The Organisms

The sand fly transmits the infective promastigotes during a bite. The promastigotes rapidly change to amastigotes after phagocytosis by macrophages or monocytes, and then multiply, filling the cytoplasm of the cell. The infected cells burst, and the released parasites are again phagocytosed. This process is repeated, producing a cutaneous lesion or visceral infection depending on the species of parasite and the host response. The amastigotes are ovoid and approximately 2–3 μm in size. The nucleus and a dark-staining, rod-like kinetoplast can be seen as a “dot” and a “dash.”

The genus Leishmania, widely distributed in nature, has a number of species that are nearly identical morpho logically. Clinical characteristics of the disease are traditional differentiating characteristics, but many exceptions are now recognized. The different leishmanias present a range of clinical and epidemiologic characteristics that, for convenience only, are combined under three clinical groupings: (1) cutaneous leishmaniasis (Oriental sore, Baghdad boil, wet cutaneous sore, dry cutaneous sore, chiclero ulcer, uta, and other names), (2) mucocutaneous leishmaniasis (espundia), and (3) visceral leishmaniasis (kala-azar— Hindi for black fever).

There are strain differences in virulence, tissue tropism, and biologic and epidemiologic characteristics, as well as in the serologic and biochemical criteria. Some species can induce several disease syndromes (eg, visceral leishmaniasis from organisms of cutaneous leishmaniasis or cutaneous leishmaniasis from organisms of visceral leishmaniasis). Similarly, the same clinical condition can be caused by different agents.

Pathology and Pathogenesis

 Leishmania tropica, Leishmania major, Leishmania mexicana, Leishmania braziliensis, and other cutaneous forms induce a dermal lesion at the site of inoculation by the sand fly (cutaneous leishmaniasis, Oriental sore, Delhi boil, etc). The dermal layers are first affected, with cellular infiltration and proliferation of amastigotes intracellularly and spreading extracellularly, until the infection penetrates the epidermis and causes ulceration. Satellite lesions may be found (hypersensitivity or recidivans type of cutaneous leishmaniasis) that contain few or no parasites, do not readily respond to treatment, and induce a strong granulomatous scarring reaction. In Venezuela, a cutaneous disseminating form, caused by L. mexicana pifanoi, is known.

In Ethiopia, a form known as Leishmania aethiopica causes a similar nonulcerating, blistering, spreading cutaneous leishmaniasis. Both forms are typically anergic and nonreactive to skin test antigen and contain large numbers of parasites in the dermal blisters.

L. braziliensis braziliensis causes mucocutaneous or nasopharyngeal leishmaniasis in Amazonian South America. It is known by many local names. The lesions are slow growing but extensive (sometimes 5–10 cm). From these sites, migration appears to occur rapidly to the nasopharyngeal or palatine mucosal surfaces, where no further growth may take place for years. After months to more than 20 years, relentless erosion may develop, destroying the nasal septum and surrounding regions. In some instances, death occurs from asphyxiation due to blockage of the trachea, starvation, or respiratory infection. This is the classic clinical picture of espundia (Figure 1), most commonly found in the Amazon basin. At high altitudes in Peru, the clinical features (uta) resemble those of Oriental sore. L. braziliensis guyanensis infection frequently spreads along lymphatic routes, where it appears as a linear chain of nonulcerating lesions. L. mexicana infection is more typically confined to a single, indolent, ulcerative lesion that heals in about 1 year, leaving a characteristic depressed circular scar. In Mexico and Guatemala, the ears are frequently involved (chiclero ulcer), usually with a cartilage-attacking infection without ulceration and with few parasites.

Fig1. A patient with espundia caused by L. braziliensis. (Reproduced with permission from WHO/TDR image library.)

Leishmania donovani, which causes visceral leishmaniasis or kala-azar, spreads from the site of inoculation to multiply in reticuloendothelial cells, especially macrophages in spleen, liver, lymph nodes, and bone marrow (Figure 2). This is accompanied by marked hyperplasia of the spleen. Progressive emaciation is accompanied by growing weakness. There is irregular fever, sometimes hectic. Untreated cases with symptoms of kala-azar usually are fatal. Some forms, especially in India, develop a post cure florid cutaneous resurgence, with abundant parasites in cutaneous vesicles, 1–2 years later (post-kala-azar dermal leishmanoid).

Fig2. Leishmania donovani amastigotes (arrows) from a liver biopsy. (Courtesy of Pathology, UCSF.)

Epidemiology

It is estimated that the prevalence of leishmaniasis is approximately 4.8 million worldwide (GBD 2016 Disease and Injury Incidence and Prevalence Collaborators, 2017) and 20,000 30,000 deaths occur annually (WHO Leishmaniasis, 2018). Oriental sore occurs mostly in the Mediterranean region, North Africa, and the Middle and Near East. The “wet” type, caused by L. major, is rural, and burrowing rodents are the main reservoir; the “dry” type, caused by L. tropica, is urban, and humans are presumably the only reservoir. For L. braziliensis, there are a number of wild animal hosts, but apparently there are no domestic animal reservoirs. Sand fly vectors are involved in all forms.

L. donovani is found focally in most tropical and subtropical countries. Its local distribution is related to the prevalence of specific sand fly vectors. In the Mediterranean littoral and in middle Asia and South America, domestic and wild canids are reservoirs, and in the Sudan, various wild carnivores and rodents are reservoirs of endemic kala-azar. Control is aimed at destroying breeding places and dogs, where appropriate, and protecting people from sand fly bites.

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مواضيع ذات صلة

Trypanosoma cruzi (Blood Flagellate)

Trypanosoma brucei Rhodesiense and Trypanosoma brucei gambiense (Blood Flagellates)

Cryptosporidium (Intestinal Sporozoa)

Entamoeba histolytica (Intestinal and Tissue Ameba)

Giardia lamblia (Intestinal Flagellate)

Classification of Parasites

Toxoplasmosis

The Lung Flukes

The Liver Flukes

Echinococcus granulosus

Taenia saginata

Taenia solium