Leishmania brasiliensis are small, flagellated protozoa belonging to the bacterial phylum Leishmania, subgenus Viannia. They live parasitically in macrophages, into which they have entered by phagocytosis without causing harm. They are causative agents of American cutaneous leishmaniasis and require host switching via the sand fly of the genus Lutzomyia to spread.
What is Leishmania brasiliensis?
Leishmania brasiliensis is the principal causative agent of American cutaneous leishmaniasis. It is a very small flagellated bacterium in the Leishmania family that is equipped with a nucleus and its own genetic material, so it is also classified in the large group of protozoa. Leishmania brasiliensis represents the main pathogen of American cutaneous leishmaniasis, which is comparable 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 replicate within macrophages by division, converting to the amastigote (flagellar) form. After programmed cell death (apoptosis) of the affected macrophage, they are released in the tissue and phagocytosed unnoticed by further macrophages together with the fragments of “their” macrophage, without being lysed, i.e. without lysosomes, the weapons of the macrophages, emptying their decomposing substances over the bacteria. Onward dissemination of the bacteria occurs via host exchange with the blood-sucking sand fly of the genus Lutzomyia.
Occurrence, distribution, and characteristics
Leishmania brasiliensis, as its name suggests, is distributed in South and Central America up to and including Mexico. A striking feature of the pathogen is that, because of its characteristic intracellular life form in macrophages, it cannot jump to other individuals and thus ensure its own persistence. For this, Leishmania brasiliensis requires the sandfly of the genus Lutzomyia as an intermediate host. The blood-sucking mosquito ingests infected macrophages with its blood, which are digested in the mosquito’s intestine and release the amastigote leishmania. They subsequently transform into the flagellated (promastigote) form and actively move toward the mosquito’s biting apparatus. When bitten again with their proboscis, the pathogens enter the skin tissue of the bitten individual and are recognized as foreign by the first wave of immune defenses and phagocytosed by polymorphonuclear neutrophil granulocytes (PMNs). To escape the lysis that normally follows, the pathogens secrete certain chemokines that prevent lysis in granulocytes. In addition, they know how to prolong the life of “their” granulocyte from two to three hours to two to three days until the arrival of the macrophages, the actual host cells of the pathogen, which are also attracted by cytokines. Interestingly, the Leishmania assist the PMN in attracting the macrophages, but at the same time prevent other white blood cell species 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, also picking up the Leishmania unnoticed. As with phagocytosis by granulocytes, macrophages fail to subsequently lyse the bacteria, allowing them to develop and multiply intracellularly. The Leishmania thus know how to switch off an important immune response, lysis after phagocytosis, and use macrophages for their protection. The pathogens ensure their survival by host switching with the sandfly, which is simultaneously associated with a relatively minor shape change from promastigote to amastigote form. However, the leishmania relies on the human or other vertebrate and sandfly cycle never being broken, as no form of the bacterium exists that would be viable outside of either host.
Diseases and ailments
Infection with Leishmania brasiliensis, with an incubation period of two to three months on average, causes American cutaneous leishmaniasis, which occurs primarily in three different manifestations. Most commonly, the disease manifests in the purely cutaneous form, also known as warty leishmaniasis.Initially, a papule forms near the injection site, which grows into one or more painless ulcers within a few weeks. Flat, visually somewhat unsightly skin lesions form, which scar over time. In most cases, cutaneous leishmaniasis heals on its own 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 then colonizes the mucous membranes of the nasopharynx. The first symptoms are a permanently blocked or runny nose with frequent nosebleeds. If left untreated, this form of leishmaniasis can lead to serious ulcers and tissue changes in the nasopharynx as well as degeneration of the nasal septum. Overall, the untreated mucocutaneous form of leishmaniasis shows a poor prognosis. The ability of the pathogen to manipulate immune defenses and thus usually survive phagocytosis makes it possible for the bacteria to be transported to other regions of the body with the bloodstream or lymph. This is then disseminated cutaneous leishmaniasis. This form of the disease is recognizable by different presenting skin lesions and papules in different regions of the body. In rare cases, the pathogen travels via the lymph to internal organs such as the liver and spleen, causing the visceral form of leishmaniasis.
