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PubMed1976

The microsporidian spore invasion tube. The ultrastructure, isolation, and characterization of the protein comprising the tube.

The extrusion apparatus of the microsporidian parasitic protozoan Nosema michaelis discharges an invasion (or polar) tube with a velocity suitalbe for piercing cells and injecting infective sporoplasm. The tube is composed of a polar tube protein (PTP) which consists of a single, low molecular weight polypeptide slightly smaller than chymotrypsinogen-A. Assembled PTP tubes resist dissociation in sodium dodecyl sulfate and brief exposures in media at extreme ends of the pH range; however, the tubes are reduced by mercaptoethanol and dithiothreitol. When acidified, mercaptoethanol-reduced PTP self-assembles into plastic, two-dimensional monolayers. Dithiothreitol-reduced PTP will not reassemble when acidified. Evidence is presented which indicates that PTP is assembled as a tube within the spore; that the ejected tube has plasticity during sporoplasm passage; and, finally, that the subunits within the tube polymer are bound together, in part, by interprotein disulfide linkages.

Amino Acids↗
PubMed1990

CD4+ cytolytic T cell clone confers protection against murine malaria.

A CD4+ T cell clone (A1.6) was derived from spleen cells of mice immunized with irradiated sporozoites. This T cell clone recognizes an antigen that is shared by sporozoites and blood forms of Plasmodium berghei and differs from the circumsporozoite protein. Clone A1.6 displays cytotoxic activity, produces IFN-gamma and IL-2 in vitro, and recognizes the plasmodial antigen in the context of the class II I-Ed molecule. Passive transfer of this CD4+ clone into naive mice resulted in a high degree of protection against sporozoite challenge.

Animals↗
PubMed1994

Structural and functional properties of region II-plus of the malaria circumsporozoite protein.

During feeding, infected mosquitos inject malaria sporozoites into the host circulation. Within minutes, the parasites are found in the liver where they initiate the first stage of malaria infection. All species of malaria sporozoites are uniformly covered by the circumsporozoite protein (CS), which contains a conserved COOH-terminal sequence called region II-plus. We have previously shown that region II-plus is the parasite's hepatocyte-binding ligand and that this ligand binds to heparan sulfate proteoglycans (HSPGs) on the hepatocyte membrane. Using a series of substituted region II-plus peptides, we show here that the downstream basic amino acids as well as the interdispersed hydrophobic residues are required for binding of CS to hepatocyte HSPGs. We also show that this positively charged stretch of amino acids must be aggregated in order to bind to the receptor. On the basis of this information, we have synthesized a multiple antigen peptide that mimics the hepatocyte-binding ligand. This construct inhibits both CS binding to HepG2 cells in vitro as well as CS clearance in mice.

Amino Acid Sequence↗
PubMed2002

The shikimate pathway and its branches in apicomplexan parasites.

The shikimate pathway is essential for production of a plethora of aromatic compounds in plants, bacteria, and fungi. Seven enzymes of the shikimate pathway catalyze sequential conversion of erythrose 4-phosphate and phosphoenol pyruvate to chorismate. Chorismate is then used as a substrate for other pathways that culminate in production of folates, ubiquinone, napthoquinones, and the aromatic amino acids tryptophan, phenylalanine, and tyrosine. The shikimate pathway is absent from animals and present in the apicomplexan parasites Toxoplasma gondii, Plasmodium falciparum, and Cryptosporidium parvum. Inhibition of the pathway by glyphosate is effective in controlling growth of these parasites. These findings emphasize the potential benefits of developing additional effective inhibitors of the shikimate pathway. Such inhibitors may function as broad-spectrum antimicrobial agents that are effective against bacterial and fungal pathogens and apicomplexan parasites.

Amino Acid Sequence↗
PubMed2006

Interactions between the parasite's previous and current environment mediate the outcome of parasite infection.

