بسم الله الرحمن الرحيم

Visceral, Mucocutaneous and Cutaneous Leishmaniasis

Leishmaniasis is a diseases of different clinical manifestations.

1. 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

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).

Morphology

-Amastigote (leishmanial form) is oval and measures 2-5

microns -Leptomonad (promastigote form) measures 14 - 20 microns a similar size to trypanosomes

EpidemiologyLeishmaniasis is prevalent world wide:

- South east Asia, Indonesia, Pakistan, - Mediterranean, - North and central Africa,- South and central America.

Species Disease

Leishmania tropica* Leishmania major* Leishmania aethiopica Leishmania mexicana

Cutaneous leishmaniasis

Leishmania braziliensis

Mucocutaneous leishmaniasis

Leishmania donovani* Leishmania infantum* Leishmania chagasi

Visceral leishmianiasis

* Endemic in Saudi Arabia

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.

Leishmania major –wet lesion

Leishmania tropica: dry type

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.

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

1 2

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.

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.

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.

mucocutaneous leishmaniasis

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.

Treatment No treatment- It self healing

lesions.

• Medical pentavalent antimony

(Pentostam), Amphotericin B.• +/- Antibiotics for secondary

bacterial infection.

• Surgical - Cryosurgery - Excision - Curettage

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).

Leishmania donovanivisceral leishmaniasis

L.infantum :mainly in infantL.donovani :mainly in adult

Species Disease

Leishmania tropica* Leishmania major* Leishmania aethiopica Leishmania mexicana

Cutaneous leishmaniasis

Leishmania braziliensis

Mucocutaneous leishmaniasis

Leishmania donovani* Leishmania infantum* Leishmania chagasi

Visceral leishmianiasis

* Endemic in Saudi Arabia

L.Donovani -visceral leishmaniasis

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.

• 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.

Post kala- azar dermal leishmaniasis

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.

Parasitological diagnosis*. bone marrow aspirate or spleen

puncture and stain (Giemsa) . *.culture material aspirated on (NNN). .Lymph node least sensitive. .tissue biopsy

1-Bone marrow biopsy

2- rosette shape promastigotes

3-promastigotes2

1

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

Treatment - Pentavalent antimony

(Pentostam) is the drug of choice.

- Amphotericin B. - Treatment of anemia, bleeding,

and infection.

African trypanosomiasis

African trypanosomiasis

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

•The reservoir Humans and wild animals (zoonosis)

• The vector Glossina (Tsetse) flies 

 

Glossina

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..

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.

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.

Lymphatic &

•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.

Clinical picture

- trypanosomal chancre- parasitemia with fever

- lymphadenopathy generalized organ involvement. - central nervous system meningoencephalitis, coma and death

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

Winterbottom's sign

Lymphatic involvement

imp

lymphadenopathy

central nervous system meningoencephalitis, coma and death

Leptomeningitis in brain

Diagnosis•Trypanosomes found in

blood lymph and cerebrospinal fluid

.

•Serological tests (IFAT)

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)

•Major problems 

- how to control Tsetse fly -(killing off all wild animal

reservoirs?)- vaccine production very difficult

because of antigenic variation of trypanosome

•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)

•American trypanosomiasis

Chagas' disease

Triatoma winged bug

SymptomsChagas' 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)

•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.

•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 .

Diagnosis• Trypanosomes found in blood • Serological tests (IFAT or ELISA) • Polymerase chain reaction PCR

•Xenodiagnosis imp

Treatment• Supportive • Benznidazole or nifurtimox

لله الحمد