PARASITOLOGY TLA 3: (Handwritten)

1. Leishmania braziliensis
o Other name & associated disease:
– Mucocutaneous leishmaniasis
– chiclero ulcer (Mexico)
– espundia
– forest yaws (Guyana)
– pian bois or uta (Peru)

o Morphology:

o Clinical symptoms:
– occur within a few weeks to months after transmission
– Large ulcers in the oral or nasal mucosa areas (mucocutaneous)
 large cutaneous lesions
 mucosal lesions
– Cutaneous: affecting or relating to the skin
– Affected parts: skin, mucous membrane, lips, nose, and surface rounding soft
parts.
– Causes the face to disfigure

o Treatment:
– Antimony compounds
– Liposomal amphotericin B (Ambisome)
– Oral antifungal drugs:
 Fluconazole (Diflucan)
 Ketoconazole (Nizoral)
 Itraconazole (Sponorox)

o Laboratory diagnosis:
– Biopsy of the infected ulcer
– Culturing the infected material (promastigote stage & serologic stage)

o Life cycle:
– Sandflies transmit promastigotes into unsuspecting humans via a blood meal
(skin bite)
– Promastigotes invade the reticuloendothelial cells; transform to amastigotes
then reproduce.
– Infective stage & Diagnostic stage: Amastigote (sandfly)
– On ingestion, amastigotes transform back to promastigotes in the fly midgut;
promastigotes multiply; migrate into salivary gland of the fly; transferred to a new
human during a blood meal.

o Epidemiology:
– Leishmania braziliensis (from Mexico to Argentina)
 – Leishmania panamensis (Panama to Colombia)
– Leishmania peruvania (Peruvian Andes)
– Leishmania guyanensis (Guiana, parts of Bazil and Venezuela)
– Rain forest regions; harvested chicle sap for chewing gum
– Vector: Lutzomyia or Psychodopygus sandfly
– Reservoir host: forest rodents & dogs

2. Leishmania donovani
Other name & associated disease:
- Visceral leishmaniasis
- kala-azar (black fever)
- dum dum fever
Morphology:

Clinical symptoms:
- nondescript abdominal illness
- hepatosplenomegaly (enlargement of the spleen and liver)
- Early stages: malaria or typhoid fever
- Incubation period: 2 weeks to 18 months
- Often present: diarrhea and anemia
- Weight loss and emaciation – occur ff. parasitic invasion of the liver and spleen
- Skin lesions are ABSENT
- Advanced stages: kidney damage, granulomatous areas of skin
- Kala azar: skin darkening
Treatment:
 - Liposomal amphotericin B (Ambisome)
- Sodium stibogluconate (Pentosam)
- Gamma interferon with pentavalent antimony
- Paramomycine and miltefosine
Laboratory diagnosis:
- Montenegro skin test: not good method for diagnosing active disease
- Diagnosing amastigote form: Giemsa-stained slides
- Diagnosing promastigote form: cultured blood, bone marrow, and other tissues
- Serologic testing (IFA, ELISA, DAT)
Life cycle:
- Identical to L. braziliensis, except:
o the specific sandfly species responsible for L. donovani transmission vary with
each of the three subspecies
o L. donovani primarily affects the visceral tissue of the infected human.
Epidemiology:
- L. donovani (India, Pakistan, Thailand, parts of Africa, and the Peoples Republic of
China)
o Vector: phelobotomus sand fly
o Reservoir host: India, none; china, dogs
- L. infantum (Mediterranean area, Europe, Africa, the Near East, and parts of the former
Soviet Union)
o Vector: phelobotomus sandfly
o Reservoir host: dogs, foxes, jackals, procupines
- L. chagasi (Central and South America)
o Vector: lutzomyia sandfly
o Reservoir host: dogs, cats, foxes
- L. donovani and L. infantum (Middle East, including Yemen, Oman, Kuwait, Iraq, Saudi
Arabia, the United Arab Emirates, and Bahrain)

3. Leishmania tropica
Other names & associated disease:
- Old World cutaneous leishmaniasis
- oriental sores
- Delhi boils
- Baghdad boils
- dry or urban cutaneous leishmaniasis
Morphology:
Clinical symptoms:
- one or more ulcers containing pus that self-heal
- a small red papule develops for infected patients
Treatment:
- sodium stibogluconate (Pentosam)
- steroids, application of heat to infected lesions, meglumine antimonite (Glucantine),
pentamidine, oral ketoconazole
- paromomycin ointment
Laboratory diagnosis:
- microscopic examination of Giemsa-stained slides
- culture of the tissue (reveal promastigote forms)
- serologic tests (IFA)
Life cycle:
- identical to L. braziliensis
- transmitted by the Phlebotomus sandfly
- attacks the human lymphoid tissue of the skin
Epidemiology
- L. tropica (Mediterranean region, Middle East, Armenia, Caspian region, Afghanistan,
India, Kenya); VECTOR: Phlebotomus sandfly; RESERVOIR HOST: dogs
- L. major (Former Soviet Union, Iran, Israel, Jordan, parts of Africa, Syria, rural areas);
VECTOR: Phlebotomus sandfly; RESERVOIR HOST: Gerbils, other rodents
- L.aethiopica (highlands of Ethiopia, Kenya, Southern Yemen); VECTOR: Phlebotomus
sandfly; RESERVOIR HOST: Rock hyrax

