Sukmab,2019 Sukmab,2017

TRYPANOSOMA AND
LEISHMANIA

Sukmawati Basuki

Department of Medical Parasitology

Faculty of Medicine, Universitas Airlangga
Surabaya, 2020

Sukmab,2017 Sukmab,2017

Phylum Class Genera

Sarcomastigophora Zoomastigophora Giardia, Leishmania,
(Motile by flagella) Trichomonas,
Trypanosoma
Lobosea/Sarcodina Acanthamoeba,
(Motile by pseudopodia & Entamoeba, Naegleria
amoeboid movement)
Apicomplexa Sporozoa Cryptosporidium,
(Most have complex life cycles Isospora,
with both sexual & asexual Plasmodium,
stages. Adult forms are non Toxoplasma
motile)
Ciliophora Kinetofragminophorea Balantidium
(Motile by cilia)

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Taxonomy

Kingdom : Animalia
Sub kingdom : Protozoa
Phylum : Sarcomastigophora
Sub phylum : Mastigophora
Class : Zoomastigophora
Order : Kinetoplastida
Family : Trypanosomatidae
Genus :
Trypanosoma
Leishmania

Amastigote Promastigote
Sukmab,2017

Trypomastigote
Epimastigote

Sukm ab,2015

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Trypanosoma
TRYPANOSOMA Gruby, 1843

Sukmawati Basuki
Sukmawati Basuki
Department of Medical Parasitology
Faculty of Medicine Department of Parasitology, Faculty of Medicine
Universitas Airlangga Universitas Airlangga, Surabaya
2020
Sukmab,2019

Sukmab,2017 Sukmab,2017
TRYPANOSOMA GAMBIENSE
• Disease : Trypanosomiasis Causes : Sleeping sickness
Vector : Glossina palpalis (tsetse flies), male and female,
T. brucei gambiense, T. brucei rhodesiense ® Glossina (vektor)® direct mechanical transmission
African trypanosomiasis (in human, under natural conditions)
Disease distibution : Endemic in Africa, from west part (Senegal) to the
T. cruzi ® infected feces of a bug (vector)® American north part (Angola).
trypanosomiasis or Chagas disease (in human) Morphology :
in the blood ® 1 forms : trypomastigote
Longitudinal binary fussion
T. cruzi : leishmania stage (amastigote, intercellular life) and Habitat : Early/ febrile stage ® blood, lymph node,
does not multiply in the trypanosoma stage cerebral symptoms ® cerebrospinal fluid. Does not
invade or live within tissue cells but inhabits
1. Basal body of flagellum replicates connective tissue spaces of various organs and reticular
2. Kinetoplast divides tissue of lymph node and spleen, intercellular spaces of brain.
3. Nucleus divides
4. Longitudinal cleavage commences at the anterior end ® 2 Cultivation : Can not be mantained as culture on N,N,N
daughter flagellates medium, but will grow in Weinman s medium

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MORPHOLOGY Sukm ab,2017

LIFE CYCLE Sukmab,2017

§ 14-32 µm in length and

1.5-3.5 µm in breadth
• a long typical trypanosome in the
blood of man
• cytoplasma: granular, vacuolated (blue)
T. gambiense
• nucleus: central (reddish/reddish purple)
• undulating membrane (pale blue)
• free flagellum at the anterior end of
the body
§ S shape
§ Giemsa, Wright s staining

T. rhodesiense

Axoneme Undulating membrane

Kinetoplast

Flagella
Para basal
body Nucleus and karyosome
Blepharoplast Volutin granules
http://www.dpd.cdc.gov/dpdx

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TRYPANOSOMA GAMBIENSE TRYPANOSOMA GAMBIENSE
Siklus hidup :
Pathogenesis and pathology:
Tsetse fly Chronic disease

