaced by mechanisms not fully understood, but probably
induced by antibodies
• During each peak parasitemia, a mixture of variable antigenic
types of parasites is present, but the dominant antigens
determine the specific antibody response
• Antigenic variation in trypanosomes is dependent on a
protective protein coat that covers the entire surface of the
trypanosome
• The coat is composed of a single protein, the variant surface
glycoprotein (VSG), that protects the plasma membrane from
complement and invariant cell surface proteins from
recognition by host immunoglobulins .
• An infecting population expresses a series of VSGs from a large
reservoir of VSG sequences in the genome
• Different VSGs are antigenically distinct due to extreme
variation in sequence but have a conserved structure,
presumably necessary for their function as a protective barrier
• These antibodies kill off the dominant population, leaving
others with different dominant antigens; these multiply, and
the process continues in cycles until the animal dies or the
immune mechanisms catch up with the parasite and the
animal recovers.
• This phenomenon is also responsible for the successive
waves of parasitemia in infected animals
• Following repeated episodes of infection and recovery (with
or without treatment) in an endemic area,
• animals will encounter a variety of antigenic types and
therefore become less susceptible to strains/serodemes in
that area.
Economic importance
• Tsetse flies infest 10 million square kilometers of Africa
involving 37 countries
• Hence, nagana is today the most important disease of
livestock in the continent
• The added risk of human infections has greatly affected
social, economic, and agricultural development of rural
communities
• Since nagana is a wasting disease, affected animals are
chronically unproductive in terms of milk, meat, manure, and
traction, and the mortality rate can be high.
• Nagana in most species is a progressive, but not always fatal
disease and the main features are anemia, tissue damage,
and immunosuppression
• Metacyclic trypanosomes are inoculated intradermally as
the fly feeds
• They multiply at this site provoking a local skin reaction
(chancre), which is most pronounced in a fully susceptible
host and may be slight or absent with some strains or
species of trypanosomes
• Within the chancre, metacyclic parasites change to
trypomastigote form, enter the bloodstream directly or
through the lymphatics, and initiate characteristic
intermittent parasitemias
• T. vivax usually multiplies rapidly in the blood of cattle, sheep and
goats, and is evenly dispersed throughout the cardiovascular
system
• T. congolense tends to be aggregated in small blood vessels and
capillaries of the heart, brain, and skeletal muscle, and rarely
causes heavy parasitemias in ruminants
• Both species exert their effect mainly by causing severe anemia
and mild to moderate organ damage
• The anemia has a complex pathogenesis involving mainly
increased erythrophagocytosis, some hemolysis, and
dyshemopoiesis
• Very acute infections with T. vivax in cattle or T. simiae in pigs
result in fulminating parasitemias and disseminated intravascular
coagulation with hemorrhages
• Such syndromes resemble a septicemia, and anemia may not be
severe
• T brucei and, rarely, T vivax, have the added capability of
escaping from capillaries into interstitial tissues and serous
cavities where they continue to multiply
• Such infections result in more severe organ damage in
horses, sheep, and goats, in addition to anemia
• The cerebrospinal fluid is often invaded by T brucei alone
• Animals chronically infected with any pathogenic
trypanosome may develop concurrent and even fatal
bacterial, viral, and other protozoan infections as a result of
immunosuppression
• Pregnant animals may abort, and transplacental fetal
infections occasionally occur
• Trypanotolerant animals control parasitemias better and
have less severe anemia and organ damage.
• They usually recover from the disease, but may act as
carriers
 CLINICAL FINDINGS
• There are no pathognomonic signs that would help in
pinpointing a diagnosis.
• The general clinical picture is as follows but there are many
variations determined by the level of tsetse challenge, the
species and strain of the trypanosome, and the breed and
management of the host
• Acute episodes last for a few days to a few weeks from which
the animal dies or lapses into a subacute to chronic stage, or
the illness may be chronic from the beginning
• Chronic cases may run a steady course, may be interrupted by
periodic incidents of severe illness, or undergo spontaneous
recovery.
• The basic clinical syndrome appears after an incubation period of
8-20 days
• There is fever, which is likely to be intermittent and to last for a
long period
• Affected animals are dull, anorexic, apathetic, have a watery
ocular discharge, and lose condition
• Superficial lymph nodes become visibly swollen, mucous
membranes are pale, diarrhea occasionally occurs, and some
animals have edema of the throat and underline
• Estrus cycles become irregular, pregnant animals may abort, and
semen quality progressively deteriorates.
