Diphyllobothriasis occurs in different areas of the world. In North America, there are endemic foci in the smaller lakes of the Great Lakes region. Outbreaks of this infection have been reported in Alaska. Western Europe, especially Finland, had high prevalence rates, but there has been a significant decline over the last few decades. Other endemic regions include South America (Uruguay, Chile) and Asia (Japan, Russia). Diphyllobothriasis is rare in Africa and Australia. Infections can occur in nonendemic areas when infected fish are transported under refrigeration and eaten insufficiently cooked.
Humans acquire the parasite by ingesting raw or undercooked freshwater fish. The lifecycle of the worm is complex and requires 3 hosts. The definitive hosts are humans and other fish-eating carnivores, in whom the mature adult worm inhabits the ileum and jejunum. Eggs are released in feces and mature in freshwater to develop into an embryo (coracidium), which is ingested by the first intermediate host, a crustacean such as Cyclops. In Cyclops, the coracidium develops into a larva (procercoid larva). When the procercoid larva-containing Cyclops are ingested by small freshwater fish such as minnows (second intermediate host), the larva matures into the plerocercoid larva (sparganum). Generally, humans do not eat small freshwater fish. Bigger predator fish such as trout, pike, or salmon eat them and harbor the plerocercoid larva. When these larger fish are eaten by humans after insufficient cooking, the larva matures into the adult form in the human body. The larva is not affected by pickling or smoking. Hence, infection occurs not only with eating raw or undercooked fish, but also with pickled fish. The cycle is completed in nature when carnivores such as bears and seals eat the plerocercoid larva-harboring freshwater fish.
Most infections with Diphyllobothrium are asymptomatic. Some infected persons may present with nonspecific symptoms such as weakness, dizziness, or salt craving, or gastrointestinal symptoms such as vague abdominal pain, discomfort, constipation, or diarrhea. Rarely, mechanical intestinal obstruction may occur if worms get entangled, necessitating urgent medical attention. Other uncommon manifestations such as cholecystitis or cholangitis may occur from migration of the proglottids (segments of worm's body). At times, patients may seek medical attention after passing a large section of proglottids in their feces.
One unique medical issue with diphyllobothriasis is the development of anemia secondary to vitamin B12 deficiency. Interestingly, with a high burden of infection or prolonged infection, the parasite may dissociate the B12-intrinsic factor complex in the human intestine (rendering the human host unable to absorb vitamin B12), and the parasite itself absorbs around 80% of the vitamin B12. Resultant deficiency of vitamin B12 may cause megaloblastic anemia and a myriad of neurological manifestations.
B70.0 – Diphyllobothriasis
187151009 – Diphyllobothriasis
Differential Diagnosis & Pitfalls
Hookworm infection with Ancylostoma duodenale or Necator americanus may cause anemia. However, anemia from hookworm infestation is that of iron deficiency (microcytic-hypochromic), in contrast to macrocytic-hyperchromic anemia seen with diphyllobothriasis. The thicker shell and the operculum of the fish tapeworm egg help distinguish it from the ovum of hookworm.
Diphyllobothriasis may be incidentally detected on stool examination being performed for other reasons. Presence of the ova should prompt clinician to check for anemia, especially B12 deficiency.