Trypanosome (trypomastigote) ® lumen of mid and hind gut, 10 days ® ü Trypanosomes predominantly in the blood stream
trypanosome (procyclic trypomastigote) ­­ + critidial forms (epimastigote): ü Trypanosomes predominantly in lymph node
slender organism, produced from the broad forms and called proventicular ü Invasion of central nervous system Chancre
forms, multiply; binary fusion ® migrate to esophagus, pharynx, labrum-
epipharynx, prestonum, salivary gland ® attached to epithelium ® broad Infected Tsetse fly ® human skin, local inflammatory (1-2 weeks),
critidia (epimastigote), multiply ® metacyclic trypanosome/ metacyclic Chancre [elevated, indurated and painful touch] ® blood
trypomastigote (2-5 days) stream, multiply, parasitemia ® lymph node, proliferation endothelial cells
lining sinuses, infiltration of leukocytes ® CNS, arachnoid spaces, brain
Development in tsetse fly: 20 days substances, infiltration of plasma cells and lymphocytes, perivascular
proliferation of endothelial and neuroglia cells between blood stream and
perivascular sheath
Incubation: 2-23 days, symptomless

Sukmab,2017
TRYPANOSOMA GAMBIENSE
Winterbottom’s sign
Pathogenesis and pathology :

Symptoms: in natives parallel the invasion of lymph node;

attack of fever ± 1 week. Fever: continous,
but usually irregular and reach maximum in the evening.
Enlargement spleen, liver, lymph node,
postcervical triangle (Winterbottom s sign) ® axilla, groin: headache,
neuralgia pains, joints: weakness in the legs, cramps, erythematous eruptions on
the skin ® Delayed sensation to pain, Kerandel s sign: present and localized
edema of hips, hands, legs and eyes ® cardiac pain, disturbed vision, anemia,
nephritis

Some cases: spontaneous recovery during acute febrile period

Invasion of nervous system: sleeping sickness stage: severe headache, mental
dullness, apathy, muscle spasm, trembling hands and trunk, disturbances of
coordination and reflex mechanism, pain and stiffness in the neck, spastic or
flaccid paralysis ® increase day to day ® fall asleep ® general paresis,
convulsion ® death

Complications: lobar bronchopneumonia, meningitis, rapid hearth failure Sukmab,2019

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TRYPANOSOMA GAMBIENSE
Diagnosis :

Based on characteristic symptoms, history of living/having live in

endemic area, demonstration of parasite in blood, lymph node juices,
sternal bone marrow, or cerebrospinal fluid ® methods: direct
microscopic examination: stained or unstained preparations, cultivation,
animal inoculation, serological technics

Treatment : Tryparsamide USP, Suramin USP, Pentamidine,

Melarsen, Berenil
Prognosis : Good at early, poor after CNS involvement
Prevention : Pentamidine, clearing of riverine vegetation,
killing potential wild animal hosts on which tsetse feed, dieldrin and
isobenzan spraying

Sukmab,2017 Sukmab,2019
TRYPANOSOMA RHODESIENSE
Causes : Sleeping sickness
Vector : Glossina palpalis, G. morsitans, G. swynnertoni,
G. pallidipes (tsetse flies), male and female, direct mechanical transmission
Disease distribution : Limited area in Africa; Rhodesia, Malawi,
Tanzania, Rwanda, Uganda, Sudan, Kenya.
Morphology : Identical with T. gambiense
Habitat : similar to T. gambiense
Cultivation : in Weinman s medium
Life cycle : similar to T. gambiense
Pathogenesis and pathology : symptoms develop more rapidly, febrile
paroxysms, edema, weakness, rapid loss of weight, myocarditis, but lymph
node enlargement is less pronounced
Treatment : More resistant to treatment: Tryparsamide
Suramin USP → effective
Pentamidine → control epidemics
• Prognosis : Similar to T. gambiense
• Prevention : see to T. gambiense

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[Bouteille B., & Buguet A., 2012]

Sukmab,2017 Sukmab,2017
TRYPANOSOMA CRUZI
Causes : Chagas disease, zoonosis
Vector : Insects: Panstrongylus megistus, Triatoma
infestans, Rhodnius prolixus ® larva, nymph, adult in the bug s
intestinal tract (Reduviid bug)
Disease distribution : Western hemisphere, Brazil (State of Minas
Gerais), Argentina, Paraguay, Chile, Uruguay, Bolivia, Peru, Texas
USA

Reservoir : Dog, cat, armadillo, fox, bat, monkey, squirrels.

