Blood and Tissue Flagellates Overview for Medtech Students

Blood and Tissue Flagellates Overview for Medtech Students

Blood and tissue flagellates, including Leishmania and Trypanosoma species, are critical topics for second-year Medtech students. This resource explores the life cycles, pathogenesis, and clinical manifestations of these parasites. Key areas include cutaneous leishmaniasis, visceral leishmaniasis, and the various forms of trypanosomiasis. Understanding these pathogens is essential for diagnosing and treating related diseases in clinical settings. This overview is tailored for students preparing for exams in clinical parasitology.

Key Points

  • Explains the life cycle of Leishmania spp. and its transmission via sandflies.
  • Describes clinical manifestations of cutaneous and visceral leishmaniasis.
  • Covers Trypanosoma cruzi and its role in Chagas disease.
  • Details the pathogenesis of African trypanosomiasis caused by Trypanosoma brucei.
  • Includes diagnostic techniques for identifying blood and tissue flagellates.
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  • Krissia Gracelle Cernal
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C L I N I C A L P A R A S I T O L O G Y
LEC 12: BLOOD AND TISSUE FLAGELLATES
MS. MARTINA DEANNE C. MENDOZA, RMT
Page 1 of 4
Leishmania SPP
Early descriptions of leishmaniasis have been found as
eaerly as the first century A.D., where American Indians
documented the disease in pottery figures
Cunningham studied the “Delhi boil” in INdia back in 1885,
and Leishman has properly identified the intracellular
parasites in 1903
Leishmania braziliensis was later indentified in 1911 by
Gaspar Viana, as was the insect vector which transmitted
the parasite in 1922 by Henrique Aragao
Leishmaniasis is a zoonotic infection in which dogs and
rodents serve as the primary reservoir hosts for all
species, and humans serve as an accidental host
The life cycle of the parasite involves a vector, the female
sandlfy of the Phlebotomus and Lutzomyia genera
It is an obligate intracellular parasite
It has three morphologic forms:
1. Amastigote - pathogenic stage and diagnostic form;
found primarily in tissue and muscle, as well as the
CNS within macrophages and in cells of the
reticuloendothelial system
2. Promastigote - may be seen only if a blood sample is
collected and examined immediately after
transmission
3. Epimastigote - found primarily in the vector
The typical amastigote is round to oval in shape and
contains a nucleus, a basal body structure called a
blepharoblast, and a small parabasal body located
adjacent to the blepharoblast
Both the blepharoblast and parabasal body are collectively
known as the kinetoplast
The promastigote is long and slender, with a kinetoplast
located in its anterior end, and a single flagellum extending
from the anterior portion
Epidemiology
Epidemiologically, the Leishmania spp. Are divided into Old
World and New World Leishmaniasis
Old World Leishmaniasis - arthropod is of the genera
Phlebotomus
L. tropica (Asia and Eastern Europe)
L. aethiopica (Africa)
L. major
New World Leishmaniasis - arthropod is of the genera
Lutzomyia
L. mexicana
L. amazonensis
L. guyanensis
L. braziliensis
L. chagasi
Leishmaniasis is primarily a disease of poverty. It affects
people living in squalid conditions, and is associated with
poor housing, malnutrition, a weak immune system, and
lack of resources
Life Cycle
Leishmaniasis is transmitted by the bite of infected female
phlebotomine sandflies
It may also be transmitted congenitally, through blood
transfusion, by contamination of the bite wounds, and by
direct contact with contaminated specimens
1. The sandflies inject the infective stage (i.e., promastigotes)
from their proboscis during blood meals
2. Promastigotes that reach the puncture wound are
phagocytized by macrophages and other types of
mononuclear phagocytic cells
3. Promastigotes transform in these cells into the tissue stage
of the parasite (i.e., amastigotes), which multiply by simple
division and proceed to infect other mononuclear
phagocytic cells
→ parasite, host, and other factors affect whether the
infection becomes symptomatic and whether cutaneous or
visceral leishmaniasis results
4. Sandlfies become infected by ingesting infected cells during
blood meals
5. In sandflies, amastigotes transform into promastigotes,
develop in the gut, and migrate to the proboscis
→
in the hindgut for leishmanial organisms in the Viannia
subgenus
→ In the midgut for organisms in the Leishmania subgenus
Page 2 of 4
Pathogenesis and Clincial Manifestations
Cutaneous Leishmaniasis (CL)
Most common form of the disease
Caused by several species of Leishmania including
L. tropica - dry or urban oriental sore
L. major - moist or rural oriental sore
L. mexicana - chiclero ulcer, usually affecting the ears
Incubation period: 2 weeks to several months
An erythematous papule or nodule, called an “oriental
button”, is produced at the inoculation site. The lesion has
raised edges and a central crater
During the course of several weeks, the papules form a
violaceous ulcer as it enlarges in size
The lesion may heal spontaneously after a few months,
leading to a disfiguring scar; in the case of New World
Leishmaniasis, CL may progress to other forms of
Leishmaniasis
Diffuse Cutaneous Leishmaniasis (DCL)
The manifestation of DCL, also called anergic or
lepromatous leishmaniasis, is characterized by a
localized, non-ulcerating papule, eventuallly developing
