Héctor H. García and Robert H. Gilman
Infection with fish tapeworms of the genus Diphyllobothrium is called diphyllobothriasis. Humans become infected by eating raw or poorly cooked fish. The most frequent species found in humans is the broad fish tapeworm, Diphyllobothrium latum, geographically located in regions of North America, especially Alaska and northern Canada, Europe, Japan, and Russia, including Siberia. In Latin America, D pacificum has also been found in humans on the Pacific coast of Peru, Chile, and Ecuador (where raw marine fish are prepared with lemon as cebiche), and Japan.1 Several other species of Diphyllobothriumalso infect humans, especially in Alaska. Usually, other definitive hosts, such as bears, dogs, and cats, maintain the infections in nature, and humans are incidentally involved.1,2
The adult tapeworm lives in the small intestine, where it may attain a length greater than 10 m. The proglottids are wider than they are long, hence the name broad fish tapeworm. Gravid proglottids continuously expel eggs into the intestinal lumen through a uterine pore. More than 1 million eggs may be passed in the feces each day. The eggs measure approximately 60 μm by 40 μm and have a lidlike structure called an operculum. If the eggs reach water, a ciliated embryo develops within the egg in about 2 weeks. This ciliated stage or coracidia then hatches through the opened operculum and is ingested by one of several species of copepod (water flea). In this minute crustacean, the embryo develops into a first-stage, or procercoid, larva in 2 to 3 weeks. When a freshwater fish eats the infected copepod, the larva penetrates the fish’s intestinal wall and migrates to the muscles, where it grows into a ribbonlike plerocercoid larva (also called a sparganum) in approximately 1 month. Larger fish such as salmon, pike, perch, and trout may eat the initial fish host, and the larva again invades the muscle of the second fish. If the game fish is eaten raw or inadequately cooked, the plerocercoid larva develops in the small intestine of the definitive host into a mature adult after approximately 5 weeks (eFig. 336.1 ).3,4
Most patients with diphyllobothriasis are asymptomatic and only recognize their infection when they pass a chain of proglottids in their stool. Gastrointestinal complaints are uncommon, but there are isolated reports of intestinal obstruction associated with vomiting of masses of tapeworm. As many as 2% of individuals infected with D latum in northern Europe may develop a megaloblastic anemia that is indistinguishable from pernicious anemia (rare or nonexistent in D pacificum–infected individuals). This “tapeworm anemia” is rare in other parts of the world. This condition is the result of several factors, including (1) the location of the tapeworm high in the jejunum, (2) an affinity of the geographic strain of D. latum for uptake of vitamin B 12 that is 7 times that of strains from North America, and (3) a reduced level of intrinsic factor or a decreased ability to absorb vitamin B12 in the affected population. Neurologic complications of vitamin B12 deficiency may develop even in the absence of anemia. The megaloblastic anemia associated with diphyllobothriasis usually affects individuals over the age of 50, but may be seen in children.
DIAGNOSIS AND TREATMENT
Fecal examination should easily reveal the characteristic eggs of Diphyllobothrium. The central uterine rosette and the dimensions of the proglottids are also diagnostic.
Praziquantel in a single dose of 5 to 10 mg/kg provides highly effective treatment. Patients should be informed that the drug is considered investigational by the FDA if used for this purpose. Niclosamide is also effective, but is no longer available in the United States. If present, anemia should be treated concomitantly with vitamin B12.3