Malaria
Plasmodium
Plasmodium falciparum
Parasitemia
Plasmodium vivax
Antigens, Protozoan
Erythrocytes
Malaria Vaccines
Antimalarials
Merozoite Surface Protein 1
Mice, Inbred C57BL
Malaria, Falciparum
Drug Resistance
Host-Parasite Interactions
Mice, Inbred A
Pyrimethamine
Mice, Inbred CBA
Mice, Inbred BALB C
Plasmodium malariae
Plasmodium knowlesi
Immunization, Passive
Malaria, Vivax
Interferon-gamma
Plasmodium ovale
Chloroquine
gammadelta T cells contribute to control of chronic parasitemia in Plasmodium chabaudi infections in mice. (1/267)
During a primary infection of mice with Plasmodium chabaudi, gammadelta T cells are stimulated and their expansion coincides with recovery from the acute phase of infection in normal mice or with chronic infections in B cell-deficient mice (mu-MT). To determine whether the large gammadelta T cell pool observed in female B cell-deficient mice is responsible for controlling the chronic infection, studies were done using double-knockout mice deficient in both B and gammadelta cells (mu-MT x delta-/-TCR) and in gammadelta T cell-depleted mu-MT mice. In both types of gammadelta T cell-deficient mice, the early parasitemia following the peak of infection was exacerbated, and the chronic parasitemia was maintained at significantly higher levels in the absence of gammadelta T cells. The majority of gammadelta T cells in C57BL/6 and mu-MT mice responding to infection belonged predominantly to a single family of gammadelta T cells with TCR composed of Vgamma2Vdelta4 chains and which produced IFN-gamma rather than IL-4. (+info)Identification of the Plasmodium chabaudi homologue of merozoite surface proteins 4 and 5 of Plasmodium falciparum. (2/267)
Previous studies of Plasmodium falciparum have identified a region of chromosome 2 in which are clustered three genes for glycosylphosphatidylinositol (GPI)-anchored merozoite surface proteins, MSP2, MSP5, and MSP4, arranged in tandem. MSP4 and MSP5 both encode proteins 272 residues long that contain hydrophobic signal sequences, GPI attachment signals, and a single epidermal growth factor (EGF)-like domain at their carboxyl termini. Nevertheless, the remainder of their protein coding regions are quite dissimilar. The locations and similar structural features of these genes suggest that they have arisen from a gene duplication event. Here we describe the identification of the syntenic region of the genome in the murine malaria parasite, Plasmodium chabaudi adami DS. Only one open reading frame is present in this region, and it encodes a protein with structural features reminiscent of both MSP4 and MSP5, including a single EGF-like domain. Accordingly, the gene has been designated PcMSP4/5. The homologue of the P. falciparum MSP2 gene could not be found in P. chabaudi; however, the amino terminus of the PcMSP4/5 protein shows similarity to that of MSP2. The PcMSP4/5 gene encodes a protein with an apparent molecular mass of 36 kDa, and this protein is detected in mature stages of the parasite. The protein partitions in the detergent-enriched phase after Triton X-114 fractionation and is localized to the surfaces of trophozoites and developing and free merozoites. The PcMSP4/5 gene is transcribed in both ring and trophozoite stages but appears to be spliced in a stage-specific manner such that the central intron is spliced from the mRNA in the parasitic stage in which the protein is expressed. (+info)Transforming growth factor beta-induced failure of resistance to infection with blood-stage Plasmodium chabaudi in mice. (3/267)
The role of transforming growth factor beta (TGF-beta) in infection with Plasmodium chabaudi was investigated with resistant and susceptible mouse models. C57BL/10 mice produced gamma interferon (IFN-gamma) and nitric oxide (NO) shortly after infection and cleared the parasite spontaneously. In contrast, BALB/c mice showed a transient enhancement of TGF-beta production, followed by a relative lack of IFN-gamma and NO production, and succumbed to the infection. However, there was no correlation between levels of serum TGF-beta and splenic TGF-beta mRNA in both mouse strains before and after infection. Administration of recombinant TGF-beta (rTGF-beta) rendered resistant mice susceptible because of suppression of subsequent production of IFN-gamma and NO. Administration of anti-TGF-beta antibody to the infected BALB/c mice resulted in remarkable increases in serum IFN-gamma and NO, and the mice resisted the infection. Splenic CD4(+) T and CD11b+ cells of C57BL/10 mice were significantly activated after infection, but this was completely abrogated by administration of rTGF-beta. These results suggested that, in the P. chabaudi-susceptible but not resistant mice, production of TGF-beta was promoted, and subsequent failure of IFN-gamma- and NO-dependent resistance to the parasite was induced. This study is the first to indicate that TGF-beta production was the key event in failure of resistance to mouse malaria. (+info)Deficiency in tumor necrosis factor alpha activity does not impair early protective Th1 responses against blood-stage malaria. (4/267)
