Neurocysticercosis (NCC) is a parasitic infection of the nervous system caused by the tapeworm Taenia solium, also known as the "pork tapeworm". The disease is caused by ingestion of tapeworm eggs, which evolve into larvae and get into tissues such as muscle, brain, and eye, and form cysts called cysticerci.[2] Neurocysticercosis manifests with various signs and symptoms, influenced by the location, number of lesions, and immune response. While some people may have no symptoms, others may experience seizures, increased pressure in the skull, cognitive impairment, or specific neurological problems. In severe cases, the condition can be life-threatening.
Diagnosis relies on imaging and blood tests. Neurocysticercosis can be prevented through improved sanitation, education, awareness, de-worming and vaccines for endemic areas. Treatment options depend on cyst viability, the host's immune response, and the location and number of lesions. Symptoms are treated with anti-seizure, antiedema, pain, or anti-inflammatory drugs. Surgery, steroids, or other medications are used to treat intracranial hypertension. Anti-parasitic medications are used for treating earlier stages of the disease. Steroids are used to manage inflammation in the central nervous system. Surgery can be used to remove cysts.
Neurocysticercosis is common in developing regions, such as Latin America, China, Nepal, Africa, India, and Southeast Asia. Although rare in Europe and the US, immigration has increased its prevalence. Taenia solium has been recognized since 1500 BC and found in ancient Egyptian mummies. The first recorded cases of neurocysticercosis were likely in 1558. In 1792, a Peruvian physician reported simultaneous taeniasis, tapeworm infection in the intestines, and cysticercosis in the same individual. In the 19th century, German pathologists found similarities between T. solium and cysticercus scolex and discovered that consumption of cysticercus in pork caused human intestinal taeniasis.
The figure summarizes the stages of NCC lesions: living viable cysts (left), degenerating dying lesions with inflammation (center), and dead calcified lesions (right). Markers that are increased in those with active epilepsy compared with NCC-infected subjects without epilepsy are shown: 1) pro-inflammatory cytokines (tumor necrosis factor-α, interferon-γ, and interleukin 1-β) and blood–brain barrier breakdown molecules (MMP-9); 2) lymphocyte adhesion molecules; and 3) mutations in regulators of lymphocyte adhesion (Toll-like receptor 4) associated with pro-inflammatory conditions.
In areas where neurocysticercosis is common, adult-onset seizures are heavily correlated with the condition.[8] Seizures are more common in parenchymal neurocysticercosis than in other forms of neurocysticercosis;[3] they can occur at any stage of the disease.[5]Partial seizures, which affect only one side of the brain at first, are the most common type of seizures.[9] If neurocysticercosis is left untreated, seizures often persist and recur despite treatment.[10] Seizures are more commonly associated with degenerating cysts,[5] which are often accompanied by swelling, inflammation, nerve damage, and gliosis.[11][12] They are caused by inflammatory responses in the brain and the space-occupying effect of the cysts.[13][14] Multiple lesions increase the risk of seizures. Active cysts are associated with first-time seizures while calcified granulomas are associated with chronic epilepsy.[8]
Focal deficits
Those with neurocysticercosis can exhibit a variety of specific neurologic symptoms determined by the size, number, and location of the parasites. Pyramidal tract symptoms, such as weakness, Babinski's sign, spasticity, and overactive reflexes are the most common; however sensory impairments, parkinsonian rigidity, involuntary movements, language disturbances, and signs of brain-stem dysfunction can also occur. Focal neurologic symptoms are most commonly seen in those with large subarachnoid cysts compressing the brain parenchyma.[6] Inflammation in the arachnoid layer can cause focal signs, ischaemic strokes caused by intracranial artery blockage, cranial nerve compression, hearing loss, and facial nerve palsy or trigeminal neuralgia. There may also be focal neurological symptoms caused by brainstem damage. Cysticercosis of the spinal cord often causes radicular pain, weakness, and sensory impairments due to localized mass effects or inflammation in the subarachnoid space.[9]
