Short communication

Trypanosomiasis by Trypanosoma vivax in cattle in the

Brazilian semiarid: Description of an outbreak
and lesions in the nervous system
J.S. Batista
a
, F. Riet-Correa
b,
*
, M.M.G. Teixeira
c
,
C.R. Madruga
d
, S.D.V. Simoes
b
, T.F. Maia
e
a
Escola Superior de Agricultura de Mossoro, Av. Francisco Mota S/N, Br 110, Km 47, 59 Rio Grande do Norte, Brazil
b
Hospital Veterinario, CSTR, Universidade Federal de Campina Grande, Patos, Para ba 58700-000, Brazil
c
Departamento de Parasitologia, Instituto de Ciencias Biomedicas, Universidade de Sao Paulo,
Av. Prof. Lineu Prestes 1374, 05508-900 Sao Paulo, Brazil
d
EMBRAPA, Centro Nacional de Pesquisa em Gado de Corte, Campo Grande, Mato Grosso do Sul, Brazil
e
Ministerio da Agricultura e do Abastecimento, Benjamim Constant 161, Patos, PB, Brazil
Received 8 November 2005; received in revised form 11 July 2006; accepted 3 August 2006
Abstract
An outbreak of trypanosomiasis by Trypanosoma vivax is reported in the semiarid of Para ba, Northeastern Brazil from May to
August 2002. Sixty-four cows out of 130 were affected; 11 died and the other recovered after treatment with diminazene aceturate.
Affected animals had fever, anemia, weight loss, hypoglycemia, increased serum levels of aspartate aminotransferase and, in nine
cows, nervous signs. All cows with nervous signs died; six of themrecovered after treatment, but the disease relapsed. Six cows aborted
and one delivered a calf that died immediately after parturition. Thirty-two out of 100 calves were affected and ve died. Nervous signs
were not observed in the calves. Gross lesions were thickening of the meninges, enlarged lymph nodes and prominent white pulp of the
spleen. The main histological lesion was meningoencephalitis and malacia in the brain of cows with nervous signs. No antibodies
against trypanosomes were found in 33 blood samples collected before the outbreak in the affected farmand in 29 samples collected at
the same time in two other neighbor farms. Until January 2003, all 89 animals tested had antibodies against T. vivax, suggesting the
occurrence of sub clinical infections in cattle without clinical signs. Only two out of 85 serum samples collected on April 2004 were
positive for T. vivax antibodies. Data obtained suggested that the semiarid region is non-endemic for trypanosomiasis and that disease
occurred due to introduction of the parasite in a susceptible population after an apparent rise in the Tabanus spp. population.
# 2006 Elsevier B.V. All rights reserved.
Keywords: Trypanosoma vivax; Trypanosomiasis; Cattle; Epidemiology; Semiarid; Brazil; Encephalomyelitis; Malacia; Nervous system
1. Introduction
In some African countries trypanosomiasis by
Trypanosoma vivax is a very important disease of
livestock (Anosa, 1983; Gardiner et al., 1989). African
isolates of T. vivax are predominantly transmitted
following cyclical development in tsetse ies. However,
it can also be mechanically transmitted by other biting
ies, and has therefore been able to spread beyond the
African tsetse belt to Central and South America. In
South America, T. vivax is only mechanically trans-
mitted by biting ies, mainly tabanids (Gardiner, 1989;
Otte and Abuabara, 1991; Jones and Davila, 2001).
www.elsevier.com/locate/vetpar
Veterinary Parasitology 143 (2007) 174181
* Corresponding author. Fax: +55 83 34213231.
E-mail address: franklin.riet@pesquisador.cnpq.br
(F. Riet-Correa).