Blood-stage Plasmodium chabaudi AS infection was controlled by 4 weeks in mice with deletion of tumor necrosis factor p55 and p75 receptors (TNFR-knockout [KO]) and control wild-type (WT) mice, although female TNFR-KO mice showed slightly but significantly higher parasitemia immediately following the peak. Serum interleukin 12 (IL-12) p70 and gamma interferon (IFN-gamma) levels were similar but tumor necrosis factor alpha levels were significantly higher in TNFR-KO mice than in WT controls. Splenic IL-12 receptor beta1 and beta2 and IFN-gamma mRNA expression, as well as spleen cell production of IFN-gamma and IL-4, were comparable in both mouse types, but IL-10 production was significantly higher in cells from TNFR-KO mice than in cells from WT mice. Lipopolysaccharide-induced NO secretion by splenic macrophages in vitro was significantly reduced but systemic NO3- levels were similar in infected TNFR-KO and WT mice. (+info)Modulation of experimental blood stage malaria through blockade of the B7/CD28 T-cell costimulatory pathway. (5/267)
Recent studies have implicated cytokines associated with CD4+ T lymphocytes of both T helper (Th)1 and Th2 subsets in resistance to experimental blood stage malaria. As the B7/CD28 costimulatory pathway has been shown to influence the differentiation of Th cell subsets, we investigated the contribution of the B7 molecules CD80 and CD86 to Th1/Th2 cytokine and immunoglobulin isotype profiles and to the development of a protective immune response to malaria in NIH mice infected with Plasmodium chabaudi. Effective blockade of CD86/CD28 interaction was demonstrated by elimination of interleukin (IL)-4 and up-regulation of interferon (IFN)-gamma responses by P. chabaudi-specific T cells and by reduction of P. chabaudi-specific immunoglobulin G1 (IgG1). The shift towards a Th1 cytokine pattern corresponded with efficient control of acute parasitaemia but an inability to resolve chronic infection. Moreover, combined CD80/CD86 blockade by using anti-CD80 and anti-CD86 monoclonal antibodies raised IFN-gamma production over that seen with CD86 blockade alone, with augmentation of this Th1-associated cytokine reducing levels of peak primary parasitaemia. These results demonstrate that IL-4 production by T cells in P. chabaudi-infected NIH mice is dependent upon CD86/CD28 interaction and that IL-4 and IFN-gamma contribute significantly, at different times of infection, to host resistance to blood stage malaria. In addition, combined CD80/CD86 blockade resulted in preferential expansion of IFN-gamma-producing T cells during P. chabaudi infection, suggesting that costimulatory pathways other than B7/CD28 may contribute to T-cell activation during continuous antigen stimulation. This study indicates a role for B7/CD28 costimulation in modulating the CD4+ T-cell response during malaria, and further suggests involvement of this pathway in other infectious and autoimmune diseases in which the Th cell immune response is also skewed. (+info)Selection for high and low virulence in the malaria parasite Plasmodium chabaudi. (6/267)
What stops parasites becoming ever more virulent? Conventional wisdom and most parasite-centred models of the evolution of virulence suppose that risk of host (and, hence, parasite) death imposes selection against more virulent strains. Here we selected for high and low virulence within each of two clones of the rodent malaria parasite Plasmodium chabaudi on the basis of between-host differences in a surrogate measure of virulence--loss of live weight post-infection. Despite imposing strong selection for low virulence which mimicked 50-75% host mortality, the low virulence lines increased in virulence as much as the high virulence lines. Thus, artificial selection on between-host differences in virulence was unable to counteract natural selection for increased virulence caused by within-host selection processes. The parasite's asexual replication rate and number of sexual transmission forms also increased in all lines, consistent with evolutionary models explaining high virulence. An upper bound to virulence, though not the asexual replication rate, was apparent, but this bound was not imposed by host mortality. Thus, we found evidence of the factors assumed to drive evolution of increased virulence, but not those thought to counter this selection. (+info)Plasticity of immune responses suppressing parasitemia during acute Plasmodium chabaudi malaria. (7/267)
gammadelta T cells have a crucial role in cell-mediated immunity (CMI) against P. chabaudi malaria, but delta-chain knockout (KO) (deltao/o) mice and mice depleted of gammadelta T cells with mAb cure this infection. To address the question of why mice deficient in gammadelta T cells resolve P. chabaudi infections, we immunized deltao/o mice by infection with viable blood-stage parasites. Sera from infection-immunized mice were tested for their ability to protect JHo/o, deltao/o double KO mice passively against P. chabaudi challenge infection. The onset of parasitemia was significantly delayed in mice receiving immune sera, compared with saline or uninfected serum controls. Immune sera were then fractionated into Ig-rich and Ig-depleted fractions by HPLC on a protein G column. Double KO mice were passively immunized with either fraction and challenged with P. chabaudi. The onset of parasitemia was significantly delayed in recipients of the Ig-rich fraction compared with recipients of the Ig-poor fraction of immune sera. We conclude that deltao/o mice, which are unable to activate CMI against the parasite, suppress P. chabaudi infection by a redundant Ab-mediated process. (+info)Early IL-12 p70, but not p40, production by splenic macrophages correlates with host resistance to blood-stage Plasmodium chabaudi AS malaria. (8/267)
