query: the infective stage of malarial parasite plasmodium that enters human body is

pos: Plasmodium first to a ring-shaped form and then to a larger form called a trophozoite. Trophozoites then mature to schizonts which divide several times to produce new merozoites. The infected red blood cell eventually bursts, allowing the new merozoites to travel within the bloodstream to infect new red blood cells. Most merozoites continue this replicative cycle, however some merozoites upon infecting red blood cells differentiate into male or female sexual forms called gametocytes. These gametocytes circulate in the blood until they are taken up when a mosquito feeds on the infected vertebrate host, taking up blood which includes the gametocytes. In

pos: Plasmodium falciparum years ago. Alphonse Laveran was the first to identify the parasite in 1880, and named it "Oscillaria malariae". Ronald Ross discovered its transmission by mosquito in 1897. Giovanni Battista Grassi elucidated the complete transmission from a female anopheline mosquito to humans in 1898. In 1897, William H. Welch created the name "Plasmodium falciparum", which ICZN formally adopted in 1954. "P. falciparum" assumes several different forms during its life cycle. The human-infective stage are sporozoites from the salivary gland of a mosquito. The sporozoites grow and multiply in the liver to become merozoites. These merozoites invade the erythrocytes (RBCs) to form

pos: Plasmodium malariae that causes fevers that recur at approximately three-day intervals (therefore occurring every fourth day, a "quartan fever"), longer than the two-day ("tertian") intervals of the other malarial parasites. In this stage, many thousands of merozoites are produced in each schizont. As the merozoites are released, they invade erythrocytes and initiate the erythrocytic cycle, where the parasite digests hemoglobin to obtain amino acids for protein synthesis. The total length of the intraerythrocytic development, is roughly 72 hours for "P. malariae". At the schizont stage, after schizogonic division, there are roughly 6–8 parasite cells in the erythrocyte. Following the erythrocytic cycle, which

pos: Plasmodium vivax process gives rise to thousands of merozoites (plasmodium daughter cells) in the circulatory system and the liver. The incubation period of human infection usually ranges from ten to seventeen days and sometimes up to a year. Persistent liver stages allow relapse up to five years after elimination of red blood cell stages and clinical cure. The "P. vivax" sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony stage. This is characterized by multiple rounds of nuclear division without cellular segmentation. After a certain number of nuclear divisions, the parasite cell will segment and merozoites are formed. There are situations where

pos: Plasmodium falciparum erythrocyte membrane protein 1 the age of five years. The parasites are transmitted through the bites of female mosquitos (of the species of "Anopheles"). Before invading the RBCs and causing the symptoms of malaria, the parasites first multiply in the liver. The daughter parasites called merozoites then only infect the RBCs. They undergo structural development inside the RBCs, becoming trophozoites and schizonts. It is during this period that malarial symptoms are produced. Unlike RBCs infected by other "Plasmodium" species, "P. falciparum"-infected RBCs had been known to spontaneously stick together. By the early 1980s, it was established that when the parasite (both the trophozoite and

pos: Plasmodium brumpti Plasmodium brumpti Plasmodium brumpti is a parasite of the genus "Plasmodium" subgenus "Lacertamoeba". Like all "Plasmodium" species "P. brumpti" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are reptiles. "Plasmodium brumpti" are differentiated from other "Plasmodium" species by several characteristics. In the blood of the reptile host, parasites in the schizont stage produce 12-22 merozoites. The gametocytes are elongated and ovular. Both schizonts and gametocytes are fairly large, more than twice the size of the host cell nucleus. "P. brumpti" has been found in reptiles in Morelos, Alpoyeca, and Puente de Ixtla, Mexico. This species was

pos: Plasmodium brumpti described by Peláez and Perez-Reyes in 1952 in the reptile "Sceloporus borridus". It was named after Alexandre Joseph Emile Brumpt (1877–1951) a French professor of parasitology. Plasmodium brumpti Plasmodium brumpti is a parasite of the genus "Plasmodium" subgenus "Lacertamoeba". Like all "Plasmodium" species "P. brumpti" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are reptiles. "Plasmodium brumpti" are differentiated from other "Plasmodium" species by several characteristics. In the blood of the reptile host, parasites in the schizont stage produce 12-22 merozoites. The gametocytes are elongated and ovular. Both schizonts and gametocytes are fairly large, more than

pos: Plasmodium polare "Plasmodium circumflexum" "Plasmodium durae" "Plasmodium fallax" "Plasmodium formosanum" "Plasmodium gabaldoni" "Plasmodium hegneri" "Plasmodium lophrae" "Plasmodium lophrae" "Plasmodium pediocetti" "Plasmodium pinotti" Plasmodium polare Plasmodium polare is a parasite of the genus "Plasmodium" subgenus "Papernaia". Like all "Plasmodium" species "P. polare" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are birds. The parasite was first described by Manwell in 1934. It is relatively small and produces on the average nine merozoites per infection. It has abundant cytoplasm. This parasite occurs in the United States. Hosts of this species include the bald eagle ("Haliaeetus leucocephalus"), the barn swallow ("Hirundo

pos: Plasmodium falciparum of its morphology on stained blood films) grows substantially before undergoing schizogony. At the schizont stage, the parasite replicates its DNA multiple times and multiple mitotic divisions occur asynchronously. Each schizont forms 16-18 merozoites. The red blood cells are ruptured by the merozoites. The liberated merozoites invade fresh erythrocytes. A free merozoite is in the bloodstream for roughly 60 seconds before it enters another erythrocyte. The duration of each blood stage is approximately 48 hours. This gives rise to the characteristic clinical manifestations of falciparum malaria, such as fever and chills, corresponding to the synchronous rupture of the infected erythrocytes.

neg: Camillo Golgi physician Charles Louis Alphonse Laveran discovered that malaria was caused by microscopic parasite (now called "Plasmodium falciparum") in 1880. But scientists were sceptical until Golgi intervened. It was Golgi who helped him prove that malarial parasite was a microscopic protozoan. From 1885, Golgi studied the malarial parasite and its transmission. He established two types of malaria, tertian and quartan fevers caused by "Plasmodium vivax" and "Plasmodium malariae" respectively. In 1886, he discovered that malarial fever (paroxysm) was produced by the asexual stage in the human blood (called erythocytic cycle, or Golgi cycle). In 1889-1890, Golgi and Ettore Marchiafava described the

neg: Giovanni Battista Grassi "Plasmodium falciparum", and discovered that only female anopheline mosquitoes are capable of transmitting the disease. His works in malaria remain a lasting controversy in the history of Nobel Prizes, because a British army surgeon Ronald Ross, who discovered the transmission of malarial parasite in birds was given the 1902 Nobel Prize in Physiology or Medicine. But Grassi, who demonstrated the complete route of transmission of human "Plasmodium", and correctly identified the types of malarial parasite as well as the mosquito vector, "Anopheles claviger", was denied. Grassi was the first to demonstrate the life cycle of human dwarf tapeworm" Taenia nana",

neg: Angelo Celli Giovanni Battista Grassi and Giuseppe Bastianelli. They were the first to use proper staining (with methylene blue) to identify malarial parasite as distinct blue-coloured pigments in the blood cells. They showed that the parasites lived inside blood cell, and that they divide by simple splitting (fission). They were the first to recognize several the stages of development of the malarial parasite in human blood. They called the new microorganism "Plasmodium" in 1885. Their works helped to differentiate different types of malaria as a result of infection with different species of "Plasmodium". Angelo Celli is famous in Rome (a marble sculpture

