Joseph J. Yoo, MD, is currently an internal medicine resident at Thomas Jefferson University Hospital. He completed his undergraduate training at Bucknell University in Lewisburg Pennsylvania, and completed medical school at Temple University College of Medicine.
Christina Tofani, MD, Leo Katz, MD, and David Kastenberg, MD, from the department of gastroenterology and hepatology at Thomas Jefferson University Hospital are co-authors of this case report.
Most cases of acute diarrheal illness can be attributed to infectious causes, including viruses, bacteria and protozoa. While viruses are thought to cause the majority of acute infectious diarrhea, estimates regarding the frequency of different pathogens vary greatly depending on the population being studied.
Joseph J. Yoo
A 34-year-old Caucasian man with no significant past medical history presented in outpatient clinic with 7 days of diarrhea and 1 day of vomiting, abdominal cramping, and chills. The patient described his diarrhea as liquid brown, associated with nocturnal bowel movements, and exacerbated by food, resulting in poor appetite. His diarrhea was alleviated only by decreasing oral intake. He denied any blood in his stool, but did present with an approximately 3-foot flatworm which he passed in his stool the evening before presentation.
The patient denied sick contacts or any recent travel outside the United States, but had visited New Zealand approximately 5 months prior. The patient also reported eating uncooked sushi approximately twice a week, with a recent fishing trip on the day his diarrhea started. Review of systems was negative for fevers, night sweats, or involuntary weight loss. Physical exam was notable for an obese abdomen, but was otherwise unremarkable. Abdomen was soft and non-tender to palpation, and had normal bowel sounds on auscultation.
Laboratory evaluation was remarkable for a hemoglobin of 13.6 with a slightly elevated absolute eosinophil count of 0.5 x 10E/uL and a normal MCV of 86. Stool cultures were negative for ova, cysts, or parasites. Cultures were negative for Salmonella, Shigella, or Campylobacter. The parasite was sent for identification, and was positively identified as Diphyllobothrium latum proglottids. The patient was prescribed a single oral dose of Praziquantel 10mg/kg (1160mg). Four days later, the patient reported that he took the Praziquantel as directed, and that his diarrhea had completely resolved.
Figure 1. Diphyllobothrium latum.
Source: Thomas Jefferson University Hospital
A 63-year-old African American male with no significant past medical history presented to the emergency department after removing a foot-long worm from his rectum during a bowel movement earlier in the day. Prior to this event, he had experienced several months of abdominal bloating and “uneasiness,” but denied any abdominal pain, diarrhea, fevers, chills, or unintentional weight loss. He reported eating uncooked sushi about 2 times a week for the past 6 months. He also frequently fishes on the Delaware, typically cooking and eating what he catches. He denied any international travel.
Physical exam revealed a well-nourished, well-appearing male, with normal bowel sounds and no abdominal tenderness or distension. Laboratory evaluation was remarkable for a hemoglobin of 14.7, with macrocytosis (MCV 100), and no eosinophilia. Vitamin B12 level was not checked in the emergency department. The parasite was sent for identification, and was positively identified as Diphyllobothrium latum proglottids. The patient was discharged from the emergency department with a prescription for a single dose of Praziquantel 600mg. He reported no side effects from the medication, and experienced complete resolution of his symptoms.
The first documented case of Diphyllobothrium latum in the United States was in 1906, in Minnesota. Since then, most cases of Diphyllobothrium infection in the United States have been attributed to Diphyllobothrium latum, with the majority of those cases being attributed to ingestion of freshwater fish from the Great Lakes region and Alaska. Until 1982, infection with Diphyllobothrium was a reportable disease in the United States, and the Centers for Disease Control and Prevention (CDC) estimated between 125 to 200 cases between 1977 and 1981.
Over the past 100 years, there has been a considerable decline in cases of diphyllobothriosis. However, higher risks for urban populations may be on the horizon with globalization of the food market and increasing incentives for exporters to ship fresh, non-frozen, fish in an effort to gain a competitive edge in the market. At the time of this report, the most recent documented case of diphyllobothriosis was of a patient in Washington State, infected with Diphyllobothrium nihonkaiense.
The main risk factor for diphyllobothriosis is ingestion of raw or undercooked fish. Salmon are likely the most common hosts to transmit diphyllobothriosis, while whitefish, trout, pike, and other species have also been known to transmit infection.
The typical life cycle of Diphyllobothrium begins as eggs, which are released into water via the stool of an infected host. It is estimated that one worm can produce up to 1 million eggs per day. Once in the water, the eggs develop into mobile coracidium, which are then ingested by various species of small crustaceans, which act as the first intermediate host. These first intermediate hosts are then ingested by freshwater fish, becoming second intermediate hosts. The most common of these freshwater fish in North America are pikeperch or walleye. Salmon and other salmoniform fish (salmon, trout, and whitefish, etc.) are the most common secondary host, however, though salmoniform fish have been historically identified as typically harboring Diphyllobothrium latum, recent data suggest that these fish more commonly harbor species other than D. latum, namely D. nihonkaiense, D. dendriticum, and D. ditremum.
After ingestion of an infected fish, the mature adult tapeworm develops and resides within the small intestine of their definitive host, which includes humans as well as other fish-eating birds or mammals such as bears, foxes, gulls, and seals.
In the case of humans, adult tapeworms usually attach to the intestinal wall at the level of the ileum, with other levels of the small intestine, and rarely, the bile duct. Though many remain asymptomatic, common symptoms include diarrhea, abdominal pain or discomfort, and constipation. Less common symptoms include headache, allergic reactions, pain in the tongue exacerbated with food, intestinal obstruction, and cholecystitis or cholangitis from migrating segments of the tapeworm.
Lab abnormalities can include low vitamin B12, present in about 40% of cases, and peripheral eosinophilia. Prolonged infection by D. latum causes the classically associated megaloblastic anemia in only 2% or less of infected hosts. The mechanism of megaloblastic anemia is not only due to the worm’s absorption of approximately 80% of the host’s B12 intake, with a preferential absorption rate of 100:1 in relation to the host, but also due to a parasite-mediated dissociation of the vitamin B12-intrinsic factor complex.
Diagnosis is made by sending stool samples on 3 consecutive days for identification of eggs in stool. It can also be made by identification of passed segments, though this is less common to occur with Diphyllobothrium compared to other tapeworms. Treatment of Diphyllobothrium is simple with a single dose of praziquantel 25mg/kg, with a repeat stool check 1 month following treatment to document cure. Other treatment strategies include niclosamide (2g in adults, 1g in children older than 6 years), and intraduodenal gastrographin, reported to be a successful strategy for the first time in 1999, resulting in the expulsion of a complete, living, 6m long D. nihonkaiense worm.
Although D. latum infection is uncommon in the United States, it has the potential to cause a severe diarrheal illness in those afflicted. This particular parasite can affect both immunocompromised and immunocompetent hosts. A high clinical suspicion can lead to accurate diagnosis and successful treatment of D. latum proglottids infection.
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