eMedicine Specialties > Infectious Diseases > Gastrointestinal Tract and Intra-abdominal Infections

Strongyloidiasis

Pranatharthi Haran Chandrasekar, MD, Director of Infectious Disease Fellowship, Professor, Department of Internal Medicine, Harper Hospital, Wayne State University School of Medicine
Ramesh A Bharadwaj, MD, Fellow in Infectious Diseases, Detroit Medical Center, Wayne State University; Hari Polenakovik, MD, Assistant Professor of Medicine, Wright State University Boonshoft School of Medicine, Dayton, OH; Sylvia Polenakovik, MD, Clinical Instructor, Internist, Department of Internal Medicine, Wayne Hospital, Wright State University

Updated: Apr 3, 2009

Introduction

Background

Strongyloidiasis is an intestinal infection caused by two species of the parasitic nematode Strongyloides. The most common and clinically important pathogenic species in humans is Strongyloides stercoralis. Strongyloides fuelleborni is found sporadically in Africa and Papua New Guinea. Distinctive characteristics of this parasite are its ability to persist and replicate within a host for decades while producing minimal or no symptoms and its potential to cause life-threatening infection (hyperinfection syndrome, disseminated strongyloidiasis) in an immunocompromised host.

For more information on cutaneous manifestations of strongyloidiasis, see the article Strongyloidiasis in eMedicine’s Dermatology volume. For additional information on pediatric strongyloidiasis, see the article Strongyloidiasis in eMedicine’s Pediatrics: General Medicine volume.

Pathophysiology

The life cycle of S stercoralis is complex and unique among the intestinal nematodes. It has two types of life cycles—a free-living life cycle and a parasitic life cycle.

Human infection is acquired via penetration of intact skin by filariform larvae during contact with contaminated soil or other material contaminated with human feces. The larvae then enter the circulation and are carried hematogenously to the lungs, where they enter the alveolar space. They then ascend the tracheobronchial tree and are swallowed. When they reach the small bowel, they molt twice and mature into adult females (2 mm X 0.05 mm in diameter). (All parasitic adult worms are female.)

First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

The parasitic females produce eggs via parthenogenesis. These eggs hatch into noninfective rhabditiform larvae, which may then be passed through the stool into the environment, where they mature into adult males and females. Alternatively, they may cause autoinfection.

Autoinfection involves premature transformation of noninfective larvae (rhabditiform, 0.25 mm X 0.015 mm) into infective larvae (filariform, 0.5 mm X 0.015 mm), which can penetrate the intestinal mucosa (internal autoinfection) or the skin of the perineal area (external autoinfection), thus establishing a developmental (parasitic) cycle within the host. Infection can be maintained by repeated migratory cycles for the remainder of the host’s life.

Autoinfection is kept in check by a normal host immune response. However, in patients with impaired cell-mediated immunity, autoinfection may give rise to the two most severe forms of strongyloidiasis: hyperinfection syndrome and disseminated strongyloidiasis.

Hyperinfection syndrome represents an acceleration of the normal life cycle of S stercoralis, leading to excessive worm burden without the spread of larvae outside the usual migration pattern (eg, gastrointestinal tract, lungs). Disseminated strongyloidiasis involves widespread dissemination of larvae to extraintestinal organs (eg, CNS, heart, urinary tract, endocrine organs), which are outside the realm of the parasite's ordinary life cycle. In these severe forms, translocation of enteric bacteria may occur, leading to polymicrobial bacteremia and occasionally meningitis with enteric pathogens. The enteric pathogens may be carried on the filariform larvae or may enter the circulation through intestinal ulcers.

Frequency

United States

Strongyloidiasis is uncommon, although endemic foci exist in rural areas of the southeastern states and the Appalachia region, with prevalence rates close to 4%. Populations in whom strongyloidiasis is more prevalent include patients in long-term institutionalized care, immigrants or refugees from tropical and subtropical countries, and persons who were stationed in Southeast Asia during World War II¹ and the Vietnam War.

International

Strongyloidiasis is endemic in tropical and subtropical countries. Prevalence rates are as high as 40% in certain areas, especially West Africa, the Caribbean, and Southeast Asia. The disease is estimated to affect more than 70 million people worldwide.

