1 of 19

file:///

Official reprint from UpToDate www.uptodate.com

2016 UpToDate

Strongyloidiasis
Authors
Peter F Weller, MD, FACP
Karin Leder, MBBS, FRACP, PhD,
MPH, DTMH

Section Editor
Edward T Ryan, MD, DTMH

Deputy Editor
Elinor L Baron, MD, DTMH

Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2016. | This topic last updated: Sep 10, 2015.
INTRODUCTION Strongyloidiasis is caused by infection with Strongyloides stercoralis.
Manifestations of infection can range from asymptomatic eosinophilia in the immunocompetent host to
disseminated disease with septic shock in the immunocompromised host.
EPIDEMIOLOGY Strongyloidiasis is endemic in tropical and subtropical regions and occurs
sporadically in temperate areas. In tropical and subtropical regions, the overall regional prevalence may
exceed 25 percent. The highest rates of infection in the United States are among residents of the
southeastern states [1,2] and among individuals who have been in endemic areas (including
immigrants, refugees, travelers, and military personnel) [3,4]. Transmission of strongyloidiasis in a
long-term care setting has also been described [2].
A Canadian study of newly arrived Southeast Asian refugees identified strongyloidiasis seroprevalence
among Kampucheans, Laotians, and Vietnamese (76, 56, and 12 percent, respectively) [4]. In another
study, over 40 percent of Cambodian immigrants to Australia had positive or equivocal strongyloides
serology indicating possible infection [5].
LIFE CYCLE The infection begins when human skin contacts filariform larvae (the infective larval
stage) of S. stercoralis, which are found in soil or other materials contaminated with human feces
(figure 1) [6,7]. The filariform larvae penetrate the skin and migrate hematogenously to the lungs
where they penetrate into the alveolar air sacs. The larvae then ascend the tracheobronchial tree and
are swallowed.
The larvae mature into adult worms that burrow into the mucosa of the duodenum and jejunum. Adult
worms may live for up to five years. The adult female produces eggs, from which noninfectious larvae
(rhabditiform larvae) develop within the lumen of the gastrointestinal tract. The rhabditiform larvae are
generally passed in the feces. The cycle from dermal penetration to appearance of larvae in the stool
requires approximately three to four weeks.
Autoinfection In contrast with other helminthic parasites, S. stercoralis can complete its life cycle
entirely within the human host [8]. As a result, the burden of adult worms in infected humans can
increase substantially through a cycle of autoinfection. During autoinfection, the rhabditiform larvae
mature into filariform larvae within the gastrointestinal tract. The filariform larvae can then penetrate
the perianal skin or colonic mucosa to complete the cycle of autoinfection. Larval transformation within
the gastrointestinal tract may also be accelerated by constipation, diverticula, other conditions that
reduce bowel motility, and steroid use.
Although autoinfection is limited by an intact immune response, a low level of autoinfection may permit
the organism to persist for decades and cause clinical manifestations long after the initial infection [9].
This has been observed in prisoners of war who were found to be infected more than 40 years after

18-May-16 10:10 PM

2 of 19

file:///

exposure in Thailand [10]. However, in patients with depressed cell-mediated immunity, autoinfection
may give rise to potentially fatal hyperinfection with disseminated disease [11,12]. (See 'Hyperinfection
syndrome' below.)
CLINICAL MANIFESTATIONS Most infected patients do not experience prominent symptoms. The
most common manifestations are mild waxing and waning gastrointestinal, cutaneous, or pulmonary
symptoms that persist for years; others simply have eosinophilia in the absence of symptoms.
Eosinophilia is not universally present in strongyloidiasis but may be the only clue that the patient
harbors a parasitic infection. One report, for example, evaluated 128 Indochinese patients with
eosinophilia, the cause of which was not apparent by routine screening [13]. Intestinal parasitism with
one or more organisms was responsible for the eosinophilia in 122; hookworm (55 percent) and S.
stercoralis (38 percent) were the most common organisms.
However, eosinophilia may be suppressed or absent in disseminated disease because of concomitant
pyogenic infection or steroid administration [14]. The serum immunoglobulin E (IgE) concentration is
often elevated in these settings [15].
Skin reactions S. stercoralis may produce cutaneous reactions when larvae penetrate the skin,
sometimes termed ground itch [16,17]. These reactions include inflammation, edema, petechiae,
serpiginous or urticarial tracts, and severe pruritus. The feet are the most commonly affected site with
initial infection, but dermal manifestations of primary infection rarely lead patients to seek medical
attention.
With chronic infection, urticaria or pruritis can develop. In addition, the dermal migration of larvae may
produce a distinctive eruption at other sites, most commonly on the buttocks. As larvae migrate, at a
rate detectable by observers, a serpiginous, raised, erythematous track develops, and these lesions are
pathognomonic of strongyloidiasis. This is known as larva currens ("running" larva). Other skin lesions
in chronic strongyloidiasis may include periumbilical purpura in disseminated infections [18],
nonpalpable purpura [19], angioedema [20,21], and erythroderma that mimics drug reaction [22].
Gastrointestinal symptoms The adult worms in the small bowel induce duodenitis, which can lead
to upper abdominal pain [23,24]. Patients may also experience diarrhea, anorexia, nausea, and
vomiting. Epigastric pain may mimic a duodenal ulcer, except that food ingestion may aggravate the
pain of strongyloidiasis. Chronic enterocolitis and malabsorption can result from a high intestinal worm
burden.
Pulmonary manifestations The transpulmonary migration of larvae can produce dry cough, throat
irritation, dyspnea, wheezing, and hemoptysis. A Loeffler's-like syndrome with eosinophilia is rarely
observed.
Some patients with chronic strongyloidiasis experience repeated episodes of fever and mild
pneumonitis, producing a picture that resembles recurrent bacterial pneumonia. Eosinophilia is often
absent initially but may develop later in the infection. Treatment of the strongyloidiasis terminates the
episodes of pneumonia.
Patients with chronic strongyloidiasis may also develop asthma that paradoxically worsens with
corticosteroid use [25,26] or dyspnea due to restrictive pulmonary disease [27]. Strongyloidiasis can
present as acute respiratory failure or pulmonary embolism [28].
Hyperinfection syndrome The cycle of autoinfection can lead to the hyperinfection syndrome by
greatly increasing the parasite burden. Autoinfection within the gastrointestinal tract begins when
rhabditiform larvae transform into filariform larvae, which penetrate the intestinal wall to enter the
bloodstream. The massive dissemination of filariform larvae to the lungs, liver, heart, central nervous
system, and endocrine glands induces inflammation that may result in symptomatic dysfunction of
these organs and even septic shock [11,29-31]. (See 'Life cycle' above.)

