The diagnostic criteria for definitive and probable neurocysticercosis are listed below:

Absolute criteria

• Biopsy of brain or spinal cord lesion showing histological evidence of tapeworm cysts
• Visualization of subretinal cysts
• Neuroimaging studies showing a scolex (head part of the tapeworm) within a cystic lesion

Neuroimaging criteria

The main neuroimaging criteria include:

• Enhancing lesions
• Cystic lesions without an apparent scolex (head part)

Confirmative neuroimaging criteria include:

• Resolution of cystic lesions following cysticidal drug therapy
• Spontaneous resolution of single small enhancing lesions
• Sequential neuroimaging studies documenting migration of ventricular cysts

Minor neuroimaging criteria include:

• Obstructive hydrocephalus (symmetric or asymmetric)
• Abnormal enhancement of basal leptomeninges

Exposure/ clinical criteria

The main exposure/clinical criteria include:

• Finding specific cysticercal antigens or anticysticercal antibodies by well-standardized immunodiagnostic tests
• Proof of household contact with tapeworm infection
• Cysticercosis outside central nervous system

Minor exposure/clinical criteria include:

• Clinical manifestations indicating neurocysticercosis
• The patient lives in region where cysticercosis is endemic

Degrees of diagnostic certainty

One of the following criteria must be met to make a definitive diagnosis:

• One absolute criterion
• Two major neuroimaging criteria along with any exposure/clinical criterion
• One confirmative and one major neuroimaging criteria along with any exposure/clinical criterion
• One major neuroimaging criterion, two exposure/clinical criteria (including at least one major exposure/clinical criteria) and exclusion of other pathologies that produce similar results.

Probable diagnosis requires one of the following:

• One major neuroimaging criteria along with any two exposure/clinical criterion
• One minor neuroimaging criteria along with at least one major exposure/clinical criterion

PORCINE CYSTICERCOSIS

Porcine cysticercosis or cysticercosis in pigs, caused by Taenia solium is a globally emerging socio-economic and public health problem. Domesticated pigs are the natural host of the parasite. They play a major role in the transmission cycle as they are close to humans and there is increase in pig farming or raising and pork consumption in many developing countries. In fact, pork is the most widely eaten meat in the world accounting for over 36% of the world meat intake. Though pigs could have massive infections, the disease is rarely associated with symptoms since most pigs are slaughtered before nine months of age, a time too short for the cysts to reach the state of degeneration and result in visible manifestations. However, the fact that Taenia solium is a leading cause of acquired epilepsy in endemic areas and the parasite was ranked first on the global scale of foodborne parasites in 2014, proves the significance and quantum of the problem.

Porcine cysticercosis is mostly caused by the larval stage of tapeworm named T. solium. Taenia asiatica is a less widespread cause of cysticercosis in pigs, with the cysts locating in the liver and viscera. Most adult and larval tapeworm infections cause little or no disease. But T. solium cysticercosis is exceptional in that the cysts are also lodged in the brain/ CNS. The caseous form of cyst contains caseous exudate which may have some calcification and develop into scars looking like rice grains. Cysticercosis in pigs are not only problematic due to the risks to humans but also cause direct problem by economic loss through condemnation of infected meat and offal.

Pigs can become infected at any age. The gravid proglottids (segment of mature worm) are shed by infected humans along with their feces. Taenia solium segments, are often passed in chains. Each of these gravid segments (proglottids) liberate up to 60,000 eggs, the greater percentage of them infective. These eggs are immediately infective when passed. Pigs feed on these feces or vegetation contaminated with these and get infected. It is possible that pigs also acquire T. solium also by ingestion of the faeces of pigs that have eaten segments. In the intestine of these pigs, the eggs hatch by shedding their outer covering and develop into oncospheres. These oncospheres traverse the intestinal wall and enter blood and lymph vessels to be carried to muscles, brain and with lesser frequency to other organs where they develop into vesicular cysticerci. In experimentally infected pigs this process takes 4 to 6 weeks after which time the immature stage of the tape worm can be identified grossly as vesicles measuring about 0.4 cm x 0.3 cm. They contain a transparent fluid with a small white structure which is the scolex (head part). Humans, in turn, ingest undercooked infected pork and thus the cycle is completed from human to pigs and from pigs, back again to humans.

Cysticercosis in pigs can be prevented by the use of chemotherapeutic agents like Oxfenbendazole and use of TSOL18 (Cysvax®) vaccine that has been registered and available for sale since November 2016. Though vaccine is effective alone, combination of vaccination and chemotherapy in pigs (99% efficacy in protecting pigs against infection when the vaccine is used in conjunction with a single dose of Oxfenbendazole) is feasible and sustainable under field conditions, taking local pig management practices into account. What is required is widespread dissemination of knowledge and use of the chemotherapeutic agents and the vaccine.