Pathogenesis (disease development)
Leishmaniasis is caused by the different species of Leishmania. These have a two-part developmental cycle, one part of which occurs in the female vector mosquito, the sandfly or butterfly mosquito (phlebotome), and the other in humans.
In the blood of the biting insect, the approximately 10-15 µm long, flagellated parasites develop and multiply (promastigote form) and subsequently migrate into the insect’s proboscis. Usually, the pathogen is destroyed at the site of inoculation (site of pathogen entry) by the host’s cellular immune response. When the affected person’s immune system is weakened, the Leishmania proliferate in the macrophages (“scavenger cells”) and monocytes (belong to the white blood cell group; cells of the immune system and precursors of macrophages) of the skin. The promastigote forms transform into amastigotes. These are unflagellated. After multiplication, the parasites destroy the cell membrane and spread hematogenously (by blood) throughout the organism. In visceral leishmaniasis, the leishmania enter the lymph nodes, spleen, liver, and bone marrow.
Old World leishmania include: L. tropica major, L. tropica minor, L. donovani, L. donovani infantum, L. archibaldi; those of the New World include: L. brasiliensis, L. mexican – mexicana, L. mexicana – pifanoi.
Etiology (causes)
Behavioral causes
- Inadequate protection against mosquito bites in endemic areas of leishmaniasis (tropics, subtropics).
- Bringing infected animals such as dogs from endemic areas.
Other causes
- Airport leishmaniasis – infection on the plane or at the airport by imported mosquitoes.
- Baggage leishmaniasis – infection by mosquitoes from airline luggage.
- Very rarely, transmission can occur through organ or blood donations.
- Diaplacental infection from mother to unborn child is possible.
