Although our knowledge of the history of leishmaniasis is incomplete, the first recognized epidemic appears to have occurred in 1824, in Jessore, in what is now Bangladesh. In 1824 there were numerous deaths. People developed chronic fever with substantial loss of weight, emaciation and dark discoloration of the skin. They died of terminal dysentery or pneumonia. After a few years this "black disease" spread over the entire Ganges plain. In 1832 the infection reached West Bengal. In 1862 the infection was seen in Jageer, Dacca district, Bangladesh. There were enormous numbers of deaths, comparable to the plague epidemics (but proceeding more slowly). Four years later Jageer was as good as wiped out. In 1875 kala azar was noted in Assam, India. Over the next 25 years 25% of the population died of the disease. At around the turn of the century the epidemic diminished in the Ganges basin. Isolated cases still persisted, but in much lower numbers than during the epidemic years. The reason for this stopping of the epidemic is unknown. Between 1918 and 1923 a further total of more than 200,000 people died of kala azar in Assam and in the Brahmaputra valley. This was followed by another epidemic in 1944. Assam fever is an old term used for kala azar.

The search for the origin of kala azar initially proceeded with great difficulty. Many hypotheses were investigated: for example, hookworm infection (ancylostomiasis) or malaria were thought to be responsible for the clinical condition. In 1900 an Irish soldier developed kala azar, after a stay in Dum Dum, near Calcutta, India. He died in England. The Scottish physician Dr. William Boog Leishman, later Director-General of the medical service of the British Army, carried out the autopsy. In spleen tissue he discovered small particles within the macrophages. He suspected that these were a sort of partly digested trypanosomes. A previously used name for visceral leishmaniasis was "Dum Dum fever" and refers to this historical event. The Irish physician Dr. Charles Donovan investigated splenic aspirates (needle biopsies of the spleen) from kala azar patients and confirmed Leishman’s discovery. The tiny particles were called Leishman-Donovan bodies.

The manner in which the transmission takes place was for a long time a mystery. The first hint of an answer was found in 1904 by Leonard Rodgers. He put some spleen tissue from a patient into a flask with simple culture medium. The parasite appeared to multiply in vitro without much difficulty. In this culture medium the form of the parasite was, however, totally different. Instead of the spherical Leishman-Donovan bodies, such as were observed in man, elongated organisms (promastigotes) that had a flagellum were now seen. This implied that the Leishman-Donovan bodies that were found in man were but one of several stages in the life cycle of the parasite. The promastigote stage would thus occur somewhere in nature, outside of man. This information was crucial. After many years of investigation with numerous false leads, the Irishman John Sinton discovered that the distribution area of kala azar in India coincided with a map of the distribution of Phlebotomus argentipes, the "silverfoot sandfly". However, it took 25 years after the first description of the parasite before Knowles in Calcutta was able to show the presence of Leishmania parasites in the tiny Phlebotomus flies. He was however not able to prove transmission itself. It took a further 14 years to discover the reason for the failure of the transmission experiments. The parasite can only maintain and fully reproduce itself in female Phlebotomus flies if the vector has first had an infected blood meal, followed by further feeding with plant sap. If the insects suck blood again too soon, the development of the parasite is disturbed in a way which makes transmission impossible. If the fly continued to feed entirely on plant sap the parasites in the insect’s intestine could multiply until they were present in such large numbers that they could almost clog up the insect’s intestine such that the gastro-oesophageal valve would totally fail. When the fly tries to take its next blood meal, parasites are regurgitated and the host infected. This was formally demonstrated in 1940. Kala azar can be transmitted in other ways, but these are exceptional, namely shared use of needles among intravenous drug users, or infected blood transfusion. Very rare cases of congenital kala azar infection have been reported.

In the same year, 1940, the Swiss chemist Paul Muller patented his discovery of DDT, the first cheap and very active insecticide. He received the Nobel Prize for this in 1948. The World Health Organization’s Global Eradication of Malaria Plan was launched several years after a big successful trial of DDT for the control of malaria in the Tennessee River valley in the USA was completed in 1945. The basic strategy was, among other things, to spray all human and animal housing twice a year with DDT. An unforeseen effect of this campaign was the effect on kala azar. Phlebotomus is a poor flyer and in India it lives around the housing of domestic animals and man. This biotope is ideal for controlling them with a residual insecticide such as DDT. In India this stopped the transmission of kala azar and up to 1955 practically no further cases of kala azar occurred.

However, after the failure of the malaria eradication programme and the end of spraying in 1970 in India, kala azar returned. The first local epidemic was in Vaishali, a small town in Bihar. In 1975 West Bengal was also affected. Around 1980 the infection was widespread from Tamil Nadu in the south of India to the regions of Nepal and Bangladesh. About 80,000 cases were reported in north-east India in 1992. In November 2000 kala azar transmission was confirmed in Calcutta city. To make matters worse, resistance to the medication has developed in the meantime so that up to 10 % of the parasites are now resistant to the antimony drugs that form the basis of therapy. This percentage still increases every year. Vector control faces many difficulties, especially with respect to organization, long-term planning and execution, as well as financing. The threat of new major epidemics remains to this day, not only in Bihar, in the east of India, but also in many other areas, such as southern Sudan and in Gedaref (eastern Sudan). The interaction between AIDS and leishmaniasis is an additional problem. In parts of Spain up to 70% of the kala azar patients are infected with HIV and 9% of the HIV patients will develop kala azar. Intravenous drug users share non-sterile needles and can transmit not only HIV, but also leishmaniasis. Here transmission is dissociated from the traditional reservoir in dogs.