The study of parasite virulence has generally focused on the conditions under which virulence is expected to increase or decrease over time and how the interactions between hosts and their environments may mediate the outcome of infection. Recently, parasite traits such as transmission, offspring production, and development have also been shown to be influenced by environmental variation. What is unclear is how variation in the parasite's environment may impact virulence. Recent theory demonstrates that plasticity can promote the evolution of decreased virulence; thus, understanding whether the parasite's environment can mediate virulence can improve predictions regarding the outcome of parasite infection. Here, an obligate mosquito parasite was reared in hosts fed high or low levels of food. Parasite oocysts (offspring) produced in these two host environments were subsequently fed to uninfected hosts. Parasites originating from well-fed hosts were found to be more virulent to these subsequent hosts compared to parasites originating from poorly fed hosts. Additionally, this effect was apparent only when current hosts were food deprived. These results demonstrate that parasite virulence was mediated by a cross-generational effect of the environment and that the overall outcome of infection was modified by variation in both the parasite's and host's environments.

Aedes↗
PubMed2003

Genomics and its impact on parasitology and the potential for development of new parasite control methods.

Parasitic organisms remain the scourge of the developed and underdeveloped worlds. Malaria, schistosomiasis, leishmaniasis, and trypanosomiasis, for example, still result in a large number of human deaths each year worldwide, while drug resistance among nematodes still poses a major problem to the livestock industries. Genome projects involving parasitic organisms are now abundant, and technologies for the investigations of the parasite transcriptome and proteome are well established. There is no doubt the era of the "omics" is with parasitology, and current trends in the discipline are addressing fundamental biological questions that can make best use of the new technologies, as well as the vast amount of new data being generated. Will this become the "golden age of molecular parasitology," leading to the control of parasitic diseases that have plagued mankind for hundreds of years? The primary aim of this paper is to review advances in the general area of parasite genomics, and to outline where the application of "omics" technologies can and have impacted on the development of new control methods for parasitic organisms.

Animals↗
PubMed2003

Parasites and immune responses: memory illusion?

Immunological memory responses to intracellular protozoa and extracellular helminths govern host resistance and susceptibility to reinfection. Humans and livestock living in parasitic disease endemic regions face continuous exposure from a very early age that often leads to asymptomatic chronic infection over their entire lifespan. Fundamental immunological studies suggest that the generation of T-cell memory is driven by tightly coordinated innate and adaptive cellular immune responses rapidly triggered following initial host infection. A key distinguishing feature of immune memory maintenance between the majority of parasitic diseases and most bacterial or viral diseases is long-term antigen persistence. Consequently, functional parasite immune memory is in a continuous, dynamic flux between activation and deactivation producing functional parasite killing or functional memory cell death. In this sense, T-cell immune memory can be regarded as "memory illusion." Furthermore, due to the finite capacity of memory lymphocytes to proliferate, continuous parasite antigen stimulation may exceed a threshold level at some point in the chronically infected host. This may result in suboptimal effector immune memory leading to host susceptibility to reinfection, or immune dysregulation yielding disease reactivation or immune pathology. The goal of this review is to highlight, through numerous examples, what is currently known about T-cell immune memory to parasites and to provide compelling hypotheses on the survival and maintenance of parasite "memory illusion." These novel concepts are discussed in the context of rationale parasite vaccine design strategies.

Animals↗
PubMed1979

Cryptosporidiosis in an immunosuppressed renal-transplant recipient with IgA deficiency.

Cryptosporidia are sporozoan parasites that infect epithelial cells of the gastrointestinal tract. Infection with cryptosporidia has been found most commonly in a variety of animal species and only rarely in man. The authors report a case of an immunosuppressed renal-transplant recipient with IgA deficiency who experienced diarrhea and fever and was found to have cryptosporidia in a jejunal biopsy specimen and in air-dried smears of the specimen. By electron microscopy, trophozoite, schizont, and macrogamete forms were identified, and these forms ahd morphologic features similar to those of cryptosporidia previously found in guinea pigs. Treatment of the cryptosporidial infection in this case was with trisulfapyrimidines. The efficacy of this treatment could not be evaluated because of complications.

Apicomplexa↗
PubMed1984

Acquired immune deficiency syndrome: postmortem findings.

