Classification: Taxonomic ranks under review (cf. Encyclopedic Reference of Parasitology, 2001, Springer-Verlag)

Metazoa (Animalia) (multicellular eukaryotes, animals)
Nemathelminthes (nematodes)
Adenophorea (Aphasmidea) (without chemoreceptors known as phasmids)
Trichocephalida (Enoplida) (thread-head)
Trichuroidea (whipworms, anterior end long and narrow, stichosome pharynx)

Family: Trichuridae
Trichurid worms are known as "whip-worms" because they have a broad short posterior end and a very long narrow whip-like anterior end (with a stichosome pharynx) which is embedded in the mucosa of the lower intestines of humans and domestic animals. Heavy infections may cause dysentery, anaemia, malnutrition, and occasionally rectal prolapse. They have simple direct life-cycles involving the faecal-oral transmission of eggs containing infective larvae. Eggs excreted with host faeces contaminate soil, food and water supplies and have a characteristic barrel-shape with mucoid polar plugs at each end.

Trichuris spp. [these species cause trichuriasis in humans and animals]

Parasite morphology: Whipworms form three different developmental stages; eggs, larvae and adults. The eggs are ellipsoidal to barrel-shaped, measuring 50-70µm in length by 25-35µm in width and have two distinct mucoid polar plugs. They are typically unembryonated in faecal samples and develop infective larvae in the external environment. Adult worms have elongate whip-like bodies (3-7cm long), with a long thin anterior end that suddenly becomes thick at the posterior end. The mouth is a simple opening without lips and the oesophagus is thin, tubular and surrounded by glandular stichocytes (whole structure referred to as stichosome pharynx). Adult female worms measure up to 7cm in length and the uterus contains many lemon-shaped eggs. Adult male worms are smaller measuring up to 5cm in length and they have a tightly coiled posterior end and a single spicule with a spiny, eversible sheath.

Host range: The species T. trichiura is found in human populations throughout the world, mainly in tropical and subtropical regions. It is estimated that around 10% of the world population (800 million people) may be infected. Parasites are very prevalent in regions where human excrement (nightsoil) is used to fertilize vegetable gardens. Infections are typically over-dispersed, where a few individuals harbour most of the worms. Other whipworm species occur in a range of domestic and wild animals, including T. ovis, T. skrjabini, T. discolor and T. globulosa in ruminants, T. vulpis, T. campanula and T. serrata in dogs and cats, T. suis in pigs and T. muris in rodents. Zoonotic transmission of T. vulpis to humans has occasionally been reported.

Site of infection: Juvenile worms develop in glands of the caecal and colonic mucosa where they moult and grow. Adult worms have their anterior ends embedded in the mucosa with their posterior ends dangling into the lumen.

Pathogenesis: Small worm burdens rarely cause disease, while heavier infections may produce a variety of conditions, ranging from local enteric disturbances to systemic conditions and occasionally death. The anterior ends of the adult worms are embedded in the mucosa where they feed on fluids, digested tissues and possibly blood. They may cause significant trauma to the mucosa with chronic haemorrhage leading to dysentery and anaemia. Pathogenesis has been related to host inflammatory responses, involving markedly reduced cell-mediated responses and elevated IgE responses, characteristic of local tissue anaphylactic responses. Persistent infections have been associated with malnutrition, growth retardation, and reduced cognitive function in children. Chronic infections may also cause finger (and occasionally toe) clubbing evident as odd thickening of the ends of the digits. Heavy infections may produce tenesmus (urgency) causing the host to strain and possibly suffer rectal prolapse.

Mode of transmission: Whipworms have a direct developmental cycle whereby embryonated eggs are directly infective to the definitive host. Infections are transmitted by the faecal-oral route, involving the ingestion of eggs with contaminated food, water or soil. Fertilized female worms produce numerous eggs (3,000-10,000 per day) which are excreted with host faecal material. The eggs embryonate in around 10 days and develop infective larvae in about three weeks in moist shady soil (or up to 4 months in cold conditions). Eggs are dispersed in the environment by anthropogenic activities as well as by wind, water and insects (houseflies can act as mechanical vectors). When ingested, infective larvae emerge from the eggs and invade the mucosa of the lower intestines where they tunnel, grow and moult to form adults. Patent infections may develop in 8-12 weeks and can persist for 1-4 years. Infections may also accumulate in hosts as they are constantly re-infected from their heavily-contaminated environments.

Differential diagnosis: Infections are routinely diagnosed by coprological examination of faecal samples, usually following concentration, and the microscopic detection of the characteristic eggs. In individuals with rectal prolapse, worms can be seen macroscopically attached to the mucosa. Colon endoscopy has also been used to reveal the presence of worms.

Treatment and control:
Whipworms are resistant to many anthelmintic treatments due to their relative inaccessibility. Mebendazole and albendazole have proven effective, and pyrantel/oxantel pamoate and flubendazole have some activity. Thiabendazole is also effective but has unpleasant side-effects. Prevention of infections is best achieved by thorough washing of vegetables, salads and fruits with clean water prior to consumption. Control measures include education programmes to improve personal hygiene and sanitary conditions, prohibiting the use of excrement as fertilizer (or ensuring it is processed by suitable microbial biocomposting prior to use) and regular deworming campaigns.


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