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1. Medical Parasitology
Dr : Ashraf Gaber Timsah
Lecturer of Parasitology
Damiatta Faculty of
Medicine
Al-Azhar university

2. •BLOOD FLAGELLATES
(Haemoflagellates)
• (Leishmania and
Trypanosoma)

3. BLOOD FLAGELLATES
(Haemoflagellates)
(Leishmania and
Trypanosoma)
• Haemoflagellates are term used
for flagellated parasite which
live in the blood or tissues of
man.

4. There are 2 types occur
in man:
• Leishmania with morphological form
amastigote in man.
• Trypanosoma with morphological form
trypomastigote. Other forms may
found in insect vectors and culture
media as epimategote and
promastigote.

5. Morphology of
haemoflagellates:
• 1. Leishmania. Has only 2 stages
during it life cycle.
• Amastigote or leshmanoid from:
found in man living intracellulary
inside reticulo-endothelial cell.
• Promastigote or leptomonad form:
found in the culture media and insect
vector living intracellulary in the cells
of the lumen of alimentary

6. 2. Trypanosoma. Have 2
stages
• Epimastigote or Crithidia.
Crithidia similar to leptomonas but
differ in following feature. Presence of
small undulant membrane.
• Trypomastigote. Similar to crithidia
but differ in the following.

7. Leishmaniaiasis
Leishmaniasis is the collective name for a
number of diseases caused by protozoan
flagellates of genous leishmania , which have
diverse clinical manifestations

8. •The leishmaniasis is endemic in 88
countries on five continents—Africa, Asia,
Europe, North America and South America.
•350 million people at risk.
•12 million people are affected by
leishmaniasis
•1.5-2 million new cases of leishmaniasis
estimated to occur annually.
• 500 000 new cases of VL which occur
annually
GEOGRAPHICAL DISTRIBUTION

9. Morphology:
As mentioned before Leishmania
occur in 2 forms during its life cycle.
The first is Leishmaniod form or
amastigote in man and reservoir host
and the second is leptomonad form or
promastigote in insect vector and
culture medi

10. Promastigote
(leptomonad) form

11. Amastigote form
Leishmania organism.

12. Vertebrate hosts

13. Vector of Leishmania
Phlebotomus(sandfly )
Larvae of sandfly

14. Classification of
leishmania:
according to clinical picture
(A) Cutaneous Leishmaniasis.
Benign self-healing lesion limited to skin
occurs in 2 forms:
Diffuse cutaneous leishmaniasis. Rare form
with L. aethiopica in Old World and with L.
mexecama in New World.
Granulomatous cutaneous. leishmaniasis.
Restricted to L. tropica infection in the Middle
East.

15. (B) Visceral
leishmaniasis.
generalized infection of the reticulo-
endothelial system with visceral and
bone marrow involvement. It occurs in
old and New Worlds.

16. Life cycle of species of
Leishmania

17. 1. Leishmaniasis is transmitted by the bite of
female phlebotomine sandflies. The sandflies
inject the infective stage, promastigotes,
during blood meals.
2. Promastigotes that reach the puncture
wound are phagocytized by macrophages.
3.They transform into amastigotes.
4. Amastigotes multiply in infected cells and
affect different tissues.
5. Sandflies become infected during blood
meals on an infected host.
6. In the sandfly's midgut, the parasites
differentiate into promastigotes.
7. They multiply and migrate to the proboscis.

18. Mode of infection:
biting of human by female sand fly
and inoculation of promastigote
in their blood which changed in to
amastigote.

19. Cutaneous Leishmaniasis
(CL)Classified according to their geographical distribution into:
(A) Old world cutaneous leishmaniasis (OWCL). Caused
by leishmania tropica complex which include.
1- L tropica. Causes dry, urban or oriental sore.
• Dry painless ulcers 25–70 mm in diameter which are self-
healing usually after 1–2 years but often leave disfiguring
scars.
• Present in Mediterranean region, Middle East, Asia and
Africa in people living in big cities.
• Dogs are reservoir hosts.
• The patient is immune to reinfection. Rarely there may
develop single or multiple unhealing lesions, often on
exposed parts specially face.