0304-4017/$ see front matter # 2006 Elsevier B.V. All rights reserved.
doi:10.1016/j.vetpar.2006.08.017
In Africa, infected cattle ranged from totally
asymptomatic chronic infections to wasting disease with
severe haematological alterations and death (Losos and
Ikede, 1972; Anosa, 1983; Gardiner, 1989). In South
America, cattle infected by T. vivax are mostly
asymptomatic (Desquesnes and Gardiner, 1993; Wells
and Betancourt, 1977; Paiva et al., 2000; Garcia et al.,
2006). However, the presence of T. vivax or antibodies
against it was frequently demonstrated in several Latin
American countries in cattle, buffaloes and sheep,
including Brazil (Shaw and Lainson, 1972; Serra Freire,
1981; Silva et al., 1999; Davila et al., 2003); French
Guiana (Desquesnes and Gardiner, 1993); Bolivia (Silva
et al., 1998); Colombia (Wells and Betancourt, 1977;
Otte et al., 1994) andVenezuela (Garcia et al., 2006). Few
outbreaks showing haematological alterations and
clinical signs were described in South America. The
rst outbreak in South America was described in 1919 in
a dairy farm in the French Guiana with high para-
sitaemias, sudden drop of milk production, anemia,
weight loss, and the death of 95 out of 180 cattle (Leger
and Vienne, 1919). In Colombia, cattle infected by T.
vivax showed anemia and progressive weight loss
(Zapata, 1931). In one outbreak reported in Bolivia, T.
vivax was detected in 25 out of 29 cattle examined and
animals showed fever, anemia, abortion, loss of appetite,
lethargy, and progressive weight loss (Silva et al., 1998).
In Brazil, T. vivax was identied by the rst time in a
buffalo with fever and weight loss (Shaw and Lainson,
1972). Later, Silva et al. (1996, 1999) reported a T. vivax
outbreak in the State of Mato Grosso, in the Pantanal
region; with parasite in the blood of 10 out of 29 cattle
and the following clinical signs: fever, anemia, abortion,
loss of appetite, lethargy, progressive weight loss,
oftalmitis, and dysentery. Further studies of naturally
infected herds demonstrated that T. vivax normally did
not cause disease in Brazil, inducing a chronic and
asymptomatic infection despite cattle, buffaloes and
sheep presented parasites detectable by microhemato-
crit and/or antibodies (Ventura et al., 2001; Davila et al.,
2003).
The identication of T. vivax in cattle in the Pantanal
region, a very important livestock-producing area, led to
the supposition that the disease will cause important
economic losses and their dissemination to other
Brazilian regions was considerer very probably (Silva
et al., 1999; Jones and Davila, 2001). Nevertheless, this
hypothesis was not conrmed, with all reported
outbreak so far restricted to Pantanal region. Nowadays,
T. vivax is commonly found in enzootic equilibrium in
the Brazilian Pantanal and surroundings (Ventura et al.,
2001; Davila et al., 2003). In this paper an outbreak of
trypanosomiasis by T. vivax is reported in cattle in the
Brazilian semiarid.
2. Materials and methods
Trypanosomiasis by T. vivax occurred in a herd of
Brown Swiss and crossbreeds cattle in a farm in the
municipality of Catole do Rocha, state of Para ba,
Northeastern Brazil, located 6820
0
38
00
Latitude West, and
37844
0
48
00
Longitude South. The climate is semiarid, hot
and dry, with a mean temperature of 27.8 8C (minimal of
20.2 8C and maxima of 35.4 8C) and a mean humidity of
50%. The meanannual rainfall is 500 mm, andthe rains
occur from JanuaryFebruary to MayJune. The
irregular distribution of the rains, a long dry period,
and the occurrence of draughts of sometimes more than 1
year are characteristic of the region. The affected herd
was grazing during the day, but at night it was kept in a
corral and supplemented with corn silage, sorghumgrain,
sugar cane, urea and a mineral supplement.
Diagnosis of T. vivax was done morphologically by
analysis on buffy coat smears and conrmed by T. vivax-
specic PCR (Ventura et al., 2001). The presence of
antibodies was detected by ELISA employing a total
extract of T. vivax as antigen. The technique was
previously standardized regarding sensitivity and speci-
city in seroepidemiological studies done in the Pantanal
region (Madruga et al., in preparation). Treatment of T.
vivax infected animals was performed by the inoculation
of 5 mg/kg bw of diminazene aceturate. Hematological
and hystopathological analysis were performed as in
previous study (Batista et al., 2006).
