Whipworm

Humans are the only known host of T trichiura and no animal reservoir is recognized.

The organism is spread via the fecal-oral route via ingestion of embyronated eggs with contaminated food or contact with contaminated hands. After ingestion the eggs hatch in the small intestine into the larval form, which penetrate the small intestinal mucosa.

After approximately one week, the immature worms move passively to the large intestine and proximal colon and penetrate the mucosal epithelial cells. The worm continues to expand intracellularly creating tunnels in the epithelium. The posterior end of the worm eventually ruptures the cell membrane and the worm protrudes partially into the lumen of the large intestine, while the anterior part still imbedded in the epithelium. Thus, the worm disrupts the normal colonic architecture; however, the host inflammatory response is the major contributor to the pathogenesis of the worm infection.

About 3 months after the ingestion, the fertilized female worm starts laying eggs. The female worm is capable of producing 3,000-20,000 eggs a day. The infected host passes unembryonated eggs in their feces and the maturation of eggs requires warm humid environment. Egg maturation occurs in approximately 2-6 weeks. T trichura eggs are bile-stained and have a characteristic barrel-shape with the presence of polar plugs in the egg shell. The embryonated egg can maintain viability for several months under suitable conditions. Destruction occurs with exposure to direct sunlight for more than 12 hours and to temperatures of less than -8°C or higher than 40°C for one hour.

The adult worm usually reaches 3-5 cm in length and has a lifespan of 1-3 years.

United States statistics

Prevalence of whipworm infestation is less than 0.1%, although adequate studies are quite outdated.[3] The most common areas of infection are the southern Appalachian range and Gulf coast states.[4]

International statistics

CDC estimated 604-795 million people in the world are infected with whipworm.

The highest prevalence rates of soil-transmitted helminthes occur in sub-Saharan Africa and southern and eastern Asia.[2] As with other soil-transmitted helminthes, the prevalence is higher in tropical and subtropical regions of the world, which provide the moist, humid environment required for the eggs to mature. Due to the poor sanitation practices in the rural areas of these regions the disease is prevalent.

Age-related demographics

Although infections are observed in all age groups, most heavy infections are observed in the pediatric population. This probably reflects the increased likelihood of children to have poor hygiene and to play in soil that carries the worms' mature eggs.

With treatment, prognosis is typically excellent.

Morbidity/mortality

Most infections are asymptomatic. Symptoms are related to the worm load or number of worms involved in an infection. Heavy infections (hundreds to thousands of worms) can lead to death secondary to GI and hematologic complications.

Mortality can result from complications such as intestinal obstruction or rectal prolapse requiring surgical intervention.

Morbidity is directly related to worm burden. Soil-transmitted helminths impair the nutritional status of the host due to intestinal bleeding, diarrhea or dysentery and malabsorption of nutrients resulting in growth delay and failure to thrive.

An estimated $4.98 million per year is lost due to disability (YLD) attributable to soil-transmitted helminths worldwide. About 13% is attributable to T trichiura.[5]

Complications

Rectal prolapse, dysentery, anemia, malnutrition, and growth retardation all can complicate heavy infections. In developing countries, T trichiura infection is a common cause of stunting and wasting among children aged younger than 5 years.[6]

Emphasize good hygiene and avoidance of pica. Proper disposal of fecal material needs to be emphasized.

When evaluating a patient suspected of having a whipworm infection, the most important part of the history is travel to or living in an area of known infestation.

Gastrointestinal complaints associated with these infections are diverse, ranging from mild to severe, including diarrhea, dysentery, abdominal discomfort, flatulence or constipation. Long-term gastrointestinal complaints with associated exposure suggest whipworm infection.

Most infections are asymptomatic. Patients with fewer than 100 worms are frequently asymptomatic; however, they may present with lower abdominal discomfort, flatulence, and diarrhea or constipation.

Patients with heavy infection have hundreds to thousands of worms and may present with lower or epigastric pain, vomiting, abdominal distension, anorexia, weight loss, anemia, diarrhea, tenesmus (painful straining), and rectal prolapse. Trichuris dysentery syndrome is observed in heavy infections and characterized by bloody mucoid diarrhea, small frequent stools, tenesmus, anemia, and growth retardation.

Polyparasitic infections can occur with whipworms, ascaris, and hookworms because these parasites live in similar environments.[7]

Generally, physical examination findings are normal.

Pallor, fatigue, and failure to thrive are common in children.

Each worm causes an estimated 5 µL of blood loss every day.

