Zoonotic hookworm infections remain a significant public health problem, causing nearly 500 million cases globally and approximately four million disability-adjusted life years lost annually. More than one-fifth of these cases are attributed to Ancylostoma ceylanicum, an emerging zoonotic health issue in the Asia-Pacific region. This review presents key research gaps regarding the epidemiology, diagnosis, control, prevention and elimination of A. ceylanicum and other canine zoonotic hookworms as neglected health threats. A. ceylanicum is the second most prevalent human hookworm in the region; it is the most common hookworm among dogs and cats-reservoirs of zoonotic infections. Previous population genetic and phylogenetic analyses revealed that A. ceylanicum has three possible transmission dynamics: zoonotic, animal-only, and human-only pathways. The actual burden of zoonotic ancylostomiasis in most endemic countries remains unknown due to the use of parasitological techniques (e.g., Kato-Katz thick smear and floatation techniques) that have reduced diagnostic performance and do not allow accurate species identification in helminth surveys. The emergence of benzimidazole resistance in soil-transmitted helminths (STHs), including hookworms, is a concern due to the protracted implementation of mass drug administration (MDA). Resistance is conferred by single nucleotide polymorphisms (SNPs) that occur in the β-tubulin isotype 1 gene. These mutations have been reported in drug-resistant A. caninum but have not been found in A. ceylanicum in the field. A. ceylanicum remains understudied in the Asia-Pacific region. The zoonotic nature of the parasite warrants investigation of its occurrence in human and animal reservoir hosts to understand the dynamics of zoonotic transmission in different endemic foci. The detection of benzimidazole resistance-associated SNPs in zoonotic hookworms from Asia-Pacific countries has yet to be thoroughly explored. Considering the high level of hookworm endemicity in the region, the circulation of resistant isolates between humans and animals potentially presents a significant One Health threat that can undermine current MDA and proposed animal deworming-based control efforts.

Co-infection with the cagA strain of Helicobacter pylori exacerbates the pathology of human liver fluke Opisthorchis viverrini (OV) infection leading to cholangiocarcinoma. However, underlying mechanisms remain unclear. We report a significant increase in cagA-positive and cagA-negative H. pylori in the stomach, blood, bile, and in the OV worms of co-infected Syrian golden hamsters at one hour, three hours, and one month, post-infection, compared to hamsters infected with either OV or H. pylori alone. Except in the worms, H. pylori numbers declined at three months post-infection, particularly in the bile fluid of co-infected animals. Both strains of H. pylori were immunohistochemically detected in the tegument of the worm, as well as in the bile duct epithelium when co-infected with O. viverrine, but not in H. pylori infection alone. Interestingly, only the cagA-positive strain was detected in the gut of the worm. Co-infection between cagA-positive H. pylori and O. viverrini resulted in a more severe biliary pathology and decreased E-cadherin expression in vivo and in vitro than those of the cagA-negative strain. These data suggest that O. viverrini acts as a carrier of cagA-positive H. pylori and co-migrates to the bile ducts, whereas O. viverrini facilitates H. pylori colonization and enhances the biliary pathogenesis and carcinogenesis.