Human African trypanosomiasis has not been reported in Nigeria since 2012. Nevertheless, limitations of current surveillance programs mean that undetected infections may persist. We report a recent case of stage 2 trypanosomiasis caused by Trypanosoma brucei gambiense acquired in Nigeria and imported into the United Kingdom

Brooks, Tim

Brown, Mike

Büscher, Philippe

Cooper, Anneli

Lowe, Patricia

Luintel, Akish

MacLeod, Annette

Emerging Infectious Diseases

Akish Luintel

Patricia Lowe

Anneli Cooper

Annette MacLeod

Philippe Büscher

Tim Brooks

Mike Brown

Directory of Open Access Journals

Case of Nigeria-Acquired Human African Trypanosomiasis in United Kingdom, 2016

LSHTM Research Online

Luintel, A; Lowe, P; Cooper, A; MacLeod, A; Buscher, P; Brooks,T; Brown, M (2017) Case of Nigeria-Acquired Human African Try-panosomiasis in United Kingdom, 2016. Emerging infectious diseases,23 (7). pp. 1225-1226. ISSN 1080-6040 DOI: https://doi.org/10.3201/eid2307.170695Downloaded from: http://researchonline.lshtm.ac.uk/4328611/DOI: 10.3201/eid2307.170695Usage GuidelinesPlease refer to usage guidelines at http://researchonline.lshtm.ac.uk/policies.html or alterna-tively contact researchonline@lshtm.ac.uk.Available under license: http://creativecommons.org/licenses/by/2.5/  7. Maurer-Stroh S, Mak TM, Ng YK, Phuah SP, Huber RG, Marzinek JK, et al. South-east Asian Zika virus strain linked to cluster of cases in Singapore, August 2016. Euro Surveill. 2016;21:30347. http://dx.doi.org/10.2807/1560-7917.ES.2016.21.38.30347Address for correspondence: Satoshi Kutsuna, National Center for Global Health and Medicine—Disease Control and Prevention  Center, 1-21-1, Toyama Shinjuku, Tokyo 162-8655, Japan; email:  sonare.since1192@gmail.com Case of Nigeria-Acquired  Human African  Trypanosomiasis in  United Kingdom, 2016Akish Luintel, Patricia Lowe, Anneli Cooper, Annette MacLeod, Philippe Büscher, Tim Brooks, Mike BrownAuthor affiliations: University College London Hospital,  London, UK (A. Luintel, P. Lowe, M. Brown); University of Glasgow, Glasgow, Scotland, UK (A. Cooper, A. MacLeod);  Institute of Tropical Medicine, Antwerp, Belgium (P. Büscher);  Public Health England, London (T. Brooks); London School of Hygiene and Tropical Medicine, London (M. Brown)DOI: https://dx.doi.org/10.3201/eid2307.170695Human African trypanosomiasis has not been reported in Nigeria since 2012. Nevertheless, limitations of current sur-veillance programs mean that undetected infections may persist. We report a recent case of stage 2 trypanosomiasis caused by Trypanosoma brucei gambiense acquired in Ni-geria and imported into the United Kingdom.Human African trypanosomiasis (HAT), known as Af-rican sleeping sickness, is a protozoal infection, the West African form of which is caused by Trypanosoma brucei gambiense. We report a case of imported T. brucei gambiense HAT, acquired in Nigeria, where no cases have been reported since 2012 (1).The case-patient, a 58-year-old Nigerian woman, lived near Warri, in Delta State, Nigeria. She traveled in-frequently to towns within Delta State, across the Niger River into Bayelsa State, and to larger cities in Nigeria, but never outside Nigeria. She reported no history of tse-tse fly bites.In January 2016, the patient experienced leg tremors and lethargy. These symptoms persisted until arrival in the United Kingdom in May 2016. Over the next 2 months, increasing malaise and unsteadiness in walking developed. In August 2016, the patient was admitted to a regional hos-pital with confusion and drowsiness. She was febrile at admission but had no lymphadenopathy; neurologic exami-nation revealed no neck stiffness or photophobia, but did show