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Taenia Infection

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Of the 32 recognized species of Taenia, only Taenia solium (pork tapeworm) and Taenia saginata (beef tapeworm) are medically important. However, recent epidemiologic studies in Southeast Asia have identified a third Taenia species in humans, known as Taenia asiatica. [1, 2] Taeniasis is an infection due to an adult tapeworm in the intestine. Humans acquire taeniasis from ingestion of undercooked pork containing cysticerci. Cysticercosis is the development of extraintestinal encysted larval forms of T. solium in various organs. Humans develop cysticercosis from ingestion of T. solium egg excreted by themselves (autoinfection), or by a human tapeworm carrier which means humans can have cysticercosis even though they do not eat pork. (see Cysticercosis). The CNS is involved in 60-90% of cases; this condition is termed neurocysticercosis (NCC). For more information, see Neurocysticercosis.

Differentiating between T. solium and T. saginata infections is important because infection with T. solium can cause neurocysticercosis, which is one of the leading cause of deaths from food-borne illnesses, resulting in a total of 2.8 million disability-adjusted life-years (DALYs) according to the World Health Organization (WHO). [3] Cysticercosis caused by T. saginata is rare; T. saginata has far lower impact on human health than T. solium. Both infections are endemic in Southeast Asia, Africa, Europe, and Central and South America. Infection in children usually goes unrecognized. [4]  WHO developed a roadmap for control and eradication of T. solium taeniasis/cysticercosis to be implemented in selected countries by 2020. [3]

Humans are the definitive host. Adult tapeworms live in the human small intestine. Humans pass gravid eggs in feces; these mature eggs contaminate pastures and barnyards, where cattle and pigs ingest them. Upon reaching the alimentary canal of infected animals, the embryos are released, penetrate the gut wall, and enter the circulation. The embryos filter from the circulation and encyst in muscular tissue. Larvae (ie, cysticerci) become infectious within 2-3 months. Humans develop a tapeworm infection by eating raw or undercooked beef or pork containing cysticerci. The cysticercus becomes activated, attaches to the wall of the small intestine by the scolex, and becomes a mature tapeworm. This maturation process takes 10-12 weeks for T. saginata and 5-12 weeks for T. solium. A single tapeworm produces an average of 50,000 eggs per day and may live up to 25 years.

Pigs are the intermediate host for T. solium and T. asiatica. The larvae of T. solium has predilection to infect the muscles and brain of pigs, however, the larvae of T. asiatica tends to infect pig viscera especially pig liver. Cows are the intermediate host for T. saginata with the larvae predominantly found in the muscle.

Humans can also act as an intermediate host for T. solium. Cysticercosis results from human ingestion of T. solium eggs through fecal contamination, reverse peristalsis of gravid proglottids, or autoinfection. The cysticerci may develop in any organ, and their effects depend entirely on the location of the cysticerci.

A coenurus is the larval stage of Taenia multiceps, Taenia serialis, and Taenia brauni. Adult tapeworms develop in dogs or other canids that ingest coenurus larvae in the tissues of various intermediate hosts. These hosts include sheep, goats, hares, rabbits, and other herbivores for T multiceps; hares, rabbits, and other rodents for T. serialis; and gerbils for T. brauni. Each protoscolex within a coenurus can mature into an adult tapeworm after ingestion by a canid host. Adult worms produce eggs, which are passed in feces; these eggs are morphologically similar to taeniid eggs. Ingestion of eggs by an appropriate intermediate host or by humans leads to development of coenurus. Coenuri are cysts that contain many protoscolices attached in rows on the internal membrane of the cyst.

United States

Cysticercosis is primarily an imported disease. Approximately 1000 cases are diagnosed each year. Most occur in persons who have immigrated, primarily from Latin America. [5] Cysticercosis has also developed following close contact with recently immigrated, infected individuals. Although some patients with NCC are born in the United States, many have traveled to rural areas in countries where the condition is endemic. Locally acquired infections have been confirmed in Los Angeles, New York, Chicago, Oregon, [6, 7] and elsewhere. Although T. saginata infection occurs worldwide, prevalence in the United States is less than 1% because most US cattle are free of the parasite.

A study analyzed in-patient records using the Nationwide Inpatient Sample for 1998-2011 to estimate cysticercosis-related hospitalizations and patient/institutional characteristics in the United States. The study reported that there were an estimated 33,060 cysticercosis-related hospitalizations nationwide, representing a hospitalization rate of 8.03 per million population. The study further reported that the highest proportion of cases were male (54.8%), Hispanic (62.0%), aged 18-44 (58.8%), and occurred in the West (45.1%). An estimated 459 deaths occurred, representing an in-hospital case-fatality rate of 1.4%. [8]

International

Approximately 50 million people worldwide are infected by T. saginata or T. solium. Approximately 50,000 people die annually of cysticercosis. T. saginata is common in cattle-breeding regions. Areas with the highest (ie, >10%) prevalence are central Asia, the Near East, and central and eastern Africa. [9, 10, 11] Areas with low (ie, 1%) prevalence are Southeast Asia, Europe, and Central and South America.

T. solium is endemic in Central and South America, Southeast Asia, [12, 13, 14] India, the Philippines, Africa, [15] Eastern Europe, and China. Areas of highest prevalence include Latin America and Africa. In some regions of Mexico, prevalence may reach 3.6% of the general population.

A study of school aged children from 27 schools in China showed overall prevalence of T. solium cysticercosis to be 6%. In three schools the prevalence was 15% or more. Risk factors for cysticercosis included pig ownership, feeding pigs with human feces, and worms in their feces. Schools with higher prevalence had more students with households that have free range pigs and practice open defecation. [16]

T. multiceps has been reported in the Americas and parts of Europe and Africa.

T. serialis infections occur in the United States and Canada.

T. brauni has been reported in Africa.

Most intestinal taeniid infections are asymptomatic. When symptoms occur, they are usually mild and involve abdominal pain, anorexia, weight loss, or malaise. Cysticercosis causes a mass effect in various vital organs (eg, brain, eye, heart). The mortality rate for cysticercosis is low and is generally caused by complications such as encephalitis, increased intracranial pressure secondary to edema and/or hydrocephalus, and stroke.

All races are equally affected.

Both genders are equally affected.

All ages are susceptible to infection. The age at which raw meat consumption begins is the primary determinant. T. solium taeniasis has been reported in children older than 2 years in certain rural communities of Mexico.

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Supatida Tengsupakul, MD Assistant Professor of Pediatrics, University of South Alabama College of Medicine; Pediatric Hospitalist and Pediatric Infectious Diseases Specialist, Department of Pediatrics, USA Children’s and Women’s Hospital

Supatida Tengsupakul, MD is a member of the following medical societies: American Academy of Pediatrics, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Ashir Kumar, MD, MBBS FAAP, Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS is a member of the following medical societies: Infectious Diseases Society of America, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Sowmya Nanjappa, MD Assistant Member, Department of Internal Medicine, Moffitt Cancer Center; Assistant Professor of Medicine, Department of Internal Medicine and Department of Oncologic Sciences (Joint Appointment), University of South Florida Morsani College of Medicine

Sowmya Nanjappa, MD is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Physicians, American Medical Association, Infectious Diseases Society of America, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Michael D Nissen, MBBS, FRACP, FRCPA Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children’s Hospital

Disclosure: Nothing to disclose.

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