Protozoal infections

Blood and tissue infection


Three clinical entities caused by Leishmania have been described:
1 Visceral leishmaniasis (kala-azar)
2 Cutaneous leishmaniasis of the New World
3 Cutaneous leishmaniasis of the Old World.
The life-cycle of the parasite involves two stages:
1 The amastigote (Leishman-Donovan body) occurs in vertebrate hosts such as humans, dogs or rodents. The parasites infect macrophages and reticuloendothelial cells and multiply until the cells rupture, releasing the organisms into the circulation. When the female sandfly (Phlebotomus or Lutzomyia) bites an infected host, it draws blood containing the amastigotes.
2 In the sandfly the parasites develop into the infective promastigotes, which move to the salivary glands in about 10 days.
The cycle is completed by the sandfly biting another vertebrate.
The presentation in humans is dependent on the patient’s cellular immunity as well as the parasite species.
In the kala-azar syndrome there is little or no immune response and the reticuloendothelial system is laden with amastigote-Iaden histiocytes. In subjects with an increased immune response, hepatic and lymph node granulomas are found and either there are no clinical symptoms or a localized lesion is seen.
Inapparent infection is common in endemic areas and is recognized by the high incidence of leishrnanin-positive skin tests. There is usually no previous history of skin ulceration or systemic disease. Infection is eradicated by the immune system and the subject is left with permanent immunity to that species of Leishmania.

Leishmaniasis-geographical distribution.
Leishmaniasis-geographical distribution.

exhibit a characteristic biphasic pattern. Cough is frequent and diarrhoea may occur. The skin is dry and rough and with time becomes pigmented. Splenic enlargement may be massive and hypersplenism is chiefly responsible for the pancytopenia seen. Epistaxis may occur due to thrombocytopenia. Hepatomegaly is less prominent than the splenomegaly. In African kala-azar, warty skin eruptions and lymphadenopathy also occur. If left untreated, death occurs within 3 years in the majority of patients and is due to pulmonary or gastrointestinal superinfection, to which these patients are predisposed.
INFANTILE KALA-AZAR is seen chiefly in the Mediterranean region and is a disease of children below the age of 5 years.
POST-KALA-AZAR DERMAL LEISHMANIASIS (PKDL) occurs 1-2 years after successful treatment for visceral leishmaniasis in a small proportion of patients in India and less often in Africa. It is characterized by macular, erythematous lesions and pale pink nodules on the face.


CHARACTERISTIC LEISHMAN-DoNOVAN BODIES may be demonstrated in buffy coat preparations of blood or in bone-marrow smears or lymph node, liver or spleen aspirates.
CULTURE. The organism can be cultured in the Nicolle- Novy-McNeal culture medium.
COMPLEMENT-FIXING ANTIBODIES may be detected by indirect immunofluorescence, ELISA and haemagglutination.
FORMOL GEL TEST is positive owing to hypergJobulinaemia. An intradermal leishmanin skin test (a test of delayed hypersensitivity) is of no value in diagnosis since it is negative early in the course of the disease.


Response to therapy varies. African kala-azar is relatively resistant to treatment and the duration of therapy is necessarily longer. Pentavalent antimony compounds are the drugs of choice. Sodium stibogJuconate 30 mg kg-I in adults should be continued for at least 40 days. Meglumine antimonate 50 mg kg-I daily for 10-30 days is a useful alternative. Intercurrent pulmonary infections should be treated with appropriate antibiotics. Blood transfusions are rarely required. Intravenous amphotericin or pentamidine (up to fourdestroying infected animals and treating infected humans early. courses of 3 mg kg-I daily for 10 days) may be required for patients whose initial response to therapy is poor.
Pentamidine is ineffective in the treatment of PKDL.


In endemic areas control of vectors plays an important part. Spraying with an effective insecticide should be carried out at regular intervals. There should also be an attempt to decrease the reservoir of infection by destroying infected animals and treating infected humans early.

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