Morphology :
Man or mammalian reservoir host:
Trypanosome (trypomastigote) ® blood, not divide in the blood stream
Leishmania form (amastigote) ® reticuloendothelial and other tissue
cells. Multiply as a leptomonas and critidia form when it is about to
escape from intracellular location ® trypanosome ® peripheral blood

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TRYPANOSOMA CRUZI
Kissing bugs
Habitat : Blood, reticuloendothelial cells of spleen, liver,
lymph nodes, lymphatic tissues, in myocardium, striated cells/muscle cells,
bone marrow, suprarenal glands, testes, ovary, nervous system, histiocytes
of cutaneous tissue, epidermis cells, intestinal mucosa membrane

Cultivation :
Easy in N,N,N media
Chick-embryo cultures (Carrel technic), HeLa cancer cells

Transmission :
1. Feces of arthropod containing trypanosome rubbed into the wound
2. By coitus, or through the milk of an infected nursing mother
3. By accidental ingestion of parasitized arthropods
4. Blood transfussion

MORPHOLOGY Sukmab,2017
LIFE CYCLE Sukmab,2017

Darah
§ 20 µm in length
§ a long typical trypanosome in the
blood of man
§ cytoplasma: granular, vacuolated (blue)
§ nucleus: central (reddish/reddish purple)
§ a narrow undulating membrane (pale blue)
§ free flagellum at the anterior end of
the body
§ C shape
§ Giemsa, Wright s staining

Jaringan
amastigote

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[Wanderley de Souza, et al, 2010]

Sukmab,2017 Sukmab,2017
TRYPANOSOMA CRUZI

Pathogenesis and pathology :

Intact skin, deposition of semiliquid feces of the infected triatomid bug ®

taking the blood meal ® invading organism, engulfed by histiocytes in
corium ® adipose tissue, nearby muscle cells ® 3 days, multiply ®
rupture ® infitrate PMNs, monocytes, lymphocytes ® rupture ® blood
stream, found temporary circulating as trypanosome forms
(trypomastigote), typically accompany by fever (do not multiply)

Characteristic primary lession (chagoma): block lymphatic capillaries and

produce edema of the area

Destruction of reticuloendothelial cells in various organs and blockage

reticuloendothelial system ® may finally cause death
Incubation: 7-14 days

Acute and Chronic form ® in children

[Wanderley de Souza, et al, 2010]

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 Sukmab,2017 Sukmab,2017
TRYPANOSOMA CRUZI Chagoma

Pathogenesis and pathology :

Acute form:
• 20-30 days
• High fever ® 2 weeks, deposit of mucoid material in tissues ®
tumefaction (does not pit), entire body
• Face swollen, edema eyelids (Romana s sign) ® myxedema, Romana sign
unilateral palpebral edema
• Fever: intermittent, remitting or cuntinuous
• Keratitis
• Anemia
• Typhoid-like syndrome; fever, enlargement of spleen and liver, without
edema
• Psychological symptoms: nervous ® encephalomyelitis,
meningoencephalitis
• Death; 2-4 weeks

Sukmab,2017 Sukmab,2017
TRYPANOSOMA CRUZI
Pathogenesis and pathology :
Chronic form:
• In adult
• Related to damage sustained during acute phase
• Depends upon localization of intracellular parasites
• Cardiac (50%, A-V block, Adam-Stokes syndrome, ECG: ventricular
hypertrophy), meningoencepalitic, myxedematous,
pseudomyxedematous, suprarenal types
• Megaesophagus, megacolon
• Deranged peristalsis ¬ destruction of autonomic ganglia within the wall
of the viscus

Diagnosis :
Blood or tissue of T. cruzi
Inoculation guinea pigs ® as a diagnostic measure (Chronic stage)
Chagomas ® making smears, sections, staining ® leishmania
form(amastigote)
Xenodiagnostic: trypanosome-free laboratory-bred triatomids
Kelser s complement-fixation test

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TRYPANOSOMA CRUZI
Treatment :
1. Unfruitfull
2. Suramin and diamidines ® leishmania form
3. Isoniazide, tetracycline, corticosteroids ® aggravate the infection
4. 8-aminoquinolines ® blood and tissue
5. Chronic form ® symptomatic relief is available