numerous diffuse satellite lesions that affect the face and
extremeties
This type of leishmaniasis may be initially diagnosed as
lepromatous leprosy
Mucocutaneous Leishmaniasis (MCL)
Develops in about 2 - 5% of persons infected with L.
braziliense
It may also be due to the contagious spread of cutaneous
leishmaniasis caused by L. tropica
Involvement of the mucous membranes of the nasal and
oral cavities results in nasal stuffness discharge, epistaxis,
and destruction of the nasl septum. This disfiguration is
often called espundia
Systemic Th1 (cellular immunity) response is strong in
cases of MCL, with increased levels of peripheral
mononuclear cells in the blood
Visceral Leishmaniasis (VL)
Also known as kala azar, is a disseminated parasitosis
primarily caused by L. donovani complex: L. donovani, L.
chagasi, and L. infantum
Incubation period: 2 - 8 months
The manifestation of the disease stems from the spread of
parasites into the bone marrow, spleen, and liver
Acute phase - twice-daily fever spikes (double quotidian)
accompanied with chills
→ can be mistaken for malaria
Post-kala azar dermal leishmaniasis (PKDL) - it
manifests as a cutaneous eruption resulting in
hypopigmented macules, malar erythema, nodules, and
ulcerations
→
lesions usually manifest a few months to several
years after treatment
It is an important opportunistic infection in AIDS patients
Immunosuppression from HIV predisposes to VL, while VL
infection accelerates HIV replication and progression to
AIDS
Leishmania tropica
amastigotes from an
impression smear of a biopsy
specimen from a skin lesion. In
this figure, an intact
macrophage is practically filled
with amastigotes (arrows),
several of which have a clearly
visible nucleus and
kinetoplast.
Leishmania sp. promastigotes
from culture.
Trypanosoma SPP
The trypanosomes are also hemoflagellates like Leishmania
The major difference between the two lines in their
diagnostic stages, which is the amastigote for Leishmania
and the trypomastigote for the trypanoosomes
The trypomastigotes are curved, assuming the shape of
the letters C, S, or U
The trypomastigotes are visible in the peripheral blood
Trypanosoma Cruzi
The parasite is found primarily in South and Central
America
It is transmitted by the bite of the reduviid or triatomid
bug (Triatoma or “cone-nose” bug or “kissing bug”)
Page 3 of 4
It is usually transferred to a human host when the feces of
the bug containing the infective trypomastigotes is
deposited near the bite site
Other routes of transmission:
Blood transfusion
Sexual intercourse
Transplacental transmission
Through the mucous membranes when the bite site is
near the eye or mouth
Life Cycle
An infected triatomine insect vector (or “kissing” bug) takes
a blood meal and releases trypomastigotes in its feces near
the site of the bite wound
Trypomastigotes enter the host through the bite wound or
intact musocal memnbranes, such as the conjunctiva
Inside the host, the trypomastigotes invade cells near the
site of inoculation, where they differentiate into
intracellular amastigotes
The amastigotes multiply by binary fission and differentiate
into trypomastigotes, and then are released into the
circulation as bloodstream trypomastigotes
Pathogenesis and Clinical Manifestations
Acute phase
Incubation period: 2 - 4 weeks
As the organisms enter the blood, the acute phase begins
and lasts 4 to 8 weeks
Infected individuals may be asymptomatic or have local
symptoms, including the presence of a Chagoma, an
ulcerative skin lesion at the site of the insect bite, or
unilateral edema around the eye (Romaña sign) if the bite
is near the ocular conjunctiva
Systemic manifestations include fever, lymphadenitis,
hepatosplenomegaly, malaise, muscular pains, and diarrhea
and vomiting
Latent Phase
It develops as the trypomastigotes disappear from the
circulation and invade the cells of the cardiac or GI system
Chronic form
30% to 40% of patient develop cardiomyopathy
Chronic myocarditis develops with damage to all heart
chambers and the conduction system. This may progress to
tachycardia and eventually congestive heart failure
Laboratory Diagnosis
Direct visualization of the parasites in thick and thin
blood smears using Giemsa stain
Trypomastigotes:
C or U shaped
Large nucleus midbody
Single anterior flagellum
Posterior kinetoplast
In chronic stage, the organism may be seen as an
amastigote in a cardiac or other tissue biopsy
specimen
Only in the first two months of acute disease can T.
cruzi trypomastigotes be seen by direct examination
Cerebrospinal fluid (CSF), tissue samples, or lymph can
also be used for parasite visualization
Other diagnostic techniques
Concentration methods (microhematocrit)
Blood culture
PCR
Xenodiagnosis
A laboratory-raised triatomid bug is allowed to feed
on patients suspected of having T. cruzi infection
The insect’s feces are examined on a regular basis for
the presence of a trypomastigote
Presence of the parasite in the insect’s feces indicates
that the patient was infected
This method is most helpful for diagnosisng infections
in the chronic stage, when fewer parasites are present
Trypanosoma Brucei Gambiense
Trypanosoma Brucei Rhodesiense
The causative agents of human Africa trypanosomiasis
(HAT) or sleeping sickness
A third subspecies, T. brucei, primarily affects wild and
domestic animals
The tsetse fly (genus Glossina) serves as the insect vector
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FAQs of Blood and Tissue Flagellates Overview for Medtech Students