3. Results and discussion
The rst cases occurred in the beginning of May 2002,
ina herd of 120cows (100milkingand30drycows), with
cattle presenting a drop in milk production from a mean
of 62.5 l daily per cow. In addition, clinically affected
animals had depression, anorexia, fever, severe anemia,
and progressive weight loss. Eight cows had nervous
signs of incoordination, hypermetry, muscular tremors,
fasciculations, opisthotonos, blindness, and strabismus.
In ve cows, nervous signs, including blindness, were
transitory and the animals recovered after treatment, but
later the disease relapsed with nervous signs, and the
cows died. Before the diagnosis of trypanosomiasis,
affected cattle were treated with tetracycline, amino
acids, physiologic serum, vitamins of the Bcomplex, and
uprednisolone. Some animals recovered, others died in
810 days, and others had a chronic phase with
continuous weight loss of up to 23% of their live weight,
J.S. Batista et al. / Veterinary Parasitology 143 (2007) 174181 175
recurrent fever of 4041 8C, anorexia, mild yellow
discoloration of the mucosal membranes, anemia, and
increased cardiac and respiratory rates.
On 5June 2002, 1 month after the start of the outbreak,
31 cows had been affected. From these, 15 recovered,
eight still with clinical signs (two acute and four chronic
cases), and eight with nervous signs died. All affected
cows except two were in lactation. Six cows, including
four lactating and two dry cows, aborted, whereas one
delivered a calf that died immediately after parturition.
On that day blood samples from four cows were
analyzed: PCV values was 16% and 20% for the two
acute cases. The two chronic cows had PCV values of
10% and 26%, besides leukopenia with 1.55 and 2.85
leukocytes per ml/10
3
of blood. Most cows presented
large amounts of T. vivax in the buffy coat smears and this
diagnosis was conrmed by PCRspecic for this species
(Ventura et al., 2001).
After the conrmation of the diagnosis of trypano-
somiasis by T vivax, in 5 June 2002, all affected animals
were treated with 5 mg/kg bw of diminazene aceturate.
All treated animals recovered, and started to gain
weight. Between 5 June and 7 July the prevalence of the
disease was evaluated in 76 cows. T. vivax was identied
in blood smears or buffy coats in 31 cows. Most of these
cows showed anemia, depression, and weight loss, and
one had also nervous signs. They were treated with
diminazene aceturate and recovered. Antibodies against
T. vivax were detected by ELISA in 34 out of 45 serum
samples from cows without clinical signs and negative
for trypanosomes in the blood examination.
A hundred calves, born between January and May
2002, were kept on a different pen than the cows. In the
start of July 2002 some calves showed low weight gains
and some had nasal discharge, dyspnoea and coughing.
Five calves died. Between 5 June and 7 July, 92 calves
were examined clinically, and samples of blood were
collected for parasitological examination. Twenty-seven
samples were positive for T. vivax, with parasitaemia
varying from 1.4 10
5
to 125 10
5
trypanosomes/ml
of blood. There was a positive linear regression between
the rectal temperature and parasitaemia. (Y = 0.0362x +
37.04; R
2
= 0.92; P < 0.05). Mean PCV of affected
calves was 21.6 5.1%. In August 2002 the PCV from
27 calves treated successfully with diminazene aceturate
returned to normal ranges (29.7 6.9%). From65 calves
negative for trypanosomes in the blood analysis, 44 had
antibodies against T. vivax. Until 14 August other two
cows were affected immediately after parturition. Both
animals did not respond to the treatment and died after a
clinical manifestation period of 1224 h. In one cowwith
nervous signs and in eight calves the disease relapsed
after treatment, withtrypanosomes observedinthe blood.
All these animals were treated and recovered. At the end
of August the cow recovered from nervous signs had
another relapse, and was euthanized after been in lateral
recumbence.
From the 130 cows in the farm at the start of the
outbreak, 64 (49.2%) had clinical signs, and 11 (8.4%)
died. All the nine cows that had nervous signs died, six
of them after the clinical relapse of the disease. From
the 100 calves in the farm, 32 (32%) had clinical signs
and ve died. Eight calves had clinical relapse after the
rst treatment, but had no nervous signs, and recovered
after a second treatment. Necropsies were performed in
four cows and one calf. In one cow(No. 1) the meninges
in the brain stem were thickened and yellowish, some
lymph nodes were enlarged and in the spleen the white
pulp was prominent. No signicant gross lesions were
found in the other animals.
