Transactions of the Royal Society of Tropical Medicine and Hygiene (2006) 100, 989—991

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CASE REPORT

Treatment and follow-up of the first case of

human trypanosomiasis caused by
Trypanosoma evansi in India
P.P. Joshi a, A. Chaudhari b, V.R. Shegokar c, R.M. Powar c, V.S. Dani a,
A.M. Somalwar a, J. Jannin d, P. Truc e,∗

a
Department of Medicine, Government Medical College, Nagpur, India
b
Directorate of Health Services, Nagpur, Maharashtra State, India
c
Department of Microbiology, Government Medical College, Nagpur, India
d
World Health Organization, Communicable Diseases Control, Prevention and Eradication, 1211 via Appia, Geneva, Switzerland
e
Institut de Recherche pour le Développement, UR 117 Trypanosomoses Africaines, LRCT, Montpellier, 34398, France

Received 3 October 2005; received in revised form 4 November 2005; accepted 4 November 2005
Available online 7 February 2006

KEYWORDS Summary The first reported human case of trypanosomiasis caused by Trypanosoma evansi
was treated using suramin. Patient follow-up indicates that the drug and specific regimen used
Human
were well tolerated. Clinical, serological and parasitological investigations at 6 months indicate
trypanosomiasis;
complete cure of the patient. Suramin should be considered in the treatment of other cases of
Trypanosoma evansi;
human T. evansi infection, if they occur.
Treatment;
© 2005 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights
Suramin;
reserved.
India

1. Introduction for 5 months, with no central nervous system (CNS) inva-

Human trypanosomiasis is generally distributed in Africa
(sleeping sickness) and South America (Chagas disease).
Recently, a human case of trypanosomiasis caused by Try-
panosoma evansi was identified in India (Joshi et al., 2005).
This latter parasite had previously been believed to be non-
infective to humans owing to the effects of a trypanolytic
factor contained in normal human serum (Hawking, 1978).
However, this patient harboured trypanosomes in his blood
∗
Corresponding author. Tel.: +33 6 11 888 828;
fax: +33 4 67 593 920.
E-mail address: truc@ird.fr (P. Truc).
sion (Joshi et al., 2005). Therefore it was decided to treat
the patient using suramin (Germanin; Bayer, Wuppertal,
Germany), a drug used to cure the first stage of the acute
form of sleeping sickness (human African trypanosomiasis
(HAT)) due to Trypanosoma brucei rhodesiense (WHO, 1998).
In the present report, we describe follow-up over 6 months
after initial treatment of this first extraordinary case found
in India.
2. Description of treatment
Suramin is produced by Bayer under the trade name of Ger-
manin and is available in vials containing 1 g of off-white
powder. The treatment regimen for HAT is usually five i.v.

