Strongyloidiasis

Classification and external resources

Strongyloides stercoralis larva. Source: CDC

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
[hide]

• 1 Life cycle
• 2 Geographic distribution
• 3 Clinical features
 o 3.1 Uncomplicated strongyloidiasis
o 3.2 Disseminated strongyloidiasis
• 4 Laboratory diagnosis
• 5 Treatment
• 6 References

• 7 External links

[edit] Life cycle

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.

[edit] 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.

[edit] Clinical features

[edit] 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 generally 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.

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.
[edit] 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.

[edit] 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.

[edit] 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—400 mg 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]

Levamisole and Mimosa pudica extract each immobilize filariform larvae of Strongyloides
stercoralis in less than one hour.[5]

Eryngial, a patented extract of Eryngium foetidum,[6] has been investigated as a treatment for
strongyloidiasis.[7]

Folk remedies for strongyloidiasis include: wormwood (Artemisia absinthium); sweet

wormwood (Artemisia annua); pumpkin seeds; astragalus root (Astragalus membranaceus);
culantro leaves (Eryngium foetidum); noni juice (Morinda citrifolia); and temple tangor/royal
mandarin/temple orange (Citrus reticulata).