20. 2- L. major. Infection is often
referred to as wet or rural
××××oriental sore.
• Present in middle east, Asia and in rural area of
Africa. The early papule is often multiple,
inflamed and resembles a boil of 5–10 mm in
diameter which rapidly develops into a large ulcer
which is self-healing within 3–6 months. Lesion
occurs in the lower limbs with moist serous
exudates and tends to ulcerate early with secondary
bacterial infection. L. major infections protect
against reinfection and also against infection with L.
tropica.

21. 3- L. aethiopica. Can cause diffuse
cutaneous leishmaniasis
• A cutaneous lesion is produced that is similar to
typical oriental sore with healing in 1–3 years. L.
aethiopica can cause diffuse cutaneous
leishmaniasis (DCL) in patients with little or no cell
mediated immunity against the parasite. This
condition characterized by the formation of
disfiguring nodules over the surface of the body
resembling lepromatous leprosy.
• L. aethiopica can also cause mucocutaneous
leishmaniasis.

22. (B)New world cutaneous leishmaniasis
(NWCL).
Present in the central and south
America.
Rodents, cats and dogs are reservoir
hosts.
Vector by Lutzomyia species. It is
caused by

23. •L. Mexicana. Causes chiclero’s
ulcer or ‘bay sore’
• Lesions of the body tend to be self-
healing but those on the ear may last
up to 30 years and entirely destroy
the ear pinna and cartilage. It occurs
in forest worker who collect the chicle
gum.
• L. peruviana. Mainly infect children.
Single or few lesions are painless, L
.tropica. The infection is known
locally as ‘uta’. It occurs at high
altitudes in dry valleys.

24. • L. guyanensis. May give rise to
painless dry single ulcers or multiple
lesions scattered all over the body.
The disease is often referred to as
‘forest yaws’ (‘pianbois’).
• L. panamensis. Causes single or few
skin ulcers which are not self-healing.
Lymphatic involvement is common,
resulting in secondary nodules.
• L.pifanoi. lesion starts single and
spread slowly like lepromatous
leprosy and does not ulcerate or heal.

25. NB. Other type of leishmania is
mucocutaneous leishmaniasis
(MCL) or ‘Espundia’.
MCL is caused by New World
Leishmania species, L. braziliensis, L.
panamensis and occasionally by L.
guyanensis.
MCL is the most severe and
destructive form of cutaneous
leishmaniasis in South America.
Lesions are similar in development to
those of oriental sore and the
resulting ulcers may become very

26. Different clinical form of
Cutaneous Leishmaniaiasis
1) Old world C.L.
2) New world C.L.
AnthroponoticC.L.(L.tropica(
(Dry sore or Urban C.L.(
C.L.( L.major(
(Wet sore or Rural C.L.(
Diffuse or Disseminated C.L.
(L. aethiopica(
Cutaneous L.(L. mexicana Complex(
(Chiclero ulcer(
CL ( L. braziliensis(
(spoundia or Uta(

27. Urban C. leishmaniasis
(Dry sore)

28. Lesions of C.L.
( Wet sore)

29. Reservior hosts
of C.L

30. Different form of
C. leishmaniasis

31. DIAGNOSIS OF CUTANEOUS AND
MUCOCUTANEOUS LEISHMANIASIS
• Clinically.
• Detecting amastigotes in smears taken from infected
ulcers or nodules. In MCL, the parasites are scanty
and difficult to find in smears.
• Culturing ulcer material and examining cultures for
promastigotes.
• Serological diagnosis of CL and MCL. Because of
the poor antibody response in CL, serological tests
are of little value in diagnosis.
• Leishmanin skin test (Montenegro test).

32. Visceral leishmaniasis
(kala-Azar, black fever or Dum-dum
fever)
• This disease caused by leishmania donovani
complex which is.
• L. donovani. Present in India, China, Africa, East
and scattered area of central Africa. Common in
young adults from 10-25 years.
• L. infantum (L. chagasi). In the Mediterranean
region, Europe, Middle east and parts of Africa
common below the age of four years.
• L. amazonensis. Central and south America. can
affect children.

33. • Reservoir hosts: dogs except in India man
is only reservoir and rodents.
• Vector: are Lutzomia species of sand fly.

