Strongyloides stercoralis: A possible involvement with Morgellons Syndrome?

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Part 1

It is easy to understand why some people feel that the nematode, Strongyloides stercoralis, could be involved with our symptoms, at least for some. This is one of the best, easy to read article about this parasite I have found so far. I am not saying that this is what causes Morgellons or even that it is part of the symptom pattern for all, but perhaps some will find some similarities between this parasite and what they are experiencing as a parasitic infection:

Strongyloides stercoralis 2011/09/03 18:37:55.486 GMT-4

By Jason Hallman

Kingdom: Animalia Phylum: Nematoda Class: Secernentea Order: Rhabditida Family: Strongyloididae Genus: Strongyloides Species: Strongyloides stercoralis Geographic Range

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. (Cheng, 1986; Roberts and Janovy, 2000)

Biogeographic Regions: nearctic ; palearctic ; oriental ; ethiopian ; neotropical .

Other Geographic Terms: cosmopolitan . Habitat

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. (Cheng, 1986)

These animals are found in the following types of habitat: 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: urban ; suburban ; agricultural . Physical Description Length 0.90 to 2.50 mm (0.04 to 0.1 in)

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. (Cheng, 1986; Roberts and Janovy, 2000)

Some key physical features: ectothermic ; heterothermic ; bilateral symmetry .

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Notice that the description at the bottom of this post describes the food that these critters eat as being body fluids and detritivore (they are carnivores).

Definition from free dictionary: Detritivores include microorganisms such as bacteria and protists as well as larger organisms such as fungi, insects, worms, and isopod crustaceans. In a food chain, detritivores are primary consumers.:

Development

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. (Cheng, 1986; Roberts and Janovy, 2000) Reproduction

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. (Barnes, 1987; Cheng, 1986; Roberts and Janovy, 2000)

Key reproductive features: sexual ; fertilization (internal ); oviparous .

Behavior

Rhabitiform larvae of Strongyloides stercoralis molt four times becoming sexually mature adults. However, if the external environment becomes unfavorable, they will metamorphose into non-feeding filariform larvae that can infect humans or some other host. As mentioned earlier, if the filariform larvae enter the host through the skin, they must migrate to the intestine via the host's tissues. For years, it has been thought that the larvae are carried to the lungs by the blood. It is believed that they inhabit the alveoli by traveling through the right atrium and ventricle of the heart. The pulmonary artery eventually brings them to the lungs where they move up the bronchi and trachea and eventually are coughed up and swallowed. The filariform larvae then mature in the intestine. This has only proven to be the case in humans. In dogs the filariform larvae do not seem to travel through the lungs but seem to get to the intestine through any route.

During the autoinfective phase, filariform larvae reenter the host through the lower gut mucosa or the perianal skin. (Cheng, 1986; Roberts and Janovy, 2000)

Key behaviors: parasite ; motile ; sedentary . Communication and Perception

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). (Barnes, 1987; Roberts and Janovy, 2000)

Communicates with: tactile ; chemical .

Other communication keywords: pheromones .

Perception channels: tactile ; chemical . Food Habits

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. (Barnes, 1987; Cheng, 1986)

Primary Diet: carnivore (eats body fluids); detritivore .

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I hope this discussion highlights why it may be important, if parasitic infection is suspected, to treat any microbial infection which one might have. This particular parasite uses microbes as food and I suspect that it is not the only parasite that does this to thrive in the host's body. This was a concept that was first introduced to me by my infectious disease doctor. I was first treated for the viral infections which had been reactivated by the bad fish I ate (most likely I had ciguatera poisoning, again according to the ID doctor I saw three years later).

Right now I am just through taking cipro for an ear problem (no pain really, but I could not hear out of the ear and the ear drum was red). I now am noticing more energy as a result of using that drug. Perhaps there are fewer microbes to feed the parasites I feel are the main issue in my version of this syndrome. I also believe that using herbs and using some alternative methods of treatment helped me too over time. I think that sometimes we may have to use Western drugs for part of our issues, especially any serious infection that crops up (such when I lost my hearing in my ear, I was not going to wait around for herbs for, by the time they might work, I could also have lost my hearing in that ear). I feel that it is important to treat microbial infections if there are any parasitic infections in the mix of symptoms. And I agree with Scabdrrgr, that the use of stromectal (ivermectin) has improved my symptoms. While I have not used it as often as he describes I feel that over time this drug has helped diminish the worst of the parasitic involvement that I have experienced.

I do not think that the goal is that we all agree about what M is or is not. The goal is to get as well as we can in whatever way works for us. Until we know exactly what we have (in common) the paths used for improved health will probably differ, just the infections we might have vary from person to person. Even if we ever do know what the common thread to this illness is, I suspect that treatment will vary, at in at least some aspects.

