Strongyloides stercolaris, also known as threadworm, and the disease it causes, Strongyloidiasis, are primarily found in tropical and subtropical areas of the world. Strongyloides stercolaris lavae was discovered by Louis Alexis Normand (1876) after observing the minute cylindrical worms in the diarrhoeic feces and intestinal walls of some French soldiers in Cochin-China. The parasite was named Strongyloides stercoralis (strongylus—round; eidos—resembling; stercoralis-fecal).
It is has been reported in areas of the South that are mostly rural and in the Appalachian Mountain region. Areas of poor sanitation, in which feces are disposed in the warm moist soil, provide a wonderful atmosphere for the organism to exist, especially when participating in the indirect cycle of reproduction. It is also common in Brazil, Columbia and in the Far East Myanmar, Thailand, Vietnam, Malaysia and Philippines. Strongyloides stercolaris has also been isolated in stool samples from Cameroon.
Morphology of Strongyloides stercolaris
The Egg of Strongyloides stercolaris
Strongyloides stercoralis eggs have traditionally been thought to be indistinguishable from hookworm eggs. However, there are two characteristics that, when present, which aid in the identification of the eggs. To begin, the standard Strongyloides stercoralis egg is only slightly smaller than hookworm eggs, measuring 48 by 35 m on average. Second, unlike hookworm, Strongyloides stercoralis eggs almost always contain fully formed larvae. Both organisms’ eggs are identical in that the two-four-, or eight-cell stage of embryonic cleavage is enclosed by a thin hyaline shell when present.
|Size||Average, 48 by 35 µm|
|Typical growth phase||Contains well-developed larvae|
|Embryonic cleavage||Two-, four-, or eight-cell stage, when present|
Rhabditiform Larvae of Strongyloides stercolaris
The actively feeding Strongyloides stercoralis rhabditiform larva measures 220 by 15 m on average. The larva has a short buccal cavity and a prominent genital primordium, while the hookworm larva has a long buccal cavity and a small genital primordium.
Filariform Larvae of Strongyloides stercolaris
The rhabditiform type molts into the long, slender, nonfeeding fiariform larva. The total length of this morphologic type is 690 m. The larva of Strongyloides stercoralis fiariform varies from that of the hookworm in two ways. First, it has a longer esophagus than the hookworm. Second, unlike S. stercoralis hookworm, the tail of S. stercoralis is notched or pointed.
Adult Female Strongyloides stercolaris
S. stercoralis has only been identified as a female adult. This tiny female worm, measuring about 2 by 0.4 mm, has a narrow buccal cavity as well as a long and slender esophagus. The body is colorless and seems almost translucent. The body is covered by a finely striated cuticle. Since no adult male S. stercoralis is known to exist, the adult female is thought to be parthenogenic, as there are no apparent morphologic structures indicating that a male is not needed for fertilization.
|Approximate size||2 by 0.4 mm|
|Other features||Colorless, transparent body; finely striated cuticle; short buccal cavity; Long and slender esophagus|
Life Cycle of Strongyloides stercolaris
Strongyloides stercoralis’ life cycle is complicated due to the numerous pathways by which it can mature. It is unusual among human nematodes in that, in addition to the parasitic cycle, it has a free-living soil cycle in which it can persist in soil for long periods of time, feeding on soil bacteria and passing through many generations.
The adult worm is present in the human intestine, lodged in the duodenum and upper jejunum mucosa. Individual worms have a lifespan of 3 to 4 months, but since they can cause autoinfection, the infection can last for years. In the intestine, only female worms are visible. It was thought that they were parthenogenetic, meaning that they could produce offspring without being fertilized by a male. However, it has since been shown that parasitic males do exist. They are both shorter and wider than females. They can be demonstrated in infected dogs in an experimental environment. They are not seen in human infections because they do not penetrate the intestinal wall and are hence removed from the intestine shortly after infection. They are not seen in human infections because they do not penetrate the intestinal wall and are thus removed from the intestine shortly after the females begin to oviposit. The majority of females, however, are most likely parthenogenetic.
The female worm is small and translucent, measuring about 2.5 mm in length and 0.05 mm in width. It has a cylindrical oesophagus in the anterior third of the body and intestines in the posterior two-thirds that open through the anus, which is located ventrally, just in front of the pointed tail tip. Paired uteri contribute to the vulva, which is located at the intersection of the middle and lower thirds of the body. The uteri of a gravid female produce thin-walled transparent ovoid eggs measuring 50 m by 30 m in dimension. The worm is an ovoviviparous parasite. The eggs laid in the mucosa hatch immediately, releasing rhabditiform (first stage) larvae that are about 0.25 mm long and have a relatively short muscular oesophagus that ends in an expanded bulb. The rhabditiform larvae migrate into the lumen and then down the gut, where they are excreted. They moult twice after reaching the soil to become infective filariform (third stage) larvae. The filariform larvae are slender, measuring about 0.55 mm in length, and have a long, uniformly widened oesophagus. It has a notched tail tip that is finely triradiate. The filariform larvae do not feed and can only survive in soil for around 12 days.
When a person walks barefoot on infective filariform larvae-infested dirt, the larvae penetrate the skin, typically on the sides of the feet or between the toes, enter the cutaneous lymphatics or blood vessels, and are brought along the venous circulation to the right side of the heart and the lungs. They escape from the pulmonary capillaries into the alveoli, travel up the respiratory tract to the pharynx, and are swallowed, eventually reaching the duodenum and jejunum, where they burrow into the mucosa. They reach maturity in 15 to 20 days and begin laying eggs. This mode of life cycle is known as direct growth, and it is the most common mode of human infection. It resembles the life cycle of the hookworm.
