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One Health is a collaborative, interdisciplinary effort that seeks optimal health for people, animals, plants, and the environment. Toxoplasmosis, caused by Toxoplasma gondii, is an intracellular protozoan infection distributed worldwide, with a heteroxenous life cycle that practically affects all homeotherms and in which felines act as definitive reservoirs. Herein, we review the natural history of T. gondii, its transmission and impacts in humans, domestic animals, wildlife both terrestrial and aquatic, and ecosystems. The epidemiology, prevention, and control strategies are reviewed, with the objective of facilitating awareness of this disease and promoting transdisciplinary collaborations, integrative research, and capacity building among universities, government agencies, NGOs, policy makers, practicing physicians, veterinarians, and the general public.

Marked phenotypic variation characterizes isolates of Toxoplasma gondii, a ubiquitous zoonotic parasite that serves as an important experimental model for studying apicomplexan parasites. Progress in identifying the heritable basis for clinically and epidemiologically significant differences requires a robust system for describing and interpreting evolutionary subdivisions in this prevalent pathogen. To develop such a system, we have examined more than 950 isolates collected from around the world and genotyped them using three independent sets of polymorphic DNA markers, sampling 30 loci distributed across all nuclear chromosomes as well as the plastid genome. Our studies reveal a biphasic pattern consisting of regions in the Northern Hemisphere where a few, highly clonal and abundant lineages predominate; elsewhere, and especially in portions of South America are characterized by a diverse assemblage of less common genotypes that show greater evidence of recombination. Clustering methods were used to organize the marked genetic diversity of 138 unique genotypes into 15 haplogroups that collectively define six major clades. Analysis of gene flow indicates that a small number of ancestral lineages gave rise to the existing diversity through a process of limited admixture. Identification of reference strains for these major groups should facilitate future studies on comparative genomics and identification of genes that control important biological phenotypes including pathogenesis and transmission.

Toxoplasma gondii is among the most prevalent parasites worldwide, infecting many wild and domestic animals and causing zoonotic infections in humans. T. gondii differs substantially in its broad distribution from closely related parasites that typically have narrow, specialized host ranges. To elucidate the genetic basis for these differences, we compared the genomes of 62 globally distributed T. gondii isolates to several closely related coccidian parasites. Our findings reveal that tandem amplification and diversification of secretory pathogenesis determinants is the primary feature that distinguishes the closely related genomes of these biologically diverse parasites. We further show that the unusual population structure of T. gondii is characterized by clade-specific inheritance of large conserved haploblocks that are significantly enriched in tandemly clustered secretory pathogenesis determinants. The shared inheritance of these conserved haploblocks, which show a different ancestry than the genome as a whole, may thus influence transmission, host range and pathogenicity. Toxoplasma gondii is a parasite that causes zoonotic infections in humans. Here, the authors identify tandem amplification and diversification of secretory pathogenesis determinants in the T. gondii genome and show that clade-specific inheritance of conserved haploblocks enriched for these determinants shapes population structure.

Coyotes are exposed to many parasites and pathogens of veterinary and zoonotic concern. To assess the prevalence of the diseases caused by these microbes, we opportunistically obtained coyote samples from a variety of sources including a GPS collaring study, rabies testing facilities, wildlife resources agents, and road-side mortalities. We performed necropsies, serological testing, fecal flotations, and molecular analyses on coyotes from Tennessee and South Carolina. Dirofilaria immitis (heartworm) infected 46% (41/89) of coyotes and was associated with eosinophilic alveolitis and arteritis. Paragonimus kellicotti, a zoonotic lung fluke, was found in 24% (17/71) of Tennessee coyotes, including one coyote with extrapulmonary infection affecting the liver and lymph nodes. Trichinella spp., a zoonotic nematode, was present in 17% (12/71) of Tennessee coyotes but was not associated with muscular inflammation. Sarcoptes scabiei, the causative agent of sarcoptic mange, was detected in one Tennessee coyote. Most coyotes (86% [90/105]) were seropositive for Toxoplasma gondii, while 8.5% (9/106) were seropositive for Trypanosoma cruzi, an emerging zoonotic, vector-borne parasite. This study demonstrated that coyotes are commonly exposed to numerous parasites and pathogens that affect people and pets and are excellent sentinels for these diseases.