On histological examination, the white pulp of the
spleen was hyperplasic in all animals examined. A mild
interstitial nephritis was observed in Cows 1 and 2. The
more signicant lesions were in the central nervous
system, characterized by meningitis (Cows 2 and 3),
meningoencephalitis (Cow 1), meningoencephalomye-
litis (Cow 4), and malacia (Cows 1 and 4). The
meningitis and encephalitis were characterized by the
presence of lymphocytes, plasma cells, unidentied
mononuclear cells, the so-called morula cells (Mott
cells), and macrophages, sometimes containing hemo-
siderin. The meningitis was localized in parietal and
temporal cortex, cerebellum (Fig. 1) and medulla (Cow
1), temporal cortex (Cows 2 and 3) and temporal cortex,
cerebellummedulla and cervical spinal cord (Cow4). In
Cow 1, the encephalitis affected the thalamus, basal
J.S. Batista et al. / Veterinary Parasitology 143 (2007) 174181 176
Fig. 1. Cerebellum. Cow1. Severe meningitis mainly by mononuclear
cells. HE, 100.
nuclei and internal capsule, and geniculate body. In the
thalamus and geniculate body the perivascular cufngs
were more severe, affecting all blood vessels and
formed sometimes by up to 12 cells tick. Diffuse lesions
of malacia with large amounts of guitter cells
distributed within the parenchyma were observed in
those regions (Fig. 2). Axonal spheroids were observed
within the areas of malacia. In the internal capsule the
malacia was mild with few guitter cells. In Cow 4, the
encephalitis affected the cerebellum, cerebellar ped-
uncles, pons, mesencephalus, and thalamus. The
perivascular cufngs were more severe in cerebellar
white matter (Fig. 3) and pons, where all blood vessels
were affected, occasionally with perivascular cufng
with up to 10 cells tick. Areas of malacia were observed
in the cerebellar white matter (Fig. 3), with pale
vacuolated neuropil, associated with mild amounts of
guitter cells, lymphocytes and axonal spheroids. In the
mesencephalus and thalamus the lesions were less
severe. This animal had also myelitis with severe
perivascular cufngs (Fig. 4), mainly in the grey
substance of the cervical spinal cord. In the white matter
the inammatory lesions were less severe, but the
neuropil was vacuolated and the roots of the spinal
nerves had Wallerian-like degeneration. No lesions
were found in the central nervous system of the calf.
Hematological analysis were done monthly, between
July and December 2002, in three groups of eight cows
each: group 1, cows with clinical signs and trypano-
somes in the blood, treated with diminazene aceturate;
group 2, cows with antibodies against T. vivax, but
without clinical signs; group 3, cows from another farm,
of the same breed and similar age than the other groups,
without antibodies to T. vivax. In hematological analysis
done in cows of group 1 the values obtained in July and
August were, respectively: (a) red blood cells, 3.78
2.9 (N 10
6
ml) and 4.42 5.1; (b) PCV, 17.5 0.9%
and 20.2 1.3%; (c) hemoglobin, 5.6 1.5 g/dl and
6.71 1.7; (d) white blood cells, 3.40 1.6 (10
3
ml
1
) and 4.95 2.1; (e) glucose, 34.6 8.3 mg/day
and 39.0 10.6. All values in cows of group 1 were
signicantly lower (P < 0.05) than those in cows of
groups 2 and 3. On September these hematological and
biochemical values returned to normal. Also in July the
serum activity of aspartate aminotransferase (AST)
(151.3 13.6 UI/l) in cows from group 1 were
signicantly higher (P < 0.05) than in the other groups
(without AST alterations), returning to normal in
August. There were no signicant differences among
the three groups of cattle in the mean corpuscular
J.S. Batista et al. / Veterinary Parasitology 143 (2007) 174181 177
Fig. 2. Thalamus. Cow 1. Perivascular cufngs formed mainly by
mononuclear cells and macrophages, and malacia with inltration by
guitter cells (arrows). HE, 200.
