Fazal Rahim ( DHQ Hospital, Timergara, District Dir, N.W.F.P. )
Fazal Rehman ( DHQ Hospital, Timergara, District Dir, N.W.F.P. )
Shuaib Ahmad ( DHQ Hospital, Timergara, District Dir, N.W.F.P. )
Bakht Zada ( DHQ Hospital, Timergara, District Dir, N.W.F.P. )
Visceral leishmaniasis is endemic in District Dir, NWFP. We evaluated 10 patients with visceral Ieishmaniasis at DHQ Hospital Timergara District Dir, N.W.F.P. All patients were in the age range 2 to 10 years. The predominant clinical features in these were chronic fever (10), splenomegaly (10), hepatomegaly (10), weight loss (10) and abdominal distention (5). Lymphadenopathy was absent. Common laboratory abnormalities included anaemia (10), leucopenia (7), thrombocytopenia (10) and hypergammaglobulinaemia (10). Formal Gel test w.as positive in all patients (100%) and all had positive bone marrow smears for Leishmania Donovani (L.D.) bodies (10). The response to stibogluconate (Glucantime Sodium) therapy was good with a 100 percent cure rate (JPMA 48:161,1998).
Visceral leishmaniasis, also known as Kala-azar is caused by a protozoa called leishmania donovani1. It was named after the discoverers, Leishman from London in May 1903 and Donovan from Madras 19032. It is conveyed to man by the female phiebotomine sand flies where the flagellate (promastigote) forms of leishmania develop3. The disease is prevalent in many countries of the world1, more so in sub-tropical and tropical areas as Mediterranean, Central Asia, China, Middle East, India, Northern Pakistan, Africa and South as well as Central America4,5. Multiplication by simple cell division of leishmania takes place in the monocytes and macrophages in various organs of the body6. The spleenis massively enlarged7. There is involvement of the bone marrow, resulting in granulocytopenia, thrombocytopenia, anaemia and occasionally pancytopenia may be present8. ESR is markedly raised. The incubation period is from ito 2 months but may be upto 10 years8. There is either continuous low grade fever or high grade intermittent rise of temperature, pallor, weakness, emaciation, enlargement of the lymph nodes, distentionof abdomen due to massive splenornegaly and chronic ill health are associated features. In neglected cases there may be bleeding from various sites of the body9. The diagnosis is based on the demonstration of Leishmania Donovani (L.D.) bodies in smears obtained from bone marrow, spleen, liver and lymph nodes10. In cutaneous Leishmaniasis, the parasites are isolated from the active lesions11.
Patients and Methods
This study was conducted at DHQ Hospital, Timergara, District Dir, NWFP. Patients diagnosed as visceral leishmaniasis, confinned by identifying Leishmania donovani in bone marrow srneaxs, were indcluded in the study. Each patient had a thorough clinical evaluation. Data recorded ineluded age, sex history of fever, weight loss, anorexia, nausea, vomitipg, diarrhoea, abdominal distension, iespiratory symptoms, temperature at presentation, lymphadenopathy, hepatosplenomgealy and skin changes. Investigations peifonned for each patient were CBC, ESR, platelets count, special smear, formal gel test, smear for malaria! parasites (thick and thin films) and urinalysis. Bone marrow aspirates were taken forLeishmaniaDonovanibodies. Patients were treated with sodium stibogluconate 15mg/kg daily for 15 days. Response was assessed by improvement of general condition, weight and anaemia, regression of organomegaly and normality of blood counts. Patients were followed up for three to sixmonths to assess relapses.
Ten patients, 7 males and 3 females, with visceral leishmaniasis were admitted to DHQ Hospital, Timergara, District Dir, from May 1996 to November, 1997. The ages ranged between 2 and 10 years. All patients presented with a history of fever for one month or more. Other symptoms included abdominal distension, weight loss and anorexia. Vomiting, diarrhoea and cough were less common. On examination, half of the children were afebrile. Bleeding was present inone patient. The liverand spleenwere enlarged in all subjects. Eighty cases had massive splenomegaly (more than 5 cm below the costal margin). The main clinical features are shown in the Table.
All the patients were anaemic with Hb <7 0%. Total leucocyte count was less than 4x109/L in 70% of patients and polymorphonuclear cells were less than 3x109/L in all the cases. Lymphocytic count was normal in majority of patients. Platelets were less than 100x109/L, formal gel test was positive and bone marrow smears for Leishmania Don vani bodies were positive in all .the paients. Response to sodium stibogluconate therapy was excellent with a cure rate of 100 percent. Fever subsided within the first week and hepatosplenomegaly regressed gradually. No relapses were seen, during the six months follow-up.