Intracranial hypertension
CT scan of the head of a patient with neurocysticercosis showing presence of hydrocephalus and dilation of ventricles
Intracranial hypertension – a build-up of pressure around the brain – is associated with neurocysticercosis and may be accompanied by other symptoms.[6] More common in extraparenchymal neurocysticercosis,[5] it is most frequently caused by buildup of cerebrospinal fluid in the brain.[6][9] Hydrocephalus can be related to granular ependymitis, compression of the CSF pathways by cysts, cysticercotic arachnoiditis, and inflammation or cysts blocking ventricles.[6][5] Large subarachnoid cysts and cyst clumps can also cause a mass effect and intracranial hypertension, with or without hydrocephalus.[16] Intracranial hypertension can present as episodic loss of consciousness when moving the head, known as Bruns syndrome; [6] it may be subacute or chronic.[9] Cysticercotic encephalitis, which is a severe type of neurocysticercosis usually affecting younger women and children can also cause intracranial hypertension.[5] Cysticercotic encephalitis is characterized by seizures, intracranial hypertension, clouding of consciousness, optic disc swelling, headache, reduction of visual acuity, and vomiting.[17][18]
Spinal arachnoiditis can cause subacute root pain and weakness. Cysts in the spinal cord are typically associated with motor and sensory impairments that vary depending on the location of the lesion. Those with cysticerci in the sellar region may have vision and hormonal issues. In the eyes, cysticerci are usually found in the subretinal space, causing a gradual reduction in visual acuity or visual field abnormalities. The cysts can cause inflammation of the vitreous membrane, uveitis, and endophthalmitis, which is the most serious complication of ocular cysticercosis and can result in eye shrinkage. Cysticercal infection in striated muscles can cause weakening and englargment over time.[17]
Causes
Neurocysticercosis is caused by the larvae of the tapeworm Taenia solium.[20] Neurocysticercosis often results from undercooked infected pork or other food, or contaminated water.[21][22] Once someone consumes Taenia solium, cysticerci are released into the small intestine.[21] The head of the tapeworm (scolex) then evaginates and attaches to the intestinal wall. When the scolex attaches, it grows into a tapeworm which penetrates the intestinal wall and gets into the bloodstream where it can travel the rest of the body.[23][24]
Taenia solium is a tapeworm in the Cestoda class and is a species of the genus Taenia.[23] It has two hosts, pigs and humans. Pigs and humans can act as intermediate hosts for the larval form, but humans are the only definitive hosts for the adult tapeworm. The larvae are cystic, fluid-filled sacs containing a tapeworm head (scolex) with four suckers and a double row of hooks, along with a narrow neck and a body made up of hundreds of segments called proglottids. When a person eats pork infected with cysts, the scolex (the head of the tapeworm) evaginates and clings to the intestinal wall using its suckers and hooks. Once attached, the segments of the tapeworm, called proglottids, multiply and grow. Within about four months, the tapeworm matures into a ribbon-like structure, measuring 2–4 meters long.[21][24]
When humans consume T. solium eggs, the eggs hatch into larvae, which penetrate the intestinal wall and spread throughout the body, leading to cysticercosis. Although the cysts can form in any tissue, they are most commonly found in the central nervous system, skeletal muscle, skin, and eyes.[25] Cysticerci enter the central nervous system as live parasites (vesicular stage) with a transparent membrane, clear fluid, and a scolex (head) tucked inside. They can survive for years, but the host’s immune response may sometimes cause them to degenerate into inactive nodules. In the colloidal stage, the fluid inside the cyst becomes cloudy, and the scolex begins to break down. Next, the cyst wall thickens, and the scolex hardens into small mineralized granules, marking the granular stage when the cyst is no longer active. Eventually, the parasite remnants fully calcify, forming hardened nodules in the calcified stage.[23][26]
