Tick-borne piroplasms and trypanosomes incidentally detected in eastern grey kangaroos () during a mortality and morbidity event in southern New South Wales, Australia.

Tick-borne haemoparasites, including piroplasms and trypanosomes, are almost ubiquitous in Australian wildlife, with some associated with health impacts to individual animals and declining wildlife populations. An array of ecologically distinct piroplasm and trypanosome species occur throughout Australia although many of these species and their sylvatic ecologies are poorly characterised. Between May 2022 and October 2023, an anecdotally reported localised eastern grey kangaroo () morbidity/mortality event occurred in coastal southern New South Wales, Australia, characterised by animals presenting with blindness, emaciation, lethargy, ataxia, and astasia.

Lipid droplet dynamics are essential for the development of the malaria parasite Plasmodium falciparum.

Lipid droplets (LDs) are organelles that are central to lipid and energy homeostasis across all eukaryotes. In the malaria-causing parasite Plasmodium falciparum the roles of LDs in lipid acquisition from its host cells and their metabolism are poorly understood, despite the high demand for lipids in parasite membrane synthesis. We systematically characterised LD size, composition and dynamics across the disease-causing blood infection.

Harnessing cholesterol uptake of malaria parasites for therapeutic applications.

Parasites, such as the malaria parasite P. falciparum, are critically dependent on host nutrients. Interference with nutrient uptake can lead to parasite death and, therefore, serve as a successful treatment strategy.

Curiosities take the stage - role-play in parasitology teaching.

Careful observation of parasites, masters of camouflage, reveals an ingenious and fascinating world. However, students often perceive parasitology as impenetrable. What if a flamboyant flea circus director passionately introduced the multidimensional contexts of this discipline? Will role-play capture the imagination of students and guide them in their future learning?

Analysis of Mitochondrial Electron Transport Chain Activity Using Seahorse XFe96 Extracellular Flux Assays.

The mitochondrial electron transport chain (ETC) is a multi-component pathway that mediates the transfer of electrons from metabolic reactions that occur in the mitochondrion to molecular oxygen (O). The ETC contributes to numerous cellular processes, including the generation of cellular ATP through oxidative phosphorylation, serving as an electron sink for metabolic pathways such as de novo pyrimidine biosynthesis and for maintaining mitochondrial membrane potential. Proper functioning of the mitochondrial ETC is necessary for the growth and survival of apicomplexan parasites including , a causative agent of malaria.

Plasmodium falciparum gametocytes display global chromatin remodelling during sexual differentiation.

Background: The protozoan malaria parasite Plasmodium falciparum has a complex life cycle during which it needs to differentiate into multiple morphologically distinct life forms. A key process for transmission of the disease is the development of male and female gametocytes in the human blood, yet the mechanisms determining sexual dimorphism in these haploid, genetically identical sexual precursor cells remain largely unknown. To understand the epigenetic program underlying the differentiation of male and female gametocytes, we separated the two sexual forms by flow cytometry and performed RNAseq as well as comprehensive ChIPseq profiling of several histone variants and modifications.

7--Substituted-3-oxadiazole Quinolones with Potent Antimalarial Activity Target the Cytochrome Complex.

The development of new antimalarials is required because of the threat of resistance to current antimalarial therapies. To discover new antimalarial chemotypes, we screened the Janssen Jumpstarter library against the asexual parasite and identified the 7--substituted-3-oxadiazole quinolone hit class. We established the structure-activity relationship and optimized the antimalarial potency.

The enemy within: lipid asymmetry in intracellular parasite-host interactions.

Eukaryotic pathogens with an intracellular parasitic lifestyle are shielded from extracellular threats during replication and growth. In addition to many nutrients, parasites scavenge host cell lipids to establish complex membrane structures inside their host cells. To counteract the disturbance of the host cell plasma membrane they have evolved strategies to regulate phospholipid asymmetry.

The role of cholesterol in invasion and growth of malaria parasites.

Malaria parasites are unicellular eukaryotic pathogens that develop through a complex lifecycle involving two hosts, an anopheline mosquito and a vertebrate host. Throughout this lifecycle, the parasite encounters widely differing conditions and survives in distinct ways, from an intracellular lifestyle in the vertebrate host to exclusively extracellular stages in the mosquito. Although the parasite relies on cholesterol for its growth, the parasite has an ambiguous relationship with cholesterol: cholesterol is required for invasion of host cells by the parasite, including hepatocytes and erythrocytes, and for the development of the parasites in those cells.

Pas-de-deux: African Plasmodium falciparum adaptations to sickle hemoglobin.

The molecular arms race between humans and Plasmodium falciparum in Africa resulted in selection of sickle-cell disease, which, on balance, protects heterozygote carriers against severe malaria. Band et al. discovered that parasites counter-adapt and can overcome disease resistance by identifying parasite genome signatures, termed P.

