Trichuriasis

Introduction

Trichuris trichiuria, meaning 'hairy tail', is actually a misnomer, since it is the proximal end that is hairlike. The popular name is whipworm, with the whip as the long thin pharynx (stichostome) and the whip handle as the posterior end with reproductive organs and intestine (Figure 11.3).

Life cycle

A mature female worm produces up to 20 000 eggs/day, which are 50 |im long and not infectious until the larval stage develops in the soil over 2-4 weeks. Warm damp soil is ideal for embryonation,

Worms Damp Soil
Figure 11.3 Trichuris trichiura worms attached to the colon. Courtesy of UK Tropical International Health.

and environmental exposure is associated with poor hygiene practices. Once ingested, larvae penetrate the epithelium of the mucosal crypt in the cecum, where they moult and the hair-like stichosome remains attached while the broader distal end extends into the lumen. The adult worm is 4 cm long and survives for 1-2 years in the host.

Epidemiology

Trichuriasis is a very common infestation with an estimated 1049 million cases worldwide, including 114 million preschool and 233 million schoolage children.68 Most of these infections are asymptomatic, but children suffer greater morbidity than adults. There appears to be a genetic or immuno-logical predisposition to heavy infection, which may be HLA group-mediated.69 There also appears to be some epidemiological 'synergism' between ascariasis and trichuriasis in that high-intensity infections occur together more often than by chance.70

Pathophysiology

With severe infection, the cecal mucosa becomes inflamed and edematous, but there are only minor changes in histology (increased IgM lamina propria plasma cells and calprotectin-secreting cells, crypt epithelial cell proliferation, distended goblet cells).71 The cytokine response in colonic mucosa involves both interferon-y (Th1) and IL-4 (Th2), but results in neither worm expulsion nor obvious protection from reinfection. There may be a protein-losing enteropathy proportional to the worm burden.72 There is an acute-phase response with intense trichuriasis, including increases in plasma tumor necrosis factor (TNF)-a, C-reactive protein (CRP), globulins, viscosity and fibronectin with decreased insulin-like growth factor (IGF)-I73-75. There is also development of an IgE-mediated immediate hypersensitivity reaction in the colon,76 usually, but not always, with systemic eosinophilia.

Clinical features

Most infections in children are light (<20 adult worms) and asymptomatic, with symptoms developing in < 10% of infected children. Occult blood in feces is uncommon even with heavy infestations, although even light infections incite a local inflammatory response involving eosinophils and neutrophils in the colon.77,78 With heavy infestations, frequent watery or mucous stools occur, sometimes with frank blood. Rectal prolapse can occur with heavy infestations.79,80 A very small minority of heavily infected children (>200 worms in the rectum, colon and often terminal ileum) develop the Trichuris dysentery syndrome,81,82 characterized by chronic dysentery, stunting, anemia and finger clubbing.

Diagnosis

The diagnosis is based on finding eggs on stool microscopy, with more than 10 000 epg generally associated with heavy infection, although there is considerable individual variation in eggs to worm load. Trichuris dysentery in children must be differentiated from amebic and bacilliary causes. Most cases of rectal prolapse in malnourished children are not due to trichuriasis.

Prevention

The use of proper latrines, good hygiene with handwashing and washing of vegetables will interrupt the life cycle. Overcrowded urban slums with limited water supply and heavily fecally contaminated soil for growing vegetables place children at particular risk. Mass chemotherapy is highly effective, but reinfection occurs rapidly in this setting.

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