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Year : 2013  |  Volume : 6  |  Issue : 3  |  Page : 355-357
Kala-azar-A case series from nonendemic area, Uttarakhand

1 Department of Medicine, Government Medical College, Haldwani, Nainital, Uttarakhand, India
2 Department of Microbiology, Government Medical College, Haldwani, Nainital, Uttarakhand, India
3 Department of Pathology, Government Medical College, Haldwani, Nainital, Uttarakhand, India

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Date of Web Publication7-Nov-2013


Resurgence of kala-azar in India has posed many problems. Apart from endemic areas, cases are being reported from nonendemic area. Other than diagnostic difficulties, resistance to stibogluconateand relapses are common problem in sporadic visceral leishmaniasis (VL). We present one case in detail and give brief description of nine other cases, hailing from nonendemicarea, Uttarakhand, during the period from December 2005 to September 2011, diagnosed in our teaching hospital. The patients in our study were diagnosed as VL by clinical findings and confirmed by demonstration of LD bodies in splenic or bone marrow smears. Six cases were treated successfully with amphotericin. One case died during treatment and three cases lost to follow up.Clinician should suspect and investigate for VL in patients with pyrexia of unknown origin even when the disease is not endemic in a specific region for early diagnosis.

Keywords: Kala-azar, nonendemic area, visceral leishmaniasis

How to cite this article:
Kumar A, Rawat V, Thapliyal N, Saxena SR. Kala-azar-A case series from nonendemic area, Uttarakhand. Ann Trop Med Public Health 2013;6:355-7

How to cite this URL:
Kumar A, Rawat V, Thapliyal N, Saxena SR. Kala-azar-A case series from nonendemic area, Uttarakhand. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Aug 8];6:355-7. Available from:

   Introduction Top

Leishmaniasis is a major public health problem causing significant morbidity and mortality in Africa, Asia, and Latin America. The present foci of VL in India are Bihar, West Bengal, Uttar Pradesh, and Jharkhand. Sporadic cases have also been reported from Gujarat (west India), [1] and sub-Himalayan parts of north India including Uttar Pradesh, Himachal Pradesh, Uttarakhand, and Jammu andKashmir. [2],[3],[4] However, the incidence of disease is still increasing in Uttarakhand. In this report, we present results of clinical investigative and therapeutic features of 10 cases identified in this new focus.

   Case Report Top

A 21-year-old male, resident of Kuamun region of Uttarakhand, presented to us with complaints of prolong intermittent fever, anorexia, weight loss, generalized body ache,and malaise for 6-7 months and yellow discoloration of eye for 4-5 months. The patient was investigated at his native place; however, no cause could be ascertained for his fever. He then reached our hospital, which is a tertiary care center. His general examination revealed significant pallor and jaundice. Per abdomen examination revealed splenomegaly (15 cm below the left costal margin) and hepatomegaly (4cm below right costal margin). His respiratory and cardiovascular systems were within normal limits.

Hematological parameter revealed pancytopenia, total leucocytes count 1000/cumm, P60, L-38, E-01, M-01, platelet count 2214/cumm, reticulocyte count 2%, and Hb 4.2g%. Peripheral smear showed normochromic normocytic anemia and was negative for haemoparasites. MP card test was also negative.

Liver function tests on admission were as follows: SGPT131 IU/L, SGOT201 IU/L,serum alkanise phosphate 200 IU/Land serum bilirubin 11.9 mg% (indirect 4.9 mg%, direct 7.0 mg%). and albumin: globulin ratio was 2.1:11.4.

Initially it was suspected as a case of malaria, but since investigations for malaria were negative. A bone marrow aspiration was done, which revealed LD bodies [Figure 1]. Hepatitis was an unusual feature in our case. To rule out other co-infection, the serological tests for typhoid, HIV, HCV, HBs Ag, HEV, HAV and cytomegalovirus were carried out, which were negative.Final diagnosis of kala-azar was made.The patient was immediately treated with amphotericin- B (1 mg/kg body wt/day) for 15 days. Patient became afebrile after 4-5days,appetite was improved, spleen was regressed to 4-5 cm after 10 days but his pancytopenia did not improve.For that repeated blood transfusion (7units) were given to maintain hematocrit. After 15 days of treatment his total serum bilirubin, SGOT, and SGPT level did not improve. Patient left against medical advice and was lost to follow up.
Figure 1: Giemsa stained bone marrow smear showing LD bodies

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Rest, nine cases, reported with fever, malaise, and weight loss. The duration between the onset of fever till diagnosis varied from 6 to 8 months. Hepatosplenomegaly were found in all cases. Eight cases [Table 1], case no 3-10] were HIV negative, case number 1 and 2 were not screened for HIV. Their hematological parameter revealed pancytopenia. Peripheral smears showed normochromic normocytic anemia and were negative for hemoparasites. MP card tests were negative in all cases. Two cases were initially treated with sodium stibogluconate (case 6 and 7). When there was no response, the treatment was changed to amphotericin-B. One case died during treatment. Six cases were successfully treated with amphotericin and in three cases were lost to follow up. [Table 1]
Table 1: Clinico-pathological findings

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   Discussion Top

Leishmaniasis, a vector-born disease caused by obligate intra-cellular protozoa of the genus Leishmania, is capable of causing a spectrum of clinical syndromes affecting millions of people in endemic areas of the tropics and subtropics. It affects other regions of the world as well with the only exception of Australia and Antarctica. Leishmaniasis is transmitted by sandflies (Phlebotomusspecies). In the human host, Leishmaniaare intra-cellular parasites that infect the mononuclear phagocytes when a vector (sandfly) transmits the parasite between vertebrate hosts. In visceral leishmaniasis (VL), the amastigotes replicate in macrophages of the mononuclear phagocyte system and then spread to the entire reticuloendothelial system, resulting in "kala-azar". [5],[6]

The visceral form of leishmaniasis is endemic in eastern states of India. However, in last quarter of the twentieth century migration of disease was noticed and new foci of this disease were reported from previously nonendemic regions. [7] VL is a disease of low altitude; it does not occur in altitudes over 2000 feet (600 m). However, cases have been reported from natives of sub-Himalayan region (above 2000 feet), India. Few sporadic cases have been reported from Kumaun in the past. [3] However, the incidence of the disease is still increasing, and 10 cases of VL have since been recorded from November 2005 to September 2011.

