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Details of Cysticercosis IgG ANTIBODY
What is Cysticercosis IgG ANTIBODY?
Cysticercosis is caused by infection with Taenia solium, a tapeworm (cestode). In this form of infection, humans and pigs serve as the intermediate host and have the cystic larval form in their tissues. Humans can also serve as the definitive host for T solium and have the adult form in their intestines (known as taeniasis).
Humans acquire cysticercosis by ingesting microscopic T solium eggs in contaminated food, water, or fomites. The eggs enter the environment when they are shed in stool from a person with the intestinal form of infection; this could be the same patient (autoinfection) or a different patient. Once ingested, the eggs hatch in the intestine to release oncospheres, which invade the intestinal wall and disseminate via the blood to muscles, liver, brain, and other tissues where they form cysts (cysticerci).
Taeniasis occurs when cysticerci are ingested in the undercooked flesh of an infected intermediate host (eg, pig). In the small intestine, cysticerci will evaginate and attach via a scolex to the intestinal wall. They then grow to become mature adult tapeworms. Adults can reside in the intestine for years and grow from 2 to 7 meters with over 500 proglottids, each filled with 50,000 eggs.
While cysticercosis and taeniasis occur globally, in the United States, infections are predominantly encountered in immigrants from Latin and Central America who acquired the infection locally.
The symptoms associated with cysticercosis depend on where the cysticerci localize, their size, number, and stage (degenerating, calcified, etc). The time between initial infection and symptom onset may vary from several months to years. The presence of cysts in the brain or spinal cord, referred to as neurocysticercosis, is the most serious form of the disease and, while some individuals may be asymptomatic, many presents with seizures (70%-90%), headache, confusion, and difficulty with balance. Cysts present in striated muscle are typically asymptomatic.
Diagnosis of cysticercosis relies on both imaging studies and serologic testing results. Importantly, detection of T solium eggs or proglottids in stool by an ova and parasite exam is diagnostic for taeniasis, not cysticercosis. Individuals with taeniasis should be evaluated for cysticercosis by serology since autoinfection can occur.
Due to imperfect sensitivity and specificity of commercially available enzyme-linked immunosorbent assays (ELISA) for cysticercosis, it is recommended that both positive and negative results by commercial ELISA be confirmed by a cysticercosis immunoblot offered through the Centers for Disease Control and Prevention (www.cdc.gov/dpdx/cysticercosis/index.html) for patients strongly suspected to have cysticercosis. Currently, available antibody detection assays are unable to distinguish between active and inactive infections.
Reference values apply to all ages.
Results suggest infection with Taenia solium (cysticercosis). Confirmatory testing through the Centers for Disease Control and Prevention is recommended. False-positive results may occur in patients with other helminth infections (eg, Echinococcus).
No antibodies to Taenia solium (cysticercosis) were detected. A negative result may not rule out infection as the sample may have been collected prior to the development of a detectable level of antibodies. Sensitivity is negatively impacted by the presence of few cysticerci or locations in areas less accessible to the immune system. Repeat testing on a new sample is recommended for patients at high risk of cysticercosis.
Diagnosis of cysticercosis should be based on exposure history, clinical presentation, other laboratory findings, and imaging studies.
False-negative results may occur in severely immunosuppressed patients.