The autopsies of 13 male homosexuals with acquired immune deficiency syndrome (AIDS) were reviewed. All patients had laboratory evidence of cellular immune dysfunction. The most common diagnoses made were disseminated cytomegalovirus infection in 12 patients and Kaposi's sarcoma in 10. All patients infected with cytomegalovirus had pulmonary compromise. The adrenal glands and gastrointestinal tract also were involved often by cytomegalovirus. Cytomegalovirus infection of organs uncommonly affected such as heart, meninges, cerebrum, and peripheral nerves was documented in two patients. Skin most frequently was involved by Kaposi's sarcoma, followed by gastrointestinal tract and lymph nodes. Two patients had visceral and/or nodal Kaposi's sarcoma with no skin compromise. Other important diagnoses were Pneumocystis carinii pneumonia, cryptosporidiosis, fungal infections, toxoplasmosis, and brain lymphoma. The cause of death was due to one or more infections in most patients. Kaposi's sarcoma did not contribute substantially to the cause of death, except in one patient with massive multifocal and multiorgan involvement.

Acquired Immunodeficiency Syndrome↗
PubMed1975

Specific immunity and nonspecific resistance to infection: listeria, protozoa, and viruses in mice and hamsters,.

Specific immunity developed by mice against protozoan (Toxoplasma gondii and Besnoitia jellisoni) and bacterial (Listeria monocytogenes) infections was compared with nonspecific protection conferred by prior infections. The results indicated that homologous immunity protected mice from more than 10-5 LD50 of T. gondii or B. jellisoni, but from only 10-2 LD50 of L. monocytogenes. Heterospecific protection among these organisms was for 10-0.4 minus 10-1.2 LD50. In studies in hamsters specific immunity to protozoan (T. gondii and B. jellisoni) and viral (equine Herpesvirus type 1 and Oriboca virus) infections was compared with nonspecific protection conferred by prior infections with several heterospecific agents: T. gondii; B. jellison; equine Herpesvirus type 1; Oriboca, Ossa, vesicular stomatitis, yellow fever, and Newcastle disease viruses; L. monocytogenes; and the bacillus Calmette-Guerin strain of Mycobacterium tuberculosis. The results indicated that homologous immunity in hamsters was effective against 10-6 minus 10-7 LD50 of T. gondii, B. jellisoni, equine Herpesvirus type 1, or Oriboca virus. Prior infection with Newcastle disease virus protected (probably by interferon induction) against 10-3 LD50 of equine Herpesvirus type 1. Heterospecific protection among other agents was for less than 10 LD50. This insignificant heterospecific protection in infections in which cellular immunity plays a role suggests that both the induction phase and the expression phase are specific.

Animals↗
PubMed1975

Resistance to infection with Nocardia asteroides.

Mechanisms of host resistance to Nocardia asteroides were studied in mice. Two to six weeks after intraperitoneal or intravenous immunization with viable N. asteroides, mice were significantly resistant to intraperitoneal challenge with LD50-100 of N. asteroides in gastric mucin when compared with control (unimmunized) mice (P smaller than 0.03). Resistance could not be transferred to normal mice with serum (1.5 ml administered intraperitoneally) or spleen cells (10-8 cells administered intravenously) from immune donor mice. Peritoneal macrophages from mice immunized with N. asteroides were activated by an in vitro L-cell inhibition assay, and these mice were resistant to challenge with Listeria monocytogenes. Mice with infections caused by Toxoplasma gondii or L. monocytogenes--infections producing activated macrophages--were resistant to challenge with N. asteroides.

Animals↗
PubMed1976

Role of activated macrophages in resistance of mice to infection with Trypanosoma cruzi.

The role of the activated macrophage in resistance of mice to infection with Trypanosoma cruzi was investigated with use of mice that had not been infected with T. cruzi but whose macrophages were activated by Toxoplasma gondii or Besnoitia jellisoni. Mice with activated macrophages were significantly more resistant to intra-peritoneal challenge with the Tulahuen strain of T. cruzi than were controls. The role of serum factors in resistance to T. cruzi was excluded by the demonstration of no difference between survival of T. cruzi in serum from mice with activated macrophages and in that from controls. As the only modality of resistance to T. cruzi in this in vivo model appeared to be the activated macrophage, this cell was investigated in vitro. Activated macrophages were shown to be able to inhibit completely multiplication of T. cruzi, whereas significant multiplication of the parasite occurred in control macrophages. Both in vivo and in vitro data suggest that the activated macrophage may play a major role in resistance to infection with T. cruzi.

Animals↗