The female T. trichiura produces 2,000–10,000 single-celled eggs per day.[3] Eggs are deposited from human feces to soil where, after two to three weeks, they become embryonated and enter the "infective" stage. These embryonated infective eggs are ingested by hand-mouth or through fomites and hatch in the human small intestine, exploiting the intestinal microflora as a stimulus to hatching.[4] This is the location of growth and molting. The infective larvae penetrate the villi and continue to develop in the small intestine. The young worms move to the caecum and penetrate the mucosa, and there they complete development as adult worms in the large intestine. The life cycle from the time of ingestion of eggs to the development of mature worms takes approximately three months. During this time, there may be limited signs of infection in stool samples, due to a lack of egg production and shedding. The female T. trichiura begin to lay eggs after three months of maturity. Worms commonly live for about one year,[5] during which time females can lay up to 20,000 eggs per day.
Recent studies using genome-wide scanning revealed that two quantitative trait loci on chromosome 9 and chromosome 18 may be responsible for a genetic predisposition or susceptibility to infection of T. trichiura by some individuals.[6]
Morphology
Trichuris trichiura has a narrow anterior esophageal end and shorter and thicker posterior end. These pinkish-white worms are threaded through the mucosa. They attach to the host through their slender anterior end and feed on tissue secretions instead of blood. Females are larger than males; approximately 35–50 mm long compared to 30–45 mm.[7] The females have a bluntly round posterior end compared to their male counterparts with a coiled posterior end. Their characteristic eggs are barrel-shaped and brown, and have bipolar protuberances.
Trichuriasis, also known as whipworm infection, occurs through ingestion of whipworm eggs and is more common in warmer climates. Whipworm eggs are passed in the feces of infected persons, and if an infected person defecates outdoors or if untreated human feces is used as fertilizer, eggs are deposited on soil where they can mature into an infective stage.[5] Ingestion of these eggs "can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled."[5] The eggs hatch in the small intestine, then move into the wall of the small intestine and develop. On reaching adulthood, the thinner end (the anterior of the worm) burrows into the large intestine, the thicker (posterior) end projecting into the lumen, where it mates with nearby worms. The females can grow to 50 mm (2.0 in) long.[3]
Trichuris trichiura can cause the serious disease Trichuris dysentery syndrome (TDS), with chronic dysentery, anemia, rectal prolapse, and poor growth.[8] TDS is treated with anthelminthics as well as iron supplementation for anemia.[9]
Trichuris trichiura can be treated with a single dose of albendazole.[11] In Kenya, half of a group of children, 98% of whom had Trichuris trichiura with or without infections by other soil-transmitted helminths, were given albendazole, while the other half of the children received placebos. It was found that the children who received the drug grew significantly better than the group of children who did not receive the treatment.[12] Another treatment that can be used is mebendazole, or flubendazole.[13] The medication interferes with the parasite’s nutrient intake, which eventually leads to death.
However, it has been shown that both albendazole and mebendazole have low cure rate for Trichuris thrichiura specifically, with treatments only achieving cure rates 30,7% for albendazole and 42,1% for mebendazole.[14]
Epidemiology
There is a worldwide distribution of Trichuris trichiura, with an estimated one billion human infections.[15][16][17][8] However, it is chiefly tropical, especially in Asia and, to a lesser degree, in Africa and South America. Within the United States, infection is rare overall but may be common in the rural Southeast, where 2.2 million people are thought to be infected. Poor hygiene is associated with trichuriasis as well as the consumption of shaded moist soil, or food that may have been fecally contaminated. Children are especially vulnerable to infection due to their high exposure risk. Eggs are infective about 2–3 weeks after they are deposited in the soil under proper conditions of warmth and moisture, hence its tropical distribution.
A closely related species, Trichuris suis, which typically infects pigs, is capable of infecting humans. This shows that the two species have very close evolutionary histories. However, morphology and developmental stages remain different, making them two separate species.[18]
WHO have since 2001 had a strategy for control of soil-transmitted helminths, including whipworms. This strategy entails treating at-risk individuals in the endemic areas. Risk groups for whipworm infections are children at preschool and school-aged children, people with specific high-risk jobs, women in reproductive and pregnant and breastfeeding women. The periodic treatment of the risk groups is done through either deworming campaigns or preventative chemotherapy.[19]
The hygiene hypothesis suggests that various immunological disorders that have been observed in humans only within the last 100 years, such as Crohn's disease, or that have become more common during that period as hygienic practices have become more widespread, may result from a lack of exposure to parasitic worms (helminths) during childhood. The use of Trichuris suis ova (TSO, or pig whipworm eggs) by Weinstock, et al., as a therapy for treating Crohn's disease[20][21][22] and to a lesser extent ulcerative colitis[23] are two examples that support this hypothesis. There is also anecdotal evidence that treatment of inflammatory bowel disease (IBD) with TSO decreases the incidence of asthma,[24][self-published source?]allergy,[25] and other inflammatory disorders.[26] Some scientific evidence suggests that the course of multiple sclerosis may be very favorably altered by helminth infection;[27] TSO is being studied as a treatment for this disease.[28][29]
^Stephenson LS, Latham MC, Kurz KM, Kinoti SN, Brigham H (July 1989). "Treatment with a Single Dose of Albendazole Improves Growth of Kenyan Schoolchildren with Hookworm, Trichuris Trichiura, and Ascaris Lumbricoides Infections". The American Journal of Tropical Medicine and Hygiene. 41 (1): 78–87. doi:10.4269/ajtmh.1989.41.78. PMID2764230.
^Stephenson LS, Latham MC, Adams EJ, Kinoti SN, Pertet A (1993). "Physical Fitness, Growth and Appetite of Kenyan School Boys with Hookworm, Trichuris trichiura and Ascaris lumbricoides Infections Are Improved Four Months After a Single Dose of Albendazole". The Journal of Nutrition. 123 (6): 1036–1046. doi:10.1093/jn/123.6.1036 (inactive 1 November 2024). PMID8505663.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
^Beer, RJ (January 1976). "The relationship between Trichuris trichiura (Linnaeus 1758) of man and Trichuris suis (Schrank 1788) of the pig". Research in Veterinary Science. 20 (1): 47–54. doi:10.1016/S0034-5288(18)33478-7. PMID1257627.
^Buning, J; et al. (March 2008). "Helminths as governors of inflammatory bowel disease". Gut. 57 (8): 1182–1183. doi:10.1136/gut.2008.152355. PMID18628388. S2CID29967284. in our patient Treg [regulatory T cells] activated by helminthosis [T. suis infestation] were most likely the key element protecting a host with latent ulcerative colitis against development of a severe protcocolitis. (1183)
^Correale J, Farez M (2007). "Association between parasite infection and immune responses in multiple sclerosis". Annals of Neurology. 61 (2): 97–108. doi:10.1002/ana.21067. PMID17230481. S2CID1033417.