Strongyloidiasis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin of the host, enter a venous or lymphatic channel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host's intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis.
Pathophysiology
Pathogenesis
Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin of the host, enter a venous or lymphatic channel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host's intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis. [1][2][3][4]
Transmission
- Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities
Incubation period
- The incubation period of strongyloidiasis is unknown but it takes 28 days for larvae to appear in urine after the initial exposure.
Life cycle
- The principal definitive hosts of S.stercoralis are humans, but infection in dogs can also occur. The Strongyloides life cycle includes the following stages:
Free-living cycle:
- The rhabditiform larvae passed in the stool can either become infective filariform larvae (direct development) or free living adult males and females.
- These adult forms mate and produce eggs from which rhabditiform larvae hatch, which eventually become infective filariform larvae.
- The filariform larvae penetrate the human host skin to initiate the parasitic cycle.
Parasitic cycle:
- Filariform larvae in contaminated soil penetrate the human skin and by various, often random, routes migrate into the small intestine.
- The larvae migrates via the bloodstream to the lungs, where they are eventually coughed up and swallowed.
- There is also evidence that larvae can migrate directly to the intestine via connective tissues.
- In the small intestine, they molt twice and become adult female worms.
- The female worms live in the epithelium of the small intestine and produce eggs through parthenogenesis, which yield rhabditiform larvae.
- The rhabditiform larvae can either be passed in the stool or cause autoinfection.
- In autoinfection, the rhabditiform larvae can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection).
- In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunosuppressed individuals.
Immune response
- The initial host immune response to Strongyloides infection is production of immunoglobulin E and eosinophilia in blood and tissues, which presumably prevents dissemination and hyper-infection in the immunocompetent host.[5][6]
- Adult female worms in otherwise healthy and asymptomatic individuals may persist in the gastrointestinal tract for years.
- If infected persons become immunocompromised, the reduction in cellular and humoral immunity may lead to an abrupt and dramatic increase in parasite load with systemic dissemination.
Associated Conditions
Prevalence of strongyloidiasis is higher in patients with conditions such as:
- Systemic rheumatic diseases
- Chronic renal failure
- Diabetes mellitus
- Malnutrition
- Alcoholism
Microscopic Pathology
- Strongyloides stercoralis is a nematode.
- Female worms can grow 2.5 mm-long, male worms can grow to only about 0.9 mm (0.04 in) in length.[7]
- Both sexes worms possess a tiny buccal capsule and cylindrical esophagus without a posterior bulb.
- 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.
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References
- ↑ Beknazarova M, Whiley H, Ross K (2016). "Strongyloidiasis: A Disease of Socioeconomic Disadvantage". Int J Environ Res Public Health. 13 (5). doi:10.3390/ijerph13050517. PMC 4881142. PMID 27213420.
- ↑ Ardiç N (2009). "[An overview of Strongyloides stercoralis and its infections]". Mikrobiyol Bul (in Turkish). 43 (1): 169–77. PMID 19334396.
- ↑ Keiser PB, Nutman TB (2004). "Strongyloides stercoralis in the Immunocompromised Population". Clin. Microbiol. Rev. 17 (1): 208–17. PMC 321465. PMID 14726461.
- ↑ "CDC - Strongyloides - Biology".
- ↑ Anthony RM, Rutitzky LI, Urban JF, Stadecker MJ, Gause WC (2007). "Protective immune mechanisms in helminth infection". Nat. Rev. Immunol. 7 (12): 975–87. doi:10.1038/nri2199. PMC 2258092. PMID 18007680.
- ↑ O'Connell EM, Nutman TB (2015). "Eosinophilia in Infectious Diseases". Immunol Allergy Clin North Am. 35 (3): 493–522. doi:10.1016/j.iac.2015.05.003. PMC 4515572. PMID 26209897.
- ↑ Roberts, Larry (2013). Gerald D. Schmidt & Larry S. Roberts' foundations of parasitology. New York: McGraw Hill. ISBN 0073524190.