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Whipworm infection

This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Trichuris trichiura.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2], Aravind Kuchkuntla, M.B.B.S[3], Usama Talib, BSc, MD [4], Syed Hassan A. Kazmi BSc, MD [5]

Synonyms and keywords: Trichuriasis, Human whipworm infection, Trichocephalus, Trichuriose

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

Trichuris trichiura is the third most common nematode worldwide, following Ascaris and Enterobius infections. Infection is acquired by the ingestion of embryonated eggs from contaminated drinking water and food. Whipworm causes disease by colonic mucosal invasion by the adult worm, resulting in inflammation of the colonic mucosa. In most cases, whipworm infection causes no clinical symptoms, but a severe infection can cause abdominal pain, diarrhea, constipation, weight loss, and anemia. The diagnosis of whip worm infection is confirmed by a stool examination for ova and parasites, which may demonstrate the presence of whipworm eggs. Whip worm eggs are barrel-like with two polar plugs. Medical therapy with antihelminthic medications is the primary modality of treatment, using albendazole, mebendazole, and ivermectin. Primary prevention measures include maintaining proper hygiene, hand washing, encouraging people not to defecate outdoors, and improving sewage disposal systems.

Historical Perspective

In 1761, Roederer described whipworm for the first time. In 1771, Carl Linnaeus coined the binomial name for human whipworm as Trichuris trichiura. The human whipworm (Trichuris trichiura) is generally considered “heirloom,” since it is found in African non-human primates, and parasite eggs were found in fossilized human feces in archaeological sites before animal domestication and before the Columbian colonization. The origin of human Trichuris is believed to be in Africa, where the parasite was transmitted to humans through early primates.

Classification

Trichuriasis infection is classified by the World Health Organization (WHO) for helminth control programs based on the number of eggs per gram of feces into light, moderate, and heavy infection.

Pathophysiology

Infection is acquired by the ingestion of embryonated eggs from contaminated drinking water and food. The eggs, once ingested, hatch in the small intestine, and the larvae enter the intestinal crypts. The larve migrate to the proximal colon and mature into adult worms. The females begin to oviposit 60 to 70 days after infection and shed between 3,000 and 20,000 eggs per day. Whipworm causes disease by colonic mucosal invasion of the adult worms, resulting in inflammation of the colonic mucosa.

Causes

The human whipworm (Trichuris trichiura or Trichocephalus trichiuris) is a round worm that causes trichuriasis. It is commonly known as the whipworm which refers to the shape of the worm; it looks like a whip with wider “handles” at the posterior end.

Differentiating whipworm infection from other diseases

Trichuris trichiura must be differentiated from other nematode infections, such as ascariasis, hook worm infection, and Strongyloides stercoralis, that can present with diarrhea and abdominal pain.

Epidemiology and Demographics

Trichuris trichiura is the third most common nematode worldwide following Ascaris and Enterobius; in total, the three infections affect approximately 1 billion people. Whip worm infection is endemic in tropical and subtropical countries. The prevalence of Trichuris trichiura is high, affecting 95% of children in countries where protein energy malnutrition and anemias are prevalent.

Risk Factors

Risk factors predisposing patients to the development of whip worm infection include low socio-economic status, low levels of education, poor sanitation, and poor hygiene.

Screening

There is insufficient evidence to recommend routine screening for Whipworm infection.

Natural History, Complications and Prognosis

In most cases, whipworm infection causes no clinical symptoms. A heavy whipworm infection (greater than 10,000 eggs per gram of feces) infection can cause abdominal pain, diarrhea, constipation, weight loss, and anemia. If left untreated, severe infection can result in Trichuris dysentery syndrome. Complications of heavy whipworm infection include chronic dysentry, rectal prolapse, and growth retardation. Prognosis is excellent with antihelminthic treatment and complete recovery occurs in 1 to 2 weeks.

Diagnosis

History and Symptoms

The majority of patients with light trichuriasis infection are asymptomatic. Trichuriasis presents with weight loss, bloody diarrhea, abdominal pain, tenesmus, and rectal prolapse in patients with moderate to heavy infection.