Diagnosis
Diagnosing neurocysticercosis can be challenging, especially in resource-limited areas, as available methods are often unreliable or inaccessible.[27] Physical examination and laboratory testing are often not helpful in diagnosing neurocysticercosis.[28] Diagnosis mainly relies on neuroimaging and blood tests.[29] Diagnostic criteria have also been created to help with the diagnostic process.[30]
Immunodiagnosis
The lentil lectin purified glycoprotein (LLGP) enzyme-linked immunoelectrotransfer blot (EITB) assay, is the most reliable test for detecting T. solium antibodies in the blood. This method uses specific proteins to identify the presence of these antibodies.[27] Antibodies can be identified in EITB as early as five weeks after infection. The LLGP-EITB has a sensitivity of 98% for individuals with multiple brain cysts and a specificity of 100%. However, its sensitivity is lower in cases with just one cyst.[28] The ELISA test for detecting anticysticercal antibodies in cerebrospinal fluid (CSF) is 89% sensitive and 93% specific for active neurocysticercosis infections. It is often used as an alternative when the EITB test is unavailable.[31]
Different presentation patterns of extraparenchymal neurocysticercosis as revealed by brain MRI
As many as 37% of those with neurocysticercosis have high eosinophils, making it the most common blood abnormality in neurocysticercosis. The number of people with positive stool tests for Taenia solium eggs in neurocysticercosis varies and seems to depend on how severe the infection is. Recognizing Taenia eggs is difficult, and many cases may go undetected during testing.[17]
Neuroimaging
CT and MRI give objective information about number and pattern of lesions, the stage of healing, and how the immune system is responding to the parasites.[17] MRI is better for evaluating different spatial planes and provides clearer images, which helps in identifying small lesions at the back of the brain or near the skull that may be missed on CT scans. CT is more sensitive at detecting calcium buildup in the brain due to its ability detect calcifications in the brain.[28]
Live vesicular cysts are small, round lesions with little swelling around them and do not need contrast for imaging. The tapeworm head (scolex) usually appears as an asymmetric nodule inside the cysts. Multiple live cysts with these heads corroborate the diagnosis. Once the cysts begin to break down (colloid cysts), their borders become unclear, they are surrounded by swelling and exhibit significant ring or nodular contrast enhancement. Calcified cysticerci are shown on CT scans as non-enhancing hyperdense nodules without swelling.[18]
Diagnostic criteria
(A) Gadolinium-enhanced magnetic resonance imaging (MRI) of the brain showing evidence of a fourth ventricular cystic structure. (B) Histopathology of a surgically removed cyst with i) cuticular layer with microvilli, ii) cellular layer, and iii) reticular layer. (C) Dissected cyst (neurocysticercosis) protruding from fourth ventricle. (D) Cyst post-excision.
Resolution of cystic lesions after antiparasitic drug therapy.
Spontaneous resolution of single small enhancing lesions.[d]
Migration of ventricular cysts[e] documented on sequential neuroimaging studies.
Minor neuroimaging criteria:
Obstructive hydrocephalus (symmetric or asymmetric) or abnormal enhancement of basal leptomeninges.
Clinical/exposure criteria:
Major clinical/exposure:
Detection of specific antibodies or antigens related to cysticercosis by well-standardized immunodiagnostic tests.[f]
Cysticercosis outside the central nervous system.[g]
Evidence of household contact with T. solium infection.
