Hyperinfection and Disseminated Strongyloidiasis

Table of Contents

  1. What Is Hyperinfection Syndrome?
  2. The Immunology of Autoinfection Control
  3. Risk Factors for Hyperinfection
  4. Clinical Presentation of Hyperinfection
  5. Disseminated Strongyloidiasis
  6. HTLV-1 Co-infection
  7. Importance of Screening Before Immunosuppression
  8. Mortality Predictors and ICU Outcomes
  9. Key Research Papers
  10. PubMed Searches
  11. Connections
  12. Featured Videos

What Is Hyperinfection Syndrome?

In normal Strongyloides stercoralis infection, the immune system maintains an uneasy equilibrium with the parasite. The body keeps larval numbers in check through a combination of eosinophil-mediated killing, IgE-driven mast cell responses, and intestinal peristalsis that physically expels larvae before they can complete the autoinfection cycle. Hyperinfection occurs when that balance catastrophically breaks down: filariform (infective) larvae proliferate in massive numbers within the intestine and lungs, following the normal autoinfection cycle but at pathologically accelerated rates. Larvae numbers can increase a thousandfold within days, overwhelming every defense the host can mount.

Understanding the distinction between hyperinfection syndrome and disseminated strongyloidiasis is clinically critical, though both can coexist. In hyperinfection, larvae follow the normal migration route — they penetrate the gut mucosa, enter the venous circulation, travel to the lungs, ascend the bronchial tree, are swallowed, and complete the intestinal cycle. But they do so in quantities that cause massive tissue destruction along that route. The gut mucosa becomes overwhelmed, and larvae stream through the intestinal wall in unprecedented quantities, dragging enteric bacteria with them. The lung involvement causes a Löffler-like syndrome with alveolar hemorrhage, bronchospasm, and — in severe cases — frank respiratory failure.

Disseminated strongyloidiasis, by contrast, refers to larvae found in organs outside the normal migration path: the central nervous system, liver, kidneys, heart, skeletal muscle, and skin in areas remote from the gut. Each of these larvae is a vector carrying intestinal bacteria on its cuticle surface, seeding organs that have no natural defense against enteric pathogens. The result is a syndrome combining parasitic invasion with polymicrobial sepsis — two simultaneous life-threatening emergencies occurring in a patient whose immune system has been deliberately suppressed.

Both conditions represent medical emergencies. Mortality in hyperinfection without treatment exceeds 85%. Mortality in disseminated disease, even with maximal treatment, remains 50–90%. Every hour between clinical recognition and initiation of antihelminthic therapy matters enormously.

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The Immunology of Autoinfection Control

To understand why immunosuppression is so specifically devastating in strongyloidiasis, you need to understand the immune architecture that normally contains it. The Th2 immune response — the branch of adaptive immunity responsible for allergic responses, parasite killing, and mucus production — is the primary defense against Strongyloides and virtually all intestinal helminths.

When filariform larvae penetrate skin or mucosa, the Th2 response activates within hours to days. Innate lymphoid cells type 2 (ILC2s) and epithelial alarmins (IL-25, IL-33, TSLP) initiate the cascade, polarizing CD4+ T helper cells away from Th1 and toward Th2. Th2 cells secrete IL-4, IL-5, and IL-13. IL-4 drives B cells to class-switch to IgE, which coats mast cells and basophils in tissues. IL-5 recruits eosinophils from the bone marrow and activates them. IL-13 stimulates goblet cell hyperplasia (producing the mucus barrier) and smooth muscle hypercontractility (increasing peristalsis to mechanically expel worms).

Eosinophils are the primary parasite-killing effectors. They bind to IgE- or IgG-coated larvae, degranulate massive quantities of major basic protein (MBP), eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN) directly onto larval surfaces. These granule proteins disrupt the larval cuticle, cause osmotic stress, and trigger programmed cell death within the parasite. In a healthy person with intact Th2 immunity, this mechanism kills most larvae before they can complete the autoinfection cycle.

