1. بسم الله الرحمن الرحيم

4. Visceral, Mucocutaneous and Cutaneous Leishmaniasis
Leishmaniasis is a diseases of different clinical manifestations .
Leishmania donovani
home the liver and spleen causing (usually fatal) visceral leishmaniasis;
2. Leishmania brasiliensis
homes the lining of the nose and throat causing the mucocutaneous disease,
3.Leishmania tropica
homes the skin causing the self limiting skin ulcers, called cutaneous leishmaniasis

5. L. tropica L. braziliensis LEISHMANIASIS species of Leishmania :
L. donovani
causes visceral leishmaniasis
(Kala-azar, black disease, dumdum fever);
L. tropica
(L.t.major, L.t. minor and L.ethiopica) cause
cutaneous leishmaniasis
(oriental sore, Delhi ulcer, Aleppo,or Baghdad
boil).
L. braziliensis
( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).

6. -Amastigote (leishmanial form) is oval and measures 2-5 microns
Morphology
-Amastigote (leishmanial form)
is oval and measures 2-5 microns
-Leptomonad (promastigote form)
measures microns
a similar size to trypanosomes

7. South east Asia, Indonesia, Pakistan, Mediterranean,
Epidemiology Leishmaniasis is prevalent world wide:
South east Asia, Indonesia,
Pakistan,
Mediterranean,
North and central Africa,
South and central America.

9. * Endemic in Saudi Arabia
Disease
Species
Cutaneous leishmaniasis
Leishmania tropica*
Leishmania major*
Leishmania aethiopica
Leishmania mexicana
Mucocutaneous
leishmaniasis
Leishmania braziliensis
Visceral leishmianiasis
Leishmania donovani*
Leishmania infantum*
Leishmania chagasi
* Endemic in Saudi Arabia

10. zoonotic cutaneous leishmaniasis: wet lesion with sever reaction.
Types of cutaneous leishmaniasis
* L.major:
zoonotic cutaneous leishmaniasis:
wet lesion with sever reaction.
. * L.tropica:
Anthroponotic cutaneous leishminiasis: dry lesions with minimal ulceration.
Oriental sore (most common)
classical self-limited ulcer.

11. Leishmania major –wet lesion

12. Leishmania tropica: dry type

16. Uncommon types
* Diffuse cutaneous leishmaniasis (DCL): caused by L. aethiopica, diffuse nodular non-ulcerating lesion.
low immunity to leishmania antigens, numerous parasites.
* Leishmaniasis recidiva
(lupoid leishmaniasis):
sever immunological reaction to leishmania antigen leading to persistent dry skin lesions,
few parasites.

17. 1-Diffuse cutaneous leishmaniasis 2-leishmaniasis recidiva (lupoid)

20. Life cycle
The organism is transmitted by blood-feeding sand flies (Phlebotomus) which carry the promastigote .
The parasites gain to mononuclear phagocytes where they transform into amastigotes and divide, infected cell ruptures. The released organisms infect other cells.
The sand fly take the organisms during the blood meal; the amastigotes transform into flagellate promastigotes and multiply in the gut.
Dogs and rodents are common reservoirs.

22. Cutaneous leishmaniasis
Pathology
Cutaneous leishmaniasis
(Oriental sore, Delhi ulcer, Baghdad boil):
the organism (L.tropica) multiplies locally, producing a papule .
The papule gradually grows to form a relatively painless ulcer.
The ulcer heals in 2-10 months, even if untreated but leaves a disfiguring scar .
The disease may disseminate in the case of depressed immune function.

24. Mucocutaneous leishmaniasis
(espundia, Uta, chiclero)
It is the same as those of cutaneous leishmaniasis, but the lesions spread to near mucous membrane (oral, pharyngeal and nasal) lead to their destruction and hence sever deformity .
The organisms responsible are L. braziliensis, L. mexicana.

25. mucocutaneous leishmaniasis

26. Cutaneous and mucocutaneous
Diagnosis:
Cutaneous and mucocutaneous
1. aspirate material from edge of ulcer and
stain (Giemsa). 2. biopsy - pathology sections.
(amastigotes = Leishmania donovani
bodies =LD bodies) are seen in
macrophages of aspirate and biopsy. 3. culture aspirate or biopsy material in
special media (NNN) producing
promastigotes.

27. Treatment Medical pentavalent antimony Surgical
No treatment- It self healing lesions.
Medical pentavalent antimony
(Pentostam), Amphotericin B.
+/- Antibiotics for secondary bacterial
infection.
Surgical
- Cryosurgery
- Excision
- Curettage

29. L. tropica L. braziliensis LEISHMANIASIS species of Leishmania :
L. donovani
causes visceral leishmaniasis
(Kala-azar, black disease, dumdum fever);
L. tropica
(L.t.major, L.t. minor and L.ethiopica) cause
cutaneous leishmaniasis
(oriental sore, Delhi ulcer, Aleppo,or Baghdad
boil).
L. braziliensis
( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).

30. Leishmania donovani visceral leishmaniasis L
Leishmania donovani visceral leishmaniasis L.infantum :mainly in infant L.donovani :mainly in adult

33. * Endemic in Saudi Arabia
Disease
Species
Cutaneous leishmaniasis
Leishmania tropica*
Leishmania major*
Leishmania aethiopica
Leishmania mexicana
Mucocutaneous
leishmaniasis
Leishmania braziliensis
Visceral leishmianiasis
Leishmania donovani*
Leishmania infantum*
Leishmania chagasi
* Endemic in Saudi Arabia

36. L.Donovani -visceral leishmaniasis

37. (kala-azar, dumdum fever)
pathology
Visceral leishmaniasis
(kala-azar, dumdum fever)
Organismes are localized and multiply in the mononuclear phagocytic cells of spleen, liver, lymph nodes, bone marrow, intestinal mucosa and other organs.
fever.
Hepatosplenomegaly.

