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NAME: Trichuris trichiura

SYNONYM OR CROSS REFERENCE: Trichocephalus trichiurus , Trichocephalus dispar , Trichocephalus hominis , trichuriasis, whipworm, trichocephaliasis, and trichocephalosis(1,2,3,4,5,6,7,8)

CHARACTERISTICS: Trichuris trichiura is a gastrointestinal nematode in the family Trichuridae , genus Trichuris(5). T. trichiura adult parasites are characterized by a long thin anterior end that lies in a burrow in the host mucosa, and thicker end that extends into the intestinal lumen. The worms are white in colour and roughly 30 to 50 mm in length(3,7). The male worm, which is smaller than the female, has a coiled posterior end when viewed in vitro(3,5,8). The female worm sheds between 3,000 and 20,000 eggs per day(2). The distinguishing feature of T. trichiura is the stichosome, which is a glandular structure encircling the slender oesophagus of the thin anterior half of the worm(2,5).

Adult worms are long lived, typically living for up to 5 years in their host(7). At the second stage of T. trichiura 's life cycle, the larva measures roughly 260 μm x 15 μm in length(5). The eggs of T. trichiura are lemon (or barrel) shaped with a characteristic plug at either end, giving it a tea tray appearance(2,3,5,8). They are usually brown in human stool samples and typically measure from 50-55 μm by 22-24 μm; however, much larger (78 by 30 μm) eggs gave been observed in stool samples from humans infected with T. trichiura, and for that reason it is somewhat difficult to distinguish the eggs of T. trichiura from those of other members of the Trichuris genus ( T. suis and T. vulpis ) by measurement alone(3,4,7,9).


PATHOGENICITY/TOXICITY: The whip-like anterior portion of the worm usually attaches itself to the mucosa of the caecum and upper colon(3). The severity of the disease is dependant on the intensity of the infection in the gastrointestinal tract, and the variables associated with the host, such as age, general health, and iron reserves(8). In supersensitive persons, infection can lead to non-specific responses such as nervousness, anorexia and urticaria. In light infections, most cases are asymptomatic(1,8). In moderate infections of 20 adult worms or less, the worms are confined to the caecum and the ascending colon. Symptoms include epigastric and lower abdominal pain, diarrhoea (rarely bloody), vomiting, flatulence and distention, headache, weight loss, and increased blood and iron loss(2,3,4,8). In heavy infections of 200 adults worms or more (Trichuris dysentery syndrome), the worms are in the distal colon and rectum; therefore, symptoms include bloody diarrhoea with profuse mucous, abdominal pain and tenesmus, weight loss leading to cachexia, severe anaemia, rectal prolapse, moderate eosinophilia, and the "clubbing" of fingers(1,2,3,8). Chronic infection leads to impaired childhood growth, poor physical fitness and nutritional status(6). T. trichiura is also believed to suck blood from the colon and it is estimated that about 0.005 ml of blood is lost per day per worm(2,3). In heavy infections, as much as 4 to 5 ml can be lost per day per worm. Combination infections with other worm type organisms such as Ascaris lumbricoides , Necator amercanus, and Ancylostoma duodenale can lead to growth stunting, intellectual retardation, and cognitive educational defects(6).

EPIDEMIOLOGY: Worldwide, although T. trichiura is most common in warm, moist, tropical and sub-tropical countries(1,2,3,4,7,8). Prevalence in children can be over 90%(6). An estimated 604 to 795 million persons harbour T. trichiura(6). Typically the most intense infections are in children aged 5 to 15 years(3,6,7), with a decline in intensity and frequency in adulthood(6).

HOST RANGE: Humans are the principal host, although infections in chimpanzees, pigs, lemurs, and monkeys have also been reported(2,3,4,10).


MODE OF TRANSMISSION: Ingestion of infective eggs from contaminated soils, hands, food, or water (eggs require a minimum of 15 to 30 days in warm moist soil to become infective)(3,4,5,6,11). After the ingestion of Trichuris eggs, the released larvae moult in the small intestine, lodge into the crypts for about 2 to 3 days, and then move to the caecum and colon where they burrow into the epithelia and develop into adult whipworm within about 12 weeks(4,7). Eggs appear in faeces about 70 to 90 days after ingestion and carriers may shed eggs for years if not treated(1).

INCUBATION PERIOD: Uncertain, however the period from egg ingestion to egg production is reported to occur in three months(2,4,7).

COMMUNICABILITY: No clear evidence for direct human-to-human transmission(1).


RESERVOIR: Humans are the primary reservoir(1,2,3,4,5,6,7,8,9,10,12).

ZOONOSIS: None(1,2).

VECTORS: None known.


DRUG SUSCEPTIBILITY: T.trichirua is more resistant to drugs than other soil transmitted nematodes. Several anthelminthics, including ivermectin, effective against Ascaris, fail against Trichuris(13). Mebendazole or albendazole, however, are effective and recommended(3,4,5,6,8).

