Alveolar echinococcosis (AE), a lethal disease caused by the parasite Echinococcus multilocularis, is characterized by tumor-like growths in a host-derived oxidative microenvironment. The mechanisms that enable the parasite to adapt its central carbon metabolism to the host's oxidative microenvironment remain poorly understood. Here, we report that oxidative stress serves as a key environmental cue that induces a profound metabolic rewiring. We identified pyruvate dehydrogenase kinase (EmPDK) as the central regulator governing this metabolic adjustment, favoring glycolysis and lactate production over oxidative phosphorylation (OXPHOS). Suppressing EmPDK activity enhances oxidative metabolism and impairs metacestode proliferation, whereas augmenting its function (via H2O2-induced upregulation) promotes glycolysis and growth. Reactive oxygen species (ROS) drive this metabolic reprogramming through the transcription factor EmHIF1α, forming an axis of ROS/EmHIF1α/EmPDK that modulates parasite metabolic plasticity. Our findings define EmPDK as a critical mediator of oxidative stress adaptation in E. multilocularis and support its further exploration as a candidate target for AE intervention.

Echinococcosis is a parasitic zoonosis caused primarily by Echinococcus granulosus (cystic echinococcosis, CE) and Echinococcus multilocularis (alveolar echinococcosis, AE). While CE typically manifests with well-formed unilocular cysts, AE presents as an infiltrative, tumour-like process. Mixed or atypical presentations pose diagnostic and therapeutic challenges. We describe a 24-year-old man from Morocco residing in Poland, who presented with progressive abdominal distension, pain, and subacute gastrointestinal obstruction. CT and ultrasound revealed multiple large, septated cysts involving the liver, spleen, peritoneum, and right lung. Serological findings were inconsistent across timepoints, alternating between positivity for E. granulosus and E. multilocularis. No molecular confirmation was available at the time of clinical decision-making. Albendazole therapy led to partial regression of intra-abdominal lesions but not pulmonary ones. Radiological findings were compatible with WHO CE2/CE3b stages, yet extensive dissemination and serological fluctuation suggested AE or a mixed pattern. A retrospective research-based molecular analysis later confirmed E. granulosus sensu stricto (G1 genotype), supporting a CE diagnosis. This case emphasizes the diagnostic uncertainty in disseminated echinococcosis with serological discordance and highlights the value of comprehensive diagnostic strategies, especially in-migrant populations from endemic areas and highlights the importance of emerging molecular diagnostics.

Echinococcosis most commonly presents as a slowly enlarging hepatic cyst, whereas extensive inflammatory extension with colonic involvement is uncommon. We report the case of an 80-year-old man who presented with abdominal pain and fever and reported having been aware of a hepatic echinococcal cyst for approximately 30 years. CT showed a giant calcified hepatic cyst containing an air-fluid level and intralesional gas, suggestive of secondary infection; intraoperative cyst-fluid culture subsequently grew Escherichia coli. Emergency laparotomy revealed dense inflammatory adherence to the transverse mesocolon and colon with obliteration of the dissection planes, necessitating right hemicolectomy with ileotransverse anastomosis, partial cyst wall excision, and drainage. Histopathology confirmed echinococcosis with extensive fibrosis, abscess formation, necrosis, and intestinal-surface involvement. The morphology raised suspicion for alveolar echinococcosis, although species-level confirmation was unavailable. The patient recovered uneventfully and received albendazole. This case highlights that chronically infected hepatic echinococcosis may mimic locally invasive disease and require adjacent-organ resection even without a demonstrable cystocolonic fistula.

Alveolar echinococcosis (AE), caused by Echinococcus multilocularis infection, leads to destructive hepatic lesions and severe hepatic fibrosis. Lactylation, a post-translational modification, has been linked to fibrotic progression in hepatocytes. However, the role of E. multilocularis infection in hepatic lactylation remains unclear. This study aims to elucidate the relationship between hepatic fibrosis and lactylation induced by E. multilocularis infection and fill this knowledge gap. The results showed that lactate concentrations in the livers and sera of AE mice were significantly elevated compared with those in the control group. The relative mRNA expression of hexokinase isoforms in the liver tissue of AE mouse models revealed significant upregulation of hexokinase-3 (HK3), a key enzyme regulating lactate production. Immunofluorescence staining revealed substantial colocalization between HK3 and TGF-β1 in hepatic lesions of AE mice. Western blot analysis using a pan-lactylation antibody showed significantly elevated lactylation levels in the livers of AE mice compared with controls, with a significant increase in histone H3 lysine 18 lactylation (H3K18la). CUT&Tag analysis revealed differential enrichment of H3K18la at multiple fibrosis-associated genes in AE mouse liver. In vitro, AML-12 hepatocytes exposed to E. multilocularis culture supernatant showed significant upregulation of TGF-β1, HK3, and histone lactylation. HK3 knockdown significantly reduced the induction of H3K18la and fibrosis-related proteins, whereas exogenous lactate supplementation significantly increased these responses despite HK3 silencing, confirming that lactate acts downstream of HK3 to drive histone lactylation and fibrogenesis. Corosolic acid, a compound that limits HK3-mediated lactate production, attenuated histone lactylation and fibrosis-related protein expression. These findings indicate that HK3-driven histone lactylation at H3K18 contributes to hepatic fibrosis in AE, and suggest that HK3 may serve as promising therapeutic targets for AE.