Mortality/Morbidity

Severe strongyloidiasis carries a high mortality rate (up to 80%) because the diagnosis is often delayed. This relates to its nonspecific presentation and the host's immunocompromised status. Most immunocompetent individuals who develop strongyloidiasis have asymptomatic chronic infections that result in negligible morbidity.

Race

Strongyloidiasis has no predilection for any racial or ethnic group.

Sex

Strongyloidiasis has no predilection for either sex.

Age

Strongyloidiasis occurs in all age groups, although acquisition is more common during childhood.

Clinical

History

• Acute strongyloidiasis
  • Lower-extremity itch (eg, mild rash at the site of larval skin penetration, usually on feet)
  • Cough, dyspnea, wheezing, and low-grade fever (due to larval migration through lungs)
  • Epigastric discomfort, diarrhea, occasional nausea, and vomiting
• Chronic strongyloidiasis
  • Asymptomatic or vague abdominal discomfort (most patients)
  • Abdominal pain, burning, and cramping (sometimes worse after eating)
  • Intermittent diarrhea (eg, alternating with constipation)
  • Occasional nausea and vomiting
  • Weight loss (if heavier infestation)
  • Recurrent maculopapular or serpiginous rashes (larva currens)
• Severe strongyloidiasis
  • Insidious and occasionally abrupt onset
  • Nausea, vomiting, and severe abdominal pain
  • Diarrhea, occasionally bloody
  • Cough, hemoptysis, dyspnea, and wheezing
  • Stiff neck, headache, and confusion (if CNS involvement)
  • Rash
  • Fever, chills

Physical

• Acute strongyloidiasis
  • Pruritic erythematous maculopapules at the site of larval skin penetration, usually on the feet
  • Wheezing
  • Low-grade fever
  • Epigastric tenderness
• Chronic strongyloidiasis
  • Epigastric tenderness
  • Chronic urticaria
  • Larva currens ("racing larva") - Rapidly progressive serpiginous wheals beginning perianally and extending to the buttocks, upper thighs, and abdomen at a rate of 5-10 cm/h; pathognomonic lesion of strongyloidiasis possibly due to an external autoinfection (ie, filariform larvae in feces penetrate perianal skin, producing local allergic reaction)
• Severe strongyloidiasis
  • Diffuse abdominal tenderness; abdominal distension; hyperactive, hypoactive, or absent bowel sounds; vomiting; hematemesis; and hematochezia
  • Altered mental status and meningismus (if CNS involvement)
  • Rash (petechiae, purpura) over the trunk and proximal extremities caused by small dermal blood vessel disruption due to massive migration of filariform larvae within the skin
  • Cough, respiratory distress, wheezing, hemoptysis, and crackles
  • Fever, chills

Causes

• Risk factors for severe strongyloidiasis
  • Corticosteroid therapy - Most important risk factor; other immunosuppressive agents (eg, chemotherapeutic agents, tacrolimus, tumor necrosis factor [TNF] modulators)
  • Human T-cell leukemia virus type 1 infection^2,3
  • Neoplasms, particularly hematologic malignancies (lymphoma, leukemia)
  • Organ transplantation^4,5,6
  • Malabsorption states
  • End-stage renal disease
  • Diabetes mellitus
  • Advanced age
  • HIV infection
  • No obvious precipitating factor

Differential Diagnoses

Workup

Laboratory Studies

• CBC count with differential
  • WBC count is usually within the reference range in acute and chronic strongyloidiasis; it is often elevated in severe strongyloidiasis.
  • Eosinophilia (>600/mL) is common during acute infection, intermittent during chronic infection, and frequently absent in severe strongyloidiasis.
  • Suspect and evaluate for strongyloidiasis in any patient who presents with persistent, mild, or moderate-to-high eosinophilia and who has lived in or traveled to an area endemic for S stercoralis.
• Stool for ova and parasites
  • Microscopically identify S stercoralis larvae (definitive diagnostic test).
  • Ova are almost never observed during a strongyloidiasis infection; results from this examination are typically negative during acute infection.
  • Examine stool directly in wet mounts (very low yield) or after ethyl acetate-formalin concentration occurs.
    