SUSCEPTIBILITY TO DISINFECTANTS: Unknown; however, 30% (v/v) ammonia in combination with temperatures above 30°C is documented to inactivate T. muris (mouse whipworm) eggs(12).

PHYSICAL INACTIVATION: T. trichiura eggs are sensitive to sunlight and will perish below -9 °C and above 52 °C(3,8).

SURVIVAL OUTSIDE HOST: T. trichiura eggs will survive in soil for around 2 weeks(4).


SURVEILLANCE: Monitor for symptoms. Eggs can be identified in faeces. Confirm presence of T. trichiura adult parasites within the large intestine by colonoscopy(3,8). The intensity of infection is measured by the number of eggs per gram of faeces, generally by the Kato-Katz faecal thick-smear technique(6).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: The benzimidazole anthelmintics, mebendazole, and albendazole are commonly used to treat trichuriasis(6,8). Mebendazole is poorly absorbed from the gastrointestinal tract so its therapeutic activity is largely confined to adult worms(6). Albendazole is better absorbed, especially when ingested with fatty meals, and the drug is metabolised in the liver to a sulphoxide derivative, which has a high volume of distribution in the tissues.


PROPHYLAXIS: Mebendazole and albendazole are used for large-scale prevention of morbidity in children living in endemic areas(6). Other measures include the improvement of environmental hygiene through adequate disposal of excreta to avoid contamination of the soil, personal hygiene, washing of raw foods and of hands, and the boiling or filtering of suspicious water(3,4).



SOURCES/SPECIMENS: Faeces and infective eggs(1,2,3,4,5,6,8,9,10).

PRIMARY HAZARDS: Ingestion of infective eggs(1,2,3,4,5,6,8,9,10).




CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

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 to splashes(14).

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(14). Additional precautions should be considered with work involving animals or large scale activities(14).


SPILLS: Allow aerosols to settle and while wearing protective clothing, gently cover the spill with paper towels and apply suitable disinfectant, starting at the perimeter, working inwards towards the centre. Allow sufficient contact time before clean up (30 minutes)(14).

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and/or incineration(14).

STORAGE: In sealed containers that are appropriately labelled(14).


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: August 2010.

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.

Copyright ©
Public Health Agency of Canada, 2010


  1. Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th Edition ed.). Washington, D.C.: American Public Health Association.
  2. Bundy, D. A., & Cooper, E. S. (1989). Trichuris and trichuriasis in humans. Advances in Parasitology, 28 , 107-173.
  3. Wolfe, M. S. (1978). Oxyuris, trichostrongylus and trichuris. Clinics in Gastroenterology, 7(1), 201-217.
  4. Acha, P. N., & Szyfres, B. (2003). Trichuriasis of Animal Origin. Zoonoses and Communicable Diseases Common to Man and Animals (3rd ed., pp. 302-304). Washington D.C.: Pan American Health Organization.
  5. Holland, C. V. (2006). Gastrointestinal nematodes - Ascaris , hookworm, Trichuris , and Enterobius . In F. E. G. Cox, D. Wakelin, S. H. Gillespie & D. D. Despommier (Eds.), Topley & Wilson's Microbiology and Microbal Infections (10th ed., pp. 713-736). Oxford U.K.: Wiley-Blackwell.
  6. Bethony, J., Brooker, S., Albonico, M., Geiger, S. M., Loukas, A., Diemert, D., & Hotez, P. J. (2006). Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm. Lancet, 367 (9521), 1521-1532.
  7. Ash, L. R., & Orihel, T. C. (2003). Intestinal Helminths. In P. R. Murrary (Ed.), Manual of Clinical Microbiology (8th ed., pp. 2031-2060). Washington D.C.: ASM Press.
  8. Stephenson, L. S., Holland, C. V., & Cooper, E. S. (2000). The public health significance of Trichuris trichiura. Parasitology, 121 (SUPPL.), S73-S95.
  9. Yoshikawa, H., Yamada, M., Matsumoto, Y., & Yoshida, Y. (1989). Variations in egg size of Trichuris trichiura. Parasitology Research, 75 (8), 649-654.
  10. Horii, Y., & Usui, M. (1985). Experimental transmission of Trichuris ova from monkeys to man. Transactions of the Royal Society of Tropical Medicine and Hygiene, 79 (3), 423.
  11. (2004). In D. L. Heymann (Ed.), Control of Communicable Diseases Manual (18th ed., pp. 551-552). Washington, D.C.: American Public Health Association.
  12. Ghiglietti, R., Rossi, P., Ramsan, M., & Colombi, A. (1995). Viability of Ascaris suum, Ascaris lumbricoides and Trichuris muris eggs to alkaline pH and different temperatures. Parassitologia, 37 (2-3), 229-232.
  13. Ranque, S., Chippaux, J. P., Garcia, A., & Boussinesq, M. (2001). Follow-up of Ascaris lumbricoides and Trichuris trichiura infections in children living in a community treated with ivermectin at 3-monthly intervals. Annals of Tropical Medicine and Parasitology, 95 (4), 389-393. doi:10.1080/00034980120065822
  14. 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.