In this study, we compared synthesis of IL-12, a potent Th1-inducing cytokine, by splenic macrophages recovered from resistant C57Bl/6 (B6) mice, which develop predominantly Th1 responses, and susceptible A/J mice that mount primarily Th2 responses during early Plasmodium chabaudi AS infection. Quantitative analysis of IL-12 p40 and p70 release by ELISA revealed significant differences between resistant B6 and susceptible A/J mice in the synthesis of biologically active IL-12 p70, but not p40, by splenic macrophages during early blood-stage P. chabaudi AS infection. Despite up-regulation in p40 and p35 mRNA levels, spontaneous release of p40 in vitro by splenic macrophages was not significantly increased following infection in either mouse strain. In contrast, spontaneous release of p70 by splenic macrophages was increased in cells from B6 mice and levels were significantly higher compared with A/J mice. Furthermore, compared with infected A/J hosts, splenic macrophages recovered from infected B6 mice produced significantly greater quantities of IL-12 p70, but not p40, in vitro, following stimulation with lipopolysaccharide (LPS) or malaria parasite antigen (PRBC). Moreover, we found significant increases in the percentage of macrophages earlier in the spleens of infected B6 mice that could further contribute to differences in total p70 levels in vivo. Taken together, these data suggest that macrophage IL-12 synthesis may contribute to the polarization of Th responses seen in resistant B6 and susceptible A/J mice during acute blood-stage malaria. (+info)"Plasmodium chabaudi" is a species of parasitic protozoa belonging to the genus Plasmodium, which includes the causative agents of malaria in various animals and humans. "P. chabaudi" primarily infects rodents, particularly mice, and serves as a model organism for studying the fundamental biology and pathogenesis of malaria.
The life cycle of "P. chabaudi" involves both sexual and asexual reproduction, similar to other Plasmodium species. The parasite is transmitted through the bite of an infected Anopheles mosquito, which injects sporozoites into the host's bloodstream. These sporozoites then infect liver cells, where they undergo schizogony (asexual reproduction) and produce merozoites.
Merozoites released from the liver invade red blood cells, initiating the erythrocytic stage of the life cycle. Within the red blood cells, the parasites multiply by schizogony, forming new merozoites that are eventually released to infect other red blood cells. Some of these parasites differentiate into male and female gametocytes, which can be taken up by a mosquito during a blood meal, completing the life cycle.
"P. chabaudi" infections in mice can lead to various pathological changes, including anemia, splenomegaly (enlarged spleen), and immune responses that contribute to disease progression. Researchers use this model organism to investigate aspects of malaria biology, such as host-parasite interactions, immunity, drug development, and vaccine design.
Malaria is not a medical definition itself, but it is a disease caused by parasites that are transmitted to people through the bites of infected female Anopheles mosquitoes. Here's a simple definition:
Malaria: A mosquito-borne infectious disease caused by Plasmodium parasites, characterized by cycles of fever, chills, and anemia. It can be fatal if not promptly diagnosed and treated. The five Plasmodium species known to cause malaria in humans are P. falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi.
"Plasmodium" is a genus of protozoan parasites that are the causative agents of malaria in humans and other animals. There are several species within this genus, including Plasmodium falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi, among others.
These parasites have a complex life cycle that involves two hosts: an Anopheles mosquito and a vertebrate host (such as humans). When a person is bitten by an infected mosquito, the parasites enter the bloodstream and infect red blood cells, where they multiply and cause the symptoms of malaria.
Plasmodium species are transmitted through the bites of infected female Anopheles mosquitoes, which become infected after taking a blood meal from an infected person. The parasites then develop in the mosquito's midgut, eventually making their way to the salivary glands, where they can be transmitted to another human through the mosquito's bite.
Malaria is a serious and sometimes fatal disease that affects millions of people worldwide, particularly in tropical and subtropical regions. It is characterized by fever, chills, headache, muscle and joint pain, and anemia, among other symptoms. Prompt diagnosis and treatment are essential to prevent severe illness and death from malaria.
'Plasmodium falciparum' is a specific species of protozoan parasite that causes malaria in humans. It is transmitted through the bites of infected female Anopheles mosquitoes and has a complex life cycle involving both human and mosquito hosts.
In the human host, the parasites infect red blood cells, where they multiply and cause damage, leading to symptoms such as fever, chills, anemia, and in severe cases, organ failure and death. 'Plasmodium falciparum' malaria is often more severe and life-threatening than other forms of malaria caused by different Plasmodium species. It is a major public health concern, particularly in tropical and subtropical regions of the world where access to prevention, diagnosis, and treatment remains limited.
