Phylum Sarcomastigophora Subphylum Mastigophora
Family Trypanosomatidae
Blood and Tissue Flagellates
Have not been diagnosed in the Philippines
Because of fast and easy travel as well as an increase in human migration imported cases may become the future source of infection
Vectors: Triatoma and Rhodnius, Phlebotomus spp. bugs are found in the country
Characteristics of Trypanosomatidae
All have single nucleusAll have single epitheliumDuring one stage of their lives they live in the blood or
tissue of all classes of vertebratesAnd one stages they live in the intestine of blood
sucking invertebrates
Trypanosome cellular architecture
Nucleoulus
Nucleus
Kinetoplast
Flagellum
Kinetosome
Kinetoplast
Nucleus
Undulating membrane
Four Morphological
Forms
Morphological forms
Leishmania spp. – amastigote and promastigote forms only
Trypanosoma brucei – epimastigote and trypomastigote forms only
Trypanosoma cruzi – contains all 4 morphological forms
Trypanosoma brucei
Trypanosoma brucei gambienseTrypanosoma brucei rhodesiense
There are two groups of trypanosomes
Develop in the posterior digestive tract of the insect (Salivaria)
Develop in the posterior digestive tract (Stercoraria)
T. brucei group - African sleeping sickness
Gambian or West African sleeping sickness
West and Central Africa
Rhodesian or East African sleeping sickness
East and South Africa
Morphology
T. brucei group exhibits only the epimastigote and trypomastigote forms
Typical trypomastigote stages with a posterior kinetoplast, a centrally located nucleus, an undulating membrane, and an anterior flagellum
polymorphic (slender, short, stumpy forms
Tsetse flyThe tsetse fly feeds on the blood of animals and
humans. Once inoculated by an infected fly, the
trypanosomes proliferate and gradually invade all the organs of the host.
Most of the parasites are effectively destroyed by the host's natural defenses,
but some trypanosomes manage to evade the immune system by modifying their surface membrane, a process known as antigenic variation.
The trypanosome can express thousands of variants, multiplying with each new surface change.
Well fed tsetse
T. brucei in blood smear
tsetse fly feeding
Pathogenesis
Stage 1 (early, or hemolymphatic, stage)
Painless skin chancre that appears about 5-15 days after the bite
Intermittent fever (refractory to antimalarials), general malaise, myalgia, and headache usually 3 weeks after bite
Generalized lymphadenopathy
Pruritus, urticaria, and facial edema (minority of patients)
Stage 2 (late, or CNS, stage)
Persistent headaches (refractory to analgesics)
Daytime somnolence followed by nighttime insomnia
Behavioral changes, mood swings, and, in some patients, depression
Loss of appetite, wasting syndrome, and weight loss
Seizures in children (rarely in adults)
African Trypanosomiasis
Characterized by irregular episodic fever
Lymphadenopathy
Progressive central nervous system
Coma
death
DIAGNOSISLymph node and chancre aspirate
Lymph node is commonly used as a rapid test for trypanosomes at a high dry magnification (X 400). It requires immediate search for parasites because they are mobile for only 15-20 minutes.
Chancre aspirate can be used as a wet preparation, especially in the East African form of the disease, but a blood smear is more sensitive.
Blood smear
A wet smear of unstained blood or Giemsa-stained thick smear (more sensitive) is used to observe the mobile trypanosomes, for 15-20 minutes. Wright and Leishman stains are inadequate
hematocrit centrifugation technique for buffy coat examination
miniature anion-exchange centrifugation technique, which filters out the red cells but not the trypanosomes.
Serology
The standard assay is the card agglutination test for trypanosomiasis (CATT) to diagnose West African trypanosomiasis.
The CATT can be conducted in the field without electricity-results are available in 10 minutes.
highly sensitive (96%) but less specific because of cross-reactivity with animal trypanosomes.