    

    

    Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

    
    
  • Single stool examination yields a low sensitivity (approximately 30%) in chronic strongyloidiasis because larval output is low and intermittent. Perform at least 3 stool examinations on consecutive days because this may increase the sensitivity to 70-80%.
  • To establish a diagnosis, enhance larvae recovery by using special methods such as the Baermann funnel method, the Harada-Mori filter paper method, and the agar plate method, when needed. The latter appears to be the most sensitive and efficient method.
  • Obtain blood cultures in all patients presenting with possible severe strongyloidiasis. Blood cultures often yield growth of enteric pathogens, most commonly Escherichia coli and/or Klebsiella species.
• Strongyloides serology (eg, enzyme immunoassay, indirect fluorescent antibody)
  • With 88-95% sensitivity, it is the most sensitive test for detecting strongyloidiasis in immunocompetent patients. Sensitivity may be lower in severely immunocompromised patients, however, and this test cannot be used to differentiate between past and present infection.
  • If results are positive, continue efforts to establish a parasitologic (microscopic) diagnosis because of cross-reactivity with other nematode infections (8-16%).
  • This test is also useful for monitoring a patient's response to therapy (antibody titers decrease markedly within 6-12 mo of successful therapy).
• Sputum cultures: These occasionally suggest Strongyloides infection; when observing the agar plate, the microorganisms that are part of the normal respiratory flora may be found outside the area of streaking as groups of colonies arranged in a characteristic pattern. This laboratory phenomenon is a result of migrating larvae on the agar plates, and, in an appropriate clinical setting, is considered diagnostic of S stercoralis infection.

Imaging Studies

• Obtain a chest radiograph to reveal possible patchy alveolar infiltrates in acute strongyloidiasis. In severe strongyloidiasis, findings are diverse; the chest radiograph may depict diffuse interstitial infiltrates, segmental or diffuse alveolar infiltrates, or pleural effusions.
• A plain abdominal radiograph may reveal loops of a dilated small bowel, or ileus, in severe strongyloidiasis.
• Barium swallow and barium enema findings may be normal, may exhibit bowel dilatation, or may indicate stenosis with ulceration.
• Obtain a CT scan of the abdomen and pelvis to reveal any nonspecific thickening of the bowel wall.

Procedures

• Findings from upper and lower gastrointestinal endoscopy may range from normal-appearing mucosa to severe duodenitis and colitis. The most common abnormal duodenal endoscopic finding is edematous mucosa, white villi, and erythematous mucosa. In some cases, the larvae are identified with duodenal biopsy.⁷
• Conduct an Enterotest (string test) or duodenal aspiration to examine duodenal fluid for Strongyloides species larvae. These tests produce more positive results than a stool examination.
• Perform sputum examinations, bronchial washings, and bronchoalveolar lavages in cases of severe strongyloidiasis. These procedures frequently reveal filariform and/or rhabditiform larvae.
• Perform a lumbar puncture if CNS involvement is suspected.
  • Perform cerebrospinal fluid analysis (elevated protein levels, decreased glucose levels, pleocytosis with neutrophilic predominance) to evaluate for acute bacterial meningitis.
  • A Gram stain may exhibit gram-negative rods or, rarely, gram-positive cocci in chains (Enterobacteriaceae, Streptococcus species).
  • A wet mount preparation may reveal S stercoralis larvae.

Histologic Findings

S stercoralis larvae are typically found in the proximal part of the small intestine, embedded in the mucosal lamina propria, where they produce mild-to-moderate degrees of edema, cellular infiltration, partial villous atrophy, and, occasionally (in severe strongyloidiasis), ulcerations. In long-standing infections, fibrosis may develop.

Treatment

Medical Care

• Administer anthelmintic therapy.
• Provide supportive treatment as indicated (eg, intravenous fluids if volume depletion, blood transfusion if gastrointestinal or alveolar hemorrhage, mechanical ventilation if respiratory failure).
• Provide antibiotic therapy directed toward enteric pathogens if bacteremia or meningitis is present or suggested.
• Reduce immunosuppression, if possible.

Surgical Care

Perform surgery in patients with acute abdominal symptoms (peritonitis due to bowel perforation or infarction) in the context of severe strongyloidiasis.

