Parasitology最新文献

Toxoplasma gondii (T. gondii), a zoonotic parasite, can cause severe disease in warm-blooded animals. Pathological changes in murine tissues infected with different T. gondii isolates were studied to establish factors influencing lesion severity and parasite burden. In Study A, mice were orally inoculated with genotype #3, #6 or #8 oocysts. In Study B, mice were inoculated intraperitoneally with genotype #1, #3, #6, #13, #141 or #265 tachyzoites. Mice were euthanised serially and tissues processed for histopathology. In Study A, genotype #6 caused pathology in the liver, brain, lung, intestine and kidney, predominantly associated with tachyzoites, while #8 caused mainly moderate pathology in the brain, lung and liver, usually associated with tissue pseudocysts/cysts. Genotype #3 occasionally caused mild pathology, but the parasite was not visible in examined tissues. In Study B, genotypes #13 and #6 caused systemic infections associated with tachyzoites. Genotypes #3, #141 and #265 caused moderate pathology associated with pseudocysts/cysts in the brain and tachyzoites in peripheral organs. Genotype #1 caused mild pathology associated with pseudocysts/cysts in organs assessed. Comparison of genotype #6 between studies showed parasite stage and inoculation method did not affect the severity of pathology, but for #3, pathology was more severe when mice were inoculated intraperitoneally with tachyzoites compared to those inoculated orally with oocysts. This study confirmed route of infection, T. gondii strain, life stage and dose influence infection outcome and ultimately contributes to the refinement of T. gondii pathogenesis knowledge, which is fundamental for toxoplasmosis management and treatment.

Historical accounts suggest that malaria was endemic in ancient southern Anatolia, possibly as early as 800 BCE, but overwhelmingly from classical antiquity onwards. However, measuring the level and extent of malaria risk for premodern periods remains difficult, given the lack of quantifiable data. Surviving records indicate a particularly high prevalence of malaria-like symptoms in lowlands of Cilicia Pedias (southeastern Anatolia, modern Türkiye), especially with travellers for whom the region was a vital transit zone between Anatolia and Mesopotamia or the Levant. A geographic information system (GIS)-based multilayer malaria risk model developed for application to antiquity highlights the insalubrious nature of the region. For references to apparent malarial infection with spatial specificity, it provides quantified confirmation of malaria risk in the indicated locations. Combined with a new method for mapping ancient road paths, the model assigns risk figures to travel along those routes by merchants, pilgrims and armies throughout antiquity. Model-produced maps depict risk for Cilicia Pedias and its major roads. Modelled risk data correlate extremely well with historical accounts of malaria-like illness related to victims' known itineraries from the 4th century BCE through the 12th century CE. These results support interpretation of reported sicknesses as malarial infection, and highlight the peril of the disease for immune-naïve travellers through the region; and, indeed, the impact of Plasmodium parasites on outcomes of certain historical events. This replicable model provides a case-study for combining GIS and text-based methodologies in evaluating malaria's impact in the premodern Mediterranean, and application of similar techniques in other regions.

Clinical toxoplasmosis is a rare but often fatal disease that impacts several medical fields, including obstetrics, ophthalmology, transplantation, oncology and the context of the AIDS pandemic. The prognosis for patients with toxoplasmosis largely depends on timely treatment, which makes early diagnosis a priority for clinicians. However, diagnosing toxoplasmosis is a significant challenge due to the lack of specific clinical symptoms. This issue is further complicated by the high seroprevalence of Toxoplasma in the general population, which is far higher than the incidence of the disease. There are currently no clinically useful predictors for toxoplasmosis. Epidemiological studies and host-parasite interactions suggest that the incidence of toxoplasmosis depends on a combination of host and parasite factors. Significant risk factors include immunodeficiency, in utero exposure, genetic predisposition, anti-Toxoplasma antibody levels, older age, virulence of the strain, parasite burden and the infectious form of the parasite. Understanding these risk factors is important for clarifying the uncertainties regarding the incidence of toxoplasmosis and improving patient outcomes. In this review, we discuss the significance of these factors and current measurements for parasite-related factors. Additionally, we discuss potential preventive strategies that focus on screening as well as control of modifiable risk factors.