Analysis of sex-specific lipid metabolism of Plasmodium falciparum points to the importance of sphingomyelin for gametocytogenesis.

Male and female Plasmodium falciparum gametocytes are the parasite lifecycle stage responsible for transmission of malaria from the human host to the mosquito vector. Not only are gametocytes able to survive in radically different host environments, but they are also precursors for male and female gametes that reproduce sexually soon after ingestion by the mosquito. Here, we investigate the sex-specific lipid metabolism of gametocytes within their host red blood cell.

Role of the J Domain Protein Family in the Survival and Pathogenesis of Plasmodium falciparum.

Plasmodium falciparum has dedicated an unusually large proportion of its genome to molecular chaperones (2% of all genes), with the heat shock protein 40 (Hsp40) family (now called J domain proteins, JDPs) exhibiting evolutionary radiation into 49 members. A large number of the P. falciparum JDPs (PfJDPs) are predicted to be exported, with certain members shown experimentally to be present in the erythrocyte cytosol (PFA0660w and PFE0055c) or erythrocyte membrane (ring-infected erythrocyte surface antigen, RESA).

Sex-specific Separation of Gametocyte Populations.

is a unicellular eukaryotic parasite that causes malaria in humans. The parasite is spread by mosquitoes after ingestion of sexual stage parasites known as gametocytes. Malaria transmission depends on parasites switching from the disease-causing asexual blood forms to male and female gametocytes.

Of membranes and malaria: phospholipid asymmetry in Plasmodium falciparum-infected red blood cells.

Malaria is a vector-borne parasitic disease with a vast impact on human history, and according to the World Health Organisation, Plasmodium parasites still infect over 200 million people per year. Plasmodium falciparum, the deadliest parasite species, has a remarkable ability to undermine the host immune system and cause life-threatening disease during blood infection. The parasite's host cells, red blood cells (RBCs), generally maintain an asymmetric distribution of phospholipids in the two leaflets of the plasma membrane bilayer.

Breakdown in membrane asymmetry regulation leads to monocyte recognition of P. falciparum-infected red blood cells.

The human malaria parasite Plasmodium falciparum relies on lipids to survive; this makes its lipid metabolism an attractive drug target. The lipid phosphatidylserine (PS) is usually confined to the inner leaflet of the red blood cell membrane (RBC) bilayer; however, some studies suggest that infection with the intracellular parasite results in the presence of this lipid in the RBC membrane outer leaflet, where it could act as a recognition signal to phagocytes. Here, we used fluorescent lipid analogues and probes to investigate the enzymatic reactions responsible for maintaining asymmetry between membrane leaflets, and found that in parasitised RBCs the maintenance of membrane asymmetry was partly disrupted, and PS was increased in the outer leaflet.

An apicoplast-resident folate transporter is essential for sporogony of malaria parasites.

Malaria parasites are fast replicating unicellular organisms and require substantial amounts of folate for DNA synthesis. Despite the central role of this critical co-factor for parasite survival, only little is known about intraparasitic folate trafficking in Plasmodium. Here, we report on the expression, subcellular localisation and function of the parasite's folate transporter 2 (FT2) during life cycle progression in the murine malaria parasite Plasmodium berghei.

Novel Method for the Separation of Male and Female Gametocytes of the Malaria Parasite That Enables Biological and Drug Discovery.

We developed a flow-cytometry-based method to separate and collect cocultured male and female gametocytes responsible for malaria transmission. The purity of the collected cells was estimated at >97% using flow cytometry, and sorted cells were observed by Giemsa-stained thin-smear and live-cell fluorescence microscopy. The expression of validated sex-specific markers corroborated the sorting strategy.

Distinct adaptations of a gametocyte ABC transporter to murine and human Plasmodium parasites and its incompatibility in cross-species complementation.

Parasites of the genus Plasmodium infect a wide range of mammalian hosts including humans, primates, bats and arboreal rodents. A hallmark of Plasmodium spp. is the very narrow host range, indicative of matching parasite-host coevolution.

-infected erythrocytes induce secretion of IGFBP7 to form type II rosettes and escape phagocytosis.

In malaria, rosetting is described as a phenomenon where an infected erythrocyte (IRBC) is attached to uninfected erythrocytes (URBC). In some studies, rosetting has been associated with malaria pathogenesis. Here, we have identified a new type of rosetting.

Plasmodium falciparum.

Plasmodium falciparum is the etiological agent of malaria tropica, the leading cause of death due to a vector-borne infectious disease, claiming 0.5 million lives every year. The single-cell eukaryote undergoes a complex life cycle and is an obligate intracellular parasite of hepatocytes (clinically silent) and erythrocytes (disease causing).