Physical Examination

There are no specific physical examination findings associated with whip worm infection. Patients with severe infection may present with pallor, finger nail clubbing, rectal prolapse, and abdominal tenderness.

Laboratory Findings

The diagnosis of whip worm infection is confirmed by a stool examination for ova and parasites. It will demonstrate the presence of whipworm eggs. There are no specific laboratory findings associated with whip worm infection. Chronic blood loss may demonstrate an iron deficiency anemia on peripheral blood smear with microcytic and hypochromic anemia.

EKG

There are no specific EKG findings associated with whipworm infection.

Chest X-Ray

There are no specific chest X-Ray findings associated with whipworm infection.

CT Scan

CT scan findings are non specific in patients with whipworm infection, but irregular nodular colonic thickening of the cecum and the ascending colon may be present.

Other Imaging Findings

A double contrast barium enema will demonstrate the presence of multiple tiny target-like or pinwheel shaped collections of barium, associated with s-shaped filling defects and appearance characteristic of a male worm with a coiled tip.

Other Diagnostic Findings

The other diagnostic studies for whip worm infection include stool examination for ova and parasitescolonoscopy, and an abdominal ultrasound. Whip worm eggs are barrel-like with two polar plugs. Colonoscopy is not routinely indicated, but it can be performed in patients with non specific symptoms and a negative stool test for the presence of eggs.

Treatment

Medical Therapy

Medical therapy with antihelminthic medications is the primary modality of treatment. The treatment options include albendazolemebendazole, and ivermectin.

Surgery

Surgery is not recommended for the treatment of whipworm infection.

Prevention

Primary Prevention

Primary prevention measures include maintaining proper hygiene, hand washing, encouraging people not to defecate outdoors, and improving sewage disposal systems.

Secondary Prevention

Secondary preventive measures for whip worm infection are similar to the primary preventive measures.

References

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2], Syed Hassan A. Kazmi BSc, MD [3]

Overview

In 1761, Roederer described whipworm for the first time. In 1771, Carl Linnaeus coined the binomial name for human whipworm as Trichuris trichiura. The human whipworm (Trichuris trichiura) is generally considered “heirloom,” since it is found in African non-human primates, and parasite eggs were found in fossilized human feces in archaeological sites before animal domestication and before the Columbian colonization. The origin of human Trichuris is believed to be in Africa, where the parasite was transmitted to humans through early primates.

Historical Perspective

Whipworm and Humans: An evolutionary perspective

  • Since the evolution of humans and the genus Homo, for the past four million years, there has been continuous contact between humans and many parasites.
  • Parasites infecting humans today have different evolutionary origins and can be broadly divided into two groups:
    • Parasites transmitted to humans through primates, which are referred to as “heirloom.”
    • Parasites acquired more recently through contact with animals (e.g. during animal domestication in the Neolithic period roughly 10,000 years ago), which are referred to as “souvenirs.”[1]
  • The human whipworm (Trichuris trichiura) is generally considered “heirloom,” since it is found in African, non-human primates, and parasite eggs were found in human fossilized feces in archaeological sites before animal domestication and before the Columbian colonization.[2]

Demographic History

  • Discovery of whipworm in different parts of the world may be explained by human migrations to various parts of the world.[3]
  • The origin of human Trichuris is believed to be in Africa, where the parasite was transmitted to humans through early primates. When pigs evolved in China, they presumably acquired whipworms.[4][5]
  • Phylogenetic analysis shows that the human whipworm clustered into separate clades demographically. The first divergence for human T. trichiura occurred between the Ugandan and China/Ecuador populations (over 500,000 generations ago). Then, a second split between the China and Ecuador populations (120,000 generations) occurred. This again supports the theory of T. trichiura originating in Africa and spreading to Asia and South America by human activity.

Discovery and Binomial Nomenclature

  • In 1761, Roederer described whipworm for the first time.[6]
  • In 1771, Carl Linnaeus coined the binomial name for human whipworm as Trichuris trichiura.

