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- Taxonomic lineage
- Brief facts
- Cell transformations
- Life cycle
- Cellular structures
- Transmission pathways
- Chagas disease stages
General informationTrypanosoma cruzi, a flagellate eukaryote of the order Kinetoplastida, is a member of Trypanosomatidae family that comprises a large number of species of pathogens that have a major impact on human and animal health by causing such diseases as sleeping sickness African trypanosomaniasis), Chagas disease (American trypanosomiasis) and leishmaniasis.
ImportanceTrypanosoma cruzi is causative agent of Chagas disease, which is one of most important health problem in large regions of South and Central America, affecting about 14 million people, with about 100 million people remaining at risk.
Geographic distributionEndemic foci of the human disease (also called Chagas disease) range from Mexico to the Northern half of Argentina and Chile, mostly in poor rural areas where houses are infested with domestic species of Triatominae (kissing bugs).
Triatominae, kissing bugs, vectors of Chagas disease at MetaPathogen
As for animal trypanosomiasis, its distribution is widespread from the Southern United States to Patagonia (roughly 40° N to 45° S).
PhylogenyPhylogenetic analyses have placed the protozoan T. gray that can be found in the blood of crocodiles and possibly date to around 480 million years ago, at the root of the kinetoplastids, next to bodonids (Bodo saltans). The life-cycles of trypanosomatids account for their major division into Salivarian and Stercorarian branches, completing the infective metacyclic stages, respectively, in the salivary gland and in the hind gut of invertebrate vectors.
DiscoveryT. cruzi was discovered by Carlos Chagas, a Brazilian physician who worked at the Oswaldo Cruz Institute, Rio de Janeiro, in 1909. He recognized it as the etiological agent of American trypanosomiasis (Chagas' disease).
Generalist parasiteTrypanosoma cruzi is characterized by heterogeneity and plasticity. It is capable of infecting more than a hundred species of mammals and nearly all the tissues. The organism also infects dozens of triatomine species from the Reduviidae family (commonly called "kissing bugs"), which serve as vectors.
PaleoparasitologyIt is estimated that the parasite emerged as a species over 150 million years ago, originally infecting mammals throughout Laurasia and Gondwanaland. The first contact with humans occurred more recently, in the late Pleistocene, 30,000–15,000 years ago, when humans first populated the Americas. There is molecular evidence for the presence of T. cruzi DNA in Chile mummies dated from 470 BC. Humans have probably contracted the parasite through different routes, depending on how they interacted with the environment. Hunters and gatherers were described as consumers of raw meat because remnants of raw bones and rodent fur have been detected in human coprolites. The oral route is efficient for T. cruzi transmission: not only the metacyclic forms are capable of invading intact mucous membranes, but also the stomach's acid exposes epitopes on the parasite's surface that increase their infectivity. The interactions with the parasites intensified in prehistoric populations 8,000-6,000 years ago when first settlements were established and the triatomine vectors, especially the T. infestans species, found shelter and blood meals in the primitive dwellings containing both humans and their animals.
Animal reservoirRecent studies have shown that in a non-endemic area of the Brazilian Atlantic coastal rainforest, 50% of the triatomine vectors, marsupials as well as several species of New World primates were naturally infected with T. cruzi. Moreover, in the US T. cruzi has been found in 11.4% of opossums and 22% of raccoons, together with infected triatomine bugs in the state of Georgia. In certain areas of that state, up to 43% of the raccoons were infected. Another study has shown that 3.6% of rural hunting dogs in Oklahoma were seropositive for T. cruzi. Furthermore, the complete T. cruzi lifecycle was observed in an ecosystem located in Baja California, Mexico in lizards that were infected by ingestion of the infected triatomine bug Dipetalogaster maximus, and thereafter uninfected D. maximus acquired the parasite upon feeding from that lizard. Thus, the ultimate reservoirs of these trypanosomes may not be mammalian.