neg: Plasmodium berghei with the genome of the human malaria parasite "Plasmodium falciparum". A number of genetically modified "P. berghei" lines have been generated which express fluorescent reporter proteins such as Green Fluorescent Protein (GFP) and mCherry (red) or bioluminescent reporters such as Luciferase. These transgenic parasites are important tools to study and visualize the parasites in the living host. "P. berghei" is used in research programs for development and screening of anti-malarial drugs and for the development of an effective vaccine against malaria. Plasmodium berghei Plasmodium berghei is a protozoan parasite that causes malaria in certain rodents. Originally, isolated from thicket rats

neg: Duffy antigen system Duffy antigen system Duffy antigen/chemokine receptor (DARC), also known as Fy glycoprotein (FY) or CD234 (Cluster of Differentiation 234), is a protein that in humans is encoded by the "DARC" gene. The Duffy antigen is located on the surface of red blood cells, and is named after the patient in which it was discovered. The protein encoded by this gene is a glycosylated membrane protein and a non-specific receptor for several chemokines. The protein is also the receptor for the human malarial parasites "Plasmodium vivax", "Plasmodium knowlesi" and simian malarial parasite "Plasmodium cynomolgi". Polymorphisms in this gene are the basis

neg: Plasmodium falciparum erythrocyte membrane protein 1 Plasmodium falciparum erythrocyte membrane protein 1 "Plasmodium falciparum" erythrocyte membrane protein 1 (PfEMP1) is a family of proteins present on the membrane surface of red blood cells (RBCs or erythrocytes) that are infected by the malarial parasite "Plasmodium falciparum". PfEMP1 is synthesized during the parasite's blood stage (erythrocytic schizogony) inside the RBC, during which the clinical symptoms of falciparum malaria are manifested. Acting as both an antigen and adhesion protein, it is thought to play a key role in the high level of virulence associated with "P. falciparum". It was discovered in 1984 when it was reported that infected RBCs

neg: Plasmodium coulangesi Plasmodium coulangesi Plasmodium coulangesi is a parasite of the genus "Plasmodium" subgenus "Vinckeia". Like all "Plasmodium" species "P. coulangesi" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are mammals. The parasite was first described by Lepers "et al." in 1989. The only known host for this species is the lemur "Lemur macaco macaco". The shape, size and colour of the host erythrocyte are unaltered by the presence of the parasite. The mature schizonts produce 6 schizonts. The malarial pigment lies apart from the parasitic mass and is connected to it by only a wisp of cytoplasm.

neg: Plasmodium coulangesi Plasmodium coulangesi Plasmodium coulangesi is a parasite of the genus "Plasmodium" subgenus "Vinckeia". Like all "Plasmodium" species "P. coulangesi" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are mammals. The parasite was first described by Lepers "et al." in 1989. The only known host for this species is the lemur "Lemur macaco macaco". The shape, size and colour of the host erythrocyte are unaltered by the presence of the parasite. The mature schizonts produce 6 schizonts. The malarial pigment lies apart from the parasitic mass and is connected to it by only a wisp of cytoplasm.

neg: Plasmodium falciparum erythrocyte membrane protein 1 targeting VAR2CSA will be able to prevent the effects of malaria, and for this reason VAR2CSA is the leading candidate for development of a PAM vaccine. Plasmodium falciparum erythrocyte membrane protein 1 "Plasmodium falciparum" erythrocyte membrane protein 1 (PfEMP1) is a family of proteins present on the membrane surface of red blood cells (RBCs or erythrocytes) that are infected by the malarial parasite "Plasmodium falciparum". PfEMP1 is synthesized during the parasite's blood stage (erythrocytic schizogony) inside the RBC, during which the clinical symptoms of falciparum malaria are manifested. Acting as both an antigen and adhesion protein, it is thought to

neg: Plasmodium falciparum erythrocyte membrane protein 1 protect them the placenta-attacking malarial parasite. They are noted for giving birth to heavier babies. In a normal human immune system, malarial parasite binding to RBCs stimulates the production of antibodies that attack the PfEMP1 molecules. Binding of antibody with PfEMP1 disables the binding properties of DBL domains, causing loss of cell adhesion, and the infected RBC is destroyed. In this scenario, malaria is avoided. However, to evade the host's immune response, different "P. falciparum" switch on and off different "var" genes to produce functionally different (antigenically distinct) PfEMP1s. Each variant type of PfEMP1 has different binding property, and thus,

neg: Plasmodium falciparum Plasmodium falciparum Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of "Plasmodium" that cause malaria in humans. It is transmitted through the bite of a female "Anopheles" mosquito. It is responsible for roughly 50% of all malaria cases. It causes the disease's most dangerous form called falciparum malaria. It is therefore regarded as the deadliest parasite in humans, causing 435,000 deaths in 2017. It is also associated with the development of blood cancer (Burkitt's lymphoma) and is classified as Group 2A carcinogen. The species originated from the malarial parasite "Laverania" found in gorillas, around 10,000

neg: Ettore Marchiafava malariae") discovered by Alphonse Laveran, finding it in the blood of the many patients suffering from malaria fever. They were the first to use proper staining (with methylene blue) to identify malarial parasite as distinct blue-coloured pigments in the blood cells. They showed that the parasites lived inside blood cell, and that they divide by simple splitting (fission). They were the first to recognize several the stages of development of the malarial parasite in human blood. They called the new microorganism "Plasmodium" in 1885. Their works helped to differentiate different types of malaria as a result of infection with different

neg: Elizabeth A. Winzeler treatments for infections with malaria. "Plasmodium falciparum", the malaria parasite, enters red blood cells of a human host in part of its life cycle and thus protects itself, but Winkeler saw that details of the genome annotationand of the transcriptome (the gene expression viewed as messenger RNAs present)could open new avenues for attack.She used the information her laboratory developed to design high-throughput drug discovery protocols.In addition, Winzeler has discovered the basis of some of the drug resistance mutations in the parasite.The laboratory has discovered several potential malarial treatment drugs,resulting in a $4.7 million dollar grant from the Gates Foundation to

neg: Parasitism as "Strongyloides stercoralis". Vector-transmitted parasites rely on a third party, an intermediate host, where the parasite does not reproduce sexually to carry them from one definitive host to another. These parasites are microorganisms, namely protozoa, bacteria, or viruses, often intracellular pathogens (causing disease). Their vectors are mostly hematophagic arthropods such as fleas, lice, ticks, and mosquitoes. For example, the deer tick "Ixodes scapularis" acts as a vector for diseases including Lyme disease, babesiosis, and anaplasmosis. Protozoan endoparasites, such as the malarial parasites in the genus "Plasmodium" and sleeping sickness parasites in the genus "Trypanosoma", infective stages in the host's blood

neg: Giovanni Battista Grassi "neutral arbitrator" in the committee; and as reported, "[He] threw the full weight of his considerable authority in insisting that Grassi did not deserve the honor" (Grassi would later point out flaws in Koch own methodology on malarial research). Ross was the first to show that malarial parasite was transmitted by the bite of infected mosquitoes, in his case the avian "Plasmodium relictum". But Grassi's work revealed that human malarial parasites were carried only by female "Anopheles". He identified the mosquito species correctly, in his case "P. claviger". By today's standard, they are likely to have shared the Nobel prize.