Minor clinical/exposure:
Clinical manifestations suggestive of neurocysticercosis.[h]
Individuals coming from or living in an area where cysticercosis is endemic.[i]
Classification
Neurocysticercosis can be classified into two main types: parenchymal, which affects the brain tissue, and extraparenchymal, which occurs outside the brain tissue.[35]
Parenchymal neurocysticercosis: neurocysticercosis lesions within brain parenchyma.[35]
Viable parenchymal cysts: contains the scolex, typically between 0.5 and 2 cm in diameter.[36]
Single enhancing lesion (solitary cysticercal granuloma): One or two smaller cysts.[36]
Massive infections: hundreds of cysts and a large number of larvae.[36]
Extraparenchymal neurocysticercosis: lesions in ventricles or subarachnoid spaces.[35]
Ventricular neurocysticercosis: cysts in the brain ventricles.[37]
Subarachnoid neurocysticercosis: cysticerci in the subarachnoid space.[38]
Other locations
Spinal neurocysticercosis: neurocysticercosis in the spine, often the extramedullary subarachnoid spaces.[12]
Retinal neurocysticercosis: cysts effecting the retina.[12]
Prevention
Neurocysticercosis is preventable.[39] Some factors that make T. solium potentially eradicable are humans being the only definitive host, the intermediate host being an animal whose exposure to ova can be controlled, well-developed diagnostic testing allowing infected individuals to be identified, effective treatments available, and the availability of pig vaccines.[40]
Neurocysticercosis is more prevalent in areas where the transmission of T. solium is more likely, such as areas with improper disposal of waste, lower levels of education, improper slaughter of pigs, and free-roaming pigs.[41] Unsanitary conditions and domestic pigs are required for T. solium to be transmitted. Urbanization and development reduce these factors, therefore transmission goes down. Because neurocysticercosis takes years to develop, intervention programs can take decades.[42]
To prevent neurocysticercosis, interventions such as increasing education, improving sanitary conditions, and strict animal husbandry and meat inspection procedures are needed. Medical prevention includes de-worming people with medications such as niclosamide or praziquantel, and vaccinating and treating pigs with oxfendazole.[39] Raised awareness of neurocysticercosis in non-endemic countries where rates are increasing is also important. The TSOL18 vaccine, which is made up of a recombinant protein from a T. soliumoncosphere is a promising solution for the prevention and control of neurocysticercosis. Increasing public health surveillance, such as obligatory notification of neurocysticercosis cases, could also be beneficial. Properly identifying neurocysticercosis is needed to target interventions.[43]
In 1985 in Ecuador praziquantel was used for de-worming, and was eventually used in other countries. In Honduras, transmission and morbidity decreased after the health education and control program. A big elimination program managed to eliminate transmission in 105 out of 107 villages by using pig vaccines, human and porcine mass chemotherapy, and stool coproantigen case confirmation.[44]
Treatment
A single treatment method is not appropriate for every person with neurocysticercosis. The disease has to be characterized in terms of cyst viability, the degree of the host's immunological response to the parasite, and the location and number of lesions to provide proper treatment.[45] Symptomatic and antiparasitic medications are typically used in conjunction for treatment. Surgery can also be used to remove cysts.[46][47]
Brain CT of neurocysticercosis before (A and B) and after (C and D) treatment with albendazole
Neurocysticercosis is a persistent infection, with symptoms appearing months or years later. As a result, removing the parasite is not an emergency, and the first step in treating those with neurocysticercosis is often aimed at minimizing the symptoms. This may be done with the use of antiepileptic, antiedema, analgesic, or anti-inflammatory drugs.[49]Carbamazepine is commonly used to control seizures.[42][50] Antiepileptic medications may be used till after a year without seizures.[51] Surgery, acetazolamide, steroids, or mannitol may be used to help manage intracranial hypertension.[49]
Steroid administration is an important step in the modulation of neurocysticercosis-related inflammation in the central nervous system, since it controls the acute inflammatory response that occurs following the destruction of live cysts. Prednisolone and dexamethasone are frequently used as adjuncts to antiparasitic therapy.[45][52][53]
