Trypanosomatids are unicellular protozoa parasites known for causing a variety of critical diseases in humans and animals. Trypanosomatids belong to class Kinetoplastida, which is restricted to the invertebrate hosts since Trypanosomatids possess monoxenous life-cycle. However, it is revealed that different genera of Trypanosomatids are pathogenic to living things (humans, animals, and plants) (Kaufer, Ellis and Stark 3). For example, Phytomonas is a form of dixenous trypanosomatid genus, whose transmission is facilitated through phytophagous insects and parasitizing, which are a variety of plants.
The prominence of Trypanosomatids is attributed to Trypanosoma and Leishmania, which are two dominant genera when it comes to their significant role as pathogens causing parasites to humans. Trypanosoma and Leishmania genera are dixenous, possessing anthroponotic life-cycles, with their transmission achieved through hematophagous insects (Kaufer, Ellis and Stark 3). The parasites from these families are known for causing severe human diseases such as Human African Trypanosomiasis (TAT), Chagas disease and leishmaniases. These diseases are characterized by a wide array of symptoms, depicting different methods of pathogenesis. As part of dixenous species, Trypanosomatids can develop from within various parts of the invertebrates, depending on their preferred sites, thus influencing the phenotype and severity of the disease.
Diseases caused by Trypanosomatids in human beings, who are identified to be the primary reservoirs, are predominantly zoonotic. On the other hand, the animal reservoirs play a critical role when it comes to sustaining endemicity. This is an indication that Trypanosomatid parasites pose a critical health concern, which is affecting a significant number of people globally (Bacazar and Vanrell 3). For instance, it is reported that TAT has become endemic in over 36 sub-Saharan countries. It is also estimated that 61 million people are exposed to the risks of contracting TAT as transmitted by vectors such as tsetse flies.
Protozoan parasites usually adapt to a broad spectrum of hosts and vector environments in a different manner. This implies that various stages of parasite life stages possess different characteristic morphologies. Apparently, Trypanosomatid parasite usually depicts a wide array of morphological variations between the species of Trypanosomatid family and its growth patterns, irrespective of having similar cytoskeletal and membranous structures (Wheeler, Gluenz and Gull 5). The life cycles of Trypanosomatid are characterized by designated proliferative and transmissive growing trends which are a representation of a variety of hosting environments. This implies that the life stages of a Trypanosomatid parasites include different linked proliferative cycles.
Trypanosomatids are parasitic protozoa, which possess a monoxonous life cycle as depicted hosting vectors or insects, which can be invertebrates or vertebrates. Trypanosoma and Leishmania genera are dixenous, maintaining anthroponotic life-cycles, with their transmission achieved through hematophagous insects. When the infected sand-fly comes in contact with blood meal, it injects, ultimately depositing metacyclic promastigotes into the vertebrate host. While residing in the vertebrate hosts, promastigotes attack macrophages before developing into non-motile amastigotes. This process is achieved through binary fission mechanisms (Kaufer, Ellis and Stark 3). For instance, replication of the Leishmania occurs within macrophages in different locations depending on the type of the species. This process of differentiation paves the way for three categories of clinical leishmaniasis which include: cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis (MCL) and visceral leishmaniasis (VL). These types are formed as the result of parasite development taking place in the reticuloendothelial system for the skin, nasopharynx, and viscera.
Cutaneous leishmaniasis is considered to be the popular clinical form of the disease, which is characterized by multiple manifestations of signs and symptoms. Some of the common morbidities or associated signs include new skin lesions with a broad spectrum of morphologies that can lead to substantial disfiguring scars. On the other hand, Mucocutaneous leishmaniasis is the worst form of Cutaneous leishmaniasis when it comes to the degrees of the disfiguring scars. Over 90% of the Mucocutaneous leishmaniasis patients might have suffered from Cutaneous leishmaniasis associated diseases before depicting the manifestations of Mucocutaneous leishmaniasis (Bacazar and Vanrell 3). Some of the symptoms portrayed by diseases linked to Mucocutaneous leishmaniasis consist of ulceration in the nasal sites, before the inception of the fever and hepatomegaly. The critical stages of Mucocutaneous leishmaniasis involve ulceration of the oronasopharyngeal mucosa. This can lead to the occurrence of erythema and edema in the regions affected by the Trypanosomatids bacteria.
Just like it is the case with Leishmania family of Trypanosomatids, the cell morphology of Phytomonas depict features of promastigote morphology as far its cell growth is concerned. The promastigote morphology exhibits a detached flagellum, which projects from a flagellar pocket at the interior of the cell. Typically, the cell morphologies of the Trypanosomatids bacteria replicate with a high fidelity as facilitated by cell division cycle. The cells are also profoundly altered when transitioning between various developmental stages, which is determined by the type of the host, organ or nature of the tissues (Jaskowska, Butler and Preston 5). The significance of the cell forms assumed by Trypanosomatids bacteria promastigote and amastigote can be attributed to motility and sensory functionalities of the flagellum.
