Leishmania species are protozoan parasites that cause leishmaniasis. They are transmitted through the bite of infected sand flies. The life cycle involves promastigotes that develop in the sand fly gut and amastigotes that multiply within human macrophages. Leishmaniasis exists in visceral, cutaneous, and muco-cutaneous forms depending on the infecting species and affected tissues. Diagnosis involves identifying amastigotes in tissue samples through microscopy or culturing. Control relies on reducing reservoir hosts and applying preventative measures against sand fly bites.

1. LEISHMANIA SPECIES
By
MontasirGhaneimAlzain
M.Sc in Medical Parasitology / UOF

2. Learning objectives
 By the end of this presentation each student should:
 Know the vectors that transmit the disease.
 Understand the life cycle of leishmania parasite.
 Know the morphology of parasite stages and where they found.
 Know the forms of Leishmaniasis.
 Know the epidemiology of Leishmaniasis forms.
 Know what species of leishmania parasite cause the forms of the
disease.
 Know the laboratory diagnosis of Leishmaniasis.

3. Introduction
 Obligate intracellular parasites which cause a protozoan infection
called Leishmaniasis.
 Discovered in 1900 by William Leishman in the spleen of a soldier
at Dum Dum, India (Dum-dum Fever).
 21 out of the 30 mammalian-infecting species of Leishmania cause
disease in humans
 Transmitted by bite of infected sandy fly (vector borne disease).
 Infection with leishmania spp. can result in three types; visceral
(VL), cutaneous (CL) and muco-cutaneous (MCL) leishmaniasis.

4. Vectors
 6 genus of sand flies are world
wide distribution.
 98 species of genus
Phlebotomus & Lutzomyia
transmit disease to human.
 Most sand flies feed mainly on
plant juices, but female flies
also require blood meals for egg
development.

5. Life cycle
 The parasite are transmitted by the bite of an infected female sand
fly, belonging to the genus Phlebotomus (Africa, Asia and Europe)
and the genus Lutzomyia (in the Americas).
 A person becomes infected when promastigotes are inoculated when
the vector takes a blood meal.
 The macrophages engulph promastigotes which develop into
intracellular forms called amastigotes.
 The amastigote multiply, rupture from the macrophages and infect
new cells.

6. Life cycle
 In visceral leishmaniasis the amastigotes multiply in the macrophages of
the spleen, liver, bone marrow, lymph glands (tissues of the
reticuloendothelial system). Blood monocytes are also infected.
 In cutaneous and muco-cutaneous leishmaniasis the parasites multiply in
skin macrophages (histiocytes).
 The intracellular and free amastigotes are ingested by a female sand fly.
 After about 72 hours, the amastigotes become flagellated promastigotes in
the midgut of the sand fly. They multiply and fill the lumen of the gut.
 After 14–18 days (depending on species), the promastigotes move forward
to the head and mouth-parts of the sand fly.

8. Morphology of amastigotes & Promastigotes
Amastigotes:
 The amastigote of VL, CL and MCL are similar,
but there are variations in size between species.
 Small, round to oval bodies measuring 2–4µm.
 Can be seen in groups inside blood monocytes
(less commonly in neutrophils), in macrophages
in aspirates or skin smears, or lying free between
cells.
 The nucleus and rod-shaped kinetoplast in each
amastigote stain dark reddish-mauve.
 The cytoplasm stains palely and is often difficult
to see when the amastigotes are in groups.

9. Morphology of amastigotes & Promastigotes
Promastigote:
 Long slender body.
 Size 9-15 μm in length.
 The large single nucleus is
located in or near the center.
 The kinetoplast is located in
the anterior end.
 A single free flagellum
extends anteriorly from the
axoneme.

10. VISCERAL LEISHMANIASIS

11. Introduction
 Called Dumdum fever or Kalaazar.
 Caused by Leishmania donovani complex (L. donovani,
Leishmania infantum, and Leishmania chagasi).
 The disease may also be referred to as Old or New World
according to geographic location of the species of
Leishmania involved.
 After inoculation, parasites infect the reticuloendothelial
system and live inside the macrophages (intracellular).

12. Epidemiology
 The L. donovani complex is composed of:
 L.donovani (India, Pakistan, Thailand, parts of Africa and China).
 L. infantum (Mediterranean area, Europe, Africa, and parts Soviet Union).
 L. chagasi (Central and South America).
 Transmitted by Phlebotomus sand fly (L. donovani and L. infantum) and Lutzomyia sand fly
(L. chagasi).
 Dogs, cats and foxes are reservoir host.
 In 2014, more than 90% of visceral leishmaniasis cases occurred in six countries: Brazil,
Ethiopia, India, Somalia, South Sudan and Sudan.
 Visceral Leishmaniasis in Sudan reported from the Upper Blue Nile, Blue Nile and Kassala,
Darfur and Kordofan. Outbreaks have also occurred north of Khartoum along the Nile River.