Parasitemia is a medical term that refers to the presence of parasites, particularly malaria-causing Plasmodium species, in the bloodstream. It is the condition where red blood cells are infected by these parasites, which can lead to various symptoms such as fever, chills, anemia, and organ damage in severe cases. The level of parasitemia is often used to assess the severity of malaria infection and to guide treatment decisions.
"Plasmodium berghei" is a species of protozoan parasites belonging to the genus Plasmodium, which are the causative agents of malaria. This particular species primarily infects rodents and is not known to naturally infect humans. However, it is widely used in laboratory settings as a model organism to study malaria and develop potential interventions, such as drugs and vaccines, due to its similarities with human-infecting Plasmodium species.
The life cycle of P. berghei involves two hosts: an Anopheles mosquito vector and a rodent host. The parasite undergoes asexual reproduction in the red blood cells of the rodent host, leading to the symptoms of malaria, such as fever, anemia, and organ damage. When an infected mosquito bites another rodent, the parasites are transmitted through the saliva and infect the new host, continuing the life cycle.
While P. berghei is not a direct threat to human health, studying this species has contributed significantly to our understanding of malaria biology and the development of potential interventions against this devastating disease.
"Plasmodium vivax" is a species of protozoan parasite that causes malaria in humans. It's one of the five malaria parasites that can infect humans, with P. falciparum being the most deadly.
P. vivax typically enters the human body through the bite of an infected Anopheles mosquito. Once inside the human host, the parasite travels to the liver where it multiplies and matures. After a period of development that can range from weeks to several months, the mature parasites are released into the bloodstream, where they infect red blood cells and continue to multiply.
The symptoms of P. vivax malaria include fever, chills, headache, muscle and joint pain, and fatigue. One distinctive feature of P. vivax is its ability to form dormant stages (hypnozoites) in the liver, which can reactivate and cause relapses of the disease months or even years after the initial infection.
P. vivax malaria is treatable with medications such as chloroquine, but resistance to this drug has been reported in some parts of the world. Prevention measures include using insecticide-treated bed nets and indoor residual spraying to reduce mosquito populations, as well as taking prophylactic medications for travelers visiting areas where malaria is common.
Antibodies, protozoan, refer to the immune system's response to an infection caused by a protozoan organism. Protozoa are single-celled microorganisms that can cause various diseases in humans, such as malaria, giardiasis, and toxoplasmosis.
When the body is infected with a protozoan, the immune system responds by producing specific proteins called antibodies. Antibodies are produced by a type of white blood cell called a B-cell, and they recognize and bind to specific antigens on the surface of the protozoan organism.
There are five main types of antibodies: IgA, IgD, IgE, IgG, and IgM. Each type of antibody has a different role in the immune response. For example, IgG is the most common type of antibody and provides long-term immunity to previously encountered pathogens. IgM is the first antibody produced in response to an infection and is important for activating the complement system, which helps to destroy the protozoan organism.
Overall, the production of antibodies against protozoan organisms is a critical part of the immune response and helps to protect the body from further infection.
Antigens are substances (usually proteins) found on the surface of cells, or viruses, that can be recognized by the immune system and stimulate an immune response. In the context of protozoa, antigens refer to the specific proteins or other molecules found on the surface of these single-celled organisms that can trigger an immune response in a host organism.
Protozoa are a group of microscopic eukaryotic organisms that include a diverse range of species, some of which can cause diseases in humans and animals. When a protozoan infects a host, the host's immune system recognizes the protozoan antigens as foreign and mounts an immune response to eliminate the infection. This response involves the activation of various types of immune cells, such as T-cells and B-cells, which recognize and target the protozoan antigens.
Understanding the nature of protozoan antigens is important for developing vaccines and other immunotherapies to prevent or treat protozoan infections. For example, researchers have identified specific antigens on the surface of the malaria parasite that are recognized by the human immune system and have used this information to develop vaccine candidates. However, many protozoan infections remain difficult to prevent or treat, and further research is needed to identify new targets for vaccines and therapies.
'Plasmodium yoelii' is a species of protozoan parasite belonging to the genus Plasmodium, which causes malaria in rodents. It is primarily used as a model organism in malaria research due to its similarity to the human malaria parasites, Plasmodium falciparum and Plasmodium vivax. The life cycle of P. yoelii involves two hosts: an Anopheles mosquito vector and a rodent host. The parasite undergoes asexual reproduction in the red blood cells of the rodent host, leading to the symptoms of malaria such as fever, anemia, and organ failure if left untreated. P. yoelii is not known to infect humans.
Erythrocytes, also known as red blood cells (RBCs), are the most common type of blood cell in circulating blood in mammals. They are responsible for transporting oxygen from the lungs to the body's tissues and carbon dioxide from the tissues to the lungs.
Erythrocytes are formed in the bone marrow and have a biconcave shape, which allows them to fold and bend easily as they pass through narrow blood vessels. They do not have a nucleus or mitochondria, which makes them more flexible but also limits their ability to reproduce or repair themselves.
