Chae MJ, et al. Korean Circ J. 2013 Apr;43(4):239-245. https://doi.org/10.4070/kcj.2013.43.4.239

The red fox (Vulpes vulpes) is a known host for various parasites, including numerous helminths and protozoans. Among these, certain species in the genus Sarcocystis (phylum Apicomplexa) have been documented to possess the capability to infect red foxes as definitive hosts. In South Korea, red foxes have been introduced and released as part of a re-introduction program. However, two months after its release, one of the foxes was found dead because of illegal trapping. The fox was necropsied, and a subsequent coprological study revealed oocysts of Sarcocystis sp. in the intestinal contents. The oocysts were identified as Sarcocystis pilosa based on the 18S rRNA and cytochrome c oxidase subunit 1 (cox1) gene sequences. It exhibited a 99.7–100% identity with 18S rRNA gene sequences and 99.1–99.8% identity with cox1 gene sequences from other previously reported S. pilosa samples. Additionally, it showed identities of 95.4–96.4% and 91.1–91.5% with the cox1 gene sequences of S. hjorti and S. gjerdei, while demonstrating 99.6 and 98.1% identity with the 18S rRNA gene sequences of S. hjorti and S. gjerdei, respectively. This is the first report from mainland Asia, excluding the Japanese archipelago, indicating that the life cycle of S. pilosa persists in South Korea.

Sarcoptic mange is a highly contagious and often lethal parasitic skin disease caused by the mite Sarcoptes scabiei, which is frequently reported in red foxes (Vulpes vulpes). However, there is a lack of documented cases and treatment strategies for sarcoptic mange in reintroduced red fox populations, particularly in South Korea. This study describes 27 cases of sarcoptic mange outbreaks in 26 red foxes reintroduced into South Korea between 2019 and 2024. Of these, 15 foxes were rescued alive, while 12 were found dead. Blood tests of the surviving animals (n = 15) showed significant leukocytosis, anemia, decreased albumin levels, increased globulin levels, elevated blood urea nitrogen levels, and decreased creatinine levels, indicative of a chronic wasting infection. Treatment with ivermectin or fluralaner resulted in complete recovery in 12 of 15 animals, while three animals died during treatment. Necropsy of the deceased animals (n = 12) revealed characteristic skin lesions, such as alopecia, hyperkeratosis, epidermal hyperplasia, and dermatitis. The study findings highlight the importance of long-term monitoring and active, continuous treatment of sarcoptic mange, a major threat, for the stable re-establishment of reintroduced foxes in South Korea.

Background: Inflammasomes recognize endogenous and exogenous danger signals, and subsequently induce the secretion of IL-1β. Studying inflammasomes in the red fox (Vulpes vulpes) is crucial for wildlife veterinary medicine, as it can help control inflammatory diseases in foxes. Methods: We investigated the activation and intracellular mechanisms of three inflammasomes (NLRP3, AIM2, and NLRC4) in fox peripheral blood mononuclear cells (PBMCs), using established triggers and inhibitors derived from humans and mice. Results: Fox PBMCs exhibited normal activation and induction of IL-1β secretion in response to representative inflammasome triggers (ATP and nigericin for NLRP3, dsDNA for AIM2, flagellin for NLRC4). Additionally, PBMCs showed normal IL-1β secretion when inoculated with inflammasome-activating bacteria. In inhibitors of the inflammasome signaling pathway, fox inflammasome activation was compared with mouse inflammasomes. MCC950, a selective NLRP3 inhibitor, suppressed the secretion of dsDNA- and flagellin-mediated IL-1β in foxes, unlike mice. Conclusions: These findings suggest that NLRP3 may have a common role in dsDNA- and flagellin-mediated inflammasome activation in the red fox. It implies that this fox inflammasome biology can be applied to the treatment of inflammasome-mediated diseases in the red fox.

Background: Inflammasomes recognize cytosolic danger signals, including pathogens, and subsequently induce the secretion of pro-inflammatory cytokines, such as interleukin (IL)-1β. Studying inflammasomes in the red fox (Vulpes vulpes) is crucial from a wildlife veterinary and public health perspective, as it can be used to help control and prevent the transmission of zoonotic pathogens. The understanding of how diversity in inflammasomes across species affects pathogen carriage in the red fox is still limited. Methods: We investigated the activation and intracellular mechanisms of three inflammasomes (NLRP3, AIM2, and NLRC4) in fox peripheral blood mononuclear cells (PBMCs), using established triggers and inhibitors derived from humans and mice. Results: Fox PBMCs exhibited normal activation and induction of IL-1β secretion in response to representative inflammasome triggers (ATP and nigericin for NLRP3, dsDNA for AIM2, flagellin for NLRC4). However, in inhibitor studies, MCC950, a selective NLRP3 inhibitor, suppressed IL-1β secretion mediated by the fox AIM2 and NLRC4 inflammasomes. Conclusions: These findings suggest that NLRP3 may have a common role in dsDNA- and flagellin-mediated inflammasome activation in the red fox. In conclusion, this fox inflammasome biology can be applied to the control of zoonotic infections and the treatment of inflammasome-mediated diseases in the red fox.