The worm also has an autoinfection cycle. During their passage down the intestine, the rhabditiform larvae develop into infective third stage larvae. Reinfection is caused by filariform larvae piercing the perianal and perineal skin during defecation. The larvae spend some time in the dermis of the perianal area, triggering a radiating perianal creeping eruption, which is a form of cutaneous larva migrans. They eventually enter the lymphatics or venules and travel to the right heart and lungs to complete the life cycle as mentioned above. This capacity to cause autoinfection explains why the infection can linger in patients for long periods of time, including up to 30 to 40 years after leaving endemic areas.
In another type of autoinfection, commonly seen in immunocompromised hosts, rhabditiform larvae released into the bowel walls mature into infective filariform larvae. They pass through the deeper layers of the intestine to meet the mesenteric venules and then circulate to complete the life cycle. Internal reinfection is a form of autoinfection. It may cause a severe infection, resulting in serious and, in some cases, fatal illness.
The rhabditiform larvae found in stools develop into free-living males and females in moist soil. The female is 1 mm long, while the male is 0.7 mm long. They mate in the ground. The fertilized female lays eggs, which hatch and give rise to the next generation of rhabditiform larvae. This can either repeat the free-living cycle or grow into filariform larvae that infect humans and start the parasitic process.
Strongyloides stercoralis’ primary host is humans, but dogs and cats have been found infected with morphologically indistinguishable strains. Strongyloides fullerborni is common in African monkeys. It infects pygmies in Zaire and Zambian forests.
It also infects humans in Papua New Guinea. Trichostrongylus, a parasite of sheep and goats found in Africa and Asia (including India), can cause asymptomatic human infection.
Pathogenesis and Clinical Features
Strongyloidosis is usually asymptomatic, with the only signs of infection being blood eosinophilia and larvae in stools. However, it may sometimes cause clinical manifestations that are serious and even fatal, particularly in those with a compromised immune response. The clinical disorder can be divided into three types: cutaneous, pulmonary, and intestinal. Hyper infection is the term used to describe the overwhelming severity of disease seen in the immunocompromised. AIDS patients can develop generalized strongyloidosis.
There may be dermatitis, with erythema and itching at the site of filariform larvae penetration, particularly if a large number of larvae reach the skin.
An allergic reaction can occur in those who have been sensitized by prior infection. This may prevent larvae from circulating in their blood, causing them to migrate in their skin, resulting in a creeping eruption or larva migrans. This rapidly progressing linear urticarial track caused by migrating strongyloides larvae has been given the name larva currens (meaning “racing larva”). These are frequently associated with autoinfection and begin perianally.
Small haemorrhages occur during the larvae’s escape from the pulmonary capillaries into the alveoli, as well as cellular penetration into the alveoli and bronchioles.
Bronchopneumonia may be present, which may progress to chronic bronchitis and asthmatic symptoms in some people. Larvae can be discovered in the sputum.
The symptoms may be similar to those of a peptic ulcer or malabsorption syndrome. Mucus diarrhoea is often present. In severe cases, the mucosa may be honeycombed with the worm and there may be excessive sloughing, resulting in dysenteric stools.
Extensive internal reinfection occurs in debilitated individuals, especially those with cellular immune defects, resulting in massive numbers of adult worms in the intestines and lungs, as well as larvae in various tissues and organs. This is referred to as hyperinfection. Severe malnutrition, lepromatous leprosy, lymphoreticular malignancies, AIDS, immunosuppressive drugs, and other conditions characterized by deficient cellmediated immunity predispose to this disease. Hyperinfection is a significant risk of steroid therapy and other forms of chronic immunosuppression, such as in transplant patients. The manifestations differ depending on the places affected. Brain abscess, meningitis, and peritonitis are also possible complications.
It has been reported that circulating strongyloides larvae carry intestinal bacteria that can cause septicaemia.
Diagnosis of Strongyloides stercolaris
- The most effective method of specific diagnosis is the demonstration of rhabditiform larvae in freshly passed stools. Larvae discovered in stale stools must be distinguished from larvae hatching from hookworm eggs. Larvae are also found in sputum and gastric aspirates.
- When larvae are scarce in stools, stool culture can help with diagnosis. The larvae grow into free-living forms and multiply in stools-filled charcoal cultures. After 7 to 10 days, there will be a large number of free-living larvae and adults.
- Serological tests using strongyloides or filarial antigens have been identified.
- There have been reports of complement fixation, indirect haemagglutination, and ELISA. However, the antigens are not widely available, and the tests’ usefulness is limited by extensive cross reactions.
- Radiological manifestations of intestinal infection are said to be distinctive and useful in diagnosis.
- The presence of peripheral eosinophilia is a common finding. However, in cases of extreme hyper infection, eosinophilia may be absent.
Treatment of Strongyloides stercolaris
To avoid serious invasive disease, all cases of Strongyloidiasis, whether symptomatic or not, should be treated. Ivermectin, thiabendazole, and mebendazole are all effective against Strongyloidiasis
Prevention of Strongyloides stercolaris
The general methods of prevention include avoiding contact with infective soil and polluted surface waters, as well as avoiding soil contamination with feces.