poor coordination with slow cognitive processes.Laboratory investigations revealed microcytic anemia with a C-reactive protein level of 13 mg/L (reference val-ue <5 mg/L) and a total serum IgM of 13.7 g/L (reference range 0.5–2.0 g/L). A blood film was negative for malaria. Confirmatory assays after positive screening assay results for HIV and syphilis antibodies showed the original results to be false positive.Cerebrospinal fluid (CSF) examination revealed 331 leukocytes/mm3, 99% lymphocytes; CSF protein level 0.82 g/L (reference range 0.23–0.38 g/L); and glucose level was >50% plasma glucose. Results of CSF PCR for herpesvi-ruses, enterovirus, and JC virus were negative. Results of GeneXpert (Cepheid, Buckinghamshire, UK) tests of CSF and mycobacterial culture were negative. Magnetic reso-nance imaging of the brain showed, on T2 weighted and flair images, bilateral diffuse hyperintensities within white matter located in the periventricular regions, basal ganglia, cerebellum, and brainstem.Treatment with ceftriaxone, acyclovir, antitubercu-lous treatment and prednisolone was stopped at 14 days because of a lack of clinical improvement and drug-in-duced transaminitis.The patient’s lethargy, intermittent confusion, and pe-riods of somnolence became more severe. Examination in August 2016 revealed intention tremor in all limbs and myoclonic jerks. Her case was discussed with the Imported Fever Service at Public Health England. A serum sample was sent to the Hospital of Tropical Diseases in London, UK for T. brucei gambiense indirect fluorescent antibody testing (IFAT), which showed a positive result (titer 1:400). The patient was transferred to this hospital.Repeat CSF examination revealed a protein level of 1.14 g/L, CSF glucose level of 2.3 mmol/L (serum 5.5 mmol/L), and 1,140 leukocytes/mm3 (90% mononuclear). No trypanosomes were seen in the buffy coat of peripheral blood or CSF. CSF total IgM of 1.98 mg/L (reference range 0–0.9 mg/L) and IgG of 306 mg/L (reference range 10–40 mg/L) were markedly raised (2).T. brucei gambiense IFAT results for CSF (titer 1:4) and blood (titer 1:400) were positive. DNA extracted from CSF was positive for trypanosomes of the subge-nus Trypanozoon by PCR (3) and confirmed as T. brucei gambiense group 1 by diagnostic PCR with TgsGP prim-ers (4). The result of immune trypanolysis was negative  Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017 1225RESEARCH LETTERSwhen T. brucei gambiense variable antigen type LiTat 1.3 was used but positive when using LiTat 1.5 (4). The patient had a titer of 1:32 in the CATT/T. brucei gam-biense test (5,6).We administered nifurtimox/eflornithine combina-tion therapy, according to World Health Organization guidelines, for treatment of stage 2 T. brucei gambiense. By the end of treatment, the patient’s cognitive function, myoclonus, tremor, and ataxia had all improved, and she was discharged.A posttreatment CSF examination revealed 4 leuko-cytes/mm3 and a protein level of 1.17 g/L. Six months after discharge, the patient had made a full functional recovery. Repeat CSF examination revealed 4 leukocytes/mm3 and a protein level of 0.63 g/L, and MRI of the brain showed improvement. The CSF T. brucei gambiense IFAT titer de-clined to 1:2.No cases of HAT in Nigeria have been reported to the World Health Organization since 2012 (1). The last report-ed patients were from the Abraka region, in Delta State, ≈50 km from this case-patient’s residence (7). We do not have a clear exposure time for this patient, which is likely to have been within 2–3 years before her hospitalization, although we have reported a case-patient with an exposure >29 years prior to illness onset; the