Leishmania infantum is a small bacterium of the Leishmania family and lives as a parasite obligate intracellularly in macrophages of humans and other vertebrates. The bacterium undergoes host switching between sandflies and humans or vertebrates to maintain its species, switching from the flagellated (mosquito) to the unflagellated form (human or vertebrate). Leishmania infantum can be the causative agent of both cutaneous and visceral leishmaniasis simultaneously.
What is Leishmania infantum?
Leishmania infantum, a small bacterium of the Leishmania family, lives as a parasite obligate intracellularly in macrophages of humans or other vertebrates. To maintain its species, the bacterium undergoes host switching, which is associated with a slight change in its external appearance. In Europe, North Africa and Asian countries, the sandfly of the genus Phlebotomus serves as an intermediate host, while in South American and Central American regions, the sandfly of the species Lutzomyia plays this part. The sandfly ingests macrophages with its blood meal in infected humans, which may contain larger amounts of Leishmania. The bacteria are released in the mosquito’s digestive tract and transform from the unflagellated (amastigote) to a flagellated (promastigote) form. In the flagellated form, the bacteria can actively move toward the mosquito’s biting apparatus and, during the next blood meal, are transferred by the mosquito’s proboscis to humans or another vertebrate, where the bacteria transform back to the amastigote form.
Occurrence, distribution, and characteristics
Leishmania infantum is distributed in all continents except Australia. In South American countries, the pathogen has been referred to as Leishmania chagasi. Experts now agree that the two bacteria are identical, so the name Leishmania infantum has become widely accepted. It is one of the few Leishmania that can cause both the cutaneous and visceral forms of leishmaniasis. The name suffix “infantum” indicates that it is a disease that primarily affects children and infants. This was already the case in the past, although it was mainly the visceral form of the disease, that which affects the internal organs, that was meant. Due to the fact that for therapeutic reasons many people are now undergoing immunosuppression, the clinical picture has changed. Increasingly, adults with disease-related or artificially weakened immune competence are also affected. Infection occurs through the proboscis of an infected sandfly. The promastigote pathogens are carried by the proboscis into skin areas, where they are recognized as foreign by polymorphonuclear neutrophil granulocytes (PMNs), the guardians of the immune system in skin tissue, and are immediately phagocytosed. However, the bacteria are able to secrete certain chemokines that prevent the PMN from secreting the contents of their substances over the leishmania following phagocytosis. In addition, the bacteria use other chemokines to assist in attracting phagocytes, which the pathogens seek to invade as their true host. Thus, while macrophages are attracted, the attraction of other immune cells such as NK cells (natural killer cells) and monocytes is simultaneously suppressed. Since the arrival of the macrophages takes about one to two days, but the activated PMNs normally disintegrate after several hours by programmed cell death (apoptosis), the bacteria help them to live longer so that they can wait for the arrival of the macrophages in the protected intracellular space of the PMNs. After the arrival of the macrophages, the PMN undergo apoptosis so that the arrived macrophages phagocytose the fragments along with the released bacteria without showing any reactions towards the Leishmania. The pathogens can now multiply, protected in a vacuole of the macrophage, and after some time cause the macrophage to burst, so that more macrophages step in and phagocytose the fragments along with the bacteria. When a sandfly now ingests blood through its proboscis, infected macrophages enter its digestive tract and the pathogens are released. They manage to escape digestion and transform back into the promastigote form. They then actively move to the mosquito’s biting apparatus and stand ready for re-infection.
Diseases and ailments
Infection with Leishmania infantum can cause visceral leishmaniasis, which affects internal organs such as the liver and spleen. In particular, children between one and five years of age and adults with naturally or artificially weakened immune systems are at increased risk of disease outbreak in endemic areas. It is striking 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, which is why it is more susceptible to diseases of all kinds. 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 also become apparent, such as swollen lymph nodes, enlarged liver and spleen, and pain in the left upper abdomen. A very specific clue to visceral leishmaniasis is the two-peaked fever. There are two clearly identifiable temperature maxima during the course of the day. If left untreated, the infection can take a serious course. In most cases, the infection goes unnoticed in adults and is overcome and suppressed by the body’s own immune defenses. However, symptoms can occur for many years after infection if the immune system is weakened by any circumstances. Infection with Leishmania infantum can also lead to a cutaneous form of leishmaniasis, which usually has a mild course.