Heavy infections are required to cause anemia.

Prolonged infections are reported to lead to growth failure, intellectual delays, and digital clubbing; however, growth and intellectual delays are likely to be multifactorial.

Diagnosis is based on the microscopic detection of eggs or larvae in fresh or fixed stool samples.[8] The eggs are bile stained with characteristic barrel (American football) shape with translucent polar plugs.

The stool commonly contains RBCs and WBCs, including eosinophils.

No serological tests or PCR testing in stool have been validated to detect infection with Trichuris.

Other laboratory findings are nonspecific. Peripheral CBC may reveal anemia (iron deficiency anemia), and ESR could be elevated due to ongoing inflammation.[9]

Anoscopy

Anoscopy may be useful. In heavy infections, worms can be directly visualized.

Biopsy

The pathologic changes are noted in the large intestine, confined primarily to the mucosal epithelium. This differentiates whipworm infection with IBD as there is little or no involvement of the submucosa and muscularis layer.

The anterior part of the worm is embedded in the mucosa and the posterior two-fifth floats in the lumen. On biopsy there is intense eosinophilic infiltrate noted around the worm.[10]

Treatment with broad-spectrum anthelminthic agents is key. Most infections can be treated successfully with mebendazole, albendazole, or ivermectin. These anthelminthic medications should be taken for 3 days. Dosage guidelines and important drug interactions are summarized in the medication section. Albendazole should be taken with food. Ivermectin should be taken with water on an empty stomach and the safety of ivermectin for children weighing less than 15 kg has not been established. Neither albendazole nor ivermectin has been approved by the US Food and Drug Administration (FDA) for treating whipworm.

A systematic review and network meta-analysis by Moser et al reported that T. trichiura cure rates with albendazole and mebendazole were 30.7% and 42.1%, respectively. The study also reported that between 1995 to 2015, albendazole cure rates decreased from 38.6% to 16.4% and egg-reduction rates decreased from 72.6% to 43.4% for albendazole and 91.4% to 54.7% for mebendazole.[11]

The combination of single dose of ivermectin and albendazole, or ivermectin and mebendazole, improves cure rates of 38% and 55% respectively.[12]  Studies have shown that combination therapy with ivermectin and albendazole has higher cure rates than monotherapy with albendazole alone.[13]

Emodepside, a veterinary drug, has shown superior activity against T trichiura when compared with albendazole. It is being studied as a therapeutic candidate to treat trichuriasis and other helminth infections.[14]

Further outpatient care

Reexamination of stool specimens 2 weeks after therapy to determine whether the worms have been eliminated is helpful for assessing therapy. Retreatment may be necessary if symptoms persist 2-3 weeks after initial therapy.

Prevention

Proper disposal of fecal material is indicated. Mass treatment of infected school-aged populations can reduce whipworm transmission in communities with endemic infection.

Some clinicians have suggested periodic deworming programs for children in endemic areas.[15]

Consultations with the following specialists may be appropriate:

• Infectious diseases specialist

• Gastroenterologist

• Hematologist

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Albendazole (Albenza)

A benzimidazole carbamate drug that inhibits tubulin polymerization, resulting in degeneration of cytoplasmic microtubules. Decreases ATP production in worms, causing energy depletion, immobilization, and, finally, death. Converted in the liver to its primary metabolite, albendazole sulfoxide. Less than 1% of the primary metabolite is excreted in the urine. Plasma level is noted to rise significantly (as much as 5-fold) when ingested after high-fat meal. Experience with patients < 6 y is limited.

To avoid inflammatory response in CNS, patient must also be started on anticonvulsants and high-dose glucocorticoids.

Well tolerated and does not appear to increase risk of worm obstruction. For pregnant women, pyrantel pamoate is the DOC.

Mebendazole (Vermox)

Well tolerated and does not appear to increase risk of worm obstruction. Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in 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.

Pyrantel pamoate (Pin Rid, Pin X)

Neuromuscular blocking agent used to slowly paralyze worm to be eliminated from GI tract. DOC during pregnancy.

Nitazoxanide (Alinia)

Inhibits growth of Cryptosporidium parvum sporozoites and oocysts and Giardia lamblia trophozoites. Elicits antiprotozoal activity by interfering with pyruvate-ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction, which is essential to anaerobic energy metabolism. Available as a 20-mg/mL oral susp. May have activity in trichuriasis.

Ivermectin (Stromectol)

Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death. Half-life is 16 h; metabolized in liver. Off-label use for T trichiura in combination with albendazole or mebendazole.