0035-9203/$ — see front matter © 2005 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.trstmh.2005.11.003
990
injections of 10% solution in distilled water at intervals
of 5—7 days (20 mg/kg with a maximum of 1 g per injec-
tion; WHO, 1998). Given that suramin is also used to treat
T. evansi in animals in India, this treatment was consid-
ered to be the most appropriate for the consenting patient.
The suramin solution was administrated by slow i.v. infu-
sion over 90 min (1 g of suramin i.v.). Owing to the risk of
a possible severe anaphylactic reaction, a sensitivity test
was performed before starting the treatment by injecting
0.1 g of suramin i.v. over a period of 3 min (Joshi et al.,
2005). No adverse effects of the suramin treatment were
observed.
3. Post-treatment follow-up
At the end of treatment (24 h after the last injection) and
at 3 and 6 months following the initial treatment, clini-
cal, serological and parasitological investigations were per-
formed using blood, plasma and cerebrospinal fluid (CSF)
to check treatment efficiency. Because invasion of the
CNS is inevitable in HAT caused by T. b. gambiense and
T. b. rhodesiense, the CSF was also checked in spite of
the fact that no CNS invasion was initially detected. The
Card Agglutination Test for Trypanosomiasis (CATT)/T. evansi
(Pathak et al., 1997), provided by the Institute of Tropi-
cal Medicine in Antwerp, Belgium, was employed. This is
a specific direct agglutination test that uses the RoTat 1.2
antigen. The test was performed using whole blood and dilu-
tions of serum from 1:2 to 1:64. The mini anion-exchange
centrifugation technique (Lumsden et al., 1979), which is
a chromatography-based system permitting concentration
and purification of trypanosomes from 300 ␮l of heparinised
blood (provided by the Institute of Tropical Medicine in
Antwerp, Belgium), was also used. The latex IgM aggluti-
nation test is a direct agglutination test using CSF (Lejon et
al., 2002) and has been shown to reveal blood—brain bar-
rier dysfunction effectively owing to the detection of IgM in
CSF, using detection after 1:8 dilution as a positive indica-
tion. The test was performed using CSF dilutions from 1:2 to
1:128. Centrifugation at 3000 rpm for 10 min of 1.5 ml of CSF
using a sealed Pasteur pipette was employed to concentrate
trypanosomes (Miézan et al., 2000). The base of the pipette
was examined for trypanosomes by bright field microscopy
at a 400-fold magnification.
Clinical examinations indicated no signs of continuing
trypanosome infection. However, the patient’s immature
bilateral cataract (present 5 months before treatment)
had progressed rapidly and 6 months after treatment the
patient had developed bilateral mature cataract with con-
siderable diminution of vision. Surgery for cataract is now
planned.
Serological tests indicated a positive result for 1:16 and
1:4 plasma dilutions performed 24 h and 3 months after
initial treatment, respectively. By 6 months, however, the
CATT test yielded a positive result only for 1:2 plasma
dilution, indicative of a falling antibody titre and proba-
bly a loss of trypanosomes. Latex IgM agglutination using
CSF was negative at 3 months and 6 months after ini-
tial treatment. No trypanosomes were detected either in
blood or CSF at 24 h, 3 months or 6 months after initial
treatment.
P.P. Joshi et al.
4. Discussion
We report here the successful treatment using suramin of a
patient presenting with trypanosomiasis caused by T. evansi
in India.
Some cases of drug resistance have been described when
using suramin both against T. b. rhodesiense in humans
(Wéry, 1994) and T. evansi in animals (Gill, 1971). Relapse
does not appear to have occurred in the case reported here.
However, given that pharmacokinetic profiles for suramin
vary from one individual to another and there are no previ-
ous cases of suramin use in patients infected by T. evansi, it
is difficult to compare directly the regimen used here with
those used in the treatment of rhodesiense HAT or animal
trypanosomiasis caused by T. evansi. Since several attempts
to cultivate in vivo the parasites isolated from this individual
by inoculation of infected blood into rodents failed (Joshi et
al., 2005), and since this strain has not adapted to growth
in vitro, we have not been able to determine the precise
sensitivity of these parasites to the drug.
Serological testing of the patient showed that CATT-
positive results decrease over time post treatment, with
1:16, 1:4 and 1:2 dilutions being required to yield a pos-
itive result at 24 h, 3 months and 6 months after initial
treatment, respectively. The same test was positive at 1:64
plasma dilution before treatment (Joshi et al., 2005), indi-
cating a loss of trypanosomes and confirming that suramin
treatment using this particular schedule has been a success.
Although follow-up will continue for another 6 months, with
a final check 12 months after treatment, as suggested for
HAT caused by T. b. rhodesiense and T. b. gambiense, treat-
ment of the first human case of T. evansi trypanosomiasis
appears to have been effective. Accordingly, the same reg-
imen should be considered in the treatment of other cases
of human T. evansi infection, if they occur.
Conflicts of interest statement
The authors have no conflicts of interest concerning the work
reported in this paper.
References
Gill, B.S., 1971. Resistance of Trypanosoma evansi to quinapyra-
mine, suramin, stilbamidine and tryparsamide and analy-
sis of cross-resistance. Trans. R. Soc. Trop. Med. Hyg. 65,
352—357.
Hawking, F., 1978. The resistance of Trypanosoma congolense, T.
vivax and T. evansi to human plasma. Trans. R. Soc. Trop. Med.
Hyg. 72, 405—407.
Joshi, P.P., Shegokar, V.R., Powar, R.M., Herder, S., Katti, R., Salkar,
H.R., Dani, V.S., Bhargava, A., Jannin, J., Truc, P., 2005. Human
trypanosomiasis caused by Trypanosoma evansi in India: the first
case report. Am. J. Trop. Med. Hyg. 73, 491—495.
Lejon, V., Legros, D., Richer, M., Ruiz, J.A., Jamonneau, V., Truc, P.,
Doua, F., Djé, N., N’Siesi, F.X., Bisser, S., Magnus, E., Wouters, I.,
Konings, J., Vervoort, T., Sultan, F., Büscher, P., 2002. IgM quan-
tification in the cerebrospinal fluid of sleeping sickness patients
by a latex card agglutination test. Trop. Med. Int. Health 7,
685—692.
Lumsden, W.H.R., Kimber, C.D., Evans, D.A., Doig, S.J., 1979.
Trypanosoma brucei: miniature anion-exchange centrifugation
technique for detection of low parasitemias: adaptation for field
use. Trans. R. Soc. Trop. Med. Hyg. 73, 312—317.
Treatment of human T. evansi trypanosomiasis in India
Miézan, T.W., Meda, H.A., Doua, F., Djè, N.N., Lejon, V., Büscher,
P., 2000. Single centrifugation of cerebrospinal fluid in a sealed
pasteur pipette for simple, rapid and sensitive detection of try-
panosomes. Trans. R. Soc. Trop. Med. Hyg. 94, 293.
Pathak, K.M.L., Singh, Y., Van Meirvenne, N., Kapoor, M., 1997.
Evaluation of various diagnostic techniques for Trypanosoma
evansi infections in naturally infected camels. Vet. Parasitol.
69, 49—54.
991
Wéry, M., 1994. Drug used in the treatment of sleeping sick-
ness (human African trypanosomiasis: HAT). Int. J. Antimicrob.
Agents 4, 227—238.
WHO, 1998. Control and surveillance of African trypanosomiasis.
World Health Organization, Geneva, Technical Report Series No.
881.