: A Drive to Survive.

is an obligate intracellular protozoan parasite that causes zoonotic disease. Central to its pathogenesis is the ability of the parasite to invade host red blood cells of diverse species, and, once in the host blood stream, to manipulate the composition of its population to allow it to endure unfavorable conditions. Here we will review key in vitro studies relating to the survival strategies that adopts during its intraerythrocytic development to persist and how proliferation is restored in the parasite population once optimum conditions return.

Altered parasite life-cycle processes characterize infection in human sickle cell anemia.

is an intra-erythrocytic parasite that causes malaria-like symptoms in infected people. As the erythrocyte provides the parasite with the infra-structure to grow and multiply, any perturbation to the cell should impact parasite viability. Support for this comes from the multitude of studies that have shown that the sickle trait has in fact been selected because of the protection it provides against a related Apicomplexan parasite, , that causes malaria.

Robust adaptive immune response against infection marked by low parasitemia in a murine model of sickle cell disease.

The intraerythrocytic parasite is the number 1 cause of transfusion-transmitted infection and can induce serious, often life-threatening complications in immunocompromised individuals including transfusion-dependent patients with sickle cell disease (SCD). Despite the existence of strong long-lasting immunological protection against a second infection in mouse models, little is known about the cell types or the kinetics of protective adaptive immunity mounted following infection, especially in infection-prone SCD that are thought to have an impaired immune system. Here, we show, using a mouse infection model, that infected wild-type (WT) mice mount a very strong adaptive immune response, characterized by (1) coordinated induction of a robust germinal center (GC) reaction; (2) development of follicular helper T (T) cells that comprise ∼30% of splenic CD4 T cells at peak expansion by 10 days postinfection; and (3) high levels of effector T-cell cytokines, including interleukin 21 and interferon γ, with an increase in the secretion of antigen (Ag)-specific antibodies (Abs).

A novel flow cytometric application discriminates among the effects of chemical inhibitors on various phases of Babesia divergens intraerythrocytic cycle.

Human babesiosis is a global emerging infectious disease caused by intraerythrocytic parasites of the genus Babesia. Its biology has remained largely unexplored due to a lack of critical tools and techniques required to define the various stages and phases of the parasite's cycle in its host RBC and the interplay between host and parasite. This article presents a powerful set of tools combining stage synchronization of the parasite with a platform that encompasses both a flow cytometric evaluation of the subpopulation structure of the parasite population together with a morphological assessment of the population parasites using light microscopy of conventional Giemsa stained smears.

Identification and Characterization of the Rhoptry Neck Protein 2 in Babesia divergens and B. microti.

Apicomplexan parasites include those of the genera Plasmodium, Cryptosporidium, and Toxoplasma and those of the relatively understudied zoonotic genus Babesia In humans, babesiosis, particularly transfusion-transmitted babesiosis, has been emerging as a major threat to public health. Like malaria, the disease pathology is a consequence of the parasitemia which develops through cyclical replication of Babesia parasites in host erythrocytes. However, there are no exoerythrocytic stages in Babesia, so targeting of the blood stage and associated proteins to directly prevent parasite invasion is the most desirable option for effective disease control.

Babesia divergens builds a complex population structure composed of specific ratios of infected cells to ensure a prompt response to changing environmental conditions.

Babesia parasites cause a malaria-like febrile illness by infection of red blood cells (RBCs). Despite the growing importance of this tick-borne infection, its basic biology has been neglected. Using novel synchronization tools, the sequence of intra-erythrocytic events was followed from invasion through development and differentiation to egress.

Identification and characterization of the RouenBd1987 Babesia divergens Rhopty-Associated Protein 1.

Human babesiosis is caused by one of several babesial species transmitted by ixodid ticks that have distinct geographical distributions based on the presence of competent animal hosts. The pathology of babesiosis, like malaria, is a consequence of the parasitaemia which develops through the cyclical replication of Babesia parasites in a patient's red blood cells, though symptoms typically are nonspecific. We have identified the gene encoding Rhoptry-Associated Protein -1 (RAP-1) from a human isolate of B.

Identification of binding domains on red blood cell glycophorins for Babesia divergens.

Background: Invasion of red blood cells (RBCs) is one of the critical points in the lifecycle of Babesia. The parasite does not invade other host cells. Earlier work has shown that GPA and GPB function as putative receptors during parasite invasion.

Babesia: impact of cold storage on the survival and the viability of parasites in blood bags.

Background: Babesia represents one of the major infectious threats to the blood supply since clinically silent infections in humans are common and these can be life-threatening in certain recipients. It is important to understand the effect of blood storage conditions on the viability of Babesia as this will impact the occurrence and severity of transfusion-transmitted babesiosis.

Study Design And Methods: Babesia divergens was introduced into blood bags containing leukoreduced red blood cells (RBCs) and stored at 4°C for 0 to 31 days.

The Microsporum canis genome is organized into five chromosomes based on evidence from electrophoretic karyotyping and chromosome end mapping.

The karyotype of Microsporum canis was analyzed by contoured-clamped homogeneous electric field (CHEF) gel electrophoresis. Four chromosomal bands that correspond to five chromosomes ranging from 3.0-6.

Babesia and red cell invasion.

Purpose Of Review: Babesiosis is a zoonosis, a disease communicable from animals to humans and an important blood-borne human parasitic infection. Despite its public health impact, its study has largely been neglected. The objective of this review is to present up-to-date information on both parasite and red blood cell molecules that function at the host-parasite interface to facilitate successful invasion.

Transcriptional profiling reveals the expression of novel genes in response to various stimuli in the human dermatophyte Trichophyton rubrum.

Background: Cutaneous mycoses are common human infections among healthy and immunocompromised hosts, and the anthropophilic fungus Trichophyton rubrum is the most prevalent microorganism isolated from such clinical cases worldwide. The aim of this study was to determine the transcriptional profile of T. rubrum exposed to various stimuli in order to obtain insights into the responses of this pathogen to different environmental challenges.

A single amino acid substitution in one of the lipases of Aspergillus nidulans confers resistance to the antimycotic drug undecanoic acid.

A plausible approach to evaluate the inhibitory action of antifungals is through the investigation of the fungal resistance to these drugs. We describe here the molecular cloning and initial characterization of the A. nidulans lipA gene, where mutation (lipA1) conferred resistance to undecanoic acid, the most fungitoxic fatty acid in the C(7:0)-C(18:0) series.

Evolution of hepatitis C virus infection under host factor influence in an ethnically complex population.

Background: The ethnic influence makes it difficult to reach a consensual definition of host-dependent genetic factors controlling the hepatitis C virus (HCV) disease course.

Aims: To investigate, in an ethnically complex Brazilian population, whether human leucocyte antigen (HLA) molecules are associated with susceptibility to HCV infection, self-limiting viral clearance and predisposition to chronic disease.

Methods: One hundred and four HCV-antibody-positive patients (stratified into groups with spontaneous viral clearance and chronic HCV infection) and 166 healthy controls were submitted to HLA genotyping.

Analysis of Trichophyton rubrum gene expression in response to cytotoxic drugs.

Suppressive subtractive hybridization was used to isolate transcripts specifically upregulated during Trichophyton rubrum exposure to acriflavin, fluconazole, griseofulvin, terbinafine or undecanoic acid. Macro-array dot-blot and sequencing of 132 clones, which correspond to genes differentially expressed after exposition of T. rubrum to at least one of these cytotoxic drugs, revealed 39 unique genes.