Pathogen safety data sheet: Infectious substances - Taenia solium
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- Section I: Infectious agent
- Section II: Hazard identification
- Section III: Dissemination
- Section IV: Stability and viability
- Section V: First aid and medical
- Section VI: Laboratory hazards
- Section VII: Exposure controls and personal protection
- Section VIII: Handling and storage
- Section IX: Regulatory and other information
Section I: Infectious agent
Name: Taenia solium
Synonym or cross reference: Pork tapeworm, taeniasis, cysticercosis, neurocysticercosisFootnote 1, Cysticercus cellulosaeFootnote 2Footnote 3.
Characteristics: Taenia solium is a tapeworm of the class cestoidea, order cyclophyllidea, and family TaeniidaeFootnote 1.
Adult worm: Mature worms are found only in humans. Adult worm grows to approximately 2-4 m. Scolex has 4 suckers and the rostellum has two crowns of horns. Gravid proglottids are 1 by 1 cm. The ovary consists of 2 lobes, 1 accessory lobe, and 1 genital pore. The gravid proglottids of T. solium have 12 lateral branches and no vaginal sphincter muscle.
Larvae (cysticerci): The larval stage of the T. solium is known as Cysticercus cellulosae. Cysticerci are 8-10 mm and are encompassed in a fluid filled bladder. Cysticerci may be found in the eye, spinal cord, or muscles of the intermediate hosts, and in the brain in the case of neurocysticercosis.
Eggs: Eggs are spherical with a diameter of 30-40 μm. They have a think yellow-brown radiated shell and contain a 6 hooked embryo (oncosphere). They are morphologically indistinguishable from the eggs of Taenia saginata but, unlike the eggs of T. saginata, they are infectious to humans.
Section II: Hazard identification
Pathogenicity/toxicity: Infection with an adult tapeworm is known as taeniasis and occurs only in humans, the sole definitive hostFootnote 1Footnote 4. Cysticercosis is caused by the larval stage of T. solium.
Taeniasis: Most carriers of T. solium are asymptomatic but some symptoms may occur including obstruction, diarrhea, hunger pains, weight loss and discomfortFootnote 4Footnote 5.
Cysticercosis: Larval stage can cause infection in different areas of the bodyFootnote 6. Carriers of T. solium are at substantial risk acquiring cysticercosis due to exposure to T.solium eggs via faeco-oral autoinfectionFootnote 5. Carriers can also infect members of their household, causing cysticercosis. Subcutaneous cysticercosis is more common in Asia and Africa and presents as small nodules in the arm and chest, which gradually disappear within months or years. Muscular cysticercosis is more common and show calcifications when radiographed. Opthalmic cysticercosis is rare and is caused by cysts floating in the eye. If found in the vitreous humour, they can result in impaired vision, and if found in the subretinal space, they can lead to retinal detachment. Neurocysticercosis is the result of infection in the central nervous system. Neurocysticercosis may be initially asymptomatic for many years and then present with varied nonspecific neurologic manifestations including headaches, confusion, ataxia, seizures, and meningismusFootnote 7. Epileptic seizures are the most common symptom; neurocysticercosis is the leading cause of adult onset epilepsy. Adverse affects occur when the cysticerci degenerate, eliciting an immune response.
Epidemiology: WorldwideFootnote 1Footnote 6. There is a greater prevalence in Latin America, Asia, sub-Saharan Africa, Eastern Europe and some areas of OceaniaFootnote 6Footnote 8.
Host range: Humans are the definitive hostFootnote 1Footnote 4Footnote 9Footnote 10. Cats and dogs have been shown, under strict experimental conditions to be able to act as the temporary hosts of T. solium, however the worm did not develop into the adult stage. A gibbon was experimentally infected and a gravid proglottids was recovered, showing it may act as a definitive hostFootnote 11. Pigs serve as the intermediate hostFootnote 4Footnote 9Footnote 10, however humans and dogs are also recognised as intermediate hostsFootnote 2Footnote 12.
Infectious dose: Unknown.
Mode of transmission: The intermediate host will contract T. saginata by ingesting the eggsFootnote 1Footnote 2. The eggs develop into the infective cysticercus in the tissues of the infected intermediate host. Humans contract Taeniasis by ingesting undercooked pork infested with T solium cysticerci.
