Site of infection: Parasitic female worms become embedded in the small intestinal mucosa, forming tunnels in the epithelium at the bases of villi in the small intestines. Eggs and first-stage larvae are passed with host faeces. Infective third-stage larvae penetrate the skin and undergo pulmonary migration before forming parthenogenetic females in the intestines.

Pathogenesis: Light thread-worm infections remain asymptomatic, even though they may persist for years due to auto-infection or re-infection. Heavier infections, however, can cause several forms of disease in humans; including dermal, pulmonary, enteric and disseminated disease. Migrating larvae can race through the skin (up to 10 mm per hour) causing larval currens, characterized by urticaria, pruritis, eosinophilia, dermatitis, and inflammation. Pulmonary migration may cause a mild transient pneumonia, with coughing, wheezing, shortness of breath, and transient pulmonary infiltrates (Loeffler’s syndrome). Lesions caused by adult worms generally consist of catarrhal inflammation, although severe infections may result in necrosis and sloughing of the mucosa, haemorrhage, epigastric pain (may mimic peptic ulcer or Crohn’s disease), vomiting, abdominal distention, diarrhoea with voluminous stools and a malabsortion syndrome with dehydration and electrolyte disturbance, peripheral eosinophilia, and possibly reactive arthritis. Hyper-infections can develop when individuals are stressed or immuno-compromised resulting in the production of large numbers of filariform larvae which can penetrate the bowel and disseminate, causing colitis, polymicrobial sepsis, pneumonitis or neurological manifestations, such as meningitis and cerebral or cerebellar abscesses.

Mode of transmission: Even though thread-worms may form parasitic or free-living adults, they all have direct life-cycles involving a geo-helminth phase where infective larvae in soil penetrate the skin of their hosts. Parasitic parthenogenetic females produce partially embryonated eggs (several dozen per day) which hatch prior to excretion with host faeces. The emergent rhabditiform larvae (L1) feed on bacteria and organic debris, moult to second-stage larvae (L2) which feed and then develop either as parasitic or free-living stages. Homogonic strains develop directly into infective third-stage filariform larvae (L3) which can live in moist soil for several weeks. Heterogonic strains moult twice to form a generation of free-living males and females which feed on bacteria with a rhabditiform pharynx before producing unembryonated eggs which grow and moult twice to form infective filariform larvae. All filariform larvae penetrate the skin (or oral mucosa) of their hosts where they enter the circulation. Most larvae are carried to the lungs where they undergo pulmonary migration by penetrating alveoli and moving up the trachea to be swallowed (other routes of larval migration have been shown in experimental animal models). Parthenogenetic female worms parasitize the small intestines and only live for a few months, yet infections can continue indefinitely because hosts undergo self-infection (auto-infection). This occurs when eggs hatch in the intestines and develop into infective larvae which directly penetrate the lower gut or peri-anal region, thus leading to a new cycle of infection.

Differential diagnosis: Infections are diagnosed by the detection of larvae in faecal samples, as most eggs hatch internally within the host releasing rhabditiform larvae. Filariform larvae may occasionally be detected, especially during hyper-infection, and they can be identified by their notched tails. Although eggs are rarely detected in faeces, they are similar in size, shape and appearance to hook-worm eggs. Faecal culture can increase the sensitivity of microscopic diagnosis, by either concentrating larvae (Harada Mori technique) or amplifying populations through a generation of free-living males and females. Larval cultures also differentiate between thread-worm (Strongyloides) and hook-worm (Ancylostoma and Necator) infections, an important undertaking as treatment options differ (thread-worm larvae have a smaller buccal cavity and a larger genital primordium). Non-nutrient agar plate cultures of faeces have also been used to detect motile larvae. Several immunoserological tests have also been developed to detect host antibodies against thread-worm antigens, but they have difficulty in distinguishing between past and active infections.

Treatment and control: Several anthelmintics are reasonably effective against threadworm infections, but none are entirely satisfactory. Thiabendazole has been widely used but it has unpleasant side-effects, including nausea, vomiting, dizziness, malaise and smelly urine. Albendazole and levamisole have also shown some activity, but infections are not responsive to mebendazole or pyrantel. Treatment should be repeated after a week because of difficulty in confirming cure. Immuno-suppressive treatments should be avoided as they can result in rampant auto-infection. Preventive measures include the wearing of solid shoes in endemic areas, thoroughly washing salad vegetables, prohibiting the use of nightsoil to fertilize gardens, the sanitary disposal of faeces, the provision of latrines in poor areas, and public education campaigns.

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