Genome and lineagesT. cruzi genome has been recently sequenced and is estimated to be between 106.4-110.7 Mb in size (diploid). At least 50% of the parasite's genome is repetitive sequence, consisting mostly of large gene families of surface proteins, retrotransposons and subtelomeric repeats. Two major evolutionary divergent lineages of the parasite, named zymodeme I (ZI, now TcI) and zymodeme II (ZII, now TcIIb), have been identified. Zymodeme is a group of strains that have the same isozyme profile. The two lineages are predominant in two distinct ecological environments: the sylvatic and domestic transmission cycles of Chagas disease, respectively. Lineages are also called Discrete Typing Units (DTUs). Molecular data showed that lineage II is further subdivided into five smaller lineages. However, there are some parasite strains that cannot be properly grouped into any one of these two major lineages. Differences between clinical manifestations of Chagas disease in different geographical regions (megaesophagus and megacolon are prominent in the southern countries of South America but either absent or rare in northern South America and Central America) can be circumstantially linked to the radical genetic differences between the strains of T. cruzi that predominantly cause Chagas disease in Brazil (ZII/TcIIb) and in Venezuela (ZI/TcI).
The amastigotes are generally 3–5 µm in diameter,
with a short round cell body and a very short flagellum, replicative.
In the environment of the reduviid midgut, amastigotes transform into
epimastigotes. At the start of the transformation, they
swell and extend their flagella, which begin to beat visibly. At this
stage, the forms are sometimes referred to as spheromastigotes.
The intracellular amastigotes can persist dormant in the host body for decades, hidden in muscle cells without causing significant damage to the tissues.
Spindle-shaped, 20–40 µm long with kinetoplast located anterior to the nucleus.
These forms are able to divide and are observed at the logarithmic phase
of growth in axenic cultures and in the intestine of the invertebrate host.
Epimastigotes are also found within vertebrate cells towards the end of the
intracellular cycle when the spheromastigotes transform into trypomastigotes
or at the beginning of a new cycle when the trypomastigotes transform into
Since amastigotes, spheromastigotes and epimastigotes are proliferative, the transition from one of these forms to another appears to be a continuum, rather than a one-step differentiation event which co-ordinates gross cellular change with exit from or re-entry to the cell cycle.
Due to the ability to obtain in vitro axenic cultures, most of the studies on T. cruzi have been done with the epimastigote form.
These forms are about 25 µm in length and about
2 µm in diameter. The kinetoplast is located posterior to the nucleus.
They can be observed (i) in the tissue cells and in the blood of
the vertebrate host, (ii) in the posterior intestine, in the feces,
and in the urine of the invertebrate host, (iii) at the stationary
phase of growth in axenic cultures, and (iv) in the liquid phase of
cell cultures. These forms are not able to divide.
trypomastigote Contrary to what is known for the African trypanosomes, the trypomastigote form of T. cruzi does not divide in the bloodstream.
trypomastigote Elongated nucleus, a subterminal kinetoplast, and a short free flagellum. It has been suggested that the slender forms are mainly responsible for the infection of the vertebrate cells
trypomastigote An oval nucleus, an almost terminal kinetoplast, and a long free flagellum. The broad forms are more able to infect the invertebrate host.
trypomastigote In contrast with pleomorphic bloodform trypomastigotes that appear not to truly exit from the cell cycle, but to merely exist in a protracted G1 phase, the monomorphic metacyclic forms, that were formed in bug's hindgut, shows characteristics of true cell cycle arrest and could be considered to be resident in G0 until triggered to re-enter the cell cycle upon host cell invasion. This, coupled with documented differences in gene expression, justifies the discrimination of bloodstream and metacyclic forms as physiologically distinct life cycle stages.
trypomastigotes The biological cycle of T. cruzi starts when the invertebrate host feeds on the vertebrate host by sucking blood and ingests a pleomorphic population of bloodstream trypomastigotes, consisting of both slender and broad forms, and up to 10% amastigotes.
in stomach It has been assumed that in the stomach of the insect most of the bloodstream trypomastigotes transform into two forms of epimastigotes (short and long) and some of them transform into spheromastigotes.
in midgut In the intestine the short-form epimastigotes and spheromastigotes divide repeatedly by a process of binary fission while long epimastygotes that are unable to divide move to the more posterior region of the digestive tract of the bug.
in hindgut Metacyclogenesis. Prior to differentiating into non-replicative metacyclic forms, elongate epimastigotes attach to the waxy cuticle of the hindgut wall. Once formed, metacyclics detach from the waxy cuticle and are excreted. Contamination of the reduviid bite wound or mucous membrane of a vertebrate host with these excreta leads to infection.