The two most commonly used antiparasitic medications are albendazole, an imidazole that inhibits glucose absorption and metabolism in the parasite, and praziquantel,[52] an isoquinoline which triggers parasite paralysis by altering calcium pathways and homeostasis.[45] Taking days to months to work,[54][42] antiparasitic drugs are only appropriate for the treatment of vesicular viable cysts or cysts in the early colloidal phases of development, and are ineffective against calcified cysts,[45] nor can they be given when there is a preexisting risk of developing hydrocephalus, such as with sub-arachnoid neurocysticercosis or encephalitic neurocysticercosis; in these cases, the inflammation that occurs after treatment may pose a significant risk of rapidly raising intracranial pressure and death.[55]
Antiparasitic medication may be ineffective in cases of severe infection due to the hazards associated with mass inflammation, but these forms of neurocysticercosis carry a high risk of consequences if left untreated. In some circumstances, a more aggressive treatment plan, including surgery, may be required.[43] Surgical treatments include ventricle-peritoneal shunts and excision of cysts.[42][46]
Outlook
The prognosis for neurocysticercosis depends on the number and location of the cysts. Single enhancing lesion neurocysticercosis typically has a good prognosis, with lesions resolving within 6 months in over 60% of cases. Multiple or calcified lesions increase the risk of seizure relapses.[39] Although psychiatric and cognitive changes are common with neurocysticercosis, they are usually not severe enough to affect day-to-day behaviour.[56]
Parenchymal neurocysticercosis also has a good prognosis.[56] Parenchymal neurocysticercosis prognosis is mediated by the number of lesions and the severity of the inflammation.[9] Over half of those with calcified parenchymal neurocysticercosis have relapses in seizures and need antiseizure medications long-term.[56]
Extraparenchymal neurocysticercosis does not respond to antiparasitic treatment as well as parenchymal neurocysticercosis, meaning that multiple types or courses of treatment are sometimes needed. Complications from treatment such as shunt blockage or vasculitis are also more prevalent with extraparenchymal neurocysticercosis.[56] Extraparenchymal neurocysticercosis can lead to obstructive hydrocephalus and death.[57]
Epidemiology
Geographic maps of Indonesia (upper) showing endemic areas of three human Taenia species ( T. asiatica, endemic in North Sumatra; T. saginata and T. solium, endemic in Bali; and T. solium, endemic in Papua) and Bali (lower)
Neurocysticercosis is endemic in most developing countries, except predominantly Muslim countries.[59][60] It is endemic in Latin America, China, Nepal, Africa, India, and Southeast Asia. It is more common in poorer countries with improper sanitation and a lack of clean water.[23]Taenia solium is considered rare in developed countries and is usually a result of people contracting Taenia solium while travelling or immigration. Reports of neurocysticercosis are growing from several wealthy nations, including the USA and the UK, as a result of increased globalization and worldwide travel.[60] Most cases of neurocysticercosis in the US have been reported in the southwestern states. Around 90% of neurocysticercosis diagnoses in the US were immigrants from Mexico or South America.[61]
Studies conducted in endemic countries have shown that neurocysticercosis is a common cause of increased rates of epilepsy.[61] In endemic regions, CNS infection is extremely common; in many of these groups, the frequency of certain serum antibodies is more than 10%, and residual intraparenchymal brain calcifications on CT scans are seen in 10–20% of the general population.[60] Neurocysticercosis is estimated to affect 29% of those with epilepsy.[60] About 15% of the pig farming community in India has asymptomatic neurocysticercosis.[60] According to a North Indian study, the prevalence of neurocysticercosis in rural India was 4.5 per 1000.[60] Twenty-five percent of individuals with active epilepsy had antibodies against T. solium, based on another study from North India.[60] In an Indian hospital series, neurocysticercosis was responsible for more than half of the instances of children with partial seizures.[60]
History, society, and culture