Prognosis :
No certain cure
1. Is grave in children
2. Unsatisfactory in adults
Parasite is known to survive at least 12 years in mild chronic infections

Prevention :
1. To destroy bugs by application of effective insecticides (DDT, BHC or
gammexane) to the walls and thatched roofs of the dwellings
2. Education individuals, families, or communities
https://www.iamat.org/risks/chagas-disease
3. Repair of the habitations at minimum cost
4. Prevent infection due to blood transfussion

Sukmab,2019
Sukmab, 2017
PREVENTION

[Hemmige V. et al, 2012]

[Rassi A. et al, 2009]

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Leishmania
LEISHMANIA Ross, 1903

Sukmawati Basuki
Sukmawati Basuki
Department of Medical Parasitology
Faculty of Medicine Department of Parasitology, Faculty of Medicine
Universitas Airlangga Universitas Airlangga, Surabaya
Surabaya, 2020 2020

Sukmab,2017

[WHO, 1990]

Disease : Leishmaniasis, a zoonosis

Sukm ab,2017 [Richard Reithinger et al, 2007]

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MORPHOLOGY Sukmab,2017 Sukmab,2017

Reproduksi secara binary fission:

Amastigote Promastigote
Leishmania form [amastigote]
blepharoplast dan parabasal bodi (kinetoplast)
pertama membelah, kemudian diikuti dengan
nukleus dan sitoplasma

Leptomonas form [promastigote]

Membelah longitudinal fission menjadi 2 individu.
Pembelahan seperti pada Leishmania form; flagela
tidak memisah, tapi flagela kedua dibentuk oleh
axoneme yang berkembang dari daughter
• a round or oval body • a long and slender body blepharoplast.
• 2-6 µm • 15-30 µm X 2-3 µm
• a nucleus • a nucleus
Terjadi di usus Phlebotomus.
• a kinetoplast • a kinetoplast Di kultur, memberikan perkembangan dan
• internal flagellum • a long free anterior flagellum pembelahan yang cepat ® rosette form
• Leishmania form • Leptomonas stage/form

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LIFE CYCLE Sukmab,2017

Usual tropism Species Clinical Expression

usual exceptional
Viserotropic L. donovani VL LCL
species L. infantum VL LCL, DCL*

Dermatropic L. aethiopica LCL DCL

species L. kilicki LCL
L. major LCL DCL*
L. tropica LCL VL
L. amazonensis LCL DCL, VL
L. colombonensis LCL
L. guyanensis LCL MCL
L. mexicana LCL
L. laisoni LCL DCL, VL*
L. naiffi LCL
L. peruviana LCL
L. shawi LCL
L. venezuelensis LCL

Dermomucotropic L. braziliensis LCL, MCL DCL*, VL*

species L. panamensis LCL MCL, DCL*

VL: visceral leishmaniasis LCL: localized cutaneous leishmaniasis

[wikipedia, 2013] DCL: diffuse cutaneous leishmaniasis MCL: mucocutaneous leishmaniasis
* : during immunosuppression (Manson s tropical diseases, 21st ed)

Leishmania tropica
Sukmab,2017 Sukmab,2017

Cause : Urban cutaneous leishmaniasis, oriental sore

Vector : Phlebotomus papatasii, P. sergenti, P. perfilievi, P.

caucasicus, P. perniciosus
Resevoar : gerbil (rodent) ® Central Asia,
Rhombomysopinus (rodent) ® Central Iran, anjing

Disease distribution : Endemic in Africa, some areas in America, Asia

and Europe
Habitat : in skin, inside endothelial cell of capillary
surrounding the infection areas, near lymph node and inside
mononuclear cell. It is not found inside the peripheral blood
streams.
Cultivation : N.N.N. medium (Nicolle, 1908), Schneider s
Drosophila medium
Skin lesions ® N.N.N. medium ® leptomonas stage
Transmission : Inoculation and Autoinoculation (scratching®
[Sharma U. et al., 2008] multiple sores). Leishmaniases do not penetrate to unbroken
skin.