emerging scientific con-sensus is that trypanotolerance may exist among some in-fected patients, leading to delay in diagnosis and premature confidence of disease elimination (8,9).A clue to diagnosis, alongside clinical and travel his-tory, was a high serum IgM level, a prominent feature in T. brucei gambiense–infected patients, as a result of poly-clonal B-cell activation (10). False-positive antibody test results specific for pathogens have been reported; multiple positive antibody tests may aid the clinician in considering HAT as a differential diagnosis (10).This case shows that HAT transmission continues in Nigeria and surveillance in Delta state is warranted. There may be a role for additional diagnostic tools if we are to achieve the goal of eliminating HAT by 2030.AcknowledgmentsWe thank Jose Ramon Franco Minguell, the HAT Control and Surveillance Programme, and the World Health Organization for releasing the nifurtimox/eflornithine combination therapy  medication and for providing advice on the manuscript.Dr. Luintel is a specialty registrar in infectious diseases at University College London Hospital in London, UK.References  1. World Health Organization. Number of new reported cases  (T.b. gambiense). Data by country. 2016 [cited 2016 Dec 18].  http://apps.who.int/gho/data/node.main.A1636?lang=en   2. Greenwood BM, Whittle HC. Cerebrospinal-fluid IgM in  patients with sleeping-sickness. Lancet. 1973;302:525–7.  http://dx.doi.org/10.1016/S0140-6736(73)92348-9  3. Masiga DK, Smyth AJ, Hayes P, Bromidge TJ, Gibson WC.  Sensitive detection of trypanosomes in tsetse flies by DNA amplification. Int J Parasitol. 1992;22:909–18. http://dx.doi.org/ 10.1016/0020-7519(92)90047-O  4. Morrison, LJ, Tait A, McCormack G, Sweeney L, Black A,  Truc P, et al. Trypanosoma brucei gambiense type 1 populations from human patients are clonal and display geographical genetic differentiation. Infect Genet Evol. 2008;8:847–54. http://dx.doi.org/ 10.1016/j.meegid.2008.08.005  5. Van Meirvenne N, Magnus E, Büscher P. Evaluation of variant specific trypanolysis tests for serodiagnosis of human infections with Trypanosoma brucei gambiense. Acta Trop. 1995;60:189–99. http://dx.doi.org/10.1016/0001-706X(95)00127-Z  6. Magnus E, Vervoort T, Van Meirvenne N. A card-agglutination  test with stained trypanosomes (C.A.T.T.) for the serological  diagnosis of T. b. gambiense trypanosomiasis. Ann Soc Belg Med Trop. 1978;58:169–76.  7. Nmorsi O, Isaac C, Igbinosa I, Umukoro D, Aitaikuru D. Human African trypanosomiasis in endemic focus of Abraka, Nigeria. Asian Pac J Trop Med. 2010;3:448–50. http://dx.doi.org/10.1016/S1995-7645(10)60107-1  8. Checchi F, Funk S, Chandramohan D, Haydon DT, Chappuis F. Updated estimate of the duration of the meningo-encephalitic stage in gambiense human African trypanosomiasis. BMC Res Notes. 2015;8:292. http://dx.doi.org/10.1186/s13104-015-1244-3  9. Sudarshi D, Lawrence S, Pickrell WO, Eligar V, Walters R,  Quaderi S, et al. Human African trypanosomiasis presenting  at least 29 years after infection—what can this teach us about the pathogenesis and control of this neglected tropical disease?  PLoS Negl Trop Dis. 2014;8:e3349. http://dx.doi.org/10.1371/ journal.pntd.000334910. Lejon V, Boelaert M, Jannin J, Moore A, Büscher P.  The challenge of Trypanosoma brucei gambiense sleeping  sickness diagnosis outside Africa. Lancet Infect Dis. 2003;3:804–8. http://dx.doi.org/10.1016/S1473-3099(03)00834-XAddress for correspondence: Akish Luintel, Division of Infection and Immunity, University College London, Euston Rd, London W1E 6BT, UK; email: akish.luintel@nhs.net1226 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017RESEARCH LETTERS