The northern hookworm, Uncinaria stenocephala, is the primary hookworm infecting dogs in temperate regions, but red foxes (Vulpes vulpes) are also frequent hosts. The extent to which fox-derived U. stenocephala contributes to canine transmission remains unclear. In this study, we assembled complete mitochondrial genomes (mitogenomes) from two adult U. stenocephala worms collected from red fox and two mitogenomes recovered via genome skimming from dog faecal egg isolates. Comparative analysis revealed >99% identity across all U. stenocephala mitogenomes with no discernible genetic differences for dog- and fox-derived U. stenocephala, supporting their conspecificity. Phylogenetic analysis confirmed paraphyly of the genus Uncinaria and clear distinction of U. stenocephala from the badger hookworm U. criniformis, resolving historical taxonomic ambiguity. We applied a 3% nucleotide divergence threshold to assess species boundaries across hookworm mitogenomes, confirming potential cryptic diversity in Necator americanus, U. sanguinis and A. caninum. Our findings demonstrate the utility of genome skimming for recovering hookworm mitogenomes from faecal samples and highlight the need for broader mitogenomic characterization across hookworm taxa to refine taxonomy and understand host associations.

The probability that a disease will manifest is highly variable. Susceptibility to disease is influenced by genetic background, environment and lifestyle choices. In this review, we put forward the premise that evolution of disease susceptibility may be partially influenced by the interaction of divergent pathogen DNA-binding proteins with variable binding sites in the host genome. The hypothesis put forward is derived from recent data obtained from work on the protozoan parasite, Theileria annulata, together with related evidence from viral and bacterial pathogens that have been postulated to modulate host epigenome architecture. The pathogen proteins highlighted have the potential to mimic functions of mammalian epigenome organisers linked to a range of disease syndromes. It is feasible, therefore, that the evolutionary relationship between pathogen and host impacts susceptibility to a range of conditions, such as autoimmune disorders and cancer, which are not directly linked to pathogen infection.

Toxoplasma gondii (T. gondii) is a neurotropic parasite that establishes latent infection in the central nervous system (CNS), and may alter behaviour and contribute to neuronal dysfunction. However, its impact on cognitive performance and CNS pathophysiological alterations in people with HIV (PWH) remains unclear. A cross-sectional study of adult PWH was conducted, assessing latent T. gondii infection through serum IgG levels in the absence of neurotoxoplasmosis. Neurocognitive impairments were assessed through neurocognitive testing across 6 domains, along with depressive and anxiety symptoms evaluation, and educational attainment. CNS pathophysiological alterations were assessed through amyloid-β1-42, total tau, phosphorylated tau, neopterin, and S-100β quantification in cerebrospinal fluid (CSF). Fifty-eight PWH were included, and T. gondii seropositivity was detected in 46.5% of participants (27/58). Overall, cognitive performance was largely comparable between groups, although subtle, non-significant declines were observed across several domains. T. gondii-seropositive individuals demonstrated a faster completion of Trail Making Test Part B (β = -35.79 sec; 95% CI: -67.78 to -3.86), lower educational attainment (β = -1.92 years; 95% CI: -3.76 to -0.09), without different levels of CSF biomarkers for neuronal-synaptic degeneration, Alzheimer's pathology, beta-amyloid deposition, macrophage-derived inflammation and glial activation-degeneration. In PWH with low CD4 counts, latent T. gondii infection was not associated with overt cognitive impairment or detectable CNS pathophysiological alterations. Instead, an atypical profile emerged, combining faster task-switching with lower educational attainment and subtle, non-significant declines in other domains. These findings highlight the complex nature of T. gondii-host interactions and need for longitudinal studies to clarify long-term neurocognitive outcomes.

Ascaridia galli and Heterakis gallinarum, the most prevalent nematodes of chickens, inhabit the small intestine and caeca, respectively, and often co-occur. Current excreta egg count (EEC) methods do not differentiate between their eggs, and although chickens produce two distinct excreta types - intestinal excreta (IE) and caecal excreta (CE) - the distribution of eggs of these species across them remains poorly understood. Forty Hy-Line Brown laying hens (40 weeks, mean body weight (BW) 2·07 ± 0·02 kg), cleared of prior nematode infection and artificially infected with A. galli (n = 20) or H. gallinarum (n = 20) were housed in separate floor pens and monitored for 26 weeks. Assessments included clinical signs, EECs from IE, CE and mixed excreta (ME), and worm recovery from subsets of birds at 8, 14, 20 and 26 weeks. Neither infection resulted in clinical signs, but A. galli slightly reduced BW gain (0·5 g/week/hen) than H. gallinarum (2·8 g/week/hen). Egg detection aligned with worm predilection sites: A. galli eggs were predominantly found in IE, while H. gallinarum eggs were largely confined to CE. In ME samples, egg counts were reduced by 45% relative to IE for A. galli and 60% relative to CE for H. gallinarum. EECs showed a negative but non-significant association with excreta moisture content. Natural re-infection produced a stable adult worm population in both infections. These findings demonstrate that analysing IE and CE separately provides a practical, non-lethal approach for differentiating these infections, while ME appears to have limited diagnostic utility. Further studies should evaluate these patterns across broader conditions and individual variation.