It has previously been reported that Strongyloides stercoralis is amazingly divergent from Strongyloides ratti. ssrRNA sequencing found that there was only a 70% similarity between gene sequences. This is unusual because two members of the same genus are never found to be that different. The divergence has recently been found to be a result of the fact that the gene sequence of S. stercoralis used in the study were hybrids of nematode and fungal sequences. It has now been confirmed that the ssrRNA between the two species' is just over 90% similar.
Nematodes within the Secernentea have phasmids, which are unicellular glands. Phasmids likely function as chemoreceptors. Females may produce pheromones to attract males.
Nematodes in general have papillae, setae and amphids as the main sense organs. Setae detect motion (mechanoreceptors), while amphids detect chemicals (chemoreceptors).
Communication Channels: tactile ; chemical
Other Communication Modes: pheromones
Perception Channels: tactile ; chemical
There is no conservation status for Strongyloides stercoralis.
There are three stages in the life-cycle of Strongyloides stercoralis: free-living, parasitic, and autoinfection. After copulation, the free-living female accumulates eggs in her uterus that contain partially developed larvae. The eggs are laid in the soil where further development occurs. The rhabitiform larvae either become free-living adults or they become infective (filariform) 3rd stage larvae. Only females can enter the next phase of development, the parastitic stage.
To continue development, the filariform larvae must penetrate a host's skin or be ingested. If they enter the host through the skin, they must travel through host tissues in order to reach the final destination, the intestine. There, the females lay parthenogenetic eggs which give rise to rhabitiform larvae. These eventually leave the host via the feces and develop into free-living adults or metamorphose into filariform larvae.
Another variant of the life cycle is the autoinfective phase. Filariform larvae, migrating to the exterior, can reinfect the host by penetrating the skin and traveling in the blood to the lungs.
Strongyloides stercoralis causes strongyloidiasis in humans. Infection occurs via contact with filariform larvae in water or soil. The disease is most prevalent in areas of poor sanitation such as those that have poor sewage disposal sites.
Strongyloidiasis occurs in three phases: invasive, pulmonary, and intestinal. Filariform larvae that penetrate the skin cause itching at the the entry site. Slight hemorrhage and swelling may appear as well and if bacteria get into the site, inflammtion is likely.
The pulmonary phase of the disease is characterized by wheezing, a burning sensation in the chest, sputum production, as well as other symptoms of bronchial pneumonia. People who are thought to have a pulmonary infection are diagnosed with a chest x-ray. Pulmonary infection can be fatal because it can eventually result in repiratory failure. Elderly people, those with AIDS, and people who have had organ transplants have a very high risk of pulmonary strongyloidiasis. AIDS patients and those with organ transplants are at such a high risk because they are immunosuppressed, an effect most likely due to corticosteroid use in the latter group. The immune system is not able to fight off the parasite and this results in a high rate of autoinfection. Much care should be taken to diagnose pulmonary strongyloidiasis properly because the symptoms of it are very similar to those of asthma and asthma is treated with corticosteroids, which could result in increased autoinfection.
The intestinal phase occurs when the parasite penetrates the intestinal mucosa. Large patches of mucosa can be sloughed off in the process. An aching pain is felt in the abdomen and in chronic cases, relapsing colitis is very likely. Ulceration of the intestine can occur in some cases if not treated properly and this can lead to septicemia which is, more often than not, fatal.
Strongyloidiasis is most often diagnosed by a fecal smear, but in some cases, where infection is not rampant, agar plate culture to detect Strongyloides stercoralis is most effective (more so than the conventional filter paper culture). Sometimes, embryonated eggs may even be seen in the stool of patients. However, different numbers of juveniles pass through the feces each day and as autoinfection occurs, the numbers of juveniles exiting the body decreases markedly.
There are three drugs that are primarily used to treat strongyloidiasis. Each regimen needs to be repeated after one or two weeks because it is difficult to confirm a patient as cured. In a study conducted by Japanese doctors, ivermectin proved to be most effective in treating the disease with a 97% rate of eradication. It was given in a 6 mg single dose. The next most successful drug was albendazole (400 mg/day for three days) with a cure rate of 77.4%. Pyrvinium pamoate once only found to cure about 23.3% of those tested. This drug was given at 5 mg/kg/day for 3 days. Thiabendazole was once thought to be an effective drug, but side effects like nausea, vomiting, and smelly urine have caused the drug to lose favor among doctors.
