A 17-year-old boy from Kansas decides to spend his summer in Australia, working on his uncle's sheep ranch. (It's actually winter in Australia at that time of the year, but this has nothing to do with the case.) About one month into his visit, the boy begins to experience pain in the upper right quadrant, along with chills and fever. These symptoms persist over several days, so he his taken to the local physician. On examination, he is found to have fever (38.5ºC), point tenderness over the liver, and pronounced hepatomegaly. The doctor asks him if he has consumed uncooked sheep liver or watercress since arriving in Australia. The boy says that he saw watercress growing in a pond on the farm and ate some of it because he is fond of it and eats it frequently in the U.S. In fact, he found it odd that his Australian family never used it in their salads, but he didn't want to say anything because he was a guest. On hearing this, the physician examines a stool sample microscopically, but he fails to find anything remarkable. At that point, he sends the boy to the nearest hospital for a CT scan of his liver and other tests. The scan reveals the presence several small track-like features that do not appear to be normal. A CBC shows a marked eosinophilia.

Question 3.1: What is the most likely diagnosis?

The upper-right-quadrant pain, point tenderness, and hepatomegaly indicate some form of liver involvement. The symptoms are not typical of any type of viral hepatitis. The eosinophilia implies that a parasitic infection is occurring. The patient's history involving residence on a sheep farm and consumption of uncooked watercress strongly suggest an infection by Fasciola hepatica, a helminthic pathogen that is commonly known as the sheep liver fluke. The features seen on the CT scan are most likely migration tracks that were created as larvae of this organism migrated through the liver parenchyma.

NOTE: The diagnosis of infection with F. hepatica depends on a high degree of suspicion, the elicitation of an appropriate geographic history, and stool examination for the characteristically shaped parasite ova. (In this case, the ova were not yet being produced in substantial numbers; see below.) Additional evidence may be obtained by documenting eosinophilia or by imaging the liver.

Question 3.2: What is the life cycle of this pathogen?

Humans are infected when they ingest encysted metacercariae of F. hepatica. The metacercarie excyst in the intestine and produce larvae that migrate through the duodenal wall and across the peritoneal cavity to reach the liver. The larvae then penetrate the liver capsule, pass through the liver parenchyma, and enter the bile ducts, where they mature into adult worms. Approximately 3 to 4 months after the initial infection, the adult flukes start producing operculated eggs that are shed in the stool. When contaminated fecal material is deposited in water, the eggs are taken up by the snail that serves as the intermediate host for F. hepatica. Development of the organism in the snail results in the release of free swimming cercaria that ultimately encyst to form metacercaria, thereby completing the life cycle.

The local physician in the present case, suspecting that it might be fascioliasis, checked the stool for the operculated eggs, but did not see them because it was a little too early in the course of the disease for substantial egg production.

Question 3.3: How is this disease transmitted?

Sheep are the principal mammalian host for F. hepatica. Infections in humans have been reported worldwide in sheep-raising areas, with the appropriate species of snail acting as an intermediate host. Humans typically acquire the disease by consumption of uncooked aquatic plants such as watercress. Infection may also be acquired by consumption of contaminated water or of food items that are rinsed with contaminated water. Infection by consumption of freshly prepared raw liver containing immature flukes has also been reported. In the present case, the boy was probably infected by consuming the watercress, especially if sheep happen to have access to the pond on the farm and sometimes deposit fecal material therein.

Question 3.4: What may happen if this case is not treated?

The acute symptoms described in this case are caused by tissue irritation that occurs as the larvae of F. hepatica migrate through the liver parenchyma. These symptoms often subside as the parasite reaches its final destination in the bile ducts. The adult worms mechanically irritate the bile ducts and secrete toxic substances. In chronic infections, this can lead to a number of problems, including hepatitis, hyperplasia of the epithelium, and biliary obstruction. Some of the bile duct worms may penetrate eroded areas in the ducts and invade the liver to produce necrotic foci that are referred to as liver rot. In severe infections, secondary bacterial infections might occur, and portal cirrhosis is possible.

Question 3.5: How is this disease treated?

F. hepatica responds poorly to praziquantel. Triclabenzadole (10 mg/kg, once) is a much better choice for this disease. Bithionol is another viable possibility.