- Ingestion of
vertebrate host Vertebrate host acquires infection by eating the infected insect, by ingestion of the insect's feces or when infected feces contaminate a bite spot or another break in the skin.
trypomastigotes Upon entry into bloodstream of vertebrate host, trypomastigotes invade the host's cells. Studies have shown that the parasite always penetrates the host cell by an endocytic process: the microtubule cytoskeleton of the mammalian cell is directed to recruit lysosomes to the point of parasite attachment. These lysosomes fuse with the plasma membrane, first forming a junction with the parasites and then a vacuolar compartment (parasitophorous vacuole or PV) allowing parasite's entry.
- Epimastigotes When inside the cell, the trypomastigotes transform into amastigotes. This process is characterized by shortening of the flagellum and rounding of the cell body. During the trypomastigote-spheromastigote transformation there is an intermediary phase, which is designated as epimastigote, although this form is somewhat different from the epimastigote observed in axenic cultures.
- Amastygotes Two hours after penetration, a gradual lysis of the membrane lining the PV occurs due the release of a trypsin-sensitive parasite enzyme known as TcTox. After the complete rupture of the PV membrane, the amastigote form establishes direct contact with the host cell cytoplasmic structures and organelles and after 24 to 35 hours starts to divide by binary fission. The doubling time of the parasite is about 14 hours. The process of cytokinesis requires about 25 minutes for completion. Proliferating amastigotes form a pseudocysts; after several successive divisions they asynchroniously transform into trypomastigotes, via an epimastigote intermediate stage. In several hours pseudocysts become packed with trypanosomes in different stages of differentiation from amastigote to trypomastigote. Five distinct morphologies were observed in this population – amastigote, epimastigote, and three morphologies of trypomastigote: slender, broad and lozenge-shaped.
Trypomastigotes At high density, amastigotes give rise to bloodstream trypomastigotes via intermediate forms, some of which have epimastigote morphology. Once formed, trypomastigotes generally escape from the pseudocyst into the blood and lymph as slender forms, which can invade new cells in a manner essentially similar to metacyclic invasion. Slender forms which fail to invade a new cell undergo morphological change, first the broad form and then to the amastigote. This default pathway of differentiation is presumably the cause of the observed pleomorphism in the trypomastigotes of the peripheral blood. Cells that are prematurely lysed may also release amastigotes, which are observed in the bloodstream during the acute phase of infection. These amastigotes too are able to infect cells, particularly phagocytic cells, albeit by a different mechanism than trypomastigotes. Finally, the mixture of trypomastigotes and amastigotes present in the blood of an infected mammal serves to complete the life cycle when taken up in a blood meal by a reduviid bug.
- Invasion of
The nucleus is elongate and localized in the central portion of the cell.
In spheromastigotes and epimastigotes it has a rounded shape.
There is continuity between the outer nuclear membrane and
the endoplasmic reticulum.
- Nucleolus The nucleolus may be found in the center of the nucleus. The nucleolus is dispersed during division, reappearing at the final phases of the cell division. It has been shown that a nucleolus is not observed in trypomastigote forms and that there is a decrease in the transcription rates by RNA polymerases I and II when epimastigote forms transform into trypomastigote forms.
The cell surface of trypanosomatids can be considered as composed by two
components: the plasma membrane and a layer
formed by the subpellicular microtubules.
Cell surface-associated components that face the extracellular medium and form the glycocalyx (also known as the cell coat or the surface coat) include the mucins, transialidase and the Tc85 family of glycoproteins.
The surface of trypomastigotes is very rugous, probably due to exposed proteins.
It is possible to identify at least
three macrodomains of the membrane that in turn
possess specific microdomains.
- Flagellum All members of the Trypanosomatidae family have a flagellum. In developmental stages such as promastigote, paramastigote, opisthomastigote, and choanomastigote, the flagellum emerges at the anterior tip whereas in epimastigote and trypomastigote forms it emerges somewhere along the side. The proportion of the total flagellar length to that inside the flagellar pocket region varies according to the developmental stage. Even in amastigote form, a short flagellum is present.
- Flagellar pocket Consists of flagellar necklace (structure localized at the basal portion of the flagellum) and flagellum attachment zone. All trypanosomatids possess a region known as the flagellar pocket which appears as a depression found in the anterior region of the cell from where the flagellum emerges. It is formed by an invagination of the plasma membrane that establishes a direct continuity with the membrane of the flagellum.
