Site of infection: Adult hook-worms use their bent mouths to attach to the small intestinal mucosa. Infective larvae invade dermal tissues, particularly in sites which have come into close contact with the ground (feet, hands and buttocks). Migrating larvae move through the lungs (pulmonary migration) and some may undergo arrested development deeper in the gut tissues or in muscles (hypobiotic larvae of A. duodenale).

Pathogenesis: Many people may be infected with hook-worms but remain asymptomatic. In general, disease development depends on the parasite species involved, the intensity of infection, and the nutritional condition of the individual. Sequential parasite development causes three phases of disease; a cutaneous phase where invading larvae may cause dermatitis, a pulmonary phase where migrating larvae may cause pneumonitis, and an intestinal phase where adult worms may cause anaemia. Infective larvae penetrate the skin and invade blood vessels in the dermis, moderate to heavy infections giving rise to an allergic dermatitis with papular, and sometimes vesicular, focal rash and pruritis (condition known as ground itch). Larvae from animal hook-worms (especially A. caninum and A. braziliense) can also penetrate human skin but do not complete their development. Instead, they aimlessly tunnel through the skin for several days or weeks leaving red itchy wounds that may become secondarily infected. The resultant condition is known as cutaneous larval migrans (or creeping eruption) and is characterized by local dermatitis, pruritis (itching) and inflammation (oedema, erythema). The next phase of disease occurs when larvae undergo pulmonary migration, having been carried to the lungs where they break out into airspaces (alveoli) causing focal haemorrhages and allergic pneumonia (severity dependent on numbers). Once worms reach the small intestines, they attach to the mucosa by ingesting a tissue plug into their mouths and commence feeding on blood. They have voracious appetites and individual adult Necator worms may consume 0.03 ml blood per day, while those of Ancylostoma may take up to 0.26 ml blood per day. Blood loss from the host may result in a profound iron-deficiency anaemia and hypoproteinaemia. The worms appear to be wasteful feeders as not all blood ingested is digested, some is apparently used for respiration and passes through the worm but degrades in the intestines resulting in black tarry faeces (melena). Blood loss is further exacerbated by intestinal lacerations as worms move to new feeding sites from time to time, secreting proteolytic enzymes and anticoagulants, and leaving microscopic ulcers. Infections involving <100 Necator are frequently mild whereas >100 worms produce more damage and >1,000 may be fatal. Fewer Ancylostoma cause greater disease because they suck more blood, 100 worms may cause severe disease. Patients with heavy infections have severe protein deficiency, dry skin and hair, oedema, and potbelly in children with delayed puberty, mental dullness, heart failure and death. Disease is intensified by malnourishment and immunological impairment.

Mode of transmission: Hook-worms have direct life-cycles involving a geo-helminth stage where infective larvae in the soil actively penetrate the skin or oral mucosa of their hosts. Female worms produce numerous eggs (up to 9,000 eggs per day for Necator and 30,000 eggs per day for Ancylostoma) which are excreted with host faeces. The eggs embryonate rapidly in warm moist conditions and hatch within 1-2 days, releasing free-living rhabditiform larvae which feed on bacteria and organic debris. The larvae moult once after ~3 days and then transform 2-5 days later into non-feeding ensheathed filariform larvae (L3) which are the infective stages. They remain viable for several weeks in light sandy soils under warm moist conditions. The larvae also exhibit short vertical migration, moving to the surface in moist conditions and host-seeking by rhythmically waving back and forth, but retreating back into the soil in dry conditions. Necator larvae must penetrate the skin to infect humans (transdermal or percutaneous transmission), but Ancylostoma can penetrate the skin or oral mucosa, be passed in mother’s milk (transmammary transmission) and even cross the placenta to infect the foetus (transplacental transmission). Some evidence suggests that A. duodenale larvae may survive in paratenic hosts and lead to human infection through the ingestion of undercooked meat, including rabbit, lamb, beef and pork. Ingested larvae may undertake pulmonary migration, but most undergo a histotrophic stage by penetrating mucosal glands before returning to the lumen and maturing into adults. Larvae which penetrate the skin actively secrete collagenase to break down basement membranes and dermal ground substances. The larvae enter the circulation and migrate over 2-7 days to the lungs where they break into respiratory alveoli and move up the trachea to be swallowed. Once they reach the small intestines, they moult, attach to mucosa and become sexually differentiated, moult again and grow into adult worms. The prepatent period (from infection to egg excretion) ranges from 4-7 weeks, although A. duodenale may undergo arrested larval developmental for up to 38 weeks. Hypobiotic larvae remain dormant in gut or muscles and recommence their development later coinciding with the seasonal return of environmental conditions more favourable to transmission. Infections may persist for years, as Ancylostoma adults have been found to live for up 5 years, and Necator adults for up to 15 years.

Differential diagnosis: The diagnosis of hookworm disease on the basis of clinical symptomatology (notably chronic anaemia and debility) is highly suggestive, but requires confirmation by the detection of parasite eggs in faecal samples by microscopy, preferably after concentration. Because the eggs of hookworms (Ancylostoma and Necator) and thread-worms (Strongyloides) are virtually identical, faeces should be kept for larval cultures (on moistened filter paper in a closed tube for a few days) to differentiate infections (hook-worm larvae have a larger buccal cavity and smaller genital primordium), since treatment options are quite different. Several immunoserological tests have been developed to detect host antibodies against hookworm antigens, but they generally do not discriminate between patent or previous infections. Radiographic findings include intestinal hypermotility, proximal jejunal dilatation and coarsening of the mucosal folds.

Treatment and control: Various anthelmintic drugs have been used to cure infections, and are best used in conjunction with dietary supplementation, especially iron replacement. The most effective drugs are mebendazole, albendazole and pyrantel pamoate. Levamisole is less effective and treatment has adverse side-effects. Older drugs, such as bephenium and tetrachlorethylene, are still used in many areas throughout the world because they are cheap. Salicylanilides have also proven effective against animal Ancylostoma infections. While chemotherapy works, mass treatment programmes are only partly effective as most cured individuals return to heavily contaminated areas and rapidly become re-infected. Infection appears to stimulate little protective immunity. Control programmes must include prophylaxis to prevent infections as well as environmental management to reduce soil contamination. People should be encouraged to wear solid shoes in endemic regions and to thoroughly wash salad vegetables. Building and education campaigns should be introduced to improve sanitary conditions, as promiscuous defaecation, associated with poverty and ignorance, keeps soil contamination high. Nightsoil (faecal waste) should not be used to fertilize gardens or vegetable crops. Dog faeces should not be left on lawns or parks (especially well-watered ones) where people congregate. Several countries have successfully controlled infections, mainly through regular periodic mass treatment, the provision of latrines and institutionalized public education.

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