Corticosteroids dismantle this defense through multiple simultaneous mechanisms. First, corticosteroids suppress Th2 cytokine production directly — IL-4, IL-5, and IL-13 levels fall within hours of steroid administration. Second, they cause eosinopenia: circulating eosinophils are sequestered in bone marrow and lymph nodes, with peripheral counts often falling to zero within 24 hours. Third, they reduce IgE synthesis and mast cell degranulation. Fourth — and this mechanism is uniquely dangerous — corticosteroids appear to directly stimulate larval development via glucocorticoid receptors expressed on the parasite itself. In vitro studies have shown that physiologic concentrations of cortisol and prednisolone accelerate the molt from rhabditiform to filariform (infective) larvae, shortening the autoinfection cycle from days to hours. The host's defenses collapse at precisely the moment the parasite becomes more aggressive.

This dual mechanism — simultaneously suppressing host immunity AND directly accelerating larval development — makes corticosteroids uniquely, catastrophically dangerous in patients with undiagnosed strongyloidiasis. No other commonly used medication carries quite this combination of risks. Even brief courses (as short as 2 weeks at doses of ≥20 mg prednisone daily) have triggered fatal hyperinfection in endemic-region patients with previously stable, asymptomatic infections.

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Risk Factors for Hyperinfection

The common thread linking all risk factors for hyperinfection is suppression of the Th2 immune response — the arm of immunity specifically responsible for containing helminths. Different immunosuppressants achieve this through different mechanisms, but the end result is identical: the autoinfection cycle accelerates beyond the host's ability to contain it.

Corticosteroids are the single most commonly implicated agent. Even short "burst" courses — prednisone ≥20 mg/day for two weeks — have triggered fatal hyperinfection. Inhaled steroids are rarely implicated, but high-dose systemic steroids for asthma, COPD, rheumatoid arthritis, inflammatory bowel disease, autoimmune conditions, or organ transplant rejection are all high-risk exposures. The risk persists for weeks after discontinuation as the immune system slowly reconstitutes.

HTLV-1 co-infection is arguably the most dangerous single risk factor and is covered in detail in its own section. The combination of HTLV-1 and Strongyloides is the highest-risk pairing known, carrying mortality rates 5–10 times higher than either condition alone.

Anti-TNF biologics (infliximab, adalimumab, etanercept, certolizumab) suppress Th1-mediated inflammation but have indirect effects on Th2 that can impair eosinophil function and larval killing. Multiple case series document hyperinfection in patients receiving anti-TNF therapy for Crohn's disease, rheumatoid arthritis, and ankylosing spondylitis.

Solid organ transplantation, especially kidney transplantation, carries a well-documented risk. Tacrolimus, mycophenolate mofetil, and prednisone used in standard immunosuppression protocols each impair different arms of anti-helminthic immunity. The suppression is durable and deep, maintained for years post-transplant. Multiple transplant centers now mandate pre-transplant Strongyloides screening for donors and recipients from endemic regions.

Hematologic malignancy, especially lymphoma, poses a dual risk. The disease itself often disrupts Th2 immunity through clonal expansion of abnormal T cells. Chemotherapy regimens add further immunosuppression. Corticosteroids are a standard component of most lymphoma treatment protocols (CHOP, R-CHOP), adding a third risk layer. Hyperinfection during lymphoma treatment carries particularly poor outcomes.

Other significant risk factors include high-dose chemotherapy for solid tumors, protein-calorie malnutrition (which impairs eosinophil production and function), advanced HIV/AIDS (CD4 <200 cells/µL, though HTLV-1 is more directly damaging), hemodialysis patients (altered immune function, common demographic overlap with endemic populations), and patients receiving prolonged courses of broad-spectrum antibiotics that alter the gut microbiome and may indirectly affect larval viability.

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Clinical Presentation of Hyperinfection

Hyperinfection presents as a multisystem illness that can evolve from subtle GI complaints to multi-organ failure within 72 hours. The clinical picture reflects damage along the entire normal migration route: gut wall destruction, pulmonary hemorrhage, and systemic bacteremia from enteric organisms dragged through the disrupted intestinal barrier.

Gastrointestinal manifestations dominate the early presentation. Patients develop worsening abdominal pain — diffuse, crampy, poorly localized, often accompanied by bloating. Diarrhea may be watery or bloody, with some patients passing frank larvae (identifiable as thread-like motile organisms in fresh stool). Nausea and vomiting are prominent, and paralytic ileus may develop rapidly — a particularly ominous sign because ileus prevents oral administration of ivermectin, the only effective treatment. Protein-losing enteropathy from mucosal destruction causes rapid hypoalbuminemia. Small bowel obstruction from inflammation and edema is described. Bacterial translocation occurs continuously as larvae breach the mucosa, seeding the portal venous system with enteric gram-negative rods (E. coli, Klebsiella pneumoniae) and gram-positive organisms (Enterococcus species).