Colony of Trypanosomatids Bacteria
Ability to grow or differentiate on axenic liquid or solid media is the fundamental feature that distinguishes trypanosomatids from the rest of the protozoans. Colonies are considered to be a suitable approach of delineating trypanosomatids species as well as isolating trypanosomatids just like it is the case with microorganisms. Whenever the humidity reaches adequate levels, it is demonstrated that colonies of trypanosomatids start developing the flagella, which cover the cells (Podlipaev and Naumov 114). For example, the Colonies of Leptomonas seymouri of depict inner structures of cell morphologies.
Towards the end of the 2000s, the colonies polymorphism which are about 15 species, which are considered to be isolates of insect trypanosomatids, had been investigated. As for the colonies of L. peterhoffi, it is revealed that they form a massive covering layer, with the inner cells appearing crumply packed as well as possessing a protruding free flagellum (Podlipaev and Naumov 116). It is observed that the approach of isolating trypanosomatids from a host or vector to the culture of culture and their self-cultivation can result in a selective retention particular genotypes of in parasite population.
Diseases Caused by TrypanosomatidsTrypanosomatid parasite are known for causing various diseases in animals and plants. In 2010 it was published that close to 37 million people were suffering from the diseases caused by Trypanosomatid protozoa, with Trypanosoma brucei (Chagas disease), Trypanosoma cruzi and s leishmaniasis, Human African Trypanosomiasis (HAT), is the standard types of trypanosomatids diseases. These diseases are categorized as critical causes of morbidity and mortality in various regions, especially third world countries (Setzer 2). The mortality rates attributed to trypanosomatid parasites is predominantly determined by accessibility and availability of the treatment as well as the growing resistance by these protozoa towards the drugs used. The medication process can also be hampered by the severity of adverse reactions or high toxicity.
Leishmaniasis Diseases are caused by a broad spectrum of the species categorized under the protozoan genus called Leishmania. Some of the common morbidities or associated signs include extra skin lesions with a wide range of morphologies that can lead to huge disfiguring scars. On the other hand, Mucocutaneous leishmaniasis is the worst form of Cutaneous leishmaniasis when it comes to the degrees of the disfiguring scars (Bacazar and Vanrell 3). Over 90% of the Mucocutaneous leishmaniasis patients might have suffered from Cutaneous leishmaniasis associated diseases before depicting the manifestations of Mucocutaneous leishmaniasis.
Some of the symptoms depicted by diseases linked to Mucocutaneous leishmaniasis consist of ulceration in the nasal sites, before the inception of the fever and hepatomegaly. The critical stages of Mucocutaneous leishmaniasis involve ulceration of the oronasopharyngeal mucosa. This can lead to the occurrence of erythema and edema in the regions affected by the Trypanosomatids bacteria. HAT (Sleeping sickness) is caused by Trypanosoma brucei with vectors such as tsetse flies used in the transmission of the parasite to the host (Bacazar and Vanrell 3). Trypanosoma brucei (Chagas disease) can either be in acute or chronic phase. Typically, during the acute infection stages, the patients are considered to be asymptomatic prompting them to exhibit a variety of general symptoms such as headaches, fever and heart inflammation.
Trypanosomatids are unicellular protozoa associated with different morbidity. As part of dixenous species, Trypanosomatids can develop from within various parts of the invertebrates, depending on their preferred sites, thus influencing the phenotype and severity of the disease. There is the need of establishing appropriate mechanisms to contain the severity of Trypanosomatids.
BIBLIOGRAPHY Balcazar, Dario and Maria Vanrell. "The superfamily keeps growing: Identification in trypanosomatids of RibJ, the first riboflavin transporter family in protist." Neglected Tropical Diseases (2017): 1-4. Web.
Jaskowska, Eleanor, Claire Butler and Gail Preston. "Phytomonas: Trypanosomatids Adapted to Plant Environments." PLOS Pathogens (2015): 2-6. Web.
Kaufer, Alexa, John Ellis and Damien Stark. "The evolution of trypanosomatid taxonomy." Parasites and Vectors (2017): 1-4. Web.
Podlipaev, Sergei A. and Andrew D. Naumov. "Colonies of trypanosomatids on agar plates: the tool for differentiation of the species and isolates." Protistology (2000): 113-119. print.
Setzer, William N. "Trypanosomatid disease drug discovery and target identification." Future Science (2013): 1-2. print.
Wheeler, Richard John, Eva Gluenz and Keith Gull. "The Limits on Trypanosomatid Morphological Diversity." Peer-Reviewed open Access (2013): 1-8. print.
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