Negative Impacts: injures humans (causes disease in humans ); causes or carries domestic animal disease
Strongyloides stercoralis has no positive effects on humans.
The three most important definitive hosts for Strongyloides stercoralis are humans, dogs, and cats. They frequently use other mammals as hosts as well, though with much less frequency.
Ecosystem Impact: parasite
Species Used as Host:
The three most important definitive hosts for Strongyloides stercoralis are humans, dogs, and cats. They frequently use other mammals as hosts as well, though with much less frequency. Parasitic females feed on the tissue of the host's internal organs which includes the intestines as well as the lungs. Free-living adults and rhabitiform larvae feed on organic debris in soil or water.
Pharyngeal glands and intestinal epithelium produce digestive enzymes to feed on the hosts’ body fluids. Extracellular digestion begins within the lumen and is finished intracellularly.
Other Foods: detritus ; microbes
Primary Diet: carnivore (Eats body fluids); detritivore
Strongyloides stercoralis is most notably found in the tropics and the subtropics, but it can occur in temperate climates as well. Because of the variety of hosts which it can parasitize, the worm can be found in various areas around the world. In North America, it has primarily been found in large cities, specifically, New York City, Chicago, and Montreal. There is also a high incidence of Strongyloides stercoralis in Asia, Africa, tropical America, the Pacific Islands, and even in parts of the former Soviet Union.
Biogeographic Regions: nearctic ; palearctic ; oriental ; ethiopian ; neotropical
Other Geographic Terms: cosmopolitan
Free-living Strongyloides stercoralis prefer the moist soil of warm climates. In the parasitic generation, the most common habitat in the host is the mucosal lining of the small intestine. Rarely, filariform larvae have been observed to take up residence in the lining of the bronchi and trachea and lay their eggs there after transforming to adults.
Habitat Regions: temperate ; tropical ; terrestrial ; freshwater
Terrestrial Biomes: desert or dune ; savanna or grassland ; chaparral ; forest ; rainforest ; scrub forest ; mountains
Aquatic Biomes: lakes and ponds; rivers and streams; temporary pools
Wetlands: marsh ; swamp
Other Habitat Features: urban ; suburban ; agricultural
Strongyloides stercoralis is generally very long and cylindrical. It has four layers of cuticle that are typical of most nematodes. The epicuticle is the outer-most layer and the exocuticle is immediately beneath it. The mesocuticle is beneath the exocuticle and is generally composed of very well organized fibrous layers. The endocuticle is the innermost cuticle and although its makeup is similar to the meso, its fibers are not well ordered.
On the body surface, there are amphids which act as chemoreceptors and they open to the outside via pores which are located on the lips or on other anterior extremities. The worm has lateral alae, which can be seen as ridges which extend, in some cases, across the body.
The mouth of Strongyloides stercoralis opens into a buccal capsule, which, in both sexes, is very small. From the buccal capsule, food moves into the esophagus which is very long, cylindrical, and lacking a bulb at its posterior end unlike most other nematodes. The esophagous is connected to the intestine via an esophago-intestinal valve. The intestine is divided into three parts and is lined with a single layer of epithelium. The most anterior region of the intestine is the ventricular region and it has a secretory function. The midregion, and the posterior prerectal region function primarily in absorption. The intestine ends in the rectum and the alimentary tract eventually opens posteriorly through the anus.
The Strongyloides stercoralis body cavity is known as a pseudocoel. The reproductive system of males consists of vas deferens which extend from the testes and they enlarge in the posterior portion of the body to form the seminal vesicle. Males possess two copulatory spicules in addition to a gubernaculum. Females, on the other hand, usually have two ovaries and an oviduct which extends from it. At the terminal end of the oviduct is a seminal receptacle, which connects the oviduct to the uterus. Free-living females have uteri which contain more eggs than parasitic females. In parasitic females, the uteri are convergent and the vulva is in the posterior portion of the body. The free-living female has a vulva that is more equatorial.
