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Strongyloidiasis

 
Sci-Tech Dictionary: strongyloidiasis
(′strän·jə′löi′dī·ə·səs)

(medicine) An infestation of humans with one of the roundworms of the genus Strongyloides.


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Medical Dictionary: stron·gy·loi·di·a·sis
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(strŏn'jə-loi-dī'ə-sĭs) or stron·gy·loi·do·sis (-dō'sĭs)
n.

Infection with the nematode Strongyloides stercoralis.

Veterinary Dictionary: strongyloidiasis
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Infection with Strongyloides spp. See also strongyloidosis.

Wikipedia: Strongyloidiasis
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Strongyloidiasis
Classification and external resources

Strongyloides stercoralis larva. Source: CDC
ICD-10 B78.
ICD-9 127.2
DiseasesDB 12559
MeSH D013322

Strongyloidiasis is a human parasitic disease caused by the nematode (roundworm) Strongyloides stercoralis. Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

Contents

Life cycle

Strongyloides LifeCycle.gif

The Strongyloides' life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:

  • Free-living cycle: The rabditiform larvae passed in the stool can either molt twice and become infective filariform larvae (direct development) or molt four times and become free living adult males and females that mate and produce eggs from which rabditiform larvae hatch. The latter in turn can either develop into a new generation of free-living adults, or into 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 are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine. In the small intestine they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rabditiform larvae. The rabditiform larvae can either be passed in the stool (see "Free-living cycle" above), or can cause autoinfection. In autoinfection, the rabditiform 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 follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into adults; or they may disseminate widely in 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 immunodepressed individuals.

Geographic distribution

Tropical and subtropical areas, but cases also occur in temperate areas (including the South of the United States). More frequently found in rural areas, institutional settings, and lower socio-economic groups.

Clinical features

Uncomplicated strongyloidiasis

Frequently asymptomatic. Gastrointestinal system symptoms include abdominal pain and diarrhea. Pulmonary symptoms (including Löffler's syndrome) can occur during pulmonary migration of the filariform larvae. Dermatologic manifestations include urticarial rashes in the buttocks and waist areas. Blood eosinophilia is ? present.

Strongyloidiasis can become chronic and then become completely asymptomatic.

Strongyloidiasis resulting from persistent infection can greatly mimic peptic ulcer and gallbladder disease. Many individuals with persistent strongyloidiasis undergo treatment or surgery for both peptic ulcer and gallbladder disease and then they fail to respond to the surgery or treatment. b Giving proton pump inhibitors, such as Nexium, Prilosec, Protonix and the likes, greatly reduces the HCl content of the stomach and allows the strongyloides to thrive. That is why often individuals with strongyloidiasis develop worse epigastric distress when placed on PPI's.

Finding strongyloides in the stool is negative in up to 70% of tests. It is important to undergo frequent stool sampling as well as duodenal biopsy if a bad infection is suspected. Treatment of strongyloides can be difficult and has been known to live in individuals for upwards of 1-2 years after treatment. Continued treatment may be necessary if symptoms persist. Treatment should be continued until symptoms resolve themselves.

In more advanced cases strongyloidiasis can create nodulation to begin to form in the lymphatic system of the small bowel. This can mimic Crohn's disease. It is important not to initiate steroid treatment for Crohn's if strongyloides is suspected. Doing so can result in disseminated infection.

Disseminated strongyloidiasis

Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become immunosuppressed. It presents with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia, and is potentially fatal. Eosinophilia is often present but is sometimes absent.

Dissemination can occur many decades after the initial infection[1] and has been associated with high dose corticosteroids, organ transplant, HIV,[2][3] lepromatous leprosy, tertiary syphilis, aplastic anemia, malnutrition, advanced tuberculosis and radiation poisoning.[4] It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are often unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is very small, so screening is usually not cost-effective, except in endemic areas.

Laboratory diagnosis

Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid. Examination of serial samples may be necessary, and not always sufficient, because direct stool examination is relatively insensitive.

The stool can be examined in wet mounts:

  • directly
  • after concentration (formalin-ethyl acetate)
  • after recovery of the larvae by the Baermann funnel technique
  • after culture by the Harada-Mori filter paper technique
  • after culture in agar plates

Culture techniques are the most sensitive, but are not routinely available in the West. Direct examination must be done on stool that is freshly collected and not allowed to cool down, because hookworm eggs hatch on cooling and the larvae are very difficult to distinguish from strongyloides.

The duodenal fluid can be examined using techniques such as the Enterotest string or duodenal aspiration. Larvae may be detected in sputum from patients with disseminated strongyloidiasis.

Treatment

The drug of choice for the treatment of uncomplicated strongyloidiasis is ivermectin. Ivermectin does not kill the strongyloides larvae only the adult worms therefore repeat dosaging may be necessary to properly eradicate the infection. There is an auto-infective cycle of roughly two weeks in which Ivermectin should be re-administered however additional dosaging may still be necessary as it will not kill strongyloides in the blood or larvae deep within the bowels or diverticuli. Other drugs that are effective are albendazole and thiabendazole (25 mg/kg twice daily for 5 days-- 400mg maximum (generally)).[3] All patients who are at risk of disseminated strongyloidiasis should be treated. It is not clear what the optimal duration of treatment for patients with disseminated infectious should be.[2]

References

  1. ^ Gill GV, Beeching NJ, Khoo S, et al. (2004). "A British Second World War veteran with disseminated strongyloidiasis". Trans R Soc Trop Med Hyg 98 (6): 382–6. doi:10.1016/j.trstmh.2003.11.002. PMID 15099996. http://linkinghub.elsevier.com/retrieve/pii/S0035920304000173. 
  2. ^ a b Kramer MR, Gregg PA, Goldstein M, Llamas R, Krieger BP. (1990). "Disseminated strongyloidiasis in AIDS and non-AIDS immunocompromised hosts: diagnosis by sputum and bronchoalveolar lavage". South Med J 83 (10): 1226–9. PMID 2218668. 
  3. ^ a b Gompels MM, Todd J, Peters BS, Main J, Pinching AJ. (1991). "Disseminated strongyloidiasis in AIDS: uncommon but important". AIDS 5 (3): 329–32. doi:10.1097/00002030-199103000-00015. PMID 2059374. 
  4. ^ Purtilo DT, Meyers WM, Connor DH (1974). "Fatal strongyloidiasis in immunosuppressed patients". Am J Med 56 (4): 488–93. doi:10.1016/0002-9343(74)90481-1. PMID 4818417. http://linkinghub.elsevier.com/retrieve/pii/0002-9343(74)90481-1. 

External links


 
 
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