In humans, cysticercosis occurs during an infection by the larval stage of T. solium when ova are ingested. The ova develop into larvae, penetrate the intestinal wall, disseminate throughout the body via the vascular system, and encyst in tissue as cysticerciFootnote 13. However, taeniasis occurs during an infection by the adult tapeworm of T solium when the human definitive host ingests cysticerci.
Incubation period: Cysticerci take 2-3 months to develop in muscle following ingestion of eggs; proglottids appear in stool within 2 months of ingestion of cysticerci Footnote 6.
Communicability: Humans acquire the infection through fecal oral contamination by infected individual hosting the mature adult parasiteFootnote 6Footnote 9 or by ingesting undercook pork infested with T solium cysticerci. Autoinfection is also possible.
Section III: Dissemination
Reservoir: Humans and pigs are the most common reservoirsFootnote 4Footnote 9Footnote 10. Dogs, cats, and non-human primates are very rarely reservoirsFootnote 2Footnote 11Footnote 12.
Zoonosis: Yes. Humans contract the pork tapeworm by ingestion raw or uncooked porkFootnote 1Footnote 2Footnote 4Footnote 14Footnote 15.
Section IV: Stability and viability
Drug susceptibility: Sensitive to albendazole and praziquantelFootnote 1Footnote 4Footnote 16.
Susceptibility to disinfectants: Susceptible to 1% sodium hypochloriteFootnote 17 and 2% glutaraldehydeFootnote 18.
Physical inactivation: Irradiation and cooking will inactivate the cycticerciFootnote 19. A minimum temperature of 60°C is required for inactivationFootnote 4. Freezing at a temperature of -10°C for 4 days will inactivate cysticerciFootnote 20.
Survival outside host: Cysticerci can survive up to 30 days in the carcass of pigs at 4°CFootnote 20. Eggs can persist in the environment for monthsFootnote 2.
Section V: First aid and medical
Surveillance: Monitor for symptoms. Microscopy is used to diagnose taeniasis by visualization of eggs and proglottids in faecesFootnote 6. However, excretion is intermittent and usually stool examination for eggs or parasites are negative. Cysticercosis is diagnosed using serological testing such as antigen detection in serum or CSF or feces. The enzyme-linked immunoelectrotransfer blot (EITB) is used to increase the specificityFootnote 21.
First aid/treatment: Infection is treated with albendazole or praziquantelFootnote 5.
Section VI: Laboratory hazards
Laboratory-acquired infections: NoneFootnote 3.
Sources/specimens: FaecesFootnote 3, muscle, brain, organs, cerebral spinal fluid (CSF)Footnote 12.
Primary hazards: Ingestion of infectious eggs or cysticerciFootnote 3.
Special hazards: During the identification process caution should be taken until a definitive identification as non-infectious T. saginata is not made confirmed as the eggs are morphologically identicalFootnote 14. The eggs are highly infectious and remain viable within the environment for many months. Taeniasis (intestinal tapeworm) is prevented by destruction, freezing or adequate heating of cysticercotic pork. In contrast human cysticercosis results from fecal-oral contamination with material containing T. solium eggs.
Section VII: Exposure controls and personal protection
Risk group classification: Risk Group 2.
Containment requirements: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or culturesFootnote 22.
Protective clothing: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashesFootnote 22.
Other precautions: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activitiesFootnote 22.
Section VIII: Handling and storage
Spills: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean upFootnote 23.
Disposal: Decontaminate all wastes that contain or have come in contact with the infectious organism by autoclave, chemical disinfection, gamma irradiation, or incineration before disposingFootnote 23.
Storage: The infectious agent should be stored in leak-proof containers that are appropriately labelledFootnote 23.
Section IX: Regulatory and other information
Updated: December 2011
Prepared by: Pathogen Regulation Directorate, Public Health Agency of Canada.
Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.
Public Health Agency of Canada, 2011
- Footnote 1
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- Footnote 2
Gajadhar, A. A., Scandrett, W. B., & Forbes, L. B. (2006). Overview of food- and water-borne zoonotic parasites at the farm level. Revue Scientifique Et Technique (International Office of Epizootics), 25(2), 595-606.
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Biosafety in Microbiological and Biomedical Laboratories (BMBL) (2007). In Richmond J. Y., McKinney R. W. (Eds.),. Washington, D.C.: Centers for Disease Control and Prevention.