Case of Nigeria-Acquired Human African Trypanosomiasis in United Kingdom, 2016.

Enlighten: Publications

  7. Maurer-Stroh S, Mak TM, Ng YK, Phuah SP, Huber RG, Marzinek 
JK, et al. South-east Asian Zika virus strain linked to cluster of 
cases in Singapore, August 2016. Euro Surveill. 2016;21:30347. 
http://dx.doi.org/10.2807/1560-7917.ES.2016.21.38.30347
Address for correspondence: Satoshi Kutsuna, National Center for 
Global Health and Medicine—Disease Control and Prevention  
Center, 1-21-1, Toyama Shinjuku, Tokyo 162-8655, Japan; email:  
sonare.since1192@gmail.com 
Case of Nigeria-Acquired  
Human African  
Trypanosomiasis in  
United Kingdom, 2016
Akish Luintel, Patricia Lowe, Anneli Cooper, 
Annette MacLeod, Philippe Büscher, Tim Brooks, 
Mike Brown
Author affiliations: University College London Hospital,  
London, UK (A. Luintel, P. Lowe, M. Brown); University of 
Glasgow, Glasgow, Scotland, UK (A. Cooper, A. MacLeod);  
Institute of Tropical Medicine, Antwerp, Belgium (P. Büscher);  
Public Health England, London (T. Brooks); London School of 
Hygiene and Tropical Medicine, London (M. Brown)
DOI: https://dx.doi.org/10.3201/eid2307.170695
Human African trypanosomiasis has not been reported in 
Nigeria since 2012. Nevertheless, limitations of current sur-
veillance programs mean that undetected infections may 
persist. We report a recent case of stage 2 trypanosomiasis 
caused by Trypanosoma brucei gambiense acquired in Ni-
geria and imported into the United Kingdom.
Human African trypanosomiasis (HAT), known as Af-rican sleeping sickness, is a protozoal infection, the 
West African form of which is caused by Trypanosoma 
brucei gambiense. We report a case of imported T. brucei 
gambiense HAT, acquired in Nigeria, where no cases have 
been reported since 2012 (1).
The case-patient, a 58-year-old Nigerian woman, 
lived near Warri, in Delta State, Nigeria. She traveled in-
frequently to towns within Delta State, across the Niger 
River into Bayelsa State, and to larger cities in Nigeria, 
but never outside Nigeria. She reported no history of tse-
tse fly bites.
In January 2016, the patient experienced leg tremors 
and lethargy. These symptoms persisted until arrival in the 
United Kingdom in May 2016. Over the next 2 months, 
increasing malaise and unsteadiness in walking developed. 
In August 2016, the patient was admitted to a regional hos-
pital with confusion and drowsiness. She was febrile at 
admission but had no lymphadenopathy; neurologic exami-
nation revealed no neck stiffness or photophobia, but did 
show poor coordination with slow cognitive processes.
Laboratory investigations revealed microcytic anemia 
with a C-reactive protein level of 13 mg/L (reference val-
ue <5 mg/L) and a total serum IgM of 13.7 g/L (reference 
range 0.5–2.0 g/L). A blood film was negative for malaria. 
Confirmatory assays after positive screening assay results 
for HIV and syphilis antibodies showed the original results 
to be false positive.
Cerebrospinal fluid (CSF) examination revealed 331 
leukocytes/mm3, 99% lymphocytes; CSF protein level 0.82 
g/L (reference range 0.23–0.38 g/L); and glucose level was 
>50% plasma glucose. Results of CSF PCR for herpesvi-
ruses, enterovirus, and JC virus were negative. Results of 
GeneXpert (Cepheid, Buckinghamshire, UK) tests of CSF 
and mycobacterial culture were negative. Magnetic reso-