TREATMENTTripanosomias Medications
Stage 1 (Hemolymphatic
Stage)MedicationsStage 2 (Neurologic [CNS] Stage)
East African TrypanosomiasisTrypanosoma brucei rhodesiense
Suramin 100-200 mg IV test dose,
Eflornithine 400 mg/kg/d
Melarsoprol 2-3.6 mg/kg/d IV for 3 d;
Eflornithine 400 mg/kg/dWest African TrypanosomiasisTrypanosoma brucei gambiense
Pentamidine isethionate 4 mg/kg/d IM for 10 dSuramin 100-200 mg IV test dose, orEflornithine 400 mg/kg/d IV
Melarsoprol 2-3.6 mg/kg/d IV for 3 d; after 1 wk, 3.6 mg/kg/d for 3 days; Eflornithine 400 mg/kg/d IV in 4 divided doses for 14 d
Prevention and ControlA vaccine is not available.Effective prophylaxis in not available. Tsetse fly trapping is possible but costly. Treatment of asymptomatic carriers is possible, and infection can be
detected by CATT or node aspirate and confirmed with smears.Wear protective clothing with dull colors and use bed nets in areas
with tsetse flies. Insect repellant is not as effective in preventing illness transmitted by
tsetse flies compared to other insect-borne diseases.Avoid areas where African trypanosomiasis (sleeping sickness) is
endemic.
Trypanosoma cruzi
Trypanosoma cruzi
The parasite is found throughout much of central and northern South America, Central America, and Mexico
In humans, T. cruzi is found as both an intracellular form, the amastigote, and as a trypomastigote form in the blood.
The vector for Chagas' disease, a "true bug" (Hemiptera) such a Triatoma or Rhodnius
Morphology
Exhibits all four stages
Trypomastigotes found in the bloodstream in man
Amastigotes in tissue cells
T. cruzi trypomastigote is similar in form to T. brucei
VECTOR - genera
Triatoma, Panstrongylus, and Rhodnius
- common names: cone-nosed bug, assassin bug, kissing bug, vinchuca
.
Triatoma and Rhodnius bugs-vector
Chagas’ disease/American trypanosomiasis
Intracellular parasite
Humans:trypomastigotes-bloodstream
Amastigotes-tissue cells
Bugs:amastigote, epimastigote and promastigote-midgut
Pathogenesis
American trypanosomiasis
At the site of inoculation – inflammation known as “chagoma” – reddish nodule from acute to chronic cases
Fever and lymphadenopathy – acute disease
May enter through the conjunctiva of the eye – causing edema of the eyelid “romana sign”
Pathogenesis
In the human host, Chagas' disease affects primarily nervous system and heart.
Chronic infections result in various neurological disorders, including dementia, megacolon, and
megaesophagus, and damage to the heart muscle. Left untreated, Chagas' disease is often fatal.
Diagnosisobservation of the parasite in a blood smear (acute
phase)demonstration of trypanosomes in blood, CSF, fixed
tissue or lymphBlood culture and xenodiagnosisSerological
IFAT, Compliment fixation test, IHAT, PCR
Dot-immunobinding assay – using antigen bound to nitrocellulose paper
PCR
Prevention and Control
Vector control
Screening and sterilization of transfusion blood
Health education
Insecticide spraying and housing improvement to reduce breeding sites of triatome bugs.
Leishmanias
Leishmania tropicaLeishmania braziliensisLeishmania donovani
Leishmanias
Occur in the southern region of North AmericaMediterranean basinEast and North AfricaArabian PeninsulaPersian Gulf regionChina, and Southern Soviet UnionMost severe forms are found in Africa, Latin America
and India
Parasite biologyLeishmanias
produce amastigotes intracellularly in the mammalian host
Promastigote in the midgut and proboscis of the insect vector
LeishmaniasisAmastigote
Ovoid or rounded
Live intracellularly in monocytes, polymorphonuclear leukocytes, endothelial cells
Nucleus is large
Promastigote
Have single free flagellum arising from the kinetoplast at the anterior end
Leishmania spp.