18-May-16 10:10 PM

3 of 19

file:///

The most common manifestations of the hyperinfection syndrome include [23,29,32]:

Fever
Nausea and vomiting
Anorexia
Diarrhea
Abdominal pain
Dyspnea
Wheezing
Hemoptysis
Cough
The chest radiograph reveals pulmonary infiltrates that consist of foci of hemorrhage, pneumonitis, and
edema (image 1) [33]. Rarely, adult parasites localize in the bronchial tree and lay eggs that develop
into larvae in the airway. Bronchospasm frequently accompanies this manifestation of hyperinfection
[34].
The clinical findings in the hyperinfection syndrome may be attributable to the direct consequences of
organ invasion by the filariform larvae or to secondary gram-negative bacteremia, pneumonia, or even
meningitis due to bloodstream seeding originating from the gastrointestinal tract or lungs [35,36].
Eosinophilia may be absent when complications such as gram-negative bacteremia ensue [33].
Mortality rates of 10 to >80 percent have been reported in the hyperinfection syndrome. (See 'Whom
to test' below.)
Role of immunosuppression The likelihood of developing the hyperinfection syndrome is
increased if cell-mediated immunity is impaired by congenital immunodeficiency, underlying
malignancy, malnutrition, alcoholism, hematopoietic stem cell transplantation (HSCT), or the
administration of corticosteroids or cytotoxic drugs [11,37-49]. Even short courses of corticosteroids of
6 to 17 days have led to overwhelming hyperinfection and death [50]. The pathophysiology underlying
these risk factors, whether disease related or iatrogenically induced, is a compromised immune system
leading to dysfunction of TH-2 helper cells [51]. It is therefore important to detect and eradicate
Strongyloides infection prior to initiation of immunosuppressive therapy. (See 'Whom to test' below.)
In comparison with steroids and cytotoxic agents, cyclosporine has activity against Strongyloides [52].
It is unknown, however, whether this effect is sufficient to reduce the risk of hyperinfection in patients
receiving cyclosporine.
Underlying human T-lymphotropic virus (HTLV)-1 infection is also a significant risk factor for
disseminated disease with strongyloidiasis [53-55]. Patients with HTLV-1 infection have high levels of
interferon-gamma production, which decreases the production of interleukin (IL)-4, IL-5, IL-13, and
IgE, important molecules in host defense against Strongyloides [15,56,57]. Regulatory T cells may play
a role in susceptibility to Strongyloides hyperinfection; among patients with HTLV-1 and Strongyloides
coinfection, regulatory T cell counts are increased and correlate with both low circulating eosinophil
counts and reduced antigen-driven IL-5 production [58].
Disseminated strongyloidiasis can occur in patients with AIDS [59,60], but it occurs less frequently
than in patients with HTLV-1 and is much less common than might be predicted given the
co-endemicity of the two infections. However, immune reconstitution may be a risk factor for
disseminated strongyloidiasis [61-63] and HIV-infected patients may be at risk for Strongyloides
treatment failure [64].

18-May-16 10:10 PM

4 of 19

file:///

Other conditions or medications may be associated with an increased risk of strongyloidiasis:

Hypogammaglobulinemia [65,66]
Antitumor necrosis factor receptor therapy [67,68]
Organ transplantation from an uninfected donor to an infected recipient with previously subclinical
infection that is unmasked by immunosuppression [69-71]
Organ transplantation from an infected donor to an uninfected recipient [49]
WHOM TO TEST Testing for strongyloidiasis is appropriate for individuals in the following
categories:
Patients with clinical manifestations and epidemiologic exposure as described above (including
unexplained eosinophilia, urticarial or serpiginous skin lesions, or pulmonary or gastrointestinal
symptoms)
Immunosuppressed patients (steroid and other immunosuppressive treatments, HTLV-1 infection,
hematologic malignancy, malnutrition, AIDS) with unexplained eosinophilia, history of characteristic
skin lesions, or epidemiologic exposure [14,72]. Transplant candidates should also be tested prior to
immunosuppression if they have a potential exposure history [73].
Asymptomatic individuals such as immigrants, refugees, long-term travelers, or military personnel
who have been in areas known to be endemic for strongyloidiasis, even if their last exposure was
decades prior [3,74-77].
In endemic regions, patients with invasive infections caused by enteric organisms (especially systemic
gram-negative bacterial infections) without an obvious cause [78,79].
DIAGNOSIS The diagnosis of uncomplicated strongyloidiasis is usually made by detecting
rhabditiform larvae in concentrated stool or via serologic methods. As noted above, larvae first appear
in the stool three to four weeks after initial dermal penetration (picture 1) [80].
Detection of larvae Standard stool examination is notoriously insensitive for detecting
strongyloides (<50 percent sensitivity) [81]. This is because larvae are excreted only intermittently,
and many patients have a low burden of infectious organisms. Specialized tests on stool specimens,
including the Baerman concentration technique, the Harada-Mori filter paper technique, and a modified
agar plate method, can increase the yield, but even three or more stool examinations can fail to detect
Strongyloides [82,83]. Of the specialized techniques, the agar plate method is used most commonly
and is most sensitive [84]. It involves inoculating agar plates with stool and incubating for two days at
room temperature. Larvae crawl on the agar and spread bacteria in their paths, creating bacterial
growth patterns on the agar surface. Larvae can be seen by macroscopic examination of the plates and
their presence confirmed with formalin washing of the plate surface and examination of the sediment
from the washing [85].
Aspiration of duodenojejunal fluid or the use of a string test (Enterotest) is sometimes used to detect
Strongyloides larvae in patients with negative stool samples [80]. Alternatively, serologic testing may
be helpful (see 'Serology' below).
In disseminated strongyloidiasis, filariform larvae can be found in stool, sputum, bronchoalveolar
lavage fluid, pleural fluid, peritoneal fluid, and surgical drainage fluid [42,86-90]. Sputum should also
be examined for larvae if disseminated strongyloidiasis is suspected [88,90,91]. For patients with rash,
larvae may be visualized by skin biopsy.
Polymerase chain reaction (PCR) tests have also been developed for detection of Strongyloides in stool
samples but are not widely available. In one study, stool samples analyzed by microscopic examination
were positive for strongyloides in 0.1 percent, compared with 0.8 percent positivity when the same

18-May-16 10:10 PM

5 of 19

file:///

samples were tested via PCR [92].

