Leishmania are human pathogenic protozoa. The parasites spread through two host organisms and alternate their host between insect and vertebrate. Infection with Leishmania results in leishmaniasis.
What are leishmania?
Protozoa are primordial animals or protozoa that can be classified as animal eukaryotic protozoa because of their heterotrophic lifestyle and mobility. According to Grell, they are eukaryotes that occur as single cells and can form colonial associations. Leishmania or Leishmania form a genus of flagellated protozoa that colonize the blood of macrophages and multiply there. In this context, there is also talk of hemoflagellates. Leishmania are obligate intracellular parasites that switch hosts between insect species such as sand flies or butterfly midges and vertebrates such as sheep, dogs or humans. The parasite genus was named after William Boog Leishman, who is considered the first describer. Like other flagellates, organisms of the genus Leishmania change the shape and position of their flagella with their current host and stage of development. Basically, leishmania turn out to be small on average. Parasites live and grow at the expense of their hosts. This means that parasites always have disease value and cause more or less severe damage to the host organism. Leishmania, for example, cause the clinical picture of leishmaniasis and are basically considered to be human pathogens. The parasites have now spread from Australia throughout the world and cause numerous animal diseases worldwide. Not all strains of the genus infect humans. Nevertheless, according to the WHO, about 1.5 million new cases occur worldwide each year. About one third of these are prevalent in visceral leishmaniasis. Currently, twelve million people are considered carriers of the infection.
Occurrence, distribution, and characteristics
Leishmania reproduces in two hosts. The first site of reproduction is the organism of the sandfly. With the mosquito’s saliva, they migrate to the bitten organism in a flagellated form when it bites. In the vertebrate organism, they are phagocytosed by macrophages or phagocytes. This principle is also known as passive invasion and results in the metamorphosis of the Leishmania. With the silent invasion of the phagocytes, the organisms transform their shape to an amastigote or unflagellated form. Within the macrophages, the parasites reproduce by division. When they have destroyed the host cell, they reassume amastigote form. In the flagellated form, the parasites are exceptionally motile and thus able to re-invade new macrophages. Once the pathogen is reabsorbed from the blood of an infected vertebrate by a sandfly or similar insect, the cycle is completed. In the insect’s intestine, the leishmania again becomes a promastigote organism, which becomes an amastigote form within the intestinal epithelium, reaching the mosquito’s salivary glands. A new infection can occur during the next stick of a vertebrate. One pathogenicity factor of Leishmania is the “Trojan horse” strategy. They carry a signal on their surface that suggests harmlessness to the immune system. The memory function is thus bypassed. In addition, the parasites of the species Leishmania major reverse the effect of the defense reaction to their benefit. They use the phagocytosis-promoting neutrophil granulocytes to their purpose by invading long-lived macrophages unrecognized and multiplying inside them. In tissue infection, granulocytes are attracted to the affected area by chemokines. In the case of an insect bite, this area corresponds to the skin. They phagocytize the invaded organisms based on their surface structures and allow a local inflammatory process to develop. Activated gray leukocytes then secrete chemokines to attract more granulocytes. The phagocytized leishmania promote the formation of further chemokines inside the phagocytes. The pathogens multiply undetected and unchallenged in the infected tissue. Leishmania also produce chemokines themselves that stop the formation of the interferon-inducible chemokine within the infected granulocytes, thus preventing activation of NK or Th1 cells.
Diseases and medical conditions
The processes described above make infection with Leishmania an insidious disease.In phagocytosis, Leishmania survive by their primary host cells signaling the absence of pathogens to the immune system. The natural lifespan of granulocytes is short. Apoptosis sets in after about ten hours. In granulocytes with the infection, caspase-3 activation is inhibited, so they live up to three days, longer. The pathogens also stimulate the granulocytes to attract macrophages, which clear cellular toxins and proteolytic enzymes from the granulocytes from the surrounding tissue. Thus, Leishmania are taken up by macrophages via physiological clearance processes, and the uptake of apoptotic material dampens macrophage activity. Defense mechanisms against intracellular parasites are disabled, allowing the pathogen to survive. Intracellularly in granulocytes, the pathogens have no direct macrophage surface receptor contact and remain unseen. Thus, the scavenger cells of the immune system are not activated. In visceral leishmaniasis, the internal organs are affected. The most common pathogens are Leishmania donovani and infantum. Without therapy, about three percent of cases end lethally. In skin leishmaniasis or cutaneous leishmaniasis, the internal organs are spared. The most important pathogens of this infection are Leishmania tropica major, tropica minor, tropica infantum and aethiopica. The skin reddens after transmission by the insect. Itchy nodules form, which gradually become papules and later form an ulcer of up to five centimeters. In addition to moist skin infections, dry or diffuse infections of the skin also occur. In addition to these forms of leishmaniasis, mucocutaneous leishmaniasis exists, which affects the mucous membrane in addition to the skin.
