AFRICAN TRYPANOSOMIASIS: A UNIQUE EXPERIENCE AT UNITED NATION MISSION IN LIBERIA - CASE REPORT.
African Trypanosomiasis (sleeping sickness) is caused by Trypanosoma brucei, a hemoflagellate protozoan parasite, transmitted to human by an insect vector Tsetse fly (Glossina spp) found in some parts of rural Africa. Two subspecies are responsible for human disease; T. brucei rhodensiense in East Africa and T. brucei gambiense in West Africa. Morphologically, both are indistinguishable but differ in clinical course and geographic distribution, East African being more rapidly progressive disease as compared to West African sleeping sickness. The disease is reasonably well controlled at present, with about 10,000 cases occurring annually with over 95% cases from Congo, Angola, Sudan, Chad, Central African republic and northern Uganda1. Still most of cases remain undiagnosed, unreported due to lack of proper laboratory facilities and technical expertise.
We present a case of African Trypanosomiasis from Liberia in a middle-aged individual having nonspecific symptoms. The importance of the case is that the disease can be suspected and diagnosed in patients with nonspecific symptoms as well, thereby cured at early stages thus not only reducing morbidity and mortality in civilians as well as UN peace keepers but also decreasing reservoir of the disease.
A 56-years-old man, resident of Maryland county-Harper, Liberia, businessman by profession, presented in medical reception centre of Pak-Field level II hospital, Harper with complaints of headache, body aches, intermittent fever and night time sleep disturbance for last one month. There was no history of flee bite, boil, ulcer, skin rash or itching. He was not diabetic or hypertensive. History revealed extensive traveling to other African countries including Ghana, Cote D Ivoire and Guinea during last 3 years. He has previously been treated as a case of typhoid fever at a local hospital.
On examination, he was looking weak but well oriented in time, place and person. He was afebrile with pulse 70 /min, blood pressure 140/100 mmHg and respiratory rate 18 breaths/min. There was no visible boil, ulcer or enlarged lymph nodes. Examination of chest, heart, abdomen and CNS was unremarkable. Blood complete picture revealed haemoglobin 11.3gm/dL, other indices were within normal limits, ESR was 40 mm at the end of 1st hour. Urine routine examination, X-ray chest, ultrsosnograhy abdomen and pelvis did not reveal any abnormality. Onsite typhoid IgG/IgM rapid test and thick and thin blood films for malarial parasite were also negative. Serum Widal test revealed titre of less than 1/20 for each of TO, TH, AO, BO antibodies.
Keeping in view the endemicity, peripheral blood film for Trypanosoma was prepared using concentration technique (centrifugation and preparation of blood film from buffy coat). Leishmain stain of blood film revealed trypomastigote form of Trypanosoma brucei having long cylinder body, central nucleus and undulating membrane with long flagellum arising from kinetoplast located at posterior end (Fig 1).
To rule out central nervous involvement lumbar puncture was performed. CSF examination did not reveal trypomastigote form or increase in cell count or proteins. With fianl diagnosis of African Trypanosomiasis (1st stage), patient was given inj. Pentamidine (Lomidine) 4 mg/kg /d intramuscularly for 10 days. Follow up blood films were negative for Trypomastigote form. He was discharged with advice for regular follow ups of blood films at 6 monthly intervals for up to 2 year to rule out any relapse.
Awareness lectures / presentations regarding the disease and its prevention were regularly delivered to locals and especially troops for prevention
Over 35 million people occupying Tsetse fly belt of Africa are at risk of developing sleeping sickness2,3. The causative agent, found in mammalian blood as elongated trypomastigote, evades host antibody response by developing series of genetically controlled surface coats resulting in successive waves of parasite each with different coat4. The clinical course has two stages: in first, the parasite is found in the peripheral circulation while in second, it invades central nervous system. After infective bite, most patients develop fever, headache, muscle/joint aches and enlarged lymph nodes within one to two weeks. Some patients may also develop rash or large sore at the site of bite. CNS involvement results in 'sleeping sickness syndrome' comprising changes in personality, increased day time sleepiness with disturbed night sleep, and progressive confusion, coma and death if untreated5.
East African sleeping sickness is rapidly progressive disease causing mental deterioration, neurological problems and death ithin months. While West African sleeping sickness is slowly progressive disease, CNS involvement occurs in 1-2 years and death usually occurs within 3 years but may be prolonged for up to 6-7 years.
Definitive diagnosis depends upon demonstration of trypomastigotes in the blood, lymph node/primary lesion aspirate, bone marrow or CSF. Gimesa/Leishmain's stain of thick, thin blood films and buffy coat concentration method are recommended for parasite detection2. Multiple slides should be prepared with multiple blood examinations to rule out trypanosomiasis. We were successful in our very first attempt in identifying the organism; following proper technique was the main reason. All patients must undergo CSF examination to determine CNS involvement as trypomastigotes can be demonstrated in centrifuged sediments. The WHO criteria for CNS involvement includes increased protein in CSF and white cell count of greater than 51. Serologic techniques like Card agglutination trypanosomiasis test, ELISA, IHA and IFA are available but not proven to be useful for routine diagnosis, as local population already have elevated levels due to exposure to non-infectious animal trypanosomes.
For T. brucei rhodensiense, Suramin 1 g intravenously on day 1, 3, 5, 14 and 21, is a drug of choice in haemolymphatic stage, while Melarsoprol 2-3.6 mg/ kg/day for three days (3 courses; 7 days apart) is suggested for CNS disease. For T. brucei gambiense, Pentamidine 4 mg/kg/d intramuscular or intravenous, for 7-10 days in haemolymphatic stage and Eflornithine 400 mg/kg/d in 4 doses for 14 days is recommended in patients with CNS involvement5,6. In our case, timely diagnosis followed by petamidine treatment for ten days proved effective.
Patients should be followed up every six month for two years to detect any relapse. As there is no prophylactic vaccine or drug, therefore prevention and control mainly depends upon decreasing the reservoir; searching for, isolating and treating patients with the disease; controlling the tsetse fly vector by traps or screens, usage of insecticides and insect repellents, avoiding contact with bushes, wearing long sleeved shirts and paints.
To conclude, most cases of African Trypanosomiasis remain undiagnosed and unreported not only due to lack of diagnostic facilities but also due to non specific symptoms early in the disease. Therefore, the disease should always be kept in differential diagnosis in endemic areas not only to reduce mortality but also to decrease reservoir, helping prevention and control.
1. African Trypnosomiasis. Atlanta, Centre for Disease Control and Prevention, Nov 2, 2010. Availablefrom:URL:http://www.cdc.gov/-parasites/sleepi-gsickness/disease.html. access-ed on: 16 Sept 2011.
2. David BA, Labarca JA. Leishmania and Trypanosoma. In: Murray PR, Baron EJ, Jorgensen JM, Yolken RH (eds). Mannual of Clinical Microbiology, 8th ed.Washington: American Society for Microbiology Press, 2003; 1960-9.
3. Ford LB, Odiit M, maiso F, Toews DW, McDermott J. Sleeping Sickness in Uganda: revis
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|Author:||Hussain, Wajid; Khan, Ahmed Mushtaque; Ali, Muhammad Zeeshan; Rashid, Abdul; Ikram, Aamer|
|Publication:||Pakistan Armed Forces Medical Journal|
|Article Type:||Clinical report|
|Date:||Jun 30, 2012|
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