Post by ::gazal:: on Mar 25, 2007 7:37:57 GMT -5
Emerging Infections and the Skin
Journal of Investigative Dermatology Symposium Proceedings (2001) 6, 175–182; doi:10.1046/j.0022-202x.2001.00038.x
Leishmaniasis as an Emerging Infection
Christine M Choi and Ethan A Lerner*
1. Boston University School of Medicine
2. *Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School
Correspondence: Ethan A. Lerner, CBRC/MGH-East, Building 149, 13th Street, Charlestown, MA 02129. Email: ethan.lerner@cbrc2.mgh.harvard.edu
Received 9 August 2001; Accepted 9 August 2001.
Abstract
Leishmaniasis is a protozoan disease whose diverse clinical manifestations are dependent both on the infecting species of Leishmania and the immune response of the host. Transmission of the disease occurs by the bite of a sand fly infected with Leishmania parasites. Infection may be restricted to the skin in cutaneous leishmaniasis, limited to the mucous membranes in mucosal leishmaniasis, or spread internally in visceral leishmaniasis or kala azar. The overall prevalence of leishmaniasis is 12 million cases worldwide, and the global yearly incidence of all clinical forms approaches 2 million new cases (World Health Organization WHO/LEISH/200.42, Leishmania/HIV Co-Infection in Southwestern Europe 1990–98: Retrospective Analysis of 965 Cases, 2000). In the last two decades, leishmaniasis, especially visceral leishmaniasis, has been recognized as an opportunistic disease in the immunocompromised, particularly in patients infected with human immunodeficiency virus.
Abbreviations:
CL, cutaneous leishmaniasis; HIV, human immunodeficiency virus; ML, mucocutaneous leishmaniasis; VL, visceral leishmaniasis
Top of page
History
The increases in travel and the number of immunocompromised individuals allows leishmaniasis to be considered an "emerging disease". The purpose of this paper is to highlight selected clinical, histopathologic, and immunologic features of leishmaniasis as well as therapies and vector biology.
The cutaneous afflictions of leishmaniasis have been known since antiquity (Peters, 1988). Descriptions of the cutaneous disease in the Old World are found from the first century AD. New World pottery from Peru and Ecuador dating from AD 400–900 illustrates faces afflicted with a process consistent with leishmaniasis (Lainson et al, 1987). The first description in English of a lesion resembling leishmaniasis was made in 1756 by Russell, who described the "Aleppo evil" from Syria. In 1885, Cunningham observed organisms in macrophages from lesions of "Delhi boil" in India. A Russian army physician named Borovsky noted the protozoal nature of the organism in 1898 in biopsy specimens from skin lesions. In 1903 Leishman published his identification of the parasite in the spleen of an English private who had died of Dumdum fever in Dum-Dum, India in 1900. A few months later Donovan described identical organisms in a splenic puncture specimen from a living child. The distinctive histologic feature of this 2–5 microm parasite was the presence of both a nucleus and a smaller rod-shaped structure consisting of mitochondrial DNA called the kinetoplast. Ross named the parasite "Leishmania donovani" later the same year. Other names of leishmaniasis include Oriental sore, Aleppo evil, Delhi boil, Baghdad sore, Rose of Jericho, Chiclero's ulcer, uta, espundia (mucous form), forest yaws, Dumdum fever (visceral form), kala-azar, and black fever.
Top of page
Clinical features
Localized cutaneous leishmaniasis (LCL)
Leishmaniasis in its various forms is present on all continents except Australia and Antarctica (Lerner and Von Lichtenburg, 1991). LCL is widespread throughout the Old World and is primarily caused by the organisms Leishmania tropica and Leishmania major. New world LCL is endemic in Central and South America. Two independent species or "complexes" of parasites are responsible for New World LCL: Leishmania braziliensis and Leishmania mexicana.
LCL usually affects unclothed parts of the body easily bitten by the sand fly vector, including the face, neck, and arms. New World leishmaniasis commonly presents with a solitary primary lesion, whereas multiple primary lesions are often found in Old World disease. After an average incubation period of 1 wk to 3 mo, a red papule appears that enlarges to a plaque or nodule. The lesion often develops into an ulcer, which is well circumscribed with a violaceous border. The ulcer base is granulomatous and crusted, and the margins are hypertrophic but without extensive undermining (Figure 1). Painless, rubbery subcutaneous nodules or cords rarely develop around the ulcer due to local lymphangitic spread of the organism. Draining lymph nodes may be enlarged and reveal parasites on biopsy (Al-Gindan and Kubba, 1989). Occasionally, inflammatory satellite papules and subcutaneous induration may develop around the primary lesion representing a reaction to local dissemination of the parasite or its antigenic products (Kubba et al, 1987,1988). Itching and pain are mild, if present. The wound may become superinfected, leading to misdiagnosis. Between 1 and 36 mo, depending upon both the patient and the infecting organism, the ulcer spontaneously regresses leaving a scar with hypo- or hyper-pigmentation. Immunity is considered complete but one study in a Saudi Arabian population found subsequent re-infection in up to 10% of individuals (Killick-Kendrick et al, 1985).