13. Signs & symptoms
 Often present with a nondescript abdominal illness and
hepato-splenomegaly.
 A papule occurs rarely at the bite site.
 Early stages of disease may resemble malaria or typhoid fever
with the development of fever and chills.
 The onset of these symptoms is gradual and follows an
incubation period ranging from 2 weeks to 18 months.
 Diarrhea, anemia and jaundice may be present.

14. Signs & symptoms
 Weight loss and emaciation tend to occur following
parasitic invasion of the liver and spleen.
 In advanced stages of disease, kidney damage occurs.
 A characteristic darkening of the skin may be noted
(this symptom is referred to by the common disease
name, kalazar, which means black sickness.
 Chronic cases usually lead to death in 1 or 2 years.

15. hepatosplenomegaly

16.  weight loss
 Emaciation

17. Jaundiced hands

18. Black skin (KALAZAAR)

19. Post kala-azar dermal leishmaniasis (PKDL)
 Its a cutaneous form of leishmaniasis which present in India and
occasionally in East Africa (endemic in India and Sudan).
 Can occur about 2 years after treatment and recovery from visceral
leishmaniasis.
 Hypopigmented and raised patches can be found on the face, body
and limbs. These may develop into nodules similar to those of
lepromatous leprosy, fungal infections or other skin disorders.
 Occasionally there is ulceration of the lips and tongue.
 Amastigotes are present in the papules and nodules.

20. PKDL

21. Lab diagnosis
 Aspiration (spleen, bone marrow or an enlarged lymph
node).
 Peripheral blood monocytes and less commonly in
neutrophils (buffy coat preparations).
 Spleen aspirate . . . . .. . . . . . . . . .. . 95–98%
 Bone marrow aspirate . . . . . . . . . . 64–86%
 Enlarged lymph node aspirate . . . . 55–64%
 Buffy coat ……….. . . . . . . . . . . . . . . 67–99%

22. Lab diagnosis
 Culture technique.
 Serological test:
 IFA (indirect fluorescent antibody).
 ELISA (enzyme-linked immunosorbent assay).
 DAT (direct agglutination test).
 The Montenegro skin test.

23. CUTANEOUS & MUCO-CUTANEOUS
LEISHMANIASIS

24. Introduction
 Skin ulcers on some parts of the body, such as the face, arms and legs
which caused by Leishmania mexicana complex, Leishmanina braziliensis
complex and Leishmania tropica complex.
 Painless lesion at site of bite, multiplication of parasite in histocytes, Kill
histocytes, Necrosis of epidermis , which lead to ulceration.
 Old world cutaneous Leishmaniasis (oriental sores, Baghdad boils), which
caused by Leishmania tropica complex.
 New world cutaneous and muco-cutaneous Leishmaniasis (chiclero ulcer
or bay sore), which caused by Leishmania mexicana complex and
leishmanina braziliensis complex.

25. Epidemiology
 L. mexicana complex is composed of:
 L. mexicana (Guatemala and Mexico).
 L. pifanoi (Amazon River basin and Venezuela).
 L. amazonensis (Amazon basin of Brazil).
 L. venezuelensis (Venezuela).
 L. garnhami (Venezuela).
 The Leishmania tropica complex is composed of:
 L. tropica (Mediterranean region, Middle East, Armenia, Afghanistan, India, and Kenya).
 L. aethiopica (Ethiopia, Kenya, and Southern Yemen).
 L. major (Sudan, Turkmenistan, Uzbekistan, and Kazakhstan, Northern Africa, Iran, Syria
and Jordan).

26. Epidemiology
 L. braziliensis complex is composed of:
 L. braziliensis.
 L. panamensis.
 L. peruvania.
 L.b.braziliensis causes the most sever form and destructive
form of Muco-cutaneous leishmanaisis, parasites migrate to
tissues of nasopharynx and the palate.
 This may lead to complete destruction of nasal septum and
perforation of the palate.

27. Epidemiology
 Members of L. mexicana and L.barzilinesis complex are
transmitted by Lutzomyia sand fly while Leishmania tropica
complex by Phlebotomus sand fly.
 Forest rodents are the reservoir host in L. mexicana complex
while dogs and rodent in Leishmania tropica complex.
 Areas with cutaneous Leishmaniasis in Sudan include Darfur,
Kordofan, central Sudan, and north of Khartoum along the
Nile River.

28. Signs and symptoms
 Usually characterized by a single
or more ulcer looks like (volcano
crater), which is generally self
healing.
 Approximately 40% of
infections affect the ear and can
cause serious damage to the
surrounding cartilage (New
world).

32. Lab diagnosis
 By using Giemsa-stained prepared smears
from ulcers material for the typical
amastigotes.
 Culture technique.
 Serologic test.

33. Prevention & control
 Public awareness through education programs in endemic areas
and exercising personal protection against contact with sand flies.
 Treatment of infected patients.
 Suppress the reservoir such as dogs, rats, and rodents
 Suppress the vector: Critical to preventing disease spreading.
 Prevent sand fly bites by Personal Protective Measures such as
clothes and insect repellent.
 Production of a vaccine against Leishmania spp. is ongoing.