Descriptions of Taenia solium tapeworms date back to 1500 BC.[62]Taenia solium cysticerci have even been found in ancient Egyptian mummies.[59] The first recorded cases of neurocysticercosis were most likely described by German physician John Wolfgang Rumler in 1558.[62][63]Hipólito Unanue, a Peruvian physician and journalist, is believed to have first recorded simultaneous taeniasis and cysticercosis in the same individual in 1792: he reported a case involving a soldier with taeniasis who died following a violent seizure.[62][59][64] During the 19th century, German pathologists noticed the morphological parallels between the adult T. solium head and the cysticercus scolex. Friedrich Küchenmeister showed that the consumption of cysticercus from pork caused human intestinal taeniasis by feeding a prisoner food that included cysticerci gathered from a recently killed pig.[59][62] In the second part of the 19th century, research showed that feeding Taenia eggs from infected humans to pigs caused cysticercosis.[59][64]
Neurocysticercosis was featured in the "Pilot" episode of House M.D. The episode followed a young woman who contracted neurocysticercosis after eating contaminated ham.[65]
↑ Round, well-defined lesions filled with fluid that looks similar to cerebrospinal fluid on CT or MRI scans.[34]
↑ One or more ring-shaped or nodular lesions, 10-20mm in size, with or without swelling, without displacing midline structures.[34]
↑ One or more solid lesions, usually smaller than 10mm.[34]
↑ The administration of corticosteroids renders this criterion invalid.[34]
↑ Follow-up CT or MRI scans show that the locations of the cystic lesions in the ventricles change over time.[34]
↑ Antibody identification by enzyme-linked immunoelectrotransfer blot test employing lentil lectin-purified T. solium antigens, and cysticercal antigen detection by monoclonal antibody-based ELISA.[34]
↑ Cysticerci can be identified through a biopsy of subcutaneous lumps, X-ray films or CT scans that reveal cigar-shaped calcifications in soft tissues, or detection of the parasite in the anterior chamber of the eye.[34]
↑ Mostly seizures (typically beginning in persons aged 20-49 years; the diagnosis of seizures in this setting is not disregarded if patients are outside of the normal age range), but other signs include chronic headaches, focal neurologic impairments, intracranial hypertension, and cognitive deterioration.[34]
↑ A location where active transmission is recorded.[34]
Related Research Articles
Brain abscess is an abscess within the brain tissue caused by inflammation and collection of infected material coming from local or remote infectious sources. The infection may also be introduced through a skull fracture following a head trauma or surgical procedures. Brain abscess is usually associated with congenital heart disease in young children. It may occur at any age but is most frequent in the third decade of life.
Cysticercosis is a tissue infection caused by the young form of the pork tapeworm. People may have few or no symptoms for years. In some cases, particularly in Asia, solid lumps of between one and two centimetres may develop under the skin. After months or years these lumps can become painful and swollen and then resolve. A specific form called neurocysticercosis, which affects the brain, can cause neurological symptoms. In developing countries this is one of the most common causes of seizures.
Praziquantel (PZQ), sold under the brandname Biltricide among others, is a medication used to treat a number of types of parasitic worm infections in mammals, birds, amphibians, reptiles, and fish. In humans specifically, it is used to treat schistosomiasis, clonorchiasis, opisthorchiasis, tapeworm infections, cysticercosis, echinococcosis, paragonimiasis, fasciolopsiasis, and fasciolosis. It should not be used for worm infections of the eye. It is taken by mouth.
Taenia solium, the pork tapeworm, belongs to the cyclophyllid cestode family Taeniidae. It is found throughout the world and is most common in countries where pork is eaten. It is a tapeworm that uses humans as its definitive host and pigs as the intermediate or secondary hosts. It is transmitted to pigs through human feces that contain the parasite eggs and contaminate their fodder. Pigs ingest the eggs, which develop into larvae, then into oncospheres, and ultimately into infective tapeworm cysts, called cysticerci. Humans acquire the cysts through consumption of uncooked or under-cooked pork and the cysts grow into adult worms in the small intestine.
Taenia is the type genus of the Taeniidae family of tapeworms. It includes some important parasites of livestock. Members of the genus are responsible for taeniasis and cysticercosis in humans, which are types of helminthiasis belonging to the group of neglected tropical diseases. More than 100 species are recorded. They are morphologically characterized by a ribbon-like body composed of a series of segments called proglottids; hence the name Taenia. The anterior end of the body is the scolex. Some members of the genus Taenia have an armed scolex ; of the two major human parasites, Taenia saginata has an unarmed scolex, while Taenia solium has an armed scolex.