nance imaging of the brain showed, on T2 weighted and 
flair images, bilateral diffuse hyperintensities within white 
matter located in the periventricular regions, basal ganglia, 
cerebellum, and brainstem.
Treatment with ceftriaxone, acyclovir, antitubercu-
lous treatment and prednisolone was stopped at 14 days 
because of a lack of clinical improvement and drug-in-
duced transaminitis.
The patient’s lethargy, intermittent confusion, and pe-
riods of somnolence became more severe. Examination 
in August 2016 revealed intention tremor in all limbs and 
myoclonic jerks. Her case was discussed with the Imported 
Fever Service at Public Health England. A serum sample 
was sent to the Hospital of Tropical Diseases in London, 
UK for T. brucei gambiense indirect fluorescent antibody 
testing (IFAT), which showed a positive result (titer 1:400). 
The patient was transferred to this hospital.
Repeat CSF examination revealed a protein level of 
1.14 g/L, CSF glucose level of 2.3 mmol/L (serum 5.5 
mmol/L), and 1,140 leukocytes/mm3 (90% mononuclear). 
No trypanosomes were seen in the buffy coat of peripheral 
blood or CSF. CSF total IgM of 1.98 mg/L (reference range 
0–0.9 mg/L) and IgG of 306 mg/L (reference range 10–40 
mg/L) were markedly raised (2).
T. brucei gambiense IFAT results for CSF (titer 1:4) 
and blood (titer 1:400) were positive. DNA extracted 
from CSF was positive for trypanosomes of the subge-
nus Trypanozoon by PCR (3) and confirmed as T. brucei 
gambiense group 1 by diagnostic PCR with TgsGP prim-
ers (4). The result of immune trypanolysis was negative 
 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017 1225
RESEARCH LETTERS
when T. brucei gambiense variable antigen type LiTat 
1.3 was used but positive when using LiTat 1.5 (4). The 
patient had a titer of 1:32 in the CATT/T. brucei gam-
biense test (5,6).
We administered nifurtimox/eflornithine combina-
tion therapy, according to World Health Organization 
guidelines, for treatment of stage 2 T. brucei gambiense. 
By the end of treatment, the patient’s cognitive function, 
myoclonus, tremor, and ataxia had all improved, and she 
was discharged.
A posttreatment CSF examination revealed 4 leuko-
cytes/mm3 and a protein level of 1.17 g/L. Six months after 
discharge, the patient had made a full functional recovery. 
Repeat CSF examination revealed 4 leukocytes/mm3 and 
a protein level of 0.63 g/L, and MRI of the brain showed 
improvement. The CSF T. brucei gambiense IFAT titer de-
clined to 1:2.
No cases of HAT in Nigeria have been reported to the 
World Health Organization since 2012 (1). The last report-
ed patients were from the Abraka region, in Delta State, 
≈50 km from this case-patient’s residence (7). We do not 
have a clear exposure time for this patient, which is likely 
to have been within 2–3 years before her hospitalization, 
although we have reported a case-patient with an exposure 
>29 years prior to illness onset; the emerging scientific con-
sensus is that trypanotolerance may exist among some in-
fected patients, leading to delay in diagnosis and premature 
confidence of disease elimination (8,9).
A clue to diagnosis, alongside clinical and travel his-
tory, was a high serum IgM level, a prominent feature in 
T. brucei gambiense–infected patients, as a result of poly-
clonal B-cell activation (10). False-positive antibody test 
