Visceral leishmniasis: The disease



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The disease manifestation and symptoms

Various terms have been used to describe visceral leishmaniasis including Dum-dum fever, Sikari disease, Burdwan fever, Shahib's disease and tropical splenomegaly. However, the most commonly used term is Kala azar, which in Hindi means black sickness or black fever. The terms originally referred to Indian VL due to its characteristic symptoms, blackening or darkening of the skin of the hands, feet, face and the abdomen (Lainson and Shaw, 1987).

Visceral leishmaniasis is caused by the parasites Leishmania donovani donovani, Leishmania donovani infantum and Leishmania donovani archibaldi in the old world and by Leishmania donovani chagasi in the new world. In endemic cases of VL, the disease is chronic and onset is gradual. Although people of all ages are susceptible in the old world, children below the age of 15 are more commonly affected with L.d infantum being largely responsible (Rab et al, 1995). In sporadic and epidemic cases of VL the disease is usually acute and symptoms appear suddenly with people of all ages being at risk except those who have conferred immunity due to a past infection.

The symptoms of VL vary between individuals and according to geographical foci. However, some of the common symptoms include high undulating fever often with two or even three peaks in 24 hours and drenching sweats which can easily be misdiagnosed as malaria, Chills, rigors, weight loss, fatigue, poor appetite, cough, burning feet, insomnia, abdominal pain, joint pain, anorexia, epistaxis and diarrhoea. Clinical sings include splenomegaly, hepatomegaly and lymphadenopathy (Hashim et al, 1994). The incubation period is highly variable, the disease can appear anything between ten days to over one year. Even longer incubation periods have been documented (WHO WWW site, 1997). The duration of the disease can be 1-20 weeks, in endemic areas of Western Sudan the illness usually lasts about 12-16 weeks with and average of about 6 weeks (Hashim et al, 1994).

Visceral leishmaniasis can be complicated by serious secondary bacterial infections such as pneumonia, dysentery and pulmonary tuberculosis, which often contribute to the high fatality rate of VL patients. Other complications, though rare include haemolytic anemia, acute renal damage and sever mucosal haemorrhage (WHO expert committee report, 1991).


Post Kala azar Dermal Leishmaniasis (PKDL)

Post Kala azar dermal leishmaniasis (PKDL) occurs in India and mainly in Sudan and Kenya in Africa (Hashim et al, 1995). Reports of PKDL in China and Iraq have also been documented (Ramesh et al, 1995). In the new world PKDL is extremely rare (WHO expert committee report, 1991). Usually PKDL follows recovery from a Kala azar infection, though less commonly, it has been known to occur in patients who have not suffered previously from Kala azar (Hashim et al, 1995). Both the Indian and the African PKDL display similar symptoms.The disease begins with small measel-like lesions (hypopigmented macules, papules or nodules) appearing on the face, and gradually increase in size ( Rarely greater than 1cm in diameter). Eventually the lesions spread to the upper trunk, arms, forearms, thighs, legs, abdomen, the neck and the back.The multiple lesions can coalesce to form larger lesions and can lead to the gross enlargement of facial features such as the nose and lips, giving an appearence similar to leprosy. The disease is particularly severe if the lesions spread to the mucosal surfaces of the nasal septum, hard and soft palate, oropharynx, larynx or the eye lids and the cornea leading to blindness (Hashim et al, 1995; Ramesh et al, 1995). Potentially the lesions can appear on any part of the body. There have been reports of lesions occurring on the glans of the penis and genital mucosa. Hence the possibility of PKDL being transmitted sexually. In addition to the disease being confused with leprosy, PKDL can also resemble cutaneous leishmaniasis, secondary syphillis and sarcoidosis (Ramesh et al, 1995). The lesions are usually self-limiting, however those that do not heal spontaneously within six months have to be treated (Hashim et al, 1995). Pentavalent antimonials remain the drugs of choice for treating PKDL. Sodium stibogluconate at adose of 20 mg/Kg of body weight administered intramuscularly for 4-5 months is recomended. In addition Ketoconazole and allopurinol can be given orally to improve response. In antimony resistant cases amphotericin B is an effective replacement (Ramesh et al, 1995). Indian PKDL appears anything between 1-7 years after apparent cure of Kala azar, although longer periods of upto 20-30 years have been reported (Zijlstra et al, 1995). The African form of the disease usually appears within a few months after cure, in most cases within 6 months, on average within 56 days. However it can develop during the treatment Kala azar, in which case the term Para Kala azar dermal leishmaniasis would seem more fitting (Hashim et al, 1995; Zijlstra et al, 1995).


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