Cysticercosis

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

Cysticercosis is an infection caused by the larval stages of the parasite Taenia solium, after a person ingests tapeworm eggs. The larvae embed in tissues such as muscle and brain, forming cysticerci (cysts).

The earliest reference to tapeworms was found in the works of ancient Egyptians that date back to almost 2000 BC.^[1].Cysticercosis is caused by the infestation of the larvae of Taenia Solium to various tissues (brain, muscles, eye .. etc).

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.

Cysticercosis is classified according to the site of cysticerci into Neurocysticercosis and extraneural cysticercosis. Neurocysticercosis is further subdivided into Parenchymal and extra-parenchymal.

Cysticercosis is more prevalent in underdeveloped countries in Africa, Latin America and Southeast Asia, especially in rural areas where humans are in direct contact with pigs and sanitary conditions, are not optimum.

Poor sanitary habits, contact with pigs and living in an endemic area are the main risk factors for having cysticercosis.

Patients with cysticercosis and their household should be screened for intestinal tapeworm. High-risk persons should be screened for cysticercosis if they are to be employed as food handlers or housekeepers.

Cysticercosis is treated easily with antihelminthic drugs and even untreated patients can remain silent for long periods. Complications can develop in the intestine if the tapeworm grows enough to cause obstructions or at the sites of cysticerci when they start to degenerate and provoke the immune system.

Presenting symptoms differ according to the site of the cysticerci. Parenchymal neurocysticercosis causes all the symptoms and signs of space occupying lesions. Extraparenchymal neurocysticercosis causes manifestations of increased intracranial pressure if cysts are present in the subarachnoid space or in the ventricles, manifestations of spinal cord compression if present in the spinal cord or causes eye disease if cysts are present in the orbit.

There is no single gold standard for diagnosing cysticercosis (except for biopsy which is rarely done). Diagnosis is made by combing data from various investigation and suspecting the disease. A set of diagnostic criteria was proposed in 2001 based on a combination of epidemiological factors, clinical manifestations, laboratory and radiological investigations.

Computerized tomography (CT) is superior to magnetic resonance imaging (MRI) for demonstrating small calcifications. However, MRI shows cysts in some locations (cerebral convexity, ventricular ependyma) better than CT, is more sensitive than CT to demonstrate surrounding edema and may show internal changes indicating the death of cysticerci.

Cysticercosis is generally treated with a combination of both anti-parasitic drugs and anti-inflammatory drugs. Symptomatic treatment is the mainstay therapy for neurocysticercosis. Surgical removal is sometimes necessary to treat ophthalmic cysticercosis and subcutaneous cysticercosis.

Surgery is not the first line of treatment except in ocular cysticercosis and other certain cases of neurocysticercosis.

Prevention against intestinal taeniasis is the main strategy for prevention of cysticercosis.

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

The earliest reference to tapeworms was found in the works of ancient Egyptians that date back to almost 2000 BC.^[1]

• The description of pork measles in the History of Animals written by Aristotle (384–322 BC) showed that the infection of pork with tapeworm was known to ancient Greeks at that time.^[1]
• It was also known to Jewish^[2] and later to early Muslim physicians and has been proposed as one of the reasons for pork being forbidden by Jewish and Islamic dietary laws.^[3]
• Recent examination of evolutionary histories of hosts, parasites, and DNA evidence show that over 10,000 years ago, ancestors of modern humans in Africa became exposed to tapeworm when they scavenged for food or preyed on antelopes and bovids, and later passed the infection on to domestic animals such as pigs.^[4]
• An African cysticercosis research was allegedly referred to by Du Huan in the 8th century inChina.
• Cysticercosis was described by Johannes Udalric Rumler in 1555; however, the connection between tapeworms and cysticercosis had not been recognized at that time.^[5]
• Around 1850, Friedrich Küchenmeister fed pork containing cysticerci of T. solium to humans awaiting execution in a prison, and after they had been executed, he recovered the developing and adult tapeworms in their intestines.^[1][5]
• By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T. solium.^[6]

Template:WikiDoc Sources

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

Cysticercosis is classified according to the site of cysticerci into neurocysticercosis and extraneural cysticercosis. Neurocysticercosis is further subdivided into Parenchymal and extra-parenchymal.

