KALA AZAR disease ,classes of KALA AZAR ,life cycle ,symptoms diagnosis , laboratory test and treatment of KALA AZAR.

KALA AZAR disease ,classes of KALA AZAR ,life cycle ,symptoms diagnosis , laboratory test and treatment of KALA AZAR.

KALA AZAR disease ,classes of KALA AZAR ,life cycle  ,symptoms diagnosis , laboratory test and treatment of KALA AZAR.

8.KALA  AZAR

Leishmaniasis is a disease caused by the flagellate protozoan genus Leishmania, which is transmitted through the bite of sand flies of the genus Lutzomyia in the New World and Phlebotomus in the Old World. The disease was named after Scottish pathologist William Boog Leishman in 1901.

This disease is also known as Leishmaniasis, Baghdad Boil, kala azar, black fever, sand fly disease, Dum-Dum fever, and espundia. Human infection is caused by approximately 21 species of Leishmania, including the L. donovani-complex with three species (L. donovani, L. infantum, and L. chagasi); the L. mexicana-complex with three main species (L. mexicana, L. amazonensis, and L.venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Vi The different species are morphologically indistinguishable, but isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies can differentiate them.
Leishmaniasis is common in Mexico, Central America, and South America, ranging from northern Argentina to southern Texas (but not in Uruguay, Chile, or Canada), as well as in southern Europe, Asia (but not Southeast Asia), the Middle East, and Africa (particularly East and North Africa). Australia and Oceania are not affected by the disease.

Leishmaniasis is classified into four types:

  1. Visceral leishmaniasis is the most serious form and can be fatal if left untreated.



2.Cutaneous leishmaniasis is the most common type, causing a sore at the bite site that heals in a few months to a year, leaving an unsightly scar. This form has the potential to progress to any of the other three forms.

3.Diffused cutaneous leishmaniasis is particularly difficult to treat because it causes widespread skin lesions that resemble leprosy.

4.Mucocutaneous leishmaniasis begins with skin ulcers that spread and cause tissue damage to the nose and mouth.

LIFE CYCLE

The bite of female phlebotomine sand flies transmits leishmaniasis. During blood meals, sand flies inject the infective stage, metacyclic promastigotes, into human blood. Macrophages phagocytize metacyclic promastigotes that reach the puncture wound but are not digested and transform into amastigote form. Amastigotes multiply in infected cells and affect various tissues depending on the Leishmania species involved.

The various clinical manifestations of leishmaniasis are caused by differences in tissue specificities. Sand flies become infected when they consume macrophages infected with amastigote forms and sucking blood meals from the infected host. The parasites transform into promastigote forms in the sandfly's midgut, multiply, differentiate into metacyclic promastigotes, and migrate to the proboscis, where they can be easily transferred into human blood while the sand-fly feeds.

SYMPTOMS

A nodule, rash, or ulceration may form in the area of the sand fly bite. The following symptoms appear four to six months after the bite: Fevers with chills and sweats twice a day, cough, weakness, diarrhea, weight loss, gums and nose may bleed, and skin or eyes may turn yellow.

DIAGNOSIS

The spleen swells and hardens dramatically. The liver enlarges. The skin becomes darker in color, and warty eruptions or ulcers may form. Rashes of a small, red color appear, as do raised lesions.

LABORTERY TEST

The following tests can detect Leishmania donovani infection:

Buffy coat blood preparation is a technique for preparing blood film on slides, bone marrow, liver, lymph nodes, or the spleen for identification of the causative organism. It is also possible to culture the organism and then identify it.

Infected people have a positive IgM (antibody reaction to the organism) agglutination test.

Patients typically have a low white blood cell count.

Total protein levels in the blood rise to 10g/dL or higher, while albumin levels fall to 3g/dL.

TREATMENT

The most commonly used treatment for visceral leishmaniasis was developed in the 1930s using antimony derivatives. Sodium stibogluconate (SSG) is administered intramuscularly over a period of 30 days or more. It's sold under the brand name Pentostam. Meglumine antimoniate, sold under the brand name Glucantime, is another antimonial medication. It is not entirely clear how these drugs work against the parasite. They could be interfering with its energy production or trypanothione metabolism. Unfortunately, the parasite for visceral or mucocutaneous leishmaniasis has become resistant to antimony drugs in many parts of the world, though the level of resistance varies by species.

Amphotericin is now the preferred treatment. AmBisome is an intravenous infusion of amphotericin B liposome formulation. AmBisome was approved for the treatment of VL in the United States and Europe in the 1990s, and it has demonstrated remarkable efficacy even after a single dose in India.

Miltefosine (Impavido) is a brand-new treatment for visceral and cutaneous leishmaniasis. Miltefosine orally was approved in India in 2002 and is now in Phase IV trials.
Two drugs are currently in development: one to treat Chagas disease in Latin America and another, Paromomycin, to treat visceral leishmaniasis in India. Paromomycin (aminosidine) is a low-cost intramuscular formulation that was approved in India in late 2006 and is currently being tested in Phase III trials in East Africa.

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