neg: Nobel Prize controversies authority in insisting that Grassi did not deserve the honor". The indelible irony was that Ross was definitely the first to show that malarial parasite was transmitted by the bite of infected mosquitoes, in his case the avian "Plasmodium relictum". But Grassi's work was much more directly relevant to human health as he demonstrated that human malarial parasites were incriminated only by female "Anopheles" (Ross never identified the mosquito species, being not a zoologist, "grey mosquito with dappled wings" was all that he could offer). Grassi identified the species correctly, and in 1898 who first established the complete life cycle

neg: Plasmodium malariae it arrives. Microscopically, the parasitised red blood cell (erythrocyte) is never enlarged and may even appear smaller than that of normal red blood cells. The cytoplasm is not decolorized and no dots are visible on the cell surface. The food vacuole is small and the parasite is compact. Cells seldom host more than one parasite. Band forms, where the parasite forms a thick band across the width of the infected cell, are characteristic of this species (and some would say is diagnostic). Large grains of malarial pigment are often seen in these parasites: more so than any other "Plasmodium" species,

neg: Plasmodium polymorphum in southern Italy. Because the host carries out an annual migration the parasite may also occur elsewhere. Not known. "P. accipiteris" infects the skylark ("Alauda arvensis"). Plasmodium polymorphum Plasmodium polymorphum is a malarial parasite of the genus "Plasmodium". Currently its only known host is the Eurasian skylark, "Alauda arvensis". This species was described by Zehtindjiev "et al". This species shows a marked preference of its blood stages for immature erythrocytes, including erythroblasts. Uniquely for an avian malaria species development and maturation of the gametocytes occur in immature red blood cells. Also uniquely the margins of nuclei in blood stages of

neg: Culex quinquefasciatus primary vector of "Wuchereria bancrofti", a nematode that causes lymphatic filariasis. It acts as an intermediate host for the helminth parasite by harbouring the larval stages. It also transmits "Plasmodium relictum", a malarial parasite of birds, and is its principal vector in Hawaii. It is the definitive host for the malarial parasite as it harbours the sexual cycle. It breeds profusely in dirty water collections, including stagnant drains, cesspools, septic tanks with leaks, burrow pits, and almost all organic polluted water collections. In optimum temperature and humidity, the lifecycle will be completed in seven days, passing through the egg, larval,

neg: Plasmodium falciparum tertian malaria by "Haemamoeba vivax" (now "P. vivax"), and quartan malaria by "Haemamoeba malariae" (now "P. malariae"). The British physician Patrick Manson formulated the mosquito-malaria theory in 1894; until that time, malarial parasites were believed to be spread in air as miasma, a Greek word for pollution. His colleague Ronald Ross, a British Army surgeon, travelled to India to test the theory. Ross discovered in 1897 that malarial parasite lived in certain mosquitoes. The next year, he demonstrated that a malarial parasite of birds could be transmitted by mosquitoes from one bird to another. Around the same time, Grassi demonstrated

neg: Plasmodium falciparum erythrocyte membrane protein 1 a family of proteins called "Plasmodium" helical interspersed subtelomeric (PHIST) proteins. Of the PHIST proteins, PFI1780w and PFE1605w bind the intracellular ATS of PfEMP1 during transport to the RBC membrane. The PfEMP1 molecule is deposited at the RBC membrane at the knobs. These knobs are easily identified as conspicuous bumps on the infected RBCs from the early trophozoite stage onward. The malarial parasite cannot induce its virulence on RBCs without knobs. As many as 10,000 knobs are distributed throughout the surface of a mature infected RBC, and each knob is 50-80 nm in diameter. The export of pfEMP1 from Maurer's

neg: Carcinogenic parasite liver cirrhosis and jaundice. The most severe infections cause cholangiocarcinoma and hepatic carcinoma. Infection with malarial parasite "Plasmodium falciparum" is classified by IARC as probable (Group 2A) carcinogen. "Schistosoma japonicum" is a possible (Group 2B) carcinogen. There is a close association between the cat liver fluke "Opisthorchis felineus" and bile duct cancer among people in Russia. "Toxoplasma gondii" and eye cancer (intraocular lymphoma) was detected by PCR from two human cases. "Strongyloides stercoralis" eggs and adult worms may be linked with gastric adenocarcinoma and colon adenocarcinoma in Korea. The roundworm "Trichuris muris" infection can increase the number of tumours in

neg: Plasmodium knowlesi a person and the parasites can be seen in the blood between 10 – 12 days after infection. The parasite may multiply rapidly resulting in very high parasite densities that may be fatal. Although the current infection rate with "Plasmodium knowlesi" is relatively low, one risk it presents is misdiagnosis with other forms of malarial parasites such as "P. malariae" especially when microscopy is used. "P. knowlesi" can only be accurately distinguished from "P. malariae" using PCR assay and/or molecular characterization. Symptoms of "P. knowlesi" in humans include headache, fever, chills and cold sweats. Singh "et al." (2004) showed clinical

neg: Plasmodium cynomolgi Plasmodium cynomolgi Plasmodium cynomolgi is a non-human primate parasite which usually been found in the Asian Old World monkeys. This species has been used as a model for human "Plasmodium vivax" because "Plasmodium cynomolgi" shares the same life cycle and some important biological features with "P. vivax". "Plasmodium cynomolgi" has a similar life cycle to "P. vivax". The sexual reproduction stage occurs in the mosquito (definitive host), and the asexual reproduction stage occurs in the monkey (intermediate host) in this case. The whole life cycle contains 12 steps: 1. Sporozoites in mosquito’s salivary glands 2. The Sporozoites would infect into

neg: Plasmodium malariae "P. malariae.". A pattern has emerged in which an infection of short duration causes a rapidly declining immune response, but upon re-infection or recrudescence, the IFA level rises significantly and remains present for many months or years. The increasing need to correctly identify "P. malariae" infection is underscored by its possible anti-malarial resistance. In a study by Müller-Stöver "et al.," the researchers presented three patients who were found to be infected with the parasite after taking anti-malarial medications. Given the slower pre-erythrocytic development and longer incubation period compared to the other malaria causing "Plasmodium" species, the researchers hypothesized that the

neg: Y. D. Sharma the understanding of the parasites' resistance to chloroquine and antifolate drugs. He is credited with the identification of "P. falciparum" strains in India, isolation of "P. falciparum" and "Plasmodium vivax", another non-cultivable protozoan parasite, as well as the development of a genomic library of "Plasmodium vivax". It was his group which reported the first incidence of malaria in humans caused by "Plasmodium knowlesi", a primate malarial parasite. These studies are reported to have relevance in developing immunotherapeutic reagents. His researches have been documented by way of several articles and the online repository of scientific articles of the Indian Academy of

neg: Plasmodium fragile "Macaca radiata" monkeys in South India and "Macaca sinica" in Sri Lanka. Transmission of this parasite to "Macaca mulatta" and Aotus species using sporozoites produced in "Anopheles dirus" mosquitoes has been reported previously. "P. fragile" has been successfully transmitted to splenectomized squirrel monkeys by both blood stage and sporozoite transmission. "Plasmodium fragile" has also been used in squirrel monkeys for vaccine trials and cross-protection trials. Plasmodium fragile Plasmodium fragile is a malaria parasite found naturally in Bonnet macaques from India and toque macaques from Sri Lanka. "Plasmodium fragile" is considered a second malaria species, a simian counterpart to the human

neg: Strongylus vulgaris very similar in appearance. The best diagnostic method to determine if a horse has a S. vulgaris infection is through a fecal culture. Here the eggs grow and develop into the infective larval stage that is specific to the large strongyle parasite. The S. vulgaris adults are primarily found in the cecum and colon of infected equids and it is here that the females will lay their eggs. These eggs will pass out of the horses body in the feces. Once outside the body the eggs will hatch and develop into the infective larval stage L3. The larvae enter the

neg: Plasmodium polymorphum Plasmodium polymorphum Plasmodium polymorphum is a malarial parasite of the genus "Plasmodium". Currently its only known host is the Eurasian skylark, "Alauda arvensis". This species was described by Zehtindjiev "et al". This species shows a marked preference of its blood stages for immature erythrocytes, including erythroblasts. Uniquely for an avian malaria species development and maturation of the gametocytes occur in immature red blood cells. Also uniquely the margins of nuclei in blood stages of are markedly smooth and distinct. It appears morphologically to be related to the "Huffia" subgenus but this has yet to be established. This species was isolated

