. Treatment of associated bacterial infection – e. g. pneumonia (aspiration or spontaneous), gram negative bacteremia

Ventilation. 12. Treatment of associated bacterial infection – e. g. pneumonia (aspiration or spontaneous), gram negative bacteremia, urinary tract infection, etc Combined treatment with benzyl penicillin and gentamicin, or cefoperazone is useful in patients who deteriorate clinically without identifiable source of infection (b) Diamidines - (i) Pentamidine isethionate - 4 mg. /kg. body weight on alternate day V or IM for 7-10 days (ii) Hydroxystilbamidine - 5 mg/kg body weight IV daily for 10- days, the course is repeated after 10 days Less potent than antimonials but may be adequate for the less resistant forms, or useful for alternating with antimonials when repeated courses are required Danger of primary trigeminal neuropathy Severe side-effects including hypoglycemia, hypotension, arrhythmia and pancreatitis (c) Amphotericin B - For refractory cases found effective in some advanced infections. 1 0 mg/kg body weight IV in 5% glucose solution on alternat e days over 4-6 hours for 45-700 days Toxic but useful in patients resistant -to antimonials and diamidines (d) Aminosidine 15 mg/kg/day for 20 days (e) a-interferon - combined with antimony compounds Dose - 100-400/mg/m2/day i.m. for 10-40 days Side effects -Fever and pain at site of injection (f) Allopurinol - 16-24 mg/day in 3 divided doses for 10 weeks The drug prevents growth and division of amastigotes (g) Ketoconazole 600 mg/day p o x 28 days. 2. Supportive treatment - (a) Antibiotics for secondary bacterial infection (b) Iron and folate for anemia (c) Relapse and resistance -Further SB therapy once or twice a day for prolonged period or alternative drugs. 3. Splenectomy - only if spleen is much enlarged and several courses of treatment have been unsuccessful. 4. Post-kala-azar dermal Leishmaniasis (PKDL) - is a cutaneous manifestation of L. donovani disease that occurs after re-treatment and recovery from kala-azar. Macules, papules and nodules all over the body particularly on face which do not ulcerate. Nodules can occur on tongue and mucous membranes. Hypopigmented or hyper pigmented skin areas may also be seen. Parasites can be isolated from the papular or nodular lesions of the skin. PKDL has also been described in acute visceral Leishmaniasis and in patients who have been symptom less previously or who have not been treated for kala-azar. Tr - Antimony gluconate 15-20 mg/kg i.m. for 4 months to one year Nodules and macules disappear quickly but depigmented macules are the last to disappear. Cutaneous Leishmaniasis Cutaneous leishmaniasis is classified according to the geographical area to which Leishmania spp. are restricted Old world cutaneous leishmaniasis - is caused by L major (desert areas), L tropica (urban areas) and L. aethiopica. It occurs in middle East, East Africa and some Mediterranean areas: It is transmitted by Phlebotomus spp and main reservoirs are rodents (L major) and hyrax (L aethiopica). Cl. Fs. - The lesion begins as small erythematous papules where the sandfly has fed. After inbubation period of 1-8 weeks, the lesion gradually enlarges, forming a nodule which later ulcerates. Multiple lesions can coexist in different areas of the skin. Lesions heal spontaneously leaving a hypopigmented area but may persist for months or years. DIFFUSE CUTANEOUS LEISHMANIASIS caused by L. aethiopica is characterised by an initial papular lesion that does not ulcerate Satellite lesions develop and eventually multiple cutaneous nodules appear on face and