Toxoplasma gondii , a major zoonotic pathogen, possess a significant genetic and phenotypic diversity that have been proposed to be responsible for the variation in clinical outcomes, mainly related to reproductive failure and ocular and neurological signs. Different T. gondii haplogroups showed strong phenotypic differences in laboratory mouse infections, which provide a suitable model for mimicking acute and chronic infections. In addition, it has been observed that degrees of virulence might be related to the physiological status of the host and its genetic background. Currently, mortality rate (lethality) in outbred laboratory mice is the most significant phenotypic marker, which has been well defined for the three archetypal clonal types (I, II and III) of T. gondii ; nevertheless, such a trait seems to be insufficient to discriminate between different degrees of virulence of field isolates. Many other non-lethal parameters, observed both in in vivo and in vitro experimental models, have been suggested as highly informative, yielding promising discriminatory power. Although intra-genotype variations have been observed in phenotypic characteristics, there is no clear picture of the phenotypes circulating worldwide; therefore, a global overview of T. gondii strain mortality in mice is presented here. Molecular characterization has been normalized to some extent, but this is not the case for the phenotypic characterization and definition of virulence. The present paper proposes a baseline (minimum required information) for the phenotypic characterization of T. gondii virulence and intends to highlight the needs for consistent methods when a panel of T. gondii isolates is evaluated for virulence.

Whereas in Europe most of Toxoplasma gondii genotypes belong to the type II lineage, in Latin America, type II is rare and atypical strains predominate. In North America, data on T. gondii genotypes in humans are scarce. In this study, T. gondii DNA samples from 67 patients with diagnosed toxoplasmosis in the United States were available for genotyping. Discriminant analysis of principal components was used to infer each atypical genotype to a geographic area where patients were probably infected. Associations between genotype, disease severity, immune status, and geographic region were also estimated. Of 67 DNA samples, 41 were successfully genotyped: 18 (43.9%) and 5 (12.2%) were characterized as types II and III, respectively. The remaining 18 genotypes (43.9%) were atypical and were assigned to a geographic area. Ten genotypes originated from Latin America, 7 from North America, and 1 from Asia (China). In North America, unlike in Europe, T. gondii atypical genotypes are common in humans and, unlike in Latin America, type II strains are still present with significant frequency. Clinicians should be aware that atypical genotypes are common in North America and have been associated with severe ocular and systemic disease and unusual presentations of toxoplasmosis in immunocompetent patients.

Toxoplasma gondii causes lifelong infection in most definitive and intermediate hosts. Clinical cases of toxoplasmosis in captive cheetahs have been reported. However, there are few reports of viable T. gondii strains isolated from cheetahs. Here, T. gondii infection was investigated using molecular and serological assays in cheetahs from China. Modified agglutination test (MAT) (cut-off: 1:25) indicated that all six examined cheetahs ( n  = 6) showed T. gondii antibodies. Toxoplasma gondii DNA was detected in three out of five cheetahs. Two viable T. gondii strains were isolated from the striated muscles of two cheetahs using mice bioassay. They were designated as TgCheetahCHn1 and TgCheetahCHn2. Genetic characterization of DNA derived from tachyzoites was performed using RFLP-PCR of 10 markers. Toxoplasma gondii TgCheetahCHn1 is ToxoDB PCR-RFLP genotype #319, and the alleles of ROP18/ROP5 types were 3/7. TgCheetahCHn2 is ToxoDB genotype #9, and the alleles of ROP18/ROP5 were 3/6. The average survival time of TgCheetahCHn1-infected Swiss mice was 22 ± 1 days ( n  = 23), and the mice did not have detectable T. gondii -specific antibodies until 117 ± 30 days post-inoculation ( n  = 8), therefore, TgCheetahCHn1 had intermediate virulence. TgCheetahCHn2 was avirulent for Swiss mice. Few brain tissue cysts (0–50) were observed in the mice inoculated with TgCheetahCHn1 or TgCheetahCHn2. The results provide direct evidence of cheetah as intermediate host of T. gondii .

Previous studies have reported high diversity between and within populations of Toxoplasma gondii in South America. In the present study, isolates of T. gondii from chickens were obtained from the Amazon region. Adult free-range chickens were acquired from 29 municipalities in the Brazilian Amazon region that included Acre (n = 9 municipalities), Amapá (n = 6), Amazonas (n = 6), Pará (n = 6), and Roraima (n = 2) states and from two municipalities in Peru, three in Bolivia, one in Guyana, and one in Venezuela. Heart, brain, and blood samples were collected from 401 chickens. Anti- T. gondii serum antibodies were detected in 273 (68.1%) chickens using the Modified Agglutination Test (MAT ≥ 5), and bioassays in mice were performed using 220 birds. Isolates were obtained from 116 (52.7%) chickens with antibody titers ≥ 20. Of these isolates, 93 (84.5%) led to acute sickness in more than 50% of the infected mice within 30 days post-inoculation. The 116 isolates were genotyped using multilocus nested polymerase chain reaction-restriction fragment length polymorphism (Mn-nPCR-RFLP) with 12 markers and 15 microsatellite (MS) markers. PCR-RFLP analysis revealed 42 genotypes from the 116 isolates. Of these, 20 (46.51%) genotypes are described for the first time. The most abundant genotype was ToxoDB PCR-RFLP genotype #7 with 40 isolates. A total of 83 genotypes were observed from the 116 isolates by MS analysis. The phylogenetic network constructed of T. gondii genotypes from current and previously reported isolates, using PCR-RFLP data, revealed five groups with clear indication of geographical separation of T. gondii population in the Amazon region versus the Southeastern region of Brazil. Such spatial diversity was also observed within the Amazon region. This study expands our knowledge of T. gondii population in South America and emphasizes the importance of genetic diversity and high mouse-virulence of the parasite in the Amazon region.