References

  1. Cox FE (2002). “History of human parasitology”. Clin. Microbiol. Rev. 15 (4): 595–612. PMC 126866. PMID 12364371.
  2. Cox FE (2002). “History of human parasitology”. Clin. Microbiol. Rev. 15 (4): 595–612. PMC 126866. PMID 12364371.
  3. Hawash MB, Betson M, Al-Jubury A, Ketzis J, LeeWillingham A, Bertelsen MF, Cooper PJ, Littlewood DT, Zhu XQ, Nejsum P (2016). “Whipworms in humans and pigs: origins and demography”. Parasit Vectors. 9: 37. doi:10.1186/s13071-016-1325-8. PMC 4724142. PMID 26800683.
  4. Hawash MB, Betson M, Al-Jubury A, Ketzis J, LeeWillingham A, Bertelsen MF, Cooper PJ, Littlewood DT, Zhu XQ, Nejsum P (2016). “Whipworms in humans and pigs: origins and demography”. Parasit Vectors. 9: 37. doi:10.1186/s13071-016-1325-8. PMC 4724142. PMID 26800683.
  5. “Whipworms in humans and pigs: origins and demography | Parasites & Vectors | Full Text”.
  6. Tokmak N, Koc Z, Ulusan S, Koltas IS, Bal N (2006). “Computed tomographic findings of trichuriasis”. World J Gastroenterol. 12 (26): 4270–2. PMC 4087392. PMID 16830393.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

Trichuriasis infection is classified by the World Health Organization (WHO) for helminth control programs based on the number of eggs per gram of feces into light, moderate, and heavy infection.

Classification

Trichuriasis infection is classified by the WHO for helminth control programs based on the number of eggs per gram of feces: [1]

  • Light infection: 1-999 eggs per gram of feces
  • Moderate infection: 1000 – 9999 eggs per gram of feces
  • Heavy infection: Greater than 10,000 eggs per gram of feces

References

  1. Stephenson, L.S.; Holland, C.V.; Cooper, E.S. (2001). “The public health significance of Trichuris trichiura”. Parasitology. 121 (S1): S73. doi:10.1017/S0031182000006867. ISSN 0031-1820.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Usama Talib, BSc, MD [2], Syed Hassan A. Kazmi BSc, MD [3]

Overview

Infection is acquired by the ingestion of embryonated eggs from contaminated drinking water and food. The eggs, once ingested, hatch in the small intestine, and the larvae enter the intestinal crypts. The larve migrate to the proximal colon and mature into adult worms. The females begin to oviposit 60 to 70 days after infection and shed between 3,000 and 20,000 eggs per day. Whipworm causes disease by colonic mucosal invasion of the adult worms, resulting in inflammation of the colonic mucosa.

Pathophysiology

Life cycle

Life Cycle of Trichiuris trichiura – Source: https://www.cdc.gov/

1. The eggs develop into a two-cell stage.

2. The two-cell stage then leads to an advanced cleavage stage.

3. The eggs embryonate.

4. Eggs become infective in 15 to 30 days.

5. Mature adult worms travel in the colon.

6. The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The life span of the adult worm is approximately 1 year.

Transmission

  • Whipworm infection is acquired by the ingestion of embryonated eggs from contaminated drinking water and food.

Pathogenesis

Molecular pathology

Secreted molecules by whipworm Role in pathogenesis
Trichuris trichiura 47 (TT47) Forms pores in cecal epithelial cells[4]
Excretory secretory products (ES products) Promote Th2/Treg response that decreases intestinal inflammation[5]
Trichinella spiralis macrophage inhibitory factor (TsMIF) Inhibits migration of macrophages by inhibiting host macrophage inhibitory factor[6]

Host response

Associated Conditions

Gross Pathology

Rectal prolapse in whipworm infection

Microscopic Pathology

Colonic Biopsy

Black arrows showing worm embeded in mucosa of colon and white arrow showing one end of worm in lumen

