|Classification: Taxonomic ranks under review (cf. Encyclopedic Reference of Parasitology, 2001, Springer-Verlag)|
Metazoa (Animalia) (multicellular eukaryotes, animals)
Secernentea (Phasmidea) (with chemoreceptors known as phasmids)
Rhabditida (early-stage larvae with rhabditiform pharynx)
Rhabdiasoidea (threadworms, parthenogenetic females embedded in mucosa)
These slender cylindrical worms have a long oesophagus and uterus intertwined, giving the appearance of a twisted thread, hence their common name of ‘thread-worms’. They are unique amongst nematodes, being capable of both parasitic and free-living reproductive cycles. Only parthenogenetic female worms are parasitic, living in the small intestinal mucosa of various mammals, birds, reptiles and amphibians. Transmission involves a geo-helminth phase, where rhabditiform larvae in the soil form infective filariform larvae which penetrate the skin of their hosts. Sometimes, however, larvae develop into male and female worms which undergo one or more free-living cycles in the soil before producing infective larvae again.Strongyloides stercoralis [this species causes enteritis, Cochin diarrhoea, larval currens in humans]Parasite morphology: The parasite has an unusual developmental cycle involving the formation of eggs, free-living and parasitic larvae, free-living male and female adult worms, as well as parasitic parthenogenetic female worms. Eggs appear as small oval thin-shelled bodies, measuring 50-58µm in length by 30-34µm in width, and are partially embryonated at the 2-8 cell stage of development. Free-living larvae (L1 and L2) measure up to 350µm in length and have a rhabditiform pharynx (with a muscular oesophagus for feeding on particulate material). Infective third-stage larvae (L3) measure up to 600µm in length and have a filariform pharynx (with a long fine oesophagus for sucking fluids after penetrating host tissues). These larvae do not feed in the soil and are ensheathed with a closed mouth and a pointed notched tail. Parasitic worms are all parthenogenetic females, measuring from 2-3mm in length and characterized by the presence of an extremely long filariform pharynx (one third of body length) and a blunt pointed tail. Free-living male and female worms have a rhabditiform pharynx and are smaller in size, measuring up to 1mm in length. Males have two simple spicules and a gubernaculum, and a pointed tail curved ventrally. Females are stout with the vulva located around the middle of the body.
Host range: Thread-worm infections occur in a range of mammalian species throughout the world, particularly in tropical and temperate regions with warmer climates favouring the survival of parasite developmental stages in soil. Different species vary in their host-specificity, the species S. stercoralis being found in humans and companion animals, and thus should be considered zoonotic.
StrongyloidesspeciesHostsLocationClinical signsGeographic distribution
S. stercoralis – humans, primates, dogs, cats. Small intestine, bloody diarrhoea.Worldwide, esp. warmer regions in South America and southeast Asia
S. fuelleborni – apes, humans. small intestine, bloody diarrhoea. Africa, Asia
S. ransomi – pigs, small intestine, bloody diarrhoea. worldwide
S. planicepscatssmall intestinenon-pathogenicworldwide
S. cati (felis)catssmall intestinenon-pathogenicworldwide
S. tumefacienscatslarge intestinesmucosal tumoursworldwide
S. papillosussheep, cattlesmall intestinediarrhoea, anorexiaworldwide
S. westerihorses, donkeys, zebra, pigssmall intestinediarrhoeaworldwide
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.