Back to the discussion of Strongyloides stercoralis:

Other Foods: detritus ; microbes. Predation

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. Ecosystem Roles

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.

Key ways these animals impact their ecosystem: parasite . Species (or larger taxonomic groups) used as hosts by this species

Humans, Homo sapiens
Dogs, Canis lupus
Cats, Felidae
mammals, Mammalia

Economic Importance for Humans: Negative

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. (Roberts and Janovy, 2000; Ting, May 2000; Toma et al., March 2000; Zaha et al., Sept. 2000)

Ways that these animals might be a problem for humans: injures humans (causes disease in humans ); causes or carries domestic animal disease .

Economic Importance for Humans: Positive

Strongyloides stercoralis has no positive effects on humans.

Conservation Status

There is no conservation status for Strongyloides stercoralis.

Other Comments

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. (Dorris and Blaxter, July 2000) For More Information

To cite this page: Hallman, J. 2003. 'Strongyloides stercoralis'(On-line), Animal Diversity Web. Accessed October 21, 2011 animaldiversity.ummz.umich.edu/site/accounts/information/Strongyloides_stercoralis.html.

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This is a great description of how this parasite is introduced into the body in two ways. So many with Morgellons have symptoms which follow this parasite's route throughout the body (the coughing out of the lungs as it passes into the intestinal area to reproduce, the fact that it often migrates to the feet as well as gaining entry to the body in this manner). While this parasite is capable of living free and is often introduced into the body via the skin from dirt, it is also capable of auto-infection within the body itself. In this form, it would not necessarily be contagious unless it were introduced to another person from larvae or eggs on improperly washed hands.

This next sentence I extracted from the article is very important. If this infection becomes pervasive and frequent it may infect areas of the body this parasite would not normally invade and that is the CNS:

'If autoimmune infections become frequent, hyperinfection is said to occur allowing the parasite to migrate and cause pathological changes in areas of the body that they do not normally invade, including the central nervous system (CNS).'

This is the other sentence I feel has great significance:

'Unlike other helminthic parasites found in humans, adult worms of S. stercoralis reproduce in the GI tract “parthogenetically”3 (ie, development of a gamete without fer- tilization) resulting in an increase in worm burden without envi- ronmental re-exposure. It is this ability to multiply in the definitive host (ie, humans) that is the basis for the persistence of this organism over many years.'

This following discussion contains the long version of the life cycle of the Strongyloides stercoralis nematode. At the bottom of this post I will add the short version of its life cycle which in the book was accompanied by a line drawing of the stages of this parasite:

Strongyloides stercoralis life cycle--LONG version

Strongyloides stercoralis occurs when the free-living filariform larval form found in the soil comes in contact with skin. The larvae pene- trate the skin and migrate to the small vessels of the lungs by way of the venous circulation.3 The larvae then travel to the alveolar spaces, are coughed up and swallowed, and further mature into adult worms in the duodenum and jejunum. Adult females bury deep into the crypts of the duodenum and jejunum and penetrate the mucosa and submucosa to lay their eggs (ova) approximately 28 days after infection.3,4 Rhabditi- form larvae are released from the eggs and passed into the stool, and the infective form (filariform) develops in the soil by either direct transformation from the rhabditiform or indirectly from intermediate, free-living forms: the major route by which these parasites develop.

Rhabditiform larvae can be identified by their well-defined muscular esophagus and prominent esophageal bulbs. Unlike other helminthic parasites found in humans, adult worms of S. stercoralis reproduce in the GI tract “parthogenetically”3 (ie, development of a gamete without ferilization) resulting in an increase in worm burden without environmental re-exposure. It is this ability to multiply in the definitive host (ie, humans) that is the basis for the persistence of this organism over many years.

Rhabditiform larvae can also develop into the infective filariform larvae in the GI tract. or after passage into the feces. When the rhafditiform larvae emerge before being passed through the bowel, internal (in the bowel) or external autoinfection (perianal skin penetration) occurs, which initiates migration to and development in the lungs. If autoinfections become frequent, hyperinfection is said to occur allowing the parasite to migrate and cause pathological changes in areas of the body that they do not normally invade, including the central nervous system (CNS).3

Epidemiology:

Strongyloides stercoralis infection is endemic in Africa, Asia, Latin America, and areas of Southern and Eastern Europe. Prevalence rates of rhabditiform larvae in stool samples have been shown to vary between >40% in Africa to 1% to 7% in Europe. Endemic infection can be seen in areas of the United States as well, specifically in rural Appalachia and other southern areas, ranging from a prevalence of 0.4% to 3%.3 The frequency of S. stercoralis infection in homosexual men is approximately 3.9%; however, this estimate of prevalence is likely to be low because of the poor sensitivity of a single stool exam.

