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We present a case of disseminated congenital toxoplasmosis in a newborn born to a mother who had been immunized against toxoplasmosis before conception. The mother was reinfected, likely by ingestion of imported raw horse meat during pregnancy. This clinical presentation is exceptional in France and raised the possibility of infection by a highly virulent Toxoplasma strain. The strain responsible was isolated from the peripheral blood of the newborn, and when genotyped with microsatellite markers, it exhibited an atypical genotype, one which is very uncommon in Europe but had been described in South America. We tested the hypothesis of a reinfection with a different genotype by using an experimental mouse model, which confirmed that acquired immunity against European Toxoplasma strains may not protect against reinfection by atypical strains acquired during travel outside Europe or by eating imported meat.

According to the hygiene hypothesis, parasites could have a protective role in the development of Multiple Sclerosis (MS). Our aim was to assess the association between presence of anti- Toxoplasma gondii antibodies and MS. MS patients were randomly selected from a population-based incident cohort of MS patients in the city of Catania. Age and sex-matched controls were randomly selected from the general population. Clinical and sociodemographic variables were recorded with a structured questionnaire and a blood sample was taken for serological analysis. Specific T. gondii IgG have been detected with a commercial kit. Adjusted Odds Ratios (ORs) were estimated using unconditional logistic regression. 129 MS subjects (66.7% women with a mean age 44.7 ± 11.0 years) and 287 controls (67.3% women with a mean age 48.1 ± 15.6 years) have been enrolled in the study. Anti- T. gondii antibodies were found in 38 cases (29.5%) and 130 controls (45.4%) giving an adjusted OR of 0.56 (95%CI 0.34–0.93). History of mononucleosis and high educational level were significantly associated with MS (adjOR 2.22 and 1.70 respectively) while an inverse association was found between high educational level and T. gondii seropositivity (adjOR 0.42). Our results further support the protective role of parasitic infections in MS.

Felidae as definitive hosts for Toxoplasma gondii play a major role in transmission to all warm-blooded animals trough oocysts dissemination. Therefore the current comprehensive study was performed to determine the global status of T. gondii infection in domestic and wild felids aiming to provide comprehensive data of interest for further intervention approaching the One Health perspective. Different databases were searched by utilizing particular key words for publications related to T. gondii infecting domestic and wild feline host species, worldwide, from 1970 to 2020. The review of 337 reports showed that the seroprevalence of T. gondii in domestic cats and wild felids was estimated in 37.5% (95% CI 34.7–40.3) ( I 2  = 98.3%, P  < 0.001) and 64% (95% CI 60–67.9) ( I 2  = 88%, P < 0.0001), respectively. The global pooled prevalence of oocysts in the fecal examined specimens from domestic cats was estimated in 2.6% (95% CI 1.9–3.3) ( I 2  = 96.1%, P  < 0.0001), and that in fecal samples from wild felids was estimated in 2.4% (95% CI 1.1–4.2) ( I 2  = 86.4%, P  < 0.0001). In addition, from 13,252 examined soil samples in 14 reviewed studies, the pooled occurrence of T. gondii oocysts was determined in 16.2% (95% CI 7.66–27.03%). The observed high rates of anti- T. gondii antibodies seroprevalence levels and oocyst excretion frequency in the felids, along with soil (environmental) contamination with oocysts may constitute a potential threat to animal and public health, and data will result of interest in further prophylaxis programs.