Stool Examination

  • A stool examination for ova and parasites reveals the presence of whipworm eggs.
  • The diagnostic characteristics are:[14]
    • A typical barrel shape
    • Two polar plugs that are unstained
    • Size: 50 to 54 µm by 22 to 23 µm
    • The external layer of the shell of the egg is yellow-brown (in contrast to the clear polar plugs).
T. trichiura egg


References

  1. Elston DM (2006). “What’s eating you? Trichuris trichiura (human whipworm)”. Cutis. 77 (2): 75–6. PMID 16570666.
  2. Elsayed S, Yilmaz A, Hershfield N (2004). “Trichuris trichiura worm infection”. Gastrointest Endosc. 60 (6): 990–1. PMID 15605023.
  3. Tilney LG, Connelly PS, Guild GM, Vranich KA, Artis D (2005). “Adaptation of a nematode parasite to living within the mammalian epithelium”. J Exp Zool A Comp Exp Biol. 303 (11): 927–45. doi:10.1002/jez.a.214. PMID 16217807.
  4. Drake L, Korchev Y, Bashford L, Djamgoz M, Wakelin D, Ashall F, Bundy D (1994). “The major secreted product of the whipworm, Trichuris, is a pore-forming protein”. Proc. Biol. Sci. 257 (1350): 255–61. doi:10.1098/rspb.1994.0123. PMID 7991635.
  5. Parthasarathy G, Mansfield LS (2005). “Trichuris suis excretory secretory products (ESP) elicit interleukin-6 (IL-6) and IL-10 secretion from intestinal epithelial cells (IPEC-1)”. Vet. Parasitol. 131 (3–4): 317–24. doi:10.1016/j.vetpar.2005.03.043. PMID 15978725.
  6. Tan TH, Edgerton SA, Kumari R, McAlister MS, Roe SM, Nagl S, Pearl LH, Selkirk ME, Bianco AE, Totty NF, Engwerda C, Gray CA, Meyer DJ, Rowe SM (2001). “Macrophage migration inhibitory factor of the parasitic nematode Trichinella spiralis”. Biochem. J. 357 (Pt 2): 373–83. PMC 1221963. PMID 11439086.
  7. “Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm – ScienceDirect”.
  8. Maizels RM, Bundy DA, Selkirk ME, Smith DF, Anderson RM (1993). “Immunological modulation and evasion by helminth parasites in human populations”. Nature. 365 (6449): 797–805. doi:10.1038/365797a0. PMID 8413664.
  9. Bethony J, Brooker S, Albonico M, Geiger SM, Loukas A, Diemert D, Hotez PJ (2006). “Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm”. Lancet. 367 (9521): 1521–32. doi:10.1016/S0140-6736(06)68653-4. PMID 16679166.
  10. Shin JL, Gardiner GW, Deitel W, Kandel G (2004). “Does whipworm increase the pathogenicity of Campylobacter jejuni? A clinical correlate of an experimental observation”. Can. J. Gastroenterol. 18 (3): 175–7. PMID 15054492.
  11. “CDC – Trichuriasis”.
  12. Kaur G, Raj SM, Naing NN (2002). “Trichuriasis: localized inflammatory responses in the colon”. Southeast Asian J Trop Med Public Health. 33 (2): 224–8. PMID 12236416.
  13. Ok KS, Kim YS, Song JH, Lee JH, Ryu SH, Lee JH, Moon JS, Whang DH, Lee HK (2009). “Trichuris trichiura infection diagnosed by colonoscopy: case reports and review of literature”. Korean J. Parasitol. 47 (3): 275–80. doi:10.3347/kjp.2009.47.3.275. PMC 2735694. PMID 19724702.
  14. Bethony J, Brooker S, Albonico M, Geiger SM, Loukas A, Diemert D, Hotez PJ (2006). “Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm”. Lancet. 367 (9521): 1521–32. doi:10.1016/S0140-6736(06)68653-4. PMID 16679166.

