“…Over fourteen Leishmania species are harmful to mammals, nine of which are identified as human parasites. , Based on the morphological characterization, Leishmania exists in two different forms: a promastigote stage that penetrates inside the host’s phagocytic cell and later transforms into an obligatory intracellular amastigote stage. This parasite performs a digenetic life cycle; each time the parasite shuttles between the host and the carrier, it undergoes morphological differentiation. , The female sandfly (Old World: genus Phlebotomus and New World: Lutzomyia and Psychodopygus ) becomes infected after consuming blood from a diseased host. Once the parasite is inside the sandfly, it goes through the first stage of differentiation and becomes a procyclic promastigote.…”
Section: Introductionmentioning
confidence: 99%
“…The amastigotes grow and multiply within the parasitophorous vacuole until the macrophage breaks off, secreting all matured amastigotes. These released amastigotes set off a chain reaction that finally develop into leishmaniasis as shown in Figure . , …”
Section: Introductionmentioning
confidence: 99%
“…These released amastigotes set off a chain reaction that finally develop into leishmaniasis as shown in Figure 1. 3,4 According to the World Health Organization (WHO), leishmaniasis is a parasitic infection that causes tropical and subtropical illnesses that are spread in over 89 countries including Africa, Asia, America, and the Mediterranean, thereby creating a global health crisis. About 10 to 15 million individuals worldwide are affected, with an annual incidence of new infections exceeding 0.7−1 million.…”
Section: Introductionmentioning
confidence: 99%
“…This parasite performs a digenetic life cycle; each time the parasite shuttles between the host and the carrier, it undergoes morphological differentiation. 3 , 4 The female sandfly (Old World: genus Phlebotomus and New World: Lutzomyia and Psychodopygus ) becomes infected after consuming blood from a diseased host. Once the parasite is inside the sandfly, it goes through the first stage of differentiation and becomes a procyclic promastigote.…”
Leishmaniasis, which is caused by a parasitic protozoan of the genus Leishmania, is still a major threat to global health, impacting millions of individuals worldwide in endemic areas. Chemotherapy has been the principal method for managing leishmaniasis; nevertheless, the evolution of drug resistance offers a significant obstacle to therapeutic success. Drug-resistant behavior in these parasites is a complex phenomenon including both innate and acquired mechanisms. Resistance is frequently related to changes in drug transportation, drug target alterations, and enhanced efflux of the drug from the pathogen. This review has revealed specific genetic mutations in Leishmania parasites that are associated with resistance to commonly used antileishmanial drugs such as pentavalent antimonials, miltefosine, amphotericin B, and paromomycin, resulting in changes in gene expression along with the functioning of various proteins involved in drug uptake, metabolism, and efflux. Understanding the genetic changes linked to drug resistance in Leishmania parasites is essential for creating approaches for tackling and avoiding the spread of drug-resistant variants. Based on which specific treatments focus on mutations and pathways could potentially improve treatment efficacy and help long-term leishmaniasis control. More study is needed to uncover the complete range of genetic changes generating medication resistance and to develop new therapies based on available information.
“…Over fourteen Leishmania species are harmful to mammals, nine of which are identified as human parasites. , Based on the morphological characterization, Leishmania exists in two different forms: a promastigote stage that penetrates inside the host’s phagocytic cell and later transforms into an obligatory intracellular amastigote stage. This parasite performs a digenetic life cycle; each time the parasite shuttles between the host and the carrier, it undergoes morphological differentiation. , The female sandfly (Old World: genus Phlebotomus and New World: Lutzomyia and Psychodopygus ) becomes infected after consuming blood from a diseased host. Once the parasite is inside the sandfly, it goes through the first stage of differentiation and becomes a procyclic promastigote.…”
Section: Introductionmentioning
confidence: 99%
“…The amastigotes grow and multiply within the parasitophorous vacuole until the macrophage breaks off, secreting all matured amastigotes. These released amastigotes set off a chain reaction that finally develop into leishmaniasis as shown in Figure . , …”
Section: Introductionmentioning
confidence: 99%
“…These released amastigotes set off a chain reaction that finally develop into leishmaniasis as shown in Figure 1. 3,4 According to the World Health Organization (WHO), leishmaniasis is a parasitic infection that causes tropical and subtropical illnesses that are spread in over 89 countries including Africa, Asia, America, and the Mediterranean, thereby creating a global health crisis. About 10 to 15 million individuals worldwide are affected, with an annual incidence of new infections exceeding 0.7−1 million.…”
Section: Introductionmentioning
confidence: 99%
“…This parasite performs a digenetic life cycle; each time the parasite shuttles between the host and the carrier, it undergoes morphological differentiation. 3 , 4 The female sandfly (Old World: genus Phlebotomus and New World: Lutzomyia and Psychodopygus ) becomes infected after consuming blood from a diseased host. Once the parasite is inside the sandfly, it goes through the first stage of differentiation and becomes a procyclic promastigote.…”
Leishmaniasis, which is caused by a parasitic protozoan of the genus Leishmania, is still a major threat to global health, impacting millions of individuals worldwide in endemic areas. Chemotherapy has been the principal method for managing leishmaniasis; nevertheless, the evolution of drug resistance offers a significant obstacle to therapeutic success. Drug-resistant behavior in these parasites is a complex phenomenon including both innate and acquired mechanisms. Resistance is frequently related to changes in drug transportation, drug target alterations, and enhanced efflux of the drug from the pathogen. This review has revealed specific genetic mutations in Leishmania parasites that are associated with resistance to commonly used antileishmanial drugs such as pentavalent antimonials, miltefosine, amphotericin B, and paromomycin, resulting in changes in gene expression along with the functioning of various proteins involved in drug uptake, metabolism, and efflux. Understanding the genetic changes linked to drug resistance in Leishmania parasites is essential for creating approaches for tackling and avoiding the spread of drug-resistant variants. Based on which specific treatments focus on mutations and pathways could potentially improve treatment efficacy and help long-term leishmaniasis control. More study is needed to uncover the complete range of genetic changes generating medication resistance and to develop new therapies based on available information.
“…Procyclic promastigotes develop from amastigotes in the insect's gut, multiply, and migrate to the anterior midgut (stomodeal valve), where they undergo metacyclogenesis and differentiate into metacyclic infective forms. Regurgitation is then used to transmit these forms to a new mammalian host during a blood meal (5,6).…”
Toxoplasma gondii is the most prevalent parasite that mostly affects warm-blooded animals, including humans. According to the Center for Disease Control (CDC), this parasite infects about one-third of the world's population of people. Lack of information regarding toxoplasmosis in the population of domestic and stray dogs and cats in Khyber Pakhtunkhwa was a major factor in the decision to conduct this study. Our aim was to use serological technique to establish the seroprevalence of T. gondii in dogs and cats. In this study, 405 dogs and 405 cats, blood samples were collected from various veterinary hospitals and privates pet clinics and an ELISA test was used to determine anti-Toxoplasma IgG antibodies. Information on four risk factors age, sex, deworming of dogs and cats and, area was collected from the owners by questionnaire. Total seroprevalence in dogs, and cats was 45.18% (183/405), and 51.60% (209/405), respectively. No significant difference was documented on basis of age and gender between dogs, and cats. Dogs and cats from urban areas showed lower seroprevalence than rural areas. Dogs that had received deworming showed lower seroprevalence. This research indicates that neglected parasite Toxoplasma gondii is prevalent in dogs and cats in Pakistan, which may have great public health importance
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