- Footnote 4
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (2003). Parasitic Zoonoses. Zoonoses: Infectious Diseases Transmissible from Animals to Humans. (3rd ed., pp. 261-403). Washington, DC.: ASM press.
- Footnote 5
Cook, G. C., & Zumla, A. I. (Eds.). (2008). Manson's Tropical Diseases (22nd Edition ed.). London: Elsevier Harcourt Brace Publishing Group.
- Footnote 6
García, H. H., Gonzalez, A. E., Evans, C. A. W., & Gilman, R. H. (2003). Taenia solium cysticercosis. The Lancet, 362(9383), 547-556. doi:DOI: 10.1016/S0140-6736(03)14117-7
- Footnote 7
Carpio, A. (2002). Neurocysticercosis: an update. The Lancet Infectious Diseases, 2(12), 751-762.
- Footnote 8
Taenia solium Cysticercosis: From Basic to Clinical Science. Taenia solium cysticercosis: An overview of global distribution and transmission. (2002). In Singh G. P. S. (Ed.),. Oxford, UK: CABI.
- Footnote 9
Saini, P. K., Webert, D. W., & McCaskey, P. C. (1997). Food Safety and Regulatory Aspects of Cattle and Swine Cysticercosis. Journal of Food Protection, 60, 447.
- Footnote 10
Sinha, S., & Sharma, B. S. (2009). Neurocysticercosis: a review of current status and management. Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia, 16(7), 867-876. doi:10.1016/j.jocn.2008.10.030
- Footnote 11
Flisser, A., Avila, G., Maravilla, P., Mendlovic, F., Leon-Cabrera, S., Cruz-Rivera, M., Garza, A., Gomez, B., Aguilar, L., Teran, N., Velasco, S., Benitez, M., & Jimenez-Gonzalez, D. E. (2010). Taenia solium: current understanding of laboratory animal models of taeniosis. Parasitology, 137(3), 347-357. doi:10.1017/S0031182010000272
- Footnote 12
Sciutto, E., Chavarria, A., Fragoso, G., Fleury, A., & Larralde, C. (2007). The immune response in Taenia solium cysticercosis: protection and injury. Parasite Immunology, 29(12), 621-636. doi:10.1111/j.1365-3024.2007.00967.x
- Footnote 13
DeGiorgio, C. M., Medina, M. T., Duron, R., Zee, C., & Escueta, S. P. (2004). Neurocysticercosis. Epilepsy Currents / American Epilepsy Society, 4(3), 107-111. doi:10.1111/j.1535-7597.2004.43008.x
- Footnote 14
Parasitology. (2003). In L. S. Garcia (Ed.), Manual of Clinical Microbiology (8th ed., pp. 1895). Washington, D.C.: ASM Press.
- Footnote 15
Youn, H. (2009). Review of zoonotic parasites in medical and veterinary fields in the Republic of Korea. The Korean Journal of Parasitology, 47 Suppl, S133-41. doi:10.3347/kjp.2009.47.S.S133
- Footnote 16
Craig, P., & Ito, A. (2007). Intestinal cestodes. Current Opinion in Infectious Diseases, 20(5), 524-532. doi:10.1097/QCO.0b013e3282ef579e
- Footnote 17
Mackie, A., & Parnell, I. W. (1967). Some Observations on Taeniid Ovicides: The Effects of Some Organic Compounds and Pesticides on Activity and Hatching. J. Helmith., 41, 167.
- Footnote 18
Block, S. S. (Ed.). (2001). Disinfection, Sterilization, and Preservation (5th ed.). Philidelphia: Lippincott Williams & Wilkins.
- Footnote 19
Gamble, H. R. (1997). Parasites associated with pork and pork products. Revue Scientifique Et Technique (International Office of Epizootics), 16(2), 496-506.
- Footnote 20
Fan, P. C., Ma, Y. X., Kuo, C. H., & Chung, W. C. (1998). Survival of Taenia solium cysticerci in carcasses of pigs kept at 4 C. The Journal of Parasitology, 84(1), 174-175.
- Footnote 21
Deckers, N., & Dorny, P. (2010). Immunodiagnosis of Taenia solium taeniosis/cysticercosis. Trends in Parasitology, 26(3), 137-144. doi:10.1016/j.pt.2009.12.008
- Footnote 22
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).
- Footnote 23
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
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