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Causes
This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Trichuriasis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The human whipworm (Trichuris trichiura or Trichocephalus trichiuris) is a round worm (a type of helminth) that causes trichuriasis (a type of helminthiasis which is one of the neglected tropical diseases) when it infects a human large intestine. It is commonly known as the whipworm which refers to the shape of the worm; it looks like a whip with wider “handles” at the posterior end.

Life cycle

Life cycle of Trichuris trichiura inside and outside the human body

The female T. trichiura produces 2,000–10,000 single-celled eggs per day.[1] 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 and hatch in the human small intestine exploiting the intestinal microflora as hatching stimulus.[2] 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 cecum and penetrate the mucosa and there they complete development to adult worms in the large intestine. The life cycle from time of ingestion of eggs to development of mature worms takes approximately three months. During this time, there may be limited signs of infection in stool samples due to lack of egg production and shedding. The female T. trichiura begin to lay eggs after three months of maturity. Worms can live up to five years, during which time females can lay up to 20,000 eggs per day.

Recent studies using genome-wide scan revealed two quantitative trait loci on chromosome 9 and chromosome 18 may be responsible for genetic predisposition or susceptibility to infection of T. trichiura by some individuals.

Morphology

Trichuris trichiura has a narrow anterior esophageal end and shorter and thicker posterior anus. 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.[3] 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.

Infection

Infection occurs through ingestion of eggs and is more common in warmer areas. Whipworms eggs are passed in the feces of infected persons, and if an infected person defecates outside or if untreated human feces as used as fertilizer, eggs are deposited on soil where they can mature into an infective stage. 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.”[4] The eggs hatch in the small intestine, and then move into the wall of the small intestine and develop. On reaching adulthood, the thinner end (the front of the worm) burrows into the large intestine and the thicker end hangs into the lumen and mates with nearby worms. The females can grow to 50 mm (2 inches) long. Neither the male nor the female has much of a visible tail past the anus.[1]

Whipworm commonly infects patients also infected with Giardia, Entamoeba histolytica, Ascaris lumbricoides, and hookworms.

Epidemiology

There is a worldwide distribution of Trichuris trichiura, with an estimated 1 billion human infections.[5][6][7] 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.

Other animals

Egg of Trichuris vulpis
Egg of Trichuris trichura

Whipworms develop when a dog swallows whipworm eggs, passed from an infected dog. Symptoms may include diarrhea, anemia, and dehydration. The dog whipworm (Trichuris vulpis) is commonly found in the U.S. It is hard to detect at times, because the numbers of eggs shed are low, and they are shed in waves. Centrifugation is the preferred method. There are several preventives available by prescription from a veterinarian to prevent dogs from getting whipworm.

The cat whipworm is a rare parasite. In Europe, it is represented mostly by Trichuris campanula, and in North America it is Trichuris serrata more often.[8][9] Whipworm eggs found in cats in North America must be differentiated from lungworms, and from mouse whipworm eggs just passing through.

Treatment of inflammatory disorders

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 (also called 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[10][11][12] and to a lesser extent ulcerative colitis[13] 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,[14] allergy,[15] and other inflammatory disorders. Some scientific evidence suggests that the course of multiple sclerosis may be very favorably altered by helminth infection;[16] TSO is being studied as a treatment for this disease.[17][18]

