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leishmania (kala-azar)

 Leishmania (kala azar)

The parasite leishmania cause leishmaniasis.

An infection with leishmania parasite spread by sandflies.

It is a parasite of reticuloendothelial system.

Visceral leishmaniasis caused by leishmania.


Sources and Modes of Transmission

Parasite is transmitted by sand fly.

Parasite pathology survives inside cell of; 

Liver, Spleen, Lymph nodes, WBCs, Inner lining of blood capillaries.

Pathogenesis and clinical manifestations

Parasite enter in host by bite of infected sand fly.

Parasite through blood enter in liver, spleen, lymph glands, WBCs and inner lining of blood capillaries, bone marrow.

Symptoms

Continous fever

Enlargement of liver, spleen,

Jaundice may be developed

Skin sores

Life cycle

Leishmania parasite passes it's life cycle, in two host; 

1. Man and animal

2. Sand fly (insect vector)

In human, it become adult (round or with flagella) and called rhizoblast, where it multiply sexually.

But in sand fly parasite multiple asexually binary fission but don't form cyst.

Leishmania parasite has two stages in it's life cycle.

1. Amastigote form

Seen in human and animals.

2. Promastigote form

Seen in sandfly (insect vector).

Inflected sand fly when bite human skin, it inject flagella promastigotes in skin.

Promastigote form loose their flagella called amastigote form in humans.

Amastigotes enter into reticuloendothelial system of human involving; spleen, liver, bone marrow.

Amastigotes multiply in reticuloendothelial system of humans.

When sand fly bites infected person, acquire amastigotes.

Amastigotes divide in sand fly gut and produce promastigotes.

Life cycle of parasite repeated.


1. Infected sandfly bite human skin, it inject flagella promastigotes in skin.

2. Promastigotes form changes into amastigotes in humans.

3. In human, Amastigotes enter into reticuloendothelial system of human; spleen, liver, and bone marrow.

4. When amastigotes multiply in reticuloendothelial system of human; spleen, liver, bone marrow.

5. Sand fly bites an Infected person and acquire amastigotes.

6  Amastigotes divide in sand flys gut and produce promastigotes.

Laboratory Diagnosis

Specimen collection

(Include tissue and fluid sample)

Laboratory diagnosis of kalaazar depend upon;

1. Direct Evidences

2. Indirect Evidence

1. Direct Evidences

a. Peripheral blood smear

Thick blood film is examined for demonstration of amastigotes forms.

2. Blood culture

Blood culture can be done in Novy-macNeal-Nicolle medium and incubated at 22-24 degee celcius.

Promastigotes forms can be demonstrated.

3. Bone marrow aspiration

Bone marrow aspiration is useful method for diagnosis.

4. Splenic puncture

It is one of the most valuable methods for diagnosis.

The amastigotes are found in stained films and promastigotes in culture.


2. Indirect Evidences

1. Blood count

There is progressive leucopenia.

The proportion of leucocytes to erythrocytes is greatly altered.

2. Haemoglobin estimation

It reveals anaemia

3. Non-specific serological tests

a. Napier's aldehyde test

This test indicates increased serum gammaglobulins and thus is non- specific.

It is positive when disease is of at least 3-months duration.

b. Chopra's antimony test

This test also depends upon increased serum gammaglobulins.

It is less reliable than aldehyde test.


c. Complement fixation test

It detects antibodies in sera of kala-azar patients.

4. Specific test

IFAT

IHA

ELISA

Treatment

Pentavalent antimonial are conventional therapy with pentamidine and Amphotericin B as second line antiparasitic agent.

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