Taeniasis: Pathophysiology of Taenia Solium - Dr. John Bartlett

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From the course by Duke University

Tropical Parasitology: Protozoans, Worms, Vectors and Human Diseases

134 ratings

Duke University

Tropical Parasitology: Protozoans, Worms, Vectors and Human Diseases

134 ratings

This course provides students an understanding of important human parasitic diseases, including their life cycles, vectors of transmission, distribution and epidemiology, pathophysiology and clinical manifestations, treatment, and prevention and control. Tropical Parasitology is taught by faculty from an area highly impacted by tropical parasites- the Kilimanjaro Christian Medical University College in Moshi, Tanzania. The faculty include Drs. Frank Mosha and Mramba Nyindo (and two lecturers, Drs. Johnson Matowo and Jovin Kitau). Dr. John Bartlett, Professor of Medicine, Global Health and Nursing at Duke University, joins his faculty colleagues in this effort.

From the lesson

Cestodes

The Cestodes cluster focuses on taeniasis and echinococcosis. One example of their impact is neurocysticercosis, which is estimated as the leading cause of epilepsy in low- and middle-income countries. This cluster has a total of 41 minutes of video and 31 pages of reading spread out over two lessons. You will have unlimited opportunities to take an untimed quiz after you’ve mastered the material, and you have two quizzes to complete for this cluster. This cluster begins by looking at the acquisition, manifestation, diagnosis, and treatment of neurocysticercosis, a helminthic infection of the nervous system caused by Taenia solium.

Taeniasis: Due to Taenia Saginatum - Dr. Mramba Nyindo5:46

Taeniasis: Pathophysiology of Taenia Saginatum - Dr. John Bartlett2:22

Taeniasis: Interview with Dr. Venance Maro 1:58

Taeniasis: Due to Taenia Solium - Dr. Mramba Nyindo6:45

Taeniasis: Pathophysiology of Taenia Solium - Dr. John Bartlett5:07

Meet the Instructors

John A. Bartlett, M.D.
Professor of Medicine, Global Health and Nursing at Duke University Medical Center
Duke Global Health Institute
Franklin Mosha, Ph.D.
Professor of Parasitology and Medical Entomology
Mramba Nyindo, Ph.D.
Associate Professor, Kilimanjaro Christian Medical University College (KCMU Co.)

Now let's discuss Taenia solium,

pathophysiology, clinical manifestations, and treatment.

Humans become infected with Taenia solium when eating

poorly cooked pork containing the cysts.

After ingestion, the oncospheres exocyst and migrate to the small intestine.

They mature into adults cestodes,

2 to 8 meters in length over the next three months.

Gravid segments containing eggs may be released into

the small intestine where they can invade the mucosa and disseminate.

Autoinfection may also occur through ingestion of

eggs via the fecal-oral route.

During dissemination, eggs migrate to muscle, brain,

intraocular locations, subcutaneous locations, or other tissue.

Once in tissue, they encyst themselves.

This is the phase known as cysticercosis.

The cysts are several millimeters to 1 to 2 centimeters in size.

In the brain, they most commonly are located in

the cerebral hemispheres at the gray-white matter junction.

They may also be found in the cerebellum, ventricles, brain stem,

subarachnoid space, basal cisterns, and spine.

Following ingestion of oncospheres, infected persons may have

GI complaints 6 to 8 weeks later as the adult worms mature.

The adult worms may live for many years causing no symptoms.

Symptoms are typically caused by encysted eggs and relate to

the organ system where they're located, most commonly the central nervous system.

Neurocysticercosis is a common cause of epilepsy in low and

middle income countries.

Neurocysticercosis may also cause headaches, hydrocephalus, and

eosinophilic meningitis.

Occasionally, cysts may degenerate and cause local inflammation.

The laboratory findings of Taenia solium infection relate to

the involved organ system.

Neurocysticercosis is commonly seen at the gray-white matter junction

on CT or MR scan.

Cysts with dead eggs may calcify.

Cysts adjacent to meningeal surfaces may rupture into ventricles or

cause eosinophilic meningitis.

During active infection, the diagnosis is made when eggs are found in the stool.

During chronic infection, biopsy will demonstrate typical cysts with eggs.

In specialized settings, there is a serologic test available.

Most commonly, the diagnosis of Cysticercosis is made based

upon clinical findings with characteristic radiological results.

Treatment of Taenia solium is offered with Albendazole,

15 milligrams per kilogram for eight days.

Alternatives include praziquantel or niclosamine.

Calcified lesions may not need treatment because the organisms are dead.

Clinicians should be aware that treatment may cause inflammation and

high risk lesions may require concurrent steroids.

Rarely, surgical resection is needed.

Let's review a case history.

A 23 year old presented at the hospital after the new onset of

generalized seizures.

His exam was unremarkable.

He was given phenytoin and his seizures resolved.

CT scan showed multiple 0.5 to

1.0 centimeter lesions in his cerebral hemispheres.

None were located near meninges or ventricles.

A clinical diagnosis of neurocysticercosis was established.

He was treated with albendazole 15 milligrams per kilogram daily for 8 days.

Importantly, he was continued on,

indefinitely, on phenytoin due to the risk of recurrent seizures.

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