References

  1. 1.0 1.1 Cross, John H. (1996). “Enteric Nematodes of Humans”. In Baron, Samuel. Medical Microbiology (4th ed.). Galveston: University of Texas Medical Branch at Galveston. ISBN 0-9631172-1-1.
  2. Hayes, K. S.; Bancroft, A. J.; Goldrick, M.; Portsmouth, C.; Roberts, I. S.; Grencis, R. K. (2010). “Exploitation of the Intestinal Microflora by the Parasitic Nematode Trichuris muris”. Science. 328 (5984): 1391–4. doi:10.1126/science.1187703. PMC 3428897. PMID 20538949.
  3. “Trichuris trichiura definition – Medical Dictionary definitions of popular medical terms easily defined on MedTerms”. Medterms.com. 2000-04-15. Retrieved 2009-05-19.
  4. http://www.cdc.gov/parasites/whipworm/
  5. Crompton, DW (1999). “How much human helminthiasis is there in the world?”. The Journal of Parasitology. 85 (3): 397–403. PMID 10386428.
  6. de Silva, Nilanthi R; Brooker, Simon; Hotez, Peter J; Montresor, Antonio; Engels, Dirk; Savioli, Lorenzo (2003). “Soil-transmitted helminth infections: updating the global picture”. Trends in Parasitology. 19 (12): 547–51. doi:10.1016/j.pt.2003.10.002. PMID 14642761.
  7. “Trichuris trichiura”. WrongDiagnosis.com. 2009-05-06. Retrieved 2009-05-19.
  8. “Whipworms”. VeterinaryPartner.com. 24 September 2007. Retrieved 2009-05-19.
  9. Hendrix CM, Blagburn BL, Lindsay DS (1987). “Whipworms and intestinal threadworms”. Vet. Clin. North Am. Small Anim. Pract. 17 (6): 1355–75. PMID 3328393.
  10. Hunter MM, McKay DM (2004). “Review article: helminths as therapeutic agents for inflammatory bowel disease”. Aliment. Pharmacol. Ther. 19 (2): 167–77. doi:10.1111/j.0269-2813.2004.01803.x. PMID 14723608.
  11. Summers RW, Elliott DE, Urban JF, Thompson R, Weinstock JV (2005). “Trichuris suis therapy in Crohn’s disease”. Gut. 54 (1): 87–90. doi:10.1136/gut.2004.041749. PMC 1774382. PMID 15591509.
  12. Summers RW, Elliott DE, Qadir K, Urban JF, Thompson R, Weinstock JV (2003). “Trichuris suis seems to be safe and possibly effective in the treatment of inflammatory bowel disease”. Am. J. Gastroenterol. 98 (9): 2034–41. doi:10.1111/j.1572-0241.2003.07660.x. PMID 14499784.
  13. Buning, J; et al. (March 2008). “Helminths as governors of inflammatory bowel disease”. Gut. 57 (8): 1182–1183. doi:10.1136/gut.2008.152355. PMID 18628388. Retrieved 2010-12-10. 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)
  14. “Helminthic Therapy: How to put your Asthma, Colitis, IBD, Crohn’s or Multiple Sclerosis into remission with hookworm”. Asthmahookworm.com. Retrieved 2009-05-19.
  15. “Allergies: Trichuris suis Ova (TSO) Therapy to Treat Food Allergies”. Allergizer.com. Retrieved 2009-05-19.
  16. Correale J, Farez M. (2007). “Association between parasite infection and immune responses in multiple sclerosis”. Annals of Neurology. 61 (2): 97&ndash, 108. doi:10.1002/ana.21067. PMID 17230481.
  17. “Asphelia Announces Initiation of an Independent TSO Trial for Multiple Sclerosis”. redOrbit. 2008-04-07. Retrieved 2009-05-19.
  18. Klaver, Elsenoor J.; Kuijk, Loes M.; Laan, Lisa C.; Kringel, Helene; van Vliet, Sandra J.; Bouma, Gerd; Cummings, Richard D.; Kraal, Georg; van Die, Irma (2013). “Trichuris suis-induced modulation of human dendritic cell function is glycan-mediated”. International Journal for Parasitology. 43 (3–4): 191–200. doi:10.1016/j.ijpara.2012.10.021. PMID 23220043.

Template:Helminthiases

Differentiating Whipworm Infection from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2] Furqan M M. M.B.B.S[3]

Overview

Trichuriasis must be differentiated from other nematode infections, such as ascariasis, hook worm infection, and Strongyloides stercoralis, that can present with diarrhea and abdominal pain.

Differential Diagnosis

Trichuriasis must be differentiated from other nematode infections, such as ascariasis, hook worm infection, and Strongyloides stercoralis infection, that can present with diarrhea and abdominal pain.