Taenia saginata, commonly known as the beef tapeworm, is a zoonotic tapeworm belonging to the order Cyclophyllidea and genus Taenia. It is an intestinal parasite in humans causing taeniasis and cysticercosis in cattle. Cattle are the intermediate hosts, where larval development occurs, while humans are definitive hosts harbouring the adult worms. It is found globally and most prevalently where cattle are raised and beef is consumed. It is relatively common in Africa, Europe, Southeast Asia, South Asia, and Latin America. Humans are generally infected as a result of eating raw or undercooked beef which contains the infective larvae, called cysticerci. As hermaphrodites, each body segment called proglottid has complete sets of both male and female reproductive systems. Thus, reproduction is by self-fertilisation. From humans, embryonated eggs, called oncospheres, are released with faeces and are transmitted to cattle through contaminated fodder. Oncospheres develop inside muscle, liver, and lungs of cattle into infective cysticerci.
Echinococcus granulosus, also called the hydatid worm or dog tapeworm, is a cyclophyllid cestode that dwells in the small intestine of canids as an adult, but which has important intermediate hosts such as livestock and humans, where it causes cystic echinococcosis, also known as hydatid disease. The adult tapeworm ranges in length from 3 mm to 6 mm and has three proglottids ("segments") when intact—an immature proglottid, mature proglottid and a gravid proglottid. The average number of eggs per gravid proglottid is 823. Like all cyclophyllideans, E. granulosus has four suckers on its scolex ("head"), and E. granulosus also has a rostellum with hooks. Several strains of E. granulosus have been identified, and all but two are noted to be infective in humans.
Taenia crassiceps is a tapeworm in the family Taeniidae. It is a parasitic organism whose adult form infects the intestine of carnivores, like canids. It is related to Taenia solium, the pork tapeworm, and to Taenia saginata, the beef tapeworm. It is commonly found in the Northern Hemisphere, especially throughout Canada and the northern United States.
Taenia pisiformis, commonly called the rabbit tapeworm, is an endoparasitic tapeworm which causes infection in lagomorphs, rodents, and carnivores. Adult T. pisiformis typically occur within the small intestines of the definitive hosts, the carnivores. Lagomorphs, the intermediate hosts, are infected by fecal contamination of grasses and other food sources by the definitive hosts. The larval stage is often referred to as Cysticercus pisiformis and is found on the livers and peritoneal cavities of the intermediate hosts. T. pisiformis can be found worldwide.
Taeniasis is an infection within the intestines by adult tapeworms belonging to the genus Taenia. There are generally no or only mild symptoms. Symptoms may occasionally include weight loss or abdominal pain. Segments of tapeworm may be seen in the stool. Complications of pork tapeworm may include cysticercosis.
Eucestoda, commonly referred to as tapeworms, is the larger of the two subclasses of flatworms in the class Cestoda. Larvae have six posterior hooks on the scolex (head), in contrast to the ten-hooked Cestodaria. All tapeworms are endoparasites of vertebrates, living in the digestive tract or related ducts. Examples are the pork tapeworm with a human definitive host, and pigs as the secondary host, and Moniezia expansa, the definitive hosts of which are ruminants.
Sparganosis is a parasitic infection caused by the plerocercoid larvae of the genus Spirometra including S. mansoni, S. ranarum, S. mansonoides and S. erinacei. It was first described by Patrick Manson in 1882, and the first human case was reported by Charles Wardell Stiles from Florida in 1908. The infection is transmitted by ingestion of contaminated water, ingestion of a second intermediate host such as a frog or snake, or contact between a second intermediate host and an open wound or mucous membrane. Humans are the accidental hosts in the life cycle, while dogs, cats, and other mammals are definitive hosts. Copepods are the first intermediate hosts, and various amphibians and reptiles are second intermediate hosts.