Fig. 3. Cerebellar white matter. Cow 4. Severe perivascular cufngs,
and malacia characterized by pale vacuolated neuropil. HE, 100.
Fig. 4. Cervical spinal cord. Cow 4. Myelitis with severe perivascular
cufngs. HE, 100.
volume and hemoglobin concentration, percentage of
neutrophils, lymphocytes, monocytes, eosinophils and
basophils, serum concentrations of total proteins,
albumin, and globulins, and serum activity of alkaline
phosphatase.
In 22 January 2003 for recommendation of another
practitioner all adult cows present in the farm were
treated with 1 mg/kg of isometamidium chloride.
The evolution of the disease in the herd was followed
each 2 months from July 2002 to January 2003, and in
May 2003, in two groups of cattle: group A, constituted
by 31 cows which showed clinical signs during the
outbreak and were treated successfully with diminazene
aceturate; group B, composed for 31 cows without
clinical signs, but with antibodies against T. vivax. In July
2002, the PCVof 18out of 31cows of groupAwere below
normal values, with very low values in four of these
animals (11%, 12%, 13% and 14%). The mean PCV
(21.6 5.0%) for cattle of group A was signicantly
lower (P < 0.05) than values for cattle of group B.
Among animals of group B (non-treated), only one cow
had a mild PCV reduction (22%). In September the PCV
fromcows of group Awere within normal values, and no
signicant differences were observed among animals
from both groups from September 2002 to May 2003.
Antibodies against T. vivax were evaluated in serum
samples from 15 cows of each group, A and B. In July
2002, antibodies were found in six out of 15 cows of
group A (treated), and in 13 out of 15 of group B (non-
treated). In January 2003, all animals from both groups
had antibodies, except one from group A previously
positive. In May 2003, one cow from group A and three
from B, which were previously positive, became
negative.
In 30 April 2004, 2 years after the occurrence of the
outbreak, clinical, parasitological and serological eva-
luation were performed in the following groups of cows:
(a) 30 non-treated cattle born between May 2003 and
April 2004; (b) 30 cows which showed clinical signs
during the outbreak, when were treated with diminazene
aceturate, and with isometamidium chloride in January
2003; (c) 25 adult cattle born immediately before or
during the outbreak and submitted to different treat-
ments: 15were treatedwithdiminazene aceturate, but not
with isometamidium; 10 were not treated. ELISA was
negative for most cows, excepting for one of the group
(a), and one of group (b). The PCVof all these 85 cattle
were within normal values and no trypanosomes were
found in the buffy coat.
A retrospective study of antibodies against T. vivax
was performed using serum samples from 62 adult
cattle, stocked at the University of Campina Grande,
Bacteriology Laboratory, which had been collected
during 2000 and 2001 for routine brucellosis and
leptospirosis examination. For this analysis, we used 36
serum samples collected in the same farm where the
outbreak occurred and 29 collected in two neighboring
farms. All these samples were negative for T. vivax
antibodies, suggesting that T. vivax was not present in
cattle in the farm before May 2002. High parasitaemia
and antibodies in all cattle tested until January 2003
suggest that cattle in the farm became infected during
the outbreak described in this study, which extended for
approximately 4 months.
There is no clear indication about the possible origin
of the outbreak. It is probably that a subclinically infected
animal was introduced in the herd; the farmer had other
four farms in the region and cattle were frequently
changedfromone farmtoanother. Besides asymptomatic
cows, we cannot discharge the possibility of other
possible reservoir, including goats and sheep, which are
common host of T. vivax (Applewaite, 1990; Vokaty
et al., 1993; Kalu et al., 2001), and very abundant in the
semiarid region. We are currently examining goats
aiming to detect reservoirs of T. vivax in this region.
Buffaloes and cervids, which are considered important
reservoirs of T. vivax inAfrica (Gardiner, 1989) and inthe
Brazilian Pantanal region (Davila et al., 2003) are not
present in the studied area.