Parasitic adult females range in length from 2.0 to 2.5 mm, larvae range in length from 300-800 micrometers, while the free-living male can grow up to 0.9 mm in length and 40 to 50 micrometers in width.
Range length: 0.9 to 2.5 mm.
Other Physical Features: ectothermic ; heterothermic ; bilateral symmetry
Sexual Dimorphism: female larger; sexes shaped differently
These parasites are probably not preyed on directly, but are ingested. Larval mortality is high as most of the parasites do not reach appropriate hosts.
Females may produce a phermomone to attract males. The male coils around a female with his curved area over the female genital pore. The gubernaculum, made of cuticle tissue, guides spicules which extend through the cloaca and anus. Males use spicules to hold the female during copulation. Nematode sperm are amoeboid-like and lack flagella.
There are three stages in the life-cycle of Strongyloides stercoralis: free-living, parasitic, and autoinfection. After copulation, the free-living female accumulates eggs in her uterus that contain partially developed larvae. The eggs are laid in the soil where further development occurs. The rhabitiform larvae either become free-living adults or they become infective (filariform) 3rd stage larvae. Only females can enter the next phase of development, the parastitic stage.
Key Reproductive Features: sexual ; fertilization (Internal ); oviparous
Parental Investment: pre-fertilization (Provisioning)
Strongyloides stercoralis is a human pathogenic parasitic roundworm causing the disease strongyloidiasis. Its common name in the US is threadworm. In the UK and Australia, however, the term threadworm can also refer to nematodes of the genus Enterobius, otherwise known as pinworms.[1]
The Strongyloides stercoralis nematode can parasitize humans. The adult parasitic stage lives in tunnels in the mucosa of the small intestine. The genus Strongyloides contains 53 species,[2][3] and S. stercoralis is the type species. S. stercoralis has been reported in other mammals, including cats and dogs. However, it seems that the species in dogs is typically not S. stercoralis, but the related species S. canis. Non-human primates are more commonly infected with S. fuelleborni and S. cebus, although S. stercoralis has been reported in captive primates. Other species of Strongyloides that are naturally parasitic in humans, but with restricted distributions, are S. fuelleborni in central Africa and S. kellyi in Papua New Guinea.
S. stercoralis infection is associated with fecal contamination of soil or water. Hence, it is a very rare infection in developed economies. In developing countries, it is less prevalent in urban areas than in rural areas (where sanitation standards are poor). S. stercoralis can be found in areas with tropical and subtropical climates.[4]
Strongyloidiasis was first described in the 19th century in French soldiers returning home from expeditions in Indochina. Today, the countries of the old Indochina (Vietnam, Cambodia, and Laos) still have endemic strongyloidiasis, with the typical prevalences being 10% or less. Regions of Japan used to have endemic strongyloidiasis, but control programs have eliminated the disease. Strongyloidiasis appears to have a high prevalence in some areas of Brazil and Central America. It is endemic in Africa, but the prevalence is typically low (1% or less). Pockets have been reported from rural Italy, but the current status is unknown. In the Pacific islands, strongyloidiasis is rare, although some cases have been reported from Fiji. In tropical Australia, some rural and remote Australian Aboriginal communities have very high prevalences of strongyloidiasis.[5]
In some African countries (e.g., Congo), S. fuelleborni was more common than S. stercoralis in parasite surveys from the 1970s, but the current status is unknown. In Papua New Guinea, S. stercoralis is endemic, but prevalence is low. However, in some areas, another species, S. kellyi,[6] is a very common parasite of children in the New Guinea Highlands and Western Province.[6]
Knowledge of the geographic distribution of strongyloidiasis is of significance to travelers who may acquire the parasite during their stays in endemic areas.
Because strongyloidiasis could theoretically be transmittable through unsanitary bedclothes care must be taken never to use unclean hotel bed sheets in endemic areas. Using plastic slippers when showering may be very important when travelling in tropical regions.
