Cysticercosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Humans develop cysticercosis by ingesting embryonated Taenia solium eggs or gravid proglottids. Following ingestion, oncospheres hatch and develop into tissue cysticerci over a period of several weeks. During the viable phase, cysts do not cause marked inflammation. As the cysts degenerate, they lose the ability to modulate immune response and result in immune attack and tissue injury and edema. Eventually, the cysts either resolve or form calcified granuloma, which is associated with seizures when present in the brain.

Pathophysiology

Life cycle of T. solium with resulting cysticercosis

The cestode (tapeworm) Taenia solium (pork tapeworm) is the main cause of human cysticercosis. In addition, the larval stage of other Taenia species (e.g., multiceps, serialis, brauni, taeniaeformis, crassiceps) can infect humans in various sites of localization including the brain, subcutaneous tissue, eye, or liver.

Pathogenesis & life cycle

• Cysticercosis is transmitted to the human host via ingesting embryonated Taenia solium eggs or gravid proglottids in contaminated foods or drinks..(1)
• Following ingestion, oncospheres hatch from the eggs, penetrate the intestinal wall into the circulation then penetrate the tissues of several organs [neural (parenchymal and extraparenchymal) or extraneural (striated muscle, liver , etc ..)] to form cysticerci in them.
• During early stages when the cysticerci are viable, they can evade the immune system so, no inflammatory response is triggered by their presence & patient remains asymptomatic. (can remain asymptomatic for years.
• But later in the disease, they degenerate and lose the ability to evade the immune system resulting in an inflammatory response. This inflammatory response is responsible for the presenting symptoms.

In other words, the cysticerci themselves are not the cause of the symptoms but it is the inflammatory response that is triggered (usually late when they degenerate)

N.B.

• Pigs can get infected by eating human feces infected with the eggs but ingestion of undercooked pork containing larval cysts does not cause cysticercosis . It only causes intestinal tapeworm (taeniasis). (2)

• Humans with cysticercosis only are dead end hosts .. meaning that they are not able to transmit the infection while humanis having intestinal tapeworm disease (teniasis) are the source of infection.

Gross

• Cysts are round to oval.
• Contain lucent or semi tranclucent fluid
• Size usually range from 1-2 cm.
• Their number vary from patient to patient (can be hundreds)

© Copyright UAB and the UAB Research Foundation, 1999-2013. All rights reserved

Microscopic

There are 4 identified microscopic pictures which correlate with the stages of the disease (6)

Vesicular stage

• The cysticerci are viable.
• Composed of a cavity containing a clear fluid and inside it lies the larvae.
• Each one is composed of finger-like invaginations and lined by a double layered, eosinophilic membrane.
• The reactive inflammatory response is usually absent (more likely to occur with degenerating cysts and with the onset of symptoms).

Colloidal stage

• Cysts start to degenerate.
• Fluid around larvae becomes turbid.
• Larvae become hyalinized.
• The inflammatory response becomes more severe and extend further.

granular-nodular stage

• Vesicle becomes involuted & its wall becomes thickened.
• Calcium starts to deposit in the larvae.

nodular-calcified stage

• Replacement of cysticerci by Calcium and collagen tissue.
• Reactive inflammation resolves but gliosis and giant cells may persist.

Gallery

• 
  This image reveals some of the cytoarchitectural features seen in a lymph node specimen that had been extracted from a patient suspected of a Hantavirus illness. From Public Health Image Library (PHIL).

References

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