Visceral Leishmaniasis: clinical features

At present 90% of all visceral leishmaniasis occurs in India, Bangladesh, Sudan and Brazil.

After an initial multiplication in the skin, causing a transient small lesion, the parasites can further multiply in bone marrow, liver and spleen. This causes visceral leishmaniasis. The incubation period is usually 2 to 6 months. The pathogens are usually Leishmania donovani and L. infantum or sometimes Leishmania tropica. L. chagasi is possibly identical to L. infantum and was possibly introduced into the New World via infected dogs or rats at the time of the Spanish and Portuguese conquests, though there are doubts about this.

The disease is characterised by chronic fever, enlarged liver and spleen and a low blood count (pancytopaenia = anaemia + leukopaenia + thrombocytopaenia). This must be distinguished from an aplastic bone marrow. The patient becomes very susceptible to other infections (pneumonia, tuberculosis, dysentery) which can sometimes prove fatal. Low blood platelet counts result in a bleeding tendency (nosebleeds, bruising, etc.). Sometimes there are also other symptoms, such as swollen lymph nodes. Weight loss and emaciation are frequent and substantial. The skin can turn a dark colour: kala azar (Hindi) means “black disease” and refers to this hyperpigmentation. The infection can proceed atypically in HIV patients (for example, without fever or splenomegaly, or with negative serology). When immunosuppression is induced by chemotherapy, latent kala azar can become clinically apparent.

A skin condition, called post-kala azar dermal leishmaniasis (PKDL), can occur after a patient has suffered from kala azar. PKDL rarely occurs without being preceded by kala azar. This disease (PKDL) was originally described by Brachmachari in India. PKDL occurs on average 4 months after kala azar, though there are strong regional variations. This disease occurs mainly in India (up to 20% of kala azar patients), and to a much lesser extent in the Middle East. In Sudan the disease occurs regularly (56% of kala azar patients in one study). It is virtually unknown in the Mediterranean Basin or in South and Central America. It involves discoloured patches and painless nodules on the skin that usually contain few, but sometimes moderate numbers of amastigotes. Most of the lesions occur on the face (98%) and to a lesser extent on the thorax (80%), arms (70%), legs (40%), tongue (40%) and genitals (6%). Various degrees of severity can be clinically distinguished in PKDL. Grade 1 includes an extensive maculopapular to nodular rash, principally around the mouth, and possibly somewhat lesser lesions on the thorax and upper arms. Grade 2 is a similar but denser rash that covers the whole face and is also present on the chest, back, upper arms and legs, with fading of the lesions in more distal regions of the body. Grade 3 is a generalised dense rash with ulcers, scabs, cheilitis and possibly lesions of the palate (roof of the mouth). This disease has a very chronic course (years) and is therefore important for transmission. Parasites do not affect internal organs in PKDL. There is sometimes a concomitant neuritis, which can further contribute to the clinical resemblance to leprosy.

Category: Medicine Notes