Estimates of the number of people infected vary with one estimate putting the figure at 370 million worldwide.[7][8] Local prevalence can exceed 40% in some tropical and subtropical countries.[9]
The life cycle of this parasite is more complex than that of most nematodes, with its alternation between free-living and parasitic cycles, and its potential for autoinfection (the parasite has the ability to complete its life cycle without the involvement of another host) and multiplication within the host. The parasitic cycle is homogonic, while the free-living cycle is heterogonic. The heterogonic life cycle is advantageous to the parasite because it allows reproduction in the absence of a host.
In the free-living cycle, the rhabditiform larvae passed in the stool can either molt twice and become infective filariform larvae (direct development) or molt four times and become free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. In the direct development, first-stage larvae (L1) transform into infective larvae (IL) via three molts. The indirect route results first in the development of free-living adults that mate; the female lays eggs, which hatch and then develop into IL. The direct route gives IL faster (three days) versus the indirect route (seven to 10 days). However, the indirect route results in an increase in the number of IL produced. Speed of development of IL is traded for increased numbers. The free-living males and females of S. stercoralis die after one generation; they do not persist in the soil. The latter, in turn, can either develop into a new generation of free-living adults or develop into infective filariform larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle. Upon contact with contaminated soil, infectious larvae contained in the soil can penetrate the skin. While S. stercoralis is attracted to chemicals such as carbon dioxide or sodium chloride, these chemicals are not specific. Larvae have been thought to locate their hosts via chemicals in the skin, the predominant one being urocanic acid, a histidine metabolite on the uppermost layer of skin that is removed by sweat or the daily skin-shedding cycle.[10] Urocanic acid concentrations can be up to five times greater in the foot than any other part of the human body. Some of them enter the superficial veins and are carried in the blood to the lungs, where they enter the alveoli. They are then coughed up and swallowed into the gut, where they parasitise the intestinal mucosa of the duodenum and jejunum. In the small intestine, they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and, by parthenogenesis, produce eggs, which yield rhabditiform larvae. Only females will reach reproductive adulthood in the intestine. Female strongyloids reproduce through parthenogenesis. The eggs hatch in the intestine and young larvae are then excreted in the feces. It takes about two weeks to reach egg development from the initial skin penetration. By this process, S. stercoralis can cause both respiratory and gastrointestinal symptoms. The worms also participate in autoinfection, in which the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine, where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons not having been in an endemic area and of hyperinfections in immunodepressed individuals.
Dogs can act as a host for this parasite both in the wild and in the laboratory but transmission from dog to human has been difficult to prove. Molecular genetic analyses have shown that there are two populations of this parasite in dogs, one of which (type B) is exclusive to dogs and a second (type A) that is common to dogs and humans.[11][12] These two genotypes may be separate species. The identity of the genes suggests that dog to human transmission may occur.
Whereas males grow to only about 0.9 mm (0.04 in) in length, females can grow from 2.0 to 2.5 mm (0.08 to 0.10 in). Both sexes also possess a tiny buccal capsule and cylindrical esophagus without a posterior bulb.[13] In the free-living stage, the esophagi of both sexes are rhabditiform. Males can be distinguished from females by two structures: the spicules and gubernaculum.
An unusual feature of S. stercoralis is autoinfection. Only one other species in the genus Strongyloides, S. felis, has this trait. Autoinfection is the development of L1 into small infective larvae in the gut of the host. These autoinfective larvae penetrate the wall of the lower ileum or colon or the skin of the perianal region, enter the circulation again, travel to the lungs, and then to the small intestine, thus repeating the cycle. Autoinfection makes strongyloidiasis due to S. stercoralis an infection with several unusual features.
Persistence of infection is the first of these important features. Because of autoinfection, humans have been known to still be infected up to 65 years after they were first exposed to the parasite (e.g., World War II or Vietnam War veterans). Once a host is infected with S. stercoralis, infection is lifelong unless effective treatment eliminates all adult parasites and migrating autoinfective larvae.