results specific for pathogens have been reported; multiple 
positive antibody tests may aid the clinician in considering 
HAT as a differential diagnosis (10).
This case shows that HAT transmission continues in 
Nigeria and surveillance in Delta state is warranted. There 
may be a role for additional diagnostic tools if we are to 
achieve the goal of eliminating HAT by 2030.
Acknowledgments
We thank Jose Ramon Franco Minguell, the HAT Control and 
Surveillance Programme, and the World Health Organization for 
releasing the nifurtimox/eflornithine combination therapy  
medication and for providing advice on the manuscript.
Dr. Luintel is a specialty registrar in infectious diseases at 
University College London Hospital in London, UK.
References
  1. World Health Organization. Number of new reported cases  
(T.b. gambiense). Data by country. 2016 [cited 2016 Dec 18].  
http://apps.who.int/gho/data/node.main.A1636?lang=en 
  2. Greenwood BM, Whittle HC. Cerebrospinal-fluid IgM in  
patients with sleeping-sickness. Lancet. 1973;302:525–7.  
http://dx.doi.org/10.1016/S0140-6736(73)92348-9
  3. Masiga DK, Smyth AJ, Hayes P, Bromidge TJ, Gibson WC.  
Sensitive detection of trypanosomes in tsetse flies by DNA 
amplification. Int J Parasitol. 1992;22:909–18. http://dx.doi.org/ 
10.1016/0020-7519(92)90047-O
  4. Morrison, LJ, Tait A, McCormack G, Sweeney L, Black A,  
Truc P, et al. Trypanosoma brucei gambiense type 1 populations 
from human patients are clonal and display geographical genetic 
differentiation. Infect Genet Evol. 2008;8:847–54. http://dx.doi.org/ 
10.1016/j.meegid.2008.08.005
  5. Van Meirvenne N, Magnus E, Büscher P. Evaluation of variant 
specific trypanolysis tests for serodiagnosis of human infections 
with Trypanosoma brucei gambiense. Acta Trop. 1995;60:189–99. 
http://dx.doi.org/10.1016/0001-706X(95)00127-Z
  6. Magnus E, Vervoort T, Van Meirvenne N. A card-agglutination  
test with stained trypanosomes (C.A.T.T.) for the serological  
diagnosis of T. b. gambiense trypanosomiasis. Ann Soc Belg Med 
Trop. 1978;58:169–76.
  7. Nmorsi O, Isaac C, Igbinosa I, Umukoro D, Aitaikuru D. Human 
African trypanosomiasis in endemic focus of Abraka, Nigeria. 
Asian Pac J Trop Med. 2010;3:448–50. http://dx.doi.org/10.1016/
S1995-7645(10)60107-1
  8. Checchi F, Funk S, Chandramohan D, Haydon DT, Chappuis F. 
Updated estimate of the duration of the meningo-encephalitic stage 
in gambiense human African trypanosomiasis. BMC Res Notes. 
2015;8:292. http://dx.doi.org/10.1186/s13104-015-1244-3
  9. Sudarshi D, Lawrence S, Pickrell WO, Eligar V, Walters R,  
Quaderi S, et al. Human African trypanosomiasis presenting  
at least 29 years after infection—what can this teach us about the 
pathogenesis and control of this neglected tropical disease?  
PLoS Negl Trop Dis. 2014;8:e3349. http://dx.doi.org/10.1371/ 
journal.pntd.0003349
10. Lejon V, Boelaert M, Jannin J, Moore A, Büscher P.  
The challenge of Trypanosoma brucei gambiense sleeping  
sickness diagnosis outside Africa. Lancet Infect Dis. 2003;3:804–8. 
http://dx.doi.org/10.1016/S1473-3099(03)00834-X
Address for correspondence: Akish Luintel, Division of Infection and 
Immunity, University College London, Euston Rd, London W1E 6BT, 
UK; email: akish.luintel@nhs.net
1226 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017
RESEARCH LETTERS