Figure 1.
www.nature.com/jidsp/journal/v6/n3/full/5640053a.html
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By: Crack_Smoke_Republican
A little history on the "Baghdad Boil"
iraqwar.mirror-world.ru/article/122206
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Journal of Investigative Dermatology Symposium Proceedings (2001) 6, 175–182; doi:10.1046/j.0022-202x.2001.00038.x
Leishmaniasis as an Emerging Infection
Christine M Choi and Ethan A Lerner*
1. Boston University School of Medicine
2. *Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School
Correspondence: Ethan A. Lerner, CBRC/MGH-East, Building 149, 13th Street, Charlestown, MA 02129. Email: ethan.lerner@cbrc2.mgh.harvard.edu
Received 9 August 2001; Accepted 9 August 2001.
Abstract
Leishmaniasis is a protozoan disease whose diverse clinical manifestations are dependent both on the infecting species of Leishmania and the immune response of the host. Transmission of the disease occurs by the bite of a sand fly infected with Leishmania parasites. Infection may be restricted to the skin in cutaneous leishmaniasis, limited to the mucous membranes in mucosal leishmaniasis, or spread internally in visceral leishmaniasis or kala azar. The overall prevalence of leishmaniasis is 12 million cases worldwide, and the global yearly incidence of all clinical forms approaches 2 million new cases (World Health Organization WHO/LEISH/200.42, Leishmania/HIV Co-Infection in Southwestern Europe 1990–98: Retrospective Analysis of 965 Cases, 2000). In the last two decades, leishmaniasis, especially visceral leishmaniasis, has been recognized as an opportunistic disease in the immunocompromised, particularly in patients infected with human immunodeficiency virus.
Abbreviations:
CL, cutaneous leishmaniasis; HIV, human immunodeficiency virus; ML, mucocutaneous leishmaniasis; VL, visceral leishmaniasis
Top of page
History
The increases in travel and the number of immunocompromised individuals allows leishmaniasis to be considered an "emerging disease". The purpose of this paper is to highlight selected clinical, histopathologic, and immunologic features of leishmaniasis as well as therapies and vector biology.
The cutaneous afflictions of leishmaniasis have been known since antiquity (Peters, 1988). Descriptions of the cutaneous disease in the Old World are found from the first century AD. New World pottery from Peru and Ecuador dating from AD 400–900 illustrates faces afflicted with a process consistent with leishmaniasis (Lainson et al, 1987). The first description in English of a lesion resembling leishmaniasis was made in 1756 by Russell, who described the "Aleppo evil" from Syria. In 1885, Cunningham observed organisms in macrophages from lesions of "Delhi boil" in India. A Russian army physician named Borovsky noted the protozoal nature of the organism in 1898 in biopsy specimens from skin lesions. In 1903 Leishman published his identification of the parasite in the spleen of an English private who had died of Dumdum fever in Dum-Dum, India in 1900. A few months later Donovan described identical organisms in a splenic puncture specimen from a living child. The distinctive histologic feature of this 2–5 microm parasite was the presence of both a nucleus and a smaller rod-shaped structure consisting of mitochondrial DNA called the kinetoplast. Ross named the parasite "Leishmania donovani" later the same year. Other names of leishmaniasis include Oriental sore, Aleppo evil, Delhi boil, Baghdad sore, Rose of Jericho, Chiclero's ulcer, uta, espundia (mucous form), forest yaws, Dumdum fever (visceral form), kala-azar, and black fever.
Top of page
Clinical features
Localized cutaneous leishmaniasis (LCL)
Leishmaniasis in its various forms is present on all continents except Australia and Antarctica (Lerner and Von Lichtenburg, 1991). LCL is widespread throughout the Old World and is primarily caused by the organisms Leishmania tropica and Leishmania major. New world LCL is endemic in Central and South America. Two independent species or "complexes" of parasites are responsible for New World LCL: Leishmania braziliensis and Leishmania mexicana.
LCL usually affects unclothed parts of the body easily bitten by the sand fly vector, including the face, neck, and arms. New World leishmaniasis commonly presents with a solitary primary lesion, whereas multiple primary lesions are often found in Old World disease. After an average incubation period of 1 wk to 3 mo, a red papule appears that enlarges to a plaque or nodule. The lesion often develops into an ulcer, which is well circumscribed with a violaceous border. The ulcer base is granulomatous and crusted, and the margins are hypertrophic but without extensive undermining (Figure 1). Painless, rubbery subcutaneous nodules or cords rarely develop around the ulcer due to local lymphangitic spread of the organism. Draining lymph nodes may be enlarged and reveal parasites on biopsy (Al-Gindan and Kubba, 1989). Occasionally, inflammatory satellite papules and subcutaneous induration may develop around the primary lesion representing a reaction to local dissemination of the parasite or its antigenic products (Kubba et al, 1987,1988). Itching and pain are mild, if present. The wound may become superinfected, leading to misdiagnosis. Between 1 and 36 mo, depending upon both the patient and the infecting organism, the ulcer spontaneously regresses leaving a scar with hypo- or hyper-pigmentation. Immunity is considered complete but one study in a Saudi Arabian population found subsequent re-infection in up to 10% of individuals (Killick-Kendrick et al, 1985).
Figure 1.
www.nature.com/jidsp/journal/v6/n3/full/5640053a.html
-----------------
By: Crack_Smoke_Republican
A little history on the "Baghdad Boil"
iraqwar.mirror-world.ru/article/122206
------------------