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Leishmania Spp.

Leishmania spp. causes Leishmaniasis, a disease transmitted by female sandflies, categorized into Old World and New World types based on geographical distribution. Old World leishmaniasis includes cutaneous and visceral forms, while New World leishmaniasis primarily involves mucocutaneous leishmaniasis. Diagnosis and treatment vary by type, with prevention strategies focusing on reducing sandfly exposure and controlling reservoirs.

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26 views3 pages

Leishmania Spp.

Leishmania spp. causes Leishmaniasis, a disease transmitted by female sandflies, categorized into Old World and New World types based on geographical distribution. Old World leishmaniasis includes cutaneous and visceral forms, while New World leishmaniasis primarily involves mucocutaneous leishmaniasis. Diagnosis and treatment vary by type, with prevention strategies focusing on reducing sandfly exposure and controlling reservoirs.

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Leishmania spp.

causes Leishmaniasis disease spread by the bite of certain types of adult female
sandflies which is a bloodsucker, usually feeding at night. Geographical
distribution divided the disease to 1- Old world leishmaniasis caused by L.
donovani, L. infantum, L. tropica, L. major, L. aethiopica are transmitted by
the sandflies genus Phlebotomus; 2- New world leishmaniasis caused by L.
mexicana, L. braziliensis and etc... are transmitted by the sandflies genus
Lutzomyia and Psychodopygus. The term ‘New World’ refers to the Americas and
the ‘Old World’ is used for the rest of the world
Morphology and Life cycl:-The life cycle of Leishmania is completed in two
hosts, humans and sandflies. Two stages are known; the amastigote which is
spherical or subspherical and the promastigote which is pyriform or spindle
shape with flagellum. Natural reservoir hosts humans, dogs and wild rodents.
When the fly bites a reservoir host or infected person with Leishmania, the
pathogen reaches the stomach of the sandfly, the amastigotes quickly transform
into elongated and motile forms called the promastigotes. The promastigotes
live extracellularly in the alimentary canal, reproducing asexually, then migrate to
the proximal end of the gut. As the fly bites, the promastigotes are released from
the proboscis and introduced locally at the bite site. Once inside the human host,
promastigotes invade macrophages. Inside the cells they transform back into
the smaller amastigote form. The amastigotes replicate in the macrophage cell.
After repeated multiplication, they break down their host cell by complete
pressure of mass. The daughter cells protozoans then migrate to fresh cells
(Cutaneous or mucocutaneous leishmaniasis) or through the bloodstream
(visceral leishmaniasis) to find new hosts. In this way the infection is progressive,
spreading to the host's mononuclear phagocyte system, particularly the spleen
and liver. The free amastigotes in peripheral tissues are then ingested by sandfly
to enter another cycle. Risk factors include poverty, malnutrition,
deforestation, lack of sanitation and urbanization. Leishmaniasis is mainly a
zoonotic disease.

A- Old world leishmaniasis


1-Cutaneous leishmaniasis (oriental sore)
Is the most common form caused by L. tropica, L. major, L. aethiopica, found in
88 tropical and subtropical countries which causes an open sore at the bite sites,
which heals in a few months to a year and half, leaving an unpleasantlooking
scar. Diffuse cutaneous leishmaniasis produces widespread skin lesions which
resemble leprosy, and may not heal on its own. Habitat is inside
reticuloendothelial cells of the skin.
Pathogenesis: Leishmania invades human macrophages and replicates
intracellularly. A raised, red lesion develops at the site of the bite (Incubation
period varies from a few weeks to 6 months and in some cases it may be 1–2
years). Clinically, the lesion begins as a raised papule about 2.5 cm in diameter.
The lesion then ulcerates and may become secondarily infected with bacteria.
One factor restricting the parasites causing cutaneous leishmaniasis to the skin may
simply be temperature.
Diagnosis : 1-A skin scraping with microscopic analysis using Wright or Giemsa
stain. 2-Needle aspiration of tissue fluid from the margin of a lesion can yield fluid
for culture (can be on NNN medium) to isolate the organism and identify the
species. 3-DNA testing (PCR). 4-Leishmanin skin test (Montenegro test) delayed-
type hypersensitivity reaction to intradermal crude Leishmania antigen.
Visceral leishmaniasis (kala-azar)
Also known as black fever, and Dumdum fever, is the most severe form of
leishmaniasis and, without proper diagnosis and treatment, is associated with
high fatality. Caused by obligate intracellular parasite Leishmania
donovani, L. infantum (infantile visceral leishmaniasis).
Pathogenesis:The parasite spreads from the site of inoculation to multiply in
reticuloendothelial cells (the Habitat), especially in the liver, spleen, bone
marrow and lymph nodes. The most typical symptoms are fever and the
progressive enlargement of the spleen, liver and lymph nodes, anaemia,
leucopenia, and skin changes. Death is due to secondary infections.
Sometime after successful treatment—generally a few months with African kala-
azar, or as much as several years with the Indian strain—a secondary form of the
disease may set in, called post kala-azar dermal leishmaniasis, or PKDL. This
condition caused by the reversal of L.donovani from viscerotropic to
dermatotropic, manifests first as small, measle-like skin lesions on the face,
which gradually increase in size and spread over the body. PKDL is not seen with
L. infantum infection .
Diagnosis:
Non specific tests: blood count, haemoglobin and serum protein estimation.
Parasitological diagnosis: blood film stained with Leishman or Giemsa stain,
culture in specific media, visualization of the amastigotes in splenic or bone marrow
aspirate, PCR (polymerase chain reaction) tests for the detection of Leishmania
DNA. Immunological tests: Serological testing is much more frequently used in
areas where leishmaniasis is endemic. Leishmanin test is negative in active
cases of kala-azar because the Cellmediated immunity is impaired in active
kala-azar patients who consequently lack a delayed hypersensitivity response.
Diagnosis of PKDL: can be established by demonstration of amastigote form of L.
donovani by a microscope of Leishman-stained smear prepared from the biopsy
material obtained from nodular lesions.

B-New world leishmaniasis


Mucocutaneous leishmaniasis (espundia)
It causes both skin and mucosal ulcers with damage primarily of the nose and
mouth. It can be highly disfiguring if not promptly treated. Caused by L.
braziliensis and, L. mexicana, which are mainly found in certain South
America, and Central America respectively.
Pathogenesis: Habitat of these parasites occur as intracellular parasites
(amastigote form) inside the macrophages of the skin and mucous
membrane of the nose and buccal cavity. Leishmania invades human
macrophages and replicates intracellularly. A raised, red lesion develops at the site
of the bite. The lesion may spontaneously heal with scarring, but then
reappear elsewhere (especially as destructive mucocutaneous lesions).
Diagnosis: It is the same process in cutaneous leishmaniasis.
Treatments: The treatment needed is determined by where the disease is
acquired, the species of Leishmania, and the type of infection. Some possible
medications used for visceral disease include liposomal amphotericin B, a
combination of pentavalent antimonials and paromomycin, and miltefosine.
For cutaneous disease, paromomycin, fluconazole, or pentamidine may be
effective.
Prevention: Leishmaniasis can be partly prevented by: 1-sleeping under nets
treated with insecticide. 2-spraying insecticides to kill sandflies. 3-treating people
with the disease early to prevent further spread. 4-reservoir control programs.
Vaccination: leishmania is an intracellular pathogen since it requires strong cell
mediated immunity to be controlled. However most of vaccines trials provide
humoral response.

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