English

Case of Nigeria-acquired Human African trypanosomiasis in United Kingdom, 2016

Crossref

Enlighten

  7. Maurer-Stroh S, Mak TM, Ng YK, Phuah SP, Huber RG, Marzinek JK, et al. South-east Asian Zika virus strain linked to cluster of cases in Singapore, August 2016. Euro Surveill. 2016;21:30347. http://dx.doi.org/10.2807/1560-7917.ES.2016.21.38.30347Address for correspondence: Satoshi Kutsuna, National Center for Global Health and Medicine—Disease Control and Prevention  Center, 1-21-1, Toyama Shinjuku, Tokyo 162-8655, Japan; email:  sonare.since1192@gmail.com Case of Nigeria-Acquired  Human African  Trypanosomiasis in  United Kingdom, 2016Akish Luintel, Patricia Lowe, Anneli Cooper, Annette MacLeod, Philippe Büscher, Tim Brooks, Mike BrownAuthor affiliations: University College London Hospital,  London, UK (A. Luintel, P. Lowe, M. Brown); University of Glasgow, Glasgow, Scotland, UK (A. Cooper, A. MacLeod);  Institute of Tropical Medicine, Antwerp, Belgium (P. Büscher);  Public Health England, London (T. Brooks); London School of Hygiene and Tropical Medicine, London (M. Brown)DOI: https://dx.doi.org/10.3201/eid2307.170695Human African trypanosomiasis has not been reported in Nigeria since 2012. Nevertheless, limitations of current sur-veillance programs mean that undetected infections may persist. We report a recent case of stage 2 trypanosomiasis caused by Trypanosoma brucei gambiense acquired in Ni-geria and imported into the United Kingdom.Human African trypanosomiasis (HAT), known as Af-rican sleeping sickness, is a protozoal infection, the West African form of which is caused by Trypanosoma brucei gambiense. We report a case of imported T. brucei gambiense HAT, acquired in Nigeria, where no cases have been reported since 2012 (1).The case-patient, a 58-year-old Nigerian woman, lived near Warri, in Delta State, Nigeria. She traveled in-frequently to towns within Delta State, across the Niger River into Bayelsa State, and to larger cities in Nigeria, but never outside Nigeria. She reported no history of tse-tse fly bites.In January 2016, the patient experienced leg tremors and lethargy. These symptoms persisted until arrival in the United Kingdom in May 2016. Over the next 2 months, increasing malaise and unsteadiness in walking developed. In August 2016, the patient was admitted to a regional hos-pital with confusion and drowsiness. She was febrile at admission but had no lymphadenopathy; neurologic exami-nation revealed no neck stiffness or photophobia, but did show poor coordination with slow cognitive processes.Laboratory investigations revealed microcytic anemia with a C-reactive protein level of 13 mg/L (reference val-ue <5 mg/L) and a total serum IgM of 13.7 g/L (reference range 0.5–2.0 g/L). A blood film was negative for malaria. Confirmatory assays after positive screening assay results for HIV and syphilis antibodies showed the original results to be false positive.Cerebrospinal fluid (CSF) examination revealed 331 leukocytes/mm3, 99% lymphocytes; CSF protein level 0.82 g/L (reference range 0.23–0.38 g/L); and glucose level was >50% plasma glucose. Results of CSF PCR for herpesvi-ruses, enterovirus, and JC virus were negative. Results of GeneXpert (Cepheid, Buckinghamshire, UK) tests of CSF and mycobacterial culture were negative. Magnetic reso-nance imaging of the brain showed, on T2 weighted and flair images, bilateral diffuse hyperintensities within white matter located in the periventricular regions, basal ganglia, cerebellum, and brainstem.Treatment with ceftriaxone, acyclovir, antitubercu-lous treatment and prednisolone was stopped at 14 days because of a lack of clinical improvement and drug-in-duced transaminitis.The patient’s lethargy, intermittent confusion, and pe-riods of somnolence became more severe. Examination in August 2016 revealed intention tremor in all limbs and myoclonic jerks. Her case was discussed with the Imported Fever Service at Public Health England. A serum sample was sent to the Hospital of Tropical Diseases in London, UK for T. brucei gambiense indirect fluorescent antibody testing (IFAT), which showed a positive result (titer 1:400). The patient was transferred to this hospital.Repeat CSF examination revealed a protein level of 1.14 g/L, CSF glucose level of 2.3 mmol/L (serum 5.5 mmol/L), and 1,140 leukocytes/mm3 (90% mononuclear). No trypanosomes were seen in the buffy coat of peripheral blood or CSF. CSF total IgM of 1.98 mg/L (reference range 0–0.9 mg/L) and IgG of 306 mg/L (reference range 10–40 mg/L) were markedly raised (2).T. brucei gambiense IFAT results for CSF (titer 1:4) and blood (titer 1:400) were positive. DNA extracted from CSF was positive for trypanosomes of the subge-nus Trypanozoon by PCR (3) and confirmed as T. brucei gambiense group 1 by diagnostic PCR with TgsGP prim-ers (4). The result of immune trypanolysis was negative  Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017 1225RESEARCH LETTERSwhen T. brucei gambiense variable antigen type LiTat 1.3 was used but positive when using LiTat 1.5 (4). The patient had a titer of 1:32 in the CATT/T. brucei gam-biense test (5,6).We administered nifurtimox/eflornithine combina-tion therapy, according to World Health Organization guidelines, for treatment of stage 2 T. brucei gambiense. By the end of treatment, the patient’s cognitive function, myoclonus, tremor, and ataxia had all improved, and she was discharged.A posttreatment CSF examination revealed 4 leuko-cytes/mm3 and a protein level of 1.17 g/L. Six months after discharge, the patient had made a full functional recovery. Repeat CSF examination revealed 4 leukocytes/mm3 and a protein level of 0.63 g/L, and MRI of the brain showed improvement. The CSF T. brucei gambiense IFAT titer de-clined to 1:2.No cases of HAT in Nigeria have been reported to the World Health Organization since 2012 (1). The last report-ed patients were from the Abraka region, in Delta State, ≈50 km from this case-patient’s residence (7). We do not have a clear exposure time for this patient, which is likely to have been within 2–3 years before her hospitalization, although we have reported a case-patient with an exposure >29 years prior to illness onset; the emerging scientific con-sensus is that trypanotolerance may exist among some in-fected patients, leading to delay in diagnosis and premature confidence of disease elimination (8,9).A clue to diagnosis, alongside clinical and travel his-tory, was a high serum IgM level, a prominent feature in T. brucei gambiense–infected patients, as a result of poly-clonal B-cell activation (10). False-positive antibody test results specific for pathogens have been reported; multiple positive antibody tests may aid the clinician in considering HAT as a differential diagnosis (10).This case shows that HAT transmission continues in Nigeria and surveillance in Delta state is warranted. There may be a role for additional diagnostic tools if we are to achieve the goal of eliminating HAT by 2030.AcknowledgmentsWe thank Jose Ramon Franco Minguell, the HAT Control and Surveillance Programme, and the World Health Organization for releasing the nifurtimox/eflornithine combination therapy  medication and for providing advice on the manuscript.Dr. Luintel is a specialty registrar in infectious diseases at University College London Hospital in London, UK.References  1. World Health Organization. Number of new reported cases  (T.b. gambiense). Data by country. 2016 [cited 2016 Dec 18].  http://apps.who.int/gho/data/node.main.A1636?lang=en   2. Greenwood BM, Whittle HC. Cerebrospinal-fluid IgM in  patients with sleeping-sickness. Lancet. 1973;302:525–7.  http://dx.doi.org/10.1016/S0140-6736(73)92348-9  3. Masiga DK, Smyth AJ, Hayes P, Bromidge TJ, Gibson WC.  Sensitive detection of trypanosomes in tsetse flies by DNA amplification. Int J Parasitol. 1992;22:909–18. http://dx.doi.org/ 10.1016/0020-7519(92)90047-O  4. Morrison, LJ, Tait A, McCormack G, Sweeney L, Black A,  Truc P, et al. Trypanosoma brucei gambiense type 1 populations from human patients are clonal and display geographical genetic differentiation. Infect Genet Evol. 2008;8:847–54. http://dx.doi.org/ 10.1016/j.meegid.2008.08.005  5. Van Meirvenne N, Magnus E, Büscher P. Evaluation of variant specific trypanolysis tests for serodiagnosis of human infections with Trypanosoma brucei gambiense. Acta Trop. 1995;60:189–99. http://dx.doi.org/10.1016/0001-706X(95)00127-Z  6. Magnus E, Vervoort T, Van Meirvenne N. A card-agglutination  test with stained trypanosomes (C.A.T.T.) for the serological  diagnosis of T. b. gambiense trypanosomiasis. Ann Soc Belg Med Trop. 1978;58:169–76.  7. Nmorsi O, Isaac C, Igbinosa I, Umukoro D, Aitaikuru D. Human African trypanosomiasis in endemic focus of Abraka, Nigeria. Asian Pac J Trop Med. 2010;3:448–50. http://dx.doi.org/10.1016/S1995-7645(10)60107-1  8. Checchi F, Funk S, Chandramohan D, Haydon DT, Chappuis F. Updated estimate of the duration of the meningo-encephalitic stage in gambiense human African trypanosomiasis. BMC Res Notes. 2015;8:292. http://dx.doi.org/10.1186/s13104-015-1244-3  9. Sudarshi D, Lawrence S, Pickrell WO, Eligar V, Walters R,  Quaderi S, et al. Human African trypanosomiasis presenting  at least 29 years after infection—what can this teach us about the pathogenesis and control of this neglected tropical disease?  PLoS Negl Trop Dis. 2014;8:e3349. http://dx.doi.org/10.1371/ journal.pntd.000334910. Lejon V, Boelaert M, Jannin J, Moore A, Büscher P.  The challenge of Trypanosoma brucei gambiense sleeping  sickness diagnosis outside Africa. Lancet Infect Dis. 2003;3:804–8. http://dx.doi.org/10.1016/S1473-3099(03)00834-XAddress for correspondence: Akish Luintel, Division of Infection and Immunity, University College London, Euston Rd, London W1E 6BT, UK; email: akish.luintel@nhs.net1226 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 23, No. 7, July 2017RESEARCH LETTERS

https://wwwnc.cdc.gov/eid/article/23/7/pdfs/17-0695.pdf

Case of Nigeria-Acquired Human African Trypanosomiasis in United Kingdom, 2016.

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