Differentiating Trichuriasis from other Nematode infections[1][2][3]
Infection Nematode Transmission Direct Person-Person Transmission Duration of Infection Pulmonary Manifestation Location of Adult worm(s) Treatment
Trichuriasis (whipworm infection) Trichuris trichiura

(whipworm)

Ingestion of infective ova No
  • 1-3 years
  • No pulmonary migration, therefore, no pulmonary manifestation
Anchored in the superficial mucosa of cecum and colon
Strongyloidiasis Strongyloides stercoralis Filariform larvae penetrate skin or bowel mucosa Yes
  • Lifetime of the host
Embedded in the mucosa of the duodenum, jejunum
Ascariasis Ascaris lumbricoides Ingestion of infective ova No
  • 1-2 years
Free air in the lumen of the small bowel (jejunum)
Hookworm infection Necator americanus and Ancylostoma duodenale Skin penetration by filariform larvae No Attached to the mucosa of mid-upper portion of the small bowel
Enterobiasis Enterobius vermicularis

(pinworm)

Ingestion of infective ova Yes
  • 1 month
  • Extraintestinal migration is very rare
Free air in the lumen of cecum, appendix, adjacent colon

References

  1. Durand, Marlene (2015). “Chapter 288:Intestinal Nematodes (Roundworms)”. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.
  2. Kim, Kami; Weiss, Louis; Tanowitz, Herbert (2016). “Chapter 39:Parasitic Infections”. Murray and Nadel’s Textbook of Respiratory Medicine Sixth Edition. Elsevier. pp. 682–698. ISBN 978-1-4557-3383-5.
  3. Serpytis M, Seinin D (2012). “Fatal case of ectopic enterobiasis: Enterobius vermicularis in the kidneys”. Scand J Urol Nephrol. 46 (1): 70–2. doi:10.3109/00365599.2011.609834. PMID 21879805.

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2], Syed Hassan A. Kazmi BSc, MD [3]

Overview

Trichuris trichiura is the third most common nematode worldwide following Ascaris and Enterobius; in total, the three infections affect approximately 1 billion people. Whip worm infection is endemic in tropical and subtropical countries. The prevalence of Trichuris trichiura is high, affecting 95% of children in countries where protein energy malnutrition and anemia are prevalent.

Epidemiology and Demographics

Prevalence

Incidence

Age

Gender

Race

Geographic distribution

  • Whip worm infection is endemic in tropical and subtropical countries.[5]
  • Incidence and prevalence rates are highest in children living in sub-Saharan Africa, followed by Asia, then Latin America and the Caribbean.[6][7]
  • Worldwide, infections are more frequent in areas with tropical weather and poor sanitation practices.[8]
Prevalence of Trichuris trichiura among school-aged children in Sub-Saharan Africa, courtesy of the Global Land Information System (GLIS) of the United States Geological Survey (http://edcwww.cr.usgs.gov/landdaac/gtopo30/)

References

  1. “CDC – Trichuriasis – Epidemiology & Risk Factors”.
  2. Starr MC, Montgomery SP (2011). “Soil-transmitted Helminthiasis in the United States: a systematic review–1940-2010”. Am. J. Trop. Med. Hyg. 85 (4): 680–4. doi:10.4269/ajtmh.2011.11-0214. PMC 3183777. PMID 21976572.
  3. Stephenson, L.S.; Holland, C.V.; Cooper, E.S. (2001). “The public health significance of Trichuris trichiura”. Parasitology. 121 (S1): S73. doi:10.1017/S0031182000006867. ISSN 0031-1820.
  4. Brooker S, Clements AC, Bundy DA (2006). “Global epidemiology, ecology and control of soil-transmitted helminth infections”. Adv. Parasitol. 62: 221–61. doi:10.1016/S0065-308X(05)62007-6. PMC 1976253. PMID 16647972.
  5. Manz KM, Clowes P, Kroidl I, Kowuor DO, Geldmacher C, Ntinginya NE; et al. (2017). “Trichuris trichiura infection and its relation to environmental factors in Mbeya region, Tanzania: A cross-sectional, population-based study”. PLoS One. 12 (4): e0175137. doi:10.1371/journal.pone.0175137. PMC 5383155. PMID 28384306.
  6. de Silva NR, Brooker S, Hotez PJ, Montresor A, Engels D, Savioli L (2003). “Soil-transmitted helminth infections: updating the global picture”. Trends Parasitol. 19 (12): 547–51. PMID 14642761.
  7. Brooker S, Clements AC, Bundy DA (2006). “Global epidemiology, ecology and control of soil-transmitted helminth infections”. Adv. Parasitol. 62: 221–61. doi:10.1016/S0065-308X(05)62007-6. PMC 1976253. PMID 16647972.
  8. Brooker S, Clements AC, Bundy DA (2006). “Global epidemiology, ecology and control of soil-transmitted helminth infections”. Adv. Parasitol. 62: 221–61. doi:10.1016/S0065-308X(05)62007-6. PMC 1976253. PMID 16647972.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

