Pathogenicity and virulence of the liver flukesFasciola hepaticaandFasciolaGiganticathat cause the zoonosis Fasciolosis

Abstract

Fasciolosis caused by the liver flukes Fasciola hepatica and Fasciola gigantica is one of the most important neglected parasitic diseases of humans and animals. The ability of the parasites to infect and multiply in their intermediate snail hosts, and their adaptation to a wide variety of mammalian definitive hosts contribute to their high transmissibility and distribution. Within the mammalian host, the trauma caused by the immature flukes burrowing through the liver parenchyma is associated with most of the pathogenesis. Similarly, the feeding activity and the physical presence of large flukes in the bile ducts can lead to anemia, inflammation, obstruction and cholangitis. The high frequency of non-synonymous polymorphisms found in Fasciola spp. genes allows for adaptation and invasion of a broad range of hosts. This is also facilitated by parasite’s excretory-secretory (ES) molecules that mediate physiological changes that allows their establishment within the host. ES contains cathepsin peptidases that aid parasite invasion by degrading collagen and fibronectin. In the bile ducts, cathepsin-L is critical to hemoglobin digestion during feeding activities. Other molecules (peroxiredoxin, cathepsin-L and Kunitz-type inhibitor) stimulate a strong immune response polarized toward a Treg/Th2 phenotype that favors fluke’s survival. Helminth defense molecule, fatty acid binding proteins, Fasciola -specific glycans and miRNAs modulate host pro-inflammatory responses, while antioxidant scavenger enzymes work in an orchestrated way to deter host oxidant-mediated damage. Combining these strategies Fasciola spp. survive for decades within their mammalian host, where they reproduce and spread to become one of the most widespread zoonotic worm parasites in the world.

Exploring the role of macrophages in determining the pathogenesis of liver fluke infection

“…After ingestion of the metacercariae by mammalian hosts, a series of stimuli (including temperature, pH and bile salts) in the digestive tract activates the excystment of the newly excysted juvenile (NEJ) worms (Andrews, 1999; Sithithaworn et al ., 2014; Cwiklinski et al ., 2018; Lalor et al ., 2021). At this developmental stage, Opisthorchiidae migrate to the ampulla of Vater and ascend into the bile ducts where the parasites mature (Fig.…”

The Differences in the Susceptibility Patterns to Triclabendazole Sulfoxide in Field Isolates of Fasciola hepatica Are Associated with Geographic, Seasonal, and Morphometric Variations

“…Although altitude is associated with a higher prevalence of fascioliasis, temperature and solar radiation are associated with snail populations, infection prevalence, incubation periods, and cercariae production [40][41][42][43]. Resistant and susceptible parasites have also been shown to have different pre-patent periods, production of cercariae per snail, and infectivity capacity, which may give them a transmission advantage depending on the region [23,44,45]. Importantly, patterns of TCBZ use in each region could have also affected the proportions of susceptible and resistant parasites by selective pressure [46,47].…”

Fasciolosis—An Increasing Challenge in the Sheep Industry

“…The juvenile and adult flukes have an outer surface called the tegument that protects the fluke from enzymes and immune attacks, but also suppresses the host’s immune system [ 17 ]. The flukes mechanically damage the liver tissue while moving, in addition to feeding on the tissue.…”

“…When the flukes end up in the bile ducts, they start to feed on blood, bile, lymph and tissue, and anemia and hypoproteinaemia develop. The tegument has spines that can be used for puncturing blood vessels [ 17 ]. Sheep do not develop protective immunity against F. hepatica [ 11 ].…”