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 Leishmania tropica
Sukmab,2017 Sukmab,2017

Pathogenesis and pathology :

Sand fly carrying promastigote blood meal, promastigotes ®
macrophages ® amastigote ® multiply ® rupture ® penetrate other
macrophages. First infection occurs in the stratum corneum, then perform
crateriform lesion® ulcer; granulation form in the centre and induration at
the periphery. The current location of Leishmania is in the lymph nodes ->
at the edge of the crater region.
ü Hypertrophy of the stratum corneum
ü Hyperplasia and hyperplasia of the papilla
ü Infiltrated plasma cells, lymphocyte cells, mononuclear cells contain
parasites, epithelioma cells
ü Necrosis and ulceration LCL: LCL: LCL:
ü Secondary infection (bacteria) Typically volcano- Lesion is Typically ulcerated
Incubation : several days - months like lession with surrounded by with a raised
Metastase : may occur on the cheek mucosa, pharynx, nose sloping sides smaller daughter inflammatory
Symptoms : variations, fever, chills, symptoms of inflammation may papules outline
arise.
In some cases: papules ® disappear (ulcer - ) after a few weeks or
months, uncomplicated case ® ulcers heal in 2 - 12 months. (Manson s tropical diseases, 21st ed)

Sukmab,2017 Sukm ab,2017

[Richard Reithinger et al, 2007]

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 Leishmania tropica
Sukmab,2017
Therapy : Antimonial compunds Leishmania tropica
In Turkestan areas : Effective for sores > 3

2 types of infection form : dry type moist type 1. Injection i.m. barberine sulfat (2% aqueous solution) / stibophen 2 ml,
Incubation : lama cepat 2 times per week for 8 weeks
Leishmania at lesion: numerous few 2. Glucantime; 0.1 g /body weight/day for 15-20 days.
Virulent in rodent : rendah tinggi
Lesion : unbroken dry papules ulcerating rapidly Effective for sores < 3 : Local infiltration of the drug at the ulcer margins
persisting for months
(delayed ulceration) Prognose : Prompt treatment ® good
Prevention:
Diagnosa : 1. Protection of lesions from insects with a gauze bandage ® prevents
1. Microscopy examination with Giemsa or Wright stains: smear of transmission
punctures in the area of induration at the edge of the ulcer, tissue 2. Autoinuculation education
smear 3. Residual spraying: chlorinated hydrocarbon (DDT) on windows, doors
2. Biopsy of lymphoid material from under the ulcer's edge 4. Repellents: dimethylphthalate
3. Cultivation: observation every week for 4 mg 5. Bednets
4. Inoculation in animals (the golden hamster) 6. Vaccination
5. Serology: Leishmanin (Montenegro) test 7. Natural reservoir detruction/eradication: rodents with chloropicrin
6. Molecular analysis Sukmab,2017

Sukmab,2017 Sukm ab,2017

[Richard Reithinger et al, 2007]

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 Leishmania braziliensis Leishmania braziliensis
Sukmab,2017 Sukmab,2017

General synonym : L. tropica var americana Pathogenesis and pathology :

Cause : American leishmaniasis, cutaneous- Promastigotes are inoculated by sand fly biting ® small papules ®
mucocutaneous leishmaniasis redness, vesicles, and itching ® 1-4 weeks, round or oval ulcers develop,
Disease distribution : in America areas; from South Mexico to with uneven edges. Another type arises a protruding edge of induration
Paraguay and northern part of Argentina, South Iran. Generally in Primary lesions:
hot areas with forest humidity and an altitude of 2,500 feets - Epithelial hyperplasia
Habitat : - Dermal inflammation with edema
Live in tissue cells, endothelial cells, mononuclear cells in the skin - Epithelial proliferation and therein leishmania zone in necrotic dermal
and on the mucosa of the nose, mouth and pharynx. It may be papillae.
found in neutrophil cells, but not in peripheral blood. - Self-healing within 6-15 months, if not accompanied by the development
Cultivation : of a second invasion. Even though the lesion was healed, Leishmania
N.N.N. medium by Pedrosa and da Silva, 1911, Schneider’s was still alive ® relapsed
Drosophila medium
Vector : P. migonei, P. whitmani, P. intermedius, P.monticolus, P. Cutaneous lesions are present on the lower extremities, face and earlobes
cruciatus, P. panamensis, dll In tropical America, the tendency for Leishmania to migrate from primary
Reservoar : dog, Syrian hamster, spiny rat (Proechimys semispinosus lesions to the muco-cuntaneous junction; nasal septum, cheek mucosa,
panamensis), kinkajou (Potos flavus) nasopharynx mucosa, and larynx ® degenerative erosive appearance of
soft tissue and cartilage ® deformity