Professor Marshall Lightowlers began his career in the field of parasitology during a post-doctoral appointment at the Institute of Medical and Veterinary Science in Adelaide where he undertook research on ovine sarcocystosis. In 1981 he began a post-doctoral position at The University of Melbourne, Veterinary Clinical Centre and commenced a research career focusing on the immunology and molecular biology of taeniid cestode parasites. His initial research at the University of Melbourne investigated the immunochemistry of antigens of Taenia taeniaeformis and Echinococcus granulosus. Subsequently he was a member of a team of scientists that developed a vaccine against Taenia ovis infection in sheep, the first recombinant vaccine against a parasitic disease. In 1989 Lightowlers took over leadership of the molecular parasitology research laboratories at the University of Melbourne and began applying the lessons learnt with T. ovis to the development of similar vaccines against infection with the larval stages of other cestode parasites. This led to the development of highly effective, recombinant vaccines against cysticercosis in cattle due to Taenia saginata (TSA9/TSA18) and in pigs due to Taenia solium. In collaboration with Dr David Heath at the Wallaceville Animal Research Centre in New Zealand, he and his colleagues also developed the EG95 recombinant vaccine against cystic echinococcosis.
Human parasites include various protozoa and worms.
Coenurosis is a parasitic infection that results when humans ingest the eggs of dog tapeworm species Taenia multiceps, T. serialis, T. brauni, or T. glomerata.
Taenia asiatica, commonly known as Asian taenia or Asian tapeworm, is a parasitic tapeworm of humans and pigs. It is one of the three species of Taenia infecting humans and causes taeniasis. Discovered only in 1980s from Taiwan and other East Asian countries as an unusual species, it is so notoriously similar to Taenia saginata, the beef tapeworm, that it was for a time regarded as a slightly different strain. But anomaly arose as the tapeworm is not of cattle origin, but of pigs. Morphological details also showed significant variations, such as presence of rostellar hooks, shorter body, and fewer body segments. The scientific name designated was then Asian T. saginata. But the taxonomic consensus turns out to be that it is a unique species. It was in 1993 that two Korean parasitologists, Keeseon S. Eom and Han Jong Rim, provided the biological bases for classifying it into a separate species. The use of mitochondrial genome sequence and molecular phylogeny in the late 2000s established the taxonomic status.
Taenia serialis, also known as a canid tapeworm, is found within canines such as foxes and dogs. Adult T. serialis are parasites of carnivores, particularly dogs, with herbivorous lagomorph mammals such as rabbits and hares, serving as intermediate hosts. In definitive hosts, T. serialis is acquired by eating tissues from a variety of intermediate hosts. Accidental infection of humans though, can occur when eggs are ingested from food or water contaminated with dog feces and the human then becomes the T. serialis intermediate host.
Taenia hydatigena is one of the adult forms of the canine and feline tapeworm. This infection has a worldwide geographic distribution.
Taeniasis-Cysticercosis may refer to different presentations of Taenia-tapeworm infection:
Cysticercus is a scientific name given to the young tapeworms (larvae) belonging to the genus Taenia. It is a small, sac-like vesicle resembling a bladder; hence, it is also known as bladder worm. It is filled with fluid, in which the main body of the larva, called scolex, resides. It normally develops from the eggs, which are ingested by the intermediate hosts, such as pigs and cattle. The tissue infection is called cysticercosis. Inside such hosts, they settle in the muscles. When humans eat raw or undercooked pork or beef that is contaminated with cysticerci, the larvae grow into adult worms inside the intestine. Under certain circumstances, specifically for the pork tapeworm, the eggs can be accidentally eaten by humans through contaminated foodstuffs. In such case, the eggs hatch inside the body, generally moving to muscles as well as inside the brain. Such brain infection can lead to a serious medical condition called neurocysticercosis. This disease is the leading cause of acquired epilepsy.
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