- Cytostome Observed in epimastigote and amastigote forms. The cytostome is an invagination of the plasma membrane followed by a few specialized microtubules that penetrate so deeply into the cell that they may reach the nuclear region. The opening of the cytostome can reach a diameter of up to 0.3 µm; however, it is significantly smaller in the deeper portion, the cytopharynx, which resembles a funnel. When epimastigotes are incubated in the presence of gold labeled macromolecules such as transferrin, LDL, etc., they initially bind to the cytostome region. Following binding to the cytostome macromolecules are rapidly internalized via the cytopharynx and appear in small endocytic vesicles which bud from the deepest region of this structure. Subsequently, these vesicles fuse to each other to form tubular structures that can be observed in the most central portion of the protozoan. Later on the macromolecules are concentrated in structures known as the reservosome.
microtubules One of the characteristic features of protozoa Trypanosomatidae is the presence of a layer of microtubules localized below the plasma membrane and designated as subpellicular microtubules. It has been observed that the microtubules are connected to each other and to the plasma membrane by short filaments. This association is probably responsible for the rigidity of the cell and the difficulties found in the disruption of the cell by mechanical means.
- Plasma membrane It is possible to identify at least three macrodomains of the membrane that in turn possess specific microdomains.
Kinetoplast T. cruzi, as well as other members of the Trypanosomatidae family, possesses only one mitochondrion that extends throughout the cell body. At a portion of the mitochondrion, localized near the basal body of the flagellum, there is a complex array of DNA fibrils which forms the characteristic structure known as kinetoplast. There is a space between the kinetoplast and the inner mitochondrial membrane in which mitochondrial cristae can be seen. At least some fibrils of the kinetoplast DNA make contact with the inner mitochondrial membrane. The kinetoplast DNA represents between 20 and 25% of the total DNA of epimastigotes of T. cruzi. It consists of a network of 20,000 to 30,000 so-called kDNA minicircles. Each minicircle has a length of about 0.45 µm, which corresponds to about 1440 base pairs. In addition to the minicircles there are 20–50 maxicircles of ~36 kb. The division of the kinetoplast is coordinated with cell division. Division in T. cruzi begins with the replication of the basal body and flagellum, followed by the division of the kinetoplast.
Maxicircles are homogeneous circular DNA molecules that encode proteins involved in energy production and are similar to conventional mitochondrial DNA; minicircles, are more heterogeneous, can be separated into sequence classes whose number and type differ between species, and encode guide RNAs for editing mitochondrial mRNAs. Each minicircle is organized into four 120 bp highly conserved regions separated by four highly variable regions. Parasite populations displaying identical or similar kDNA minicircle restriction patterns have been called schizodemes.
The structure and function of the kDNA complex is not completely elucidated. The revelation that minicircles are integrating into the host genome and correlated to the pathology of Chagas has renewed interest in understanding the composition of minicircles within the known sub-groups of T. cruzi. Minicircle kDNA integrations behave as mutagens in the host.
Or glycosome. Membrane-bound cytoplasmic structures
resembling peroxisomes in mammalian cells.
In the case of mammalian cells, these structures contained catalase, an enzyme involved in the degradation of hydrogen peroxide formed in metabolic reactions. A major breakthrough in this area was the discovery that most of the glycolytic pathway takes place in this organelle; thus it was eventually designated as the glycosome. In other cell types, glycolysis takes place in the cytosol. Since glycosomes found in the monogenetic trypanosomatids contain catalase, but those found in the digenetic ones do not, they are now considered to be a special type of peroxisome.
- Acidocalcisome Vacuolar structures containing electron-dense deposits. Functions of these organelles are not completely elucidated. Researchers consider four possibilities: (a) a role in the process of Ca2+ storage to be used in certain moments of the parasite's life cycle (amastigote forms live in the cytoplasm of the host cell where the concentration of Ca2+ is in the range of 0.1 mM, in contrast to the trypomastigote form which lives in a environment where the concentration is around 2 mM); (b) an energy storage (the organelle contains a large amount of inorganic PPi; (c) a possible role in the regulation of the cytoplasmic pH; (d) the control of the process of osmoregulation.