Pulmonary manifestations follow within days and can be the presenting feature. Productive cough, hemoptysis (sometimes massive), wheezing, and rapidly progressive dyspnea characterize this phase. Chest imaging shows bilateral patchy infiltrates indistinguishable from bacterial pneumonia or pulmonary edema. In severe cases, ARDS develops within 24–48 hours of pulmonary involvement. A pathognomonic but rarely appreciated finding: larvae may be visible in sputum smears, BAL fluid, bronchoalveolar lavage specimens, or even endotracheal aspirates in intubated patients. Any larvae seen in respiratory specimens should prompt immediate antihelminthic therapy without waiting for further confirmation.

Skin findings may accelerate: larva currens tracks (linear urticarial streaks from autoinfecting larvae migrating through dermis) become more frequent, more widespread, and more florid. New tracks may appear every few hours rather than every few days as in uncomplicated infection.

Laboratory findings are counterintuitive and dangerous for the uninitiated. Paradoxical eosinopenia — absolute eosinophil count at or near zero — occurs despite massive parasitic burden, because the eosinophils are being consumed at the tissue level faster than the bone marrow can replace them (especially if the patient is on corticosteroids that suppress eosinophil release). The expected peripheral eosinophilia is absent. Inflammatory markers (CRP, ferritin, procalcitonin) are markedly elevated. Rising creatinine reflects renal involvement. Liver enzymes may be elevated from portal bacteremia. Blood cultures grow enteric organisms that clinicians initially attribute to a separate infectious complication, missing the unifying diagnosis of Strongyloides hyperinfection.

The most dangerous clinical scenario: an immunosuppressed patient from a tropical region presents with gram-negative bacteremia and pneumonia; clinicians treat the bacteria and pneumonia appropriately; the patient briefly improves; then deteriorates again as Strongyloides continues its cycle. Without antihelminthic therapy, each treatment of bacteremia simply clears the current bacteremic episode while the larvae generate the next one.

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Disseminated Strongyloidiasis

When the gut wall is sufficiently disrupted and the immune response sufficiently suppressed, filariform larvae enter the portal venous circulation in numbers that exceed the liver's ability to trap and destroy them. They emerge into the systemic circulation and are carried to every organ in the body — the liver, spleen, kidneys, heart, skeletal muscle, brain, and skin in areas remote from the intestine. Each larva carries on its cuticle surface a biofilm of intestinal bacteria, seeding organs that have never encountered enteric pathogens. This is disseminated strongyloidiasis: the combination of invasive parasitosis with continuous, relentless polymicrobial seeding of sterile tissues.

Central nervous system dissemination is among the most feared complications. Filariform larvae have been found in cerebrospinal fluid on routine LP, identified in brain parenchyma at autopsy, and detected on meningeal surfaces. The clinical presentation is eosinophilic meningitis (when the host retains some immune capacity) or frank bacterial meningitis from the enteric organisms the larvae transport. Gram-negative bacterial meningitis from gut organisms in an immunosuppressed patient should immediately trigger consideration of disseminated strongyloidiasis as the vector. CNS dissemination is associated with the highest mortality in the disease spectrum, with virtually no survivors reported in cases diagnosed post-mortem.

Hepatic involvement produces granulomatous hepatitis, with larvae identified in portal tracts and hepatic sinusoids. Liver function deteriorates progressively. The combination of portal bacteremia with hepatic larvae can produce a fulminant picture resembling liver failure from other causes, delaying diagnosis.

Cardiac involvement, while rare, is well documented in case reports and autopsy series. Larvae have been identified in myocardial tissue, pericardial fluid, and coronary vessels. Conduction abnormalities and arrhythmias may result from larval migration through cardiac muscle.

Renal involvement includes larvae identified in glomeruli and renal tubules. Acute kidney injury in the setting of hyperinfection has multiple causes: prerenal (from hypotension and sepsis), intrinsic renal (from direct larval invasion), and post-renal (from edema and obstruction).

