- Email: [email protected]
African trypanosomiasis acquired in an urban area
EUROPEAN
JOURNAL
OF
INTERNAL MEDICINE ELSEVIER
European
Journal
of Internal
Medicine
14 (2003)
390-391 www.elsevier.com/locate/ejim
Brief report
African trypanosomiasis acquired in an urban area Cedric Landron*, France Roblot, Gwenael Le Moal, Bertrand Becq-Giraudon Department
of Internal
Medicine
Received
and Infectious Diseases, Hospital BP 577, F-86021 Poitiers
6 March
2003;
received
in revised
de la Miletrie, cedex, France
form
13 May
CHU
2003;
La MilPtrie,
accepted
Avenue
de La Milttrie,
10 June 2003
Abstract A 28-year-old Zairian woman was presented with a diurnal somnolence, cervical polyadenopathy, elevated IgM. A diagnosis of West African trypanosomiasis was confirmed and the patient improved 0 2003 Elsevier B.V. All rights reserved. Keywords:
African
trypanosomiasis;
Urban
transmission;
Hyper
IgM;
Eflornithine
1. Introduction African trypanosomiasis is caused by West Trypanosoma brucei gambiense, which is transmitted by the tsetse fly. In most cases, the infection is contracted in the bush. We report the case of a young Zairian woman who presented with a trypanosomiasis but who denied ever living outside the urban area of Kinshasa.
2. Case report A 28-year-old Zairian woman was hospitalized in September 2001 because of fatigue and weight loss (5 kg). She also reported having headaches, cervicodynias, loss of memory, and diurnal somnolence. The symptoms had started 5 months
earlier.
The patient
was born in the center
of Kinshasa and had never been in the bush or elsewhere in Zaire. She first came to France in April 2001 and so she had only been out of Africa for 5 months prior to presentation. Physical examination revealed axillary and cervical
adenomegalies and splenomegaly without hepatomegaly. Neurological examination showed no focal deficit or confusion, but there was somnolence associated with visual and auditory hallucinations. Laboratory investigations revealed WBC, 6.6X 109/l (eosinophils 1.58X 109/l); hemoglobin, 103 g/l; platelets, 210X1012/1; and C-reactive protein, 5.5 mg/l (normal<5 mg/l). There was a polyclonal hypergammaglobulinemia with a total serum protein level of 100 g/l and a serum IgM level of 12.2 g/l (normal< 1.9 g/l). HIV serology and tests for syphilis were negative. No malaria parasites were seen on a blood film. CT brain scan revealed a diffuse cerebral edema. Brain MRI showed T2-weighted hyperintense signals of the white
matter
that was enhanced
author.
Tel.:
+33-5-49-44-44-22;
c.landron@chu-poitiersfr
0953-6205/03/$ - see front doi:lO.l016/S0953-6205(03)00139-O
matter
fax:
endemic patient’s
+33-5-49-44-
2003 Elsevier
B.V. All rights
of contrast
area
associated
blood,
with
elevated
IgM
levels
and
Trypanosomes were not found in the
CSF, bone marrow,
or lymph
node aspira-
tions. However, Mott’s cells were found in the bone marrow and in lymph node aspiration, and serology
(C. Landron). 0
after injection
product, findings compatible with subacute meningitis. Cerebrospinal fluid (CSF) contained 290X 109/l leukocytes (100% polymorphonuclears), 0.6 g/l protein, 3 mmol/l glucose, 12.1 mmol/l lactic acid, and elevated polyclonal IgM (249 mg/l). The diagnosis of African trypanosomiasis was suggested by the clinical findings in a patient coming from an hypereosinophilia.
*Corresponding 43-83. E-mail address:
splenomegaly, eosinophilia, and after treatment with eflornithine.
reserved
C. Landron
et al. I European
Journal
Table 1 Results of the serology Blood
test
Direct immunofluorescence T. brucei gambiense LiTat 1.3 antigen (positive ?1:50) Direct agglutination T. brucei gambiense LiTat 1.3 antigen (positive 215)
November 2001
July 2002
December 2002
1:400
1:200
1:50
1:20
1:lO
15
strongly suggested infection with T. brucei gambiense (Table 1). Furthermore, CSF serology was positive for T. brucei gambiense (IgG). After a 14-day course of eflornithine (100 mg/kg every 6 h), the patient’s hypersomnia and hallucinations disappeared, as did her adenomegalies and splenomegaly. Also, her neurological examination and serum protein levels returned to normal. One year later, her eosinophilia remained ( 1.12 X 109 cells/l); however, her IgM level had decreased (2.37 mg/l). The patient refused a repeat CSF examination. Repeat serology 6 and 12 months after the treatment confirmed infection with T. brucei gambiense (Table 1).