All our patients had contracted the disease indigenously is suggestive of a local vector and or probably a zoonotic reservoir. Since none of our patients reported to have been out of the state or district during the 3 years preceding the onset of symptoms. Six species of Phlebotomus and 15 species of Sergentomyia have been found in the northern mountain ranges of the Himalayas (Kumaun is situated in these ranges), with their distribution limited to particular ecoclimatic zones. [8] Survey of sandflies in the Himalayan region has established the presence of Phlebotomusargentipes, P. longiductus, and P. major (Diptera: Psychodidae) in this area. [9]

The recent emergence of VL in this area of Uttarakhand appears to be due to construction activities, horticulture development, and establishment of new residential, large water resources schemesleading to destruction of forests and intrusion into the sylvatic cycle. The laborers employed are mainly from the known endemic areas of Bihar, Jharkhand, Uttar Pradesh, and Nepal. [4]

In our case pathognomonic feature of kala-azar like hepatosplenomegaly with pancytopenia was found in all cases but in one case [case no 10, [Table 1] it was associated with severe jaundice. Functional derangement of liver in VL is reported infrequently in literature. [10] Because of this, many cases are misdiagnosed as malaria or hepatitis. Mathur et al. [11] also found severe hepatitis associated with kala-azarin a 4 year child but in their case hepatitis was found to be due to hemophagositic syndrome (HPS) secondary to infection. In our case we did not find picture of HPS in bone marrow aspirate.

One patient died. The delay in diagnosis and treatment may also be contributory factor for fatal outcome. In the remote, backward area of hills, where infection is predominant, expert bone marrow microscopic facilities are rarely available. In such circumstances, many cases may go undetected.In the present cases, there was a prolonged delay in the initiation of treatment due to its failure to be diagnosed as a case of kala-azar at their native places. Lack of awareness of the occurrence of kala-azarin a nonendemic area and the unusual manifestation may cause considerable difficulties in establishing the diagnosis. Two of our cases did not respond to sodium stibogluconate. Resistance to this drug in nonendemic area is also a matter of great concern.

Our cases emphasize the need for careful examination of clinical material and consideration of nonendemic diseases in the differential diagnoses of fever with moderate-to-severe hepatosplenomegaly. Patients with pyrexia of unknown origin should be investigated for VL, even when the disease is not endemic in a specific region for early diagnosis, to prevent mortality and morbidity. This report also highlights the changing geographic distribution and spread of leishmaniasis in India with implications for its control as a public health problem. Epidemiological work is required in this area to substantiate the presence or absence of any zoonotic reservoir.

   References Top

1.Sharma U, Redhu NS, Mathur P, Singh S. Re-emergance of visceral leishmiasis in Gujrat, India. J Vector Borne Dis 2007;44:230-2.  Back to cited text no. 1
2.Naik SR, Rao PN, Datta DV, Mehta SK, Mahajain RC, Mehta S, et al. Kala-azar in north-westwrn India: A study of 23 patients. Trans R Soc Trop Med Hyg1979;73:61-5.  Back to cited text no. 2
3.Singh S, Biswas A, Wig N, Aggarwal P, Sood R, Wali JP. A new focus of visceral leishmaniasis in sub-Himalayan (Kumaon) region of northern India. J Commun Dis 1999;31:73-7.  Back to cited text no. 3
4.Raina S, Mahesh DM, Kaul R, Satindera KS, Gupta D, Sharma A, et al. A new focus of visceral leishmaniasis in the Himalayam India. J Vector Borne Dis 2009;46:303-6.  Back to cited text no. 4
5.Murray W, Leismaniasis. In: Feigin Cherry JD, editor. Textbook of pediatric infectious diseases. 4 th ed. Phildelphia: WB Saunders; 1918.  Back to cited text no. 5
6.Herwadt BL. Leishmaniasis. Lancet 1999;353:1191-9.  Back to cited text no. 6
7.Dev A, Sharma U, Singh S. First case of indigenous visceral leishmaniasis from central India. Am J Trop Med Hyg 2007;77:95-8.  Back to cited text no. 7
8.Kaul SM, Jain DC. Distribution of Phlebotomine sandflies (Diptera: Psychodidae) according to the physiographic divisions of India. J Commun Dis 1995;27:155-63.  Back to cited text no. 8
9.Kulkarni SM, Bhat HR, Modi GB. Survey of Phlebotomid sandflies from the Himalayan region, India (Diptera: Phlebotomidae). Indian J Med Res 1978;67:583-8.  Back to cited text no. 9
10.Mittal V, Bhatia R, Seghal S. Clinicoepidemiological profile of kalaazar patients in Delhi. J Commun Dis 1989;21:255-61.  Back to cited text no. 10
11.Mathur P, Samantray JC, Samanta P. Fatal haemophagocytic syndrome and hepatitis associated with visceral leishmanaiasis. Indian J Med Microbiol2007;25:416-8.  Back to cited text no. 11
[PUBMED]  Medknow Journal  

Correspondence Address:
Vinita Rawat
Department Microbiology, Government Medical College, Haldwani, Nainital, Uttarakhand
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1755-6783.121008

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