Leishmania braziliensis
Sukmab,2017 Sukmab,2017

Pathogenesis dan pathology :

Secondary lesions in the mucous membrane may be ulcerative and
indurative, invasion from plasma cells, endothelial cells,
macrophage cells filled with Leishmania, and oedema.
.
Incubation : Several days - weeks
Symptoms : Primary lesions (papules ® ulcers) painless ® heals
within months - 2 years or ® develops open ulcers with secondary
infection ® develops pain. Secondary lesions appear before the
primary lesions heal, if the deformity + voice disappears,
complications: septicemia, bronchopneumonia ® fever, anemia,
pain, malaise.
MCL: MCL:
Extensive lesion of Obtained regional lymph node enlargement, or
Nasal septum
the palate hepatosplenomegaly

Differential Diagnosis :
Furuncles, Eczema, Tropical ulcers, Impetigo, Pemphigus,
sporotrichosis, syphilis, leprosy, yaws, cutaneous tuberculosis
(Manson s tropical diseases, 21st ed)

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 Diagnosis : Leishmania braziliensis Sukmab,2017
Leishmania braziliensis
Sukmab,2017

1. Microscopic with Giemsa or Wright's stain: smear of punctures in the

induration area of the periphery of primary ulcers, nodules, and ulcers Prognose : good before there was metastasis.
Prevention :
on mucus membranes
2. Biopsy of lymphoid material from under the ulcer's edge
3. Cultivation: observation every week for 4 weeks 1. Protection of lesions from insects with a gauze bandage ®
prevents transmission
4. Inoculation in animals
2. Autoinuculation education
5. Serology tests; Montenegro skin test
6. Molecular analysis 3. Residual spraying: chlorinated hydrocarbon (DDT) on windows,
doors
4. Repellents: dimethylphthalate
Treatment :
5. Bednet
6. Vaccination
1. Stibophen, or ethylstilbamine, i.m. good for kids
7. Reservoir destruction/eradication
2. If it fails with antimonial treatment compunds ® Amphotericin B
Pentamidine, or a combination of interferon gamma with Glucantime. Leishmaniasis recidivans
3. Glucantime is infiltrated in the primary lesion
4. Meta arsenite, good for secondary lesions Chronic form of leishmaniasis caused by L. tropica and L. braziliensis.
The location of the lesion was on the face, followed by acute lesions,
5. ollow-up therapy: with smears and cultures after 1-2 weeks of treatment
after several months of evolution. There is an active zone in the
6. Antibiotic
7. Topical disinfection, curettage, cauterization, coagulation diathermy, periphery with healing in the central part, containing several parasites.
DD: Lupus vulgaris
excision, plastic surgery

Sukmab,2017

Leishmania donovani
Sukmab,2017

Synonym : Piroplasma donovani (Laveran dan Mesnil, 1903)

Cause : Visceral leishmaniasis, tropical splenomegali,
kala azar, dundum fever
Disease distribution : America, Africa: endemic in Sudan, Ethiopia,
Somalia, North Kenya, West Africa, Morocco, Algeria, and Tunisia,
Asia: China, Turkey, Jordan, Syria, Lebanon, Israel, and Saudi
Arabia, Europe: endemic in Portugal, Spain, Italia, Corsican,
Albania, Yunani, Bulgaria, and USSR

Habitat : In the reticuloendothelial tissues : spleen, liver,

bone marrow, intestinal mucosa, and mesenteric lymph nodes, it
may be found in renal endothelial cells, suprarenal capsule, lung,
meninges, and in cerebrospinal fluid.