of Internal
West African sleeping sickness is due to T. brucei gambiense, which is transmitted by the tsetse lly in west and central African countries [l]. Measures were introduced in the middle of the 20th century to reduce the spread of the tsetse fly. Neglect of these vector eradication campaigns may explain the current rising incidence of trypanosomiasis in Africa. Although the habitat of the
14 (2003)
390-391
391
tsetse fly is the bush, other cases of urban transmission of the sleeping sickness, similar to that of our patient, have recently been described. This may indicate a change in the epidemiology of this disease. Moreover, trypanosomiasis has been described in travelers who were only in an endemic area for a short time [2]. Eflomithine has been recommended for the treatment of second-stage T. brucei gambiense infection, but it is difficult to administer as it requires four daily infusions for 7 or 14 days [3]. Clinical and biological supervision is recommended for 2 years after the treatment. The differential diagnoses include any angiitis of the central nervous system, HIV infection with opportunistic infection, and neurosyphilis, as well as other parasitic infections [4]. The increasing spread of the tsetse fly makes it likely that trypanosomiasis will be encountered with greater frequency in people from, and travelers to, Africa. The condition should be suspected in any patient from an endemic area who has eosinophilia and elevated gamma globulins.
References [II
3. Discussion
Medicine
Sinha A, Grace C, Alston WK, Westenfeld F, Maguire JH. African trypanosomiasis in two travelers from the United States. Clin Infect Dis 1999;29:840-4. PI Moore DAJ. Edwards M, Escombe R. Agranoff D. Bailey JW. Squire SB et al. African trypanosomiasis in travelers returning to the United Kingdom. Emerg Infect Dis 2002;8:74-6. G, Gastellu-Etchegorry M, Paquet C, Burri C. [31 Legros D, Ollivier Jannin J et al. Treatment of human African trypanosomiasispresent situation and needs for research and development. Lancet, Infect Dis 2002;2:437-40. JD, Janevski J, Detski AS. Out of Africa. N [41 Sahlas DJ. Maclean Engl J Med 2002;347:749-53.
JOURNAL
OF
INTERNAL MEDICINE ELSEVIER
European
Journal
of Internal
Medicine
14 (2003)
390-391 www.elsevier.com/locate/ejim
Brief report
African trypanosomiasis acquired in an urban area Cedric Landron*, France Roblot, Gwenael Le Moal, Bertrand Becq-Giraudon Department
of Internal
Medicine
Received
and Infectious Diseases, Hospital BP 577, F-86021 Poitiers
6 March
2003;
received
in revised
de la Miletrie, cedex, France
form
13 May
CHU
2003;
La MilPtrie,
accepted
Avenue
de La Milttrie,
10 June 2003
Abstract A 28-year-old Zairian woman was presented with a diurnal somnolence, cervical polyadenopathy, elevated IgM. A diagnosis of West African trypanosomiasis was confirmed and the patient improved 0 2003 Elsevier B.V. All rights reserved. Keywords:
African
trypanosomiasis;
Urban
transmission;
Hyper
IgM;
Eflornithine
1. Introduction African trypanosomiasis is caused by West Trypanosoma brucei gambiense, which is transmitted by the tsetse fly. In most cases, the infection is contracted in the bush. We report the case of a young Zairian woman who presented with a trypanosomiasis but who denied ever living outside the urban area of Kinshasa.
2. Case report A 28-year-old Zairian woman was hospitalized in September 2001 because of fatigue and weight loss (5 kg). She also reported having headaches, cervicodynias, loss of memory, and diurnal somnolence. The symptoms had started 5 months
earlier.
The patient
was born in the center
of Kinshasa and had never been in the bush or elsewhere in Zaire. She first came to France in April 2001 and so she had only been out of Africa for 5 months prior to presentation. Physical examination revealed axillary and cervical
adenomegalies and splenomegaly without hepatomegaly. Neurological examination showed no focal deficit or confusion, but there was somnolence associated with visual and auditory hallucinations. Laboratory investigations revealed WBC, 6.6X 109/l (eosinophils 1.58X 109/l); hemoglobin, 103 g/l; platelets, 210X1012/1; and C-reactive protein, 5.5 mg/l (normal<5 mg/l). There was a polyclonal hypergammaglobulinemia with a total serum protein level of 100 g/l and a serum IgM level of 12.2 g/l (normal< 1.9 g/l). HIV serology and tests for syphilis were negative. No malaria parasites were seen on a blood film. CT brain scan revealed a diffuse cerebral edema. Brain MRI showed T2-weighted hyperintense signals of the white
matter
that was enhanced
author.