- Golgi complex The secretory pathway in T. cruzi is formed by the ER, Golgi complex and a system of vesicles that bud from the Golgi cisternae and migrate toward the flagellar pocket where they fuse and discharge their contents into the flagellar pocket. ER cisternae are seen around the nucleus and radiate towards all cell regions, especially the peripheral region where microtubules are located. Both rough and smooth ER cisternae can be seen. The Golgi complex is always located close to the flagellar pocket and is has morphology similar to that described in other cells.
- Reservosome Each epimastigote form possesses several reservosomes, mainly localized in the posterior region of the cell. Usually it is a spherical organelle, with a mean diameter of 0.7 µm, surrounded by a unit membrane. The matrix of the reservosome is slightly dense and possesses some inclusions. The organelle was designated as reservosome based on two criteria: (1) because all macromolecules ingested by the parasite through an endocytic process, accumulate in the organelle; (2) because it gradually disappears when epimastigotes are incubated in a poor culture medium, conditions which trigger the process of transformation of non infective epimastigote into infective trypomastigote forms. Reservosomes were found to be the main functional site of cruzipain in epimastigotes, pointing to a lysosome function, although no other lysosome markers has been identified in the organelle. During metacyclogenesis, when epimastigotes differentiate to infective trypomastigote forms, the organelle disappears. Reservosomes have been described as an exclusive structure of epimastigote forms.
- Fecal contamination of bite wound.
- Ingestion of uncooked meat of infected animal.
- Ingestion of food contaminated with feces or crushed parts of infected bug.
- Placental (from mother to child) transmission.
Blood-borne transmission pathways:
- Blood transfusion.
- Organ transplant.
- Accidental self-inoculation by hospital personnel.
- Chagas disease (American trypanosomiasis) is the clinical condition
in human triggered by
infection with the protozoan Trypanosoma cruzi.
In nature the infection is enzootic (i.e.
is constantly present in an animal population, but usually
causes fatal pathologies only in a small number of animals).
Field studies predict that one
third of an estimated 18 million T. cruzi-infected humans in
Latin America will die of Chagas disease. The pathogenesis of
Chagas disease appears to be related to a parasite-induced
mutation of the vertebrate genome. Currently,
treatment is unsatisfactory.
Although immunity represents a barrier against parasite circulation in the blood, it does not eliminate parasites that colonize non-phagocytic muscle cells, allowing the protozoa to persist throughout its host's life. Thus, vaccination against Chagas disease is not possible with the currently available biotechnologies. Currently available chemotherapy with anti-trypanosome nitroderivatives shows severe toxicity and does not provide a complete cure.
Two theories have been set forth to explain the pathogenesis
of the lesions in Chagas disease. The parasite persistence
theory postulates that Chagas lesions could be a direct
consequence of the mechanical rupture of the parasitized
host cells and subsequent inflammation. The autoimmune
theory ascribes Chagas lesions to the rejection of parasite-free
target cells by immune lymphocytes.
These theories may not be mutually exclusive.
A unique pathological feature seen in every chagasic individual is inflammatory mononuclear cell infiltrates and lysis of target cells. This minimal rejection unit can be used to define pathology accordingly to the target tissue involved. In this respect, target units could affect either striated or smooth muscles, or neurons of the sympathetic and parasympathetic nervous systems. Although each of these pathologic lesions is detected in every chagasic, the hallmark heart lesions are associated with 94.5% of deaths. Another key feature of T. cruzi infection is the integration of kDNA minicircles into the host genome followed by vertical transmission to the progeny. The integration-induced mutations can enter multiple loci in diverse chromosomes, generating new genes, pseudo genes and knock-outs, and resulting in genomic shuffling and remodeling over time.
- Acute stage Infection with T. cruzi leads to an acute phase during which circulating parasites are numerous and able to infect several tissues in the host, including skeletal muscle, lymphoid tissues, nervous tissues, and glands. In humans, the acute phase lasts for about two months. In 95% of the cases, the acute phase is asymptomatic or is not percieved by the patient. In the remaining symptomatic cases, the clinical manifestations of acute Chagas disease are fever, malaise, muscle and joint pains, somnolence, cramps and diarrhea, edema, respiratory disturbances, and inflammatory reaction at the vector's biting site (chagoma). The acute phase usually goes into remission spontaneously and the infection enters the chronic stage.