Visceral leishmanias is prevalent in Pakistan and affects predominantly infants and young children4. The main clinical features seen among our patients were fever, weight loss, anorexia, abdominal distension and hepatosplenomegaly. Lymphadenopathy was rare. This is similar to the Indian and Saudi experience5. Lymphadenopathy is commonly seen in the African type of the diseases8. The hematological findings were anaemia, leukopenia and thrombocytopenia. Anaemia is probably due to a combination of iron deficiency, hemolysis and bone marrow suppression (anaemia of chronic disease)9. Neutmpema and thrombocytopema are likely to be due to hypersplemsm as they are absent in patients who have had splenectomy. Fonnal gel test was positive in all patients, but this test is known to have a low specificity. Cross-reactions occur with leprosy. malaria, schistosomiasis and cutaneous leishmaniasis . Definite diagnosis of visceral leishmaniasis depends on demonstration of amastigotes in bone marrow, spleen, liver, lymph nodes10 and in the case of cutaneous leishmaniasis in active lesions11. These results are comparable to those reported in the literature4,10. The response to sodium stibogluconate in our series was excellent. This is similar to another Pakistani expenence4. The Indian variety of the disease also responds well to therapy4. Visceral leishmaniasis in Africa seems to be less responsive5. Patients who do not respond to the initial course of antimony may respond to a second or even a third course1.
In many ways, visceral leishmaniasis in Pakistan bears many clinical similarities to the Indian and Mediterranean type of the disease. All are known to have good response to therapy4. Visceral leishmaniasis is endemic in District Dir, NWFP. It is simple to diagnose if the physician has a high degree of suspicion. The symptoms are typical and the laboratory tests are easy to perform and inexpensive. The response to therapy is excellent with a 100 percent cure rate. Left untreated visceral Leishmaniasis can prove to be fatal.
1. Farthing MJG, Jefihes DJ, Anderson J. Infectious diseases, tropical medicine and sexually transmitted diseases In: Kumar. P. J. and Clark, M. (eds), Clinical Medicine 3rd ed., London, BailliereTindall, 1995, pp. 1-106.
2. Chatterjee KD (ed). Parasitology, 12th ed., Calcutta, Chatterjee Medical Publishers, 1997, pp. 9-107.
3. Bauer JD, Ackermann PG, Toro G. Methods in parasitology, In: Clinical Laboratory Methods. (8th ed), Saint Louis, C.V. Mosby Company. 1997,pp. 547-601.
4. Hassan M, Baat BD Hassan K A. New Breakthrough in treatment of Visceral Leishmaniasis in children. J. Pak. Med. Assoc., 199S;45:155-157.
5. Al-OraivyIO,Qasim IV. SingLMetal. Visceral leishmaniasis in Gizen, Saudi Arabia. Ann. Saudi Med., 1994;14:396-398.
6. HeyneD. Medical parasitology. in: Brook, OF., Butel, J.S., Omston, L.N. et al. (eds) Medical Microbiology, 19th ed. London, Prentic Hall International, 1991, pp.332-365.
7. Firkin F, Cheseterman C, Penington D et al. (eds). de Gruchy’s Clinical Haematology in Medical Practice. 5th ed. London, Black well Scientife Publications, 1989, pp. 346-359.
8. Wyler DJ and Horowitz HW. Leishmaniasis, Infectious Diseases: Parasitic Infections. In: Behrrnan, R.E. and Vaughan, V.C. (eds). Nelson Textbook of Paediatrics. 13th ed., London, W.B. Saunders Company, 1987, pp. 736-738.
9. Lockaley RN. Leishmaniasis. In: Isselbacher KJ, Braunwald E. Wilson JD (eds). Harrison’s Principles of Internal Medicine, 13th ed. London, McGraw-Hill, 1994, pp.896-899.
10. Rab MA. Laboratory diagnosis ofvisceral leishmaniasis. J. Pak. Med. Assoc., 1996;46:187-188.
11. Rab MA. Cutaneous Leishmaniasis: Iso-Enzymes Characterization of Leishmania Trophic. J. Pak. Med. Assoc., 1997;47:270.273.