Tel.:
+33-5-49-44-44-22;
c.landron@chu-poitiersfr
0953-6205/03/$ - see front doi:lO.l016/S0953-6205(03)00139-O
matter
fax:
endemic patient’s
+33-5-49-44-
2003 Elsevier
B.V. All rights
of contrast
area
associated
blood,
with
elevated
IgM
levels
and
Trypanosomes were not found in the
CSF, bone marrow,
or lymph
node aspira-
tions. However, Mott’s cells were found in the bone marrow and in lymph node aspiration, and serology
(C. Landron). 0
after injection
product, findings compatible with subacute meningitis. Cerebrospinal fluid (CSF) contained 290X 109/l leukocytes (100% polymorphonuclears), 0.6 g/l protein, 3 mmol/l glucose, 12.1 mmol/l lactic acid, and elevated polyclonal IgM (249 mg/l). The diagnosis of African trypanosomiasis was suggested by the clinical findings in a patient coming from an hypereosinophilia.
*Corresponding 43-83. E-mail address:
splenomegaly, eosinophilia, and after treatment with eflornithine.
reserved
C. Landron
et al. I European
Journal
Table 1 Results of the serology Blood
test
Direct immunofluorescence T. brucei gambiense LiTat 1.3 antigen (positive ?1:50) Direct agglutination T. brucei gambiense LiTat 1.3 antigen (positive 215)
November 2001
July 2002
December 2002
1:400
1:200
1:50
1:20
1:lO
15
strongly suggested infection with T. brucei gambiense (Table 1). Furthermore, CSF serology was positive for T. brucei gambiense (IgG). After a 14-day course of eflornithine (100 mg/kg every 6 h), the patient’s hypersomnia and hallucinations disappeared, as did her adenomegalies and splenomegaly. Also, her neurological examination and serum protein levels returned to normal. One year later, her eosinophilia remained ( 1.12 X 109 cells/l); however, her IgM level had decreased (2.37 mg/l). The patient refused a repeat CSF examination. Repeat serology 6 and 12 months after the treatment confirmed infection with T. brucei gambiense (Table 1).
of Internal
West African sleeping sickness is due to T. brucei gambiense, which is transmitted by the tsetse lly in west and central African countries [l]. Measures were introduced in the middle of the 20th century to reduce the spread of the tsetse fly. Neglect of these vector eradication campaigns may explain the current rising incidence of trypanosomiasis in Africa. Although the habitat of the
14 (2003)
390-391
391
tsetse fly is the bush, other cases of urban transmission of the sleeping sickness, similar to that of our patient, have recently been described. This may indicate a change in the epidemiology of this disease. Moreover, trypanosomiasis has been described in travelers who were only in an endemic area for a short time [2]. Eflomithine has been recommended for the treatment of second-stage T. brucei gambiense infection, but it is difficult to administer as it requires four daily infusions for 7 or 14 days [3]. Clinical and biological supervision is recommended for 2 years after the treatment. The differential diagnoses include any angiitis of the central nervous system, HIV infection with opportunistic infection, and neurosyphilis, as well as other parasitic infections [4]. The increasing spread of the tsetse fly makes it likely that trypanosomiasis will be encountered with greater frequency in people from, and travelers to, Africa. The condition should be suspected in any patient from an endemic area who has eosinophilia and elevated gamma globulins.
References [II
3. Discussion
Medicine
Sinha A, Grace C, Alston WK, Westenfeld F, Maguire JH. African trypanosomiasis in two travelers from the United States. Clin Infect Dis 1999;29:840-4. PI Moore DAJ. Edwards M, Escombe R. Agranoff D. Bailey JW. Squire SB et al. African trypanosomiasis in travelers returning to the United Kingdom. Emerg Infect Dis 2002;8:74-6. G, Gastellu-Etchegorry M, Paquet C, Burri C. [31 Legros D, Ollivier Jannin J et al. Treatment of human African trypanosomiasispresent situation and needs for research and development. Lancet, Infect Dis 2002;2:437-40. JD, Janevski J, Detski AS. Out of Africa. N [41 Sahlas DJ. Maclean Engl J Med 2002;347:749-53.