Key Points The parasite Toxoplasma gondii is extremely widespread in animals and is a common cause of food- and water-borne infection in people. Although most infections are benign, they can have severe consequences in immunocompromised patients and following congenital infection. T. gondii is regarded as a model intracellular parasite for which forward- and reverse-genetics tools are available. In combination with the mouse model of toxoplasmosis (including the many genetic knockout and transgenic mouse lines that are available), these tools for genetic manipulation of the parasite have enabled researchers to explore the molecular determinants of T. gondii pathogenesis and host defence. Forward-genetics crosses conducted in T. gondii , using strains of different genotypes and virulences in mice, revealed that acute virulence is largely mediated by a family of effector proteins that are secreted into the host cell cytoplasm during parasite invasion. These proteins are derived from a secretory organelle called the rhoptry and, hence, are called ROP effectors. ROPs include a family of serine/threonine kinases that affect host targets and have important roles in infection in the mouse. Among these, ROP18 phosphorylates immunity-related GTPases, thus promoting parasite survival in activated macrophages, whereas ROP16 phosphorylates signal transducer and activator of transcription 3 (STAT3) and STAT6 and, hence, alters host gene transcription. Curiously, the activity of ROP18 is mediated by another family member called ROP5, which is a pseudokinase. Although a limited subset of ROP kinases can largely explain the virulence of T. gondii in the mouse, their role in other hosts has not been established. The genome encodes more than 40 ROPs, and these different proteins might have distinct roles during infection in the wide range of hosts infected by T. gondii . Understanding these patterns might help in the prevention and treatment of human infections. The intracellular parasite Toxoplasma gondii can infect a range of hosts and occasionally causes serious disease in humans. In this Review, Hunter and Sibley summarize recent studies that implicate rhoptry kinases and a dense-granule protein as mediators of acute virulence in the mouse model. They also describe the complex interplay between these parasite effector proteins and the innate immune system. Toxoplasma gondii is a common parasite of animals and humans and can cause serious opportunistic infections. However, the majority of infections are asymptomatic, possibly because the organism has co-evolved with its many vertebrate hosts and has developed multiple strategies to persist asymptomatically for the lifetime of the host. Over the past two decades, infection studies in the mouse, combined with forward-genetics approaches aimed at unravelling the molecular basis of infection, have revealed that T. gondii virulence is mediated, in part, by secretion of effector proteins into the host cell during invasion. Here, we review recent advances that illustrate how these virulence factors disarm innate immunity and promote survival of the parasite.

Acute infection with Toxoplasma gondii during pregnancy and its potentially tragic outcome for the fetus and newborn continue to occur in the United States, as well as worldwide, despite the fact that it can be prevented. The infection can be acquired through ingestion of infected, undercooked meat or contaminated food or water. Transmission to the fetus occurs almost solely in women who acquire their primary infection during gestation and can result in visual and hearing loss, mental and psychomotor retardation, seizures, hematological abnormalities, hepatosplenomegaly, or death. Systematic education and serological screening of pregnant women are the most reliable and currently available strategies for the prevention, diagnosis, and early treatment of the infection in the offspring; this is largely because toxoplasmosis in pregnant women most often goes unrecognized. Treatment of the infection in the fetus and infant during the first year of life has been demonstrated to significantly improve the clinical outcome.

Toxoplasma gondii infection disrupts the gut microbiota and host systemic metabolism, which plays a key role in the pathophysiology of toxoplasmosis. To investigate these interactions, we conducted metagenomic sequencing and untargeted serum metabolomics on 18 Sprague-Dawley rats across control, acute, and chronic stages of infection. De novo assembly of 148 Gb of high-quality reads produced a comprehensive non-redundant microbial gene catalog comprising over 5.7 million genes. Infection led to a marked reduction in microbial diversity and significant shifts in community structure. Chronic infection, in particular, was characterized by the enrichment of Lactobacillus johnsonii , Lactobacillus intestinalis , and Limosilactobacillus reuteri , alongside a marked depletion of Akkermansia muciniphila and Rothia nasimurium . These compositional changes coincided with reduced abundance of carbohydrate-active enzymes, suggesting impaired microbial metabolic capacity. Pathway analysis revealed distinct, stage- and gut-region-specific metabolic disruptions, including suppressed amino acid and energy metabolism, and enhanced glycan and carbohydrate pathways during chronic infection. Untargeted LC-MS/MS profiling uncovered 883 differentially abundant serum metabolites, enriched in pathways related to amino acid metabolism, bile acid transformation, and aromatic compound processing. Importantly, L. johnsonii and L. reuteri were positively correlated with metabolites implicated in immune modulation and oxidative stress response, whereas A. muciniphila showed negative associations. These findings demonstrate that T. gondii infection orchestrates a coordinated host–microbiota–metabolome network, advancing our understanding of disease mechanisms and pointing to novel microbial and metabolic targets for therapy.

