life cycle, distrbution, clinical picture, laboratory diagnosis and control measures

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.