parasitic protozoa

Old World Cutaneous Leishmaniasis (Oriental sore)
Clinical disease
Leishmania tropica minor - dry or urban cutaneous leishmaniasis
Leishmania tropica major - wet or rural cutaneous leishmaniasis

Important features
These are parasites of the skin found in endothelial cells of the capillaries of the infected site, nearby lymph nodes, within large mononuclear cells, in neutrophilic leukocytes, and free in the serum exuding from the ulcerative site.





Life Cycle
The amastigotes are present in the skin, within large mononuclear cells, in neutrophils, inside capillary endothelial cells and also free in the tissues. They are ingested by sandflies feeding near the skin lesions. In the midgut of the sandfly, the amastigotes develop into promastigotes which replicate profusely. These are in turn transmitted to the skin of persons bitten by the sandflies. In the skin, the promastigotes are phagocytosed by the mononuclear cells, in which they become amastigotes and multiply.

Clinical features
The first sign, a red papule, appears at the site of the fly’s bite. This lesion becomes irritated, with intense itching, and begins to enlarge & ulcerate.
Gradually the ulcer becomes hard and crusted and exudes a thin, serous material. At this stage, secondary bacterial infection may complicate the disease.
They may also give rise to diffuse cutaneous leishmaniasis (DCL) in patients who produce little or no cell mediated immunity against the parasite. This leads to the formation of disfiguring nodules over the surface of the body.

Treatment
The drug of choice is sodium stibogluconate, with an alternative treatment of
applying heat directly to the lesion. Treatment of L. tropica remains to be a
problem as there is no safe and effective drug.

Prevention
- Prompt treatment & eradication of ulcers
- Control of sand flies & reservoir hosts.
Balantidiasis

The intestinal protozoan Balantidium coli is the only member of the ciliate group that is pathogenic for humans. Disease produced by B. coli is similar to amebiasis, because the organisms elaborate proteolytic and cytotoxic substances that mediate tissue invasion and intestinal ulceration.





Balantidium coli tphozoite (A), cyst (B)



Life cycle
The life cycle of B. coli is simple, involving ingestion of infectious cysts, excystation, and invasion of trophozoites into the mucosal lining of the large
intestine, caecum, and terminal ileum. The trophozoite is covered with rows of hair like cilia that aid in motility. Morphologically more complex than amebae, B. coli has a funnel-like primitive mouth called a cytostome, a large (macro) nucleus and a small (micro) nucleus involved in reproduction.


life cycle of Balantidium coli


Clinical features
As with other protozoan parasites, asymptomatic carriage of B. coli can exist. Symptomatic disease is characterized by abdominal pain, tenderness, tenesmus, nausea, anorexia, and watery stools with blood and pus. Ulceration of the intestinal mucosa, as with amebiasis, can be seen; a secondary complication caused by bacterial invasion into the eroded intestinal mucosa can occur. Extra intestinal invasion of organs is extremely rare in balantidiasis.


Treatment
The drug of choice is tetracycline; iodoquinol and metronidazole are alternative agents.