neg: Sanaria Sanaria Sanaria is a biotechnology company developing vaccines protective against malaria, as well as related products for use in malaria research. Sanaria’s vaccines are based on the use of the sporozoite (SPZ) stage of the malaria "Plasmodium" parasite as immunogen. The SPZ stage of the malaria parasite is inoculated into humans by mosquito bite. Sanaria has developed the technology to grow and harvest large quantities of aseptic, purified "Plasmodium falciparum" (Pf) SPZ and formulate them for use in vaccines for human use. Pf is responsible for the most of the approximately 500,000 deaths caused by malaria annually. Sanaria's most advanced

neg: Sanaria Health Institute and the Swiss Government, and the Tanzanian Commission on Science and Technology. Sanaria Sanaria is a biotechnology company developing vaccines protective against malaria, as well as related products for use in malaria research. Sanaria’s vaccines are based on the use of the sporozoite (SPZ) stage of the malaria "Plasmodium" parasite as immunogen. The SPZ stage of the malaria parasite is inoculated into humans by mosquito bite. Sanaria has developed the technology to grow and harvest large quantities of aseptic, purified "Plasmodium falciparum" (Pf) SPZ and formulate them for use in vaccines for human use. Pf is responsible for

neg: Plasmodium vivax Plasmodium vivax Plasmodium vivax is a protozoal parasite and a human pathogen. This parasite is the most frequent and widely distributed cause of recurring (Benign tertian) malaria, "P. vivax" is one of the five species of malaria parasites that commonly infect humans. Although it is less virulent than "Plasmodium falciparum", the deadliest of the five human malaria parasites, "P. vivax" malaria infections can lead to severe disease and death, often due to splenomegaly (a pathologically enlarged spleen). "P. vivax" is carried by the female "Anopheles" mosquito; the males do not bite. "Plasmodium vivax" is found mainly in Asia, Latin America,

neg: Plasmodium gaboni that the ancestor of this parasite clade could have been already present in hominid ancestors. "Plasmodium gaboni" is 10-fold more diverse than human parasite "Plasmodium falciparum", indicating a very recent origin of the latter. "Plasmodium gaboni" is similar to both "Plasmodium falciparum" and to "Plasmodium reichenowi" in microscopic studies, seeming likely that all of these ape Laverania parasites represent morphologically indistinguishable species. "Plasmodium gaboni" can be found in Western Africa. Study has confirmed the presence of "Plasmodium gaboni" in wild chimpanzees (subspecies "Pan troglodytes troglodytes" and "Pan troglodytes vellerosus"). Due to the close proximity between "Plasmodium gaboni" and the most

neg: History of malaria 30 million years old. Human malaria likely originated in Africa and coevolved with its hosts, mosquitoes and non-human primates. Malaria protozoa are diversified into primate, rodent, bird, and reptile host lineages. Humans may have originally caught "Plasmodium falciparum" from gorillas. "P. vivax", another malarial "Plasmodium" species among the six that infect humans, also likely originated in African gorillas and chimpanzees. Another malarial species recently discovered to be transmissible to humans, "P. knowlesi", originated in Asian macaque monkeys. While "P. malariae" is highly host specific to humans, there is some evidence that low level non-symptomatic infection persists among wild chimpanzees. About

neg: Plasmodium malariae of species, which vary by geographic region. Information about the prepatent period, or the period of time between the infection of the parasite and demonstration of that parasite within the body, of "P. malariae" associated malaria is limited, but the data suggests that there is great variation, often the length of time depending on the strain of "P. malariae" parasite. Usually, the prepatent period ranges from 16 to 59 days. "Plasmodium malariae" causes a chronic infection that in some cases can last a lifetime. The "P. malariae" parasite has several differences between it and the other "Plasmodium" parasites, one being

neg: Plasmodium reichenowi host range for P. reichenowi. Plasmodium reichenowi Plasmodium reichenowi is a malaria parasite that infects chimpanzees. "Plasmodium reichenowi" is classified into the subgenus Laverania. It is a chimpanzee malaria parasite that is evolutionarily related to the human malaria parasite "P. falciparum". "P. reichenowi" and "P. falciparum" are phylogenetically close to each other. A high-quality reference genome for "P. reichenowi" was produced from Illumina reads using de novo assembly and post hoc improvement. Excluding the subtelomeres, the genome is almost completely co-linear with "P. falciparum" and share almost identical gene content emphasizing their recent shared ancestry. The vast majority of these

neg: Plasmodium reichenowi Plasmodium reichenowi Plasmodium reichenowi is a malaria parasite that infects chimpanzees. "Plasmodium reichenowi" is classified into the subgenus Laverania. It is a chimpanzee malaria parasite that is evolutionarily related to the human malaria parasite "P. falciparum". "P. reichenowi" and "P. falciparum" are phylogenetically close to each other. A high-quality reference genome for "P. reichenowi" was produced from Illumina reads using de novo assembly and post hoc improvement. Excluding the subtelomeres, the genome is almost completely co-linear with "P. falciparum" and share almost identical gene content emphasizing their recent shared ancestry. The vast majority of these approximately 5,000 ‘core’ genes are

neg: Jay Keasling a global health problem that threatens 300-500 million people and kills more than one million people annually. The chloroquine-based drugs that were used widely in the past have lost effectiveness because the Plasmodium parasite that causes malaria has become resistant to them. Artemisinin, a sesquiterpene lactone endoperoxide, extracted from "Artemisia annua" L is highly effective against Plasmodium spp. resistant to other anti-malarial drugs. However, there are several problems with current production methods for artemisinin. First, artemisinin combination therapies (ACTs) are too expensive for people in the developing world to afford. Second, artemisinin is extracted from "A. annua", and its yield

neg: Avadhesha Surolia green tea catechins as anti-cancer and anti-malarial agents. He has developed a rhodanine, BCFMT, as a potential therapeutic for cancer. Surolia co-discovered the existence of the fatty acid synthesis (FAS) pathway in Plasmodium and demonstrated its remarkable distinction from that of its human host. He co-identified triclosan, a widely used biocide, to compromise the growth of the parasite by inhibiting its enoyl-ACP reductase (FabI). Recently, Surolia and colleagues have identified Pranlukast (an FDA approved drug for asthma) as novel inhibitor of Mtb ArgJ, an enzyme of the arginine biosynthesis pathway, essential for pathogenicity and survival in host cells. Pranlukast demonstrated

neg: Doxorubicin unique to the malarial parasite "Plasmodium falciparum". The pharmaceutical company GlaxoSmithKline (GSK) later identified doxorubicin in a set of compounds that inhibit parasite growth Doxorubicin is also known to be fluorescent. This has often been used to characterize doxorubicin concentrations, and has opened the possibility of using the molecule as a theranostic agent. However, there are significant limitations, as doxorubicin's fluorescence spectrum is known to depend on a variety of factors, including the pH of the environment, solvent dielectric constant and others. Doxorubicin fluorescence is quenched by binding to DNA, and shielded by micelle encapsulation. It is also known to

neg: Antimalarial medication can be complicated and varies between "Plasmodium" species. It is generally accepted to be initiated primarily through a spontaneous mutation that provides some evolutionary benefit, thus giving the anti-malarial used a reduced level of sensitivity. This can be caused by a single point mutation or multiple mutations. In most instances a mutation will be fatal for the parasite or the drug pressure will remove parasites that remain susceptible, however some resistant parasites will survive. Resistance can become firmly established within a parasite population, existing for long periods of time. The first type of resistance to be acknowledged was to chloroquine