Consultations

Notify the microbiology laboratory when strongyloidiasis is suspected to ensure that specific tests are performed for optimal larval detection in stool specimens. Other consultations include the following:

• Infectious disease specialist
• Pulmonologist or critical care specialist
• General surgeon

Diet

No specific diet is required in patients with strongyloidiasis.

Activity

Limit activity as tolerated by the patient.

Medication

The goal of therapy in strongyloidiasis is eradication of the parasite by using anthelmintic drugs.

Anthelmintics

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Ivermectin (Stromectol, Mectizan)

DOC for acute and chronic strongyloidiasis, hyperinfection syndrome, and disseminated strongyloidiasis. Binds selectively to glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death. Half-life is 16 h; metabolized in liver.

Dosing

Adult

200 mcg/kg/d PO for 2 d; may repeat course in 14 d

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; do not use in first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Treat mothers who intend to breast feed only when risk of delayed treatment outweighs possible risks to newborn caused by ivermectin excretion in milk; repeat courses may be required in immunocompromised patients; may cause nausea, vomiting, mild CNS depression, and drowsiness

Albendazole (Albenza, Eskazole, Valbazen, Zentel)

Alternative to ivermectin for treatment of acute and chronic strongyloidiasis. Decreases ATP production in worm, causing energy depletion, immobilization, then death. To avoid inflammatory response in CNS, administer with anticonvulsants and high-dose glucocorticoids.

Dosing

Adult

400 mg/d PO for 3 d; may repeat course in 14-21 d

Pediatric

<2 years: 200 mg/d PO for 3 d
>2 years: Administer as in adults

Interactions

Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity

Contraindications

Documented hypersensitivity; do not use in first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue use if LFTs increase significantly (resume when levels decrease to pretest values); caution in women who are breastfeeding

Thiabendazole (Mintezol)

Alternative to ivermectin for acute and chronic strongyloidiasis, hyperinfection syndrome, and disseminated infection. For mixed helminthic infections; inhibits helminth-specific mitochondrial fumarate reductase.

Dosing

Adult

Acute or chronic strongyloidiasis: 1.5 g PO bid for 2 d
Hyperinfection syndrome or disseminated infection: 1.5 g PO bid for 7-14 d

Pediatric

Acute or chronic strongyloidiasis: 25 mg/kg PO bid for 2 d; not to exceed 3 g/d
Hyperinfection syndrome or disseminated infection: 25 mg/kg PO bid for 7-14 d; not to exceed 3 g/d

Interactions

May elevate theophylline serum levels, increasing toxicity (monitor serum levels and reduce dose prn)

Contraindications

Documented hypersensitivity; do not use in the first trimester of pregnancy and avoid use until after delivery if possible

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Closely monitor in hepatic or renal dysfunction; prior to initiating therapy, supportive therapy is necessary for anemia, dehydration, or malnutrition; use in confirmed worm infestation (not prophylactically); may cause nausea, vomiting, and mild CNS depression

Follow-up

Further Inpatient Care

• Consider contact isolation in patients with severe strongyloidiasis because sputum, stool, vomitus, and other bodily excreta may contain infective (filariform) larvae.

Further Outpatient Care

• Medication: Repeat courses of ivermectin in immunocompromised patients because relapse is common in this population.
• Follow-up examination
  • To ensure a parasitologic cure, repeat stool examinations and/or duodenal aspirations every 2-3 months.
  • Alternatively, schedule follow-up strongyloides serology studies (4-8 mo after therapy) to monitor the patient's response to therapy.
  • Ensure that the Strongyloides antibody titer declines to low or undetectable levels within 6-18 months after successful treatment.
  • A nondeclining titer may indicate a need for additional anthelmintic therapy.

Inpatient & Outpatient Medications

• Conduct definitive treatment with anthelmintic drugs (see Medication).
• Treat bacterial complications (eg, bacteremia, meningitis) for 2-4 weeks with antibiotics according to the results of in vitro testing against the bacterial isolate(s).

Deterrence/Prevention

• Instruct travelers to endemic areas to avoid walking barefoot in places or soil that potentially contain infective larvae. Shoes help protect against infection.
• No prophylactic regimens are accepted, and no vaccines are available for strongyloidiasis.