Cysticercosis can be classified according to the site of infestation by the cysts into:^[1]

• Inside brain parenchyma (most common site)^[1]

• Eyes (ocular cysticercosis)
• Meninges
• Brain ventricles
• Subarachnoid space
• Spinal cord

• Cutaneous cysticercosis
• Muscular cysticercosis

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

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.

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.

• 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)

• 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 humans having intestinal tapeworm disease (teniasis) are the source of infection.

• 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

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

• 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)

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

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

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

• 
  Image reveals the presence of numbers of pork tapeworm, Taenia solium cysticerci, which had contaminated this sample of porcine muscle tissue. From Public Health Image Library (PHIL). ^[4]
• 
  Image reveals the presence of numbers of pork tapeworm, Taenia solium cysticerci, which had contaminated this sample of porcine muscle tissue. From Public Health Image Library (PHIL). ^[4]

Template:WikiDoc Sources

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

Cysticesrosis is caused by infestation of the larvae of Taenia solium to various tissues (Brain, Muscles, eye ,etc).

• Cysticercosis is caused by the larval form of Taenia solium (pork tapeworm). Taenia solium is a member of Phylum Platyhelminthes, class Cestoda, Order Cyclophyllidea and family Taeniidae. The common larval stage of Taenia solium was also known as Cysticercus cellulosae.
• T. solium worms may reach a length of several meters.
• The scolex has four suckers, and a double crown of prominent hooks, which attach to the intestinal mucosa.T. solium eggs are spherical and 30 to 40 µm in diameter.^[1]
• The cysticercus larva completes development in about 2 months. It is semi-transparent, opalescent white, and elongate oval in shape and may reach a length of 0.6 to 1.8  cm.

• 
  Micrograph reveals the morphology of a Taenia solium tapeworm scolex with its four suckers, and two rows of hooks. From Public Health Image Library (PHIL). ^[2]
• 
  Iimage depicts two Taenia solium cysticerci, which represent the larval, or intermediate, immature developmental stages of this pork tapeworm. From Public Health Image Library (PHIL). ^[2]
• 
  Photomicrograph depicted the “scolex”, or head region of the cestode, Taenia saginata tapeworm. From Public Health Image Library (PHIL). ^[2]
• 
  Photomicrograph of a brain tissue specimen revealed the presence of cysticerci in a case of cysticercosis, an infection due to the ingestion of eggs of a pork tapeworm, Taenia solium. Infestation of the brain tissue by larval tapeworms is known as neurocysticercosis (100X mag). From Public Health Image Library (PHIL). ^[2]
• 
  Photomicrograph depicts some of the ultrastructural details exhibited by a Taenia sp. ovum, i.e., egg (400X mag). From Public Health Image Library (PHIL). ^[2]
• 
  Photomicrograph depicts some of the ultrastructural morphology exhibited by three Taenia solium proglottids (8X mag). From Public Health Image Library (PHIL). ^[2]

Template:WikiDoc Sources

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

Cysticercosis must be differentiated from other diseases that cause brain cystic lesions (as brain abscess and brain tumors) or ocular lesions (as retinal detachment and coats disease).

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

Cysticercosis is more prevalent in underdeveloped countries in Africa, Latin America and Southeast Asia, especially in rural areas where humans are in direct contact with pigs and sanitary conditions, are not optimum.

• It is estimated that 50 million human have cysticercosis (may be an underestimate due to the high number of asymptomatic cases).^[1]

• Cysticercosis is widely endemic in rural areas of Latin America, Asia, and Africa. In these countries, prevalence is highest in rural areas where humans are in close contact with pigs and sanitary conditions are poor.