3 Pathogenesis:

When the adult worms and larvae pene- trate the upper intestine, or when the filariform larvae infect the lungs, an inflammatory response ensues consisting of eosinophil and mononuclear cell infiltrates.

3 Autoinfection

leading to high worm burdens and disseminated strongyloidiasis may occur in patients with decreased cell-mediated immunity.

6 Individuals at risk for autoinfection include those chronically taking steroids, renal transplant recipients, and patients with leukemia or lymphomas.7,8

Although S. stercoralis can persist as a latent infection for decades, it is important to recognize that changes in immune competency can initiate a conversion from asymptomatic disease to hyperinfection.

BRIEF description of Strongyloides life cycle

[F1] Life Cycle of Strongyloides stercoralis. Infection with S. stercoralis occurs when the free-living filariform larvae found in the soil penetrates the skin and migrates to the lungs via the venous circulation. After entering the alveolar spaces, they are coughed up, swallowed, and mature in the small intestine. Female rhabditiform larvae continue their life cycle by 3 different pathways:

1) development into infective filariform larvae and release from the GI tract (internal autoinfection),

2) release from the bowel and re-entry into the host via penetration of peri-anal skin (external autoinfection), or 3) release eggs and development into infective filariform larvae in the soil.

3) Excretion into the soil (free-living and filariform larvae)

labmed.ascpjournals.org/content/35/6/346.full.pdf

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Treating parasitic infections is very important to the health of those who have such infections. This is why I believe that it is unconscionable that those with pretty symptomatic parasite infections are turned away with a DOP diagnosis without any testing ever taking place. As already stated I do not know that strongyloides is common to all who have M, but there are many similarities between M symptoms and this parasite. If strongyloides spreads hyperinfection may occur. Steroid drugs are known to worsen strongyloides as it may lead to hyperinfection (sudden increase in parasite load) or disseminated infection (into various organs). Strongyloides are also known to cause central nervous system symptoms in patients.

Successful Ivermectin Treatment of Hepatic Strongyloidiasis Presenting with Severe Eosinophilia
Gulbas, Zafer MD; Kebapci, Mahmut MD; Pasaoglu, Ozgul MD; Vardareli, Eser MD


From the Departments of Hematology, Radiology, Pathology, and Gastroenterology, Osmangazi University Medical Faculty, Eskisehir, Turkey.

Reprint requests to Mahmut Kebapci, MD, Department of Radiology, Osmangazi University Medical Faculty, Meselik, 26480, Eskisehir, Turkey.

Accepted September 4, 2003. Abstract

A 49-year-old, previously healthy nurse presented with hepatic lesions and severe peripheral eosinophilia due to strongyloidiasis. Imaging studies of the abdomen showed predominantly peripheral, confluent hepatic lesions. The hepatic lesions and eosinophilia did not show any improvement with albendazole, but completely resolved with ivermectin treatment. Our findings suggest that Strongyloides stercoralis can present with isolated focal hepatic lesions and severe eosinophilia, and resolves with ivermectin treatment.

Key Points

* Strongyloides stercoralis can present with isolated focal hepatic lesions and severe peripheral eosinophilia.

* The clinical diagnosis of hepatic strongyloidiasis may be delayed because the clinical findings are nonspecific. The presence of eosinophilia warrants a search for this nematode.

* Imaging features are helpful in the diagnosis of hepatic strongyloidiasis.

* Ivermectin is a useful drug for the treatment of hepatic strongyloidiasis.

* Hepatic strongyloidiasis is exceedingly unusual; this case serves to remind physicians that isolated hepatic involvement and eosinophilia are features of strongyloidiasis.

Description of the severe form of strongylodiasis:

There are two severe forms of strongyloidiasis: hyperinfection syndrome and disseminated strongyloidiasis. A massive infection of the gastrointestinal tract and lungs is termed hyperinfection syndrome. Disseminated strongyloidiasis occurs when other organs are involved. These forms of strongyloidiasis may be seen in patients with chronic diseases, in patients on corticosteroids, and those who are immunocompromised.1,7 It is postulated that a large proportion of activated natural killer cells, perhaps producing interferon, suppressed the T-helper 2 response that controlled the strongyloides infection8 in patients with natural killer lymphocytosis. However, our patient did not have natural killer lymphocytosis.

If interested entire article is online here:

journals.lww.com/smajournalonline/Fulltext/2004/09000/Successful_Ivermectin_Treatment_of_Hepatic.33.aspx