Leishmania are human pathogenic protozoa. The parasites spread via two host organisms and change their host between insect and vertebrate. An infection with Leishmania leads to leishmaniasis.

What are Leishmania?

Protozoa are primitive animals or protozoa, which, because of their heterotrophic lifestyle and mobility, are classified as animal eukaryotic protozoa. According to Grell, they are eukaryotes that can occur as single cells and form colonial associations. Leishmania or Leishmania form a genus of flagellated protozoa that colonize and multiply the blood of macrophages. In this context, also of hemoflagellates the speech.

Leishmania are obligate intracellular parasites, which make a host change between insect species such as sandflies or butterfly mosquitoes 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 location of their flagellum with their current host and stage of development. Basically, Leishmania are on average small.

Parasites live and grow at the expense of their hosts. This means that parasites always have disease value and inflict more or less damage on the host organism. Leishmania, for example, cause the symptoms of leishmaniasis and are generally considered to be pathogenic to humans.

The parasites have now spread from Australia around the world and cause numerous animal diseases worldwide. Not all strains of the genus infest humans. Despite this, according to the WHO, there are around 1.5 million new cases every year worldwide. Around one third of these are the prevalence of visceral leishmaniasis. Currently, twelve million people are carriers of the infection.

Occurrence, distribution & characteristics

Leishmania multiply in two hosts. The first place of reproduction is the sandfly organism. With the saliva of the mosquito, they migrate to the stung organism in the lurch in flagellate form. In the organism of vertebrates, they are phagocytosed by macrophages or phagocytes. This principle is also known as passive invasion and results in the transformation of Leishmania. With the silent invasion of the phagocytes, the organisms transform their shape into an amastigote or unsophisticated form.

Within the macrophages, the parasites multiply by division. When they have destroyed the host cell, they take amastigote form again. In the flagellated form, the parasites are extremely motile and thus capable of invading new macrophages. Once the pathogen is taken up by a sandfly or similar insect from the blood of an infected vertebrate, the cycle closes. In the intestine of the insect, the Leishmania again become a promastigote organism, which becomes an amastigote form within the intestinal epithelium, reaching the salivary glands of the mosquito. The next stick of a vertebrate can be a new infection.

A pathogenicity factor of Leishmania is the strategy of the "Trojan horse". They carry a signal on their surface, which suggests to the immune system harmlessness. The memory function has been bypassed. In addition, the parasites of the species Leishmania major reverse the action of the defense reaction to their benefit. They use the phagocytosis-friendly neutrophilic granulocytes for their purpose by invading undetectedly into long-lived macrophages and multiplying in their interior.

In the case of an infection in the tissue, granulocytes are attracted to the affected area by chemokines. In an insect bite this area corresponds to the skin. They phagocytose the invaded organisms because of their surface structures and cause a local inflammation process. Activated graunocytes then secrete chemokines to attract more granulocytes. The phagocytic Leishmania promote the formation of additional chemokines inside the phagocytes. The pathogens multiply unrecognized and unmarked in the infected tissue. In addition, Leishmania produce chemokines that stop the formation of interferon-inducible chemokines within the infected granulocytes, thereby preventing the activation of NK or Th1 cells.

Diseases & complaints

The processes described above make the infection with Leishmania a treacherous disease. In phagocytosis, Leishmania survive by their primary host cells signaling to the immune system the absence of pathogens. The natural life span of granulocytes is short. Apoptosis sets in after about ten hours. In granulocytes infected with the infection, caspase-3 activation is inhibited, allowing them to live up to three days longer. The pathogens also stimulate the granulocytes to attract macrophages, which remove cell toxins and proteolytic enzymes of the granulocytes from the surrounding tissue. Thus, the Leishmania are absorbed by physiological Abrauma processes of macrophages, the absorption of the apoptotic material attenuates the macrophage activity.

Defense mechanisms against intracellular parasites are deactivated so that the pathogen survives. Intracellularly in the granulocytes, the pathogens have no direct macrophage surface receptor contact and remain unseen. The phagocytes of the immune system are not activated.

Visceral leishmaniasis affects the internal organs. The most common pathogens are Leishmania donovani and infantum. Without therapy, about three percent of the cases end lethal. Skin sensitization or cutaneous leishmaniasis does not damage the internal organs. The main pathogens of this infection are Leishmania tropica major, tropica minor, tropica infantum and aethiopica.

The skin becomes red after transmission through the insect. It causes the formation of itchy nodules, which gradually become papules and later form an ulcer of up to five centimeters. In addition to moist skin infections, dry or diffuse skin infections also occur. In addition to these forms of leishmaniasis, there is a mucocutaneous leishmaniasis, which affects the mucous membrane in addition to the skin.

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