Transmission :
In India: Human – sand fly – Human
In China, Mediterranean, Brazil : 1. Dog – sand fly – Human
2. Dog – sand fly - Human
Vector : Generally in the 2,000 ft ® rural area

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 Leishmania donovani Leishmania donovani Sukmab,2017

Pathogenesis and pathology : Post-kala azar dermal leishmanoid: nodules due to inadequate
Promastigotes are inoculated by sand fly biting ® macrophages ® treatment of antimonial compounds. White patches on the skin ®
amastigote ® slow developing ® multiply ® macrophages containing nodules (parasites are not found in the blood or spleen)
parasites ® blood circulation ® to tissues, fast growing ® macrophage
production ­­ ® neutropenia (secondary infection +), granulocytopenia, Differential diagnosis : Schistosomiasis, malaria, typhoid fever,
monocytosis, erythrocyte production ¯ ( anemia) ® infected histiocyte cells relapsing fever, dysentery, visceral syphilis, influenza, tubercolosis
ü Splenomegaly Diagnosa :
ü Hepatomegaly 1. Blood smear, spleen, lymph nodes, liver, bone marrow, nasal
ü Enlarged kidneys secretions
ü Enlarged lymph glands 2. Cultivation
ü Ulcers in the intestine: Peyer's patch 3. Serology: precipitation test (serum g globulin ­, albumin ¯),
complement fixation test, Montenegro skin test,
Incubation : 10 days –1 year (2 – 4 months). The infection is sudden 4. Molecular analysis
onset 5. Inoculation of animals is not carried out - it takes several months
Symptoms : malaise, headache, irregular-interval fever, progressive Treatment :
enlargement of the spleen, acute abdominal pain, anemia, leukopenia, 1. Supportive
periosteum skin oedema, dysentery/diarrhea, cachexia accompanied by 2. Specific
enlarged spleen and liver. Death may occur within weeks in acute Antimonial compounds
infections, within 1 year in subacute infections, and within 2-3 years in pentavalent antimony: Pentostam, Glucantime, i.v
chronic infections. Complications ® death. Sukm ab,2017
sodium or potassium antimonyl tartrate in 2 % solution – i.v.

Leishmania donovani
Sukm ab,2017 Sukmab,2017

Treatment (continued) :
Ethylstibamine (Neostibosan), i.m. atau i.v.
Sodium antimony gluconate (Solustibosan)
Diamidine compunds
hidroxy-stilbamidine isethionate, i.v

Alternative therapy (Resistance +): Amphotericin B,

Liposomal Amphotericin B, Pentamidine isethionate,
Allupurinol + antimony, Aminosidine, Aminosidine +
antimony,

Antibiotics

VL: Follow up therapy: clinical observation accompanied

Protuberant by smears and cultures 1-2 weeks after treatment
abdomen caused
by voluminous
enlargement of Prognose : Prompt treatment ® good. Resistant to
spleen and liver antimony or diamidine ® poor.
(Manson s tropical diseases, 21st ed)

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 Leishmania donovani
Sukmab,2017 Sukmab,2017

Prevention :

1. Adequate treatment
2. Avoid and destroy in infected dogs
3. Control vectors: extermination of sand fly nests, catching adult sand
fly morning and night, spraying: residual chlorinated hydrocarbon
insecticides (DDT), organophosphate, carbamate, pyrethroid
4. Bednets: Permethrine-treated (300 mg / m2), Deltamethrine (15-25
mg / m2), lamdacyhalothrine (10 mg / m2)
5. Repellents: dimethylphthalate
6. Home ventilation +

Sukmab,2017 Sukmab,2017

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 Sukmab,2017
Sukmab,2017
MACROPHAGE INVASION AND Routes by which humans acquire parasitic infections
SURVIVAL STRATEGIES OF INTRACELLULAR MICROBE

Coiled phagosome
Legionella
Vacuola lysis
Listeria fusion
Trypanosoma cruzi
no fusion

Lysosomal
Restricted fusion/acidification Histoplasma
Mycobacteria Leishmania
Toxoplasma gondii

Sukm ab,2015 Figure 23.1

Sukmab,2017 Sukmab,2019

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