The farmer reported a considerable increase in the
number of tabanids before and during the outbreak,
which started at the end of the rainy period. Previous
papers associated the increase of Tabanus spp., which are
conrmed mechanical vectors of South American T.
vivax (Otte and Abuabara, 1991), with high prevalence of
T. vivax infection in cattle (Desquesnes and Gardiner,
1993; Silva et al., 1996). Contribution of H. irritans in the
transmission of T. vivax in this outbreak could not be
dismissed. However, this y occurred in large number
even when cases of the disease were not observed. Taken
together, clinical disease in 64 (49.2%) cows and 32
(32%) calves, high parasitaemia, and antibodies against
T. vivax detected in all cows until January 2003, these
data suggest that all cattle of this farm were infected in
this outbreak. Probably, this outbreak was due introduc-
tion of T. vivax in an area of enzootic instability, where
cattle do not live in contact with this parasite.
Antibodies against T. vivax in cattle that did not
showed clinical signs suggest the occurrence of
subclinical disease, which has been associated to the
low efciency of the mechanical transmission, animal
resistance or low virulence of T. vivax isolate. The
frequent inoculation of small amounts of T. vivax by
mechanical vectors in endemic areas contribute to the
J.S. Batista et al. / Veterinary Parasitology 143 (2007) 174181 178
development of protective antibodies, and the coex-
istence of the parasite with cattle without causing
disease. The virulence of the T. vivax isolate responsible
for the outbreak was demonstrated by the inoculation in
sheep, which presented severe clinical signs of the
disease (Batista et al., 2006).
Analysis of ribosomal gene sequences showed that T.
vivax from the Paraiba outbreak is closely phylogenetic
related to isolates from symptomatic (Silva et al., 1996,
1999) or asymptomatic (Paiva et al., 2000; Cortez et al.,
2006) cattle fromBrazil. Moreover, Brazilian isolates are
very similar to isolates from West Africa (Ventura et al.,
2001; Cortez et al., 2006), where cattle infected by T.
vivax could be symptomatic (Gardiner, 1989). Different
breeds of cattle showed different degree of susceptibility
to T. vivax (Gardiner, 1989). The outbreak reported in the
semiarid region affected Brown Swiss breed cattle
(taurine-cattle), whereas in the Pantanal region, Nelore
breed (Zebu-cattle) were reported with bothsymptomatic
and asymptomatic infection. Thus, whether outbreaks
and different pathologies are associated with particular T.
vivax isolates, and/or with host features such as breed,
health conditions and immunity to T. vivax remain to be
elucidated.
Subclinical T. vivax infections are common in Africa
(Gardiner et al., 1989) and in endemic regions of South
America (Otte et al., 1994; Paiva et al., 2000; Ventura
et al., 2001; Davila et al., 2003; Garcia et al., 2006).
Desquesnes and Gardiner (1993) suggested that the
absence of clinical disease in the Americas is not due to
the low pathogenicity of the T. vivax isolates, but to the
different epidemiological conditions. In contrast to
African T. vivax, which is cyclically transmitted by
tsetse ies, express a larger repertoire of variable surface
glycoproteins (VSG) and generate different serodemes,
South American T. vivax is mechanically transmitted and
shows smaller number of serodemes. The continuous
infections by few serodemes contribute to the rapid
disease equilibrium and even to elimination of the
parasite (Uzoigwe, 1986; Nantulya et al., 1986; Gardiner,
1989).
Fever, anemia, leukopenia, hypoglycemia, and high
serum ASTactivity were observed when affected cattle
had high parasitaemia. The anemia caused by T. vivax is
considered multifactorial being attributed to intra- and
extra-vascular haemolisis, decreased erytropoiesis, and
hemorrhages (Holmes, 1997). The association of
leukopenia with parasitaemia is also an important
factor in the pathogenesis of trypanosomiasis in cattle,
sheep and goats. Hypoglycemia in the acute phase of
trypanosomiasis occurs also in experimentally infected
cattle (Kadima et al., 2000). The high serum AST
activity suggests a hepatic lesion probably caused by
anemia, but no histological lesions were observed in the
liver of necropsied animals.
