In eastern Asia, human fasciolosis appears to be sporadic. Few cases were documented in Japan, Koreas, Vietnam, and Thailand. Australia and the Oceania
In Australia, human fasciolosis is very rare (only 12 cases documented). In New Zealand, F. hepatica has never been detected in humans. Other animals
A number of drugs have been used in control fasciolosis in animals. Drugs differ in their efficacy, mode of action, price, and viability. Fasciolicides (drugs against Fasciola spp.) fall into five main chemical groups:Halogenated phenols: bithionol (Bitin), hexachlorophene (Bilevon), nitroxynil (Trodax)
Salicylanilides: closantel (Flukiver, Supaverm), rafoxanide (Flukanide, Ranizole)
Benzimidazoles: triclabendazole (Fasinex), albendazole (Vermitan, Valbazen), mebendazol (Telmin), luxabendazole (Fluxacur)
Sulphonamides: clorsulon (Ivomec Plus)
Phenoxyalkanes: diamphenetide (Coriban)Triclabendazole (Fasinex) is considered as the most common drug due to its high efficacy against adult as well as juvenile flukes. Triclabendazole is used in control of fasciolosis of livestock in many countries. Nevertheless, long-term veterinary use of triclabendazole has caused appearance of resistance in F. hepatica. In animals, triclabendazole resistance was first described in Australia, later in Ireland and Scotland and more recently in the Netherlands. Considering this fact, scientists have started to work on the development of new drug. Recently, a new fasciolicide was successfully tested in naturally and experimentally infected cattle in Mexico. This new drug is called Compound Alpha and is chemically very similar to triclabendazole.
In the case of CyN, the mutation variants have been found to mostly cluster in intron 4 and exon 4 and 5, but were also located in intron 3, and exon 2 and 3. Some mutation variants have been found in both Cyn and SCN, which indicates they are phenotypes of the same disease with different severity.It is considered that the mutation causes a decrease in the "neutrophil production or excessive apoptosis (shorter half-life)" which results in a deficiency of mature neutrophils in the blood. The exact pathological mechanism is still researched, with the main hypotheses being mislocalization of ELANE or unfolded protein response (UPR) induced by mutant ELANE, however according to Mehta et al. (2016), the "UPR induction by mutant ELANE is not strong enough to promote cell death and that mutant ELANE causes SCN through an alternative mechanism". According to Garg et al. (2020), new "findings challenge the currently prevailing model that SCN results from mutant ELANE, which triggers endoplasmic reticulum stress, UPR, and apoptosis". The expression of the ELANE gene has been linked to GFI1 gene, and some considered that interaction with other genes causes the emergence and severity of one or the other phenotypic disorder. It is unclear what causes the cyclic aspect in CyN. According to Donadieu et al. (2011), the "cyclic aspect ... suggests the existence of a cryptic biological clock that regulates granulopoiesis. This putative clock might be revealed by particular mutations".