neg: Plasmodium knowlesi Plasmodium knowlesi Plasmodium knowlesi is a primate malaria parasite commonly found in Southeast Asia. It causes malaria in long-tailed macaques ("Macaca fascicularis"), but it may also infect humans, either naturally or artificially. "Plasmodium knowlesi" is the sixth major human malaria parasite (following the division of "Plasmodium ovale" into 2 subspecies). It may cause severe malaria as indicated by its asexual erythrocytic cycle of about 24 hours, with an associated fever that typically occurs at the same frequency (i.e. the fever is quotidian). This is an emerging infection that was reported for the first time in humans in 1965. It accounts

neg: Climate change in Africa The increase in mosquitoes will thus increase the opportunity for both "Plasmodium falciparum" and "Plasmodium vivax" parasites to proliferate. Exposure to malaria will become a greater risk to humans as the number of female "Anopheles" mosquitos infected with either the "Plasmodium falciparum" or "Plasmodium vivax" parasite increases. The mosquito will transmit the parasite to the human host through a bite, resulting in infection. Then, when an uninfected mosquito bites the now infected human host, the parasite will be transmitted to the mosquitoes which will then become an exposure to other uninfected human hosts. Individuals who are constantly exposed to the

neg: Plasmodium berghei Plasmodium berghei Plasmodium berghei is a protozoan parasite that causes malaria in certain rodents. Originally, isolated from thicket rats in Central Africa, "P. berghei" is one of four "Plasmodium" species that have been described in African murine rodents, the others being "Plasmodium chabaudi", "Plasmodium vinckei", and "Plasmodium yoelii". Due to its ability to infect rodents and relative ease of genetic engineering, "P. berghei" is a popular model organism for the study of human malaria. Like all malaria parasites of mammals, including the four human malaria parasites, "P. berghei" is transmitted by "Anopheles" mosquitoes and it infects the liver after being

neg: Merozoite surface protein Merozoite surface protein Merozoite surface proteins are both integral and peripheral membrane proteins found on the surface of a merozoite, an early life cycle stage of a protozoan. Merozoite surface proteins, or MSPs, are important in understanding malaria, a disease caused by protozoans of the genus Plasmodium. During the asexual blood stage of its life cycle, the malaria parasite enters red blood cells to replicate itself, causing the classic symptoms of malaria. These surface protein complexes are involved in many interactions of the parasite with red blood cells and are therefore an important topic of study for scientists aiming to

neg: Gongylonema pulchrum in buccal cavity of human host, ingested eggs locate near esophagus, develop and mature into adult worms after two subsequent molting stages, migrate into buccal cavity, no eggs are ever found in human feces, which strengthens the assumption that humans are solely incidental, accidental, and dead end hosts for the "Gongylonema pulchrum" parasite life cycle. The "G. pulchrum" parasite has also been studied in vivo in rabbits. The life cycle is as follows: Infective third stage larva from naturally infected dung beetles (intermediate hosts and vectors), were orally given to rabbits. The larvae entered the upper gastrointestinal tract of the

neg: Pentose phosphate pathway SIRT2-mediated deacetylation and activation of G6PD stimulates oxidative branch of PPP to supply cytosolic NADPH to counteract oxidative damage or support "de novo" lipogenesis. Several deficiencies in the level of activity (not function) of glucose-6-phosphate dehydrogenase have been observed to be associated with resistance to the malarial parasite "Plasmodium falciparum" among individuals of Mediterranean and African descent. The basis for this resistance may be a weakening of the red cell membrane (the erythrocyte is the host cell for the parasite) such that it cannot sustain the parasitic life cycle long enough for productive growth. Pentose phosphate pathway The pentose phosphate

neg: Mosquito-malaria theory one type (which he called "brown type" or more commonly "dappled-winged mosquitoes", not knowing the species, which in fact was "Anopheles") acquired the malarial parasites in its stomach. This was the first evidence for Manson's theory that mosquito did carry the malarial parasite, and Ross would later famously call 20 August as "Malaria Day" (now adopted as World Mosquito Day). The second experimental evidence came in the mid-1898 when Ross demonstrated the transmission of bird malaria "Proteosoma relictum" (now "Plasmodium relictum") between larks and mosquitoes, which he called "grey mosquitos" (which were "Culex fatigans", but now renamed "Culex quinquefasciatus"). He

neg: Plasmodium malariae Plasmodium malariae Plasmodium malariae is a parasitic protozoa that causes malaria in humans. It is one of several species of "Plasmodium" parasites that infect humans including "Plasmodium falciparum" and "Plasmodium vivax" which are responsible for most malarial infection. While found worldwide, it is a so-called "benign malaria" and is not nearly as dangerous as that produced by "P. falciparum" or "P. vivax". It causes fevers that recur at approximately three-day intervals (a "quartan fever"), longer than the two-day (tertian) intervals of the other malarial parasites, hence its alternative names quartan fever and quartan malaria.. Malaria has been recognized since the

neg: Parasitic nutrition B, which may be important in nutrient acquisition. Malaria, caused by the apicomplexan parasite "Plasmodium falciparum", is an intracellular endoparasite. This parasite relies on a third organism, in the form of an "Anopheles" mosquito vector. The host blood provides an ideal rich source of glucose and amino acids to the parasite, particularly during blood stage infection where "Plasmodium" infects erythrocytes. To acquire essential nutrients "Plasmodium" has to compete with both the vertebrate and insect host and therefore must be highly efficient, regulating uptake according to nutrient availability. "Plasmodium", along with many other endoparasitic parasites, have numerous channels in their parasitophorous

neg: Ronald Ross bird parasites, very closely related to the human malarial parasites. Using more convenient model of birds, by July 1898 he established the importance of mosquitoes as intermediate hosts in avian malaria. On 4 July he discovered that the salivary gland was the storage sites of malarial parasites in the mosquito. By 8 July he was convinced that the parasites are released from the salivary gland during biting. He later demonstrated the transmission of malarial parasite from mosquitoes (in this case "Culex" species) to healthy birds from an infected one, thus, establishing the complete life cycle of malarial parasite. In September

neg: Angelo Celli Angelo Celli Angelo Celli (25 March 1857 – 2 November 1914) was an Italian physician, hygienist, parasitologist and philanthropist known for his pioneering works in malarial parasite and control of malaria. He was Professor of Hygiene at the University of Palermo, and then at the Sapienza University of Rome. He founded Pasteur Institute of Italy. With wife Anna Fraentzel he established a number of medical schools in Roman Campagna and dispensaries in Rome. He and Ettore Marchiafava correctly described the protozoan parasite that caused malaria and gave the scientific name "Plasmodium" in 1885. Understanding the nature of malaria, he was

neg: Plasmodium knowlesi out experiments on rhesus macaques in a Memphis laboratory with the assumption that humans were not susceptible to “monkey malaria.” Early research had concluded that macaques could not host "Plasmodium vivax", the human malaria parasite. This led Eyles and Coatney to begin working with "Plasmodium cynomolgi", a parasite similar enough to "P. vivax" to model the human malaria infection. The two exposed themselves to the infection, noting the causal itchy bite as a mere annoyance; however, Eyles fell ill with fever soon after the experiment. It was not until several days later that the two accepted the possibility that Eyles

neg: Plasmodium falciparum membrane. Infected erythrocytes are often sequestered in various human tissues or organs, such as the heart, liver and brain. This is caused by parasite-derived cell surface proteins being present on the erythrocyte membrane, and it is these proteins that bind to receptors on human cells. Sequestration in the brain causes cerebral malaria, a very severe form of the disease, which increases the victim's likelihood of death. After invading the erythrocyte, the parasite loses its specific invasion organelles (apical complex and surface coat) and de-differentiates into a round trophozoite located within a parasitophorous vacuole. The young trophozoite (or "ring" stage, because