Toxoplasma gondii , an obligatory intracellular parasite, is the causative agent of toxoplasmosis, a widespread disease affecting approximately one-third of the global population. This study investigates the strain-specific effects of T. gondii infection on immune responses, reproductive physiology, and oxidative stress in Wistar rats, comparing the highly virulent RH strain to the less virulent VEG strain. The results show that the RH strain significantly reduced levels of the anti-inflammatory cytokine IL-10 ( p  < 0.01) while increasing pro-inflammatory IFN-γ ( p  < 0.05), suggesting a strong inflammatory response. In contrast, the VEG strain produced a more balanced immune profile, with no significant change in IL-10 and a moderate rise in IFN-γ. Although no visible damage to ovarian tissue was observed in any group, the RH strain resulted in a higher number of growing follicles ( p  < 0.05), while the VEG strain led to significantly larger follicles ( p  < 0.05). Both strains elevated CRP levels, with the RH strain inducing a more significant inflammatory response. However, oxidative stress markers showed no significant differences among the experimental groups. In conclusion, the findings indicate that the highly virulent RH strain elicits a strong inflammatory response, whereas the less virulent VEG strain induces a more moderate immune reaction, without causing significant damage to ovarian tissue.

Toxoplasma gondii is a protozoan parasite that is responsible for approximately 24% of all estimated deaths attributed to foodborne pathogens in the United States. Human infection results from accidental ingestion of oocysts from the environment, in water, or on insufficiently washed produce or from consumption of raw or undercooked meat products that contain T. gondii tissue cysts. This review focused on studies of T. gondii in meat because many human T. gondii infections are acquired through consumption of raw or undercooked meat. Prevalence of T. gondii is higher in conventionally reared pigs, sheep, and poultry than in cattle and is greater in meat products from organic than from conventionally reared meat animals because of outdoor access, which poses substantially greater opportunities for exposure to infected rodents, wildlife, and oocyst-contaminated feed, water, or environmental surfaces. Risk factors related to T. gondii exposure for livestock include farm type, feed source, presence of cats, methods of rodent and bird control, methods of carcass handling, and water quality. This review serves as a useful resource and information repository for informing quantitative risk assessment studies for T. gondii infection in humans through meat consumption.

Abstract Toxoplasma gondii is an obligate intracellular protozoan parasite that causes opportunistic disease, particularly in immunocompromised individuals. Central to its transmission and pathogenesis is the ability of the proliferative stage (tachyzoite) to convert into latent tissue cysts (bradyzoites). Encystment allows Toxoplasma to persist in the host and affords the parasite a unique opportunity to spread to new hosts without proceeding through its sexual stage, which is restricted to felids. Bradyzoite tissue cysts can cause reactivated toxoplasmosis if host immunity becomes impaired. A greater understanding of the molecular mechanisms orchestrating bradyzoite development is needed to better manage the disease. Here, we will review key studies that have contributed to our knowledge about this persistent form of the parasite and how to study it, with a focus on how cellular stress can signal for the reprogramming of gene expression needed during bradyzoite development. This review describes the molecular mechanisms orchestrating the development of latent tissue cysts of the protozoan parasite Toxoplasma gondii, a process that is critical to pathogenesis and transmission.

Toxoplasma gondii is a highly ubiquitous and prevalent parasite. Despite the cat being the only definitive host, it is found in almost all geographical areas and warm blooded animals. Three routes of transmission are recognised: ingestion of oocysts shed by the cat, carnivory and congenital transmission. In natural populations, it is difficult to establish the relative importance of these routes. This paper reviews recent work in our laboratory which suggests that congenital transmission may be much more important than previously thought. Using PCR detection of the parasite, studies in sheep show that congenital transmission may occur in as many as 66% of pregnancies. Furthermore, in families of sheep on the same farm, exposed to the same sources of oocysts, significant divergent prevalences of Toxoplasma infection and abortion are found between different families. The data suggest that breeding from infected ewes increases the risk of subsequent abortion and infection in lambs. Congenital transmission rates in a natural population of mice were found to be 75%. Interestingly, congenital transmission rates in humans were measured at 19·8%. The results presented in these studies differ from those of other published studies and suggest that vertical transmission may be much more important than previously thought.