Trichuriasis, which is infection with the parasite Trichuris trichiura, or whipworm, is a very common intestinal helminthic infection worldwide.[1, 2] About one quarter of the world's population is thought to carry the parasite. Principally a problem in tropical Asia and, to a lesser degree, in Africa and South America, a lack of a tissue migration phase and a relative lack of symptoms characterize whipworm infection. Trichuris is notable for its small size compared with Ascaris lumbricoides. Only individuals with heavy parasite burden become symptomatic. Vitamin A deficiency has been seen in patients with trichuriasis.
Poor hygiene is associated with T trichiura transmission, and children are especially vulnerable because of their high exposure risk. This is particularly true in developing countries, where poor sanitary conditions correlate with heavy disease burden and infections. One study in Nigeria was undertaken to determine helminth infection status and hygienic conditions in primary schools. Prevalence of helminth infection was higher in the schools where hygiene conditions (ie, tapwater, handwashing soap) were lacking. The study results recommended that the school health programs include deworming, health education, and improvement of hygiene conditions.[3]
The whipworm derives its name from its characteristic whiplike shape; the adult (male, 30-45 mm; female, 35-50 mm) buries its thin, threadlike anterior half into the intestinal mucosa and feeds on tissue secretions, not blood. This relative tissue invasion causes occasional peripheral eosinophilia. The cecum and colon are the most commonly infected sites, although in heavily infected individuals, infection can be present in more distal segments of the GI tract, such as the descending colon and rectum.
Note that T trichiura is usually found in association with other helminths that flourish under similar conditions, a common pathogen being A lumbricoides.
Trichuris, as with Ascaris lumbricoides, is spread via fecal-oral transmission. Eggs are deposited in soil through human feces. After 10-14 days in soil, eggs become infective. In contrast to other parasites, such as A lumbricoides, no tissue migratory phase occurs with Trichuris organisms, confining infection to the GI tract. Larvae hatch in the small intestine, where they grow and molt, finally taking up residence in the cecum and ascending colon. In people with a heavy burden of infection, the entire colon and rectum may be infested with worms. The time from ingestion of eggs to development of mature worms is approximately 3 months. During this time, there may be no shedding of eggs and only limited evidence of infection in stool samples. Worms may live from 1-5 years, and adult female worms lay eggs for up to 5 years, shedding up to 20,000 eggs per day.
Immunologically, cytokines such as interleukin 25 (IL-25) mediate type 2 immunity and are required for the regulation of inflammation in the gastrointestinal tract.
Recent linkage analyses of a genome-wide scan revealed that two quantitative trait loci on chromosomes 9 and 18 may be responsible for the susceptibility to trichuriasis in some genetically predisposed individuals.[4]
United States
Whipworm infection is rare overall but is more common in the rural Southeast, where 2.2 million people are thought to be infected.
International
Whipworm infection is more common in less-developed countries. T trichiura is carried by nearly 1 bilion of the world's population.
Whipworm infection is rarely fatal and is usually asymptomatic, but symptoms may be present in heavily infected individuals.[1, 2] Loose stools may be present with minimal blood with the development of chronic anemia if bleeding is chronic. Nocturnal stooling is quite common. In individuals with a heavy burden of worms, dysentery and colitis may be seen. Fingernail clubbing also may be present. In children, vitamin deficiencies (vitamin A) may contribute to developmental delay and growth retardation. Rectal prolapse may occur in heavily infected hosts.
Trichuriasis has no racial predilection.
Boys are more likely to be infected with T trichiura because they are thought to eat more dirt than girls.
Children are more commonly infected than adults due to poor hygiene and increased consumption of soil. Children are also more heavily infected.[1, 2] Furthermore, it is widely believed that partial protective immunity develops with age and children are not protected initially.
The prognosis of trichuriasis is excellent with proper treatment; however, without education and changes in behavior/waste management, re-infection is very common.
Good personal hygiene is highly recommended. Where relevant, community waste management systems should be developed to reduce exposure to potentially infected waste.
Most individuals with whipworm infection (trichuriasis) are asymptomatic. Clinical symptoms are limited to patients with heavy infection, who tend to be small children or others with significant exposure. Note that there is no pulmonary migration and, thus, no pulmonary or extra-gastrointestinal symptoms. Symptoms include the following[1, 2] :
Nocturnal loose stools
Dysentery can occur in patients with greater than 200 worms.
Rectal prolapse
Failure to thrive
Symptoms of anemia (massive infection only)
Vague abdominal discomfort
Stunted growth
Physical findings include the following:
Trichuriasis is caused by consumption of soil or food that has been fecally contaminated. (Eggs are infective or embryonated about 2-3 weeks after being deposited in the soil).
Potential complications of whipworm infection (trichuriasis) include the following:
Rectal prolapse or anemia
Vitamin deficiency
Other parasitic helminth infections
The following are laboratory studies used in the diagnosis of whipworm infection (trichuriasis):
Endoscopy often shows adult worms attached to the bowel mucosa.
Obtain a stool smear for ova and parasites (as above).
No procedures are indicated in the absence of complications. However, endoscopy may be warranted in instances of severe anemia or refractory infection.
Effective anthelmintic therapy is available for whipworm infection (trichuriasis) (see Medication).
Specialty consultation for trichuriasis is not necessary unless rectal prolapse or severe anemia is present; both are rare.
Household contacts are at low risk because of life-cycle requirements.
If fecal contamination of soil is possible (eg, children defecating in the back yard, human waste used as fertilizer), consider the possibility of household transmission.
Contacts may be screened for asymptomatic carrier state.
Improved sanitation is the best way to eradicate whipworm infection (trichuriasis).
Careful washing of vegetables and fruits grown in contaminated areas is also important.
Inpatient care for whipworm infection (trichuriasis) may be warranted for patients with rectal prolapse or severe anemia.
The drug of choice for trichuriasis is mebendazole. A single 500-mg dose can result in a cure rate of 40-75%. Albendazole is an alternative drug. However, its efficacy for trichuriasis is slightly lower than for mebendazole.[5, 6]
Recent studies have shown combination therapy with Ivermectin and Albendazole has higher cure rates than monotherapy with Albendazole alone.[22]
Oxantel pamoate (not currently available in the United States) has shown efficacy in the treatment of trichuriasis. Using oxantel pamoate in combination with either mebendazole or albendazole results in a much higher cure rate than monotherapy.
Emodepside, a veterinary drug, has shown superior activity against trichuria when compared to Albendazole. It is currently being studied as a leading therapeutic candidate to treat trichuriasis and other helminth infections.[23]
Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.
Causes worm death by selectively and irreversibly blocking glucose uptake and other nutrients in the susceptible adult intestine where helminths dwell. Available as a 100-mg chewable tablet that can be swallowed whole, chewed, or crushed and mixed with food.
Administer a second course if patient is not cured within 3-4 wk.
Decreases whipworm ATP production, causing energy depletion, immobilization, and death.
Increases nerve and muscle cell membrane permeability when it binds to chloride ion channels causing paralysis and subsequent death of parasite