• The animal becomes very emaciated and cachectic and dies within
2-4 months or longer
• Thin, rough-coated, anemic, lethargic cattle with generalized
lymph node enlargement are said to have a 'fly-struck'
appearance.
• T congolense is more pathogenic to cattle in eastern
and southern Africa
• T vivax produces a more serious disease in West Africa.
• However, severe outbreaks of T. vivax involving exotic
dairy animals in East Africa occur; affected animals
show mucosal petechiation, rhinorrhagia, dysentery,
and death after an illness of only a few weeks
• Mixed infections are common and are usually more
severe
• intercurrent bacterial, viral, or other parasitic infections
may mask or complicate the basic clinical syndrome
 T. vivax
• affects all agricultural species except pigs
• Acute and chronic outbreaks occur, anemia is severe, and
fever is usually associated with high parasitemia
• A chronic form of the disease is more usual in East Africa, but
an acute hemorrhagic form can occur with exotic cattle
• T. vivax is less commonly seen in trypanotolerant cattle
breeds
• T. congolense
• affects all species, usually with an acute disease lasting 4-6
weeks, but some chronic cases occur, especially in West
Africa.
• Anemia and emaciation are severe
• T. brucei affects all species with a subacute to chronic
disease in which subcutaneous edema and
keratoconjunctivitis may be marked
• Nervous signs are manifested in horses, pigs, and small
ruminants by ataxia, circling, head pressing, and paralysis.
• Cattle are usually asymptomatic
• T. simiae
• affects exotic pigs with a fulminating infection in which the
animal dies within hours or a few days of first appearing ill
• There is fever, stiff gait, dyspnea, and cutaneous hyperemia,
but no significant anemia.
 DIAGNOSIS
• Blood sampling
• T.evansi is parasite of blood and tissues often inhabiting the
deep blood vessels in low parasitemia
• Blood for diagnosis obtained from both peripheral and deep
blood vessels
• Only 50% of affected animals identified by blood smear
examination
• The anemia results in a progressive drop in packed cell volume, a
non-specific but useful indicator in endemic areas
• The classic method of confirming diagnosis is to demonstrate
parasites in a wet blood film, and in a thin or thick blood smear
stained with Giemsa. This is easiest in the early stages of the
disease when parasitemic peaks correspond with fever
• To increase the accuracy of parasitological diagnosis, it is now
routine to concentrate the parasites in the buffy coat layer of a
microhematocrit capillary tube
• The buffy layer is then examined directly at low power
(Woo's method) or in a wet preparation with a dark
ground/phase contrast microscope (Murrays method)
• Both tests are simple, sensitive, and applicable to field use
on individual animals as well as in herds
• Blood should be examined fresh but may be refrigerated for
up to 24 hours, beyond which most parasites will die and
disappear from the sample
• To detect antitrypanosome antibodies in sera or other body
fluids.
• The three tests used most often are the indirect
immunofluorescent antibody test (IFAT), the capillary
agglutination test (CAT), and the ELISA.
• These tests have the disadvantage that they indicate past as
well as present infections, are difficult to standardize for
different laboratories, and are not species specific
• The ELISA technique was modlified to detect Circulating
trypanosome antigens (antigen-ELISA) using monoclonal
antibodies that would distinguish between T. vivax, T.
congolense, and T. brucei, and would detect only current or
very recent
• The polymerase chain reaction (PCR) technique can be used
to detect trypanosome DNA in tsetse tissues and in blood.
• The test is sensitive and species specific and can be
combined with ELISA.
• Dried blood spots on filter papers are also a useful source of
DNA for the detection of T. congolense and T. brucei by PCR
• But the test is expensive and can only be done in specialized
laboratories
 TREATMENT
• The number of trypanocidal drugs available for treating and
preventing infections in endemic areas is limited
• The drugs have been in the market for over 30 years, their
range of therapeutic safety is small, many of them cause
severe local reactions especially in horses, and some may be
fatal in high dose
• drugs are not always available and they are expensive,
underdosing is common
• These, plus the fact that some drugs are used both
prophylactically and therapeutically, have led to cases of drug
resistance
• Diminazene aceturate (Berenil) is used widely against T. vivax
and T. congolense as a curative and sanative drug at 3.5-7 mg/kg
BW.