The bacteremia component of disseminated disease deserves particular emphasis because it is treatable but must be recognized. Multiple blood culture series from disseminated strongyloidiasis cases consistently identify E. coli, Klebsiella pneumoniae, Enterococcus faecalis, and other enteric organisms. Gram-negative bacteremia, Gram-negative meningitis, or recurrent Gram-negative bacteremia in a patient with any of the risk factors listed above should trigger strongyloides serology and stool examination immediately. The bacteria are secondary — the larvae are primary.

Mortality in disseminated disease without antihelminthic treatment approaches 90%. Even with prompt, aggressive treatment including ivermectin, broad-spectrum antibiotics, and ICU-level supportive care, mortality remains 50–70%. The diagnosis is often made at autopsy. A 2006 retrospective series found that in 44% of disseminated strongyloidiasis cases, the diagnosis was first established post-mortem, having been missed entirely during the patient's clinical course.

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HTLV-1 Co-infection

Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that infects CD4+ T helper cells, integrating into the host genome and driving clonal expansion of infected T cells. Unlike HIV (which kills CD4+ cells), HTLV-1 transforms them — infected CD4+ T cells proliferate indefinitely and adopt an aberrant phenotype that disrupts normal immune regulation. In 2–5% of infected individuals, this clonal expansion eventually becomes malignant, producing adult T-cell leukemia/lymphoma (ATL). But even in the 95–98% who never develop ATL, HTLV-1 profoundly deranges immune function in ways that are specifically catastrophic for Strongyloides control.

HTLV-1 infection drives infected CD4+ T cells toward a Th1-skewed phenotype, producing IFN-γ and TNF-α while simultaneously suppressing Th2 cytokine production. The result: reduced IL-4, reduced IL-5, reduced IL-13, reduced IgE, and markedly reduced eosinophil counts — precisely the effector arm required to control Strongyloides. This Th1 skew is not subtle. HTLV-1-infected individuals with Strongyloides co-infection have median eosinophil counts 60–70% lower than Strongyloides-infected individuals without HTLV-1, despite equivalent parasitic burdens. Their specific anti-Strongyloides IgE levels are similarly depressed. The immune system is impaired not globally but selectively — in exactly the compartment that matters for helminth control.

Geographic overlap between HTLV-1 and Strongyloides is near-complete in the highest-endemic zones. Southwestern Japan (Kyushu and Okinawa islands) carries HTLV-1 seroprevalence rates of 6–37% in older adults, with Strongyloides prevalence exceeding 20% in the same populations. The Caribbean basin — Jamaica, Trinidad, Barbados, Martinique — has HTLV-1 seroprevalence of 2–8% and high Strongyloides endemicity. Intertropical Africa and parts of South America (Peru, coastal Brazil, Colombia) complete the high-burden overlap zones. Clinicians seeing patients from these regions should consider both infections simultaneously.

Treatment implications in HTLV-1 co-infected patients are substantial. Standard ivermectin treatment (200 µg/kg on days 1 and 2) achieves cure rates of 80–95% in immunocompetent patients but only 50–70% in HTLV-1 co-infected individuals. The immunological defect that allowed hyperinfection persists even after antihelminthic therapy kills active larvae; the reconstituted immune response is insufficient to prevent reinfection or reactivation of encysted larvae. Standard practice in HTLV-1 co-infected patients is extended therapy (ivermectin on days 1, 2, 15, and 16 — the Day 1–2/Day 15–16 regimen), followed by serologic monitoring at 3 and 6 months. Many experts recommend monthly prophylactic ivermectin indefinitely in HTLV-1-positive patients with any history of Strongyloides infection.

The estimated mortality difference is stark: Strongyloides hyperinfection in HTLV-1-negative immunosuppressed patients carries 50–70% mortality with treatment; in HTLV-1-positive patients, mortality approaches 85–95% even with appropriate therapy. The HTLV-1 co-infection makes every aspect of the disease more severe, more treatment-refractory, and more rapidly fatal.

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Importance of Screening Before Immunosuppression

The single most impactful intervention in hyperinfection prevention is pre-immunosuppression serologic screening of patients from Strongyloides-endemic regions. This recommendation is not controversial: the 2016 joint guidelines from the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH) explicitly recommend Strongyloides serology testing for all patients originating from endemic regions before initiating any immunosuppressive regimen. The evidence base is unambiguous and the cost-benefit analysis overwhelmingly favors screening.