Serology Diagnosis of strongyloidiasis by enzyme-linked immunosorbent assay (ELISA) has proven
useful in immunocompetent individuals, both in symptomatic and asymptomatic strongyloidiasis
[93,94]. The ELISA may be positive even if repeated examinations of stool samples are unrevealing
[95]. The ELISA for detecting S. stercoralis infection detects immunoglobulin G (IgG) to filariform
larvae. Negative test results in immunocompetent individuals decrease the likelihood that infection is
present; however, some ELISA serologies run by commercial laboratories are of variable reliability. In
addition, ELISA results can be falsely negative in immunocompromised hosts [91]. False-positive
results may occur in the presence of other helminth infections [85].
The ELISA may be positive even when repeated examinations of stool samples have been unrevealing
[95]. However, ELISA can be falsely negative in immunocompromised hosts [91]. In addition, some
ELISA serologies run by commercial laboratories are of variable reliability.
In one study, two commercially available ELISAs (IVD-ELISA and Bordier-ELISA) were found to have
sensitivity of 89 and 83 percent, respectively, and specificity of 97.2 percent for both in the diagnosis of
intestinal strongyloidiasis [96].
Indirect immunofluorescence assays have also been developed, as has a gelatin particle agglutination
test [97]. A newer technique, luciferase immunoprecipitation system (LIPS), is another attractive
alternative to ELISA-based methods [98].
Endoscopy Upper endoscopy is not usually needed to establish a diagnosis of strongyloidiasis.
However, it may be performed in patients with gastrointestinal symptoms with unsuspected disease.
Strongyloidiasis has a broad range of endoscopic features [99]:
In the duodenum, the findings included edema, brown discoloration of the mucosa, erythematous
spots, subepithelial hemorrhages, and megaduodenum.
In the colon, the findings include loss of vascular pattern, edema, aphthous ulcers, erosions,
serpiginous ulcerations, and xanthoma-like lesions.
In the stomach, thickened folds and mucosal erosions are seen [100].
Larvae may be demonstrated on biopsies of the affected mucosa [14,101].
Strongyloides colitis can sometimes mimic ulcerative colitis, but distinctive features of the
strongyloidiasis include skip pattern of the inflammation, distal attenuation of the disease,
eosinophil-rich infiltrates, relatively intact crypt architecture, and frequent involvement of submucosa
(picture 2) [102].
DIFFERENTIAL DIAGNOSIS The differential diagnosis of strongyloidiasis includes:
Ascariasis and hookworm Strongyloidiasis, ascariasis, and hookworm can all cause nonspecific
gastrointestinal and/or pulmonary symptoms or chronic urticaria and/or pruritus. In addition, all can be
associated with eosinophilia in the presence or absence of other symptoms. Coinfection can occur; the
diagnoses are distinguished by stool microscopy. (See "Approach to stool microscopy".)
Cutaneous larva migrans The strongyloidiasis skin reaction known as larva currens must be
distinguished from cutaneous larva migrans; both are associated with migratory serpiginous lesions
that are erythematous, raised, and pruritic. The conditions usually can be distinguished clinically based
on the speed of advancement; larva currens can progress approximately 1 cm in 5 minutes and 5 to 15
cm per hour, while the larval track of cutaneous larva migrans progresses approximately 1 to 2 cm per
day. (See "Hookworm-related cutaneous larva migrans".)
Tropical filarial pulmonary eosinophilia Disseminated strongyloidiasis may resemble tropical filarial
pulmonary eosinophilia; symptoms include dry cough, wheeze, and fatigue. Tropical pulmonary

18-May-16 10:10 PM

6 of 19

file:///

eosinophilia is characterized by eosinophilia above 3000/microL; the diagnosis can be confirmed by

filarial antibody titers. (See "Tropical pulmonary eosinophilia".)
TREATMENT
Uncomplicated infection In the past, thiabendazole was administered for uncomplicated infection.
However, thiabendazole is now rarely used due to the availability of more efficacious and better
tolerated medications. The treatment of choice for strongyloidiasis at present is ivermectin with
albendazole as an alternative [103,104].
Ivermectin Ivermectin is usually administered as two single 200 mcg/kg doses of ivermectin
administered either on two consecutive days or two weeks apart [103,105].
In a study of 88 patients with strongyloidiasis, 31 patients received thiabendazole 25 mg/kg/12 hours
for three consecutive days; 22 patients received ivermectin 200 mcg/kg as a single dose, and 35
patients received ivermectin for two consecutive days [104]. The efficacy rates were 78, 77, and 100
percent in the thiabendazole, ivermectin single dose, and ivermectin two-dose regimens, respectively.
Sixteen percent of patients taking thiabendazole experienced side effects in contrast with three percent
in the combined ivermectin groups.
In immigrants from areas of Africa endemic for loiasis, patients should be screened to exclude high
levels of Loa loa microfilaremia because administration of ivermectin to highly microfilaremic subjects
can precipitate life-threatening encephalopathy.
Albendazole Albendazole (400 mg by mouth twice daily for three to seven days) also has
activity against Strongyloides [106,107]. In varied studies, the efficacy of albendazole has been lower
than that of ivermectin, with a mean of 60 percent effectiveness for three days of albendazole versus
92 percent for ivermectin [108]. One study of 42 Thai patients with chronic strongyloidiasis noted a
cure rate of 90 percent following a single dose of ivermectin compared with 50 percent for seven days
of albendazole 800 mg/day [109].
Disseminated disease/hyperinfection syndrome The optimal treatment of disseminated disease
and hyperinfection is uncertain, as data are limited. In immunocompromised patients with
disseminated disease, reduction of immunosuppressive therapy, if possible, is an important adjunct to
any anthelminthic therapy. In such cases, it is also usually necessary to prolong or repeat ivermectin
therapy, although there is no generally agreed upon regimen.
Some experts give five to seven days of ivermectin in disseminated disease or combine ivermectin with
albendazole until the patient responds. Often the duration of treatment is determined clinically; daily
ivermectin should be administered until symptoms resolve and daily stool examinations have been
negative for at least two weeks (one autoinfection cycle) or longer if patient remains
immunosuppressed [110].
The optimal treatment of critically ill patients with the hyperinfection syndrome is uncertain; data
regarding the ideal dose, duration, and route of therapy is limited. In patients with hyperinfection
strongyloidiasis who were not able to receive oral therapy due to ileus or obtundation, alternative (not
US Food and Drug Administrationapproved) regimens including subcutaneous ivermectin (200
mcg/kg) [111-113], per rectal ivermectin administration [114], and a parenteral veterinary formulation
of ivermectin [115-117] have been used with variable success. Combined longer-term ivermectin and
albendazole have been successful in a case of refractory strongyloidiasis [118]. Ongoing monthly doses
of ivermectin for at least six months may be given in the setting of ongoing immunosuppression among
survivors of the hyperinfection syndrome.
Blood cultures should be obtained in the setting of hyperinfection syndrome, and broad spectrum
empiric antibiotics that include coverage of enteric gram-negative bacteria should be administered.
PATIENT MONITORING Patients who are being treated for strongyloidiasis should have follow-up