Risk factors predisposing patients to the development of whip worm infection include low socioeconomic status, low levels of education, poor sanitation, and poor hygiene.

Risk Factors

The following risk factors predispose patients to whip worm infection:[1][2]

  • Low socioeconomic status[1]
  • Low levels of education
  • Poor sanitation
  • Close proximity to water sources
  • Co-infection with A. lumbricoides and T. trichiura can occur in:
    • Students
    • Fishermen
    • Farmers

References

  1. 1.0 1.1 Ross AG, Olveda RM, McManus DP, Harn DA, Chy D, Li Y; et al. (2017). “Risk factors for human helminthiases in rural Philippines”. Int J Infect Dis. 54: 150–155. doi:10.1016/j.ijid.2016.09.025. PMID 27717859.
  2. Diniz-Santos DR, Jambeiro J, Mascarenhas RR, Silva LR (2006). “Massive Trichuris trichiura infection as a cause of chronic bloody diarrhea in a child”. J Trop Pediatr. 52 (1): 66–8. doi:10.1093/tropej/fmi073. PMID 16000342.

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]

Overview

In most cases, whipworm infection causes no clinical symptoms, but a severe infection can cause abdominal pain, diarrhea, constipation, weight loss, and anemia. If left untreated, severe infection can result in Trichuris dysentery syndrome. Complications of heavy whipworm infection include chronic dysentry, rectal prolapse, and growth retardation. Prognosis is excellent with antihelminthic treatment and complete recovery occurs in 1 to 2 weeks.

Natural History, Prognosis and Complications

Natural History

In most cases, whipworm infection causes no clinical symptoms, but a severe infection can cause abdominal pain, diarrhea, constipation, weight loss, and anemia.[1] If left untreated, severe infection can result in Trichuris dysentery syndrome, which presents with features of chronic dysentery, rectal prolapse, anemia, poor growth, and clubbing of the finger nails.[2][3]

Complications

In patients with heavy infection, the following complications may develop:[2][4]

Prognosis

The prognosis of trichuriasis is excellent with anti-helminthic treatment. All the patients recover completely with treatment.

References

  1. Tokmak N, Koc Z, Ulusan S, Koltas IS, Bal N (2006). “Computed tomographic findings of trichuriasis”. World J Gastroenterol. 12 (26): 4270–2. PMC 4087392. PMID 16830393.
  2. 2.0 2.1 Stephenson, L.S.; Holland, C.V.; Cooper, E.S. (2001). “The public health significance of Trichuris trichiura”. Parasitology. 121 (S1): S73. doi:10.1017/S0031182000006867. ISSN 0031-1820.
  3. Elsayed S, Yilmaz A, Hershfield N (2004). “Trichuris trichiura worm infection”. Gastrointest Endosc. 60 (6): 990–1. PMID 15605023.
  4. Kim JB, Seo KI, Moon W (2017). “Trichuris trichiura Infection in North Korean Defector Resulted in Chronic Abdominal Pain and Growth Retardation”. Korean J Gastroenterol. 69 (4): 243–247. doi:10.4166/kjg.2017.69.4.243. PMID 28449427.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings |Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

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