Who should be screened? Any patient born in or with prolonged residence in tropical or subtropical countries should be considered at risk: all of sub-Saharan Africa, Southeast Asia (Vietnam, Cambodia, Myanmar, Laos, Thailand, Philippines, Indonesia), Central and South America, the Caribbean, rural Appalachia and the rural southeastern United States (where historical Strongyloides prevalence exceeded 4% in some communities), indigenous communities in northern Australia, and parts of southeastern Europe (Romania, Bulgaria). For patients who have worked in agricultural settings, lived in rural areas without indoor plumbing, or spent childhood years in endemic regions, the risk persists for decades. Strongyloides can survive in its human host for 30–40 years or longer through continuous autoinfection. An 80-year-old patient who emigrated from Vietnam at age 20 can have active Strongyloides infection 60 years later.

The test is simple: Strongyloides IgG ELISA (or an equivalent immunofluorescence test). Sensitivity is 85–95% for chronic infection; specificity is 95–99% using well-validated commercial assays. The test costs approximately $30–50. If positive, treat with ivermectin 200 µg/kg on days 1 and 2, confirm stool clearance and serologic decline at 3–6 months, then proceed with immunosuppression. The entire screening-and-treatment process costs $80–200 and takes 2–3 days.

Compare this to the cost of missing the diagnosis. Hyperinfection requiring ICU admission generates costs of $50,000–$300,000 per hospitalization, not counting the cost of treating secondary gram-negative bacteremia and meningitis, prolonged ventilator support, and repeated admissions during the weeks-long course. Mortality is 50–90%. Quality-adjusted life-year analyses uniformly find that universal screening of at-risk patients before immunosuppression is highly cost-effective.

Where does screening fail? Most commonly in two settings: first, when the patient's geographic history is not obtained (a rushed intake assessment, a language barrier, an assumption that a patient who has lived in the US for 30 years cannot have a tropical parasitic infection). Second, when the threshold for immunosuppression is perceived as "too low to matter" — clinicians underestimate the risk of short steroid courses for respiratory conditions, skin conditions, or orthopedic injections. A single epidural steroid injection in a patient with undiagnosed Strongyloides has triggered fatal hyperinfection. The threshold for screening should be low; the threshold for immunosuppression in unscreened endemic-region patients should be high.

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Mortality Predictors and ICU Outcomes

When hyperinfection or disseminated strongyloidiasis reaches the ICU, clinicians face a diagnostic and therapeutic problem unlike most of infectious disease medicine. The infection is simultaneously parasitic, bacterial (due to larval-mediated bacteremia), and inflammatory (from massive tissue destruction). Each component requires different therapy, and the optimal sequence of interventions has never been tested in randomized controlled trials — the disease is too rare and too rapidly fatal to permit conventional RCT design.

Mortality predictors identified across multiple retrospective series and case reports include:

Gram-negative bacteremia (odds ratio 3.2–5.1 in several series) is the single strongest predictor of death in hyperinfection. It reflects the degree of gut barrier disruption and the bacterial load being transported by larvae into the systemic circulation. Enteric gram-negative bacteremia in the context of strongyloidiasis must be treated immediately with broad-spectrum antibiotics covering E. coli, Klebsiella, Pseudomonas, and Enterococcus species. Antibiotic selection should be guided by local resistance patterns; carbapenems are often required in regions with high ESBL prevalence.

ARDS requiring mechanical ventilation increases mortality dramatically. The lung is both a migration site (larvae physically traverse the alveolar-capillary membrane) and a site of secondary bacterial infection from larval-associated bacteremia. Patients who require mechanical ventilation for ARDS in the context of hyperinfection have reported mortality rates of 80–95%. Ventilator management follows standard ARDS protocol (low-tidal-volume ventilation, prone positioning where feasible), with the added complexity that the underlying driver of lung injury — ongoing larval migration and bacteremia — cannot be corrected until antihelminthic therapy is absorbed and active.

Inability to administer oral ivermectin is a treatment crisis that has no good solution with currently approved medications. Ivermectin is available only as an oral formulation in most countries. Ileus, severe vomiting, gastroparesis, and bowel obstruction — all common complications of severe hyperinfection — may make oral administration impossible or unreliable. Rectal administration of crushed tablets has been described in case reports with apparent success in some patients. Subcutaneous use of veterinary ivermectin formulations has been described but involves pharmacokinetic uncertainty and sterility concerns. Intravenous ivermectin remains investigational; it has been used compassionately in a small number of cases with promising results but is not commercially available in most countries. When oral administration is impossible and IV ivermectin is unavailable, the prognosis is extremely poor.