The control of the disease on the farm, with the
treatment of the clinical cases, was efcient, since in
September 2002, 4 months after the start of the
outbreak, all cattle examined had normal hematological
values. The rapid stabilization of the disease, apparently
followed by elimination of T. vivax infection in the farm
suggest that the epidemiology of trypanosomiasis in the
semiarid of northeastern Brazil is different from
endemic regions like Brazilian Pantanal, where the
disease is endemic. The absence of antibodies against T.
vivax in 83 out of 85 cattle of different ages, 2 years
after the start of the outbreak suggest that T. vivax was
eliminated from blood of cows in the studied farm,
indicating that animals were again susceptible to the T.
vivax infection. Data suggested that Brazilian semiarid
is non-endemic (marginal) for trypanosomiasis, prob-
ably because the environmental conditions, long dry
periods and high temperatures, are not favorable to the
development of vectors during most part of the year. In
the Pantanal region, the favorable climate conditions
permit the development of the mechanical vectors
during the whole year. In this region, where the presence
of T. vivax is rarely associated with disease, cattle,
buffalo and cervids can be potentially be reservoirs of
this trypanosome (Ventura et al., 2001; Davila et al.,
2003). As a consequence of continuous existence of
vectors and reservoirs, cattle are frequently inoculated
by mechanical vectors and do not loss their protective
immune response against T. vivax, which appear to be
observed only in infected animals.
The absence of signicant gross lesions observed in
this outbreak is common in T. vivax infections (Losos and
Ikede, 1972). Macroscopic lesions intrypanosomiasis are
occasionally associated with some African T. vivax
isolates, which cause a severe hemorrhagic syndrome
(Gardiner et al., 1989; Mwongela et al., 1981). The
nervous signs, and the meningoencephalomyelitis and
malacia observed in this outbreak had not been reported
before in any infection by T. vivax in cattle, whereas
meningoencephalitis was already reported in goats
experimentally infected by T. vivax (Whitelaw et al.,
1988). Meningoencephalitis and malacia are caused by
Trypanosoma congolense in cattle (Losos and Ikede,
1972), Trypanosoma evansi in horses (Seiler et al., 1981;
Rodrigues et al., 2006), and Trypanosoma brucei in man
(Poltera et al., 1977). One characteristic of the menin-
goencephalitis caused by these trypanosomes is the
presence of Mott cells, which are plasma cells containing
large amounts of immunoglobulins with marginal
J.S. Batista et al. / Veterinary Parasitology 143 (2007) 174181 179
nucleus. Nervous system lesions caused by these
trypanosomes has been associated to: (a) the presence
of trypanosomes in the nervous tissues and cerebrospinal
uid (Losos and Ikede, 1972; Whitelaw et al., 1988;
Tuntasuvan et al., 1997, 2000); (b) circulatory alterations
caused by embolus formed by trypanosomes, leukocytes,
and brin in capillaries and venules of the brain (Losos
and Ikede, 1972); (c) autoimmune reaction, because
antibodies against nervous tissues had been detected in
the cerebrospinal uid (Dumas and Bouteille, 1996); (d)
apoptosis of endothelial cells of the blood vessels of the
cerebrum and cerebellum (Stiles et al., 2004).
Clinical and parasitological relapses after treatment,
observed in six animals with nervous signs, have been
associated with the location of the parasite in nervous
tissue, cerebrospinal uid, and aqueous humor, where
trypanosomes are protected from trypanosomicides
drugs. These extra-vascular foci are indicative of poor
prognosis and are thought to be important in the
maintenance of livestock trypanosomiasis (Whitelaw
et al., 1988). In humans infected by T. brucei, relapses
occur because the trypanosomicides drugs do not pass
through the hematoencephalic barrier (Brun et al.,
2001).
In conclusion, this study of trypanosomiasis by T.
vivax in Brazilian semiarid region demonstrated that T.
vivax can cause nervous signs due to inammatory and
degenerative brain lesions in cattle. The disease can be
controlled by the treatment with diminazene aceturate,
with good results when administered in the early acute
cases of disease. However, in cattle with nervous signs
these treatment is not efcient, the disease relapse and
the animals died. The absence of antibodies in cattle of
the same farm 2 years after the occurrence of the
outbreak suggest that the semiarid region is non-
endemic for T. vivax trypanosomiasis, and that cured
animals are again susceptible to new outbreaks.
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