Leishmania infantum is a small bacterium from the Leishmania family and lives as a parasite obligate intracellularly in macrophages in humans and other vertebrates. In order to preserve its species, the bacterium changes host between sand flies and humans or vertebrates and changes from the flagellated (mosquito) to the non-flagellated form (human or vertebrate). Leishmania infantum can be the causative agent of both cutaneous and visceral leishmaniasis.
Leishmania infantum, a small bacterium from the Leishmania family, lives as an obligate parasite intracellularly in macrophages in humans or other vertebrates. To maintain its species, the bacterium changes host, which is associated with a slight change in its external shape.
The sand fly of the genus Phlebotomus serves as an intermediate host in Europe, North Africa and the Asian countries, while the sand fly of the type Lutzomyia plays this role in South American and Central American regions. The sand fly ingests macrophages with its blood meal from infected people, which can contain large amounts of leishmania.
The bacteria are released in the mosquito's digestive tract and transform from the non-flagellated (amastigote) to a flagellated (promastigote) form. In the flagellated form, the bacteria can actively move in the direction of the mosquito bite and are transferred to humans or another vertebrate during the next blood meal through the mosquito's proboscis, where the bacteria convert back into the amastigote form.
Leishmania infantum is common in all continents with the exception of Australia. In South American countries the pathogen was identified as Leishmania chagasi designated. Experts now agree that the two bacteria are identical, so that the name Leishmania infantum has largely established itself.
It is one of the few leishmanias that can cause both the cutaneous and visceral forms of leishmaniasis. The addition of "infantum" to the name indicates that it is a disease that mainly affects children and toddlers. This has been the case before, mainly referring to the visceral form of the disease that affects the internal organs.
Because many people are now immunosuppressed for therapeutic reasons, the clinical picture has changed. Adults with disease-related or artificially weakened immune skills are also increasingly affected.
The infection occurs through the proboscis of an infected sand fly. The promastigote pathogens are brought into the skin with the proboscis, where they are recognized as foreign by polymorphic neutrophil granulocytes (PMN), the guardians of the immune system in the skin tissue, and immediately phagocytosed. However, the bacteria are able to secrete certain chemokines which prevent the PMN from secreting the contents of their substances via the leishmanias following phagocytosis. In addition, the bacteria use other chemokines to help attract phagocytes into which the pathogens want to invade as their actual host.
So while macrophages are attracted, the attraction of other immune cells such as NK cells (natural killer cells) and monocytes is suppressed at the same time. Because the arrival of the macrophages takes about one to two days, but the activated PMNs normally decompose after several hours via programmed cell death (apoptosis), the bacteria help them to live longer so that they can arrive in the protected intracellular space of the PMN the macrophages can wait. After the macrophages arrive, the PMN undergo apoptosis, so that the macrophages that have arrived phagocytize the fragments together with the released bacteria without showing any reactions to the leishmanias.
The pathogens can now, protected in a vacuole of the macrophage, multiply and after a while cause the macrophage to burst, so that further macrophages step in and phagocytize the fragments along with the bacteria. When a sandfly ingests blood through its proboscis, infected macrophages get into their digestive tract and the pathogens are released. They know how to escape digestion and transform themselves back into the promastigote form. They then move actively to the mosquito bite and are ready for a new infection.
Infection with Leishmania infantum can cause visceral leishmaniasis, which affects internal organs such as the liver and spleen. Children between the ages of one and five years and adults with naturally or artificially weakened immune systems are particularly at increased risk of the disease in endemic areas.
It is noticeable that in endemic areas the risk of infection increases with malnutrition, so that the disease is often referred to as the disease of the poor. The less balanced the diet, the harder it is for the body to build a strong immune system, making it more prone to disease of any kind.
The infection is not always correctly diagnosed because, for example, abdominal pain, diarrhea and weight loss (the typical initial symptoms of the disease) are difficult to interpret correctly. As the disease progresses, more specific symptoms such as swollen lymph nodes, enlarged liver and spleen, and pain in the left upper abdomen will also appear. A very specific indication of visceral leishmaniasis is bimodal fever. During the day there are two clearly recognizable temperature maxima.
If left untreated, the infection can be severe. In most cases, the infection goes unnoticed in adults and is overcome and suppressed by their own immune system. However, if the immune system is weakened by any circumstance, symptoms can still appear many years after infection. An infection with Leishmania infantum can also lead to a cutaneous form of leishmaniasis, which usually show a mild course.