Cysticercosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Overview

Humans develop cysticercosis by ingesting Taenia solium eggs. Following ingestion, oncospheres hatch, have access to the circulation and infect various tissues. During the viable phase, cysts do not cause marked inflammation nor symptoms. As the cysts degenerate, they lose the ability to modulate the immune response and result in an immune attack and tissue injury and edema. Eventually, the cysts either resolve or form a calcified granuloma, which is associated with seizures if it is located in the brain.

Pathophysiology

Life cycle of T. solium with resulting cysticercosis - Source: https://www.cdc.gov/

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. Infection can remain asymptomatic for years.
  • But later in the disease, cysts degenerate and cysticerci 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.

Gross Pathology:

  • Cysts round to oval
  • Contain lucent or semi tranclucent fluid
  • Size usually ranges from 1-2 cm
  • Cyst numbers vary from patient to patient (can be hundreds)

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

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

Microscopic Pathology:

There are 4 identified microscopic pictures which correlate with the stages of the disease.[3]

Taenia solium scolex - By https://es.wikipedia.org/wiki/User:Rjgalindo, class="extiw" title="es:User:Rjgalindo">Rjgalindo</a> from <a href="https://es.wikipedia.org/wiki/" class="extiw" title="es:">es</a>, <a href="http://creativecommons.org/licenses/by-sa/3.0/" title="Creative Commons Attribution-Share Alike 3.0">CC BY-SA 3.0</a>, <a href="https://commons.wikimedia.org/w/index.php?curid=2496706">Link</a>

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

Gallery

References

  1. "Clinical manifestations and diagnosis of cysticercosis".
  2. "CDC - Cysticercosis".
  3. "www.archivesofpathology.org".
  4. 4.0 4.1 "Public Health Image Library (PHIL)".


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