38. (relative monocytosis and lymphocytosis) -anemia and thrombocytopenia
Bone marrow:
-leukopenia
(relative monocytosis and lymphocytosis)
-anemia and thrombocytopenia
hyperpigmented granulomatous skin
(kala-azar means black disease).
Chronic disease renders patients susceptible to other infections.
Untreated disease results in death.

39. Post kala- azar dermal leishmaniasis

40. Presentation Fever . splenomegaly, hepatomegaly, hepatosplenomegaly
Weight loss.
Anemia, Epistaxis.
Cough, Diarrhea.
Untreated case can be fetal.
After recovery may be post
kala –azar dermal leishmaniasis.

41. Parasitological diagnosis
*. bone marrow aspirate or spleen
puncture and stain (Giemsa) .
*.culture material aspirated on
(NNN).
.Lymph node least sensitive.
.tissue biopsy

42. 1-Bone marrow biopsy 1 2
3-promastigotes
2- rosette shape promastigotes

43. Serological diagnosis:
- direct agglutination test, ELISA,
IFAT.
- Skin test leishmanin test for survey
and follow up after treatment.
- non spesfic detection of
hyper-gammaglobulinemia by
formaldehyde (formol gel test ) or
by electrophoresis.
- PCR

44. Treatment - Pentavalent antimony
(Pentostam) is the drug of choice.
- Amphotericin B.
- Treatment of anemia, bleeding, and
infection.

46. African trypanosomiasis

47. African trypanosomiasis
2 species:  
-Trypanosoma brucei gambiense
(Africa :west of Rift valley) -Trypanosoma brucei rhodesiense
(Africa :east of Rift valley)

49. The reservoir Humans and wild animals (zoonosis) The vector
Glossina (Tsetse) flies   

50. Glossina

51. African Trypanosomiasis
(African Sleeping Sickness) A hemo-flagylate found only in Africa.
In East Africa disease, transmitted from resevoir animal to man by the vector tsetse fly (Glossina) zoonosis.
In west Africa it is transmitted by tsetse human to human..

53. Life cycle
The infective metacyclic trypanosome is injected into host during a bite by tsetse fly .
it enters the draining lymphatic and blood stream.
The trypanosomal form enters the vector during the blood meal and travels through the alimentary canal to the salivary gland where it proliferates as epimastigotes form and matures to infectious metacyclic forms.

55. Pathogenesis
Tsetse bites man and injects saliva containing trypanosomes into the wound.
These multiply locally producing a local lesion.
trypanosome multiplies by binary fission extracellularly producing fever and lymphadenopathy .
then reaches the central nervous system producing a meningoencephalitis.

56. Lymphatic &

57. Trypomastigotes can traverse the walls of blood and lymph capillaries into the connective tissues
at a later stage, cross the choroid plexus into the brain and cerebrospinal fluid.
The organism can be transmitted through blood transfusion.

58. Clinical picture - trypanosomal chancre - parasitemia with fever
- lymphadenopathy
generalized organ involvement. - central nervous system meningoencephalitis, coma and death

59. Bite reaction:
T.chancre
A non-pustular, painful, itchy chancre appears 1-3 weeks after the bite and lasts 1-2 weeks. It leaves no scar

62. Winterbottom's sign
lymphadenopathy
Lymphatic involvement
imp

63. central nervous system
meningoencephalitis, coma and death

64. Leptomeningitis in brain

65. Trypanosomes found in blood Serological tests (IFAT)
Diagnosis
Trypanosomes found in blood
lymph and cerebrospinal fluid .
Serological tests (IFAT)

67. Treatment Suramin Pentamidine (T.gambiense only)
Cases with CNS involvement
should be treated with Mel-
arsoprol, an organic arsenic
compound.
-di-fluoro-methly-ornithine
(DFMO)

68. Major problems - how to control Tsetse fly
-(killing off all wild animal reservoirs?)
- vaccine production very difficult because of antigenic variation of trypanosome

70. Losses due to nagana are estimated at $ 1.5 - 4 billion annually ,
estimated to be new cases of human sleeping sickness with deaths annually (WHO)

71. American trypanosomiasis
Chagas' disease

74. Triatoma winged bug

75. 1-The primary lesion, chagoma, appearing at the site of bite
Symptoms Chagas' disease can be divided into three stages:
1-The primary lesion, chagoma, appearing at the site of bite
. Infection in the eyelid, resulting in a unilateral conjunctivitis and orbital edema (Ramana's sign)

78. 2-Acute Stage: Fever, bone and muscle pains. hepatomegaly, and rash.
lymphadenopathy.
Diffuse myocarditis, sometimes pericarditis and endocarditis.
In children, Chagas' disease may cause meningo-encephalitis and coma.
Death occurs in 5-10 percent.

79. 3-The chronic: stage results in an abnormal function of the hollow organs, particularly the heart, esophagus and colon.
The cardiac changes include myocardial insufficiency, cardiomegaly.
Disturbances of peristalsis lead to megaesophagus and megacolon .

84. Treatment Xenodiagnosis imp Diagnosis Trypanosomes found in blood
Serological tests (IFAT or ELISA)
Polymerase chain reaction PCR
Xenodiagnosis imp
Treatment
Supportive
Benznidazole or nifurtimox

86. الحمد لله

87. الحمد لله