leishmaniasis(redirected from Sir William Boog Leishman)
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leishmaniasis(lēsh'mənī`əsĭs), any of a group of tropical diseases caused by parasitic protozoansprotozoan
, informal term for the unicellular heterotrophs of the kingdom Protista. Protozoans comprise a large, diverse assortment of microscopic or near-microscopic organisms that live as single cells or in simple colonies and that show no differentiation into tissues.
..... Click the link for more information. of the genus Leishmania. The parasites live in dogs, foxes, rodents, and humans; they are transmitted by the bites of sand flies. There they infect the very white blood cells that normally would defend the body from such invaders. There are two forms of leishmaniasis. The more serious, called visceral leishmaniasis, affects the internal organs, causing fever, anemia, splenomegaly, and discoloration of the skin. Untreated, it can be fatal. The term kala-azar may be used as a synonym for visceral leishmaniasis, or reserved for more advanced cases of the form. The second, or cutaneous form, leaves deep, disfiguring sores at the site of the bite. The cutaneous form may result in mucosal leishmaniasis, typically several years to decades later, if the parasites move from the skin to the mucous membranes of the pharynx. Research suggests that the visceral form results at least in part from a genetic susceptibility. Treatment is mainly with meglumine antimoniate, sodium stibogluconate, and other drugs that contain antimony. Leishmaniasis is rarely seen in the United States, but is prevalent in South Asia, the Middle East, much of Africa, and parts of Central and South America.
a group of infectious diseases of man and certain animals, occurring with ulcers of the skin and mucous membranes (cutaneous leishmaniasis) or with severe visceral lesions (visceral leishmaniasis, or kala-azar). The causative agent is the unicellular protozoan Leishmania, named after W. Leishman (1865–1926), who described the causative agent of visceral leishmaniasis in 1900. It is transmitted by the bite of the sandfly, the vector of the disease.
Leishmaniasis occurs mainly in tropical and subtropical countries (in the USSR, chiefly in Middle Asia and Transcaucasia) where sandflies are prevalent. The leishmanias that parasitize man are Leishmania tropica, the causative agent of cutaneous leishmaniasis; L. brasiliensis, the causative agent of mucocutaneous leishmaniasis; and L. donovani, the causative agent of visceral leishmaniasis.
Cutaneous leishmaniasis, or Borovskii’s disease (named after the Russian physician P. F. Borovskii, who discovered and described the causative agent of cutaneous leishmaniasis in 1898), occurs in two forms: late ulcerating (urban leishmaniasis, Ashkhabadka) and acute necrotizing (rural leishmaniasis, Penjdeh sore). The process is generally confined to the exposed areas of the body, especially the face and hands. The papules that appear at the sites of the sandfly bites, called leishmaniomas (1–2 cm and more in diameter), eventually break down to form ulcers, which heal with a scar. The incubation period for urban leishmaniasis varies from two months to one or two years and more. The entire process, from the formation of the tubercle, takes a year, on the average, but sometimes as much as 1.5–2 years. Persons affected with the disease are also a source of infection. Rural leishmaniasis is a natural-nidal zoonosis that occurs more acutely: the incubation period ranges from one week to two months. The process, from the appearance of the leishmaniomas to the formation of the scars, takes from three to six months. Diseased rodents (for example, gerbils) are the source of infection. Patients who have recovered from the disease acquire immunity to both types. However, persons who have had urban leishmaniasis may contract rural leishmaniasis.
Mucocutaneous leishmaniasis (American leishmaniasis) occurs in South and Central America.
Visceral leishmaniasis, or kala-azar (Hindi for “black fever”), is a transmissible tropical disease. The source of the causative agent is an infected person or dog. The disease strikes mainly children. Recovery is accompanied by future immunity. Visceral leishmaniasis develops gradually. After an incubation period ranging from 20 days to ten months or more (usually from three to five months), the temperature rises, takes on a wavelike pattern, and fluctuates during the course of the day. The characteristic black color of the skin seems to be due to adrenal insufficiency. The liver and spleen enlarge. Anemia intensifies and the leukocyte count drops. The lymph nodes often become involved.
Cutaneous leishmaniasis is treated with antimony preparations (Solyusurmin), quinacrine hydrochloride, and Monomycin. Visceral leishmaniasis is treated with Solyusurmin and symptomatic therapy. The diseases are prevented by guarding against sandflies with screens and repellents, by exterminating sandflies and rodents, by destroying diseased animals, and by the early detection and treatment of infected individuals. Persons settling for a long time in foci of cutaneous leishmaniasis are inoculated with a live culture of rural-type leishmanias. The inoculation is made on a nonexposed part of the body, no later than three months before a swarm.
REFERENCESKozhevnikov, P. V., N. V. Dobrotvorskaia, and N. I. Latyshev. Uchenie o kozhnom leishmanioze. Moscow, 1947.
Latyshev, N. I., P. V. Kozhevnikov, and T. P. Povalishina. Bolezn’ Borovskogo. Moscow, 1953.
Kassirskii, I. A., and N. N. Plotnikov. Bolezni zharkikh stran, 2nd ed. Moscow, 1964.
R. S. BABAIANTS