Trypanosoma cruzi, the protozoan etiologic agent of Chagas disease, was first described in 1909 by Carlos Chagas and remains one of the most important zoonotic parasitic pathogens in the Americas. Echinococcus granulosus and Echinococcus multilocularis are emerging zoonotic tapeworms and the causative agents of cystic echinococcosis and alveolar echinococcosis, respectively. Collectively, echinococcosis affects millions of people worldwide and are considered one of the 20 Neglected Tropical Diseases by the World Health Organization with low mortality and high morbidity rates. Dogs are clinically relevant veterinary hosts because they increase the risk of zoonotic transmission to humans.

Echinococcosis is a chronic parasitic disease and a serious zoonotic infection caused by the adult or larval stages of Echinococcus tapeworms. The transmission of Echinococcosis depends on carnivores as definitive hosts and various animals as intermediate hosts. According to current epidemiological reports, the liver is the most commonly affected organ. Clinically, Hepatic Echinococcosis is classified into hepatic alveolar Echinococcosis and hepatic cystic Echinococcosis, both of which pose a serious threat to the quality of life of residents in endemic areas. Currently, surgical treatment combined with benzimidazole medication is the main therapy; however, there are few chemotherapeutic drugs and targeted treatments available, and clinical treatment still has limitations. Therefore, there is an urgent need for new exploration in the molecular immunology, cellular directions. In recent years, with the development of high-throughput sequencing technology, integrated analyses of spatial transcriptomics and single-cell transcriptomics have become more accessible in clinical research, providing new approaches for the study of hepatic Echinococcosis. This review focuses on the application of single-cell RNA sequencing in hepaticEchinococcosis in recent years, as well as research on molecular immunopathogenesis, moleculardiagnostics, metastasis, cellular heterogeneity, growth and development, and the interactions between human hosts and echinococcosis. We pay particularly attentionto the heterogeneity of infiltrating immune cells around lesions, classification of cell subpopulations, immune suppression, and the immune microenvironment, which can help clinicians better understand the molecular immune mechanisms and biological characteristics of hepatic Echinococcosis, providing references for exploring new drug therapeutic targets.

Echinococcosis, a zoonotic disease caused by larval Echinococcus tapeworms, manifests primarily as Cystic Echinococcosis (CE) and Alveolar Echinococcosis (AE). It poses a serious threat to the global livestock industry and public health. Based on a systematic review of the disease's epidemiological features, pathogen biology, life cycle, and clinical management, this review systematically assesses the progress, core strengths, and key translational barriers of four mainstream anti-echinococcosis drug development avenues over the past five years. It was emphasized that the in vivo and in vitro efficacy and mechanisms of action of these emerging therapeutic agent classes critically evaluate the current landscape and core challenges of the field, and offer forward- looking perspectives for future research. This review aims to provide a crucial theoretical foundation and practical reference for precise disease control, optimized clinical strategies, and the development of novel therapeutics.

Long-term outcomes after hepatectomy for alveolar echinococcosis (AE) in immunosuppressed patients remain poorly investigated. This study evaluated recurrence rates and recurrence-free/overall survivals (RFS/OS) after AE resection in immunocompromised and immunocompetent patients. Consecutive patients operated for liver AE in two university hospitals were retrospectively collected (2000-2021). Immunosuppressed patients were defined as patients who had a reduced ability to fight infection due to certain diseases or treatments. 195 patients had hepatectomy for liver AE. Preoperative albendazole was given in 111 cases (57%). Fifty-two patients (27%) were considered immunosuppressed. Patients in the immunosuppressed and immunocompetent cohorts had similar preoperative characteristics. Recurrences occurred in 10 patients (immunosuppressed group: 4, non-immunosuppressed group: 6) within a median follow-up of 58 months (95%CI 48-68). No significant differences in RFS and OS were found between the immunosuppressed and immunocompetent groups (212 vs. 206 months, p = 0.625 and 236 vs. 210 months, p = 0.282). Two-year recurrence rates were 0% in the immunosuppressed cohort and 1% (1/142) in the immunocompetent patients (p = 0.466). Absence of preoperative albendazole and lesion size were predictive of recurrence after hepatectomy. Immunosuppression was not found to be a risk factor for recurrence (HR 1.4, p = 0.626). In this bicentric study, immunocompromised patients did not have significantly different recurrence rates, RFS, and OS than immunocompetent patients.

Echinococcus multilocularis and Echinococcus canadensis (genotypes G8 and G10) are emerging parasites of concern across North America. Historically confined to northern and western regions, both species have been detected with increasing frequency in new geographic areas in wildlife, domestic dogs, and humans. Both Echinococcus spp have indirect life cycles involving carnivore definitive hosts (domestic and wild canids) and either herbivore intermediate hosts (for E canadensis) or rodents (for E multilocularis). For E multilocularis, domestic dogs can serve as both definitive hosts, shedding eggs into the environment, and aberrant intermediate hosts that can develop severe, often fatal alveolar echinococcosis (AE). Clinical presentations in dogs with AE include hepatic masses, abdominal distension, anorexia, and hematological abnormalities. Intestinal Echinococcus spp infections in canids can be treated with products that contain praziquantel, but treatment of canine AE cases is complicated and has a poor prognosis. Intestinal infections can be diagnosed by fecal examinations and detection of eggs; however, importantly, the eggs are morphologically indistinguishable from Taenia spp. Molecular testing is therefore essential to definitively determine the parasite species. Given expanding parasite ranges, the close human-dog bond, and the severity of disease in both dogs and people, enhanced surveillance programs and routine veterinary testing and treatment protocols are important to minimize the risk of infection. Because diagnosis is important to prevent infection, the companion Currents in One Health by Garrett et al, AJVR, July 2026, investigates different methods of detection using fecal testing.