18-May-16 10:10 PM

7 of 19

file:///

stool examinations, complete blood counts with eosinophilia, and serologies.

Treatment failures may occur even with ivermectin in nonimmunocompromised hosts. If stool exams
were positive for larvae prior to treatment, repeat stool exams should be performed about two to four
weeks after treatment. In the setting of the hyperinfection syndrome, treatment should be
administered until symptoms resolve and daily stool examinations have been negative for at least two
weeks. However, a negative stool exam is not definitive proof of parasitologic cure since stool exams
are insensitive for detecting larvae. Persistent symptoms following treatment for strongyloidiasis should
raise the possibility that initial ivermectin treatment was not fully curative.
Decreasing titers of anti-Strongyloides antibodies may also be useful to assess treatment adequacy of
treatment; we recommend repeat serologies at three to six months [119]. One retrospective study of
31 patients treated for strongyloidiasis noted a significant reduction in blood eosinophilia and serologic
antibody titer after an average of 96 and 270 days, respectively [74]. In another study among
Cambodian refugees, 65 percent of patients followed with serial serology reached levels consistent with
cure 6 to 12 months after treatment [120]. Eosinophilia persisting for several months after treatment
suggests either failure to eradicate strongyloides and/or other etiologies for eosinophilia [104]. (See
"Approach to the patient with unexplained eosinophilia".)
PROGNOSIS The prognosis of strongyloidiasis is good except in the hyperinfection syndrome. The
latter patients have high case-fatality rates that are increased by concomitant immunosuppression,
bacteremia, and delayed diagnosis [121]. Failure to respond to ivermectin raises the possibility that the
patient has underlying human T-lymphotropic virus (HTLV)-1 [122,123].
PREVENTION Prevention of disease is mainly achieved by wearing shoes in endemic areas to avoid
contact with infected soil.
SUMMARY AND RECOMMENDATIONS
Strongyloidiasis is endemic in tropical and subtropical regions and occurs sporadically in temperate
areas. (See 'Introduction' above.)
The burden of adult worms in infected humans can increase substantially via autoinfection. Among
immunocompromised hosts, autoinfection can lead to the hyperinfection syndrome where there is
massive dissemination of filariform larvae to the lungs, liver, heart, central nervous system, and
endocrine glands. (See 'Life cycle' above and 'Hyperinfection syndrome' above.)
Most infected patients do not experience prominent symptoms. The most common manifestations are
mild waxing and waning gastrointestinal, cutaneous, or pulmonary symptoms that persist for years;
others simply have eosinophilia in the absence of symptoms. (See 'Clinical manifestations' above.)
For diagnosis, we recommend that at least two concentrated stool specimens be examined for the
presence of rhabditiform larvae as well as serologic testing. If these diagnostic tests are negative and
clinical suspicion of strongyloidiasis remains, we recommend either examination of duodenal fluid for
larvae or empiric ivermectin therapy. (See 'Diagnosis' above.)
We recommend treatment with ivermectin for uncomplicated strongyloidiasis (Grade 1A). The typical
dose of ivermectin is 200 mcg/kg administered in two single doses, usually given two weeks apart.
(See 'Ivermectin' above.)
In patients with disseminated disease (hyperinfection syndrome), we suggest extended dosing of
ivermectin (Grade 2C). The typical dose schedule is 200 mcg/kg daily for at least five to seven days.
Ivermectin can also be combined with albendazole. Daily stool examinations should be performed
during treatment to determine the effect on larval burden, and treatment should be administered daily
until symptoms resolve and stool tests have been negative for at least two weeks. (See 'Disseminated
disease/hyperinfection syndrome' above.)

18-May-16 10:10 PM

8 of 19

file:///

In patients with eosinophilia that persists for more than three months despite therapy, we recommend
evaluation for treatment failure or other causes of eosinophilia. (See "Approach to the patient with
unexplained eosinophilia".)
Use of UpToDate is subject to the Subscription and License Agreement
REFERENCES