In humans, erythrocytes are typically disc-shaped and measure about 7 micrometers in diameter. They contain the protein hemoglobin, which binds to oxygen and gives blood its red color. The lifespan of an erythrocyte is approximately 120 days, after which it is broken down in the liver and spleen.
Abnormalities in erythrocyte count or function can lead to various medical conditions, such as anemia, polycythemia, and sickle cell disease.
I'm sorry for any confusion, but "Protozoan Proteins" is not a specific medical or scientific term. Protozoa are single-celled eukaryotic organisms, and proteins are large biological molecules consisting of one or more chains of amino acid residues. Therefore, "Protozoan Proteins" generally refers to the various types of proteins found in protozoa.
However, if you're looking for information about proteins specific to certain protozoan parasites with medical relevance (such as Plasmodium falciparum, which causes malaria), I would be happy to help! Please provide more context or specify the particular protozoan of interest.
Malaria vaccines are biological preparations that induce immunity against malaria parasites, thereby preventing or reducing the severity of malaria disease. They typically contain antigens (proteins or other molecules derived from the parasite) that stimulate an immune response in the recipient, enabling their body to recognize and neutralize the pathogen upon exposure.
The most advanced malaria vaccine candidate is RTS,S/AS01 (Mosquirix), which targets the Plasmodium falciparum parasite's circumsporozoite protein (CSP). This vaccine has shown partial protection in clinical trials, reducing the risk of severe malaria and hospitalization in young children by about 30% over four years. However, it does not provide complete immunity, and additional research is ongoing to develop more effective vaccines against malaria.
Antimalarials are a class of drugs that are used for the prevention, treatment, and elimination of malaria. They work by targeting the malaria parasite at various stages of its life cycle, particularly the erythrocytic stage when it infects red blood cells. Some commonly prescribed antimalarials include chloroquine, hydroxychloroquine, quinine, mefloquine, and artemisinin-based combinations. These drugs can be used alone or in combination with other antimalarial agents to increase their efficacy and prevent the development of drug resistance. Antimalarials are also being investigated for their potential use in treating other diseases, such as autoimmune disorders and cancer.
Merozoite Surface Protein 1 (MSP1) is a malarial antigen, which is a protein present on the surface of merozoites, which are the invasive forms of the Plasmodium parasites that cause malaria. MSP1 plays a crucial role in the invasion of red blood cells by the merozoites during the erythrocytic stage of the parasite's life cycle.
The MSP1 protein is synthesized and processed through several stages, resulting in multiple fragments, including the C-terminal 42 kDa fragment (MSP1-42) that is further cleaved into four smaller fragments (MSP1-19, MSP1-33, MSP1-38, and MSP1-42). These fragments are involved in the recognition and attachment of merozoites to the red blood cells, followed by the formation of a tight junction between the parasite and the host cell membranes.
MSP1 is one of the most abundant and immunogenic proteins on the surface of the merozoites, making it an attractive vaccine candidate. However, despite extensive research, a successful MSP1-based malaria vaccine has yet to be developed due to challenges in eliciting a protective immune response against this complex antigen.
The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:
1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.
The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.
C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.
The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.
C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.
One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.
Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.
There doesn't seem to be a specific medical definition for "DNA, protozoan" as it is simply a reference to the DNA found in protozoa. Protozoa are single-celled eukaryotic organisms that can be found in various environments such as soil, water, and the digestive tracts of animals.
Protozoan DNA refers to the genetic material present in these organisms. It is composed of nucleic acids, including deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), which contain the instructions for the development, growth, and reproduction of the protozoan.
The DNA in protozoa, like in other organisms, is made up of two strands of nucleotides that coil together to form a double helix. The four nucleotide bases that make up protozoan DNA are adenine (A), thymine (T), guanine (G), and cytosine (C). These bases pair with each other to form the rungs of the DNA ladder, with A always pairing with T and G always pairing with C.
The genetic information stored in protozoan DNA is encoded in the sequence of these nucleotide bases. This information is used to synthesize proteins, which are essential for the structure and function of the organism's cells. Protozoan DNA also contains other types of genetic material, such as regulatory sequences that control gene expression and repetitive elements with no known function.
Understanding the DNA of protozoa is important for studying their biology, evolution, and pathogenicity. It can help researchers develop new treatments for protozoan diseases and gain insights into the fundamental principles of genetics and cellular function.
Malaria, Falciparum is defined as a severe and often fatal form of malaria caused by the parasite Plasmodium falciparum. It is transmitted to humans through the bites of infected Anopheles mosquitoes. This type of malaria is characterized by high fever, chills, headache, muscle and joint pain, and vomiting. If left untreated, it can cause severe anemia, kidney failure, seizures, coma, and even death. It is a major public health problem in many tropical and subtropical regions of the world, particularly in Africa.