neg: Plasmodium eylesi Plasmodium eylesi Plasmodium eylesi is a parasite of the genus "Plasmodium" subgenus "Plasmodium". Like all "Plasmodium" species "P. eylesi" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are mammals. The parasite was first described by Warren "et al." in 1965. and is named after the malariologist Dr. Don E. Eyles. It is believed that this species is related to "Plasmodium hylobati", "Plasmodium jefferyi" and "Plasmodium youngi" but this putative relationship awaits examination by DNA based methods. The parasite prefers to infect reticulocytes but will infect older erythrocytes. Multiple infections like those of "Plasmodium falciparum" are common

neg: Plasmodium knowlesi knowlesi edesoni" was described by Garnham in 1963. It was named after the parasitologist J F B Edeson. It is not known if there are any clinical differences between these two subspecies. Plasmodium knowlesi Plasmodium knowlesi is a primate malaria parasite commonly found in Southeast Asia. It causes malaria in long-tailed macaques ("Macaca fascicularis"), but it may also infect humans, either naturally or artificially. "Plasmodium knowlesi" is the sixth major human malaria parasite (following the division of "Plasmodium ovale" into 2 subspecies). It may cause severe malaria as indicated by its asexual erythrocytic cycle of about 24 hours, with an

neg: Asif Mohmmed Asif Mohmmed Asif Mohmmed is an Indian cell biologist, parasitologist and a professor at the International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi. At ICGEB, he leads a research group on Parasite Cell Biology and is one of the key collaborators of the Tewari Lab at the School of Life Science of the University of Nottingham. He is known for his studies on Plasmodium falciparum proteases with regard to cellular Stress and parasite cell-death and protein-trafficking machinery in the pathogen, as well as the development of new anti-malarial drugs. His studies have been documented by way of a

neg: Plasmodium eylesi the author was not certain of the infecting species. Plasmodium eylesi Plasmodium eylesi is a parasite of the genus "Plasmodium" subgenus "Plasmodium". Like all "Plasmodium" species "P. eylesi" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are mammals. The parasite was first described by Warren "et al." in 1965. and is named after the malariologist Dr. Don E. Eyles. It is believed that this species is related to "Plasmodium hylobati", "Plasmodium jefferyi" and "Plasmodium youngi" but this putative relationship awaits examination by DNA based methods. The parasite prefers to infect reticulocytes but will infect older erythrocytes.

neg: Plasmodium falciparum The parasite forms a parasitophorous vacuole, to allow for its development inside the erythrocyte. This infection cycle occurs in a highly synchronous fashion, with roughly all of the parasites throughout the blood in the same stage of development. This precise clocking mechanism has been shown to be dependent on the human host's own circadian rhythm. Within the erythrocyte, the parasite metabolism depends on the digestion of hemoglobin. The clinical symptoms of malaria such as fever, anemia, and neurological disorder are produced during the blood stage. The parasite can also alter the morphology of the erythrocyte, causing knobs on the erythrocyte

neg: Plasmodium vivax gram stain (negative vs. positive) and may appear as either. "P. vivax" was used between 1917 and the 1940s for malariotherapy, that is, to create very high fevers to combat certain diseases such as tertiary syphilis. In 1917, the inventor of this technique, Julius Wagner-Jauregg, received the Nobel Prize in Physiology or Medicine for his discoveries. However, the technique was dangerous, killing about 15% of patients, so it is no longer in use. Plasmodium vivax Plasmodium vivax is a protozoal parasite and a human pathogen. This parasite is the most frequent and widely distributed cause of recurring (Benign tertian) malaria,

neg: Plasmodium brasilianum mosquitoes infected by feeding on a platyrrhine spider monkey ("Ateles geoffroyi geoffroyi") from Panama carrying "P. brasilianum", have been shown to transmit the parasite through biting to five human volunteers. Investigations in the 1960s demonstrated that humans could be experimentally infected with "P. brasilianum" from monkeys and vice versa. In addition to humans, "P. brasilianum" has been transmissible experimentally to marmosets. In 1908, a quartan malaria parasite was identified by Gonder and von Berenberg-Gossler in an imported bald uakari ("Cacajao calvus") and named "Plasmodium brasilianum", the quartan malaria parasite of New World monkeys in Latin America. It resembled the human

neg: Andamanese both Fya antigen in another two areas (Jirkatang and Tirur). There was an absence of malarial parasite "Plasmodium vivax" infection though "Plasmodium falciparum" infection was present in 27·59% of cases. A very high frequency of Fy (a–b–) in the Jarawa tribe from all the four jungle areas of Andaman Islands along with total absence of "P. vivax" infections suggests the selective advantage offered to Fy (a–b–) individuals against "P. vivax" infection. Overall, the Andamanese showed closest relations with other Asian populations. The Nicobarese also were observed to share close genetic relations with adjacent Indo-Mongoloid populations of Northeast India. Bulbeck (2013)

neg: Loma salmonae Loma salmonae Loma salmonae is a species of microsporidian parasite, infecting Pacific salmon ("Oncorhynchus" spp.). "L. salmonae" is the causative agent of microsporidial gill disease of salmon. It is an intracellular parasite which induces respiratory distress, secondary infection, and increased mortality rates. "Loma salmonae" enters the "Oncorhynchus" host's gut via an infective spores. Once in the gut, the spore injects its sporoplasm into an epithelial cell. From there, it migrates to the heart for a two-week merogony-like phase. In the heart, the host's immune system phagocytizes the parasite. Following macrophage mediated transportation, "L. salmonae" enters into the host's gills where

neg: Plasmodium cynomolgi described. In addition to a few naturally occurring cases, human infection by "P. cynomolgi" has been verified in laboratories both by experimental infection of human volunteers and by laboratory accidents resulting in human infection. Transmission of "P. cynomolgi" from human to human by a mosquito vector has also been shown in laboratory experiments, although it appears to occur rarely if at all in the environment. "P. cynomolgi" is the second-most studied malaria parasite of non-human primates after "Plasmodium knowlesi", primarily due to its similarity to the human parasite "P. vivax". Both its blood stages and liver stages can be maintained

neg: Taenia taeniaeformis and is treated with the same medications (i.e., antihelminthics). The definitive host must ingest the strobilocercus stage of the tapeworm in order to acquire the parasite. The strobilocercus is a larval stage that has a terminal bladder and a rather long segmented body that is in crowned with the scolex that looks very similar to that found on the adult form. It seems that the strobilocercus must attain an age of about 2 months before it is in infective to a cat upon ingestion. Once a cat ingests the strobilocercus, the posterior portion of the larva is in digested away

neg: Circumsporozoite protein Circumsporozoite protein Circumsporozoite protein (CSP) is a secreted protein of the sporozoite stage of the malaria parasite ("Plasmodium" sp.) and is the antigenic target of RTS,S, a pre-erythrocytic malaria vaccine currently undergoing clinical trials. The amino-acid sequence of CSP consists of an immunodominant central repeat region flanked by conserved motifs at the N- and C- termini that are implicated in protein processing as the parasite travels from the mosquito to the mammalian vector. The structure and function of CSP is highly conserved across the various strains of malaria that infect humans, non-human primates and rodents. It can first be detected

neg: Plasmodium knowlesi other four types of human malaria. Infective mosquitoes are restricted to the forest areas. Non-infective mosquitoes are typically found in the urban areas but transmission may occur due to the abundance of mosquitoes in this region. particularly Malaysia, but there are also reports on the Thai-Burmese border. One fifth of the cases of malaria diagnosed in Sarawak, Malaysian Borneo are due to "P. knowlesi". "Plasmodium knowlesi" is absent in Africa. This may be because there are neither long-tailed nor pig-tailed macaques (the reservoir hosts of "P. knowlesi") in Africa, and many West Africans lack the Duffy antigen - a protein