1. Centers for Disease Control and Prevention. Notes from the field: Strongyloidiasis in a rural
setting--Southeastern Kentucky, 2013. MMWR Morb Mortal Wkly Rep 2013; 62:843.
2. Centers for Disease Control and Prevention. Notes from the field: strongyloides infection among
patients at a long-term care facility--Florida, 2010-2012. MMWR Morb Mortal Wkly Rep 2013;
62:844.
3. Posey DL, Blackburn BG, Weinberg M, et al. High prevalence and presumptive treatment of
schistosomiasis and strongyloidiasis among African refugees. Clin Infect Dis 2007; 45:1310.
4. Gyorkos TW, Genta RM, Viens P, MacLean JD. Seroepidemiology of Strongyloides infection in the
Southeast Asian refugee population in Canada. Am J Epidemiol 1990; 132:257.
5. Caruana SR, Kelly HA, Ngeow JY, et al. Undiagnosed and potentially lethal parasite infections
among immigrants and refugees in Australia. J Travel Med 2006; 13:233.
6. Schupf N, Ortiz M, Kapell D, et al. Prevalence of intestinal parasite infections among individuals
with mental retardation in New York State. Ment Retard 1995; 33:84.
7. Lindo JF, Robinson RD, Terry SI, et al. Age-prevalence and household clustering of Strongyloides
stercoralis infection in Jamaica. Parasitology 1995; 110 ( Pt 1):97.
8. Siddiqui AA, Genta RM, Berk SL. Chapter 111. In: Infectious Diseases - Principles, Practices and
Pathogens, Guerrant RL, Walker DH, Weller PF (Eds), Churchhill-Livingstone Elsevier, Philadelphia
2006. p.1274.
9. Chu E, Whitlock WL, Dietrich RA. Pulmonary hyperinfection syndrome with Strongyloides
stercoralis. Chest 1990; 97:1475.
10. Pelletier LL Jr, Baker CB, Gam AA, et al. Diagnosis and evaluation of treatment of chronic
strongyloidiasis in ex-prisoners of war. J Infect Dis 1988; 157:573.
11. Keiser PB, Nutman TB. Strongyloides stercoralis in the Immunocompromised Population. Clin
Microbiol Rev 2004; 17:208.
12. Haque AK, Schnadig V, Rubin SA, Smith JH. Pathogenesis of human strongyloidiasis: autopsy and
quantitative parasitological analysis. Mod Pathol 1994; 7:276.
13. Nutman TB, Ottesen EA, Ieng S, et al. Eosinophilia in Southeast Asian refugees: evaluation at a
referral center. J Infect Dis 1987; 155:309.
14. Arsi-Arsenijevi V, Dzami A, Dzami Z, et al. Fatal Strongyloides stercoralis infection in a young
woman with lupus glomerulonephritis. J Nephrol 2005; 18:787.
15. Robinson RD, Lindo JF, Neva FA, et al. Immunoepidemiologic studies of Strongyloides stercoralis
and human T lymphotropic virus type I infections in Jamaica. J Infect Dis 1994; 169:692.
16. Mackey SL, Wagner KF. Dermatologic manifestations of parasitic diseases. Infect Dis Clin North Am
1994; 8:713.
17. Meinking TL, Burkhart CN, Burkhart CG. Changing paradigms in parasitic infections: common
dermatological helminthic infections and cutaneous myiasis. Clin Dermatol 2003; 21:407.
18. Salluh JI, Bozza FA, Pinto TS, et al. Cutaneous periumbilical purpura in disseminated
strongyloidiasis in cancer patients: a pathognomonic feature of potentially lethal disease? Braz J
Infect Dis 2005; 9:419.
19. Reddy TS, Myers JW. Syndrome of inappropriate secretion of antidiuretic hormone and

18-May-16 10:10 PM

9 of 19

file:///
nonpalpable purpura in a woman with Strongyloides stercoralis hyperinfection. Am J Med Sci
2003; 325:288.
20. Van Dellen RG, Maddox DE, Dutta EJ. Masqueraders of angioedema and urticaria. Ann Allergy
Asthma Immunol 2002; 88:10.
21. Mehta RK, Shah N, Scott DG, et al. Case 4. Chronic urticaria due to strongyloidiasis. Clin Exp
Dermatol 2002; 27:84.
22. Ly MN, Bethel SL, Usmani AS, Lambert DR. Cutaneous Strongyloides stercoralis infection: an
unusual presentation. J Am Acad Dermatol 2003; 49:S157.
23. Scowden EB, Schaffner W, Stone WJ. Overwhelming strongyloidiasis: an unappreciated
opportunistic infection. Medicine (Baltimore) 1978; 57:527.
24. Berkmen YM, Rabinowitz J. Gastrointestinal manifestations of the stongyloidiasis. Am J Roentgenol
Radium Ther Nucl Med 1972; 115:306.
25. Sen P, Gil C, Estrellas B, Middleton JR. Corticosteroid-induced asthma: a manifestation of limited
hyperinfection syndrome due to Strongyloides stercoralis. South Med J 1995; 88:923.
26. Wehner JH, Kirsch CM, Kagawa FT, et al. The prevalence and response to therapy of Strongyloides
stercoralis in patients with asthma from endemic areas. Chest 1994; 106:762.
27. Lin AL, Kessimian N, Benditt JO. Restrictive pulmonary disease due to interlobular septal fibrosis
associated with disseminated infection by Strongyloides stercoralis. Am J Respir Crit Care Med
1995; 151:205.
28. Newberry AM, Williams DN, Stauffer WM, et al. Strongyloides hyperinfection presenting as acute
respiratory failure and gram-negative sepsis. Chest 2005; 128:3681.
29. Longworth DL, Weller PF. Hyperinfection syndrome with strongyloidiasis. In: Current Clinical Topics
in Infectious Diseases, Remington JS, Swartz MN (Eds), McGraw-Hill, New York 1986. p.1.
30. Woodring JH, Halfhill H 2nd, Reed JC. Pulmonary strongyloidiasis: clinical and imaging features.
AJR Am J Roentgenol 1994; 162:537.
31. Cebular S, Lee S, Tolaney P, Lutwick L. Community-acquired pneumonia in immunocompromised
patients. Opportunistic infections to consider in differential diagnosis. Postgrad Med 2003; 113:65.
32. Strazzella WD, Safirstein BH. Asthma due to parasitic infestation. N J Med 1989; 86:947.
33. Lam CS, Tong MK, Chan KM, Siu YP. Disseminated strongyloidiasis: a retrospective study of clinical
course and outcome. Eur J Clin Microbiol Infect Dis 2006; 25:14.
34. Nwokolo C, Imohiosen EA. Strongyloidiasis of respiratory tract presenting as "asthma". Br Med J
1973; 2:153.
35. Ghoshal UC, Ghoshal U, Jain M, et al. Strongyloides stercoralis infestation associated with
septicemia due to intestinal transmural migration of bacteria. J Gastroenterol Hepatol 2002;
17:1331.
36. Walker M, Zunt JR. Parasitic central nervous system infections in immunocompromised hosts. Clin
Infect Dis 2005; 40:1005.
37. Schaeffer MW, Buell JF, Gupta M, et al. Strongyloides hyperinfection syndrome after heart
transplantation: case report and review of the literature. J Heart Lung Transplant 2004; 23:905.
38. Adam M, Morgan O, Persaud C, Gibbs WN. Hyperinfection syndrome with Strongyloides stercoralis
in malignant lymphoma. Br Med J 1973; 1:264.
39. Cruz T, Reboucas G, Rocha H. Fatal strongyloidiasis in patients receiving corticosteroids. N Engl J
Med 1966; 275:1093.
40. Higenbottam TW, Heard BE. Opportunistic pulmonary strongyloidiasis complicating asthma treated
with steroids. Thorax 1976; 31:226.
41. Purtilo DT, Meyers WM, Connor DH. Fatal strongyloidiasis in immunosuppressed patients. Am J
Med 1974; 56:488.
42. Smith SB, Schwartzman M, Mencia LF, et al. Fatal disseminated strongyloidiasis presenting as