chronic phase Following the acute phase, the patient enters into a long indeterminate latent phase with no symptoms and very low parasitism. The latent infection remains silent for 10 to 30 years. About one third of infected patients in the latent phase develop clinical symptoms such as chronic cardiac dysfunction (cardiomyopathy), megacolon, or megaesophagus. People considered to be in the indeterminate chronic phase of the infection do not die of Chagas disease. The chronically infected individual remains a life-long source of the parasite as an indeterminate phase reservoir. Approximately one third of all individuals with indeterminate infections will develop chronic Chagas disease.
disease The symptomatic disease affects the heart in 94.5% of cases; these patients are considered to have chronic Chagas heart disease. Heart insufficiency is related to the cause of death in 58% of patients, whereas arrhythmias have been associated with unexpected deaths in 36.5%. Many patients (58%) with chronic Chagas heart disease frequently die within 7 months to 2 years after the onset of symptoms. The size of the heart of a patient with congestive heart failure is markedly increased and often reaches twice the normal size. The main microscopic findings always present in a patient with chronic Chagas heart disease are inflammatory infiltrates and target heart cell lyses.
disease The remaining 4.5% of patients with chronic Chagas infection show mega syndromes, a disease state that involves esophagus (megaesophagus) and colon (megacolon). Megaesophagus and megacolon consist of gross dilation of the organs and thickening of their walls accompanied by loss of motility of these segments because of inflammatory infiltrates in smooth muscles as well as because of loss of the parasympathetic neurons within the walls.
- Megaesophagus Megaesophagus can manifest clinically as early as 2 years of age, although the majority of cases are seen in men between 20 and 40 years old. The disease manifests by dysphagia, heartburn, hiccups, regurgitation of food, and increasing salivation.
- Megacolon Megacolon is seen later in the course of Chagas disease in comparison with megaesophagus. The main symptom is constipation. The hardened bolus leads to dilation and thickening of the walls of the colon (usually the sigmoid colon and rectum). Difficulty with passing of bolus leads to dilation of the remaining intestines, increasing bowel movements, pain, and constant physical distress. Typical complications of megacolon are intestinal obstruction and rupture.
- Trypanosoma cruzi - free articles in PubMed
Franco-Paredes C, Von A, Hidron A, Rodríguez-Morales AJ, Tellez I, Barragán M, Jones D, Náquira CG, Mendez J. Chagas disease: an impediment in achieving the Millennium Development Goals in Latin America. BMC Int Health Hum Rights. 2007 Aug 28;7:7.
Title Cycle of transmission of Trypanosoma cruzi and its vectors to humans. Triatomine bugs live in the crevices of poorly constructed houses in impoverished areas in Latin America. Metacyclic trypomastigote is the infecting form to humans, while the amastigote is the intracellular form responsible for the immunopathogenesis in target human organs.
Hecht MM, Nitz N, Araujo PF, Sousa AO, Rosa Ade C, Gomes DA, Leonardecz E, Teixeira AR. Inheritance of DNA transferred from American trypanosomes to human hosts. PLoS One. 2010 Feb 12;5(2):e9181.
Model of Trypanosoma cruzi minicircle integration and replication in the human genome.
(A) Infection-induced host DNA (green) double strand-break (DSB) and integration of kDNA minicircle sequence (blue) mediated by microhomology end-joining.
(B) Replication of the kDNA-LINE sequence by target-primed reverse-transcription using the autonomous recombination machinery of the LINE-1. The kDNA sequence repeat received a specific cut, and free-end pairing with a first strand transcript (green). A complementary second strand transcript is made, which can transpose to different chromosomes.
Nóbrega AA, Garcia MH, Tatto E, Obara MT, Costa E, Sobel J, Araujo WN. Oral transmission of Chagas disease by consumption of açaí palm fruit, Brazil. Emerg Infect Dis. 2009 Apr;15(4):653-5.
Trypanosoma cruzi (arrow) in a peripheral blood smear of a patient at a local health facility in a rural area of Pará State, Brazil (Giemsa stain, magnification x100). Image provided by Adriana A. Oliveira, Brazilian Field Epidemiology Training Program, Brasilia, Brazil.
Barrias ES, Reignault LC, De Souza W, Carvalho TM. Dynasore, a dynamin inhibitor, inhibits Trypanosoma cruzi entry into peritoneal macrophages. PLoS One. 2010 Jan 20;5(1):e7764.
