Fasciolopsiasis is known to be endemic in freshwater habitats of Cambodia, China, the Indian subcontinent, Laos, Myanmar, Taiwan, Thailand and Vietnam [
1,
6]. The disease occurs focally and linked to freshwater habitats associated with common social and agricultural practices and promiscuous defecation [
2]. Humans commonly become infected by eating raw or undercooked aquatic plants, but infection can be also contracted by the drinking or use of contaminated water or processing of the water-derived plants, e.g., using teeth to peel plants.
The present case is the second report of
F. buski human infection, but the first case of autochthonous transmission in Nepal. Dutt et al. [
7] reported a case of fasciolopsiasis in a 14 months-old child resident of Terai (Far Western) region of Nepal. Although stool routine examination of the child was negative, the patient coughed out a live adult worm after antihelminthic treatment. The authors suggested that infection was imported and related to drinking water from a pond during a stay of the child in India. The case presented herein appears to be the first reported case of autochthonous transmission of
F. buski in Nepal and related to the habit of the patient to eating aquatic plants and snails from ponds and rivers near his home, which suggest the presence of this parasite in Nepal. The ingestion of aquatic vegetables is a common source of human infection [
6].
The low number of cases of human fasciolopsiasis in Nepal is surprising since this country has been qualified as probably endemic area of foodborne trematode infections [
8] and, moreover, human cases of
Fasciolopsis buski have been described from the Nepal bordering states of Bihar and Uttar Pradesh in India [
9–
11]. Probably, the impact of human fasciolopsiasis in Nepal is underestimated in relation to the vague and unspecified symptoms of most light infections with
F. buski and the poor development of health systems in developing countries, especially in the remote rural environments [
2]. The severity of the disease is usually directly associated with the number of parasites involved: an infection with one or few worms may be subclinical but a heavy parasitic load can lead to severe tissue damage and complications such as ulcerations, abscesses and hemorrhages with the eventuality of intestinal obstruction and perforation [
1,
3]. When present, symptoms include abdominal pain, nausea, diarrhea and headache, while marked eosinophilia, leukocytosis and B12 deficiency are common reports only in severe infections [
3]. Allergic reaction to the toxic metabolites of the worm may manifest as facial-orbital edema, and anasarca [
3,
6]. The diagnosis is usually suggested by the clinical presentations in endemic areas and confirmed by detecting the ellipsoidal, yellowish-brown, large (130–140×85 μm), thin shell, operculated eggs in the stool [
2,
3]. It should be noted that the eggs of
F. buski are almost indistinguishable from those of
Fasciola species (
F. hepatica and
F. gigantica) [
5,
12,
13], and those of other lesser common intestinal trematode such as
Echinostoma ilocanum [
14], making necessary further investigations in areas where these parasites overlaps. In our case, identification of the adult worm was made on the basis of morphological keys and its differences with
F. hepatica are evident, specifically,
F. buski lacks the cephalic cone and is usually longer [
3].