18-May-16 10:10 PM

10 of 19

file:///
acute abdominal distress in an urban child. J Pediatr 1977; 91:607.
43. Stemmermann GN. Strongyloidiasis in migrants. Pathological and clinical considerations.
Gastroenterology 1967; 53:59.
44. Davidson RA. Infection due to Strongyloides stercoralis in patients with pulmonary disease. South
Med J 1992; 85:28.
45. Safdar A, Malathum K, Rodriguez SJ, et al. Strongyloidiasis in patients at a comprehensive cancer
center in the United States. Cancer 2004; 100:1531.
46. Lemos LB, Qu Z, Laucirica R, Fred HL. Hyperinfection syndrome in strongyloidiasis: report of two
cases. Ann Diagn Pathol 2003; 7:87.
47. Hira PR, Al-Ali F, Shweiki HM, et al. Strongyloidiasis: challenges in diagnosis and management in
non-endemic Kuwait. Ann Trop Med Parasitol 2004; 98:261.
48. Orlent H, Crawley C, Cwynarski K, et al. Strongyloidiasis pre and post autologous peripheral blood
stem cell transplantation. Bone Marrow Transplant 2003; 32:115.
49. Centers for Disease Control and Prevention (CDC). Transmission of Strongyloides stercoralis
through transplantation of solid organs--Pennsylvania, 2012. MMWR Morb Mortal Wkly Rep 2013;
62:264.
50. Ghosh K, Ghosh K. Strongyloides stercoralis septicaemia following steroid therapy for eosinophilia:
report of three cases. Trans R Soc Trop Med Hyg 2007; 101:1163.
51. Concha R, Harrington W Jr, Rogers AI. Intestinal strongyloidiasis: recognition, management, and
determinants of outcome. J Clin Gastroenterol 2005; 39:203.
52. Schad GA. Cyclosporine may eliminate the threat of overwhelming strongyloidiasis in
immunosuppressed patients. J Infect Dis 1986; 153:178.
53. Porto MA, Alcntara LM, Leal M, et al. Atypical clinical presentation of strongyloidiasis in a patient
co-infected with human T cell lymphotrophic virus type I. Am J Trop Med Hyg 2005; 72:124.
54. Satoh M, Kiyuna S, Shiroma Y, et al. Predictive markers for development of strongyloidiasis in
patients infected with both Strongyloides stercoralis and HTLV-1. Clin Exp Immunol 2003;
133:391.
55. Rahim S, Drabu Y, Jarvis K, Melville D. Strongyloidiasis: a mistaken diagnosis and a fatal outcome
in a patient with diarrhoea. Trans R Soc Trop Med Hyg 2005; 99:215.
56. Carvalho EM, Da Fonseca Porto A. Epidemiological and clinical interaction between HTLV-1 and
Strongyloides stercoralis. Parasite Immunol 2004; 26:487.
57. Plumelle Y, Pascaline N, Nguyen D, et al. Adult T-cell leukemia-lymphoma: a clinico-pathologic
study of twenty-six patients from Martinique. Hematol Pathol 1993; 7:251.
58. Montes M, Sanchez C, Verdonck K, et al. Regulatory T cell expansion in HTLV-1 and
strongyloidiasis co-infection is associated with reduced IL-5 responses to Strongyloides stercoralis
antigen. PLoS Negl Trop Dis 2009; 3:e456.
59. Celedon JC, Mathur-Wagh U, Fox J, et al. Systemic strongyloidiasis in patients infected with the
human immunodeficiency virus. A report of 3 cases and review of the literature. Medicine
(Baltimore) 1994; 73:256.
60. Lessnau KD, Can S, Talavera W. Disseminated Strongyloides stercoralis in human
immunodeficiency virus-infected patients. Treatment failure and a review of the literature. Chest
1993; 104:119.
61. Kim AC, Lupatkin HC. Strongyloides stercoralis infection as a manifestation of immune restoration
syndrome. Clin Infect Dis 2004; 39:439.
62. Taylor CL, Subbarao V, Gayed S, Ustianowski AP. Immune reconstitution syndrome to
Strongyloides stercoralis infection. AIDS 2007; 21:649.
63. Brown M, Cartledge JD, Miller RF. Dissemination of Strongyloides stercoralis as an immune
restoration phenomenon in an HIV-1-infected man on antiretroviral therapy. Int J STD AIDS 2006;