Drug resistance, also known as antimicrobial resistance, is the ability of a microorganism (such as bacteria, viruses, fungi, or parasites) to withstand the effects of a drug that was originally designed to inhibit or kill it. This occurs when the microorganism undergoes genetic changes that allow it to survive in the presence of the drug. As a result, the drug becomes less effective or even completely ineffective at treating infections caused by these resistant organisms.
Drug resistance can develop through various mechanisms, including mutations in the genes responsible for producing the target protein of the drug, alteration of the drug's target site, modification or destruction of the drug by enzymes produced by the microorganism, and active efflux of the drug from the cell.
The emergence and spread of drug-resistant microorganisms pose significant challenges in medical treatment, as they can lead to increased morbidity, mortality, and healthcare costs. The overuse and misuse of antimicrobial agents, as well as poor infection control practices, contribute to the development and dissemination of drug-resistant strains. To address this issue, it is crucial to promote prudent use of antimicrobials, enhance surveillance and monitoring of resistance patterns, invest in research and development of new antimicrobial agents, and strengthen infection prevention and control measures.
Host-parasite interactions refer to the relationship between a parasitic organism (the parasite) and its host, which can be an animal, plant, or human body. The parasite lives on or inside the host and derives nutrients from it, often causing harm in the process. This interaction can range from relatively benign to severe, depending on various factors such as the species of the parasite, the immune response of the host, and the duration of infection.
The host-parasite relationship is often categorized based on the degree of harm caused to the host. Parasites that cause little to no harm are called commensals, while those that cause significant damage or disease are called parasitic pathogens. Some parasites can even manipulate their hosts' behavior and physiology to enhance their own survival and reproduction, leading to complex interactions between the two organisms.
Understanding host-parasite interactions is crucial for developing effective strategies to prevent and treat parasitic infections, as well as for understanding the ecological relationships between different species in natural ecosystems.
Inbred A mice are a strain of laboratory mice that have been produced by many generations of brother-sister matings. This results in a high degree of genetic similarity among individuals within the strain, making them useful for research purposes where a consistent genetic background is desired. The Inbred A strain is maintained through continued brother-sister mating. It's important to note that while these mice are called "Inbred A," the designation does not refer to any specific medical condition or characteristic. Instead, it refers to the breeding practices used to create and maintain this particular strain of laboratory mice.
'Anopheles' is a genus of mosquitoes that are known for their role in transmitting malaria parasites to humans. These mosquitoes have a distinctive resting posture, with their abdomens raised and heads down, and they typically feed on human hosts at night. Only female Anopheles mosquitoes transmit the malaria parasite, as they require blood meals to lay eggs.
There are over 400 species of Anopheles mosquitoes worldwide, but only about 30-40 of these are considered significant vectors of human malaria. The distribution and behavior of these mosquitoes can vary widely depending on the specific species and geographic location.
Preventing and controlling the spread of malaria involves a variety of strategies, including the use of insecticide-treated bed nets, indoor residual spraying, antimalarial drugs, and vaccines. Public health efforts to reduce the burden of malaria have made significant progress in recent decades, but the disease remains a major global health challenge, particularly in sub-Saharan Africa.
Pyrimethamine is an antiparasitic medication that is primarily used to treat and prevent protozoan infections, such as toxoplasmosis and malaria. It works by inhibiting the dihydrofolate reductase enzyme, which is essential for the parasite's survival. By doing so, it interferes with the synthesis of folate, a vital component for the growth and reproduction of the parasite.
Pyrimethamine is often used in combination with other medications, such as sulfonamides or sulfones, to increase its effectiveness and prevent the development of drug-resistant strains. Common side effects of pyrimethamine include nausea, vomiting, loss of appetite, and headache. It is important to note that pyrimethamine should only be used under the supervision of a healthcare professional due to its potential for serious side effects and interactions with other medications.
A protozoan genome refers to the complete set of genetic material or DNA present in a protozoan organism. Protozoa are single-celled eukaryotic microorganisms that lack cell walls and have diverse morphology and nutrition modes. The genome of a protozoan includes all the genes that code for proteins, as well as non-coding DNA sequences that regulate gene expression and other cellular processes.
The size and complexity of protozoan genomes can vary widely depending on the species. Some protozoa have small genomes with only a few thousand genes, while others have larger genomes with tens of thousands of genes or more. The genome sequencing of various protozoan species has provided valuable insights into their evolutionary history, biology, and potential as model organisms for studying eukaryotic cellular processes.
It is worth noting that the study of protozoan genomics is still an active area of research, and new discoveries are continually being made about the genetic diversity and complexity of these fascinating microorganisms.
"CBA" is an abbreviation for a specific strain of inbred mice that were developed at the Cancer Research Institute in London. The "Inbred CBA" mice are genetically identical individuals within the same strain, due to many generations of brother-sister matings. This results in a homozygous population, making them valuable tools for research because they reduce variability and increase reproducibility in experimental outcomes.
