What is Leishmania brasiliensis?
Leishmania brasiliensis is the main causative agent of American cutaneous leishmaniasis. It is a very small flagellated bacterium of the family Leishmania, which is equipped with nucleus and own genetic material, so that it is also assigned to the large group of protozoa.
Leishmania brasiliensis is the main causative agent of American cutaneous leishmaniasis, which is similar to cutaneous leishmaniasis caused, for example, by Leishmania tropica in other regions.
The bacterium lives parasitically intracellularly in protected small vacuoles in the cytoplasm of macrophages. They proliferate within the macrophages by division and thereby transform themselves into the amastigote (flagellum) form. After the programmed cell death (apoptosis) of the affected macrophages they are released in the tissue and phagocytosed unnoticed by other macrophages together with the fragments of "their" macrophages without being lysed, ie without lysosomes, the weapons of the macrophages, their decomposing substances on the Empty bacteria.
The propagation of the bacteria happens via the host change with the bloodsucking sandfly of the genus Lutzomyia.
Occurrence, distribution & characteristics
Leishmania brasiliensis is - as its name suggests - widespread in South and Central America up to and including Mexico. What is striking about the pathogen is that, because of its characteristic intracellular life form in the macrophages, it can not skip over to other people and thus ensure its own survival. For this Leishmania brasiliensis needs the sandfly of the genus Lutzomyia as an intermediate host.
The blood-sucking mosquito absorbs macrophages infected with the blood, which are digested in the intestine of the mosquito and release the amastigote Leishmania. They then transform into the flagellated (promastigote) form and actively move towards the mosquito's stinging apparatus. In a renewed stab with their Stechrüssel enter the pathogens in the skin tissue of the stung man and are recognized by the first wave of the immune system as foreign and phagocytosed by polymorphic neutrophilic granulocytes (PMN).
In order to avoid the usually subsequent lysis, the pathogens release certain chemokines, which prevent the lysis of the granulocytes. In addition, they understand how to extend the life of "their" granulocyte from two to three hours to two to three days until the macrophages, which are also attracted by cytokines, the actual host cells of the pathogen, arrive.
Interestingly, Leishmania support PMN in attracting macrophages, but at the same time prevent other species of white blood cells, such as monocytes and NK cells (natural killer cells) from being attracted.
After apoptosis, the programmed cell death of the PMN, the macrophages phagocytose the fragments of the PMN and, unnoticed, also take Leishmania with them. As with the phagocytosis by the granulocytes, the subsequent lysis of the bacteria does not occur with the macrophages, so that they can develop and multiply intracellularly. The Leishmania thus understand how to eliminate an important immune response, lysis after phagocytosis, and to use macrophages for their protection.
The pathogens ensure their survival by the host change with the sandfly, which is connected at the same time with a relatively small change in shape from the promastigoten to the amastigote form. The Leishmania, however, rely on the fact that the cycle human or another vertebrate and sandfly is never interrupted, since no form of the bacterium exists, which would survive beyond the two hosts.
Diseases & complaints
An infection with Leishmania brasiliensis with an average incubation period of two to three months triggers the American cutaneous leishmaniasis, which occurs mainly in three different manifestations. The most common form of the disease is the cutaneous form, also known as warty leishmaniasis.
First, near the puncture site, a papule forms, which within a few weeks grows into one or more painless ulcers. It forms flat, visually a little unsightly skin lesions that scar in the course of time. In most cases, cutaneous leishmaniasis heals by itself within a few months, without acquiring immunity to the pathogen.
In less frequent cases there is an additional infection of the mucous membranes (mucocutaneous leishmaniasis). In most cases, the pathogen colonizes the mucous membranes of the nasopharyngeal space. The first symptoms are a permanently congested or runny nose with frequent nosebleeds. Left untreated, this form of leishmaniasis can lead to severe ulcers and tissue changes in the nasopharyngeal space as well as to a breakdown of the nasal septum.
Overall, the untreated mucocutaneous form of leishmaniasis shows a poor prognosis. The ability of the pathogen to manipulate the immune system, and thus to survive phagocytosis, makes it possible for the bacteria to be transported to other regions of the body with the blood stream or with the lymph. It is then the disseminated cutaneous leishmaniasis.
This form of the disease is recognizable by different presenting skin lesions and papules in different parts of the body. In rare cases, the pathogen migrates via the lymph to internal organs such as the liver and spleen and causes the visceral form of leishmaniasis.