Clinical manifestations and diagnosis of cysticercosis
- A Clinton White, Jr, MD, FACP, FIDSA
A Clinton White, Jr, MD, FACP, FIDSA
- Paul R Stalnaker Distinguished Professor of Medicine and Director, Infectious Disease Division
- Department of Internal Medicine
- University of Texas Medical Branch
Cysticercosis is caused by the larval stage (metacestode) of the pork tapeworm Taenia solium. Clinical syndromes related to this parasite are divided into neurocysticercosis (NCC) and extraneural cysticercosis. Neurocysticercosis, in turn, is divided into parenchymal and extraparenchymal forms. Extraparenchymal forms include intraventricular, subarachnoid, intraocular, and spinal disease.
The clinical features and diagnosis of cysticercosis will be reviewed here. The epidemiology, life cycle, transmission and treatment of this infection are discussed separately. (See "Epidemiology, transmission, and prevention of cysticercosis" and "Treatment of cysticercosis" and "Intestinal tapeworms".)
Tissue cysticerci develop over a period of three to eight weeks following ingestion of T. solium eggs shed in the stool of a human tapeworm carrier. Cysticerci can develop at one or multiple sites; during the initial viable phase, cysticerci do not cause much inflammation in surrounding tissues. This phase of infection is usually asymptomatic, and cysticerci typically remain in this stage for many years. (See "Epidemiology, transmission, and prevention of cysticercosis".)
Taenia parasites have sophisticated means of evading destruction, and a number of mechanisms for host immune tolerance have been postulated. Metacestodes elaborate a variety of substances, including prostaglandins, taeniaestatin (a parasite serine proteinase inhibitor), paramyosin, sulfated polysaccharides, and secretory proteases, that inhibit or divert host inflammatory responses [1,2]. Parasite molecules may interfere with lymphocyte proliferation and macrophage function, thereby inhibiting normal cellular immune defenses [1,2]. Secreted proteases degrade host molecules including cytokines. In addition, humoral antibodies do not kill the mature metacestode.
Eventually (after a variable number of years) the cysts degenerate and lose their ability to modulate the host immune response . Host immune and inflammatory cells attack the cysticercus, which leads to the appearance of edema and/or contrast enhancement on imaging studies. This inflammatory response is associated with onset of seizures. Host inflammatory molecules such as substance P may be key mediators of seizures [4,5].
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- CLINICAL MANIFESTATIONS
- Parenchymal NCC
- Extraparenchymal NCC
- - Intraventricular cysts
- - Subarachnoid cysts
- - Spinal cysticercosis
- - Ocular cysticercosis
- Extraneural cysticercosis
- - Subcutaneous and intramuscular cysticercosis
- Laboratory tests
- Clinical approach
- Diagnostic tools
- - Imaging
- - Serology
- - Funduscopic exam
- - Spinal fluid studies
- - Pathology
- DIFFERENTIAL DIAGNOSIS
- SUMMARY AND RECOMMENDATIONS