Leishmania tropica – seen around the Mediterranean Sea, Middle East to Central Asia, China and India
Leishmania donovani – Mediterranean Sea, in Africa, India, China, and also in South AmericaTransmitted by sand flies of the genus Phlebotomus
Leishmania braziliensis – Mexico through Central America to South AmericaTransmitted by sand fly genus Lutzomyia
Cutaneous leishmaniasisLeishmania tropica minor – usually features single
solitary ulcerating lesions on the exposed parts of the skin
Leishmania tropica major – is the common important species responsible for zoonotic leishmaniasis and features multiple cutaneous lesions
Leishmania aethiopica – causes a range of lesions from solitary lesions to diffuse cutaneous involvement and to mucocutaneous leishmaniasis
Clinical feature
Incubation period varies between 2-8 moLesion starts at the site of infection → nodule →
ulceratesThis heals in about 6 moThere is an assoc. life long immunity from disease
Cutaneous leishmaniasis is marked by sores that often look like
volcanoes: they have a central pit and a raised
rim. They can be painful or painless and
may be covered by scabs. The sores tend to appear on the face,
arms, and legs, and some people have as many as 200 of them.
Patients with cutaneous leishmaniasis also may have swollen lymph nodes* near the sores
Mucocutaneous leishmaniasis
Caused by Leishmania brazillensis
Vector is Lutzomyia sand fly
Disease starts as cutaneous leishmaniasis
During the course of primary infection or several yrs after healed there is metastatic spread to involve the oronasal or the pharyngeal mucous membrane
Disease is called espundia
Mucocutaneous…
Mucosal involvement takes the form of an ulceration and erosion of soft tissues and cartilage with serious deformities
It may be painful or painlessDisease does not heal spontaneously and death is
due to malnutrition or secondary bronchopneumoniaIndividual w/ mucocutaneous leishmaniasis show both
a strong cell mediated immune rxn and presence of circulating ab.
Mucocutaneous Leishmaniasis
Ulcers on the oral or nasal mucosa. If untreated, all of the nasal mucosa will be infected and the septum will be destroyed.
This form of the disease usually spreads more widely than the cutaneous form.
Leishmania braziliensis pathology1. Promastigotes inoculated into skin transform into amastigotes
and enter skin macrophages
2. Amastigotes metastasize and spread to the mucocutaneous zones
• secondary lesion:nasal system and buccal mucosa causing degeneration of cartilage and soft tissues.
• ulceration may involve mucous membranes and cartilaginous tissues of the lips, nose, palate, and pharynx are destroyed; larynx may also be involved, destroying voice
Leishmania donovani
Causative agent of visceral leishmaniasis
Identified by William Leishman in 1900 from a soldier who died of fever in Dum-Dum, India. Charles Donovan identified the parasites in the spleen of an infected person in 1903. Parasite is named in honor of these two men.
Vector – Phlebotomus spp.
Leishmania donovani
• Amastigotes multiply in macrophage, eventually rupturing the cell
• Free amastigotes then invade the circulatory system.
Pathogenesis
May range from asymptomatic to fully develop kala-azar
Fever, malaise
Wasting and anemia
Protrusion of abdomen from enlarged liver and spleen leading to death
Pathogenesis
Visceral leishmaniasis may be viewed as disease of RES, the phagocytic cells:habitat of parasiteBlood forming organ:bone marrow and spleen
undergo production of macrophages and other phagocytes to the detriment of red cells production.
The spleen and liver become greatly enlarge “hepatospleenomegaly”
Visceral LeishmaniasisAbdominal swelling without
definite illness, anemia, dermal nodules or lesions resembling leprosy. Diagnosis is made by visualizing the parasite. Samples taken from a sternal marrow aspiration
Leishmania donovani
DIAGNOSISDIAGNOSIS
visceral leishmaniasis-blood sample and/or taking a biopsy from the bone marrow to show the parasite.
cutaneous leishmaniasis will require a small biopsy or scraping of the ulcer.
mucocutaneous leishmaniasis requires a biopsy of the affected tissues.
Biopsy samples are examined by microscopy, culture and other methods to look for the parasite and identify the specific kind of Leishmania causing the ulcer. Some of these methods will give results within a few days, but culture may take 2-4 weeks to demonstrate the parasite.
Prevention
Control of sand flies
Protect wound from insect bite
Health Education in endemic areas
End of Blood and Tissue Flagellates….
Thank you!By: Hazel Carbon-Granil, RMT, MiB, MSMT