Strongyloidiasis pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
*Strongyloides stercoralis is a nematode, 2.5 mm-long, | *Strongyloides stercoralis is a nematode, females can grow 2.5 mm-long, males grow to only about 0.9 mm (0.04 in) in length.<ref>{{cite book | last = Roberts | first = Larry | title = Gerald D. Schmidt & Larry S. Roberts' foundations of parasitology | publisher = McGraw Hill | location = New York | year = 2013 | isbn = 0073524190 }}</ref> | ||
*Both sexes 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. | |||
{{#ev:youtube|TSwN602mcn4}} | {{#ev:youtube|TSwN602mcn4}} | ||
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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 classified as a soil-transmitted helminth. The primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they are able to penetrate it and migrate through the body, eventually finding their way to the small intestine where they burrow and lay their eggs. Unlike other soil-transmitted helminths such as hookworm and whipworm, whose eggs do not hatch until they are outside the body, the eggs of Strongyloides hatch into larvae in the intestine. Most of these larvae will be excreted in the stool, but some of the larvae may molt and immediately re-infect the host either by burrowing into the intestinal wall or by penetrating the perianal skin. This characteristic of Strongyloides is termed auto-infection. The significance of auto-infection is that if left untreated, patients may remain infected throughout their lifetime.[1][2][3][4]
Pathophysiology
Pathogenesis
Strongyloides is a soil-transmitted helminth. The primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they are able to penetrate it and migrate through the body, eventually finding their way to the small intestine, where they burrow and lay their eggs. The eggs of Strongyloides hatch into larvae in the intestine. The majority of these larvae will be excreted in the stool, but some of the larvae may molt and immediately re-infect the host either by burrowing into the intestinal wall or by penetrating the perianal skin. This characteristic of Strongyloides is termed autoinfection. The significance of autoinfection is that, unless treated for Strongyloides, persons may remain infected throughout their lifetime.
Transmission
Contact with soil and autoinfection are the most common modes of transmission, though there have been rare cases of person-to-person transmission in:
- Organ transplantation
- Long-term care facilities
- Daycare centers
Incubation period
The incubation period of strongyloidiasis is unknown but it takes 28 days for larvae to appear in urine after the initial exposure. Local rash is the initial manifestation that can occur immediately(within a week of skin penetration). Abdominal symptoms typically occur approximately two weeks later.
Life cycle
The Strongyloides life cycle is more complex than that of most nematodes because of its alternation between free-living and parasitic cycles and its potential for autoinfection and multiplication within the host.
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.
- Historically it was believed that the larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed.
- However, 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 females live threaded 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 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 disseminate throughout 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 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, females can grow 2.5 mm-long, males grow to only about 0.9 mm (0.04 in) in length.[7]
- Both sexes 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.
{{#ev:youtube|TSwN602mcn4}}
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.