Toxoplasma gondii is an obligate intracellular protozoan that infects humans and other mammals. The C57BL/6J mouse strain is regarded as an ideal model organism for studying T. gondii due to its susceptibility to T. gondii infection and its other advantages over other laboratory animals. However, systematic studies on the response dynamics of the susceptible C57BL/6J mice after oral infection with T. gondii cysts are lacking. To address this research gap, we investigated the spatiotemporal dynamics of infection, colonization, and antibody fluctuations in susceptible C57BL/6J mice orally infected with Type II T. gondii ME49 strain cysts. Mice were orally challenged with T. gondii cysts to examine the infection dynamics. Daily monitoring was conducted for 60 days post-infection (dpi) to assess animals’ clinical signs and survival rates. The parasite burden in various organs was quantified using qPCR targeting the T. gondii B1 gene. The serum antibody responses were evaluated using ELISA. The cyst burden in the mouse brain was assessed via histology and immunofluorescence. T. gondii infection induced clinical symptoms in the mice, including fever and weight loss. T. gondii rapidly invaded the mice’s small intestine, spleen, lungs, liver, and heart via the bloodstream within 1–5 dpi. T. gondii had breached the blood–brain barrier and colonized the brain by 7 dpi. The levels of Toxoplasma-specific IgG antibodies increased and stabilized for two months (until the experiment ended). Systemic parasite dissemination occurred rapidly, infiltrating most tissues and organs, leading to pronounced enteritis and multi-organ damage due to inflammation. The tachyzoites differentiated into bradyzoites when T. gondii infection progressed from the acute to the chronic phase in mice, forming tissue cysts in organs, including the muscles and brain. As a result, the predilection site of T. gondii in mice is the brain, which is where the cysts persisted for the host’s lifetime and continuously induced meningitis. These findings provide valuable insights into the spatiotemporal diffusion, colonization, predilection sites, temporal antibody dynamics, pathogen detection methodologies, and histopathological changes in C57BL/6J mice following oral infection with T. gondii cysts. These insights are important for elucidating T. gondii’s pathogenesis and host–T. gondii interaction.

Avian haemosporidia infect both domestic and wild birds, causing anemia, acute tissue degeneration, and depopulation in wild birds. Poultry and wild birds have been reported as common reservoirs of haemosporidia, but limited information is available for red junglefowl (Gallus gallus) in China. The present study investigated the prevalence and molecular characterization of haemosporidia in red junglefowl. Blood samples were collected from 234 red junglefowl from Jinghong City of Yunnan Province, and genomic DNA was extracted from these samples. The prevalence of haemosporidia was determined by nested PCR targeting the mitochondrial cytochrome b (cytb) gene. Molecular characterization was investigated based on phylogenetic analysis of cytb sequences, and associated risk factors were analyzed using the Chi-square (χ²) test. The overall prevalence of haemosporidia was 74.8% (175/234), and three species were identified, namely Haemoproteus enucleator, Leucocytozoon californicus, and Plasmodium juxtanucleare. The prevalence of haemosporidia in adult fowl (81.1%, 107/132) was significantly higher (χ² = 6.32, df = 1, P = 0.012) than that in juveniles (66.7%, 68/102). Three novel haemosporidian lineages were revealed. This study examined the prevalence and identified species of avian haemosporidians in red junglefowl, providing new information on the molecular epidemiology and geographical distribution of haemosporidian parasites. Our results indicated high prevalence and diverse species distribution of these haemosporidians in red junglefowl. To the best of our knowledge, this is the first record of haemosporidian infection in red junglefowl in China.

The accumulation of mitochondrial DNA (mtDNA) mutations is a primary driver of mitochondrial dysfunction, which is intrinsically linked to aging and various pathologies. POLG, the catalytic subunit of DNA polymerase gamma, is essential for mtDNA replication; notably, a deficiency in its proofreading function precipitates the accumulation of mtDNA mutations. In this study, by combining prime editing with somatic cell nuclear transfer technology, we successfully generated a mitochondrial mutator pig model expressing proofreading-deficient POLG. These pigs exhibited elevated somatic mtDNA mutation loads and recapitulated key premature aging phenotypes, including weight loss, rough hair coat, anemia, structural alterations in the skin and testicular interstitium, increased apoptosis, and the up-regulation of senescence-associated markers, culminating in shortened life span. Given the physiological and metabolic similarities between pigs and humans, this mitochondrial mutator pig model represents an ideal preclinical tool for dissecting the mechanistic role of mtDNA mutations in aging and age-related pathologies and for accelerating the translation of therapeutic strategies.

Toxoplasma gondii is a significant foodborne parasite. However, the precise thermal conditions required to inactivate its tissue cysts in meat remain poorly defined. This study systematically determined the effects of temperature (45–70 °C) and time (10–30 min) on cyst viability. Cysts treated under each condition were orally administered to susceptible C57BL/6J mice, and infectivity was comprehensively assessed through survival, clinical signs, serology (IgG), qPCR, and histopathology. Results demonstrated that treatment at 60 °C for 10 min or under more stringent conditions completely abolished infectivity, as evidenced by 100% survival, the absence of specific antibodies, and the non-detection of parasite DNA or lesions in tissues. Thus, 60 °C for 10 min is established as a critical inactivation threshold, providing a definitive reference for developing science-based thermal processing guidelines to enhance meat safety.