Trypanosoma cruzi can enters into host cells both by anterior and posterior ends. Observation by field emission electron microscopy (FESEM) of control peritoneal macrophages and trypomastigotes or epimastigotes.
A: Trypomastigote invasion by the posterior body region (white arrow).
B: Trypomastigote invasion by the anterior body region (white arrowhead).
C and D: Epimastigote internalization by the flagella (anterior region - black arrow and arrowhead).
Note that in D the epimastigote is internalized by coiled phagocytosis (black arrowhead) and in C the epimastigote is internalized by a funnel-like host cell plasma membrane structure (black arrow). Bars=1 µm.
Tarleton RL, Reithinger R, Urbina JA, Kitron U, Gürtler RE. The challenges of Chagas Disease-- grim outlook or glimmer of hope. PLoS Med. 2007 Dec;4(12):e332.
Chest X-Ray of 4 Different Patients with Chagas Heart Disease.
B: mild cardiomegaly;
C: moderate cardiomegaly;
D: severe cardiomegaly with pulmonary congestion.
De Souza W. From the cell biology to the development of new chemotherapeutic approaches against trypanosomatids: dreams and reality. Kinetoplastid Biol Dis. 2002 May 31;1(1):3.
Copyright © 2002 De Souza; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
Light microscopy of stained cells showing the developmental stages found in the members of the Trypanosomatidae family.
High voltage electron microscopy showing an intact tyrypomastigote form of T. cruzi.
- Elias MC, Nardelli SC, Schenkman S. Chromatin and nuclear organization in Trypanosoma cruzi. Future Microbiol. 2009 Oct;4:1065-74.
- Bern C, Kjos S, Yabsley MJ, Montgomery SP. Trypanosoma cruzi and Chagas' Disease in the United States. Clin Microbiol Rev. 2011 Oct;24(4):655-81.
- Pena SD, Machado CR, Macedo AM. Trypanosoma cruzi: ancestral genomes and population structure. Mem Inst Oswaldo Cruz. 2009 Jul;104 Suppl 1:108-14.
- Souza W. Structural organization of Trypanosoma cruzi. Mem Inst Oswaldo Cruz. 2009 Jul;104 Suppl 1:89-100.
- Araújo A et al. Paleoparasitology of Chagas disease--a review. Mem Inst Oswaldo Cruz. 2009 Jul;104 Suppl 1:9-16.
- de Meis J et al. Differential regional immune response in Chagas disease. PLoS Negl Trop Dis. 2009 Jul 7;3(7):e417.
- Teixeira AR et al. Environment, interactions between Trypanosoma cruzi and its host, and health. Cad Saude Publica. 2009;25 Suppl 1:S32-44.
- Noireau F, Diosque P, Jansen AM. Trypanosoma cruzi: adaptation to its vectors and its hosts. Vet Res. 2009 Mar-Apr;40(2):26.
- Lima VS et al. Chagas disease in ancient hunter-gatherer population, Brazil. Emerg Infect Dis. 2008 Jun;14(6):1001-2.
- Tarleton RL et al. The challenges of Chagas Disease-- grim outlook or glimmer of hope. PLoS Med. 2007 Dec;4(12):e332.
- Teixeira AR et al. Chagas disease. Postgrad Med J. 2006 Dec;82(974):788-98.
- Teixeira AR et al. Evolution and pathology in chagas disease--a review. Mem Inst Oswaldo Cruz. 2006 Aug;101(5):463-91.
- Cunha-e-Silva N et al. Reservosomes: multipurpose organelles? Parasitol Res. 2006 Sep;99(4):325-7.
- Vaidian AK, Weiss LM, Tanowitz HB. Chagas' disease and AIDS. Kinetoplastid Biol Dis. 2004 May 13;3(1):2.
- Macedo AM et al.Chagas disease: role of parasite genetic variation in pathogenesis. Expert Rev Mol Med. 2002 Mar 5;4(5):1-16.
- De Souza W.From the cell biology to the development of new chemotherapeutic approaches against trypanosomatids: dreams and reality. Kinetoplastid Biol Dis. 2002 May 31;1(1):3.
- Tyler KM, Engman DM. The life cycle of Trypanosoma cruzi revisited. Int J Parasitol. 2001 May 1;31(5-6):472-81.