The CBA strain is known for its susceptibility to certain diseases, such as autoimmune disorders and cancer, which makes it a popular choice for researchers studying those conditions. Additionally, the CBA strain has been widely used in studies related to transplantation immunology, infectious diseases, and genetic research.
It's important to note that while "Inbred CBA" mice are a well-established and useful tool in biomedical research, they represent only one of many inbred strains available for scientific investigation. Each strain has its own unique characteristics and advantages, depending on the specific research question being asked.
BALB/c is an inbred strain of laboratory mouse that is widely used in biomedical research. The strain was developed at the Institute of Cancer Research in London by Henry Baldwin and his colleagues in the 1920s, and it has since become one of the most commonly used inbred strains in the world.
BALB/c mice are characterized by their black coat color, which is determined by a recessive allele at the tyrosinase locus. They are also known for their docile and friendly temperament, making them easy to handle and work with in the laboratory.
One of the key features of BALB/c mice that makes them useful for research is their susceptibility to certain types of tumors and immune responses. For example, they are highly susceptible to developing mammary tumors, which can be induced by chemical carcinogens or viral infection. They also have a strong Th2-biased immune response, which makes them useful models for studying allergic diseases and asthma.
BALB/c mice are also commonly used in studies of genetics, neuroscience, behavior, and infectious diseases. Because they are an inbred strain, they have a uniform genetic background, which makes it easier to control for genetic factors in experiments. Additionally, because they have been bred in the laboratory for many generations, they are highly standardized and reproducible, making them ideal subjects for scientific research.
"Plasmodium malariae" is a species of protozoan parasite that causes malaria in humans. It's one of the five Plasmodium species known to cause malaria in humans, with the other four being P. falciparum, P. vivax, P. ovale, and P. knowlesi.
P. malariae is transmitted through the bites of infected Anopheles mosquitoes. Once inside the human body, the parasites travel to the liver where they multiply and then infect red blood cells. The infection caused by P. malariae can persist for several years, even a lifetime, if not treated properly.
The symptoms of P. malariae infection include fever, chills, headache, muscle and joint pain, and anemia. However, the severity of these symptoms is generally less than that caused by P. falciparum, which is the most deadly form of malaria.
It's worth noting that while P. malariae can be effectively treated with antimalarial drugs such as chloroquine and primaquine, drug resistance has been reported in some areas, making accurate diagnosis and treatment even more critical for controlling the spread of this disease.
"Plasmodium knowlesi" is a species of protozoan parasite that causes malaria in certain primates, particularly macaques. It can also infect humans, and has been identified as a significant cause of malaria in Southeast Asia. The life cycle of P. knowlesi involves two hosts: anopheline mosquitoes and primates. The parasite is transmitted to the host through the bite of an infected mosquito, and then invades and reproduces within the host's red blood cells, leading to symptoms such as fever, chills, headache, and muscle and joint pain. In severe cases, P. knowlesi infections can lead to complications such as respiratory distress, kidney failure, and coma.
It is important to note that "Plasmodium knowlesi" malaria is different from the more common forms of human malaria caused by Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. P. knowlesi infections can be effectively treated with antimalarial drugs, but early diagnosis and prompt treatment are crucial to prevent severe disease and complications.
Passive immunization is a type of temporary immunity that is transferred to an individual through the injection of antibodies produced outside of the body, rather than through the active production of antibodies in the body in response to vaccination or infection. This can be done through the administration of preformed antibodies, such as immune globulins, which contain a mixture of antibodies that provide immediate protection against specific diseases.
Passive immunization is often used in situations where individuals have been exposed to a disease and do not have time to develop their own active immune response, or in cases where individuals are unable to produce an adequate immune response due to certain medical conditions. It can also be used as a short-term measure to provide protection until an individual can receive a vaccination that will confer long-term immunity.
Passive immunization provides immediate protection against disease, but the protection is typically short-lived, lasting only a few weeks or months. This is because the transferred antibodies are gradually broken down and eliminated by the body over time. In contrast, active immunization confers long-term immunity through the production of memory cells that can mount a rapid and effective immune response upon re-exposure to the same pathogen in the future.
Malaria, Vivax:
A type of malaria caused by the parasite Plasmodium vivax. It is transmitted to humans through the bites of infected Anopheles mosquitoes. Malaria, Vivax is characterized by recurring fevers, chills, and flu-like symptoms, which can occur every other day or every third day. This type of malaria can have mild to severe symptoms and can sometimes lead to complications such as anemia and splenomegaly (enlarged spleen). One distinguishing feature of Malaria, Vivax is its ability to form dormant stages in the liver (called hypnozoites), which can reactivate and cause relapses even after years of apparent cure. Effective treatment includes medication to kill both the blood and liver stages of the parasite. Preventive measures include using mosquito nets, insect repellents, and antimalarial drugs for prophylaxis in areas with high transmission rates.
