2. • Leishmaniasis is a parasitic disease spread
introduction by the bite of infected sand flies. There
are several different forms of
leishmaniasis. The most common are
cutaneous and visceral. The cutaneous
type causes skin sores. The visceral type
affects internal organs such as the
spleen, liver and bone marrow. People
with this form usually have fever, weight
loss and an enlarged spleen and liver.
• Leishmaniasis is found in parts of about
88 countries. Most of these countries are
in the tropics and subtropics. It is possible
but very unlikely that you would get this
disease in the United States. But you
should be aware of it if you are traveling
to the Middle East or parts of Central
America, South America, Asia, Africa or
southern Europe.
3. Types
• Infection with Leishmania species can result in 3 main types of disease depending on the
species, geographic region and host immune response.
• Leishmania donovani produces visceral leishmaniasis (kala-azar). Symptoms include fever (often 2
fever spikes per day), enlargement of the spleen and liver, weakness, and progressive emaciation. The
disease is often fatal without treatment, but survivors often develop immunity.
• Leishmania tropica and L. mexicana produce cutaneous leishmaniasis which is characterized by skin
lesions (oriental sore). Infected macrophages containing amastigotes are found primarily at the site of
infection around the sores. The sores are chracterized by an elevated rim encircling the lesion.
• Leishmania braziliensis produces mucocutaneous leishmaniasis, characterized by lesions near mucosal
membranes. The intitial site if infection is a small red papule that ulcerates in a few weeks. The lesions
are flat (no raised rim) and often oozing. Infections of the ear, nose and mouth area lead to
degeneration of the cartilage and soft tissues, resulting in disfigurement.
4. Types
• Cutaneous leishmaniasis
Americas -Leishmania tropica mexicana, Leishmania
braziliensis, and Leishmania amazonensis
Old World -Leishmania tropica, Leishmania major, L
infantum, and Leishmania aethiopica
• Mucocutaneous leishmaniasis
Americas -L braziliensis
Old World -L aethiopica
• Visceral leishmaniasis
India, Kenya -Leishmania donovani
South Europe and North Africa -L infantum
Americas -Leishmania chagasi
5. • Amastigote of leishmania
are spherical to ovoid .
Leishmania measure 1-5 µm long by 1-2
µm wide
They possess a large
nucleus, a prominent
kinetoplast, and a short
axoneme
The organisms reside in
macrophages of the host and
can be found throughout the
body.
6. • promastigate: Promastigote
10-20 X 7-4 micrometers in
Leptomonad stage size, fusiform in shape, it has
one nucleus.central in
position, and one anterior
flagellum which is just as long
as its body length.
Promastigotes are found in
the digestive tract of
sandflies. which serve as an
arthropod vector, and they
can also be found in culture
medium.
7. Leishmaniasis Life Cycle
Infection occurs when infected sandfly regurgitates infective promastigotes into the blood while
feeding.
The promatigotes are phagocytized by macrophages and transform into amastigotes.
The amastigoteThe life cycle is continued when a sandfly feeds on an infected person and
ingests the amastigotes in the macrophages.multiply by binary fission in the macrophages.
8. transmission
• Human Stages
• Sand fly injects promastigotes into the skin during a blood meal. *infective stage
• Promastigotes are phagocytized by neutrophils that are rapidly recruited to the bite site.
• Infected neutrophils release the parasites which are then consumed by macrophages.
• Promastigotes transform into amastigotes inside macrophages. *diagnostic stage
• Amastigotes multiply in cells (including macrophages) of various tissues. *diagnostic stage
• Sand Fly Stages
• Sand fly ingests infected macrophages when it takes a blood meal.
Ingestion of parasitized cell.
• Amastigotes transform into promastigotes in midgut.
• Promastigotes divide and migrate to the anterior midgut and foregut.
• Sand fly injects promastigotes into the skin during a blood meal. *infective stage
9. Risk factors
• Children are at greater risk than adults in endemic areas.
• Malnutrition has been shown to contribute to the development of disease.
• Persons with AIDS are at 100-1000 times greater risk of developing visceral
leishmaniasis in certain areas.
• Incomplete therapy of initial disease is a risk factor for recurrence of leishmaniasis.
• Some studies have shown protection against cutaneous leishmaniasis with
vaccination of killed Leishmania promastigotes and live bacillus Calmette-Guérin
(BCG). However, this does not seem to be protective against visceral leishmaniasis.
• Of note, the bite of one infected sandfly is sufficient to cause the disease, since a
sandfly can egest more than 1000 parasites per bite.
11. Cutaneous leishmania
Leishmania tropica Most
Cutaneous leishmaniasis common form Characterized by
one or more sores, or nodules
on the skin
Sores can change in size and
appearance over time.
Often described as looking
somewhat like a volcano with a
raised edge and central crater
Sores are painless or painful
12. Cutaneous leishmaniasis
• 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
13. 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.
14. Sores usually are found on exposed areas of skin, especially the
extremities and face.
15. Cutaneous leishmaniasis
• Regional
adenopathy, satellite
lesions, and subcutaneous
nodules can be present.
• Untreated sores can leave
depigmented retracted
scars.
