Ascariasis pathophysiology: Difference between revisions
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{{Ascariasis}} | {{Ascariasis}} | ||
{{CMG}}; '''Associate Editor-In-Chief:''' Imtiaz Ahmed Wani, [[M.B.B.S]] | {{CMG}}; '''Associate Editor-In-Chief:''' Imtiaz Ahmed Wani, [[M.B.B.S]] | ||
==Life cycle== | ==Overview== | ||
==Pathophysiology== | |||
===Life cycle=== | |||
[[Image:Ascariasis LifeCycle - CDC Division of Parasitic Diseases.gif|thumb|left|260px|Adult worms (1) live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3), depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (6) (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small intestine, they develop into adult worms (8). Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.]]First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever; observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during migration of the larvae. However there are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and [[eosinophilia]]. | [[Image:Ascariasis LifeCycle - CDC Division of Parasitic Diseases.gif|thumb|left|260px|Adult worms (1) live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks (3), depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (6) (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon reaching the small intestine, they develop into adult worms (8). Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.]]First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever; observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during migration of the larvae. However there are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and [[eosinophilia]]. | ||
==Source== | ===Source=== | ||
The source of transmission is from soil and vegetation on which fecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves by a different type of roundworm can cause infection with that type of worm (Toxocara canis, etc) as occasionally occurs with groomers. | The source of transmission is from soil and vegetation on which fecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves by a different type of roundworm can cause infection with that type of worm (Toxocara canis, etc) as occasionally occurs with groomers. | ||
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Transmission from human to human by direct contact is impossible.[http://www.cdc.gov/ncidod/dpd/parasites/ascaris/factsht_ascaris.htm#contagious] | Transmission from human to human by direct contact is impossible.[http://www.cdc.gov/ncidod/dpd/parasites/ascaris/factsht_ascaris.htm#contagious] | ||
==Animal models for Ascaris infestation== | ===Animal models for Ascaris infestation=== | ||
There are two animal models for studying Ascaris infection: | There are two animal models for studying Ascaris infection: | ||
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* ''Ascaris suum'' in experimentally infected pigs. (Lichtensteiger CA et al; 1999) | * ''Ascaris suum'' in experimentally infected pigs. (Lichtensteiger CA et al; 1999) | ||
==Trivia== | ===Trivia=== | ||
*Ascariasis may result in allergies to shrimp and dustmites due to the shared [[antigen]], [[tropomyosin]]. | *Ascariasis may result in allergies to shrimp and dustmites due to the shared [[antigen]], [[tropomyosin]]. | ||
*Ascaris have an aversion to some general anesthetics and may exit the body, sometimes through the mouth.[http://arpa.allenpress.com/arpaonline/?request=get-document&doi=10.1043%2F0003-9985(2000)124%3C0174:AL%3E2.0.CO%3B2] | *Ascaris have an aversion to some general anesthetics and may exit the body, sometimes through the mouth.[http://arpa.allenpress.com/arpaonline/?request=get-document&doi=10.1043%2F0003-9985(2000)124%3C0174:AL%3E2.0.CO%3B2] | ||
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==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WikiDoc Help Menu}} | {{WikiDoc Help Menu}} | ||
{{WikiDoc Sources}} | {{WikiDoc Sources}} | ||
Revision as of 20:26, 23 August 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Imtiaz Ahmed Wani, M.B.B.S
Overview
Pathophysiology
Life cycle
First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever; observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during migration of the larvae. However there are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and eosinophilia.
Source
The source of transmission is from soil and vegetation on which fecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves by a different type of roundworm can cause infection with that type of worm (Toxocara canis, etc) as occasionally occurs with groomers.
Transmission also comes through municipal recycling of wastewater into crop fields. This is quite common in emerging industrial economies, and poses serious risks for not only local crop sales but also exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable exports.
Transmission from human to human by direct contact is impossible.[2]
Animal models for Ascaris infestation
There are two animal models for studying Ascaris infection:
- Mouse-Ascaris suum test model. (Howes HL Jr. J Parasitol. 1971 Jun; 57(3): 487-93.)
- Ascaris suum in experimentally infected pigs. (Lichtensteiger CA et al; 1999)
Trivia
- Ascariasis may result in allergies to shrimp and dustmites due to the shared antigen, tropomyosin.
- Ascaris have an aversion to some general anesthetics and may exit the body, sometimes through the mouth.[3]
| Genus and Species | Ascaris lumbricoides |
|---|---|
| Common Name | Giant Intestinal Roundworm |
| Etiologic Agent of: | Ascariasis |
| Infective stage | Embryonated Egg |
| Definitive Host | Man |
| Portal of Entry | Mouth |
| Mode of Transmission | Ingestion of Embryonated egg through contaminated food or water |
| Habitat | Small Intestine |
| Pathogenic Stage | Adult Larva |
| Mode of Attachment | Retention in the mucosal folds using pressure |
| Mode of Nutrition | Feeding of Chyme |
| Pathogenesis | Larva – pneumonitis, Loeffler’s syndrome;
Adult – Obstruction, Liver abscess, Appendicitis. With Blood-Lung Phase along with Hookworms and Strongyloides stercoralis. |
| Laboratory diagnosis | Concentration methods and Direct Fecal Smear: Kato-Katz |
| Treatment | Albendazole, Mebendazole, or Pyrantel Pamoate |
| Diagnostic Feature - Adult | Female - prominent genital girdle |
| Diagnostic Feature - Egg | Coarse mammilated albuminous coating |