[1] It is prevalent in Bangladesh, India, Burma, China, Kazakhstan, Philippines, Thailand, Vietnam, and the Volga Delta of Russia,[2][3] with isolated cases from Africa, such as Nigeria.
Its natural habitat is the colon of pigs, and has also been found in rhesus monkeys, orang-utans, fish, field rats and Napu mouse-deer.
The worm was discovered and described by two British medical doctors, Timothy Richard Lewis and James McConnell, in 1876, from the caecum of an indigenous Assamese man in India.
[8] The currently accepted nomenclature was fortified by the British parasitologist J. J. C. Buckley, at the London School of Hygiene and Tropical Medicine (where he was then a Milner Research Fellow), whose descriptions were based on high incidence of the parasitism among the native Assamese ethnic groups in Northeastern India.
[12] The alimentary canal is incomplete, consisting of a pair of lateral pouches arising from the oral sucker and a pharyngeal tube, which bifurcates into two gut caeca.
[13] The body covering, called a tegument, is smooth in appearance, but contains a fine structure in a series of concentric folds bearing numerous tightly packed tubercles.
[14][15] The incomplete alimentary canal consists of a pair of lateral pouches arising from the oral sucker and a slightly tortuous pharyngeal tube, which bifurcates into two gut caeca.
The oval-shaped ovary lies just posterior to the testes in the middle, and the loosely coiled uterus opens to the genital pore.
In water, eggs hatch into miracidia, which then infect a mollusc, in which larval development and fission occurs.
In an experimental infection of the mollusc Helicorbis coenosus, miracidum develops into cercaria after 28-153 days of ingestion.
[16] In the snail, mother and daughter rediae are found in the digestive gland, and are about 148-747/45-140 μm in size, sausage-shaped, and lack collar and locomotory organs.
The complete life cycle is not yet observed in nature,[18] and the tiny snail, H. coenosus, remains the most commonly accepted vector, as it is coincidentally found in abundance in the pigsties.
It is hypothesised that the free cercaria in water bodies accidentally find and penetrate these animals as second intermediate host, where they encyst as metacercaria.
Heavy infection in humans is suspected to cause diarrhoea, fever, abdominal pain, colic, malnutrition, anaemia, and even death.
[2][4] Gastrodiscoidiasis is an infection that is usually asymptomatic and affects the small intestine in animals, such as pigs, to a very mild symptom, but when it occurs in humans it can cause serious health problems and even death.
The submucosa can show oedema and thickening, resulting in a subacute inflammation of the caecum and mucoid diarrhoea.
[1] First described from a native Assamese patient, it was initially believed to have a distribution restricted to NE India and the southeast Asia.
Later investigations revealed that it is widespread, and is further spread by infected persons to other parts of the world, such as Guyana.
[13] Regions of high incidence can be attributed to low standard of sanitation, such as rural farms and villages where night soils are used.
It is also assumed that transmission from infected fish that is under-cooked or eaten raw, as common among southeast Asian.
[19] There is a unique case report of a seven-year-old Nigerian who showed symptoms of malnutrition and anaemia and was eventually diagnosed with infections of G. hominis and Ascaris lumbricoides.