17. • Mucotaneous leishmaniasis (MCL)
cases are focused in South
America, especially in
Mucotaneous leishmaniasis
Brazil, Paraguay, Ecaudor, Bolivia, Peru,
Colombia, andVenezuela. Ninety
percent of the cases occur in
Brazil, Bolivia, and Peru. Twenty
percent of leishmaniasis patients in
Brazil develop MCL. In Ecuador, many
of the cases seem to be focused in the
Amazon region. During the 1990-2003
period, there were 21,805 reports of
MCL mostly from the Amazonian
lowlands, some inter-Andean
valleys, and throughout the Pacific
coastal region. Other infections caused
by various Leishmania species have
occurred in
Ethiopia, Kenya, Namibia, Central
America, Guyana, Surinam, Panam, an
d Sudan.
18. 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.
19. Mucocutaneous leishmaniasis
• 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 (as depicted
below) but usually spares bony structures, and it
can leave extreme disfigurement.
20. Mucocutaneous leishmaniasis
• Cutaneous lesions can be single or multiple.
• Secondary mucosal lesions often develop after the
primary lesion has healed.
• Signs include gingival edema, periodontitis, and
adenopathy.
21. single or multpile lesions and ulcers develop at the mucosal regions
(nose, mouth, throat cavities) and in the adjacent tissue
extensive disfiguring of the nasal septum, lips, and palate (does not include the bones)
23. • L. donovani produces visceral
leishmaniasis or Kala-azar.
Visceral leishmaniasis Kala-azar is an Indian
name, meaning "black fever"
(darkening of the skin).
• Most severe form of the
disease, usually fatal if left
untreated Usually associated
with fever, weight loss, and an
enlarged spleen and liver.
24. • Habitat:- internal organ
(liver, lymph nodes, spleen
Visceral leishmaniasis
,bone marrow)
Disease- Visceral
leishmaniasis, Kala
azar, Dum Dum fever
Transmission- VL. is
transmitted chiefly by
female Sandflies
(Phlebotomus spp.)
25. 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.
26. 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
28. Mucocutaneous leishmaniasis
• Diagnosis preferably is made by culture of the
organism, but organisms are often scant.
• Results from the leishmanin skin test are positive
after 2-3 months of infection.
• Serologic tests are available in some centers and, as
in the cutaneous form, PCR is becoming more
common as a method of diagnosing the disease.
• Because the organisms often are scarce, the
diagnosis often is epidemiologic (travel to endemic
area, clinical picture coupled with laboratory data).
29. Visceral leishmaniasis
• Definitive diagnosis is made by observing the parasite (more
specifically, amastigotes in tissue) on stained Giemsa smears
or by observing the culture of bone
marrow, splenic, hepatic, or lymph node aspirates.
• Cultures are grown on NNN medium
• Serologic testing is useful with the indirect fluorescent
antibody test
• An enzyme-linked immunosorbent assay (ELISA)
• Obtain a complete blood count. Bone marrow infiltration may
cause anemia, thrombocytopenia, and leukopenia with a
relative monocytosis and lymphocytosis.
• Perform liver function tests (LFTs).
• Run a coagulation panel.
30. Cutaneous leishmaniasis
• Diagnosis usually is based on the appearance of the
lesion.
• microscopy of the parasite in Giemsa stains or
histological section can reveal the parasite and should
be attempted first.
• The leishmaniasis skin test (Montenegro test) produces
positive results 3 months after the appearance of
lesions.
• polymerase chain reaction (PCR) is being used more
frequently and is more accurate in determining new-
onset leishmaniasis than serum tests.
32. Cutaneous leishmaniasis
• Treatment of cutaneous leishmaniasis differs according to the
etiology and geographic location of the infection. For certain types
of cutaneous leishmaniasis where the potential for mucosal spread
is low, topical paromycin can be used. If only one or a few small
lesions are present (excluding face or over a joint), careful follow-
up without drug treatment may be appropriate.
• For more invasive lesions (eg, those failing to respond to topical
treatment; metastatic spread to the lymph nodes; or
large, disfiguring, and multiple skin lesions, especially those on the
face, near mucosal surfaces, or near joints), sodium stibogluconate
or pentamidine can be used.
• Other reported treatments include topical imiquimod
cream, cryotherapy, thermotherapy, ketoconazole, photodynamic
therapy, itraconazole, allopurinol, and miltefosine (not FDA
approved, requires Investigation New Drug [IND] application and
local Institutional Review Board [IRB] approval).
33. Mucosal leishmaniasis
• Amphotericin B deoxycholate may be first-line
therapy for advanced mucosal disease.
• Pentavalent antimony for a course of 4 weeks
has been recommended.
• Miltefosine is the only oral medication
approved for both VL and ML.
34. Visceral leishmaniasis
• Be alert for complications related to reticuloendothelial system failure. Patients
may have bleeding or neutropenia leading to infectious conditions such as
pneumonia or diarrhea. Transfusions may be necessary for severe bleeding or
anemia. Antibiotics are indicated to treat intercurrent infectious conditions.
• Outside of India, treatment with a pentavalent antimonial compound usually is
effective. The use of an alternative parenteral agent should be considered even for
first-line therapy in areas where resistance to pentavalent antimony therapy is
prevalent, as it is in India, or if nonantimonial therapy would be advantageous for
other reasons (eg, toxicity profile, duration of therapy).
• A major advance has been the advent of liposomal formulations of amphotericin
B, in which various alternative lipids have replaced deoxycholate.
• Other parenteral alternatives that have merit include amphotericin B (not only in
deoxycholate form but also in liposomal forms) and have generally replaced
pentamidine. Miltefosine, a chemotherapeutic agent, is the first extremely
effective oral agent for visceral leishmaniasis but is not currently available in the
United States. Injectable paromycin has also been reported to be noninferior to
amphotericin B but also is not currently FDA approved.