18-May-16 10:10 PM

11 of 19

file:///
17:560.
64. Viney ME, Brown M, Omoding NE, et al. Why does HIV infection not lead to disseminated
strongyloidiasis? J Infect Dis 2004; 190:2175.
65. Seet RC, Lau LG, Tambyah PA. Strongyloides hyperinfection and hypogammaglobulinemia. Clin
Diagn Lab Immunol 2005; 12:680.
66. Sathiyasekaran M, Shibalan S. Intestinal strongyloidiasis and common variable immunodeficiency
syndrome. Indian Pediatr 2005; 42:391.
67. Boatright MD, Wang BW. Clinical infection with Strongyloides sterocoralis following etanercept use
for rheumatoid arthritis. Arthritis Rheum 2005; 52:1336.
68. Krishnamurthy R, Dincer HE, Whittemore D. Strongyloides stercoralis hyperinfection in a patient
with rheumatoid arthritis after anti-TNF-alpha therapy. J Clin Rheumatol 2007; 13:150.
69. Marty FM. Strongyloides hyperinfection syndrome and transplantation: a preventable, frequently
fatal infection. Transpl Infect Dis 2009; 11:97.
70. Vilela EG, Clemente WT, Mira RR, et al. Strongyloides stercoralis hyperinfection syndrome after
liver transplantation: case report and literature review. Transpl Infect Dis 2009; 11:132.
71. Valar C, Keitel E, Dal Pr RL, et al. Parasitic infection in renal transplant recipients. Transplant Proc
2007; 39:460.
72. Mejia R, Nutman TB. Screening, prevention, and treatment for hyperinfection syndrome and
disseminated infections caused by Strongyloides stercoralis. Curr Opin Infect Dis 2012; 25:458.
73. Roxby AC, Gottlieb GS, Limaye AP. Strongyloidiasis in transplant patients. Clin Infect Dis 2009;
49:1411.
74. Nuesch R, Zimmerli L, Stockli R, et al. Imported strongyloidosis: a longitudinal analysis of 31
cases. J Travel Med 2005; 12:80.
75. Gill GV, Welch E, Bailey JW, et al. Chronic Strongyloides stercoralis infection in former British Far
East prisoners of war. QJM 2004; 97:789.
76. Johnston FH, Morris PS, Speare R, et al. Strongyloidiasis: a review of the evidence for Australian
practitioners. Aust J Rural Health 2005; 13:247.
77. Lim S, Katz K, Krajden S, et al. Complicated and fatal Strongyloides infection in Canadians: risk
factors, diagnosis and management. CMAJ 2004; 171:479.
78. Agrawal V, Agarwal T, Ghoshal UC. Intestinal strongyloidiasis: a diagnosis frequently missed in the
tropics. Trans R Soc Trop Med Hyg 2009; 103:242.
79. Al-Hasan MN, McCormick M, Ribes JA. Invasive enteric infections in hospitalized patients with
underlying strongyloidiasis. Am J Clin Pathol 2007; 128:622.
80. Beal CB, Viens P, Grant RG, Hughes JM. A new technique for sampling duodenal contents:
demonstration of upper small-bowel pathogens. Am J Trop Med Hyg 1970; 19:349.
81. Boulware DR, Stauffer WM 3rd, Walker PF. Hypereosinophilic syndrome and mepolizumab. N Engl J
Med 2008; 358:2839; author reply 2839.
82. Rosenblatt JE. Clinical importance of adequately performed stool ova and parasite examinations.
Clin Infect Dis 2006; 42:979.
83. Hirata T, Nakamura H, Kinjo N, et al. Increased detection rate of Strongyloides stercoralis by
repeated stool examinations using the agar plate culture method. Am J Trop Med Hyg 2007;
77:683.
84. Ramanathan R, Nutman T. Strongyloides stercoralis infection in the immunocompromised host.
Curr Infect Dis Rep 2008; 10:105.
85. Greiner K, Bettencourt J, Semolic C. Strongyloidiasis: a review and update by case example. Clin
Lab Sci 2008; 21:82.
86. Eveland LK, Kenney M, Yermakov V. Laboratory diagnosis of autoinfection in strongyloidiasis. Am J
Clin Pathol 1975; 63:421.

18-May-16 10:10 PM

12 of 19

file:///

87. Schainberg L, Scheinberg MA. Recovery of Strongyloides stercoralis by bronchoalveolar lavage in a

patient with acquired immunodeficiency syndrome. Am J Med 1989; 87:486.
88. Smith B, Verghese A, Guiterrez C, et al. Pulmonary strongyloidiasis. Diagnosis by sputum gram
stain. Am J Med 1985; 79:663.
89. Williams J, Nunley D, Dralle W, et al. Diagnosis of pulmonary strongyloidiasis by bronchoalveolar
lavage. Chest 1988; 94:643.
90. Harris RA Jr, Musher DM, Fainstein V, et al. Disseminated strongyloidiasis. Diagnosis made by
sputum examination. JAMA 1980; 244:65.
91. Abdalla J, Saad M, Myers JW, Moorman JP. An elderly man with immunosuppression, shortness of
breath, and eosinophilia. Clin Infect Dis 2005; 40:1464, 1535.
92. ten Hove RJ, van Esbroeck M, Vervoort T, et al. Molecular diagnostics of intestinal parasites in
returning travellers. Eur J Clin Microbiol Infect Dis 2009; 28:1045.
93. Carroll SM, Karthigasu KT, Grove DI. Serodiagnosis of human strongyloidiasis by an enzyme-linked
immunosorbent assay. Trans R Soc Trop Med Hyg 1981; 75:706.
94. Neva FA, Gam AA, Burke J. Comparison of larval antigens in an enzyme-linked immunosorbent
assay for strongyloidiasis in humans. J Infect Dis 1981; 144:427.
95. Savage D, Foadi M, Haworth C, Grant A. Marked eosinophilia in an immunosuppressed patient with
strongyloidiasis. J Intern Med 1994; 236:473.
96. van Doorn HR, Koelewijn R, Hofwegen H, et al. Use of enzyme-linked immunosorbent assay and
dipstick assay for detection of Strongyloides stercoralis infection in humans. J Clin Microbiol 2007;
45:438.
97. Boscolo M, Gobbo M, Mantovani W, et al. Evaluation of an indirect immunofluorescence assay for
strongyloidiasis as a tool for diagnosis and follow-up. Clin Vaccine Immunol 2007; 14:129.
98. Ramanathan R, Burbelo PD, Groot S, et al. A luciferase immunoprecipitation systems assay
enhances the sensitivity and specificity of diagnosis of Strongyloides stercoralis infection. J Infect
Dis 2008; 198:444.
99. Sreenivas DV, Kumar A, Kumar YR, et al. Intestinal strongyloidiasis--a rare opportunistic infection.
Indian J Gastroenterol 1997; 16:105.
100. Thompson BF, Fry LC, Wells CD, et al. The spectrum of GI strongyloidiasis: an endoscopicpathologic study. Gastrointest Endosc 2004; 59:906.
101. Overstreet K, Chen J, Rodriguez JW, Wiener G. Endoscopic and histopathologic findings of
Strongyloides stercoralis infection in a patient with AIDS. Gastrointest Endosc 2003; 58:928.
102. Qu Z, Kundu UR, Abadeer RA, Wanger A. Strongyloides colitis is a lethal mimic of ulcerative
colitis: the key morphologic differential diagnosis. Hum Pathol 2009; 40:572.
103. Drugs for Parasitic Infections, 3rd Ed, The Medical Letter, New Rochelle, NY 2013.
104. Igual-Adell R, Oltra-Alcaraz C, Soler-Company E, et al. Efficacy and safety of ivermectin and
thiabendazole in the treatment of strongyloidiasis. Expert Opin Pharmacother 2004; 5:2615.
105. Zaha O, Hirata T, Kinjo F, et al. Efficacy of ivermectin for chronic strongyloidiasis: two single doses
given 2 weeks apart. J Infect Chemother 2002; 8:94.
106. Marti H, Haji HJ, Savioli L, et al. A comparative trial of a single-dose ivermectin versus three days
of albendazole for treatment of Strongyloides stercoralis and other soil-transmitted helminth
infections in children. Am J Trop Med Hyg 1996; 55:477.
107. Archibald LK, Beeching NJ, Gill GV, et al. Albendazole is effective treatment for chronic
strongyloidiasis. Q J Med 1993; 86:191.
108. Muennig P, Pallin D, Challah C, Khan K. The cost-effectiveness of ivermectin vs. albendazole in the
presumptive treatment of strongyloidiasis in immigrants to the United States. Epidemiol Infect
2004; 132:1055.
109. Suputtamongkol Y, Kungpanichkul N, Silpasakorn S, Beeching NJ. Efficacy and safety of a