What are the main types of leishmaniasis?
Leishmaniasis is primarily classified into cutaneous leishmaniasis (CL), visceral leishmaniasis (VL), and mucocutaneous leishmaniasis (MCL). CL is the most common form, characterized by skin ulcers, while VL, also known as kala azar, affects internal organs and can be fatal if untreated. MCL involves lesions in the mucous membranes, often resulting from the spread of CL. Each type is caused by different Leishmania species and has distinct clinical presentations.
How is Trypanosoma cruzi transmitted?
Trypanosoma cruzi is primarily transmitted through the bite of infected triatomine bugs, commonly known as 'kissing bugs.' These bugs deposit feces containing trypomastigotes near the bite site, allowing the parasites to enter the host through the wound or mucous membranes. Other transmission routes include blood transfusions, congenital transmission, and through mucosal contact. Understanding these transmission pathways is crucial for preventing Chagas disease.
What are the symptoms of visceral leishmaniasis?
Visceral leishmaniasis, caused by the Leishmania donovani complex, presents with symptoms such as prolonged fever, weight loss, splenomegaly, and anemia. The incubation period can range from 2 to 8 months, and without treatment, it can be fatal. Patients may experience double quotidian fever spikes and systemic manifestations as the parasites invade the bone marrow, spleen, and liver. Early diagnosis and treatment are essential for improving patient outcomes.
What diagnostic methods are used for trypanosomiasis?
Diagnosis of trypanosomiasis involves several methods, including direct visualization of trypomastigotes in blood smears, serological tests, and PCR. Wet preparations can reveal highly motile trypomastigotes, while thick and thin blood smears stained with Giemsa help identify the parasites. In chronic cases, amastigotes may be found in tissue biopsies. These diagnostic techniques are crucial for timely and accurate identification of the disease.
What is the significance of antigenic variation in Trypanosoma brucei?
Antigenic variation is a key survival mechanism for Trypanosoma brucei, allowing the parasite to evade the host's immune response. By continuously changing its surface glycoproteins, the parasite can avoid detection by antibodies, leading to recurrent waves of parasitemia. This ability complicates treatment and contributes to the chronic nature of African sleeping sickness. Understanding this mechanism is vital for developing effective therapeutic strategies.

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