Complications

• Gastrointestinal
  • GI hemorrhage
  • Malabsorption
  • Intestinal obstruction
  • Peritonitis
  • Appendicitis
  • Obstructive jaundice
  • Ileus
  • Pneumatosis intestinalis
  • Intestinal perforation
  • Intestinal infarction
• Respiratory
  • Asthma or exacerbation of preexisting obstructive pulmonary disease
  • Pneumonitis
  • Respiratory failure⁸
  • Acute respiratory distress syndrome
  • Alveolar hemorrhage
  • Pleural effusion
  • Granulomatous lung disease
• Dermatologic
  • Larva currens
  • Purpura of the trunk and proximal extremities
  • Chronic urticaria
• Neurologic
  • Meningitis due to enteric bacteria
  • Brain abscess
• Vascular - Hyperinfection syndrome presenting as bacteremia (occasionally recurrent) due to enteric microorganisms (eg, E coli, Klebsiella pneumoniae, Enterococcus species including vancomycin-resistant Enterococcus faecium, Streptococcus bovis)
• Renal -Nephrotic syndrome (rare)⁹
• Musculoskeletal -Reactive arthritis (rare)
• Death

Prognosis

• Acute and chronic strongyloidiasis carry a good prognosis.
• Hyperinfection syndrome and disseminated strongyloidiasis carry a poor prognosis.

Miscellaneous

Medicolegal Pitfalls

• The diagnosis of strongyloidiasis requires a high index of suspicion, as patients with the infection present with no distinctive clinical features, and ancillary laboratory, imaging, and endoscopic findings are often nonspecific.
• Obtaining an appropriate travel and residence history is important. Furthermore, the possibility of strongyloidiasis should always be considered in any immunocompromised patient who suddenly deteriorates.
• Delay in diagnosing strongyloidiasis frequently results in death, despite vigorous treatment.

Special Concerns

• Pregnancy: Clinicians may prefer to defer treatment for strongyloidiasis until after the first trimester. All of the medications listed are FDA category C agents.
• Immunocompromise: In patients with an appropriate geographic history, rule out strongyloidiasis by means of thorough evaluation, including several stool examinations for ova and parasites, special larvae detection techniques, and/or serology in all transplant candidates or others who are likely to receive a prolonged course of steroids or other immunosuppressive medications. Among the immunosuppressive agents, only cyclosporine A is known to possess anthelmintic activity. This was initially confirmed in animal models and subsequently observed in clinical practice. To date, no cases of severe strongyloidiasis developing in transplant recipients treated with cyclosporine have been reported.

Multimedia

Media file 1: First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Media file 2: Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Media file 3: Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Media file 4: Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Media file 5: Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Media file 6: Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

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Keywords

strongyloidiasis, hyperinfection syndrome, disseminated strongyloidiasis, Strongyloides, threadworm infection, Cochin China diarrhea, parasitic nematodes, Strongyloides stercoralis, S stercoralis, Strongyloides fuelleborni, S fuelleborni, bacterial meningitis, rhabditiform larvae, parthenogenesis, filariform, bacteremia, Escherichia coli, E coli, Klebsiella species, helminth, strongyloidosis, acute strongyloidiasis, chronic strongyloidiasis, intestinal strongyloidiasis

Contributor Information and Disclosures

Author

Pranatharthi Haran Chandrasekar, MD, Director of Infectious Disease Fellowship, Professor, Department of Internal Medicine, Harper Hospital, Wayne State University School of Medicine
Pranatharthi Haran Chandrasekar, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Ramesh A Bharadwaj, MD, Fellow in Infectious Diseases, Detroit Medical Center, Wayne State University
Ramesh A Bharadwaj, MD is a member of the following medical societies: American College of Physicians and Michigan State Medical Society
Disclosure: Nothing to disclose.

Hari Polenakovik, MD, Assistant Professor of Medicine, Wright State University Boonshoft School of Medicine, Dayton, OH
Hari Polenakovik, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Sylvia Polenakovik, MD, Clinical Instructor, Internist, Department of Internal Medicine, Wayne Hospital, Wright State University
Sylvia Polenakovik, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Wesley W Emmons, MD, FACP, Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE
Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Managing Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
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CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
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Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
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