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1. Epimastigote
Hemoflagellates of medical importance
There are 4 parasitic stages (or forms):
• Amastigote & Trypomastigote occur in vertebrate hosts
• Promastigote & Epimastigote occur in invertebrate hosts
Amastigote Trypomastigote Promastigote
Leishmania spp. & Trypanosoma spp.
have digenetic life cycles, involving vertebrate hosts (Man &
reservoir animals) and invertebrate hosts (arthropods) 

2. Leishmaniasis
Genus: Leishmania
Disease: Leishmaniasis.
• Leishmaniasis is classified according to
its clinical picture & geographical
distribution:
I- Cutaneous leishmaniasis
• A- Old World Cutaneous leishmaniasis.
• B- New World Cutaneous leishmaniasis.
II- Mucocutaneous leishmaniasis
• A- New World Mucocutaneous
leishmaniasis.
III- Visceral Leishmaniasis.
• A- Old World Visceral leishmaniasis.
• B- New World Visceral leishmaniasis.
• --

3. Geographical distribution of cutaneous
leishmaniasis

4. Geographical distribution of cutaneous
leishmaniasis in Saudi Arabia.

5. Cutaneous Leishmaniasis
Infective stage
Promastigote or Amastigote.
Transmission
1- Biological:
Bite of infected female ♀ sand flies.
(Infective stage >>> Promastigote form).
2- Mechanical:
Direct contact and autoinfection.
(Infective stage >>> Amastigote form).
Most common form(s) of Leishmaniasis.

6. 6
Female sand flies
Male
Female
Vector

7. The life cycle of Leishmania

8. The life cycle of Leishmania

9. Life cycle of Leishmania [Cutaneous and
Mucocutaneous] in humans and reservoir animals

10. Life cycle of Leishmania species
The infective stage is transmitted by the bite of
blood-feeding female sand flies (Phlebotomus or
Lutzomyia) which carries the promastigote in the
anterior gut and pharynx.
It get engulfed by local macrophages where it
transform into amastigotes and divides until the
infected cell ruptures. The released organisms
infect other cells.
The sand fly acquires the organisms during its meal,
the amastigotes transform into flagellate
promastigotes and multiply in the gut until the
anterior gut and pharynx are packed.
Salivary glands are not invaded.

11. Cutaneous leishmaniasis gives solid immunity

12. C/P of Cutaneous leishmaniasis
Clinically differs according to the species of the parasite & the
immunity of the patient
 Old World CL: caused by
L. tropica complex (L. tropica, L. major & L. aethiopica).
 New World CL: caused by
L. mexicana & L. braziliensis complexes.
Classical lesion
The lesion starts at the site of insect bite as a Papule >>> Nodule;
due to multiplication of Leishmania form in skin macrophages
followed by granulomatous reaction around them; then >>>
ulcerates and the ulcer heals leaving a disfiguring scar.

13. A- Old World Cutaneous Leishmaniasis
L. tropica complex
Leishmania tropica
causing
Chronic, dry or urban Cutaneous Leishmaniasis:
Painless ulcer or Oriental sore.
Leishmania major
causing
Acute, wet or rural Cutaneous Leishmaniasis.
Leishmania aethiopica
Causing
Diffuse (Disseminated) Cutaneous Leishmaniasis.

14. Chronic, Dry or Urban OWCL
[caused by L. tropica].
Reservoir host: Dogs.
Incubation period: 2-8 months.
Distribution:
Occurs in Mediterranean region, Middle East, parts of
Africa & Asia (mainly in urban areas).
It give the following lesions:

15. Painless ulcer or Oriental sore
 The lesion starts as a single red prurtic papule on the exposed parts
of the body.
 It is dry, painless, increases in size, ulcerates and crusts after
several months.
• The ulcer [Oriental sore] has sharp cut edges, raised indurated
margin (volcano like), with scanty exudates.
• 2nd bacterial infection may occurs.
• Healing takes place spontaneously in about 1-2 years leaving
depigmented flat, atrophic, disfiguring scar.
• parasites are seen only in the edges
 This lesion is common in Saudi Arabia.

16. Painless ulcer or Oriental sore

17. Acute, Wet or Rural OWCL
[caused by L. major]
Reservoir host: Rodents.
Incubation period: 2-6 weeks.
Distribution: Occurs in the desert areas of Middle
East, Asia, Africa [mainly in rural areas].
It is common in Saudi Arabia
The Lesions are multiple, painless, severely
inflamed, moist with serous exudates and rapidly
ulcerating.
2nd bacterial infection is common.
Healing takes place within 3-6 months, leaving large
disfiguring scars.