18-May-16 10:10 PM

13 of 19

file:///
single-dose veterinary preparation of ivermectin versus 7-day high-dose albendazole for chronic
strongyloidiasis. Int J Antimicrob Agents 2008; 31:46.
110. Segarra-Newnham M. Manifestations, diagnosis, and treatment of Strongyloides stercoralis
infection. Ann Pharmacother 2007; 41:1992.
111. Pacanowski J, Santos MD, Roux A, et al. Subcutaneous ivermectin as a safe salvage therapy in
Strongyloides stercoralis hyperinfection syndrome: a case report. Am J Trop Med Hyg 2005;
73:122.
112. Leung V, Al-Rawahi GN, Grant J, et al. Case report: failure of subcutaneous ivermectin in treating
Strongyloides hyperinfection. Am J Trop Med Hyg 2008; 79:853.
113. Turner SA, Maclean JD, Fleckenstein L, Greenaway C. Parenteral administration of ivermectin in a
patient with disseminated strongyloidiasis. Am J Trop Med Hyg 2005; 73:911.
114. Tarr PE, Miele PS, Peregoy KS, et al. Case report: Rectal adminstration of ivermectin to a patient
with Strongyloides hyperinfection syndrome. Am J Trop Med Hyg 2003; 68:453.
115. Marty FM, Lowry CM, Rodriguez M, et al. Treatment of human disseminated strongyloidiasis with a
parenteral veterinary formulation of ivermectin. Clin Infect Dis 2005; 41:e5.
116. Salluh JI, Feres GA, Velasco E, et al. Successful use of parenteral ivermectin in an
immunosuppressed patient with disseminated strongyloidiasis and septic shock. Intensive Care
Med 2005; 31:1292.
117. Miller MA, Church LW, Salgado CD. Strongyloides hyperinfection: a treatment dilemma. Am J Med
Sci 2008; 336:358.
118. Pornsuriyasak P, Niticharoenpong K, Sakapibunnan A. Disseminated strongyloidiasis successfully
treated with extended duration ivermectin combined with albendazole: a case report of intractable
strongyloidiasis. Southeast Asian J Trop Med Public Health 2004; 35:531.
119. Kobayashi J, Sato Y, Toma H, et al. Application of enzyme immunoassay for postchemotherapy
evaluation of human strongyloidiasis. Diagn Microbiol Infect Dis 1994; 18:19.
120. Biggs BA, Caruana S, Mihrshahi S, et al. Management of chronic strongyloidiasis in immigrants
and refugees: is serologic testing useful? Am J Trop Med Hyg 2009; 80:788.
121. El Masry HZ, O'Donnell J. Fatal stongyloides hyperinfection in heart transplantation. J Heart Lung
Transplant 2005; 24:1980.
122. Terashima A, Alvarez H, Tello R, et al. Treatment failure in intestinal strongyloidiasis: an indicator
of HTLV-I infection. Int J Infect Dis 2002; 6:28.
123. Jeyamani R, Joseph AJ, Chacko A. Severe and treatment resistant strongyloidiasis--indicator of
HTLV-I infection. Trop Gastroenterol 2007; 28:176.
Topic 5714 Version 19.0
2016 UpToDate, Inc. All rights reserved.

18-May-16 10:10 PM

14 of 19

file:///

Pulmonary Strongyloides on radiography and CT

scan

The posterior-anterior radiograph (A) shows a diffuse reticulonodular

pattern scattered diffusely throughout both lung fields. Image B is a
magnified view of A and shows extensive micronodularity (arrows) and

18-May-16 10:10 PM

15 of 19

file:///

coarsened interstitial markings. Image C is a coronal reformat of a CT

scan and shows multiple peripheral nodules (arrows).
CT: computed tomography.
Images A and C courtesy of Augustine Andoh-Duku, MD.

Graphic 97783 Version 4.0

18-May-16 10:10 PM

16 of 19

file:///

Strongyloides life cycle

Causal agent: The nematode (roundworm) Strongyloides stercoralis. Other Strongyloides

include S. flleborni, which infects chimpanzees and baboons and may produce limited
infections in humans.
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 rhabditiform larvae passed in the stool (1) (see "Parasitic cycle"
below) can either molt twice and become infective filariform larvae (direct development) (6),
or molt four times and become free living adult males and females (2) that mate and produce
eggs (3) from which rhabditiform larvae hatch (4). The latter in turn can either develop (5)
into a new generation of free-living adults (as represented in [2]), or into infective filariform
larvae (6). The filariform larvae penetrate the human host skin to initiate the parasitic cycle
(see below) (6).
Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin (6), 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 (7). In
the small intestine they molt twice and become adult female worms (8). The females live
threaded in the epithelium of the small intestine and by parthenogenesis produce eggs (9),
which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool (1)
(see "Free-living cycle" above), or can cause autoinfection (10). 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 follow the previously described route,

18-May-16 10:10 PM

17 of 19

file:///

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 socioeconomic groups.
Reproduced from: Centers for Disease Control and Prevention. DPDx: Strongyloidiasis. Available at:
http://www.cdc.gov/dpdx/strongyloidiasis/index.html.

Graphic 87284 Version 3.0

18-May-16 10:10 PM

18 of 19

file:///

Strongyloides stercoralis

Wet mount of stool (x100) shows the diagnostic larval form of

Strongyloides stercoralis.
Courtesy of Harriet Provine.

Graphic 63898 Version 2.0

18-May-16 10:10 PM

19 of 19

file:///

Endoscopy - strongyloidiasis

Colonoscopic view of multiple 2 mm diameter nodules with surrounding

erythema.
Reproduced from: Goh S-K, Chow P, Chung AY, et al. Strongyloides colitis in
a patient with Cushing's syndrome. Gastrointest Endosc 2004; 59:738.
Illustration used with the permission of Elsevier Inc. All rights reserved.

Graphic 51753 Version 1.0

18-May-16 10:10 PM