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Most of the clinical knowledge about fascioliasis is based on cases caused by Fasciola hepatica. However, the same principles and clinical features are thought to apply to F. gigantica.
Fasciola parasites do not multiply in people. Therefore, the parasite burden depends on the inoculum, including the potential for reinfection. The large size of the parasite also can be problematic—for example, can compound the tissue damage and increase the abdominal pain when larval flukes migrate through the liver and can predispose to biliary obstruction during the chronic phase.
Both the acute and chronic phases of infection can be symptomatic or symptom free. Nonspecific clinical features of both phases can include the following:
- Fever, which can be intermittent;
- Abdominal pain, in the right upper quadrant, epigastrium, or more diffuse/generalized;
- Other abdominal symptoms (such as anorexia, nausea, vomiting, diarrhea, change in bowel habits, and weight loss) and signs (such as hepatomegaly and jaundice);
- Eosinophilia, which is more prominent and less variable during the acute phase than in the chronic phase;
- Anemia, especially in children; and
- Transaminitis (during the chronic phase, laboratory testing also can indicate hepatobiliary obstruction).
The Acute Phase (Acute Fascioliasis)
The acute phase is also referred to as the migratory, invasive, hepatic, parenchymal, or larval phase. Immature larval flukes migrate through the intestinal wall, the peritoneal cavity, the liver capsule, and hepatic tissue and, ultimately, to the bile ducts. The acute phase lasts up to approximately 3 to 4 months and ends when the larvae reach and mature in the bile ducts. Larval migration, especially through the liver, can result in tissue destruction, inflammation, local or systemic toxic/allergic reactions, and internal bleeding. Symptoms, in addition to those listed above, can include urticaria, cough, and shortness of breath. This phase can be life threatening in sheep infected with large inocula of parasites. However, severe illness is uncommon in people, although some young children have intense abdominal pain.
The Chronic Phase (Chronic Fascioliasis)
The chronic phase is also referred to as the biliary or adult phase. The chronic phase begins when immature larvae reach the bile ducts, mature into adult flukes, and start producing eggs. The eggs are passed from the bile ducts into the intestines and then into the feces. During this phase, the patient may be asymptomatic for months, years, or indefinitely. The only finding on routine blood testing might be peripheral eosinophilia, which typically is less prominent than during the acute phase.
Some experts differentiate between an asymptomatic latent phase and a symptomatic obstructive phase, which only some patients experience. The symptoms, if any, can be similar to those during the acute phase or can be more focal/discrete, such as clinical manifestations associated with cholangitis and biliary obstruction, which can be intermittent; cholecystitis and gallstones; or pancreatitis (also see below regarding ectopic infection). Fibrosis of the liver may occur.
On the basis of limited data, the life span of adult flukes in people might be 5 to 10 years or even longer (up to 13.5 years has been reported).
Involvement of Ectopic Sites
Fasciola parasites usually go to the liver and bile ducts. However, larval flukes also can migrate to ectopic (aberrant) sites, such as the pancreas, lungs, subcutaneous tissue, genitourinary tract, eyes, or brain. Fasciola parasites at ectopic sites may or may not mature into adult flukes. For example, subadult worms might emerge through the skin.
In addition, in the past, some cases of a syndrome known as Halzoun (a local, Middle Eastern term) —i.e., an acute hypersensitivity reaction involving the buccopharyngeal mucosa and upper respiratory tract in persons who ingested raw or undercooked sheep or goat liver—were attributed to temporary pharyngeal attachment of larval Fasciola flukes. However, whether Fasciola spp. (versus other parasites or agents) can cause this pharyngeal syndrome is unclear.
A high index of suspicion is important, especially because the clinical manifestations are nonspecific and the parasitologic tools are suboptimal.
The most widely used diagnostic approach is direct detection of Fasciola eggs, by light-microscopic examination of stool or of duodenal or biliary aspirates. However, egg production typically does not start until approximately 3 to 4 months after the exposure, whereas antibodies to the parasite may become detectable 2 to 4 weeks postexposure. (See below.) Even during the chronic phase of infection, more than one stool specimen may need to be examined to find the parasite, especially in people with light infections.