18. [2] a- Acute, wet or rural OWCL

19. Diffuse; Disseminated; Cutaneous Leishmaniasis
[Caused by Leishmania aethiopica]
Distribution:
L. aethiopica occurs mainly in Ethiopia,
Kenya & south Yemen.
The parasite causes chronic form with late
ulceration but is usually proliferate
indefinitely [due to deficient cell-mediated
immunity] Producing
Diffuse Cutaneous Leishmaniasis

20. Diffuse; Disseminated; Cutaneous Leishmaniasis
[Cont.].
It takes the form of widely
disseminated thickening of the skin
(papules or multiple non ulcerative
nodules) on the face & exterior surface
of limbs.
The lesion is non self healing &
similar to Lepromatous leprosy

21. Parasite:
L. braziliensis complex & L. mexicana complex.
Distribution: Occurs in Central & South America.
Reservoir hosts: Forest rodents & dogs.
Vector: ♀ Sand fly, genus Lutzomyia.
The clinical features are similar to those of OWCL but lesions
tend to be more severe & chronic.
B- New world cutaneous and mucocutaneous
leishmaniasis [NWCL]

22. B- New world cutaneous and mucocutaneous
leishmaniasis [NWCL]
[1] Leishmania braziliensis complex
 a. Mucocutaneous Leishmaniasis or Espundia:
Caused by L. braziliensis.
 b. Uta: Caused by L. peruviana;
Single or few painless skin ulcers that heal spontaneously.
[2] Leishmania Mexicana complex
 a. Chiclero’s ulcer or Bay sore.

23. II- Mucocutaneous Leishmaniasis or Espundia
Pathology & Clinical picture
 L. braziliensis produces single or
multiple lesions;
 Similar to oriental sore; that undergo
extensive ulceration.
 After months or years, lymphatic spread
to mucous membranes of nose, mouth &
ear may occur >>>
 hypertrophy, destruction, severe pain &
great deformity .

24. Mucocutaneous Leishmaniasis or Espundia
[Cont.]
Disfiguration is often extreme with
complete destruction of the nasal
septum, perforation of the palate and
damage to the tissues of the lips and
larynx.
It is accompanied with fever,
anaemia & loss of weight.
Death occurs as a result of 2nd bacterial
infections or malnutrition.

25. Chiclero’s ulcer or Bay sore
Occurs in forest workers [Chicle collectors].
It is a single painless lesion mainly affects the ear
causing
destruction of cartilage & heal spontaneously within 6 months.
Chiclero’s ulcer or Bay sore

26. Diagnosis of Cutaneous leishmaniasis
I. Clinical Diagnosis:
- History: Residence or traveling to endemic area.
- Clinical picture.
II. Laboratory Diagnosis
1- Direct Methods.
2- Indirect methods:
a- Intradermal skin test
[Leishmanin or Montenegro's test]:
It is a delayed hypersensitivity skin test.
Positive test [˃ 95%] >>> induration more than 5 mm at
site of injection after 48 hours.
It is –ve in D.C.L. (since there is deficiency in cell
mediated immunity).
b- Aspirate or biopsy >>> PCR
to diagnose & type the species.
Killed Leishmania
from culture
(leishmanin antigen)
are injected in the
arm

27. 1- Direct Laboratory Methods
a- Aspirated tissue juice, scraping or biopsy
material from raised nodule or raised edge of the
ulcer & from mucosal scraping in
mucocutaneous type to detect the parasite after:
 preparing smears & staining with Giemsa or
Leishman stains >>> Amastigote form.
b- Inoculation in culture [NNN medium] >>>
Promastigote form.
c- Animal inoculation >> Amastigote form.
Amastigote
Promastigote

28. Aspiration and biopsy from the ulcer
Aspiration
Scrape or take biopsy
Leishmania
amastigotes
(Giemsa stained)

29. Laboratory Diagnosis
Sample collection
From the edge of the ulcer

30. Treatment
1- Non inflamed-non ulcerated lesion:
Intra- lesional injection of pentavalent antimonial or 5%
mepacrine, 1-3 times at 3-5 days interval.
2- Inflamed or ulcerated lesions, multiples lesions,
or lesions on sites where scarring might produce
disability or disfigurement: Pentostam I.V or I.M.,
10:20 mg/kg/day for 10 days.
3- I.D. injection of interferon gamma around the
lesion to promote healing of the ulcer.
4- Antibiotics: for 2nd bacterial infections
5- Local application of heat to 37- 43 ºC.
6- Surgical removal, CO2 snow or X-ray.

31. Prevention & control
 1- Treatment of cases, control of vector &
reservoir hosts.
 2- Proper dressing of the ulcer [Why ???].
 3- Active immunization on concealed parts of
body in endemic areas.
 4- Protection: by using wire screens, repellents
& mosquito nets

32. Leishmaniasis in KSA
L. major
L. tropica
L. infantum
Species
L. tropica
L. major
L. infantum
Regions
(CL) Al-Ahsa,
Ha’il, Medinah
(VL) Jazan,
Aser, Bishah
Type of Disease
Oriental sore
Wet, acute, rural sore
80-90% in < 10 years old

33. Disease
SPECIES
Cutaneous
Leishmaniasis
Leishmania tropica *
Leishmania major *
Leishmania aethiopica
Leishmania mexicana
Mucocutaneous
Leishmaniasis
Leishmania braziliensis
Visceral
Leishmaniasis
Leishmania donovani *
Leishmania infantum *
Leishmania chagasi
* Endemic in Saudi Arabia
Leishmania species & Disease