34. Life cycle and pathology:
• Life cycle as before in cutaneous leishmaniasis but
in visceral leishmaniasis the amastigotes multiply in
the macrophages of the spleen, liver, bone marrow,
lymph glands, mucosa of the small intestine and
other tissues of the reticuloendothelial system.
Blood monocytes are also infected. In cutaneous
leishmaniasis the parasites multiply in skin
macrophages (histocytes).

35. The affected organ shows.
• Erythropiosis. Become depressed and life span of
granulocytes and erythrocytes is reduced
granulocytopenia and anaemia.
• Spleen. demonstrates atrophy of white pulp with
necrosis and fibrosis.
• The liver. show atrophy of liver cell with cloudy
swelling and fatty degeneration.
• Some liver function remains normal but there is
hypoalbuminaemia with oedema and ascites.
• Intestine. Atrophy of velli and crypts

36. CLINICAL PICTURE:
This is the most severe form of leishmaniasis, adults
and children are being affected.
Incubation period 4 to 6 months.
• Local lesion in small non ulcerating cutaneous
nodule (leishmanioma) that precedes systemic
manifestation.
• fever (double daily rise with chills and sweating).
• Diarrhea and dysentery are common.
• Splenomegaly (hard, huge and not tender),
Hepatomegaly and generalized lymphadenopathy.

37. • Pancytopenia (anaemia, leucopenia,
lymphocytosis and thrombocytopenia).
• Epistaxis (nose bleed) and bleeding from the
gums.
• Hypeprigmentation especially on hand, feet,
forehead and abdomen.
• Jaundice and oedema

38. Post kala-azar dermal
leishmaniasis (PKDL).
• In India and occasionally in East Africa, a cutaneous
form of leishmaniasis can occur about 2 years after
treatment and recovery from visceral leishmaniasis
or incomplete treatment. This is referred to as post
kala-azar dermal leishmaniasis. It appears as
Hypopigmented patches or may develop as nodules
and resemble 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
of this lesion.

39. Clinical Features of
visceral leishmaniasis

40. Complication:
• As immunosuppression and secondary infection as
pulmonary T.B.Progressive loss of weight and
weakness in limbs and chest wall. Death occur from
month to 1 or 2 years due to intercurrent infection
• Relapse: Recurrence of clinical attack similar to
primary disease resulting from in sufficient
treatment or intercurrent infection.

41. Diagnosis
• Clinicl picture.
• Detection of the parasite
-Sample: Bone marrow, spleen and lymph node
aspirations.
-Detection methods: the sample taken may be
Smeared on to a microscopic slide and stained by
leishman OR Giemsa stain for (amastigote).
Amastigotes are typically intramonocytic (the
nucleus and kinetoplast staining purple).
-Cultured on NNN media for (promastigotes):
-PCR technique for detection parasite DNA.

42. Microscopy finding
A B

43. • Immunological diagnosis: detect circulating
specific antibodies IgG.
• Indirect fluorescent antibody technique (IFAT, the
most commonly used).
• Immuno-electrophoresis.
• Indirect haemagglutination test
• Immunoblot, ELISA and fast-ELISA.
• The leishmanin test (Montengro): The leishmanin
skin test measures delayed-type hypersensitivity.

44. Treatment
• Visceral leishmaniasis:
• pentavalent antimonial (Pentostam) at a dose of 20
mg /kg per day for 28 day.
• pentamidine. 2–4 mg/kg intramuscular every other
day up to 15 doses.
• Allopurinol : 20 mg/kg daily in 3 divided dose
orally for AIDS patients.
• Amphotericin B. used in first intention, with five
daily injections (3 mg/kg per injection), and a final
injection on the 10th day.
• Correcting nutritional deficiencies and ttt of

46. • Localized cutaneous leishmaniasis:
• Diffuse cutaneous Leishmaniasis.
Combination of paromomycin and antimonial.
• Mucocutaneous Leishmaniasis.
Systemic treatment of the primary cutaneous lesion
by pentavalent antimonial, 20-day course of i.m.
injections, 20 mg /kg per day.

47. prevention and control of leishmaniasis.
• Early detection and treatment of infected persons.
• Vector control.
• Destruction of stray dogs and infected domestic
dogs.
• vaccination in endemic.