neg: Artesunate and debatable. Artesunate is a prodrug that is rapidly converted to its active form dihydroartemisinin (DHA). This process involves hydrolysis of the 4-carbon ester group via plasma esterase enzyme. It is hypothesized that the cleavage of endoperoxide bridge in the pharmacophore of DHA generates reactive oxygen species (ROS), which increases oxidative stress and causes malarial protein damage via alkylation. In addition, Artesunate potently inhibits the essential "Plasmodium falciparum" exported protein 1 (EXP1), a membrane glutathione S-transferase. As a result, the amount of glutathione in the parasite is reduced. In 2016, artemisinin has been shown to bind to a large number

neg: Plasmodium gaboni Plasmodium gaboni Plasmodium gaboni is a parasite of the genus "Plasmodium". "Plasmodium gaboni" was given its name in reference to Gabon, where the parasite was discovered in two wild-borne chimpanzees kept as pets in villages in that country. "Plasmodium gaboni" is phylogenetically very close to "Plasmodium billbrayi". In 2009, Ollomo et al. published the complete mitochondrial genome of "Plasmodium gaboni", which was not yet named at the time. The parasite belongs to the "P falciparum/P reichenowi" lineage. It has been proposed that "Plasmodium gaboni" diverged from the "P falciparum/P reichenowi" lineage about 21 million years ago, leading to the conclusion

neg: Plasmodium malariae "Plasmodium" parasite. It can be found at the following link: http://cdc.gov/malaria/map/index.html. "P. malariae" can infect several species of mosquito and can cause malaria in humans. "P. malariae" can be maintained at very low infection rates among a sparse and mobile population because unlike the other "Plasmodium" parasites, it can remain in a human host for an extended period of time and still remain infectious to mosquitoes. The vector of transmission of the parasite is the female Anopheles mosquito, but many different species have been shown to transmit the parasite at least experimentally. Collins and Jeffrey report over thirty different types

neg: Apicoplast the phylum Apicomplexa. Among the most infamous Apicomplexan parasites is "Plasmodium falciparum", a causative agent of severe malaria. Because apicoplasts are vital to parasite survival, they provide an enticing target for antimalarial drugs. Specifically, apicoplasts' plant-like properties provide a target for herbicidal drugs. And, with the emergence of malarial strains resistant to current treatments it is paramount that novel therapies, like herbicides, are explored and understood. Furthermore, herbicides may be able to specifically target the parasite's plant-like apicoplast and without any noticeable effect on the mammalian host's cells. Evidence suggests that the apicoplast is a product of secondary endosymbiosis, and

neg: Intermittent fever types. Bouts of fever occurs daily (24-hour periodicity) for few hours, typical of Plasmodium falciparum or Plasmodium knowlesi. Fever occurs after an interval of two days (48-hour periodicity), typical of Plasmodium vivax and Plasmodium ovale. Fever occurs after an interval of three days (72-hour periodicity), typical of Plasmodium malariae. Following examples of infectious diseases show intermittent fever. Antipyretics like ibuprofen and paracetamol are used for fever and body aches. Antibiotics are also used for any underlying infection. For treating malaria, anti-malarial drugs like quinine, chloroquine and primaquine are given. Intermittent fever Intermittent fever is a type or pattern of fever

neg: Plasmodium tropiduri Plasmodium tropiduri Plasmodium tropiduri is a parasite of the genus "Plasmodium" subgenus "Lacertaemoba". Like all "Plasmodium" species "P. tropiduri" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are reptiles. This species is closely related to "Plasmodium floridense" and "Plasmodium minasense". The parasite was first described by Aragão and Neiva in 1909. It had been previous discovered by Carlos Chagas but not formally described. Later it was realised that this species was in fact a species complex. This complex was divided into a number of subspecies by Telford in 1979. "Plasmodium tropiduri aquaticum" is found in "Anolis

neg: Malaria originated through the endosymbiosis of algae and play a crucial role in various aspects of parasite metabolism, such as fatty acid biosynthesis. Over 400 proteins have been found to be produced by apicoplasts and these are now being investigated as possible targets for novel anti-malarial drugs. With the onset of drug-resistant "Plasmodium" parasites, new strategies are being developed to combat the widespread disease. One such approach lies in the introduction of synthetic pyridoxal-amino acid adducts, which are taken up by the parasite and ultimately interfere with its ability to create several essential B vitamins. Antimalarial drugs using synthetic metal-based complexes

neg: ACDC domain ACDC domain The "A"P2-"C"oincident "D"omain mainly at the "C"arboxy-terminus, or ACDC domain, is a protein domain that occurs in proteins from apicomplexan parasites. It is found exclusively in apicomplexan proteins that also contain AP2 (Apetala 2-integrase) DNA binding domains (ApiAP2 proteins). In 8 of 9 known examples in the malarial parasite "Plasmodium falciparum" it is near the carboxy terminus, with the remaining one being at the amino terminus. As yet, beyond its identification and the observation that it occurs only in ApiAP2 proteins, the function of the ACDC domain is unknown. Two proteins with the ACDC domain were found in

neg: Plasmodium gaboni virulent agent of malaria, "Plasmodium falciparum", it has been considered the possibility of transfer risk of this species to humans. Plasmodium gaboni Plasmodium gaboni is a parasite of the genus "Plasmodium". "Plasmodium gaboni" was given its name in reference to Gabon, where the parasite was discovered in two wild-borne chimpanzees kept as pets in villages in that country. "Plasmodium gaboni" is phylogenetically very close to "Plasmodium billbrayi". In 2009, Ollomo et al. published the complete mitochondrial genome of "Plasmodium gaboni", which was not yet named at the time. The parasite belongs to the "P falciparum/P reichenowi" lineage. It has been

neg: Plasmodium falciparum that help in suppressing communication of the immune cells. Even at the height of the infection when RBCs are ruptured, the immune signals are not strong enough to activate macrophages or natural killer cells. Although "P. falciparum" is easily recognized by human immune system while in the bloodstream, it evades immunity by producing over 2,000 cell membrane antigens The initial infective stage sporozoites produce circumsporozoite protein (CSP), which binds to hepatocytes. Binding to and entry into the hepatocytes is aided by another protein, thrombospondin-related anonymous protein (TRAP). TRAP and other secretory proteins (including sporozoite microneme protein essential for cell traversal

neg: Barbigerone Barbigerone Barbigerone is one of a few pyranoisoflavones among several groups of isoflavones. It was first isolated from the seed of a leguminous plant "Tephrosia barbigera"; hence the name "barbigerone". Members of the genus "Millettia" are now known to be rich in barbigerone, including "M. dielsiena", "M. ferruginea", "M. usaramensis", and "M. pachycarpa". It has also been isolated from the medicinal plant "Sarcolobus globosus". Barbigerone from "S. globosus" is validated to have significant antioxidant property. Barbigerone exhibits profound antiplasmodial activity against the malarial parasite "Plasmodium falciparum". It is also demonstrated that it has anti-cancer potential as it causes apoptosis of

neg: Barbigerone murine lung-cancer cells. Barbigerone Barbigerone is one of a few pyranoisoflavones among several groups of isoflavones. It was first isolated from the seed of a leguminous plant "Tephrosia barbigera"; hence the name "barbigerone". Members of the genus "Millettia" are now known to be rich in barbigerone, including "M. dielsiena", "M. ferruginea", "M. usaramensis", and "M. pachycarpa". It has also been isolated from the medicinal plant "Sarcolobus globosus". Barbigerone from "S. globosus" is validated to have significant antioxidant property. Barbigerone exhibits profound antiplasmodial activity against the malarial parasite "Plasmodium falciparum". It is also demonstrated that it has anti-cancer potential as it

neg: Premunition Premunition Premunition, also known as infection-immunity, is a host response that protects against high numbers of parasite and illness without eliminating the infection. This type of immunity is relatively rapid, progressively acquired, short-lived, and partially effective. For malaria, premunition is maintained by repeated antigen exposure from infective bites. Thus, if an individual departs from an endemic area, he or she may lose premunition and become susceptible to malaria. Antibody action contributes to premunition. However, premunition is probably much more complex than simple antibody and antigen interaction. In the case of malaria, the sporozoite and merozoite stages of "Plasmodium" elicit the