• Prevalence is low in areas inhabited by Muslims and Jews (who do not eat pork due to religious beliefs), proving the importance of pigs as an intermediate host.

• During the 1980s, however, neurocysticercosis has been increasingly recognized in the United States through improved brain imaging by CT and MRI. Most cases have been diagnosed in the western states among immigrants from areas with endemic cysticercosis. In addition, from 1988 through 1990, 7.3% of 138 cases reported to the Los Angeles Department of Health Services were acquired locally (i.e., in patients born in the United States who had not traveled to foreign countries with endemic cysticercosis). Epidemiologic investigation of these cases identified as possible sources of infection household contact with persons who had imported tapeworm infections.

• A subtype might be prevalent in certain areas regardless of the total prevalence of the disease. For example, cutaneous cysticercosis is more prevalent in India than it is in Latin America despite the fact that cysticercosis is generally more prevalent in Latin America.

Template:WikiDoc Sources

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

Poor sanitary habits, contact with pigs and living in an endemic area are the main risk factors for having cysticercosis.

Statistically proven risk factors are:^[1]

1. Poor defaecating habits
2. Inability to identify pork infected with cysticercosis
3. History of passing Taenia proglottides
4. History of raising pigs
5. Feeding human faeces to pigs
6. Using pigs barn as a toilet
7. Using dipping method for washing hands ^[2]

Template:WikiDoc Sources

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

Patients with cysticercosis and their household should be screened for intestinal tapeworm. High risk persons should be screened for cysticercosis if they are to be employed as food handlers or housekeepers.

• Patients with cysticercosis, their household and other personal contacts should be screened for tapeworm infection since treatment with a single dose of niclosamide or praziquantel will eradicate the tapeworm and remove a potential source of transmission.
• Consideration should be given to screening persons at high risk for T. solium infections for intestinal parasites if those persons are to be employed as food handlers or housekeepers.
• Persons having household or other close contact (i.e., contact that exposes them to inadvertent infection through the fecal-oral route) with a person with a documented tapeworm should be screened for cysticercosis by medical history and serologic testing; if such an assessment suggests cysticercosis, neurologic examination and brain scan is advised.

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

Cysticercosis is treated easily with antihelminthic drugs and even untreated patients can remain silent for long periods. Complications can develop in the intestine if the tapeworm grows enough to cause obstructions or at the sites of cysticerci when they start to degenerate and provoke the immune system.

Most of the cases remain asymptomatic for long periods. Symptoms and signs arise in some patients with cyst degeneration and subsequent provocation of the immune system.

Tapeworm can grow inside the digestive tract and reach a length of 30 feet. It can cause obstruction at various sites in the GIT as:

• Appendix
• Bile duct
• Pancreatic duct

• Seizures
• Neurological deficits
• Hydrocephalus (80%)^[1]
• Cerebral infarcts (64%)
• Mental disorders (43%)

Cysticerci can be located anywhere in the orbit: in the retina, subretinal space, vitreous, anterior chamber or even in the extraocular muscles. Many patients go asymptomatic while others may have:

• Chorioretinitis
• Retinal detachment
• Blindness in advanced cases after 3-5 years^[2]

• Prognosis differs from patient to patient and depends on the site and number of cysts.
• On neuroimaging, single ring enhancing lesion is associated with better prognosis.^[3]
• Retinal and subretinal infestation have the worst prognosis and are the most difficult to treat.
• In 13 years (1990 – 2001), deaths from cysticercosis in the united states were 221 cases.^[4]

• The greater majority of the cases were Latinos followed by whites .. The ethnicity of the cases were as the following:

1. Latinos: 84.6%
2. White: 6.8%
3. Blacks: 5.9%
4. Asian: 2.3%
5. Native American: 0.5%

Template:WikiDoc Sources