A cautionary note is that Fasciola eggs can be difficult to distinguish on the basis of morphologic criteria from the eggs of Fasciolopsis buski, which is an intestinal fluke. This distinction has treatment implications. Infection with Fasciolopsis buski is treated with praziquantel, which typically is not effective therapy for fascioliasis.
False fascioliasis (pseudofascioliasis) refers to the presence of Fasciola eggs in the stool because of recent ingestion of contaminated liver (containing noninfective eggs). The potential for misdiagnosis can be avoided by having the patient follow a liver-free diet for several days before repeating stool examinations. In addition, serologic testing may be useful to exclude infection.
Various types of immunodiagnostic tests for Fasciola have been developed. CDC provides serologic testing using an immunoblot assay that detects IgG antibody to FhSAP2, a recombinant antigen derived from Fasciola hepatica. As always, test results should be interpreted in context, with expert consultation. In general, serologic testing can be useful
- During the acute phase of infection, before the onset of egg production;
- During the chronic phase, in cases with low-level or sporadic production of eggs; and
- In cases of ectopic infection, in which eggs are not found in stool.
Other types of testing can provide supportive evidence (such as eosinophilia) or parasitologic confirmation (for example, if flukes are seen by imaging or by histopathology). The following are examples of additional types of testing:
- Routine blood work, including a complete blood count (with a differential white blood cell count) and blood chemistries;
- Abdominal imaging, such as ultrasonography, computerized axial tomography (CAT scan), magnetic resonance imaging (MRI scan), and endoscopic retrograde cholangiopancreatography (ERCP); and
- Histopathologic examination of a biopsy specimen of liver or other pertinent tissue.
More on: Laboratory Diagnosis
Triclabendazole, a benzimidazole compound active against immature and adult Fasciola parasites, is the drug of choice for treatment of fascioliasis. In February 2019, the U.S. Food and Drug Administration (FDA) approved triclabendazole for treatment of fascioliasis in patients at least 6 years of agepdf iconexternal icon.
As with all medications, use of triclabendazole should be individualized.
Triclabendazole is given orally, with food, to improve absorption. According to the FDA-approved product labelpdf iconexternal icon, the recommended dosage regimen (for patients at least 6 years of age) is two doses of 10 mg/kg given 12 hours apart.
Triclabendazole resistance has been documented, particularly in infected animals but also in some infected humans.
Additional Perspective About Therapy
On the basis of limited data, nitazoxanide might be effective therapy in some patients. The drug is given orally, with food. The dosage regimen for adults is 500 mg po bid (twice a day) for 7 days.
Praziquantel, which is active against most trematodes (flukes), typically is not active against Fasciola parasites. Therefore, praziquantel therapy is not recommended for fascioliasis.
In some patients who have biliary tract obstruction, manual extraction of adult flukes (e.g., via endoscopic retrograde cholangiopancreatography [ERCP]) may be indicated.
There are no available data on the use of triclabendazole in pregnant women to inform a drug-associated risk for major birth defects, miscarriage, or adverse maternal or fetal outcomes. See additional perspective in the product labelpdf iconexternal icon.
According to the product labelpdf iconexternal icon, there are no data on the presence of triclabendazole in human milk, the effects on the breastfed infant, or the effects on milk production. Published animal data indicate that triclabendazole is detected in goat milk when administered as a single dose to one lactating animal. When a drug is present in animal milk, it is likely that the drug will be present in human milk. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for triclabendazole and any potential adverse effects on the breastfed infant from the medication or from the underlying maternal condition.
According to the product labelpdf iconexternal icon, which addresses treatment of fascioliasis, the safety and effectiveness of triclabendazole have been established for pediatric patients aged 6 years and older (the age group for which the drug has been approved by FDA for treatment of fascioliasis) but have not been established for younger patients.