Interferon-gamma (IFN-γ) is a soluble cytokine that is primarily produced by the activation of natural killer (NK) cells and T lymphocytes, especially CD4+ Th1 cells and CD8+ cytotoxic T cells. It plays a crucial role in the regulation of the immune response against viral and intracellular bacterial infections, as well as tumor cells. IFN-γ has several functions, including activating macrophages to enhance their microbicidal activity, increasing the presentation of major histocompatibility complex (MHC) class I and II molecules on antigen-presenting cells, stimulating the proliferation and differentiation of T cells and NK cells, and inducing the production of other cytokines and chemokines. Additionally, IFN-γ has direct antiproliferative effects on certain types of tumor cells and can enhance the cytotoxic activity of immune cells against infected or malignant cells.
"Plasmodium ovale" is a species of protozoan parasites that are transmitted to humans through the bites of infected female Anopheles mosquitoes. This parasite causes a type of malaria known as "ovale malaria," which is generally milder than other forms of malaria caused by Plasmodium falciparum or Plasmodium vivax.
The life cycle of Plasmodium ovale involves two hosts: the mosquito and humans. When an infected mosquito bites a human, the parasites are injected into the skin along with the mosquito's saliva. The parasites then enter the liver where they multiply and form dormant stages called hypnozoites. After a period of time (usually several weeks to months), the hypnozoites become activated and begin to infect red blood cells, leading to the symptoms of malaria.
The symptoms of ovale malaria are similar to those of other forms of malaria and include fever, chills, headache, muscle and joint pain, and fatigue. However, ovale malaria is less likely to cause severe complications or death than falciparum malaria. Diagnosis of ovale malaria is typically made through microscopic examination of blood smears or by using rapid diagnostic tests (RDTs) that detect parasite antigens in the blood. Treatment usually involves the use of antimalarial drugs such as chloroquine or primaquine.
Chloroquine is an antimalarial and autoimmune disease drug. It works by increasing the pH or making the environment less acidic in the digestive vacuoles of malaria parasites, which inhibits the polymerization of heme and the formation of hemozoin. This results in the accumulation of toxic levels of heme that are harmful to the parasite. Chloroquine is also used as an anti-inflammatory agent in the treatment of rheumatoid arthritis, discoid or systemic lupus erythematosus, and photodermatitis.
The chemical name for chloroquine is 7-chloro-4-(4-diethylamino-1-methylbutylamino)quinoline, and it has a molecular formula of C18H26ClN3. It is available in the form of phosphate or sulfate salts for oral administration as tablets or solution.
Chloroquine was first synthesized in 1934 by Bayer scientists, and it has been widely used since the 1940s as a safe and effective antimalarial drug. However, the emergence of chloroquine-resistant strains of malaria parasites has limited its use in some areas. Chloroquine is also being investigated for its potential therapeutic effects on various viral infections, including COVID-19.
Anemia is a medical condition characterized by a lower than normal number of red blood cells or lower than normal levels of hemoglobin in the blood. Hemoglobin is an important protein in red blood cells that carries oxygen from the lungs to the rest of the body. Anemia can cause fatigue, weakness, shortness of breath, and a pale complexion because the body's tissues are not getting enough oxygen.
Anemia can be caused by various factors, including nutritional deficiencies (such as iron, vitamin B12, or folate deficiency), blood loss, chronic diseases (such as kidney disease or rheumatoid arthritis), inherited genetic disorders (such as sickle cell anemia or thalassemia), and certain medications.
There are different types of anemia, classified based on the underlying cause, size and shape of red blood cells, and the level of hemoglobin in the blood. Treatment for anemia depends on the underlying cause and may include dietary changes, supplements, medication, or blood transfusions.
Innate immunity, also known as non-specific immunity or natural immunity, is the inherent defense mechanism that provides immediate protection against potentially harmful pathogens (like bacteria, viruses, fungi, and parasites) without the need for prior exposure. This type of immunity is present from birth and does not adapt to specific threats over time.
Innate immune responses involve various mechanisms such as:
1. Physical barriers: Skin and mucous membranes prevent pathogens from entering the body.
2. Chemical barriers: Enzymes, stomach acid, and lysozyme in tears, saliva, and sweat help to destroy or inhibit the growth of microorganisms.
3. Cellular responses: Phagocytic cells (neutrophils, monocytes, macrophages) recognize and engulf foreign particles and pathogens, while natural killer (NK) cells target and eliminate virus-infected or cancerous cells.
4. Inflammatory response: When an infection occurs, the innate immune system triggers inflammation to increase blood flow, recruit immune cells, and remove damaged tissue.
5. Complement system: A group of proteins that work together to recognize and destroy pathogens directly or enhance phagocytosis by coating them with complement components (opsonization).
Innate immunity plays a crucial role in initiating the adaptive immune response, which is specific to particular pathogens and provides long-term protection through memory cells. Both innate and adaptive immunity work together to maintain overall immune homeostasis and protect the body from infections and diseases.