• It is well tolerated by ruminants and it is one of the two
recommended drugs for bovine trypanosomosis.
• It is not well tolerated by horses
• Homidium bromide (ethidium) and homidium chloride
(novidium) are also widely used against T. congolensc and T.
vivax as curative and sanative drugs at 1 mg/kg BW
• Isometamidium (Samorin or Trypamidium) is the other
preferred drug against T. vivax and T. congolense in
ruminants.
• It is used as a curative and prophylactic drug at 0.25-1 mg/kg
BW. At much higher doses (12.5-35 mg/kg BW)
• it can be used prophylactically against T. simiae in pigs but
not without the risk of death from acute cardiovascular
collapse
• Pyrithidium bromide (prothridium)
• less widely used against T. congolense and T. vivax as
prophylaxis at 2 mg/kg BW
• Quinapyramine sulfate (Antrycide) is no longer used
extensively in cattle, but it is the preferred curative drug (at
5 mg/kg BW) against T. brucei in horses.
• Quinapyramine sulfate and chloride (Antrycide prosalt) is
used prophylactically at 7.4 mg/kg BW
• Suramin (naganol) may also be used against T. brucei as a
curative and prophylactic drug at 10 mg/kg BW in horses and
camels
• Q Antrycide-Suramin complex is the only other drug against
T. simiae in pigs and it is used prophylactically at 40
mg/kgBW
• The control of trypanosomosis in enzootic countries involves
control of tsetse fly population, prophylactic treatment,
good husbandry of animals at risk, and use of
trypanotolerant animals
• There is no vaccine against the disease and, in spite of
intensive research, none appears likely in the near future
because of the ability of trypanosomes to readily change
their glycoprotein surface coat through a process called
antigenic variation.
• Control of tsetse has been successfully attempted in some
African countries, but reinvasion is frequent if the land is not
properly utilized
• The earliest methods involved bush clearing and elimination
of game animals on which tsetse feed.
• These methods were effective in eradicating or controlling
tsetse in some parts of the continent, especially in southern
Africa, but they resulted in destroying valuable plant and
animal resources, and also led to soil erosion.
• use of insecticides, especially DDT and endosulfan, applied
strategically in the form of ground and aerial spraying over
large expanses of land
• As tsetse are sensitive to insecticides and no resistance has
developed, considerable successes were achieved in some
countries
• However, spraying insecticides is costly and harmful to the
environment
• These harmful effects are considerably reduced if the
insecticides, for example, synthetic pyrethroids, are applied
directly on the animal in the form of spray or pour-on
formulation.
• The latter offers great promise and also reduces tick
infestation in treated animals.
• targets impregnated with insecticides and traps that attract
and catch tsetse. These are simple and cheap and can be
constructed and maintained by local communities.
• They do not pollute the environment and are suitable for
both small- and large-scale fanning.
• sterile male technique.
• Since the female tsetse only mates once in a lifetime, this
technique is theoretically able to eradicate a targeted tsetse
species in areas where other methods have been used to
reduce its density
• But it is expensive.
• development of the land for agriculture, industries,
highways, etc. will effectively destroy the habitat for tsetse
flies. This has occurred significantly in Nigeria where there
were rapid economic activities and expanding human
population in the 1970s and 1980s
• Attempts at trypanosomosis control have also been directed
to prophylactic dosing with chemicals such as suramin,
prothridium, and isometamidium (Samorin)
• Prophylaxis is used along with other methods in areas
where there is a heavy tsetse challenge.
• The prophylactic effect is supplemented by the development
of antibodies, and the total period of protection may be as
long as 5 months.
• Trypanotolerant animals are being used to establish ranches
in areas where tsetse challenge is not too heavy, but they
have not been readily accepted in some countries,
supposedly because they are smaller in size and they
produce less milk than other indigenous breeds and crosses
with exotic breeds
• headaches, fever, weakness, pain in the joints,
lymphadenopathy, and stiffness.
• People who become infected may or may not show signs
of illness immediately, but over time the parasite crosses
the blood-brain barrier and migrates to the central
nervous system.
• Here it causes various neurological changes which include
the sleep disorder (hence the name “sleeping sickness”),
deep sensory disturbances, abnormal tone and mobility,
ataxia, psychiatric disorders, seizures, coma and
ultimately death.