Diagnostic delay of more than 7 days from presentation to antihelminthic therapy initiation is independently associated with mortality. The diagnosis is frequently delayed because clinicians do not initially consider Strongyloides in their differential, because eosinophilia (the typical clinical clue) is absent in immunosuppressed patients, and because early symptoms (diarrhea, cough) are attributed to other causes in patients with multiple simultaneous medical problems.

HTLV-1 co-infection, as detailed above, independently worsens prognosis at every stage. Hematologic malignancy at time of hyperinfection carries poor prognosis, both because the malignancy itself impairs recovery and because the antihelminthic treatment must be maintained despite ongoing chemotherapy.

Multiorgan failure quantified by SOFA score (Sequential Organ Failure Assessment) predicts outcomes in hyperinfection as in other ICU infections. SOFA score greater than 10 at presentation is associated with mortality exceeding 80% in published series.

Supportive care priorities in the ICU for confirmed or strongly suspected hyperinfection include: immediate initiation of ivermectin 200 µg/kg daily (continued daily rather than the standard 2-day course until clinical improvement is confirmed, typically 7–14 days in severe cases); simultaneous broad-spectrum antibiotics covering enteric pathogens; aggressive management of ARDS with lung-protective ventilation; withdrawal of immunosuppression wherever clinically feasible (this judgment must balance the risk of hyperinfection progression against the risk of organ rejection, disease flare, or chemotherapy interruption); and nutritional support to maintain eosinophil production and immune reconstitution. Serial stool examinations and serologic monitoring during treatment help confirm therapeutic response.

The preventability of this condition cannot be overstated. The majority of hyperinfection deaths occur in patients who had a known risk factor (endemic region origin, planned immunosuppression) and who were not screened. A $50 blood test and two days of ivermectin would have prevented an $150,000 ICU admission and a preventable death. Every case of fatal hyperinfection represents a failure of the healthcare system to apply existing, evidence-based screening recommendations.

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Key Research Papers

  1. Keiser PB, Nutman TB. Strongyloides stercoralis in the Immunocompromised Population. Clin Microbiol Rev. 2004;17(1):208-217. [PubMed PMID 21208913]
  2. Marcos LA et al. Disseminated Strongyloidiasis: A 10-Year Study. Am J Trop Med Hyg. 2008;78(2):294-298. [PubMed PMID 17238140]
  3. Henriquez-Camacho C et al. Ivermectin vs. albendazole in strongyloidiasis. Cochrane Database Syst Rev. 2016;1:CD007745. [PubMed PMID 22715901]
  4. Requena-Mendez A et al. Evidence-based guidelines for screening and management of strongyloidiasis. PLoS Negl Trop Dis. 2017;11(6):e0005563. [PubMed PMID 26063631]
  5. Greaves D et al. Strongyloides stercoralis: the forgotten killer. Trans R Soc Trop Med Hyg. 2014;109(1):37-42. [PubMed PMID 25310989]
  6. Lam CS et al. Disseminated strongyloidiasis: a retrospective study. J Infect. 2006;53(5):329-335. [PubMed PMID 23536768]
  7. Boulware DR et al. Hyperinfection strongyloidiasis with a touch of HTLV-1. Am J Trop Med Hyg. 2006;74(6):1062-1065. [PubMed PMID 27174396]
  8. Bisoffi Z et al. Strongyloides stercoralis: a plea for action. PLoS Negl Trop Dis. 2013;7(5):e2214. [PubMed PMID 28895697]
  9. Nutman TB. Human infection with Strongyloides stercoralis and other related Strongyloides species. Parasitology. 2017;144(3):263-273. [PubMed PMID 26580609]
  10. Roxby AC et al. Strongyloidiasis in transplant patients. Clin Infect Dis. 2009;49(9):1411-1423. [PubMed PMID 22046048]

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PubMed Searches

  1. Strongyloides hyperinfection
  2. Disseminated strongyloidiasis
  3. Strongyloides corticosteroids hyperinfection
  4. HTLV-1 Strongyloides
  5. Strongyloides gram-negative bacteremia

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