Diphyllobothriasis

While the infection is generally mild, complications may occur. Complications are predicated on parasite burden, and are generally related to vitamin B12 deficiency and related health conditions.[8]

Vitamin B12 deficiency with subsequent megaloblastic anaemia (which is indistinguishable from pernicious anaemia) may occur in some instances of the disease.[10] Anaemia may in turn result in subacute combined degeneration of the spinal cord and cognitive decline.[8]

D. latum competes with the host for vitamin B12 absorption,[11] absorbing some 80% of dietary intake and causing deficiency and megaloblastic anaemia in some 40% of cases.[12] Vitamin B12 uptake is enabled by the position of the parasite which usually lodges in the jejunum.[13] Vitamin B12 deficiency is - according to research - conversely seldom seen in D. pacificum infection.[11]

Rarely, massive infections may result in intestinal obstruction. Migration of proglottids can cause cholecystitis or cholangitis.[7]

Humans are one of the definitive hosts of Diphyllobothrium tapeworms, along with other carnivores; fish-eating mammals (including canids, felids, and bears), marine mammals (dolphins, porpoises, and whales), and (a few) birds (e.g. gulls) may also serve as definitive hosts.[7]

Definitive hosts release eggs in faeces; the eggs then mature in ~18–20 days if under favourable conditions. Crustaceans serve as the first intermediate hosts, and Diphyllobothrium larvae develop. The larvae are released when crustaceans are consumed by predators, which serve as second intermediate hosts (these are mostly small fish). Larvae move into deeper tissues in the second intermediate host. Second intermediate hosts do not serve as an important source of infection of humans as these are not regularly consumed raw. Consumption of infected second intermediate hosts by larger predatory fish, which serve as paratenic hosts; the parasites thereupon migrate into the musculature awaiting consumption by definitive hosts in which adult tapeworms will then finally develop in the small intestine to release up to a million immature eggs per day per parasite. Hosts begin to release eggs 5–6 weeks after infection.[7]

Diphyllobothriasis is postulated to cause changes in neuromodulator concentrations in host tissue and serum. D. latum infection has been shown to cause local changes in the host, leading to altered GI function (including motility) via neuroendocrine modulation.[8]

Diphyllobothriasis causes mast cell and eosinophil degranulation, leading to pro-inflammatory cytokine release.[8]

Diagnosis is usually made by identifying proglottid segments, or characteristic eggs in the faeces.[14] Eggs are usually numerous and can be demonstrated without concentration techniques. Morphologic comparison with other intestinal parasites may be employed as a further diagnostic approach.

These simple diagnostic techniques are able to identify the nature of the infection to the genus level, which is usually sufficient in a clinical setting.[6] Though it is difficult to identify the eggs or proglottids to the species level, the distinction is of little clinical importance because - like most adult tapeworms in the intestine - all members of the genus respond to the same treatments. Treatment may distort morphological features of expelled pathogen tissues and complicate subsequent morphological diagnosis attempts.[7]

When the exact species need be determined (e.g. in epidemiological studies), restriction fragment length polymorphisms can be effectively used. PCR can be performed on samples of purified eggs, or on native fecal samples following sonication of the eggs to release their contents.[6] Molecular identification is currently generally only used in research.[7]

A potential diagnostic tool and treatment is the contrast medium gastrografin which, when introduced into the duodenum, allows both visualization of the parasite, and has also been shown to cause detachment and passing of the whole parasite.[15]

Diphyllobothriasis occurs in areas where lakes and rivers coexist with human consumption of raw or undercooked freshwater fish.[24] Such areas are found in Europe, newly independent states of the former Soviet Union, North America, Asia, Uganda, Peru (because of ceviche), and Chile.[24] Many regional cuisines include raw or undercooked food, including sushi and sashimi in Japanese cuisine, carpaccio di persico in Italian, tartare maison in French-speaking populations, ceviche in Latin American cuisine and marinated herring in Scandinavia. With emigration and globalization, the practice of eating raw fish in these and other dishes has brought diphyllobothriasis to new parts of the world and created new endemic foci of disease.[6]

Infections in Europe and North America were traditionally associated with Jewish women due to the practice of tasting bits of uncooked fish during preparation of the gefilte fish dish,[25] and also occurred in Scandinavian women for the same reason. Diphyllobothriasis was thus also referred to as the "Jewish housewife's disease" or the "Scandinavian housewife's disease".[26]

Diphyllobothriasis nihonkaiense was once endemic to coastal provinces of central and northern Japan, where salmon fisheries thrived.[24] In recent decades, regions with endemic diphyllobothriasis nihonkaiense have disappeared from Japan, though cases continue to be reported among urbanites who consume sushi or sashimi.[24] In Kyoto, it is estimated that the average annual incidence in the past 20 years was 0.32/100,000, and that in 2008 was 1.0 case per 100,000 population, suggesting that D. nihonkaiense infection is equally as prevalent in Japan as D. latum is in some European countries.[24]

The disease is rare in the United States.