Cutaneous leishmaniasis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Promastigotes of leishmania are transmitted to human skin by the bite of a sandfly. Leishmania then invades human macrophages and replicates intracellularly.
The risk is highest from dusk to dawn because sand flies typically feed (bite) at night and during twilight hours. Although sand flies are less active during the hottest time of the day, they may bite if they are disturbed (for example, if hikers brush up against tree trunks or other sites where sand flies are resting). Vector activity can easily be overlooked: sand flies do not make noise, they are small (approximately one-third the size of mosquitoes), and their bites might not be noticed.
A raised, red lesion develops at the site of the bite (often weeks or sometimes years afterwards). The lesion then ulcerates and may become secondarily infected with bacteria. In many species (for example, Leishmania major) the lesion often spontaneously heals with atrophic scarring. In some species (for example, L. viannia braziliensis) the lesion may spontaneously heal with scarring, but then re-appear elsewhere (especially as destructive mucocutaneous lesions). Lesions of other leishmania species may spontaneously heal and then re-appear as satellite lesions around the site of the original lesion, or along the route of lymphatic drainage.
Some species tend to cause cutaneous leishmaniasis (e.g., Leishmania major and L. tropica), whereas some species tend to cause visceral leishmaniasis (e.g., Leishmania infantum and Leishmania donovani).
Post kala-azar dermal leishmaniasis
Post kala-azar dermal leishmaniasis(PKDL) is a sequel of Kala-azar that may appear on skin of affected individuals upto 20 years after the being partially treated, untreated or in those considered adequately treated[1][2]. Though any organism causing Kala-zar can lead to PKLD, it is commonly associated with L. donovani which gives different disease patterns in India and Sudan. In Indian variant nodules enlarge with time and form plaques but rarely ulcerate but African variety often ulcerate as they progress. Nerve involvement is common in African variety but rare in Indian subcontinent[3]. Histology demonstrates mixture of chronic inflammatory cells; there can be macrophage or epitheloid granuloma[4]. Parasite concentration is not consistent among studies perhaps reflecting low sensitivity of diagnostic methods used in earlier entries.
Mucocutaneous leishmaniasis
Mucocutaneous leishmaniasis is the most feared form of cutaneous leishmaniasis because it produces destructive and disfiguring lesions of the face. It is most often caused by Leishmania (Viannia) braziliensis, but cases caused by L. aethiopica have also been rarely described.
References
- ↑ Banerjee N (1973). "Role of I.M.A. during natural calamities and national emergencies". Journal of the Indian Medical Association. 61 (11): 477–81. PMID 4600129.
- ↑ Rathi SK, Pandhi RK, Chopra P, Khanna N (2005). "Post-kala-azar dermal leishmaniasis: a histopathological study". Indian journal of dermatology, venereology and leprology. 71 (4): 250–3. PMID 16394433.
- ↑ Salotra P, Singh R (2006). "Challenges in the diagnosis of post kala-azar dermal leishmaniasis". Indian J. Med. Res. 123 (3): 295–310. PMID 16778312.
- ↑ Singh N, Ramesh V, Arora VK, Bhatia A, Kubba A, Ramam M (1998). "Nodular post-kala-azar dermal leishmaniasis: a distinct histopathological entity". J. Cutan. Pathol. 25 (2): 95–9. PMID 9521498.