Many people infected are asymptomatic at first. Symptoms include dermatitis: swelling, itching, larva currens, and mild hemorrhage at the site where the skin has been penetrated. Spontaneous scratch-like lesions may be seen on the face or elsewhere. If the parasite reaches the lungs, the chest may feel as if it is burning, and wheezing and coughing may result, along with pneumonia-like symptoms (Löffler's syndrome). The intestines could eventually be invaded, leading to burning pain, tissue damage, sepsis, and ulcers. Stools may have yellow mucus with a recognizable smell. Chronic diarrhea can be a symptom.[14] In severe cases, edema may result in obstruction of the intestinal tract, as well as loss of peristaltic contractions.[15]
Strongyloidiasis in immunocompetent individuals is usually an indolent disease. However, in immunocompromised individuals, it can cause a hyperinfective syndrome (also called disseminated strongyloidiasis) due to the reproductive capacity of the parasite inside the host. This hyperinfective syndrome can have a mortality rate close to 90% if disseminated.[16][17][18]
Immunosuppressive drugs, especially corticosteroids and agents used for tissue transplantation, can increase the rate of autoinfection to the point where an overwhelming number of larvae migrate through the lungs, which in many cases can prove fatal. In addition, diseases such as human T-lymphotropic virus 1, which enhance the Th1 arm of the immune system and lessen the Th2 arm, increase the disease state.[17] Another consequence of autoinfection is the autoinfective larvae can carry gut bacteria back into the body. About 50% of people with hyperinfection present with bacterial disease due to enteric bacteria. Also, a unique effect of autoinfective larvae is larva currens due to the rapid migration of the larvae through the skin. Larva currens appears as a red line that moves rapidly (more than 5 cm or 2 in per day), and then quickly disappears. It is pathognomonic for autoinfective larvae and can be used as a diagnostic criterion for strongyloidiasis due to S. stercoralis.
Locating juvenile larvae, either rhabditiform or filariform, in recent stool samples will confirm the presence of this parasite.[19] Other techniques used include direct fecal smears, culturing fecal samples on agar plates, serodiagnosis through ELISA, and duodenal fumigation. Still, diagnosis can be difficult because of the day-to-day variation in juvenile parasite load.
Ideally, prevention, by improved sanitation (proper disposal of feces), practicing good hygiene (washing of hands), etc., is used before any drug regimen is administered.
Ivermectin is the drug of choice for treatment, due to its low side effect profile.[20] Albendazole is also effective in treating strongyloidiasis. Mebendazole has a much higher failure rate in clinical practice than albendazole or ivermectin.[21] However, these drugs have little effect on the autoinfective larvae. Hence, repeat treatments with ivermectin or albendazole must be administered to kill newly matured parasites that have developed from the autoinfective larvae. This means a full treatment dose every two weeks until all larvae capable of maturing into adults have been extirpated. Follow-up stool samples, potential additional treatment, and blood tests are necessary to ensure a cure.[22]
This parasite depends on chemical cues to find a potential host. It uses sensor neurons of class AFD to identify cues excreted by the host.[23] S. stercoralis is attracted to nonspecific attractants of warmth, carbon dioxide, and sodium chloride. Urocanic acid, a component of skin secretions in mammals, is a major chemoattractant. Larvae of S. stercoralis are strongly attracted to this compound.[10] This compound can be suppressed by metal ions, suggesting a possible strategy for preventing infection.
Strongyloides stercoralis is a human pathogenic parasitic roundworm causing the disease strongyloidiasis. Its common name in the US is threadworm. In the UK and Australia, however, the term threadworm can also refer to nematodes of the genus Enterobius, otherwise known as pinworms.
The Strongyloides stercoralis nematode can parasitize humans. The adult parasitic stage lives in tunnels in the mucosa of the small intestine. The genus Strongyloides contains 53 species, and S. stercoralis is the type species. S. stercoralis has been reported in other mammals, including cats and dogs. However, it seems that the species in dogs is typically not S. stercoralis, but the related species S. canis. Non-human primates are more commonly infected with S. fuelleborni and S. cebus, although S. stercoralis has been reported in captive primates. Other species of Strongyloides that are naturally parasitic in humans, but with restricted distributions, are S. fuelleborni in central Africa and S. kellyi in Papua New Guinea.
