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The medications nifurtimox and benznidazole are effective treatments during the acute phase of Chagas disease. The efficacy of these drugs is much lower when the disease is in the chronic phase. Avoiding exposure to the pathogen through vector control is the most effective method of limiting this disease.

a) Micrograph of red blood cells with crescent-shaped cells outside. These parasitic cells are about the length of 2 red blood cells. B) photo of a triatomine bug.
(a) Trypanosoma cruzi protozoan in a blood smear from a patient with Chagas disease. (b) The triatomine bug (also known as the kissing bug or assassin bug) is the vector of Chagas disease. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Erwin Huebner)
  • How do kissing bugs infect humans with Trypanosoma cruzi ?

Leishmaniasis

Although it is classified as an NTD, leishmaniasis is relatively widespread in tropical and subtropical regions, affecting people in more than 90 countries. It is caused by approximately 20 different species of Leishmania , protozoan parasites that are transmitted by sand fly vectors such as Phlebotomus spp. and Lutzomyia spp. Dogs, cats, sheep, horses, cattle rodents, and humans can all serve as reservoirs.

The Leishmania protozoan is phagocytosed by macrophages but uses virulence factors to avoid destruction within the phagolysosome. The virulence factors inhibit the phagolysosome enzymes that would otherwise destroy the parasite. The parasite reproduces within the macrophage, lyses it, and the progeny infect new macrophages (see Micro Connections: When Phagocytosis Fails ).

The three major clinical forms of leishmaniasis are cutaneous (oriental sore, Delhi boil, Aleppo boil), visceral (kala-azar, Dumdum fever), and mucosal (espundia). The most common form of disease is cutaneous leishmaniasis , which is characterized by the formation of sores at the site of the insect bite that may start out as papules or nodules before becoming large ulcers ( [link] ).

It may take visceral leishmaniasis months and sometimes years to develop, leading to enlargement of the lymph nodes, liver, spleen, and bone marrow. The damage to these body sites triggers fever, weight loss, and swelling of the spleen and liver. It also causes a decrease in the number of red blood cells (anemia), white blood cells (leukopenia), and platelets (thrombocytopenia), causing the patient to become immunocompromised and more susceptible to fatal infections of the lungs and gastrointestinal tract.

The mucosal form of leishmaniasis is one of the less common forms of the disease. It causes a lesion similar to the cutaneous form but mucosal leishmaniasis is associated with mucous membranes of the mouth, nares, or pharynx, and can be destructive and disfiguring. Mucosal leishmaniasis occurs less frequently when the original cutaneous (skin) infection is promptly treated.

Definitive diagnosis of leishmaniasis is made by visualizing organisms in Giemsa-stained smears, by isolating Leishmania protozoans in cultures, or by PCR-based assays of aspirates from infected tissues. Specific DNA probes or analysis of cultured parasites can help to distinguish Leishmania species that are causing simple cutaneous leishmaniasis from those capable of causing mucosal leishmaniasis.

Questions & Answers

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Source:  OpenStax, Microbiology. OpenStax CNX. Nov 01, 2016 Download for free at http://cnx.org/content/col12087/1.4
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