4. Trypanosoma cruzi
Other names and associated disease:
- Chagas’ disease (Carlos Chagas)
- American trypanosomiasis

Morphology:
Clinical symptoms:
- Asymptomatic, chronic, or acute in nature
- Development of erythematous nodule (CHAGOMA)
- Edema, rash around the eyes and face
- Romana’s sign (conjunctivitis and unilateral edema of the eyelids)
- Fever, chills, fatigue, myalgia, malaise
- Most commonly seen in children (younger than 5 yrs)
Treatment:
- Nifurtimox (Lampit)
- Benznidazole, allopurinol, anti-fungal agent (ketoconazole)
Laboratory diagnosis:
- SPECIMEN OF CHOICE: Giemsa-stained blood slides
- Rarely seen in circulating blood: epimastigotes
- Blood culture (reveal amastigotes)
- Serologic tests (Complement fixation, DAT, indirect immunofluorescence)
- PCR and ELISA
Life cycle:
- Reduviid bug (vector) defecates infective trypomastigotes
- As the host scratches the bite area (itching sensation), trypomastigotes gain entry into
the host by literally being rubbed into the bite wound
- Additional routes or transmission: blood transfusions, sexual intercourse,
transplacental transmission, entry through the mucous membranes when the bug bite
near the eye or mouth
- After entering the host, trypomastigotes invade surrounding cells, and transform into
AMASTIGOTES
- Amastigotes then multiply, destroy host cells, then convert back into trypomastigotes
- The resulting trypomastigotes migrate through the blood, penetrate additional cells,
transform back to amastigotes, and replication and destruction cycle repeats.
- Trypomastigotes are transmitted back to reduviid bug when it feeds, via a blood meal on
an infected human.
- On ingestion, trypomastigotes transform into epimastigotes in the MIDGUT;
multiplication of epimastigotes produces parasites then convert back to trypomastigotes
when they reach hindgut
Epidemiology:
- Found in South and Central America
- BRAZIL (highest known prevalence of disease)
- First isolated in Panstrongylus megistus
- Vectors: kissing bug, conenose bug, triatomid bug, reduviid bug
- Reservoir hosts: dogs and cats

5. Trypanosoma rhodesiense
Other names and associated disease:
- East African sleeping sickness
- Rhodesian trypanosomiasis

Morphology:

Clinical symptoms:
- Fever, myalgia, rigors
- Winterbottom’s sign (may or may not be present)
- Lymphadenopathy (absent)
- Rapid weight loss
- Mental disturbance, lethargy, anorexia
- Death (kidney damage); myocarditis (inflammation of the heart); occurs within 9-12
months in untreated patients
Treatment:
- Identical to T. gambiense
Laboratory diagnosis:
- Blood slides stained with Giemsa and microscopic examination of CFS sediment
- Protein and IgM studies on CSF
- Serologic tests
Life cycle:
- Vectors: Glossina morsitans and Glossina pallidipes
- Attacking game animals may also transmit this organism
Epidemiology:
- Found in East and Central Africa (brush areas)
- Reservoir hosts: Cattle and sheep, wild game animals

6. Trypanosoma gambiense
Other names and associated disease:
- West African sleeping sickness
- Gambian trypanosomiasis
Morphology:
Clinical symptoms:
- Painful chancre (ulcer), surrounded by a white halo at the bite site
- Fever, malaise, headache, generalized weakness, anorexia
- Lymph node enlargement (lymphadenopathy)
- Winterbottom’s sign – enlargement of cervical lymph nodes
 - Erythematous (red) rash, puritis, Edema (swelling), Kerandel’s sign (delayed sensation
to pain)
- In patients involved CNS, mental retardation, tremors, meningoencephalitis, somnolence
(excessive sleepiness), character changes
- Final stages: coma and death; pneumonia or malaria
Treatment:
- Melasorsoprol, suramin, pentamidine, eflornithine
Laboratory diagnosis:
- Blood, lymph node aspirations, CSF are the specimens of choice for diagnosing
- Giemsa-stained slides of blood and lymph nodes aspirations (reveal trypomastigote
morphologic forms)
- Serologic tests
Life cycle:
- Humans become infected following the injection of trypomastigotes by the tsetse fly
during its blood meal
- The entering trypomastigotes migrate through blood streams and into lymphatic system,
multiply by binary fission
- Although the host’s immune system is activated and some trypomastigotes are
destroyed, mutations of parasites manage to escape and continue to reproduce
- Trypomastigotes are transmitted back to tsetse fly vector
- Once ingested by the tsetse fly, trypomastigotes continue to multiply and migrate back to
salivary gland, converting into epimastigotes
- Once in the salivary gland, epimastigotes transform back to trypomastigotes, and
completes the cycle.
Epidemiology:
- found in tropical West Africa and Central Africa (shaded areas along stream banks
where tsetse fly vector breeds)
- VECTORS: Glossina palpalis & Glossina tachinoides