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Thread: Leishmaniasis : An Overview

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    Leishmaniasis : An Overview


    Introduction

    Leishmaniasis is a disease caused by the protozoa of the Leishmania species, which is transmitted by the bite of a female sandfly. While several ways to classify leishmaniasis (eg, by geography or taxonomy) are available, clinically, it can present itself in various ways, and is more easily classified as cutaneous, mucocutaneous, and visceral leishmaniasis.

    The typical lesions of cutaneous leishmaniasis were described as early as 900 BC and have been referred to as the "Balkan sore" in the Balkans, the "Delhi boil" in India, the "Baghdad boil" in Iraq, and "saldana" in Afghanistan.
    Pathophysiology

    Leishmaniae spend part of their life cycle in the gut of the sandfly, but their life cycle is completed in a vertebrate host.

    Within the sandfly gut, the protozoa are carried as extracellular promastigotes. Over the course of 4-25 days, these parasites multiply in the gut and migrate toward the pharynx. As the leishmaniae replicate, they create a blockage in the fly's esophagus. The feeding sandfly then clears out its esophagus by expelling leishmaniae into the skin of the host, from where they pass into the blood and tissues of the human host. Promastigotes are phagocytosed into macrophages of the reticuloendothelial system, where they shed their flagella and become amastigotes that multiply by binary fission. When the infected cells rupture, the infection spreads to other macrophages and is carried throughout the body. Temperature is an important factor that helps determine the localization of leishmanial lesions. Species causing visceral leishmaniasis are able to grow at core temperatures, while those responsible for cutaneous leishmaniasis grow best at lower temperatures.

    Although the Leishmania species differ clinically and biologically, their characteristics overlap and each clinical syndrome can be produced by multiple species of Leishmania.

    In cutaneous leishmaniasis, the hallmark of the disease is skin lesions, which can spontaneously heal in 2-10 months.

    In mucocutaneous leishmaniasis, mucosal ulcerations usually develop by metastasis from disseminated protozoa rather than by local spread. Secondary infection plays a prominent role in the size and persistence of ulcers. Ulcer progression is slow and steady.

    Typically, visceral leishmaniasis incubates for weeks to months before becoming clinically apparent. The disease can be subacute, acute, or chronic, and can manifest in patients who are immunocompromised years after they have left endemic regions.
    Clinical

    History
    In some endemic areas, natives have recognized that immunity occurs as a natural course of the disease. Some cultures deliberately inoculate their children on a part of the body that is not usually exposed to avoid later development of a disfiguring scar on an exposed part of the body.

    Cutaneous leishmaniasis
    ◦The broad spectrum of clinical manifestations of cutaneous leishmaniasis is often compared with that of leprosy. Cutaneous leishmaniasis can be simple or diffuse.
    ◦Different species, as well as host factors, can also affect the clinical picture, where some species cause "wet" ulcers and others "dry" ulcers.
    ◦After the bite of an infected sandfly, the incubation period is usually several weeks after inoculation, but this incubation period is variable. Initial lesions can appear immediately after a bite, or the incubation period may last for several months. These lesions are usually painless.
    ◦Skin trauma can result in activation of seemingly latent cutaneous infection long after the initial bite.
    ◦Over a period of weeks to years, some lesions may resolve spontaneously without pharmacotherapy.


    Mucocutaneous leishmaniasis
    ◦The incubation period is from 1-3 months. Mucocutaneous leishmaniasis can be the primary manifestation of the disease, but the primary lesions may also be limited to cutaneous manifestations, with mucosal lesions appearing only later in the course of disease when untreated cutaneous lesions progress to involve the oral and nasal surfaces. Cases in which the time between the primary lesion and the appearance of mucosal involvement is up to 2 decades have been reported.
    ◦Initial symptoms related to mucosal lesions may include nasal obstruction and bleeding.
    ◦Mucosal lesions become painful gradually and can become sites of infection, sometimes leading to sepsis.
    Visceral leishmaniasis
    ◦Kala azar is the Indian name for visceral leishmaniasis. The term means "black disease," which is a reference to the characteristic darkening of the skin that is seen in patients with the disease.
    ◦Many subclinical cases occur and go unrecognized for each clinically recognized case.
    ◦Malnutrition has been shown to contribute to the development of clinical disease.
    ◦Like cutaneous leishmaniasis, visceral leishmaniasis can take different forms ranging from asymptomatic or self-resolving disease to fulminant disease.
    ◦Onset can be insidious or sudden.
    ◦In endemic areas, kala azar may be suspected in a patient with persistent, irregular, or remittent fever; leukopenia; and splenomegaly. Other accompanying symptoms may be lymphadenopathy and weight loss.
    ◦Fever can be continuous, intermittent, or remittent, and it can recur at irregular intervals.

    Physical

    Cutaneous leishmaniasis
    ◦Systemic signs usually are absent.
    ◦Initially, the lesion is a small, red papule up to 2 cm in diameter. Over several weeks, the papule becomes darker and will crust in the center, eventually ulcerating to present a typical appearance of an ulcer with raised edges and surrounding dusky red skin. The ulcers can be moist or open with seropurulent exudate or dry with a crusted scab. After about 3-6 months, the ulcers heal, leaving a raised border.
    ◦Sores usually are found on exposed areas of skin, especially the extremities and face.
    ◦Regional adenopathy, satellite lesions, and subcutaneous nodules can be present.
    ◦Untreated sores can leave depigmented retracted scars.

    Mucocutaneous leishmaniasis
    ◦Cutaneous lesions can be single or multiple.
    ◦Secondary mucosal lesions often develop after the primary lesion has healed.
    ◦Mucosal lesions can progress to involve the entire nasal mucosa and the hard and soft palates. Without treatment, the entire nasal mucosa and palates become deformed with ulceration and erosion of the nasal septum, lips, and palate. The disease attacks cartilaginous areas but usually spares bony structures, and it can leave extreme disfigurement.
    ◦Signs include gingival edema, periodontitis, and adenopathy.
    Visceral leishmaniasis
    ◦Bouts of fever occur.
    ◦Hepatosplenomegaly occurs secondary to compensatory production of phagocytic blood cells.
    ◦Wasting and weakness are observed.
    ◦Darkening of the skin is characteristic (thus, the name kala azar or black fever).
    ◦Diarrhea may occur.
    ◦Lymphadenopathy is often present.
    ◦In visceral leishmaniasis, patients may die of hemorrhage (secondary to infiltration of the hematopoietic system), severe anemia, secondary bacterial infections of mucous membranes, bacterial pneumonia, septicemia, tuberculosis, dysentery, or measles.



    Leishmaniasis.




    Leishmaniasis.


    Leishmaniasis.


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    Last edited by trimurtulu; 02-04-2009 at 10:31 PM.

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