neg: ACDC domain the nucleus of "P. falciparum", as detected by a proteomic method, suggesting a role in nuclear biology. ACDC domain The "A"P2-"C"oincident "D"omain mainly at the "C"arboxy-terminus, or ACDC domain, is a protein domain that occurs in proteins from apicomplexan parasites. It is found exclusively in apicomplexan proteins that also contain AP2 (Apetala 2-integrase) DNA binding domains (ApiAP2 proteins). In 8 of 9 known examples in the malarial parasite "Plasmodium falciparum" it is near the carboxy terminus, with the remaining one being at the amino terminus. As yet, beyond its identification and the observation that it occurs only in ApiAP2 proteins,

neg: Rufigallol Rufigallol Rufigallol or 1,2,3,5,6,7-hexahydroxy-9,10-anthraquinone is an organic compound with formula , which can be viewed as a derivative of anthraquinone through the replacement of six hydrogen atoms (H) by hydroxyl groups (OH). The compound is soluble in dioxane, from which it crystallizes as red needles that sublime without melting at 365 °C. It can be obtained by treating gallic acid with concentrated sulfuric acid and then with sodium hydroxide. Rufigallol is particularly toxic to the malarial parasite "Plasmodium falciparum" and has a synergistic effect in combination with the antimalarial drug exifone, which has structural sumilarities to rufigallol. Rufigallol forms a

neg: Plasmodium fieldi Plasmodium fieldi Plasmodium fieldi is a parasite of the genus "Plasmodium" sub genus "Plasmodium" found in Malaysia. This species is related to "Plasmodium ovale" and "Plasmodium simiovale". Like all "Plasmodium" species "P. fieldi" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are primates. This species was first described by Eyles, Laing and Fong in 1962. The parasite was identified in a pig-tailed macaque ("Macaca nemestrina") that Eyles purchased in peninsular Malaysia in mid-August 1960. It was named after the malariologist Dr. John W. Field. The asexual cycle is 48 hours in length Ring forms: These measure

neg: Giovanni Battista Grassi that the roundworm is transmitted through direct ingestion from contaminated source. Grassi made his first contribution on malaria in 1890, when he (with Raimondo Feletti) discovered "Haemamoeba vivax", later renamed "Plasmodium vivax". He described "Proteosoma praecox", the malaria parasite of birds. In 1891 he performed the first inoculation of malaria parasites from one bird into another. He was the first to compile a comprehensive monograph on the identity and impact of different malarial parasites. His work "Studi di uno Zoologo Sulla Malaria " in 1891 is as relevant today as it was in his time. His description of the specific

neg: Giovanni Battista Grassi produce the final proof of mosquito transmission of malaria when they fed local mosquitoes ("A. claviger") on infected patients and found that uninfected individuals developed malaria through the mosquito bite. The 1902 Nobel Prize in Physiology or Medicine was awarded to Ronald Ross for his discovery of the life cycle of malarial parasite (or as the Nobel citation goes: "for his work on malaria, by which he has shown how it enters the organism..."). However, this was disputed and continues to be disputed to this day. Grassi was the first to suggest that there must be some developmental stage of

neg: DNA vaccination TH2 responses. This is true for intracellular and plasma membrane-bound antigens, but not for secreted antigens, which seem to generate TH2 responses, regardless of the method of delivery. Generally the type of T-cell help raised is stable over time, and does not change when challenged or after subsequent immunizations that would normally have raised the opposite type of response in a naïve specimen. However, Mor "et al.". (1995) immunized and boosted mice with pDNA encoding the circumsporozoite protein of the mouse malarial parasite "Plasmodium yoelii" (PyCSP) and found that the initial TH2 response changed, after boosting, to a TH1 response.

neg:
Plasmodium pinotti Plasmodium pinotti Plasmodium pinotti is a parasite of the genus "Plasmodium" subgenus "Giovannolaia". Like all "Plasmodium" species "P. pinotti" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are birds. The parasite was first described by Muniz and Soares in 1954. It was named after the Dr Mario Pinotti. It is related to the following species "Plasmodium asanum"
 "Plasmodium circumflexum"
 "Plasmodium durae"
 "Plasmodium fallax"
 "Plasmodium formosanum"
 "Plasmodium gabaldoni"
 "Plasmodium hegneri"
 "Plasmodium lophrae"
 "Plasmodium pediocetti"
 "Plasmodium polare" This species is found in Jamaica. Known hosts of this species include the bananaquit ("Coereba flaveola"), orangequit ("Euneornis campestris"), yellow-shouldered grassquit

neg:
Plasmodium pinotti ("Loxipasser anoxanthus"), the large toucan ("Ramphastos toco") and the black-faced grassquit ("Tiaris bicolor"). Plasmodium pinotti Plasmodium pinotti is a parasite of the genus "Plasmodium" subgenus "Giovannolaia". Like all "Plasmodium" species "P. pinotti" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are birds. The parasite was first described by Muniz and Soares in 1954. It was named after the Dr Mario Pinotti. It is related to the following species "Plasmodium asanum"
 "Plasmodium circumflexum"
 "Plasmodium durae"
 "Plasmodium fallax"
 "Plasmodium formosanum"
 "Plasmodium gabaldoni"
 "Plasmodium hegneri"
 "Plasmodium lophrae"
 "Plasmodium pediocetti"
 "Plasmodium polare" This species is found in Jamaica. Known hosts

neg: Plasmodium tejerai Plasmodium tejerai Plasmodium tejerai is a parasite of the genus "Plasmodium" subgenus "Haemamoeba". Like all "Plasmodium" species "P. tejerai" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are birds. The parasite was first described by Gabaldon and Ulloa in 1977. This parasite is found in Brazil and Venezuela. Not known. This organism infects the domestic turkey ("Meleagris gallopavo") and the South American penguin ("Spheniscus magellanicus"). Morphologically this parasite resembles "Plasmodium relictum" closely. In the penguin infection may be fatal with splenomegaly,hepatomegaly, hydropericardium and pulmonary oedema. Tissue meronts may occur in the macrophages and endothelial cells of

neg: Émile Brumpt Émile Brumpt Alexandre Joseph Émile Brumpt (10 March 1877, Paris – 8 July 1951) was a French parasitologist. He studied zoology and parasitology in Paris, obtaining his degree in science in 1901, and his medical doctorate in 1906. In 1919 he succeeded Raphaël Blanchard (1857-1919) as professor of parasitology to the Faculté de Médecine de Paris, a position he maintained until 1948. Much of his career was spent performing research in Africa and Latin America. Brumpt is credited for introducing a technique known as xenodiagnosis into parasitological research. In 1935 he described "Plasmodium gallinaceum", an avian malarial parasite that infects

neg:
Plasmodium durae Plasmodium durae Plasmodium durae is a parasite of the genus "Plasmodium" subgenus "Giovannolaia". Like all "Plasmodium" species "P. durae" has both vertebrate and insect hosts. The vertebrate hosts for this parasite are birds. The parasite was first described by Herman in 1941. Mature gametocytes tend to lie obliquely within the host cell, displace the nucleus to one pole of the cell and possess one or more clumps of clear pigment granules. It is related to the following species: "Plasmodium asanum"
 "Plasmodium circumflexum"
 "Plasmodium fallax"
 "Plasmodium formosanum"
 "Plasmodium gabaldoni"
 "Plasmodium hegneri"
 "Plasmodium lophrae"
 "Plasmodium lophrae"
 "Plasmodium pediocetti"
 "Plasmodium pinotti"
 "Plasmodium polare"