Visceral,%20Mucocutaneous%20and%20Cutaneous%20Leishmaniasis

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• 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

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• 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).

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• Morphology
• -Amastigote (leishmanial form)
• is oval and measures 2-5 microns
• -Leptomonad (promastigote form)
• measures 14 - 20 microns
• a similar size to trypanosomes

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• EpidemiologyLeishmaniasis is prevalent
  world wide
• South east Asia, Indonesia,
• Pakistan,
• Mediterranean,
• North and central Africa,
• South and central America.

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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
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• 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.

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Leishmania major wet lesion
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Leishmania tropica dry type
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• 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.

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

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• 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.

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• 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.

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mucocutaneous leishmaniasis
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• 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.

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

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• 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).

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Leishmania donovanivisceral leishmaniasisL.infa
ntum mainly in infantL.donovani mainly in adult
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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
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L.Donovani -visceral leishmaniasis
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• 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.

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• 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.

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Post kala- azar dermal leishmaniasis
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• 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.

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

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1-Bone marrow biopsy
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2
3-promastigotes
2- rosette shape promastigotes
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• Serology 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

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

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• Trypanosomiasis

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African trypanosomiasis
2 species   -Trypanosoma brucei gambiense
(Africawest of Rift valley)-Trypanosoma
brucei rhodesiense (Africaeast of Rift
valley)
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• The reservoir
• Humans and wild animales
• The vector
• Glossina (Tsetse) flies   

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Glossina
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• African Trypanosomiasis
• (African Sleeping Sickness) A
  hemo-flagylate found only in Africa.
• zoonosis with a resevoir host,
• in East African form of disease, transmitted
  from resevoir animal to man by the vector tsetse
  fly (e.g. Glossina palpalis).
• In west African form it is transmitted by tsetse
  human to human..

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• 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 the epimastigotes form and matures to
  infectious metacyclic forms.

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

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• 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.

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

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• 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

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Winterbottom's sign
lymphadenopathy
Lymphatic involvement imp
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central nervous system
meningoencephalitis, coma and death
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Leptomeningitis in brain
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• Diagnosis
• Trypanosomes found in
• blood, lymph and cerebrospinal
• fluid .
• Serological tests (IFAT)

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• 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)

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

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• Losses due to nagana are estimated at 1.5 - 4
  billion annually ,
• estimated to be 500 000 new cases of human
  sleeping sickness with 45 000 deaths annually
  (WHO)

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• American trypanosomiasis
• Chagas' disease

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Triatoma winged bug
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• SymptomsChagas' disease can be divided into
  three stages
• 1-The primary lesion, chagoma, appearing at the
  site of bite, within a few hours. Infection in
  the eyelid, resulting in a unilateral
  conjunctivitis and orbital edema (Ramana's sign)
  is the commonest finding

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• 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.

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• 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
  atrio-ventricular conduction and the Adams-Stoke
  syndrome.
• Disturbances of peristalsis lead to megaesophagus
  and megacolon .

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

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