Background Toxoplasma gondii infections are common in humans and animals worldwide. Among all intermediate hosts of T. gondii , captive marsupials from Australia and New Zealand are highly susceptible to clinical toxoplasmosis. However, most free-range marsupials establish chronic T. gondii infection. Infected marsupial meat may serve as a source of T. gondii infection for humans. Differences in mortality patterns in different species of kangaroos and other marsupials are not fully understood. Lifestyle, habitat, and the genotype of T. gondii are predicted to be risk factors. For example, koalas are rarely exposed to T. gondii because they live on treetops whereas wallabies on land are frequently exposed to infection. Methods The present review summarizes worldwide information on the prevalence of clinical and subclinical infections, epidemiology, and genetic diversity of T. gondii infecting Australasian marsupials in their native habitat and among exported animals over the past decade. The role of genetic types of T. gondii and clinical disease is discussed. Results Fatal toxoplasmosis has been diagnosed in captive Australasian marsupials in Argentina, Chile, China, Germany, Hungary, Japan, Spain, Turkey, and the USA. Most deaths occurred because of disseminated toxoplasmosis. Genetic characterization of T. gondii strains isolated from fatal marsupial infections identified Type III as well as atypical, nonclonal genotypes. Fatal toxoplasmosis was also diagnosed in free-ranging wombats ( Vombatus ursinus ) in Australia. Genetic characterization of DNA amplified directly from host tissues of subclinical culled kangaroos at slaughter identified many mixed-strain infections with both atypical and recombinant genotypes of T. gondii . Conclusions Most Australasian marsupials in their native land, Australia and New Zealand, have high prevalence of T. gondii , and kangaroo meat can be a source of infection for humans if consumed uncooked/undercooked. The genotypes prevalent in kangaroos in Australia and New Zealand were genetically distinct from those isolated or genotyped from most macropods in the USA and other countries. Thus, clinical toxoplasmosis in marsupials imported from Australia is most likely to occur from infections acquired after importation. Graphical Abstract

Background In changing northern ecosystems, understanding the mechanisms of transmission of zoonotic pathogens, including the coccidian parasite Toxoplasma gondii , is essential to protect the health of vulnerable animals and humans. As high-level predators and scavengers, foxes represent a potentially sensitive indicator of the circulation of T. gondii in environments where humans co-exist. The objectives of our research were to compare serological and molecular assays to detect T. gondii , generate baseline data on T. gondii antibody and tissue prevalence in foxes in northern Canada, and compare regional seroprevalence in foxes with that in people from recently published surveys across northern Canada. Methods Fox carcasses ( Vulpes vulpes / Vulpes lagopus , n  = 749) were collected by local trappers from the eastern (Labrador and Québec) and western Canadian Arctic (northern Manitoba, Nunavut, and the Northwest Territories) during the winters of 2015–2019. Antibodies in heart fluid were detected using a commercial enzyme-linked immunosorbent assay. Toxoplasma gondii DNA was detected in hearts and brains using a magnetic capture DNA extraction and real-time PCR assay. Results Antibodies against T. gondii and DNA were detected in 36% and 27% of foxes, respectively. Detection of antibodies was higher in older (64%) compared to younger foxes (22%). More males (36%) than females (31%) were positive for antibodies to T. gondii . Tissue prevalence in foxes from western Nunavik (51%) was higher than in eastern Nunavik (19%). At the Canadian scale, T. gondii exposure was lower in western Inuit regions (13%) compared to eastern Inuit regions (39%), possibly because of regional differences in fox diet and/or environment. Exposure to T. gondii decreased at higher latitude and in foxes having moderate to little fat. Higher mean infection intensity was observed in Arctic foxes compared to red foxes. Fox and human seroprevalence showed similar trends across Inuit regions of Canada, but were less correlated in the eastern sub-Arctic, which may reflect regional differences in human dietary preferences. Conclusions Our study sheds new light on the current status of T. gondii in foxes in northern Canada and shows that foxes serve as a good sentinel species for environmental circulation and, in some regions, human exposure to this parasite in the Arctic. Graphical Abstract